MODIFIED INFECTIOUS .... Ok

01. 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
SOURCES OF INFECTIOUS AGENTS

- Human – patient or carrier (from the end of the incubation period; prodromal
period; climax period; convalescence, when microorganism excretion occur) -
antroponosis
-Animals (domestic, wild) – zoonosis
-Antropozoonosis (both man and animal can be the source)
-Environment – sapronosis (tetanus, legionellosis)
MECHANISM OF TRANSMISSION
4 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)
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
02. Classification of infectious diseases.
1.GROUPS OF INFECTIOUS DISEASES BY GROMASHEVSKY
- 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
03. 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, drugs such
as immunoglobulins, glucocorticoids and antibacterial drugs
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
04. 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
• Tested for antibodies, produced by the person's immune system in
response to the microorganism
• Tested for a microorganism's antigens (molecules from the
microorganism that can trigger an immune response in the body)
• Tested for genetic material (such as DNA or RNA) from the
microorganism
• Testing of a Microorganism's Susceptibility to Antimicrobial Drugs
05. 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
• Chemotherapy: Antibacterial (antibiotics, sulfonamides,
nitrofurans, and others), antiviral(viroleks, rimantadine, acyclovir),
antiprotozoal (yatren, delagil, primaquine), antihelmintic (naftamon,
decaris) • Natural biological products: interferon, deoxyribonuclease
• bacterial preparations: laktobakterin, colibacterin, baktisubtil
Serotherapy: immune serum, immunoglobulins, bacteriophages
06. 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
• Deratization
• Prophylaxis: Chemoprophylaxis, Vaccines
07. 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.
08.STAGES OF TYPHOID FEVER PATHOGENESIS

Quick epidemiology of typhoid fever (you can go straight to the answer or can say
something about the epidemiology)
Typhoid fever is anthroponosis. The source of infection is sick man or bacteriocarrier.
The patients with typhoid fever discharge the agent with stool, urine, rarely – with
saliva and milk.
The discharge of the agent is observed at the and of incubation period, during all
disease, and sometimes in the period of reconvalescence. in some cases the discharge
continues till three months (acute carriers) or more than three months (chronic
carriers). Chronic carriers may be from six months till some years. The mechanism
of the infection transmission is fecal-oral. The factors of transmission may be water,
milk, various food-stuffs and contaminated feces of the patient or bacterial carriers
STAGES( 8 stages)
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 is the reproduction of the agents and formation of the focus of
infection)
3. Bacteremia(Bacteria in blood)
In clinic bacteremia 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.
The fifth phase of a pathogenesis is parenchymatous diffusion of microbes. 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
09.CLASSIFICATION OF TYPHOID
-Typhoid fever is anthroponosis.
-The source of infection is sick man or bacteriocarrier.
-The patients with typhoid fever discharge the agent with stool, urine, rarely – with
saliva and milk.
-The mechanism of the infection transmission is fecal-oral.
-The factors of transmission may be water, milk, various food-stuffs and
contaminated feces of the patient or bacterial carriers
THE CLASSIFICATION ARE
• According to forms:
A.typical
B. Atypical: aborted, effaced ( ambulant,afebrile, mildest),
disguised (pneumotyphus, colotyphus, meningotyphus,
apendicotyphus, colotyphus, nephrotyphus, sepsis) •
According to severity:
mild, moderate, severe, exacerbation, relapse
• According to complications: enterorrhagia, perforation of intestine, bleeding from
intestine, infectious shock
• According to bacteria carriage: convalescent, chronic
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 patients with typhoid fever discharge the agent with stool,
urine, rarely – with saliva and milk.
-The mechanism of the infection transmission is fecal-oral. The factors of
transmission may be water, milk, various food-stuffs and contaminated feces of the
patient or bacterial carriers Typhoid is characterized by cyclical course of the
disease.
-There are such periods during course of the infectious process: incubation, initial,
period of climax, early reconvalescence and outcomes.
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): Tempertaure 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): Tempertaure 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
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 apathethic.
• Intoxication is increased.
• Temperature is constant and most typical syndrome of typhoid fever and
paratyphoid. The phase of climax is near two weeks. The phase of decrease of the
temperature is near one week. • Chills and diaphoreses 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
fluidfilled loops of bowel on palpating of the abdomen is considered to be
characteristic
- 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
• Neuropsychiatries manifestations, including confusion, dizziness,

seizures, or acute psychotic behavior, may be predominant in an occasional
case.
• Status typhosus is observed in serious course of the disease.- Cervical
lymphoadenopathy may be present
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 dissapears,
sometimes exist longer than fever.
•usually are present only in half of the patients
• Often new elements appear
13.PECULIARITIES OF PARATYPHI 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 shorter than in typhoid fever. It's duration is 8-

10 days.
• The onset of the disease is an acute. Sometimes, the onset of the disease is
accompanied by cough, catarrh.
• Facial hyperemia, blood injection of the sclera’s vessels, herpes on the lips are
observed during examination.
• The temperature is wave-like or remittent. The fever is accompanied by chills and
than by diaphoreses.
• . In paratyphoid A the rash appears more early than in typhoid fever. The rash is
polymorphic. Roseolas, petechias and measles-like rash may be observed. The
intoxication is temperate. • There is no status typhosus.
• There is normal quantity of leukocytes in peripheral blood. But leukocytosis and
lymphocytosis may occur too.
• In majority of the patients the disease has a moderate course. The relapses are
frequently observed in case of paratyphoid A.
14.PERCULIARITIES OF PARATYPHI B
Paratyphi B
Source of infection –(humans and cattle)
Mechanism of transmission –fecal oral
Paratyphoid B incubation period is 5-10 days.
• The onset of the disease is acute, 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 disappears 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
15 SIGNS OF POSSIBLE RELAPSE OF TYPHOID FEVER
Relapse, a recurrence of the manifestation of typhoid fever after initial clinical
response,It s occur 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
• Aneozynophylia
16. Differential diagnosis of typhoid fever and influenza.

Typhoid is caused by bacteria by Salmonella Typhi .
The source infection is sick man or bacteriocarrier.
-The patients with typhoid fever discharge the agent with stool, urine, rarely – with
saliva and milk.
-The mechanism of the infection transmission is fecal-oral. The factors of
transmission may be water, milk, various food-stuffs and contaminated feces of the
patient or bacterial carriers
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 Influenza
Incubation period starts from Incubation period is few
1-12 or 21 days hours to 1-2 days
Clinical (Usually presents with Usually presents as upper

presentation gastrointestinal respiratory symptoms
symptoms) fever, chills, (cough,sneezing,rhinorrhe
myalgia, nausea, a, sore throat)
vomiting, rash,,
constipation Sudden onset of fever,
chills or rigors,
headache, malaise, diffuse
myalgia,
Physical Maculopapular rash, high temperature,

Exam coated tongue, jaundice, headaches, dizziness, a
splenomegaly, delirium syncope condition, fever,
malaise, pains in different
parts of the body i.e. the
symptoms of general
intoxication. The headache
is located in the forehead,
temples and over the
brows, neurologic
symptoms(unconsciousnes
s
, delirium, convulsions)
Diagnostic Hemoculture,serological,copro Rapid diagnostic test from
Investigation c ulture nasopharyngeal secretions,
chest radiography
based on physical
findings
Management Ciprofloxacin or Supportive care and
ofloxacin rehydration.
Antivirals for early
treatment or
prophylaxis (osetalmivir,
zanamivir)
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), 3 secondary to prolonged severe illness (suppurative parotitis and
pneumonia).
4 secondary to growth and persistence of typhoid fever bacilli (relapse, localized
infection - meningitis, endocarditis, osteomyelitis or arthritis
5 secondary to therapy (bone marrow suppression, hypersensitive reactions and toxic
shock
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
• Important symptom of peritonitis – local 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
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
secondor 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
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 fluorescen, and 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
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 that is characterized by a cyclic course with intestinal
bacterial invasion, lesions of the small intestine lymphatic apparatus, bacteremia,
intoxication and fever, skin rash and diarrhea (which is sometimes bloody).
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 **
22. Etiology and epidemiology of salmonellosis.

Salmonellosis is an anthropozoonotic, foodborne infection, characterized by essential
damage of the gastrointestinal tract leading to diarrhea (sometimes bloody),
abdominal cramps, fever, and more rarely, by typhus-like or septicopyemic
manifestation.
Etiology
It is caused by Salmonella species of bacteria from the Enterobacteriaceae family. All
nontyphoid species of Salmonella may cause Salmonellosis.
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. **
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.
It may either be
Foodborne infections – Whereby there is ingestion of viable pathogens e.g. Typhoid
fever, Salmonellosis, Cholera, Shigellosis, etc
Foodborne intoxication – Whereby the is ingestion of preformed toxins e.g.
Botulism and Staphylococсal poisoning
Food Toxicoinfection – Whereby microbes produce toxins insitu when ingested with
the food e.g. Bacillus cereus poisoning
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.
** 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. **
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.
25. Clinical signs of salmonellosis generalized forms.

The Generalized forms of Salmonellosis cause systemic affection and there is the
- Typhus-like form; and
- 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.
Sometimes the typhus-like variant may occur without appearances of gastroenteritis
and the principal symptoms in such cases are usually fever, chills, headache,
weakness.
In the climax period of such cases there may be adynamia, pale skin, injections of
scleras, observed.
In rare cases there may be marked catarrh, hyperemia of pharynx and
laryngotracheobronchitis.
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 complicatioms 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.
26. Clinical manifestation of food toxicoinfection.

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 Clinical Manifestation According to etiology
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 symptoms include 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 symptoms include 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. Because the toxin is thermostable, once it forms
in cells, heating food containing viable microbial cells before eating it is what leads
to the symptoms.
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.
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.
27. The differential diagnosis of salmonellosis and shigellosis.

And
Shigellosis is an acute intestinal infection, caused by Shigella species of bacteria
that is characterized by bloody diarrhea. Differential Diagnosis
SALMONELLOSIS SHIGELLOSIS
SOURCES OF Usually associated with Most significant sources

INFECTION the consumption of are sick persons and
contaminated Poultry, carriers; also from
eggs and milk; also from ingestion of contaminated
sick persons and carriers food and water
and contact infected
animals and their feces
MECHANISM OF Fecal-oral route Fecal-oral route;
TRANSMISSION personperson transmission
is also
common
CHARACTER OF Mucous, watery green Watery stools with gross
DIARRHEA stools which smells like blood and mucus;
rotten eggs. tenesmus is often present
(false urgency to defecate)
LABS High WBC with left shift; High WBC and bands
Positive stool culture for increase;
nontyphoid Salmonella Positive stool culture for
species of bacteria Shigella bacteria;
Positive stool Guaiac Test
28. Clinical manifestations of dehydration shock.
Dehydration shock also known as hypovolemic shock is a serious and sometimes
lifethreatening complication of dehydration, characterized by severe hypotension and
disturbance ofhemodynamic stability and vital signs.
Clinical Manifestation
• 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
29. Methods of salmonellosis specific diagnostics.

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
30. The peculiarities of food toxicoinfection specific diagnostics.

food e.g. Bacillus cereus poisoning
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.
clinical symptoms:. Nausea, explosive vomiting for up to 24hours.
Abdominal cramps or pain. Headache, weakness, diarrhea and subnormal body
temperature.
31. Emergency aid at a localized form of salmonellosis and at food

toxicoinfection.
And
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
32. Treatment of salmonellosis and food toxicoinfection patients.

And
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
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*****
34. Clinical manifestations of different dehydration degrees at 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.
According to the 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.
Clinical Manifestations According to the degree of

dehydration In mild course (First degree of dehydration):
• The stool frequency is till about 10 times in a day in scanty portions.
• In some patients vomiting may occur 1-2 times
• Thirst, light dizziness, weakness may present
• The mucous of the mouth is dry
• There are no changes of the pulse and arterial pressure.
• No or slight pain during palpation of the stomach. • Subfebrile temperature
may be present
• There is no change in electrolytes and blood pH
• Their state is satisfactory.
In moderate course (Second degree of dehydration):

• The stool frequency is from 10 to 20 times in a day.
• The character of the stool is liquid, rice-water-like and plentiful. • There
is considerable 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
• There may be moderate cyanosis of lips and extremities may be in some
patients.
• There is occurrence of muscle cramps
• The pulse is frequent up to about 100 per minute, Hypotension.
• Hematocrit is increased, Erythrocyte sedimentation rate (ESR) is slightly
increased, Leukocytosis with left shift, and eosinophilia may occur in some
patients
• The change of electrolytes is insignificant but Hypokalemia and
hypochloremia are more expressed.
In Severe course (Third degree of dehydration):

• The 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. **
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:
1. 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.
2. 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 **
36. Laboratory diagnosis of cholera.

•
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. 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
37. Differential diagnosis of cholera and salmonellosis.

And
CHOLERA SALMONELLOSIS
MODE/FACTORS OF Majorly associated with Majorly associated with

TRANSMISSION contaminated water and ingestion of contaminated
seafood (e.g. Shellfish, food, especially poultry,
clams, mussels) eggs and milk.
CLINICAL Explosive Watery, Mucus, green stools, that
RPESENTATION: ricewater-like stools smell like rotten eggs
CHARACTER OF (quantity is dependent on
DIARRHEA severity)
PHYSICAL Severe dehydration Mild dehydration that
EXAMINATION: occurs does not or only mildly
HEMODYNAMIC that may lead to affects Hemodynamic
STABILITY hypovolemic shock stability in most cases
DIAGNOSIS Stool culture is done on Stool culture is done on
sucrose agar plates and McConkey agar plates
reveals yellow colonies to and reveals colourless
confirm Cholera; Vibrio colonies and sometimes
bacteria species are colour change of the
revealed from medium from orange to
bacteriological study amber; Nontyphoid
Salmonella bacteria
species are revealed from
bacteriological study
38. Differential diagnosis of cholera and shigellosis.
And
Shigellosis is an acute intestinal infection, caused by Shigella species of bacteria that
is characterized by bloody diarrhea.
CHOLERA SHIGELLOSIS
MODE/FACTORS OF Majorly associated with Most significant sources

TRANSMISSION contaminated water and are sick persons and
seafood (e.g. Shellfish, carriers; also from
clams, mussels) ingestion of contaminated
food and water
MECHANISM OF Fecal-oral route Fecal-oral route;
TRANSMISSION personperson transmission
is also
common
CLINICAL Explosive Watery, Watery stools with gross
RPESENTATION: ricewater-like stools blood and mucus;
CHARACTER OF (quantity is dependent on tenesmus is often present
DIARRHEA severity) (false urgency to defecate)
PHYSICAL Severe dehydration occurs May lead to septic shock;
EXAMINATION: that may lead to may also cause severe
HEMODYNAMIC hypovolemic shock dehydration that may lead
STABILITY to hypovolemic shock
DIAGNOSIS Stool culture is done on Stool culture is done on
sucrose agar plates and McConkey agar plates
reveals yellow colonies to and reveals circular,
confirm Cholera; Vibrio colourless or translucent
bacteria species are colonies of Shigella
revealed from bacteria; Shigella species
bacteriological study are revealed from
bacteriological study;
Positive stool Guaiac Test
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.
40. Rehydration therapy at cholera.

Rehydration therapy is a fluid replacement therapy
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
Make ORS with safe water, which is water that has been boiled or treated for at least
15 minutes. 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.
- If ORS is not available, water, broth, or other fluids should be provided.
Drinks with a high sugar content, such as juice, soft drinks, or sports
drinks are contraindicated because they can worsen diarrhea.
• 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
Indications:
- severe dehydration,
- stupor, coma
- uncontrollable vomiting
- extreme fatigue that prevents drinking.
• 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.
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, Other
enteroviruses 68-71; also Rhinovirus
Epidemiology:
! Source of infection: patients and carriers
! Mechanism of transmission: Inhaling contaminated airborne droplets droplets,
fecaloral ( Swallowing food or water contaminated with stool from aninfected
person), transplacenta;
! Contact with infected hands !
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. Incubation period; 3-5 days lasting up to 10days
● Seasonality- summer and early autumn
42.Clinical forms 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.
CLINICAL FORMS
• Asymptomatic Infection ( most common)
• 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

This is the most common presentation of enterovirus infection.
Most present with an illness that manifests as sudden fever. The fever may last for as
long as a week, Patients may also report myalgia, headache, sore throat, nausea,
vomiting, mild abdominal discomfort, and diarrhea.
Aspetic Meningitis
Mainly caused by Enteroviruses of group B coxsackievirus and echovirus
The clinical course typically involves an initial episode of nonspecific fevers in
conjunction with CNS symptoms.Symptoms may also include headache, malaise,
nausea, and vomiting.,photophobia. Physical examination typically demonstrates
generalized muscle stiffness or spasm.
Infection With Poliovirus

Acute paralytic disease may be caused by naturally occurring wild polioviruses or
by mutated vaccine-derived polioviruses. In classic paralytic polio, the 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.
OPV ( oral polio vaccine ) remains the vaccine of choice.
Encephalitis
Frank encephalitis is an unusual manifestation of enterovirus infection.
Echovirus 9 is the most common etiologic agent.
Clinical manifestations include lethargy, drowsiness, and personality change to
seizures, paresis, and coma. Children with focal encephalitis present with partial
motor seizures, hemichorea, and acute cerebellar ataxia
Rashes
Certain coxsackieviruses, echoviruses,.Rashes are usually nonpruritic, do not
desquamate, and occur on the face, neck, chest, and extremities. They are sometimes
maculopapular but occasionally hemorrhagic, petechial, or vesicular. Fever is
common. Aseptic meningitis may develop simultaneously.
Ocular Infections
Outbreaks of acute hemorrhagic conjunctivitis are typically due to Echovirus 70 or
Coxsackie virus.Presentation is characterized by a sudden onset of severe eye pain
and associated photophobia. Subconjunctival hemorrhages are frequently present.
Systemic symptoms, including fever, are rare.
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.
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.
The usual presentation is 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. Bronchitis
and interstitial pneumonia occasionally occur in adults and children. The course is
usually mild but can be severe as evidenced by the 2014 enterovirus D68
outbreak.
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.
43.The main symptoms of enteroviral diseases.

small, single-stranded, RNA viruses. (members include- Polio Virus, ECHO and
Coxackie A and B, Other enteroviruses, also Rhinovirus)
Symptoms may vary based on clinical form of enterovirus infection but main
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
******* (NOT MAIN!!)
CLINICAL FORMS
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

This is the most common presentation of enterovirus infection.
Most present with an illness that manifests as sudden fever. The fever may last for as
long as a week, Patients may also report myalgia, headache, sore throat, nausea,
vomiting, mild abdominal discomfort, and diarrhea.
Aspetic Meningitis
Mainly caused by Enteroviruses of group B coxsackievirus and echovirus
The clinical course typically involves an initial episode of nonspecific fevers in
conjunction with CNS symptoms.Symptoms may also include headache, malaise,
nausea, and vomiting.,photophobia. Physical examination typically demonstrates
generalized muscle stiffness or spasm.
Infection With Poliovirus

Acute paralytic disease may be caused by naturally occurring wild polioviruses or
by mutated vaccine-derived polioviruses. In classic paralytic polio, the 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.
OPV ( oral polio vaccine ) remains the vaccine of choice.
Encephalitis
Frank encephalitis is an unusual manifestation of enterovirus infection.
Echovirus 9 is the most common etiologic agent.
Clinical manifestations include lethargy, drowsiness, and personality change to
seizures, paresis, and coma. Children with focal encephalitis present with partial
motor seizures, hemichorea, and acute cerebellar ataxia
Rashes
Certain coxsackieviruses, echoviruses,.Rashes are usually nonpruritic, do not
desquamate, and occur on the face, neck, chest, and extremities. They are sometimes
maculopapular but occasionally hemorrhagic, petechial, or vesicular. Fever is
common. Aseptic meningitis may develop simultaneously.
Ocular Infections
Outbreaks of acute hemorrhagic conjunctivitis are typically due to Echovirus 70 or
Coxsackie virus.Presentation is characterized by a sudden onset of severe eye pain
and associated photophobia. Subconjunctival hemorrhages are frequently present.
Systemic symptoms, including fever, are rare.
Herpangina.
Hand-foot-and-mouth Disease.
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.
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.
The usual presentation is 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. Bronchitis
and interstitial pneumonia occasionally occur in adults and children. The course is
usually mild but can be severe as evidenced by the 2014 enterovirus D68
outbreak.
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.
44.Laboratory diagnosis of enteroviral infections.

Coxackie A and
B, Other enteroviruses, also Rhinovirus)
! 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 (or Pandy's reaction) is done on the CSF (cerebrospinal fluid) to
detect the elevated levels of proteins (mainly globulins).
45.Principles of enteroviral diseases therapy.

