Etiology: Salmonella typhi (gr-)

Source of infection: patient or carrier

Transmission mechanism: fecal-oral
Transmission routes: food, water, contact
Anthroponosis
Pathogenesis: stomach-small intestine - lymphoblastic intestine - lymphogenous dissemination -
bacteremia - parenchymal diffusion - secondary bacteremia - excretory excretion with feces, urine -
sanation of the body
Pathomorphology: 1 week - "cerebral swelling" of Peyer's plaques and solitary follicles; 2 week -
necrosis; 3 week - the formation of "dirty" ulcers; 4 week - the stage of "clean" ulcers; 5-6 weeks -
healing of ulcers.
Clinic: gradual (less often acute) onset, staged-like fever, headache, insomnia, loss of appetite,
flatulence, adynamia, characteristic language, hepatosplenomegaly, relative bradycardia,
hypotension, roseolean rash on days 8-11, leukopenia with lymphocytosis and aneosinophilia
Diagnosis: hemoculture, RNGA with O-, H- and Vi-diagnosticums (1: 200)
Treatment: SPR up to 10 days of normal temperature
Antibacterial therapy: ciprofloxacin, levomycetin, cephalosporins 2-3 pcs. up to 10 days of normal
temperature

Dysentery
Etiology: Shigella (dysenteriae, flexneri, boydii, sonnei) (gr-)
Transmission mechanism: fecal-oral
Transmission routes: food, water, contact-household
Anthroponosis
Pathogenesis: stomach-intestine (production of entero, cytotoxins, endotoxins, diarrhea syndrome) -
invasion in colon epithelium (colitis)
Pathomorphology: acute catarrhal inflammation, fibrinous-necrotic inflammation, stage of
ulceration, healing of ulcers
Clinic: the most characteristic is the colitis variant: acute developing fever and intoxication, which
outstrip the development of gastrointestinal damage; distal colitis: pain cramping in the left ileal
region, tenesmus, spasmodic sigmoid colon, stools frequent, diluted, with an admixture of mucus
and blood, in the form of rectal spitting
Diagnosis: feces investigation, EIA, RPGA, RNGA, coprogram, sigmoidoscopy
Treatment: fluoroquinolones, aminoglycosides, cephalosporins 3 p., Bacteriophage, rehydration,
enterosorbents, enzymes, antispasmodics.

Salmonellosis
Etiology: Salmonella (enteritidis, typhimurium, panama, infantis, newport)
(gr-)
Transmission mechanism: fecal-oral
Transmission routes: food, water, contact-household
Anthropozoonosis
Pathogenesis: gastrointestinal tract - adhesion, colonization of enterocytes - production of
enterotoxin - exudative diarrhea, intoxication
Pathomorphology: hyperemia, edema, spot hemorrhages in the mucosa of the small and partially
large intestine
Clinic: syndrome of intoxication (fever, chills, weakness, adynamia, headache); Gastrointestinal
syndrome - predominantly gastroenteritis (nausea, vomiting, periodic pains in epigastric, umbilical,
ileacinal areas ("salmonella" triangle), stool disorder - feces malodorous, abundant, watery, with
undigested food, color of swampy mud, possible mucus and blood admixture (less often than with
dysentery), dehydration syndrome.
Diagnosis: fakisledovanie excrement, vomit, IFA, RPGA, express methods: RIF, RLA
Treatment: diet, rehydration, fluoroquinolones, intetriks, cephalosporins 3 p., Enterosorbents,
enzymes, eubiotics, antispasmodics.

Cholera
Etiology: Vibrio cholera (classica, El-Tor) (gr-)
OOI!
Stay in the hearth!
Transmission mechanism: fecal-oral
Transmission routes: food, water, contact-household
Pathogenesis: gastrointestinal tract - adhesion, colonization of vibrios on the surface of enterocytes
and in the lumen of the small intestine - isolation of the cholerogen - activation of the secretion of
electrolytes and liquid - development of dehydration according to the isotonic type
Pathomorphology: the sharp dehydration of all tissues, the thickening of blood, the fullness of
serous membranes, in the parenchymal organs - dystrophic changes.
Clinic:
- acute onset of the disease;
- often normal body temperature;
- Frequent watery stools of turbid white color, with floating flakes, reminiscent of rice decoction;
- vomiting, which has joined after the onset of diarrhea;
- Absence of pain in the abdomen;
- decreased diuresis;
- cramps in the limbs;
- dry skin and mucous membranes, hoarseness of voice;
- tachycardia, lowering blood pressure.
Diagnosis: examination of feces, vomit, RN, IFA, RIF.
Treatment: NB! Patients with cholera (or with suspicion of cholera) are subject to mandatory
hospitalization in an infectious inpatient. rehydration !! Trisol, Acesol, Chlosol, Quartasol.
Antibiotics: fluoroquinolones, doxycycline, furazolidone

Foodborne diseases
Etiology: (gr +): staphylococci, clostridia, streptococci and (gr-): esherichia, klebsiella, enterobacter,
citrobacter
Transmission mechanism: fecal-oral
Transmission routes: food, water
Saprozooanthroponosis
Transmission factors: meat and dairy products, eggs, culinary products
Pathogenesis: the development of exotoxins (enterotoxins) - activation of the adenylate / guanylate
cyclase system and endotoxins - activators of the arachidonic cascade.
Epidemiological anamnesis: typical group morbidity, it is necessary to collect a "food" anamnesis for
1-2 days before the onset of the disease
Clinic: - acute, sudden onset;
- Short-term illness;
- the level of fever and the severity of intoxication depend on the etiology and dose of toxins;
- multiple vomiting;
- a loose stool, watery, plentiful;
- dehydration.
NB! On the call: it is necessary to take away the remains of food products.
Diagnosis: isolation of the causative agent from vomit, gastric wash and feces. Agglutination reaction
with auto-stam. Identification of the causative agent isolated from the infected product and from
the patient
Treatment:
Immediately wash the stomach first with water, and, after taking the first wash water for
bacteriological examination, rinsing is continued with 2-4% sodium hydrogen carbonate solution
until a clean wash water is obtained.
Rehydration, detoxification

Botulism
Etiology: Clostridium botulinum (anaerobic, gr-), forms spores
Toxicoinfection!
Transmission mechanism: fecal-oral or contact (with wound botulism).
Transmission routes: food, air-dust, contact-household
Main reservoirs and sources of infection:
- external environment
- warm-blooded animals
Pathogenesis:
Hit Cl. botulinum and its toxin in the digestive tract
Absorption of toxin into the blood
Binding of Toxin with Nervous Structures
The inhibition of parasympathetic nervous system activity by toxin
Paresis of the intestine and suppression of the secretion of digestive glands
Excretory excretion from the body
Clinic:
- the onset of acute;
- normal or subfebrile temperature;
- can be vomiting and loose stool, which quickly gives way to a persistent constipation;
- dry mouth;
- Muscle weakness;
- signs of damage to the nervous system: ophthalmoplegic, defeat of the nuclei of the facial nerve,
violation of swallowing and speech, paresis and paralysis, acute respiratory failure
Diagnosis: detection of botulinum toxin in blood serum, discharge of the patient, in food
Treatment: gastric lavage, hospitalization, administration of anti-butulinic serum

Pseudotuberculosis

Etiology: Yersinia pseudotuberculosis (gr-)

True Zoonosis
Source: wild and domestic animals, birds
Transmission mechanism: fecal-oral
Transmission routes: food, water, airborne and drip on contact with a sick animal
Pathogenesis: adhesion - invasion - intracellular multiplication - production of enterotoxins -
production of cytotoxins - endotoxin release - incomplete phagocytosis - granuloma formation -
bacteremia - endotoxinemia - immunocomplex pathology - autoimmune reactions - HRT
Clinic:
Initial period: acute onset, syndromes: intoxication, catarrhal, dyspeptic
Period of heat: febrile fever up to 10 days, hyperemia and swelling of the hands, feet, face and neck
(symptoms of "socks, gloves", "hood"), exanthema, gastrointestinal lesion, joint syndrome,
splenomegaly, CCC, respiratory system, kidney, CNS
The period of remission
The period of relapses and exacerbations
Period of convalescence
Clinical forms: scarlet-like, abdominal, arthralgic, icteric, septic (generalized), combined
Diagnosis: bacteriological method, serology: RA 1:80, RNGA 1:80, RPHA 1: 200; RCA, ELISA
Treatment: regardless of severity - antibiotics up to 10 days of normal temperature: amoksiklav,
cephalosporins 2-3 p., Aminoglycosides, tetracyclines, levomycetin
Disintoxication therapy, antihistamines, NSAIDs, SCS short course, immunomodulators, probiotics

Intestinal yersiniosis
Etiology: Yersinia enterocolitica (gr-)
Anthropozoonosis
Source: person (patient or carrier) and animals
Transmission mechanism: fecal-oral
Transmission routes: food, water, contact-household, aerogenic
Pathogenesis: adhesion - invasion - intracellular multiplication - production of enterotoxins -
production of cytotoxins - release of endotoxin unfinished phagocytosis - formation of granulomas -
bacteremia - endotoxinemia - immunocomplex pathology - autoimmune reactions - HRT
Clinic: there is always a loss of the gastrointestinal tract!
- fever;
- short-term nausea and vomiting;
- loose stool, mainly enteritis;
- stomach ache;
- rash - polymorphic, scarlet-like from 2-6 days;
- enlargement of the liver;
- Hyperemia and swelling of the hands, feet, face and neck (symptoms of "socks, gloves", "hood"),
hyperemia conjunctiva, injection of vessels sclera, hyperemia of the oropharynx;
- The language is bright, with hypertrophied papillae ("crimson");
- a positive symptom of Padalka;
- tenderness in palpation in iliac regions;
- Arthralgia.
Clinical forms: abdominal, hepatitis, articular, septic
Diagnosis: bacteriological method, serology: RA 1:40 - 1: 160, RNGA 1: 100 - 1: 200, RPHA 1: 400;
RCA, ELISA
Treatment: regardless of severity - antibiotics up to 10 days of normal temperature: amoksiklav,
cephalosporins 2-3 p., Aminoglycosides, tetracyclines, levomycetin
Disintoxication therapy, antihistamines, NSAIDs, SCS short course, immunomodulators, probiotics

