FINAL ANSWERS

Department of Infectious Diseases and Epidemiology

Course: 6

1. Classifications of infection disease. ............................................................................... 3

2. Slow infection. Special features of anamnesis, periods of disease, main clinical sings,
diagnostics tests, principles of therapy. ................................................................................ 6
3. Semiotics of infectious disease. Kinds of fever according to durations & elevation
level, types of temperature curves, kinds of eruption, characteristics of eruption types. ...... 9
4. Principles of infection diseases diagnostics. Collection of castу and epidemiological
histories, clinical examination, pathognomonic symptoms, bacteriological tests, serological
and immunological methods................................................................................................ 10
5. Principles of infectious disease treatment. Antibacterial therapy, chemotherapy,
serotherapy, principles of pathogenetic therapy. ................................................................. 12
6. Infectious process, its forms. ........................................................................................ 14
7. Factors of infectious process, its forms, carriage of infection, periods of infectious
disease.................................................................................................................................. 14
8. Toxic shock as complications of meningococcal infectiouns. Diagnostics, treatment.16
9. Hypovolemic shock as complications of cholera. ........................................................ 17
10. Meningococcal infection, meningococcemia. Pathogenesis, clinical forms, special
clinical features, diagnostics, treatment. .............................................................................. 19
11. Influenza. Etiopathogenesis, clinical sings, diagnostics, treatment, complications. .... 24
12. Parainfluenza infection. Etiopathogenesis, clinical sings, diagnostics, treatment,
complications. ...................................................................................................................... 27
13.Adenoviral infection Epidemiology, pathogenesis, clinical features, diagnostics, treatment. 29
14. Diphtheria of fauces. Forms, variants of the disease, clinical features, complications,
diagnostics, specific therapy. ............................................................................................... 31
15. Enteric yersiniosis. Epidemiological features, clinical forms, main clinical sings,
diagnostic tests, principles of therapy................................................................................. 35
16. Botulism. Epidemiological features, pathogenesis, clinical sings, diagnostics, specific
therapy. ................................................................................................................................ 38
17. Cholera. Stages of dehydration, маin clinical sings, diagnostics methods, etiotropic
therapy, treatment of dehydration. ....................................................................................... 42
18. Typhoid fever. Forms of disease, маin clinical sings, characteristics of feverish
reaction & status thyfosus, diagnostics tests, treatment, complications. ............................. 45
19. Hepatitis A. Clinico-biocchemical syndromes, stages of the disease, clinical sings,
laboratory findings, principles of therapy............................................................................ 50
20. Hepatitis B. Epidemiology, pathogenesis, clinical manifestations, markers of disease,
biochemical tests, treatment. ............................................................................................... 53
21. Hepatitis C. Epidemiological features, pathogenesis, clinical manifestations,
laboratory data, markers of disease, principles of therapy. ............................................. 58
22. Hepatitis E. Routes of transmission, characteristics of prodromal period, main clinical
sings, laboratory findings, markers of disease, treatment................................................... 61
23. Hepatitis D. Epidemiology, pathogenesis, clinical manifestations, markers of disease,
biochemical tests, treatment. ............................................................................................... 63
24. Shigellosis. Epidemiology, pathogenesis, clinical manifestations, diagnostics
methods, principles of therapy............................................................................................ 65
25. Salmonellosis. Epidemiological features, pathogenesis, clinical sings, diagnostics,
treatment. ............................................................................................................................. 67
26. Food poisoning. Epidemiological features, stages of pathogenesis, clinical forms, main
clinical sings, diagnostics tests, treatment. .......................................................................... 71
27. Typhus fever. Epidemiology, stages of pathogenesis, main clinical sings, diagnostics,
therapy. ................................................................................................................................ 73
28. Brill disease. Epidemiological data, pathogenesis, clinical sings, diagnostic tests,
therapy. ................................................................................................................................ 75
29. Anthrax. Etiology, epidemiology, clinical forms, diagnostics, treatment. ................... 76
30. Erysipelas. Epidemiology, clinical manifestation, treatment, prevention measures. ... 79
31. Rabies. Special features of anamnesis, periods of disease, main clinical sings,
diagnostics tests, prinсiples of therapy. ............................................................................... 81
32. Infectious mononucleosis. Epidemiology, etiopathogenesis, clinical manifestation,
diagnostic tests, therapy. ...................................................................................................... 83
33. Plague. Epidemiological situation, pathogenesis, clinical forms, diagnostics, therapy.85
34. Tularemia. Epidemiological situation, pathogenesis, clinical forms, diagnostics,
therapy ................................................................................................................................. 88
35. Staphylococcus infections. Epidemiology, pathogenesis, clinical forms, diagnostics,
treatment .............................................................................................................................. 91
36. Lyme Borreliosis. Epidemiology, pathogenesis, clinical forms, diagnostics, treatment94
37. Hemorrhagic fever with disrenal syndrome Epidemiology, pathogenesis, clinical
forms, diagnostics, treatment. .............................................................................................. 96
38. Malaria. Epidemiology, pathogenesis, clinical forms, diagnostics, treatment. ............ 99
39. Herpes virus infections. Epidemiology, pathogenesis, clinical forms, diagnostics,
treatment ............................................................................................................................ 102
40. Psittacosis (ornitosis). Epidemiology, pathogenesis, clinical forms, diagnostics,
treatment ............................................................................................................................ 104
41. Amebic infection. Epidemiology, pathogenesis, clinical forms, diagnostics, treatment106
42. Leptospirosis. Epidemiology, etiopathogenesis, clinical manifestation, diagnostic test,
therapy ............................................................................................................................... 109
43. Toxoplasmosis. Epidemiology, pathogenesis, clinical forms, diagnostics, treatment.114
44. Brucellosis. Epidemiological features, pathogenesis, clinical sings, diagnostics,
specific therapy .................................................................................................................. 117
45. Differential diagnosis of salmonellosis from shigellosis. Agent of disease, leading
syndromes, clinical manifestation, diagnostics tests. ........................................................ 120
46. Differential diagnosis of shigellosis from cholera. Agent of disease, leading
syndromes, clinical manifestation, diagnostics tests. ........................................................ 122
47. Differential diagnosis of plague from tularemia. Epidemiological features, clinical
forms, main clinical sings, diagnostics tests. ..................................................................... 124
48. Differential diagnosis of brucellosis from typhoid fever. Anamnestic data,
characteristics of temperature curves, clinical sings, blood pictures, diagnostics tests..... 128
49. Differential diagnosis of Brill disease from typhus fever. Epidemiological features,
special clinical sings, complications, serological tests, immunological tests. ................... 131
50. Differential diagnosis of typhus fever from influenza. Species features of anamnesis,
syndromes, clinical mаnifestation, blood picture, specific diagnostics. ............................ 134
51. Differential diagnosis of cholera from food poisoning. Special feature of anamnesis,
main clinical syndromes, clinical sings, diagnostics tests. ................................................ 136
52. Differential diagnosis of meningococcal meningitis from tuberculosis meningitis.
Special feature of anamnesis, main clinical syndromes, clinical sings, CFS abnormality,
specific therapy. ................................................................................................................. 138
53. Differential diagnosis of viral hepatitis A from viral hepatitis B. Special feature of
anamnesis daft, characteristics of prodromal period, main clinical symptoms, markers of
disease................................................................................................................................ 139
54. Differential diagnosis of cholera from salmonellosis. Agents, epidemiological data,
clinical manifestation, lab data, diagnostic tests................................................................ 141
55. Differential diagnosis of anthrax from erysipelas. Agents, epidemiological data,
clinical forms, course variants, clinical manifestation, diagnostic criteria. ....................... 143
56. Differential diagnosis of typhoid fever from typhus fever. Species features of
anamnesis, syndromes, clinical mаnifestation, characteristics of typhus state and
temperature curve, clinical sings, blood picture, diagnostic tests. .................................... 145
57. Differential diagnosis of meningococcal meningitis from viral meningitis. Special
feature of anamnesis, main clinical syndromes, clinical sings, CFS abnormality, specific
therapy. .............................................................................................................................. 147
58. Differential diagnosis of botulism from food poisoning. Agents, epidemiological data,
clinical manifestation, lab data, diagnostic tests................................................................ 147
59. Differential diagnosis of jaundice. Special feature of anamnesis, main clinical
syndromes, clinical sings, specific therapy. ...................................................................... 147
60. Differential diagnoses of diseases with feverish syndrome. ...................................... 147
61. Taenia. Saginana taeniasis. Epidemiology, pathogenesis, diagnostics, treatment. .... 147
62. Taenia. Solium taeniasis and cysticercosis. Epidemiology, diagnostics, treatment. .. 147
63. Enterobiasis. . Epidemiology, pathogenesis, clinical sings, diagnostics, treatment. . 147
64. Ascariasis. Epidemiology, pathogenesis, clinical sings, diagnostics, treatment. ...... 147
65. Ecyinococcosis. Epidemiological features, clinical sings, diagnostics, specific therapy.150
66. Acute hepatic encephalopathy. Clinical manifestation, diagnostic criteria, thearapy.151
67. AIDS. Epidemiological features, pathogenesis, clinical sings, diagnostics, specific
therapy. .............................................................................................................................. 155

1. Classifications of infection disease.

By the route of infection-
 intestinal diseases: salmonella, cholera, dysentery, paratyphoid A
and B, foodborne diseases, escherihiosis, typhoid fever;
 respiratory tract infections: chicken pox, SARS, measles,
influenza, mycoplasma respiratory infection
 transmissive or blood infections: malaria, plague, typhus and
relapsing, HIV infection;
 infectious diseases of integument: tetanus, anthrax;
 Infection with multiple pathways: infectious mononucleosis,
enterovirus infections.

Classification of infectious disease pathogens in nature

• viruses: measles, influenza, parainfluenza, HIV, viral hepatitis,

meningitis, cytomegalovirus infection;
• prions: Fatal familial insomnia, kuru, Creutzfeldt-Jakob disease;
• protozoal: kritosporidiosis, amebiasis, izosporiasis, babesiosis,
toxoplasmosis, blastocystosis,
malaria, balantidiasis;
• bacteria: cholera, plague, dysentery, staphylococcal and
streptococcal infections, salmonella, meningitis;
• mycosis (fungal infection): athlete’s foot, aspergillosis,
candidiasis, mucormycosis, cryptococcosis, chromomycosis.

According to the source of infection (zoonotic ones and

antropos)
• Zoonotic ( by animals) : rabies, anthrax, tularemia, foot and mouth
disease, brucellosis, leptospirosis, listeriosis.
• Anthroponotic (from person to person) -measles, typhoid,cholera,
dysentery, smallpox, typhoid fever, diphtheria
• Invasive or parasitic disease caused by parasites (insects, protozoa,
mites).
• Quarantine diseases: some of the most dangerous infections that
spread rapidly and are highly contagious and serious epidemic and
with a high risk of rapid death (plague fever, cholera,anthrax,
tularemia, malaria, etc)

From lectures-
According to clinical forms
1. Type- typical and atypical
2. Gravity- mild, moderate, severe, fulminant, hypertoxic
3. Course- acute, subacute, prolonged, chronic

According to form of interaction between host and parasite ( macro and

micro-organism)
1- Specific insusceptibilty ( eg- People with G6PD deficiency is
unsusceptible for malaria)
2- Autoinfection, endogenia, saprophytic infection
3- Inapparent (silent, subclinical)
4- Acute infections (duration 2-3 months)
5- Subacute (duration 3-6 months)
6- Chronic infections ( > 6 months)
7- Persistent infections ( 3-6 months)
8- Latent infections
9- Slow infections

Mechanism of transmission Route of transmission

Contact Water / food/ direct or indect contact
Airborne Air droplets/ air dust
 Transmissive Vertical/ blood
Insects Insects

2. Slow infection. Special features of anamnesis, periods of disease,

main clinical sings, diagnostics tests, principles of therapy.
An infection having a long incubation period, as that caused by a slow virus or
a prion.
A slow virus is a virus, or a viruslike agent etiologically associated with a
disease, having a long incubation period of months to years and
then a gradual onset of symptoms which
progress slowly but irreversibly and
terminate in a severe compromised state or, more commonly, death.

Special features of anamnesis

i) Long incubation period for months or years
ii) Steadily progressive & cyclic course, sometimes with fatal outcome
iii) Development of pathological changes, predominantly in 1 organ or
system usually in CNS –
e.g. infectious somatic & nervous system disease, AIDS, viral hepatitis, rabies,
rubella, lupus erthematousis, subacute scleroting panencephalitis

iv) Infectious disease caused by 1 type of organism is monoinfection

Simultaneous by several type of organism is mixed infection
v) Infection may be exogenous or endogenous
Most infection originate from exogenous source (eg human, animal,
environment)
Malnutrition, immunodepression, surgical intervention on certain individual
may cause inversion of normally harmless potential pathogens already on the
pt to become pathogenic

Periods of disease-having a long incubation period of months to years and

then a gradual onset of symptoms

Main clinical signs-

• cause diseases that are confined to the CNS
• have a prolonged incubation period
• follow a slow, progressive, fatal course of disease
• produce a spongiform encephalopathy
• characteristically result in vacuolation of neurons
• can cause formation of fibrillar aggregates, which contain PrP and have
amyloid-like characteristics
 Absence of immune response or an immune response that does not arrest
the disease, but may actually contribute to pathogenesis
 Genetic predisposition

diagnostics tests-
 Clinical: features depends on the sites of CNS invoved. Not definitive

Investigations
 EEG
• Shows a typical periodic pattern
• Stereotyped periodic bursts of <200ms duration, occurring every 1‐2sec
• 90% cases of sporadic CJD , Rare in new variant CJD (vJCD)
 CSF
• Protein and glucose concentration is normal
• No pleocytosis
• Elevation of protein 14‐3‐3: most useful CSF marker of CJD
• This protein is also elevated in patients with encephalitis, cerebral infarction,
and other conditions
 CT scan
• Normal/cortical atrophy
  MRI brain scan
• Shows high signal intensity in
‐ basal ganglia 70% of cases of sporadic CJD
‐ posterior thalamus in 90% of cases of vCJD

 Western blotting of PrPsc (prion in the Scrapie form )

 Conformation dependent immunoassay (CDI)
• Extremely sensitive & quantitative
• Useful for both ante & post mortem detection of prions
 Brain biopsy
• A definitive diagnosis is made by microscopic examination of brain tissue
 Neuronal loss in advance stages
• PrPsc can be detected in
‐brain tissue extracts by ELISA
‐tissue sections by immunohistochemistry
• As PrPSC not uniformly distributed throughout the CNS, absence of
PrPSC in limited sample like brain biopsy does not rule out prion disease
 Brain autopsy
• Only definitive test is post‐mortem pathology
 DNA sequencing
• Can be done on extracts from blood, brain, and other tissues
• Detects : Mutations of the PRNP gene , Codon 129 polymorphism

principles of therapy-
 Quinacrine
• Pentosan polyphosphate
• Humanized anti PrP monoclonal antibodies can be given for passive
immunizations in early pathogenesis to block the neuroinvasion.
 3. Semiotics of infectious disease. Kinds of fever according to
durations & elevation level, types of temperature curves, kinds of
eruption, characteristics of eruption types.
Kinds of fever according to durations-
 Acute ( up to 2 weeks)
 Subacute ( up to 6 weeks)
 Chonic ( > 6 weeks)

Kinds of fever according to elevation levels-

Subfebrile 37-37.9 0C
Moderate 38-39
High (pyrexia) 39-39.5
Hyperpyretic >40
Subnormal <36

Types of temperature curves-

 Febris continua- temperature fluctuation within the 10C range
(abdominal typhus, crupous pneumonia)
 Febris remittens- daily fluctuations exceeds 10C range ( exudative
pleuritis)
 Febris intermittens- daily fluctuation exceeds the 10C range,
temperature may reverse to normal ( malaria, infectious endocarditis)
 Febris hectica- the temperature fluctuation is 3 to 5 degrees ( sepsis)
 Recurrent fever / Relapsing fever- Few days with fever and few days
without fever (crisis) (Recurrent fever” disease)
 Undulant fever- Gradual elevation of temperature to high figures for
days then, decreases to normal (lysis) ( Brucellosis)
 Irregular fever- High and moderately high temperature, Different &
unpredictable daily fluctuations (Meningitis, Influenza)

Kinds of eruptions-
 Macules- flat spots
 Papules- firm, raised areas
 Vesicles- fluid filled / blisters
 Pustules- pus-filled sacs
 Ulcers- deep loss of skin
 Lesions are also characterized by color, presence/absence of
hemorrhage
→ can be – skin color
- hyperpigmented
- hypopigmented
→ Blanching erythematous ( due to vasodilation)
→ Non-blanching erythematous (extravasation)
→ Purpuric lesions (hemorrhage into skin)
• If small – petechial
• If large – ecchymotic

4. Principles of infection diseases diagnostics. Collection of castу and

epidemiological histories, clinical examination, pathognomonic
symptoms, bacteriological tests, serological and immunological
methods.
case history
should be collected carefully and in detail
i. necessary to reveal special features of the onset of the disease
(acute,gradual, incidious)
ii.fever development without or with chills. Characteristics of fever and its
types.
iii. associated non-specific symptoms. Their character and duration
iv. Indication about traumas, wounds, operation, hemoserotransfusion
v. Indications about past vaccination.

epidemiological history
i. if the patient had contact with sick person or animals
ii. if the patient is from an endemic area or epizootic foci

clinical examination
Has to be performed in an appointed order.
I. General condition of patient;
 Level of consciousness.
 Psychic balance.
 Confusions.
 Euphoria.
II. Examination of the skin;
  Color – yellow indicate jaundice, pale may due to anemia,
hyperemic may be die to inflammatory response.
 Types and location of rashes – macula, papula, urticaria,
pustules, vesicles, bulla, petechiae, exanthema

III. Examination of conjunctiva and mucous membrane;

 Presence of hyperemia.
 Patchy appearances.
 Conjunctival injection.
IV. Respiratory and CVS inspection, palpation, percussion and
auscultation.
V. Nervous and psychic activity examination.
VI. Lymphadenopathy;
 Palpable and enlargement of the lymph nodes.
 Size, consistency, mobility and pain or painless.

Pathognomonic signs
These are symptoms that are typical only for only one nosological form of
infection
Eg. Hydrophobia in rabies
Koplic spots- for measles

Bacteriological examination
Used to identify the causative agent of disease
These are 2 main stages:
i. specimen collection and transport of clinical materials
ii.isolation of the pathogen and its identification

-artificial media are used for isolation of bacteria.

-These media are usually composed of agar & often in combination with
substances to inhibit the growth of other bacterias
-once the organism is isolated, traditional methods of phenotypic
characterization are used for the identification of species of the
microorganism.
-in viral infections, culture methods are used rarely.
-Virus may be detected by direct observation of the cultured cells for
cytopathic effects or by detection of its antigens by immunoflourscent tests.
Culture and isolation of MO:
-specimen should be chosen according to the likelihood of the yield
-should be done before antimicrobial agents are administered.
-collected specimen should be immediately placed in appropriate transport
media (eg. Aerobic or anaerobic conditions)
-Culture media can be general or specific.
•general purpose media include chocolate or blood agar.
•special media
i.enriched media-nutrient media, enhances the growth of desired organisms,
rather than excluding undesirable ones
ii.selective media-contains substances that inhibit the growth of bacteria other
than the target one
Thayer-martin agar(chocolate agar +ab)
iii.differential media-allows definition of specific biochem properties of
target MO- macConkey agar.
iv.anaerobic media

serological,immunological method
Serological testing is based on antibody detection in the clinical
applications.
-when the agent is difficult to isolate eg.viral infection
-when infection is deep seated eg.brucellosis

As a rule this requires 2 blood specimens;

One during the acute phase and the second one during covalescent period.
A significant increase in time (eg. four fold or greater) between 2 specimens is
a good evidence of infection.

Immunological-
-compliment fixation tests: ELISA, direct or indirect hemoagglutinin
-indirect immunofluorescent tests
-immunodiffusion assays-used to detect fungal antibodies.

5. Principles of infectious disease treatment. Antibacterial therapy,

chemotherapy, serotherapy, principles of pathogenetic therapy.
A-Antibacterial therapy:
Antibiotics are efficacious in infectious patients. They
shorten the course of the disease
 prevent complications and
decrease the mortality rate.
When prescribing antibiotics, it is necessary to consider the type of causative
agent, its sensitivity to a given antibiotic, duration of antibiotic therapy, the
dose and route of administration (oral, intramuscular, intravenous), and
toxicity of the
antibiotic.
Antimicrobial therapy can be optimized for a given patient if you go beyond
"Drugs of Choice" lists. The usual drug of first choice may be inappropriate
for a given patient.

B-chemotherapy:
Chemical drugs that produce a specific action on the pathogenic agent can
be
synthetic or natural by their origin.
When a chemical drug is administered, it inhibits multiplication and vitality
of the pathogenic microorganisms.
Further eradication of the agent is ensured by the strength of the immune
system of the patient
Examples: Derivatives of 8-oxyquinoline (intestopan, mexaform, mexase, 5-
NOK) are used to treat intestinal infections.

C-serotherapy
Serum of immune animals and people is used to treat infectious diseases.
The preparations are classified as
• antitoxic (containing antitoxins) and
• antibacterial (containing bactericidal antibodies).
Antitoxic sera are used to treat diphtheria, botulism, tetanus, gaseous
gangrene, etc.
The serum should be administered as early as possible, before the toxins
produce irreversible changes in the organs and tissues.
Immune globulins (polyglobulins, gamma-globulins) also can be used to treat
infectious patients.
Gamma-globulins are used for therapeutic and prophylactic purposes in
influenza, pertussis, measles, seasonal encephalitis, anthrax, leptospirosis,
staphylococcal infections.
Treatment of infectious patients with immunoglobulins is often combined with
chemical drugs

D-principles of pathogenetic therapy

includes medical measures aimed at elimination of toxemia by detoxication
therapy and glucocorticoids therapy, and depending on the clinics of the
disease: restoration of water-salt equilibrium, nomalization of CVS and
Nervous system functions and also improving body functions by stimulation
therapy.
i)Decreasing intoxication and correction of homeostatsis is the main aim
ii)Corticosteroids : septic shock and in acute renal failure
eg: Diphtheria typhoid fever of inflammation present (Brucellosis)
iii)Rehydration therapy (IV saline)

6. Infectious process, its forms.

1-Types of infectious process according to duration

a)Acute infection
b) Subabute infection
c)Chronic infection
d)Latent infection
e)Persistent infection
f)Slow infections

From a previous prep

Characteristics of latent infection

i)A latent infection remains capable of producing symptoms is inactive in a
certain period
ii)Periods of inactivity present either before signs and symptoms appear or
between attacks

eg- Herpes viruses are examples of pathogens which readily enter a latent
stage during which symptoms disappear, only to reappear at a later time upon
the reactivation of the latent infection.

7. Factors of infectious process, its forms, carriage of infection,

periods of infectious disease.
a-Factors of infectious process:
Microbial invasion can be facilitated by the following:
• Virulence factors
• Microbial adherence
• Resistance to antimicrobials
• Defects in host defense mechanisms
 Susceptibility

b-its forms: Types of infectious process according to duration

a)Acute infection
b)Subacute infection
c)Chronic infection
d)Latent infection
e)Persistent infection
f)Slow infections

c-carriage of infection:

A person or animal that harbors a specific infectious agent without discernible

clinical disease and serves as a potential source of infection.
The carrier state may be
 inapparent throughout its course (commonly known as healthy or
asymptomatic carrier), or
 during the incubation period, convalescence and post-convalescence of
an individual with a clinically recognizable disease (commonly known
as
an incubatory or convalescent carrier).
Under either circumstance the carrier state may be of short or long duration
(temporary or transient carrier, or chronic carrier)

Periods of infectious diseases

4 periods of infectious diseases

i)Incubation
• Interval between acquiring infection & development of 1st symptom
• Duration vary from few hrs (eg botulism, influenza) to weeks or months (eg
viral hepatitis ), rabies till 2yrs

ii)Prodromal period
• Interval between the appearance of 1st symptom n the characteristics of
illness (eg skin rash)
• There are many symptoms that occur in this period (eg weakness, fatigue,
headache, disturbance of sleep usually insomnia, poor appetite)
• Duration = 1-3days

iii)Peak period
• Last from few days (eg rubella, influenza) to several wks (eg typhoid fever,
brucellosis, viral hep)
• Typical symptom of the disease are pronounced in this period (eg rash,
hepatosplenomegaly, enlargement of lymph nodes)

iv)Convalescent period / recovering stage

• Duration of disease differ
• Recovery may be complete but in some cases residual signs are preserved

8. Toxic shock as complications of meningococcal infectiouns.

Diagnostics, treatment.

Toxic shock in meningicoccal infections, develops as a result of Lipo-

oligosaccharide (LOS) endotoxin that interacts with human cells,
producing proinflammatory cytokines and chemokine  activation of
the complement system, coagulation hemostasis with subsequent
damage to the capillary endothelium  increased vascular
permeability  impairs circulation of blood, causes hemorrhage into
the skin, mucosa, serous membranes, and into the parenchyma of the
internal organs (shock process).

Diagnostics:

-Clinical manifestation:
Fever, chill, vertigo, weakness, confusion, myalgia, vomiting, and
convulsions.
Cyanosis, dyspnea  body temperature drops to normal.
The pulse is thread, fast, and soon becomes indeterminable.
Hypotension develops.
Hyperemic face and neck. Petechial lesions, intensive haemorrhages
develop in the skin.
Nosebleed, gastric and uterinehemorrhage.
Absence of meningismus and a rapid increase in disorders of
consciousness

Lab.:
 -CBC: Neutrophilic leukocytosis (or Leukopenia). Thrombocytopenia.
Possible Anemia. Decreased ESR.

-Biochemical blood test: Severe acidosis, Hypoproteinemia, Increased

Creatinine and urea. Increased procalcitonin.

Culture and Microscopy: G- diplococci

-CSF: Serosanguinous. Increased protein. Decreased glucose. Rough

fibrin film.

Treatment:
Intensive care unit
Chloramphenicol sodium - 0,05g-0,1g/kg for 10 days. IV
Detoxication therapy – toxic shock: 20mL/kg of 4.5% human
Albumin solution or normal saline .Ringer solution polyglucin
Glucocorticoids: In fulminant shock improves cardiovascular function
Vasoactive drug: Dopamine - After initiating therapy, increase the dose
by 1-4 mcg/kg/min every 10-30 minutes.
Acidosis correction – 4% sodium hydrocarbonate or lactate solution.
Improvement cardiovascular function: strophanthin, corglucon,
cocarboxylase, and ascorbic acid should be administered

9. Hypovolemic shock as complications of cholera.

Cholera (cholera) is an acute anthroponotic infectious disease with a

fecal-oral transmission, characterized by massive diarrhea (rice water)
with rapid development of dehydration, progressing to hypovolemic
shock.

Patho of Hypovolemic shock in Cholera:

Cholera  enterotoxin  attack membrane receptor  stimulates
adenylate cyclase → increased cyclic AMP (adenosine monophosphate)
→ increased ion (mainly chloride) and water secretion into the intestinal
lumen → profuse liquid stools (Secretory diarrhea)
↓
Increased number of defecation and volume of discharge (up to 1L,
>15x a day) and vomiting
Disease progress and if untreated
 ↓
4th degree dehydration develops  Liquid losses ≥ 10% of body weight
 Hypovolemic shock (Decrease of the plasma volume  peripheral
circulation disturbances  tissue hypoxia, decompensated metabolic acidosis and
respiratory alkalosis, Severe hypotension .Cessation of glomerularfiltration 
dysfunction and nitrogenimia)

Clinical pic Hypovolemic shock In cholera:

-Patient’s condition gets worse, supor
-Diarrhea and vomiting decrease/cease
-Temperature fall 35-36°c, clammy extremities
-Cholera’s face suffering expression, "the setting sun" eyes ( eyes
balls are deep-set, and upwards.
-Skin fold increased and doesn’t fla  cholera’s fold (decreased skin
turgor)
-Tachycardia
-BP decreased (hypotension)
-Respiratory rate 40-60 per minute
-Tonic cramps over all groups of muscles, even diaphragm 
excruciating
hiccups
-Abdomen is retracted and soft, tender during abdominal muscles
cramps

Diagnosis:
Dipstick(rapid test; initial test  antigen detection)
Stool culture (confirmatory)
PCR

LAB:
Anemia usually, leukocytosis and neutrophilic shifted to the left.
Relative density of blood rises from 1.038 to l.05.
Hematocrit index increases to 0.6-0.7
Nitrogen deficiency, potassium chlorine, and hydrocarbonates increase.

Tx:
Admission to Infectious Hospital  ICU
Correction of hypovolemic and metabolic acidosis and prevention of
hypokalemia.
Replacement fluid intravenously:
 2 stages: 1st stage: initial rehydration. 2nd stg: corrective dehydration.
↓
Polyionic solution (at 39 -40 degree) during the first 2 hours in volume
of 10% of body weight.
Firsts 2-4 liters: Stream infusion (100-120 mill /min).
After, drop infusion at the rate of 30-60 ml/min.
The general volume of infused solution may reach 20 to 80 liter for 3-5
days.

ATB: (etiotropic therapy)

Tetracycline - 500 mg orally every 6 hours for 5 days
Doxycylin (300 mg orally given 6 hours for days
Furasolidone (100 g orally given every 6 hours for 72 hours)
Cloramphenicol - 50mg/6hr (5 days)

Electrolyte repletion:  monitor serum electrolytes daily

Magnesium sulfate
Potassium Chloride
Calcium gluconate

10.Meningococcal infection, meningococcemia. Pathogenesis, clinical

forms, special clinical features, diagnostics, treatment.

Etio: Neisseria meningitides (meningococcus - Diplococci G-

Different serotypes AB,C,D
Endoxotin
Unstable in environment
Sources: Human -> sick and carrier
Transmission: air-borne (0,5m → close contact)
Suspetible → children until 5y, young adults
Risk → immunocompromised, senile complement deficiency, asplenic patients
Season dependent → Winter and spring
Immunity → Innate type, then after infection → specific immunity

Pathogenesis:
Entry  mucosa of the fauces & nasopharynx  catarrhal
inflammation of the upper respiratory tract, rhinitis, nasopharyngitis 
overcome local barrier (lymphatic throat ring) → enter blood→ various
organs and tissues →bacteremia
-If mild disease  Bacteremia  polymorphous rash, subsides in few
hours/days

-If sensitive patient  Meningococcaemia

Clinical forms:
1. Localized forms (carrier form, acute nasopharyngitis).
2. Generalized forms (meningococcemia, meningitis,
meningoencephalitis, mixed forms).
3. Rare forms (endocarditis, polyarthritis, pneumonia, iridociclitis).