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-thecounter cold medications as needed. Most people recover completely,
Hence , 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 conjuctivitis
( ***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.
**** Hand-foot-and-mouth Disease.

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.
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. Posses capsule (K
antigen) and O antigen. The Shigella bacterium is spread through contaminated water
and food or through contact with contaminated feces. The bacteria release toxins that
irritate the intestines.
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
47.Clinical classification of shigellosis.
DEFINTION- 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
irritate the intestines. The primary symptom of shigellosis is diarrhea.
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 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.
According to Pathology:
! Acute catarrhal inflammation
! Fibrinous Necrotic
! Ulcerous and folliclic-ulcerous
! Stage of formation of scars
48.Peculiarities of shigellosis, depending on the clinical form.

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 doesn’t require etiological treatment, but adequate hydration should is
key, moderate to severe may require antibiotics eg. ciprofloxacin or azithromycin.
DON’T USE ANTIDIARRHEALS Like loperamide.
49.The clinic of colitis syndrome at shigellosis.

CLINIC OF COLITIS SYNDROME

50.Laboratory diagnosis of shigellosis.

! 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
51.The treatment principles of shigellosis patients.

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.
52.Etiology and epidemiology of amebiasis.

DEFINTION - Amebiasis is a parasitic infection of the intestines
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
53. Clinical classification of amebiasis.

DEFINITION - 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.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.
54. The features of clinical duration of amebiasis intestinal forms.

weeks.
Amoebic colitis
! Symptoms present over a period of 1-2 weekks
! 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.
55. Clinical signs of extraintestinal amebiasis.

DEFINTION - Amebiasis is a parasitic infection of the intestines caused by
weeks
Extra-intestinal amoebiasis can occur if the parasite spreads to other organs,

most commonly the liver, other locations include 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.
56. Complications of amebiasis.
DEFINTION - Amebiasis is a parasitic infection of the intestines caused by

weeks
! Fulminant amebic colitis: Rapid onset of severe bloody diarrhea, severe

abdominal pain, rebound tenderness, fever.
! Toxic megacolon: Toxic megacolon is an acute form of colonic distension. It is
characterized by a very dilated colon (megacolon), accompanied by abdominal
distension (bloating), and sometimes fever, abdominal pain, or shock
! Ameboma- An 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
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
57 .Laboratory diagnosis of amebiasis.

weeks
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
58.The treatment principles of amoebiasis patients.

weeks
TREATMENT
Both symptomatic intestinal infection and extra intestinal disease as well as
Asymptomatic patients infected with E. histolytica should be treated with
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.
59.The etiology and epidemiology of giardiasis.
DEFINITION- Giardiasis is an intestinal infection marked by stomach cramps,

bloating, nausea and bouts of watery diarrhea
Etiology: Caused by Giardiasis intestinalis also called Giardia Lamblia), Giardia is
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
60.Clinical signs of giardiasis.

DEFINITION- Giardiasis is a Parasitic intestinal infection Caused by Giardiasis
intestinalis also called Giardia Lamblia).
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
61.Diagnostics of giardiasis.
Definition
Giardiasis is a diarrheal disease caused by the microscopic parasite Giardia
duodenalis (or“Giardia” for short). Once a person or animal has been infected with
Giardia, the parasite lives in the intestines and is passed in stool (poop). Once
outside the body, Giardia can sometimes survive for weeks or even months spread
by:
• Swallowing unsafe food or water contaminated with Giardia germs
• Having close contact with someone who has giardiasis, particularly in childcare
settings
• Traveling within areas that have poor sanitation
• Exposure to poop through sexual contact from someone who is sick or recently sick
with Giardia
DIAGNOSIS
•Atleast 3 stool samples in 2 days for culture: ova and parasites should be seen.
• Fresh stool+ iodine or methylene blue examination for cysts on wet mount
• Stool antigen test with immunofluorescent antibody assay or ELISA test,
PCR( especially used for identification of subjects during a pandemic )
- •upper endoscopy with biopsies and duodenal aspirated samples of duodenal

fluid (e.g., Enterotest) may demonstrate trophozoites.
•
62. The treatment principles of giardiasis.

It's caused by a microscopic parasite called Giardia lamblia and there has been no
approved human vaccine against giardiasis , and pharmacotherapy is the only
available option to treat giardiasis.
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
Incase of pregnancy can use

Paromycin
63. Differential diagnosis of amebiasis and shigellosis.

amebiasis
Source of infection
Anthroponosis
Etiology
Amebiasis is a parasitic infection of the intestines caused by the protozoan Entamoeba
histolytica, or E. histolytica.
Symptoms
The symptoms of amebiasis include loose stool, abdominal cramping, and stomach
pain Acute, bloody diarrhea, liver abscess, colic
Diagnosis
Trophozoite in stool, colonic mucosa flask ulceration, serologic test
History
•Travel to endemic area
•people who live in institutions with poor sanitary conditions, such as prisons
•men who have sex with other men
•people with compromised immune systemsand other health
conditions Shigellosis Etiology
is Gram-negative, facultative anaerobic, non-spore-forming, nonmotile, rod-
shaped It’s a bacteria caused an infection called shigellosis Source of
infection.
Sick patient and carrier
Symptoms
Watery, bloody diarrhea. Tenesmus, pain in inguinal region, Fecal leukocytes,
fever, pain and cramps. Diagnosis
Positive stool culture
History
food borne
64. The etiology and epidemiology of balantidiasis.
Balantidium (=Neobalantidium) (=Balantioides) 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.
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 smallintestine,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.
Epidiemology
Balantidium coli occurs worldwide. Because 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
●
65. Diagnostics of balantidiasis. a protozoan infection caused by

infection with Balantidium coli
Usually asymptomatic in immunocompetent individuals, but the symptoms of
balantidiasis include: Intermittent diarrhea,Constipation,Vomiting,Abdominal
pain,Anorexia,Weight loss,Headache
Balantidiasis is diagnosed by 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.
In addition, the diagnosis of balantidiasis can be made by microscopic examination
of stools in search of trophozoites or cysts,or colonoscopy or sigmoidoscopy to
obtain a biopsy from the large intestines which may provide evidence for the
presence of
66. The treatment principles of balantidiasis.

Desintoxication with oral rehydration
• Probiotics
• Vitamins
• Antibiotics: Tetracycline, metronidazole, iodoquinol,• Enzymes: pancreatin,
gordoux• Enema
Management
Avoid ingestion of material contaminated with animal feces
Treatment of infected pigs
Prevention of contaminated food
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.
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.
Botulism is not transmitted from person to person. Botulism develops if a person
ingests the toxin (or rarely, if the toxin is inhaled or injected) or if the organism
grows in the intestines or wounds and toxin is released.
Three common forms of botulism are:

• Foodborne botulism. The harmful bacteria thrive and produce the toxin in
environments with little oxygen, such as in home-canned food.
• Wound botulism. If these bacteria get into a cut, they can cause a dangerous
infection that produces the toxin.
• Infant botulism. This most common form of botulism begins after Clostridium
botulinum bacterial spores grow in a baby's intestinal tract. It typically occurs in
babies between the ages of 2 months and 8 months.
Mechanism of transmission: food borne(canned foods) contact, airborne
Spores widespread in soil ,contaminated vegetables and meat
Foods canned without adequate sterilization
Sesason; summer, early fall (autumn)
The symptoms of botulism may include: double vision,blurred vision,drooping

eyelids,slurred speech,difficulty swallowing,dry mouth ,muscle weakness, and
,flaccid, symmetric, descending paralysis
68. The main clinical syndromes of botulism.

Common forms include
Food botulism,wound botulism,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
69. What are the symptoms of pharyngoplegic syndrome at botulism

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

70. What are the symptoms of ophthalmoplegic syndrome at botulism.

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

•Mouse bio-assay: serum gastric secretion or food diluted in phosphate buffer and
injected into mice peritoneum
• Culture of food samples, gastric aspirate or fecal material in anaerobic conditions
• Electrophysiological testing
• ELISA and PCR•A normal Tensilon test helps to differentiate botulism from
myasthenia gravis; borderline positive tests can occur in botulism
• 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
72. Specific therapy and management of botulism patient

Anti botulism serums are injected at first hours of the disease
Botulism antitoxin A and E (10,000IU), B (5,000IU)
Nonspecific desintoxication therapy consists of injection of glucose solution,
polyionic solutions (Lactasault, Trisault, Quartasault) and simultaneously diuretics
- Furosemid ( Lasix).
For suppression of infection in a digestive tract Ampicillin, Oxacillin, Levomycetin
or Tetracyclin are indicated. A course of antibiotic therapy lasts for 5-7 days.
In serious cases and for prophylaxy of serum disease indicate Prednisolone on 40 mg.
in day or its analogues. At disorders of respiration of the patient it is required to
hospitalize to reanimation departament and transfer on controlled 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
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

• Prodromal period: elevated temperature for short period of time (2-3hours), skin
warm to hot
• Malaise, chilliness, myalgias, headache, dizziness, syncopem malaise body pain
• Frontal retro-orbital headache
• Eyes may be red and watery
• Sore, throat, tonsillitis
• Cough
• Rhinopharyngitis, laryngotracheitis, tracheobronchitis
74. Differential diagnosis of influenza and adenoviral infection.

Influenza
Etiology
Influenza is a systemic viral illness from influenza A or B, usually occurring in an
epidemic pattern and transmitted by droplet nuclei
Mode of transmission
Aerosols , direct contact , nasal droplets
Clinical symptoms
Tracheaitis,severe intoxication,moderate rhinitis , Dry cough,absence of
conjunctivitis ,pharyngeal hyperaemia ,absent lymphadenopathy ,normal liver ,
absent diarrhoea Diagnosis with rapid antigen detection methods of swabs or
washings of nasopharyngeal secretions.
Treatment
Specific antiviral medications for both influenza A and B are the neuraminidase
inhibitors oseltamivir and zanamivir.
Adenovirus infection
Etiology
Adenoviral
Mode of transmission
They’re very contagious. They can spread when someone who's infected coughs or
sneezes.
Droplets containing the virus fly into the air and land on surfaces.
You can catch the virus when they touch the handof someone t and then touches
their mouth, nose, or eyes.. You also can get sick from eating food prepared by
someone
who didn't wash their hands properly after going to the bathroom
Clinical symptoms
Pharyngotonsilitis,moderate intoxication,expressed cattharal stmptoms,moderate
myalgia & althgragia,expressed rhinitis,rare occurrence of cough ,often conjunctivitis
,pharyngeal hyperaemia ,lymphadenopathy ,enlarged liver, diarrhoea might be
present
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
75. Laboratory diagnosis of flu.

Diagnosis is initially confirmed with rapid antigen detection methods of swabs or
washings of nasopharyngeal secretions. Viral culture is the most accurate test but is
usually not available rapidly enough to make it useful in acute patient management.
Leukopenia, relative lymphopenia
• Viral culture of nasopharyngeal samples and/ or throat samples.
• Hemadsorption is positive
• Stain with fluorescent antibody
76. Specific treatment of influenza.

Symptomatic therapy with acetaminophen and antitussives is useful
. Specific antiviral medications for both influenza A and B are the 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
The most important candidates for vaccination are those with chronic lung and
cardiac disease, pregnant women in any trimester, residents of chronic care facilities,
health-care workers, immunosuppressed patients, and those with diabetes and renal
dysfunction. Influenza vaccine is contraindicated in those who are highly allergic to
eggs and which would result in anaphylaxis.
77. Clinical signs of adenoviral infection.

Epidemiology: Source: infected pt, transmitted by contact, fecal oral, waterborne
Clinical• 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
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 of the disease symptoms of 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
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
RSV can spread when

• An infected person coughs or sneezes
• You get virus droplets from a cough or sneeze in your eyes, nose, or mouth
• You touch a surface that has the virus on it, like a doorknob, and then touch your
face before washing your hands
• You have direct contact with the virus, like kissing the face of a child with RSV
Clinic:
• Incubation 4-5 days
Runnyw nose,Decrease in appetite,Coughing,Sneezing,Fever,Wheezing
• Cough, subfebrile temperature with shivering, 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
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)
● 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
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
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
They are facultative intra cellular parasites
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
It is a respiratory infection
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
Highest incidence – During the warmer months when air conditioning systems are
used more frequently
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
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
infections Human herpesvirus type 6 causes childhood illness known as roseola
infantum or sixth disease.
Human herpesvirus type 7 cause a skin condition in infants known as exanthema

subitum, Human herpesvirus type 8 cause Sarcoma Kaposi's
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 mothers genital tract to her unborn child
Source of infection
Humans (Sick persons , Carriers )
Clinical Manifestations
Herpes simplex 1
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
2) 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
3) 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.
4) 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 walled vesicles ,
then they become pustular and ulcerate
5) Skin infections ( herpetic whitlow, herpes gladiatorum , eczema herpeticum )
6) 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
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),
• 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
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),
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
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
88.DIFFERENTIAL DIAGNOSIS OF HERPES ZOSTER AND

CHICKENPOX
Chicken Pox Herpes zoster
Transmission Through respiratory secretions By reactivation of latent

or vesicular fluid Varicella zoster virus
Signs and Malaise, fever, rash Neuralgia, dermatomal rash,
symptoms weakness of affected nerve
Distribution of rash Trunk initially, progressing to Dermatomal - Primarily

face, extremities, mucosa or thoracic, cranial, cervical,
combination, it involves the lumbar
whole body
Character of rash Non-grouped, itchy vesicles Grouped along affected
nerve, erythematous, severely
painful vesicles
In chicken pox the rash crust by the 7th day, in herpes zoster they crust by the
14th day In chicken pox rash is itchy , in herpes zoster rash is painful
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
90. THE SOURCE OF INFECTION AND MECHANISM OF TRANSMISSION

AT
EBSTEIN-BARR INFECTION
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
91. CLINICAL FORMS OF EBSTEIN-BARR VIRAL INFECTION
Epstein- Barr virus causes Infectious mononucleosis which is an infectious
widespread disease which infects B-cells (B-lymphocytes), producing a reactive
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
92. 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
• Helatosplenomegaly
• 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 OR
• 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.
93. Laboratory diagnosis of infectious mononucleosis.
Infectious mononucleosis is an infectious widespread disease caused by the Epstein-

Barr virus which infects B-cells (B-lymphocytes), producing a reactive
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)
Criteria
CBC – Lymphocytosis
Peripheral blood smear – presence of at least 10% atypical lymphocytes on smear(a
type of mononuclear cells – big monocytes with deformed big nucleus and widened
cytoplasm ) Positive serological test for EBV
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
94. Differential diagnosis of infectious mononucleosis with diphtheria.
Infectious mononucleosis Diphtheria

Lymphoproliferative
syndrome, tonsillitis is Fibrinous inflammation in
Leading symptoms not obvious throat, toxic syndrome
Absent or bright
Throat changes hyperemia Cyanotic, hyperemia, edema
Grey or white yellow
membranes can spread outside
Purulent in follicles or in the tonsils. They are dense,
lacunas, white-yellowish hard to remove and bleed if
only on tonsils. Can be you remove them. After
Character of easily removed without removal, they reappear again
tonsillar exudates bleeding and cannot be separated
Lymphadenitis General Regional
Hepatosplenomegal
y Present absent
Prolonged with gradual Proportional to surface of
development (moderate or inflammation. (mild, moderate
Toxic sign severe) and severe)
Subcutaneous fat Over the regional lymph Typical for toxic forms (bull
edema nodes in severe cases neck sign)
Changes on the
tongue Coated Coated
95.Differential diagnosis of infectious mononucleosis with acute tonsillitis.

.
Infectious mononucleosis Acute tonsilitis
Leading symptoms Lymphoproliferative Intoxication syndrome,

syndrome, tonsillitis is not Inflammation of tonsils
obvious
Throat changes Absent or bright Hyperemia of throat
hyperemia
Character of tonsillar Purulent in follicles or in Red, swollen tonsils which can
exudates lacunas, white-yellowish cause patient to have Dysphagia
only on tonsils. Can be (difficult to swallow or
easily removed without odynophagia (pain when
bleeding swallowing), changes of voice
Lymphadenitis General Regional (in neck region)
Hepatosplenomegaly Present absent
Toxic sign Prolonged with gradual cough, headache, chills,

development (moderate or tiredness, pain in ears or neck
severe)
Airway obstruction Absent Present: Mouth breathing,
snoring, nocturnal breathing,
pauses or sleep apnea
96.The source of infection and the mechanism of transmission at diphtheria.

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
97. The classification of clinical forms of diphtheria.
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 mainly with the formation
of fibrinogenous fur and typical complications on the part of the nervous system,
cardiovascular system and excretory system
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

● Form: Localized, widespread,
● Nature of process: catarrhal, island like, membranous
● Complicated and without complications
Complications include : myocarditis, neuritis, nephritis
98) Clinical features of the tonsils lesions at diphtheria.

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
99. Clinical features of the larynx diphtheria
Croup (true, diphtheric) can be primary – at the primary localization

of the diphtheria process in the larynx. Secondary- if it develops after
the affection of the fauces or the nose.
The course of croup can be divided into three stages.

1) Catarrhal croup
2) Stenosis (compensated , subcompensated , decompensated )
3) Asphyxia
A 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.
A 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 )
An asphyxia stage.
• In the struggle with stenosis the child exhausts, the respiratory muscles get
tired. The child becomes calm, sleepy, he inditfferently 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.
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, following improvement in the pharyngeal phase of the
disease Cardiac involvement is thought to be responsible for 50-60% of deaths
associated with diphtheria:
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-toproximal 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
101.Laboratory diagnosis of diphtheria.
Corynebacterium diphtheriae is the leading cause of diphtheria.

It is transmitted between humans via droplets, secretions or direct contact.
The two major sites of infection are the respiratory mucosa and skin.
The initial 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.
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
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 severe pain in Fibrinous inflammation in throat, toxic
symptoms mouth and gums, syndrome
foul smelling breath
Throat changes Grey-white pseudo Cyanotic, hyperemic, edema
membrane on gums
that can ulcerate
and
cause bad taste in
mouth
Character of Grey-white pseudo Grey or white yellow membranes can
tonsillar membrane on spread outside the tonsils. They are dense,
exudates tonsils that can hard to remove and bleed when removed.
ulcerate and After removal, they reappear and cannot
become necrotic. be separated
Easily removable
Lymphadenitis Cervical Regional
lymphadenopathy
Toxic sign Absent or minor Proportional to surface of inflammation.
(mild, moderate and severe)
Subcutaneous Absent Typical for toxic forms (bull neck sign)
fat edema
Changes on the Absent Coated
tongue
103.Specific treatment of diphtheria.
Diphtheria is caused by Corynebacterium diphtheriae.

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.
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.
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
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.
106. Peculiarities of rubella in adults.

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
107. Peculiarities of mumps in adults.

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
108. Peculiarities of chickenpox in adults.
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).
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
109. Classification of meningococcal infection.
Meningococcal infection is an acute infectious disease caused by

meningococcous Neisseria Meningitigis.
Mechanism of transmission- (air-drop)
It is characterized by damage of mucous membrane of nasopharynx

(nasopharingitis), generalization of the process in form of specific septicemia
(meningococcemia) and inflammation of the soft cerebral membranes
(meningitis). 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
● Complicalions: sepsis, DIC syndrome, toxic shock, brain edema
110. Clinic of meningococcal generalized forms.

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.
111. Complications of meningococcal disease.

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.
112.Diagnostics of meningococcal infection.

● 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
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)
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)
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.
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.
According to Seupaul, the following 3 findings on CSF analysis have clinically useful
likelihood ratios for the diagnosis of bacterial meningitis in adults [28] :
• 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
114.Treatment of meningococcal disease.

