P 1 Infectious

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.

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
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

DEFINITION - Diphtheria is an acute infectious disease caused by Corynebacterium 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

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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.