Infectious Orals

INFECTIOUS DISEASE
Q.1 The peculiarities of infectious diseases.

Infectious diseases are diseases caused by microbes such as (viruses, bacteria, fungi etc) and
are able to spread among individuals.
PERCULIARITIES OF INFECTIOUS DISEASES
❑ Contagenicity – dangerous for surrounding people
❑ Specificity – every disease has the specific infectious agent
❑ Periodicity –
▪ incubation period;
▪ initial (prodromal) period;
▪ period of acute illness;
▪ period of convalescence or reconvalescence.
❑ Post-infection immunity
❑ Cyclicity – ability to epidemic spreading after some period of time
Sources of infectious agents:
• Human – sick patient or carrier (from the end of the incubation period; prodromal period; climax
period; convalescence, when microorganism excretion occur) – anthroponoses.
• Animals (domestic, wild) – zoonosis.
• Antropozoonoses (both man and animal can be the source).
• Environment – sapronoses (tetanus, legionellosis)
Mechanism of transmission:
Four mechanisms of transmission are distinguished according to the primary localization of pathogenic
agents in macroorganisms:
1. Fecal-oral (intestinal localization);
2. Air-borne (respiratory tract);
3. Transmissive (blood circulating system);
4. Contact (wound) (biological fluids).
Q.2 Classification of infectious diseases.

1.GROUPS OF INFECTIOUS DISEASES BY GROMASHEVSK
- Intestinal infections – are transferred by fecal-oral mechanism
- Respiratory infections – are transferred by the droplet mechanism
- Blood infections – by means of transmissive mechanism of transfer
- Infections of external covers – by means of contact or contact-wound mechanism
BY DURATION
• Acute- develops and runs its course quickly
• Chronic- develops more slowly and is usually less severe, but may persist for a long,
indefinite period of time
• Latent- characterized by periods of no symptoms between outbreaks of illness
BY LOCALISATION
• Local- confined to specific area of the body
• Systemic- a generalized illness that infects most of the body with pathogens distributed widely in
tissues
BY THE TIME
• Primary- initial infection in a previously healthy person
• Secondary- infection that occurs in a person weakened by a primary infection
MICROBIAL CLASSIFICATION
• Bacteria: Gram positive, Gram negative
• Virus- obligate intracellular parasites which only replicate intracellularly: DNA virus, RNA virus,
Enveloped, non-enveloped
• Fungal- non-motile filamentous, branching strands of connected cells: disseminated, localized
• Parasitic: Protozoa (single cell organisms with a well-defined nucleus), helminths
• Prions: unique proteins lacking genetic molecules
Q.3 Principles of infectious diseases diagnosis.

DIAGNOSIS INCLUDE: history taking, clinical examination and lab diagnosis
• Anamnesis of the disease: onset of disease, fever, chills, degrees of increase in
temperature, its oscillation, duration.
• Character of stool.
• Localization and intensity of pains. Violation of sleep.
• Epidemiological anamnesis. Food of patient, insect bites, traumas, operations.
• Prophylactic vaccinations
Clinical examination:
• Inspect skin and mucous membranes for exanthema or enanthema.
• Lymph nodes examination. Examination of different organs and systems, Fever.
• Vital signs. Identification of main syndromes
Laboratory methods:
• Bacteriological: sowing of material on nutritive medium, isolation of the clean
culture of the agent from blood, urine, stool, CSF.
• Parasitological: microscopy of thick drop and blood smears (malaria), smears of
blood and bone marrow (leishmaniasis), smears of gland, stool.
• Virological: culture if tussues and hen embryos are used
Q.4 Methods of infectious diseases specific diagnostics.

• Stained and examined under a microscope: e.g: gram stain
• Cultured (placed in conditions that encourage the growth of microorganisms):
inoculated on nutrient media
• Testing for antibodies, produced by the person's immune system in response to the
microorganism
• Testing for a microorganism's antigens (molecules from the microorganism that can
trigger an immune response in the body)
• Testing for genetic material (such as DNA or RNA) from the microorganism
• Testing of a Microorganism's Susceptibility to Antimicrobial Drugs
Q.5 Principles of infectious diseases treatment.

Pathogenetic treatment:
• correction of violation of homeostasis: (correction of water electrolyte, protein
balance, acid-alkaline state.
• Liver, kidney, respiratory and cardiovascular failure.
• Decrease allergic manifestation)
Etiotropic treatment
1. Chemotherapy:
• Antibacterial (antibiotics, sulfonamides, nitrofurans, and others),
• Antiviral(viroleks, rimantadine, acyclovir),
• Antiprotozoal (yatren, delagil, primaquine),
• Antihelmintic (naftamon, decaris)
2. Natural biological products:
• Interferon, deoxyribonuclease
• Bacterial preparations: laktobakterin, colibacterin, baktisubtil
• Serotherapy: immune serum, immunoglobulins, bacteriophages
Q.6 Principles of infectious diseases prevention

Control infection source:
Timely revealing of sick persons.
Active detection is performed by medical personnel at hospitals, polyclinics, medical posts
Isolation (in hospital, at home)
Treatment
Examination for the carrier state (sanation)
Disruption of infection transmission pathways

General sanitary measures (community hygiene)
Health education of population
Disinfection
Sterilization
Disinsection
Prophylaxis: Chemoprophylaxis, Vaccines
Q.7 Indications for hospitalization of patients with infectious diseases.

• Patients that are highly infective
• Patients that are unable to swallow medications or has regurgitation
• Patient with moderate-severe state: eg. Cholera
• Patients that live in unsanitary areas
• Patients that live in crowded homes or areas e.g. hostel
• Diseases that need to be quarantined: plague, hemorrhagic fever, small pox, swine flu, bird flu etc.
Q.8 stages of typhoid fever pathogenesis

There are 8 main stages of typhoid fever pathogenesis:
1. Penetration of the causative agent into the organism.
(The first phase is penetration of the agent in the salmonella.
However, penetration does not always lead to the development of the pathological process. It
depends on the quantity of the agent and the state of barrier functions (stomach in this case)
2. Development of lymphadenitis and lymphangitis.
(Salmonellae achieve the small intestine and actively penetrate into solitary follicules, Peyer’s
patches. There occurs reproduction of the agents and formation of the focus of infection)
3. Bacteraemia (Bacteria in blood)
In clinic bacteraemia means the end of incubation period and beginning of the clinical
manifestations.
4. Intoxication.
The action of endotoxins causes changes of the state of the central nervous system, adynamia, fever,
headaches, violations of dream, appetite.
5.Parenchymatous diffusion.
By the flow of the blood Salmonella of typhoid fever and paratyphoid enter into all organs.
Microbes are fixated especially in liver, spleen, bone marrow, skin.
Secondary focuses are formed (typhoid granulomas), from which bacteria likewise from the primary
focuses (lymphatic apparatus of the intestine) enter into the blood, supporting bacteremia
6.Discharge of the agent from the organism (excretory phase).
The agents enter into the intestine from the liver through the bile ducts. They are excreted into the
external environment with feces of the patient.
7.Allergic reaction, mainly, of lymphoid tissue of the small intestinum.
The part of the agents repeatedly penetrates from the small intestine into lymphatic apparatus of the
intestine and cause sensibilization to microbes.
The expressive changes of lymphoid tissue develop due to repeated implantation of Salmonella typhi
with development of morphological changes from cerebral-like swelling to necrosis and formation
of ulcers.
This process is considered as the seventh phase of pathogenesis – allergic response of lymphoid
tissue of the small intestine.
8.Formation of immunity
Q.9 classification of typhoid

-Typhoid fever is anthroponosis.
-The source of infection is sick man or bacteriocarrier.
-The mechanism of the infection transmission is fecal-oral.
-The factors of transmission may be various food-stuffs and beverages contaminated by feces of the
patient or bacterial carriers.
Q.10 main signs of typhoid in the initial period of the disease

• Typhoid fever is anthroponosis.
• The source of infection is sick man or bacteriocarrier.
• The mechanism of the infection transmission is fecal-oral.
The initial manifestations are nonspecific and consist of fever, malaise, anorexia, headache
and myalgias.
• Inverse sleep pattern: patient sleeps in afternoon, awake at night
• Diarrhoea on first days then constipation
• Typhoid tongue: large tongue with white coating only in the center of tongue.
EXAMPLE OF TEMPERATURE CURVES IN TYPHOID FEVER
• Trapezium (Wunderlich’s): Temperature increases from normal to 40-41 degrees in the first
week, remains high in second week and gradually decreases in third week
• Triangular (kildushevsky’s): Temperature increases from normal to 40-41degrees in the first
week. Gradually decreases from second week
• Undulating (Botkins): Temperature changes from high to normal every week
• Intermittent: high or very high and normal temperature with daily fluctuations of 3 — 4°C
Q.11 The pathognostic (main) symptoms of typhoid fever in the

climax of the disease.
Typhoid disease turns into the climax of the disease at the end of the first week. The appearance
of the patients is very typical in this period
• The skin is pale.
• Patient is apathetic.
• Intoxication is increased.
• Temperature is constant and most typical syndrome
• Chills and diaphoresis are seen in patients even in the absence of antimicrobial therapy.
• Either constipation or diarrhea may occur.
• Respiratory symptoms, including cough and sore throat may be prominent.
• Examination of the chest may reveal moist rales-
• The abdomen is tender, especially in the lower quadrants.
• Abdominal distention is common, and peristalsis is often hypoactive.
• The sensation of displacing air - and fluid filled loops of bowel on palpating of the abdomen
• Rose spots, 2-4 mm erythematous, maculopapular lesions that blanch on pressure, appear on the
upper abdomen or on the lateral surface of the body
• Neuropsychiatric manifestations: confusion, dizziness, seizures, or acute psychotic behavior,
• Status typhosus is observed in serious course of the disease.
• Cervical lymphadenopathy may be present
Q.12 Description, terms of beginning and dynamics of rash in patients

with typhoid fever.
• Rashes appear as rose spots which is 2-4 mm and is erythematous and maculopapular lesions that
blanch on pressure - appear on the upper abdomen or on the lateral surface of the body.
• Roseolas also appear and are few (5-15) in number
• The lesions are transient and resolve in hours to days.
• Rose spots are observed on the 7-10 day of the disease near in half of patients.
• Sometimes they disappear, sometimes exist longer than fever.
• usually are present only in half of the patients
• often new elements occur
Q.13 peculiarities of paratyphoid A
Paratyphi A is also having similar properties as salmonella typhi
Source of infection –sick person or carrier
Mechanism of transmission –fecal oral
• In paratyphoid A incubation period is 8-10 days, shorter than typhoid fever

• The onset of the disease is an acute.
• Sometimes accompanied by cough, catarrh.
• Facial hyperemia, herpes on the lips are observed during examination.
• The temperature is wave-like or remittent. The fever is accompanied by chills and then by
diaphoresis.
• In paratyphoid A the rash appears more early than in typhoid fever
• Rash is polymorphic. Roseolas, petechias and measles-like rash may be observed. The
intoxication is temperate.
• Leukocytosis and lymphocytosis may occur
• In majority of the patients the disease has a moderate course. The relapses are frequently
observed in case of paratyphoid A.
Q.14 Peculiarities of paratyphoid B

Paratyphi B
Source of infection – (humans and cattle)
Mechanism of transmission – fecal oral
Paratyphoid B incubation period is 5-10 days.
• Acute onset of the disease with expressive chill, myalgia and weakness
• At the initial period of the disease the intoxication may be combined with symptoms of acute
gastroenteritis
• The temperature is not prolonged. Status typhosus is absent in majority of the patients.
• The symptoms of intoxication disappear very quickly
• The rash is polymorphic, plenty. It appears at the earlier period.
• In some cases the course of paratyphoid B may be severe with septic manifestations
Q.15 Signs of possible relapse of typhoid fever

Relapse, a recurrence of the manifestation of typhoid fever after initial clinical response.
It occurs in patients who have not received antimicrobial therapy,
Some possible signs include
▪ Subfebrile temperature
▪ Increasing of pulse rate
▪ Presence of rash
▪ Rashes appear as rose spots which is 2-4 mm and is erythematous and maculopapular lesions
that blanch on pressure
▪ Hepato-Splenomegaly
▪ Eosinophilia
Q.16 Differential diagnosis of typhoid fever and influenza.

• Typhoid is caused by bacteria Salmonella Typhi.
• The mechanism of the infection transmission is fecal-oral.
• Influenza is caused by a RNA virus (orthomyxovirus).

• Spread is through respiratory droplets and aerosol.
• A sick person is the only source of the disease.
Incubation period Typhoid fever- 1-12 or 21 days Influenza- few hours to 1-2
days
Clinical presentation (Usually presents with Usually presents as upper

gastrointestinal symptoms) fever, respiratory symptoms (cough,
chills, myalgia, nausea, vomiting, sneezing, rhinorrhea, sore
rash, constipation throat)
Sudden onset of fever, chills or
rigors, headache, malaise,
diffuse myalgia,
Physical Exam Maculopapular rash, coated tongue, high temperature, headaches,

jaundice, splenomegaly, delirium dizziness, a syncope condition,
fever, malaise, pains in
different parts of the body
The headache is located in the
forehead, temples and over the
brows, neurologic symptoms
(unconsciousness, delirium,
convulsions)
Diagnostic Hemoculture, serological, coproc Rapid diagnostic test from
Investigation ulture nasopharyngeal secretions,
chest radiography based on
physical findings
Management Ciprofloxacin or ofloxacin Supportive care and
rehydration.
Antivirals for early treatment or
prophylaxis (osetalmivir,
zanamivir)
Q.17 Specific complications of typhoid fever.
Most common complications due to gastrointestinal are:
• Intestinal bleeding of the bowel
• Intestinal perforation of the bowel
• Infectious-toxic shock
Other complications include
1.secondary to toxemia (myocarditis, hyperpyrexia, hepatic and bone marrow damage),
2. Secondary to prolonged severe illness (suppurative parotitis and pneumonia).
3.Secondary to growth and persistence of typhoid fever bacilli (relapse, localized infection -
meningitis, endocarditis, osteomyelitis or arthritis
4.Secondary to therapy (bone marrow suppression, hypersensitive reactions and toxic shock
Q.18 Pathogenesis, clinical manifestations of small intestine perforation

at typhoid fever, time of onset.
• They occur in third week of the disease
• Perforation occurs in the terminal ileum where the number of lymphoid aggregates is the largest
and ulcerations most frequent
• Pathogenesis: hyperplasia, necrosis and sloughing, ulcerations, perforation
• Mostly weak abdominal pain, sudden acute pain occur rarely
• tension of abdominal muscles
• Signs of peritoneal irritation are weak or absent.
• Positive Blumberg sign,
• Guarding and forced position of the patient
Emergency AID
The only treatment is emergency surgery to close perforation. Abdominal lavage with antibiotic
solutions and IV antibiotics
Q.19 Pathogenesis, clinical manifestations of intestinal bleeding at

typhoid, time of onset. Pathogenesis
▪ Interstinal bleeding occurs because there is formation of ulcers in the intestinal mucosa due to
infiltration of the mucosa with Salmonella typhi.
▪ As the ulcer erodes the vessels of the intestinal mucosa, it causes bleeding to occur.
▪ Major intestinal hemorrhage is usually a late complication that occur during the secondary
third week of illness.
▪ There is an important sign of the massive intestinal hemorrhage symptom of “scissors” that is
when Suddenly the temperature is decreased up to normal or subnormal. But tachycardia is
observed or increased
Clinical manifestation:
▪ increase pulse rate and decreased temperature.
▪ Signs of hemorrhagic anemia: anemia, pallor, unconsciousness
Emergency aid
Can be stopped endoscopically or with hemostatics such as tranexamic acid, aminocapronic acid,
vikasol.
In some of cases, bleeding can be rapidly fatal if large vessels is involved and in such cases only
surgery is uses
Q.20 Methods of specific diagnostics of typhoid fever. Interpretation of

results depending on the duration of illness and material for research.
• Hemoculture on meat peptone agar. In the first week collect 10ml of blood and use 100ml
medium. On the second week collect 15ml of blood and use 150ml of medium. On the third
week collect 20ml of blood and use 200ml of medium.
• Widals test: detect O and H antigen of S.typhi
• Indirect hemagglutination,
• indirect fluorescent test,
• indirect enzyme-linked immunosorbent assay (ELISA) for immunoglobulin M (IgM)
and IgG antibodies to S typhi polysaccharide
Other tests
-Stool culture less sensitive to test for S.typhi
-Cultures of punch-biopsy samples of rose spots and rectal swabs
Q.21 The principles of typhoid fever treatment.

Typhoid fever is an acute intestinal disease transmitted by fecal-oral route from a sick person or
carrier to a healthy person. It is caused by Salmonella Typhi bacteria and leads to intestinal infection
Principles of Treatment
Etiotropic and Symptomatic Therapy
• Antibiotics depending on bacterial sensitivity test results
- Cephalosporins – e.g. Cefixime, Ceftriaxone
- Quinolones – e.g. Ciprofloxacin, Ofloxacin
- Macrolides – e.g. Azithromycin
- Sulfonamides – e.g. Co-trimoxazole
- Levomycetin (Chloramphenicol)
• Disintoxication therapy and Treatment of Infectious Toxic Shock where it develops
- Intravenous glucose and fluids
- Reopolyglycin
- Quartasault (lactosault)
- Dopamine
- Prednisolone
• Treatment of gastrointestinal bleeding
- Blood transfusion
- Vicasol, Calcium chloride
Supportive Therapy
• Bed rest and liquid diet during the fever period
• Adequate hydration
• Dietary Supplements with Ascorbic acid and vitamins
• Probiotics to prevent intestinal dysbiosis
** Prevention
• TAB Vaccine (Typhoid-paratyphoid A and B Vaccine) – 5-7years immunity
• Vi capsular polysaccharide Vaccine against the capsular (Vi) antigen **
Q.22 Etiology and epidemiology of salmonellosis.

Etiology
Caused by Salmonella species of bacteria from the Enterobacteriaceae family.
All nontyphoid species of Salmonella may cause Salmonellosis.
E.g. Salmonella typhimurium, Salmonella enteritidis,
* NB: Hence, S. Typhi, S. Paratyphi A, B and C do not cause Salmonellosis. **
Epidemiology
• Source of infection: contaminated food (poultry, eggs, beef, etc), contaminated water, contact
with infected animals or their fecal matter, sick people or carriers
• Mode of transmission: Unhygienic cooking environments and persons, improperly cooked foods
• Vectors of the infection: Flies, cockroaches, rats
• Mechanism of transmission: Fecal-oral route
• Mode of occurrence: Occur as separate sporadic cases and as outbreaks
• Incubation period is 12-72 hours but can be longer
• Susceptibility of a person depends on the premorbid state of the macroorganism and the quantity
and variety (serotypes) of Salmonella present.
• Seasonality; mostly summer
** NB: Salmonella can remain viable in water for 11-120 days, in the sea water – 15-27 days, in soil
– 1-9 months , in sausage products – 60-130 days, in the eggs, vegetables and fruits till 2,5 months. **
Q.23 Etiology and epidemiology of food poisonings.

Food poisoning is a foodborne illness resulting from eating contaminated, spoiled or toxic food that
manifests with symptoms such as nausea, vomiting and diarrhea.
ETIOLOGY
• Bacteria (either by bacterial endotoxin or exotoxin contamination)
- Campylobacter (most common cause)
- Salmonella (most commonly associated with contaminated poultry and eggs)
- E. Coli (most common cause of traveller's diarrhea; some species are associated with contaminated
hamburger meat)
- Clostridium species (associated with canned foods – Clostridium Botulinum; unrefrigeration of
meat causing it to go bad – Clostridium Perfringens)
- Bacillus cereus (associated with fried rice)
- Vibrio (associated with contaminated water; some species are associated with contaminated sea
food e.g. shellfish, clams, mussels)
• Viruses
- Rotavirus (commonly associated with outbreaks in children)
- Norovirus (commonly associated with outbreaks in children)
- Hepatitis A
• Parasites
- Giardia intestinalis (associated with contaminated water)
- Taeniasis
• Protozoa
- Cryptosporidium parvum (associated with HIV especially in profound immunosuppression and
low levels of CD4 cells)
Toxoplasma (associated with cat feces)
Epidemiology
• Source of food poisoning: contaminated food (poultry, sausages, eggs, beef, vegetables, canned
foods, milk, etc), water or soil, contact with infected animals or their fecal matter, sick people or
carriers
• Mode of transmission: Unhygienic cooking environments and persons, improperly cooked foods
• Mode of occurrence: Occur as outbreaks with an explosive character of illness affecting a mass of
people that fall ill over a short period of time (e.g. After visiting a restaurant); and may also occur as
separate sporadic cases
• Incubation period: A few hours
• Susceptibility of a person to this group of diseases is very high, sometimes up to about 90-100%.
• Seasonality: Toxic food-borne infections may occur during the whole the year, but occur more
especially in summer.
It may either be
Foodborne infections – ingestion of viable pathogens e.g. Typhoid fever, Salmonellosis, Cholera,
Shigellosis, etc
Foodborne intoxication – ingestion of preformed toxins e.g. Botulism and Staphylococсal
poisoning
Food Toxicoinfection – microbes produce toxins insitu when ingested with the food e.g. Bacillus
cereus poisoning
** NB:
There are 2 types of Bacterial toxins: Exotoxins & Endotoxins
• Exotoxins are the toxic products of bacteria which are actively secreted into environment.
Some exotoxin-releasing bacteria are Clostridium species, Enterobacter, Proteus, etc. There
are 2 types of Enterotoxins (Exotoxins) of bacteria: thermolabile and thermostable. They
increase the secretion of the fluids and salts into the stomach and intestine and damage the
membranes of the epithelial cells. Majority of enterotoxins are thermolabile.
• Endotoxins are toxic substances which are liberated only during the lysis of microbial cells.
Some endotoxin-releasing bacteria are Salmonella. **
Q.24 Clinical signs of salmonellosis localized forms.

Salmonellosis is an anthropozoonotic, foodborne infection, caused by nontyphoid Salmonella
species of bacteria that is characterized by the essential damage of the gastrointestinal tract.
Localized forms of Salmonellosis are restricted to the gastrointestinal system and occur in most
cases.
There is the
- Gastritic variant;
- Gastroenteritic variant; and
- Gastroenterocolitic variant.
Clinical Signs of the Localized Forms
• Onset of the disease is acute with an incubation period 4-6 hours
• Prodromal period is not typical or very short with weakness, malaise, slight chills
• Subfebrile temperature may occur in moderate to severe forms
• Nausea and vomiting
• Diarrhea with
- loose stools of moderate volume without visible blood.
- stool is green and smells like rotten eggs (with fatty droplets).
- In exceptional cases, the stools may be watery and of great volume
(“choleralike”), or, of small volume and associated with tenesmus and gross blood
(“shigellosis-like”)
• Diffuse mild abdominal pain in the epigastrium or right iliac region.
• Signs of Dehydration – Decreased skin turgor, Dry, tacky skin, increased capillary refill
time, etc
• Hyperactive bowel sounds.
** NB: Tenesmus is the false urge to defecate.
Q.25 Clinical signs of salmonellosis generalized forms.

The Generalized forms of Salmonellosis cause systemic affection and there is the
- Typhus-like form;
- Septic form (septicopyemia)
Clinical Signs of the Generalized Forms
Typhus-like form:
• Acute onset from high temperature (39-40°C) lasting 1-2 weeks
• Vomiting
• Diarrhea
• Tenderness in right inguinal region
• Hepato-splenomegaly from 5-6 days of disease
• Typhoid tongue (coated tongue)
• Skin rash on trunk
• Hallucinations
• Leukocytosis is observed only in early period of the disease. Then marked leukopenia, but
with neutrophilia.
In the climax period of such cases there may be a dynamia, pale skin, injections of scleras,
Septic form:
Sepsis develops when there is a sharp decrease in the immune system function of the patient and it
is characterized by symptoms such as
• Acute onset from hectic or prolonged fever, chills and sweating, after an Incubation period
of about 5-10 days
• Pallor, rash may appear on the skin (petechiae or large hemorrhages).
• Purulent metastases in different organs and tissues
• Presence of septic focus may cause complications such as meningitis, pneumonia,
osteomyelitis, pyelonephritis, enterocolitis, etc
• Hepatosplenomegaly sometimes with the development of jaundice
• Toxic-dystrophic syndrome (dystrophic changes to parenchyma of organs e.g. liver)
• The influence of intoxication on the central nervous system leads to irritation, violations of
sleep, and sometimes delirium.
Q.26 Clinical manifestation of food toxicoinfection.

Food Toxicoinfection is a group of foodborne illnesses resulting from eating contaminated food,
whereby microbes produce toxins in situ when ingested with the food e.g. Bacillus cereus poisoning.
Clinical Manifestation
According to etiology
1) Caused by Bacillus Cereus:
There are 2 types of enterotoxins of Bacillus cereus associated with 2 forms of symptoms
• Thermolabile toxin associated with the Diarrheal Form
• Thermostable toxin associated with the Emetic Form
In the Diarrheal Form: profuse watery diarrhea and abdominal pain.
They occur 6-12 hours after the ingestion of viable microbial cells and usually resolve within
24hours.
In the Emetic Form: nausea, vomiting and abdominal pain. Diarrhea may sometimes be present.
They occur 1-5hours after the ingestion of viable microbial cells and last for 24hours.
2) Caused by Clostridium perfringens:

• Incubation period is 8-24hours after ingestion of large number of viable microbial cells
• Fever
• Abdominal pain and cramps
• Diarrhea
• Nausea and vomiting
Symptoms lasts 24 hours, and the disease is termed as a mild one.
3) Caused by Staphylococcus species:

• Rapid onset within 1-6hours.
• Nausea and explosive vomiting for up to 24hours.
• Abdominal cramps or pain.
• Headache, weakness
• Diarrhea
• Increased body temperature. Symptoms last less than 12hours.
Q.27 The differential diagnosis of salmonellosis and shigellosis.

Shigellosis is an acute intestinal infection, caused by Shigella species of bacteria that is
characterized by bloody diarrhea.
Differential Diagnosis
SALMONELLOSIS SHIGELLOSIS
SOURCES OF INFECTION • contaminated Poultry, • sick persons and

eggs and milk; carriers; also from
• sick persons and • ingestion of
carriers and contaminated food and
• contact infected water
animals and their feces
MECHANISM OF Fecal-oral route Fecal-oral route;
TRANSMISSION person-person transmission
CHARACTER OF Mucous, watery green Watery stools with gross blood

DIARRHEA stools which smells like and mucus; tenesmus is often
rotten eggs. present (false urgency to
defecate)
LABS High WBC with left shift; High WBC and bands
Positive stool culture for increase;
nontyphoid Salmonella species Positive stool culture for
of bacteria Shigella bacteria;
Positive stool Guaiac Test
Q.28 Clinical manifestations of dehydration shock.
Dehydration shock also known as hypovolemic shock is a serious and sometimes life threatening
complication of dehydration, characterized by severe hypotension and disturbance of
hemodynamic stability and vital signs.
• Patient is drowsy
• Cold extremities
• Lethargy and weakness
• Eyes are sunken and dry with absence of tears
• Mouth and tongue is dry
• Skin turgor and elasticity decreased
• Tachycardia, Hypotension
• Tachypnea with Deep and rapid breathing
• Increased capillary refill time
• Urine output reduced or absent
• Increased hematocrit
• Electrolytes imbalance
Q.29 Methods of salmonellosis specific diagnostics.

Salmonellosis is an anthropozoonotic, foodborne infection, caused by nontyphoid Salmonella species
of bacteria that is characterized by the essential damage of the gastrointestinal tract.
Specific Diagnostic Methods
• Stool or urine culture: On McConkey agar media, Eosin-methylene blue agar and xylose-
lysine doxycholate
• Blood cultures may be positive
• Serological tests for bacterial antigens
• Anamnesis and presenting signs and symptoms
Other Diagnostic Methods include:
• CBC - increased or normal WBC; increased or normal hematocrit
• Biochemical blood analysis - Electrolyte imbalance in case of dehydration
• pH metry – Metabolic alkalosis
Q.30 The peculiarities of food toxicoinfection specific diagnostics.
Food Toxicoinfection is a group of foodborne illnesses resulting from eating contaminated food,
whereby microbes produce toxins insitu when ingested with the food e.g. Bacillus cereus poisoning
Nausea,
explosive vomiting for up to 24hours.
Abdominal cramps or pain.
Headache,
weakness,
diarrhea
subnormal body temperature.
Specific Diagnostic Methods
• Stool culture: Reveals pathologic microbe e.g. Bacillus cereus, Clostridium perfringens,
etc
• Blood cultures may be positive for the causative agents in severe cases with toxicosis
• Serological tests reveal bacterial antigens
• Anamnesis and presenting signs and symptoms may be characteristic for specific
microbial course of presentation
Diagnosis is made according to anamnesis, presenting clinical symptoms, epidemiological data
and laboratory data such as CBC, biochemical and serological tests, culture for bacterial
examination using stool, vomitus, gastric lavage material and analysis of food products.
Q.31 Emergency aid at a localized form of salmonellosis and at food

toxicoinfection.
• Salmonellosis is an anthropozoonotic, foodborne infection, caused by nontyphoid
Salmonella species of bacteria that is characterized by the essential damage of the
gastrointestinal tract.
• Food Toxico-infection is a group of foodborne illnesses resulting from eating
contaminated food, whereby microbes produce toxins in situ when ingested with the food.
Emergency aid at a localized form of salmonellosis and at food toxicoinfection:
• Perform a standard evaluation of airway, breathing, and circulation.
• Provide oral rehydration fluids if signs or symptoms of dehydration are present.
• Disintoxication therapy with Reopolyglycin
• Sorbents: Activated charcoal, enterosgel, cytoxil
• Symptomatically manage pain, nausea, vomiting, and diarrhea.
- Analgesics e.g. Ibuprofen
- Antiemetics e.g. metoclopramide
- Compensate fluid loss from diarrhea and vomiting
It is not advised to give antidiarrheal drugs to allow pathological bacterial excretion
• Send to hospital
Q.32 Treatment of salmonellosis and food toxicoinfection patients.
o Salmonellosis is an anthropozoonotic, foodborne infection, caused by nontyphoid Salmonella
o Food Toxicoinfection is a group of foodborne illnesses resulting from eating contaminated
food, whereby microbes produce toxins insitu when ingested with the food.
Treatment of salmonellosis and food toxicoinfection:

• Gastric lavage: with 10L warm water
• Rehydration: trisol, quartasol, rehydron
• Disintoxication therapy: Reopolyglycin
• Antibiotic in severe cases: ciprofloxacin, levofloxacin (salmonella)
• Probiotics
• Spasmolytics: nospa, spasmolgon
• Ferments: Mezim, pancreatin, festal, gordoux
Q.33 Etiology and epidemiology of cholera.

Cholera is an acute anthroponosic infectious disease caused by eating contaminated food or drinking
contaminated water that leads to severe watery diarrhea and vomiting, which can result in
dehydration and even death if untreated.
Etiology:
Vibrio Cholera Bacteria
Classical biotype, which was discovered by Koch and El Tor biotype.
Epidemiology:
• Source of infection: sick person, reconvalescent after cholera or clinically healthy vibrio-
carriers
• Mode of transmission: Contaminated food and water use, contact with fecal matter of
infected persons, ingestion of contaminated seafood
• Mode of occurrence: Occur as outbreaks with an explosive character of illness affecting
a mass of people that fall ill over a short period of time
• Incubation period: 48hours-5days
• Susceptibility of a person is general and high.
• In endemic areas morbidity is observed more frequently in children and elderly
persons.
• Endemic areas: Most especially in the tropics.
• SEASON- spring, winter*****
Q.34 Clinical manifestations of different dehydration degrees at
cholera.
According to the classification of Pocrovsky,
o The first degree of dehydration (Mild) is with fluid loss of 1-3 % of body weight.
o The second degree of dehydration (Moderate) is with fluid loss of 4-6 % of body weight.
o The third degree of dehydration (Severe) is with fluid loss of 7-9 % of body weight.
o The fourth degree of dehydration (Extremely severe) is with fluid loss of more then 10 % of
body weight.
Clinical Manifestations
In mild course (First degree of dehydration):
• Stool frequency about 10 times in a day
• Vomiting 1-2 times
• Thirst, light dizziness, weakness may present
• The mucous of the mouth is dry
• Subfebrile temperature may be present
• Their state is satisfactory.
In moderate course (Second degree of dehydration):
• Stool frequency is from 10 to 20 times in a day.
• The character of the stool is liquid, rice-water-like and plentiful.
• Weakness, dizziness, and thirst in patients.
• Dehydration appears after a few defecations in many patients.
• Turgor and elasticity of the skin decreases, dry mucus membranes, increased capillary
refill time - Oliguria may be present
• Vomit is rice-water-like.
• The skin is pale
• Moderate cyanosis of lips and extremities
• There is occurrence of muscle cramps
• The pulse is 100 per minute, Hypotension.
• Hematocrit is increased, ESR is slightly increased,
• Leukocytosis with left shift,
• The change of electrolytes is insignificant but Hypokalemia and hypochloremia are more
expressed.
In Severe course (Third degree of dehydration):
• Stool frequency is more than 20 times in a day; Sometimes the patient cannot count a
quantity of defecations.
• The stool is watery, rice-water-like and abundant from the first hours of the disease.
Frequent vomiting
• Grave weakness, adynamia, severe thirst and cramps of the muscles are observed.
• Cyanosis of lips and extremities is observed
• Marked dehydration
- eyes are deeply sunken in the orbits
- symptom of “black eyeglasses” is observed
- Dry oral cavity and mucous membranes, the lips are dry too. Tongue is dry and
coated.
- skin is cold and shrivelled with decreased turgor and elasticity
• Muscle cramps are often of long duration, with tonic character, accompanied with pain
• Tachycardia, marked Hypotension , Tachypnea or Dyspnea and Hypothermia
• Signs of Renal failure is manifested
- Protein and leukocytes are observed in urine
• Hematocrit and Erythrocyte sedimentation rate (ESR) is markedly increased,
Leukocytosis with left shift, and eosinophilia
• Fluid-electrolyte imbalance occurs • The state of the patient is grave or severe.
• Rarely occurs.
In Extremely Severe Course (Fourth degree of dehydration/ decompensated dehydration):
• It leads to hypovolemic shock.
• Marked organ dysfunction and renal failure
• Paresis of the stomach and intestine muscles, with hypokalemia and metabolic acidosis
occurs
• Relapsing vomiting and very frequent stooling are observed.
• Severe dehydration
- Cold, clammy skin
- eyes deeply sunken in orbits
- skin is shrivelled, with decreased turgor and elasticity (“washwoman’s hands”)
• Intensive total cyanosis.
• Decompensated dehydration may develop as early as in the first few hours
• Generalized tonic muscle cramps are observed, including muscles of the abdomen and
back
• Agonizing hiccup due to clonic spasm of diaphragm.
• There is no pulse, the arterial pressure is not determined, the breathing is frequent and
superficial and Hypothermia is present
• There is impression of the suffering on the face (facies cholerica).
• Voice becomes hoarse.
• Marked fluid-electrolyte imbalance
• In the last hours diarrhoea and vomiting may be absent • The state of the patient is very
grave.
• Untreated patients die. The cause of the death is an acute heart failure or renal failure •
Most rarely occurs.
** NB:
According to the WHO classification, patients with cholera may be divided into three groups by
their degree of dehydration:
The first degree of dehydration (Mild) - Patients who have loss of fluid volume equal to 5
% of their body weight.
• The second degree of dehydration (Moderate) - Patients who have loss of fluid volume
equal to 6-9 % of their body weight.
• The third degree of dehydration (Severe) - Patients who have loss of fluid volume over
10% of their body weight. This dehydration is dangerous for life if the reanimation
measures are not done. **
Q.35 Classification of cholera.