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
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 40-

50ml/kg. Diuretics to prevent brain edema (mannitol). Hydrocortisone (3-
7mg/kg/day) or Prednisolone 1-2mg/kg/ day in severe cases.
● Oxygen therapy
● Symptomatic therapy: antipyretics, anti-convulsants as needed
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 auxillary 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
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
Stage:
● 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
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
● Shock
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
01.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
02.The main pathogenic syndromes of viral hepatitis.
Viral hepatitis is an infection that causes liver inflammation and damage.
● Intoxication syndrome: general weakness, fatigue, headache, insomnia and change

in behavior. Increased body temperature
● Catarrhal syndrome: flu-like syndrome, sore throat, dry cough. Hyperemia of
conjunctiva and mucus of soft palate. Edema of nose making it hard to breathe
● Dyspeptic syndrome: anorexia, nausea, vomiting, abdominal pain, diarrhea
● Arthralgic syndrome: Pain in large joints only, no deformation of joints ●
Cholestatic syndrome: Jaundice
03.Clinical and epidemiological features of hepatitis A.
Hepatitis A is an intestinal anthroponotic viral infection.
Epidemiology
• Fecal-oral mechanism of transmission
Watery route
Alimentary route
Contact way (dirty hands, towels, dishes etc)
• Source of infection
Patients in the incubation, prodromal period and climax of the disease
• Susceptibility
Children after the first year of life, teenagers, young people up to 35 years, patients
with immunosuppression.
• Factors
Contaminated Water, infected food products and household items.
Clinic presentation
● Onset of fever, poor apetite, nausea, pain in the Right Upper Quadrant
● Within few days Jaundice, dark urine, clay coloured stools
● Usually mild and self limiting.
04. Clinical and epidemiological features of hepatitis E.
Definition: Hepatitis E is a liver disease caused by infection with a virus known as
hepatitis E virus (HEV).
Epidemiology:
Source of infection: sick people
Mechanism of transmission: fecal oral
Incubation period: 2-6 weeks
Susceptibility : high
Factors of transmission: water, food.
Clinic:
Onset of fever, poor apetite, nausea, pain in RUQ
Within few days Jaundice, dark urine, clay coloured stools
Usually mild and self limiting
05.Changes in the biochemical blood analysis at viral hepatitis.
Definition: Hepatitis E is a liver disease caused by infection with a virus known as

hepatitis E virus (HEV).
Epidemiology:
Source of infection: sick people
Mechanism of transmission: fecal oral
Incubation period: 2-6 weeks
Susceptibility : high
Factors of transmission: water, food.
Clinic:
Onset of fever, poor apetite, nausea, pain in RUQ
Within few days Jaundice, dark urine, clay coloured stools
Usually mild and self limit
Biochemical Blood analysis
● Cytolytic syndrome: increased ALT, AST, LDH, Cu. Decreased albumin,
prothrombin
● dysproteinemia
● Mesenchymal-inflammation: increased alpha and gamma globulins, tymol-test
● Cholestasis: increased bilirubin, bile acids, cholesterine, GGTP and alkaline
phosphatase ● Urine: urobilinogen, stool absent stercobillin
06.Clinical and laboratory predictors of acute hepatic encephalopathy.
Definition: Hepatic encephalopathy is a brain dysfunction caused by liver

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

may present in acute form as a recent infection with relatively rapid onset, or in
chronic form.
The most common causes of viral hepatitis are the five unrelated hepatotropic viruses
hepatitis A, B, C, D, and E.
Haemolytic Jaundice: Hemolytic jaundice occurs as a result of hemolysis, or an
accelerated breakdown of red blood cells, leading to an increase in production of
bilirubin.
Parameter Viral hepatitis Hemolytic jaundice
Type of serum bilirubin Unconjugated and Unconjugated
increased conjugated
Urine urobillinogen Increased/decreased/ normal Increased
PTT Abnormal, not corrected Normal
with vitamin K
Additional features Increase ALT/AST Blood smear:
hemolytic anemia
08.Differential diagnosis of viral hepatitis with obstructive jaundice.

chronic form. The most common causes of viral hepatitis are the five unrelated
hepatotropic viruses hepatitis A, B, C, D, and E.
Obstructive Jaundice: Obstructive jaundice occurs as a result of an obstruction in
the bile duct. This prevents bilirubin from leaving the liver.
Parameter Viral hepatitis Obstructed jaundice
Type of serum Unconjugated and Conjugated
bilirubin conjugated
increased
Urine Increased/decreased Decreased or absent
urobillinogen / normal
PTT Abnormal, not Abnormal, corrected with Vitamin K
corrected with
vitamin K
Additional Increase ALT/AST. Increased Serum ALP> 3 times
features Jaundice normal. Itching Jaundice with
greenish tinge
09.Differential diagnosis of viral hepatitis with leptospirosis.

chronic form. The most common causes of viral hepatitis are the five unrelated
hepatotropic viruses hepatitis A, B, C, D, and E.
Leptospirosis: Leptospirosis is a blood infection caused by the bacteria
Leptospira. Signs and symptoms can range from none to mild (headaches, muscle
pains, and fevers) to severe (bleeding in the lungs or meningitis).
Parameter Viral hepatitis Leptospitosis
Source of Sick people or Zoonosis/environment
infection carriers
Main features Flu-like symptoms Flu like symptoms with myositis of calf
with myalgia, muscles and acute renal failure, jaundice
jaundice
Hepatobilliary Hepatitis Hepatitis, acalculous cholecystitis
sysytem
Diagnosis Blood ELISA test Tissue biopsy microscopic agglutination
test
10.The specific diagnostic of hepatitis A and E.
Definition: Hepatitis A virus (HAV) and hepatitis E virus (HEV) are the most
common causes of acute hepatitis in humans worldwide. Most HAV and HEV
infections are acquired through contaminated water and food. Symptoms include:
Fever, Fatigue, Loss of appetite, Nausea, Vomiting, Abdominal pain, Jaundice.
● CBC: leukopenia with neutropenia.
● Biochemical: increased AST,ALT, ALP
● Serological diagnoses IgM Anti-HAV for hepatitis A, IgM Anti-HEV for recent
infection.
If IgG anti-HAV, it’s for vaccinated patients
11.The principles of viral hepatitis A and E treatment .
Definition: Hepatitis A virus (HAV) and hepatitis E virus (HEV) are the most
common causes of acute hepatitis in humans worldwide. Most HAV and HEV
infections are acquired through contaminated water and food. Symptoms include:
Fever, Fatigue, Loss of appetite, Nausea, Vomiting, Abdominal pain, Jaundice.
● Bed rest
● Supportive and symptomatic therapy
● Adequate nutrition: diet low fat, carbohydrates.
● Desintoxication therapy: glucose, rheosorbilact, isotonic solution
● Sorbents
● Ferments: mezim, contrical
● Lactulose
● Postexposure therapy
12.Treatment of patients with hepatic encephalopathy.
Definition: Hepatic encephalopathy is a brain dysfunction caused by liver

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

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

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

ELISA or PCR
Hepatitis B
● Acute infection: HBsAg+, HBeAg+, Anti-HBs-
● Past Hepatitis B infection: IgG anti-HBc+, HBsAG-, IgG-Anti-HBs –
● Chronic carrier: HBsAg+, IgG Anti-HBc-, Anti-HBe
● Window period: IgG (or IgM) Anti-HBc+, HBsAg-, IgG anti-HBs-
17. Specific laboratory diagnosis of hepatitis C
Hepatitis C: determine the genotype 1-5, A or B. Usually IgG anti-HCV. If IgM and
IgG anti-HCV present it is chronic re-infection.
18.Specific etiological Therapy of hepatitis B
Definition: Hepatitis B is an infectious disease caused by the hepatitis B virus

(HBV) that affects the liver; it is a type of viral hepatitis. It can cause both acute and
chronic infection. Many people have no symptoms during the initial infection.
Epidemiology
stomatologists, tattoo. Hepatitis B can stay on tools for long, not killed by normal
anesthetic ● Incubation period 6 weeks- 6months
● Susceptibility: high Clinic:
● Gradual onset of dyspeptic and intoxication syndrome
● Early in course of disease athralgic syndrome develops
● Progressive appearance of jaundice: 2 weeks and more. Jaundice is prolonged and
severe. ● Presence of asthenic (intoxication) syndrome throughout the whole period
of the disease
Antiviral medications
● Entecavir
● Tenofovir
● Lamivudine
● Adefovir
● Telbivudine
19.Specific etiological therapy of hepatitis C.
Definition: Hepatitis C is an infectious disease caused by the hepatitis C virus

(HCV) that primarily affects the liver; it is a type of viral hepatitis. During the initial
infection people often have mild or no symptoms. Occasionally fever, dark urine,
abdominal pain, and yellow tinged skin occurs.
Epidemiology
stomatologists, tattoo. Hepatitis C can stay on tools for long, not killed by normal
anesthetic ● Susceptibility: high Clinic
● Asymptomatic or mild course of disease. Usually manifests years later with
complications ● Mild prodromal period lasting more than 2 weks: dyspeptic
syndrome, mild arthralgic syndrome, intoxication syndrome
● Mild cholestatic syndrome
● Usually present much later with complicatons such as liver cirrhosis
Antiviral medications
● Pegylated Interferon
● Ribavirin
● Protease inhibitors (simeprevir, paritaprevir, glecaprevir, grazoprevir)
20.The epidemiology of HIV, persons with increased risk of HIV infection .
Definition: HIV (human immunodeficiency virus) is a virus that attacks the body’s
immune system. If HIV is not treated, it can lead to AIDS (acquired
immunodeficiency syndrome. Epidemiological data: HIV is spread primarily by
unprotected sex (including anal and oral sex), contaminated blood transfusions,
hypodermic needles, and from mother to
child during pregnancy, delivery, or breastfeeding.[13] Some bodily fluids, such as
saliva, sweat and tears, do not transmit the virus. South Africa, Nigeria, India, South
East Asia, Carribbean Sea, Eastern Europe
Epidemiology
● Ways of transmission: Sexual contact, iv drug abusers, infection of medical
personell.
Risk group
● Homosexuals unprotected sex
● Multi sexual partners (prostitutes), unprotected sex
● IV drug abusers
● Infected mothers to child
● Viral Hepatitis B, C, D
● Recipients of blood transfusion or organs
21.Clinical stages of HIV infection, its stages.
hypodermic needles, and from mother to child during pregnancy, delivery, or
breastfeeding.[13] Some bodily fluids, such as saliva, sweat and tears, do not
transmit the virus. South Africa, Nigeria, India, South East Asia, Carribbean Sea,
Eastern Europe
● Stage 1: asymptomatic, persistent generalized lymphadenopathy. Level of

functional ability 1: asymptomatic course and normal course of daily activity
● Stage 2: Weight loss less than 10%, minimum defeat of skin and mucous
(seborrhea dermatitis, mycotic defeat of nails, recurrent ulcers of mucous of oral
cavity, angular cheilitis i.e, inflammation of one or both corners of the mouth ).
Episodes of herpes zoster, recurrent episodes of upper respiratory tract (bacterial
sinusitis), Level of functional ability 2 (WHO: performance status 2): symptomatic
course, normal level of daily activity
● Stage 3: weight loss > 10%, hyperthermia more than 1 month, pneumocyst
pneumonia, cerebral toxoplasmosis, extrapulmonary criptococosis,
cryptosporidiosis with diarrhea more than 1 month. Cytomegalovirus infection with
defect of any organs except liver, spleen and lymph nodes. Level of functional
ability 3 (Performance status 3): patient lay in bed less than 50% of daily time
● Stage 4: Severe weight loss, cerebral toxoplasmosis. Pneumocystic carinii

pneumonia (jirovacii pneumonia), cryptosporidiosis with diarrhea.
Cytomegalovirus infection involving all organs except liver and spleen. Kaposi
Sarcoma, invasive cervical carcinoma. Progressive multifocal
leukoencephalopathy, atypical mycobacteriosis. Non-typhoid salmonella
bacteremia, HIV encephalopathy, disseminated mycosis. Extra pulmonary TB
Level functional ability: full bed rest. Decreased T-helpers less than 0.5X10^9.
22.Opportunistic infections at AIDS.
Acquired immunodeficiency syndrome (AIDS) is a chronic, potentially life-

threatening condition caused by the human immunodeficiency virus (HIV). By
damaging your immune system, HIV interferes with your body's ability to fight
infection and disease.
● Pneumocystis pneumonia
● Toxoplasma gondii
● Microsporidiosis
● Disseminated mycobacterium infection
● Bartonellosis
● Mucosal candidiasis
● Cryptococcal meningitis
● Herpes simplex with chronic ulcers,
23.Epidemiological and clinical criteria for the diagnosis of HIV

infection.
hypodermic needles, and from mother to child during pregnancy, delivery, or
breastfeeding.[13] Some bodily fluids, such as saliva, sweat and tears, do not
transmit the virus. South Africa, Nigeria, India, South East Asia, Carribbean Sea,
Eastern Europe Clinical data:
● prolonged fever more than 1 month
● generalized lymphadenopathy: more than 3 lymph nodes enlarged in different
anatomical groups of lymph nodes ● Diarrhea more than 1 month
● weight loss more than 10%
● opportunistic infection,
● Wasting syndrome (cachexia)
24.Laboratory diagnosis of HIV infection.

● Stage 1: Lab confirmation of HIV infection with no AIDS defining condition
and CD4 + T lymphocyte count of > 500 cells/ micro litre or CD4+ T
lymphocyte percentage of total lymphocytes of > 26%
● Stage 2: Lab confirmation of HIV infection with no AIDS defining condition
and CD4 + T lymphocyte count of 200-499 cells/micro litre or CD4 + T
lymphocyte percentage of total lymphocytes of 14-25%
● Stage 3 (AIDS; greater than 6years): Lab confirmation of HIV infection and
CD4 + T lymphocyte count less than 200 cells/micro litre or CD4 + T
lymphocyte percentage of total lymphocytes of less than 14%.
● Stage 3 defining opportunistic illnesses in HIV: bacterial infections (multiple or
recurrent in children), candidiasis of bronchi, trachea, lungs, or esophagus.
Cervical cancer invasive in adults, adolescents. Coccidioidomycosis,
disseminated or extrapulmonary. Extrapulmonary cryptocorccosis,
cryptosporidiosis (chronic intestinal> 1 month)
25.Etiological treatment of HIV infection.

Antiretroviral drugs
● Nucleoside and Nucleotide reverse transcriptase inhibitors (NRTI):
Abacavir 300 mg twice daily
, Didanosine, , Lamivudine 300 mg once daily,
 Non-nucleoside Reverse transcriptase inhibitor (NNRTI)-
Delaviridine, Efavirenz, Nevirapine
● Protease Inhibitors:
Atazanavir + Ritonavir; 300mg + 100mg once daily.
Darunavir, Fosamprenavir, Indinavir, Lopinavir, Nelfinavir, Saquinavir,
Tipranavir
● Integrase Strand Inhibitors (INST):
Dolutegravir, Elvitegravir and Raltegravir.
● Fusion inhibitors: Enfuvirtide
● Chemokine receptor antagonists: Maraviroc
26.The basic treatment of opportunistic infections.

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

Malaria; An infectious disease caused by protozoan parasites from the Plasmodium
family that can be transmitted by the bite of the Anopheles
Infectious agent : Plasmodium Falciparum, P.vivax, P.ovale, P.malariae, P.knowlesi
Incubation period: 7-30 days
Source of infection: Sick people, carrier
Mechanism of transmission: blood meal ,
*transplacenta*congenital transmission
Vectors: Female mosquitos of anopheles
genus. Season : summer autumn
High susceptibility
28.The pathogenesis of malaria attacks.

● Mosquito infects a person by taking a blood meal. They release sporozoites

from their salivary glands. Infects the organism in 2 phases
● Exoerythrocytic phase: sporozoutes enter blood stream and migrate to hepatic
system. In hepatocytes they multiply into merozoites, rupture the liver cells and
escape into blood stream
● Erythrocytic phase: the merozoites infect the red blood cells where they
develop into ring forms Trophozoites and schizonts which in turn produce more
merozites. Pathogenesis
- Tissue schizogony (incubation period)
- Erythrocyte schizogony
- Typical attack- massive destruction of erythrocytes, massive appearance of parasites
and products of their metabolism
- Disturbance of thermoregulation centre, increasing of vessels penetration
- Disturbance of microcirculation, water electrolytes balance, vegetative neurotic
system - Development of hemolytic anemia
- Hepatosplenomegaly
- Developmnt of coma
An attack of malaria may either be a primary attack or a relapse.

A primary attack normally develops after an incubation period of 10-14 days; by
direct blood inoculation it is about 11 days.
Relapses are defined as recurrences of malarious symptoms and the reappearance of

malaria parasites in the peripheral blood, following recovery from the initial attack.
29.The types of temperature curves at different forms of malaria.

● Febris intermittens; It is alternating fever. It is characterized by the rising

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

● Cyclical occurrence of coldness followed by rigor and then fever and sweating
lasting 4-6 hours every 2 days in P.vivax and P.ovale infections, while every 3 days
for P.malariae, P.falciparum can have recurrent fever every 36-48 hours or less.
● Shivering, arthralgia
● Anemia and jaundice. because of the loss of red blood cells, hemoglobinuria
● Retinal damage
● Convulsions
● P.falciparum causes severe malaria: coma, splenomegaly, severe headache, cerebral
ischemia, hepatomegaly, hypoglycemia and hemoglobinuria with renal failure.
● Chronic malaria P.vivax, P.ovale
31.Differential diagnosis of malaria and leptospirosis.

Leptospirosis is a blood infection caused by the bacteria Leptospira. Signs and

symptoms can range from none to mild (headaches, muscle pains, and fevers) to
severe (bleeding in the lungs or meningitis).
Parameter Malaria Leptospiriosis

Transmission Mosquito water exposure of contaminated
animal urine
Fever Undulating high fever with Mild to high fevers

cold, hot and sweating phases
Rash Absent Conjunctival rash
Chief symptoms Flu like symptoms, weakness, Flu smptoms, headache, back or
malaise calf pain, jaundice
Lab Anemia, thrombocytopenia, Leukocytosis, severe cholestasis,

abnormalities hypoglycemia renal failure, thrombocytopenia
32.Differential diagnosis of malaria with viral hepatitis.

family that can be transmitted by the bite of the Anopheles.
Viral hepatitis is liver inflammation due to a viral infection. The most common
causes of viral hepatitis are the five unrelated hepatotropic viruses hepatitis A, B,
C, D, and E.
Parameter Malaria Viral hepatitis

Transmission Mosquito Fecal-oral, contact
Incubation Max 21 days 2 weeks- 6 months
period
Fever Undulating high fever with Subfebrile
cold, hot and sweating phases
Signs and headache, malaise, myalgia, Fever, malaise, arthralgia,
symptoms anorexia, chills, faints, rigors. anorexia, nausea, abdominal
Jaundice with pain, diarrhoea, itching.
hepatosplenomegaly in severe Jaundice, hepatosplenomegaly
cases
Lab Anemia, thrombocytopenia, Increased ALT, AST
abnormalities hypoglycemia
33.Complications of malaria.
● Plasmodium falciparum: Cerebral Malaria (seizures and coma), acute renal failure,
non cardiogenic pulmonary edema, tropical splenomegaly
● Plasmodium Vivax: late splenic rupture (2-3 months after initial infection)
● Plasmodium Malariae: immune complex glomerulonephritis
● In pregnant women it can lead to still birth, infant mortality, low birth weight
34.The principles of malaria treatment.

● Plasmodium Falciparum: Artmether(20mg Lumefantrine(120mg), Atovaquone

(250mg)-proguanil (100mg), 4 tablets 4 times a day for 3 days.
mefloquine(250mg). Or Quinine Sulfate plus doxycycline, tetracycline,
clindamycin. Hydroxychloroquine 620mg
● P.vivax, P.ovale: chloroquine plus primaquine
● P maleriae, P.Knowlesi: chloroquine
● Severe cases: artesunate-quinine
● No diet diet or activity restrictions
● quinine and clindamycin is the recommended treatment for women in the first
trimester of pregnancy
35.Prevention of malaria.
Eradication of mosquito is the primary aim.
● Avoid mosquito bites
● Sleep in rooms properly screened with gauze over windows and doors
● Spray room with insecticides before entering
● Wear long sleeve shirts
● Use mosquito repellant cream
● Clean environment by getting rid of mosquito breeding sites
● Take antimalarial drugs when prescribed by doctor
36.The epidemiology of brucellosis.

Brucellosis is a bacterial infection that spreads from animals to people caused by a
type of bacteria called Brucella. Most commonly, people are infected by eating raw
or unpasteurized dairy products.
Clinical manifestations; Fever, Chills, Loss of appetite, Sweats, Weakness, Fatigue,
Joint, muscle and back pain, Headache.
Source of infection : Brucella Melitensis, Abortus, suis, canis

Factors of transmission : Zoonosis (goat, cow, sheep, dog, pig, camel, rodents),
unpasteurized milk
Mechanism of transmission: air borne, fecal oral, contact
The incubation period is highly variable, usually 2-4 weeks, can be 1 week to 2
months or longer.
37. Clinical classification of brucellosis.

or unpasteurized dairy products.
● Subclinical: usually asymptomatic
● Acute 2-3months
● Subacute 3-12months
● Chronic: 1 year: low grade fevers and neuropsychiatric symptoms predominate ●
Relapsing: every 2-3months.
Clinical features:
● GI symptoms: nausea, vomiting, constipation, diarrhea, abdominal pain
● Pulmonary symptoms: dry cough, pleural effusion
● Chest signs: hilar lymphadenopathy, pleural effusion, pneumothorax, lung nodules
● Generalized lymphadenopathy
● Men can have testicular pain
● Arthralgia of knees, hips and spine
● Focal CNS symptoms in severe cases: mild to moderate neuropsychiatric
symptoms, headache, fatigue, depression
● Uncommon signs: red eye, cranial nerve palsy, neck stiffness
(meningoencephalitis), ● Skin rash: non specific maculopapular rash
38.Laboratory diagnosis of brucellosis.

or unpasteurized dairy products of an infected animal.
Lab tests
● Blood culture in Castaneda’s medium
● Serological: ELISA, agglutination, microagglutination, PCR
● CSF, synovial fluid analysis: increased protein, low glucose, lymphocytes
predominate
● CSF culture, synovial fluid culture
● CBC: anemia, thrombocytopenia, leukopenia or leukocytosis more prominent is
leukopenia
● Liver function test: slight increase AST, ALT
39. Differential diagnosis of brucellosis and flu.