I. Primarily localized forms:

a) meningococcal carrier state (clinical manifestations are absent)
b) acute nasopharyngitis;
c) pneumonia.

II. Hematogenously generalized forms:

a) meningococcemia: typical, fulminant; chronic;
b) meningitis; meningoencephalitis;
c) mixed forms (meningococcemia + meningitis, meningoencephalitis).
d) rare forms (endocarditis, arthritis, iridocyclitis).

Special Clinical features:

Meningococcaemia
-Begins suddenly w/ chills headache
-High fever >40°C (intermittent or continuous fever)
-Hemorrhagic rash (petechias – with irregular size, slight elevated. At
lower extremities  buttocks, dorsal surface of thights and shins) 
purpura  ecchymosis.
- Hemorrhage into sclera, faucial mucosa
-Micro/macrohematuria
-Lesions of joints
-Pneumonia
-Endocarditis
-Toxemia sympt.: Tachycardia, BP decrease, cyanosis, dyspnea, dry
skin,
-Absent symptoms Meningitis.

Severe case
-pupuric parts, echimos, petichia
-arthralgia, myalgia, endocarditis, myocarditis, myocardial failure,
pericarditis
-Meningococcemia

Fulminating meningococcal sepsis(Hypertoxic fulminant form)

Supor  Shock and Adrenal hemorrhage (Waterhouse-Fridereichsen
sd)
Adrenal insufficiency
Sudden high fever (40-41°), chill, vertigo, confusion, vomiting, diarrhea
Myalgia, convulsion
Hyperemic face and neck
↓
Then:
Cyanosis, dyspnea
Decreased BP, cold extremities
Intensive petechial lesions and hemorrhages  at skin, nosebleed,
stomach and uterine bleeding.
Marked meningitis symptoms (mixed form)
IN CSF  Serosanguineous

Chronic
-fever (intermittent), rash, arthralgia
-hepatomegaly, petichia, nephritis, carditis

Acute nasophyringitis: (extra)

Independent manifestation, or Prodromal stg of meningitis,
meningococcaemia.
SYMPTOMS:
Temperature increased (for 1-3 days)
Headache,
Stuffy nose
Dry cough
Sore throat
Edema and hyperemia of posterior pharyngeal wall
Hyperplasia of lymphoid follicles, herpes

Meningitis: (extra)
Acute onset, w shaking chills
Fever 39-40°C
Drowsiness, confusion, delirum can develop
Vomiting recurrent, severe headache (usually frontal), vertigo,
convulsion.
Fontanelle Triad: Protusion, tension as absence normal pulsation of
frontal fontanelle.
Skin hypersesthesia, hypersensitivity of light
Signs of meningitis - stiff neck(can bend neck), kerning symptom (cant
extend leg when thight is flexed on abdômen), brudzinski sign (when
flex neck -> flexion of thigh and leg)
Specific Posture -> knee flexed on abdômen, head tilted backwards
(Pointing dog posture)

CN involvement  strabismus, nisocoriam facial nerve paresis

Tachycardia  Bradycardia (due swelling and brain edema)

Meningoencephalitis: (extra)
Deranged consciousness
Muscle cramping
Paralysis and paresis

Diagnostics:
-CBC:
Leukocytosis shift to the left, Eosinophilia can be presente. Increased
ESR
-CSF (Lumbar puncture):
Cloudy purulent, Gray color
Increased WBC > 1000/ml, neutrophilic pleocytotosis (12-30 x 109/1)
- high cytosis,
Increased opening pressure.
High protein contente (1-3 g/1)
Decreased glucose
High viscosity (slow drops puncture)
Rough fibrin film formation
Serosanguineous CSF in Fulminating meningococcal sepsis

-Culture & microscopy:

Nasopharynx swab, blood ,CSF – Positive microscopy & culture (G-
diplococci)

Treatment:

Acute nasopharynx Moderate degree:

ATB:
Sulfa drugs (Adults: 4-6 g a day. Children: 0.3 g/kg. Course of 3-5
days)
Sulphapyridazine or sulphadimethoxin  Adults 2 g during 1st
day and 1g during subsequent 4 days.

Meningitis and meningococcaemia:

ATB:
Penicillin I.M (Adults: 300 000 U/kg daily,
Infants <3 months 300000-400000 U/kg, 4h interval btw
doses
Infants <2 months 300000-400000 U/kg, 3 hours intervals
Course: 5-8 days or until CSF normalizes.

Chloramphenicol sodium succinate dose of 0.05-0.1 g/kg for 6-8 days

(Specially for Fulminant form)

Ampicillin (0.15-0.2 g/kg a day).

 Detoxification therapy:
Fluids
If toxic shock  Polyglucin, ringer solution, 5% glucose, Albumin

Correction electrolyte disbalance

Acidosis is corrected by 4% sodium hydrocarbonate or lactate solution.

Brain edema:
Diuretics, manitol

Improve CVS function (specially in fulminante shock):

Glucocorticoids, strophanthin, corglucon, cocarboxylase and ascorbic
acid.

Continuous monitoring
If in CSF neutrophils > 100  need to change Antibiotics, use 2 ATB
together, or add sulfa drugs.

11.Influenza. Etiopathogenesis, clinical sings, diagnostics, treatment,

complications.

Etiology:
Single-stranded RNA Virus. Family: Orthomyxoviridae.
Antigens: Neuraminidase(Sialidase), Hemagglutinin
Types/Serotypes: (A, B, and C) → A and B = most disease. C - mostly
children, sporadically.
Antroponotic disease
Source infection: Diseased human -> Transmission: Air Droplets -Air-
borne
Antigenic drift: Changes in superficial/surface antigen HA protein ->
new virus (accumulation of Minor gene mutations within the antigen-
binding sites)
Antigenic Shift -> Novelinfluenza A subtype virus-> ability
transmission human to human → Due to Direct Introduction of Avian
strain or new strain produced by recombination of 2 different influenza
viruses.  forms a new subtype
Etiopathogenesis:
Infected human with Influenza virus  Droplets/Airdust by
cough/sneezing/speaking -> Infection mucosa of upper airways ->
Columnar epithelium of trachea → Cause degeneration necrosis: ( =
Edema, epistaxis, blood in sputum)
Toxemia can occur (due toxins)  lesion cns and cvs.
Interferon of infected cells inhibits multiplication of virus in first hours.
At end 1st week production of specific antibodies (Type-specific for
20 yrs

Clinical signs:
(Incubation 1-2 days
Immunity: A virus 2-3 years. B virus till 6 years
Susceptible: Cardio and resp. diseased pt)

SYNDROMES:
Intoxication sd (since 1st day)
Catarrhal sd (start after 2 days) -> stuff nose, rhinorrhea, hyperemic
fauces, edema of fauces

CLINICAL PIC:
Forms: Mild, moderate, severe
Typical or Atypical (Atypical wont have one of the syndromes)

Typical:
Acute onset:
Increased temp → 38.7-40°C. (for 2-4 days)
If mild → Subfebrile
Headache → Frontal, retro-ocular(mov. eyes)
Algias Pain muscle and bones → myalgias, arthralgias
Dry Cough (10 days), Sneezing ,Nasal obstruction, Dry throat,
Tracheitis
Sweating, Weakness
Hoarseness of the voice.
Physical Examination: hyperemic face and neck, and injected scleral
vessels. Coated tongue, hyperemic fauces

CNS manifestations:
Neuralgia, neuritis
Symptoms of encephalitis

Severe (toxic) form:

Toxemia sympt:
Severe headache
Hyperpyrexia >40°C
Dyspnea
Cyanosis
Hypotension
Delirium
Nausea vomiting
Loss of consciousness
Symptoms of meningitis
Skin hemorrhage

Diagnosis:
LAB:

CBC:
Leucopenia(viral), relative lymphocytosis, neutrophilic shift to left,
eosinophilia
Transaminase can be mildly elevated

Nasopharyngeal/ Nasal swabs aspirates:

PCR
Rapid influenza diagnostic test
Immunofluorescence assay
Serologic -> do after 5-7 day

Treatment:
Bed rest
Milk-vegetable diet. Vit.C, tea, milk w/honey ⇒ 1.5L of fluids at least
Pharmaco:
Oseltamivir(Tamiflu) - 75 mg - 2 times daily in capsules for 5 days.
Zanamivir - 10 mg - 2 times daily inhalation for 5 days
 Interferons - nasal drops
Detoxication: Fluid therapy: Sodium Chloride, Ringer lactate, glucose
1.5L + Lasix (diuretics), or Urea and mannitol.
Antipyretics: Acetaminophen (for fever more than 38.8)
If secondary Bacterial infection (Complications)  ATB therapy.

HOSPITALIZATION:
Children, Elderly w/ chronic diseases, High fevers, Severe dyspnea

Complications:
-Pneumonias -> Secondary bacterial infection (pneumococci,
staphylococci,hemolytic streptococci)
-Acute cardiovascular failure, laryngitis, tracheobronchitis, bronchitis,
bronchiolitis, frontal sinusitis, maxillary sinusitis, otitis and various
hemorrhages (epistaxis  hemorrhagic)

12.Parainfluenza infection. Etiopathogenesis, clinical sings,

diagnostics, treatment, complications.

Etiopathogenesis:
Etiology:
Parainfluenza virus (RNA virus).
Family: Paramyxoviridae
4 serotypes

Pathogenesis:
Infected human with Parainfluenza virus  Droplets/Airdust by
cough/sneezing/speaking -> Infection mucosa of upper airways ->
Columnar epithelium of trachea -> Inflammation upper airways w/
edema formation

In smaller children also more common affection of Lower respiratory

tract too → spread to lower respiratory tract by secretions 
Bronchiolitis, Pneumonitis
 In older children and adults – asymptomatic, febrile rhinitis, common
cold

Clinical signs:
Incubation: 3-4 days  gradually onset, w/ sluggish course.

(In adults  Milder, asymptomatic, a common cold)

Mild intoxication → Subfebrile fever, Headache.
Mild rhinorrhea, cough

(More common in younger children) :

Laryngitis, Laryngotracheitis, bronchiolitis, pneumonitis  Laryngeal
stenosis and croup can develop (subglottic narrowing)
Croup = Laryngotracheobronchitis → Hoarness of voice, chest pain

Barking Cough,
Inspiratory stridor
Dyspnea
In severe cases  thoracic retraction, tachydyspnea  resp. failure 
cyanosis  hypoxemia  bradycardia  altered mental status

Diagnosis:
LAB:
Virological tests:
Nasopharyngeal swabs  PCR, culture (monkey cell culture)

Serological (blood serum test)  ELISA

Immunofluorescence

(X-ray  can detect subglottic narrowing in Croup)

Treatment:
Symptomatic treatment ( no specific tx)
Anti-influenza Immunoglobulin can be given IM
Bronchodilators
Dexamethasone  reduces airway swelling (Croup)
Oxygen therapy

If secondary complications (bacterial infection)  ATB, sulpha drugs

 Complications:
Croup
Pneumonia
Acute tonsillitis, sinusitis, otitis

13.Adenoviral infection Epidemiology, pathogenesis, clinical features,

diagnostics, treatment.

Epidemiology:
-Source infection: carriers, sick person  nasal, nasopharyngeal mucus,
sputum, and conjunctival discharge (during first 5-6 days of diseases)

-Transmission: air-borne, fecal-oral. (More stable in the environment

than the influenza virus)

-Mostly affected person: Infants 6 months – 3 years

-Type specific immunity – produced in convalescence

-Sporadic, epidemic outbreaks in children's institutions.

-Increased morbidity in autumn and winter.

- Incubation period 3-12 days  Outbreak last longer than influenza

Pathogenesis:
Infection is usually transmitted in droplets of respiratory or ocular
secretions  Replicate in the epithelial cells that line the lungs,
conjuctiva, intestinal mucosa also affected.
The lymphoid tissue of the regional lymph nodes is damaged, the
vegetative nervous and endocrine systems are also upset with
subsequent vascular disorders (pallor, tachycardia).

Clinical features:
Incubation: 3-12 (freq. 5-6 days)
Rhinopharyngitis,
Rhinopharyngotonsillitis (more common)
Rhinopharyngoconjunctivitis (more common)
Rhinopharyngobronchitis,
Pharyngoconjunctival fever,
Membranous/folicular conjunctivitis (KeratoConjunctivitis) Days to
>2wks
Pneumonia
Gastroenteritis
Myocarditis

General symptoms:
Fever, subfebrile  2-7 days
malaise, chilliness, headache

Local symptoms:
Respiratory: Stuffy nose, hyperemia of the fauces and the posterior wall
of the pharynx, difficult swallowing, cough (dry or with expectoration
of sputum) and chest pain.

Pneumonia: Bronchopneumonia, usually infants <1y.o; Dyspnea,

cyanosis, toxemia.

Conjunctivitis: eyelids, mucosa and eyeballs are injected, edema,

granularity, eye secretion (serous)
GIT: Abdominal pain, intestinal disorders, sometimes hepatic
enlargement

Diagnostics:
LAB:
Virologically  tissue culture, PCR
Serological
Immunofluorescence

Treatment:
Supportive:
Bed rest
Analgesics
Antitussives
Hydration therapy
NSAIDs

Severe cases:
 Immunoglobulin
Interferon
Desoxyribonuclease

14.Diphtheria of fauces. Forms, variants of the disease, clinical

features, complications, diagnostics, specific therapy.

Corynebacterium diphtheria – Gram + bacilli bacteria.

Faucial diphtheria - tonsillar pharyngeal diphtheria.

Forms:
Local
Diffuse
Toxic
Hypertoxic
Hemorrhagic

Clinical features Fauces diphtheria:

Local:
1- Catarrhal:
-Without membrane

2- Insular:
-Separate islands of membrane on the tonsils.

-Gradual onset
-Fever to 38°C, malaise, headache, poor appetite
-Slight Pain Swallowing
-Hyperemic fauces on firsts days
 Greyish-white membrane
-Deep and thick grey-white membrane
-When removed (cotton/spatula)  Bleeding surface is exposed
-Submandibular and Anterior neck Lymph Nodes Enlarged
-Toxemia signs Absent

Diffuse:
-Acute onset
-Body temp. rise 38,5-39°C
 -Chill, weakness, headache
- Tonsils: Edematous and Enlarged
Thick grey membrane  extends to palatine arches,soft palate
and nasopharynx.
-Lymph Nodes are more tender and enlarged than local form.
-Can occur as result of untreated local form

Toxic:
-Onset: Fulminant
-Fever: 39-40°C
-Severe weakness
-Dull heartsound, tachycardia (140-160 bpm)
-Membrane: thick, greyish-white/brownish-grey
Covers tonsils, extends to soft hard palate
-Nasopharynx & nasal cavity can be involved  serosanguineous
discharge
-Breath is foul and sweetish
-Edema of faucial mucosa & membrane  Mechanically impede
respiration: Noisy and hoarse respiration.
-Degrees:
Degree I - Edema extends to the middle of the neck,
Degree II - Edema extends to the clavicle
Degree III - Below the clavicle.

-Hypertoxic form:
-Severe fulminant local process in fauces
-Tomexia: Quickly developing Cardiovascular failure
-Patient dies in 4-5 days

-Hemorrhagic form:
Nasal bleeding, gum bleeding

EXTRA: Laryngeal diphtheria (Diphtheric or True Croup):

-Independent form or Secondary, from Faucial or Nasal Diphtheria.
-3 stg:
1-Dysphonic: fever, malaise, hoarsness, barking cough
dysphonia/aphonia
2-Stenotic phase: (after 1-3d). Noisy respiration(saw cutting wood),
chest retraction during inspiration, use of accessory muscles in
respiration.
3-Asphyxia (if pt not treated, after hrs to 2-3days). Anxiety, drowsiness,
cyanosis (lips,nose,nails), fast & shallow respiration, BP decreased, cold
sweat, convulsions  death.

EXTRA: Nasal Diphtheria:

Usually in infants
Subfebrile/Normal temperature
Mild toxemia
Blocked nose
Serosanguineous nasal discharge
Excoriation, fissures at nostrils
Membranes and ulcers covered with crusts on nasal mucosa

EXTRA: Rare location diphtheria:

Secondary from faucial or nasal diphtheria
Clinical picture as Catarrhal or lacunar tonsillitis.

Complications:
Myocarditis:
-Can occur early or late
-Cardiac toxicity occurs in 2nd week of illness
-Signs: Soft heart sound, gallop rhythm, signs congestive heart failure
(less common). 50% mortality.
-ECG abnormalities: Supraventricular & ventricular ectopic,
Tachyarrhythmia, broad QRS complex, ST and T wave changes, Heart
blocks, Bradyarrhythmia. BBB and Complete heart block 80%
moratlity.
-Cardiac enzymes: Increased acc. damage – Creatinine phosphokinase
MB, Myoglobin, Troponin.

Neuropathy:
-Late development (3-8wks after local sympt.)
-Exotoxin  Degeneration myelin sheath
-Polyneuritis, mononeuritis  in moderate/severe cases 
-Paralysis of soft palates (local toxin spread)  Nasal voice,
regurgitation ingested fluids through nose
-Paralysis of pharynx, larynx, respiratory muscles
-Affection of Cranial nerves IX, X  VII  II, IV and VI
-Quadriparesis  death from respiratory failure: Respiratory muscle
paralysis or Paralytic closure of the larynx

Diagnostics:
LAB:
2 swabs  Nasal & Tonsils(Take before ATB therapy) 1st,2nd, 3rd
day.
↓
Micro, Culture, PCR.

If myocarditis signs  Cardiac enzymes (CPK MB, Tropo,myoglobin),

ECG.

Treatment:

Bed rest
Detox therapy -> saline, dextrose, glucose, Riopolyglycin
Diphtheria Antitoxin:
→ 20.000 - 40.000 Units for Faucial diphtheria <48h
40.000 – 80.000 Units for faucial diphtheria > 48h
80.000 – 100.000 Units for Malignant (Toxic state, bull
neck)
(need to test hypersensitivity reaction -> can give anaphylactic
shock)
Test: 1 ampule diluted, another non diluted
Inject diluted intracutaneosly, wait 20-40 min -> check size of
hyperemia infiltration at the place of injection, if hyperemia <0,9
cm (1cm), you take 0,1 ml of diluted and inject subcutaneously,
wait 20-30 min, if size the same (<0,9cm) → negative reaction =
Use all dosage. If + & anaphylatcit reaction  Adrenaline

ATB:
Penicillin G 50.000 units/kg 4x day.
Erythromycin 5mg/kg Parenteral/Orally. 4x day
cephalosporins, and tetracycline
 If cardiac involvement  ACEI (Captopril),
Completer heart block  Pacing

Intubation/ Emergency Tracheostomy  In respiratory obstruction -

laryngeal diphtheria

Corticosteroids in severe case Laryngeal diphtheria  reduces swelling

15.Enteric yersiniosis. Epidemiological features, clinical forms, main

clinical sings, diagnostic tests, principles of therapy.
Yersiniosis is a sapronosis, which is characterized by worldwide
spreading, intoxication syndrome development, damaging of the
gastrointestinal tracts predominantly, polyorganic damaging in
generalized form, tendency to reccurents

Epidemiological features:
 Main reservoir: soil
 Secondary reservoir: animals and birds
 Main source: rodents and animaisls (swines, rabbits, dogs, cats)
 Mechanism of transmission: fecal oral
 Incubation period: 4-6 days (1-14days)

The susceptibility to this infection is high, some people have risk for
yersiniosis. They are people working in poultry farming, cattle
breeding.
Yersinia enterocolitica infection is registered anywhere, more often in
Europe, Great Britain, USA, Canada, Japan, Russia. More rarely the
disease is registered in Africa, Asia. The many cases of their disease
occur from March, still during 4-5 months and decreased to August. Its
secondary cases may appear at the end of the years

Clinical forms:
 Gastrointestinal form
‐ Variants: gastroenteritis, enterocolitis, gastroenterocolitis.
‐ Enterocolitis occurs predominantly in children.
 ‐ Onset of the disease is acute.
‐ Prodromal symptoms: anorexia, headache, listlessness
followed by watery mucoid diarrhea, low- grade fever ,
colicky abdominal pain . In some patients catarrhal
symptoms, exanthema appear.
‐ The symptoms of gloves, socks, hood hands are typical.
‐ On the 2-6 days point like macular papula and urticaria rash
appear on palms, hands, soles, chest with following
desquamation. Hyperemia of conjunctiva, mouth,
lymphadenopathy, hepatosplenomegaly can be noted.
Fondue becomes raspberry jelly on the 5-6 days of
yersiniosis.
‐ The temperature becomes normal 4-5 days after the
beginning of the disease. In most cases yersinia disease is
self- limited.

 Abdominal form
‐ Variants: mesenteric, amenities, terminal ileitis, acute
appendicitis, pseudo appendicitis syndrome is most
common in children and young adults.
‐ Onset of the disease is similar with gastrointestinal form.
But after 1-3 days’ fever, intensive abdominal pain in
ileocaecal and umbilical regions, sometimes nausea,
vomiting appear. This signs are accompanied by fever and
leucocytosis. In mesenteric lymphadenitis non intensive
pain in right lower quadrant pain appears on 2-4 days of the
disease and accompanied by fever and lasts until 2 months.
‐ Sometimes during palpation of the abdomen painful
mesenteric lymph nodes in umbilical region can be noted.
The terminal ileitis is characterized by prolonged pain in
right lower quadrant of abdomen and enterocolitic signs.
‐ During laparoscopy inflammation and edema of distal part
is observed.
‐ This abnormalities disappear after 2 to 6 days.
‐ The prognosis is favorable

 Generalized form (septic and mixed variants)

 ‐ Characterized by the different organs and tissues damaging
‐ Acute onset , high fever , intoxication catarrhal signs,
abdominal pain in epigastric and umbilical regions
sometimes vomiting, watery diarrhea are characteristics.
‐ The fever lasts about 2 weeks on the 2-3 days of the disease
polymorphic rash with itching appears and lasts 3-6 days
with following desquamation.
‐ Arthralgia is noted on the first week, large and small joints
can be damaged. Arthritis is not typical conjunctivitis,
jaundice, exanthemas.

Clinical signs: (AMBOSS)

 Duration: 12-22 days
 Low-grade fever, vomiting
 Invasive diarrhea (may be bloody in severe cases)
 Pseudoappendicitis: mesenteric lymphadenitis, particularly in
ileum, with typical signs of appendicitis. (right lower quadrante
abdominal pain)

Diagnostic tests:

Laboratory:
 CBC: leukocytosis with left shift (eosoinophilia and
lymphopenia), increase ESR (in generalized form)
 Biochemical blood analysis: increase AST and ALT, increase level
of biluribin in some cases
 Bacteriological investigations: blood, feces, urine swabs from
the faucets are used, taking in the first 7 days after onset of
disease
 Immunological methods: revealing of yersinia enterocolitica
antigens in clinical material in first 10 days of disease
 Serological methods (ELISA, agglutination test): revealing of the
antibody from the second week of disease in pain serum with
interval 10-14 days, using 2-3 methodics. For their aim aT, CFT,
HATare used
 Instrumental (Imaging studies help in the diagnostics of
different forms of yersinia enterocolitica disease):
 X-ray of the chest
 ECI
 ultrasound investigation
 colonoscopy
 laparoscopy

Principle of therapy:
There are some indications for the patients, hospitalization. They are
clinical indications (severe course of disease). Complications
development, (severe additional diseases) and epidemiological
indications (focus of disease and patients from the group risks).

(AMBOSS)
 Supportive therapy for gastroenteritis: bland diet, oral
rehydration therapy
 Antibiotic therapy: based on culture susceptibility, indicated for
severe cases (they dont shorten disease course)
‐ Trimethorim/Sulfamethoxazole OR
‐ Fluoroquinolones (Ciprofloxacin) OR
‐ 3rd generation cephalosporins (Cefotaxime)

16.Botulism. Epidemiological features, pathogenesis, clinical sings,

diagnostics, specific therapy.
Botulism is a life-threatening condition of neuroparalysis that is caused
by a potent neurotoxin produced by the spore-forming bacteria
Clostridium botulinum.
Botulism (from Latin botulus sausage) is caused by spore-forming
Clostridia (Clostridium botulinum). Seven serologic types of these
motile anaerobes are distinguished by the structure of the antigen and
exotoxin: A, B, C, D, E, F, and G types. Types A, B and E are commonly
found in soil; these are responsible for the onset of botulism in
humans.
Botulinum toxin: protease that cleaves SNARE proteins and prevents
fusiono f transmitter-containing vesicles with the presynaptic
membrane  inhibition of acetylcholine release from the presynapctic
axon terminals.

Epidemiological features:
Pathogen: Clostridium botulinum  stable in the e in the environment
because they can form spores
Transmission: fecal-oral (ingestion of pickled or salted mushrooms, or
home-canned vegetables, home-smoked meat, and other foods
infected with botulism spores. Industrially canned food is safe because
it is treated in autoclaves in which the spores are quickly killed)
Incubation period: 6-30 hours (2 hours – 12 days) /12-36 hours
(AMBOSS)

Botulism microorganisms and their toxins propagate in separate foci

rather than in the whole bulk of smoked meat, fish or sausage. This
explains the fact that only few people may be infected, v/hile others,
who took the same food, may remain healthy. Botulism occurs
sporadically; group morbidity is less frequent.

Clinical signs:
The onset of the disease is acute: nausea, vomiting, abdominal pain,
muscular debility, lassitude, headache, and vertigo. Diarrhoea is rare.
More characteristic are constipation and flatulence due to atonia and
paresis of the gastrointestinal tract. Simultaneously with dyspepsia, or
3-4 hours later, the specific symptoms of botulism develop. The body
temperature is usually normal but it can rise to 37.7-38 °C.
The muscles of the eye are affected and the patient complains of
dimmed vision, indistinct contours (especially in the near sight) and
diplopia. Examination reveals ptosis of the upper eyelid, strabismus,
anisocoria, and stable mydriasis (morbid dilatation of the pupils).
Speech and swallowing are difficult due to lesion of the 9th and 12th
pairs of the cranial nerves. The voice first becomes hoarse, then it
weakens and becomes whispered. Speech becomes inarticulate and
nasal (rhinolalia); aphonia is possible. Secretion of the saliva and
mucus can be upset. The mucosa of the mouth, nose and throat
becomes dry. Thirst develops. The muscles of the throat may be
paralyzed to cause difficult swallowing. The soft palate can also be
paralyzed and liquid food then returns through the nose; the tongue
movement is upset. The motor function of the stomach is terminated.
Pylorospasm is followed by a complete relaxation of the pylorus;
gastric secretion decreases.
Respiratory distress develops in severe cases. The patient experiences
compression of the chest; dyspnoea develops (tachypnoea of 40-50
per minute); inspiration is difficult, asphyxia and complete cessation of
respiration occur. Respiratory disorders develop due to lesion of the
intervertebral muscles and the diaphragmatic muscles.
The pulse is first slow but later it accelerates and becomes small;
"cyanosis and pallor develop. Combination of tachycardia with low
body temperature are characteristic. Consciousness is normal.
The blood is characterized by neutrophilosis with a shift to the left.
If the disease is mild, only several symptoms of botulism can be
observed and the patient recovers in 2-3 weeks. The severe course of
the disease is characterized by the presence of all symptoms and the
patient recovers only in 2-3 months. Death from botulism is due to
respiratory paralysis.

Diagnostics:
 Anamnesis and clinical Picture
 Neutralization reaction on albino mice (One pair of mice is
inoculated intraperitoneally with 0.5-0.8 ml of the patient's
blood, filtrate of the vomitus, gastric washings, extract of the
 suspected food or of the biopsied specimens. Another (control)
pair of mice is given a mixture of the material with antibotulism
vaccine (A, B, C, E, F), 0.05 ml of each type. If the experimental
pair of mice dies, while the controls survive, a reaction of
neutralization is performed with separate monovalent vaccines.)

Specific therapy:
 Erradication of toxin though bowel empitying (induced by
medication) and stomach lavage with 5% sodium bicarbonate
 Horse derived heptavalent botulismo antitoxin (after
determination of sensitivity to equine protein  skin test; test is
negative if <1cm after 20 min). If positive test: donor
antibotulinus immunoglobulin or antibotulinus bovine serum
should be used OR Prednisolone 60mg and anithistamine
preparations are are injected subcutaneously and only after, the
horse serum diluted 1:100 is injected subcutaneously at 20-min
interval in doses of 0.5, 2.0 and 5.0 ml. In the absence of
reaction to these doses, 0.1 ml undiluted antibotulinus serum is
injected subcutaneously. In the absence of reaction to this dose,
the entire dose of the serum is injected intramuscularly.)
If the patient has developed a positive reaction to one of this
dose, he/she is given 180-240 ml prednisolone as an intravenous
infusion, and the total therapeutic dose of antibotulinus serum is
injected after 30 min
The only contraindication for administration of antibotulinus
serum is anaphylactic shock that develops during determination
of sensitivity to a foreign protein.
 Polyvalent vaccine ( A,B,C and E antitoxins) IM once a day during
3-4 days (In severe cases, or if the treatment begins late after
the onset of the disease, the vaccine is administered at 6-8 hour
intervals for 2-3 days, and then 2 times a day)
 Chloraphenicol (500mg 4x/day) and Tetracycline (300mg 4x/day)
for 7-8days
17.Cholera. Stages of dehydration, маin clinical sings, diagnostics
methods, etiotropic therapy, treatment of dehydration.
Cholera is an acute intestinal disease which has tendency to pandemic
spread. This disease is common in many countries of the world.