Cholera is an acute anthroponosic infectious disease caused by eating food or drinking water
contaminated by Vibrio bacteria species, that leads to severe watery diarrhea and vomiting, which
can result in dehydration and even death if untreated.
Classification
According to degree of dehydration:
WHO classification –
• The first degree of dehydration (Mild) - Patients who have loss of fluid volume equal
to 5 % of their body weight.
• The second degree of dehydration (Moderate) - Patients who have loss of fluid volume
equal to 6-9 % of their body weight.
• The third degree of dehydration (Severe) - Patients who have loss of fluid volume over
10% of their body weight. This dehydration is dangerous for life if the reanimation
measures are not done.
Classification of Pocrovsky - patients can be divided into four groups by their degree of
dehydration:
• The first degree of dehydration (Mild) is with fluid loss of 1-3 % of body weight.
• The second degree of dehydration (Moderate) is with fluid loss of 4-6 % of body
weight.
• The third degree of dehydration (Severe) is with fluid loss of 7-9 % of body weight.
• The fourth degree of dehydration (Extremely severe) is with fluid loss of more then 10
% of body weight.
According to Clinical forms:

1. Typical
2. Atypical
According to the Degree of Severity:

1. Mild,
2. Moderate,
3. Severe, 4. Very severe
** NB:
Complications: collapse, renal failure, cardiac failure,, pneumonia, abscess, phlegmon **
Q.36 Laboratory diagnosis of cholera.
LABORATORY DIAGNOSIS
Specific Tests:
• Stool culture and bacteriological studies
- Stool specimen appears like rice water
- Culture on sucrose agar plates (thiosulfate-citrate-bile-sucrose agar) reveals growth of yellow
colonies to confirm Cholera
- Gram stain, with Dark field microscopy reveals Gram negative, non motile Vibrios
- Bacteriological studies reveal lactose negative, sucrose positive, oxidase positive microbes
• Serological tests reveal cholera Antigens and host Antibodies to antigens as well as serotypes O1
and O139.
Non-specific Tests:
• CBC reveals Increased Hematocrit and ESR, Leukocytosis with left shift, neutrophylia and
eosinophilia. May reveal lymphopenia and monocytopenia in some cases.
• Biochemical Blood Analysis reveals
- fluid-electrolyte imbalance (sodium, potassium, chlorine, etc)
- elevations of LDH, AST and ALT enzymes (during complications)
• Renal Function tests may reveal kidney failure
• Urine Analysis may reveal signs of kidney failure
Q.37 Differential diagnosis of cholera and salmonellosis.

o Cholera is an acute anthroponosic infectious disease caused by eating food or drinking water
contaminated by Vibrio bacteria species, that leads to severe watery diarrhea and vomiting,
which can result in dehydration and even death if untreated.
o Salmonellosis is an anthropozoonotic, foodborne infection, caused by nontyphoid Salmonella
CHOLERA SALMONELLOSIS
Mode/factors of contaminated water and seafood ingestion of contaminated
transmission (e.g. Shellfish, clams, mussels) food, especially poultry, eggs
and milk.
Clinical presentation: Explosive Watery, ricewater-like Mucus, green stools, that smell
Character of Diarrhea stools (quantity is dependent on like rotten eggs
severity)
Physical examination: Severe dehydration occurs Mild dehydration that
Hemodynamic that may lead to
Stability hypovolemic shock
Diagnosis Stool culture is done on sucrose Stool culture is done on
agar plates and reveals yellow McConkey agar plates and
colonies to confirm Cholera; reveals colourless colonies and
Vibrio bacteria species are revealed sometimes colour change of
from bacteriological study the medium from orange to
amber; Nontyphoid
Salmonella bacteria species
are revealed from
bacteriological study
Q.38 Differential diagnosis of cholera and shigellosis.

o Cholera is an acute anthroponosic infectious disease caused by eating food or drinking water
contaminated by Vibrio bacteria species, that leads to severe watery diarrhea and vomiting,
which can result in dehydration and even death if untreated.
o Shigellosis is an acute intestinal infection, caused by Shigella species of bacteria that is
characterized by bloody diarrhea.
CHOLERA SHIGELLOSIS
MODE/FACTORS OF contaminated water and sick persons and carriers;
TRANSMISSION seafood (e.g. Shellfish, also from ingestion of
clams, mussels) contaminated food and water
MECHANISM OF Fecal-oral route Fecal-oral route; person to
TRANSMISSION person transmission is also
common
CLINICAL Explosive Watery, ricewater- Watery stools with gross
RPESENTATION: like stools (quantity is blood and mucus; tenesmus is
CHARACTER OF dependent on severity) often present (false urgency
DIARRHEA to defecate)
PHYSICAL Severe dehydration occurs May lead to septic shock;
EXAMINATION: that may lead to hypovolemic may also cause severe
HEMODYNAMIC shock dehydration that may lead to
STABILITY hypovolemic shock
DIAGNOSIS Stool culture is done on Stool culture is done on
sucrose agar plates and McConkey agar plates and
reveals yellow colonies to reveals circular, colourless or
confirm Cholera; Vibrio translucent colonies of
bacteria species are revealed Shigella bacteria; Shigella
from bacteriological study species are revealed from
bacteriological study;
Positive stool Guaiac Test
Q.39 The principles of cholera treatment.

The principles of Treatment include:
• Immediate hospitalization
• Use of special bed
• Compensation of fluid-electrolyte loss and metabolic changes by giving - Oral Rehydration
therapy in first and second stages
• IV Polyphonic Solutions: Trisol, Acesolum, Lactasol, Quartasol under control of sodium and
potassium
• Close monitoring of Hemodynamics and Vital Signs – Blood pressure, pulse, respiratory rate,
body temperature
• At a pernicious vomiting and cramps, use of Dimedrol or Suprastin with Promedol are
indicated
• Antibiotics: cotrimoxazole, erythromycin, doxycycline, chloramphenicol
• Panangin or Asparcam during 1 month are indicated during early reconvalescence.
Q.40 Rehydration therapy at cholera.
Rehydration therapy for patients with cholera can include
• adequate volumes of a solution of oral rehydration salts,
• intravenous (IV) fluids when necessary, and
• electrolytes.
For Oral Rehydration Therapy
Add prepackaged oral rehydration salts which contains glucose and electrolytes, to 1 liter of the
safe water.
• Give oral rehydration solution (ORS) immediately to dehydrated patients who can sit up and
drink.
• Give ORS frequently - measure the fluid lost from diarrhea and vomitus and measure the
amount of ORS to compensate the loss
- for older children and adults is 100 ml of ORS every 5 minutes, until the patient stabilizes.
- adults can consume as much as 1,000 ml of ORS per hour, if necessary, during the initial
stages of therapy
• Give small, frequent sips of ORS to patients who vomit, or give ORS by nasogastric tube.
• If the patient requests more than the prescribed ORS solution, give more.
• Patients should continue to eat a normal diet or resume a normal diet once vomiting stops.
Intravenous Rehydration Therapy
• start IV fluids immediately.
• If the patient can drink, give ORS by mouth while the IV drip is set up. Ringer’s lactate IV
fluid is preferred. If not available, use normal saline or dextrose solution.
• Measure the amount of IV fluids delivered to compensate the amount of fluid lost from di
Primary rehydration: IV fluids i.e %of weight loss given in litres in 2 hours.
Secondary rehydration: daily rehydration
• IV: Trisol, Acesolum, Lactasol, Quartasol under control of sodium and potassium
• In first and second stage, oral rehydration with standard salt solutions: oralyte, rehydron.
First degree give 30ml/kg, second degree give 60-70ml/kg
• IV Lactated ringer solution 10-20ml/kg/hour
• ORS 500-1000ml arrhea and vomitus
Q.41 Etiology and epidemiology of enteroviral infection.

DEFINITION- Enteroviral infections cover a wide range of illnesses that are caused by
enteroviruses (EVs).
They are members of the Picornaviridae family, which are small, single-stranded, RNA viruses.
Etiology: Main class - Polio Virus, ECHO and Coxackie A and B,
Epidemiology:
• Source of infection: patients and carriers
• Mechanism of transmission: Inhaling contaminated airborne droplet- droplets, fecal-oral
(Swallowing food or water contaminated with stool from an infected person),
transplacenta
! Contact with infected hands!
• Incubation period: 3-5 days lasting up to 10days
• Risk Populations:
- Overcrowded
- Poor hygienic and poor economic status populations
- Immuno compromised patients
- Infants and young adults
• Distribution: Worldwide distribution, Infections occur often in summer and fall.
• Seasonality- summer and early autumn
Q.42 Clinical forms of enteroviral diseases.

DEFINITION - Enteroviral infections cover a wide range of illnesses that are caused by
enteroviruses (EVs). They are members of the Picornaviridae family, which are small, single-
stranded, RNA viruses.
CLINICAL FORMS
• Asymptomatic Infection
• Non specific Febrile illness
• Aseptic Meningitis
• Paralytic polio disease
• Encephalitis
• Hand foot and mouth disease
• Herpangina
• acute hemorrhagic conjunctivitis
• Generalized Disease of Newborn
• Skeletal Muscle Infection Manifest as Pleurodynia
• Myopericarditis
• Clinic with respiratory infection
➢ Asymptomatic Infection
More than 50% of EV infections are asymptomatic or result only in Nonspecific febrile
illness. Young age is associated with higher frequency of symptomatic infection.
➢ Nonspecific febrile illness
• Illness that manifests as sudden fever. The fever may last for as long as a week
• myalgia, headache, sore throat, nausea, vomiting, mild abdominal discomfort, and diarrhea.
➢ Aspetic Meningitis
• Caused by Enteroviruses of group B coxsackievirus and echovirus
• Nonspecific fevers with CNS symptoms.Symptoms may also include headache, malaise,
nausea, and vomiting.,photophobia. Physical examination typically demonstrates
generalized muscle stiffness or spasm.
➢ Paralytic Polio disease
• Rapid onset of paralysis occurs 1 to 3 days after a minor febrile illness with sore throat,
headache, and myalgias.
• The paralysis is asymmetric and affects the proximal muscles more than the distal muscles.
• Lower limbs are more frequently affected and sensation is usually intact except in severe
cases.
➢ Encephalitis
• Echovirus 9 is the most common etiologic agent.
• lethargy, drowsiness, and personality change to seizures, paresis, and coma. Children with
focal encephalitis present with partial motor seizures, hemichorea, and acute cerebellar
ataxia
➢ Herpangina.
• This is an enanthematous (mucous membrane) disease that
• Painful vesicles of the oral mucosa along with fever and sore throat,
• The onset is sudden, with high temperatures [39.4-40°C].
• The oropharyngeal lesions usually erupt around the time of first fever.The duration of
illness is 3 to 6 days.
➢ Hand-foot-and-mouth Disease.
• Manifests as a vesicular skin rash on the hands and feet along with vesicles in the oral
cavity.
• Mainly caused by Coxsackie virus and echovirus.
• The oral vesicles usually are located on the buccal mucosa and tongue and are only mildly
painful.
• The exanthem involves vesicles on the palms, soles, and the interdigital surfaces of the
hands and feet.
➢ Skeletal Muscle Infection
• Manifest as Pleurodynia (Bornholm disease) which is characterized by an acute onset of
severe muscular pain in the chest and abdomen accompanied by fever.
• Coxsackie Virus 5 are the major causes.
• The muscular pain is sharp and spasmodic, with episodes typically lasting 15 to 30 minutes.
• During spasms, patients can have signs of respiratory distress or appear in shock, with
diaphoresis and pallor.
➢ Heart Infections
• In myopericarditis, Coxscakie virus B5 the most common causative agent.
• Fever, fatigue, and dyspnea on exertion, but more fulminant symptoms, including heart
failure or dysrhythmia, can occur.
➢ Respiratory infections
• These infections may result from enteroviruses.
• Symptoms include fever, coryza, pharyngitis, and, in some infants and children,
vomiting and diarrhea.
➢ Generalized Disease of Newborn-
• Develop during the first week of life
• Resembles bacterial sepsis with fever, irritability and lethargy.
• This illness is complicated by; Myocarditis, Hypotension, Disseminated Intravascular
Coagulation, Fulminant hepatitis, Meningitis, Pneumonia.
Q.43 The main symptoms of enteroviral diseases.
Defintion- Enteroviral infections include a wide range of illnesses that are caused by enteroviruses
(EVs). They are members of the Picornaviridae family, which are small, single-stranded, RNA
viruses. (members include- Polio Virus, ECHO and Coxackie A and B, Other enteroviruses, also
Rhinovirus)
Symptoms include
• A Latent period lasts 2-10 days
• Acute beginning from toxic syndrome (high body temperature 39-40 degree, headache,
malaise, fatigue, repeated vomiting, decreased apetite), abdominal pain and catarrhal syndrome
• Hyperemia of overhead half of trunk, skin, neck and face
• Injection of sclera vessels
• Hyperemia, gaininess of soft palate, and back pharyngeal wall
• Neck catarrhal lymphadenitis, or polyadenitis, may be hepatosplenomegaly
CLINICAL FORMS
• Asymptomatic Infection
• Non specific Febrile illness
• Aseptic Meningitis
• Paralytic polio disease
• Encephalitis
• Hand foot and mouth disease
• Herpangina
• acute hemorrhagic conjunctivitis
• Generalized Disease of Newborn
• Skeletal Muscle Infection Manifest as Pleurodynia
• Myopericarditis
• Clinic with respiratory infection
➢ Asymptomatic Infection
More than 50% of EV infections are asymptomatic or result only in Nonspecific febrile illness.
Young age is associated with higher frequency of symptomatic infection.
➢ Nonspecific febrile illness
• Illness that manifests as sudden fever. The fever may last for as long as a week
• myalgia, headache, sore throat, nausea, vomiting, mild abdominal discomfort, and diarrhea.
➢ Aspetic Meningitis
• Caused by Enteroviruses of group B coxsackievirus and echovirus
• Nonspecific fevers with CNS symptoms.Symptoms may also include headache, malaise,
nausea, and vomiting.,photophobia. Physical examination typically demonstrates
generalized muscle stiffness or spasm.
➢ Paralytic Polio disease
• Rapid onset of paralysis occurs 1 to 3 days after a minor febrile illness with sore throat,
headache, and myalgias.
• The paralysis is asymmetric and affects the proximal muscles more than the distal muscles.
• Lower limbs are more frequently affected and sensation is usually intact except in severe
cases.
➢ Encephalitis
• Echovirus 9 is the most common etiologic agent.
• lethargy, drowsiness, and personality change to seizures, paresis, and coma. Children with
focal encephalitis present with partial motor seizures, hemichorea, and acute cerebellar
ataxia
➢ Herpangina.
• This is an enanthematous (mucous membrane) disease that
• Painful vesicles of the oral mucosa along with fever and sore throat,
• The onset is sudden, with high temperatures [39.4-40°C].
• The oropharyngeal lesions usually erupt around the time of first fever.The duration of
illness is 3 to 6 days.
➢ Hand-foot-and-mouth Disease.
• Manifests as a vesicular skin rash on the hands and feet along with vesicles in the oral
cavity.
• Mainly caused by Coxsackie virus and echovirus.
• The oral vesicles usually are located on the buccal mucosa and tongue and are only mildly
painful.
• The exanthem involves vesicles on the palms, soles, and the interdigital surfaces of the
hands and feet.
➢ Skeletal Muscle Infection
• Manifest as Pleurodynia (Bornholm disease) which is characterized by an acute onset of
severe muscular pain in the chest and abdomen accompanied by fever.
• Coxsackie Virus 5 are the major causes.
• The muscular pain is sharp and spasmodic, with episodes typically lasting 15 to 30 minutes.
• During spasms, patients can have signs of respiratory distress or appear in shock, with
diaphoresis and pallor.
➢ Heart Infections
• In myopericarditis, Coxscakie virus B5 the most common causative agent.
• Fever, fatigue, and dyspnea on exertion, but more fulminant symptoms, including heart
failure or dysrhythmia, can occur.
➢ Respiratory infections
• These infections may result from enteroviruses.
• Symptoms include fever, coryza, pharyngitis, and, in some infants and children,
vomiting and diarrhea.
Q.44 Laboratory diagnosis of enteroviral infections.

stranded, RNA viruses (members include- Polio Virus, ECHO and Coxackie A and B, Other
enteroviruses, also Rhinovirus).
LABORATORY-
• Virological investigation of nasopharyngeal smears, feces, Cerebrospinal fluid
• Serological investigations (CBR with paired sera) titre enlargement 4 times and more
• CBC: leukopenia with neutrophylosis, lymphopenia, eosinophilia, elevated ESR
• CSF: moderate neutrophil-lymphocyte, then lymphocyte pleocytosis, normal or slightly
elevated protein. Pandy’s test is negative, sugar and chlorides are normal or slightly
decreased
• Reverse transcription-Polymerase Chain Reaction (RT-PCR)- This test is highly sensitive
and specific for detecting enterovirus RNA in cerebral spinal fluid specimens
• Cardiac enzyme levels and troponin 1 - These levels may be elevated in persons with
myopericarditis caused by enter viral infection (majorly caused by coxsaxkie B virus)
• *** Pandy's test done on the CSF to detect the elevated levels of proteins (mainly
globulins).
Q.45 Principles of enteroviral diseases therapy.

stranded, RNA viruses (members include- Polio Virus, ECHO and Coxackie A and B, Other
enteroviruses, also Rhinovirus).
PRINCIPLE OF THERAPY
• There is no specific treatment for non-polio enterovirus infection.
• People with mild illness caused by non-polio enterovirus infection typically only need to treat
their symptoms.
• This includes drinking enough water to stay hydrated and taking over-the counter cold
medications as needed. Most people recover completely,
Recommendations are
• Bed regimen in acute period
• Control of fever
• NSAIDs for pain relieve (ibuprofen, paracetamol), or opiate analgesics (morphine) in clinical
forms with severe pain
• Physiotherapy (in case of epidemic myalgia or paralytic form)
• Mechanical ventilation may be required if respiratory muscles are affected in paralytic form
• Patients with weakness or paralysis of the bladder may be treated with cholinergic agents, the
sound of running water, or catheterization.
• Cold compresses may be used, along with antihistamine/decongestant eye drops in case of
enteroviral infection presenting as acute hemorrhagic conjunctivitis (***mainly caused by Echo
or Coxsackie virus)
• Topical anesthetics, and saline rinses may be used in enteroviral infection presenting as
Herpangina and hand-foot-and-mouth disease
Herpangina
This is an enanthematous (mucous membrane) disease that presents with painful vesicles of the oral
mucosa along with fever and sore throat. The onset is sudden, with high temperatures [39.4-40°C].
The oropharyngeal lesions usually erupt around the time of first fever. The duration of illness is 3
to 6 days.
Hand-foot-and-mouth Disease
This common clinical syndrome manifests as a vesicular skin rash on the hands and feet along with
vesicles in the oral cavity. Mainly caused by Coxsackie virus and echovirus. Fever could also be
present. The oral vesicles usually are located on the buccal mucosa and tongue and are only mildly
painful. The exanthem involves vesicles on the palms, soles, and the interdigital surfaces of the
hands and feet.
Q.46 Etiology and epidemiology of shigellosis.
DEFINITION- Shigellosis is a bacterial infection that affects the digestive system. Shigellosis is
caused by a group of bacteria called Shigella. Gram negative bacteria from the family
enterobacteriaceae, most non-motile, non-sporing. Possess capsule (K antigen) and O antigen
Etiology: 4 subgroup based on biological and serological characteristics
Shigella dysenteriae
Shigella flexneri,
Shigella boydii
Shigella sonnei
Epidemiology
• Source- Sick patients, patients in period of convalescence and carriers.
• Mechanism of transmission: fecal-oral
• Ways of transmission: water (Shigella,.flexneri), food stuffs (Shigella .sonnei), dishes, dirty
hands, flies ! Epidemic features:
• season: summer & fall
• age: affects younger children more
• Incubation period 2-5 days
*** Shigella dysenteriae causes the most serious form of bacillary dysentery
Q.47 Clinical classification of shigellosis.

DEFINITION- Shigellosis is a bacterial infection that affects the digestive system caused by a
group of bacteria called Shigella. They are Gram negative bacteria from the family
enterobacteriaceae, most non-motile, non-sporing. Posses capsule (K antigen) and O antigen.
The Shigella bacterium is spread through contaminated water and food or through contact with
contaminated feces.
CLINICAL CLASSIFICATION
Duration
• Acute; up to 1 and a half months
• Subacute: up to 3months
• Chronic: more than 3 months
Clinical variants:
• Colitic variant
• Gastroenterocolitic variant
• Gastroenteric variant
Clinical form:
• Typical: with dominant toxicosis
• with dominant local inflammation
• mixed
Depending on severity:
• Mild form: acute diarrhea 5-8 times per day with mucus and blood. Mild abdominal pain,
normal temperature. Loss of appetite, could be vomiting
• Moderate form: acute onset of diarrhea, symptoms of toxicosis, temperature 3839 degrees,
anorexia, crampy abdominal pain, stool 10-15 times per day with mucus and blood. Pain
during palpation of left inguinal region
• Severe form: vomiting with or without food, stool more than 15 times per day with mucus and
blood. General condition sharply worsened. Sopor, loss of consciousness, cramps. Severe
toxicosis, weight loss and dehydration.
According to Pathology:
• Acute catarrhal inflammation
• Fibrinous Necrotic
• Ulcerous and folliclic-ulcerous
• Stage of formation of scars
Q.48 Peculiarities of shigellosis, depending on the clinical form.

group of bacteria called Shigella.
They are Gram negative bacteria from the family enterobacteriaceae, most non-motile, non-sporing.
Posses capsule (K antigen) and O antigen.
contaminated feces. The bacteria release toxins that irritate the intestines. The primary symptom of
shigellosis is diarrhea.
PECULIARITIES
With dominance of toxicosis:
• Toxicosis is the first sign (loss of appetite, headache, fatigue, vomiting, hallucinations,
unconsciousness, seizures, febrile temperature 39-40 degrees
• Colitis is secondary: abdominal pain, tenesmus, false urge to defecate, sigmoid colon is
tender, spastic, anus is open in severe cases. Feces in the form of spit of mucus and blood
(rectal spit), enlargement of number of defecation
With dominance of local inflammation:
! Sudden onset of high grade fever
! Abdominal cramping
! Abdominal pain
! Tenesmus
! Large volume of mucus, cylindrical epithelial cells diarrhea
! Fecal incontinence, small volume, mucous diarrhea with frank blood
According to severity
• Mild form: acute diarrhea 5-8 times per day with mucus and blood. Mild abdominal pain,
normal temperature. Loss of appetite, could be vomiting
• Moderate form: acute onset of diarrhea, symptoms of toxicosis, temperature 3839 degrees,
anorexia, crampy abdominal pain, stool 10-15 times per day with mucus and blood. Pain
during palpation of left inguinal region
• Severe form: vomiting with or without food, stool more than 15 times per day with mucus
and blood. General condition sharply worsened. Sopor, loss of consciousness, cramps.
Severe toxicosis, weight loss and dehydration.
Q.49 The clinic of colitis syndrome at shigellosis.
group of bacteria called Shigella.
They are Gram negative bacteria from the family enterobacteriaceae, most non-motile, non-sporing.
Posses capsule (K antigen) and O antigen.
contaminated feces. The bacteria release toxins that irritate the intestines. The primary symptom of
shigellosis is diarrhea.
CLINIC OF COLITIS SYNDROME
➢ Mild form: acute diarrhea 5-8 times per day with mucus and blood.
Mild abdominal pain, normal temperature.
Loss of appetite, could be vomiting
➢ Moderate form: acute onset of diarrhea, symptoms of toxicosis, temperature 38-39 degrees,
anorexia, crampy abdominal pain, stool 10-15 times per day with mucus and blood.
Pain during palpation of left inguinal region
➢ Severe form: vomiting with or without food, stool more than 15 times per day with mucus and
blood. General condition sharply worsened.
Sopor, loss of consciousness, cramps. Severe toxicosis, weight loss and dehydration.
Q.50 Laboratory diagnosis of shigellosis.

DEFINITION- Shigellosis is a bacterial infection that affects the digestive system. caused by a
group of bacteria called Shigella. They are Gram negative bacteria from the family
enterobacteriaceae most non-motile, non-sporing. Posses capsule (K antigen) and O antigen.
contaminated feces.
The bacteria release toxins that irritate the intestines. The primary symptom of shigellosis is
diarrhea.
LABORATORY-
• CBC: left shift leukocytosis, increased ESR
• Stool, feces, vomiting mass or gastric lavage culture for Shigella, colorless colonies on
mackonkey agar or Eosin methylene blue agar
• Serological reactions: increasing antibody titre to shigella
• PCR: detection of shigella DNA in feces and scrapping of the rectum mucous
Q.51 The treatment principles of shigellosis patients.

DEFINITION- Shigellosis is a bacterial infection that affects the digestive system. caused by a
group of bacteria called Shigella.They are Gram negative bacteria from the family
enterobacteriaceae
TREATMENT
In mild cases, treatment with antibiotics may not be indicated however adequate hydration is vital.
In more severe cases:
! Antibiotic therapy- Ciprofloxacin, Ceftriaxone, Azithromycin
! Probiotics: collibacterin, bifidumbacterin
! Rehydration: trisol, quartasol, saline
! Spasmolytics: no shpa. Spasmolgon
DON’T USE ANTIDIARRHEALS Like loperamide.
Q.52 Etiology and epidemiology of amebiasis.

DEFINTION- Amebiasis is a parasitic infection of the intestines caused by Entamoeba
histolytica.
Etiology-
• Protozoa called Entamoeba histolytica
• It exists in two forms- Vegetative (trophozoite) and cystic forms (cyst).
• Trophozoites multiply and encyst in the colon.
• The cysts are excreted in stool and are infective to humans.
• Cysts remain viable and infective for several days in faeces, water, sewage and soil in the
presence of moisture and low temperature.
Epidemiology
• Worldwide distribution (more predominant in tropical regions, with poor sanitary and
economic conditions)
• Source of infection: sick people, carriers
• Mechanism of transmission: fecal-oral, contact
• Ways of transmission: food-borne, anal sex, contaminated water
• Incubation period 2-4 weeks
• Seasonality; rainy season more and any other season
Q.53 Clinical classification of amebiasis.

DEFINITION - Amebiasis is a parasitic infection of the intestines caused by Entamoeba
histolytica,
Mechanism of transmission: fecal-oral, contact.
It has an incubation period of 2-4 weeks
CLINICAL CLASSIFICATION
Asymptomatic infection: (cyst passers/carriers)
Symptomatic infection (Intestinal Amebiasis & Extraintestinal)
➢ Intestinal Amoebiasis: Acute dysentery, Chronic non-dysentry, colitis,
- Symptoms present over a period of 1-2 weeks, Diarrhea with cramping, abdominal pain,
watery or bloody diarrhea and weight loss or anorexia. Stool looks like raspberry jelly. Fever
➢ Extraintestinal Amoebiasis: liver, skin, lung, pleura and brain
- Hepatic amebiasis: abdominal pain, weight loss,
- Amebic liver abscess: fever, right upper quadrant pain, weight loss, hepatomegaly,
jaundice, weight loss. Could be associated GI symptoms such as nausea, vomiting,
abdominal distention, diarrhea and constipation
!
- Rupture of amebic hepatic abscess: pleuropulmonary amebiasis: liver abscess rupture,
cough, pleuritic chest pain, dyspnea, necrotic sputum. amebic peritonitis or amebic
pericarditis can also occur due to rupture of liver
- Cerebral amebiasis: mental status changes and focal neurological deficits.
Q.54 The features of clinical duration of amebiasis intestinal forms.

histolytica, whose of source of infection are sick people and carriers.
It has an incubation period of 2-4 weeks.
Intestinal Amoebiasis:
Acute dysentery, Chronic non-dysentry, colitis,- Symptoms present over a period of 1-2 weeks,
Diarrhea with cramping, abdominal pain, watery or bloody diarrhea and weight loss or anorexia.
Stool looks like raspberry jelly. Fever
Amoebic colitis
• Symptoms present over a period of 1-2 weeks
• Diarrhea with cramping, abdominal pain, watery or bloody diarrhea and weight loss or
anorexia.
• Stool looks like raspberry jelly.
• Fever
Chronic amoebic colitis
Recurrent episodes of bloody diarrhea and vague abdominal discomfort, plus fatigue, weight loss
and occasional fever.
Fulminnt amebic colitis:
Rapid onset of severe bloody diarrhea, severe abdominal pain, rebound tenderness, fever.
Toxic megacolon:
Very dilated colon (megacolon), accompanied by abdominal distension (bloating), and sometimes
fever, abdominal pain, or shock
Q.55 Clinical signs of extraintestinal amebiasis.

DEFINTION - Amebiasis is a parasitic infection of the intestines caused by Entamoeba
histolytica, whose of source of infection are sick people and carriers
Extra-intestinal amebiasis can occur if the parasite spreads to other organs, most commonly the
liver, other locations include skin, lung, pleura and brain
• Extraintestinal Amoebiasis: liver, skin, lung, pleura and brain
• Hepatic amebiasis: abdominal pain, weight loss,
• Amebic liver abscess: fever, right upper quadrant pain, weight loss, hepatomegaly, jaundice,
weight loss. Could be associated GI symptoms such as nausea, vomiting, abdominal
distention, diarrhea and constipation
• Rupture of amebic hepatic abscess: pleuropulmonary amebiasis: liver abscess rupture, cough,
pleuritic chest pain, dyspnea, necrotic sputum. amebic peritonitis or amebic pericarditis can
also occur due to rupture of liver
• Cerebral amebiasis: mental status changes and focal neurological deficits.
Q.56 Complications of amebiasis.
DEFINTION - Amebiasis is a parasitic infection of the intestines caused by Entamoeba
histolytica, whose of source of infection are sick people and carriers Mechanism of transmission:
fecal-oral, contact.
Complications of amoebic liver abscess include the following:
Intraperitoneal, intrathoracic, or intrapericardial rupture, with or without secondary bacterial
infection
Direct extension to pleura or pericardium
Dissemination and formation of brain abscess
Other complications due to amoebiasis include the following:
Bowel perforation
Gastrointestinal bleeding
Stricture formation
Intussusception
Peritonitis
Empyema
! Ameboma- also known as an amebic granuloma, is a rare complication of Entamoeba histolytica
infection with formation of annular colonic granulation, which results in a large local lesion of the
bowel.
! Rectovaginal fistula
Q.57 Laboratory diagnosis of amebiasis.

histolytica, whose of source of infection are sick people and carriers.
LABORATORY DIAGNOSIS
! Microscopic identification of cysts and trophozoites in the stool is the common method for
diagnosing E. histolytica
! Stool or liver abscess aspirate culture, E. histolytica trophozoites can also be identified in
biopsy samples
! Stool antigen test with monoclonal antibodies
! Serum anti-amoebic antibody: PCR and DNA probes for E.histolytica
! CT with contrast: amebic liver abscess
Q.58 The treatment principles of amoebiasis patients.

histolytica, whose of source of infection are sick people and carriers
TREATMENT
Antiamoebic drugs, to prevent spread of infection and latent infection
• Metronidazole 500mg PO tid 7days ( main therapy)
• Tinidazole- intestinal amebiasis: 600mg PO: bid 3 days with food
• Iodoquinol
• Chloroquine + metronidazole and diloxande for Liver absceses
• Increase fluid intake
• Surgical drainage of hepatic abscess with Liver aspiration- Liver aspiration is indicated only
if abscesses are large (> 12 cm), abscess rupture is imminent, medical therapy has failed, or
abscesses are present in the left lobe.
Q.59 The etiology and epidemiology of giardiasis.

DEFINITION- Giardiasis is a parasitic intestinal infection caused by Giardiasis intestinalis also
called Giardia Lamblia, it is marked by stomach cramps, bloating, nausea and bouts of watery
diarrhea
Etiology:
Caused by Giardiasis intestinalis also called Giardia Lamblia),
Found on surfaces or in soil, food, or water that has been contaminated with feces from infected
humans or animals.
The life cycle is composed of 2 stages:
(1) The trophozoite which exists freely in the human small intestine
(2) The cyst, which is passed into the environment.
Epidemiology
• It has a Worldwide distribution (prevalent throughout the world increasing in areas with poor
sanitation)
• Source of infection: zoonosis: beavers, dogs, cats, rodents
• Mechanism of transmission: fecal oral
• Way of transmission: water-borne, food-borne
• Incubation period 1- 2 weeks
Q.60 Clinical signs of giardiasis.

DEFINITION- Giardiasis is a parasitic intestinal infection caused by Giardiasis intestinalis also
called Giardia Lamblia, it is marked by stomach cramps, bloating, nausea and bouts of watery
diarrhea
CLINICAL SIGNS
• Diarrhea,
• abdominal distention, abdominal cramps, flatulence.
• Malodorous, greasy stools.
• Malaise, weakness, low grade fever, anorexia
• Nausea, vomiting
• CNS symptoms: irritability, sleep disorder, mental depression, neurasthenia
Q.61 Diagnostics of giardiasis.

Giardiasis is a parasitic intestinal infection Caused by Giardiasis intestinalis also called Giardia
Lamblia. It is marked by stomach cramps, bloating, nausea and bouts of watery diarrhea.
DIAGNOSIS
o Atleast 3 stool samples in 2 days for culture: ova and parasites should be seen
o Fresh stool+ iodine or methylene blue examination for cysts on wet mount
o Stool antigen test with immunofluorescent antibody assay or ELISA test, PCR (especially
used for identification of subjects during a pandemic
o Upper endoscopy with biopsies and duodenal aspirated samples of duodenal fluid (e.g.,
Enterotest) may demonstrate trophozoites.
CLINICAL SIGNS
• Diarrhea,
• abdominal distention, abdominal cramps, flatulence.
• Malodorous, greasy stools.
• Malaise, weakness, low grade fever, anorexia
• Nausea, vomiting
• CNS symptoms: irritability, sleep disorder, mental depression, neurasthenia
Q.62 The treatment principles of giardiasis.

Giardiasis is a parasitic intestinal infection Caused by Giardiasis intestinalis also called Giardia
Lamblia. It is marked by stomach cramps, bloating, nausea and bouts of watery diarrhea.
TREATEMENT
It’s treated with antibiotics which have anti parasitic effects (nitroimidazole drugs)
• Metronidazole: (contraindicated in first trimester of pregnancy )250mg
• Tinidazole 2g orally once
• Nitazoxanide 20mg/ml orally
•Albendazole
In case of pregnancy can use Paromycin
Q.63 Differential diagnosis of amebiasis and shigellosis.
Q.64 The etiology and epidemiology of balantidiasis.

ETIOLOGY:
• Balantidium coli, a large ciliated protozoan, is the only ciliate known to be capable of
infecting humans.
• It is often associated with swine, the primary reservoir host.
EPIDEMIOLOGY:
• Pigs, are the primary reservoir, human infections occur more frequently in areas where pigs
are raised and sanitation is inadequate.
• Source of infection: pork excrement(zoonosis)
• Mechanism of transmission: fecal oral, Person-to-person spread, including through food
handlers.
PATHOGENESIS
Cysts are the stage responsible for transmission of balantidiasis
1.The host most often acquires the cyst through ingestion of contaminated food or water
2. Following ingestion, excystation occurs in the small intestine, and the trophozoites colonize
the large intestine
3.The trophozoites reside in the lumen of the large intestine and appendix of humans and animals,
where they replicate by binary fission, during which conjugation may occur .
4. Trophozoites undergo encystation to produce infective cysts
5. Some trophozoites invade the wall of the colon and multiply, causing ulcerative pathology in
the colon wall. Some return to the lumen and disintegrate. Mature cysts are passed with feces.
Q.65 Diagnostics of balantidiasis.
A protozoan infection caused by infection with Balantidium coli
SYMPTOMS:
Usually asymptomatic in immunocompetent individuals, but the symptoms of balantidiasis
include: Intermittent diarrhea, Constipation, Vomiting, Abdominal pain, Anorexia, Weight loss,
Headache
DIAGNOSIS:
Balanitis can usually be diagnosed during a physical examination because most of its symptoms are
visible.
• Microscopic examination of a patient’s feces:
• A stool sample is collected and a wet mount is prepared.
• Cysts or trophozoites can be detected in the feces.
• Balantidium coli is passed periodically, therefore stool,samples should be collected
frequently and examined immediately in order to make a definitive diagnosis.
• colonoscopy or sigmoidoscopy to obtain a biopsy from the large intestines which may
provide evidence for the presence of balantidiasis
Q.66 The treatment principles of balantidiasis.