Influenza; commonly called "the flu", is an infectious disease caused by influenza
viruses. Symptoms range from mild to severe and often include fever, runny nose,
sore throat, muscle pain, headache, coughing, and fatigue.
Parameter Brucellosis Flu

Transmission ingestion of unpasteurized goat Air droplets
milk
Fever Fever with relative bradycardia Severe
Signs and anorexia, asthenia, fatigue, Dry cough, rhinitis,
symptoms weakness, malaise. Bone and joint headache, tracheitis,
pain. Neuropsyciatric symptoms. myalgia, malaise,
Can be abdominal pain, catarrhal signs
constipation, diarrhea
Diagnosis Anemia, Serology Nasopharyngeal swab,
leukopenia with
lymphocytosis
40. Treatment of brucellosis.

● No diet or activity restriction

● Gentamycin 5mg/kg/d IV or IM 10-14 days
● Streptomycin 1g IM/d 10-14 days
● Doxycycline 100mg orall bid 10-14 days
● Quinolones and rifampin
● Doxycycline, rifampin therapy
● Tripple therapy: above drugs plus amino glycoside
● Pregnant women: Rifampin 600mg orally daily for 6 weeks
● Neurological manifestation: treat 3-6months: triple therapy with ceftriaxone
41. Clinical signs of sepsis.

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

Epidemic typhus is caused by Rickettsia prowazekii. Symptoms are prolonged high
Fever, intractable headache and macolopapular rash.
Brill-Zinsser disease is a recrudescence of epidemic typhus, occurring years after an

initial attack.
Epidemic typhus occurs in Central and South America, Africa, northern China, and
certain regions of the Himalayas. Outbreaks may occur when conditions arise that
favor the propagation and transmission of lice. Brill-Zinsser disease develops in
approximately 15% of people with a history of primary epidemic typhus.
● Etiology: Rickettsia prowazekii

● Source of infection: sick person
● Mechanism of transmission: transmissive ● Vectors: Pediculus humanus (human
lice)
● Incubation 1-2 weeks
Brill zinesser disease

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

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

It occurs due to reoccurrence of epidemic louse-borne typhus caused by Rickettsia
prowazekii years after initial attack.
Brill-Zinsser disease can occur >40 years after primary
infection It has same clinical presentation as Epidemic typhus
but milder.
● Abrupt onset of high fever,chills, headache (unremitting).
● Enanthema **
● Rash: maculopapular/ petechial rash on 4-7 day on chest then axilla, trunk and
spread peripherally
● Rigors, myalgia, malaise
● CNS symptom: mental dullness to coma, stupor, sensitivity to light and delirium
● Regional and generalized lymphadenopathy. Mild hepatosplenomegaly
45.Complications of epidemic typhus.

Epidermic Typhus also called louse-borne typhus, is an uncommon disease caused by
a bacteria called Rickettsia prowazekii.
Epidemic typhus is spread to people through contact with infected body lice.
It’s complications include
● Vasculitis which may result in hypovolemia
● Thromboses of various vessels
● Bronchitis, pneumonia,
● Otitis media
● Parotitis
● nephritis
46. Laboratory diagnosis of epidemic typhus and Brill-Zinsser disease.

Epidermic Typhus also called louse-borne typhus, is an uncommon disease caused
by a bacteria called Rickettsia prowazekii.
Brill-Zinsser disease occurs due to reoccurrence of epidemic louse-borne typhus
caused by Rickettsia prowazekii years after initial attack.
So,
Suspect epidemic typhus based on clinical manifestations and signs of louse
infestation; such as abrupt headaches and fever , hepatomegaly, maculopapular
rashes etc
We can confirm with fluorescent antibody staining of skin biopsy.
Can only be made by serological

● Complement fixation test
● Indirect hemagglutination
● Indirect immunofluorescens
47.Differential diagnosis of epidemic typhus with typhoid fever.

Typhoid fever : It's caused by a bacterium called Salmonella typhi, which is related to
the bacteria that cause salmonella food poisoning.
48.Differential diagnosis of epidemic typhus with leptospirosis.
Leptospirosis is a non rickettsial infection that at some time during its course may
mimic louse- borne typhus ( epidemic typhus )
Leptospirosis generally presents after contact with urine of infected animals. with
cough, jaundice, chest pain, lymphadenopathy, hepatosplenomegaly and is diagnosed
by PCR.
Epidemic typhus caused by Rickettsia prowazekii occurs after being bitten by a tick
or louse, can only be transferred human to human: presented by high fever, cough,
rash, muscles and joint pain. Sometimes liver and spleen can be enlarged. Eyes look
like Rabbits eye. Enanthema on uvula, tremor of tongue. Diagnosed by serology
49.Treatment of epidemic typhus and Brill-Zinsser disease.

Brill-Zinsser disease occurs due to reoccurrence of epidemic louse-borne typhus
caused by Rickettsia prowazekii years after initial attack.
So the treatment :
● Etiotropic therapy: tetracycline (0.3-0.4g), chloramphenicol (0.5g) four times a day

● Pathogenetic treatment: heart (corglycon, strophantin), Vascular (cordiamin,
ephedrine, mezaton).
● Syptomatic therapy
● Desintoxication and dehydrative therapy
50. Epidemiology of Lyme borreliosis.
Lyme borreliosis also known as Lyme disease, is an infectious disease caused by the
Borrelia bacterium which is spread by ticks.
Etiology: Borrelia burgdorferi

Epidemiology:
● Source of infection: . ticks, Zoonosi
● Infective agent: Borrelia burgdorferi
● Mechanism of transmission: transmissive, vectors
● Vectors: tick ixode
● Incubation period: 1-2 weeks
The disease is currently recognized as the most common vector-borne disease in

Europe and North America.
Registration of Lyme borreliosis in humans in Ukraine began in 2000. It was proved

that the incidence of the disease in the country was growing each year from 58 cases
in 2000 (incidence: 0.12/100,000) to 3413 in 2015 (incidence: 7.96/100,000) (2).
The western part of Ukraine, including the Ternopil area, is recognised as an endemic
region for LB, as it is located in the forest-steppe region with mixed forests, fertile
soils, as well as adequate moisture and optimal temperatures.
51.The epidemiology of tick-borne encephalitis(TBE)

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

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

The most common sign of infection is an expanding red rash, known as erythema
migrans, that appears at the site of the tick bite about a week after it occurred.
Methods for diagnosis
1. Usually based on History of tick bites or bulls eye rash, endemic areas.
2. Serological tests: Western blot and ELISA or PCR of blood via venipuncture or
CSF
55.Etiological therapy of Lyme borreliosis.

1. To treat the Erythrema migrans: we give doxycycline 100mg PO bid 10-15 days,
Amoxicillin 500mg P0 tid, Cefuroxime: 500mg bid. If allergy to above give
Azithromycin 500mg single dose, erythromycin 500mg qid, clarithromycin.
2. AV block, CNS: IV antibiotics ceftriaxone 2g IV once/day 14 days.
Benzylpenicillin IV or IM 2.4g every 4-6hours. Cefotaxime 2g tid.
3. To treat Arthritis: antibiotic + NSAID, diclofenac 50mg tid, ibuprofen 300-400mg
tid (max 2400mg). Recurrent arthritis: antibiotics + arthroscopic synovectomy +
intraarticular injection.
56. Emergent prevention of Lyme borreliosis.

Preventions include:
- Application of DEET cream 20-30% on skin before going out
-Permethrine spray on clothes
-Shower within 2hours after coming indoors
-Patients are advised to call the doctor if they experience fever or rash
-After exposure to tick, promptly remove attached ticks without crushing tick before
transmission of Borrelia spirochetes and wash area with antiseptics, soaps and water.
- Give an Antimicrobial prophylactics after tick bites such as doxycycline within 72
hours 100mg single dose.
- Carefully inspect the entire body and remove any attached ticks. Ticks may feed
anywhere on the body. Tick bites are usually painless and, consequently, most
people will be unaware that they have an attached tick without a careful check.
57.Classification of erysipelas.
Erysipelas is an infection of the upper layers of the skin (superficial). The most
common cause is group A streptococcal bacteria, especially Streptococcus
pyogenes. Erysipelas results in a fiery red rash with raised edges that can easily
be distinguished from the skin around it. Classification:
1. According to etiology: Streptococcal Group A, Streptococcal group B,
staphylococcus, 2. According to clinical form(ie. The character of local changes ) :
Erysipelas erythematosum, erysipelas vasiculosum, erysipelas haemorrhagicum,
erysipelas abscedens, erysipelas gangrenosum
3. According to complication: abscess, gangrene, thrombophlebitis, bacteremia,
streptococcal toxic shock syndrome
58.Clinic of erysipelas erythematous form.
Erysipelas is a human infectious disease infectious disease of streptococcal
etiology with acute and chronic forms and is characterized by intoxication
syndrome and local changes looking like circumscribed locus of serous
hemorrhagic inflammation of skin . Clinical signs of the erythematous form is :
• It has an acute onset
• Intoxication syndrome (High fever, shaking, chills, fatigue, headache, vomiting
• Early signs of the disease before the local changes include:
1. Regional lymphadenitis and lymphangitis
2. Burning pain in erysipelas Can occur on skin of face that starts 5-6 hours before the
local inflammatory focus forms
• Local process is characterized by sharply circumscribed hyperemia with peripheral
inflammatory wall, edge painfulness , and local temperature reactions (erythematous
forms ) • Local process is associated with lymphatic edema of various degree.
• Re-infection causes lymphadenitis
59.Treatment of primary erysipelas.
Erysipelas is a human infectious disease infectious disease of streptococcal etiology

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

with acute and chronic forms and is characterized by intoxication syndrome and local
changes looking like circumscribed locus of serous hemorrhagic inflammation of skin
.
Treatment
1. Etiotropic therapy
Penicillin is the antibiotic of choice
Depending on the severity can be given for 7 days , 10 days or 14 days
2. Pathogenetic therapy
E. Detoxification therapy
Oral – (enterodez, regidron , etc )
Parenteral – crystalloids ( polyionic solutions , trisol , 5% glucose etc) and Low
molecular colloids
F. Desensibilisation therapy- Antihistamine drugs ( dimerol , tavegil, suprastin ,
pipolfen,… )
G. Correction of the Haemostasis alterations according to the coagulogram control :
disaggregants ( eg. Trental etc ) , direct acting anticoagulant (eg. Heparin ,
fraxiparin , calciparin etc ) , indirect acting anticoagulant ( kumadin,
pelentan , etc)
H. Immunocorrection with the control of the control of immune status
( Immunoglobulins IV and IM , interferons , primidines ( eg. methyluracil )
3. Local treatment
• Don’t touch erythematous forms
• Emulsions ,Ointments and antiseptic solutions are meant only for bullous forms
4. Ambulatory monitoring:
• finishing treatment
• Sanitation of the chronic focuses of infection
• Relapse prophylaxis: bicillin once a month for 6 months after disease
1. Penicillin V 2million units daily for 8 days then

2. Penicillin V 1 million units daily for 3 weeks
61.Epidemiology of nosocomial infections.

A nosocomial infection is contracted because of an infection or toxin that exists in a
certain location, such as a hospital. People now use nosocomial infections
interchangeably with the terms health-care associated infections (HAIs) and hospital-
acquired infections.
1. Etiology: Most common causes are Pseudomonas aeruginosa and E.coli,
Methicillin resistant staphylococcus resistant aureus. Clostridium difficile, TB
2. Source of infection: sick people
3. Mechanism of transmission: contact, droplet, airborne, fecal oral
Bacteria Infection type
Staphylococcus aureus(S.
blood
aureus)
Escherichia coli (E. coli) UTI
blood, UTI,
Enterococci
wound
Pseudomonas aeruginosa (P. kidney, UTI,
aeruginosa) respirator
Incidence of nosocomial infections

The most common nosocomial infection was pneumonia (517 cases, 64%), followed
by sepsis (106 cases, 13%), wound infection (102 cases, 13%), urinary tract infection
(43 cases, 5%) and catheter-related bloodstream infection (42 cases, 5%).
62.Clinical classification of toxoplasmosis.

Toxoplasmosis is a disease that results from infection with the Toxoplasma gondii
parasite, one of the world's most common parasites. Infection usually occurs by
eating undercooked contaminated meat, exposure from infected cat feces, or mother-
to-child transmission during pregnancy.
Classification:
1. Acute or chronic
2. Congenital or acquired
There are three forms of Toxoplasma gondii:

1. the tachyzoite (the rapidly reproducing form),
2. the bradyzoite (a slower reproducing form contained in tissue cysts), and
3. the sporozoite (contained in oocysts).
63.Peculiarities of toxoplasmosis at pregnancy and congenital toxoplasmosis.
Congenital toxoplasmosis is a group of symptoms that occur when an unborn baby
(fetus) is infected with the parasite Toxoplasma gondii.
1. Pregnant women generally are asymptomatic or have flu like symptoms. Higher
risk of transmission to infant. Can lead to premature birth 2. Congenital
toxoplasmosis:
1. Cerebral calcifications
2. Microcephaly
3. Hydrocephaly
4. Bilateral Chorioretinitis
5. Convulsions
Other: organomegaly, jaundice, rashes and fever, psychomotor retardation
64. Laboratory diagnosis of toxoplasmosis.
● Blood, tissue or amniotic fluid examination (ELISA) with Sabin Feldman dye
test for Toxoplasma gondii.
● Indirect fluorescent antibody test
65.Treatment principles of patients with congenital and acquired toxoplasmosis.

● Most healthy people recover from toxoplasmosis without treatment.
● Sulfadiazine 75mg/kg PO qid, plus Pyrimethamine 50-200mg for 3-6 weeks

plus folinic acid
● Clindamycin 600mg PO IV qid 3-6 weeks
● Azithromycin: 500mg PO on day one, then 250mg/day for 3 weeks or
Spiramycin 3g/day orally for 3 weeks, discontinue for 2 weeks, then continue
for 3 weeks. Done for a total of 5 cycles.
66.Clinical syndromes of leptospirosis.

• Leptospirosis can present in two distinct clinical syndromes, icteric or anicteric.
• The anicteric syndrome is self-limited and presents with a nonspecific flu-like
illness. The onset is usually sudden and can present with a headache, cough, non-
pruritic rash, fever, rigors, muscle pain, anorexia, and diarrhea. This symptoms may
last a few days before resolution of the fever. This form of leptospirosis is rarely
fatal and represents approximately 90% of all documented cases of Leptospirosis.
• The anicteric syndrome can also have recurrence several days later, and this phase is
called the immune stage during which aseptic meningitis can occur. These patients
can recover fully but may suffer from chronic, episodic headaches.
• Icteric syndrome: called weils disease, usually severe. Fever, renal failure, jaundice,
hemorrhage and respiratory distress. May involve heart, CNS and muscles. It
present with vascular collapse, thrombocytopenia , hemorrhage,
• Hemorrhagic syndrome
• Asthenovegetative syndrome
• Intoxication syndrome
• Hepatomegaly
• Pneumonia syndrome
• Meningeal syndrome
67. Clinical signs of leptospirosis.

• The clinical course of leptospirosis is variable. Most cases are mild and self-limited
or subclinical, while some are severe and potentially fatal. The illness generally
presents with the abrupt onset of fever(38-40)
rigors, myalgias, and headache in 75 to 100 percent of patients, following an

incubation Fever 38-40 degrees, warm and flushed skin
• nausea and vomiting, Anorexia, diarrhea
• Cough
• Muscle pain: especially gastrocnemius (calf), muscles of scalp, neck and abdomen,
lumbar area. Muscle tenderness and myositis. Increase during palpation
• oliguria,red urine with moderate proteinuria, fresh erythrocytes and leukocytes.
• Hypotension, oliguria
• Hepatosplenomegaly with jaundice:
• pneumonia
• Rare: Cardiovascular: dull heart sounds, relative bradycardia, arrhythmia,
extrasystole.
• CNS: disorders of consciousness, headache, insomnia, delirium. Meningitis on 5-8th
day of disease
• Hemorrhagic syndrome: petechial rash on skin, conjunctivitis, epistaxis,
hemorrhage in stomach, intestine and uterus. Can lead to anemia
68. Diagnosis of leptospirosis.

• The most common way to diagnose leptospirosis is through serological tests either
the Microscopic Agglutination Test (MAT) which detects serovar-specific
antibodies, or a solidphase assay for the detection of Immunoglobulin M (IgM)
antibodies.
• CBC: anemia, low reticulocyte number, thrombocytopenia in hemorrhagic
syndrome. Left shift leukocytosis with neutrophilia and lymphopenia. Increased
ESR 40-60
• Biochemical: increased direct and indirect bilirubin, slightly increased AST and
ALT. decrease prothrombin time. Increased urea nitrogen and creatinine.
• Urine analysis: moderate proteinuria, fresh erythrocytes, leukocytes, hyaline casts
and cells of epithelium
• CSF analysis: increased pressure, moderate lymphocytic pleocytosis, increased
protein • Culture of urine, CSF or tissues for leptospiriosis for bacteriologic (water
medium with native rabbit serum) and bacterioscopic exam
• Biologic: using guinea pigs, inject infected material. If they die, it confirms
diagnosis
69. Treatment of leptospirosis.

• Bed rest, diet with adequate rehydration • Antimicrobial
therapy
● Antibiotic
● Antibiotic: Benzylpenicillin G 6-24millionU every 4 hours. Cephalosporins bid
1g. period of temperature plus 2 days
● Desintoxication therapy
● Antileptospirosis immunoglobulin
● Diuretics: lasix
● Glucocorticoids in severe forms
• : Bed rest, diet with adequate rehydration
Mild disease — For outpatients with mild disease, we favor treatment with
doxycycline (adults: 100 mg orally twice daily for 7 days; children: 2 mg/kg per day
in two equally divided doses [not to exceed 200 mg daily] for 7 days) or azithromycin
(adults: 500 mg orally once daily for three days; children: 10 mg/kg orally on day 1
[maximum dose 500 mg/day] followed by 5 mg/kg/day orally once daily on
subsequent days [maximum dose 250 mg/day]).
For pregnant women, we favor treatment with either azithromycin (500 mg orally
once daily for three days) or amoxicillin (25 to 50 mg/kg in three equally
divided doses [maximum 500 mg/dose] for seven days). Azithromycin is
preferred over amoxicillin if the differential diagnosis includes rickettsial
infection.
For hospitalized adults with severe disease, we favor treatment with penicillin (1.5
million units intravenously [IV] every six hours), doxycycline (100 mg IV
twice daily), ceftriaxone (1 to 2 g IV once daily), or cefotaxime (1 g IV every
six hours). The duration of treatment in severe disease is usually seven days.
For hospitalized children with severe disease, we favor treatment with penicillin
(250,000 to 400,000 units/kg IV per day in four to six divided doses [maximum dose
6 to 12 million units daily]), doxycycline (4 mg/kg IV per day in two equally divided
doses [maximum dose 200 mg/day]), ceftriaxone (80 to 100 mg/kg IV once daily
[maximum dose 2 g daily]), or cefotaxime (100 to 150 mg/kg IV per day in three to
four equally divided doses). For children who cannot tolerate the above agents,
azithromycin is an acceptable alternative agent (10 mg/kg IV on day 1 [maximum
dose 500 mg/day], followed by 5 mg/kg/day IV once daily on subsequent days
[maximum dose 250 mg/day]). The duration of treatment in severe disease is usually
seven days.
• Tetracycline antibiotics may cause permanent tooth discoloration for children <8
years if used repeatedly. However, doxycycline binds less readily to calcium than
other tetracyclines and may be used for ≤21 days in children of all ages
• Glucocorticoids in severe forms
70. Etiology and epidemiology of tetanus.