Pathogen: Vibrio cholerae (gram negative)

Most common in developing countries
Transmission: fecal oral (undercooked seafood or contaminated water)
Incubation period: some hours – 5 days (average 2 days)
Pathogenesis: cholera toxin  stimulate adenylate cyclase via
activation of Gs  increase cyclic AMP - decrease absorption of
sodium and chloride by villous cell and increase ion (mainly chloride)
and water secretion into the intestinal lumen  profuse liquid stools

Stages of dehydration:
 1st stage (1-3% of body weight)
 2nd stage (4-6%) - slight decrease in volume of circulatory
plasma
 3rd stage (7-9%) - accompanied by a grater decrease in the
volume of circulating plasma, drop in pulse pressure, renal flow
 4th stage (10%) – development of dehydration shock (decrease
of the plasma volume оf peripheral circulation disturbances,
tissue hypoxia, decompensated metabolic acidosis and
respiratory alkalosis, severe hypotension cessation of
glomerularfiltration leads to dysfunction and nitrogenimia take
place)

Main clinical signs:

Typical form:
 Acute onset
 Abdominal disconfort and murmur
 Frequent stools (3-10x/day) – rice water appearance (clear fluid
with only flecks and mucus visible) and a slight fishlike odor
 Hypothermia (in severe cases may be subfebrile)
 Objective examination: tachycardia, xerostomia, and abdominal
murmur, painless and retracted belly.
2nd stage: recurrent abundant vomiting and repeated stools (15-
20x/day)
 Unstable cyanosis
 Muscle cramps of short duration in the feet and hands
 Skin turgor decreases
 Compensative metabolic acidosis
 Diuresis decrease
 Rise of relative density of blood increase (1.026-1.029) compared
to normal one 1.025
 Hematocritic index increases. (0.51-0.54) compared to normal
one 0.4-0.5

3rd stage:
 The cyanosis spreads over grater area of the body
 Tonoclonic cramps take place in separate muscle groups
 There is a further decrease of skin turgor, that is the patient's
features look sharpened, the skin on the hands becomes
wrinkled (this is so called hands of lawn - dress)
 The temperature is normal or drops below the normal
 The development of oliguria takes place
 The relative density of blood rises to 1.03-1.035
 Hematocritic index increase to 0.55-0.65
 There is further development of metabolic acidosis, hypokalimia,
hypochlorimia and compensative hyponatrimioa appear.

4th stage: shock develops; may occur in first 12h of disease

 Diarrhea and recurrent vomiting becomes more rare or they
cease at all
 The temperature falls to 35-34 C
 The cyanosis become diffuse
 The patient features sharpen still more; the “dark glasses” will
appear (symptoms). There is another symptom "the setting sun"
that is when the eyeballs are deep-set and turned upwards.
There is an expression of suffering which appears on the patient
face and called “faces cholera”
  The skin can be easily gathered into folds and doesn't flatten out
for a long time (sometimes during one hour) it is called “cholera
fold”
 Cardiovascular changes include tachycardia, thread like pulse,
arterial blood pressure is difficult to be taken as for the sounds
are hardly heard
 Breathlessness increases, the breath is arrhythmic and shallow,
the respiratory rate is 40 to 60 per minute
 The tonic cramps spread over to all groups of muscles including
the diaphragm which leads to excruciating hiccup
 The abdomen is retracted and soft, tender during abdominal
muscles cramps
 Usually anemia takes placed.
 Due to blood thickening the erythrocyte count rises to 6-8 in 10
liter of blood, leukocytosis and neutrophilic shifted to the left.
 The relative density of blood rises from 1.038 to l.05. Hematocrit
index increases to 0.6-0.7
 Nitrogen deficiency as well as potassium chlorine, and
hydrocarbonates increase.

Atypical forms:
 Dry: in weakened patient and it is characterized in acute onset
and rapid development of dehydration. Diarrhea and vomiting
are absent
 Fulminant: sudden onset and intensive development of
dehydrative chock with great liquid loss

Diagnostic methods:
 Dipstick test (rapid test)
 Stool culture (confirmatory): usually reveals fewer than 5
polymorph nuclear cells (high power field)
 Serological test: determining vibriosidal agglutinating and toxin-
neutralizing antibodies, the peak titers usually occur 7-14 days
after the onset of the illness. Vibriocidal and agglutination
antibody titers return to base line levels 8-12 week after the
onset, antitoxin titer remain elevated for up 12- 18 mo.
(retrospective diagnosis)
 Etiotropic therapy
Antibiotic therapy :
Tetracycline 500mg PO every 6h for 5days OR
Doxycycline 300mg PO single dose OR
Furasolidone 100mg PO 6/6h for 3days OR
Chloramphinicol 500mg PO 6/6h for 5 days

Before discharge from the hospital bacteriological investigation of

feces must be carry out after the end of treatment of antibiotics
following the cessation of treatment 24 -36 hours

Treatment of dehydration:
Initial rehydration: restore defict
Glucose electrolyte solution PO for 2-4h in value equal to the defict of
liquid and salt after Orealit and Rehydron are administered in volume
of electrolyte and liquid loses, which are determined by the volume of
excrement every 2 or 4 hours. Oral rehydration should be continued till
the cessation of diarrhea for one or 2 days.

Corrective rehydration: compesation of electrolytes and liquid losses

Polyionic solution should be warmed to 39 -40 degree before use. They
are usually giving during the first 2 hours in volume of 10% of body
weight. First 2-4 liters of solution are given through by stream infusion
(100-120 mill /min) after that solution are given by drop infusion at the
rate of 30-60 ml/min.

18.Typhoid fever. Forms of disease, маin clinical sings, characteristics

of feverish reaction & status thyfosus, diagnostics tests, treatment,
complications.
Typhoid fever is a severe multisystemic illness characterized by the
classic prolonged fever, sustained bacteremia without endothelial or
endocardial involvement, and bacterial invasion of and multiplication
within the mononuclear phagocytic cells of the liver,spleen,lymph
nodes, and Peyer patches.
  Pathogen: Salmonella typhi (gram negative rod, facultative
anaerobe, flagellated)
 Reservoir: humans
 Transmission: fecal oral
‐ Direct: person-to-person (handshake)
‐ Indirect: contaminated food and water
 Incubation period: 3-60 days (most commonly 7-14 days)

Forms of disease: (found in a lecture on google)

 Typical forms (mild, moderate and severe)
 Atypical forms
‐ Abortive - beginning is as typical, then the course is suddenly
disrupted and convalescence begins.
‐ Subtle - The main symptoms are not manifested.
Recognition is possible only in epidemic situations, using
bacteriological and serological examinations. Sometimes is
recognized only after specific complications
 Masked forms (pneumotyphus, colitis like, cholangitis like,
meningitis like, encephalitis like, sepsis like): In the clinical
picture there is a background of not clearly expressed symptoms
and domination of organ or organsystem signs. The most severe
masked form is colitis like typhus, which has high case fatality
rate. Post mortem diagnosis is common.

Main clinical signs:

The classic sings of enteric fever include fever, toxemia, delirium,

abdominal discomfort, constipation and hepatosplenomegaly

Bacteremia: chills, diaphoresis, anorexia, dry cough, a dull frontal

headache, and myalgias before onset of high fever.

 1 week: swell of lymph nodes in ileum.

‐ Body temperature rises gradually
‐ Relative bradycardia (Physiologically, the heart rate increases
in proportion to body temperature (for every degree Fahrenheit,
the heart rate should increase ∼ 10 beats/min). In typhoid fever,
 this physiologic response is typically reduced. Thus, the heart
rate is only moderately increased despite a high fever.)
‐ Constipation or diarrhea (Foul-smelling diarrhea, comparable to
pea soup, often occurs after generalized dissemination of the
pathogen (week 2))
‐ Headache

 2 week: central part of lymphoid formation, lymphoid folliculs

become dirty grey-green color.
‐ Persistent fever without chills; mostly unresponsive to
antipyretics (>38º with diurnal variation of <1º)
‐ Rose colored spots: exanthema in lower chest and abdômen
(most commonly around navel) - subtle, extremely sparse (often
< 5 spots), salmon- colored, blanching, truncal, maculopapular
rash with 1-4 cm lesion that generally resolve within 2-5 days
‐ Typhoid tongue: greyish/yellowish-coated tongue with red edges
‐ Non specific abdominal pain and headache
‐ Yellow-green diarrhea – comparable to pea soup (caused by
purulent, bloody necrosis of peyers patches), or obstipation and
bowel obstruction (as a result of swollen peyers patches in
ileum) – 6-8x/day
‐ Neurological symptons (delirium, coma) – S.typhii toxins can
cross BBB leadin to confusion and drowsiness

 3 week: deep mucosa and submucosa defected.

Clinical features of week 2 + possible complications, that include:
‐ Gastrointestinal ulceration with bleeding and perforation
(pathogen induce necrotic inflammation)
‐ Hepatosplenomegaly
‐ In rare cases: sepsis, meningitis, myocarditis and renal failure

 4 week: period of clear ulcer: ulcer with clear fundus and slightly
swelled adjacent.
the fever, mental state, and abdominal distension slowly improve
over a few days, but intestinal complications may still occur in
surviving untreated individuals
  5 week: heal of ulcer with slight pigmentation.

Characteristic of feverish reaction and status typhosus:

Status typhosus (neurotropic action) –

occurs classically with typhoid and typhus fevers but is also seen in
other infectious diseases. Clinical descriptions of this state as
"muttering delirium" or "coma vigil" refer to the peculiar preoccupied
nature of the stupor. Picking at the bedclothes and at imaginary
objects (carphology and floccillation) are characteristic, as is muscular
twitching (subsultus tendinum).

Diagnostic test:

Laboratory:
 CBC: anemia, relative leucopenia (absolute eosinopenia and
relative lymphocytosis), thrombocytopenia, increase ESR (in
adults – leucopenia; children – leukocytosis)
 Biochemical blood: incrreased ALT, AST and bilirubin levels; mild
hyponatremia ad hyppokalemia
 Serological tests: Indirect hemmaglutination, indirect
fluorescence Vi antibody and ELISA, Widal test (will be positive
from 2 week)
 Bacteriological examination: e, blood, intestinal secretions, and
stool culture results are usually positive in approximately 85-
90% of patients with typhoid fever. It can also be isolated from
the cerebrospinal fluid, peritoneal fluid, mesenteric lymph
nodes, resected intestine, pharynx, tonsils, abscess, bone and
urine, among others.
Bacteremia is detectable in week 1 of disease. Stool culture may
be positive from week 2-3. Bone marrow culture may be positive
even after antibiotic treatment
 DNA testing: PCR

Serological tests supports diagnosis but should be confirmed with

cultures or DNA evidence
Instrumental exam:
Radiography of the kidneys, ureters, and bladder are useful in the
clinician suspects bowel perforation. CT scanning or MRTI may be
warranted to investigate abscesses that may occur in, among other
sites, the liver or bones.

Treatment
 Antibiotic therapy:
‐ Fluroquinolones: Ciprofloxacin OR
‐ 3rd generation Cephalosporin: Ceftriaxone or Cefotaxime

Cefixime is a suitable oral alternative. Antibiotics, such as ampicillin,

chloramphenicol, trimethoprim-sulfamethoxazol, amoxicillin and
ciprofloxacin, have been commonly used to treat typhoid fever in
developed countries.

 Supportive treatment: Fluids, electrolytes and nutrition

Complications

 Chronic Salmonella carriage (positive stool culture 12 months

after disease; asymptomatic; Tx: ciprofloxacin at least 1 month)
 Intestinal perforation
 GIT bleeding
 Infectious toxic shock (profound hemodynamic disorder,
pulmonary and brain edema, acute adrenal failure)
 Jaundice – may be due to hepatitis, cholangitis, cholecystitis or
hemolysis
 Pancreatitis and simultaneous acute renal failure and hepatitis
with hepatomegaly have been reported
 Toxic myocarditis - in patients who are severely ill and toxemic
and is characterized by tachycardia, weak pulse and heart
sounds, hypotension, and electrocardiographic abnormalities
 Pericarditis
 Toxic confusional state - disorientation, delirium, and
restlessness, is characteristic of late-stage typhoid
  Convulsions
 Meningismus
 Immune complex glomerulitis and proteinuria, nephritic
syndrome

19.Hepatitis A. Clinico-biocchemical syndromes, stages of the disease,

clinical sings, laboratory findings, principles of therapy.
 Pathogen: hepatitis A vírus (HAV) (Family:Picornaviridae, genus:
hepatovirus)
 Reservoir: humans
 Transmission: fecal oral (contaminated water and food)
 Incubation period: 7-50 days (more commonly 15-30 days)
 Infectious period: 2 weeks before – 1 week after the onset of
illness

HAV is not cytopathic in itself, research suggest that liver damage is

caused by cellular immunity (especially CD8+ T cells)

Clinico-biochemical syndromes:
 Influenza like syndrome: fever (38ºC), chill, headache,
lassitude, and catarrhs
 Dyspeptic syndrome: poor or completely lost appetite,
nausea, vomiting, discomfort, distension in the epigastrium
or dullpain in the epigastrium and right hypochondrium
 Asthenovegetative syndrome: radually develops lassitude,
the working capacity decreases,the patient becomes irritable,
his sleep deranges, he develops headache.
 Arthralgic syndrome: myalgia, pain in the bones andjoints in
the absence of visible deformations, erythema or swelling.
 Jaundice syndrome: Icteric sclera, skin and visible musoca.
Liver is enlarged, the urinebecomes dark (beer-coloured) due
to increased urobilinogen content. Faeces are sometimes
discoloured (clay-coloured), the bilirubin(especially
conjugated bilirubin) in the blood serum increases
 Cytolysis syndrome: elevation of ALT, AST
  Cholestatic syndrome: ↑ bilirubin,, ↑ cholesterol, ↑ akaline
phosphatase, ↑ gamma glutamyl transferase (+ jaundice with
pruritus)

Stages of the disease and clinical signs:

1. Prodormal phase (1-2 weeks on avarage, but can last till 30

days)
 Right upper quadrante pain, tender hepatomegaly
 Fever (38ºC), malaise
 Anorexia, náusea, vomiting
Influenza like syndrome, Dyspeptic syndrome,
Asthenovegetative syndrome, Arthralgic syndrome

2. Icteric phase (7-15 days) – Jaundice syndrome

 Jaundice
 Dark urine and pale stools
 Pruritus

3. Resolution of symptons
 Lessening and then disappearance of jaundice, normalization
of the faecal colour and excretion of a great amount of light
urine.
 The clinical symptoms of the disease rapidy subside with the
onset of the recovery phase.
 The serum bilirubin and the activity of alaninetransaminase
normalize.
 The index of the thymol turbidity testremains high for a long
time.

*HAV infection in children is typically asymptomatic. The risk of

symptomatic disease increases with age and coinfection (ex.: with
hepatitis B)

Laboratory findings:
  CBC: ↑ ESR
 Biochemical blood analysis:
‐ ↑ AST and ALT ( >1000 IU/L) – serum ALT > AST (AST/ALT
ratio < 1) preceeds bilirubin elevation
‐ ↑ Bilirubin
‐ ↑ Alkaline phosphatase
‐ ↑ acute phase proteins
 Immunogram: ↑ immunoglobulin levels
 Serological exam:
‐ anti-HAV IgM – acute HAV infection; peaks during the
acute or early convalescent phase of the disease and
remains positive for approximately 4-6 months. It may
persist at a low titre for 12-14 months in patients with a
protracted or relapsing course
‐ anti-HAV IgG – appear early in the convalescent phase of
the disease and remain detectable for decades. In adults
who are vaccinated against HAV, antibodies become
detectable 2 weeks after vaccination, but titres are 10-
100-fold lower than levels induced by wild-type infection.
 Virological exam: PCR (from stool, body fluids, serum and
liver tissue) – may be detected for at least 81 days after onset
of disease

Principle of therapy:
Disease is self limited, so treatment is mainly supportive

Mild disease:
 Bed rest as long as needed
 Sparing liver diet: Fried, smoked or pickled food, and also
alcohol should be excluded. Taking much liquid (2-3 litres a
day) as stewed fruits, tea with lemon, fruit juices, and the
like, is recommended.

Moderate disease with toxemia:

 Detoxification therapy - A 5-10 per cent glucose solution,
Ringer-Locke solution (250-500 ml each) with an addition of
 10 ml of a 5 per cent ascorbic acid solution should be given
by drip infusion. Nicotinic acid (60 mg), thiamine (6 mg),
riboflavin and pyridoxine should also be given

Severe form:
 Move to intensive therapy unit or other ward where they can
be properly observed by a neurologist (twice a day).
 Their acid-base and water-salt equilibria should be
controlled; coagulograms should be taken, and daily diuresis
measured.
 Detoxicating preparations should be given.
 Oliguria should be treated with furosemide (0.02- 0.04 g) in
combination with verospiron (0.025 g 3-4 times a day).
 In order to eliminate hypokalaemia, panangin (10-20 ml)
should be administered. Vikasol (1 per cent solution, 2-5 ml)
should be given intramuscularly for haemorrhage.
Prednisolone is indicated of encephalopathy.

20.Hepatitis B. Epidemiology, pathogenesis, clinical manifestations,

markers of disease, biochemical tests, treatment.

Epidemiology

 Pathogen: hepatitis B vírus (HBV) (Family: Hepadnavirus) – doble

strand DNA
 Reservoir: humans
 Transmission: sexual, parenteral/percutaneous, perinatal
 Incubation period: usually 60-120 days (6 weeks – 6 months)

 HBV is a global public health problem with more than 350

million persons estimated to be chronically infected with the
virus.
 HBV can present with a variety of clinical syndromes
including acute hepatitis, chronic liver disease, cirrhosis or
hepatocellular carcinoma (HCC).
  HBV-related liver disease accounts for more than half a
million deaths per year and 5-10% of cases of liver
transplantation.
 The outcome of HBV infection depends on the age at
infection, level of HBV replication, immune status of the host,
co-infection with other viruses and comorbidities such as
alcohol abuse and obesity
 The younger when infected, the more likely a patientt
develops chronic HBV
 Hepatitis B virus can be found in the blood 2-8 weeks before
the onset of the disease during the prodromal period and
during 2-3weeks of the clinically manifest jaundice.
 Hepatitis B virus persists in the organism for a long time after
convalescence (from 4 months to13 years and longer)
 Virus B can be found in the saliva, urine, semen and other
biologic fluids or faeces

Pathogenesis
Virus enter in blood  carried to liver, macrophages and other
organs  vírus alters composition of hepatocyte plasma menbrane
 immune resposnse  cytolysis and mesenchymal inflammatory
changes  disturbed liver architecture  cholestasis

Secondary and subsequent invasions of the virus in the blood

accounts for the unduiant course of the disease, its exacerbations,
and transition into the chronic form. Increasing specific immunity
eradicates the virus from the patient.

Clinical Manifestations

1. Pre-icteric period ( 1st day to several weeks, or can be absent)

 Body temperature rises in some patients.
 Dyspepsia, arthralgia and the as the no vegetative
symptoms are more common for hepatitis B.
 The liver is enlarged, some patients complain of pruritus
and urticaria like allergic itching rash.
Serum-sickeness like syndrome (rash, arthralgia, myalgias, fever)
 2. Icteric period/Clinical jaundice
 yellow colouration of the sclera, visible mucosa, and skin
 Right upper quadrante pain
 clinical symptoms of the prodromal period intensify.
 The liver enlargement continues, its edge is tender to
palpation.
 The spleen is also enlarged in many cases.

3. Recovery phase
The disease ismore severe and is likely to transform into a
protracted (from 3 to 6months) chronic active hepatitis or
chronic persistent hepatitis. A persistent elevation of serum
ALT for longer than 6 months indicates a progression to chronic
hepatitis.

4. Chronic hepatitis B:
 Many patients are asymptomatic while others have non-
specific symptoms such as fatigue.
 Some patients experience flares of disease which may be
asymptomatic or mimic acute hepatitis.
 Physical examination may be unremarkable or there may be
stigmata of chronic liver disease and splenomegaly.
 Patients with decompensated cirrhosis may present with
jaundice, ascites, peripheral oedema and encephalopathy.

Markers of disease:

HBV surface antigen (HBsAg) is the key marker of HBV infection,

present in serum during acute and chronic infection. HBsAg appears
in serum 1–10 weeks after exposure, before the onset of symptoms
or raised ALT. Inpatients who recover, HBsAg becomes undetectable
after 4–6 months. Persistence of HBsAg for more than 6 months
implies chronic infection. Clearance of HBsAg is followed by
development of anti-HBs. Rarely, anti-HBs may not appear until
several weeks after HBsAg is lost. During this ‘window period’,
diagnosis is by the detection of IgM anti-HBc. Some HbsAg+ patients
also have anti-HBs. They should be regarded as carriers.

HBV core antigen (HBcAg) is an intracellular protein, which is not

found in serum. Anti-HBcIgM is detected during acute infection and
may be the only indicator of HBV if there is a window period (see
above). IgM may remain detectable up to years after the acute
infection, and may reappear during exacerbations of chronic
hepatitis B. IgG anti-HBc persists life long, with anti-HBs in patients
who recover, and with HBsAg in chronic infection. Isolated anti-HBc
with neither HBsAg nor anti-HBs sometimes occurs and indicates
either:
‐ the window period of acute hepatitis B (mostly IgM);
‐ many years after recovery from acute hepatitis B when anti-
HBs has fallen to undetectable levels;
‐ after many years of chronic HBV infection when the HBsAg has
been cleared (which occurs in 1% of carriers).
Individuals with isolated anti-HBc may be infectious, and will not be
detected if HBsAg is used as the only screening test for infectivity.

Hepatitis B e antigen (HBeAg) is a marker of viral replication and

high infectivity; usually associated with the presence of HBV DNA in
serum. Loss of HBeAg and development of anti-HBe occurs early
during acute infection, before HBsAg to anti-HBs seroconversion. In
chronic infection, HBeAg may persist and is associated with high
infectivity (‘supercarriers’)and active liver disease. Loss of HBeAg
and development of anti-HBe is usually associated with the loss of
HBV DNA from serum and remission of hepatitis. Some patients
continue to have active liver disease and detectable HBVDNA after
HBeAg seroconversion. In some cases, this is due to the presence of
a mutation that prevents the production of HBeAg (so called‘precore
mutants’).
During window period, anti-HBc IgM and anti-HBe may be the only
markers available to diagnose na acute HBV infection
Seroconversion of HBsAg to anti-HBs indicates immune clearance of
HBV

Biochemical tests:

Acute hepatitis:
 ↑ AST and ALT
 AST/ALT ratio <1 (>1 in fulminante infection)
 ↑ gamma-glutamyl transferase
 ↑ ferritin
 ↑ bilirubin
 ↑ Alkaline phosphatase
 Hypoalbuminemia, hypergammaglobulinemia

Chronic hepatitis:
 High variablility: mildly ↑ or unchanged AST and ALT
 AST/ALT ratio >1
 ↑ gamma-glutamyl transferase
 Treatment:
LIFESTYLE CHANGES:
 Weight loss
 Cessation of substance use (alcohool)
 Discontinuation of hepatotoxic medication (ex.:
acetoaminophen)

PHARMACOLOGICAL:
 Interferon alpha (IFN) - recommended for patients with
positive HBeAg, positive HBV DNA, raised ALT and chronic
hepatitis on liver biopsy. Duration of therapy 3-6 months
 Pegylated IFN - Lamivudine (appears to be effective in
patients with precore mutants) – indicated specially in
young patients with compensated liver disease

SURGICAL:
Liver transplantation in end-stage liver disease due to HBV or
fulminante hepatic failure

21.Hepatitis C. Epidemiological features, pathogenesis, clinical

manifestations, laboratory data, markers of disease, principles of
therapy.

Epidemiological features:

 Pathogen: Hepacivirus C (HCV) – Hepacivirus genus, Flaviviridae

family (single strand RNA)
 Reservoir: humans
 Transmission: parenteral/percutaneous, organ transplant,
perinatal, sexual (rare)
 Incubation period: 2 weeks – 6 months
 HCV is a major global cause of chronic liver disease with an
estimated 130 million people infected worldwide.
 Acute infection is often asymptomatic and liver failure is rare.
 Acute HCV infection usually leads to chronic infection: 60-80% of
cases develop chronic HCV infection and 20-30% of these
develop cirrhosis over a 20-30-year period.
 Acute HCV infection accounts for 10-20% of cases of acute
hepatitis.
 Chronic HCV infection is the most frequent indication for liver
transplantation.
 Hepatitis С is the cause of 27% of cirrhosis cases and 25% of
hepatocellular carcinoma worldwide

Pathogenesis:
HCV is not cytopathic, but the host’s immune response in an
attempt to fight the virus is the cause of liver damage due to long-
lasting inflammation. Acute selflimiting HCV infection is associated
with a strong and consistent multi-specific CD4+ and C8+ T cell
responses against the epitopes of viral proteins, whereas the
probable reasons for the persistence of HCV despite such responses
are:
‐ extensive mutations during HCV replication, leading to
multiple viral species in a single patient;
‐ Mutations that prevent antigen presentation;
‐ the inhibition of intracellular interferon (IFN) signalling;
‐ the functional impairment of CD8+ T lymphocyte responses;
‐ viral inhibition of host defences.

Clinical manifestations:
Most acute infections are asymptomatic (80%) or have a clinically
mild course lasting 2-12 weeks:
 Malaise, fever, myaalgia, arthralgia
 RUQ pain, tender hepatomegaly
 Náusea, vomiting, diarrhea
 Jaundice, possibly pruritus (< 25% of symptomatic cases)

Chronic infection:
  Findings are often mild, nonspecific (ex.: fatigue)
 Liver cirrhosis (up to 25% of cases) within 20 years of infection
 Extrahepatic features are common ( HCV may trigger
autoimune and immune complex reactions), such as: Mixed
cryoglobulinemia, lymphoproliferative disorders, thyroid
autoimmune disorders and type 2 diabetes

Laboratory data: (AMBOSS)

Biochemical blood:
 ↑ AST and ALT with AST/ALT ratio:
‐ < 1: acute hepatitis
‐ >1: chronic hepatitis
 ↓ Total protein/albumin, acoagulation (particularly ↑
prothrombin time), ↓ cholinesterase
 Cholestasis parameters: ↑ gamma-glutamyl transferase, ↑
alcaline phosphatase, ↑ bilirubin

Inflammatory markers:
 Leukocytosis
 ↑ ferritin

Liver biopsy:
 Acute: macrovesicular steatosis, bile duct injury, sinusoidal
inflammation of hepatocytes
 Chronic: lymphoid follicles in portal triad, necroinflammation
of periportal liver cells, variable degree of fibrosis, severe
hepatocyte injury

Markers of disease:
 Anti-HCV antibodies - positive in case of acute, chronic and
previous HCV infection (20-150 days; mean 50 days after
acute expousure)
 HCV RNA (PCR) – detectable 7-21 days after acute expousure
‐ If positive PCR: active HCV infection (may be acute or
chronic)
‐ If negative PCR: no infection, but prior infection (In these
cases, the infection has either cleared spontaneously or
 been successfully treated. However, it is also possible that
the HCV titer may be temporarily below the level of
detection. In such cases, HCV infections should be
monitored for a period of one year.)
Spontaneous clearance of HCV infection, however, confers no
protection against reinfection

Principles of therapy
General recommendations: avoid hepatotoxic (ex.: acetaminophen)
and alcohol use

Pharmacological:
The goal of antiviral therapy is to eradicate HCV RNA and achieve a
sustained virological response (SVR), defined as being HCV RNA
negative 6 months after completing antiviral therapy
The decision to treat patients with chronic HCV infection is based on
a number of factors including HCV RNA positivity, liver biopsy with
chronic hepatitis and fibrosis, compensated liver disease, acceptable
haematological and biochemical indices, ability to adhere to
treatment and no contraindications to treatment. Additional factors
such as alcohol or drug use, chronic kidney disease or prior liver
transplantation may also influence treatment decisions.
 Pegylated interferon alfa and Ribavirin

22.Hepatitis E. Routes of transmission, characteristics of prodromal

period, main clinical sings, laboratory findings, markers of disease,
treatment.

Routes of transmission
 waterborne or enterical transmission through contaminated water
 faeco-oral transmission since the HEV is excreted in stool
 In endemic areas - transmitted by blood transfusion and vertically from mother to
child during the third trimester of pregnancy

characteristics of prodromal period

 The incubation period of HEV infection ranges from 15 to 60 days
Associated with symptoms such as,
 Jaundice
  Fever
 loss of appetite
 abdominal pain
 lethargy
 myalgias
 arthralgias
 Prominent GIT dyspepsia: anorexia and distaste for cigarettes are frequent, and
nausea, vomiting, diarrhea may follow; with a steady upper abdominal pain

main clinical sings

Jaundice is usually accompanied by
 Malaise
 Anorexia
 Nausea
 Vomiting
 abdominal pain
 fever and hepatomegaly.
Other less common features include,
 Diarrhoe
 Arthralgia
 pruritus and an urticarial rash.

According to old prep,???

1. Prodromal period: symptoms of intoxication, subfebrile temperature, abdominal
pain and dyspepsia
• End of pre-icteric period:
- Dark urine with pale feces, hepato+/- splenomegaly
• Clinical jaundice (2-3 weeks):
- Sclera, visible mucosa and skin become icteric (jaundice), +/- pruritus; with transient
worsening of prodromal symptoms
- tender hepato+/- splenomegaly
• Recovery/ convalescence:
- gradual constutitional symptoms improvement
- recedes jaundice and regresses liver enlargement
- majority patients recover in the course of 3-6 weeks

laboratory findings
Through biochemical blood analysis

a)Cytolytic
• Increase serum ALT, AST and Increase serum bilirubin level (unconjugated level
increase) - which usually resolve 1-6 weeks after the onset of the illness.
• Decrease prothrombin index, protein, serum albumin level
b) Mesenchymal
• Increase beta & gamma globulin
• Thymol test increase
• Sublimate test decrease
c) Cholestasis
• Increase conjugated bilirubin level
• Increase bile acid level
• Increase of cholesterol (beta-lipoproteins)
• Increase alkaline phosphatase activity

And stool analysis - HEV can be detected in the stool one week after the onset of illness

markers of disease
 antibodies to HEV
 detection of HEV in serum or stool by PCR.
 Anti-HEV IgM - appears early in the course of illness and disappears over 4-5
months.
 Anti-HEV IgG - appears shortly after the anti-HEV IgM and increases
 through the acute phase and convalescent phase, remaining elevated for up to 14
years.
 anti-HEV IgA – improve specificity as the IgM assay may cross-react with other
IgM-based assays such as rheumatoid factor IgM.
 And other laboratory markers as indicated above

Treatment
 Mainly supportive treatment – oral ribavirin
Other than that,
 Travellers to endemic areas should avoid drinking water that is not boiled or
purified and consuming uncooked fruits, vegetables, meat and shellfish
 vaccination

23.Hepatitis D. Epidemiology, pathogenesis, clinical manifestations,

markers of disease, biochemical tests, treatment.