OCI
Etiology: bacteria (shigella, staphylococcus, escherichia, salmonella, campylobacter, etc.); viruses
(rotaviruses, enteroviruses, noroviruses, adenoviruses, etc.); protozoa (amoeba, balantidia, lamblia,
etc.)
Transmission mechanism: fecal-oral
Transmission routes: food, water, contact-household
Transmission factors: food, water, household items, toys, flies
Pathogenesis: adhesion, invasion, production of enterotoxins, production of cytotoxins
Syndromes: diarrhea, intoxication, dehydration
Diarrhea is an unformed or loose stool three times or more for 24 hours (or more often than usual
for a particular person).
Types of diarrhea: secretory (watery, enterotoxigenic), hyperosmolar, hyperexcudative
(enteroinvasive, inflammatory), hyper- and hypokinetic, mixed
Clinical syndromes: enteritis, gastroenteritis, enterocolitis, gastroenterocolitis, colitis
The severity of the course of the disease: mild, moderate, severe
Dehydration (exsicosis): isotonic, hypertonic, hypotonic
4 degrees (in children - 3 degrees)
1 degree - deficiency of body weight to 3% ;. 2 degree - 4-6%, 3 degree - 7-9%, 4 degree - 10% and
more
Intoxication (mild, moderate, severe). Symptoms: weakness, chills, fever, dry mucous membranes,
cyanosis and acrocyanosis, musculo-articular pain, tachypnea, heart tones, tachycardia, hypotension,
ECG changes, vomiting, stools, headache, dizziness, abdominal pain, lethargy, fainting , muscle
cramps of extremities, ITSH
The extreme degree of manifestation is neurotoxicosis, ITSH, HUS

Treatment: diet,
rehydration (oral and infusion), enterosorption, antiemetic, antispasmodics, enzymes, etiotropic
therapy, phagotherapy, immunotherapy, probiotics

Helminthiases
Morphological classification:
Cestodes (ribbon):
• Teniosis
• Teniarinhoz
• Cysticercosis
• Diphyllobothriasis
• Hymenolepidosis
• Echinococcosis (alveococcosis)
Trematodes (flukes)
• Schistosomiasis
• Opisthorchiasis
• Fasciolia
Nematodes (roundworms)
• Askaridosis
• Enterobiasis
• Trichocephalosis
• Trichinosis
• Ankylostomidosis
• Strongylodosis
• Filariatoses
Epidemiology:
• Biohelminths are helminths, the life cycle of which is associated with development in various
organisms (ie, intermediate hosts - teniosis, opisthorchiasis)
• Geohelminths are helminths whose life cycle is associated with the development of eggs or larvae
in the earth (ascariasis, trichocephalus)
• Contact helminths are helminths, the life cycle of which does not require additional development
in the earth, and the spreading occurs by self-infection or by contact-household (enterobiosis,
hymenolepiasis)

Teniosis
The causative agent is an armed thyme (pig), the length is up to 2 m. The head is 4 suckers, hooks.
The ultimate host is a man
Intermediate host - pig
Infection of man through pork meat
Source of infection - a man with a shadow

Teniarinhoz
The causative agent is tamarin unarmed (bullish), length 4-6 m, head with suckers. The segments can
actively creep out of the anus
The ultimate host is a man
Intermediate host - cattle
Infection of a person through poorly digested meat
The source of the invasion is a person with a teniarinchiasis

Diphyllobothriasis
The causative agent - a wide ribbon, 10 m long and longer, the head is equipped with suction slots
(botryas).
The ultimate host is a person and fish-eating animals (cats, dogs, bear, fox)
1 intermediate host - copepods (cyclops)
2 intermediate host - fish
Infection of a person through fish (pike, burbot, perch, ruff)
Source of invasion - a patient with diphyllobothriasis

Echinococcosis (single-chambered)
Pathogen - echinococcus, small cestode 3-4 mm long
Final hosts - dogs, wolves, jackals
Intermediate hosts are all ungulate mammals and humans (a larval vesicular stage develops)
A person is involved in the epidemiological process accidentally, contracting helminth eggs in contact
with sick dogs

Opisthorchiasis
The causative agent is a trematode (cat's flailer) 4-13 mm in length
The ultimate host is a person and fish-eating animals
1 intermediate host - freshwater mollusc
2 intermediate host - fish of the Cyprinidae family
Infection of humans when eating inadequately thermally processed fish
The source of the infection is a sick person, a lesser role is played by domestic and wild animals

Ascaridosis
Pathogen - ascaris, length up to 40cm
The only owner is a man, helminth lives 9-11 months
The infection of a person occurs mainly through the hands contaminated in field work, with the use
of fresh fruits and vegetables grown on soil fertilized by uncleared human feces

Enterobiosis
Pathogen - pinworm, life expectancy 3-4 weeks
Only one owner is a person, mostly children
For laying eggs, the female crawls out of the intestine (more often at night), causing severe itching in
the anal region
Source of infection - a sick person (self-infection)

Toxocarosis
Pathogen - larvae of nematodes of the genus Toksokara, geogelmint
The ultimate host is dogs and other dogs
Infection of a person with ingestion of toxocar eggs on the skin of hands, in food and water
Source of infestation - dogs, less often cats

Liver failure

Complex clinical and pathogenetic syndrome caused by acute or chronic impairment of liver function
with characteristic toxic encephalopathy, hemorrhagic manifestations and development of multiple
organ failure

Causes of hepatic insufficiency

● Viral hepatitis
● Cirrhosis of the liver
● Herpes infection
● Poisoning with mushrooms
● Hepatotropic poisoning
● Drug poisoning
● Yellow fever
● Leptospirosis
● Regional hypoxia of the liver, associated with NK, trauma, abscesses, parasitic liver lesions
● Cirrhosis of the liver against galactosemia, cystic fibrosis, fructoseemia

Morphology of liver failure

● Diffuse liver damage
● Total or submissive necrosis
● Cirrhosis (with cirrhosis)
● Fatty degeneration of the liver (with Ray syndrome)

Hepatic coma
● Endogenous (decay, destructive, hepatic-cellular)
● Exogenous (shunt, bypass, portosystemic) (more often with cirrhosis)
● Mixed
● Electrolyte, false hepatic coma, pseudocoma (against the background of long-term saluretics in
large doses - hypokalemia)

Periods (stages) of liver failure

Stage 1 - hemorrhagic syndrome, jaundice, hiccup, shortening of the liver, fever, fainting, dizziness,
"flies" before the eyes, flushing of the face with perspiration, adequate but slow answers to
questions
Stage 2 - toxic dyspnea, oliguria, flatulence, sweet liver odor, tachycardia, increased hemorrhagic
syndrome, vomiting of the "coffee" thick, progressive jaundice, sharp painfulness of the liver and its
further contraction, absence of abdominal reflexes, convulsive syndrome, somnolence, confused
consciousness with a change in psychomotor agitation (hepatic delirium resembles alcoholic)
Stage 3 - aggravation of symptoms of stage 2, bladder paresis or involuntary urination and
defecation, progression of DIC syndrome, melena, progressive cerebral edema
Stage 4 - absence of reflexes (including pupillary), Cheyne-Stokes or Kussmaul respiration,
gastrointestinal bleeding, decreased PTI, leukocytosis, thrombocytopenia, hypoalbuminemia,
hyperbilirubinemia, bilirubin-enzyme dissociation, oliguria, generalized secondary infection (before
sepsis ). Stop breathing. Death.
Hepatic encephalopathy:
precoma of the first stage - forerunners of coma: a sharp general weakness, dizziness at rest, a sense
of "failure in the abyss," adynamia, inhibition, slow thinking, impaired coordination of movement,
emotional lability, anxious sleep with bright "nightmarish" dreams, vegetative disorders (yawning,
sweating, tinnitus), slight tremor of fingers and eyelids; repeated unmotivated vomiting.
precoma II stage - somnolence, threatening coma: confusion, disorientation in time and space,
memory loss, speech and behavior stereotypes, rapid exhaustion with possible short-term loss of
consciousness, acute psychomotor agitation (delirium), "clapping tremor", tremor language
sopor: loss of consciousness, persistence of reaction to strong irritants, "floating" eyeballs;
coma: the appearance of pathological reflexes, involuntary urination and defecation
deep coma: loss of consciousness with areflexia

Treatment:
● Access to the Vienna
● Ensuring airway patency, ventilation according to indications, fighting with hypoxia
● Probe in the stomach, cleansing enemas
● Catheterization of the bladder
● Dietotherapy (unloading fruit-sugar day, for 3-5 days protein-free diet, then diet with protein
restriction)
● Detoxification therapy (infusion, extracorporeal detoxification)
● Correction of electrolyte disturbances
● Prevention of intestinal auto-toxicity
● Treatment of cerebral edema, anticonvulsant therapy
● Treatment of DIC syndrome, control of bleeding
● A / b therapy taking into account hepatotoxicity
● Treatment of acute renal failure (including hemodialysis according to indications)
● Protease inhibitors, vitamin therapy, metabolic therapy
● Prednisolone 5-10 mg / kg per day in / in
● Symptomatic treatment according to indications
● HSS