• Etiology: Tetanus is due to infection from the bacterium, Clostridium tetani,
which is found in soil, dust, or animal feces. It is a gram-positive, spore-forming,
obligate anaerobic bacillus. This bacteria and its spores are found worldwide,
however, it is more frequently found in hot and wet climates where the soil is rich
with organic matter.
• The source of infection, in most cases, is a wound, usually from a minor injury.
A very common cause of tetanus is a lack of immunization.
• Epidemiology: C tetani is found worldwide in soil, on inanimate objects, in
animal feces, and, occasionally, in human feces. Tetanus is predominantly a disease
of underdeveloped countries. It is common in areas where soil is cultivated, in rural
areas, in warm climates, during summer months, and among males. In countries
without a comprehensive immunization program, tetanus predominantly develops in
neonates and young children.
•
71.Classification of tetanus.
o Generalised: trismus (lock jaw), repeated painful spasms any part of the body.
Restlessness, irritability, dysphagia. Opisthotonus: spasm of muscles causing
backward arching of head, neck and spine. Seizures can be seen and respiratory
failure o o Grade 1(mild): mild trismus (lock jaw), general spasticity, little or no
dysphagia ▪ Grade 2 (moderate): moderate trismus and generalized spasticity,
mild dysphagia and fleeting spasms. Moderate respiratory embarrassment
▪ Grade 3a(severe): severe trismus and generalized spasticity. Severe dysphagia and
respiratory difficulties. Severe and prolonged spasms
▪ (both spontaneous and on stimulation
• Grade 3b: same as 3a with autonomic dysfunction o
Localised: muscle spasms on one extremity or one body
region
o Cephalic: due to head injury or middle ear infection: cranial nerve palsies which
progress to generalized tetanus o Neonatal: associated with umbilical stump infection
in neonates born to mothers who have not been immunized. o Maternal: tetanus
during pregnancy and 6 weeks after.
72. Clinical signs of tetanus.

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

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

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

• Rabies is a zoonotic, fatal and progressive neurological infection caused by rabies
virus of the genus Lyssavirus and family Rhabdoviridae. It affects all warm-
blooded animals and the disease is prevalent throughout the world and endemic in
many countries except in Islands like Australia and Antarctica.
• transmission : Bite of rabid animals and saliva of infected host
• reservoirs: wildlife like raccoons, skunks, bats and foxes.
76.The stages of rabies.

• Incubation period: 1week-3years : The closer the bite is to the brain, the sooner the
effects are likely to appear.
• Prodromal period: virus enters CNS. Lasts 2-10days. Paraesthesia or pain at
inoculation site. Malaise, headache, anorexia, fever of 38 degrees and above, chills,
pharyngitis and laryngitis by spasm with hydrophobia, nausea, emesis, diarrhea,
anxiety, insomnia and depression. Aerophobia
• Excitation period: patient has furious episodes of agitation, hyperactivity,
restlessness, thrashing, biting, confusions or hallucinations lasting less than 5
minutes. Seizures may occur. This phase may end in cardiorespiratory arrest or
progress to next stage.
Hydrophobia, aerophobia.
• Paralysis: begins within 10 days of onset. Can lead to respiratory depression, arrest
and death.
77.Clinical signs of rabies
• At first, there's a tingling, prickling, or itching feeling around the bite area. A
person also might have flu-like symptoms such as a fever, headache, muscle aches,
loss of appetite, nausea, and tiredness.
• After a few days, neurological symptoms develop, including:
• irritability or aggressiveness
• excessive movements or agitation
• confusion, bizarre or strange thoughts, or hallucinations
• muscle spasms and unusual postures
• seizures (convulsions)
• weakness or paralysis (when a person cannot move some part of the body)
• extreme sensitivity to bright lights, sounds, or touch
• Classic encephalitic (furious) rabies: hydrophobia and hyperexcitability
• Paralytic (dumb) rabies: flaccid muscle paralysis
• Non-classic atypical rabies (bite of bat): neuropathic pain, focal brainstem sign and
myoclonus
78.The treatment of rabies.

• After exposure and before symptoms begin, a series of shots can prevent the virus
from thriving. Strategies include:
• A fast-acting dose of rabies immune globulin: Delivered as soon as possible, close

to the bite wound, this can prevent the virus from infecting the individual.
• A series of rabies vaccines: These will be injected into the arm over the next 2 to 4
weeks. These will train the body to fight the virus whenever it finds it.
•
• Rabies vaccine 1ml on days 0,3,7 and 14. Rabies immunoglogulin 20IU/kg when
incubation period is less than 4 weeks. • Intensive cardiopulmonary supportive care
• Symptomatic treatment
79.Prevention of rabies.
• regular antirabies vaccinations for all pets and domestic animals
• bans or restrictions on the import of animals from some countries
• widespread vaccinations of humans in some areas
• educational information and awareness
• If bitten by animal: animal should be caged and monitered for 10 days to see if
signs of rabies appear.
• If animal with rabies attack you, step outside their visual acuity
• Vaccinate animals and humans with rabies vaccine
• Post exposure prophylaxis with rabies vaccine
80. Clinic of Ebola hemorrhagic fever.

•
• Caused by bunyaviridae family from hantaan kind

• Incubation period: 10-15 days
• Acute and adrupt onset of symptoms including,
• extremely strong chills with fever.
• Decreased visual acuity (mist before eyes), sharp headache, backache, muscles of
extremities, photophobia
• Nausea and vomiting. Pale nasolabial triangle with hyperemia of face, neck and
trunk
• Oral mucosa are bright red with hemorrhages
• Meningeal syndrome
• Then ptechia in axillary fossa, above clavicles.
• Nasal, intestinal and pulmonary bleeding
• Tachycardia initially, then bradycardia. Hypotonia. Dull cardiac sounds
• The course of the illness can be split into five phases:

Febrile phase:
• Symptoms include redness of cheeks and nose, fever, chills, sweaty palms, diarrhea,
malaise, headaches, nausea, abdominal and back pain, respiratory problems such as
the ones common in the influenza virus, as well as gastro-intestinal problems. These
symptoms normally occur for three to seven days and arise about two to three weeks
after exposure.[4] Hypotensive phase:
• This occurs when the blood platelet levels drop and symptoms can lead to
tachycardia and hypoxemia. This phase can last for 2 days.
Oliguric phase:
• This phase lasts for three to seven days and is characterised by the onset of renal
failure and proteinuria. Diuretic phase :
• This is characterized by diuresis of three to six litres per day, which can last for a
couple of days up to weeks. Convalescent phase :
• This is normally when recovery occurs and symptoms begin to improve. This
syndrome can also be fatal. In some cases, it has been known to cause permanent
renal failure.
81.Clinic of yellow fever.

• Yellow fever is a potentially life threatening viral illness that is found in tropical
areas of Africa and South and Central America.
• It is transmitted by the bite of an infected mosquito.
▪ Incubation period 3-6 days
• Symptoms are divided into the acute phase and the toxic phase.
▪ The acute phase presents with non specific symptoms of a viral infection such as
sudden high fever, headache, muscle ache, nausea and vomiting and loss of appetite.
Pain in head, back, lower back, bones.
▪ Hyperemia and edema of face, neck and eye injected by blood
▪ Mucosa, pharynx or tongue is bright red colour, photophobia, tachycardia
• Around 15% progress from the acute phase to the toxic phase which usually begins
on 3rd day
▪ On 3rd day: jaundice, hemorrhagic rash on skin, hepatosplenomegaly
▪ 5th day: pale face with cyanotic tint, delirium. Nausea and vomiting. Dark brown
or black emesis. Ptechia and ecchymoses on trunk and extremities. Nasal and gum
bleeding • followed by death in 50% of cases within 10-14 days.
82.The main symptoms of cutaneous leishmaniasis.
o Leishmaniasis is a disease caused by the Leishmania parasite. This parasite

typically lives in infected sand flies and is transmitted by the bite of infected sand
fly • Cutaneous leishmaniasis includes the following features:
• Localized cutaneous leishmaniasis: Crusted papules or ulcers on exposed skin;
lesions may be associated with sporotrichotic spread
• Diffuse (disseminated) cutaneous leishmaniasis: Multiple, widespread
nontender, nonulcerating cutaneous papules and nodules; analogous to lepromatous
leprosy lesions ▪ CL is characterized by skin lesions (open or closed sores), which
typically develop within several weeks or months after exposure. They typically
progress from small papules to nodular plaques, and often lead to open sores with a
raised border and central crater (ulcer), which can be covered with scales or crust.
The lesions usually are painless but can be painful, particularly if open sores become
infected with bacteria.
▪ Satellite lesions, regional lymphadenopathy, and nodular lymphangitis can be
noted. The sores usually heal eventually, even without treatment. However, they can
last for months or years and typically result in scarring ▪ Treatment: fluconazole and
amphotericin B
• Other consequences, which can become manifest anywhere from a few months
to years after infection, include fever, damage to the spleen and liver, and anemia
83. The main symptoms of visceral leishmaniasis.

▪ Visceral leishmaniasis – the most serious form and potentially fatal if untreated.
Also known as kala-azar
• Symptoms often don’t appear for months after the bite with this type of
leishmaniasis. Most cases are apparent two to six months after the infection
occurred. The incubation period typically ranges from weeks to months.
Common signs and symptoms include:
• weight loss
• weakness
• fever that lasts for weeks or months
• enlarged spleen
• enlarged spleen
• enlarged liver
• decreased production of blood cells
• bleeding
• other infections
• swollen lymph nodes
▪ Treatment: Amphotericin B, Meglumine antimoniate
84.The epidemiology of anthrax.

Epidemiology: Anthrax is an infection caused by gram positive rod shaped bacteria
called bacillus anthracis which is transmitted by contact with the bacterium’s spores
from affected sick animals
-All ages and gender are affected
-it occurs worldwide
-it’s is mainly found in endemic areas such as Africa and Asia
-anthrax spores can be infectious for decades and survive for extended periods
-it mainly affects livestock and wild game
-humans are infected through direct or indirect contact with sick animals
-It’s natural reservoir is considered to be the soil
It’s occurs in four forms: cutaneous/skin form, inhalation/ pulmonary form, intestinal
form, injection form
•Etiology: Bacillus anthracis
• Source of infection: infected animals which ingested or inhaled anthrax spores
while grazing
• Mode of transmission: fecal-oral or contact
-contact with infected tissues of dead animals which can lead to cutaneous
anthrax -consumption of contaminated undercooked meat which can lead to
gastrointestinal or oropharangeal anthrax
-contact with contaminated hair, wool, or hides which can lead to either inhalational
or cutaneous anthrax
85.The clinic of anthrax cutaneous form.

Anthrax is an infection caused by gram positive rod shaped bacteria called bacillus
anthracis which is transmitted by contact with the bacterium’s spores from affected
sick animals
• Incubation 1-7 days

• A pruritic papule that enlarges 24-48hours to form ulcer surrounded by a satellite
bulbous/ lesion edematous halo
-lesions located on the head or neck
-Presence of systemic symptoms(fever, malaise, headache, tachycardia,
tachypnea, hypotension, hyper/hypothermia) -presence of extensive edema
-multiple extensive or bulbous lesions
• Lesion is 2-3cm n diameter and has a round, regular raised edge. Painless
• Regional lymphadenopathy
• 7-10 days: ulcer evolve into black eschar for 7-14 days them evolve leaving a
permanent scar.
86.The clinic of anthrax pulmonary form.

sick animals
• Incubation: 1-3 days
• flu like symptoms which may last for a few hours to days such as Low grade fever,
nonproductive cough, sore throat, fatigue, muscle aches
-mild chest discomfort
-Nausea
-trouble breathing
• Hemorrhagic mediastinitis(condition which causes fluid to accumulate in the chest
cavity/ mediastinum) which will cause high fever, severe shortness of
breath,tachypnea, cyanosis, profuse diaphoresis, hematemesis ,and chest pain
-painful swallowing
-shock
87.Laboratory diagnosis of anthrax.

sick animals
• Staining ulcer exudates with giemsa stain or methylene blue for microscopic
investigation
• Ulcer, blood or CSF culture on sheep blood or peptone agar
• Serological: ELISA
-tissue biopsy to check for cutaneous anthrax
-Chest x-ray or CT scan
88.The treatment of anthrax.

sick animals
• Bed rest with no dietry restrictions Antibiotics such as:
• Penicillin G. Dose- 4 million units IV qid
• Amoxicillin. Dose 500mg PO tid
• Ampicillin. Dose 2g IV every 4 hours
-Ciprofloxacin, levofloxacin, Chloramphenicol
-Monoclonal antibodies such as Raxibacumab
89.Epidemiology of plague.
Plague is a disease caused by Yersinia pestis usually found in small mammals and
their fleas
Source of infection: zoonosis (rodent and fleas)
Epidemiology: it occurs in various countries such as Africa, Asia , south America and
the USA
-it is gram negative , non motile, non spore forming bacillus
- it is resistant to freezing temperatures
-human plague occurs from bite of an infected flea
-outbreaks are cyclical corresponding to rodent reservoirs and arthropod vector
correspondents
-Vectors are rodents, carnivorous mammals(cats,foxes,dogs), patient with pneumonic
plague
Mechanism of transmission: droplet contact, physical contact, sexual contact,

touching soil, airborne/aerogenic , fecal-oral
90.The clinic of skin and bubonic plague.

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

Pneumonic plague is a disease caused by Yersinia pestis usually found in small
mammals and their fleas
The symptoms include:

• Chilly sensations. Headache, loss of appetite, tachycardia and fever
• Painless Cough and dyspnea appear within 24 hours after onset
• Expectoration is clear at first and then becomes blood tinge. Sputum then becomes
thinner and bright red contains enormous number of plague bacilli
• Conjunctiva injected and tongue coated with white or brownish layer
• Anxious facial expression with dusky hue
• Dyspnea can become severe leading to cyanosis
92.The clinic of plague intestinal form.

their fleas
The symptoms are:

• Mucous membrane of mouth and throat are hyperemic with occasional hemorrhagic
patches
• Tonsils may be swollen and hyperemic.
-A bubo may form in the tonsils and cause edema of glottis.
• Vomiting preceded by nausea containing blood.
• Constipation is common but Bleeding in intestine causes blood to appear in
stool.
93.Laboratory diagnosis of plague.

their fleas
• Bacteriological examination of material collected from bubo by syringe and

inoculated into infusion broth or blood agar or mcconkey agar, some can be
examined by smear • Blood taken from patients vein inoculated into guinea pig
subcutaneously.
• Sputum exam by direct microscopy.
-staining- gram and Watson’s or gemsa
-dfa testing
-Serological- fourfold rising in antibody titter (F1 Ag), single tiger of >1:128
94.Treatment of plague.
their fleas
• Hospitalization and quarantine

• Antibiotics immediately streptomycin 1g IM tid. Tetracyclines, Monomycin,
Ampicillin
• Prophylactic plague vaccine for anyone who came in contact with patients -oxygen,
iv fluids and respiratory support is usually needed
95.The clinical forms of tularemia.

Tularemia is a rare infectious disease caused by Francisella tularensis.Also known as
rabbit fever or deer fly fever, it typically attacks the skin, eyes, lymph nodes and
lungs. The disease mainly affects rabbits, hares, and rodents, such as muskrats and
squirrels.
The clinics forms are

• Bubonic form
• Ulcer-bubonic form
• Eye-bubonic form
• Anginous-bubonic form
• Abdominal form
• Pulmonic form
96.The epidemiology of tularemia.

squirrels.
Epidemiology: Francisella tularensis, a small gram negative cocco-bacillus and the

causative agent of tularemia, exists as two major subspecies called biovars. F.
tularensis biovar tularensis (type A) is a virulent strain responsible for most infections
in North America. F. tularensis palaearctica (type B) causes milder disease and is
prevalent in Europe and Asia.
- The disease occurs naturally in the south- central and western states of the U.S. and
northern and central Europe.
• Source of infection (rodents and blood sucking insects)
• Mechanism of transmission: Contact, insects bite from affected Arthropoda, Rarely
fecal oral and air droplets • Incubation period 2-7 days
97.The clinic of tularemia bubonic form.

squirrels.
• Prodromal period: shivering, fever, headache, malaise, muscle ache, dizziness,

anorexia. Sleep disturbance with night sweating. Vomiting, nose bleeds, loss of
consciousness and delirium. Conjunctivitis
• Period of high point of disease: Primary buboes (inflammatory changes in lymph
node) in region near site of inoculation of disease. Secondary buboes occurs due to
hematogenous spread of disease. Buboes can be as big as nut or egg. They are
dense, painful with no periadenitis. Buboes can become completely dissolved,
suppurated, ulcerated and eventually scarred.
• Convalescence: softening e.g. Bubo after 2-3 weeks. First hyperemia of skin then
buboes break and drain, the pus is thick, white and no smell.
clinical signs of tularemia eye-bubonic form.

• If pathogen penetrated the eye mucous
membrane
• Expressed conjunctivitis. Eyelids are swollen, dense with tenderness of moving.
There is moderate mucopurulent discharge from eye
• On eyelid mucous membrane, there are small foci in the form of the cone
• Sometimes the presence of papules and ulcers of regional lymph nodes (buboes)
such as parotid, anterior cervical and submaxillary on the side of affected eye.
• Inflammatory small foci with a bunch of superficial widened vessels on conjunctiva
• Rarely, lachrymal sac phlegmon
98.Laboratory diagnosis of tularemia.

squirrels.
• Direct bacterioscopy of blood or bulbo aspiration material

• Agglutination test, Compliment binding reaction, hemagglutination test
• Subcutaneous allergic reaction with allergen tularin 1ml test
-chest X-ray to check for signs of pneumonia
-Blood test (to check for antibodies in bacteria)
99.Treatment of tularemia.
squirrels.
• Bed rest, quarantine

• Antibiotics Streptomycin 0,5-2g per day IM for period of fever plus 2 days.
Tetracylcline, doxycycline, levomycetin, kanamycin, gentamycin
• Inactive vaccine
• Desintoxication therapy with glucose
• Vitamins
• Eye-bubonic form: 20-30% sulfacil-natrii solution
• Calcium gluconate, diphenylhydramine to decrease allergic manifestation
• Compress, ointment, bandages on area of buboes at stage of dissolving
100.Clinical forms of intestinal Yersiniosis.

Yersiniosis is an infection that affects the intestinal tract caused most often by eating
raw or undercooked pork contaminated with Yersinia enterocolitica bacteria.
• Scarlatinic form characterized by general intoxication symptoms: fine-dot rash,
fever • Arthralgic form
• Abdominal form: gastro intestinal, hepatic, pseudo appendicitis • Generalized form
with affection of different organs and systems
• Icteric form:
101.Clinical features of intestinal Yersiniosis.

Yersiniosis is an infection caused most often by eating raw or undercooked pork
contaminated with Yersinia enterocolitica bacteria.
• Pain in epigastric region of abdomen, umbilical or right iliac area, less often in right
hypochondrium and left iliac area
-fever
-nausea
-vomiting
-bloody diarrhea
• In the form of mesenteric lymphadenitis, terminal ileitis, acute appendicitis
• Enlarged, painful and grumbling cecum and mesenteric lymph nodes
.
102.Clinical features of pseudotuberculosis.
Yersinia pseudotuberculosis is a, gram-negative bacillus bacterium that causes Far
East scarlet-like fever in humans, who occasionally get infected zoonotically, most
often through the food-borne route.
Clinical features:
• catarrhal syndrome: Pharyngeal and tonsilar erythema without the exudates,
erythema of the soft palate, conjunctivitis, coryza • intoxication syndrome: fever,
headache
• Abdominal syndrome; tenderness during the palpation of abdomen, may be acute
appendicitis
• Dyspepsia: nausea, vomiting, liquid feces.
• Rashes: maculopapulous (like in scarlet fever), may be erythematosus or even
erythema nodosum may developed. rash appears on face and intensifies periorbitally
and neck
• Arthritis of knees , elbows, foot and hand small joints .
• Presence of “strawberry” tongue.
***Source of infection-wild and home animals (rats, dogs, foxes, cats and other);
• Way of transmitting – alimentary;
• Susceptible organism – children (not infants), adults.
103.Laboratory diagnosis of Yersiniosis.

Yersiniosis is an infection caused by the bacteria of the genus Yersinia
-phage typing of bacterial culture or antibodies for F-antigen

Agglutination test
• Complete blood analysis: leucocytosis, neutrophilosis with left shift, eosynophylia,
ERS is enlarged.
• Urinalysis: slight proteinuria, leucocituria, casts uin small amount in case of toxic
damage of kidneys.
• Bacteriological – Yersinia enterocolitica may be found in feces, urine, blood, pus,
lymph nodes and pharyngeal mucus.
• Coprogram: Increasing of red blood cells and leukocytes, mucus.
-Dfa testing
• Serological - increasing of special antibodies 4 times and more in 2- 4 wks in paired
sera (IHAR 1:200, AR 1:40 – 1:160). -Staining- gram , waysons, methylene blue
104. Principles of Yersiniosis treatment.