Epidemiology

 HDV infection is endemic in the Mediterranean basin where infection occurs in

children and young adults through mucosal or percutaneous spread, which is usually
inapparent.
 Transmission within families is common and may be associated with poor hygiene
and lower socioeconomic status
 The prevalence of HDV among HBV carriers in the Far East is variable, ranging
from 90% in the Pacific islands to 5% in Japan
 HDV transmission has been associated with sexual transmission in Taiwan and
injection drug use in Hong Kong
  HDV infection is uncommon in industrialized countries and is mainly confined to
certain populations, e.g. injection drug, users, haemophiliacs and multiply
transfused patients.
 The epidemiology of HDV is changing with in certain countries, e.g. falling rates in
Italy as a result of improved socioeconomic conditions and HBV vaccination and
prevention programmes.
 In contrast, other areas of the Mediterranean and Central Europe report rising rates,
which may be related to immigration from endemic countries or highrisk behaviours
such as injection drug use

Pathogenesis

2 forms are present

• HDV- HBV Co-infection
• HDV – Super infection
Majority of cases are HDV – HBV – co-infection
The liver cell destruction associated with 3 main factors
1. HDV-related factors (e.g. HDV genotype and expression of specific HDAg species)
2. HBV-related factors (e.g. HBV genotype and level of replication)
3. host immune response.
And also direct cytopathic damage during acute infection and immune mediated damage
during chronic infections

clinical manifestations

it is varying from the asymptomatic state to decompensated chronic liver disease

A) HDV-HBV co-infection resembles uncomplicated HBV infection. There are four main
stages:
o Incubation period: 30 – 180 days ( 1 – 6 months)
o Prodromal 4-10 days à dyspeptic syndrome, asthenovegetative, athralgia, mixed
o Icteric period (the condition worsens with icteric period)
o Convalescence
• The onset can be with nausea, vomiting, decrease appetite, fatigue, malaise, myalgia,
urticaria, and macular popular rashes with polyarthritis, maybe present too
• Dark colored urine and clay colored stool at the end of prodromal period with the
appearance of jaundice the condition of pt worsens
• Hepatomegaly and splenomegaly may be present during recovery must of the clinical
signs disappear
• But liver enlargement and biochemical changes may be present
• Recovery usually in 3-4 months
B) In HDV superinfection: acute disease is more likely to be progressive and severe leading
to cirrhosis and persistant HDV à hepatic failure

markers of disease
 HBsAg – positive
 acute HBV/HDV co-infection are also positive for anti-HBcIgM
  HDV super-infection or chronic HDV infection are negative for anti-HBcIgM.
 Serum HDV RNA also appears early in the course of acute HBV/HDV co-infection
and HDV superinfection; in the former HDV RNA is transient whereas in the latter
it is persistent
 Serum total anti-HDV antibody is usually detectable 4 weeks after acute HDV
infection

biochemical tests
Elisa ( serum ab to ag HCV), serum anti – HVC ↑
- Aminotransferase ↑
- Recombinant immunoblot assay (RIBA) HVC RNA determination
- PCR
- Hepatitis C ab tests, genotyping, qualitative & quantitative RNA test

Treatment
 the primary aim is suppression of HDV replication (HDV RNA negativity in blood)
which is accompanied by normalization of the serum ALT and improvement in
hepatic inflammation
 A secondary aim is to eradicate HBV infection with conversion of HBsAg to anti-
HBs and thus to protect the patient from reinfection with HBV or HDV.
 Interferon-α treatment
 Liver transplantation for fulminant acute & end stage chronic
 Prevention : vaccination for early hepatitis B , education to avoid risk factors

24.Shigellosis. Epidemiology, pathogenesis, clinical manifestations,

diagnostics methods, principles of therapy.

Epidemiology
 One hundred eighty-eight million cases of Shigella diarrhea or dysentery occur
annually worldwide, with 164,000 associated deaths .
 Among children under the age of five years in low and middle income
countries, Shigella species are the most common cause of dysentery and the second
most common cause of diarrhea overall.
 Shigella transmission can occur through direct person-to-person spread or from
contaminated food and water. The minimal infectious dose can be transmitted
directly from contaminated fingers, since intermediate bacterial replication is not
required to achieve the low infectious dose.
 In resource-rich countries, most cases are transmitted by fecal-oral spread from
people with symptomatic infection.
 Outbreaks among men who have sex with men, particularly with drug-resistant
isolates are increasingly reported .
 In resource-limited countries, both fecal-oral spread and contamination of common
food and water supplies are important mechanisms of transmission.
 Pathogenesis
 After oral inoculation, Shigella pass to the terminal ileum and colon where invade
and proliferate within epithelial cells, spreading from cell to cell.
 Bacillary dysentery is an invasive infection of the colonic and rectal mucosa
that tends to remain local.
 In severe cases, the invasive process also may affect the terminal ileum. The disease
process is cauterized by an acute inflammation of the intestinal mucosa with
ulceration of the epithelium

clinical manifestations
 Mild fever with mild diarhhea
 frequent passage (usually 10 to 30 times per day) of small-volume stools consisting
of blood, mucus, and pus, this diarrhea is accompanied by abdominal pain,
especially in the left lower quadrant
 Tenesmus - the painful straining with stooling that may lead to rectal prolapse.
 Severe shigellosis can progress to toxic dilatation and colonic perforation. Rarely,
Shigella bacteria can affect other parts of the- body that are far from the digestive
tract.
 When this happens, there can be seizures, confusion or coma, kidney failure,
arthritis, rashes or other symptoms shigellosis can be severe and lead to life-
threatening dehydration and other complications within a few days

Diagnostic methods
Laboratory examination
 Stool analysis – culture of shigella
 PCR
 Serological tests -antibodies to somatic antigens develop early in the acute phase of
disease
 Common blood analysis – neutrophilic leukocytosis, anemia due to blood loss with
hemorrhagic diarrhea, prerenal azotemia, or (if watery diarrhea has been
pronounced) hyperchloremic acidosis

Instrumental examination
 Sigmoidoscopy - reveal hyperemia and whitish exudates, and in severe
cases an extensive pseudomembranous colitis may be present.

Principles of therapy

Lifestyle modification
 Good hygiene, especially frequent hand washing.
 Wash your hands immediately after changing a child's diaper, especially if the child
has diarrhea.
 Dispose of soiled diapers in closed-lid garbage cans.
 Swim only in lakes and pools whose water quality is monitored by local health
officials.
  drinking only treated or boiled water,- and eating only foods that have been cooked
thoroughly. Never eat unpeeled fruits, and always peel fruits yourself immediately
before eating them.
Pharmacological therapy
 fluids to treat dehydration
 antibiotics such as ampicillin (Polycillin, Totacillin, Omnipen), trimethoprim –
sulfamethoxazole (Bactrim, Septra and other brand names), tetracycline (sold under
many brand names), or ciprofloxacin (Cipro).
 And other symptomatic treatment

25.Salmonellosis. Epidemiological features, pathogenesis, clinical sings,

diagnostics, treatment.

Epidemiological features
 The source of infection is man and animal.
 The main epidemiologic role belongs to animals in which the disease is clinically
manifest or is characterized by the carrier state. From an infected animal the
microorganisms are released with faeces, urine, milk, saliva, and nasal discharge.
Infected cattle and pigs are the greatest danger. Horses, sheep, cats, dogs and
rodents (mice and rats) can also be the source of infection. Birds, especially
waterfowl, in which the salmonellae can be found not only in flesh but in the eggs
as well, are also important epidemiologically.
 Examination of animals and their meat reveals salmonellae in cattle (from 1 to 5 per
cent), in pigs (from 5 to 15 per cent), in sheep (from 4 to 30 per cent), and in ducks
and geese (to 50 per cent). Mice and rats are carriers in about 40 per cent of cases,
and about 10 per cent of cats and dogs are carriers too. Human patients and carriers
are also the source of infection. People working at kindergartens, food catering and
the like establishments are a special danger for the surrounding people.
 The transmission factors are foods in which salmonellae not only survive but
also multiply. Man is usually infected by ingestion of meat, milk, fish, etc. heavily
infested with salmonellae as a result of inadequate handling, cooking, and storage.
 Meat can be infected during slaughter of the diseased animals, as a result of
neglected sanitary rules at slaughterhouses (intestinal contents of the diseased
animals can get on meat of slaughtered healthy animals), during transportation, im-
proper cooking and processing, and storage. Contact infection is possible during
intimate association with a patient or a carrier, less frequently with animals.
 Infants are mostly infected by contact.
 Nosocomial (intrahospital) outbreaks of salmonellosis are possible in children, who
are weakened by coexisting diseases, especially premature infants, neonates, infants
under two years of age, asthenic persons, patients with other diseases and the aged.
 Since salmonellae are stable in the environment, they can be distributed with
water and dust. People are quite sensitive toward toxins produced by salmonellae,
and outbreaks of the disease are therefore possible among people who ingest
foodinfected with salmonellae and their toxins.
  The incidence of salmonellosis is higher during the warm (especially hot) season
since the conditions for multiplication of salmonellae are most favourable during
this seasons, and besides, the incidence of the disease among cattle is also the
highest in summer

pathogenesis
 An infectious process can begin only after living salmonellae (not only their
 toxins) reach the gastrointestinal tract.
 Part of the microorganisms are killed in the stomach, while the surviving
salmonellae enter the small intestine and multiply in tissues (localized form).
 By the end of the incubation period, the macroorganisms are poisoned by
endotoxins that are released from the dead salmonellae.
 The local response to the endotoxins is enteritis and gastrointestinal disorder.
 In the generalized form of the disease, salmonellae pass through the lymphatic
system of the intestine into the blood of the patients (typhoid form) and are carried
to various organs (liver, spleen, kidneys) to form secondary foci (septic form).
 Endotoxins first of all acts on the vascular and nervous apparatus. This is
manifested by increased permeability and decreased tone of the vessels, upset
thermal regulation, vomiting and diarrhoea.
 In severe forms of the disease, much liquid and electrolytes are lost to upset the
water-salt metabolism, to decrease the circulating blood volume and arterial
pressure, and to cause hypovolaemic shock.
 A septic shock can develop. Shock of mixed character (with signs of hypovolaemic
and septic shock) are more common in severe salmonellosis. Oliguria and azotaemia
develop in severe cases as a result of renal involvement due to hypoxia and
toxaemia.

clinical sings

The incubation period varies depending on the mechanism of infection and

lasts from 6 to 24 hours, when salmonellae are ingested, and for 2 and more days if
infection is transmitted by contact.
The following forms of salmonellosis are distinguished:
(1) gastrointestinal (localized), that runs a coursesimilar to that of acute gastritis,
gastroenteritis, or gastroenterocolitis;
(2) generalized form, that runs a typhoid and septic course;
(3) carrier state (acute, chronic, transient).
The gastrointestinal form.
 The onset is acute.
 The body temperature rises;
 weakness, headache, chill, nausea, vomiting develop; the appetite impairs, and the
patient complains of epigastric pain.
 When the disease is at its height in 1-2 days, diarrhoea begins. Stools are usually
ample, with admixtures of mucus, or watery, without pathological admixtures. The
duration of the disease and its symptoms depend on severity of the disease. In mild
 forms the body temperature is normal or subfebrile, vomiting occurs only once,
abdominal pain is not severe, stools are watery, five times a day.
 The patient recovers in 2-3 days. The liquid loss does not exceed 3 per cent of the
body weight. The onset of salmonellosis of moderate severity is acute, the body
temperature rises to 38-39 °C and persists for 4 days; vomiting is repeated, stools
are ample and fetid, to 10 times a day, cramps in the limbs are common.
The gastroenterocolitic form is characterized by mucous stools, sometimes
with streaks of blood.
 Diarrhoea persists for 7 days.
 Tachycardia and dehydration of the first and second degree (liquid loss to 6 per
cent) are possible.
 In severe cases, the symptoms manifest to their maximum extent already during the
first hours of the disease.
 The temperature rises to39 °C, the patient develops chill, repeated vomiting, that
rapidly becomes incoercible, and frequent (10-20 times a day) am-ple, fetid, watery
stools.
 If water-salt metabolism is upset (dehydration of the second or third degree), the
patient develops cramps, pallor with a cyanotic hue, skin dryness, and hoarse voice
that transforms into aphopia.
 The loss of moisture is from 7 to 10 per cent of body weight. The amount of urine
excreted decreases; pathological admixtures appear, such as protein,
erythrocytes and casts.
 Arterial pressure falls, tachycardia develops.
The generalized form.
 The disease can begin with gastroenteritis or fever without signs of this disease,
whose clinical manifestations are similar to those of typhoid and paratyphoid fever.
 The septic form, which usually occurs in infants, is characterized by acyclic
character, prolonged and severe course, remittent fever, chills and profuse sweats,
tachycardia, spleno- and hepatomegaly.
 Secondary septicopyemic foci of various localization (pneumonia, pleurisy,
osteomyelitis, arthritis, tonsillitis, cervical purulent lymphadenitis, meningitis) are
formed.
Carrier state.
 Acute and chronic carrier state occur in convalescents.
 Acute carrier state probably lasts to 3 months, chronic over three months.
 A transient carrier state is characterized by the absence of clinical symptoms of the
disease, the bacillus is isolated only once or twice at 1 day interval with subsequent
negative cultures and reactions of indirect haemagglutination with
salmonellousdiagnosticum.

Diagnostics
 clinical findings, a thoroughly collected epidemiologic anamnesis and laboratory
findings.
 Bacteriologic studies- (before commencement of treatment).
  Blood taken from the ulnar vein in sterile conditions in quantity of 5-10 ml is
cultivated in 50-100 ml of bile culture medium or Rappoport medium. Vomitus (50-
100 g) and gastric washing water (100-200 ml) are taken in sterile flasks; excretions
(4-5 g) are taken into a sterile test tube containing a glycerol mixture; urine (20-50
ml) is taken in a sterile bottle or a test tube; pus (in septic form of the disease) is
taken from secondary foci.
 Suspected food (in the quantity of 50-60 g from various portions, taken in a
sterile bottle) should also be delivered to the laboratory.
 A preliminary result is ready in 2 days and the final result in 4 days.
 Direct and indirect haemagglutination reactions can be performed in a week (1 ml of
blood).
 The result of the indirect haemagglutination reaction is ready in 4-6 days of the
disease. The test is positive if the serum dilution is 1:160 and over.
Immunofluorescence test is used for rapid diagnosis

treatment.
 Mild forms of the disease can be treated at home.
 Detoxication therapy - perform gastric lavage with ample warm water (2-3 litres) or
a 2-3 % sodium hydrocarbonate solution.
 If salmonellosis is of mild or moderate severity, and vomiting or marked toxaemia
are absent, the patient is given salt solutions per os.
 The amount of liquid given must comply with the amount of liquid lost.
 If toxaemia is marked while dehydration is mild, these solutions must be given by
intravenous drip (40-60 drops per minute).
 If the course of the disease is severe (dehydration of the 3rd or 4th degree) a
polyionic solution should be given at a rate of 80-120 ml/min. The volume of the
solution that is given to replenish the liquid lost, depends on the degree of
dehydration (4-8 litres and over).
 After haemodynamic stabilization, termination of vomiting, and restoration of the
excretory function of the kidneys, the patient can be given liquid per os.
 If adrenal insufficiency develops, the patient should be given prednisolone (60-90
mg) or hydrocortisone (125-250 mg) intravenously; later (in 4-6 hours) these
preparations can be given by intravenous drip.
 Desoxycorticosterone acetate should be given intramuscularly (5-10 mg at
12-hour intervals).
 In order to restore the gastrointestinal function, the patient can be given festal,
panzynorm, cholenzyme, etc., and also preparations restoring the intestinal
microflora(bifidumbacterin, colibacterin, lactobacterin, etc.).
 Antacids, e.g. white clay, bismuth preparations, should also be given.
 In typhoid forms of salmonellosis the patient should be given (in addition to
detoxicating, rehydrating and desensitizing therapy) chloramphenicol sodium
succinate (30-50 mg per kg of body mass a day) or chloramphenicol (0.5 g 4 times a
day for 10-12 days), and ampicillin (1 g 4-6 times a day for 8-10 days).
 Septic forms should be treated with ampicillin in combination withsurgery
  of purulent foci. It is important to prescribe a proper diet to the patient. Vitamins are
also necessary.
 The patient is recommended to eat oat and rice porridges (without milk), boiled fish,
steam-cooked minced meat, fruit jellies, curds and sweet cheese during the first
days of the disease.

26.Food poisoning. Epidemiological features, stages of pathogenesis,

clinical forms, main clinical sings, diagnostics tests, treatment.

Epidemiological features
 food poisoning results from a reaction to food or water contaminated during
improper cooking, handling or storage
 it is caused by: Staph. aureus, E.coli enteritis, Salmonella, Shigella, Campylobacter,
Botulism, Listeria, Bacillus cereus, Fish poisoning, Yersinia. Other contaminants
include viruses,parasites and toxins.
 Food poisoning can be of two types,

1. food infection - presence of bacteria or other microbes which infect the

body after consumption.
2. food intoxication - the ingestion of toxins contained
within the food, including bacterially produced exotoxins, which can happen
even when the microbe that produced the toxin is no longer present or able to
cause infection.
 source- people, animals, sick + bacillus carriers
 agents- are detected in feces-spread onto soil,water in lakes, rivers, vegetables Eg.
In ataphylcoccus infection- source of infection is persons with purulent infection
like in pyoderma, pharyngitis, tonsillitis, stomatitis Eg. In animals-mastitis(cows or
sheeps)
 mechanism of spreading – fecal-oral

stages of pathogenesis
The pathogenesis of diarrhea in food poisoning is classified broadly into either
noninflammatory or inflammatory types.
Noninflammatory diarrhea
 It is caused by the action of enterotoxins on the secretory mechanisms of the
mucosa of the small intestine, without invasion.
 This leads to large volume watery stools in the absence of blood, pus, or severe
abdominal pain. Occasionally, profound dehydration may result. The enterotoxins
may be either preformed before ingestion or produced in the gut after ingestion.
Examples include Vibrio cholerae, enterotoxic Escherichia coli, Clostridium
perfringens, Bacillus cereus, Staphylococcus organisms , Giardia lamblia,
Cryptosporidium,rotavirus, norovirus (genus Norovirus, previously called Norwalk
virus), and adenovirus

Inflammatory diarrhea
  It is caused by the action of cytotoxins on the mucosa, leading to invasion and
destruction. The colon or the distal small bowel commonly is involved.
 The diarrhea usually is bloody; mucoid and leukocytes are present. Patients are
usually febrile and may appear toxic.
 Dehydration is less likely than with noninflammatory diarrhea because of
smaller stool volumes. Fecal leukocytes or a positive stool lactoferrin test
indicates an inflammatory process, and sheets of leukocytes indicate colitis.

clinical forms ???

Incubation period
 It is the period that the delay between consumption of a contaminated food and
appearance of the first symptoms of illness.
 From hours to days (and rarely months or even years, such as in the case of
Listeriosis or Creutzfeldt-Jacob disease), depending on the agent, and on how much
was consumed.
 If symptoms occur within 1–6 hours after eating the food, it suggests that it
is caused by a bacterial toxin or a chemical rather than live bacteria.
 During the incubation period, microbes pass through the stomach into the
intestine, attach to the cells lining the intestinal walls, and begin to multiply there.
 Some types of microbes stay in the intestine, some produce a toxin that is absorbed
into the bloodstream, and some can directly invade the deeper body tissues. The
symptoms produced depend on the type of microbe.
Infectious dose
 It is the amount of agent that must be consumed to give rise to symptoms of
foodborne illness, and varies according to the agent and the consumer's age and
overall health.
 In the case of Salmonella a relatively large in-oculum of 1 million to 1 billion
organisms is necessary to produce symptoms in healthy human volunteers as
Salmonella are very sensitive to acid.
 An unusually high stomach pH level (low acidity) greatly reduces the number of
bacteria required to cause symptoms by a factor of between 10 and 100.
main clinical sings
 Nausea
 Vomiting
 Watery or bloody diarrhea
 Abdominal pain and cramps
 Fever
 Frequent episodes of vomiting and inability to keep liquids down
 Bloody vomit or stools
 Diarrhea for more than three days
 Extreme pain or severe abdominal cramping
 An oral temperature higher than 100.4 F (38 C)
  Signs or symptoms of dehydration — excessive thirst, dry mouth, little or no
urination, severe weakness, dizziness, or lightheadedness
 Neurological symptoms such as blurry vision, muscle weakness and tingling
in the arms

diagnostics tests

 the food history, the geographic location, the season of the year, and the order and
timing of onset of symptoms.
 If symptoms continue for more than 48 hours, it may be necessary to examine a
 stool sample under a microscope.
 Also we can to take a sample from blood, stools or the food in question. The sample
can be cultured in a laboratory, which means it is placed on a special material that
encourages organisms that may be in the sample to grow, so they can be identified.
 Physical examination includes: blood pressure, pulse, breathing rate and
temperature.
 Diagnosis is easier if a number of people have had the same food or drink
and are displaying the same symptoms.
 A stool or vomit sample may be taken to see if there is any blood or mucus
 in it. A urine sample may also be taken to test for infection. Blood test also can be
used
treatment
you should get medical advice if:
- the illness lasts for more than a few days or general condition worsens
- there is blood in the stools
- the person affected is elderly, a baby or a pregnant woooman
- diarrhoea contains yellowish or greenish mucus.
Because large amounts of fluids are lost through vomiting and diarrhea,
treatment of food poisoning focuses on preventing dehydration. If you have food
poisoning, you must drink fluids/even if you have trouble keeping them down.
Once you can tolerate fluids without vomiting, you can begin to add bland foods

27.Typhus fever. Epidemiology, stages of pathogenesis, main clinical

sings, diagnostics, therapy.

Pathogenesis
 After ingestion by the host, S.typhi invades through the gut and multiplies
within the mononuclear phagocytic cells in the liver, spleen, lymph nodes, and
Peyer patches of the ileum.
 Then alters its structure to resist destruction and allow them to exist within the
macrophage. This renders them resistant to damage by complement and the immune
response.
 Then is them spread via the lymphatics while inside the macrophages.
  This give them accesses to the reticuloendothelial system and then to different
organs throughout the body. The organism is Gram-negative short bacillus that is
motile due to its peritrichous flagella. The bacterium grows best at 37 C – human
body temperature.
 Pathological changes in the intestine.
1 week: swell of lymph nodes in ileum.
2 week: central part of lymphoid formation, lymphoid folliculs become dirty
grey-green color.
3 week: deep mucosa and submucosa defected.
4 week: period of clear ulser: ulser with clear fundus and slightly swelled
adjacent.
5 week: heal of ulser with slight pigmentation.
 After primary intestinal infection, further seeding of the Peyerpaches occurs
through infected bile.
 They may become hyperplastic and necrotic with infiltration of mononuclear cells
and neutrophils, forming ulcers that may hemorrhage through eroded blood vessels
or perforate the bowell wall, causing peritonitis.
 From blood or from the liver via bile ducts, in infects the gallbladder and
reenters the gastrointestinal tract in the bile, spreading to other hosts via stool.
 In addition, it occasionally invades the urinary tract and spreads via urine

main clinical signs

 fever
 toxemia
 delirium
 abdominal discomfort
 constipation and hepatosplenomegaly.
 The incubation period may varies from 7 to 14 days (range 3-60) days. In
paratyphoid infection, the incubation period ranges from 1-10 days.
Diagnostics
Laboratory examination
 anemia, have an elevated erythrocyte sedimentation rate, thrombocytopenia, and
relative lymphopenia.
 Leucopeniawith eosinopenia and relative lymphocytosis
 Blood cultures - positive for Salmonellatyphi or paratyphi
 Widal test - negative in the first week. And In the second week of the infections the
Widal reaction is strongly positive with antiO and antiH antibody
 Liver transaminase values and serum bilirubin levels are usually elevated to twice
 the reference range biochemical blood analysis - Mild hyponatremia and
hypokalemia
 Specific serological tests: assay that identifies Salmonella antibodies or antigens
support the diagnosis but should be confirmed with cultures or DNA evidence.
 Indirect hemagglutination, indirect fluorescent Vi antibody, and indirect enzyme-
nlinked immunosorbent assay for immunoglobulin M (Ig M) and IgG antibodies to
 S typhi polysaccharide are available. Monoclonal antibodies against S typhiflagellin
are promising developments
 Definitive diagnosis of typhoid fever generally requires isolation of the organism
from blood, bone marrow, vomitus, fresk stool, or urine
 Bone marrow aspiration or punch biospy

Therapy
 Lifestyle modification -adequate hand washing and safes disposal of feces and urine
 Antibiotic therapy is essential and should begin empirically if the clinical evidence
is strong. - ampicillin, chloramphenicol, trimethoprim-sulfamethoxazol,
amoxicillinand ciprofloxacin,
 Patients must receive adequate fluids, electrolytes, and nutrition.
 Where resistance is uncommon, the treatment of choice is fluoroquinolone such as
ciprofloxacin otherwise; a third-generation cephalosporin such as ceftriaxone or
cefotaxime is the first choice. Cefixime is a suitable oral alternative.
 Surgery is usually indicated in cases of intestinal perforation

28.Brill disease. Epidemiological data, pathogenesis, clinical sings,

diagnostic tests, therapy.

Epidemiological data
 Patients who develop Brill Disease either acquired epidemic typhus earlier in life
 Lived in an endemic area
 Brill disease is caused by R.Prowazekii which remains viable long after recover in
the lymph nodes after the initial infection

the recurrent typhus
 This disease is sporadic occurring in any season and in the absence of infected louse
 Brill disease is more common in elderly people
Pathogenesis
 vector of epidemic typhus is the body louse (Pediculus corporis).
 Host – human
 Rickettsia prowazekii, which is the etiologic agent of typhus, lives in the alimentary
tract of the louse.
 A Rickettsia- harboring louse bites a human to engage in a blood meal and causes a
pruritic reaction on the host's skin. The louse defecates as it eats; when the host
scratches the site, the lice are crushed, and the Rickettsia- laden excrement is
inoculated into the bite wound. The Rickettsia travel to the bloodstream and
rickettsemia develops.
 Rickettsia parasitize the endothelial cells of the small venous, arterial, and capillary
vessels.
  The organisms proliferate and cause endothelial cellular enlargement with resultant
multiorgan vasculitis.
 This process may cause thrombosis, and the deposition of leukocytes, macrophages,
and platelets may result in small nodules.
 Thrombosis of supplying blood vessels may cause gangrene of the distal portions of
the extremities, nose, ear lobes, and genitalia. This vasculitic process may also
result in loss of intravascular colloid with subsequent hypovolemia and decreased
tissue perfusion and, possibly, organ failure.
Clinical signs
• Course of the disease is always mild (incubation period 1-2 wks)
• Starts w malaise,cough,headache,backache,arthralgia and chest pain
• Abrupt onset of t° + chills (38-39°) which lasts for about 5-7 days
• Exanthematous occur in 60-96%
• Rashes appear first on the trunk and then spreads through the body except
face,hands & sole of foot
• There are macules first then become meculo-papules à petechial à confluent
• Insomnia,some euphoria in the peak of the disease
• Meningeal symptoms occur rarely
Diagnostic test
• Should specify through the anamnesis that the symptoms has developed after
contacting with animals or after travel
Laboratory tests
• Microbiological test : culture & isolation of microoragnisms from blood
• Serological detection : (ELISA) Ab titer of Ig G first and then Ig M
• Ag detection by Immunofluorescent test
Therapy
• Supportive therapy – glucose,Ringer solution, anticoagulants ,O2, blood
transfusion
• bed regime (5-6 days)
• antibiotics - chloramphenicol 50mg /kg 4x , Tetracycline 25mg/kg 4 x /day ,
doxycycline can be given to any age of patients

29.Anthrax. Etiology, epidemiology, clinical forms, diagnostics,

treatment.

 Etiology
Anthrax is caused by gram-positive, rod-shaped bacteria known as Bacillus
anthracis.
 Epidemiology
occurs worldwide in animals, especially in Africa, Asia and in south-
eastern Australia.
  Clinical forms

Clinical features of anthrax depend on the route of exposure of the organism.

Cutaneous anthrax

o After 1-5 days, a small erythematous papule develops at the site of

inoculation then develops into a vesicle containing fluid, serosanguineous in
nature, in 1-2 more days.
o The vesicle then ruptures and a necrotic ulcer form centrally
o The ulcer then evolves into a central black eschar of 1-3 cm diameter over a
week or so.
o The eschar finally separates after 1-2 more weeks, leaving a scar.
o patients often have fever, malaise and headache.
o The skin lesion is characteristically non-pruritic and non-purulent.

Gastrointestinal anthrax
o results from the consumption of contaminated meat and is extremely rare.
o Cause full-blown hemorrhagic gastroenteritis.
o Signs and symptoms may include fever, abdominal pain that may be severe,
hematemesis, bloody diarrhea, hypovolemia and prostration.
o Complications: Intestinal obstruction or perforation and ascites may occur.
Sepsis is common and the case fatality rate is high

oropharyngeal form
o associated with spore ingestion.
o This form presents with severe sore throat, neck swelling, adenopathy,
and dysphagia.
Inhalational anthrax
o results from inhalation of infectious spores
o After an incubation period of 1-6 days, develop fever, malaise and fatigue
o chest discomfort and a non-productive cough; headache, drenching sweats,
nausea and vomiting, myalgia and confusion may also occur.
o These manifestations may last 2-3 days
 o These early phases are then followed by sudden deterioration with severe
respiratory distress, dyspnea and stridor, diaphoresis and cyanosis.

Diagnosis
o Recent history of occupational exposure or a bioterrorism attack is
helpful. Pleural fluid or CSF is often bloody.
Clinical laboratory features may include
o elevated leukocyte count, neutrophilia, elevated transaminases,
metabolic acidosis and elevated creatinine.
Definitive laboratory diagnosis
o Gram-staining: Gram-positive rods in high concentration.
o The gold standard and most sensitive test is microbiological culture of
the organism from skin lesion aspirate, blood, pleural fluid or
cerebrospinal fluid.
o IFA with microscopy, ELISA, gamma-phage sensitivity, electro-
chemiluminescence and nucleic acid amplification (PCR).
o Examination of punch biopsy specimens from a skin lesion:
characteristic rod-shaped organisms.

Treatments
treatment depend on: the potential route(s) of exposure, infectious dose to
host immunocompetence; age; possibility of pregnancy; severity of illness.
Cutaneous anthrax
o 7-10 days of antibiotics
o Oral penicillin, ciprofloxacin and doxycycline are the antibiotic
options
o A total of 60 days of treatment is recommended if there has been risk
of aerosol exposure and the possibility of retained spores in the lung.
inhalational anthrax
o penicillin, ciprofloxacin and doxycycline
 o Antibiotics should be started immediately if the disease is suspected.
o Combined antibiotics are effective.
o Other antibiotics: clindamycin, rifampin, imipenem, aminoglycosides,
chloramphenicol, vancomycin, cefazolin, tetracycline, linezolid and
the macrolides.
o antibiotic treatment for 60 days (switch to oral treatment after clinical
recovery)
Intensive supportive care: Ventilatory support, maintenance of adequate
perfusion and oxygenation, and fluid management
Newer therapies: anthrax immune globulin (AIG) and monoclonal antibody
treatments against anthrax toxins, may be important for enhanced survival.