Limit the amount of protein in the food to 1-1.5 g / kg / day (but not for long - 3-5 days);
In order to reduce intracranial hypertension, the patient's head is raised by 20 °, hypothermia is
used, mannitol or furosemide is administered.
Free the intestines from nitrogen-containing substances and bacteria that produce ammonia and
other toxins:
- Lactulose 30-40 mg 3-5 times a day, patients in coma are administered per rectum in large doses
- enemas from freshly prepared 20% of lactulose solution 2 times a day
- Antibiotics (metronidazole, ciprofloxacin, rifaximin - it is necessary to constantly change
Decrease in ammonia concentration:
Hepa-Merz (Lornithine-Laspart) inject the first 7-14 days of IV in 20-40 g, the drug is taken orally 9 to
18 g per day for 2-3 weeks
Hepasteril A in a dose of 500 ml per day
Hepasol IV drip 500 ml 40 drops per minute 2 times a day
Solutions containing a high concentration of amino acids with branched chain:
Aminoplasmal-Hepa 10% r-7-10 ml / kg iv
Aminosteril N-Hepa 5% and 8%
Falkamine - oral preparation, which is dissolved in 100-200 ml of fruit juice and taken once a day
during meals
"Recycling System of Molecular Absorbents" (MARS-molecular absorbent recirculating system)
(albumin dialysis)

Assessment of the degree of depression on the Glasgow scale

● 15 points - no disturbance of consciousness
● 14-11 points - precommission
● 10-9 points - the scoop
● 8-4 points - deep coma

Differential diagnosis of jaundice

On the intensity of dyeing of the skin:

Slightly expressed ≥ 35 μmol / l
Moderate 86 - 170 μmol / l
Bright> 170 μmol / l

On the mechanism of development:

Superhepatic (hemolytic) - decay of erythrocytes (hemolysis) - malaria, leptospirosis
Subhepatic (mechanical) - impaired patency of extrahepatic bile ducts - compression of the biliary
tract cyst in echinococcosis
Hepatic (parenchymal) - a violation of the metabolism and transport of bilirubin in the liver tissue -
viral (acute and chronic), bacterial, protozoal hepatitis; acute hepatic insufficiency, viral hepatic
cirrhosis

If jaundice is detected, it is necessary to find out:

- epidemics
- Intensity, timing of occurrence and rate of jaundice
- a shade of jaundice
- change in color of urine and feces
- itching, scratching
- smell from the mouth
- abdominal pain
- the size and consistency of the liver
- Cystic symptoms
- size of the spleen

Erys

Etiology: beta-hemolytic streptococcus group A (mostly)

The main mechanism of transmission of infection is a contact (exogenous infection)
With recurrent erysipelas, the main pathway of infection is exogenous.
Pathogenesis
▪ Introduction of MHA into the skin
▪ Multiplication of MGA in lymphatic capillaries of the dermis
▪ Toxemia
▪ Development of a local hotbed of skin inflammation
▪ Violation of capillary lymphogenesis with the formation of lymphostasis, the formation of
hemorrhages and blisters
▪ Elimination of bacterial forms with phagocytosis
▪ Formation of chronic forms of infection in some patients Provoking factors:
▪ Skin integrity disorders
▪ Sharp temperature change (overcooling, overheating)
▪ Emotional stress, insolation, bruises, trauma
Clinic. Classification
by the nature of local manifestations:
- Erythematous
- Erythematous-bullous
- Erythematous-hemorrhagic
- Bullous-hemorrhagic
by the degree of intoxication (severity of the course)
- Lightweight
- Medium-heavy
- Heavy
by the multiplicity of the flow:
- Primary
- Repeated
- Recurrent
on the prevalence of local manifestations:
- Localized
- Common (migratory)
- Metastatic
consequences of erysipelas
- Persistent lymphostasis (lymphedema)
- Secondary elephantiasis (fibredema)
Treatment: penicillins, inhibitor-protected penicillins, aminopenicillins, cephalosporins, macrolides,
lincosamides
In severe forms and delayed initiation of treatment - vancomycin in combination with macrolides or
with clindamycin
- Detoxification therapy (glucose-saline r-ry, reamberin)
- NSAIDs (orthophane, diclofenac, ibuprofen, ketonal)
- Angioprotectors, antioxidants (rutin, askorutin, trental, quarantil, vitamin E, troxevasin, troxerutin,
detralex
- Desensitizing (fenkarol, zirtek, klaritin, etc.)
- Immunomodulators (derinat, immunophane, polyoxidonium)
Chronicle Prevention:
- Bicillin 5 (1.5mln ED) or retarpen (2.4mln ED)

Malaria
Exciters - protozoa of the genus Plasmodium of the Sporozoea class:
P. vivax, P. malariae, P. falciparum, P. ovale.
Cycles of development of the pathogen: asexual development (schizogony) - a person; sexual
development (sporogony) - the mosquito genus Anopheles.
Pathogenesis:
• Impact on the thermoregulatory center
• Circulatory disorders
• Allergic sensitization
• Immune mechanisms
Source of infection - sick person
Transmission mechanism:
- transmissible
- official
- vertical
Classification
By type of pathogen:
- three-day malaria (vivax);
- three-day oval-malaria (ovale);
- four-day malaria (malariae);
- Tropical malaria (falciparum).
By the time of development of the infectious process:
- Primary;
- repeated;
- relapses (early and late)
By the nature of the clinical course:
uncomplicated;
- heavy;
- complicated
Clinic: "chills" from 30 minutes to 2-3 hours, "fever", the phase of "sweat"
Complicated malaria: drowsiness, convulsions, jaundice, hypoglycemia, acidosis, pulmonary edema,
oliguria, anemia, hemoglobinuria
Diagnosis: thick drop, immunochromatography, PCR
Treatment:
Aminoquinolines (Chlorokhin, Hydroxychloroquine, Primachin)
Quinoline methanol: (Quinine hydrochloride, Mefloquine)
Artemisinin derivatives: Artemisinin, Artesunate, Artemether
Biguanids: Proguanil
Combined preparations: Savarin, Malaron, Coartem
Pyrimethamine + other antimalarial drugs: Fansidar, Tetracycline,
Doxycycline

HFRS
Etiology: the virus of the genus Hantavirus of the family Bunyaviridae.
Natural focal zoonosis
The reservoir and source of infection are various species of wild mouse-rodents (field mouse, red
vole, gray and black rats)
Transmission routes: aspirating, alimentary, contact
Pathogenesis:
• Introduction of the virus, viremia
• Damage to the vascular wall, plasmorrhoea
• Reduction of BCC, increase of blood viscosity
• Microthrombosis, inhibition of fibrinolysis
• Mechanisms for the development of arresters:
1. serous hemorrhagic edema interstitium of the kidneys, compression of tubules and collecting
tubes → retardation of renal blood flow → aggregation of platelets → microthrombosis → occlusion
of capillaries → decrease in glomerular filtration
2. Immunopathological factor: CEC formation → fixation on basal membrane → blockage of
glomeruli → decreased glomerular filtration
Clinic:
• Disease Periods: Incubation (7 - 45 days)
Elementary
Oligouric
Polyurichesky
Reconvalescence
• Forms: - typical
- atypical (abdominal, meningoencephalitic, with prolonged manifestations of renal failure)
6 main clinical and pathogenetic syndromes:
- general toxic,
- hemodynamic disorders (central and microcirculatory disorders),
- acute renal failure (ARF),
- DIC syndrome,
- a syndrome of a hepatitis,
- respiratory syndrome.
Diagnosis: ELISA, MFA, RNIF, PCR, immunochromatographic analysis Treatment:
• Human specific immunoglobulin against HFRS, ribavirin, a-interferon preparations, interferon
inducers
• Infusion therapy
• Hyposensitizing therapy
• Management of hemorrhagic and DIC syndrome
• Spasmolytic and analgesic
• Diuretics?
• Antibiotics

Боррелиоз

Этиология: грам(-) бактерия рода Borrelia

Резервуар и источник инфекции—многие виды диких и домашних позвоночных животных и
птиц
Механизм передачи—чаще всего трансмиссивный
Пути передачи:
• при укусе клеща
• при употреблении сырого козьего молока
• трансплацентарный путь
Патогенез:
• Фаза размножения возбудителя в области входных ворот и образованием мигрирующей
эритемы
• Гематогенная диссеминация возбудителя в кожу, л/узлы, сердце, печень, мышцы, суставы,
бронхи, почки, ЦНС
• Развитие иммунопатологических механизмов
Клиника:
Инкубационный период 2 дня – 3 месяца
Иммунитет нестерильный, видоспецифический
Стадия I (локальная инфекция):
- начало болезни постепенное
- мигрирующая клещевая эритема
Стадия II (диссеминированная инфекция): развивается через 2-10 недель после острого
периода:
- поражения нервной системы
- поражения сердца
- поражения органа зрения
- поражения суставов
Поздний период боррелиоза: клинические проявления формируются через
1— 3мес после первых двух фаз, а у некоторых больных через 6—12 мес и более.
Диагноз: нРИФ, ИФА, ПЦР
Лечение: антибиотики – обязательны!
- доксициклин, амоксициллин, цефуроксим, азитромицин

Hepatitis E
Etiology: HEV (RNA, 2 species - HEV of mammals and HEV of birds)
Anthropozoonosis
Transmission mechanism: fecal-oral
Transmission routes: mainly water; food, domestic - from pigs
Pathogenesis: mouth - stomach - small intestine - blood (portal vein) - liver, replication; direct
cytopathic action: necrosis of hepatocytes; virus isolation through bile and feces
Pathomorphology: only the liver is affected, necrosis of individual hepatocytes: point, zonal
Clinic:
!! The only hepatotropic virus is deadly for pregnant women (massive necrosis, hemorrhagic
syndrome, hemolysis of erythrocytes, arthritis, fatality up to 25%))
The incubation period is 15-60 days
The cyclicity of the course (the pre-egg period is 1 to 9 days, icteric 1-3 weeks, the period of
convalescence is 1-3 months)
A gradual (acute) onset with intoxication and dyspepsia syndrome, fever is not characteristic
Pre-zheltic period: dyspeptic, asthenovegetative, mixed
Jaundice period: with jaundice, deterioration of health, increased intoxication, hepatomegaly,
sometimes splenomegaly, darkening of urine, stool clarification
Hyperbilirubinemia mainly due to bound fraction
Increase of ALT, AST, increase of thymol test
In the urine - urobilin
Diagnosis: IgM to HEV (circulate 1-3 months)
Treatment: diet, regimen, detoxification therapy (solutions, enterosorbents); sometimes UDCA,
lactulose
Pregnant: ICU, prolongation of pregnancy, prevention of bleeding
Artificial termination of pregnancy is contraindicated!