Diet number 5 for icteric form and number 4 for other forms
Etiological treatment
! in mild cases it’s not used;
! in moderate and severe cases – by chloramphenicol 10-20 mg/kg 4 times per
day orally during 6-9 days. If not effective – alternative
antibiotics: cefalosporins of the 3rd-4th generation 100-150 mg/kg,
aminoglycosides of the 3rd generation. 7-10 days
Pathogenetic treatment:
! detoxification therapy: oral to all patient and in case of mild dehydration, or
parenteral: Rheosorbilact, 0.9% NaCl, 5% glucose (moderate and severe
dehydration);
! Sorbents: enterosgel 0.5-1 g/kg, polysorb (Silix) 100-200 mg/kg per day in 3
doses for 5-7 days
! antihistamines: claritin, cetirizin, suprastin, pipolphen 1-3 mg/kg per day,
! corticosteroids 1-3 mg/kg with a short course (in severe cases, in case of
myocarditis),
! Normalisation of the intestinal flora: linex, bifi-form, acidophilus 1-2 caps 2-3
times per day not less than 2 wks;
! antipyretics: paracetamol 10 mg/kg not more than 5 times per day,
! NSAIDs in case of arthritis, carditis, nodular erythema (ibuprofen 20 mg/kg
per day, aspirin 50-75 mg/kg per day, voltaren 2-3 mg/kg per day,
indomethacin 2-3 mg/kg per day (in average doses).
SECTION 3
01. Epidemic process and its components.
Epidemiology is the study of frequency, distribution and determinants of health
related events.
Epidermic process -The continuous chain of successive transmission of infection
(patientcarrier), manifested by symptomatic or asymptomatic forms of disease.
Components
● Infectious agent
● transmission factors
● Susceptible individual ( without immunity)
02. The main motive forces of the epidemic process.

Source of infectious agent
● Mechanisms of infectious agent transfer
● Receptive organism
Secondary motive forces of epidemiological process:

● Social factors
● Environmental factors
03.Features of epidemic process at anthroponoses and zoonoses. The concept

of sapronoses.
Anthroponoses- when the source of infection is Human (Sick person or carrier )
Zoonoses- source of infection is Animal
Sapronosis - It’s transmitted from the environment to human ( soil , water , decayed
plants)
04.Anti Epidemic measures in the places of infectious diseases outbreaks.

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

The reservoir of an infectious agent is the habitat in which the agent normally lives,
grows, and multiplies. Reservoirs include humans, animals, and the environment.
Human reservoirs - Diseases that are transmitted from person to person without
intermediaries include the sexually transmitted diseases, measles, mumps,
streptococcal infection, and many respiratory pathogens.
Animal reservoirs - Many of these diseases are transmitted from animal to animal,
with humans as incidental hosts. infectious disease that is transmissible under natural
conditions from vertebrate animals to humans. Long recognized zoonotic diseases
include brucellosis (cows and pigs), anthrax (sheep), plague (rodents),
trichinellosis/trichinosis (swine), tularemia (rabbits), and rabies (bats, raccoons, dogs,
and other mammals). HIV/AIDS, Ebola infection and SARS.
Environmental reservoirs - Plants, soil, and water in the environment are also
reservoirs for some infectious agents. Many fungal agents, such as those that cause
histoplasmosis, live and multiply in the soil. Outbreaks of Legionnaires disease are
often traced to water supplies in cooling towers and evaporative condensers,
reservoirs for the causative organism Legionella pneumophila.
06. Sick person and the carrier and their epidemiological value.
Sick person is the primary source from which the infection spreads and is the most
dangerous source of infection because he or she releases a great quantity of the
pathogenic microorganisms.
A carrier is a person with infection who is capable of transmitting the pathogen to
others Carriers release pathogenic agents into the environment in a smaller quantity
than patients with clinically manifest diseases, but they are danger to community too
since they actively associate with healthy people and spread the infection.
Carriers commonly transmit disease because they do not realize they are infected, and
consequently take no special precautions to prevent transmission. Symptomatic
persons who are aware of their illness, on the other hand, may be less likely to
transmit infection because they are either too sick to be out and about, take
precautions to reduce transmission, or receive treatment that limits the disease.
****Categories of infectious diseases carriers.

Asymptomatic or passive or healthy carriers are those who never experience
symptoms despite being infected.
Incubatory carriers are those who can transmit the agent during the incubation
period before clinical illness begins.
Convalescent carriers are those who have recovered from their illness but remain
capable of transmitting to others.
Chronic carriers are those who continue to harbor a pathogen such as hepatitis B
virus or Salmonella Typhi, the causative agent of typhoid fever, for months or even
years after their initial infection.
07.Epidemiological value of animals (rodents, bats etc.)

Rodents, animals that are almost everywhere, can be reservoirs of important zoonotic
diseases such as leptospirosis, leishmaniasis, relapsing fever, tularemia, plague, Q
fever, salmonellosis, and hantavirus. These diseases can be transmitted to humans by
touch or bite of the animal, direct contact with their feces, urine and saliva, bite of
their vectors (ticks, mosquitoes, fleas, …), ingestion of food or waters contaminated
with their feces or urine, inhalation of dried feces of infected rodents or during
dissection and autopsy of these animals. With early diagnosis and prompt treatment,
most of these diseases are not a serious threat to human. This reflects the importance
of having enough knowledge about theses diseases, especially by those who deal with
them directly. Since the vaccine has not been approved for the prevention of most of
these diseases, educating of people especially those at most risk of infection, limiting
the contact with rodents, use of personal protective equipment (boots, gloves, masks,
etc.), washing the hands with soap and water regularly following close contact with
rodents and avoiding the insect bites is necessary in the prevention of these diseases.
08.Definition of meaning- Mechanism of trans mission – its chains , factors and
ways of infectious disease transmissions
Mechanism of transmission: It is a process that begins when an infectious agent or
pathogen leaves its reservoir, source, or host through a portal of exit and is conveyed
by some mode of transmission, enters the host through an appropriate portal of entry,
and infects a susceptible host.
OR
Mechanism of transmission: The combination of routes by which the pathogenic
microorganisms are transmitted from an infected macroorganism to a healthy one
Four mechanisms of infection transmission are distinguished according to the
primary localization of pathogenic agents in macroorganisms
• Faecal-oral (intestinal localization);
• Air-bome (airways localization);
• Transmissive (localization in the blood circulating system);
• Contact (transmission of infection through direct contact with another person
or environmental objects)
Main factors are involved in transmission of infection: air, water, foods, soil, utensils,
arthropods (living agents).
Three phases are distinguished in the transmission of infection from one
macroorganism to another:
● 1st phase: excretion of the causative agent from the infected macroorganism
● 2nd phase: staining of the causative agent in environment
● 3rd phase: infectious agent’s penetration into healthy (susceptible) organism.
- direct contact, droplet, indirect transmission, vectors,
09. Types of infectious diseases mechanisms of transmission.
Direct contact occurs through skin-to-skin contact, kissing, and sexual intercourse.
Direct contact also refers to contact with soil or vegetation harboring infectious
organisms. Thus, infectious mononucleosis (“kissing disease”) and gonorrhea are
spread from person to person by direct contact. Hookworm is spread by direct contact
with contaminated soil. spread refers to spray with relatively large, short-range
aerosols produced by sneezing, coughing, or even talking.
Droplet spread is classified as direct because transmission is by direct spray over a
few feet, before the droplets fall to the ground. Pertussis and meningococcal infection
are examples of diseases transmitted from an infectious patient to a susceptible host
by droplet spread.
Indirect transmission refers to the transfer of an infectious agent from a reservoir to
a host by suspended air particles, inanimate objects (vehicles), or animate
intermediaries (vectors).
Vectors such as mosquitoes, fleas, and ticks may carry an infectious agent through
purely mechanical means or may support growth or changes in the agent. Examples
of mechanical transmission are flies carrying Shigella on their appendages and fleas
carrying Yersinia pestis, the causative agent of plague, in their gut.
10.Types and methods of disinsection

Disinsection” means the procedure whereby health measures are taken to control or
kill the insect vectors of human diseases present in baggage, cargo, containers,
conveyances, goods and postal parcels.
Methods
There are four types of disinsection methods that can be used:

• Residual- is carried out while no passengers are onboard. The entire aircraft is
sprayed with a residual insecticide and lasts eight weeks
• Pre-embarkation- is carried out while no passengers are on board. Crew may
be on board as this method is completed up to 40 minutes prior to passengers
boarding the aircraft. The treatment lasts for the duration of the single flight
• Pre-flight and top of descent- refers to a two-part process consisting of pre-
flight and top of descent spraying. Pre-flight spraying is followed by a further
in-flight spray of a non-residual insecticide, carried out at top of descent as the
aircraft starts its descent into either Australia or New Zealand. The treatment
lasts for the duration of the single flight
• On-arrival- is an in-flight spray of a non- residual insecticide, carried out once
the aircraft lands in Australia or New Zealand. The treatment lasts for that one
arrival.
11.Defination of disinfection, its types and methods.
Disinfection is the process of using a disinfectant to destroy, inactivate, or
significantly reduce the concentration of pathogenic agents (such as bacteria, viruses,
and fungi) Both viruses are susceptible to disinfection by a weak solution of chlorine
bleach
Types of disinfectant
● Low-level disinfectants- kill most vegetative bacteria and some fungi as well as
enveloped (lipid) viruses example is hepatitis b, c, hantavirus hiv. They do not kill
myocobacteria or bacterial spores but typically used to clewan environmental
surface
● Intermediate-level disinfectants- the kill vegetative bacteria most viruses and fungi
but not resistant bacterial spores
● High-level disinfectants process destroy vegetative bacteria, myocobacteria, fungi
and enveloped and non enveloped virus but not necessarily bacterial spores
METHODS
Chemical and Physical Method
● Chemical
- Alcohol
- Chlorine and chlorine compounds
- Formaldehyde
- Glutaraldehyde
- Hydrogen peroxide
-Iodophors
- Halogen
- Peracetic acid
- Peracetic acid and hydrogen peroxide
Physical method
● Boiling at 100°C for 15 minutes, which kills vegetative bacteria.
● Pasteurizing at 63°C for 30 minutes or 72°C for 15 seconds, which kills food
pathogens. ● Using nonionizing radiation such as ultraviolet (UV) light. UV rays
are long wavelength and low energy.
12. Sterilization and its stages, control of quality.
Sterilization refers to any process that removes, kills, or deactivates all forms of life
(in particular referring to microorganisms such as fungi, bacteria, spores, unicellular
eukaryotic organisms such as Plasmodium, etc.) and other biological agents.
Stages:
Pre-Vacuum, Rising Temperature, Sterilizing and Vacuum-Drying
Methods
Heating in an autoclave (steam sterilization)
Exposure of microorganisms to saturated steam under pressure in an autoclave
achieves their destruction by the irreversible denaturation of enzymes and structural
proteins. The recommendations for sterilization in an autoclave are 15 minutes at
121-124 °C.
Filtration - Sterilization by filtration is employed mainly for thermolabile solutions.
These may be sterilized by passage through sterile bacteria-retaining filters, e.g.
membrane filters.
Exposure to ionizing radiation
Sterilization of certain active ingredients, drug products, and medical devices in their
final container or package may be achieved by exposure to ionizing radiation in the
form of gamma radiation from a suitable radioisotopic source such as 60Co (cobalt
60) or of electrons energized by a suitable electron accelerator.
Aqueous solutions in glass containers usually reach thermal equilibrium within 10
minutes for volumes up to 100 mL and 20 minutes for volumes up to 1000 mL.
Dry-heat sterilization
In dry-heat processes, the primary lethal process is considered to be oxidation of cell
constituents. Dry-heat sterilization requires a higher temperature than moist heat and
a longer exposure time. Preparations to be sterilized by dry heat are filled in units that
are either sealed or temporarily closed for sterilization. The entire content of each
container is maintained in the oven for the time . Temperature 160 , 170 , 180 degrees
for 180mins , 60mins and 30mims respectively..
Gas sterilization (with ethylene oxide)
The active agent of the gas sterilization process can be ethylene oxide or another
highly volatile substance. The highly flammable and potentially explosive nature of
such agents is a disadvantage unless they are mixed with suitable inert gases to
reduce their highly toxic properties and the possibility of toxic residues remaining in
treated materials.
13. Schedules of immunization.
Depend on: Need , Efficacy , Safety , Ease of administration.

Vaccination should be performed according to a predetermined plan, or for special
epidemiologic indications. Planned vaccination is performed against tuberculosis,
diphtheria, tetanus, pertussis, poliomyelitis, measles, epidemic parotitis, and against
some other infections within the confinement of separate districts or population
groups, regardless of the presence or absence of a given disease. Vaccination for
special epidemiologic indications are performed in the presence of direct danger of
spreading of a particular infection. Vaccination reports must be compiled and
special entries made in histories.
Preparations can be given parenterally (percutaneously, intracutaneously,

subcutaneously, intramuscularly, intravenously) or enterally (per os), intranasally or
by inhalation (aerosols).
When giving vaccines parenterally, it is necessary to observe sterile conditions and to

adhere to the rules specified for injection of a particular vaccine. Jet inject are widely
used now: the preparations are administered into the skin, subcutaneously and
intramuscularly using various syringes.
When given in the liquid state or in tablets, the vaccine should be taken together with
water.
Contra -indications to Vaccination

•Acute fevers and recently sustained infections
•Avoid giving live vaccines to pregnant women in the first Trimester of pregnancy.
•chronic diseases such as tuberculosis, heart diseases, severe diseases of the kidneys.
•allergic disease and states such as (bronchial asthma , hypersensitivity reaction)
•In spite of Immune suppression in HIV infected, we can still give Measles, mumps,
rubella vaccines and Oral polio drops ( But Salk killed vaccine is safe). • In HIV
patients do not give BCG vaccine Ideal vaccine.
•Promotes effective immunity.
•Controls lifelong protection.
•Safe, do not carry side effects.
•Stable, cheap,
•Acceptance by public.
Postvaccination complications. They are divided into the following groups:

● (1) complications developing secondary to
vaccination; ● (2) complications due to aseptic
conditions of vaccination; ● (3) exacerbation of a pre-
existing disease.
14. Epidemiological classification of infectious diseases.

It is based on the location of infection in the macroorganism. In accordance with the
main sign that determines the transmission mechanism, all infectious diseases are
divided by the author into 4 groups: (1) intestinal infections;
(2) respiratory infections;
(3) blood infections;
(4) skin infections.
Intestinal infections – are transferred by fecal-oral mechanism. As a microbe is

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

includes diseases whose causative agents parasitize on the respiratory mucosa and are
liberated into the environment with droplets of sputum during sneezing, cough, loud
talks, or noisy respiration.
• People get infected when the microbes contained in sputum get on the mucosa
of the upper airways.
• Transmission can be minimised by control of overcrowding, proper ventilation
and isolation of enclosures, using UV-lamps, wearing masks, respirators,
disinfection.
Blood infections –by means of transmissive mechanism of transfer.

• The diseases of this group are transmitted by blood-sucking insects, such as
fleas, mosquitoes, ticks, etc., which bite people and introduce the pathogenic
agent into the blood.
• Control of blood infections includes altering natural conditions, improvement
of soils, draining swamps, destroying sites where the insects multiply,
disinsection measures against mosquitoes, ticks, etc., detoxication of sources of
infection by their isolation and treatment, carrying out preventive measures.
Infections of external covers (skin infections –by means of contact or contact-

wound mechanism.
The diseases of this group occur as a result of contamination of the skin or mucosa
with the pathogenic microorganisms. They can remain at the portal of infection
(tetanus, dermatomycoses), or affect the skin, enter the body and be carried to various
organs and tissues with the circulating blood (erysipelas, anthrax). Pathogenic
microorganisms causing venereal diseases, rabies, AIDS.
• The main measures to control skin infections include isolation and treatment of
the source of infection, killing diseased animals, homeless dogs and cats,
improving sanitation and living conditions of population, personal hygiene,
control of traumatism, and specific prophylaxis
15.Epidemiological features of intestinal infections.
Source of infection: at typhoid fever, shigellosis , paratyphoid A, some food

poisonings – ill person or bacteriocarrier; at parathyphi B, Salmonella botulism -
more often animals.
Bacteria carrying: acute, chronic, transient.
Mechanism of transmission – fecal-oral.
Ways of transmission – by the water, foods (at botulism – caned meat, mushrooms,
as a rule homemade), household things, dirty arms; flies.
Epidemics – contacts, water, food borne.
Seasonality – summer-autumn.
subtypes
● Subtype 1 - typical intestinal infection ( agent stays in the GIT) shigellosis,
cholera, echerichiosis.
● Subtype 2 - Toxic infection ( intensive reproduction of the agent out of the
organism ) food poisoning , botulism and staphylococcal toxicosis
● Subtype 3 - intestinal infection with spreading of the agent beyond the
intestine ( amebiasis , ascaridiasis, echinococcosis)
● Subtype 4 - intestinal infection with penetration of the agent into blood with
additional outlet of the agent in the environment with the urine, secretions
( typhoid fever, brucellosis, leptospirosis)
16.Epidemiological features of respiratory infections.
This group includes diseases whose causative agents parasitize on the respiratory
mucosa and are liberated into the environment with droplets of sputum during
sneezing, cough, loud talks, or noisy respiration. People get infected when the
microbes contained in sputum get on the mucosa of the upper airways. If the
causative agent is unstable in the environment, a person can only be infected by lose
contact with the sick or carrier. Pathogenic microorganisms causing some diseases
can persist for a period of time in an enclosure where the sick is present. Infected
particles of sputum or mucus can dry and be suspended in the air. Some diseases of
this group can spread through contaminated linen, underwear, utensils, toys, etc. It is
important to timely reveal the sick and carriers, and also to break the mechanism of
infection transmission: control of overcrowding, proper ventilation and isolation of
enclosures, using UV-lamps, wearing masks, respirators, disinfection, and the like.
17.Epidemiological features of blood infections.
Source of infection - sick person , carier

Mechanism of transmission - transmissible
Vector - insects , fleas , mosquitoes , tick
Seasonality - warm season
Susceptibility - high
The diseases of this group are transmitted by blood-sucking insects, such as fleas,
mosquitoes, ticks, etc., which bite people and introduce the pathogenic agent into the
blood. Control of blood infections includes altering natural conditions, improvement
of soils, draining swamps, destroying sites where the insects multiply, disinsection
measures against mosquitoes, ticks, etc., detoxication of sources of infection by their
isolation and treatment, carrying out preventive measures. If the source of infection
are rodents, measures to control them are taken. Active immunization is also
effective.
18.Epidemiological features of infections of external coverings.
The diseases of this group occur as a result of contamination of the skin or mucosa
with the pathogenic microorganisms. They can remain at the portal of infection
(tetanus, dermatomycoses), or affect the skin, enter the body and be carried to various
organs and tissues with the circulating blood (erysipelas, anthrax).
The transmitting factors can include bed linen, clothes, plates and dishes and other
utensils, that can be contaminated with mucus, pus or scales. Pathogenic
microorganisms causing venereal diseases, rabies, AIDS, and some other diseases are
transmitted without the agency of the environmental objects.
Wound infections are characterized by damage to the skin as a result of injury

(tetanus, erysipelas). The main measures to control skin infections include isolation
and treatment of the source of infection, killing diseased animals, homeless dogs and
cats, improving sanitation and living conditions of population, personal hygiene,
control of traumatism, and specific prophylaxis.
19.Epidemiology and prevention of HIV.

HIV (human immunodeficiency virus) is a virus that attacks cells that help the body
fight infection, making a person more vulnerable to other infections and diseases.
Epidemiology: Youths tend to have the highest HIV diagnosis rates.