A protozoan infection caused by infection with Balantidium coli
TREATMENT-
o Desintoxication with oral rehydration
o Antibiotics: Tetracycline, metronidazole, iodoquinol,
o Probiotics
o Vitamins
o Enzymes: pancreatin, gordoux
Three medications are used most often to treat Balantidium coli: tetracycline, metronidazole,
and iodoquinol.
➢ Tetracycline*: adults, 500 mg orally four times daily for 10 days; children ≥ 8 years old, 40
mg/kg/day (max. 2 grams) orally in four doses for 10 days. (Note: Tetracyclines are
contraindicated in pregnancy and in children < 8 years old. Tetracycline should be taken 1 hour
before or 2 hours after meals or ingestion of dairy products.)
Alternatives:
➢ Metronidazole*: adults, 500-750 mg orally three times daily for 5 days; children, 35-50
mg/kg/day orally in three doses for 5 days.
OR
➢ Iodoquinol*: adults, 650 mg orally three times daily for 20 days; children, 30-40 mg/kg/day
(max 2 g) orally in three doses for 20 days. (Note: iodoquinol should be taken after meals.)
➢ Nitazoxanide*: has been tried in small studies, which suggest some therapeutic benefit (adults,
500 mg orally twice daily for 3 days; children age 4-11 years old 200 mg orally twice daily for
3 days; children 1-3 years old 100 mg orally twice daily for 3 days).
Management
Avoid ingestion of material contaminated with animal feces
Treatment of infected pigs
Prevention of contaminated food
Q.67 Source of infection, mechanism and factors of transmission at

botulism.
Botulism is a rare but serious condition caused by toxins from bacteria called Clostridium
botulinum.
SOURCE: Botulin toxin is ingested through improperly processed food in which bacteria or spores
survive, mainly food borne but also can be caused by wound infection of inhalation.
Botulism is not transmitted from person to person.
MECHANISM:
Botulinum toxin acts by binding presynaptically to high-affinity recognition sites on the cholinergic
nerve terminals and decreasing the release of acetylcholine, causing a neuromuscular blocking
effect.
Three common forms of botulism are:
• Foodborne botulism. The harmful bacteria thrive and produce the toxin in environments
with little oxygen, such as in home-canned food.
• Wound botulism. If these bacteria get into a cut, they can cause a dangerous infection that
produces the toxin.
• Infant botulism. This most common form of botulism begins after Clostridium botulinum
bacterial spores grow in a baby's intestinal tract. It typically occurs in babies between the ages of 2
months and 8 months.
• Eight immunologically distinct toxin

• types have been described (types A, B, C, D, E, F, G.
• Types А, В and E most commonly cause disease in man;
• types F and G have only rarely caused human illness.
• Types С and D are associated with animal botulism, especially in cattle, ducks and chickens.
Q.68 The main clinical syndromes of botulism.

botulinum.
Common forms include-
o Food botulism,
o wound botulism,
o infant botulism
CLINICAL SYNDROME:
✓ Myoplegic syndrome
✓ Pharyngeoplegic syndrome: Bilateral damage of CN IX, X and XII causes bulbar syndrome,
Dysarthria, Dysphonia, Dysphagia: can’t eat solid or drink water, regurgitation in nose
✓ Opthalomegic syndrome: Blurred vision and diplopia Ptosis, nystagmus, Anizokoria,
Mydriasis, Decreased reflex ,Net fogin in front of eyes
✓ Gastrointestinal syndrome: epigastric pain, nausea, vomiting, diarrhea
✓ Intoxication Syndrome: Sub febrile temperature, rapid fatigue, marked muscle weakness
✓ Paralytic syndrome
✓ Autonomic dysfunction: hypothermia, urine retention, dry mouth and throat, postural
hypotension, constipation
Q.69 What are the symptoms of pharyngoplegic syndrome at botulism

botulinum. The toxin blocks acetylcholine release from the presynaptic membranes resulting in
weakness, flaccid paralysis, and, often, respiratory arrest.
Pharyngeoplegic syndrome:
• Bilateral damage of Central Nervous
IX (glossopharyngeal nerve),
X (vagus nerve) and
XII (hypoglossal nerve)
causes bulbar syndrome such as; Dysarthria, Dysphonia, Dysphagia: can’t eat solid or
drink water, regurgitation in nose
Q.70 What are the symptoms of ophthalmoplegic syndrome at

botulism.
ophthalmoplegic syndrome
Damage of CN III, IV, VI i,e oculomotor, trochlear, abducens nerves
• Blurred vision and diplopia
• Ptosis, nystagmus
• Anisocoria, Mydriasis, Decreased reflex
• Net fogging in front of eyes
Q.71 Specific diagnostics of botulism.

SPECIFIC DIAGNOSTICS
o Mouse bio-assay: serum gastric secretion or food diluted in phosphate buffer and injected into
mice peritoneum
o Culture of food samples, gastric aspirate or fecal material in anaerobic conditions
o Electrophysiological testing
o ELISA and PCR
o A normal Tensilon test helps to differentiate botulism from myasthenia gravis; borderline
positive tests can occur in botulism
o Laboratory confirmation is done by demonstrating the presence of toxin in serum, stool, or
food, or by culturing C. botulinum from stool, a wound or food
Q.72 Specific therapy and management of botulism patient

• Anti botulism serums Botulism antitoxin A and E (10,000IU), B (5,000IU) are injected at
first hours of the disease
Nonspecific desintoxication therapy
• Injection of glucose solution,
• Polyionic solutions (Lactasault, Trisault, Quartasault)
• Diuretics - Furosemid ( Lasix).
For suppression of infection in a digestive tract
• Ampicillin, Oxacillin, Levomycetin or Tetracyclin for 5-7 days.
• For prophylaxy of serum disease indicate Prednisolone on 40MG/DAY
• At disorders of respiration hospitalize & artificial respiration immediately.
• HBAT which has antitoxin A,B, C, D, E, F
The principles of botulism treatment

• Gastric Lavage and Enema with Sodium carbonate
• Oxygen
• Desintoxication therapy: glucose, polyionic solutions (lactasault, threesault, quartasault),
gurosemide
• Botulism anti-toxin
• For suppression of infection: ampicillin, oxacillin, levomycetin for 5-7 days
• In severe cases Prednisolone 40mg/day
• Vitamin B complex, cocarboxylase, riboxin
Q.73 The main clinical symptoms of influenza.

Influenza is a systemic viral illness from influenza A or B, usually occurring in an epidemic
pattern and transmitted by droplet nuclei.
Influenza can lead to damage to the respiratory epithelium, leading to sinusitis, otitis media,
bronchitis, and pneumonia.
Incubation period 2-3days
Clinical symptoms of influenza:
• Prodromal period: elevated temperature for short period of time (2-3hours), skin warm to hot
• Malaise, chilliness, myalgias, headache, dizziness, syncope, body pain
• Frontal retro-orbital headache
• Eyes may be red and watery
• Sore, throat, tonsillitis
• Cough
• Rhinopharyngitis, laryngotracheitis, tracheobronchitis
Q.74 Differential diagnosis of influenza and adenoviral infection.
Parameter Influenza Adenoviral infection

Respiratory tract Tracheitis Pharyngotonsillitis
Intoxication Severe Moderate
Catarrhal symptoms Mild Expressed
Myalgia, arthralgia Expressed Moderate
Rhinitis Moderate Expressed
Cough Dry Rarely
Conjunctivitis Absent Often
Pharyngeal hyperemia Expressed Expressed tonsillitis
Lymphadenopathy Absent Polyadenopathy
Liver Normal Often enlarged
Diarrhea Absent May be present
Q.75 Laboratory diagnosis of flu.
o Diagnosis is initially confirmed with rapid antigen detection methods of swabs or washings
of nasopharyngeal secretions.
o CBC- Leukopenia, relative lymphopenia
o Viral culture of nasopharyngeal samples and/ or throat samples is the most accurate test but is
usually not available rapidly enough to make it useful in acute patient management.
o Hemadsorption is positive
o Stain with fluorescent antibody
Treatment: antiviral medications: neuraminidase inhibitors oseltamivir and zanamivir
Q.76 Specific treatment of influenza.

Influenza is a systemic viral illness from influenza A or B, usually occurring in an epidemic
pattern and transmitted by droplet nuclei.
Influenza can lead to damage to the respiratory epithelium, leading to sinusitis, otitis media,
bronchitis, and pneumonia.
TREATMENT-
Symptomatic therapy: acetaminophen and antitussives
Specific antiviral medications: neuraminidase inhibitors oseltamivir and zanamivir.
• They should be used within 48 hours of the onset of symptoms to limit the duration of
symptoms.
• Amantadine and rimantadine should not be used in the empiric therapy of influenza.
• Influenza vaccine is recommended annually in the general public Bed rest
• Rehydration
• Osteltamivir- 75mg PO bid 5 days
• Zanamivir: 5mg oral inhalation bid 5 days
• Acetaminophen for fever and headache
• Amantadine, Rimantadine blocks neuraminidase
Q.77 Clinical signs of adenoviral infection.

CLINICAL SIGNS ARE-
• Acute Respiratory disease: tracheobronchitis, bronchiolitis, pneumonia, conjunctivitis presence
of bronchitis.
• Fever, rhinorrhea, cough, sore throat.
• Enlarged adenoid lymph nodes
• Pharyngoconjunctival fever: acute conjunctivitis, fever, sore throat, coryza and red eyes
• Epidemic keratoconjunctivitis: starts as unilateral red eye then spreads to both eyes:
• Photophobia, tearing and pain. Fever, lymphadenopathy, malaise
• Acute hemorrhagic cystitis: dysuria, grossly bloody urine, nephritis, fever, flank pain
• Gastroenteritis: infantile diarrhea, hepatomegaly
• Immunocompromised patient: hemorrhagic cystitis, nephritis, pneumonitis, hepatitis, liver
failure, gastroenteritis
DIAGNOSIS:
• Nasopharyngeal swab for culture of respiratory virus
• Viral and bacterial swab cultures of conjunctival secretions
• Urine analysis
TREATMENT
• Ribavirin 30mg/kg IV qid
• Cidofovir 1mg/kg IV tid for 3 weeks
Q.78 Clinical features of parainfluenza.

Epidemiology of human parainfluenza virus (HPIV): source is sick patient, transmission
airborne
CLINIC
• Incubation hours-7 days
• HPIV 1 and 2 causes Croup, HPIV 3 causes pneumonia and bronchiolitis
• In Mild courses: laryngitis manifested by sore throat, dry rough cough, burning in trachea, hoarse
voice, subfebrile temperature.
• Symptoms of upper respiratory illness may include: fever, runny nose, cough
• Symptoms of lower respiratory illness may include:
- croup (infection of the vocal cords (larynx), windpipe (trachea) and bronchial tubes
(bronchi))
- bronchitis (infection of the main air passages that connect the windpipe to the lungs)
- bronchiolitis (infection in the smallest air passages in the lungs)
- pneumonia (an infection of the lungs)
Other symptoms of HPIV illness may include
• sore throat, sneezing, wheezing, ear pain, irritability, decreased appetite
• Croup is often the main and only manifestation of disease: fever and rough barking cough.
Hyperemia, edema and plethora of mucous membrane larynx especially in infraglottis
Diagnosis: throat or nose immunofluorescent test. Chest X-ray

Treatment: Desintoxication therapy orally. In severe cases give immunoglobulin
Q.79 Clinic signs of respiratory-syncytial infection

Causes lower respiratory tract infections such as bronchitis, bronchiolitis and pneumonia
Source of infection: sick people transmitted via airborne
Clinic:
• Incubation 4-5 days
• Runny nose,
• Decrease in appetite, Coughing, Sneezing, Fever, Wheezing
• tachypnea,
• cyanosis,
• chest retractions,
• wheezing, and rales on auscultation.
• Dry cough. Nasal breathing
DIAGNOSIS:
• CBC: mild leukocytosis
• Secretions of bronchial wash, nasopharyngeal swab for immunofluroscent exam Treatment:
Desintoxication orally or IV, Ribavirin, Bronchodilators
Q.80 Laboratory diagnostics of acute respiratory viral infection

(ARVI).
Respiratory syncytial virus, or RSV, is a common respiratory virus that usually causes mild,
cold-like symptoms. RSV is the most common cause of bronchiolitis (inflammation of the small
airways in the lung) and pneumonia (infection of the lungs)
LABORATORY-
● Blood chemistry test, CBC
● Swab from nose or mouth or sputum sample to check for the type of virus .
● Chest x-ray or CT scan
● IgM against SARS
● PCR
● Viral isolation: CRP ELEVATED
Q.81 Complications of acute respiratory viral infection (ARVI)

Acute Viral Upper Respiratory Tract Infections – is a large group of Infectious Diseases, which
are caused by viruses, transmitted by Airbone way, characterized by intoxication and catarrhal
syndrome with predominant changes in mucous membranes of the respiratory tract
The main complication is
a) Acute respiratory distress
Signs of respiratory compromise Shortness of breath (Dyspnea )
Rapid, shallow breathing (tachypnea )
Retractions
Tachycardia
Using accessory muscles to breath
Blueish tinge to extremities or lips/tongue (cyanosis)
b) Respiratory failure –the patient cannot compensate for the inadequate oxygenation despite
extra respiratory effort and rate. There will be bradycardia, bradypnea, decreased level of
consciousness
c) Pneumonia - secondary infection by bacteria (viral infection can cause impairment of the
physical barrier in the respiratory airways making it easier for bacteria to invade) resulting in
pneumonia
It can occur from bacteria like staphylococcus aureus, streptococcus pneumonia, hemophilus
influenza
There will be productive cough, headache elevated WBC count, hypoxemia, chest radiograph
will show multiple infiltrates
Empyema
Lung abscess
Orbital cellulitis
Orbital abscess Mastoiditis
Q.82 Clinical and epidemiological features of legionellosis Pneumonia

ETIOLOGY- caused by legionella pneumophila, it is an important cause of both nosocomial and
community acquired pneumonia
EPIDEMIOLOGY
o They are facultative intra cellular parasites
o Water is the major environmental reservoir for legionella
They can infect and replicate within Protozoa such as acanthamoeba and hartmannella species
that are found in water systems
o It is a respiratory infection
o Transmission- Airbone
Through Direct inhalation via inhalation of aerosolized mist from water sources ( showers,
cooling towers) that is contaminated with either the bacterium or the amoebic cells that are
contaminated with the bacteria
Nosocomial acquisition is mostly through aspiration, respiratory therapy equipments (CPAP,
ventilators , humidifiers ),nebulizers or contaminated water
o Highest incidence – During the warmer months when air conditioning systems are used more
frequently
o Features that can increase the colonization of legionellae in man-made water environments
• Stagnation
• Temperature of 25-42c
• Presence of free living water amoebas that can support the intracellular growth of legionella
Factors that increase Risk of infection

• Advanced age
• Smoking
• Chronic heart or lung disease
• Immune compromised or immunosuppressive medications
• Recent exposure to water or soil
Signs and symptoms
▪ Incubation period – 2-10 days
▪ Fever > 40C, chills
▪ Cough – Dry or productive
▪Pleuritic or nonpleuritic chest pain
▪Localized rales
▪Neurological symptoms- Headache, lethargy, Encephalopathy, mental status changes
(depressed or agitation) which is the most common neurological symptom
▪ GI symptoms- Nausea, vomiting, abdominal pain, diarhea (watery)
▪ Myalgia
▪ Relative bradycardia
▪ Other extrapulmonary manifestations can be – myocarditis, pericarditis, prosthetic valve
endocarditis, pancreatitis, peritonitis, acute renal failure
Complications
Decreased pulmonary function, abscess formation (in lungs or extra pulmonary site), pulmonary
fibrosis, fulminant respiratory failure, death
Diagnostic
▪ Definitive method – Isolation of organism in respiratory secretions (sputum, lung fluid,
pleural fluid)
▪ Serology – ELISA, immunofluorescent antibody, PCR
▪ Lab – increased C reactive protein, hypophosphatemia (specific to legionella excluding other
causes of hypo phosphatemia), increased liver enzyme, increased creatine phosphokinase
Treatment:
▪ Levofloxacin 750mg IV daily 7-14days
▪ Ciprofloxacin 400mg IV tid 7-10d
▪ Moxifloxacin 400mg orally or IV once per day for 7-10 days
▪ Azithromycin 500mg orally or IV once per day for 7 days
Q.83 The etiology of herpes viral infection

• Human Herpes Virus 1: Herpes Simplex Virus 1: Orolabial herpes
• Human herpes virus 2: Herpes Simplex virus 2 Genital herpes
• Human Herpes Virus 3: Varicella zoster virus
• Human Herpes Virus 4: Epstein Barr Virus
• Human Herpes Virus 5: Cytomegalovirus
• Human Herpes Virus 6: herpes virus 6A or 6B
• Human Herpes virus 7: herpes virus 7
• Human Herpesvirus 8: Karposi sarcoma accociated herpes virus
➢ HSV-1 causes Oral-facial infections, Gingivostomatitis and pharyngitis, conjunctivitis, herpes

labalis , skin infection ( herpetic whitlow , gladiatorum )
➢ HSV-2 is a sexually transmitted infection that causes genital herpes
➢ Varicella-zoster virus causes Shingles (herpes zoster) and Chickenpox
➢ Epstein-Barr virus causes Infectious mononucleosis
➢ Cytomegalovirus causes CMV mononucleosis and immunocompromised host infection
➢ Human herpesvirus type 6 causes childhood illness known as roseola infantum or sixth disease.
➢ Human herpesvirus type 7 causes a skin condition in infants known as exanthema subitem
➢ Human herpesvirus type 8 cause Sarcoma Kaposi's
Q.84 Clinical manifestations and clinical course of herpes Simplex
Herpes simplex is a viral disease caused by both herpes simplex virus 1 (HSV-1) and herpes
simplex virus 2
Mode of transmission – Contact wound
HSV-1 is transmitted mostly by contact with infected saliva
HSV -2 transmitted sexually or from mother genital tract to her unborn child
Source of infection- Humans (Sick persons, Carriers)
CLINICAL MANIFESTATIONS
Herpes simplex 1
Acute Herpetic Gingivostomatitis – occurs in children aged 6months – 5 years, may occasionally
be in adult
It last 5-7 days and symptoms subside in 2 weeks, viral shedding may continue for 3 weeks
Symptoms include- Abrupt onset, High temperature (39-40c), Anorexia, Gingivitis, Vesicular
lesions, Tender regional lymphadenopathy, Perioral skin involvement due to contamination with
infected saliva
In adult it causes pharyngitis and tonsillitis more often than gingivostomatitis Symptoms
• Fever, malaise, headache, sore throat
• The vesicles rupture and forms ulcerative lesions with grayish exudates on the tonsils and
posterior pharynx
Conjunctivitis - unilateral follicular conjunctivitis with regional adenopathy and/or a blepharitis
with vesicles on the lid margin. Photophobia, chemosis, excessive tearing, and edema of the
eyelids may be present.
Herpes labialis – which is the manifestation of recurrent HSV-1 infection. Symptoms
• Prodromal symptoms (Pain, burning and tingling at the site) followed by
• Development of erythematous papules that turns into tiny, thin wall vesicles, then they become
pustular and ulcerate
Skin infections (herpetic whitlow, herpes gladiatorum, eczema herpeticum )
Herpes encephalitis (fever, headache, focal signs, altered level of consciousness)
Herpes simplex 2
Primary general herpes can be caused by both
Symptoms-
• Constitutional symptoms like fever, headache, malaise, myalgia (prominent in the first 3-4 days)
• Local symptoms like pain, itching, dysuria, vaginal and urethral discharge
• Tender lymphadenopathy
• In females – herpetic vesicles appear on the external genitalia , labia majora, labia minora,
vaginal vestibule , introitus, in most areas the vesicles rupture and form ulcer , the vaginal
mucosa is inflamed and edematous
• In males – the herpetic vesicles will appear in the glans penis , shaft of penis and
sometimes scrotum , thighs , in dry areas the lesions will become pustule and encrust
Perinatal infections
Q.85 Clinical forms of herpes zoster
DEFINITION- Herpes zoster is viral infection that occurs with reactivation of the varicellazoster
virus that has remained dormant within dorsal root ganglia, often for decades after the patient’s
initial exposure to the virus in the form of varicella (chickenpox),
CLINICAL FORMS
• Thoracic, lumbar, cervical and cranial form
• Herpes zoster opthalmicus: conjunctivitis, scleritis, episcleritis, retinitis, optic atrophy,
retrobulbar neuritis, exopthalmus, ptosis
• Herpes zoster of maxillary branch of CNV: severe toothache
• Herpes zoster of mandibular branch of CNV: pain in side of head, external ear, lower lip •
Herpes zoster oticus (Ramsay Hunt Syndrome): vesicles on external ear canal or tympanic
membrane with pain
• Glossopharyngeal and vagal herpes zoster
• Herpes occipitocollaris (vertebral nerves C2 and C3)
• Herpes zoster encephalomyelitis
• Disseminated Herpes Zoster
• Unilateral herpes zoster involving multiple dermatomes
• Recurrent herpes zoster
• Herpes zoster involving urinary bladder, bronchi, pleural space, or GIT
• Herpes zoster with motor complications
Q.86 Features of rash at herpes zoster

DEFINITION- Herpes zoster is viral infection that occurs with reactivation of the varicellazoster
virus that has remained dormant within dorsal root ganglia, often for decades after the patient’s
initial exposure to the virus in the form of varicella (chickenpox),
FEATURES-
• The earliest symptoms of herpes zoster, includes headache, fever, and malaise, myalgia are
nonspecific
• Before the rash appears there is itching, paresthesia, hyperesthesia, burning pain in affected
dermatone 2 or 4 days
• After 2 days, a characteristic rash appears, painful papules on red base
• Later Rash becomes vesicular developing on an erythematous base
• The Vesicles are clear initially but eventually they become cloudy or darkened with blood,
fever and malaise continues, the vesicles rupture, crust within 7-10 days and involute
• Rash heals within two to four weeks
• After vesicular involution, hyperemic base turns pale, epithelization and slight
hyperpigmentation (in 1 week)
• Rash typically appear unilaterally (either on the left or right side of the body or face), stopping
abruptly at the midline of the limit of sensory coverage of the involved dermatome, mostly
thoracic and lumbar dermatone are affected
• some people can develop post herpetic Neuralgia ( is persistent or recurring pain lasting 30 or
more days after the acute infection or after all lesions have crusted. It is the most frequent
complication of herpes zoster,symptoms are a deep burning or aching pain, paresthesia,
dysesthesia, hyperesthesia, or electric shock–like pains.
• There can be disemninated shingles
• The skin lesions (more than 20) appears outside either the primarily affected dermatome or
dermatomes directly adjacent to it
• Affection of other organs like the brain, liver causing encephalitis and hepatitis
Q.87 Laboratory diagnosis of herpes viral infection

isolation of virus in tissue culture
Herpes simplex is best confirmed by isolation of virus in tissue culture
It can yield positive results within 48 hours of inoculation
Characteristic cytopathic effect with ballooning of cells and cell death is seen
The cytologic changes can be seen in the tzank smear
It cannot distinguish between HSV-1 and HSV -2
Tzanck smear: scraping from base of fresh vesicular lesion after rupture may be smeared, fixed
with ethanol or methanol and stained with Giemsa or Wright preparation.
Rapid diagnosis using histological appearance
Histological appearance - The presence of multinucleated giant cells and epithelial cells containing
eosinophilic inclusion bodies indicates infection with HSV or varicella-zoster virus.
PCR – to detect HSV (herpes simplex virus) DNA, in HSV encephalitis, PCR with CSF is a
sensitive rapid diagnostic technique, it can also be used to detect asymptomatic viral shedding
Direct fluorescent antibody – Cells scrapes from ulcer base can be stained with direct fluorescent
antibody and it is used to distinguish HSV-1 from HSV-2, tissue culture cells can also be stained
Brain biopsy in Herpes encephalitis
Q.88 Differential diagnosis of herpes zoster and Chickenpox
Chicken Pox Herpes zoster

Transmission Through respiratory secretions or By reactivation of latent Varicella
vesicular fluid zoster virus
Signs and symptoms Malaise, fever, rash Neuralgia, dermatomal rash,
weakness of affected nerve
Distribution of rash Trunk initially, progressing to face, Dermatomal- Primarily thoracic,
extremities, mucosa or combination, it cranial, cervical, lumbar
involves the whole body
Character of rash Non-grouped, itchy vesicles Grouped along affected nerve,

In chicken pox rash is itchy erythematous, severely painful
vesicles
In chicken pox the rash crust by the in herpes zoster rash is painful
7th day in herpes zoster they crust by the
14th day
Q.89 Treatment of herpes viral infection

Desintoxication therapy
● Antihepatic drugs: acyclovir, valaciclovir, famaciclovir
A number of nucleoside derivatives interfere with the synthesis of HSV DNA. Some of these
(trifluorothymidine, vidarabine) are useful in and licensed for the topical treatment of herpes
keratitis.
● Immune stimulators: interferon, amizone
● Symptomatic therapy: NSAID (paracetamol, ibuprofen) for pain, sitz bath, topical lidocain
Q.90 The source of infection and mechanism of transmission at

Epstein-Barr viral infection
DEFINITION- Infectious mononucleosis is an infectious widespread disease caused by the
Epstein- Barr virus which infects B-cells (B-lymphocytes), producing a reactive lymphocytosis
and atypical T-cells (T-lymphocytes) known as Downey bodies, mostly in adolescent and
characterized by fever, sore throat, leg and muscle soreness and fatigue (symptoms of a common
cold or allergies). White patches on the tonsils or in the back of the throat may also be seen
(resembling strep throat)
Source of infection – Humans (symptomatic and latent forms, EBV carriers)
Mechanism of transmission – Airbone and contact (wound)
Ways of realizing through Droplet, sexual, parenteral, through saliva during speaking, coughing,
kissing
Q.91 Clinical forms of Epstein-Barr viral infection

DEFINITION-Epstein- Barr virus causes Infectious mononucleosis which is an infectious
widespread disease which infects B-cells (B-lymphocytes), producing a reactive lymphocytosis and
atypical T-cells (T-lymphocytes) known as Downey bodies, mostly in adolescent and characterized
by fever, sore throat, leg and muscle soreness, lymphadenopathy and fatigue (symptoms of a
common cold or allergies). White patches on the tonsils or in the back of the throat may also be seen
(resembling strep throat)
CLINICAL FORMS OF INFECTIOUS MONONUCLEOSIS
a) Typical
b) Atypical (mesadenitis, pseudoappendicitis, hepatitis, nephritis, pneumonia, respiratory
mononucleosis
Course of disease – acute, subacute, chronic
Degree of severity – mild, moderate, severe
Typical clinical features
• Incubation 1-2months
• Acute beginning with intoxication (fever, headache, myalgia, malaise, arthalgia )
• Generalized lymphadenopathy especially posterior cervical, anterior cervical on both sides
• Hepatosplenomegaly
• Jaundice
• Tonsilopharyngitis, large palatine tonsils covered with whitish yellowish exudates, it is not
easily seperated but without bleeding, it doesn’t exceed tonsils, no cyanotic or edema of soft
palate
• Rash – maculopapular may confluence with erythema as a result of hypersensitivity in case of
amoxicillin or ampicillin treatment
• Neurologic: optic neuritis, transverse myelitis, aseptic meningitis, meningoencephalitis, CN
palsies
Q.92 Clinical forms of cytomegaloviral infection

There are three clinical forms of cytomegaloviral infection:
1) Congenital CMV (asymptomatic or CMV inclusion disease of the newborn)
2) Acute acquired CMV infection (cytomegalovirus mononucleosis, cytomegalovirus
hepatitis)
3) CMV in immuno-compromised persons (CMV retinitis, encephalitis, CMV pneumonia)
Congenital CMV
• Maybe asymptomatic or present as cytomegalovirus inclusion disease of newborn
• Low birth weight
• On the skin - petechiae and purpura (I.e, blueberry muffin baby)
• Jaundice, Hepatosplenomegaly
• Thrombocytopenia, hemolytic anemia
• Chorioretinitis (inflammation of choroid and retina)
• Microcephaly
• Peri ventricular cerebral calcifications
• Long term outcomes include seizures, mental retardation, sensorineural hearing loss
Primary Acquired CMV infection
Usually asymptomatic OR
• May produce mononucleosis syndrome similar to Epstein Barr virus - fever, - Fatigue
- a feeling of being not quite right (malaise),
- skeletal-muscular pain and the absence of a sore throat;
- Swelling of glands (lymphadenopathy)
But in comparison to EBV infectious mononucleosis, CMV mononucleosis has lower incidence of
pharyngitis and cervical adenopathy
• Cytomegalovirus Hepatitis
CMV in immuno-compromised persons (for instance, people who have had organ transplants or
who have HIV) with increased risk for difficult eye infections (CMV retinitis), gastrointestinal
CMV, encephalitis, CMV pneumonia.
Q.93 Laboratory diagnosis of infectious mononucleosis.
DEFINITION- Infectious mononucleosis is an infectious widespread disease caused by the
Epstein- Barr virus which infects B-cells (B-lymphocytes), producing a reactive lymphocytosis
and atypical T-cells (T-lymphocytes) known as Downey bodies, mostly in adolescent and
characterized by fever, sore throat, leg and muscle soreness and fatigue (symptoms of a common
cold or allergies).
LABORATORY EVALUATION-
a) CBC – Leukocytosis , lymphocytosis , monocytosis , increased ESR
b) Liver function test – mild increases in the serum transaminases
c) Peripheral blood smear – atypical lymphocytes
d) Heterophile Antibody test (Monospot test) –
- A titre of 1:40 or greater is considered a positive result
- The heterophile antibody is an immunoglobulin M (IgM) antibody produced by infected B
lymphocytes.
- In the heterophile test, human blood is first absorbed by a guinea pig kidney. Then, it is
tested for agglutination activity that is directed against horse, sheep, or cow erythrocytes.
- it may be negative early in the course (first week) of EBV infectious mononucleosis so
negative test can be repeated within the first 6 weeks
- It is less useful in children younger than 2 years
e) Serology –
- igM and igG antibodies against the viral capsid antigen (VCA) of Ebstein Barr virus is
useful in confirming diagnosis of EBV and differentiating acute and/or recent infection
from previous infection
- The EBV IgM viral capsid antigen titre decrease after 3-6 months
- EBV IgG viral capsid antigen (VCA) antibodies rises later than the IGM viral capsid
antigen (VCA) antibodies and remains elevated for life
Q.94 Differential diagnosis of infectious mononucleosis with
diphtheria.
Q.95 Differential diagnosis of infectious mononucleosis with acute

tonsillitis.
Infectious mononucleosis Acute tonsilitis
Leading symptoms Lymphoproliferative syndrome, Intoxication syndrome, Inflammation
tonsillitis is not obvious of tonsils
Throat changes Absent or bright hyperemia Hyperemia of throat

Character of Purulent in follicles or in Red, swollen tonsils which can cause
tonsillar exudates lacunas, white-yellowish only on patient to have Dysphagia
tonsils. Can be easily removed (difficult to swallow or odynophagia
without bleeding (pain when swallowing), changes of
voice
Lymphadenitis General Regional (in neck region)
Hepatosplenomegaly Present absent
Toxic sign Prolonged with gradual cough, headache, chills, tiredness,
development (moderate or pain in ears or neck
severe)
Airway obstruction Absent Present: Mouth breathing, snoring,
nocturnal breathing, pauses or sleep
apnea
Q.96 The source of infection and the mechanism of transmission at

diphtheria.
DEFINITION - Diphtheria is an acute infectious disease caused by Corynebacterium diphtheria,
transmitted mainly in an air-borne way and characterized by the symptoms of general intoxication,
local inflammation of the mucous membranes
ETIOLOGY- Corynebacterium diphtheria
They are gram positive, aerobic or facultative anaerobic, nonmotile rods, nonencapsulated, non-
sporing
The 3 isolated strains of C diphtheria include gravis, intermedius, and mitis
They produce exotoxins
SOURCE OF INFECTION – Humans (sick persons and asymptomatic bacteria carriers) The
most epidemically dangerous are the bacteria-carriers who discharge microbes for a long time
(up to 1 month and longer), it is more often observed in patients with chronic diseases of the
upper respiratory tracts particularly with tonsillitis.
MODE OF TRANSMISSION- Airbone respiratory droplets or contact
WAYS OF TRANSMISSION- it is realized by direct contact with droplets or contact with
infected skin lesions, nasopharyngeal secretions
It belongs to the respiratory infections
Autumn- winter seasonality is characteristic for diphtheria
Incubation period – 3-10 days
Q.97 The classification of clinical forms of diphtheria.

DEFINITION- Diphtheria is an acute infectious disease caused by Corynebacterium diphtheria,
local inflammation of the mucous membranes mainly with the formation of fibrinogenous fur and
typical complications on the part of the nervous system, cardiovascular system and excretory system
CLASSIFICATION OF CLINICAL FORMS OF DIPHTHERIA:
Based on location:
a) Diphtheria of tonsils (&pharynx)
b) Diphtheria of larynx
c) Diphtheria of nasopharynx
d) Diphtheria of anterior part of nose
e) Rarely of the eyes, ears, genitals, umblicus, wounds, lips, cheeks, combined diphtheria
Degree of severity: Mild, moderate, severe, Toxic, hyper toxic, hemorrhagic
Based on Form: Localized, widespread,
Nature of process: catarrhal, island like, membranous
Complicated and without complications
Complications include: myocarditis, neuritis, nephritis
Q.98 Clinical features of the tonsil lesions at diphtheria.

typical complications on the part of the nervous system, cardiovascular system and excretory system
CLINICAL ONSET –
• low grade fever, cough, hoarseness, sore throat, intensity of intoxication depends on the square
of affection (localized, spread, toxic form)
• Gray adherent membranous exudate on tonsils in localized form
• Localized can be (catarrhal, island, membranous), in island the thigh grey membrane covers
part of the tonsils, in membranous it covers all tonsils
• In the spread form it extends to the soft palate, cheeks, Tongues
• Not easily seperated and exudates bleed when removed
• Hyperemia of throat with cyanotic(blue) tint and edema of the mucus membrane in places not
covered by the thick grey membrane
• Regional lymph nodes are enlarged and tender (lymphadenopathy)
In toxic form - you see bull neck (due to neck subcutaneous tissue edema and the grey
membranous exudates also extends outside the tonsils
Hypertoxic form- Sudden onset, severe intoxication (temp > 40c, seizures , nausea , vomiting ,
unconsciousness )
Hemorrhagic form- Hemorrhages, membranous educates are soaked with blood
Q.99 Clinical features of the larynx diphtheria

Croup (true, diphtheric) can be:
primary – at the primary localization of the diphtheria process in the larynx.
Secondary- if it develops after the affection of the fauces or the nose.
The course of croup can be divided into three stages.
Catarrhal croup
Stenosis (compensated, subcompensated, decompensated)
Asphyxia
AT CROUP COUGH STAGE.
The first symptom is sharp loud cough, which becomes rasping and barking
• Senior children complain of the sense of pressure in the larynx; the palpation of the larynx is
painful
• At the same time the voice becomes hoarse,
• At the examination with a laryngeal mirror it is often possible to see an edema and
hyperemia of the epiglottis. This period lasts 1-2-3 days and develops into a second stage.
AT STENOSIS STAGE.
• Stenotic breathing (narrowing of airways – inspiratory Dyspnea with an elongated inspiration)
• Noisy respiration
• Participation of auxiliary muscles in respiration Aphonia develops then later inspiratory stridor.
• Signs of hypoxia; peripheral then general cyanosis, tachycardia, anxiety, retractions)
AT ASPHYXIA STAGE.
• In the struggle with stenosis the child exhausts, the respiratory muscles get tired. The child
becomes calm, sleepy, he indifferently lies in bed.
• The respiration is accelerated, but it is superficial, the retractions are already not so visible.
• The lips, tip of the nose and nails become blue, the face turns pale, sweat quite often appears on
the forehead.
• The extremities are cold, the pulse is very rapid, thready, sometimes paradoxical (abasement of
the pulse wave during the inhalation).
• From time to time there are attacks of acute dyspnea – the child jumps up, rushes because of
air-deficiency, the eyes express fright, the face becomes cyanotic; sometimes such attacks result
in the immediate death;
• in other cases the child dies after a more or less continuous agony with the symptoms of
exhaustion of respiratory and circulation centers.
Q.100 Complications of diphtheria.

Early complications- (1st – 2 week)
• Toxic shock syndrome
• DIC syndrome, nephritis
• Adrenal failure, kidney failure, respiratory failure, multi organ failure, myocarditis
Late complications (3rd – 7th week)
Myocarditis
Peripheral spinal nerve palsies
Cardiac toxicity
Cardiac complications may arise during the first 10 days of illness or may be delayed until 2-3
weeks after onset
The first sign of toxin- induced myocardiopathy is
- tachycardia disproportionate to the degree of fever
- Various dysarthymias like first- degree, second-degree, or third-degree AV blocks; ventricular
tachycardia
- congestive heart failure which is a consequence of myocardial inflammation( progressive
Dyspnea , reduced heart sounds, systolic murmur )
- Echocardiography may reveal dilated or hypertrophic cardiomyopathy;
Neurological toxicity
Demyelination of nervous tissue
There will be Frank paralysis which involves the muscles of the palate and the hypopharynx,
beginning as early as the first 10 days of illness;
Difficulty swallowing and nasal speech are often the first indications of neurologic impairment;
Cranial nerve deficit – Oculomotor, ciliary paralysis (blurred vision), facial, pharyngeal
dysfunction
involvement of the anterior horn cells of the spinal cord may be seen as late as 3 months after
initial disease, Diffuse, usually bilateral, motor function deficits with progression of weakness either
from proximal-to-distal regions or, more commonly, from distal-to-proximal regions;
Involvement of the phrenic nerve may cause diaphragmatic paralysis at any time between the
first and seventh weeks of illness;
Recovery from neurologic damage usually is complete in patients who survive.
Airway obstruction by the diphtheritic: membrane and peripharyngeal edema combine to pose a
risk of death in patients with diphtheria
Q.101 Laboratory diagnosis of diphtheria.