Hepatitis A
Etiology: HAV (RNA, 1 antigen)
Anthroponosis
Transmission mechanism: fecal-oral
Transmission ways: water, food, household; the most intensive isolation of the virus at the end of
the incubation and early icteric periods
Pathogenesis: mouth - stomach - small intestine - blood (portal vein) - liver, replication - part of the
virus is secreted through bile and feces, part of it infects adjacent hepatocytes. T-lymphocytes - lysis
of hepatocytes
Pathomorphology: only the liver is affected, necrosis of individual hepatocytes: point, zonal
Clinic:
The incubation period is 7-50 days
The cyclicity of the course (the pre-egg period is 2-14 days, icteric, the period of convalescence)
An acute onset with a syndrome of intoxication and dyspepsia, sometimes catarrhal phenomena
Pre-zheltushny period: influenza-like, dyspeptic, asthenovegetative.
Jaundice period: rapid increase of jaundice (per night), with jaundice, improvement of health,
hepatomegaly, sometimes splenomegaly, darkening of urine, clarification of feces
Hyperbilirubinemia mainly due to bound fraction
Increase of ALT, AST, increase of thymol test
In the urine - urobilin
Diagnosis: IgM to HAV (circulating 6-8 months)
Treatment: diet, regimen, detoxification therapy (solutions, enterosorbents); sometimes UDCA,
lactulose
Clinical examination for 4-6 months, vaccination against vaccinations 6 months
HAVRIX vaccine

Hepatitis D
Etiology: HDV (RNA, 7 genotypes)
Only together with hepatitis B!
Transmission mechanism: hemocontact, vertical
Transmission routes: parenteral, sexual
Pathogenesis: blood - hepatocytes; direct cytopathic and immuno-mediated action
Pathomorphology: the predominance of necrotic manifestations over inflammatory
Clinic: 2 options: co-infection and superinfection
Co-infection: similar to acute hepatitis B, inc. 6-10 weeks
In the pre-zheltushnom period, joint pain, fever, pain in the right hypochondrium, the average
duration of the period of 5 days
Jaundice period: intoxication intensifies more intensively than with hepatitis B, more often the
enlargement of the spleen
Hyperbilirubinemia mainly due to bound fraction
Increased ALT, AST is more pronounced than with hepatitis B, an increase in thymol sample, a
decrease in the sulemic test
Often the two-wave flow
5-25% - fulminant form
Superinfection of the hepatitis B virus carrier: incubation period 3-4 weeks
The pre-zheltushny period is acute, sometimes turbulent, short, with an increase in temperature,
arthralgia, pain in the right hypochondrium, a significant increase in the liver and spleen, in 40%
edematous-ascitic syndrome
Decrease in the sulemic test, increase in thymol, decrease in albumin, increase in gamma globulin
Wavy current
Recovery is extremely rare, transition to a chronic form (80%) or death
Diagnosis: HDAg, anti-HDV IgM, HDV RNA
Treatment: as fulminant hepatitis B; glucocorticosteroids are contraindicated (direct cytopathic
action of the virus)
Medical examination 12 months

Hepatitis B
Etiology: HBV (DNA, 8 genotypes, antigens HBsAg, HBeAg, HBcAg)
Anthroponosis
Transmission mechanism: hemocontact, vertical
Transmission routes: natural (contact, vertical, sexual), artificial (artificially)
Pathogenesis: blood - hepatocytes, replication of nucleocapsid, some of them - secreted into the
blood. Integration of DNA into the hepatocyte genome and extrahepatic. In hepatocyte, the DNA of
a virus can be in an integrated form and in a free form. The predominance of CD4-Th1 and CD8 is a
self-dissolving process, the predominance of CD4-Th2 is persistence.
Pathomorphology: focal, submasmatic and massive necrosis. Dystrophy, apoptosis, matte-vitreous
hepatocytes (contain HBsAg). Sand kernels in hepatocytes (contain HBcAg).
Clinic:
The incubation period is 45 - 180 days
The cyclicity of the course (1 to 5 days before the jaundice, jaundiced (from several days to several
months), the period of reconvalescence to 6 months)
Pre-zheltic period: dyspeptic, asthenovegetative, arthralgic
Jaundice period: a gradual increase in jaundice (2-3 weeks), with the appearance of jaundice,
deterioration of well-being or unchanged.
Hepatomegaly, sometimes splenomegaly, darkening of urine, stool clarification
Hyperbilirubinemia mainly due to bound fraction
Increase in ALT, AST, reduction of the sulemic test, in severe cases - decrease in albumin, PTI
Diagnosis: EIA: HBsAg, anti-HBsAg, HBeAg, anti-HBeAg, anti-HBcorAg-IgM (G), PCR method: HVB DNA
Treatment:
compulsory hospitalization
Disintoxication therapy (solutions, enterosorbents)
With cholestasis - UDCA
Lactulose
In severe current:
preparations of vitamin K,
prevention of bacterial infection
treatment of cerebral edema
bleeding prevention
Heavy current with coma - lamivudine, entecavir, telbivudine
Mortality 1%
Medical examination 12 months

Hepatitis C
Etiology: HCV (RNA, structural proteins-nucleocapsid, envelope proteins, non-structural proteins-
NS2, NS3, NS4, NS4, 6 genotypes)
High mutational variability
Anthroponosis
Mechanism and transmission pathways: natural (contact, vertical, sexual); artificial
Pathogenesis: blood - penetration into hepatocytes by endocytosis. Replication on the membranes
of the endoplasmic reticulum. Extrahepatic replication. The defeat of the liver cells is a direct
cytopathic action and immuno-mediated (including autoimmune).
Pathomorphology: lymphoid infiltration of portal tracts, lobules; stenotic necrosis, steatosis, fibrosis,
cirrhosis
Clinic:
The incubation period is 2-26 weeks
In 50 - 80% of cases occurs in an icteric form
Pregnant period from several days to 2 weeks, in 20% of patients there is no pre-zheltushnogo
period
In the pre-jaundiced period, asthenovegetative and dyspeptic symptoms prevail, much less often -
the arthralgic variant
The icteric period does not differ from other parenteral hepatitis.
Hepatomegaly, sometimes splenomegaly, darkening of urine, stool clarification
Hyperbilirubinemia mainly due to bound fraction
Increase in ALT, AST.
Recovery at acute HS - 20-50%
Criteria for recovery: well-being, normalization of liver size, normal biochemical parameters, PCR-
otrits RNA method within 2 years after OGS
Diagnosis: ELISA: anti-HCV; PCR method: HCV RNA - viral load, genotype
Chronic HS (up to 80% of acute HS) - retention in the blood of HCV RNA for more than 6 months,
often a low-symptom course, extrahepatic lesions
Treatment of chronic hepatitis C:
Pegylated interferons (algeron, pegasis, pegintron) + ribavirin: course from 24 to 48 weeks
depending on the genotype
Non-interferon treatment regimens (daklatasvir, sophosbuvir) - course of 12 weeks

Rabies

Pathogen: the virus of the genus Lissavirus family Rhabdovirida

Zoonosis
Tank and sources of infection-infected animals
Transmission mechanism-contact, aerogenic
• Infection occurs by biting and ablating the skin and mucous membranes
• Undamaged mucous membranes are permeable to the virus, and intact skin is not
Pathomorphology
• Swelling and swelling of the brain, petechial hemorrhages
• Inflammatory process in the trigeminal nerve, gasser nodes, gray matter of the brain
• Cytoplasmic inclusions - the Babesh-Negri calf
Pathogenesis
Viremia is not typical
The spread of the virus occurs through neural pathways
In the brain, neurons are infected
After replication in the brain returns to the periphery along the nerve pathways
Clinic
The incubation period is from 7 days to tens of years, more often from 30 to 90 days
1 prodromal stage
2 stage of the developed disease or stage of excitation
3rd stage of paralysis
Diagnostics
• 1. Isolation of the virus from saliva and tissues (brain) by fluorescent antibodies (MFA), including
the detection of viral antigens in the tissues of the cornea, skin - in vivo
• 2. Isolation of viral RNA by PCR
• 3. Histological method
• 4. Bioassay
Treatment
• Protective mode
• sleeping pills
• anticonvulsant
• painkillers
Brucellosis