In southern Africa, Bostwana, Lesotho, India, Mozambique and Nigeria have the
highest cases
In 2016, people age 13 to 24 accounted for 21 percent of the people diagnosed with
HIV. About 80 percent of the diagnoses in this age group (or 6,776 cases) occurred in
people between 20 and 24 years old.
As of 2018, approximately 37.9 million people are infected with HIV globally.[3]
There were about 770,000 deaths from AIDS in 2018
Source
• By having sex. You may become infected if you have vaginal, anal or oral sex
with an infected partner whose blood, semen or vaginal secretions enter your
body. ...
• By sharing needles. ...
• From blood transfusions. ...
• During pregnancy or delivery or through breast-feeding.
Ways of transmission occurs mainly through blood, semen, vaginal fluids, and breast
milk.
Mеchanism of transmission – contact
PREVENTION OF HIV
You can use strategies such as
• Abstinence (not having sex)
• Use condoms
• Avoid multiple sex partners/ Limit your sex partners
• Get tested. Be sure you and your partner are tested for HIV and other STIs
• Never reuse or "share" needles, syringes, water, or drug preparation equipment.
Only use needles and syringes that you got from a reliable source (such as
drugstores or needle exchange programs).
• You may also be able to take advantage of HIV prevention medicines such as
preexposure prophylaxis (PrEP) and post-exposure prophylaxis (PEP).
• Don't douche. Douching removes some of the normal bacteria in the vagina
that protects you from infection. This may increase your risk of getting HIV
and other STIs.
• Be monogamous. Having sex with just one partner can lower your risk for HIV
and other STIs.
20. The sanitary protection of the territory from delivery and spreading of
infections that may have international importance.
(1) mass-scale measures aimed at improvement of public health, prevention and

spread of infectious diseases;
(2) medical measures aimed at reduction of infectious morbidity and eradication of

some diseases;
(3) health education and involvement of population in prevention or restriction of the

spread of infectious diseases;
(4) prevention of import of infectious diseases from other countries.
Preventive measures aimed to control infectious diseases taken by medical

personnel are divided into: preventive and anti-epidemic
Preventive measures: are carried out regardless of the presence or absence of

infectious diseases at a given time and locality. These measures are aimed at
prevention of infectious diseases.
Anti-epidemic measures – measures must be put in place to control or terminate the
source of infection, transmission mechanism, and susceptibility of population.
Exclusion of any of these factors terminates the spread of an epidemic process.

Prophylactic and antiepidemic measures are therefore aimed at control of the source
of infection, disruption of the route by which infection spreads, and strengthening of
non-susceptibility of population. Control of infection source, The infectious patients
must also be isolated in proper time.
21.Typhoid fever. Epidemiological features (source of agent, factors of

transmission, signs of epidemic process), preventive and anti-epidemic measures.
Source of infection:– ill person or bacteriocarrier

Bacteria carrying: Salmonella Typhi
Infectiveness: last days of incubation period, all period of the disease
Mechanism of transmission – fecal-oral.
Ways of transmission – by the water, foodstuffs, household things, dirty

arms; flies. Epidemics – contacts, water, food borne. Susceptibility (index of
contagiousness) – 0,4
Seasonality – summer-autumn.
Incubation period – from 7 till 25 days .
CLINICAL SIGNS OF THE TYPHOID FEVER
1-st week:
The beginning is gradual
Complains: headache, tiredness, sleeplessness, anorexia, constipation or
diarrhea Long fever 39-40 °С (intermittent fevers)
Paleness of skin
«typhoid» tongue
Duguet's angina
Bradycardia, dicrotism of pulse,
hypotonia Symptoms of bronchitis
meteorism, positive Padalka's symptom
2nd week:
Typhoid rash – typhoid maculopapular rash(roseola elevata), some elements,
localized on the anterior abdominal wall and lateral walls («vest»), new elements can
appear , sometimes is present longer than fever.
Hepato-splenomegalia.
Status typhosus.
Serologic reactions.
Antiepidemic measures:
Examination on typhoid fever and paratyphoids all patients with fever, which last
more than
5 days (once on hemoculture, and if fever continue more than 10 days
Vidal’s reaction of hemaglutination or RIHA)
Examination of all persons, who are working at the industries dealing with food, for
detection of bacteriocarriers
Obligatory hospitalization infectious hospital of patients and carriers into infectious

hospital
Observation of contact persons during 25 days and their separation from other people
Every day thermometry, interrogation and medical examination
One analyze of feces on coproculture and blood antibodies on Vi-antibodies
Convalescents are discharged from hospital only after clinical recovery and three-
time analysis of feces and urine with 5-days interval, and bile in 10 days after
disappearing of clinical signs, if results are negative
Three-month observation and 2-years registration in sanitary-epidemic
department with several times bacterial examination Current and final
disinfection.
22.Hepatitis A. Epidemiological features (source of agent, factors of

Hepatitis A (formerly known as infectious hepatitis) is an acute infectious disease of

the liver caused by the hepatitis A virus (HAV), which is most commonly
transmitted by the fecal-oral route via contaminated food or drinking water.
the incubation period), is between two and six weeks and the average incubation
period is 28 days. The illness is usually contracted in early childhood.
Hepatitis A infection causes no clinical signs and symptoms. It does not have a
chronic stage, is not progressive, and does not cause permanent liver damage.
Following infection, the immune system makes antibodies against HAV that confer.
Prevention: Hepatitis A vaccine , also Hepatitis A can be prevented by vaccination,
good hygiene and sanitation.
23.Shigellosis. Epidemiological features (source of agent, factors of transmission,

signs of epidemic process), preventive and anti-epidemic measures.
Infective agent : Sh. Dysenteriae, Sh. Flexneri, Sh. Boydii, Sh. Sonnei
Source of infection — patients, persons in period of convalescence and

bacteriocarries. The patients with acute shigellosis are especially dangerous.
Mechanism – fecal-oral route of transmission
Ways of transmission – water (more often Sh. flexneri), food staffs (Sh. sonnei),
dishes, dirty hands, flies.
Seasonal - summer-autumn.
Immunity - type-specific
Laboratory diagnostic of Shigellosis
Etiologic diagnostic:
Detection of the agent from the feces, vomiting mass, lavage fluid
Serologic reactions (presence of antibodies to the causative agent and increasing the
titer in dynamic)
Polymerase chain reaction (PCR) – detection of shigella DNA in feces and scraping
of the rectum mucous.
Antiepidemic measures
Medical supervision after contact persons (7 days)
Bacteriological investigation of stool (decree group only)
Serological investigation
Disinfection – current, final
24. Cholera. Epidemiological features (source of agent, factors of transmission,

Infective agents – vibrio cholera (classic, El-Tor)

Source of the infection – sick, convalescents, vibriocarrier (1:100)
Mechanism of transmission – fecal-oral
Seasonal prevalence – summer-autumn
Susceptibility - high
Epidemic and pandemic spreading
Types of epidemics – water (more often); alimentary; home-contact.
Prophylaxis of Cholera
Antiepidemic measures at exposure of ill person or carrier

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

Infectious agent - corynebacterium diphtheria

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

Salmonellae are widely dispersed in nature, being found in the in the gastrointestinal
tracts of domesticated and wild mammals, reptiles, birds, and insects. May present
clinically as gastroenteritis, enteric fever, a bacteremic syndrome, or focal disease.
An asymptomatic carrier state may also occur.
Source infection - sick people and carriers

Mechanism of transmission - faecal oral
Factors of transmission - food-stuffs of animal origin and other products
which are polluted by excretions of animals and humans. Incubation period -
from 4-6 hours up to some days.
Clinical manifestations
1) Localized (gastrointestinal) forms of Salmonellosis: a) Gastritic
variant; b) Gastroenteritic variant;
c) Gastroenterocolitic variant.
2) Generalized forms:
a) Typhus-like form;
b) Septic form (septicopyemia).
3) Carrier state:
a) Acute carriers;
b) Chronic carriers;
c) Transitory carriers.
nausea and vomiting, myalgia and headache , diarrhoea with loose stool swamp like
with bad smell.
Prophylaxis
Veterinary-surveillance upon animals and production of meat and dairy industry,
laboratory control of food stuffs. It is necessary to reveal carriers on milk farms, in
foods, children’s and medical establishments. The maintenance of the rules of
personal hygiene and rules of food’s cooking plays an important role in prophylaxis
of Salmonellosis.
27. Botulism. Epidemiological features (source of agent, factors of transmission,

Causative agent - Clostridium botulinum (saprozoonosis)
Types A, B, C, D, E, F, G, Types А, В and E most commonly cause disease in man.
Types С and D are associated with animal botulism, especially in cattle, ducks and
chickens. Botulism is an acute neurologic disorder that causes potentially life-
threatening neuroparalysis due to a neurotoxin.
Resevior - grass feeding animals,
Ways of transmission -
1) botulism food poisoning results from eating food that contains preformed
toxin; 2) wound botulism occurs when toxin is produced by C. botulinum
organisms contaminating traumatic wounds;
3) infant botulism is due to toxin production by C. botulinum within the
gastrointestinal tract of infants.
Incubation period - 2 to 12hours till 10days (6-24hours)
Signs
Dysphagia , diplopia, dysphonia, dry tongue , horizontal nystagmus, blepharoptosis.
Prophylaxis
The observance of the sanitary and hygienic rules at processing, transportion, keeping
and preparing of the food-stuffs experts possibility of accumulation of botulotoxin. It
is necessary to perform the strict control under sterilization and keeping preserved
food-stuffs. Cook meats, mushrooms and vegetables properly .
28. Meningococcal infection, purulent bacterial meningitis. Epidemiological

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

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

Etiology – Hepatitis B virus

Incubation period- 45 days or more
Mechanism of transmission - contact (wound)
Ways of transmission - parenteral, sexual, through placenta from sick mother to

fetus (vertical or transplacentar).
Factors - blood, sperm, vaginal secret, milk of mother

Susceptibility to the disease is high.
Risk group - drug addicts, homosexualists, prostitutes, medical personal
Source of infection- sick person with acute or chronic form, healthy carrier.
Asymptomatic form: the specific markers of infectious agent and proper

immunological changes are exposed only
Sub-clinical form: immunologic, biochemical and histological changes, however
main clinical signs of illness are absent
Non-jaundice form: different clinical symptoms of illness are present except
jaundice
Jaundice form: jaundice, which is the main sign of hepatitis present
Fulminant (malignant) form: extremely
Symptoms
Jaundice, fever, fatigue, loss of appetite with nausea and vomiting, joint pain and
abdominal pain.
Prophylaxis
Use of disposable medical instruments, thorough sterilisation of non-expendable
instruments.
Clinical and laboratory examination of blood and organ donors.
Specific prophylaxis - vaccination against B hepatitis HB-Vax, Ingerix-B
30 .HIV-infection. Epidemiological features (source of agent, factors of

Source – sick and carrier (contagious during all life)
(Disease of «4 Н» - homosexuality, heroin (drug addicts), hemophilia, Haiti island)
Mеchanism of transmission – contact (wound), vertical
Ways of transmission : anal sex, vaginal sex, sharing needles,
Natural: sexual (homosexualists – females, males)
Vertical (transplacentar, childbirth, during breast feeding)

Artificial: parenteral manipulations and drug using, blood recipients
,transplantation of organs and tissues, artificial ingravidation. professional:
infection of medical personal, Intrahospital outbreaks
HIV High Risk Groups

● Homo- and bisexuals
● Intravenous drugs addicts
● Recipients of blood, blood preparations and organs
● Prostitutes and other persons who conduct the disorderly sexual life ● Patients with
venereal diseases and viral hepatitis B, C, D ● Children infected by HIV mothers.
Symptoms
Prolonged fever, prolonged diarrhoea, generalized lymphadenopathy, weight
loss( >10%), opportunistic infections, kaposi sarcoma
Diagnostic Criteria: epidemiological data , clinical signs and laboratory data ( IFA,
immunobloting)
Prophylaxis of HIV/AIDS in blood transfusions:

● Selection and investigation of donors (obligatory 6-months quarantine of all plasma
donors)
Medical personal prophylaxis In case of medical accident:

● Pretreatment of dirty skin with 70 % ethyl alkohol, washing by water with soap,
mucous membranes – with clean water
● To register of case in special journal
● Investigation of suffer person concerning of HIV antibodies presence (in first 5
days, then – after 1, 3 and 6 months)
● Post contact prophylaxis (scheme № 2) during 72 hours (better 24-36) after
accident ● In case of positive reaction – conclusion of special commission about
the professional contamination.
● Treatment of HIV from 28 weeks of pregnancy

● Cesarean section in 38 weeks term ● Treatment of mother and newborn ●
Prohibition of breast feeding.
31. Malaria. Epidemiological features (source of agent, factors of transmission,

Etiology - plasmodium
Types of plasmodium
Pl. malariae
Pl. falciparum
Pl. ovale
Pl. vivax
Pl. knowlesi
Source – sick person, carrier
Mechanism – transmissible after the bites of female mosquito Anopheles
Seasonal –- summer-autumn, in tropics – whole year
Susceptibility – high
Immunity – non persistent, homologous
Incubation period- 3days/10-14days
Symptoms
Attack of fever - (chills-hot-sweat), Hepatosplenomegaly, hémolytique
anemia(jaundice ), tachycardia, hypotonia , myalgia , diarrhoea, vomiting, loss of
appetite, cyanosis, herpes.
Prophylaxis
● Sanitarian patrolling of the state from delivery (quarantine infection
contamination) ● Mandatory registration
● Sterilization of toolkit
● At detection of sick or carrier – parasitoscopy examination of all family members
● Ant mosquito measures (melioration, usage of insecticides, repellents)
● Drug prophilaxis - primachinum 0,027gm/day for 14days
32. Plague. Epidemiological features (source of agent, factors of transmission,

Possible ways of transmission- transmissive, contact, alimentary and droplet

Causative agent - yersinia pestes (flea)
Clinical forms
Skin Bubonic , Primary pulmonary, secondary pulmonary, intestinal , primary septic,
secondary septic.
Complications
Infectious toxic shock , meningitis, adeno phlegmon
Symptoms
Fever
Severe intoxication
Severe hemorrhagic inflammation of lymphatic nodes , lungs and other organs
through Sepsis .
Anti-epidemic measures:
• prevention the import of infection from abroad;
• making of natural cells of plague healthy;
• urgent prophylaxis in the case of exposure of patient with a plague.
immunization of people :
● Vaccinations of population of certain territories;
● Urgent 6-daily prophylaxis by streptomycine tetracycline on suspicion of possible
infection.
33. Hemorrhagic Fevers Ebola and Marburg. Epidemiological features (source

of agent, factors of transmission, signs of epidemic process), preventive and anti-
epidemic measures.
Incubation period: Ebola (7-14days) , Marburg (4-9days)
Etiology – filoviridae
Source - mice/rat (which are excreting the virus with urine, stool and saliva)
Mechanism of transmission: - transmissive way(contact with blood n body fluids)
The contamination of the person descends by air - dust, nutritional and contact
pathes (routes). The transplacental transmission of a virus from the pregnant woman
is possible.
Symptoms
Fever (39-40degrees)
Decreased visual equity( mist before eyes)
Sharp headache
Back ache and pain in muscles of extremities
Photophobia
Nausea and vomiting
Paleness nasolabial triangle, hyperemia of a face, necks, upper half of trunk.
The palpebral fissures are narrowed down, scleratis.
A mucosa of an oral cavity and pharynx are bright red with
haemorrhages. The Kerning’s signs, Brudzinsky sign can be
determined and stiff neck. Fever 7-9 days is prolonged.
Delirium
On 3-5th day of illness on a neck, lateral areas of a thoracic cell, in axillaries fossas,
above clavicles occurs petechial eruption.
Then there are nasal, intestinal, pulmonary bleedings.
Cardiac sounds are dull; the initial tachycardia is replaced by a bradycardia,
hypotonia. Dryness of tongue, abdominal pain without definite localization, patients
enlarged a liver and spleen and the icterus are possible.
Prophylaxis
Inactivated cultural, cerebral vaccines and recombinant of a vaccine
Carry out a disinfestation in the natural locuses, puttings, and also collect of tongs
with animal and poultries. For a disinfestation will use gexachloran.
Medical observation in the focus for 10 days and Conduct mandatory final
disinfection with 3 % Chloraminum solution and chlorofos. For contact persons or
one who was bitten by tongs in endemial districts enter a specific immunoglobulin
i.m. in doses 5-7.5 ml for adult, 2.5-3.5 ml - for children.
Primary antiepidemic measures after detection of sick with contagious hemorrhagic

fevers Lassa, Ebola and Marburg, and also yellow fever same, as well as at other
quarantine infection contaminations. Patient will hospitalize in hermetic isolation
ward with independent life support, monitor behind absence of an air inflow from a
zone of isolation ward, paste vent holes. . The staff should work in a protective
clothing, including a mask or respiratory supplied with a special inhaler. Conduct
careful current and final disinfection. The specific prophylaxis contagious
hemorrhagic fever. The quarantine for arriving from epidemic areas lasts 17 day. In
endemial districts of yellow fever vaccination of the population by an alive “Dakar”
vaccine or 17-D is carried out. The immunodefence is saved 10 years, and then make
a revaccination.
34.Lyme borreliosis. Epidemiological features (source of agent, factors of

Lyme disease is spread by the bite of the Ixodes scapularis (dammini)

tick. Tick needs at least 24 hours of attachment before transmission can take
place.
Borrelia burgdorferi organism. The tick is small, and the bite is often not
remembered. Incubation period:- 3 to 30days

Symptoms
• Erythema migrans rash at the site of the bite (80% of patients)
–– An erythematous patch, which may enlarge in the first few days, may have partial
central clearing, giving it a “bull’s-eye” appearance, although this is not commonly
seen. –– The rash will resolve in several weeks, even without treatment.
• Flulike illness with fever, chills, and myalgias (50% of patients)
• Neurologic symptoms several weeks later (10–20% of patients)
–– Most common symptom is paralysis of the seventh cranial nerve (facial paralysis),
possibly be bilateral
–– Meningitis, encephalitis, headache, and memory disturbance may develop as well
• Cardiac symptoms (<10% of patients)
–– Most common symptom is AV heart block
–– Myocarditis, pericarditis, and various forms of arrhythmias may develop as well
• Joint involvement months to years later (up to 60% of patients)
–– Most commonly a migratory polyarthritis, although chronic monoarticular arthritis
(most commonly affecting the knee)
Diagnosis Criteria
Based on clinical signs especially (erythema migrans rash) and serological testing
(ELISA test and western blot).
Prophylaxis
Doxycycline (200 mg for adults or 4.4 mg/kg for children of any age weighing less
than 45 kg).
35.Enterobiasis, clinic and diagnostics.

Etiology: Enterobias vermicularis. Disease may also be called pinworm infection
Clinic: itching in anal areas more prominent at night which leads to restlessness and
difficulty in sleeping. At night, the female worm moves to anus and deposit its eggs
and dies.
Diagnosis: Eggs detected in cellulose tape preparations applied to patient’s perianal

region in the early morning prior to bathing or using toilet.
Treatment:
! Good hand hygiene and wash perianal areas well. Wash clothes and bed linen well.
! Can also give one dose of pyrantel pamoate one dose repeated in 2 weeks.
! Petroleum jelly is given to relieve itching
36. Whip-worm infection, clinic and diagnostics.