30.Erysipelas. Epidemiology, clinical manifestation, treatment,

prevention measures.

Epidemiology
o The incidence of erysipelas declined throughout the mid-20th
o Internationally: Erysipelas is somewhat more common in European
countries.
o Death as a direct result of erysipelas is exceedingly rare.
o Race: Erysipelas infections affect all races.
o Sex: Erysipelas has been reported to be more common in females
o Age: Cases of erysipelas have been reported in all age groups,
common in infants, young children and elderly patients. The peak
incidence 60-80years
o high-risk and immunocompromised or those with lymphatic drainage
problems (e.g., after mastectomy, pelvic surgery, bypass grafting).

Clinical features
 o Erysipelas begins as a small erythematous patch that progresses to a
fiery red, indurated, tense, and shiny plaque.
o The lesion exhibits raised sharply demarcated advancing margins.
o superficial blebs or bullae may form, usually 2 or 3 days after onset.
o The lesion typically develops over a few hours and is associated with
fever and chills.
o Local signs of inflammation, such as warmth, edema, and tenderness,
are universal.
o regional lymphadenopathy.
o More severe infections: vesicles and bullae along with petechial and
even frank necrosis.
Erysipelas, characteristic locations: the malar area of the face and the lower
extremities.
Classification:
1. According to clinical forms:
Erythematous erythematous-bullas, bullas-hemorrhagic.
2. According to the time of appearance:
primary, relapsing, secondary.
Primary: occurs at 1st time
Relapsing form
1. symptoms of this disease and first attack is less than 2 years.
2. Pathological process is localized at the same place.
Secondary form
1. appearing the symptoms and first attack is more than 2 years.
2. Pathological process is localized at the other place.

Treatment
o Elevation and rest of the affected limb: to reduce local swelling,
inflammation, and pain.
 o Saline wet dressings should be applied to ulcerated and necrotic lesion
and changed every 2-12 hours
o penicillin first-line therapy. orally or intramuscularly given for 10-12
days. cephalosporin or macrolide may be used if the patient has an
allergy to penicillin.
o recurrent erysipelas: patients should be educated regarding local
antisepsis and general wound care.
o Long-term: prophylactic antibiotic therapy generally is accepted.
benzathine penicillin at 2,4 MU intramuscularly every 3 weeks for up
to 2 years.

Prevention:-
B saline 5.
The prevention of an episode of erysipelas calls for correct personal hygiene
and adequate use of topical antiseptics in case of skin effraction.

31.Rabies. Special features of anamnesis, periods of disease, main

clinical sings, diagnostics tests, prinсiples of therapy.

Special features of anamnesis

The incubation period of disease depends on how far from virus must travel
to reach the CNS.
The contagious period begins 7-10 days before the clinical signs of the
disease develop, and persists till the death of the animal.
The incubation period in dogs is 14-30 days.
The incubation period depends on several factors
1. dose of inoculum
2. the severity of the wound
 3. the length of the neural path from the wound to the brain. (Wound on face
have the shorter incubation period then wound in the legs)
periods of disease
 prodrome
 excitation
 paralysis

main clinical sings

The prodrome
o pain at the site of inoculation and along the courses of the local
nervous trunk.
o The general signs of the disease develop next: apprehension, fears,
depression, deranged sleep, oppression in the chest, tachycardia and
subfebrile temperature.
o The period lasts 2-3 days
o At the place of bite- pronounced tingling pain.
The excitation period
o progressive respiratory distress and cardiovascular dysfunction
o The most pathognomonic sign soon develops: hydrophobia
o patient is excited,his behavior is maniacal.
o Aerophobia soon develops
o The pupils are irregular, pulse is fast, body temperature rises to 40 °C and
higher.
o Hallucinations, delirium, aggressiveness and hyperexcitation
o foaming at the mouth
o Photophobia, and Acoustophobia

Paralysis
 o In 2-3 days convulsions abate and paralysis develops
o The lower extremities are first involved but paralysis rapidly extends
over the whole body
o In 12-20 hours the patient dies of apnea and heart failure.

Diagnosis.
o Hematologic picture- high leucocyte count (to 30 x 109/1) combined
with neutrophilia, monocytosis, and an eosinophilia.
o fluorescent antibody test (FAT)
o an immunohistochemistry procedure, which is recommended by the
WHO
o Virus cultivation- the most definitive.

Treatment.
o Effective treatment is unknown
o As a rule, treatment is aimed at decreasing the psychomotor
excitement and at lessening the patient's sufferings
o Salt solutions, glucose and vitamins parenterally
o Chloral hydrate (2 g in 100 g of starch solution), morphine, aminazine,
dimedrol and cardiac are indicated.
o Curare-like preparations and intensive respiratory support can prolong
the life of the patient for 2-3 days.

32.Infectious mononucleosis. Epidemiology, etiopathogenesis, clinical

manifestation, diagnostic tests, therapy.

Epidemiology
o Low contagious
o Sporadic cases:- few cases during year (not epidemic or pandemic)
o But immunity is stable
 o Epidemiology: Source of infection are patients with symptomatic and
asymptomatic forms, EBV-carriers.
o There are two age group of higher incidence — children (before 5 years old)
and adolescents.

Etiology
o EBV is the most common cause
o The second common cause of IM is CMV, but in can be also observed in
patients with primary HIV, acute toxoplasmosis, rubella, viral hepatitis

pathogenesis
Mechanism of transmission is droplet, rarer is contact
Can be associated with Burkitt’s lymphoma.

After infection of B lymphocytes and the cells of oropharyngeal epithelia incubation

may last up to 50 days. In the course of immune response during IM there is
production of many antibodies against viral antigen as well as unrelated antigen
which can be found on other animals’ cells (heterophile antibodies). Less frequently
antibody can be synthesized against platelets, neutrophils and ampicillin.

Clinical features
Incubation period is 10-15 days (may be longer-2 month).
Gradual onset
o Beginning is acute from fever,
o Fever usually remittent febrile from 3 days till 3 weeks.
o Tonsilopharyngitis
o lymphoid follicles hyperplasia
o Adenoiditis, posterior rhinitis
o Generalized lymphadenopathy
o 0.5cm may be so normally cannot see enlargement, painless.
o Hepatosplenomegaly is the sign of lymphoproliferative syndrome.
o Maculopapular rashes
o skin pigmentation may occur as a sign of hypersensitivity in case of
amoxicillin, ampicillin treatment (in 70-80%).

Other signs: hepatitis (jaundice form of infectious mononucleosis); toxic

myocarditis, diarrhea.
Complete recover takes a lot of time despite of fever disappearance in 10-14 days.

Diagnosis

Heterophile antibodies
Serological identification of EBV specific antibodies
Epstein-Barrvirus nuclear antigen (EBNA)

1. Blood analyses: leucocytosis, lymphocytosis, monocytosis, appearing of atypical

mononuclear cells (virocytes) more than 10%, ESR enlarges
2. Heterophil agglutination test
3. Immune-enzyme method – VCA Ig M, EA Ig M presence in the blood.
4. PCR (measuring of EBV nucleinic acid in the blood, saliva, lymphatic tissues).

Treatment
In immunocompetent patients infection is usually self-limited and does not require
specific treatment.
1. Reduction of activity and bed rest.
2. Control of fever and myalgia: ibuprophen, not often than every 6 hours.
3. Antihistamines– pipolphen, suprastin, claritin, cetirizin.
4. Corticosteroids - in severe cases 1-2 mg/kg/day prednisone for 3-5 days.
5. In case of secondary bacterial complications macrolides, cefalosporins

Ampicillin and other semisynthetic penicillins are contraindicated!

33.Plague. Epidemiological situation, pathogenesis, clinical forms,

diagnostics, therapy.

Etiology: The disease is due to Yersinia pestis, the bacillus of the genus Yersinia,
the family Enterobacteriaceae
Epidemiology
Plague is a typical disease of rodents which are the primary source of the disease
among humans.
The primary reservoir of plague infection are sousliks, voles, marmots and rats.
Anthropozoonotic
Fleas are the main vector of infection.
Pathogenesis
The pathogenesis depends on the route
through the skin, the bacillus is carried to the regional lymph nodes. A
primary bubo is thus formed
 From the bubo, the microbes enter the blood stream. The microbes enter the
internal organs and lymph nodes and form secondary buboes are thus formed.
the air-borne route, hemorrhagic pneumonia and sepsis occur
alimentary infection, the disease is manifested by hemorrhagic enteritis and
sepsis
In primary septicemia, the lymphatic barrier is weak
The plague microbe forms exo- and end toxins which cause toxemia

Clinical picture
The incubation period lasts from 2 to 6 days
 localized form of plague
cutaneous, bubonic, cutaneous-bubonic, or tonsillar (pharyngeal)
 generalized form
primary septicemic, secondary septicemic, primary pulmonic, secondary
pulmonic or intestinal plague.

cutaneous-bubonic form
o a spot is first seen at the portal of entry
o then converted into a papule, a vesicle, a pustule, and an ulcer.
o later it becomes covered with a dark crust and does not heal for a long
time.
o As distinct from anthrax, a plague carbuncle is painful.
o Lymphadenitis (plague bubo) on 1st or 2nd day
o Pain makes him assume a forced position.
o If the bubo is the inguinal area, the patient flexes his leg.
o The bubo either resolves spontaneously or purulates and scleroses.
tonsillar (pharyngeal) plague
o lasts 2-3 days
 o The toxemia is weak, the body temperature rises to 38 °C, the
submandibular and neck lymph nodes are enlarged.
primary septicemic form
o delirious hyperactivity or complete adynamia
o Hemorrhagic rash and hemorrhages into the skin and mucosa
o Untreated patient dies during first days of the disease.
intestinal form: high body temperature, extreme weakness, loss of appetite,
nausea, recurrent vomiting, ample liquid stools with streaks of blood and mucus,
severe abdominal pain during the defecation.
Primary pulmonic plague
o fulminating course with dyspnea
o severe chest pain
o cough with liquid blood-stained foaming sputum
o Cardiovascular failure develops on the very first days of the disease.
secondary septicaemic form in 1-2 days and the patient died

Diagnosis
The diagnosis is based on clinical, epidemiologic and laboratory findings.

specimens
 bubo contents
 exudate from ruptured buboes, vesicles, pustules, carbuncles and
ulcers
 sputum is taken from patients with the pulmonic form
 Feces should be taken from patients with intestinal lesions.
 Blood specimens of patients with all forms of the disease are studied.

o smears are stained with Gram's stain and methylene blue (Loeffler)
o The serologic luminescence analysis: luminescent microscope
 o Hottinger's or Martin's culture media containing sodium sulphite and
gentian violet are inoculated
o Indirect hemagglutination and indirect agglutination inhibition tests
o positive indirect hemagglutination test
o Fleas and rodents, and also dead animals, especially camels, should be
examined bacteriologically in the focus of infection.
Treatment
o Specific treatment includes the tetracyclines (tetracycline, doxycycline,
oxycycline, methacycline) 0.2 g 6 times a day.
o to prevent complications: dimedrol,0.03 g 2-3 times a day, and
vitamins (B1; B6, B12, C, K).
o A 40 per cent glucose solution: to patients with marked toxemia (20-40
ml.)
o 5% glucose: 500-1000 ml.
o marked acidosis: Isotonic sodium chloride solution or sodium
hydrocarbonate
o for edema: Lasix, furosemide
o cardio vascular disorders: Cordiamine, camphor, caffeine, ephedrine,
adrenaline and strophanthin:

34.Tularemia. Epidemiological situation, pathogenesis, clinical forms,

diagnostics, therapy

Etiology: Francisella tularenis of the genus Francisella, the family

Brucellaceae.

Epidemiology
o The main reservoir and source of infection are rodents, hares, muskrats,
and hamsters.
 o source of the infection: Squirrels, foxes, cats, dogs, goats, cattle and
sheep are of secondary importance
o Zoonotic
o animal to human: air-borne route, by direct contact, by ingestion of and
by the bites of infected arthropods: ticks, lice, mosquitoes, etc.
o Increased risk of epidemic tularaemia exists among agricultural workers,
shepherds, farmers, hunters, laboratory workers

Pathogenesis.
o gain entrance to the human body through the skin, nasopharynx,
gastrointestinal tract, respiratory ducts and the eyes.
o rapidly reaches the regional lymph nodes and later the blood stream.
o Circulation of the tularaemia causes toxemia formation of specific
granulomas in them.
o Primary buboes are formed in the regional lymph nodes
o Tularaemia granulomas are necrotized, degraded, and look like tubercles
o As the microbes propagate, they can cause secondary buboes
Clinical picture.
disease depends on the route
incubation period lasts from 2 to 8 days
The following clinical forms of tularaemia are differentiated:
 Bubonic
 Ulceroglandular
 Oculoglandular
 Angioglandular
 Gastrointestinal
 pulmonic and primary septic (generalized) forms.

All clinical forms are characterized by some common symptoms.

a short-lasting chill is followed by elevation of temperature to 38.5-40 °C.
Remittent and intermittent fevers are common
headache, muscular and lumbar pain, weakness, hyperhidrosis, and poor appetite
hyperemic face and conjunctivitis.
The spleen and the liver are enlarged by the end of the first week.
bubonic form
 lymphadenitis (bubo)
 A group of lymph nodes is often involved. The nodes do not fuse
between themselves or with the surrounding cellular tissue.
 The nodes are only slightly tender. As the body temperature falls, the
buboes slowly resolve.
ulceroglandular tularaemia,
 vesicle, pustule, and finally transform to an ulcer
 primary bubo present
oculoglandular tularaemia,
 follicular proliferations over the conjunctiva and simultaneous
enlargement of the lymph nodes
 papules and ulcers can appear on the eye tunic.
The angioglandular form
 hyperplasia of the tonsils with subsequent formation of a greyish white
necrotic coat, formation of deep slowly healing ulcers.
 Unilateral involvement is more common.
gastrointestinal form of tularaemia
 severe abdominal pain
 nausea, vomiting and diarrhea.
pulmonic tularaemia
 development of focal pneumonia
 X-ray studies and skin-allergic tests are decisive diagnostically.
septic form of tularaemia
 Clinically this form has a more pronounced picture of toxemia
 Polymorphous erythematous rash
Diagnosis
 diagnosed on the basis of clinical, epidemiologic and (in the pulmonic form)
X-ray findings.
 Blood analysis: Leucopenia, moderate shift to the left, relative lympho- and
monocytosis are seen; ESR is high
 Skin-allergic tests can be conducted on the 3rd-5th day of disease.
 biologic tests bubonic exudates
 blood specimen: The agglutination reaction is considered positive with serum
dilutions of 1:100 and higher.
 Indirect haemagglutinationtest is more sensitive (red cells sensitized with
tularaemia antigen are used as the diagnosticum).

Treatment.
 The tetracyclines: dose of 0.2 g 4 times a day
 Chloramphenicol: dose of 0.5 g 4 times a day for 7-10 days
 Isotonic sodium acid is given intravenously
 Cardiacs are given whenever necessary.
 Vaccino therapy: subcutaneously, intramuscularly and intravenously.

35.Staphylococcus infections. Epidemiology, pathogenesis, clinical

forms, diagnostics, treatment

Etiology: staphylococci which are Gram-positive cocci

Epidemiology
o Sources of infection are patients and bacilli carriers
 o The main ways of pathogen transmission: airborne, airbornedust,
home, alimentary.
Factors contributing to the development of infection:
weakened immune system, long-term use of antibiotics, hormones or
immunosuppressant, acute exacerbation of chronic diseases, long term
chemotherapy or radiotherapy

Pathogenesis.
Staphylococci implementation develop purulonecrotic inflammation
The further process can have two scenarios:
1.Strong specific immunity does not develop the disease and contributes to
the rapid focus elimination.
2. The weakened immune system cannot fight off the infection
The pathogen and toxins being in blood develop bacteremia and intoxication
cause septicemia and septicopyemia.
Clinical signs
Clinical signs of disease are determined by the area of bacteria
implementation
 Skin- develops pyoderma, Necrotic staphylococcal skin diseases
include boils and carbuncles, abscess or cellulitis formation
 lungs- pneumonia is a heavy but quite rare pathology. intoxication and
pain syndromes, respiratory failure with pronounced dyspnea.
Complications of the disease are lung abscess and empyema.
 meninges - neurological symptoms, signs of meningism, epilepsy,
alteration of consciousness.
 Osteomyelitis - pain, tissue swelling, pus formation of fistulas,
arthrempyesis.
  Endocarditis- fever, pain in muscles and joints, chills, sweating, pale
skin, appearance of rashes and small dark red nodules on the palms
and feet, heart failure.
 Infectious-toxic shock syndrome- intoxication, dyspepsia, confusion,
symptoms of cardiovascular and kidney failure, collapse.
 Food toxicosis- severe intoxication and indigestion. Vomiting is often
the result of dehydration.

Diagnosis
o The main diagnostic method- microbiological examination of nasal
discharge.
material for the study: blood, pus, ears, nose, wound and eyes discharge,
pleural exudate, feces, gastric washings, vomit, Fluor cervical (for women), urine.
o Microbial culture in milky bile-salt or egg yolk-salt agar
o enzyme immunoassay or gel precipitation test
o Serodiagnosis- hemolysis inhibition test, passive hemagglutination,
EIA
Therapy (internet source)
o Antibiotics commonly prescribed to treat staph infections include cefazolin,
nafcillin, oxacillin, vancomycin, daptomycin and linezolid. (IV/oral/topical
creams)

o For serious staph infections, vancomycin (MRSA)

o Detoxification therapy: IV fluid

o Abscess drainage
 o Wound care

36.Lyme Borreliosis. Epidemiology, pathogenesis, clinical forms,

diagnostics, treatment

Epidemiology:

Brucellosis is a typical zoonosis because the reservoir of infection is

domestic animals. It has already been said that goats and sheep are the
commonest source of infection in man. Cattle and swine are less important. If
healthy and diseased animals of various species are raised together, brucella
migrates from goats to cattle and other animals. Outbreaks of the disease in man
thus become possible. Cats, dogs, camels, deer, horses are a secondary reservoir
of the infection. A diseased man presents no danger to the surrounding
people.The highest incidence of the disease is during the spring and summer. The
first wave of morbidity is seen in the early spring. It is associated with bearing the
young and miscarriages.
Pathogenesis:
When the pathogenic organism gets inside a human through a damaged
skin or mucosa, it passes with the lymph to regional lymph nodes where it
multiplies during the entire incubation period. By the moment when the disease
becomes clinically manifest, brucella enters the blood and is carried to various
organs and systems: the liver, spleen, bone marrow, and the lymph nodes.
Secondary foci of infection thus develop.
Clinical Forms
Acute form of brucellosis often begins with a prodromal period. The patient
complains of malaise, lassitude, depression, deranged sleep, lumbar pain, myalgia
and arthralgia, chills.
Subacute form brucellosis, in addition to the mentioned symptoms, is also
characterized by focal allergic lesions in the form of arthritis, neuritis, plexitis, etc.
Subacute brucellosis can gradually transform into chronic brucellosis which is
characterized by a further reconstruction of allergic response with involvement of
other organs and systems. The body temperature is usually subfebrile or normal
during weeks and months (remissions).
Chronic form of the disease is usually characterized by stable changes in the
locomotorium (arthritis, bursitis, tendovaginitis, periostitis, perichondritis) and in the
nervous system (radiculitis, ischioradiculitis, plexitis, neuralgia). The genitalsystem
is also involved: orchitis (inflammation of the testes), orchiepididymitis
(inflammation of the testes and the epididymis) in males and oophoritis
(inflammation of the ovaries and the tubes), endometritis, and abnormal menstrual
cycle in women.
Chronic brucellosis proceeds with relapses and remissions and can last 2-3 years.
After the patient recovers, residual phenomena are possible: pain in the joints and
muscles, headache, irritability, organic changes in the locomotorium with
deformation of the joints, etc.
The clinical picture of the disease has lately somewhat changed. Severe forms of
brucellosis are rare.

Diagnosis
Blood cultures are inoculated with 5-10 ml blood specimens taken from the ulnar
vein of patients before the antibiotic therapy is started.
The result is ready only in 5-10 days, and sometimes in 29-30 days. Serologic
tests, the immunofluorescent method, Coombs' test, direct haemagglutination test,
and intracutaneous allergic test are used for serologic diagnosis of brucellosis.
Wright and Huddleson tests are positive beginning with the 8-9th day of the
disease, while the Burnet test in 7-8 days and later. A specimen of blood taken
from the finger or the vein (1-2 ml) is tested (Wright's reaction) and result is
considered positive with serum dilution of 1:200 and more. The Burnet
intracutaneous test is performed after the 10th day of the disease. Coombs' test is
used in chronic forms of infection. The reaction is based on the detection of
incomplete antibodies using antiglobulin serum.

Treatment
Antibiotics are given to patients with acute, subacute and exacerbated
chronic brucellosis with signs of marked toxemia and high fever. The tetracyclines
and terramycin are most efficacious. Vaccine therapy is indicated after 2-3
courses. The vaccine should preferably be given intravenously. In the presence of
contraindications, it can be given intracutaneously.
Severe cases of brucellosis with involvement of the joints, the central and
peripheral nervous system, orchitis, etc., are treated with prednisolone and
prednisone (in addition to antibiotics), given in a dose of 20-30 mg for 4-6 days.
The corticosteroid therapy is combined with butadione and other anti-
inflammatory preparations. Symptomatic treatment should also be given:
invigorating measures, preparations improving appetite, vitamins B and ascorbic
acid, cardiacs and analgesics.

37.Hemorrhagic fever with disrenal syndrome Epidemiology,

pathogenesis, clinical forms, diagnostics, treatment.

Epidemiology

HFRS is caused by an airborne contact with secretions from rodent hosts, infected
with the group of viruses. The severity of this disease depends on the type of virus
and on the geographic distribution.
Inoculation of the microorganism into human in the natural body is by acrogenic
route, by contact and alimentary route. Sporadic cases of HFRS are registered
during all year, predominantly in human. Group disease occurs predominantly in
summer and autumn.

Pathogenesis
The immune mechanisms play an important role in HFRS pathogenesis. The
cytokine production, complement pathway activation or an increase in circulating
complexes occur and play an important role during febrile and hypotensive stages.
Damage of the vascular endothelium, leakage, capillary dilation are significant
features of the disease.
Nitric oxide productions increase in the active phase of disease. In the kidneys
venous stage with serous – hemorrhagic edema development causes degenerative
changes in the epithelium cells and appearing of fibrin into kidneys canicula, so
serous-hemorrhagic nephritis in both kidneys and acute destructive and obstructive
hydronephrosis may develop.

Clinical Forms
1. Febrile stage lasts about 4-6 days. The asset of disease is abrupt
with high fever up to 40C. The patient complaints are headache, chills, abdominal,
back pain and malaise. During examination of patients can be revealed blushing of
the face, neck, chest, petechiae on the soft palate, axilla. Subconjunctival
hemorrhage bradycardia may be noted.
2. The hypotensive stage lasts from a few hours to 2 days. It is
characterized by decreasing of the blood pressure, tachycardia, acute abdominal
pain, convulsion or purposeless movements. Blood examination in this stage may
reveal the changes of coagulation profile such as elevation of the prothrombin time,
activation of partial thromboplastin time, prolongation of bleeding time.
3. The oliguria stage lasts about 3 to 6 days. The main signs in this
stage are oliguria, elevation of the blood pressure, tendency to bleeding, edema
(including pulmonary edema) thrombocytopenia. Anuria may be preserved then.
 4. The diuretic stage lasts 2-3 weeks and is characterized by increasing
of the diuresis (until 3 to 6 litters daily) rapid signs of dehydration and severe shock
in some cases. The main signs of previous stage disappear in many cases.
5. The convalescent stage lasts for as long as 3 to 6 months. The main
signs of hemorrhagic fever with renal syndrome begin to disappear from the
second week of disease, glomerular filtration rate normalizes during 3 to 6 months.
The renal tubular concentrating capacity recovers many mouths.

Diagnosis
Blood picture abnormalities revealed are the following: leucocytosis,
thrombocytopenia, elevation of hematocrit; prolonged bleeding time, elevation of
prothrombin time, activation of thromboplastin time in hypo stage; elevation of live
enzymes, blood urea nitrogen; hematuria, proteinuria can be evident;
hypernatremia, hyperphosphatemia, hyperpotassemia.
Serological tests can help in diagnosis. Enzymes linked immunosorbent
assay is useful for section of antibodies. For field rise in titer IgM for 1 week against
Hantaviruses are evident.
Hantavirus antigen can be detected in different tissues, in microvasculature
by immunohistochemical methods.

Treatment
The treatment depends on the stage of the disease, status of hydration and overall
hemodynamic patient’s condition.
Maintaining fluid and electrolyte balance is mandatory in the acute disease. Early
and effective fluid therapy is the cornerstone in the renal failure. The use of
vasoactive agents and albumin is recommended in shock period: excessive
administration of fluid can lead to extravasation due by vascular leak, especially
during the febrile and hypotensive stages. In oliguric stages diuretic is
recommended.
Dialysis is indicated if the patient is oliguric for a prolonged time with no response
to diuretics and renal failure is rapid with electrolyte abnormality and worsening
fluid.
Corticosteroids, prednisolone, hydrocortisone inhibitors of proteolysis (contrical),
vitamins (C, P) other symptomatic drugs can be used. Antihypertensive agent,
vasoactive drugs, colloids or diuretics may be needed to control hypertension, treat
shock, to induce diuresis.

38.Malaria. Epidemiology, pathogenesis, clinical forms, diagnostics,

treatment.

Epidemiology

The source of infection is infected humans, whose blood contains gametocytes,

patients with primary or relapsing form of malaria, and carriers. Humans can infect
mosquitoes during the very first days of malaria induced by P. vivax, P. ovale, and
P. malariae, and remain so until the parasites are contained in the blood.
Malaria falciparum patients become contagious only in 10-12 days after
development of the first malarial attacks.
Malarial plasmodium can be transmitted from an infected mother to the fetus
through the placenta, during labor or blood transfusion, through syringes and
needles, etc.
Susceptibility to malaria is high, especially in children, who make the
prevalent incidence in endemic areas. Strictly specific immunity to a given species
and strain is induced in persons who sustained malaria. The immunity persists only
on the condition of repeated infections. Immunity can be lost if a person leaves the
endemic area.

Pathogenesis
Paroxysms of malaria are associated with the response of the thermoregulation
centers to the release into blood of a great number of merozoites and other
proteins that are formed during division of schizonts and decay of red blood cells.
Foreign proteins cause a toxic allergic response in the patient. Malarial plasmodia
and their metabolites, the malarial pigment, and the products of protein
degradation evoke anaphylaxis: hyperadrenalinaemia, hyperglycemia,
hypercholesterolemia, hyperkalemia, and relative hyponatremia.
HyperadrenalAnalinemia provokes hypertension, tachycardia, spasm of the
peripheral vessels and upsets microcirculation in the internal organs.
Increased immunoglobulins (IgM, IgG), activated phagocytosis of invaded
erythrocytes and decay of the parasites in macrophages stop the first series of
paroxysms after the second or third attack. The disease passes into its next phase,
secondary occult period, or early (short) inter paroxysmal period. Due to imperfect
initial immune reactions, the blood fails to be completely freed from the parasites.
During early relapses, the developed immunity becomes sufficiently strong to
suppress schizogony and to promote clinical recovery.

Clinical Forms
Four forms of malaria are thus distinguished: tertian or vivax malaria, quartan
malaria, falciparum malaria, and ovale malaria.
The following periods are distinguished in the course of the disease: incubation
period, primary (acute) manifestations, occult period, relapses, and the recovery
period.
Paroxysms are characteristic of the disease. A typical paroxysm includes the "cold
stage", the "hot stage" and the "wet stage". The malarial paroxysm begins with the
cold stage: the patient is attacked by shaking chill that cannot be managed by
warm cover.
The severest course is characteristic of falciparum malaria. Its fever is irregular and
the paroxysms are long (lasting 24-36 hours and longer). The afebrile periods are
less pronounced. Chills and sweating are not characteristic because the
temperature variations are not very marked.
Attacks of vivax malaria usually develops in the morning; while in ovale malaria
macroorganism and the parasites is attained.
Tertian malaria (vivax and ovale) runs a benign course.
Quartan malaria is usually benign. It is characterized by a prolonged course and a
great number of relapses over many years.
Malaria in pregnant women is the cause of frequent abortion, eclampsia, premature
labor, and stillbirth.
Diagnosis
The laboratory methods include microscopy of thin (species identification) and thick
(detect organism) blood smears in which plasmodia are detected. The number of
malarial plasmodia are not great during the first attacks. Blood should therefore be
studied up to 3 times a day during 2-3 days. Blood specimens should be taken at
the height of fever as well as during apyrexia. In the blood analyses develop
anemia. Specific diagnosis of malaria is possible with serologic studies: indirect
immunofluorescent test, indirect haemagglutination and enzyme-labelled antibody
tests.
Treatment
All antimalarial preparations are divided into four groups:
1. Gametoschizotropic drugs, preventing development of erythrocytic
schizoites: quinine, mepacrine, proguanil, derivatives of 4- aminoquinoline:
chloroquine (chloroquine diphosphate), nivaquine (chloroquine sulphate),
plaquenil, amodiaquine, pyrimethamine.
2. Histoschizotropic preparations preventing development of trophozoites:
proguanil, 8-aminoquinoline derivatives (primaquine)
3. Gametocides destroying gamonts: pyrimethamine, 8-aminoquinoline
derivatives.
4. Sporontocides preventing maturation and growth of gamonts in the
mosquito stomach: proguanil, pyrimethamine, and 8-aminoquinoline derivatives.
In order to abate acute symptoms of all types of malaria, 4-aminoquinoline
derivatives are given to adults (after meals) in the following doses: chloroquine or
nivaquine, 2-2.5 g per course. The dose for the first intake is 1 g (4 tablets of 0.25
g), 0.5 g in 6-8 hours; on the second and third day, 0.5 g given for one intake.
Malaria due to the chloroquine-resistant strains P. falciparum and P. vivax should
be treated with quinine hydrochloride. The dose of 0.65 g (3V4 tablets of 0.2 g)
should be given 3 times a day for 10-14 days.
Radical cure is attained with a combination of quinine and tetracycline (0.5 g 4
times a day for 7 days).