Pathogen: aerobic and microaerophilic immobile g-bacteria, genus Brucella

Zoonosis
The reservoir and sources of infection are sheep, goats, cattle and pigs
Ways of infection:
1. Contact
2. Alimentary
3. Aerogenic
4. Intrauterine
Pathomorphology: the formation of characteristic brucellosis granulomas consisting of Pirogov-
Langhans cells
Pathogenesis
1 phase: lymphogenous
2 phase: hematogenous drift
3 phase: formation of hematogenous metastatic foci
4 phase: poliofocal localizations
Clinic
Incubation period from 2-3 days to 3-7 weeks
Classification: acute (up to 1.5 months), subacute (up to 4 months), chronic (more than 4 months)
and residual (clinic consequences) form
Bacteremia, fever, lymphadenitis, severe sweating, fibrositis and cellulitis, enlarged liver and spleen.
Severe infection occurs due to B. melitensis
Diagnostics
• Bacteriological (sowing of blood and bone marrow)
• Biological
• Serological (agglutination reaction - lamellar (Haddleson), RPHA, ELISA)
• Allergic (intradermal Burne test)
• PCR
Treatment
- rifampicin 600-900 mg and doxycycline 200 mg daily for at least 6 weeks
- often used: tetracycline / aminoglycosides, tetracycline / rifampicin, co-trimoxazole, tetracycline /
fluoroquinolones
Immunocorrectors
Corticosteroids
Non-steroidal anti-inflammatory drugs
Desensitizing
Physiotherapeutic treatment
Vaccination is recommended only in foci of brucellosis caused by Br.melitensis, i.e. in foci of goat-
sheep type
A live anti-brucellosis vaccine prepared from strain BA-19

Leptospirosis

Pathogen: aerobic mobile spiral-like bacterium Leptospira

interrogans of the family Leptospiraceae
Zoonosis
The reservoir and sources of infection are rodents, insectivores, various domestic animals, fur
animals of cellular contents
Transmission mechanism-fecal-oral
Ways of infection:
1. Water
2. Contact
3. Nutritional
Pathomorphology: multiple hemorrhages in the kidneys, lungs, endocardium, mucous membranes,
into the skin. Dystrophic lesions of the parenchymal organs. Necrosis of hepatocytes. The kidneys
are enlarged in size, flabby, on a jaundice incision
Pathogenesis
1 phase: leptospira are introduced through the skin and mucous membranes, penetrate into the
blood (asymptomatic short-term bacteremia and primary dissemination)
2 phase: repeated entry into the blood, with blood and lymph flow, again penetrates into different
organs and tissues
3 phase: toxic, there is a universal capillarotoxicosis
4 phase: non-sterile immunity
Phase 5: Sterile immunity
Clinic
Incubation period from 3 to 20 days
Classification of VI. Pokrovsky et al. (1979)
clinical forms - icteric, anicteric;
leading syndrome - renal, hepatorenal, meningeal, hemorrhagic;
current - no relapse, with relapses; without complications, with complications;
severity: mild, moderate and severe.
Intoxication, myalgia, rash, hemorrhagic manifestations, lymphadenitis, liver, kidney (OPN), lung,
CNS
Diagnostics
OAK leukocytosis, lymphopenia, aneosinophilia, anemia, thrombocytopenia,> ESR
OAM-proteinuria, erythrocyturia, cylindruria
Biochemistry:> bilirubin, aminotransferases, urea, creatinine
The method of direct microscopy, bacteriological method, PCR, PMA, RSK, ELISA
Treatment: penicillin, cephalosporins 1-3-3., Moxifloxacin
Detoxification therapy
Antihistamines
Analgetics
Means that increase vascular resistance and blood clotting
In severe and threatened development of OPN - corticosteroids
Hemodialysis, hemosorption, HBO
Vaccination: Concentrated leptospiroznaya vaccine inactivated liquid

anthrax

Zoonotic anthropurgic disease belongs to the group

Pathogen: Gram + fixed large bacillus Bacillus anthracis, aerobic; bacilli and spores
The reservoir and sources of infection are herbivores: large and small cattle, sheep, pigs, horses,
camels
Ways of infection:
1. Contact (direct or indirect)
2. Transmissible: flies, flies
3. Alimentary
4. Aerogenic
Pathomorphology: in all cavities - transudate. On the surface of the brain - hemorrhagic overlay "cap
cardinal"
Pathogenesis: penetration through the skin, reproduction at the entrance gate, exotoxin release,
penetration into the lymphatic system, breakthrough - generalization
Clinic: incubation period from several hours to 12 days
Classification:
Cutaneous form: carbuncle, edematous, bullous, rozhistopodobnaya
Septic form: pulmonary, intestinal
Carbunclele form: stain, papule, vesicle, ulcer with a dark bottom, scab
Common phenomena - intoxication
Diagnosis: microscopy of smears, culture on nutrient media, use of MFA to detect antigens and
antibodies to them, RNGA, ELISA, PCR
Treatment: ciprofloxacin, doxycycline, levofloxacin, moxifloxacin, clindamycin
treatment of generalized form with meningitis:
The drug with bactericidal action (fluoroquinolone):
Ciprofloxacin 400 mg every 8 hours or
Levofloxacin 750 mg every 24 hours or
Moxifloxacin 400 mg every 24 hours
PLUS preparation with bactericidal action (β-lactam):
Meropenem 2 g every 8 h or
Imipenem 1 g every 6 h or
Doripenem 500 mg every 8 hours
Vaccination: live vaccine STI-1, STI PR

Plague

Acute infectious natural focal disease, belonging to the group of quarantine, OOI
Pathogen: Yersinia pestis belongs to the family Enterobacteriaceae, small rod, is an optional
anaerobic, g "-"
Reservoir and sources of infection - 200 species and subspecies of rodents; also pathogens were
found in rabbits, predators (jackals, foxes, ferrets), insectivores (hedgehogs, shrews)
Ways of infection:
1. Contact
2. Transmissible: Fleas
3. Alimentary
4. Aerogenic
Pathogenesis: overcoming of the skin-epithelial barrier, lymphatic damage (bubonic form).
With airborne transmission, the primary pulmonary form develops
In cases of insufficient barrier function of lymph nodes, septic forms of the disease develop
Clinic: incubation period from several hours to 10 days
Classification:
A. Predominantly local forms:
1. Skin
2. Bubonic
3. Skin-bubonic
B. Internal disseminated forms:
1. Primary septic
2. Secondary-septic
B. Externally disseminated forms:
1. Primary pulmonary
2. Secondary pulmonary
3. Intestinal
Common phenomena: intoxication, severe headache, febrile temperature, tongue, conjunctivitis,
hepatomegaly, splenomegaly, insomnia, delirium, hallucinations, CCC, ITH, DIC-syndrome
Local phenomena - bubo sharply painful, the skin over the bubo is tense, cyanotic-red
Pulmonary form: the most severe form in the clinical course, the most dangerous in the
epidemiological plan.
3 periods of the disease: initial feverish excitement, the height of the disease, terminal
(comparative) period
Diagnosis: bacterioscopy, bacteriology, RNGA, RPGA, ELISA, PCR
Treatment: fluoroquinolones, aminoglycosides, doxycycline, rifampicin, cephalosporins

Tularemia

Natural-focal disease, zoonosis

Pathogen: Francisella tularensis, family Francisellaceae, genus Francisella, gram-stick
The reservoir and sources of infection are rodents, insectivorous predators, ixodids, mosquitoes,
horseflies
Ways of infection:
1. Contact
2. Transmissible
3. Alimentary
4. Aspiration
Pathomorphology: specific tularemia granulomas in organs and lymph nodes, long-lasting non-
healing ulcers on the skin after opening the bubo, degenerative changes in internal organs
Pathogenesis:
1. Introduction, primary adaptation of the pathogen
2. Phase lymphogenous drift
3. Phase of primary regional - focal and general reactions
4. Phase of hematogenous drift and generalization
5. Phase of secondary polyochagism
6. Phase of reactive-allergic changes
7. Phase reverse metamorphosis and recovery
Clinic: incubation period from several hours to 2-3 weeks (3-7 days)
Classification:
► Clinical forms:
1. Ulceroglandular form (ulcerative-bubonic)
2. The glandular form (bubonic)
3. The oculoglandular form (eye-bubonic)
4. Pulmonary form (thoracic)
5. Gastrointestinal form (abdominal)
6. The generalized form (typhoid, septic)
7. Anginozno-bubonic
8. Asymptomatic, latent
► ΙΙ. Degree of severity: mild, moderate, severe.
ΙΙΙ. Current: acute, prolonged, recurrent
Diagnostics:
► Serological methods - RA, PMA, RPGA, RTPGA, ELISA, RIF
► Allergological method: skin-allergic test with tularin, leukocytolysis reaction
► Bacteriological method
► Biological sample (rarely used)
► RIF - immunofluorescent method (reveals the luminescence of a specific antigen);
► PCR
Treatment: gentamicin, amikacin, doxycline, rifampicin