Corynebacterium diphtheriae is the leading cause of diphtheria.
It is transmitted between humans via droplets, secretions or direct contact.
o The initial symptoms of respiratory diphtheria include sore throat, malaise, and low-grade
fever
o The characteristic clinical presentation is the presence of a grayish-white, fibrinous and firmly
adherent pseudomembrane that forms within the first few days and spans over the tonsils, the
pharynx, or the larynx.
o Cutaneous diphtheria can be caused by either toxigenic C. diphtheriae or Corynebacterium
ulcerans and commonly occurs on exposed limbs, particularly the legs.
LAB DIAGNOSIS:
a) Swabs from the nose, throat or suspected lesions are cultured onto blood and tellurite agar,
Löffler medium, hoyle, Mueller or tinsdale medium.
*(Tellurite inhibits growth of some normal flora and allows the Corynebacterium sp. to grow as
black or grey colonies)
b) In vitro phenotypic method for detection of toxigenicity is the Elek
immunoprecipitation (gold standard) which indicates presence of a biologically active protein.
c) PCR assay- for detection of the toxin gene (PCR positives must be confirmed by the
phenotypic Elek test)
d) Serology
Q.102 Differential diagnosis of diphtheria and Simanovsky-Plaut-
Vincent tonsillitis.
• Diphtheria- Corynebacterium diphtheriae is the leading cause of diphtheria. It is
transmitted between humans via droplets, secretions or direct contact.
• S. P. Vincent tonsillitis- also known as Vincent’s Angina is caused by Bacillus fusiformsis
and Borrelia Vincentii.
Simanovsky-Plaut Diphtheria
Vincent tonsillitis
Leading symptoms severe pain in mouth and gums, Fibrinous inflammation in throat, toxic
foul smelling breath syndrome
Throat changes Grey-white pseudo membrane on Cyanotic, hyperemic, edema
gums that can ulcerate and cause
bad taste in mouth
Character of tonsillar Grey-white pseudo membrane on Grey or white yellow membranes can
exudates tonsils that can ulcerate and spread outside the tonsils. They are
become necrotic. Easily dense, hard to remove and bleed when
removable removed. After removal, they reappear
and cannot be separated
Lymphadenitis Cervical lymphadenopathy Regional
Toxic sign Absent or minor Proportional to surface of inflammation.
(mild, moderate and severe)
Subcutaneous fat Absent Typical for toxic forms (bull neck sign)
edema
Changes on the tongue Absent Coated
Q.103 Specific treatment of diphtheria.

Diphtheria is caused by Corynebacterium diphtheriae.
o Symptoms of respiratory diphtheria include sore throat, malaise, and low-grade fever. The
characteristic clinical presentation is the presence of a grayish-white, fibrinous and firmly
adherent pseudomembrane that forms within the first few days and spans over the tonsils, the
pharynx, or the larynx.
o Cutaneous diphtheria commonly occurs on exposed limbs, particularly the legs.
TREATMENT:
● Immediate Hospitalization
● Bed regimen (localized forms - 10 days, toxic forms - not less than 35-45 days)
● Specific treatment- antitoxic antidiphtherial Serum (from 30-50 thousand IU in localized forms
and 100-120 thousand IU in toxic forms by Bezredka method)
● Glucocorticoids (In toxic forms and croup)
● Antibiotics (penicillin, tetracycline, erythromycin)
● Strychninum (in toxic forms)
● In case of croup - inhalations, broncholitics, diuretics, glucocorticoids, antibiotics,
antihistamine, lytic admixture
● under the indications - intubation, tracheotomy.
Q.104 Emergency aid at croup and diphtheria hypertoxic forms.

Diphtheria is caused by Corynebacterium diphtheriae.
Diphtheria of larynx (Emergency Aid)
● Give diphtheria anti-toxin
● Inhalation of antiedematous drugs (2% NaHCO3(sodium bicarbonate), hydrocortisone, euphillin
and mucolytics)
● Suction of membranes and mucus
● Oxygen inhalation
● III stage- intubation is required
● In case of spread croup combined with diphtheria of pharynx: tracheotomy
Diphteria toxic forms (Emergency Aid)
● Immediate IV infusion of Diphtheria antitoxin with 30-50mg prednisolone
● Prednisolone 10-20mg/kg/day in equal doses 2-4 times per day
● Desintoxication therapy, correction of acid balance and electrolytes
● Dopamine, trental, corglycon
Diphtheria of larynx: Real croup (stenosis of a larynx):
o I degree (catarrhal) - laboured inspiration, retraction of intercostal spaces, rasping “dog
barking” cough, “hoarse” voice
o II degree (stenosis) - noisy respiration (whistling sound), inspiratory dyspnea with an
elongated inspiration (inspiratory stridor), participation in respiration of axillary muscles
(intercostal, scalene, sternocleidomastoid muscles), aphonia
o III degree (asphyxia) - acute oxygen insufficiency, sleepiness, cyanosis, cold sweat.
Extremities are cold, thread paradoxical pulse. Cramps.
Q.105 Peculiarities of measles in adults.
Peculiarities:
● Incubation period 8-12 days
● Prodromal period: high fever lasting 4-7 days. Malaise, anorexia. Cough, coryza and
conjunctivitis. Koplick spots inside the cheek opposite second molar
● Period of exanthema: Erythematous Maculopapular rash that becomes confluent begins on the
face and then proceeds to trunk, extremities, palms and soles. Lasts about 5 days.
● Desquamation and brown staining which spares palms and soles
● Generalized lymphadenopathy, mild hepatomegaly and appendicitis may occur due to
generalized involvement of lymphoid tissues.
● The characteristic of measles rash is classically described as a generalized, macropapular,
erythematous rash that begins several days after the fever starts. It starts on the head before
spreading to cover most of the body, often causing itching. The rash is said to “stain”, changing
color from red to dark brown, before disappearing. The measles rash appears two to four days
after initial symptoms, and lasts for up to eight days
Q.106 Peculiarities of rubella in adults.
DEFINITION – Rubella (also known as German measles) is an infection caused by the rubella virus.
Commonly it occurs in young children but it can affect anyone. The illness is usually mild but rubella
in pregnancy can cause serious damage to the fetus.
Mode of transmission- the virus is transmitted by droplets, air-born route or direct contact
Causative organism- rubella virus is a member of togaviridae family
PECULIARITIES:
● Prodromal period (usually absent in children): eye pain on lateral and upward eye
movement, conjunctivitis, sore throat, headache, general body aches, low grade fever, chills,
anorexia. Tender lymphadenopathy particularly posterior auricular and suboccipital lymph
nodes. Forchheimer sign: pinpoint maculopapular Enanthema on soft palate.
● Exanthema (called 3 day measles): discrete rose-pink maculopapular rash which can be pruritic.
Begins on face and neck and spreads to trunk and extremities in 24 hours. Then on 2nd say they
begin to fade on face and disappear throughout the body on third day
Q.107 Peculiarities of mumps in adults.

DEFINITION- Mumps is a viral illness caused by a paramyxovirus. spreads easily from person to
person through direct contact with saliva or respiratory droplets of an infected person.
The most common symptoms of mumps that may be seen in both adults and children are:
• Discomfort in the salivary glands (in the front of the neck) or the parotid glands. These glands
may become swollen and tender.
• Other symptoms include fever, muscle aches, headache, loss of appetite, difficulty chewing.
PECULIARITIES:
● Fever lasts about a week and usually subsides before parotitis. headache, malaise, anorexia,
abdominal pain.
● Within 24 hours patients complain of ear pain near ear lobe which is aggravated by chewing
movement of jaw.
● Enlargement of parotid gland, initially unilateral then bilateral. Edema over parotid gland
typically occurs with non discrete borders, pain with pressure and obscured angle of mandible.
● Involvement of other salivary glands: submaxillary glands and sublingual glands. Orifices of
ducts may be erythematous and edematous
Q.108 Peculiarities of chickenpox in adults.

DEFINITION- Chickenpox is a highly contagious viral infection caused by varicella virus in
which a person develops extremely itchy blisters all over the body. The varicella virus can remain
in the body for decades and become active again in adults, causing herpes zoster (shingles).
Mode of transmission:
• Person-to-person by direct contact
• Droplet or airborne spread of vesicle fluid
• Secretion of the respiratory tract of chickenpox cases
• Vesicle fluid of patients with herpes zoster
• Indirectly through articles freshly soiled by discharges from vesicle and mucous membrane of
infected people
PECULIARITIES:
● Onset of myalgia, itching, nausea, fever, headache, sore throat, pain in both ears. Pressure in
head or swollen face with malaise.
● Then Erythematous vesicles mainly on the body and head. Usually pruritic and heals without
scaring
● Rash is absent on palms
● More severe in adults than children. In children rash is first then intoxication syndrome
Q.109 Classification of meningococcal infection.

DEFINITION- Meningococcal infection is an acute infectious disease caused by meningococcous
Neisseria Meningitis.
Mechanism of transmission- (air-drop)
The incubation period is 1-10 days, more frequently 5-7 days.
CLASSIFICATION:
● Primary localized forms
o Meningococcal carrier state
o Acute nasopharyngitis
● Hematogenic generalized forms
o Meningococcemia: typical acute meningococcal sepsis, chronic
o Meningitis
o Meningoencephalitis
● Mixed forms (meningococcemia and meningitis)
● Rare forms: endocarditis, arthritis, irideocyclitis, pneumonia
● Complications: sepsis, DIC syndrome, toxic shock, brain edema
Q.110 Clinic of meningococcal generalized forms.

Meningococcal infection is an acute infectious disease caused by meningococcous Neisseria
Meningitigis.
HEMATOGENIC GENERALIZED FORMS ARE:
● Meningococcemia:
- The disease is more impetuous, with symptoms of toxicosis and development of secondary
metastatic foci. The onset of the disease is an acute.
- Body temperature may increase up to 39-41 0C and lasts for 2-3 days.
- It may be continous, intermittent, hectic, wave-like.
- After a few days of upper respiratory symptoms, temperature rises abruptly often after a chill.
- Malaise, weakness, myalgia, headache, nausea and vomiting.
- Hemorrhagic rash (ptechia, ecchymoses and purpura) on whole body and fingers. Rash is star
like.
● Meningitis:
- Neck rigidity, positive brudzinski and kerning sign.
- Hemorrhagic rash (ptechia, ecchymoses and purpura) on the body.
- Severe diffuse or pulsatory headache worse at night, also increases with changing of body
position, sharp sounds and bright light.
- Fountain like Vomiting without nausea and no connection with food.
- Hyperthermia, hyperkinesia, photophobia, hyperalgesia and hpersomia.
- Assymetry of reflexes or hyporeflexia, patients lay with extended head and bent knees.
- Pathological reflexes.
- Tachycardia, tachypnea and arrhythmia.
- Tongue is dry and covered with dirty brownish coat. Loss of consciousness.
• Meningoencephalitis
- It is rare form of meningococcal infection.
- In this case the symptoms of encephalitis predominate, but meningeal syndrome is weakly
expressed.
- Meningococcal encephalitis is characterized by rapid onset and impetuous cramps, paresises
and paralyses.
- Prognosis is unfavorable. The mortality is high and recovery is incomplete even in modern
conditions.
Q.111 Complications of meningococcal disease.

Meningitigis.
COMPLICATIONS:
● Meningococcal arthritis: Can occur within the first few days of treatment, or when patient
appears to be improving from meningitis or sepsis. Severe arthralgia with few signs of joint
inflammation. Occurs mostly on wrists, elbow and ankle joints
● Pericarditis is a late complication: fever, dyspnea, substernal chest pain or cardiac tamponade
● Myocarditis
● Cranial nerve palsies, radiculitis, hemiplegia, seizures, ophthalmic complications,
hydrocephalus, arachnoiditis.
Q.112 Diagnostics of meningococcal infection.
Meningitigis.
The incubation period is 1-10 days, more frequently 5-7 days.
LABORATORY
● CBC: left shift leukocytosis with neutrophilia, increased ESR
● Bacteriological exam of nasopharyngeal mucus, blood, CSF, bacterioscopy of blood (thick
smear) and CSF
● CSF: neutrophil pleocytosis, protein increase, positive Pandy test, elevated pressure, slight
decrease of glucose level
● Serological
● Coagulogram: hypercoagulation or coagulopathy
Q.113 Changes in cerebrospinal fliud of patients with meningitis

Meningitis is an acute inflammation of the protective membranes covering the brain and spinal cord
(meninges)
Typical CSF abnormalities in meningitis include the following:
• Cloudy CSF
• Increased opening pressure in subarachnoid space (>180 mm water)
• Pleocytosis of polymorphonuclear leukocytes (white blood cell [WBC] counts between 10 and
10,000 cells/µL, predominantly neutrophils)
• Decreased glucose concentration (< 45 mg/dL)
• Increased protein concentration (>45 mg/dL)
• Gram stain and culture of CSF identify the etiologic organism, N meningitides.
According to Seupaul, the following 3 findings on CSF analysis have clinically useful likelihood
ratios for the diagnosis of bacterial meningitis in adults:
• CSF glucose−to−blood glucose ratio of 0.4 or lower
• CSF WBC count of 500/µL or higher
• CSF lactate level of 31.53 mg/dL or higher
More specialized laboratory tests:
• culture of CSF and blood specimens, are needed for identification of N meningitidis and the
serogroup of meningococci, as well as for determining its susceptibility to antibiotics
Symptoms:
Central- headache, altered mental status
Ears- Phonophobia, Eyes- photophobia, Neck stiffness
Systemic- high fever
Trunk, mucus membranes, extremities- petechiae (if it’s meningococcal infection)
Types of meningitis and their causes:
Bacterial meningitis: commonly caused by Streptococcus pneumonia (pneumococcal) bacteria
which causes ear and sinus infections but can also be caused by the Haemophilis influenza type
B bacteria, Listeria bacteria and the meningococcal bacteria.
Viral meningitis: commonly caused by enterovirus, but herpes simplex virus causing mumps,
measles, rubella and chicken pox can also cause viral meningitis.
Fungal meningitis: caused by a fungal infection and can mimic bacterial meningitis, but it is
uncommon.
Q.114 Treatment of meningococcal disease.

Meningitigis.
The incubation period is 1-10 days, more frequently 5-7 days
TREATMENT:
● Etiological treatment: benzylpenicillin 200.000-300,000 IU/kg/d, or ampicillin (or
metycillin) 200-300mg/kg/day, Chloramphenicol: 50-100mg/kg/ day, tetracycline 25mg/kg if
patient resistant to other antibiotics
● Pathogenetic treatment: salt solutions such as albumin, isotonic solution 4050ml/kg.
Diuretics to prevent brain edema (mannitol). Hydrocortisone (37mg/kg/day) or Prednisolone 1-
2mg/kg/ day in severe cases.
● Oxygen therapy
● Symptomatic therapy: antipyretics, anti-convulsants as needed
Symptoms include:
Fever and chills, Fatigue, Vomiting
Severe aches or pain in the muscles, joints, chest or abdomen
Rapid breathing
Diarrhea.
In the later stages, a dark purple rash
Q.115 The real croup: stage, clinic, emergency aid.

Laryngotracheobronchitis caused by mechanical blockage of larynx and trachea e.g. by coating as
seen in diphtheria.
Clinical triad: hoarse voice, inspiratory stridor and barking cough.
STAGES
● I degree (catarrhal)- labored inspiration, retraction of intercostal spaces, barking cough
● II degree (stenosis): Noisy respiration (whistling sound), inspiratory dyspnea with
elongated inspiration (inspiratory stridor). Participation of axillary muscles (intercostal, scalene,
sternocleidomastoid muscles)
● III degree (asphyxia): acute oxygen insufficiency, sleepiness, cyanosis. Extremities are
cold, thread paradoxical pulse. Cramps.
EMERGENCY AID:
● Treat underlying cause: In case of diphtheria, give antitoxin
● Mechanical removal of blockage, suction of membranes and mucous
● Give anti-edematic drugs (euphillin)
● Oxygen
● Intubation or tracheotomy as required in severe cases
Q.116 False croup: stage, clinic, emergency aid

Laryngotracheobronchitis caused by edema of mucous membrane causing narrowing as seen in
parainfluenza.
Clinical triad- hoarse voice, inspiratory stridor and barking cough
STAGES:
● I degree (compensated stenosis): hoarse voice, rough barking cough, compensated
hyperventilation of lungs pO2 normal
● II degree (Subcompensated stenosis): dyspnea, moist skin, pallor, perioral cyanosis. Mild
participation of auxillary muscles. Hypoventilation of lungs, tachycardia. pO2 normal.
● III degree (Decompensated stenosis)- inspiratory dyspnea, breathing with all auxiliary
muscles. Acrocyanosis, hypotonia, hypotension, superficial breathing. pO2 decreased pCO2
starts to increase
● IV degree (asphyxia): coma, cyanosis of whole body, superficial and labored breating.
Hypotonia, hypotension, bradycardia, aphonia. pCo2 increases severely.
EMERGENCY AID:
● Cool humidified oxygen. Helium-oxygen mixture to reduce work of breathing in severe
respiratory distress
● Dexamethasone 0.15-0.6mg/kg orally. Max 10mg
● Intubation if airway severely compromised
Q.117 Acute respiratory failure: clinic, emergency care.

Acute respiratory failure is a medical emergency in which the usual exchange between oxygen and
carbon dioxide in the lungs does not occur.
TYPES:
● Hypoxemic: high altitude, pneumonia, atelectasis, asthma, COPD etc. Normal pH, pCO2:
normal or decreased, pO2: decreased
● Hypercapnic: Acute upper airway obstruction, spinal cord disease, exogenous CO2 inhalation
etc. pH: decreased, pCO2: increased, pO2: decreased.
● Peri-operative: this is generally subset of type 1 failure but is sometimes considered
separately because it is common.
● Shock: it is secondary to cardiovascular instability
CLINICAL SIGNS:
● CNS: breathlessness, difficult inspiration or expiration. Restlessness, anxious. In terminal
stages: coma
● Skin: first acrocyanosis then total cyanosis
● Respiratory system: apnea, bradypnea, tachypnea, shallow breathing. Irregular breathing,
dyspnea
● Cardiovascular system: Tachycardia, hypotension
EMERGENCY CARE:
● Clean oral cavity
● Provide oxygen
● Artificial ventilation with ambu bag,
● If further inadequacy of breathing:0.5ml of 0.1% atropine and intubation
SECTION 2
Q.1 The classification of viral hepatitis.

Viral hepatitis is an infection that causes liver inflammation and damage.
Classification according to the infectious agent:
● Viral hepatitis A (Fever, headache, malaise, jaundice) 3-6weeks incubation period
● Viral hepatitis B (severe liver damage, chronic disease occurs) incubation period is more than
45 days (maximum 6 months)
● Viral hepatitis C (same symptoms as HBV but more chronic) 14-160days incubation period
● Viral hepatitis D occurs only with hepatitis B co-infection or super-infection (severe liver
damage, high mortality rate) 21-45 days incubation period
● Viral hepatitis E (pregnant women may be at high risk and show high mortality, not a chronic
disease) 15-60 days incubation period
● Viral hepatitis A, E: Acute
● Viral hepatitis C: Acute but mostly chronic
● Viral hepatitis B: acute and chronic
● Viral hepatitis D: occurs only with hepatitis B co-infection or super-infection
Classification according to clinical forms:
• cholestatic, sub-clinical (asymptotic), anicteric, icteric, fulminant
Classification according to course:
• Acute, prolonged, chronic
Degree of severity:
• Mild, moderate, severe, very severe
Q.2 The main pathogenic syndromes of viral hepatitis.
Viral hepatitis is an infection that causes liver inflammation and damage.
MAIN SYNDROMES-
● Intoxication syndrome: general weakness, fatigue, headache, insomnia and change in behavior.
Increased body temperature
● Catarrhal syndrome: flu-like syndrome, sore throat, dry cough. Hyperemia of conjunctiva and
mucus of soft palate. Edema of nose making it hard to breathe
● Dyspeptic syndrome: anorexia, nausea, vomiting, abdominal pain, diarrhea
● Arthralgic syndrome: Pain in large joints only, no deformation of joints
● Cholestatic syndrome: Jaundice
Q.3 Clinical and epidemiological features of hepatitis A.
Hepatitis A is an intestinal anthroponotic viral infection.
EPIDEMIOLOGY
• Fecal-oral mechanism of transmission- Watery route, Alimentary route, Contact way
(dirty hands, towels, dishes etc)
• Source of infection- Patients in the incubation, prodromal period and climax of the disease
• Susceptibility- Children after the first year of life, teenagers, young people up to 35 years,
patients with immunosuppression.
CLINICAL CHARACTERISTICS
Cyclical disease.
1. Incubation:
- Asymptomatic, duration 10-50 days, but on an average 28 days
- At watery and alimentary ways - incubation period is shorter
- At contact way - incubation period is longer
2. Initial period: duration is 5-7 days
- Intoxication: hyperthermia till 38-39oC; headache, weakness;
- Dyspepsia: loss of appetite, nausea, vomitinf, feeling of heaviness in the epigastrium and
right hypochondrium;
- Change (darkening) in color of urine
Initial period of HAV may occur in 3 clinical variants:
• Flu-like: hyperthermia, nasal congestion, discomfort in the oropharynx, coughing
• Dyspeptic: anorexia, nausea, vomiting, stomach pain, diarrhea
• Astheno-vegetative: general weakness, irritability, indifference, insomnia or drowsines
3. Climax (icteric) period:
Jaundice:
- With its appearance patient’s state is improved (additional diagnostic criteria
- First painted the mucosa of the oropharynx and the sclera, later the ski of the trunk, and then
extremities
- Continues 2-3 weeks
3 phases:
o Progression: 3-4 days
o Peak: 1-2 weeks
o Attenuation: 2 weeks
- Discoloured stool: dark urine (dark brown, like root beer or black tea foamy);
- Enlarged liver and spleen: palpation is painful, dense liver tissue
- Cardiovascular sd: tendency to hypotension, bradycardia
4. Reconvalescence:
• Continues 3-6 months
• Jaundice disappears gradually
• Asthenovegetative syndrome
Q.4 Clinical and epidemiological features of hepatitis E.

Definition: Hepatitis E is a liver disease caused by infection with a virus known as hepatitis E virus
(HEV).
EPIDEMIOLOGY:
Source of infection: sick people
Mechanism of transmission: fecal oral
Incubation period: 2-6 weeks
Susceptibility: high
Factors of transmission: water, food.
CLINIC:
Onset of fever, poor apetite, nausea, pain in RUQ
Within few days Jaundice, dark urine, clay colour stools
Usually mild and self-limiting
Q.5 Changes in the biochemical blood analysis at viral hepatitis.

DEFINITION: Hepatitis E is a liver disease caused by infection with a virus known as hepatitis E
virus (HEV).
EPIDEMIOLOGY:
Source of infection: sick people
Mechanism of transmission: fecal oral
Incubation period: 2-6 weeks
BIOCHEMICAL BLOOD ANALYSIS
● Cytolytic syndrome: increased ALT, AST, LDH, Cu. Decreased albumin, prothrombin
● dysproteinemia
● Mesenchymal-inflammation: increased alpha and gamma globulins, tymol-test
● Cholestasis: increased bilirubin, bile acids, cholesterine, GGTP and alkaline phosphatase
● Urine: urobilinogen, stool absent stercobilin
Q.6 Clinical and laboratory predictors of acute hepatic

encephalopathy.
DEFINITION: Hepatic encephalopathy is a brain dysfunction caused by liver impairment or
portosystemic shunting; it manifests as a wide spectrum of neurological or psychiatric abnormalities
ranging from subtle changes in cognition to clinically obvious changes in intellect, behaviour, motor
function and consciousness
CLINICAL
• First stage: inverted sleep, decreased attention, irritability, mild tremor. Jaundice increases.
Bradycardia.
• Second stage: decreased consciousness, memory loss, increased tendon reflexes. Jaundice
increases. Muffled heart sounds and hypotonia. Patient smells like ammonia. Liver decrease in
size, diuresis decreased
• Third stage: Complete loss of consciousness and disappearance of reflexes. Pathological
reflexis, convulsive syndrome. Tachycardia, hypotonia, disorder of rhythm. Anuria
• Fourth stage: Coma, cerebral edema
LABORATORY:
• Bilirubin continues to increase, Decreased ALT and AST
• Increased level of ammonia in blood
Q.7 Differential diagnosis of viral hepatitis with hemolytic jaundice.

Viral Hepatitis: Viral hepatitis is liver inflammation due to a viral infection. It may present in
acute form as a recent infection with relatively rapid onset, or in chronic form.
The most common causes of viral hepatitis are the five unrelated hepatotropic viruses hepatitis A, B,
C, D, and E.
Haemolytic Jaundice: Hemolytic jaundice occurs as a result of hemolysis, or an accelerated
breakdown of red blood cells, leading to an increase in production of bilirubin.
Parameter Viral hepatitis Hemolytic jaundice
Type of serum bilirubin Unconjugated and conjugated Unconjugated

increased
Urine urobilinogen Increased/decreased/ normal Increased
PTT Abnormal, not corrected with Normal
vitamin K
Additional features Increase ALT/AST Blood smear:
hemolytic anemia
Q.8 Differential diagnosis of viral hepatitis with obstructive jaundice.

Viral Hepatitis: Viral hepatitis is liver inflammation due to a viral infection. It may present in
acute form as a recent infection with relatively rapid onset, or in chronic form. The most common
causes of viral hepatitis are the five unrelated hepatotropic viruses hepatitis A, B, C, D, and E.
Obstructive Jaundice: Obstructive jaundice occurs as a result of an obstruction in the bile duct.
This prevents bilirubin from leaving the liver.
Viral hepatitis Obstructed jaundice
Type of serum Unconjugated and Conjugated

bilirubin increased conjugated
Urine urobilinogen Increased/decreased/ Decreased or absent
normal
PTT Abnormal, not corrected Abnormal, corrected with Vitamin K
with vitamin K
Additional features Increase ALT/AST. Increased Serum ALP> 3 times normal.

Jaundice Itching Jaundice with greenish tinge
Q.9 Differential diagnosis of viral hepatitis with leptospirosis.

o Viral Hepatitis: Viral hepatitis is liver inflammation due to a viral infection. It may present in
acute form as a recent infection with relatively rapid onset, or in chronic form. The most
common causes of viral hepatitis are the five unrelated hepatotropic viruses hepatitis A, B, C,
D, and E.
o Leptospirosis: Leptospirosis is a blood infection caused by the bacteria Leptospira.
Signs and symptoms can range from none to mild (headaches, muscle pains, and fevers) to
severe (bleeding in the lungs or meningitis).
Parameter Viral hepatitis Leptospitosis
Source of Sick people or carriers Zoonosis/environment
infection
Main features Flu-like symptoms with Flu like symptoms with myositis of calf muscles
myalgia, jaundice and acute renal failure, jaundice
Hepatobiliary Hepatitis Hepatitis, acalculous cholecystitis
system
Diagnosis Blood ELISA test Tissue biopsy microscopic agglutination test
Q.10 The specific diagnostic of hepatitis A and E.

DEFINITION: Hepatitis A virus (HAV) and hepatitis E virus (HEV) are the most common causes
of acute hepatitis in humans worldwide. Most HAV and HEV infections are acquired through
contaminated water and food.
Symptoms include:
Fever, Fatigue, Loss of appetite, Nausea, Vomiting, Abdominal pain, Jaundice.
LABORATORY-
● CBC: leukopenia with neutropenia.
● Biochemical: increased AST, ALT, ALP
● Serological diagnosis: IgM Anti-HAV for hepatitis A, IgM Anti-HEV for recent infection.
If IgG anti-HAV, it’s for vaccinated patients
Q.11The principles of viral hepatitis A and E treatment.

DEFINITION: Hepatitis A virus (HAV) and hepatitis E virus (HEV) are the most common causes
of acute hepatitis in humans worldwide. Most HAV and HEV infections are acquired through
contaminated water and food.
Symptoms include: Fever, Fatigue, Loss of appetite, Nausea, Vomiting, Abdominal pain, Jaundice.
TREATMENT:
● Bed rest
● Supportive and symptomatic therapy
● Adequate nutrition: diet low fat, carbohydrates.
● Desintoxication therapy: glucose, rheosorbilact, isotonic solution
● Sorbents
● Ferments: mezim, contrical
● Lactulose
● Postexposure therapy
Q.12 Treatment of patients with hepatic encephalopathy.

DEFINITION: Hepatic encephalopathy is a brain dysfunction caused by liver impairment or
portosystemic shunting; it manifests as a wide spectrum of neurological or psychiatric abnormalities
ranging from subtle changes in cognition to clinically obvious changes in intellect, behaviour, motor
function and consciousness.
TREATMENT-
● Prednisolone 1-3mg/kg
● Lactulose 10-30g PO 2-4 times daily
● Rifaximin 550mg PO twice daily or Canamycin
● Stop diuretic therapy
● Correct electrolyte imbalance
● Diet: high glucose, low protein
Q.13 Clinical and epidemiological features of hepatitis B.

DEFINITION: Hepatitis B is an infectious disease caused by the hepatitis B virus (HBV) that
affects the liver; it is a type of viral hepatitis. It can cause both acute and chronic infection. Many
people have no symptoms during the initial infection.
EPIDEMIOLOGY-
● Source of infection: sick people and carriers
● Mechanism of transmission: contact
● Mode of transmission: Sexual, blood transfusion, drug users, barber shops, stomatologists,
tattoo. Hepatitis B can stay on tools for long, not killed by normal anesthetic
● Incubation period 6 weeks- 6months
● Susceptibility: high
CLINIC:
● Gradual onset of dyspeptic and intoxication syndrome
● Early in course of disease athralgic syndrome develops
● Progressive appearance of jaundice: 2 weeks and more. Jaundice is prolonged and severe.
● Presence of asthenic (intoxication) syndrome throughout the whole period of the disease
Q.14 Clinical and epidemiological features of hepatitis C.

DEFINITION: Hepatitis C is an infectious disease caused by the hepatitis C virus (HCV) that
primarily affects the liver; it is a type of viral hepatitis. During the initial infection people often have
mild or no symptoms. Occasionally a fever, dark urine, abdominal pain, and yellow tinged skin
occurs.
EPIDEMIOLOGY
tattoo. Hepatitis C can stay on tools for long, not killed by normal anesthetic
● Susceptibility: high
CLINIC
● Asymptomatic or mild course of disease. Usually manifests years later with complications
● Mild prodromal period lasting more than 2 weeks: dyspeptic syndrome, mild arthralgic
syndrome, intoxication syndrome
● Mild cholestatic syndrome
● Usually present much later with complications such as liver cirrhosis
Q.15 Clinical and epidemiological features of hepatitis D.
DEFINITION: Hepatitis D, also known as the hepatitis delta virus, is an infection that causes the
liver to become inflamed. This swelling can impair liver function and cause long-term liver
problems, including liver scarring and cancer. The condition is caused by the hepatitis D virus
(HDV)
EPIDEMIOLOGY
● Source of infection: sick people with hepatitis B
● Mode of transmission: Sexual, blood transfusion, drug users, barber shops,
stomatologists, tattoo. Hepatitis B can stay on tools for long, not killed by normal anesthetic
CLINICAL
● Co-infection with hepatitis D: Identical features of hepatitis B-
- Gradual onset of dyspeptic and intoxication syndrome
- Early in course of disease athralgic syndrome develop
- Progressive appearance of jaundice: 2 weeks and more. Jaundice is prolonged and
severe.
● Can lead to fatal hepatic necrosis
● Hepatitis D Superinfection: Worsens patient’s general condition. Severe signs of Hepatitis B
Q.16 Specific laboratory diagnosis of hepatitis B.

DEFINITION - Hepatitis B is an infectious disease caused by the hepatitis B virus (HBV) that
SPECIFIC LABORATORY DIAGNOSIS:
ELISA or PCR
● Acute infection: HBsAg+, HBeAg+, Anti-HBs-
● Past Hepatitis B infection: IgG anti-HBc+, HBsAG-, IgG-Anti-HBs –
● Chronic carrier: HBsAg+, IgG Anti-HBc-, Anti-HBe
● Window period: IgG (or IgM) Anti-HBc+, HBsAg-, IgG anti-HBs-
Q.17 Specific laboratory diagnosis of hepatitis C

DEFINITION - Hepatitis C is an infectious disease caused by the hepatitis C virus (HCV) that
primarily affects the liver; it is a type of viral hepatitis. During the initial infection people often
have mild or no symptoms. Occasionally a fever, dark urine, abdominal pain, and yellow tinged
skin occurs.
SPECIFIC LABORATORY DIAGNOSIS:
ELISA or PCR
Hepatitis C: determine the genotype 1-5, A or B. Usually IgG anti-HCV. If IgM and IgG anti-
HCV present it is chronic re-infection.
Q.18 Specific etiological Therapy of hepatitis B
DEFINITION: Hepatitis B is an infectious disease caused by the hepatitis B virus (HBV) that
EPIDEMIOLOGY
tattoo.
SPECIFIC ETIOLOGIC TREATMENT- ANTIVIRAL MEDICATIONS
● Entecavir
● Tenofovir
● Lamivudine
● Adefovir
● Telbivudine
PEG IFN, entecavir, or tenofovir are recommended as first-line therapy
PEG IFN requires finite-duration therapy, achieves the highest rate of HBeAg responses after a
year of therapy
Entecavir Nucleoside analogue, inhibits reverse transcriptase 0.5 mg/day : 1 mg/day in
lamivudine or telbivudine exposed and decompensated
Pegylated Interferon (Pegasys) Long-acting interferon,is given by injection once a week usually
for 6 months to a year.
Q.19 Specific etiological therapy of hepatitis C.

DEFINITION: Hepatitis C is an infectious disease caused by the hepatitis C virus (HCV) that
primarily affects the liver; it is a type of viral hepatitis. During the initial infection people often have
mild or no symptoms. Occasionally fever, dark urine, abdominal pain, and yellow tinged skin
occurs.
Epidemiology
tattoo.
TREATMENT-
Antiviral medications
● Pegylated Interferon
● Ribavirin
● Protease inhibitors (simeprevir, paritaprevir, glecaprevir, grazoprevir)
Interferon, peginterferon, and ribavirin used to be the main treatments for hepatitis C. They can
have side effects like fatigue, flu-like symptoms, anemia, skin rash, mild anxiety, depression,
nausea, and diarrhea.
NS5A inhibitors- Odalasvir Ombitasvir Ravidasvir Samatasvir Velpatasvir Daclatasvir Elbasvir
Ledipasvir
Sofosbuvir and ledipasvir fixed drug combination of an NS5B polymerase inhibitor and an
NS5A inhibitor Daily once tablet containing 400 mg of sofosbuvir and 90 mg of ledipasvir
Q.20 The epidemiology of HIV, persons with increased risk of HIV

infection
DEFINITION: HIV (human immunodeficiency virus) is a virus that attacks the body’s immune
system. If HIV is not treated, it can lead to AIDS (acquired immunodeficiency syndrome.
EPIDEMIOLOGICAL DATA:
HIV is spread primarily by unprotected sex (including anal and oral sex), contaminated blood
transfusions, hypodermic needles, and from mother to child during pregnancy, delivery, or
breastfeeding. Some bodily fluids, such as saliva, sweat and tears, do not transmit the virus. South
Africa, Nigeria, India, South East Asia, Carribbean Sea, Eastern Europe
EPIDEMIOLOGY
● Ways of transmission: Sexual contact, iv drug abusers, infection of medical personal
RISK GROUP
● Homosexuals unprotected sex
● Multi sexual partners (prostitutes), unprotected sex
● IV drug abusers
● Infected mothers to child
● Viral Hepatitis B, C, D
● Recipients of blood transfusion or organs
Q.21 Clinical stages of HIV infection, its stages.

CLINICAL STAGES-
● Stage 1: asymptomatic, persistent generalized lymphadenopathy. Level of functional ability
1: asymptomatic course and normal course of daily activity
● Stage 2: Weight loss less than 10%, minimum defeat of skin and mucous (seborrhea dermatitis,
mycotic defeat of nails, recurrent ulcers of mucous of oral cavity, angular cheilitis i.e,
inflammation of one or both corners of the mouth).
Episodes of herpes zoster, recurrent episodes of upper respiratory tract (bacterial sinusitis),
Level of functional ability 2 (WHO: performance status 2): symptomatic course, normal level
of daily activity
● Stage 3: weight loss > 10%, hyperthermia more than 1 month, pneumocyst pneumonia,
cerebral toxoplasmosis, extrapulmonary criptococosis, cryptosporidiosis with diarrhea more
than 1 month.
Cytomegalovirus infection with defect of any organs except liver, spleen and lymph nodes.
Level of functional ability 3 (Performance status 3): patient lay in bed less than 50% of daily
time
● Stage 4: Severe weight loss, cerebral toxoplasmosis. Pneumocystic carinii pneumonia (jirovacii
pneumonia), cryptosporidiosis with diarrhea.
Cytomegalovirus infection involving all organs except liver and spleen.
Kaposi Sarcoma, invasive cervical carcinoma. Progressive multifocal leukoencephalopathy,
atypical mycobacteriosis.
Non-typhoid salmonella bacteremia, HIV encephalopathy, disseminated mycosis.
Extra pulmonary TB
Level functional ability: full bed rest.
Decreased T-helpers less than 0.5X10^9.
Q.22 Opportunistic infections at AIDS.
Acquired immunodeficiency syndrome (AIDS) is a chronic, potentially life-threatening
condition caused by the human immunodeficiency virus (HIV). By damaging your immune
system, HIV interferes with your body's ability to fight infection and disease.
OPPORTUNISTIC INFECTIONS:
● Pneumocystis pneumonia
● Toxoplasma gondii
● Microsporidiosis
● Disseminated mycobacterium infection
● Bartonellosis
● Mucosal candidiasis
● Cryptococcal meningitis
● Herpes simplex with chronic ulcers,
Q.23 Epidemiological and clinical criteria for the diagnosis of

HIV infection.
EPIDEMIOLOGICAL DATA:
HIV is spread primarily by unprotected sex (including anal and oral sex), contaminated blood
transfusions, hypodermic needles, and from mother to child during pregnancy, delivery, or
breastfeeding.
Some bodily fluids, such as saliva, sweat and tears, do not transmit the virus.
South Africa, Nigeria, India, South East Asia, Carribbean Sea, Eastern Europe
• Source of infection: sick people and carriers
• Mechanism of transmission: contact
• Ways of transmission: Sexual contact, iv drug abusers, infection of medical personnel
CLINICAL DATA:
● prolonged fever more than 1 month
● generalized lymphadenopathy: more than 3 lymph nodes enlarged in different anatomical
groups of lymph nodes
● Diarrhea more than 1 month
● weight loss more than 10%
● opportunistic infection,
● Wasting syndrome (cachexia)
Q.24 Laboratory diagnosis of HIV infection.
DEFINITION - HIV (human immunodeficiency virus) is a virus that attacks the body’s immune
system. If HIV is not treated, it can lead to AIDS (acquired immunodeficiency syndrome
LABORATORY DIAGNOSIS:
● Stage 1: Lab confirmation of HIV infection with no AIDS defining condition and CD4 + T
lymphocyte count of > 500 cells/ micro litre or CD4+ T lymphocyte percentage of total
lymphocytes of > 26%
● Stage 2: Lab confirmation of HIV infection with no AIDS defining condition and CD4 + T
lymphocyte count of 200-499 cells/micro litre or CD4 + T lymphocyte percentage of total
lymphocytes of 14-25%
● Stage 3 (AIDS; greater than 6years): Lab confirmation of HIV infection and CD4 + T
lymphocyte count less than 200 cells/micro litre or CD4 + T lymphocyte percentage of total
lymphocytes of less than 14%.
● Stage 3 defining opportunistic illnesses in HIV: bacterial infections (multiple or recurrent in
children), candidiasis of bronchi, trachea, lungs, or esophagus. Cervical cancer invasive in
adults, adolescents. Coccidioidomycosis, disseminated or extrapulmonary. Extrapulmonary
cryptocorccosis, cryptosporidiosis (chronic intestinal> 1 month)
Q.25 Etiological treatment of HIV infection.