Etiology: Trichuris Trichiura worm has whip-like form of the body
Clinic: Usually asymptomatic. A heavy worm burden may result in mechanical

damage to the intestinal mucosa due to adult work threaded into epithelium of cecum.
This can lead to abdominal cramps, tenesmus, dysentery and prolapsed rectum.
Diagnosis: Microscopic stool exam shows barrel shaped ova
37.Ascariasis, clinic and diagnostics.
Etiology: Ascaris Lumbricoides worm
Clinical signs:
! patient may have signs of pneumonitis with cough and low grade fever during
the migration of larvae through the liver and lungs. Can be accompanied by
wheezing and eosinophilia
! In heavy worm burdens, adult worms migrate in intestine resulting in intestinal
blockage which lead to vomiting, abdominal pain
!
Diagnoses:
! adult worms may be expelled through anus, mouth or nose
! Eggs seen on microscopic stool exam
38.Complications of ascariasis.
Volvulus
Intussuception
Hepatic abscess
Acute cholangitis
Peritonitis
Biliary colic
Acute cholecystitis
Acute pancreatitis
Upper GI bleeding
39.Epidemiology and pathogenesis/ life cycle of ancylostomiasis.
Etiology: Anclystoma duodenale (hookworm)
Pathogenesis
! Ingestion of worms: adult worms live in small intestine, attached firmly
to the mucous membrane of the gut lining and feed on blood and tissue !
Adult females deposit their eggs in the gut and are passed out in feces !
They survive in light sandy loam soil feeding on bacteria.
! After one week, they become infective and move to position for suitable host to
pass
! They enter organism by ingestion
! Enter blood vessels and are carried to heart, lungs and trachea
40. Clinic and complications of ancylostomiasis

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

Strongyloides stercoralis is a human parasitic roundworm, commonly known as
threadworm, Inhabit small intestine mucosa (duodenum &jejunum) and Causing the
disease strongyloidiasis.
Is transmitted by soil and can cause severe disease in immunocompromised
individuals.
Clinical pictures
-Initial skin penetration causes little reaction, repeated infections lead to
hypersensitive reactions. This leads to Larva currens: rapidly progressing urticarial
attack.
• Migration of larva to the lungs may stimulate an immune response resulting in
cough, wheezing and fever
• Ulceration of intestines, can lead to malabsorption, GI bleeding and eosinophilia
• Hyperinfection syndrome: parasite and host reach an equilibrium where neither host
nor parasite suffers adverse reactions. It leads to the infection proliferation with
immense numbers of larvae migrating to every tissue in the body especially the
lungs (pneumonitis), brain damage and respiratory failure
-Skin phase: Dermatitis; An itchy, red rash that occurs where the larva entered the
skin, creeping eruption may also occur.
-Respiratory phase: Löffler's syndrome (pneumonitis + Asma)
-Abdominal phase: Infection may be asymptomatic(light infection) • Symptoms
resemble gastric ulcer; (stomachache, bloating, and heartburn, hunger pain • Chronic
intermittent diarrhea may be with yellow mucus. Constipation, Nausea and loss of
appetite
Complication ;
-Gastric ulcer resulting from damaged mucosa by the worms
-Intestinal obstruction occur In severe cases, edema may result in obstruction of the
intestinal tract, as well as loss of peristaltic contractions.
-Immunosuppression
-Disseminated strongyloidosis- tissue damage
-Pneumonitis, brain damage
-Respiratory failure
42.Diagnostics of strongyloidosis
Strongyloides stercoralis is a human parasitic roundworm, commonly known as

threadworm, Inhabit small intestine mucosa (duodenum &jejunum) and Causing the
disease strongyloidiasis.
Faecal smear, with microscopy

Multiple stool sample test to detect larvae
sputum or duodenal aspirates by enterotest or string test
-ELISA to detect antibodies
Baermann’s Technique- involving fecal suspicion in water causing larvae
migration to settle in water.
43. Clinical features and complications of trichinellosis
Trichinellosis is a parasite disease caused by a roundworm of the genus Trichinella.
Etiology- trichinella spiralis. History of eating pork or sausage.
Clinical features These

symptoms include eye
puffiness, splinter
hemorrhage,
nonspecific
gastroenteritis,
Fever,
Muscle soreness and pain,
Gastrointestinal symptoms,
Facial edema, eosinophilia, and subconjuctival, subungual, and retinal hemorrhages."
Complications
myocarditis
pneumonia
meningoencephalitis
hepatitis
nephritis
systemic
vasculitis
thrombophlebitis
thrombocytopeni
a
44. Diagnostics of trichinellosis

Trichinellosis is a parasite disease caused by a roundworm of the genus Trichinella.
Etiology- trichinella spiralis. History of eating pork or sausage.
-CBC- leukocytosis, eosinophils ( low counts indicates an increased mortality rate),
-Blood test( microscopy) ;
-antibody detection Using ELISA test
-Muscle biopsy; reveals larvae within striated muscles
-Lactate dehydrogenase; Levels of lactate dehydrogenase isoenzymatic forms (ie,
lactate dehydrogenase fraction 4 [LD4] and lactate dehydrogenase fraction 5 [LD5])
are elevated in 50% of patients
-Immunoglobulin E; immunoglobulin E levels are typically elevated
Antibody detection ( serological test)
PCR- isolating and subsequent genetic typing
Hypertensive skin test - positive
45. Etiology and epidemiology of lymphatic filariasis?
Lymphatic filariasis commonly known as elephantiasis, is a neglected tropical
disease.
EPIDEMIOLOGY
● Infection occurs when filarial parasites are transmitted to humans through
mosquitoes.
● Lymphatic filariasis is transmitted by different types of mosquitoes for example
by the Culex mosquito, Anopheles, and Aedes,
● Lymphatic filariasis is spread from person to person by mosquitoes.
● humans are definitive hosts.
• It is endemic in many tropical & subtropical countries like Africa, Asia,
Western Pacific and parts of America.
The painful and profoundly disfiguring visible manifestations of the disease,

lymphedema, elephantiasis and scrotal swelling occur later in life and can lead to
permanent disability.
46. The clinical picture and complications of lymphatic filariasis
Lymphatic filariasis is a human disease caused by parasitic worms known as
filarial worms.
Clinical picture
• Fever
• Inguinal or axillary lymphadenopathy
• Testicular and/or inguinal pain
• Skin exfoliation
• Limb or genital swelling
• dry and paroxysmal nocturnal cough;
• wheezing
• Dyspnea
Complications
• chronic lymphedema,
• hydrocele,
• skin pigmentation,
• renal impairment (eg chyluria. )
47. Etiological therapy of nematodosis
Nematode(round worm) infections need to be identified and treated accordingly.
Antihelminthic:
- Albendazole
- Mebendazole
- Pirantel,
- Vermox,
Preventive measures are as follows:

Good hygiene and sanitation
Avoidance of sources of infection (eg, arthropod bites, rivers/streams, contaminated
soils, consumption of raw or undercooked fish, snails, and slugs) Public health
activities such as vector control.
48. Epidemiology and life cycle of beef tapeworm infection

Beef tapeworm infection( Taenia saginata) Taenia saginata commonly known as
beef tapeworm; unarmed tapeworm of man
It is an intestinal parasite of human and cattle.

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

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

-Microscopy. Proglottids or eggs can diagnosed in feces
-ELISA AND PCR
-When cysts presents in brain CT scan(computed tomography) are used o X-ray
may used
- Serologic tests
* Prevention
Make sure you cook meat thoroughly
Freezing to 5 degrees for 4days
* Treatment praziquantel , Niclosamide, Albendazole, mebendazole
51. Epidemiology and life cycle of pork tape worm infection

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

Taeniasis is the infection of humans with the adult tapeworm of Taenia solium.
Humans are the only definitive host.
Clinical picture
Most people with tapeworm infections have no symptoms or mild symptoms.
-They can cause digestive problems including abdominal pain, loss of appetite,
weight loss, and upset stomach.
-The most visible symptom of taeniasis is the active passing of proglottids
(tapeworm segments) through the anus and in the feces.
- Neurocysticerosis may include Headache.
Lethargy.
Confusion.
Vision changes
Weakness or numbness
Complications
Tapeworm can be lodged in appendix (Appendicitis), bile
duct (cholecystitis), pancreatic duct (pancreatitis)
53. The clinical picture and complications of cysticerocosis

Cysticercosis refers to tissue infection after exposure to eggs of Taenia solium,
the pork tape worm.
The disease is spread via the oral route through contaminated food and water, and
is primarily a food born disease.
Clinical picture
Cysts, called cysticerci, can develop in the muscles, the eyes, the brain, and the spinal
cord -Cyst in the brain or spinal cord causes neurocysticercosis.
- seizures and headaches
- confusion
- difficult with balance
- brain swelling and excess fluid around the brain. - stroke
- Cyst in the muscles can cause lumps under the skin ( which can be tender).
-Myositis with fever and eosinophilia and muscular pseudohypertrophy. This can
later progress to atrophy and fibrosis
-Eyes: Cysticerci may be found in eyeball, extraocular muscles and subconjunctica.

May cause retinal edema, hemorrhage, decreased vision or visual loss.
Complications
brain edema,
hydrocephalus
chronic meningitis
vasculitis paralysis
partial blindness
seizures, coma, and
death.
54. Diagnostics of pork tapeworm infection and cysticercosis.
Pork tape worm infection (taeniasis) is an intestinal infection with adult tapeworms
that follows ingestion of contaminated pork.
Diagnosis
Microscopic examination of stool for ova and proglottids
CT and/or MRI and serologic testing for patients with central nervous system
symptoms.
Cysticercosis
Cysticercosis is a parasitic tissue infection caused by larval cysts of the tapeworm
Taenia solium. Diagnosis
Biopsy of infected tissue, microscopic examination
ELISA: Antibodies to cyticerci
CT or MRI of head
CSF exam: pleocytosis, elevated protein levels and depressed glucose levels
55. Epidemiology and life cycle of echinococcosis
Echinococcosis is a parasitic disease that occurs in two main forms in humans:
cystic echinococcosis (also known as hydatidosis) and alveolar echinococcosis,
caused by the tapeworms Echinococcus granulosus and Echinococcus multilocularis,
respectively.
Epidemiology
• Cystic echinococcosis is globally distributed in most pastoral and rangeland
areas of the world, with highly endemic areas in the eastern part of the
Mediterranean region, northern Africa, southern and eastern Europe, at the
southern tip of South America, in Central Asia, Siberia and western China.
Humans are infected through ingestion of parasite eggs in contaminated food,
water or soil, or after direct contact with animal hosts( dogs)
Life cycle
-The adult Echinococcus granulosus resides in the bowel of its definite host.
-Gravid proglottids release eggs that are passed in the feces.
-These eggs are then ingested by a suitable intermediate host, including sheep,
goat, swine, cattle, horses and camels. The eggs then hatch in the bowels and
release oncospheres that penetrate the intestinal wall.
These oncospheres then migrate through the circulatory system to various organs of
the host.
-At the organ site, the oncosphere develops into a hydatid cyst. This cyst enlarges
gradually, producing protoscolices and daughter cysts that fill the cyst interior.
-These cyst-containing organs are then ingested by the definite host, causing
infection. After ingestion, the protoscolices evaginate, producing protoscolexes.
-The scolexes of the organisms attach to the intestine of the definite host and develop
into adults in 32-80 days.
The life cycle then continues in humans:
(Humans can become infected if they ingest substances infected with Echinococcus
eggs. -The eggs then release oncospheres in the small intestine.)
56. The clinical picture and complications of echinococcosis

Echinococcosis is a parasitic disease of tapeworms of the Echinococcus type, from
contamination of food by feces from infected dogs (Echinococcusspecies)
Clinical picture
Human infection with E. granulosus leads to the development of one or more
hydatid cysts located most often in the liver and lungs
-Abdominal pain, nausea and vomiting are commonly seen when hydatids occur in
the liver. - If the lung is affected, clinical signs include chronic cough, chest pain and
shortness of breath.
-Other signs depend on the location of the hydatid cysts and the pressure exerted on
the surrounding tissues. Non-specific signs include anorexia, weight loss and
weakness.
Complications: anaphylactic reaction, shock. Hepatomegaly, respiratory disease or

pulmonary eosinophilia, coin lesion in lungs, ectopic calcification
57. Diagnostics of echinococcosis

Echinococcosis is a parasitic disease of tapeworms of the Echinococcus type, from
the contamination of food by feces from infected dogs (Echinococcusspecies)
- Ultrasonography, computed tomography ( ct scan) and magnetic resonance

imaging ( MRI scan)
- serological test ( Specific antibodies are detected ) and can support the
diagnosis of early detection of E. granulosus and E. multilocularis infections,
especially in low-resource settings.
-Biopsies of cyst to differentiate it from tumour.
58. Epidemiology and life cycle of diphyllobothriasis

A fish tapeworm(diphyllobothriasis) infection can occur when a person eats raw or
undercooked fish that’s contaminated with the parasite Diphyllobothrium latum. The
parasite is more commonly known as the fish tapeworm.
This type of tapeworm grows in hosts such as small organisms in the water and large
mammals that eat raw fish. It’s passed through the feces of animals. A person
becomes infected after ingesting improperly prepared freshwater fish that contain
tapeworm cysts.
● Source of infection: zoonosis: fish

Epidemiology
This type of tapeworm parasite is most common in areas where people eat raw
or undercooked fish from lakes and rivers. Such areas include:
-Russia and other parts of Eastern Europe
-North and South America
-some Asian countries, including Japan
It may also be common in parts of Africa where freshwater fish are eaten.
Life cycle
Immature eggs are passed in feces.
The eggs mature (approximately 18 to 20 days) and yield oncospheres which
develop into a coracidia
After ingestion by a suitable freshwater the coracidia develop into procercoid
larvae...
Following ingestion of the copepod by a suitable second intermediate host,
The procercoid larvae are released from the crustacean and migrate into the fish flesh
where they develop into a plerocercoid larvae (sparganum)
The plerocercoid larvae are the infective stage for humans. Because humans do
not generally eat undercooked minnows and similar small freshwater fish, these do
not represent an important source of infection. Nevertheless, these small second
intermediate hosts can be eaten by larger predator species, e.g., trout, perch, walleyed
pike
In this case, the sparganum can migrate to the musculature of the larger predator fish
and humans can acquire the disease by eating these later intermediate infected host
fish raw or undercooked
After ingestion of the infected fish, the plerocercoid develop into immature adults
and then into mature adult tapeworms which will reside in the small intestine. The
adults of D. latum attach to the intestinal mucosa by means of the two bilateral groves
(bothria) of their scolex Eggs appear in the feces 5 to 6 weeks after infection.
59. The clinical picture and complications of diphyllobothriasis

A fish tapeworm( diphyllobothriasis) infection can occur when a person eats raw or
undercooked fish that’s contaminated with the parasite Diphyllobothrium latum.
Clinical picture
Fish tapeworm infections rarely present noticeable symptoms. Tapeworms are most
often discovered when people notice eggs or segments of the tapeworm in stool.
Symptoms may include (diarrhea,fatigue,stomach cramps and pain, chronic

hunger or lack of appetite, unintended weight loss and weakness)
Complications
-anemia, specifically pernicious anemia caused by vitamin B-12 deficiency
-intestinal blockage
-gallbladder disease
60 Diagnostics of diphyllobothriasis.
Diphyllobothriasis is a Zoonotic infection caused by the Cestode

Diphyllobothrium latum which is an intestinal tapeworm, Way of
transmission – Fecal – oral ingestion of raw, poorly cooked or pickled fresh
water fish containing larvae called plerocercoids
Diagnosis Microscopic exam of eggs or proglottids in stool
You will see characteristic eggs from formol ether concentrate of feces.
(The egg is usually ovoid and has a small knob at the opercular end and is yellowish-
brown in colour with a smooth shell, of moderate thickness. They measure 58 –
75mm by 40 – 50mm in size.)
Proglottids may also be seen in fecal samples usually in a chain of segments from a
few centimeters to about 0.5 meters in length.
CBC – can reveal eosinophilia, anemia if there is B12 deficiency

Peripheral smear – macrocytosis
Treatment: Praziquantel or Niclosamide
Symptoms- maybe absent or minimal with eosinophilia ,there can be occasional

intestinal obstruction, diarrhoea, and abdominal pain, vitamin B12 deficiency
(megaloblastic anemia)
61.Epidemiology and pathogenesis of opisthorchiasis.

Opisthorchiasis is defined as infection with Opisthorchis viverrini (Southeast Asian
liver fluke) or O. felineus (cat liver fluke)
Clinical presentation:
a) Most infections are asymptomatic.
b) Mild infections may cause dyspepsia, abdominal pain, diarrhoea or constipation.
c)Longer-term infections may cause more severe symptoms and may lead to
hepatomegaly and malnutrition.
Epidemiology:
• acquired by eating infected raw or undercooked fish (fecal-oral)
• Opisthorchis felineus is an intestinal parasite of cats, dogs, foxes, pigs, cetaceans

(such as whales and dolphins) in Eastern Europe, Siberia and other parts of Asia.
• Opisthorchis viverrini is found in domesticated and wild dogs and cats in

Southeast Asia.
• It is a very common human infection in North East Thailand.
Pathogenesis:
● Eggs are ingested by snail and undergo development (sporocyst to rediae to
cercariae). ● Cerciae are released from snails and penetrate fresh water fish
encysting as metacercariae in muscles or under scales
● Humans become infected after eating raw or undercooked fish
● Metacercariae excyst in the duodenum and ascend through the ampulla of vater
and into the biliary ducts where they attach to the mucosa and mature. Adult flukes
grow up to: 5 to 10 mm (O. viverrini) 7 to 12mm (O. felineus).
62. The clinical picture and complications of opisthorchiasis.
Definition: Opisthorchiasis is a parasitic disease caused by species in the genus

Opisthorchis (specifically, Opisthorchis viverrini and Opisthorchis felineus). Chronic
infection may lead to cholangiocarcinoma, a malignant cancer of the bile ducts.
Usually asymptomatic
● Eosinophillia,
● Diarrhea, epigastric and right upper quadrant pain, lack of appetite
● Fatigue, mild fever, weakness
● Jaundice
Complications
● Edema of legs and ascites
● Cholangitis, periductal fibrosis, cholecystitis, cholelithiasis
● Hepatitis and/or fibrosis of periportal system
● Cholangicarcinoma
63.Diagnostics of opisthorchiasis.
Opisthorchiasis is a parasitic disease caused by species in the genus Opisthorchis
(Opisthorchis viverrini and Opisthorchis felineus) acquired by eating infected raw or
undercooked fish.
The medical diagnosis is established by finding eggs of Opisthorchis in feces using

the Kato technique.
• Microscopic examination of stool; Detects the eggs in feces
• Ultrasonography, CT , MRI , cholangiography may show biliary tract abnormalities.
• ELISA Test to detect antigen 89 kDa seen in Opisthorchis viverrini
(The Kato technique is a laboratory method for preparing human stool samples prior
to searching for parasite eggs.)
Treatment: Praziquantel, Albendazole, Mebendazole

64. Etiological treatment of cestodosis (tapeworms) and trematodosis (flukes).
Tapeworm infections are all acquired by ingesting worm cysts or eggs. The most
common infections result from undercooked fish (Diphyllobothrium latum), beef
(Taenia saginata), and pork (Taenia solium). Other tapeworms can be spread person-
to-person (Hymenolepsis nana) or with contamination of food by feces from infected
dogs (Echinococcusspecies). Mature worms reside in the gut, releasing large numbers
of eggs, but usually causing little disease.
Most common syndrome of Tenia solium it causes is cysticercosis ( infection with
parasite cysts, most often in the brain, following ingestion of food contaminated with
parasite eggs from pig feces.)
Trematodiases, also known as trematode infections, are a group of diseases caused by
the parasite trematodes. Symptoms can range from mild to severe depending on the
species, number and location of trematodes in the infected organism.
Mostly causes flukes
Etiological Treatment
● Praziquantel : 75mg/kg.day orally three doses per day for 2 days
● Albendazole 10mg/kg/day for 7 days
• Mebendazole
• Triclabendazole

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01. The peculiarities of infectious diseases.

Infectious diseases are diseases caused by microbes such as (viruses,bacteria,fungi

SOURCES OF INFECTIOUS AGENTS

03. Principles of infectious diseases diagnosis.

04. Methods of infectious diseases specific diagnostics.

05. Principles of infectious diseases treatment.

06. Principles of infectious diseases prevention.

Control infection source:

• Timely revealing of sick persons. Active detection is performed by medical

08.STAGES OF TYPHOID FEVER PATHOGENESIS

The initial manifestations are nonspecific and consist of fever, malaise,

• Neuropsychiatries manifestations, including confusion, dizziness,

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

In paratyphoid A incubation period is shorter than in typhoid fever. It's duration is 8-

16. Differential diagnosis of typhoid fever and influenza.

Clinical (Usually presents with Usually presents as upper

Physical Maculopapular rash, high temperature,

17. Specific complications of typhoid fever.

18.Pathogenesis, clinical manifestations of small intestine perforation at

19.Pathogenesis, clinical manifestations of intestinal bleeding at typhoid, time of

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

21. The principles of typhoid fever treatment.

22. Etiology and epidemiology of salmonellosis.

23. Etiology and epidemiology of food poisonings.

24. Clinical signs of salmonellosis localized forms.

25. Clinical signs of salmonellosis generalized forms.

26. Clinical manifestation of food toxicoinfection.

Caused by Clostridium perfringens:

Caused by Staphylococcus species:

27. The differential diagnosis of salmonellosis and shigellosis.

SOURCES OF Usually associated with Most significant sources

29. Methods of salmonellosis specific diagnostics.

30. The peculiarities of food toxicoinfection specific diagnostics.

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

32. Treatment of salmonellosis and food toxicoinfection patients.

33. Etiology and epidemiology of cholera.

34. Clinical manifestations of different dehydration degrees at cholera.

Clinical Manifestations According to the degree of

In moderate course (Second degree of dehydration):

In Severe course (Third degree of dehydration):

2. Classification of Pocrovsky - patients can be divided into four groups by

According to Clinical forms:

According to the Degree of Severity:

36. Laboratory diagnosis of cholera.

37. Differential diagnosis of cholera and salmonellosis.

MODE/FACTORS OF Majorly associated with Majorly associated with

MODE/FACTORS OF Majorly associated with Most significant sources

40. Rehydration therapy at cholera.

• Give oral rehydration solution (ORS) immediately to dehydrated patients who

41.Etiology and epidemiology of enteroviral infection.

42.Clinical forms of enteroviral diseases.

Nonspecific febrile illness

Infection With Poliovirus

Skeletal Muscle Infection

Generalized Disease of Newborn-

43.The main symptoms of enteroviral diseases.

Nonspecific febrile illness

Infection With Poliovirus

Skeletal Muscle Infection

Generalized Disease of Newborn-

44.Laboratory diagnosis of enteroviral infections.

! Virological investigation of nasopharyngeal smears, feces, Cerebrospinal fluid

45.Principles of enteroviral diseases therapy.