Tetanus

Pathogen: Clostridium tetani, the family of Bacillaceae, g + rod, strict anaerobic. There are 2 forms -
vegetative and spore
Sources of infection are animals and humans, in the intestines of which the causative agent is
saprophytic. Transmission factors - feces and soil
Ways of infection: wound infection
Pathomorphology: in skeletal muscles, coagulation necrosis, muscle ruptures with the formation of
hematomas. In the central nervous system, edema, congestion of the brain
Pathogenesis: the entrance gates are wounds, especially the deep ones. Production of toxin. The
toxin progresses along the motor fibers of the peripheral nerves and through the blood into the
dorsal, medulla oblongata, and into the reticular formation of the trunk; fixation of toxin. In tetanus,
the intercalary neurons of the polysynaptic reflex arches are affected, the paralysis of their activity
occurs.
Clinic: incubation period - from several hours to a month, usually 6-14 days.
Classification:
Posttraumatic tetanus (wounds, punctures, splinters, burns, frostbite, bites)
Postoperative tetanus (penetrating damage to the gastrointestinal tract during emergency
operations)
Tetanus newborn (umbilical)
According to the severity of the current,
- very heavy shape
- heavy form
- moderate
- light form
The first symptoms are trismus, sardonic smile, dysphagia. Tonic tension of muscles, opisthotonus,
pain syndrome, tetanic convulsions, hyperthermia, hypersalivation, CCC lesion.
Diagnosis: according to clinical and epidemiological data. Laboratory diagnostics: seeding on the
environment of Vinyal-Veyon in anaerostat.
Treatment: obligatory surgical treatment.
Anti-tetanus serum IM once in a dose of 100-150 thousand IU or n / tetanus human immunoglobulin
(POCCH), once in the / m in a dose of 900 IU (6 ml). In the first 3 days in parallel injected n / tetanus
toxoid (AC) to 0.5-1 ml per day
Pathogenetic therapy: probing (parenteral) nutrition, arresting seizures, midokalm, antibiotics, a and
ß-blockers, correction of metabolic acidosis, prevention of pressure sores
Preventive maintenance: for planned prophylaxis use following preparations:
- DTP vaccine
- ADS - anatoxin
- ADS-M - an anatoxin with a reduced content of antigens
- AS – anatoxin

HIV infection

The causative agent: human immunodeficiency viruses HIV-1, HIV-2 belong to the family of
retroviruses (Retrovirus), a subfamily of slow viruses (Lentivirus). Proteins: p24, gp120, gp41.
Enzymes: reverse transcriptase, integrase, protease
Sources of infection - an HIV-infected person who is in any stage of the disease
Ways of infection: Natural mechanisms: during sexual intercourse (heterosexual and homosexual in
men); from mother to child (during pregnancy, childbirth); from the child to the mother (with
breastfeeding).
Artificial mechanisms: transfusion of blood and its preparations, transplantation of organs and
tissues, sperm; medical and non-medical parenteral interventions, parenteral administration of
psychoactive substances
Pathogenesis: Phases: attachment and penetration, reverse transcription, replication, virion budding
and maturation.
Target cells: T-lymphocytes-helpers (CD4); cells of mononuclear phagocyte system - monocytes,
tissue macrophages - (Langerhans cells, Kupfer cells, alveolar macrophages, microglia, etc.); CD4
receptors are found on CD8-lymphocytes, B-lymphocytes, follicular dendritic cells of lymph nodes,
oligodendroglia cells, astrocytes of the brain, epithelial cells of the intestine and cervix.
Clinic: incubation period-from 3 weeks to 3 months
Russian classification of HIV infection:
• Stage of incubation (stage 1)
• Stage of primary manifestations (stage 2):
• - 2 "A"
• - 2 "B"
• - 2 "B"
• Subclinical stage (stage 3)
• Stage of secondary diseases (stage 4):
• - 4 "A"
• - 4 "B"
• - 4 "B"
• Terminal stage (stage 5)
Diagnosis: ELISA, immune blotting, PCR
Treatment:
• Component 1 - a protease inhibitor or a non-nucleoside reverse transcriptase inhibitor
• Component # 2 - reverse transcriptase inhibitor, nucleoside analogue of thymidine derivative
• Component # 3 - reverse transcriptase inhibitor, a nucleoside analogue of a thymidine derivative

Typhus

The causative agent: Rickettcia prowazekii, "g-", has 2 antigens

Sources of infection - a sick person
Carrier - a louse
Ways of infection: rubbing the feces of lice in combs on the skin
Pathomorphology: swelling and desquamation of endothelial cells - verrucose endothelium
Pathogenesis: the gate of infection - small skin lesions, after 5-15 minutes rickettsia penetrate into
the blood. Reproduction is intracellular in the vascular endothelium. The cells that get into the blood
stream are destroyed, the rickettsia released at the same time affects the new endothelial cells.
Vascular changes are particularly pronounced in the central nervous system
Clinic: incubation period from 6 to 21 days (usually 12-14 days).
Allocate: the initial period - from the first signs to the appearance of the rash (4-5 days) and the peak
period - until the body temperature drops to the norm (lasts 4-8 days after the onset of the rash).
Acute onset, severe headache, insomnia, irritability, verbosity, hyperesthesia of the sense organs,
"red eyes on the red face", conjunctival rash - Chiari-Avtsyna spots, petechial-roseose rash on days
4-6, tachycardia, lowering of blood pressure, muffling of tones heart, ECG change, ITH; CNS: amy,
smoothing of nasolabial folds, deviation of the tongue, when protruding it, dysarthria, impaired
swallowing, nystagmus, c-m Govorov-Godel, general tremor
Diagnosis: RSK (1: 160), RNGA (1: 1000) from 5-7 days; NIRF
Treatment: doxycycline, chloramphenicol, fluoroquinolones (ciprofloxacin, ofloxacin)
Extract not earlier than 12 days of normal temperature, medical examination 3-6 months

Токсоплазмоз

Паразитарное заболевание человека и животных, вызываемое токсоплазмами, в

подавляющем большинстве случаев протекающее бессимптомно
Возбудитель: Toxoplasma gondii относится к Sporozoa, класс Coccidea, род Toxoplasma,
существуют в формах: тахизоиты (трофозоиты, эндозоиты), брадизоиты (цисты), ооцисты
Источники инфекции— домашние животные
Пути заражения: основной путь - пероральный; контаминационный путь - заражение через
слизистые и поврежденную кожу; трансплантационный; внутриутробный
Патогенез: ооцисты или цисты проникают в организм через ЖКТ, внедряются в эпителий
нижнего отдела тонкой кишки и в мезентериальные лимфузлы. Затем - гематогенная
диссеминация
Клиника: приобретенный токсоплазмоз (инаппарантный, острый, хронический)
врожденный токсоплазмоз (инаппарантный, острый, хронический)
Диагностика: РСК, ИФА, ПЦР,
Лечение: хлоридин (пириметамин, дараприм, тиндурин) по 100-200 мг в первые 2 дня, затем
по 75мг в день в сочетании с сульфадиазином или сульфадимезином (2-4 г/сут) и
тетрациклином (1,2 г/сут).
В дальнейшем (через 10-14 дней лечения) могут быть использованы спирамицин или
клиндамицин

Herpes 1-2 types

Pathogen: human herpesvirus 1 - HSV1 (HSV-1), human herpesvirus 2 - HSV-2 (HSV-2), a DNA-
containing
Source of infection: patient and virus carrier
Ways of infection: percutaneous, aerogenic, sexual, vertical, parenteral
Starting factors: IDS, hypothermia, acute infections, stress and surgeries, excessive UFD, eating
disorders, alcohol
Pathogenesis: epiteliotropnost, blood circulation in the composition of the formed elements
(changes in chromosome apparatus of lymphocytes and their functional activity -
immunosuppression), neurotropic: tropism paravertebral sensory ganglia
Clinic: clinical forms: mucosal lesions, eye damage, skin lesions, genital herpes, CNS lesions, visceral
forms.
By the prevalence of lesions: a localized form, a common form, a generalized form
Diagnostics:
• Immunofluorescent
• Virological
• Detection of DNA virus by PCR method
• Immunocytochemical
• ELISA
• DGC
Treatment: acyclovir, a single dose of 5-10 mg / kg every 8 hours for 7-10 days (with cutaneous,
mucous, genital herpes); 15 mg / kg - with visceral forms (herpes trachea, larynx, esophagitis,
hepatitis, pneumonia); 20 (30) mg / kg - with encephalitis and generalized forms in newborns
Valaciclovir, famciclovir, ganciclovir, foscarnet
Interferons
Immunocorrectors
Local treatment
Prevention: vaccine Vitagerpovac, Gerpovax
The

Toxoplasmosis

Parasitic disease of man and animals, caused by toxoplasm, in the vast majority of cases proceeding
asymptomatically
Pathogen: Toxoplasma gondii refers to Sporozoa, the Coccidea class, the genus Toxoplasma, exists in
forms: tachyzoites (trophozoites, endozoites), bradizoites (cysts), oocysts
Sources of infection - domestic animals
Ways of infection: the main route is oral; contamination path - infection through mucous and
damaged skin; transplantation; intrauterine
Pathogenesis: oocysts or cysts penetrate the body through the digestive tract, are introduced into
the epithelium of the lower part of the small intestine and into the mesenteric lymph nodes. Then -
hematogenous dissemination
Clinic: acquired toxoplasmosis (inapparent, acute, chronic)
congenital toxoplasmosis (inapparent, acute, chronic)
Diagnosis: DSC, ELISA, PCR,
Treatment: Chloridine (pyrimethamine, daraprim, tindurine) for 100-200 mg in the first 2 days, then
75 mg daily in combination with sulfadiazine or sulfadimezin (2-4 g / day) and tetracycline (1.2 g /
day).
In the future (after 10-14 days of treatment), spiramycin or clindamycin