DEFINITION - HIV (human immunodeficiency virus) is a virus that attacks the body’s immune
TREATMENT-ANTIRETROVIRAL DRUGS
● Nucleoside and Nucleotide reverse transcriptase inhibitors (NRTI):
Abacavir 300 mg twice daily, Didanosine, Lamivudine 300 mg once daily,
● Non-nucleoside Reverse transcriptase inhibitor (NNRTI)- Delaviridine, Efavirenz,
Nevirapine
● Protease Inhibitors:
Atazanavir + Ritonavir; 300mg + 100mg once daily.
Darunavir, Fosamprenavir, Indinavir, Lopinavir, Nelfinavir, Saquinavir, Tipranavir
● Integrase Strand Inhibitors (INST):
Dolutegravir, Elvitegravir and Raltegravir.
● Fusion inhibitors: Enfuvirtide
● Chemokine receptor antagonists: Maraviroc
Q.26 The basic treatment of opportunistic infections.

An infection that occurs because of a weakened immune system.
● Protozoa: Bactrim, pirimethamine sulfametoxazol, metronidazole,
● Mycosis: Amphotericin B, Ketoconazole, Fluconazole
● Pneumocystic pneumonia: co-trimoxasole
● Herpetic infection: Acyclovir, Vaaltrex, Zovirax, Interferon, Laferon
● CMV infection: Ganciclovir, forscanet
● Bacterial: Antibiotic: macrolides, cephalosporin, aminoglycosides
● Pathogenetic and symptomatic treatment
Q.27 The epidemiology of malaria.

Malaria; An infectious disease caused by protozoan parasites from the Plasmodium family that can
be transmitted by the bite of the Anopheles
EPIDEMIOLOGY
Infectious agent: Plasmodium Falciparum, P.vivax, P.ovale, P.malariae, P.knowlesi
Incubation period: 7-30 days
Source of infection: Sick people, carrier
Mechanism of transmission: blood, transplacenta*congenital transmission
Vectors: Female mosquitos of anopheles genus.
Season: summer autumn
Q.28 The pathogenesis of malaria attacks.
Malaria; An infectious disease caused by protozoan parasites from the Plasmodium family that
can be transmitted by the bite of the Anopheles
● Mosquito infects a person by taking a blood meal. They release sporozoites from their
salivary glands. Infects the organism in 2 phases
● Exoerythrocytic phase: sporozoutes enter blood stream and migrate to hepatic system. In
hepatocytes they multiply into merozoites, rupture the liver cells and escape into blood stream
● Erythrocytic phase: the merozoites infect the red blood cells where they develop into ring
forms Trophozoites and schizonts which in turn produce more merozites.
PATHOGENESIS
- Tissue schizogony (incubation period)
- Erythrocyte schizogony
- Typical attack- massive destruction of erythrocytes, massive appearance of parasites and
products of their metabolism
- Disturbance of thermoregulation centre, increasing of vessels penetration
- Disturbance of microcirculation, water electrolytes balance, vegetative neurotic system -
Development of hemolytic anemia
- Hepatosplenomegaly
- Developmnt of coma
An attack of malaria may either be a primary attack or a relapse.

A primary attack normally develops after an incubation period of 10-14 days; by direct blood
inoculation it is about 11 days.
Relapses are defined as recurrences of malarious symptoms and the reappearance of malaria
parasites in the peripheral blood, following recovery from the initial attack.
Q.29 The types of temperature curves at different forms of malaria.

be transmitted by the bite of the Anopheles
FEVER CHARACTERISTIC
● Febris intermittens; It is alternating fever. It is characterized by the rising periods of
temperature (paroxysmuses) with the periods of normal temperature (apirrhexions).
Temperature rises to 40 °С and goes down to the norm and rises again.
● The paroxysmuses can arise every fourth day (febris quartana), every third day (febris
tertiana) or daily (febris quotidiana). Periodicity of the temperature rise depends on duration of
development cycle of malarial Plasmodium
STAGES OF FEVER DEVELOPMENT
● Premonitory stage: patient may feel headache, arthralgia, nausea, vomiting
● Cold stage (1-2hours): patient feels very cold, shivers and wraps themselves in blankets.
Fingers shriveled and goose skin. This is only subjective because temperature is still rising.
Vomiting. Urine is abundant with micturition.
● Hot stage (3-4 hours): shivering episodes and alternates with sensations of great heat. Face is
flushed, pulse is full, intense headache. Vomiting, tachypnea. Skin is dry and burning with
temperature 40-41 degrees
● Sweating stage (2-4 hours): Profuse perspiration with sweat running off him in streams,
saturating clothes and bedding. With sweating headache declines, temperature is subnormal
until the next paroxysm.
Q.30 Clinical signs of malaria.

Malaria; An infectious disease caused by protozoan parasites from the Plasmodium family that
can be transmitted by the bite of the Anopheles
CLINICAL SIGNS
● Cyclical occurrence of coldness followed by rigor and then fever and sweating lasting 4-6
hours every 2 days in P.vivax and P.ovale infections, while every 3 days for P.malariae,
P.falciparum can have recurrent fever every 36-48 hours or less.
● Shivering, arthralgia
● Anemia and jaundice. because of the loss of red blood cells, hemoglobinuria
● Retinal damage
● Convulsions
● P.falciparum causes severe malaria: coma, splenomegaly, severe headache, cerebral ischemia,
hepatomegaly, hypoglycemia and hemoglobinuria with renal failure.
Q.31 Differential diagnosis of malaria and leptospirosis.
o Malaria; An infectious disease caused by protozoan parasites from the Plasmodium family
that can be transmitted by the bite of the Anopheles
o Leptospirosis is a blood infection caused by the bacteria Leptospira. Signs and symptoms can
range from none to mild (headaches, muscle pains, and fevers) to severe (bleeding in the lungs
or meningitis)
Q.32 Differential diagnosis of malaria with viral hepatitis.
o Malaria; An infectious disease caused by protozoan parasites from the Plasmodium family that
can be transmitted by the bite of the Anopheles.
o Viral hepatitis is liver inflammation due to a viral infection. The most common causes of viral
hepatitis are the five unrelated hepatotropic viruses hepatitis A, B, C, D, and E.
Parameter Malaria Viral hepatitis
Transmission Mosquito Fecal-oral, contact

Incubation period Max 21 days 2 weeks- 6 months
Fever Undulating high fever with cold, Subfebrile

hot and sweating phases
Signs and headache, malaise, myalgia, Fever, malaise, arthralgia, anorexia,
symptoms anorexia, chills, faints, rigors. nausea, abdominal pain, diarrhoea,
Jaundice with itching.
hepatosplenomegaly in severe Jaundice, hepatosplenomegaly
cases
Lab abnormalities Anemia, thrombocytopenia, Increased ALT, AST

hypoglycemia
Q.33 Complications of malaria.

be transmitted by the bite of the Anopheles.
COMPLICATIONS-
● Plasmodium falciparum: Cerebral Malaria (seizures and coma), acute renal failure, non
cardiogenic pulmonary edema, tropical splenomegaly
● Plasmodium Vivax: late splenic rupture (2-3 months after initial infection)
● Plasmodium Malariae: immune complex glomerulonephritis
● In pregnant women it can lead to still birth, infant mortality, low birth weight
Q.34 The principles of malaria treatment.
TREATMENT-
● Plasmodium Falciparum:
Artmether (20mg Lumefantrine(120mg),
Atovaquone (250mg)-proguanil (100mg), 4 tablets 4 times a day for 3 days.
mefloquine(250mg). Or Quinine Sulfate plus doxycycline, tetracycline, clindamycin.
Hydroxychloroquine 620mg
● P.vivax, P.ovale: chloroquine plus primaquine
● P maleriae, P.Knowlesi: chloroquine
● Severe cases: artesunate-quinine
● No diet diet or activity restrictions
● quinine and clindamycin is the recommended treatment for women in the first trimester of
pregnancy
Q.35 Prevention of malaria.

Mechanism of transmission: Transmissive
PREVENTIONS-
Eradication of mosquito is the primary aim.
● Avoid mosquito bites
● Sleep in rooms properly screened with gauze over windows and doors
● Spray room with insecticides before entering
● Wear long sleeve shirts
● Use mosquito repellant cream
● Clean environment by getting rid of mosquito breeding sites
● Take antimalarial drugs when prescribed by doctor
Q.36 The epidemiology of brucellosis.

DEFINITION- Brucellosis is a bacterial infection that spreads from animals to people caused by a
type of bacteria called Brucella. Most commonly, people are infected by eating raw or
unpasteurized dairy products.
EPIDEMIOLOGY-
Source of infection: Brucella Melitensis, Abortus, suis, canis
Factors of transmission: Zoonosis (goat, cow, sheep, dog, pig, camel, rodents), unpasteurized milk
Mechanism of transmission: air borne, fecal oral, contact
The incubation period is highly variable, usually 2-4 weeks, can be 1 week to 2 months or longer.
CLINICAL MANIFESTATIONS-
Fever, Chills, Loss of appetite, Sweats, Weakness, Fatigue, Joint, muscle and back pain, Headache.
Q.37 Clinical classification of brucellosis.

DEFINITION- Brucellosis is a bacterial infection that spreads from animals to people caused by a
type of bacteria called Brucella. Most commonly, people are infected by eating raw or
unpasteurized dairy products.
CLASSIFICATION-
● Subclinical: usually asymptomatic
● Acute 2-3months
● Subacute 3-12months
● Chronic: 1 year: low grade fevers and neuropsychiatric symptoms predominate
● Relapsing: every 2-3months.
CLINICAL FEATURES:
● GI symptoms: nausea, vomiting, constipation, diarrhea, abdominal pain
● Pulmonary symptoms: dry cough, pleural effusion
● Chest signs: hilar lymphadenopathy, pleural effusion, pneumothorax, lung nodules
● Generalized lymphadenopathy
● Men can have testicular pain
● Arthralgia of knees, hips and spine
● Focal CNS symptoms in severe cases: mild to moderate neuropsychiatric symptoms, headache,
fatigue, depression
● Uncommon signs: red eye, cranial nerve palsy, neck stiffness (meningoencephalitis),
● Skin rash: non-specific maculopapular rash
Q.38 Laboratory diagnosis of brucellosis.
Brucellosis is a bacterial infection that spreads from animals to people caused by a type of bacteria
called Brucella. Most commonly, people are infected by eating raw or unpasteurized dairy products
of an infected animal.
CLINICAL MANIFESTATIONS:
Fever, Chills, Loss of appetite, Sweats, Weakness, Fatigue, Joint, muscle and back pain, Headache.
LAB TESTS
● Blood culture in Castaneda’s medium
● Serological: ELISA, agglutination, microagglutination, PCR
● CSF, synovial fluid analysis: increased protein, low glucose, lymphocytes predominate
● CSF culture, synovial fluid culture
● CBC: anemia, thrombocytopenia, leukopenia or leukocytosis more prominent is leukopenia
● Liver function test: slight increase AST, ALT
Q.39 Differential diagnosis of brucellosis and flu.

o Brucellosis is a bacterial infection that spreads from animals to people caused by a type of
bacteria called Brucella. Most commonly, people are infected by eating raw or unpasteurized
dairy products of an infected animal.
Clinical manifestations; Fever, Chills, Loss of appetite, Sweats, Weakness, Fatigue, Joint,
muscle and back pain, Headache.
o Influenza; commonly called "the flu", is an infectious disease caused by influenza viruses.
Symptoms range from mild to severe and often include fever, runny nose, sore throat, muscle
pain, headache, coughing, and fatigue.
Brucellosis Flu
Transmission ingestion of unpasteurized goat milk Air droplets
Fever Fever with relative bradycardia Severe
Signs and anorexia, asthenia, fatigue, weakness, Dry cough, rhinitis,

symptoms malaise. Bone and joint pain. headache, tracheitis,
Neuropsyciatric symptoms. Can be myalgia, malaise, catarrhal
abdominal pain, constipation, diarrhea signs
Diagnosis Anemia, Serology Nasopharyngeal swab,
leukopenia with
lymphocytosis
Q.40 Treatment of brucellosis.

Brucellosis is a bacterial infection that spreads from animals to people caused by a type of bacteria
called Brucella. Most commonly, people are infected by eating raw or unpasteurized dairy products
of an infected animal.
Clinical manifestations: Fever, Chills, Loss of appetite, Sweats, Weakness, Fatigue, Joint, muscle
and back pain, Headache.
TREATMENT-
● No diet or activity restriction
● Gentamycin 5mg/kg/d IV or IM 10-14 days
● Streptomycin 1g IM/d 10-14 days
● Doxycycline 100mg orall bid 10-14 days
● Quinolones and rifampin
● Doxycycline, rifampin therapy
● Tripple therapy: above drugs plus amino glycoside
● Pregnant women: Rifampin 600mg orally daily for 6 weeks
● Neurological manifestation: treat 3-6months: triple therapy with ceftriaxone
Q.41 Clinical signs of sepsis.

Sepsis is a potentially life-threatening condition that occurs when the body's response to an
infection damages its own tissues.
CLINICAL SIGNS-
● Complaints: weakness, headache, pain in joints, chills, dry mucous membranes and poor appetite,
dry coated tongue. Dizziness, confusion
● Slurred speech
● Nausea, vomiting, diarrhea
● Hectic fever
● Skin is pale, moist or icteric in severe cases. Cold clammy skin.
● Rashes of different types, mostly hemorrhagic. Others can be present too. Localized anywhere on
the body
● Tachycardia, hypotension. Systolic murmur at apex. Heart is enlarged
● Dyspnea, tachypnea
● Hepatosplenomegaly
● Low urine output
● Loss of consciousness
Q.42 The epidemiology of epidemic typhus and Brill-Zinsser disease.

DEFINITION- Epidemic typhus is caused by Rickettsia prowazekii. Symptoms are prolonged
high Fever, intractable headache and maculopapular rash.
Brill-Zinsser disease is a recrudescence of epidemic typhus, occurring years after an initial attack.
EPIDEMIOLOGY-
Epidemic typhus occurs in Central and South America, Africa, northern China, and certain regions
of the Himalayas. Outbreaks may occur when conditions arise that favor the propagation and
transmission of lice.
Brill-Zinsser disease develops in approximately 15% of people with a history of primary epidemic
typhus.
● Etiology: Rickettsia prowazekii
● Source of infection: sick person
● Mechanism of transmission: transmissive
● Vectors: Pediculus humanus (human lice)
● Incubation period: 1-2 weeks
Brill zinesser disease

Delayed relapse of epidemic typhus
Onset of epidemic typhus is abrupt and occurs 7 to 14 days after exposure, whereas
Brill Zinsser disease can occur >40 years after primary infection
Q.43 Clinical signs of epidemic typhus.

Epidemic typhus is caused by Rickettsia prowazekii. Symptoms are prolonged high Fever,
intractable headache and macolopapular rash.
CLINICAL SIGNS-
● Abrupt onset of high fever, chills, headache, myalgia, malaise. Fever worsens and quickly
becomes unremitting. Fever on days 3-4, 8-9, 12-13.
● Giddiness, backache, anorexia, nausea.
● Face is edematous, flushed. Eyes are brilliant with injected sclera (rabbits eyes)
● Symptom of Rosenberg: Ptechial enanthema on basis of uvula 2-3rd day of disease. May be on
transitive folds of conjunctiva from third-fourth day (symptom of KjaryAcuyne)
● Govorov-Godeljae symptom: tremor of tongue declining to side.
● Rash: maculopapular/ petechial rash on 4-7 day on chest then axilla, trunk and spread
peripherally. Never on face. Disappears with decreasing temperature
● Rigors, myalgia, malaise
● CNS symptom: mental dullness to coma, stupor, sensitivity to light and delirium
● Regional and generalized lymphadenopathy. Mild hepatosplenomegaly
Q.44 Clinical features of Brill-Zinsser disease.

It occurs due to reoccurrence of epidemic louse-borne typhus caused by Rickettsia prowazekii years
after initial attack.
Brill-Zinsser disease can occur >40 years after primary infection It has same clinical presentation as
Epidemic typhus but milder.
● Abrupt onset of high fever,chills, headache (unremitting).
● Enanthema **
● Rash: maculopapular/ petechial rash on 4-7 day on chest then axilla, trunk and spread peripherally
● Rigors, myalgia, malaise
● CNS symptom: mental dullness to coma, stupor, sensitivity to light and delirium
● Regional and generalized lymphadenopathy. Mild hepatosplenomegaly
Q.45 Complications of epidemic typhus.
DEFINITION-Epidermic Typhus also called louse-borne typhus, is an uncommon disease caused
by a bacteria called Rickettsia prowazekii.
Epidemic typhus is spread to people through contact with infected body lice.
It’s complications include
● Vasculitis which may result in hypovolemia
● Thromboses of various vessels
● Bronchitis, pneumonia,
● Otitis media
● Parotitis
● nephritis
Q.46 Laboratory diagnosis of epidemic typhus and Brill-Zinsser

disease.
Epidermic Typhus also called louse-borne typhus, is an uncommon disease caused by a bacteria
called Rickettsia prowazekii.
Brill-Zinsser disease occurs due to reoccurrence of epidemic louse-borne typhus caused by
Rickettsia prowazekii years after initial attack. So,
Suspect epidemic typhus based on clinical manifestations and signs of louse infestation; such as
abrupt headaches and fever , hepatomegaly, maculopapular rashes etc
We can confirm with fluorescent antibody staining of skin biopsy.
Can only be made by serological
● Complement fixation test
● Indirect hemagglutination
● Indirect immunofluorescens
Q.47 Differential diagnosis of epidemic typhus with typhoid fever.
Typhoid fever: It's caused by a bacterium called Salmonella typhi, which is related to the bacteria
that cause salmonella food poisoning.
Q.48 Differential diagnosis of epidemic typhus with leptospirosis.

o Epidemic typhus caused by Rickettsia prowazekii occurs after being bitten by a tick or louse,
can only be transferred human to human: presented by high fever, cough, rash, muscles and joint
pain. Sometimes liver and spleen can be enlarged. Eyes look like Rabbits eye.
Enanthema on uvula, tremor of tongue.
Diagnosed by serology
o Leptospirosis is a non rickettsial infection, blood infection caused by the bacteria Leptospira
that at some time during its course may mimic louse- borne typhus (epidemic typhus)
Leptospirosis generally presents after contact with urine of infected animals.
with cough, jaundice, chest pain, lymphadenopathy, hepatosplenomegaly
diagnosed by PCR.
Q.49 Treatment of epidemic typhus and Brill-Zinsser disease.
Brill-Zinsser disease occurs due to reoccurrence of epidemic louse-borne typhus caused by
Rickettsia prowazekii years after initial attack.
TREATMENT-
● Etiotropic therapy: tetracycline (0.3-0.4g), chloramphenicol (0.5g) four times a day
● Pathogenetic treatment: heart (corglycon, strophantin), Vascular (cordiamin, ephedrine,
mezaton).
● Syptomatic therapy
● Desintoxication and dehydrative therapy
Q.50 Epidemiology of Lyme borreliosis.

Lyme borreliosis also known as Lyme disease, is an infectious disease caused by the Borrelia
bacterium which is spread by ticks.
Etiology: Borrelia burgdorferi Epidemiology:
● Source of infection: ticks, Zoonosi
● Infective agent: Borrelia burgdorferi
● Mechanism of transmission: transmissive, vectors
● Vectors: tick ixode
● Incubation period: 1-2 weeks
- The disease is currently recognized as the most common vector-borne disease in Europe and North
America
- Registration of Lyme borreliosis in humans in Ukraine began in 2000. It was proved that the
incidence of the disease in the country was growing each year from 58 cases in 2000 (incidence:
0.12/100,000) to 3413 in 2015 (incidence: 7.96/100,000) (2).
- The western part of Ukraine, including the Ternopil area, is recognised as an endemic region for
LB, as it is located in the forest-steppe region with mixed forests, fertile soils, as well as adequate
moisture and optimal temperatures.
Q.51 The epidemiology of tick-borne encephalitis (TBE)

DEFINITION - Tick-borne encephalitis (TBE) is a human viral infectious disease involving the
central nervous system. The virus is transmitted by the bite of infected ticks.
Etiology (infective agent): Flavivirus
EPIDEMIOLOGY
● Source of infection: vector, zoonosis (squirrels, moles, porcupines, rats, field mouse)
● Mechanism of transmission: focal transmissive, vector
● Vectors: Tick
● It is endemic in focal areas of Europe and Asia.
● Russia is the largest number of reported tick-borne encephalitis cases and western Siberia has
the highest incidence of tick-borne encephalitis in the world
● Most cases appear from April through November
● Incidence and severity of disease are highest in people aged ≥ 50 years.
Q.52 Clinical Stages of Lyme borreliosis.

Lyme disease, also known as Lyme borreliosis, is an infectious disease caused by the Borrelia
THE CLINICAL STAGES ARE
Stage 1: Early localized disease:
- Symptoms of Lyme disease usually start 1 to 2 weeks after the tick bite.
- One of the earliest signs of the disease is a bull’s-eye rash. (Erythema migrans)
- The rash can occur with or without systemic viral or flu-like symptoms.
- Other symptoms commonly seen in this stage of Lyme disease include: chills, fever, enlarged
lymph nodes, sore throat, vision changes, fatigue, muscle aches, headaches
Stage 2: Early disseminated Lyme disease
- Occurs several weeks to months after the tick bite.
- general feeling of being unwell, and a rash may appear in areas other than the tick bite.
- This stage of the disease is primarily characterized by evidence of systemic infection, which
means infection has spread throughout the body, including to other organs.
Symptoms can include:
1. multiple erythema multiforme (EM) lesions
2. disturbances in heart rhythm, which can be caused by Lyme carditis
3. neurologic conditions, such as numbness, tingling, facial and cranial nerve palsies, and meningitis
- The symptoms of stages 1 and 2 can overlap.
Stage 3: Late disseminated Lyme disease
Occurs when the infection hasn’t been treated in stages 1 and 2.
Stage 3 can occur months or years after the tick bite.
This stage is characterized by:
1. arthritis of one or more large joints
2. brain disorders, such as encephalopathy, which can cause short-term memory loss, difficulty
concentrating, mental fogginess, problems with following conversations and sleep disturbance
3. numbness in the arms, legs, hands, or feet
Q.53 The main symptoms in the initial period of Lyme borreliosis.

The main symptoms include:
• Circular, outwardly expanding rash erythema migrans at site of tick bite
• Rash is red, warm and painless, Innermost portion remains dark red and becomes indurated, the
outer edge remains red. The portion in between clears giving the appearance of a red oval or
bulls eye
• Red rash occurs at the site of the tick bite, usually, but not always, has a central red spot
surrounded by a clear spot with an area of redness at the edge…. Having the appearance of a red
oval or a bull eye. The rash usually is painless
• Flu like symptoms: headache, muscle soreness, fever and malaise
Q.54 Methods of Lyme disease specific diagnosis.

• Source of infection: ticks, Zoonoyic
• Infective agent: Borrelia burgdorferi
• Mechanism of transmission: transmissive, vectors
• Vectors: tick ixode
• Incubation period: 1-2 weeks
The most common sign of infection is an expanding red rash, known as erythema migrans, that
appears at the site of the tick bite about a week after it occurred.
METHODS FOR DIAGNOSIS
Usually based on History of tick bites or bulls eye rash, endemic areas.
Serological tests: Western blot and ELISA or PCR of blood via venipuncture or CSF
Q.55 Etiological therapy of Lyme borreliosis.
ETIOLOGICAL THERAPY-
1. To treat the Erythrema migrans: we give doxycycline 100mg PO bid 10-15 days,
Amoxicillin 500mg P0 tid, Cefuroxime: 500mg bid.
If allergy to above give Azithromycin 500mg single dose, erythromycin 500mg qid
clarithromycin.
2. AV block, CNS: IV antibiotics ceftriaxone 2g IV once/day 14 days.
Benzylpenicillin IV or IM 2.4g every 4-6hours. Cefotaxime 2g tid.
3. To treat Arthritis:
antibiotic + NSAID, diclofenac 50mg tid, ibuprofen 300-400mg tid (max 2400mg).
Recurrent arthritis: antibiotics + arthroscopic synovectomy + intraarticular injection.
Q.56 Emergent prevention of Lyme borreliosis.

PREVENTIONS INCLUDE:
o Application of DEET cream 20-30% on skin before going out
o Permethrine spray on clothes
o Shower within 2hours after coming indoors
o Patients are advised to call the doctor if they experience fever or rash
o After exposure to tick, promptly remove attached ticks without crushing tick before transmission
of Borrelia spirochetes and wash area with antiseptics, soaps and water.
o Give an Antimicrobial prophylactics after tick bites such as doxycycline within 72 hours 100mg
single dose.
o Carefully inspect the entire body and remove any attached ticks. Ticks may feed anywhere on the
body.
o Tick bites are usually painless and, consequently, most people will be unaware that they have an
attached tick without a careful check.
Q.57 Classification of erysipelas.
Erysipelas is an infection of the upper layers of the skin (superficial).
The most common cause is group A streptococcal bacteria, especially Streptococcus pyogenes.
Erysipelas results in a fiery red rash with raised edges that can easily be distinguished from the
skin around it.
CLASSIFICATION
• According to etiology:
- Streptococcal Group A
- Streptococcal group B
- Staphylococcus
• According to clinical form (i.e. The character of local changes):
- Erysipelas erythematosum
- Erysipelas vasiculosum
- Erysipelas haemorrhagicum
- Erysipelas abscedens
- Erysipelas gangrenosus
• According to complication:
- Local (abscess, gangrene, thrombophlebitis, phlegmona, necrosis, ulcers, suppuration of the
contents of bullas, elephantiasis)
- General (sepsis, nephritis, pneumonia)
• According to frequency:
- Primary
- Recurrent
- Relapsing
• According to severity:
- Mild
- Moderate
- Severe
• According to localisation:
- Face
- Extremities
- Mucous membranes
Q.58 Clinic of erysipelas erythematous form.

Erysipelas is a human infectious disease infectious disease of streptococcal etiology with acute
and chronic forms and is characterized by intoxication syndrome and local changes looking like
circumscribed locus of serous hemorrhagic inflammation of skin
Clinical signs of the erythematous form is:
• It has an acute onset
• Intoxication syndrome (High fever, shaking, chills, fatigue, headache, vomiting
• Early signs of the disease before the local changes include:
1. Regional lymphadenitis and lymphangitis
2. Burning pain in erysipelas Can occur on skin of face that starts 5-6 hours before the local
inflammatory focus forms
• Local process is characterized by sharply circumscribed hyperemia with peripheral inflammatory
wall, edge painfulness, and local temperature reactions (erythematous forms )
• Local process is associated with lymphatic edema of various degree.
• Re-infection causes lymphadenitis
Q.59 Treatment of primary erysipelas.

Erysipelas is a human infectious disease infectious disease of streptococcal etiology with acute
and chronic forms and is characterized by intoxication syndrome and local changes looking like
TREATMENT
• Etiotropic therapy
- Penicillin is the antibiotic of choice
- Depending on the severity can be given for 7 days, 10 days or 14 days
• Pathogenetic therapy
Detoxification therapy→
- Oral – (enterodez, regidron, etc)
- Parenteral – crystalloids (polyionic solutions, trisol, 5% glucose etc) and Low molecular
colloids
Desensibilisation therapy→ Antihistamine drugs ( dimerol , tavegil, suprastin , pipolfen)
Correction of the Haemostasis alterations according to the coagulogram control: disaggregants
(eg. Trental etc), direct acting anticoagulant (eg. Heparin, fraxiparin, calciparin etc), indirect
acting anticoagulant kumadin, pelentan, etc)
Immunocorrection with the control of the control of immune status (Immunoglobulins IV and
IM, interferons, primidines (eg. Methyluracil)
• Local treatment
- Don’t touch erythematous forms
- Emulsions, Ointments and antiseptic solutions are meant only for bullous forms
• Ambulatory monitoring:
- finishing treatment
- Sanitation of the chronic focuses of infection
- Relapse prophylaxis: bicillin once a month for 6 months after disease
1. Penicillin G: 0.6-1.2 million U IM bid for 10 days
2. Dicloxacillin 125-500mg PO qid for 10days
3. Nafcillin 1-2g IV qid for 7 days
Q.60 Treatment of recurrent forms of erysipelas.
Erysipelas is a human infectious disease infectious disease of streptococcal etiology with acute and
chronic forms and is characterized by intoxication syndrome and local changes looking like
TREATMENT
• Etiotropic therapy
- Penicillin is the antibiotic of choice
- Depending on the severity can be given for 7 days, 10 days or 14 days
• Pathogenetic therapy
Detoxification therapy→
- Oral – (enterodez, regidron, etc)
- Parenteral – crystalloids (polyionic solutions, trisol, 5% glucose etc) and Low molecular
colloids
Desensibilisation therapy→ Antihistamine drugs ( dimerol , tavegil, suprastin , pipolfen)
Correction of the Haemostasis alterations according to the coagulogram control: disaggregants
(eg. Trental etc), direct acting anticoagulant (eg. Heparin, fraxiparin, calciparin etc), indirect
acting anticoagulant kumadin, pelentan, etc)
Immunocorrection with the control of the control of immune status (Immunoglobulins IV and
IM, interferons, primidines (eg. Methyluracil)
• Local treatment
- Don’t touch erythematous forms
- Emulsions, Ointments and antiseptic solutions are meant only for bullous forms
• Ambulatory monitoring:
- finishing treatment
- Sanitation of the chronic focuses of infection
- Relapse prophylaxis: bicillin once a month for 6 months after disease
1. Penicillin V 2million units daily for 8 days then
2. Penicillin V 1 million units daily for 3 weeks
Q.61 Epidemiology of nosocomial infections.

A nosocomial infection is contracted because of an infection or toxin that exists in a certain location,
such as a hospital. People now use nosocomial infections interchangeably with the terms health-care
associated infections (HAIs) and hospital acquired infections.
• Etiology: Most common causes are Pseudomonas aeruginosa and E.coli, Methicillin resistant
staphylococcus resistant aureus. Clostridium difficile, TB
• Source of infection: sick people
• Mechanism of transmission: contact, droplet, airborne, fecal oral
Some common bacteria and the type of infection that they cause:
• Staphylococcus aureus (S. aureus) - blood
• Escherichia coli (E. coli) – UTI
• Enterococci - blood, UTI, wound
• Pseudomonas aeruginosa (P. aeruginosa) - kidney, UTI, respiratory
Incidence of nosocomial infections
The most common nosocomial infection was pneumonia (517 cases, 64%), followed by sepsis (106
cases, 13%), wound infection (102 cases, 13%), urinary tract infection (43 cases, 5%) and catheter-
related bloodstream infection (42 cases, 5%).
Q.62 Clinical classification of toxoplasmosis.