39.Herpes virus infections. Epidemiology, pathogenesis, clinical forms,

diagnostics, treatment

Epidemiology

Varicella zoster virus (VZV) causes a primary infection known as varicella (chicken
pox). The virus then migrates from the skin lesions via nerve axons and, probably
also by viremic spread, to spinal and cranial sensory ganglia where it becomes
dormant. Later in life, in some individuals the virus is reactivated (usually within a
single ganglion) to cause a secondary infection known as herpes zoster (HZ;
shingles). Individuals with HZ can transmit VZV to their seronegative contacts, who
may develop varicella, but not HZ . The household transmission rate of HZ (to
cause varicella) is 15%, making it significantly less contagious than varicella but
nevertheless of relevance to at-risk contacts.

Pathogenesis
The primary infection, chickenpox, is a contagious and usually benign febrile
illness. After this infection resolves, viral particles remain in the dorsal root or other
sensory ganglia, where they may lay dormant for years to decades.
In this latent period, host immunologic mechanisms suppress replication of the
virus, but VZV reactivates when the host mechanisms fail to contain the virus.
Such failure may result from a wide spectrum of conditions, ranging from stress to
severe immunosuppression; occasionally, it follows direct trauma. VZV viremia
occurs frequently with chickenpox but also may arise with herpes zoster, albeit with
a lower viral load.
Once VZV is activated at the spinal root or cranial nerve neurons, an inflammatory
response occurs that also encompasses the leptomeninges; both plasma cells and
lymphocytes are noted. This inflammation in the dorsal root ganglion can be
accompanied by hemorrhagic necrosis of nerve cells. The result is neuronal loss
and fibrosis.

Clinical Forms
Shingles is always localized along the nerve trunks, very often in the intercostal
nerve, and in the branches of the trigeminal nerve; one-sided destruction and pain.
In most cases, rash appear on the body, but can appear on the face and even over
the sculp. Skin rash is almost always preceded by malaise, itching, low-grade body
temperature, neuralgic pain and tingling in the future rash area.
The next stage is characterized by the appearance of swollen pink spots that within
3-4 days are grouped into erythematous rash that quickly turns into blisters. After
6-8 days’ blisters begin to dry out and crust over, the crusting skin will fall off
naturally, remaining slight pigmentation. After the rash disappearance some
patients may have postherpetic neuralgia, which is very difficult to treat.

Diagnostics

-microscopy - varicella zoster virus is large enough and is visible even in

normal light microscope.
-serologic methods, based on the determination of the titer of antibodies
specific to the virus Varicella zoster.
-immunofluorescence method.
-culture method of growing the virus in culture medium.

Treatment

The main objectives of the disease treatment:

-the acceleration of the healing process;
-maximum pain reduction;
-prevention of possible complications;
- reduction of chance of postherpetic neuralgia.
For herpes zoster treatment various antiviral medications are used: Isoprinosine,
valacyclovir, acyclovir, penciclovir, famvir.
These medications penetrate into the viral DNA, allowing to disrupt viral replication,
i.e. to suppress the process of its reproduction.
At the initial stage of the disease the use of antiviral drugs can reduce pain, reduce
the duration of the disease and reduce the chance of post-herpetic neuralgia.
Treatment of herpes zoster often involves taking pain relievers: dexketoprofen,
naproxen, ibuprofen, ketorolac and ketoprofen.

40.Psittacosis (ornitosis). Epidemiology, pathogenesis, clinical forms,

diagnostics, treatment

Epidemiology
The natural harbor of the ornithosis agent are birds (wild and domesticated).
Chlamydial psittaci has been isolated from more than 140 species of birds.
Humans are usually infected by poultry (ducks, turkeys, less frequently hens).
Pigeons are the most dangerous psittacine birds. Besides natural and secondary
foci of ornithosis, epizootics occur at poultry-raising farms the origin of which is
difficult to relate to any natural nidus or to transmission of the disease by wild birds
or pigeons. The source of infection can in such cases be birds in which the
infection is latent. The infection generalizes due to decreasing resistance during
laying eggs, overcrowding, cold, or other adverse factors. It is believed that a
ornithosis s patient is not contagious; nevertheless, hospital-acquired infections
have been reported. The main routes of infection transmission are dust- and air-
borne; hence the lungs are usually involved. Infection is transmitted through
infected down and feather, during inhalation of dust containing the bacteria, by
contamination of the mouth or eye mucosa with soiled hands. This happens in
poultry raisers, during slaughtering and processing of poultry, or eating unboil
eggs. Outbreaks of occupational disease among poultry raisers and
slaughterhouse workers usually occur during the spring or autumn which is
connected with care of the young birds and mass-scale slaughter of poultry. The
susceptibility to ornithosis is high. Women are usually affected occupationally. The
immunity produced in those who sustained the disease is unstable.

Pathogenesis
The main portal of entry is the mucosa of the upper airways. Multiplication
and accumulation of the agent occurs in the lungs where it is brought with the
blood. From the lungs, the pathogenic microbe is brought back to the blood that
carries it to the liver, spleen, adrenal glands, nervous system, or myocardium
where it multiplies to cause fine foci of degenerative and proliferative changes and
hemorrhages. The agent circulates for 7-10 days. Chlamydia produce a toxic effect
that accounts for the main clinical symptoms.
Depending on the organs and tissues involved, the following clinical forms of the
disease are distinguished: influenza-like, pneumonic, typhoid, and meningeal. The
pathogenic agent is retained in the cells of macrophage systems which causes
relapses of the disease and its conversion into chronic forms.

Clinical Forms
The incubation period usually lasts from 7 to 10 days with extremes of 6 and 25
days. The onset is usually acute: the patient develops chills, headache, myalgia
and pyrexia (remittent fever). Hyperhidrosis, nausea, vomiting and poor appetite
are also among the symptoms.
The influenza-like form is manifested by dry cough and the symptoms of laryngitis
and tracheobronchitis that develop in 2-3 days.
In pneumonia-like form, cough intensifies on the 5-7th day and the patient
expectorates mucoid or mucopurulent sputum; moist rales can be heard in the
lower portions of the lungs; respiration is weak.

The fever period lasts from 2 to 4 weeks. The body temperature decreases
lytically and the recovery phase begins slowly. Exacerbations and relapses of the
disease are possible. In severe ornithosis, coma develops in 4-5 days and the
patient dies of cardiac and/or respiratory failure. The patient can die in 2-3 weeks
due to lung edema.
The typhoid form is characterized by signs of toxemia. The patient complains of
poor appetite, constipation, aching pain in the entire body. Hepatic and splenic
enlargement becomes obvious in 5-7 days. Examination fails to reveal any
symptoms of lung involvement.
The meningeal form is rare. The disease begins acutely; the symptoms of
meningitis supervene in 2-4 days. Fever persists for 3-4 weeks.
Diagnosis

Laboratory examinations include direct and indirect complement fixation tests and
haemagglutination. A 5-ml specimen of blood is taken from the cubital vein into a
dry sterile test tube in 4-7 days after the onset of the disease. At least two portions
of the blood are tested at 7-10-day interval. Antibiotic therapy slows down
accumulation of antibodies; therefore, the third portion of blood should be tested in
20-30 days from the onset of the disease. The diagnosis of psittacosis is confirmed
if at least two-fold increase in the antibody titre is noted.
Haemagglutination reaction, inhibition of haemagglutination and indirect
haemagglutination reactions are also used.
Ornithosis agents can also be cultivated on chick embryos.

Treatment
The tetracyclines (tetracycline, oxytetracycline, terramycin, etc.) are most effective.
They are given in doses from 1.2 g to 2 g a day, depending on severity of the
disease and the body weight of the patient. Duration of the therapy is from 3-5 to 9-
10 days after normalization of body temperature.
Oxygen therapy, vitamins and cardiacs are given for special indications. Plasma or
blood (autohaemotherapy included) should be given during the recovery phase. In
the presence of contraindications, vaccine therapy should be given for chronic
psittacosis.

41.Amebic infection. Epidemiology, pathogenesis, clinical forms,

diagnostics, treatment

Epidemiology
Travelers to endemic areas are at risk for infection. Amebic liver abscess
has been reported in travel exposures as short as 4 days (median, 3 months),
whereas amebic colitis is uncommon in short-term travelers. In one study, 10% of
individuals returning with diarrhea were found to have amebiasis. In another, the
rate of acute amebic diarrhea ranged from 1.5% in travelers returning from
Southeast Asia to 3.6% in those returning from Central America, with an overall
rate of 2.7%.
E histolytica is transmitted primarily through the fecal-oral route. Infective
cysts can be found in fecally contaminated food and water supplies and
contaminated hands of food handlers. Sexual transmission is possible. Poor
nutrition, through its effect on immunity, has been found to be a risk factor for
amebiasis.

Pathogenesis
Ingestion of E histolytica cysts from the environment is followed by excystation in
the terminal ileum or colon to form highly motile trophozoites. Upon colonization of
the colonic mucosa, the trophozoite may encyst and is then excreted in the feces,
or it may invade the intestinal mucosal barrier and gain access to the bloodstream,
whereby it is disseminated to the liver, lung, and other sites. Excreted cysts reach
the environment to complete the cycle.
Spread of amebiasis to the liver occurs via the portal blood. The pathogenic strains
evade the complement-mediated lysis in the bloodstream.
Spread of amebiasis to the liver occurs via the portal blood. The pathogenic strains
evade the complement-mediated lysis in the bloodstream. Serum antibodies in
patients with amebic liver abscess develop in 7 days and persist for as long as 10
years. A mucosal IgA response to E histolytica occurs during invasive amebiasis.

Amebic colitis is gradual in onset, with symptoms presenting over 1-2

weeks; this pattern distinguishes this condition from bacterial dysentery. Diarrhea
is the most common symptom. Patients with amebic colitis typically present with
cramping abdominal pain, watery or bloody diarrhea, and weight loss or anorexia.
Fever is noted in 10-30% of patients. Intestinal amebiasis may mimic acute
appendicitis. Rectal bleeding without diarrhea can occur, especially in children.
Amebic liver abscess is the most common form of extraintestinal
amebiasis. It occurs in as many as 5% of patients with symptomatic intestinal
amebiasis and is 10 times as frequent in men as in women.
The most typical presentation of amebic liver abscess is fever (in 85-90% of
cases, in contrast to amebic colitis), right upper quadrant pain, and tenderness of
less than 10 days’ duration. Involvement of the diaphragmatic surface of the liver
may lead to right-side pleuritic pain or referred shoulder pain. Acute abdominal
symptoms and signs should prompt rapid investigation for intraperitoneal rupture.
Clinical Forms

E histolytica is capable of causing a spectrum of illnesses. Intestinal

conditions resulting from E histolytica infection include the following:
● Asymptomatic infection
● Symptomatic noninvasive infection
● Acute proctocolitis (dysentery)
● Fulminant colitis with perforation
● Toxic megacolon
● Chronic nondysenteric colitis
● Ameboma
● Perianal ulceration
Extraintestinal conditions resulting from E histolytica infection include the
following:
● Liver abscess
● Pleuropulmonary disease
● Peritonitis
● Pericarditis
● Brain abscess
● Genitourinary disease

Diagnostics

Findings from basic blood tests may include the following:

● Leukocytosis without eosinophilia (80% of patients)
● Elevated alkaline phosphatase level (80%)
● Elevated transaminase levels
● Mildly elevated bilirubin level
 ● ReducThe loop-mediated isothermal amplification (LAMP) assay has
been applied to the detection of E histolytica in cases of hepatic amebiasised
albumin level
● Mild anemia
● Elevated erythrocyte sedimentation rate (ESR)
Microscopic examination of fresh stool smears for trophozoites that contain
ingested red blood cells (RBCs) is commonly done.
Cultures can be performed either with fecal or rectal biopsy specimens or
with liver abscess aspirates.
Enzyme-linked immunosorbent assay (ELISA) is used to detect antigens
from E histolytica in stool samples.

Treatment
Metronidazole is the mainstay of therapy for invasive amebiasis. Tinidazole
has been approved by the US Food and Drug Administration (FDA) for intestinal or
extraintestinal amebiasisAmebic liver abscess of up to 10 cm can be cured with
metronidazole without drainage. Clinical defervescence should occur during the
first 3-4 days of treatment. Failure of metronidazole therapy may be an indication
for surgical intervention. Treatment with a luminal agent should also follow.
The indications for drainage of amebic liver abscess include the following:
● Presence of a left-lobe abscess more than 10 cm in diameter
● Impending rupture and abscess that does not respond to medical
therapy within 3-5 days
Percutaneous catheter drainage improves treatment outcomes in amebic
empyema and is life-saving in amebic pericarditis. It should be used judiciously in
the setting of localized intra-abdominal fluid collections.

42.Leptospirosis. Epidemiology, etiopathogenesis, clinical

manifestation, diagnostic test, therapy
Epidemiology

The reservoirs and sources of leptospirosis are subdivided into two groups.
The main natural reservoirs are rats mice, moles. The main reservoirs of infections
are dogs, rabbits, hole hogs, cows , sheep, raccoons, opossums, skunks and
marine mammals. In Africa the landed mongoose has been identified as a carrier
of the pathogen.
Humans become infected through contact with water, food, of soles,
containing urine from infected wild or domestic animals. Leptospirosis is also
transmittedvia the semen of infected animals.
Occupations at risk include farmers, veterinarians, slaughterhouse workers,
sewers maintenance workers, waist disposal facility workers, land surveyors and
people working on derelict buildings. The incidence of leptospirosis correlates
directly with the amount of rainfall, making it seasonal in driest climates and year-
round in tropical countries. Summer–autumn seasonal characteristics are more
typical for leptospirosis. The dogs may excrete leptospiras during some months
until 3-8 years, cats – until 4 months, the rodents can be reservoirs of infection
during all life.

Etiopathogenesis
Leptospirosis is caused by spirochete bacteria belonging to the genus
leptospira. 21 species of leptospira have been identified, about 250 pathogenic
serovars of leptospira are recognized.

There are some phases in pathogenesis of leptospirosis:

● Phase of invasion. Leptospira penetrates into the human body through
damaged skin and mucous membranes to the blood stream. After that the
microorganism heads to the lever, kidneys, nervous system with intensive
penetration. This phase corresponds to the incubation period.
● Phase of dissemination. This phase is characterized by the secondary
leptospiras with following damaging of the liver, spleen, kidneys, supra renal
glands, membranes of the brain. Degenerative changes, necrosis can
develop in hepatocytes, epithelium of renal caniculars, epithelium of
 erythrocytes and capillaries, Doric metabolites appeared in the blood. This
phase corresponds to the initial period of disease.
● Toxinemia phase. In this phase damaged of capillary endothelium,
increased of the vessels permeability which can lead to the hemorrhagic
syndrome development with damaging of the liver, kidneys, suprarenal
glands. It corresponds to the clinical manifestations stage. Toxins in
pathomorphological and functional changes in different organs are
pronounced Generalized cappilarytoxicosis, mereasing vessel permeability
with DTV syndrome, microcirculation disturbances, different hemorrhagic
changes (hemorrhagic rash) . Bleeding from different organs are
characteristics. Damaging of the liver is associated with mechanical invasion
of leptospira into hepatocytes, endotoxinemia. Destructive processes,
hemorrhagic, histiolymphocytic infiltrates in sceletal muscles can lead to
intensive muscles pain in this disease.
● Formation of immunity phase. Formation of immunity is associated with
specific antibody appearance and activation of fagocytes. But leptospiras
can be still in the human body. From the second week microorganism
localized in the kidneys caniculas can still be contained in urine until 40 days
from the disease onset.

Clinical manifestation
The incubation period in leptospirosis is from 7 to 14 days , but can lasts
until 1 month. There are icteric and anicteric forms of disease, mild, average
severity, severe. This disease is cyclic, biphasic, that begins suddenly.
The first phase (acute or septicemic) begins from flu-like symptoms
appearing . The temperature elevated until 39-40 C isregular , accompanied by
chills. The patient complaints are intensive headache, severe myalgia (muscle
ache), abdominal pain , weakness, poor appetite. The patient face becomes
hyperemic, edematic with herpes on the lips and nose sometimes. Conjunctival
suffusion hemorrhage onto scleras, conjunctiva, red color of oropharynx can
berevealed. Hemorrhagic syndrome: petechia, hemorrhage on injections places,
hemorrhagic rash on axillary region , upper extremities, hematuria, nasal leading
can recognized. The first stage ends after 3-7 days of illnesses. The patient is as
symptomatic during 2-4 days until the second phase begins with another episode
of fever.
The main signs of pronounced clinical manifestations in second phase are:
1. Development of DIS symptoms andmassive hemorrhage in subcutaneous
muscles and abdominal cavity, gastric, intentional, pulmonary,
uteryhemorages, hemoragic edema;
2. Nausea, vomiting pain in epigastric, right hypochondrium regions, stool
disturbances are typical sings their period;
3. Urine becomes dark or reddish, includes high number of protein, leukocytes
, erythrocytes , cards. Oliguria or anuria leads to progressive renal
insufficiency.
4. Damaging of nervous system is characterized by headache, insomnia,
aggressive patient’s condition.
5. The hallmark of the second phase is aseptic meningitis, encephalitis
6. Classic form of severe leptospirosis is known as Well’s disease which is
characterized by lever damage, kidneyfailureand bleeding.
7. Other severe manifestations are extreme fatigue, hearing loss, respiratory
distress and azotemia.
90% percent of cases of the disease are mild leptospirosis.
Myocarditis, pericarditis, uveitis are also possible features.
The illness lasts from a few days to 3 weeks or longer. Without treatment
recovery may take several months.
The second stage is called hypotensive stage. It lasts from few hours to2
days and occurs in 11% of patients. Tachycardia, decreased blood pressure
abdominal pain , convulsions or purposeless movements are characteristics.
The oliguric stage occurs in 68% of patients, lasts from 3 to 7 days. This
phase is characterized by the onset of renal failure and proteinuria. Oliguria,
hypertension ,bleeding tendency, edema, pulmonary edema sometimes are typical
signs is their stage.
 The diuretic stage lasts for 2 weeks. Diuretic is this stage range of 3-6 either
per day, rapid signs of dehydration and severe shock in some cases. Usual signs
from the previous stage of disease disappear and convalescent stage follows.
Convalescence stage lasts about 3 to 6 months. During this stage gradual
resolution of symptoms, azotemia, glomerular filtration rate is normalized and
improves.

Diagnostic

Laboratory:
A CBS count is necessary in significant anemia, platelet count diminished in
hemorages .
DIC levels of blood urea nitrogen, serum creatinen can be elevated in
oliguria and anemia. In addition, potassium wasting and renal magnesium occur in
this disease .
Serum bilirubin levels of the hepatocytes-cellular transaminase are elevated
in hepatocellular damaging.
Alkaline phosphates levels can be elevated 10 fold too .
Coagulation times can be elevated in patients with the muscular
involvement. In the signs of meningitis leptospires is routinely isolated from the
cerebrospinal fluid.
Image studies

In the chest radiography, cardiomegaly and pulmonary edema due to myocarditis

can be revealed .in patients with alveolar hemorrhage due to pulmonary capillaries
multiple patchy infiltrates can be revealed in the lung parenchyma.
Billiary tract ultrasonography can reveal an acalculous cholangitis.
For histological examination, silver staining and immunofluorescence are
used. Leptospirosis can be identified in the liver, spleen , kidney , nervous system ,
muscles, heart.

Therapy
 There are some antibiotics, which are effective: cefotaxime, ceftriaxone,
penicillin 6, doxycycline, amoxicillin. Domicile is used in dose 100 mg orally every
12 hours for 7 days , penicillin 6 1-1,5 mg every 4 hours for 1 week.
Supportive therapy measures include detoxification and normalization of the hydro-
electrolytic balance. Infusions of glucose, slot solution can be administered,
dialysis is used in serious causes.

43.Toxoplasmosis. Epidemiology, pathogenesis, clinical forms,

diagnostics, treatment.

Toxoplasmosis is an anthropozoonotic infection which is characterized by acute and

chronic course, polymorphic clinical manifestation in acquired and congenital infection.
Epidemiology
Toxoplasma Gondi infection has worldwide distribution. Distribution of this disease is in
Latin American 50-80%, Esther and Central Europe 20-60%, Southeast Asia 30-50% and
Africa 20-60%.
Toxoplasmosis occurs in more than 220 mammals and 110 kinds of birds. The main source
of toxoplasma Gondi infection is cats, more rare- rabbits, pigs and domestic birds: ducks,
chicken, geese.
Invasion of people organisms with toxoplasma Gondi maybe through the different routes.
Oral transmission may be occurred through the following:
1. Infection of raw or partly cooked meat, especially lanes, pork or venison containing
toxoplasma cysts. Rarely infection of eggs, milk with can be reason of infection
transmission.
2. Infection during hand to mouth contact after handling, uncooked meat or from using
knives, utensils or cutting boards, contaminated by raw meat.
3. Infection of unwashed fruits or vegetables that have been in contact with contaminated
by the infected cat soil,
4. Infection through the hand to mouth contact follow in gardening, cleaning a cat’s box,
contact with children’s sandpits.
Pathogenesis
T gondii oocysts are ingested in material contaminated by feces from infected cats. Oocysts
may also be transported to food by flies and cockroaches. When T gondii is ingested,
bradyzoites are released from cysts or sporozoites are released from oocysts, and the
organisms enter gastrointestinal cells. Host cell receptors consisting of laminin, lectin, and
SAG1 are involved in T gondii tachyzoite attachment and penetration. Tachyzoites
multiply, rupture cells, and infect contiguous cells. They are transported via the lymphatics
and are disseminated hematogenously throughout the tissues.
The ability of T gondii to actively penetrate host cells results in formation of a
parasitophorous vacuole that is derived from the plasma membrane, which is entirely
distinct from a normal phagocytic or endocytic compartment. Following apical attachment,
the parasite rapidly enters the host cell in a process that is significantly faster than
phagocytosis. The vacuole is formed primarily by invagination of the host cell plasma
membrane, which is pulled over the parasite through the concerted action of the actin-
myosin cytoskeleton of the parasite. During invasion, the host cell is essentially passive and
no change is detected in membrane ruffling, the actin cytoskeleton, or phosphorylation of
host cell proteins.
Tachyzoites proliferate, producing necrotic foci surrounded by a cellular reaction. Upon the
development of a normal immune response, tachyzoites disappear from tissues. In
immunodeficient individuals and in some apparently immunologically healthy patients, the
acute infection progresses, resulting in potentially lethal consequences such as pneumonitis,
myocarditis, and necrotizing encephalitis.
Tissue cysts form as early as 7 days after infection and remain for the lifespan of the host.
The tissue cysts are up to 60μm in diameter, each containing up to 60,000 organisms. They
produce little or no inflammatory response but cause recrudescent disease in
immunocompromised patients or retinochoroiditis in congenitally infected older children.
So there are some stages in toxoplasmosis development:
- Invasion of the pathogen
Lymphadenitis in regional lymph nodes with hyperplasia development and inflammatory
granulomatous process in lymph
- Hematogenous dissemination, (parasitemia)
- Development of immune responses, formation of the in trace, tissue cysts
clinical forms
There are acquired and congenital toxoplasmosis. The course of this disease may be acute,
chronic and latent
Toxoplasmosis:
1. Acquired:
-acute
- latent
- chronic
2. Congenital:
- acute
- subacute
- chronic
In 80-90% children and adults toxoplasmosis remain to be unrecognized. Often people
become infected with primary- latent toxoplasmosis development. It's asymptomatic
infection with acute acquired toxoplasmosis. Incubation period in toxoplasmosis is 3 to 14
days.
The most typical sign of their form of toxoplasmosis is enlargement of lymph nodes.
Swollen lymph nodes are found in the neck, occipital, axillary regions, followed by the
armpits and groin regions. In adults and swollen lymph nodes are recognized at single sites,
back in children generalized lymphadenopathy can be found.
Myalgias, maculopapularrash, throat pain, abdominal pain , confusion. Clinical
manifestation of acute toxoplasmosis lasts during some weeks, but enlarged lymph nodes
will resolve within once to two months in 60% , in other cases – within two to six months.
A substantial number 60% lymph nodes do not return to normal until much later.
Acute toxoplasmosis after disappearing of the symptoms lead to chronic secondary
toxoplasmosis or secondary latent toxoplasmosis.
Chronic toxoplasmosis is characterized by gradual onset the long course of disease with
remission. With damaging of the nervous system brain , eyes, endocrine system ,specific
myositis is typical, chorioretinitis, uveitis may be reveled in patients with HIV/AIDS
infection.
Acute congenital toxoplasmosis is characterized by the signs intoxication: fever,
hepatosplenomegaly with jaundice ,pneumonia myocarditis sometimes hemorrhagic
syndrome.
In subacute congenital toxoplasmosis signs of meningoencephalitis are characteristic.
For acquired toxoplasmosis there is a triad of typical manifestations. They are
hydroencephalopathy, choreoretinitis, intracerebral calcificates.
Diagnosis
Diagnostics of human toxoplasmosis is made by biological, serological, histological or
molecular methods or their combination. Toxoplasma gondii may be detected in blood ,
amniotic fluid.
The most commonly used biological tests are the Sabin Feldman dye tests, indirect
hemaggluttination assay, latex agglutination tests, Immunosorbent agglutination
assay test (enzyme linked immunosorbent assay) revealing of igM in the blood and
increasing its titers in immunodyes.
T. gondii IGM antibodies may be detected a week after acquiring primary infection and
decreases within one to six months. IgG specific antibodies appear within a week or two of
infection peak within 1 to 2 months and decline at various rates. Toxoplasma IgG
antibodies generally persist for life. They may be present in blood as result of previous
infection.
Treatment
Indications for treatment are:
• Acute toxoplasmosis
• Severe and prolonged course of toxoplasmosis, including chronic toxoplasmosis
• Preventive treatment of the pregnant women infected with toxoplasma gondi or in acute
toxoplasmosis.
• Congenital toxoplasmosis in children with clinical manifestations of this disease.
The combination of pyrymethamine-sulfa drugs is the best treatment of toxicoplasmosis.
Pyrymethamine is given orally of 50-75 mg in adults or 2mg in children once a time daily.
A leading dose can be used every 2 to 3 days after that pyrimethamine in daily dose 25 mg
for adults and 1 g/kg for children may be used during 4 – 7 days. Usually it is to use 2-3
cycles with 10 day intervals.
The dosage of sulfadiazine is 2 to 4g per day for adults and 50-100 mg/kg per day for
children in two or three divided doses.
The combination of pyrymethamine 25 and sulfadoxine in tablets is given orally at dosage
one tablet/20kg body weight every 4 to 10 days.
It is necessary to monitor the blood count, because in treatment with pyremethamine of the
bone marrow depressions, resulting of thrombocytopenia, anemia can develop. In treatment
with drugs the development of leucopenia and granulopenia is possible.
Folinic acid 50 mg orally or intramuscular injections every 3 to 6 days can prevent it.
Spiromycine (50-100 mg/kg in infants and 3 gr daily in adult can prevent mother-fetal
transmission.
It is necessary to have 7 days course of treatment with these drugs with interval of 7 to 10
days.
In immunodeficiency after the course it is necessary to prescribe pyrimethamine (20-50
mg/ kg daily dose) and sullatizine (2-4 g/daily dose) or with one pyrymethamine (50-
75mg) daily during all life.
For pregnant women spyromycine 3 ml 6 days 3 times daily during 2-3 weeks.
Specific immunotherapy with toxoplasmine must be used intracutaneously.

44.Brucellosis. Epidemiological features, pathogenesis, clinical sings,

diagnostics, specific therapy

This infection is caused by microorganisms of six species Human brucellosis is due to the
following three species: B. melitensis (goats), B. suis (hogs) and B. abortus (cattle).