Chickenpox

Causative agent: - Human herpesvirus 3 - v. herpes vericella-zoster (VVZ), DNA-containing. The

properties of the virus - volatility, low stability in the external environment
Source of infection: a patient with chicken pox and herpes zoster
The mechanism of infection: aerogenic and vertical
Ways of infection: airborne, contact, transplacental
Pathogenesis:
• Entrance gate - mucosa of the upper respiratory tract
• Introduction and multiplication of the virus at the entrance gate
• Penetration of the virus through the reticuloendothelial system into the blood - viremia
• Drift of the virus into the epithelial cells of the skin and mucous membranes, nerve tissue, visceral
organs
Clinic:
• The incubation period is 11-21 days
• The prodromal period
• Rash period: stain - papule - vesicle - crust, "false polymorphism" of the rash
• Period of crust formation
Diagnostics:
• VIRUSOSCOPIC METHOD
• PCR
• Virological method
• Serological diagnosis (DSC, ELISA, immunofluorescence method)
Treatment:
• Acyclovir is prescribed:
- Children over 1 year old with chronic skin and lung diseases receiving inhaled corticosteroids and
long courses of salicylates
- Children over 12 years of age because of the high risk of developing neurological complications
- All patients with IDS on the background of autoimmune and oncohematological diseases,
regardless of age
- Severe form of the disease, incl. hemorrhagic
- Chicken pox in newborns and prematurity
- The defeat of the nervous system (meningoencephalitis)
- Development of mixed infections
Local treatment
• Prevention: "Varilrix", "Okavaks"

Shingles Herpes

Causative agent: - Human herpesvirus 3 - v. herpes vericella-zoster (VVZ), DNA-containing. The

properties of the virus - volatility, low stability in the external environment
Pathogenesis: secondary endogenous infection in persons who have suffered chicken pox. The main
reason is the reactivation of the pathogen after latent persistence in the body.
Pathomorphology: inflammatory changes in the spinal ganglia and associated areas of the skin,
sometimes also in the hind and anterior horns of the gray matter, the posterior and anterior roots of
the spinal cord and soft meninges
Clinic:
• The incubation period may be several years from the moment of infection
Classification of clinical forms:
• 1. Ganglionic
• 2. Ear
• 3. Eye
4. Abortive
5. hemorrhagic
• 6. Gangrenous
7. Herpes zoster with lesion of vegetative ganglia
8. Meningoencephalitic
• 9. Disseminated
Disease Periods:
- prodromal (stage of prehepatic neuralgia)
- the period of herpetic manifestations (herpetic rashes)
- the period of residual phenomena (convalescence)
Diagnosis: as with chicken pox
Treatment:
• Acyclovir 800 mg 4 times a day - 7-10 days
• Valaciclovir - 1.0 g 3 times a day 7-10 days
• Famciclovir - 250 mg 3 times a day 7 days
• Groprinosin 500mg - 6-8 tablets / day - 5 days - immunomodulator
• Hangleblockers:
gangleron im / 1,5% r-r 1,0ml once a day 10-12 days or 0.04 in capsules 2 times / day 10-15 days
Carbamazepine from 0.1 g 2 times a day to 0.6 g per day (in 3-4 divided doses)
• Anesthetics, reflexology, topical therapy, B vitamins

Infectious mononucleosis

Pathogen: - Human type 4 herpesvirus, DNA-containing, can persist for a long time in a latent state
in the host cells
Source of infection: patients and virus carriers
Ways of infection: airborne, hemotransfusion, sexual, transplacental
Pathogenesis:
The phase of infection: primary reproduction and accumulation of the virus at the entrance gate
(mucous and lymphoid formations of the oropharynx); infection of B-lymphocytes in the primary
focus
B-lymphocyte-mediated generalization of infection
Hyperplastic processes in lymphoreticular organs
The phase of recovery with the mobilization of immune mechanisms
Clinic:
• Incubation period from 5 days to 1.5 months
• fever: 39-40 °, 5-14 days
• Polyadenia
• oropharyngeal lesions
• nasopharyngeal damage: absence of exudative component, posterior rhinitis and adenoiditis
• hepatolienal syndrome
• jaundice - 6-10%
Diagnostics:
EIA:
- the formation of IgM, IgG to capsid antigen (VCA) - from the first days of the disease with a
maximum at 3-4 weeks.
- IgM to VCA is determined within 3 months (the indicator of primary infection), IgG to VCA decrease
after 4 weeks, but for a long time keep the threshold level
- IgG to EA (early antigen) determine the active replication of the virus, including the activation of
chronic VEBI (during recovery, they decrease in 3-6 months).
- IgG to EBNA (nuclear antigen) appear in 2-3 months. After the acute phase and persist for life
Treatment:
Antipyretics, desensitizing, vitamin therapy, detoxification, antiseptics-topical
Antibiotics (except ampicillin) - with superposition in the oropharynx
Metronidazole is effective
Glucocorticosteroids (1-2 mg / kg / day) with a sharp increase in lymphoid tissue and severe
Immunocorrection (viferon, tsikloferon, groprinosin, bifidumbacterin in high doses)
Cytomegalovirus infection

Pathogen: - Human type 5 herpesvirus, DNA-containing, genus Cytomegalovirus, family

Herpesviridae. Expressed tropism to the tissues
salivary glands
The reservoir and sources of infection are people with acute or latent disease
Ways of infection:
• Contact - through damaged skin, genital tract
• Parenteral route (with blood transfusion, organ transplantation)
• Airborne droplets
• Vertical (from mother to child)
• Household transmission path
Pathogenesis: Entrance gates - mucosa VDP, gastrointestinal tract, genital organs. Short-term
viremia, localization of the pathogen in leukocytes and mononuclear phagocytes, there is replication.
Cells are transformed into cytomegaly. In the organs - defeat depending on the severity of the
disease
Clinic:
Characteristic subclinical forms and latent virus carrying
Classification:
• A. Acquired cytomegal:
Latent (localized) form;
• acute mononucleosis form;
• generalized form of cytomegaly.
• B. Congenital cytomegalovirus:
• acute form;
• chronic cytomegaly.
• B. Cytomegalia in HIV-infected and other immunocompromised individuals.
• Latent (localized)
• acquired form of CMV.
Diagnostics:
Virological method
Cytological
REEF
PCR
ELISA
Verification of acute CMVI:
• IgM
• Low-like CMV-IgG (avidity index up to 30%)
• DNA in real-time PCR (quantitative), or the presence of antigen of the virus in blood leukocytes
Reactivation of CMV:
• IgM
• borderline IgG level (avidity index from 30 to 40%)
• or detection of highly-invasive IgG (avidity index more than 40%)
• detection of CMV antigen in blood cells
Latent CMV:
• Detection of CMV DNA against the presence of highly-invasive IgG and absence of IgM
Treatment:
Ganciclovir (cymenevene) in a dose of 1 g 3 times a day (or 0.5 g 6 times) orally or 5 mg / kg
intravenously drip every 12 h
Valganciclovir-900 mg 1p per day. Course 1-3 months.
Alternative drugs are foscarnet (60 mg / kg 3 times intravenously drip), cidofovir and labubavir.
Newborns, pregnant - neocytotect

The

Mycoplasmosis
Pathogen: Mycoplasma pneumoniae - bacteria of the genus Mycoplasma of Mycoplasmataceae
family
Source: sick or healthy carrier
Transmission mechanism: aerogenic;
Transmission path: airborne (possibly through toys), airborne
Pathogenesis: tropism to the epithelium of the respiratory tract - the defeat of all divisions.
Hematogenous dissemination is possible. The causative agent is capable of prolonged persistence
Clinic: Clinical forms: acute respiratory infections, acute bronchitis, pneumonia
Diagnosis: PCR of nasopharyngeal mucus (quantitative method),
Serological methods of research: the growth of antibody titer, the detection of antibodies of class M
(may appear on 2-3 weeks)
Treatment: macrolides, tetracyclines, fluoroquinolones
The

Legionellosis
Sapronosis
Pathogen: "gram-" bacteria of the genus Legionella family Legionellaceae, the most frequent
causative agent of Legionella pneumophila
Transmission mechanism: - aerosol
Transmission route: infection occurs most often by inhalation of an aerosol;
It is possible to air-dust (soil) path of infection during construction and earth works.
Pathogenesis: the entrance gates are respiratory tracts, are absorbed by phagocytes, the spread
with the blood flow leads to a violation of microcirculation, inflammation with the hemorrhagic
component. Especially often affected lungs, kidneys, liver, bone marrow. The release of endotoxin is
intoxication.
Clinic: incubation period 2-10 days
Main clinical forms:
• pneumonic (actually a disease of legionaries)
• by type of acute respiratory disease (Pontiac fever - infectiousness index = 100)
• acute febrile illness with exanthema (Fort Bragg fever)
Diagnostics:
• Bacteriological method: isolation of the pathogen from pleural fluid, sputum, bronchial flushes
(culture method)
• Serodiagnostics: RSK, RGA with paired sera (slow rise of AT); ELISA
• Express method: an immunochromatographic method (a method for determining legionellosis in
the urine of urine)
Treatment: macrolides, tetracyclines, respiratory fluoroquinolones, rifampicin

Pneumocystis
Causal agent: Pneumocystis carinii (jiroveci)
Anthroponosis, an opportunistic infection, refers to AIDS-indicator diseases
Transmission mechanism: aerosol
Transmission path: airborne
Clinic: during the disease there are 3 stages:
1. Ointment, duration 1-7 weeks
2. Atelectatic - about 4 weeks
3. Emphysema
leading diagnostic sign - dyspnea with meager auscultatory symptoms
Diagnostics:
• Immunofluorescence method (staining of the pathogen)
• Serological methods - ineffective ("dance" titers IgM-AT, especially with HIV infection)
• Histological examination of bronchoalveolar lavage fluid and transbronchial biopsy specimens
• PCR
Treatment: Trimethoprim - 20 mg / kg / day every 6 hours per os or on / in day 21 with transition to
maintenance therapy
Clindamycin - 1.2 g / day per os or iv or primaquine 0.03 g / day per os