Toxoplasmosis is a disease that results from infection with the Toxoplasma gondii parasite, one of
the world's most common parasites. Infection usually occurs by eating undercooked contaminated
meat, exposure from infected cat feces, or motherto-child transmission during pregnancy.
CLASSIFICATION:
1. Acute
2. Congenital
Based on duration of symptoms:
• Acute: If the duration of symptoms is less than 4-6 weeks
• Chronic: If the symptoms persist for more than 6 weeks
Based on organs involved:
• Neurotoxoplasmosis
• Pulmonary toxoplasmosis
• Occular toxoplasmosis
There are three forms of Toxoplasma gondii:
1. the tachyzoite (the rapidly reproducing form),
2. the bradyzoite (a slower reproducing form contained in tissue cysts), and
3. the sporozoite (contained in oocysts).
Q.63 Peculiarities of toxoplasmosis at pregnancy and congenital

toxoplasmosis.
Congenital toxoplasmosis is a group of symptoms that occur when an unborn baby (fetus) is infected
with the parasite Toxoplasma gondii.
Peculiarities of toxoplasmosis at pregnancy:
• Pregnant women generally are asymptomatic or have flu like symptoms. Higher risk of
transmission to infant. Can lead to premature birth
• Congenital toxoplasmosis:
- Cerebral calcifications
- Microcephaly
- Hydrocephaly
- Bilateral Chorioretinitis
- Convulsions
- Other: organomegaly, jaundice, rashes and fever, psychomotor retardation
Q.64 Laboratory diagnosis of toxoplasmosis.
DEFINITION - Toxoplasmosis is a disease that results from infection with the Toxoplasma gondii
parasite, one of the world's most common parasites. Infection usually occurs by eating undercooked
contaminated meat, exposure from infected cat feces, or mother-to-child transmission during
pregnancy.
LABORATORY DIAGNOSTICS:
• The demonstration of the Toxoplasma gondii organism in blood, body fluids, or tissue.
• Detection of Toxoplasma gondii antigen in blood or body fluids by enzyme-linked immunosorbent
assay (ELISA) technique.
• The Sabin-Feldman dye test: is a sensitive and specific neutralization test. It measures IgG antibody
and is the standard reference test for toxoplasmosis. High titters suggest acute disease.
• Serologically: IgM fluorescent antibody test detects IgM antibodies within the first week of
infection, but titters fall within a few months.
• PCR on body fluids, including CSF, amniotic fluid, and blood.
• Skin test results showing delayed skin hypersensitivity to Toxoplasma gondii antigens.
• Antibody levels in aqueous humour or CSF may reflect local antibody production and infection.
• Animal inoculation: inoculation of suspected infected tissues into experimental animals.
• Culture: inoculation of suspected infected tissues into tissue culture.
Q.65 Treatment principles of patients with congenital and acquired

toxoplasmosis.
DEFINITION - Toxoplasmosis is a disease that results from infection with the Toxoplasma gondii
parasite, one of the world's most common parasites. Infection usually occurs by eating undercooked
contaminated meat, exposure from infected cat feces, or mother-to-child transmission during
pregnancy
Treatment of congenitally infected neonates:
• Daily oral pyrimethamine (1 mg/kg) and sulfadiazine (100 mg/ kg) with folinic acid or 1 year.
• Depending on the signs and symptoms, prednisone (1 mg/kg per day) may be used or congenital
infection
Treatment of acquired toxoplasmosis:
• Combination of Pyramethamine and Sulphadiazine or Trisulfapyramidines.
• Sulfadiazine 75mg/kg PO qid, plus Pyrimethamine 50-200mg for 3-6 weeks plus folinic acid
• Other alternative Drugs:
- Spiramycin→ Spiramycin 3g/day orally for 3 weeks, discontinue for 2 weeks, then continue
for 3 weeks. Done for a total of 5 cycles.
- Clindamycin→600mg PO IV qid 3-6 weeks
- Trimethoprim
- Sulphmethoxazole
• In pregnancy - Spriamycin is recommended drug
Q.66 Clinical syndromes of leptospirosis.
Leptospirosis is a blood infection caused by the bacteria Leptospira. Signs and symptoms can range
from none to mild (headaches, muscle pains, and fevers) to severe (bleeding in the lungs or
meningitis).
• Leptospirosis can present in two distinct clinical syndromes, icteric or anicteric.
• The anicteric syndrome is self-limited and presents with a nonspecific flu-like illness. The onset
is usually sudden and can present with a headache, cough, nonpruritic rash, fever, rigors, muscle
pain, anorexia, and diarrhea.
• The anicteric syndrome can also have recurrence several days later, and this phase is called
the immune stage during which aseptic meningitis can occur. These patients can recover fully but
may suffer from chronic, episodic headaches.
• Icteric syndrome: called weils disease, usually severe. Fever, renal failure, jaundice, hemorrhage
and respiratory distress. May involve heart, CNS and muscles. It presents with vascular collapse,
thrombocytopenia, hemorrhage,
Other syndromes that can also be present are
• Hemorrhagic syndrome
• Asthenovegetative syndrome
• Intoxication syndrome
• Hepatomegaly
• Pneumonia syndrome
• Meningeal syndrome
Q.67 Clinical signs of leptospirosis.

from none to mild (headaches, muscle pains, and fevers) to severe (bleeding in the lungs or meningitis).
CLINICAL SIGNS-
• The clinical course of leptospirosis is variable. Most cases are mild and self-limited or subclinical,
while some are severe and potentially fatal. The illness generally presents with the abrupt onset of
fever (38-40oC) rigors, myalgias, and headache in 75 to 100 percent of patients, following an
incubation.
• Fever 38-40 degrees, warm and flushed skin
• nausea and vomiting, Anorexia, diarrhea
• Cough
• Muscle pain: especially gastrocnemius (calf), muscles of scalp, neck and abdomen, lumbar area.
Muscle tenderness and myositis. Increase during palpation
• Oliguria, red urine with moderate proteinuria, fresh erythrocytes and leukocytes.
• Hypotension, oliguria
• Hepatosplenomegaly with jaundice
• Pneumonia
• Rare: Cardiovascular: dull heart sounds, relative bradycardia, arrhythmia, extrasystole.
• CNS: disorders of consciousness, headache, insomnia, delirium. Meningitis on 5-8th day of disease
• Hemorrhagic syndrome: petechial rash on skin, conjunctivitis, epistaxis, haemorrhage in stomach,
intestine and uterus. Can lead to anemia
Q.68 Diagnosis of leptospirosis.
from none to mild (headaches, muscle pains, and fevers) to severe (bleeding in the lungs or
meningitis).
DIAGNOSIS-
• The most common way to diagnose leptospirosis is through serological tests either the Microscopic
Agglutination Test (MAT) which detects serovar-specific antibodies, or a solid-phase assay for the
detection of Immunoglobulin M (IgM) antibodies.
• CBC: anemia, low reticulocyte number, thrombocytopenia in hemorrhagic syndrome. Left shift
leukocytosis with neutrophilia and lymphopenia. Increased ESR 40-60
• Biochemical: increased direct and indirect bilirubin, slightly increased AST and ALT. decrease
prothrombin time. Increased urea nitrogen and creatinine.
• Urine analysis: moderate proteinuria, fresh erythrocytes, leukocytes, hyaline casts and cells of
epithelium
• CSF analysis: increased pressure, moderate lymphocytic pleocytosis, increased protein
• Culture of urine, CSF or tissues for leptospiriosis for bacteriologic (water medium with native
rabbit serum) and bacterioscopic exam
• Biologic: using guinea pigs, inject infected material. If they die, it confirms diagnosis
Q.69 Treatment of leptospirosis.

from none to mild (headaches, muscle pains, and fevers) to severe (bleeding in the lungs or meningitis).
TREATMENT:
• Bed rest, diet with adequate rehydration
• Antimicrobial therapy
• Antibiotic:
➢ Mild disease - For outpatients with mild disease, we favor treatment with doxycycline (adults:
100 mg orally twice daily for 7 days; children: 2 mg/kg per day in two equally divided doses
[not to exceed 200 mg daily] for 7 days) or azithromycin (adults: 500 mg orally once daily for
three days; children: 10 mg/kg orally on day 1 [maximum dose 500 mg/day] followed by 5
mg/kg/day orally once daily on subsequent days [maximum dose 250 mg/day]).
➢ For pregnant women, we favour treatment with either azithromycin (500 mg orally once daily
for three days) or amoxicillin (25 to 50 mg/kg in three equally divided doses [maximum 500
mg/dose] for seven days). Azithromycin is preferred over amoxicillin if the differential diagnosis
includes rickettsial infection.
➢ For hospitalized adults with severe disease, we favour treatment with penicillin (1.5 million
units intravenously [IV] every six hours), doxycycline (100 mg IV twice daily), ceftriaxone (1
to 2 g IV once daily), or cefotaxime (1 g IV every six hours). The duration of treatment in severe
disease is usually seven days.
➢ For hospitalized children with severe disease, we favour treatment with penicillin (250,000
to 400,000 units/kg IV per day in four to six divided doses [maximum dose 6 to 12 million units
daily]), doxycycline (4 mg/kg IV per day in two equally divided doses [maximum dose 200
mg/day]), ceftriaxone (80 to 100 mg/kg IV once daily [maximum dose 2 g daily]), or cefotaxime
(100 to 150 mg/kg IV per day in three to four equally divided doses). For children who cannot
tolerate the above agents, azithromycin is an acceptable alternative agent (10 mg/kg IV on day
1 [maximum dose 500 mg/day], followed by 5 mg/kg/day IV once daily on subsequent days
[maximum dose 250 mg/day]). The duration of treatment in severe disease is usually seven days.
• Tetracycline antibiotics may cause permanent tooth discoloration for children <8 years if used
repeatedly. However, doxycycline binds less readily to calcium than other tetracyclines and may be
used for ≤21 days in children of all ages
• Glucocorticoids in severe forms
Q.70 Etiology and epidemiology of tetanus.

ETIOLOGY:
Tetanus is due to infection from the bacterium, Clostridium tetani, which is found in soil, dust, or
animal feces. It is a gram-positive, spore-forming, obligate anaerobic bacillus. This bacteria and its
spores are found worldwide, however, it is more frequently found in hot and wet climates where the
soil is rich with organic matter.
Host: humans, domestic and wild animals
Causative organism: clostridium tetani
Two forms: dormant form (spores) and active form (vegetative)
The source of infection: in most cases, is a wound, usually from a minor injury. A very common cause
of tetanus is a lack of immunization.
EPIDEMIOLOGY:
C tetani is found worldwide in soil, on inanimate objects, in animal feces, and, occasionally, in human
feces. Tetanus is predominantly a disease of underdeveloped countries. It is common in areas where
soil is cultivated, in rural areas, in warm climates, during summer months, and among males. In
countries without a comprehensive immunization program, tetanus predominantly develops in
neonates and young children.
Q.71 Classification of tetanus.

DEFINITION - Tetanus is due to infection from the bacterium, Clostridium tetani, which is found in
soil, dust, or animal feces. It is a gram-positive, spore-forming, obligate anaerobic bacillus.This
bacteria and its spores are found worldwide, however, it is more frequently found in hot and wet
climates where the soil is rich with organic matter
CLASSIFICATION:
1. Generalised: trismus (lock jaw), repeated painful spasms any part of the body. Restlessness,
irritability, dysphagia. Opisthotonus: spasm of muscles causing backward arching of head, neck and
spine. Seizures can be seen and respiratory failure.
2. Localised: muscle spasms on one extremity or one body region
3. Cephalic: due to head injury or middle ear infection: cranial nerve palsies which progress to
generalized tetanus
4. Neonatal: associated with umbilical stump infection in neonates born to mothers who have not been
immunized.
5. Maternal: tetanus during pregnancy and 6 weeks after.
Generalised is then further divided based on grade:
• Grade 1 (mild): mild trismus (lock jaw), general spasticity, little or no dysphagia
• Grade 2 (moderate): moderate trismus and generalized spasticity, mild dysphagia and fleeting
spasms. Moderate respiratory embarrassment
• Grade 3a (severe): severe trismus and generalized spasticity. Severe dysphagia and respiratory
difficulties. Severe and prolonged spasms (both spontaneous and on stimulation)
• Grade 3b: same as 3a with autonomic dysfunction
Q.72 Clinical signs of tetanus.

soil, dust, or animal feces. It is a gram-positive, spore-forming, obligate anaerobic bacillus. This
climates where the soil is rich with organic matter.
CLINICAL SIGNS-
• The classical presentation of tetanus seen in patients begins with trismus or ‘locked jaw’ due to
spasms of the masseter. Rigidity then spreads down the arms and trunks over the next 1 to 2 days,
progressing to generalized muscle rigidity, stiffness, reflex spasms, opisthotonus and dysphagia.
Even minute sensory stimulation can precipitate prolonged spasms.
• The generalized spasms are also accompanied by autonomic disturbances, such as swings in blood
pressure, arrhythmias, hyperpyrexia and sweating. Exhaustion, autonomic disturbances, and
complications from muscle spasms (for example, asphyxiation, pneumonia, rhabdomyolysis,
pulmonary emboli) can contribute to the high fatality rates observed in severe tetanus. Abdominal
muscle spasms.
• Rose tetanus local clinic
• Occurs after contact with roses infected with tetanus
• Rigidity of the muscles associated with the site of spore inoculation. Lower motor neuron
dysfunction (weakness and diminished muscle tone)
Q.73 The principles of tetanus treatment.

TREATMENT-
• The principles of management of tetanus include sedation and control of muscle spasms,
neutralization of tetanus toxin, prevention of production of tetanus toxin by use of antibiotics to
which Clostridium tetani is susceptible and by wound debridement, treatment of complications,
including autonomic dysfunction, and supportive care: Tetanus is a medical emergency requiring
• Wound care: clean wound thoroughly with soap and water to remove dirt foreign bodies and dead
tissue from wound to prevent growth of tetanus spores
• Medication: antibiotics
▪ Sedatives to control spasm
▪ Drugs like Magnesium sulfate, beta blockers, and morphine to regulate involuntary muscle
activities, regularize heartbeat and breathing
• Supportive therapy: long periods of treatment in an intensive care settings eg. Ventilator
Metronidazole 0.5g qid for 7-10 days
Q.74 Preventing of tetanus.

PREVENTION-
• Immunisation is the only effective prevention of tetanus.
• DTP vaccine (diphtheria, toxoid, pertussis) age 2mo, 4mo, 6mo, 12-15mo and 4-6years.
• Tetanus booster every 10years.
• Tetanus Immunoglobulin, antitoxin or antibiotic if patient comes with wound with no prior
vaccination
Q.75 Etiology and epidemiology of rabies.

Rabies is a zoonotic, fatal and progressive neurological infection caused by rabies virus of the
genus Lyssavirus and family Rhabdoviridae. It affects all warm-blooded animals and the disease is
prevalent throughout the world and endemic in many countries except in Islands like Australia and
Antarctica
Incubation period: 1week-3years.
Transmission: Bite of rabid animals and saliva of infected host
Reservoirs: wildlife like raccoons, skunks, bats and foxes.
Q.76 The stages of rabies.
DEFINITION - Rabies is a zoonotic, fatal and progressive neurological infection caused by rabies
virus of the genus Lyssavirus and family Rhabdoviridae. It affects all warm-blooded animals and the
disease is prevalent throughout the world and endemic in many countries except in Islands like
Australia and Antarctica.
STAGES-
• Incubation period: 1week-3years. The closer the bite is to the brain, the sooner the effects are
likely to appear.
• Prodromal period: virus enters CNS. Lasts 2-10days. Paraesthesia or pain at inoculation site.
Malaise, headache, anorexia, fever of 38 degrees and above, chills, pharyngitis and laryngitis by
spasm with hydrophobia, nausea, emesis, diarrhea, anxiety, insomnia and depression. Aerophobia
• Excitation period: patient has furious episodes of agitation, hyperactivity, restlessness, thrashing,
biting, confusions or hallucinations lasting less than 5 minutes. Seizures may occur. This phase may
end in cardiorespiratory arrest or progress to next stage. Hydrophobia, aerophobia.
• Paralysis: begins within 10 days of onset. Can lead to respiratory depression, arrest and death.
Q.77 Clinical signs of rabies

CLINICAL SIGNS:
• At first, there's a tingling, prickling, or itching feeling around the bite area. A person also might
have flu-like symptoms such as a fever, headache, muscle aches, loss of appetite, nausea, and
tiredness.
• After a few days, neurological symptoms develop, including:
- irritability or aggressiveness
- excessive movements or agitation
- confusion, bizarre or strange thoughts, or hallucinations
- muscle spasms and unusual postures
- seizures (convulsions)
- weakness or paralysis (when a person cannot move some part of the body)
- extreme sensitivity to bright lights, sounds, or touch
• Classic encephalitic (furious) rabies: hydrophobia and hyperexcitability
• Paralytic (dumb) rabies: flaccid muscle paralysis
• Non-classic atypical rabies (bite of bat): neuropathic pain, focal brainstem sign and myoclonus
Q.78 The treatment of rabies.
TREATMENT-
After exposure and before symptoms begin, a series of shots can prevent the virus from thriving.
Strategies include:
• A fast-acting dose of rabies immune globulin: Delivered as soon as possible, close to the bite wound,
this can prevent the virus from infecting the individual.
• A series of rabies vaccines: These will be injected into the arm over the next 2 to 4 weeks. These
will train the body to fight the virus whenever it finds it.
• Rabies vaccine 1ml on days 0, 3, 7 and 14. Rabies immunoglobulin 20IU/kg when incubation period
is less than 4 weeks.
• Intensive cardiopulmonary supportive care
• Symptomatic treatment
Q.79 Prevention of rabies.

PREVENTION:
• Regular antirabies vaccinations for all pets and domestic animals
• bans or restrictions on the import of animals from some countries
• widespread vaccinations of humans in some areas
• educational information and awareness
• If bitten by animal: animal should be caged and monitored for 10 days to see if signs of rabies
appear.
• If animal with rabies attack you, step outside their visual acuity
• Vaccinate animals and humans with rabies vaccine
• Post exposure prophylaxis with rabies vaccine
Q.80 Clinic of Ebola hemorrhagic fever.

Ebola haemorrhagic fever is a severe, often-fatal disease in humans and nonhumans primates caused
by infection with Ebola virus.
caused by bunyaviridae family from hantaan kind
SIGNS-
• Incubation period: 10-15 days
• Acute and adrupt onset of symptoms including, extremely strong chills with fever.
• Decreased visual acuity (mist before eyes), sharp headache, backache, muscles of extremities,
photophobia
• Nausea and vomiting. Pale nasolabial triangle with hyperemia of face, neck and trunk
• Oral mucosa are bright red with hemorrhages
• Meningeal syndrome
• Then petechia in axillary fossa, above clavicles.
• Nasal, intestinal and pulmonary bleeding
• Tachycardia initially, then bradycardia. Hypotonia. Dull cardiac sound
The course of the illness can be split into five phases:

• Febrile phase: Symptoms include redness of cheeks and nose, fever, chills, sweaty palms, diarrhea,
malaise, headaches, nausea, abdominal and back pain, respiratory problems such as the ones
common in the influenza virus, as well as gastro-intestinal problems. These symptoms normally
occur for three to seven days and arise about two to three weeks after exposure.
• Hypotensive phase: This occurs when the blood platelet levels drop and symptoms can lead to
tachycardia and hypoxemia. This phase can last for 2 days.
• Oliguric phase: This phase lasts for three to seven days and is characterised by the onset of renal
failure and proteinuria.
• Diuretic phase: This is characterized by diuresis of three to six litres per day, which can last for a
couple of days up to weeks.
• Convalescent phase: This is normally when recovery occurs and symptoms begin to improve. This
syndrome can also be fatal. In some cases, it has been known to cause permanent renal failure
Q.81 Clinic of yellow fever.

Yellow fever is a potentially life-threatening viral illness that is found in tropical areas of Africa and
South and Central America.
CLINIC-
• It is transmitted by the bite of an infected mosquito.
• Incubation period 3-6 days
• Symptoms are divided into the acute phase and the toxic phase.
• The acute phase presents with non-specific symptoms of a viral infection such as sudden high fever,
headache, muscle ache, nausea and vomiting and loss of appetite. Pain in head, back, lower back,
bones.
• Hyperemia and edema of face, neck and eye injected by blood
• Mucosa, pharynx or tongue is bright red colour, photophobia, tachycardia.
• Around 15% progress from the acute phase to the toxic phase which usually begins on 3rd day
• On 3rd day: jaundice, hemorrhagic rash on skin, hepatosplenomegaly
• On 5th day: pale face with cyanotic tint, delirium. Nausea and vomiting. Dark brown or black
emesis. Petechia and ecchymoses on trunk and extremities. Nasal and gum bleeding
• Followed by death in 50% of cases within 10-14 days.
Q.82 The main symptoms of cutaneous leishmaniasis.
Leishmaniasis is a disease caused by the Leishmania parasite. This parasite typically lives in infected
sand flies and is transmitted by the bite of infected sand fly
Cutaneous leishmaniasis includes the following features:
• Localized cutaneous leishmaniasis: Crusted papules or ulcers on exposed skin; lesions may be
associated with sporotrichotic spread
• Diffuse (disseminated) cutaneous leishmaniasis: Multiple, widespread nontender, non-ulcerating
cutaneous papules and nodules; analogous to lepromatous leprosy lesions
• CL is characterized by skin lesions (open or closed sores), which typically develop within several
weeks or months after exposure. They typically progress from small papules to nodular plaques, and
often lead to open sores with a raised border and central crater (ulcer), which can be covered with
scales or crust. The lesions usually are painless but can be painful, particularly if open sores become
infected with bacteria.
• Satellite lesions, regional lymphadenopathy, and nodular lymphangitis can be noted. The sores
usually heal eventually, even without treatment. However, they can last for months or years and
typically result in scarring
Treatment:
• fluconazole and amphotericin B
• Other consequences, which can become manifest anywhere from a few months to years after
infection, include fever, damage to the spleen and liver, and anemia
Q.83 The main symptoms of visceral leishmaniasis.

Visceral leishmaniasis - the most serious form and potentially fatal if untreated. Also known as kala-
azar
Symptoms often don’t appear for months after the bite with this type of leishmaniasis.
Most cases are apparent two to six months after the infection occurred.
The incubation period typically ranges from weeks to months.
Common signs and symptoms include:
• weight loss
• weakness
• fever that lasts for weeks or months
• enlarged spleen
• enlarged spleen
• enlarged liver
• decreased production of blood cells
• bleeding
• other infections
• swollen lymph nodes
Treatment: Amphotericin B, Meglumine antimoniate
Q.84 The epidemiology of anthrax.
Epidemiology: Anthrax is an infection caused by gram positive rod shaped bacteria called bacillus
anthracis which is transmitted by contact with the bacterium’s spores from affected sick animals
▪ Etiology: Bacillus anthracis
▪ Source of infection: infected animals which ingested or inhaled anthrax spores while grazing
▪ Mode of transmission: fecal-oral or contact
-contact with infected tissues of dead animals which can lead to cutaneous anthrax
-consumption of contaminated undercooked meat which can lead to gastrointestinal or
oropharyngeal anthrax
-contact with contaminated hair, wool, or hides which can lead to either inhalational or cutaneous
anthrax
-All ages and gender are affected

-it occurs worldwide
-it’s is mainly found in endemic areas such as Africa and Asia
-anthrax spores can be infectious for decades and survive for extended periods
-it mainly affects livestock and wild game
-humans are infected through direct or indirect contact with sick animals
-It’s natural reservoir is considered to be the soil
It’s occurs in four forms: cutaneous/skin form, inhalation/ pulmonary form, intestinal form,
injection form
Q.85 The clinic of anthrax cutaneous form.

Anthrax is an infection caused by gram- positive rod- shaped bacteria called bacillus anthracis
which is transmitted by contact with the bacterium’s spores from affected sick animals
CLINIC-
• Incubation 1-7 days
• A pruritic papule that enlarges 24-48hours to form ulcer surrounded by a satellite bulbous/ lesion
edematous halo
- lesions located on the head or neck
- Presence of systemic symptoms (fever, malaise, headache, tachycardia, tachypnea,
hypotension, hyper/hypothermia) -presence of extensive edema
- multiple extensive or bulbous lesions
• Lesion is 2-3cm n diameter and has a round, regular raised edge. Painless
• Regional lymphadenopathy
• 7-10 days: ulcer evolve into black eschar for 7-14 days them evolve leaving a permanent scar.
Q.86 The clinic of anthrax pulmonary form.
Anthrax is an infection caused by gram- positive, rod shaped bacteria called bacillus anthracis
CLINIC-
• Incubation: 1-3 days
• flu like symptoms which may last for a few hours to days such as Low-grade fever, non-
productive cough, sore throat, fatigue, muscle aches
- mild chest discomfort
- Nausea
- trouble breathing
• Hemorrhagic mediastinitis (condition which causes fluid to accumulate in the chest cavity/
mediastinum) which will cause high fever, severe shortness of breath, tachypnea, cyanosis,
profuse diaphoresis, hematemesis and chest pain
-painful swallowing
-shock
Q.87 Laboratory diagnosis of anthrax.

Anthrax is an infection caused by gram- positive, rod shaped bacteria called bacillus anthracis
LABORATORY-
• Staining ulcer exudates with giemsa stain or methylene blue for microscopic investigation
• Ulcer, blood or CSF culture on sheep blood or peptone agar
• Serological: ELISA
• tissue biopsy to check for cutaneous anthrax
• Chest x-ray or CT scan
Q.88 The treatment of anthrax.

Anthrax is an infection caused by gram-positive, rod shaped bacteria called bacillus anthracis which
is transmitted by contact with the bacterium’s spores from affected sick animals.
TREATMENT-
• Bed rest with no dietary restrictions
• Antibiotics such as:
- Penicillin G. Dose- 4 million units IV qid
- Amoxicillin. Dose 500mg PO tid
- Ampicillin. Dose 2g IV every 4 hours
• Ciprofloxacin, levofloxacin, Chloramphenicol
• Monoclonal antibodies such as Raxibacumab
• Symptomatic treatment
Q.89 Epidemiology of plague.
Plague is a disease caused by Yersinia pestis usually found in small mammals and their fleas
Source of infection: zoonosis (rodent and fleas)
Epidemiology:
o it occurs in various countries such as Africa, Asia, south America and the USA
o it is gram negative, non- motile, non- spore forming bacillus
o it is resistant to freezing temperatures
o human plague occurs from bite of an infected flea
o outbreaks are cyclical corresponding to rodent reservoirs and arthropod vector correspondent
o Vectors are rodents, carnivorous mammals (cats, foxes, dogs), patient with pneumonic plague
Mechanism of transmission: droplet contact, physical contact, sexual contact, touching soil,
airborne/aerogenic, fecal-oral
Q.90 The clinic of skin and bubonic plague.

Bubonic plague is a disease caused by Yersinia pestis usually found in small mammals and their
fleas
SYMPTOMS INCLUDE:
• Malaise and headache usually severe with mental dullness. -Backache.
• Fever with moderate rigor or repeated shivering
• Tachycardia and tachypnea
• Skin is hot and dry, face bloated, eyes injected and hearing dull
• Tongue is swollen and coated with creamy fur.
• Burning in throat or stomach with nausea and vomiting
• Constipation
• Enlarged lymph nodes
• The affected gland is hard and tender.
• Buboes (inflammatory swelling of lymphatic glands) the size of walnut or egg appear in inguinal
glands, axillary region, or cervical
• Leukocytosis, increase in polymorph nuclear leucocytes
Q.91 The clinic of pneumonic plague.

Pneumonic plague is a disease caused by Yersinia pestis usually found in small mammals and their
fleas
THE SYMPTOMS INCLUDE:
• Chilly sensations.
• Headache, loss of appetite, tachycardia and fever
• Painless Cough and dyspnea appear within 24 hours after onset
• Expectoration is clear at first and then becomes blood tinge.
• Sputum then becomes thinner and bright red contains enormous number of plague bacilli
• Conjunctiva injected and tongue coated with white or brownish layer
• Anxious facial expression with dusky hue
• Dyspnea can become severe leading to cyanosis
Q.92 The clinic of plague intestinal form.

Intestinal Plague is a disease caused by Yersinia pestis usually found in small mammals and their
fleas
THE SYMPTOMS ARE:
• Mucous membrane of mouth and throat are hyperemic with occasional hemorrhagic patches
• Tonsils may be swollen and hyperemic.
• A bubo may form in the tonsils and cause edema of glottis.
• Vomiting preceded by nausea containing blood.
• Constipation is common but Bleeding in intestine causes blood to appear in stool.
Q.93 Laboratory diagnosis of plague.

LABORATORY-
• Bacteriological examination of material collected from bubo by syringe and inoculated into
infusion broth or blood agar or mc-conkey agar, some can be examined by smear
• Blood taken from patient vein inoculated into guinea pig subcutaneously.
• Sputum exam by direct microscopy.
- staining- gram and Watson’s or gemsa
- dfa testing
• Serological- fourfold rising in antibody titter (F1 Ag), single tiger of >1:128
Q.94 Treatment of plague.

TREATMENT-
• Hospitalization and quarantine
• Antibiotics immediately streptomycin 1g IM tid. Tetracyclines, Monomycin, Ampicillin
• Prophylactic plague vaccine for anyone who came in contact with patients
• oxygen, iv fluids and respiratory support is usually needed
Q.95 The clinical forms of tularemia.
Tularemia is a rare infectious disease caused by Francisella tularensis. Also known as rabbit fever or
deer fly fever, it typically attacks the skin, eyes, lymph nodes and lungs. The disease mainly affects
rabbits, hares, and rodents, such as muskrats and squirrels.
The clinics forms are
• Bubonic form
• Ulcer-bubonic form
• Eye-bubonic form
• Anginous-bubonic form
• Abdominal form
• Pulmonic form
Ulceroglandular tularemia
The symptoms of ulceroglandular tularemia, or infection through the skin, can include:
● a skin ulcer at the point of contact with the infected animal or at the site of a bite
● swollen lymph nodes near the skin ulcer (most often in the armpit or groin)
● severe headaches
● a fever
● chills
● fatigue
Glandular tularemia
The symptoms of glandular tularemia, or infection through the skin, are similar to ulceroglandular
symptoms but without a skin ulcer.
Pneumonic tularemia
Pneumonic tularemia is the most serious form of this disease. It’s transmitted through inhalation.
The symptoms can include:
● a dry cough
Oculoglandular tularemia
The symptoms of oculoglandular tularemia, or infection of the eye, can include:
● eye irritation
● eye pain
● eye swelling
● discharge or redness of the eye
● a sore on the inside of the eyelid
● swollen lymph glands behind the ear
Oropharyngeal tularemia
The symptoms of oropharyngeal tularemia, or infection through ingestion of the bacteria, can
include:
● a sore throat
● ulcers in the mouth
● swollen lymph nodes in the neck
● tonsillitis, or swollen tonsils
● vomiting
● diarrhea
Typhoidal tularemia
The symptoms of the rarest form of this disease, typhoidal tularemia, can include:
● a very high fever
● extreme fatigue
● diarrhea
● vomiting
Typhoidal tularemia can lead to pneumonia and an enlarged liver and spleen
Q.96 The epidemiology of tularemia.

Tularemia is a rare infectious disease caused by Francisella tularensis.
Also known as rabbit fever or deer fly fever, it typically attacks the skin, eyes, lymph nodes and
lungs. The disease mainly affects rabbits, hares, and rodents, such as muskrats and squirrels.
EPIDEMIOLOGY:
• Francisella tularensis, a small gram negative cocco-bacillus and the causative agent of tularemia,
exists as two major subspecies called biovars.
• F. tularensis biovar tularensis (type A) is a virulent strain responsible for most infections in North
America.
• F. tularensis palaearctica (type B) causes milder disease and is prevalent in Europe and Asia.
• The disease occurs naturally in the south, central and western states of the U.S. and northern and
central Europe.
• Source of infection: rodents and blood sucking insects
• Mechanism of transmission: Contact, insects bite from affected Arthropoda, Rarely fecal oral and
air droplets
Q.97 The clinic of tularemia bubonic form.

Tularemia is a rare infectious disease caused by Francisella tularensis.
Also known as rabbit fever or deer fly fever, it typically attacks the skin, eyes, lymph nodes and
lungs. The disease mainly affects rabbits, hares, and rodents, such as muskrats and squirrels.
CLINIC-
• Prodromal period: shivering, fever, headache, malaise, muscle ache, dizziness, anorexia. Sleep
disturbance with night sweating. Vomiting, nose bleeds, loss of consciousness and delirium.
Conjunctivitis
• Period of high point of disease: Primary buboes (inflammatory changes in lymph node) in region
near site of inoculation of disease. Secondary buboes occurs due to hematogenous spread of disease.
Buboes can be as big as nut or egg. They are dense, painful with no periadenitis. Buboes can become
completely dissolved, suppurated, ulcerated and eventually scarred.
• Convalescence: softening e.g. Bubo after 2-3 weeks. First hyperemia of skin then buboes break and
drain, the pus is thick, white and no smell.
Clinical signs of tularemia eye-bubonic form:
• If pathogen penetrated the eye mucous membrane
• Expressed conjunctivitis. Eyelids are swollen, dense with tenderness of moving.
• There is moderate mucopurulent discharge from eye
• On eyelid mucous membrane, there are small foci in the form of the cone
• Sometimes the presence of papules and ulcers of regional lymph nodes (buboes) such as parotid,
anterior cervical and submaxillary on the side of affected eye.
• Inflammatory small foci with a bunch of superficial widened vessels on conjunctiva
• Rarely, lachrymal sac phlegmon
Q.98 Laboratory diagnosis of tularemia.

DEFINITION- Tularemia is a rare infectious disease caused by Francisella tularensis.
Also known as rabbit fever or deer fly fever, it typically attacks the skin, eyes, lymph nodes and lungs.
The disease mainly affects rabbits, hares, and rodents, such as muskrats and squirrels
• Direct bacterioscopy of blood or bulbo aspiration material
• Agglutination test, Compliment binding reaction, hemagglutination test
• Subcutaneous allergic reaction with allergen tularin 1ml test
• chest X-ray - to check for signs of pneumonia
• Blood test - to check for antibodies in bacteria
Q.99 Treatment of tularemia.

DEFINITION- Tularemia is a rare infectious disease caused by Francisella tularensis.
Also known as rabbit fever or deer fly fever, it typically attacks the skin, eyes, lymph nodes and lungs.
The disease mainly affects rabbits, hares, and rodents, such as muskrats and squirrels
TREATMENT:
• Bed rest, quarantine
• Antibiotics Streptomycin 0.5-2g per day IM for period of fever plus 2 days.
• Tetracylcline, doxycycline, levomycetin, kanamycin, gentamycin
• Inactive vaccine
• Desintoxication therapy with glucose
• Vitamins
• Eye-bubonic form: 20-30% sulfacil-natrii solution
• Calcium gluconate, diphenylhydramine to decrease allergic manifestation
• Compress, ointment, bandages on area of buboes at stage of dissolving
Q.100 Clinical forms of intestinal Yersiniosis.

DEFINITION - Yersiniosis is an infection that affects the intestinal tract caused most
often by eating raw or undercooked pork contaminated with Yersinia enterocolitica bacteria
THE CLINICAL FORMS ARE:
• Scarlatinic form: characterized by general intoxication symptoms: fine-dot rash, fever
• Arthralgic form
• Abdominal form: gastro intestinal, hepatic, pseudo appendicitis
• Generalized form: with affection of different organs and systems
• Icteric form
Enterocolitis
● Enterocolitis, the most common presentation of Y enterocolitica, occurs primarily in young
children, with a mean age of 24 months.
Mesenteric adenitis, mesenteric ileitis, and acute pseudoappendicitis
These manifestations are characterized by the following symptoms (although nausea, vomiting,
diarrhea, and aphthous ulcers of the mouth can also occur):
● Fever
● Abdominal pain
● Tenderness of the right lower quadrant
● Leukocytosis
Pseudoappendicitis syndrome is more common in older children and young adults. [46] Patients
with Y enterocolitica infection often undergo appendectomy;
Q.101 Clinical features of intestinal Yersiniosis.

DEFINITION - Yersiniosis is an infection that affects the intestinal tract caused most often by eating
raw or undercooked pork contaminated with Yersinia enterocolitica bacteria
CLINICAL FEATURES:
• Pain in epigastric region of abdomen, umbilical or right iliac area, less often in right hypochondrium
and left iliac area
- Fever,
- nausea,
- vomiting,
- bloody diarrhea
• In the form of mesenteric lymphadenitis, terminal ileitis, acute appendicitis
• Enlarged, painful and grumbling cecum and mesenteric lymph nodes
Q.102 Clinical features of pseudotuberculosis.

Yersinia pseudotuberculosis is a, gram-negative bacillus bacterium that causes Far East scarlet-
like fever in humans, who occasionally get infected zoonotically, most often through the food-borne
route.
Source of infection - wild and home animals (rats, dogs, foxes, cats and other)
Way of transmission - alimentary;
Susceptible organism - children (not infants), adults.
CLINICAL FEATURES:
• Catarrhal syndrome: Pharyngeal and tonsilar erythema without the exudates, erythema of the soft
palate, conjunctivitis, coryza
• Intoxication syndrome: fever, headache
• Abdominal syndrome: tenderness during the palpation of abdomen, may be acute appendicitis
• Dyspepsia: nausea, vomiting, liquid feces.
• Rashes: maculopapulous (like in scarlet fever), may be erythematosus or even erythema nodosum
may developed. rash appears on face and intensifies periorbitally and neck
• Arthritis of knees, elbows, foot and hand small joints.
• Presence of “strawberry” tongue.
Q.103 Laboratory diagnosis of Yersiniosis.

raw or undercooked pork contaminated with Yersinia enterocolitica bacteria
• Phage typing of bacterial culture or antibodies for F-antigen
• Agglutination test
• Complete blood analysis: leucocytosis, neutrophilia with left shift, eosinophilia, ERS is enlarged.
• Urinalysis: slight proteinuria, leucocyturia, casts in small amount in case of toxic damage of
kidneys.
• Bacteriological - Yersinia enterocolitica may be found in feces, urine, blood, pus, lymph nodes and
pharyngeal mucus.
• Coprogram: Increasing of red blood cells and leukocytes, mucus.
• Dfa testing
• Serological - increasing of special antibodies 4 times and more in 2- 4 weeks in paired sera (IHAR
1:200, AR 1:40 – 1:160).
• Staining: gram, waysons, methylene blue
Q.104 Principles of Yersiniosis treatment.

raw or undercooked pork contaminated with Yersinia enterocolitica bacteria.
TREATMENT-
Diet number 5 for icteric form and number 4 for other forms
Etiological treatment:
• In mild cases it’s not used;
• In moderate and severe cases - by chloramphenicol 10-20 mg/kg 4 times per day orally during 6-9
days.
• If not effective - alternative antibiotics: cefalosporins of the 3rd-4th generation 100-150 mg/kg,
aminoglycosides of the 3rd generation. 7-10 days
Pathogenetic treatment:
• Detoxification therapy: oral to all patient and in case of mild dehydration, or parenteral:
Rheosorbilact, 0.9% NaCl, 5% glucose (moderate and severe dehydration)
• Sorbents: enterosgel 0.5-1 g/kg, polysorb (Silix) 100-200 mg/kg per day in 3 doses for 5-7 days
• Antihistamines: claritin, cetirizin, suprastin, pipolphen 1-3 mg/kg per day
• Corticosteroids 1-3 mg/kg with a short course (in severe cases, in case of myocarditis)
• Normalisation of the intestinal flora: linex, bifi-form, acidophilus 1-2 caps 2-3 times per day not
less than 2 weeks
• Antipyretics: paracetamol 10 mg/kg not more than 5 times per day
• NSAIDs in case of arthritis, carditis, nodular erythema (ibuprofen 20 mg/kg per day, aspirin 50-75
mg/kg per day, voltaren 2-3 mg/kg per day, indomethacin 2-3 mg/kg per day (in average doses).
SECTION 3
Q.1 Epidemic process and its components.

Epidemiology is the study of frequency, distribution and determinants of health-related events.
Epidemic process - The continuous chain of successive transmission of infection (patient-carrier),
manifested by symptomatic or asymptomatic forms of disease.
Epidemic process is the process of the rise and the spreading of the infectious diseases among the
people
Components
● Infectious agent
● transmission factors
● Susceptible individual (without immunity)
The epidemic process is an evolutionarily stabilized mechanism consisting of three phases:
(1) excretion of the agent from the host’s organism (i.e., the source or donor of an infectious
disease);
(2) transmission of the agent;
(3) its entry into a susceptible host (recipient).
Source of infectious
-agent is infected (sick or carrier) agent is infected (sick or carrier) organism
- human or animal organism
- human or animal (object which is the site of natural habitation and multiplication of pathogenic
habitation and multiplication of pathogenic organisms, from where they can infect organisms, from
where they can infect healthy people)
Q.2 The main motive forces of the epidemic process.

people
Source of infectious agent
● Mechanisms of infectious agent transfer
● Receptive organism
Secondary motive forces of epidemiological process:
● Social factors
● Environmental factors
Q.3 Features of epidemic process at anthroponoses and zoonoses. The
concept of sapronoses.
According to source of agent it is divided into three groups:
• Anthroponoses - when the source of infection is Human (Sick person or carrier)
• Zoonoses - source of infection is Animal
The source of zoonotic diseases is a vertebrate animal (donor), excreting the microbial agent during
the contagious phase, sometimes being without any clinical symptoms but, more often, during the
period of fully developed clinical signs.
The excretion mechanisms include:
- urination (hantaviruses, leptospires),
- defecation (Salmonella, Giardia),
- regurgitation (the production of pellets, e.g. in raptors and owls: Mycobacterium avium),
- salivation (rabies virus),
- expectoration (coughing: e.g. Nipah or SARS viruses),
- bleeding (e.g. Lassa, Ebola or CCHF viruses),
- lactation (milk-borne zoonoses TBE, brucellosis, bovine tuberculosis),
- via pus (glanders).
• Sapronosis - It’s transmitted from the environment to human (soil, water, decayed plants)
In sapronoses, the source of infection is an abiotic substrate (e.g. soil or water in some visceral
mycoses, atypical mycobacterioses or legionellosis), in which the agent lives as a saprophyte .
Q.4 Anti Epidemic measures in the places of infectious diseases

outbreaks.
people
Measures concerning infectious agent’s source
● Disease diagnosis
● Registration
● Isolation of the patient (carrier)
● Etiological treatment
Measures concerning transmission mechanisms
● disinfection (disinsection, deratization) – current, final
Measures concerning contact persons:
● Sanitary processing
● Medical observation
● Laboratory examination
● Specific prophylaxis
Q.5 The source and reservoir of infectious diseases.