Epidemiology.
Brucellosis is a typical zoonosis because the reservoir of infection is domestic animals. It
has already been said that goats and sheep are the commonest source of infection in man.
Cattle and swine are less important. If healthy and diseased animals of various species are
raised together, brucella migrates from goats to cattle and other animals. Outbreaks of the
disease in man thus become possible. Cats, dogs, camels, deer, horses are a secondary
reservoir of the infection. A diseased man presents no danger to the surrounding people.
Diseased animals shed the pathogenic microorganisms with amniotic fluid, abortus, urine,
dung, and milk. Besides, the organisms are contained in the blood and flesh of the animals.
The infection is usually transmitted by direct contact with the animal excrements and
objects infected by these excrements. Humans get infected when taking care of the animals,
during milking, shearing, etc. Another route of infection transmission is through
infected foods, such as raw milk, curds, sheep cheese prepared from raw milk, and
also through meat of the diseased animal. There is still another, although rare, route of
infection transmission: by airborne droplets. Humans get infected during processing wool
of the diseased animals. Since brucella survives for a long time in water, water-borne
infection should not be excluded either.
Brucellosis is an occupational disease of animal breeders and farm workers.
The highest incidence of the disease is during the spring and summer. The main mechanism
is alimentary.
Pathogenesis.
When the pathogenic organism gets inside a human, through a damaged skin or mucosa, it
passes with the lymph to regional lymph nodes where it multiplies during the entire
incubation period. By the moment when the disease becomes clinically manifest, brucella
enters the blood and is carried to various organs and systems: the liver, spleen, bone
marrow, and the lymph nodes. Secondary foci of infection thus develop. In a considerable
number of persons, the acquired immunity does not ensure elimination of the causative
agent. Retention and multiplication of brucella in the infection focus, repeated release of
the organisms into the blood, and endotoxaemia account for the sensitization of the person
to various allergens. If untreated, the disease converts into its chronic form with periodic
exacerbation and remissions. Allergic changes are manifested by systemic lesion of the
vessels, inflammation in the organs, arthritis, fibrositis, etc.
Clinical picture
The incubation period lasts for 2-3 weeks, with variation from one week to two months.
The disease is sometimes asymptomatic and can only be diagnosed in the laboratory. Acute
brucellosis (lasting to 3 months from the onset of the disease), subacute (from 3 to 6
months), chronic brucellosis (longer than 6 months).
According to severity, the disease is classed as mild, moderate and severe.
An acute form of brucellosis often begins with a prodromal period. The patient complains
of malaise, lassitude, depression, deranged sleep, lumbar pain, myalgia and arthralgia,
chills. The prodromal period lasts from several days to a few weeks.
The body temperature suddenly rises to hyperpyrexia. The elevation of temperature is
attended by chills. The fever then lessens and sweating is profuse. Despite fever, the
patient's general condition remains normal and his working capacity is preserved. The
patient then complains of rapid fatigue, headache, irritability, transient pain in some large
joints. Fever can be undulant, remittent, intermittent, or, less frequently, continuous. Lymph
nodes, usually submandibular and cervical, less frequently axillary and inguinal lymph
nodes are enlarged in some patients. The spleen and liver are enlarged from the first days of
fever; the condition persists for a long time. These organs become firm.
By the end of the second week of the disease the patient develops pain in some large joints.
Pain comes in attacks (undulant). It is due to arthritis and periarthritis, periostitis, bursitis,
myositis, fibrositis, cellusitis, etc. Headache and pallor are due to the lesion of the central
nervous system. Excitability and whining are characteristic.
Subacute brucellosis, in addition to the mentioned symptoms, is also characterized by focal
allergic lesions in the form of arthritis, neuritis, plexitis, etc.
Subacute brucellosis can gradually transform into chronic brucellosis which is
characterized by a further reconstruction of allergic response with involvement of other
organs and systems. The body temperature is usually subfebrile or normal during weeks
and months (remissions). The chronic form of the disease is usually characterized by stable
changes in the locomotorium (arthritis, bursitis, tendovaginitis, periostitis, perichondritis)
and in the nervous system (radiculitis, ischioradiculitis, plexitis, neuralgia).
The genital system is also involved: orchitis (inflammation of the testes), orchiepididymitis
(inflammation of the testes and the epididymis) in males and oophoritis (inflammation of
the ovaries and the tubes), endometritis, and abnormal menstrual cycle in women.
Chronic brucellosis proceeds with relapses and remissions and can last 2-3 years. After the
patient recovers, residual phenomena are possible: pain in the joints and muscles, headache,
irritability, organic changes in the locomotorium with deformation of the joints, etc.
Diagnosis
A properly collected epidemiologic anamnesis and laboratory studies help establish a
correct diagnosis. Isolation of brucella from the blood, bone marrow, urine, and the lymph
nodes is diagnostically decisive although these studies take much time.
Blood cultures are inoculated with 5-10 ml blood specimens taken from the ulnar vein of
patients before the antibiotic therapy is started. It is recommended to cultivate specimens of
blood, bone marrow and lymph nodes of patients with chronic brucellosis during
exacerbation before treatment begins.
Serologic tests, the immunofluorescent method, Coombs' test, direct haemagglutination
test, and intracutaneous allergic test are used for serologic diagnosis of brucellosis. Wright
and Huddleson tests are positive beginning with the 8-9th day of the disease, while the
Burnet test in 7-8 days and later. A specimen of blood taken from the finger or the vein (1-
2 ml) is tested (Wright's reaction) and result is considered positive with serum dilution of
1:200 and more. The Huddleson test can be carried out at patient's bedside (1 ml of blood).
But this reaction is qualitative and the agglutination titres remain unknown. The test is
suitable for screening of population before prophylactic vaccination.
The reaction of direct haemagglutination is more specific. It is positive with the dilution of
1:100.
The Burnet intracutaneous test is performed after the 10th day of the disease. Brucellin is
injected into the skin on the palmar surface of the middle third of the forearm. A painful
edema develops in 24-48 hours (positive test). The size of the edema is measured: if the
edema is from 1 to 3 cm in diameter, the reaction is weakly positive, if 4-6 cm-positive,
and greater than 6 cm-highly positive.
Coombs' test is used in chronic forms of infection. The reaction is based on the detection of
incomplete antibodies using antiglobulin serum. The luminescent serologic test consists in
applying a fixed smear of labelled serum in the working dilution. The smear is examined in
a luminescent microscope.
Treatment
Patients with acute brucellosis and exacerbated chronic brucellosis should be taken to
hospital.
Antibiotics are given to patients with acute, subacute and exacerbated chronic brucellosis
with signs of marked toxemia and high fever. The tetracyclines and terramycin are most
efficacious. They are given in a dose of 0.3 g 4 times a day. Chloramphenicol (0.5 g 4 times
a day) and other antibiotics are also useful. The mentioned preparations are given per os for
5-7 days. The course is repeated at a 5-day interval.
Vaccine therapy is indicated after 2-3 courses. The vaccine should preferably be given
intravenously. In the presence of contraindications, it can be given intracutaneously.
The vaccine is administered intravenously in two steps. The daily dose of the vaccine is
administered not by a single injection but in two portions at a 90-120-minute interval. From
7 to 10 administrations are necessary at 3-5 day intervals between the injections.
Especially severe cases of brucellosis with involvement of the joints, the central and
peripheral nervous system, orchitis, etc., are treated with prednisolone and prednisone (in
addition to antibiotics), given in a dose of 20-30 mg for 4-6 days. The corticosteroid
therapy is combined with butadione and other anti-inflammatory preparations.
Symptomatic treatment should also be given: invigorating measures, preparations
improving appetite, vitamins B and ascorbic acid, cardiacs and analgesics. To release
arthralgia, 3, 5 or 10 ml of a 0.25 per cent Novocain solution are injected intravenously.
Physiotherapy is widely used in brucellosis. Residual phenomena should be corrected by
medical exercises and massage. Health-resort therapy is indicated in 6 months after
recovery.

45.Differential diagnosis of salmonellosis from shigellosis. Agent of

disease, leading syndromes, clinical manifestation, diagnostics tests.

Salmonellosis
1. Agent of the s.typhimurium,s.heideberg,s.london,
disease s.cholerae-suis,s.debri,s.enteridis,
s.anatum, includes 2 antigens 0-
somatic, H-flagella, grm –ve motile
2. leading -renal syndromes
syndromes (azotemia,oliguria)
-dypeptic syndrome(impaired
appetite)
-intoxication syn(weakness,
headache, Chills,nausea,vomiting)
-pain syn(epigastric pain)
Shigellosis
s.dysenteriae,flexnerii,boydii,
s.sonei, gram –ve, non motile
bacilli.
-intoxication syn(high fever,
malaise, weakness, t>40°c
- dyspeptic syn(diarrhea with
blood + mucus
-pain syn-lower part left side
of abdomen
3. special A) Gastrointestinal form
features of  Incubation period is 24-48
clinical hours
manifestations  Acute onset
 2 syndromes:-
- intoxication & dysfunction
of gastrointestinal tract
 Recurrent & abundant
vomiting
 Stool is watery profuse,
frothy & fetid
 Meteorism murmurs in
bowel
 Painfulness in epigastrium
& ileoceccal areas around the
umbilicus “Salmonellosis
Triangle”
B) Gastric variant
 Abdominal pain in
epigastrium, nausea,
recurrent vomiting
 Diarrhea is absent
C) Gastroenterocolitis
 Intoxication, diarrhea with
admixture of mucus & blood
D) General form – Typhoidal
fom
 Fever till 40 C, adynamia,
hallucination, insomnia,
hepatosplenomegaly
 Rare spots, relative
bradycardia
 Bacteremia from 1 st day
develop as sepsis
 Remittent & irregular
temperature
C/P is usually less than
48hrs:2main symptoms
1. intoxication symptoms
(inc temp,disoreders of
CNS,weakness,malaise)
2. dyspeptic symptoms
(diarrhea w mucous &
blood)
 if the disease is mild
:watery diarrhea,minimal
systemic involvement &
mild dehydration
 in severe cases: crampy
abd pain,temp. > 40°
lasting 1-3 days
,diarrhea,containing
blood &mucous,there
maybe severe
intoxication leading to
CNS involvement
(seizures,convulsions &
etc)
-Diarrhoea is charact by
10-30 x/day ,small vol
containing
mucous,pus,blood,abd
cramps & tenesmus (this
may lead to rectal
prolapse especially in
young children)
  Chill
 Profuse sweating,
hepatosplenomegaly
- Isolation from feces, blood, urine,
4. Diagnostic tests duodenal content tissue fluids
- Microscopy study of feces:-
 Polymorphonuclears, leukocytes,
mucus & RBC
- Blood picture:-
 Leukocytosis shift to the left
 Increase ESR
46.Differential diagnosis of shigellosis from cholera. Agent of disease,
leading syndromes, clinical manifestation, diagnostics tests.
Shigellosis
Causative Agent Shigella is a genus of
of disease Gram- negative, facultative
anaerobic, nonspore-forming,
nonmotile, rod-shaped bacteria
Serogroup A: S. dysenteriae
Serogroup B: S. flexneri
Serogroup C: S. boydii
Serogroup D: S. sonnei
-Rectoscopy
-Endoscopy for ulcers
Laboratory diagnosis
-general blodd test
–typical picture for
infection (leukocytosis
shift to the left)
-culture of shigella from
stool or from rectal
swabs
-serological diagnosis of
disease by ELISA/ indirect
hemagglutination
Cholera
Vibrio cholerae is a Gram-negative,
comma-shaped bacterium. V.
cholerae is a facultative anaerobe
and
has a flagellum at one cell pole as
well as pili.
Leading Intoxication- ( main )
Syndromes Pain
Dyspeptic
Enterocolitis, colitic syndr also present
Clinical 1) prodromal period with malaise, poor
manifestations appetite,
2) rumbling, inflation of the abdomen,
chills etc
3)Weakness progresses, appetite is
completely lost, headache, nausea,
vomiting, spinal & articular discomfort
develop, t rises fr subfebrile to 40 oC
& remains high for several days.
4) Abdominal pain soon develops. 1st
dull, permanent, & diffuse over entire
abdomen, then cramps appear (usually L
Gastroenterocolitis
Dehydration (Main )
1) profuse diarrhea and vomiting of
clear fluid. The diarrhea is described
as "rice water" and have a fishy odor.
2) Severe cholera without
treatment- result in life-
threatening dehydration and electrolyte
imbalances. Cholera has been
nicknamed the "blue death" because a
person's skin may turn bluish-gray
from extreme loss of fluids.
3) Fever is rare and should raise

side). suspicion for secondary infection.

4) Lethargy, sunken eyes, dry mouth,
5) Stools are liquid & frequent, 1st
formed, several days later pathological cold clammy skin, decreased
skin turgor, or wrinkled hands and
admixtures (mucus & streaks of blood)
feet. Kussmaul breathing, Blood
appear in the faeces.
pressure drops due to dehydration,
6) Spastic contractions of muscles in the
peripheral pulse is rapid and thready,
lower portions of colon → tenesmus
and urine output decreases with time.
Only a small amt of mucus with streaks
of blood is excreted after a strong Muscle cramping and weakness,
effort; the act of defaecation becomes altered consciousness, seizures, or
even coma due to electrolyte losses and
long & feeling of incomplete
ion shifts are common, especially in
defaecation develops.
children.
7) Examination – bradycardia, low
arterial pressure, dry coated tongue.
8) Palpation – spasms & tenderness of
 colon, esp L iliac region. ( palpable
sigmoid colon)

Diagnostic tests Serological : serological against O-Ag,
IFT, ELISA, skin allergic test
( S.sonnei ), neutralization, indirect agg
1:160 titer >5th day
Coprology : blood, mucus
Rectomanoscopy : ulceration seen
Culture : stool
Blood : ESR ↑, neutrophilia, WBCosis,
anemia
Serology : IFT, micro n macro
agg using anticholera O vaccine
Dark field microscopy w antisera,
microscopy of stool →motile
vibrio seen
Oliguria
Culture : stool, vomitus
Blood : ↑ blood density, ↑
Ht
(hemoconcentration ), metabolic
acidosis, RBCosis, WBCosis, K,
Cl, HCO3 ↓, azotemia,

47.Differential diagnosis of plague from tularemia. Epidemiological features, clinical forms,

main clinical sings, diagnostics tests.
 Plague
Epidemiological Plague is an infectious disease that is
features caused by the bacterium Yersinia pestis.
Depending on lung infection, or
sanitaryconditions, plague can be spread
in the air, by direct contact, or very
rarely by contaminated undercooked
food.
The epidemiological use of the
term plague is currently applied to any
severe bubo inflammation resulting
from an infection with Y. pestis.
Yersinia pestis circulates in animal
reservoirs, particularly in rodents, in the direct contact with contaminated
natural foci of infection found on all
continents except Australia.
It is mainly a disease in the fleasthat
infested the rats, making the rats
themselves the first victims of the
plague. Infection in a human occurs when
a person is bitten by a flea that has been
infected by biting a rodent that itself has
been infected by the bite of a flea
carrying the disease.
Clinical forms 1) Bubonic plague
2) Septicemic plague
3) Pneumonic plague
4) Pharyngeal plague
5) Meningeal plague
6) Other clinical forms ( asymptomatic
plague and abortive plague )
Main clinical 3 main types — bubonic, septicemic and
signs pneumonic — depending on which part
of your body is involved.
Bubonic plague- most common variety of
the disease. buboes — swollen lymph
nodes — which typically develop within
a week after an infected flea bites Buboes
may be:Situated in the groin, armpit or
neck, About the size of a chicken egg,
Tender and warm to the touch. Other
Tularemia
Tularemia is a serious infectious
disease caused by the
intracellular bacterium Francisella
tularensis.
The disease is endemic in North
America and parts of Europe and
Asia. The most common mode of
transmission is via arthropod vectors.
Tularemia can also be transmitted by
biting flies, particularly the deer
fly Chrysops discalis.
Tularemia may also be spread by
animals or material, by ingestion of
poorly cooked flesh of infected animals
or contaminated water, or by
inhalation.
1) bubonic
2) ulceroglandular (75 % )
3) oculoglandular
4)angioglandular
5)gastrointestinal
6) pulmonic
7) primary septic (generalized) forms
Depending on the site of
infection. In most susceptible
mammals, the clinical signs
include fever, lethargy, loss of
appetite, signs
of sepsis, and possibly death.
The face and eyes redden and
become inflamed. Inflammation
spreads to the lymph nodes, which
enlarge and may suppurate
signs and symptoms may include:Sudden (mimicking bubonic plague). Lymph
node involvement is
accompanied by a high fever.
 onset of fever and chills, Headache, Death occurs in less than 1% of cases if
Fatigue or malaise and Muscle aches. therapy is initiated promptly.
Septicemic plague- when plague bacteria
multiply in the bloodstream. Signs and
symptoms include:Fever and
chills,Extreme weakness, Abdominal
pain, diarrhea and vomiting, Bleeding
from the mouth, nose or rectum, or under
your skin, Shock, Blackening and death of
tissue (gangrene) in extremities, most
commonly fingers, toes and nose.
Pneumonic plague- It's the least common
variety of plague but the most dangerous,
because it can be spread from person to
person via cough droplets. Signs and
symptoms can begin within a few hours
after infection, and may include:Cough,
with bloody sputum,Difficulty breathing,
Nausea and vomiting, High fever,
Headache, Weakness. Pneumonic plague
progresses rapidly and may cause
respiratory failure and shock within two
days of infection.
Diagnostic tests -Lymph node aspirate: An affected -Growth of F. tularensis in culture is
bubo should contain numerous the definitive means of confirming the
organisms that can be evaluated diagnosis of tularemia. Appropriate
microscopically and byculture. specimens include swabs or scrapings
-Blood cultures: Organisms may be of skin lesions, lymph node aspirates
seen in blood smears if the patient is or biopsies, pharyngeal swabs, sputum
septicemic. Blood smears taken from specimens, or gastric aspirates,
suspected bubonic plague patients early depending on the form of illness.
in the course of illness are usually Paradoxically, blood cultures are
negative for bacteria by microscopic often negative.
examination but may be positive by -A presumptive diagnosis of tularemia
culture. may be made through testing of
-Sputum: Culture is possible from sputum specimens using direct fluorescent
of very ill pneumonic patients; however, antibody, immunohistochemical
blood is usually culture-positive at this staining, or PCR.
time as well. -The diagnosis of tularemia can also be
established serologically by
-Bronchial/tracheal washing may be taken
 from suspected pneumonic plague demonstrating a 4-fold change in
patients; throat specimens are not ideal specific antibody titers between acute
for isolation of plague since they often and convalescent sera. Convalescent
contain many other bacteria that can mask sera are best drawn at least 4 weeks
the presence of plague. after illness onset;
-In cases where live organisms are
unculturable (such as postmortem),
lymphoid, spleen, lung, and liver tissue or
bone marrow samples may yield evidence
of plague infection by direct detection
methods such as direct fluorescent
antibody (DFA) or PCR.

48.Differential diagnosis of brucellosis from typhoid fever. Anamnestic

data, characteristics of temperature curves, clinical sings, blood
pictures, diagnostics tests.

Question Brucellosis Typhoid Fever

Anamnestic data Brucellosis is a zoonotic infection a) Cause: Salmonella
typhi,
caused by the bacterial Salmonella paratyphi
genus Brucella. The bacteria are b) Characteristic:
Gram negative,
transmitted from animals to humans by flagellated, non-sporing,
facultative
ingestion through infected food anaerobic bacilli.
products, direct contact with an infected c) Antigens: O
(somatic), H
animal, or inhalation of aerosols. The (flagella), K (envelope)
disease is an old one that has been d) Transmission:
anthroponotic
known by various names, including e) Route: faecal-oral,
Mediterranean fever, Malta fever, contaminated food and
beverages.
gastric remittent fever, and undulant f) It is more
prevalent in warmer
fever. seasons.
Brucella organisms are small aerobic g) Some people may
be chronic
intracellular coccobacilli. Gram - carriers which spreads the
disease.
Brucella melitensis (from sheep; highest h) Patients with mild
or abortive
pathogenicity) form have the highest risk
 of
Brucella suis (from pigs; high spreading the infection.
pathogenicity)
Brucella abortus (from cattle; moderate
pathogenicity)
Brucella canis (from dogs; moderate
pathogenicity)

Charateristics of Fever is the most common symptom feverish reaction

temperature curves occurring in 80-100% of cases. It is i) Classical

intermittent in 60% of patients with (trapezoid)
acute and chronic brucellosis and Rises in steps, 39-
undulant in 60% of patients with 40C on 4th-
5th day
subacute brucellosis. Fever can be
For a period
associated with a relative bradycardia. It
of time, it may remain
is associated with chills in almost 80% constantly
of cases. Body
Acute: with high continuous fever temperature decreases to
Subacute : with fever undulating over normal in 4-5 weeks
7- 10 days ii) Undulan
t fever
Chronic: low-grade fever, complicated
Increase
with neuropsychiatric symptoms
s&
decrease
s
gradually
iii) Inclined plane
fever Increases
rapidly &
decreases
gradually
g) status thyposus:
i) On the
5th-7th day, fever
intensifies &
nervous system is
involved
ii) Dimmed
consciousness may
transform to stupor or
spoor in severe cases,
 delirium, severe
headache, meteorism,
insomnia

Clinical signs Fever a) Feverish reaction

Other clinical symptoms: b) Status thyposus
i) Sweating c) Skin
ii) Weakness i) Rose spots
iii) Headache ii) Monomorphic
iv) Anorexia rashes
v) Pain in limbs and back iii) Pale skin
vi) Rigors d) GIT
vii) Joint paints i) Enlarged &
Signs: splenomegaly thick tongue +
impression of tongue,
coated only at center &
base
ii) Hepatospleenomeg
aly
iii) Meteorism
iv) Dull sound on
percussion at
ileaocecal region
e) CVS
i) Relative
bradycardia ( PR
doesn’t agree with body
 temperature)
ii) Low BP

49.Differential diagnosis of Brill disease from typhus fever.

Epidemiological features, special clinical sings, complications,
serological tests, immunological tests.

Question Brill disease Typhus Fever

Epidemiological Brill–Zinser disease is a delayed a) Cause:
features relapse of epidemic typhus, Salmonella typhi,
caused Salmonella paratyphi
b)
by Rickettsia prowazekii. After a patient Characteristic:
contracts epidemic typhus from the Gram negative,
fecal matter of an flagellated, non-
infected louse (Pediculus humanus), sporing, facultative
the rickettsia can remain latent and anaerobic bacilli.
reactivate months or years later, c) Antigens:
with O (somatic), H
symptoms similar to or even identical to
(flagella), K
the original attack of typhus, including
(envelope)
a maculopapular rash. This reactivation
d) Transmission:
event can then be transmitted to other anthroponotic
individuals through fecal matter of the
e) Route:
louse vector, and form the focus for a
faecal-oral,
new epidemic of typhus.
contaminated food
and beverages.
f) It is more
 prevalent in warmer
seasons.
g) Some people
may be chronic
carriers which
spreads the disease.
h) Patients with
mild or abortive form
have the highest risk
of
spreading the infection.

Special clinical The incubation period of disease varies a) Feverish reaction

signs from 5 to 14 days. High body b) Status thyposus
temperature is the most common c) Skin
symptom which begins abruptly with i) Rose spots
chills, malaise, headache, rigors, post ii) Monomorphic
orbital pain, diarrhea and generalized rashes
iii) Pale skin
lymphadenopathy. A small papule may
d) GIT
appear after 2-3 days of attachment of
i) Enlarged &
larva to skin. This soon turns into a
thick tongue +
necrotic eschar developing into a black
impression of tongue,
slough which separates from the 10th
coated only at center
day onwards leaving behind a punched
& base
out ulcer. There is regional
ii) Hepatospleenome
lymphadenopathy. galy
iii) Meteorism
Fever in a case of scrub typhus iv) Dull sound
increases progressively during the first on percussion at
week. Initially it is ileaocecal region
intermittent, e) CVS
remittent or continuous i) but Relative
bradycardia ( PR
doesn’t agree with
body temperature)
ii) Low BP
iii) Weak heart
sound
 subsequently becomes continuous and
subsides by lysis on the fourteenth to
seventeenth day. Despite high
temperature, pulse is slow.

Complications By the end of first week there is a) Intestinal

generalized lymphadenopathy, a red haemorrhage and
macular rash which began on the trunk perforation are most
by 5th day, spreads to the extremities. dangerous
Pain in the chest and pneumonitis complications.
develops. Patient may go into b) Possible septic shock.
circulatory collapse myocarditis, nerve c) Ulcer is usually
deafness, photo-phobia and meningo perforated, and
encephalitis. Coma often precedes danger to the
death. patient’s life.
d) Other complication.
Gastro intestinal complications include i) Septic shock
hemorrhage and superficial mucosal ii) Pneumonia
erosion while renal involvement leads iii) Parotitis
to varying degrees of renal failure. iv) Cholecystitis
There may be jaundice along with DIC v) Myocarditis
and multiple organ failure. Neurological vi) Pyelocystitis.
features are common in seriously ill vii) Thrombophlebitis.
patients and range from restlessness, viii) Involvement
irritability, delirium, seizures to toxic of nervous
encephalopathy leading to stupor and system
coma. (meningo-
encephalitis, etc)
Serological tests Wil Felix test (WF) using a proteus Specific serologic tests-
OXK strain gives positive test in 50% The Widal test is used to
of patients during second week of measure agglutinating
illness. A minimum positive titer of 1: antibodies against H and
80 or a four fold rise over previous O antigens of S typhi.
levels is significant. Indirect hemagglutination,
indirect fluorescent Vi
Other tests include Micro immuno antibody, and indirect
fluorescence, latex agglutination, enzyme-linked
indirect haemagglutination, immuno immunosorbent assay
peroxidase assay, ELISA and (ELISA) for
immunoglobulin M (IgM)
and IgG antibodies to S
typhi polysaccharide, as well
as
monoclonal antibodies
 against S

polymerase chain reaction (PCR). A typhi flagellin.

dip stick test using a dot blot
immunoassay format for the sero
diagnosis of scrub typhus is accurate,
rapid and easy to use test.

The leucocyte count is variable and

there is neutropenia with relative
lymphocytosis.

50.Differential diagnosis of typhus fever from influenza. Species features of

anamnesis, syndromes, clinical mаnifestation, blood picture, specific
diagnostics.

Typhus fever Influenza

Special • patient has been to highly • patient has been contact

features of congested areas such as
anamnesis prisons
• usually occurs in winter
and spring
• patient is hypovitaminous
• source of infection is
human feces transmitted
by lice.
• immunity is +/- following
infection is solid and long
with people with flu.
• usually occurs in winter
and spring
• source of infection is
usually sick people
• immunity is not stable
• transmitted by air
droplets. • I.P. : 1 – 2 days.
 lasting but not sterile
• I.P. : 6 – n25 days

Leading 1.intoxication syndrome: 1. Intoxication syndrome:

syndromes • temp. : high 40oC , • Temp. : 38 – 40oC
and clinical continuous • headache, chills,
manifestations • decrease 1 – 1.5oC malaise, myalgia,
7 – 10days arthalgia, painful eye
• headache, malaise, movements
chills 2. Catarrhal syndrome
• irritability and • rinorrhea
anxiety on the 1st • hoarseness of voice
day then followed by • sometimes dry
excitation. cough
• hyperemic face and • hyperemic face and
swollen face neck
• injected and dilated • injected scleral
scleral vessels( vessels
rabbits eye) • tongue coated
• tongue is dry and • hyperemic fauces
difficult to protrude
(Godelie’s sign),
dyspnoe
• Petechial
hemorrhage can
develop in 3 days on
conjunctival folds
2. 4th – 5th day rash , rose
spots (petechias)
3. Presences of typhus
status
Blood picture • leukocytosis • Lymphocytosis
• increased ESR
• eosinophilia

Diagnostic • ELISA • Serological

method • immunoflourescent • immunoflourscent
• hemagglutination
reactions
• indirect fluorescent
 antibody (IFA)
• microscopic agglutination

51.Differential diagnosis of cholera from food poisoning. Special feature of

anamnesis, main clinical syndromes, clinical sings, diagnostics tests.
Cholera Food poisoning
Special • Patient came in contact • raw food, undercooked
features of with sick patients eggs, meat, other
anamnesis • Usually is autumn and products
summer • improper hygeine.
• Improper hygiene • occurs in children and
• Children < 3yrs of age elderly more often
are susseptible • people with sickle cell
anemia
• patient has animals
• non season dependent

Leading • Pain syndrome • Intoxication syndrome

syndromes - pain in • Gastritis
paraumbilical and • Gastroenteritis
epigastric area and • Mild dehydration
• Dehydration
syndromes -level of
dehydration depends
on level of body fluids
lost
• signs of dehydration:
according to amount
fluid lost • 1st = 1-3%,
2nd = 4-6%, 3rd =7-9%,
4th = >10%
• Signs: pale skin, dry,
loss elasticity and tugor
of skin, low BP, weak
pulse, tachycardia,
sunken eyes

Clinical • Types: 1. typical=> • I.P. : few hours

signs mild, moderate, severe • intoxication syndrome:
2. atypical=> dry, nausea, vomiting, fever(
fulminant subfebrile)[ case of staph .
• Painless, retracted aureus)
belly, no pain or • gastritis: abdominal pain ,
tenesmus, discomfort epigastric especially, nausea,
and mumurs in vomiting, acute onset of
abdomen diarrhea not typical
• stool: 3 m- 10x, rice • gastroenteritis: umbilical,
water character of iliac pain, profuse watery
stool , slight fish like diarrhea 1015x /day
adour 1.C perfringens: 10% fever,
• temp: normal or nausea, vomiting, abdominal
subnormal cramps, diarrhea 2.B. cereus:
• I.P. : few hours to 5 2 types: a)diarrheal form (
days( usually 48hrs) long incubation period= 8 –
• onset: sudden, acute 16hrs) , b) emetic form (
short I.P. =1 – 6hrs) gastritis
signs, usually without
diarrhea
3.S.aureus: decrease in
vision, gastritis

Lab data • Blood: leukocytosis, • Culture of vomit, stool,

Increased
hematocrit,anemia
• Stool: stool culture for
v. cholera( seen V.
cholera colonies) and
microscopy
• Retrospective studies:
vibrocidal agglutinating
and toxin neutralizing
antibodyes
stomach lavage
àdetect the bacteria or
its toxins (the type of
bacteria and the toxins
depends on the
causing agent)
• serological test: direct
agglutination(
diagnostic: 1 : 200
dilution )

Tests • Blood examination • culture: stool, vomit,

• Stool culture stomach lavage
• vibrocidal agglutination • serological test: direct
agglutination
 52.Differential diagnosis of meningococcal meningitis from tuberculosis
meningitis. Special feature of anamnesis, main clinical syndromes,
clinical sings, CFS abnormality, specific therapy.
Meningococcal Meningitis Tuberculous Meningitis
Special • Caused by Nesseria • Caused by Mycobacterium
features of Meningitidis Tuberculosis
anamnesis • Contact with sick • History of TB
person / carriers • Bronchoadenitis, pleuritis
• Mostly in winter & • Contact with TB patient,
spring hematogenous spread
• Common in infants • Positive skin test
• Non-seasonal dependent
• Common in children

Main clinical • Acute onset • Onset gradual

signs • Temperature – high • Temperature subfebrile
(39-41 C) (37-38 C)
• Meningial signs in 1st • M-signs on 2nd – 3rd day
days • Headache severe on 2nd -
• Severe headache from 3rd week
1st hours • Usually secondary o
• Neck stiffness primary lung foci can be
revealed in 50% cases

Examination • Color à gray / white • Color à yellow

of CSF • Pressure à increase, • Pressure à increased,
turbid transparent
• Cytosis à increased till • Cytosis à increased till
1000. Neutrophils 100’s – 700’s.
increased, protein Lymphocytes increased,
increased, protein markedly
lymphocytes increased.
decreased • PMN à 20-40
• PMN à 40-100 • CL à increase
• CL à decrease • Fragile / v soft film
• Rough film v deep

Specific • Benzyl Penicillin G (IV / • Anti TB

therapy IM) 200-300,000 • Glucocorticoids
U/kg/day (every 6 hr)
• Ampicillin 200-300,000
U/kg/day (every 4 hrs)
 • Oxacillin 300mg/kg/
1day (interval 3 hr)
• Chloramphenicol

53.Differential diagnosis of viral hepatitis A from viral hepatitis B.