Ornithosis
Causative agent: "gram-" immobile bacterium Chlamydia psittaci, genus Chlamydia family
Chlamydiacea
Zoonosis
The reservoir and sources of infection are domesticated and wild birds.
Transmission mechanism-aerosol
Transmission path: dusty, food
Clinic: incubation period - 1-3 weeks
Pneumonic form of ornithosis:
• Lack of prodromes
• Sharp beginning
• Fever with chills lasting up to 7-28 days
• Rarity of the VDP
• Clinic of pneumonia on day 4-6 of the disease
• Leukopenia, ESR
• Hepatomegaly by the end of week 1 (7%)
• The probability of relapse in 15-20%
• Long-term asthenia
Diagnostics: DSC (1: 16-1: 32), RNGA (1: 512 and above), RIF
Treatment: macrolides, tetracyclines, fluoroquinolones

Meningococcal infection
Anthroponosis
Pathogen: Neisseria meningitidis, "G-" diplococcus, is located inside and extracellularly, produces
endo- and exotoxin
Source: person
Transmission mechanism: aerosol
Transmission path: air-drip, contact-household
Pathogenesis: Meningococcus enters the mucous membrane of the nasopharynx by a drip
(nasopharyngeal stage), where it can vegetate without causing damage to the host - meningococcus.
With a decrease in the resistance of the body, it is possible to develop an inflammatory process in
the nasopharynx - meningococcal nasopharyngitis. In some cases, meningococcus enters the
lymphatic system and blood (lymphohematogenous dissemination), resulting in the development of
a generalized form of infection.
Clinic:
Classification of meningococcal infection of VI Pokrovsky:
Localized forms: meningonitis, nasopharyngitis.
Generalized forms:
- meningitis
- acute meningococcemia
- chronic meningococcemia
- meningoencephalitis,
- Combined form (meningitis + meningococcemia).
Diagnosis: UAC: neutrophilic leukocytosis, shift of formula to the left to young and myelocytes,
aneosinophilia, increased ESR, thrombocytopenia, increased ammonia, urea, creatinine, electrolyte
balance and acid-base state
CSF: cloudy, pressure increased, neutrophilic pleocytosis, increased protein
Specific diagnostics: bacterioscopy (blood, CSF), latex agglutination, bacteriological method (blood,
CSF), PCR (blood, CSF), RNGA with meningococcal erythrocyte diagnosticums A, B and C (blood)
Treatment: generalized forms: levomycetin sodium succinate in a single dose of 25 mg / kg,
benzylpenicillin in / m or iv 200,000-500,000 units / kg / day
Ceftriaxone
Cefotaxime
Cefepim
Pefloxacin
Meropenem
Vaccination - Meningococcal A vaccine; M

Vaccination - Meningococcal A vaccine; Meningo A + C; Mentsevaks ACWY; Menugate (Men C)

Flu
Pathogen: RNA-containing viruses, family-ORTHOMYXOVIRIDAE, genus-Influenza, types-A, B and C.
The most variable is the influenza A virus. The outer envelope of the virus contains 2 antigens - the
protein: haemagglutinin (H) and neuraminidase (N) - antigenic drift, antigenic shift
Source: sick person
Transmission mechanism: aerogenic
Transmission path: air-drip (aerosol) and less often - contact-household (through toys, dishes)
Pathogenesis: epitheliotropic, hematogenous distribution, endotheliotropic, immunosuppressive
action, sensitizing effect.
• Penetration of the virus through the VDP;
• Reproduction of the virus;
• Interferon production;
• Virology, toxemia;
• Vascular system damage;
• Neurotoxic syndrome;
• Secondary immunodeficiency;
• Attachment of bacterial infection
Clinic:
A. Downstream:
1. A typical (manifest)
2. Atypical (asymptomatic, erased)
B. By gravity:
1. Mild severity
2. The average severity
3. Severe severity
4. Very severe degree (hypertoxic)
C. By the nature of the current:
1. Uncomplicated
2. Complicated (specific complications, complications caused by secondary microflora, exacerbation
of chronic disease)
Diagnostics:
Detection of RNA of influenza virus by PCR method in blood, saliva and other secrets
Detection of influenza virus antigens in swabs from the nasal and oropharynx (ELISA, IFM)
Identification of antibodies to the influenza virus in peripheral blood (RTGA)
Immunochromatography (influenza, RCC)
Treatment: Oseltamivir (Tamiflu) 75 mg twice daily for 5 days, Zanamivir (Relenza) 2 inhalations 2
times a day for 5 days, Peramivir (Rapivab)
Vaccination - Grippol (Russia), Vaxigrip (France), Agrippal S, Begrivac (Germany), Influvac
(Netherlands), Fluarix (England).

Diphtheria

An acute infectious disease characterized by toxic damage to the cardiovascular, nervous, urinary
systems and local inflammation with the formation of fibrinous plaque
Anthroponosis
Pathogen: Corynebacterium diphteriae or Leffler's wand, refers to the genus Corynebacteria. They
are divided into toxigenic and non-toxic. All biotypes produce an identical toxin.
Source: person sick or carrier of toxic bacteria
Transmission mechanism: aerosol
Transmission path: air-drip, contact-household, alimentary
Pathogenesis: the rod settles in the entrance gates of the infection - on the mucous membrane of
throat, nose, VDP. Propagates, after 2-4 days begins to produce toxin.
Further, the entrance gate of the microbe does not spread; diphtheria - a toxicoinfection!
The permeability of blood vessels increases - the sweat of the liquid part of the blood in the tissue -
fibrinogen turns into fibrin - a dense fibrinous film forms on the mucosal surface. The toxin causes
porosity of the blood vessels and paresis of the lymph vessels - edema is formed. Exotoxin enters the
lympho- and bloodstream - a lesion of the CCC, the nervous and urinary system.
Clinic: the incidence period is 2-10 days.
Classification:
Localized forms (lungs): diphtheria of the oropharynx, nasopharynx, eye, etc.
Common forms of (medium severity): oropharynx, nose, eyes, genitals, etc.
Toxic forms (severe): toxic oropharyngeal diphtheria of I, II, III degrees
Diphtheria croup: localized and disseminated
Atypical form: diphtheria of the skin (wounds), ..
Combined forms
Complications: loss of SSS, kidney, nervous system
Diagnosis: bacteriological examination, PCR, serological methods: RNGA, RPGA, ELISA, ELISA, RLA
Treatment: Antidiphtheria serum (with a breakdown on Bezredka):
Localized diphtheria of the oropharynx: Ostrovchataya 10-15tys ME - single dose, 10-20 thousand IU
- course dose; filmy 15-40 (30-50);
The common diphtheria of the oropharynx is 30-50 (50-70)
Subthoxic diphtheria of the oropharynx 40-60 (60-100)
Toxic diphtheria of the oropharynx: I st. 60-80 (100-180), II tbsp. 80-100 (150-220), III st. 100-150
(220-350)
Hypertensive diphtheria of the oropharynx 150-200 (350-450)
Localized cereals 15-20 (30-40)
The common croup is 30-40 (60-80, up to 100)
Antibiotics: macrolides with localized form, cephalosporins and penicillins in / m in severe forms, 7-
20 days
Vaccination: ADS, ADS-M, D.T. Vax, Imovaks TD Adult, AD-M, as part of multicomponent vaccines:
DTP, Bubo-M, Tetrakok, Bubo-Kok, Pentaxim, Hexavac, Tritanrichs Nvinfanriks, Triazeliuvaks CDS

Trial of the Barefoot

Before the first introduction, a skin test with horse serum, diluted 1: 100 - the "ampoule is marked in
red", is mandatory, to determine the sensitivity to the horse serum protein.
Serum, diluted 1: 100, is administered in a volume of 0.1 ml intradermally, into the flexor surface of
the forearm.
Allow for reaction after 20 minutes. If the result is negative (diameter of the edema and / or redness
at the injection site of 1 cm), serum diluted (ampoule blue) in a volume of 0.1 ml is injected
subcutaneously into the middle third of the shoulder.
In the absence of a general or local reaction, after 45 ± 15 minutes, the prescribed dose of serum,
heated to a temperature of 36 ± 1 ° C, is injected in / m, the maximum volume of the drug in one
place is 8 ± 2 ml, followed for 1 hour.
If the reaction is positive (swelling and / or redness is greater than or equal to 1 cm) and in the case
of a reaction to p / c injection of 0.1 ml of serum, the drug is used only for vital indications.
To desensitize the serum diluted 1: 100, enter SC in a volume of 0.5 ml, 2.0 ml, 5.0 ml with an
interval of 15-20 minutes, then at the same interval 0.1 ml and 0.1 ml are added 1.0 ml of undiluted
serum.
In the absence of a reaction, all serum is administered. Simultaneously injected anti-shock drugs.
With anaphylactic shock, the serum is injected under anesthesia.
The primary dose of serum is 1/2 - 1/3 of the course. APDS is administered intramuscularly (in the
region of the upper third of the antero-external surface of the thigh or buttock) with localized forms
of the disease, intravenously drip in toxic forms. With the localized form of diphtheria and the early
timing of administration, a single administration of APDS is sufficient, and in severe cases it is
necessary to repeat the administration of the APDS 12-24 hours later. Introduction of APDT is
expedient and maximally effective in the early periods of diphtheria. The introduction of APDS in the
late period of the disease is ineffective. It is advisable to conduct seroterapia no later than the 4th
day after the onset of the disease in patients with a localized form of diphtheria.