The reservoir of an infectious agent is the habitat in which the agent normally lives, grows, and
multiplies. Reservoirs include humans, animals, and the environment.
Human reservoirs –
Diseases that are transmitted from person to person without intermediaries include the sexually
transmitted diseases, measles, mumps, streptococcal infection, and many respiratory pathogens.
Animal reservoirs –
- Many of these diseases are transmitted from animal to animal, with humans as incidental hosts.
- infectious disease that is transmissible under natural conditions from vertebrate animals to
humans.
- Long recognized zoonotic diseases include brucellosis (cows and pigs), anthrax (sheep), plague
(rodents), trichinellosis/trichinosis (swine), tularemia (rabbits), and rabies (bats, raccoons, dogs,
and other mammals). HIV/AIDS, Ebola infection and SARS.
Environmental reservoirs –
- Plants, soil, and water in the environment are also reservoirs for some infectious agents.
- Many fungal agents, such as those that cause histoplasmosis, live and multiply in the soil.
- Outbreaks of Legionnaires disease are often traced to water supplies in cooling towers and
evaporative condensers, reservoirs for the causative organism Legionella pneumophila.
Q.6 Sick person and the carrier and their epidemiological value.
Sick person is the primary source from which the infection spreads and is the most dangerous
source of infection because he or she releases a great quantity of the pathogenic microorganisms.
A carrier is a person with infection who is capable of transmitting the pathogen to others Carriers
release pathogenic agents into the environment in a smaller quantity than patients with clinically
manifest diseases, but they are danger to community too since they actively associate with healthy
people and spread the infection.
Carriers commonly transmit disease because they do not realize they are infected, and consequently
take no special precautions to prevent transmission. Symptomatic persons who are aware of their
illness, on the other hand, may be less likely to transmit infection because they are either too sick to
be out and about, take precautions to reduce transmission, or receive treatment that limits the
disease.
Categories of infectious diseases carriers.
• Asymptomatic or passive or healthy carriers are those who never experience symptoms
despite being infected.
• Incubatory carriers are those who can transmit the agent during the incubation period before
clinical illness begins.
• Convalescent carriers are those who have recovered from their illness but remain capable of
transmitting to others.
• Chronic carriers are those who continue to harbor a pathogen such as hepatitis B virus or
Salmonella Typhi, the causative agent of typhoid fever, for months or even years after their
initial infection.
Q.7 Epidemiological value of animals (rodents, bats etc.)

• Rodents, animals that are almost everywhere, can be reservoirs of important zoonotic diseases such
as leptospirosis, leishmaniasis, relapsing fever, tularemia, plague, Q fever, salmonellosis, and
hantavirus.
• These diseases can be transmitted to humans by touch or bite of the animal, direct contact with their
feces, urine and saliva, bite of their vectors (ticks, mosquitoes, fleas), ingestion of food or waters
contaminated with their feces or urine, inhalation of dried feces of infected rodents or during
dissection and autopsy of these animals.
• With early diagnosis and prompt treatment, most of these diseases are not a serious threat to human.
This reflects the importance of having enough knowledge about these diseases, especially by those
who deal with them directly.
• Since the vaccine has not been approved for the prevention of most of these diseases, educating of
people especially those at most risk of infection, limiting the contact with rodents, use of personal
protective equipment (boots, gloves, masks, etc.), washing the hands with soap and water regularly
following close contact with rodents and avoiding the insect bites is necessary in the prevention of
these diseases.
Q.8.Definition of meaning- Mechanism of trans mission – its chains , factors and

ways of infectious disease transmissions
Mechanism of transmission: It is a process that begins when an infectious agent or pathogen
leaves its reservoir, source, or host through a portal of exit and is conveyed by some mode of
transmission, enters the host through an appropriate portal of entry, and infects a susceptible host.
OR
Mechanism of transmission: The combination of routes by which the pathogenic microorganisms
are transmitted from an infected macroorganism to a healthy one
Four mechanisms of infection transmission are distinguished according to the primary
localization of pathogenic agents in macroorganisms
• Faecal-oral (intestinal localization);
• Air-bome (airways localization);
• Transmissive (localization in the blood circulating system);
• Contact (transmission of infection through direct contact with another person or
environmental objects)
Main factors are involved in transmission of infection: air, water, foods, soil, utensils, arthropods
(living agents).
Three phases are distinguished in the transmission of infection from one macroorganism to
another:
o 1st phase: excretion of the causative agent from the infected macroorganism
o 2nd phase: staining of the causative agent in environment
o 3rd phase: infectious agent’s penetration into healthy (susceptible) organism. - direct
contact, droplet, indirect transmission, vectors,
Q.9 Types of infectious diseases mechanisms of transmission.

• Direct contact occurs through skin-to-skin contact, kissing, and sexual intercourse. Direct
contact also refers to contact with soil or vegetation harboring infectious organisms. Thus,
infectious mononucleosis (“kissing disease”) and gonorrhea are spread from person to person by
direct contact. Hookworm is spread by direct contact with contaminated soil. spread refers to
spray with relatively large, short-range aerosols produced by sneezing, coughing, or even
talking.
• Droplet spread is classified as direct because transmission is by direct spray over a few feet,
before the droplets fall to the ground. Pertussis and meningococcal infection are examples of
diseases transmitted from an infectious patient to a susceptible host by droplet spread.
• Indirect transmission refers to the transfer of an infectious agent from a reservoir to a host by
suspended air particles, inanimate objects (vehicles), or animate intermediaries (vectors).
• Vectors such as mosquitoes, fleas, and ticks may carry an infectious agent through purely
mechanical means or may support growth or changes in the agent. Examples of mechanical
transmission are flies carrying Shigella on their appendages and fleas carrying Yersinia pestis,
the causative agent of plague, in their gut.
Q.10 Types and methods of disinfection

Disinfection” means the procedure whereby health measures are taken to control or kill the insect
vectors of human diseases present in baggage, cargo, containers, conveyances, goods and postal
parcels
Types of disinfection:
1. Concurrent: disinfection as soon as patient is discharged from the hospital. E.g. disinfection of
sputum, urine, feces, clothing, etc.
2. Terminal: disinfection of a sick room and its contents at the termination of a disease.
3. Precurrent: this is a prophylactic disinfection that is, action taken prior to the onset of infection
Methods of disinfection:
1. Physical methods:
• drying,
• heating,
• radiation,
• ultrasound waves
2. Mechanical methods:
• filtration
3. Chemical methods:
• Alcohol
• Aldehydes
• Phenols
• Halogens
• Oxidizing agents
• Heavy metal salts
• Surface active agents
• Dyes
• Gas sterlization
Q.11 Definition of disinfection, its types and methods.

Disinfection is the process of using a disinfectant to destroy, inactivate, or significantly reduce the
concentration of pathogenic agents (such as bacteria, viruses, and fungi) Both viruses are susceptible
to disinfection by a weak solution of chlorine bleach
TYPES OF DISINFECTANT
● Low-level disinfectants- kill most vegetative bacteria and some fungi as well as enveloped
(lipid) virus example is hepatitis b, c, hantavirus hiv. They do not kill mycobacteria or bacterial
spores but typically used to clean environmental surface
● Intermediate-level disinfectants- the kill vegetative bacteria most viruses and fungi but not
resistant bacterial spores
● High-level disinfectants process destroys vegetative bacteria, myocobacteria, fungi and
enveloped and non- enveloped virus but not necessarily bacterial spores
Types of disinfection:
4. Concurrent: disinfection as soon as patient is discharged from the hospital. E.g. disinfection of
sputum, urine, feces, clothing, etc.
5. Terminal: disinfection of a sick room and its contents at the termination of a disease.
6. Precurrent: this is a prophylactic disinfection that is, action taken prior to the onset of infection
METHODS
● Chemical Method
- Alcohol
- Chlorine and chlorine compounds
- Formaldehyde
- Glutaraldehyde
- Hydrogen peroxide
-Iodophors
- Halogen
- Peracetic acid
- Peracetic acid and hydrogen peroxide
● Physical method
Boiling at 100°C for 15 minutes, which kills vegetative bacteria.
Pasteurizing at 63°C for 30 minutes or 72°C for 15 seconds, which kills food pathogens.
Using nonionizing radiation such as ultraviolet (UV) light. UV rays are long wavelength and low
energy.
● Mechanical method
Cleaning, washing, filtration
Q.12 Sterilization and its stages, control of quality.

Sterilization refers to any process that removes, kills, or deactivates all forms of life (in particular
referring to microorganisms such as fungi, bacteria, spores, unicellular eukaryotic organisms such as
Plasmodium, etc.) and other biological agents.
STAGES:
- Pre-Vacuum,
- Rising Temperature,
- Sterilizing
- Vacuum-Drying
METHODS
• Heating in an autoclave (steam sterilization) - Exposure of microorganisms to saturated steam
under pressure in an autoclave achieves their destruction by the irreversible denaturation of enzymes
and structural proteins. The recommendations for sterilization in an autoclave are 15 minutes at 121-
124 °C.
• Filtration - Sterilization by filtration is employed mainly for thermolabile solutions. These may be
sterilized by passage through sterile bacteria-retaining filters, e.g. membrane filters.
• Exposure to ionizing radiation - Sterilization of certain active ingredients, drug products, and
medical devices in their final container or package may be achieved by exposure to ionizing
radiation in the form of gamma radiation from a suitable radioisotopic source such as 60Co (cobalt
60) or of electrons energized by a suitable electron accelerator.
• Aqueous solutions in glass - containers usually reach thermal equilibrium within 10 minutes for
volumes up to 100 mL and 20 minutes for volumes up to 1000 mL.
• Dry-heat sterilization - In dry-heat processes, the primary lethal process is considered to be
oxidation of cell constituents. Dry-heat sterilization requires a higher temperature than moist heat
and a longer exposure time. Preparations to be sterilized by dry heat are filled in units that are either
sealed or temporarily closed for sterilization. The entire content of each container is maintained in
the oven for the time. Temperature 160, 170, 180 degrees for 180mins, 60mins and 30mims
respectively.
• Gas sterilization (with ethylene oxide) - The active agent of the gas sterilization process can be
ethylene oxide or another highly volatile substance. The highly flammable and potentially explosive
nature of such agents is a disadvantage unless they are mixed with suitable inert gases to reduce
their highly toxic properties and the possibility of toxic residues remaining in treated materials.
Q.13 Schedules of immunization

• Vaccination should be performed according to a predetermined plan, or for special epidemiologic
indications.
• Planned vaccination is performed against: tuberculosis, diphtheria, tetanus, pertussis, poliomyelitis,
measles, epidemic parotitis, and against some other infections.
• Vaccination for special epidemiologic indications are performed in the presence of direct danger of
spreading of a particular infection.
• Preparations can be given parenterally (percutaneously, intracutaneously, subcutaneously,
intramuscularly, intravenously) or enterally (per orally), intranasally or by inhalation (aerosols).
Immunization depends on:
• Need
• Efficacy
• Safety
• Ease of administration.
Schedule of immunization:
Preparations can be given parenterally (percutaneously, intracutaneously, subcutaneously,
intramuscularly, intravenously) or enterally (per os), intranasally or by inhalation (aerosols).
Postvaccination complications. They are divided into the following groups:
(1) complications developing secondary to vaccination;
(2) complications due to aseptic conditions of vaccination;
(3) exacerbation of a pre-existing disease.
Q.14 Epidemiological classification of infectious diseases.

It is based on the location of infection in the macro-organism. In accordance with the main sign that
determines the transmission mechanism, all infectious diseases are divided by the author into 4
groups:
(1) intestinal infections;
(2) respiratory infections;
(3) blood infections;
(4) skin infections.
Intestinal infections - which are transferred by fecal-oral mechanism
• As a microbe is released into the environment with faeces, urine, vomitus (cholera), it can cause
disease in a healthy person only after ingestion with food or water.
• They are characterized by location of the causative agents in the intestine and their distribution in
the environment with excrements.
• If the causative agent circulates in the blood (typhoid fever, paratyphoid A and B, leptospirosis, viral
hepatitis, brucellosis, etc.) it can also be withdrawn through various organs of the body, e. g. the
kidneys, lungs, the mammary glands.
• The main means of control of intestinal infection are sanitary measures that prevent possible
transmission of the pathogenic microorganisms with food, water, insects, soiled hands, etc.
• Specific immunization is only of secondary importance in intestinal infections.
Respiratory infections - which are transferred by the droplet mechanism
• This group includes diseases whose causative agents parasitize on the respiratory mucosa and are
liberated into the environment with droplets of sputum during sneezing, cough, loud talks, or noisy
respiration.
• People get infected when the microbes contained in sputum get on the mucosa of the upper airways.
• Transmission can be minimised by control of overcrowding, proper ventilation and isolation of
enclosures, using UV-lamps, wearing masks, respirators, disinfection.
Blood infections - which are transferred by means of transmissive mechanism of transfer
• The diseases of this group are transmitted by blood-sucking insects, such as fleas, mosquitoes, ticks,
etc., which bite people and introduce the pathogenic agent into the blood.
• Control of blood infections includes altering natural conditions, improvement of soils, draining
swamps, destroying sites where the insects multiply, disinfection measures against mosquitoes,
ticks, etc., detoxification of sources of infection by their isolation and treatment, carrying out
preventive measures
Infections of skin and mucus membrane - which are transferred by means of contact or contact-wound
mechanism
• The diseases of this group occur as a result of contamination of the skin or mucosa with the
pathogenic microorganisms.
• They can remain at the portal of infection (tetanus, dermatomycoses), or affect the skin, enter the
body and be carried to various organs and tissues with the circulating blood (erysipelas, anthrax).
• The main measures to control skin infections include isolation and treatment of the source of
infection, killing diseased animals, homeless dogs and cats, improving sanitation and living
conditions of population, personal hygiene, control of traumatism, and specific prophylaxis.
Q.15 Epidemiological features of intestinal infections.

Source of infection: at typhoid fever, shigellosis, paratyphoid A, some food poisonings – ill person
or bacteriocarrier; at Paratyphi B, Salmonella botulism - more often animals.
Bacteria carrying: acute, chronic, transient.
Mechanism of transmission: fecal-oral.
Ways of transmission: by the water, foods (at botulism – canned meat, mushrooms, as a rule
homemade), household things, dirty arms; flies.
Epidemics: contacts, water, food borne.
Seasonality: summer-autumn.
SUBTYPES:
• Subtype 1 - typical intestinal infection (agent stays in the GIT) shigellosis, cholera, echerichiosis.
• Subtype 2 - Toxic infection (intensive reproduction of the agent out of the organism) food-
poisoning, botulism and staphylococcal toxicosis
• Subtype 3 - intestinal infection with spreading of the agent beyond the intestine (amebiasis,
ascaridiasis, echinococcosis)
• Subtype 4 - intestinal infection with penetration of the agent into blood with additional outlet of the
agent in the environment with the urine, secretions (typhoid fever, brucellosis, leptospirosis)
Additional optional information:

• As a microbe is released into the environment with faeces, urine, vomitus (cholera), it can cause
disease in a healthy person only after ingestion with food or water.
• They are characterized by location of the causative agents in the intestine and their distribution in
the environment with excrements.
• If the causative agent circulates in the blood (typhoid fever, paratyphoid A and B, leptospirosis, viral
hepatitis, brucellosis, etc.) it can also be withdrawn through various organs of the body, e. g. the
kidneys, lungs, the mammary glands.
• Intestinal infections occurs usually during the warm seasons.
• The main means of control of intestinal infection are sanitary measures that prevent possible
transmission of the pathogenic microorganisms with food, water, insects, soiled hands, etc.
• Specific immunization is only of secondary importance in intestinal infections.
Q.16 Epidemiological features of respiratory infections.

Source of infection- sick person, carries
Mechanism of transmission- Air-droplet, direct contact
• This group includes diseases whose causative agents parasitize on the respiratory mucosa and are
liberated into the environment with droplets of sputum during sneezing, cough, loud talks, or noisy
respiration.
• People get infected when the microbes contained in sputum get on the mucosa of the upper airways.
• If the causative agent is unstable in the environment, a person can only be infected by lose contact
with the sick or carrier.
• Pathogenic microorganisms causing some diseases can persist for a period of time in an enclosure
where the sick is present.
• Infected particles of sputum or mucus can dry and be suspended in the air.
• Some diseases of this group can spread through contaminated linen, underwear, utensils, toys, etc.
• Transmission can be minimised by control of overcrowding, proper ventilation and isolation of
enclosures, using UV-lamps, wearing masks, respirators, disinfection.
Q.17 Epidemiological features of blood infections.
Source of infection: sick person, carrier
Mechanism of transmission: transmissible
Vector: insects, fleas, mosquitoes, tick
Seasonality: warm season
• The diseases of this group are transmitted by blood-sucking insects, such as fleas, mosquitoes, ticks,
etc., which bite people and introduce the pathogenic agent into the blood.
• Control of blood infections includes altering natural conditions, improvement of soils, draining
swamps, destroying sites where the insects multiply, disinfection measures against mosquitoes,
ticks, etc., detoxification of sources of infection by their isolation and treatment, carrying out
preventive measures.
• If the source of infection are rodents, measures to control them are taken. Active immunization is
also effective.
Q.18 Epidemiological features of infections of external coverings.

• The diseases of this group occur as a result of contamination of the skin or mucosa with the
pathogenic microorganisms.
• They can remain at the portal of infection (tetanus, dermatomycoses), or affect the skin, enter the
body and be carried to various organs and tissues with the circulating blood (erysipelas, anthrax).
• The transmitting factors can include bed linen, clothes, plates and dishes and other utensils, that can
be contaminated with mucus, pus or scales.
• Pathogenic microorganisms causing venereal diseases, rabies, AIDS, and some other diseases are
transmitted without the agency of the environmental objects.
• The main measures to control skin infections include isolation and treatment of the source of
infection, killing diseased animals, homeless dogs and cats, improving sanitation and living
conditions of population, personal hygiene, control of traumatism, and specific prophylaxis.
Q.19 Epidemiology and prevention of HIV

HIV (human immunodeficiency virus) is a viral disease of human, which is passed mainly by sexual
and parenteral ways and characterized by long-term persistence. Defeat of the thymus glands system
of immunity, causes clinically expressed form - syndrome of acquired immune deficiency (AIDS) with
lymphadenopathy, intoxication, spreading of infectious diseases and oncological processes.
EPIDEMIOLOGY:
• Source of infection: sick and carrier (contagious during all life)
• Mechanism of transmission: contact (wound), vertical
• Ways of transmission:
- Natural: sexual, vertical (transplacenter, childbirth, during breast feeding)
- Artificial: parenteral manipulations and drug using, blood recipients, transplantation of organs,
artificial ingravidation
- Professional: infection of medical personnel
Epidemiology: Youths tend to have the highest HIV diagnosis rates.
In southern Africa, Bostwana, Lesotho, India, Mozambique and Nigeria have the highest cases
PREVENTION OF HIV
We can use strategies such as:
• Abstinence (not having sex)
• Use condoms
• Avoid multiple sex partners / Limit sex partners
• Get tested. Be sure you and your partner are tested for HIV and other STIs
• Never reuse or "share" needles, syringes, water, or drug preparation equipment.
• Only use needles and syringes that you got from a reliable source (such as drugstores or needle
exchange programs).
• HIV prevention medicines such as pre-exposure prophylaxis (PrEP) and post-exposure prophylaxis
(PEP).
Q.20 The sanitary protection of the territory from delivery and

spreading of infections that may have international importance.
• mass-scale measures aimed at improvement of public health, prevention and spread of infectious
diseases;
• medical measures aimed at reduction of infectious morbidity and eradication of some diseases;
• health education and involvement of population in prevention or restriction of the spread of
infectious diseases;
• Prevention of import of infectious diseases from other countries.
PREVENTIVE MEASURES aimed to control infectious diseases taken by medical personnel are
divided into:
1. Preventive
2. Anti-epidemic
➢ Preventive measures: are carried out regardless of the presence or absence of infectious diseases
at a given time and locality. These measures are aimed at prevention of infectious diseases.
➢ Anti-epidemic measures: measures must be put in place to control or terminate the source of
infection, transmission mechanism, and susceptibility of population.
• Exclusion of any of these factors terminates the spread of an epidemic process.

• Prophylactic and antiepidemic measures are therefore aimed at control of the source of infection,
disruption of the route by which infection spreads, and strengthening of non-susceptibility of
population.
• Control of infection source.
• The infectious patients must also be isolated in proper time.
Q.21 Typhoid fever. Epidemiological features (source of agent, factors
of transmission, signs of epidemic process), preventive and anti-
epidemic measures.
Source of infection: ill person or bacterio-carrier
Bacteria carrying: Salmonella Typhi
Infectiveness: last days of incubation period, all period of the disease
Mechanism of transmission: fecal-oral.
Ways of transmission: by the water, foodstuffs, household things, dirty arms; flies.
Epidemics: contacts, water, food borne.
Susceptibility (index of contagiousness): 0.4
Seasonality: summer-autumn.
Incubation period: from 7 till 25 days.
CLINICAL SIGNS OF THE TYPHOID FEVER:

• 1-st week:
- The beginning is gradual
- Complains: headache, tiredness, sleeplessness, anorexia, constipation or diarrhea
- Long fever 39-40°С (intermittent fevers), Paleness of skin, «typhoid» tongue, Duguet's angina
- Bradycardia, dicrotism of pulse, hypotonia
- Symptoms of bronchitis
• 2nd week:
- Typhoid rash: typhoid maculopapular rash (roseola elevata), some elements, localized on the
anterior abdominal wall and lateral walls («vest»), new elements can appear, sometimes is
present longer than fever.
- Hepatosplenomegaly,
- Status typhosus
- Serologic reactions.
ANTIEPIDEMIC MEASURES:
• Examination on typhoid fever and paratyphoids all patients with fever, which last more than 5 days
(once on hemo-culture, and if fever continue more than 10 days Widal’s reaction of
hemaaglutination or RIHA)
• Examination of all persons, who are working at the industries dealing with food, for detection of
bacteriocarriers
• Obligatory hospitalization infectious hospital of patients and carriers into infectious hospital
• Observation of contact persons during 25 days and their separation from other people
• Every day thermometry, interrogation and medical examination
• One analyze of feces on coproculture and blood antibodies on Vi-antibodies
• Convalescents are discharged from hospital only after clinical recovery and three-time analysis of
feces and urine with 5-days interval, and bile in 10 days after disappearing of clinical signs, if results
are negative
• Three-month observation and 2-years registration in sanitary-epidemic department with several
times bacterial examination
• Current and final disinfection.
Q.22 Hepatitis A. Epidemiological features (source of agent, factors of
transmission, signs of epidemic process), preventive and anti-epidemic
measures.
Hepatitis A (formerly known as infectious hepatitis) is an acute infectious disease of the liver caused
by the hepatitis A virus (HAV).
EPIDEMIOLOGY:
• Mechanism of transmission - Fecal-oral, Watery route Alimentary route Contact way (dirty hands,
towels, dishes etc.)
• Source of infection - Patients in the incubation, prodromal period and climax of the disease
• Susceptibility - Children after the first year of life, teenagers, young people up to 35 years, patients
with immunosuppression.
• Factors - Contaminated Water, infected food products and household items.
• Incubation period - between 2 and 6 weeks and the average incubation period is 28 days
Hepatitis A infection causes no clinical signs and symptoms.

It does not have a chronic stage, is not progressive, and does not cause permanent liver damage.
Following infection, the immune system makes antibodies against HAV.
PREVENTION: Hepatitis A can be prevented by vaccination, good hygiene and sanitation.
Q.23 Shigellosis. Epidemiological features (source of agent, factors of

measures.
DEFINITION- Shigellosis is a bacterial infection that affects the digestive system. Shigellosis is
caused by a group of bacteria called Shigella. Gram negative bacteria from the family
enterobacteriaceae, most non-motile, non-sporing. Possess capsule (K antigen) and O antigen.
EPIDEMIOLOGY
• Infective agent: Sh. Dysenteriae, Sh. Flexneri, Sh. Boydii, Sh. Sonnei
• Source of infection: Sick patients, patients in period of convalescence and carriers.
• Mechanism of transmission: fecal-oral
• Ways of transmission: water (Shigella flexneri), food stuffs (Shigella sonnei), dishes, dirty hands,
flies
• Epidemic features:
- season: summer & fall
- age: affects younger children more
• Immunity: type-specific
ANTI-EPIDEMIC MEASURES:
• Medical supervision after contact persons (7 days)
• Bacteriological investigation of stool (decree group only)
• Serological investigation
• Disinfection - current, final
Laboratory diagnosis:
• CBC: left shift leukocytosis, increased ESR
• Stool, feces, vomiting mass or gastric lavage culture for Shigella, colorless colonies on Mackonkey
agar or Eosin methylene blue agar
• Serological reactions: increasing antibody titre to Shigella
• PCR: detection of shigella DNA in feces and scrapping of the rectum mucous
Q.24 Cholera. Epidemiological features (source of agent, factors of

measures.
Cholera is an acute anthroponosic infectious disease caused by eating contaminated food or drinking
contaminated water that leads to severe watery diarrhea and vomiting, which can result in dehydration
and even death if untreated.
EPIDEMIOLOGY:
• Infective agents: vibrio cholera (classic, El-Tor)
• Source of infection: sick person, reconvalescent after cholera or clinically healthy vibrio-carriers
• Mode of transmission: Contaminated food and water use, contact with fecal matter of infected
persons, ingestion of contaminated seafood
• Seasonal prevalence: summer-autumn
• Mode of occurrence: Occur as outbreaks with an explosive character of illness affecting a mass of
people that fall ill over a short period of time
• Incubation period: 48hours-5days
• Susceptibility of a person is general and high.
• In endemic areas morbidity is observed more frequently in children and elderly persons.
• Endemic areas: Most especially in the tropics
Prophylaxis and Antiepidemic measures at exposure of ill person or carrier:

• Immediate isolation of sick into the extremely dangerous infections hospital and treatment
• Discharging after 3 negative results of bacteriological investigation
• Active isolation of new episodes of the disease (everyday rounds of all inhabitants of problem
settlement)
• Active isolation of new episodes of the disease (everyday rounds of all inhabitants of problem
settlement)
• Isolation for 5 days into isolation ward everybody that were in contact.
• Laboratory examination on Cholera
• Disinfection
• Quarantine
Q.25 Diphtheria. Epidemiological features (source of agent, factors of

measures.
typical complications on the part of the nervous system, cardiovascular system and excretory system.
EPIDEMIOLOGY-
Infectious agent: Corynebacterium diphtheria
Source: sick person, carriers (convalescent or healthy)
Way of transmission: airborne, contact
Sensibility: high, adults more often become sick
Season character: autumn and winter
Immuno defense: antitoxic, post vaccine
Incubation period: 2 to 10 days
PREVENTION:
• Plan immunisation (3, 4, 5 months with DTaP, revaccination in 18months, then 6, 11, 14, 18years
and adults every 10 years)
• In focus - 7 days medical observation after contact with sick person
• Bacteriological examination
• Sanitation of detected carriers
• Final disinfection
• Revaccination
CLINICAL MANIFESTATION:
• Phenomena of intoxication (high fever, malaise, general weakness, headache)
• Pharyngalgia - moderate
• Changes of a throat mucous - soft hyperemia, edema of tonsills, covers on their surface (grey colour,
dense, hard to remove with bleeding, slime), spread out of tonsills limits (palatopharyngeal arches,
uvula, soft palate)
• Augmentation and moderate morbidness of regional lymph nodes
• Edema of a hypodermic fat of a neck.
Q.26 Salmonellosis. Epidemiological features (source of agent, factors

epidemic measures.
Salmonellosis is an anthropozoonotic, foodborne infection, characterized by essential damage of the
gastrointestinal tract leading to diarrhea (sometimes bloody), abdominal cramps, fever, and more
rarely, by typhus-like or septicopyemic manifestation.
ETIOLOGY: It is caused by Salmonella species of bacteria from the Enterobacteriaceae family. All
nontyphoid species of Salmonella may cause Salmonellosis.
Eg. Salmonella typhimurium, Salmonella enteritidis
EPIDEMIOLOGY:
• Source of infection: contaminated food (poultry, eggs, beef, etc.), contaminated water, contact with
infected animals or their faecal matter, sick people or carriers.
• Mode of transmission: Unhygienic cooking environments and persons, improperly cooked foods.
• Vectors of the infection: Flies, cockroaches, rats.
• Mechanism of transmission: Faecal-oral route.
• Mode of occurrence: Occur as separate sporadic cases and as outbreaks.
• Incubation period: 12-72 hours but can be longer.
• Susceptibility of a person depends on the premorbid state of the macroorganism and the quantity
and variety (serotypes) of Salmonella present.
Salmonella can remain viable in water for 11-120 days, in the sea water - 15-27 days, in soil - 1-9
months, in sausage products - 60-130 days, in the eggs, vegetables and fruits till 2.5 months.
PREVENTION:
• Veterinary-surveillance upon animals and production of meat and dairy industry, laboratory control
of food stuffs.
• It is necessary to reveal carriers on milk farms, in foods, children’s and medical establishments.
• The maintenance of the rules of personal hygiene and rules of food’s cooking plays an important
role in prophylaxis of Salmonellosis.
Q.27 Botulism. Epidemiological features (source of agent, factors of

measures.
DEFINITION - Botulism is a rare but serious condition caused by toxins from bacteria called
Clostridium botulinum. The toxin blocks acetylcholine release from the presynaptic membranes
resulting in weakness, flaccid paralysis, and, often, respiratory arrest.
Eight immunologically distinct toxin types have been described such as types A, B, C, D, E, F, G.
Types А, В and E most commonly cause disease in man; types F and G have only rarely caused human
illness. Types С and D are associated with animal botulism, especially in cattle, ducks and chickens.
EPIDEMIOLOGY
Reservoir - grass feeding animals
Incubation period - 2 to 12hours till 10 days (6-24hours)
Three common forms of botulism are:
• Foodborne botulism: The harmful bacteria thrive and produce the toxin in environments with little
oxygen, such as in home-canned food.
• Wound botulism: If these bacteria get into a cut, they can cause a dangerous infection that produces
the toxin.
• Infant botulism: This most common form of botulism begins after Clostridium botulinum bacterial
spores grow in a baby's intestinal tract. It typically occurs in babies between the ages of 2 months
and 8 months.
Mechanism of transmission:
• Food borne (canned foods) contact, airborne
• Spores widespread in soil, contaminated vegetables and meat
• Foods canned without adequate sterilization
PREVENTION:
• The observance of the sanitary and hygienic rules at processing, transportation, keeping and
preparing of the food-stuffs expert possibility of accumulation of botulotoxin.
• It is necessary to perform the strict control under sterilization and keeping preserved food-stuffs.
Cook meats, mushrooms and vegetables properly.
Q.28 Meningococcal infection, purulent bacterial meningitis.

Epidemiological features (source of agent, factors of transmission,
signs of epidemic process), preventive and anti-epidemic measures
Etiology: Neisseria meningitidis
Serotypes: A, B, C, D, X, Y, Z
Source of infection: Carrier and sick people (patients with meningococcal nasopharyngitis and
generalized form of infection)
Mechanism of Transmission: air droplets
Seasonal occurrence: February to April
Immunity: type specific, steady
Entrance gate: upper respiratory routes
SYMPTOMS:
Fever, headache, vomiting, rigidity of neck, positive kernic sign, star-like hemorrhagic rash on thighs
buttocks and trunk, Seizures.
ANTI-EPIDEMIC MEASURES AGAINST THE SOURCE OF INFECTION:

• Revealing of patients with meningococcal meningitis and sepsis and their hospitalization.
• Patients with meningococcal nasopharyngitis should be hospitalize in infectious hospital or isolate
at home.
• Isolation of patients till their clinical convalescence and negative bacteriological investigation.
• Contact persons should be observed during 10 days with their thermometry every day, skin and
throat examination and bacteriological test
• Persons with rash and inflammatory changes in the throat should be isolated and observed
• In child's institutions apply 10-days quarantine
• Sanitation of carriers by antibiotics (ampicillin, erythromycin) and discharging after double
bacteriological investigation.
Q.29 Hepatitis B. Epidemiological features (source of agent, factors of

measures.
DEFINITION - Hepatitis B is an infectious disease caused by the hepatitis B virus (HBV) that affects
the liver; it is a type of viral hepatitis. It can cause both acute and chronic infection. Many people have
no symptoms during the initial infection.
EPIDEMIOLOGY:
• Etiology: Hepatitis B virus
• Source of infection: sick people and carriers
• Mechanism of transmission: contact
• Mode of transmission: Sexual, blood transfusion, drug users, barber shops, stomatologists, tattoo.
Hepatitis B can stay on tools for long, not killed by normal anaesthetic
• Factors: blood, sperm, vaginal secret, breastmilk
• Incubation period: 6 weeks to 6months
• Susceptibility: high
• Risk group: drug addicts, homosexuals, prostitutes, medical personal
FORMS-
• Asymptomatic form: the specific markers of infectious agent and proper immunological changes
are exposed only
• Sub-clinical form: immunologic, biochemical and histological changes, however main clinical
signs of illness are absent
• Non-jaundice form: different clinical symptoms of illness are present except jaundice
• Jaundice form: jaundice, which is the main sign of hepatitis present
• Fulminant (malignant) form: extremely
SYMPTOMS: Jaundice, fever, fatigue, loss of appetite with nausea and vomiting, joint pain and
abdominal pain.
PREVENTION:
• Use of disposable medical instruments, thorough sterilisation of non-expendable instruments.
• Clinical and laboratory examination of blood and organ donors.
• Specific prophylaxis - vaccination against B hepatitis HB-Vax, Engerix-B
Q.30 HIV-infection. Epidemiological features (source of agent, factors
epidemic measures.
DEFINITION - HIV is a viral disease of human, which is passed mainly by sexual and parenteral
ways and characterized by long-term persistence. Defeat of the thymus glands system of immunity,
causes clinically expressed form - syndrome of acquired immune deficiency (AIDS) with
lymphadenopathy, intoxication, spreading of infectious diseases and oncological processes.
EPIDEMIOLOGY:
• Source of infection: sick and carrier (contagious during all life)
• Mechanism of transmission: contact (wound), vertical
• Ways of transmission:
- Natural: sexual, vertical (transplacenter, childbirth, during breast feeding)
- Artificial: parenteral manipulations and drug using, blood recipients, transplantation of organs,
artificial ingravidation
- Professional: infection of medical personnel
HIV High Risk Groups:
• Homo- and bisexuals
• Intravenous drugs addicts
• Recipients of blood, blood preparations and organs
• Prostitutes and other persons who conduct the disorderly sexual life
• Patients with venereal diseases and viral hepatitis B, C, D
• Children infected by HIV mothers.
Symptoms: Prolonged fever, prolonged diarrhoea, generalized lymphadenopathy, weight loss (
>10%), opportunistic infections, Kaposi sarcoma
Diagnostic Criteria: epidemiological data, clinical signs and laboratory data (IFA, immunobloting)
PREVENTION MEASURES:
• Selection and investigation of blood donors (obligatory 6-months quarantine of all plasma donors)
• Medical personal prophylaxis In case of medical accident:
- Pretreatment of dirty skin with 70 % ethyl alkohol, washing by water with soap, mucous
membranes - with clean water
- To register of case in special journal
- Investigation of suffer person concerning of HIV antibodies presence (in first 5 days, then - after
1, 3 and 6 months)
- Post contact prophylaxis during 72 hours (better 24-36) after accident
- In case of positive reaction - conclusion of special commission about the professional
contamination.
• Treatment of HIV from 28 weeks of pregnancy
• Cesarean section in 38 weeks term
• Treatment of mother and newborn
• Prohibition of breast feeding.
Q.31 Malaria. Epidemiological features (source of agent, factors of

measures.
DEFINITION - An infectious disease caused by protozoan parasites from the Plasmodium family
that can be transmitted by the bite of the Anopheles
EPIDEMIOLOGY-
Mechanism of transmission: Transmissive
Season: summer autumn
Symptoms: Attack of fever (chills-hot-sweat), Hepatosplenomegaly, hemolytic anemia (jaundice),
tachycardia, hypotonia, myalgia, diarrhoea, vomiting, loss of appetite, cyanosis, herpes.
PREVENTION MEASURES:
• Sanitarian patrolling of the state from delivery (quarantine infection contamination)
• Mandatory registration
• Sterilization of toolkit
• At detection of sick or carrier - parasitoscopy examination of all family members
• Anti-mosquito measures (melioration, usage of insecticides, repellents)
• Drug prophylaxis - primachinum 0,027gm/day for 14 days
Q.32 Plague. Epidemiological features (source of agent, factors of transmission,

signs of epidemic process), preventive and anti-epidemic measures.
Plague is a disease caused by Yersinia pestis usually found in small mammals and their fleas.
EPIDEMIOLOGY-
Causative agent: Yersinia pestes (flea)
Source of infection: zoonosis (rodent and fleas)
Possible ways of transmission: transmissive, contact, alimentary and droplet
Clinical forms:
• Skin Bubonic
• Primary pulmonary
• Secondary pulmonary
• Intestinal
• Primary septic
• Secondary septic.
Complications: Infectious toxic shock, meningitis, adeno phlegmon
Symptoms: Fever, Severe intoxication, Severe hemorrhagic inflammation of lymphatic nodes, lungs
and other organs through, Sepsis
ANTI-EPIDEMIC MEASURES:
• Prevention the import of infection from abroad;
• Making of natural cells of plague healthy;
• Urgent prophylaxis in the case of exposure of patient with a plague.
• Immunization of people.
• Vaccinations of population of certain territories;
• Urgent 6-daily prophylaxis by streptomycin tetracycline on suspicion of possible infection.
Q.33 Hemorrhagic Fevers Ebola and Marburg. Epidemiological

features (source of agent, factors of transmission, signs of epidemic
process), preventive and antiepidemic measures.
Ebola haemorrhagic fever is a severe, often-fatal disease in humans and nonhumans primates caused
by infection with Ebola virus.
EPIDEMIOLOGY-
Incubation period: Ebola (7-14days), Marburg (4-9days)
Etiology: filoviridae
Source: mice/rat (which are excreting the virus with urine, stool and saliva)
Mechanism of transmission: transmissive way (contact with blood n body fluids)
The contamination of the person descends by air: dust, nutritional and contact paths (routes). The
transplacental transmission of a virus from the pregnant woman is possible.
SYMPTOMS:
• Fever (39-40 degrees)
• Decreased visual equity (mist before eyes), Sharp headache
• Back ache and pain in muscles of extremities
• Photophobia, Nausea and vomiting
• Paleness nasolabial triangle, hyperemia of a face, necks, upper half of trunk
• The palpebral fissures are narrowed down, scleratis
• A mucosa of an oral cavity and pharynx are bright red with haemorrhages
• The Kerning’s signs, Brudzinsky sign can be determined and stiff neck
• On 3-5th day of illness on a neck, lateral areas of a thoracic cell, in axillaries fossas, above clavicles
occurs petechial eruption
• Then there are nasal, intestinal, pulmonary bleedings
• Cardiac sounds are dull; the initial tachycardia is replaced by a bradycardia, hypotonia
• Dryness of tongue, abdominal pain without definite localization, patients enlarged a liver and spleen
and the icterus are possible.
PREVENTION:
• Inactivated cultural, cerebral vaccines and recombinant of a vaccine
• Carry out a disinfestation in the natural locuses, For a disinfestation will use gexachloran.
• Medical observation in the focus for 10 days and Conduct mandatory final disinfection with 3 %
Chloraminum solution and chlorofos.
• For contact persons or one who was bitten by tongs in endemic districts enter a specific
immunoglobulin i.m. in doses 5-7.5 ml for adult, 2.5-3.5 ml - for children.
PRIMARY ANTI-EPIDEMIC MEASURES:
• After detection of sick with contagious hemorrhagic fevers Lassa, Ebola and Marburg, and also
yellow fever same, as well as at other quarantine infection contaminations.
• Patient will hospitalize in hermetic isolation ward with independent life support, monitor behind
absence of an air inflow from a zone of isolation ward, paste vent holes.
• The staff should work in a protective clothing, including a mask or respiratory supplied with a
special inhaler.
• Conduct careful current and final disinfection. The specific prophylaxis contagious hemorrhagic
fever.
• The quarantine for arriving from epidemic areas lasts 17 day.
• In endemic districts of yellow fever vaccination of the population by an alive “Dakar” vaccine or
17-D is carried out.
• The immunodefence is saved 10 years, and then make a revaccination.
Q.34 Lyme borreliosis. Epidemiological features (source of agent,

factors of transmission, signs of epidemic process), preventive and anti-
epidemic measures.
DEFINITION - Lyme borreliosis also known as Lyme disease, is an infectious disease caused by the
Borrelia bacterium which is spread by ticks.
ETIOLOGY: Borrelia burgdorferi
EPIDEMIOLOGY:
• Source of infection: ticks, Zoonoyic
• Infective agent: Borrelia burgdorferi
• Mechanism of transmission: transmissive, vectors
• Vectors: tick ixode
• Incubation period: 1-2 weeks
• The disease is currently recognized as the most common vector-borne disease in Europe and North
America.
Symptoms:
• Erythema migrans rash at the site of the bite (80% of patients)
• Flulike illness with fever, chills, and myalgias (50% of patients)
• Neurologic symptoms several weeks later (10–20% of patients)
• Cardiac symptoms (<10% of patients)
• Joint involvement months to years later (up to 60% of patients)
Diagnosis Criteria: Based on clinical signs especially (erythema migrans rash) and serological testing
(ELISA test and western blot).
PROPHYLAXIS:
Doxycycline (200 mg for adults or 4.4 mg/kg for children of any age weighing less than 45 kg).
Q.35 Enterobiasis, clinic and diagnostics.

ETIOLOGY:
• Enterobias vermicularis. Disease may also be called pinworm infection
• Enterobias vermicularis is a small (1 cm in length), white, threadlike nematode
• Typically inhabits the cecum, appendix, and adjacent areas of the ileum and ascending colon
• Gravid females migrate at night to the perianal and perineal regions.
• Human infections occur by the faecal-oral route.
CLINIC:
itching in anal areas more prominent at night which leads to restlessness and difficulty in sleeping. At
night, the female worm moves to anus and deposit its eggs and dies.
DIAGNOSIS:
Eggs detected in cellulose tape preparations applied to patient’s perianal region in the early morning
prior to bathing or using toilet.
TREATMENT:
• Good hand hygiene and wash perianal areas well.
• Wash clothes and bed linen well.
• Can also give one dose of pyrantel pamoate one dose repeated in 2 weeks.
• Petroleum jelly is given to relieve itching
Q.36 Whip-worm infection, clinic and diagnostics.

ETIOLOGY:
Trichuris Trichiura worm has whip-like form of the body
CLINIC:
Usually asymptomatic. A heavy worm burden may result in mechanical damage to the intestinal
mucosa due to adult work threaded into epithelium of cecum. This can lead to abdominal cramps,
tenesmus, dysentery and prolapsed rectum.
DIAGNOSIS:
Microscopic stool exam shows barrel shaped ova
Q.37 Ascariasis, clinic and diagnostics.
DEFINITION - Ascariasis, also known as roundworm, is an intestinal infection caused by the
parasitic worm. Ascariasis lumbricoides, and is part of a family of parasites known as the soil-
transmitted helminthes.
ETIOLOGY: Ascaris Lumbricoides worm
CLINICAL SIGNS:
• Patient may have signs of pneumonitis with cough and low-grade fever during the migration of
larvae through the liver and lungs. Can be accompanied by wheezing and eosinophilia
• In heavy worm burdens, adult worms migrate in intestine resulting in intestinal blockage which lead
to vomiting, abdominal pain
DIAGNOSIS:
• Adult worms may be expelled through anus, mouth or nose
• Eggs seen on microscopic stool exam
Q.38 Complications of ascariasis.

DEFINITION - Ascariasis, also known as roundworm, is an intestinal infection caused by the
parasitic worm. Ascariasis lumbricoides, and is part of a family of parasites known as the soil-
transmitted helminthes.
ETIOLOGY: Ascaris Lumbricoides worm
COMPLICATIONS:
- Volvulus
- Intussuception
- Hepatic abscess
- Acute cholangitis
- Peritonitis
- Biliary colic
- Acute cholecystitis
- Acute pancreatitis
- Upper GI bleeding
Q.39 Epidemiology and pathogenesis/ life cycle of ancylostomiasis.

DEFINITION - Ancylostomiasis is the infection caused by hookworm Ancylostoma duodenale.
Ancylostomiasis is caused when hookworms, present in large numbers, produce an iron deficiency
anemia by sucking blood from the host's intestinal walls.
ETIOLOGY: Anclystoma duodenale (hookworm)
LIFE CYCLE:
• Ingestion of worms: adult worms live in small intestine, attached firmly to the mucous membrane
of the gut lining and feed on blood and tissue
• Adult females deposit their eggs in the gut and are passed out in feces
• They survive in light sandy loam soil feeding on bacteria.
• After one week, they become infective and move to position for suitable host to pass
• They enter organism by ingestion
• Enter blood vessels and are carried to heart, lungs and trachea
Q.40 Clinic and complications of ancylostomiasis

DEFINITION - Ancylostomiasis is the infection caused by hookworm Ancylostoma duodenale.
Ancylostomiasis is caused when hookworms, present in large numbers, produce an iron deficiency
anemia by sucking blood from the host's intestinal walls.
CLINICAL FEATURES:
• Larva penetration into skin leads to pruritus.
• Adult work in intestine may cause intestinal necrosis and blood loss: abdominal pain, diarrhea,
nausea, vomiting.
• Chronic infection can lead to iron deficiency anemia.
• Mental and physical growth is retarded in children and growing youth in ancylostomiasis
• Unchecked ancylostomiasis infection may lead to fatty degeneration of heart, liver and kidneys,
ending in death.
COMPLICATIONS:
• Iron deficiency anemia, caused by loss of blood.
• Nutritional deficiencies (malnutrition)
• Intestinal ulcers
• Severe protein loss with fluid build-up in the abdomen (ascites)
Diagnostics of ancylostomiasis:
• Microscopic exam of stool deposits reveals ova
• Because hookworm species cannot be differentiated on the basis of their eggs, it is necessary to
culture larvae or to recover adult worms for morphologic study
Q.41 The Clinical picture and complications of strongyloidosis

DEFINITION - Strongyloides stercoralis is a human parasitic roundworm, commonly known as
threadworm, Inhabit small intestine mucosa (duodenum & jejunum) and causing the disease
strongyloidiasis.
Is transmitted by soil and can cause severe disease in immunocompromised individuals.
CLINICAL PICTURES:
• Initial skin penetration causes little reaction, repeated infections lead to hypersensitive reactions.
This leads to Larva currens: rapidly progressing urticarial attack.
• Migration of larva to the lungs may stimulate an immune response resulting in cough, wheezing
and fever
• Ulceration of intestines, can lead to malabsorption, GI bleeding and eosinophilia
• Hyper-infection syndrome: parasite and host reach an equilibrium where neither host nor parasite
suffers adverse reactions. It leads to the infection proliferation with immense numbers of larvae
migrating to every tissue in the body especially the lungs (pneumonitis), brain damage and
respiratory failure
• Skin phase: Dermatitis - An itchy, red rash that occurs where the larva entered the skin, creeping
eruption may also occur.
• Respiratory phase: Löffler's syndrome (pneumonitis + Asma)
• Abdominal phase: Infection may be asymptomatic (light infection)
• Symptoms resemble gastric ulcer; (stomach ache, bloating, and heartburn, hunger pain)
• Chronic intermittent diarrhea may be with yellow mucus. Constipation, Nausea and loss of appetite
COMPLICATION:
• Gastric ulcer resulting from damaged mucosa by the worms
• Intestinal obstruction occur in severe cases, edema may result in obstruction of the intestinal tract,
as well as loss of peristaltic contractions
• Immunosuppression
• Disseminated strongyloidosis - tissue damage
• Pneumonitis, Brain damage
• Respiratory failure
Q.42 Diagnostics of strongyloidosis
DEFINITION - Strongyloides stercoralis is a human parasitic roundworm, commonly known as
threadworm, Inhabit small intestine mucosa (duodenum & jejunum) and causing the disease
strongyloidiasis.
Is transmitted by soil and can cause severe disease in immunocompromised individuals.
DIAGNOSTICS:
• Faecal smear, with microscopy
• Multiple stool sample test to detect larvae
• Sputum or duodenal aspirates by enterotest or string test
• ELISA to detect antibodies
• Baermann’s Technique - involving fecal suspicion in water causing larvae migration to settle in
water.
Q.43 Clinical features and complications of trichinellosis

Trichinellosis is a parasite disease caused by a roundworm of the genus Trichinella.
ETIOLOGY: trichinella spiralis.
History of eating pork or sausage.
CLINICAL FEATURES: These symptoms include
• Eye puffiness,
• Splinter hemorrhage,
• Nonspecific gastroenteritis,
• Fever,
• Muscle soreness and pain,
• Gastrointestinal symptoms,
• Facial edema, eosinophilia, and subconjuctival, subungual, and retinal hemorrhages."
COMPLICATIONS:
• Myocarditis
• Pneumonia
• Meningoencephalitis
• Hepatitis
• Nephritis
• Systemic vasculitis
• Thrombophlebitis
• Thrombocytopenia
Q.44 Diagnostics of trichinellosis

Trichinellosis is a parasite disease caused by a roundworm of the genus Trichinella.
ETIOLOGY: trichinella spiralis.
History of eating pork or sausage.
DIAGNOSTICS:
• CBC: leukocytosis, eosinophils (low counts indicates an increased mortality rate)
• Blood test (microscopy)
• Antibody detection Using ELISA test
• Muscle biopsy: reveals larvae within striated muscles
• Lactate dehydrogenase: Levels of lactate dehydrogenase isoenzymatic forms (i.e., lactate
dehydrogenase fraction 4 [LD4] and lactate dehydrogenase fraction 5 [LD5]) are elevated in 50%
of patients
• Immunoglobulin E: immunoglobulin E levels are typically elevated
• Antibody detection (serological test)
• PCR: isolating and subsequent genetic typing
• Hypertensive skin test - positive
Q.45 Etiology and epidemiology of lymphatic filariasis

DEFINITION - Lymphatic filariasis commonly known as elephantiasis, is a neglected tropical disease
caused by parasitic worms known as filarial worms.
EPIDEMIOLOGY
• Infection occurs when filarial parasites are transmitted to humans through mosquitoes.
• Lymphatic filariasis is transmitted by different types of mosquitoes for example by the Culex
mosquito, Anopheles, and Aedes,
• Lymphatic filariasis is spread from person to person by mosquitoes.
• humans are definitive hosts.
• It is endemic in many tropical & subtropical countries like Africa, Asia, Western Pacific and
parts of America.
• The painful and profoundly disfiguring visible manifestations of the disease, lymphedema,
elephantiasis and scrotal swelling occur later in life and can lead to permanent disability.
CLINICAL PICTURE:
• Fever
• Inguinal or axillary lymphadenopathy
• Testicular and/or inguinal pain
• Skin exfoliation
• Limb or genital swelling
• Dry and paroxysmal nocturnal cough;
• Wheezing
• Dyspnea
Q.46 The clinical picture and complications of lymphatic filariasis

DEFINITION - Lymphatic filariasis commonly known as elephantiasis, is a neglected tropical disease
caused by parasitic worms known as filarial worms.
CLINICAL PICTURE:
• Fever
• Inguinal or axillary lymphadenopathy
• Testicular and/or inguinal pain
• Skin exfoliation
• Limb or genital swelling
• Dry and paroxysmal nocturnal cough;
• Wheezing
• Dyspnea
COMPLICATIONS:
• Chronic lymphedema,
• Hydrocele,
• Skin pigmentation,
• Renal impairment (eg. chyluria)
Q.47 Etiological therapy of nematodosis

Nematodosis are round worm infections.
TREATMENT:
• Antihelminthic:
- Albendazole
- Mebendazole- 15 mg/kg BW
- Thiabendazol : 50 mg/kg BW
- Oxfendazol : 5 mg/kg BW
- Pirantel
- Vermox
Preventive measures are as follows:
• Good hygiene and sanitation
• Avoidance of sources of infection (e.g., arthropod bites, rivers/streams, contaminated soils,
consumption of raw or undercooked fish, snails, and slugs).
• Public health activities such as vector control.
Q.48 Epidemiology and life cycle of beef tapeworm infection

Beef tapeworm infection (Taenia saginata). Taenia saginata commonly known as beef tapeworm;
unarmed tapeworm of man. It is an intestinal parasite of human and cattle. Taenia saginata infection
is generally asymptomatic.
LIFE CYCLE:
• Cattles are the only intermediate host of the T. saginata.
• Cattle will eat the eggs and the oncospheres will hatch in the duodenum under the influence of
gastric juices.
• It will envaginate into the intestinal walls and travel via the general circulatory system.
• The embryos will disseminate all over the body and develop cysticercus in striated muscles of the
cow within 70 days.
• Human beings will be infected if they eat the cow meat at this time.
• The life cycle in humans begins with the ingestion of raw or undercooked beef containing T.
saginata larvae.
• The larvae gets digested out of the beef in the human intestinal system.
• The worm then attaches on the intestinal mucosa of the upper small intestine.
• The tapeworm will digest food and grow longer.
• Mature tapeworms will release 10 single gravid proglottids daily via the feces or will
spontaneous be released from the anus.
• Proglottids are motile and will shed eggs as it moves. These eggs (containing the oncosphere) can
remain viable for several days to weeks in sewage, rivers, and pastures.
Q.49 Clinic and complications of beef tapeworm infection.

CLINICAL PICTURE:
• Heavy infection causes weight loss, dizziness, abdominal pain, diarrhoea, headache, nausea,
constipation, chronic indigestion and loss of appetite.
• It also causes antigenic reaction that induce allergic reaction
• It also rarely cause Ileus: disruption of normal propulsive ability of the gastrointestinal tract.
COMPLICATIONS:
• Systemic cysticercosis.
• Cyst rupture (hydatid cyst rupture rare)
• Vitamin B-12 deficiency
• Obstruction of the appendix or pancreatic or bile ducts (rare)
• Intestinal obstruction (rare)
• Cholangitis (rare)
• Cholecystitis (rare)
• Pancreatitis.
Q.50 Diagnostics of beef tapeworm infection

CLINICAL SIGNS:
Heavy infection causes weight loss, dizziness, abdominal pain, diarrhoea, headache, nausea,
constipation, chronic indigestion and loss of appetite. It also causes antigenic reaction that induce
allergic reaction.
DIAGNOSTICS:
• Microscopy. Proglottids or eggs can diagnosed in feces
• ELISA AND PCR
• When cysts presents in brain CT scan (computed tomography) are used.
• X-ray may be used
• Serologic tests
PREVENTION:
• Make sure you cook meat thoroughly
• Freezing to 5 degrees for 4days
TREATMENT:
• Praziquantel
• Niclosamide
• Albendazole
• mebendazole
Q.51 Epidemiology and life cycle of pork tape worm infection

The pork tapeworm (Taenia solium) is a tapeworm which has humans as its definitive host and often
pigs as intermediate or secondary host.
EPIDEMIOLOGY:
• It is found throughout the world and is most common in countries where pork is eaten. Eastern
Europe, Russia, Eastern Africa. Latin America
• Source of infection: Zoonosis (pigs)
• Mechanism of transmission: Oral (eating undercooked pork)
LIFE CYCLE:
• Eggs or gravid proglottids are passed with feces; the eggs can survive for days to months in the
environment.
• Pigs (T. solium) become infected by ingesting vegetation contaminated with eggs or gravid
proglottids
• In the animal’s intestine, the oncospheres hatch. The number and invade the intestinal wall, and
migrate to the striated muscles, where they develop into cysticerci. (A cysticercus can survive for
several years in the animal.)
• Humans become infected by ingesting raw or undercooked infected meat. In the human intestine,
the cysticercus develops over 2 months into an adult tapeworm, which can survive for years.
• The adult tapeworms attach to the small intestine by their scolex and reside in the small intestine
(Length of adult worms is usually 5 m or less for T. saginata (however it may reach up to 25 m) and
2 to 7 m for T. solium)
• The adults produce proglottids which mature, become gravid, detach from the tapeworm, and
migrate to the anus or are passed in the stool (approximately 6 per day).
Q.52 The clinical picture and complications of pork tapeworm

infection
The pork tapeworm (Taenia solium) is a tapeworm which has humans as its definitive host and often
pigs as intermediate or secondary host.
CLINICAL PICTURE:
• Most people with tapeworm infections have no symptoms or mild symptoms.
• They can cause digestive problems including abdominal pain, loss of appetite, weight loss, and upset
stomach.
• The most visible symptom of taeniasis is the active passing of proglottids (tapeworm segments)
through the anus and in the feces.
• Neurocysticerosis may include Headache.
• Lethargy.
• Confusion.
• Vision changes Weakness or numbness
COMPLICATIONS:
- Tapeworm can be lodged in appendix (Appendicitis),
- bile duct (cholecystitis),
- pancreatic duct (pancreatitis)
Q.53 The clinical picture and complications of cysticerocosis

Cysticercosis refers to tissue infection after exposure to eggs of Taenia solium, the pork tape worm.
The disease is spread via the oral route through contaminated food and water, and is primarily a food
born disease.
CLINICAL PICTURE:
• Cysts, called cysticerci, can develop in the muscles, the eyes, the brain, and the spinal cord
• Cyst in the brain or spinal cord causes neurocysticercosis.
• Seizures and headaches
• Confusion
• Difficult with balance
• Brain swelling and excess fluid around the brain.
• Stroke
• Cyst in the muscles can cause lumps under the skin (which can be tender)
• Myositis with fever and eosinophilia and muscular pseudohypertrophy. This can later progress to
atrophy and fibrosis
• Eyes: Cysticerci may be found in eyeball, extraocular muscles and subconjunctica.
May cause retinal edema, hemorrhage, decreased vision or visual loss.
COMPLICATIONS:
• Brain edema
• Hydrocephalus
• Chronic meningitis
• Vasculitis
• Paralysis
• Partial blindness
• Seizures, coma, and death.
Q.54 Diagnostics of pork tapeworm infection and cysticercosis.
Pork tape worm infection (taeniasis) is an intestinal infection with adult tapeworms that follows
ingestion of contaminated pork.
Diagnosis:
• Microscopic examination of stool for ova and proglottids
• CT and/or MRI and serologic testing for patients with central nervous system symptoms.
Cysticercosis- Cysticercosis is a parasitic tissue infection caused by larval cysts of the tapeworm
Taenia solium.
Diagnosis:
• Biopsy of infected tissue, microscopic examination
• ELISA: Antibodies to cyticerci
• CT or MRI of head
• CSF exam: pleocytosis, elevated protein levels and depressed glucose levels
Q.55 Epidemiology and life cycle of echinococcosis

Echinococcosis is a parasitic disease that occurs in two main forms in humans: cystic echinococcosis
(also known as hydatidosis) and alveolar echinococcosis, caused by the tapeworms Echinococcus
granulosus and Echinococcus multilocularis, respectively.
EPIDEMIOLOGY:
• Cystic echinococcosis is globally distributed in most pastoral and rangeland areas of the world, with
highly endemic areas in the eastern part of the Mediterranean region, northern Africa, southern and
eastern Europe, at the southern tip of South America, in Central Asia, Siberia and western China.
• Humans are infected through ingestion of parasite eggs in contaminated food, water or soil, or after
direct contact with animal hosts (dogs)
LIFE CYCLE:
• The adult Echinococcus granulosus resides in the bowel of its definite host.
• Gravid proglottids release eggs that are passed in the feces.
• These eggs are then ingested by a suitable intermediate host, including sheep, goat, swine, cattle,
horses and camels. The eggs then hatch in the bowels and release oncospheres that penetrate the
intestinal wall. These oncospheres then migrate through the circulatory system to various organs of
the host.
• At the organ site, the oncosphere develops into a hydatid cyst. This cyst enlarges gradually,
producing protoscolices and daughter cysts that fill the cyst interior.
• These cyst-containing organs are then ingested by the definite host, causing infection. After
ingestion, the protoscolices evaginate, producing protoscolexes.
• The scolexes of the organisms attach to the intestine of the definite host and develop into adults in
32-80 days.
• The life cycle then continues in humans: (Humans can become infected if they ingest substances
infected with Echinococcus eggs).
• The eggs then release oncospheres in the small intestine.
Q.56 The clinical picture and complications of echinococcosis

CLINICAL PICTURE:
• Human infection with E. granulosus leads to the development of one or more hydatid cysts located
most often in the liver and lungs
• Abdominal pain, nausea and vomiting are commonly seen when hydatids occur in the liver.
• If the lung is affected, clinical signs include chronic cough, chest pain and shortness of breath.
• Other signs depend on the location of the hydatid cysts and the pressure exerted on the surrounding
tissues. Non-specific signs include anorexia, weight loss and weakness.
COMPLICATIONS:
• Anaphylactic reaction, shock.
• Hepatomegaly,
• respiratory disease or pulmonary eosinophilia, coin lesion in lungs,
• ectopic calcification
Q.57 Diagnostics of echinococcosis

CLINICAL PICTURE:
• Abdominal pain, nausea and vomiting are commonly seen when hydatids occur in the liver.
• If the lung is affected, clinical signs include chronic cough, chest pain and shortness of breath.
• Other signs depend on the location of the hydatid cysts and the pressure exerted on the surrounding
tissues.
• Non-specific signs include anorexia, weight loss and weakness.
DIAGNOSIS:
• Ultrasonography, computed tomography (CT scan) and magnetic resonance imaging ( MRI scan)
• Serological test (Specific antibodies are detected) and can support the diagnosis of early detection
of E. granulosus and E. multilocularis infections, especially in low-resource settings.
• Biopsies of cyst to differentiate it from tumour.
Q.58 Epidemiology and life cycle of diphyllobothriasis
A fish tapeworm (diphyllobothriasis) infection can occur when a person eats raw or undercooked fish
that’s contaminated with the parasite Diphyllobothrium latum. The parasite is more commonly
known as the fish tapeworm.
EPIDEMIOLOGY:
This type of tapeworm parasite is most common in areas where people eat raw or undercooked fish
from lakes and rivers. Such areas include:
• Russia and other parts of Eastern Europe
• North and South America
• Some Asian countries, including Japan
• It may also be common in parts of Africa where freshwater fish are eaten.
LIFE CYCLE:
• Immature eggs are passed in feces.
• The eggs mature (approximately 18 to 20 days) and yield oncospheres which develop into a
coracidia
• After ingestion by a suitable freshwater the coracidia develop into procercoid larvae.
• Following ingestion of the copepod by a suitable second intermediate host
• The procercoid larvae are released from the crustacean and migrate into the fish flesh where they
develop into a plerocercoid larvae (sparganum)
• The plerocercoid larvae are the infective stage for humans. Because humans do not generally
eat undercooked minnows and similar small freshwater fish, these do not represent an important
source of infection.
• These small second intermediate hosts can be eaten by larger predator species, e.g., trout, perch,
walleyed pike In this case, the sparganum can migrate to the musculature of the larger predator fish
and humans can acquire the disease by eating these later intermediate infected host fish raw or
undercooked
• After ingestion of the infected fish, the plerocercoid develop into immature adults and then into
mature adult tapeworms which will reside in the small intestine.
• The adults of D. latum attach to the intestinal mucosa by means of the two bilateral groves (bothria)
of their scolex
• Eggs appear in the feces 5 to 6 weeks after infection.
Q.59 The clinical picture and complications of diphyllobothriasis

CLINICAL PICTURE:
• Fish tapeworm infections rarely present noticeable symptoms.
• Tapeworms are most often discovered when people notice eggs or segments of the tapeworm in
stool.
• Symptoms may include: diarrhea, fatigue, stomach cramps and pain, chronic hunger or lack of
appetite, unintended weight loss and weakness.
COMPLICATIONS:
• Anemia, specifically pernicious anemia caused by vitamin B-12 deficiency
• Intestinal blockage
• Gallbladder disease
Q.60 Diagnostics of diphyllobothriasis.

Way of transmission: Fecal - oral
Symptoms: maybe absent or minimal with eosinophilia, there can be occasional intestinal obstruction,
diarrhoea, and abdominal pain, vitamin B12 deficiency (megaloblastic anemia)
DIAGNOSIS:
• Microscopic exam of eggs or proglottids in stool
• We can see characteristic eggs from formol ether concentrate of feces. (The egg is usually ovoid
and has a small knob at the opercular end and is yellowish-brown in colour with a smooth shell, of
moderate thickness. They measure 58 – 75mm by 40 – 50mm in size.)
• Proglottids may also be seen in faecal samples usually in a chain of segments from a few centimeter
to about 0.5 meters in length.
• CBC: can reveal eosinophilia, anemia if there is B12 deficiency
• Peripheral smear: macrocytosis
TREATMENT: Praziquantel or Niclosamide
Q.61 Epidemiology and pathogenesis of opisthorchiasis.

Opisthorchiasis is defined as infection with Opisthorchis viverrini (Southeast Asian liver fluke) or O.
felineus (cat liver fluke).
EPIDEMIOLOGY:
• Acquired by eating infected raw or undercooked fish (fecal-oral)
• Opisthorchis felineus is an intestinal parasite of cats, dogs, foxes, pigs, cetaceans (such as whales
and dolphins) in Eastern Europe, Siberia and other parts of Asia.
• Opisthorchis viverrini is found in domesticated and wild dogs and cats in Southeast Asia.
• It is a very common human infection in North East Thailand.
PATHOGENESIS:
• Eggs are ingested by snail and undergo development (sporocyst to rediae to cercariae).
• Cerciae are released from snails and penetrate fresh water fish encysting as metacercariae in muscles
or under scales
• Humans become infected after eating raw or undercooked fish
• Metacercariae excyst in the duodenum and ascend through the ampulla of vater and into the biliary
ducts where they attach to the mucosa and mature. Adult flukes grow up to:
- 5 to 10 mm (O. viverrini)
- 7 to 12mm (O. felineus)
CLINICAL PRESENTATION:
• Most infections are asymptomatic.
• Mild infections may cause dyspepsia, abdominal pain, diarrhoea or constipation.
• Longer-term infections may cause more severe symptoms and may lead to hepatomegaly and
malnutrition.
Q.62 The clinical picture and complications of opisthorchiasis.

Opisthorchiasis is a parasitic disease caused by species in the genus Opisthorchis (specifically,
Opisthorchis viverrini and Opisthorchis felineus). Chronic infection may lead to cholangiocarcinoma,
a malignant cancer of the bile ducts.
CLINICAL PICTURE:
• Usually asymptomatic
• Eosinophillia,
• Diarrhea, epigastric and right upper quadrant pain, lack of appetite
• Fatigue, mild fever, weakness
• Jaundice
COMPLICATIONS:
• Edema of legs and ascites
• Cholangitis, periductal fibrosis, cholecystitis, Cholelithiasis
• Hepatitis and/or fibrosis of periportal system
• Cholangicarcinoma
Q.63 Diagnostics of opisthorchiasis.

Opisthorchiasis is a parasitic disease caused by species in the genus Opisthorchis (Opisthorchis
viverrini and Opisthorchis felineus) acquired by eating infected raw or undercooked fish.
DIAGNOSIS:
• The medical diagnosis is established by finding eggs of Opisthorchis in feces using the Kato
technique. The Kato technique is a laboratory method for preparing human stool samples prior to
searching for parasite eggs.
• Microscopic examination of stool; Detects the eggs in feces
• Ultrasonography, CT, MRI, cholangiography may show biliary tract abnormalities.
• ELISA Test to detect antigen 89 kDa seen in Opisthorchis viverrini
TREATMENT:
• Praziquantel,
• Albendazole,
• Mebendazole
Q.64 Etiological treatment of cestodosis (tapeworms) and trematodosis
(flukes).
• Tapeworm infections are all acquired by ingesting worm cysts or eggs.
• The most common infections result from undercooked fish (Diphyllobothrium latum), beef (Taenia
saginata), and pork (Taenia solium).
• Other tapeworms can be spread person-to-person (Hymenolepsis nana) or with contamination of
food by feces from infected dogs (Echinococcusspecies).
• Mature worms reside in the gut, releasing large numbers of eggs, but usually causing little disease.
• Most common syndrome of Tenia solium it causes is cysticercosis (infection with parasite cysts,
most often in the brain, following ingestion of food contaminated with parasite eggs from pig feces.)
• Trematodiases, also known as trematode infections, are a group of diseases caused by the parasite
trematodes.
• Symptoms of trematodiases can range from mild to severe depending on the species, number and
location of trematodes in the infected organism. Mostly causes flukes
ETIOLOGICAL TREATMENT
- Praziquantel: 75mg/kg.day orally three doses per day for 2 days
- Albendazole 10mg/kg/day for 7 days
- Mebendazole
- Triclabendazole
- Viable or degenerating parenchymal cysts: AED, steroids, antiparasitics
- Intraventricular cysts: endoscopic removal of cysts or VPS followed by antiparasitics and
steroids
- Subarachnoid: Steroids, antiparasitics (repeated courses?) +/- VPS
- Calcifications: AED (current rec’s against use of antiparasitics)
Drugs for cestode (Tapeworm) infections are generally treated with:

Niclosamide
▪ Praziquantel 25 mg/kg 3 times a day for 2 days taken with liquids during a meal
Drugs for trematode (flukes) infections:
▪ Praziquantel 10-20 mg/kg as a single dose OR 25 mg/kg 3 times a day
▪ 2-dose regimen of Triclabendazole 10 mg/kg PO x2 doses administered 12hr apart [ Used for
Fascioliasis].
▪ ALBENDAZOLE 10mg/kg/day for 7 days + Supplements ( vitamin B12, vitamin C , Iron ) in case
of anemia and their deficiencies.

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INFECTIOUS DISEASE

Q.1 The peculiarities of infectious diseases.

Q.2 Classification of infectious diseases.

Q.3 Principles of infectious diseases diagnosis.

Q.4 Methods of infectious diseases specific diagnostics.

Q.5 Principles of infectious diseases treatment.

Q.6 Principles of infectious diseases prevention

Disruption of infection transmission pathways

Q.7 Indications for hospitalization of patients with infectious diseases.

Q.8 stages of typhoid fever pathogenesis

Q.9 classification of typhoid

Q.10 main signs of typhoid in the initial period of the disease

Q.11 The pathognostic (main) symptoms of typhoid fever in the

Q.12 Description, terms of beginning and dynamics of rash in patients

• In paratyphoid A incubation period is 8-10 days, shorter than typhoid fever

Q.14 Peculiarities of paratyphoid B

Q.15 Signs of possible relapse of typhoid fever

Q.16 Differential diagnosis of typhoid fever and influenza.

• Influenza is caused by a RNA virus (orthomyxovirus).

Clinical presentation (Usually presents with Usually presents as upper

Physical Exam Maculopapular rash, coated tongue, high temperature, headaches,

Q.18 Pathogenesis, clinical manifestations of small intestine perforation

Q.19 Pathogenesis, clinical manifestations of intestinal bleeding at

Q.20 Methods of specific diagnostics of typhoid fever. Interpretation of

Q.21 The principles of typhoid fever treatment.

• Vi capsular polysaccharide Vaccine against the capsular (Vi) antigen **

Q.22 Etiology and epidemiology of salmonellosis.

Q.23 Etiology and epidemiology of food poisonings.

Q.24 Clinical signs of salmonellosis localized forms.

Q.25 Clinical signs of salmonellosis generalized forms.

Q.26 Clinical manifestation of food toxicoinfection.

2) Caused by Clostridium perfringens:

3) Caused by Staphylococcus species:

Q.27 The differential diagnosis of salmonellosis and shigellosis.

SOURCES OF INFECTION • contaminated Poultry, • sick persons and

CHARACTER OF Mucous, watery green Watery stools with gross blood

Q.29 Methods of salmonellosis specific diagnostics.

Q.31 Emergency aid at a localized form of salmonellosis and at food

Treatment of salmonellosis and food toxicoinfection:

Q.33 Etiology and epidemiology of cholera.

Q.35 Classification of cholera.

According to Clinical forms:

According to the Degree of Severity:

Q.37 Differential diagnosis of cholera and salmonellosis.

Q.38 Differential diagnosis of cholera and shigellosis.

Q.39 The principles of cholera treatment.

Q.41 Etiology and epidemiology of enteroviral infection.

Q.42 Clinical forms of enteroviral diseases.

Q.44 Laboratory diagnosis of enteroviral infections.

Q.45 Principles of enteroviral diseases therapy.

Q.47 Clinical classification of shigellosis.

Q.48 Peculiarities of shigellosis, depending on the clinical form.

Q.50 Laboratory diagnosis of shigellosis.

Q.51 The treatment principles of shigellosis patients.

Q.52 Etiology and epidemiology of amebiasis.

Q.53 Clinical classification of amebiasis.

Q.54 The features of clinical duration of amebiasis intestinal forms.

Q.55 Clinical signs of extraintestinal amebiasis.

Q.57 Laboratory diagnosis of amebiasis.

Q.58 The treatment principles of amoebiasis patients.

Q.59 The etiology and epidemiology of giardiasis.

Q.60 Clinical signs of giardiasis.