Special feature of anamnesis daft, characteristics of prodromal period,
main clinical symptoms, markers of disease.
HEPATITIS A HEPATITIS B
Special • Picorna virus • DNA virus
features of • Source- Sick person • Source- sick person and
anamnestic no carrier carrier
data • Mechanism- Fecal • Mechanism-
oral hematological ways
• Incubation- 15- • Incubation period- 30-
50days 180 days
• Risk group- • Risk group- drug abuse ,
Children, homosexual, medical
homosexual, person , dialysis
traveler • Seasonal dependant
• Mainly Summer and • Pathogenesis- hepatic
autumn destruction is by
• Pathogenesis- immune system
Primary toxic
effect(virus has
troposin that cuase
destruction of liver
cell

Characteristics • Lasts for 5-7days n • Last 4-10days n main

of prodromal main syndromes syndromes are
period are influenza like, dyspepsia,
dyspepsia, asthenoveg,mixed
asthenovegatative, • Fatigue, malaise,
mixed myalgia, arthalgia,
• Influenza- onset is anorexia, nausea,
acute w t 38-39c, vomiting, uticaria,
coryza, cough, maculo-papular
photophobia, eruption, polyarthritis
pharyngitis, myalgia angiooedema
• Dyspepsia- nausea, • Polyarthrititis→interpha
 vomiting, abd pain langeal, appendicular
• Asthenoveg- joint
fatigue, malaise • At the end off thos
• Mixed- period→urine
influenza+dyspepsia dark,stool clay
• At the end of this color,worsen jaundice
period dark appear
urine,clay color
stool

Main clinical -Preicteric phase -Preicteric phase

symptoms • Inflammation like
symptomsà fever
(38 -39 oC),
fatigue, malaise,
headache, myalgia,
photophobias,
arhtalgias
• Dypeptic
syndromeà nausea,
vomiting
• Astenovegetative:
weakness, passive
posture
- Icteric pahase: presence
of jaundice and the
preicteric signs diminish,
enlargement of the liver ,
tenderness in the right
upper quadrant, pain and
discomfort, splenomegaly
and adenopathy
- In the recovery stage the
constitutional signs
disappear but liver
enlargement still present
and biochemical signs still
evident.
• Latent
• Dyspepticà nausea,
vomiting
• Urticaria
• Weight loss à usually
mild ( 2.5 – 5 kg).
- Icteric pahase: presence of
jaundice and the preicteric
signs diminish, enlargement of
the liver , tenderness in yhe
right upper quadrant, pain and
discomfort, splenomegaly and
adenopathy.
- In the recovery constitutionsl
signs disappear disappear but
liver enlargement still present
and biochemical signs still
evident

markers of • Anti HAV IgG • HBs Ag

disease • Anti HAV IgM • Anti HBs, HBe, HBc IgG
• HAV RNA • Anti HBc IgM
 • HBV DNA

54.Differential diagnosis of cholera from salmonellosis. Agents,

epidemiological data, clinical manifestation, lab data, diagnostic tests.
Cholera Salmonellosis
Agents • Vibrio cholera – classic , • S.enteritidis, S.typhi
Eltor mureum, S.virchaw,
• Serogroup à ogawa, S.haclav, S.heidelberg,
Inaba, Hikojema S.agona, S.indiana,
• Short, slightly curved, S.occrers
motile, gram negative • Motile, gram negative,
rod, single polar flagellated
flagellum.

Epidemiological • Anthroponotic disease • Anthropo-zoonotic

data (only humans) disease
• Mechanism of • Fecal-oral transmission
transmission is fecal • Non-season dependant
oral • High susceptibility after
• Peak in summer and gastroectomy and
autumn hypochlorhydria
• Susceptibility due to • Food à meat, poultry,
blood group O eggs, milk, water
• Suppronotc infection
(assisted by external
environment)

Clinical • Incubation period :- • Incubation period is 24-

manifestation hours - 4 days
• Sudden onset
• 2 types:-
a) typical – mild,
moderate, severe
b) atypical – dry,
fulminant
• Dehydration syndrome
• Enteritis syndrome •
• Pain syndrome absent •
• Diarrhea:- - 3-10 days -
Rice watery stool -
48 hours
• Sudden onset
• 3 forms:-
a) Gastrointestinal
b) General
c) Carriers
• Russian Classification:-
a) GIT form - gastritis -
gastroenteritis -
gastroenterocolitis
b) General form -
typhus like - septico
 Slight fish-like odour
• Thirst, depressed
appetite
• Temperature :- -
typically hypo thermia,
maybe subfebrile
• Meteorism absent
• Tachycardia, xerostomia
pyemia
c) Bacterial discharge -
acute, chronic,
transitory
• Classification in other
countries:-
• a) gastroenteritis
b) bacteremia
• Intoxication syndrome
• Dyspeptic syndrome
• Pain :- crampy
abdominal pain
• Diarrhea:- - only at
beginning large volume
of stool, bloody,
mucoid, watery,
raspberry jelly-like
• Meteorism
• Temperature (39-40 C)
• Dehydration
• Hepatosplenomegaly
• Encephalopathy

Lab data a) microscopy of stool a) microscopy of stool

• polymorphic nuclear • blood, mucoid,
cells polymorphonuclear
• < 5 cells cells, leukocytes
b) Culture b) serological test
• Comma-shaped vibrio • 1: 200 diagnostic
cholera c) Blood
c) vibriocidal agglutinating • Leukocytosis shift to
& toxin neutralizing left (gastrointestinal
antibodies form)
• four-fold or greater • Shift to left, increase
during acute disease ESR (bacteremic)
•fall in titre during • Eosinophils absent
convalescence • Leucopenia
d) blood • leukocytosis
• leukocytosis shift to d) proctosigmoidoscopy
left
• neutrophilia
• hematocrit increase
 • level of blood density
increase
e) indirect
hemagglutination test
Diagnostic tests • cholera face, cholera
yes
• physical examination à
pain due to palpation is
absent
• xray not important
• proctosigmoidoscopy
not important •
isolation from feces •
• microagglutination with
4x increase in time
55.Differential diagnosis of anthrax from erysipelas. Agents,
epidemiological data, clinical forms, course variants, clinical
manifestation, diagnostic criteria.
Anthrax Erysipelas
Agents  Bacillus anthracis
Epidemiological  Trasmited by direct or
Data indirect contact
 Airborne
 Fecal-oral
Clinical Forms  Cutaneous
 Gastrointestinal
 Inhalational
• abdomen distended
• pain due to palpation
• xray à shock ileus
• proctosigmoidoscopy à
show inflammation of
the colon & ulceration
• isolation from feces
• lood
• indirect
hemagglutination test
• 1:200 titer increase
 Streptococcus
pyogene
 Is transmited by
direct contact in skin
lesion
 The infection rapidly
invades & spreads
through the
lymphatic vessels.
 This can produce
overlying skin
"streaking" and
regional lymph node
swelling and
tenderness.
 Facial infections
 Lower extremities
infections
  Atypical

Course Variants
The disease start with mild symptoms and progress if
untreated

Clinical  Raised itching bump  Erythematous patch,

Manifestations which quickly indurated, tense with
develops into a well demarcated
painless sore with a margins and it may
black center. develop bullae in 3
 Its red and lymph days.
nodes are swelled.  Facial erysipelas
 Vomiting of blood, lesions appear on the
severe diarrhea, acute cheeks and
inflammation of the
intestinal tract, and
loss of appetite.
 Respiratory infection
initially presents with
cold or flu-like
symptoms for several
days, followed by
severe (and often
fatal) respiratory
collapse.

Diagnostic  Chest Xray Based upon the association

Criteria  CT scan of an
 acute inflammatory
plaque
 fever
 lymphagiitis
 adenopathy
 hyperleukocytosis
 56.Differential diagnosis of typhoid fever from typhus fever. Species
features of anamnesis, syndromes, clinical mаnifestation, characteristics
of typhus state and temperature curve, clinical sings, blood picture,
diagnostic tests.
Typhoid Fever Typhus Fever
Species  S. typhi  Rickettsia prowasekii
Features of  Antroponotic  Anthroponotic infectiom
anamnesis infection  Transmission is the
 Transmission if fecal- primary arthropod
oral vectors in person-to-
 Incubation period is person. If lice is infected
from 3-21 days and if they are crushed
 Has a longer cours or rubbed into the bite
wound transmission
occurs. The rickettsia is
also infectious by
inhalation or contact
with mucous
membranes.
 Incubation period is from
1-2 weeks
Syndromes  Enteric syndrome  Intoxication syndrome
 Lymphatic syndrome  Encephalitis syndrome
 Intoxication
syndrome

Clinical  1 st week: rising  -1st symptom of

Manifestations fever, headache
constipation
 2 nd week: abdominal
pain, fever increases,  Rash may develop after
diarrhea, rose spots
 3 rd week:
hepatosplenomegaly,
intestinal bleeding,
lymphatic hyperplasia
intoxication: headache,
fever, chills, prostration,
myalgia.
4-6 days(small pink
macules, first in upper
trunk and axillae then
spread to the entire
body except face, palms
and soles). As the
disease progress rash
becomes dark and
maculopapular or
petechial and
hemorrhagic if severe.
  Splenomegaly,
hypotension,nausea,
vomiting and confusion
may also be seen.
Gangrene and symptoms
of encephalitis or
pneumonia may occur

Temperature  Continuous fever up  Continuous fever from 7-

Curve to 2 weeks 10
Blood Picture  Leukopenia
 Thrombocytopenia
 Lymphocytosis
 ESR Increased
 Anemia

Diagnostic  Blood analysis  Serologic test

Tests  Blood culture  Skin biopsies
 Stool culture  PCR
 Bone marrow culture  Immunohistochemical
 Serologic tests staining
57.Differential diagnosis of meningococcal meningitis from viral
meningitis. Special feature of anamnesis, main clinical syndromes,
clinical sings, CFS abnormality, specific therapy.

58.Differential diagnosis of botulism from food poisoning. Agents,

epidemiological data, clinical manifestation, lab data, diagnostic tests.
59.Differential diagnosis of jaundice. Special feature of anamnesis, main
clinical syndromes, clinical sings, specific therapy.

60.Differential diagnoses of diseases with feverish syndrome.

61.Taenia. Saginana taeniasis. Epidemiology, pathogenesis, diagnostics,

treatment.

62.Taenia. Solium taeniasis and cysticercosis. Epidemiology, diagnostics,

treatment.
63.Enterobiasis. . Epidemiology, pathogenesis, clinical sings, diagnostics,
treatment.

64.Ascariasis. Epidemiology, pathogenesis, clinical sings, diagnostics,

treatment.

(AMBOSS and CDC)

Epidemiology:
 Pathogen: Ascaris lumbricoides (nematode/roundworm)
 Host: humans and swine
 Transmission: fecal-oral

Ascaris lumbricoides infections happen all over the world. The eggs from the
parasite are passed in human feces and can contaminate the soil. The eggs
survive best in warm, humid areas and must grow in the soil before they can
infect others. Most cases occur in tropical and subtropical areas of Asia, sub-
Saharan Africa, and the Americas

Pathogenesis:
Adult worms live in the lumen of the small intestine. A female may
produce approximately 200,000 eggs per day, which are passed with the
feces . Unfertilized eggs may be ingested but are not infective. Larvae
develop to infectivity within fertile eggs after 18 days to several weeks ,
depending on the environmental conditions (optimum: moist, warm, shaded
soil). After infective eggs are swallowed , the larvae hatch , invade the
intestinal mucosa, and are carried via the portal, then systemic circulation to
the lungs . The larvae mature further in the lungs (10 to 14 days),
penetrate the alveolar walls, ascend the bronchial tree to the throat, and are
swallowed . Upon reaching the small intestine, they develop into adult
worms. Between 2 and 3 months are required from ingestion of the infective
eggs to oviposition by the adult female. Adult worms can live 1 to 2 years.

Clinical signs:
Most patients are asymptomatic

EARLY SYMPTONS: Occur 4–16 days after egg ingestion and are caused by
migration of larvae through lungs and systemic eosinophilia (usually
transient)
 Dry cough, blood tinged sputum, wheezing
 Loeffler syndrome: transiente respiratory disorder characterized by
accumulation of eosinophils in the lungs due to certain infections
(usually parasites) or allergic reaction to drugs. Symptons are usually
mild and resolve spontaneosly

LATE SYMPTONS: Occur 6–8 weeks after egg ingestion and are caused by
mature worms in the intestinal tract
 Anorexia
 Abdominal disconfort
 Nausea, vomiting
 Diarrhea

Additional symptons due to blockage by adult worm depends on the location

of obstruction:
 Bowel obstruction, especially at ileocecal valve (may lead to intestinal
perforation)
 Obstruction of the apêndix  features of appendicitis
 Obstruction of billiary and pancreatic ducts  features of cholestasis,
pancreatitis

Diagnostic:
 CBC: eosinophilia
 Confirmatory test: stool samples show the presence of worms or
visible oval eggs with a knobby apppearance under the microscope

Treatment:
Asymptomatic patients with suspected infection should also be treated
for ascariasis due to the high risk of complications.
Antihelmintic drugs (-bendazoles):
- Albendazole 400mg PO single dose
- Mebendazole 100mg PO 2x/day for 3 days OR 500mg PO single dose
- Ivermectin 150-200mcg/kg PO single dose
During pregnancy: pyrantel pamoate 11mg/kg PO for 3 days
 65.Ecyinococcosis. Epidemiological features, clinical sings, diagnostics,
specific therapy.

Echinococcosis is a parasitic disease caused by infection with tiny tapeworms of the

genus Echinocococcus. Echinococcosis is classified as either cystic echinococcosis or
alveolar echinococcosis.
Epidemiological features
Cystic echinococcosis (CE) is caused by infection with the larval stage of Echinococcus
granulosus. CE is found in Africa, Europe, Asia, the Middle East, Central and South
America, and in rare cases, North America. The parasite is transmitted to dogs (definitive
host) when they ingest the organs of other animals that contain hydatid cysts. The cysts
develop into adult tapeworms in the dog. Infected dogs shed tapeworm eggs in their feces
which contaminate the ground. Sheep, cattle, goats, and pigs (intermediate hosts) ingest
tapeworm eggs in the contaminated ground; once ingested, the eggs hatch and develop
into cysts in the internal organs. The most common mode of transmission to humans is by
the accidental consumption of soil, water, or food that has been contaminated by the fecal
matter of an infected dog. Echinococcus eggs that have been deposited in soil can stay
viable for up to a year. The disease is most commonly found in people involved in raising
sheep, as a result of the sheep’s role as an intermediate host of the parasite and the
presence of working dogs that are allowed to eat the offal of infected sheep.
Alveolar echinococcosis (AE) is caused by infection with the larval stage of
Echinococcus multilocularis. AE is found across the globe and is especially prevalent in
the northern latitudes of Europe, Asia, and North America. The adult tapeworm is
normally found in foxes, coyotes, and dogs (definitive hosts). Infection with the larval
stages is transmitted to people through ingestion of food or water contaminated with
tapeworm eggs.
Clinical signs
Echinococcus granulosus infections often remain asymptomatic for years before the cysts
grow large enough to cause symptoms in the affected organs. The rate at which
symptoms appear typically depends on the location of the cyst. Hepatic and pulmonary
signs/symptoms are the most common clinical manifestations, as these are the most
common sites for cysts to develop In addition to the liver and lungs, other organs (spleen,
kidneys, heart, bone, and central nervous system, including the brain and eyes) can also
be involved, with resulting symptoms. Rupture of the cysts can produce a host reaction
manifesting as fever, urticaria, eosinophilia, and potentially anaphylactic shock; rupture
of the cyst may also lead to cyst dissemination.
Echinococcus multilocularis affects the liver as a slow growing, destructive tumor, often
with abdominal pain and biliary obstruction being the only manifestations evident in
early infection. This may be misdiagnosed as liver cancer. Rarely, metastatic lesions into
the lungs, spleen, and brain occur. Untreated infections have a high fatality rate.
Echinococcus vogeli affects mainly the liver, where it acts as a slow growing tumor;
secondary cystic development is common. Too few cases of E. oligarthrus have been
reported for characterization of its clinical presentation.
Diagnosis
The presence of a cyst-like mass in a person with a history of exposure to sheepdogs in
an area where E. granulosus is endemic suggests a diagnosis of cystic echinococcosis.
Imaging techniques, such as CT scans, ultrasonography, and MRIs, are used to detect
cysts. After a cyst has been detected, serologic tests may be used to confirm the
diagnosis.
Radiography permits the detection of hydatid cysts in the lungs; however, in other organ
sites, calcification is necessary for visualization. Ultrasonography has been widely used
for screening, clinical diagnosis, and monitoring of treatment of liver and intra-abdominal
cysts. Cyst viability cannot be reliably determined with radiography or parasite antigen
detection; calcification can be present in all stages of cysts.
Serologic tests, such as enzyme-linked immunosorbent assay (ELISA) and indirect
hemagglutination test, are highly sensitive methods for detecting infection. Specific
confirmation can be obtained by demonstrating echinococcal antigens by
immunodiffusion (arc 5) procedures or immunoblot assays (8-, 21 –kD bands).

Alveolar echinococcosis is typically found in older people. Imaging techniques such as

CT scans are used to visually confirm the parasitic vesicles and cyst-like structures and
serologic tests can confirm the parasitic infection.
Plain radiographs show hepatomegaly and characteristic scattered areas of radiolucency
outlined by calcific rings 2 to 4 mm in diameter. The usual CT image of E. multilocularis
infection is that of indistinct solid tumors with central necrotic areas and perinecrotic
plaque-like calcifications. Serologic test results are usually positive at high titers.
Treatment
In the past, surgery was the only treatment for cystic echinococcal cysts. Chemotherapy,
cyst puncture, and PAIR (percutaneous aspiration, injection of chemicals and
reaspiration) have been used to replace surgery as effective treatments for cystic
echinococcosis. However, surgery remains the most effective treatment to remove the
cyst and can lead to a complete cure. Some cysts are not causing any symptoms and are
inactive; those cysts often go away without any treatment.
The treatment of alveolar echinococcosis is more difficult than cystic echinococcosis and
usually requires radical surgery, long-term chemotherapy, or both.
For some patients, chemotherapy with benzimidazoles is the preferred treatment. Patients
with small cysts or multiple cysts in several organs can be treated successfully with
albendazole.
Drug* Adult Dosage Pediatric Dosage
400 mg orally twice a day for 10-15 mg/kg/day (max 800 mg) orally in two
Albendazole
1-6 months doses for 1-6 months
As a second choice for treatment, mebendazole 40-50 mg/kg body weight per day
continuously for several months have been highly effective.

66.Acute hepatic encephalopathy. Clinical manifestation, diagnostic

criteria, thearapy.
a. thearapy.
Hepatic encephalopathy (HE) may be defined as a disturbance in central nervous
system function because of hepatic insufficiency. Present in both acute and chronic
liver failure, these neuropsychiatric manifestations are potentially reversible
Pathophysiology
nitrogenous substances derived from the gut adversely affect brain function

Clinical Subtypes
The most distinctive presentation is the development of an acute confusional state
that can evolve into coma (acute encephalopathy).
recurrent encephalopathy
persistent encephalopathy
mild cognitive abnormalities only recognizable with psychometric or
neurophysiologic tests (minimal or subclinical encephalopathy

diagnostic criteria
Hepatic encephalopathy is a diagnosis of exclusion. Other metabolic
disorders, infectious diseases, intracranial vascular events, and intracranial space–
occupying lesions can present with neuropsychiatric symptomatology.
Anamnesis of acute or chronic liver disease, the existence of a precipitating
factor, and/or a prior history of HE are clinical elements needed for diagnosis.
Intrinsically linked to the diagnosis of HE is an evaluation of the degree of liver
dysfunction and possible alterations of the hepatic circulation (thrombosis, large
spontaneous portal-systemic shunt, transjugular intrahepatic portal-systemic shunt
[TIPS]).
The detection of asterixis, fetor hepaticus and fluctuating long-tract signs
are helpful clues, albeit nonspecific. The absence of such clinical signs does not
exclude the diagnosis of HE. Measurement of venous ammonia blood levels may
be helpful in the initial evaluation when there is doubt about the presence of
significant liver disease or of other causes for an abnormality in consciousness.
Follow-up with repeated ammonia levels is unnecessary and does not replace the
evaluation of the patient’s mental state. Ammonia levels should be promptly
assayed in an experienced laboratory to avoid pitfalls in its determination. Tools to
exclude other causes of an abnormal mental state include automated
electroencephalogram analysis, brain imaging (especially in patients in stupor
and coma), and lumbar puncture (for patients with unexplained fever,
leukocytosis, or other symptoms suggestive of meningeal irritation). Alterations of
the electroencephalogram are not specific for HE and are subject to variability in
interpretation; Neuropsychological testing -The Number Connection Test, parts A
and B; the Digit Symbol Test; and the Block Design Test have been the tests most
frequently employed.
Staging In patients with cirrhosis and overt encephalopathy, two staging
classifications have been used for patients with HE.
1. The West Haven criteria of altered mental state in HE (numerous
studies have employed variations of these criteria).
Stage 0. Lack of detectable changes in personality or behavior. Asterixis
absent.
Stage 1. Trivial lack of awareness. Shortened attention span. Impaired
addition or subtraction. Hypersomnia, insomnia, or inversion of sleep pattern.
Euphoria or depression. Asterixis can be detected.
Stage 2. Lethargy or apathy. Disorientation. Inappropriate behavior.
Slurred speech. Obvious asterixis.
Stage 3. Gross disorientation. Bizarre behavior. Semistupor to stupor.
Asterixis generally absent.
Stage 4. Coma.

Evaluation of the level of consciousness with the Glasgow Scale: although the
Glasgow coma scale has not been rigorously evaluated in patients with HE, its
widespread use in structural and metabolic disorders of brain function justifies its
application in acute and chronic liver disease.

Treatment options
1. Protein and Zinc
1. Nutritional Management Patients with HE should avoid prolonged periods
of dietary protein restriction and receive the maximum tolerable protein intake,
aiming at 1.2 g of protein/kg/day (range 1–1.5).
IMPLEMENTATION
 Acute encephalopathy. Protein feeding can be withdrawn for the first day.
Short term (4 days) enteral nutrition has not been shown to benefit hospitalized
cirrhotic patients.
Chronic management. An increase in protein tolerance can be achieved by
increasing protein intake in combination with other therapeutic measures, such as
nonabsorbable disaccharides. Substitution of animal protein with vegetable and/or
dairy protein should be reviewed, a process facilitated by a consultation with a
nutritional expert. Oral formulation of branched chain amino acids may provide a
better tolerated source of protein in patients with chronic encephalopathy and
dietary protein intolerance. Zinc acetate can be administered as 220 mg b.i.d. It
may reduce the absorption of other divalent cations (e.g., copper).

2. Reduction in the Nitrogenous Load Arising From the Gut

A. BOWEL CLEANSING. Bowel cleansing is a standard therapeutic
measure in HE.
Implementation. Various laxatives may be used, but nonabsorbable
disaccharides are preferred, as they result in additional effects that potentiate the
elimination or reduce the formation of nitrogenous compounds (see below).
Administration of enemas may be necessary in the patient with a severe
impairment of consciousness. Alternatively, bowel cleansing can also be achieved
after irrigation of the gut via a p.o. tube. Irrigation with a 5-L isotonic solution of
mannitol, 1 g/kg, has been shown in a controlled trial to prevent encephalopathy
after a GI hemorrhage.
B. NONABSORBABLE DISACCHARIDES. Lactulose is a first-line
pharmacological treatment of HE.
Implementation- For acute encephalopathy, lactulose (ingested or via
nasogastric tube), 45 ml p.o., is followed by dosing every hour until evacuation
occurs. Then dosing is adjusted to an objective of two to three soft bowel
movements per day (generally 15–45 ml every 8–12 h). Only one study examined
in a controlled fashion the effectiveness of Lactitol enemas. Lactulose by enema
(300 ml in 1 L of water) is retained for 1 h, with the patient in the Trendelenburg
position (to increase the possibility of access to the right colon). For chronic
encephalopathy, oral dosing of lactulose does not require the hourly initial
administration. Lactose can be used in patients with lactase deficiency. Lactitol,
more palatable, is available in Europe but not the United States.

C. ANTIBIOTICS.
Implementation. For acute encephalopathy, neomycin (3–6 g/day p.o.)
should be given for a period of 1–2 wk. For chronic encephalopathy, neomycin (1–
2 g/day p.o.) should be given, with periodic renal and annual auditory monitoring.
Neomycin can be combined with oral lactulose in problematic cases.
Metronidazole should be started at a dose of 250 mg b.i.d.

D. OTHER THERAPIES. Ornithine aspartate drug is not available in the

United States. It provides substrates for the urea cycle (ornithine) as well as for the
synthesis of glutamine (aspartate, via transamination to glutamate). It is available
in oral and i.v. formulations. Preliminary experience in both acute and chronic
encephalopathy has been encouraging.

3. Drugs That Affect Neurotransmission Flumazenil and bromocriptine

administration may have a therapeutic role in selected patients.
IMPLEMENTATION. Flumazenil (1 mg bolus i.v.) is indicated for patients
with HE and suspected benzodiazepine intake. Although flumazenil has been
reported to occasionally cause seizures, such findings have not been described in
patients with HE. Bromocriptine (30 mg p.o. b.i.d.) is indicated for the treatment of
chronic encephalopathy in patients unresponsive to other therapy. Bromocriptine
may result in elevation of prolactin levels.

4. Manipulation of the Splanchnic Circulation

The presence of large spontaneous portal-systemic shunts should be sought
in selected patients with recurrent episodes of encephalopathy despite medical
therapy, where a precipitating factor is not found.
IMPLEMENTATION. Occlusion of portal-systemic collaterals should be
undertaken only in centers with experienced interventional radiologists and after
all other medical measures have failed.

67.AIDS. Epidemiological features, pathogenesis, clinical sings,

diagnostics, specific therapy.

Epidemiological features

 HIV continues to be a major global public health issue, having claimed 36.3 million
[27.2–47.8 million] lives so far.
 There is no cure for HIV infection. However, with increasing access to effective HIV
prevention, diagnosis, treatment and care, including for opportunistic infections, HIV
infection has become a manageable chronic health condition, enabling people living with
HIV to lead long and healthy lives.
 There were an estimated 37.7 million [30.2–45.1 million] people living with HIV at the
end of 2020, over two thirds of whom (25.4 million) are in the WHO African Region.
 In 2020, 680 000 [480 000–1.0 million] people died from HIV-related causes and 1.5
million [1.0–2.0 million] people acquired HIV.
 To reach the new proposed global 95–95–95 targets set by UNAIDS, we will need to
redouble our efforts to avoid the worst-case scenario of 7.7 million HIV-related deaths
 over the next 10 years, increasing HIV infections due to HIV service disruptions during
COVID-19, and the slowing public health response to HIV.

Risk factors

 having unprotected anal or vaginal sex;

 having another sexually transmitted infection (STI) such as syphilis, herpes, chlamydia,
gonorrhoea and bacterial vaginosis;
 sharing contaminated needles, syringes and other injecting equipment and drug solutions
when injecting drugs;
 receiving unsafe injections, blood transfusions and tissue transplantation, and medical
procedures that involve unsterile cutting or piercing; and
 experiencing accidental needle stick injuries, including among health workers

AIDS can be transmitted through,

 sexual transmission
 parenteral transmission
 vertical transmission
 Infection with HIV occurs by the transfer of blood, semen, vaginal fluid, pre-ejaculate, or
breast milk.

Pathogenesis
• HIV primarily attacj to specific receptors on host cells containing CD4 using a
glycoprotein gp 120
• Secondary attachment occurs due to co receptor molecules (CCR5 OR CXR4 )
• Co receptor facilitate the tight binding of the virus to the cell membrane and
induce conformational changes in the viral envelope glycoprotein
• Mostly helper T cells and sometimes monocytes , macrophages , NK cells and
certain B cells and glial cells are targets for HIV
clinical signs
It depends on the person and what stage of the disease they are in.
Basically there are 3 stages
Stage 1 – acute HIV infection- Within 2 to 4 weeks after infection with HIV, about two-thirds
of people will have a flu-like illness. This is the body’s natural response to HIV infection.

Flu-like symptoms can include:

 Fever
 Chills
 Rash
 Night sweats
 Muscle aches
 Sore throat
 Fatigue
 Swollen lymph nodes
 Mouth ulcers
Stage 2: Clinical Latency- In this stage, the virus still multiplies, but at very low levels. People in
this stage may not feel sick or have any symptoms. This stage is also called chronic HIV infection.
Stage 3: AIDS -If you have HIV and you are not on HIV treatment, eventually the virus will weaken
your body’s immune system and you will progress to AIDS (acquired immunodeficiency
syndrome). This is the late stage of HIV infection.
Symptoms of AIDS can include:

 Rapid weight loss

 Recurring fever or profuse night sweats
 Extreme and unexplained tiredness
 Prolonged swelling of the lymph glands in the armpits, groin, or neck
 Diarrhea that lasts for more than a week
 Sores of the mouth, anus, or genitals
 Pneumonia
 Red, brown, pink, or purplish blotches on or under the skin or inside the mouth, nose, or
eyelids
 Memory loss, depression, and other neurologic disorders

Diagnostics

 HIV ELISA and HIV Western blot tests detect antibodies to the HIV virus in the blood
 RNA/DNA test
 Antibody test
 The HIV ELISA and HIV Western blot tests detect antibodies to the HIV virus in the
blood. Both tests must be positive to confirm an HIV infection. Having these antibodies
means you are infected with HIV.
 If the test is negative (no antibodies found) and you have risk factors for HIV such
as Sore throat and Swollen lymph glands
 The HIV ELISA and HIV Western blot tests detect antibodies to the HIV virus in the
blood. Both tests must be positive to confirm an HIV infection. Having these antibodies
means you are infected with HIV. If the test is negative (no antibodies found) and you
have risk factors for HIV infection, you should be retested in 3 months. If the HIV
ELISA and HIV Western blot tests are positive, other blood tests can be done to
determine how much HIV is in your bloodstream. A complete blood count (CBC) and
white blood cell differential may also show abnormalities. A lower-than-normal CD4 cell
count may be a sign that the virus is damaging your immune system.

Other than that

 Serologic tests are the most important studies in the evaluation for HIV infection.
 Secondary testing that may be performed to assist with diagnosis or staging includes the
following:
 Viral culture
 Lymph node biopsy
 Proviral DNA polymerase chain reaction (PCR)
 Genotyping of viral DNA/RNA
 Screening assays
 A high-sensitivity enzyme-linked immunosorbent assay (ELISA) should be used for
screening. Most ELISAs can be used to detect HIV-1 types M, N, and O and HIV-2.
 CD4 + T-cell Count
 Viral Load
 Baseline Studies
 Baseline studies for other infections that are important in the initial workup of a patient
with newly diagnosed HIV infection include the following:
 Purified protein derivative (PPD) skin testing for tuberculosis
 Cytomegalovirus (CMV) testing
 Syphilis testing
 Rapid amplification testing for gonococcal and chlamydial infection
 Hepatitis A, B, and C serology
 Anti-Toxoplasma antibody

specific therapy.
Currently, there's no cure for HIV/AIDS. However we use medications to control and prevent
complications of HIV -These medications are called antiretroviral therapy (ART). - ART is
usually a combination of two or more medications from several different drug classes.
Two drugs from one class, plus a third drug from a second class, are typically used.
Anti – HIV drugs include,
 Non-nucleoside reverse transcriptase inhibitors (NNRTIs) turn off a protein
needed by HIV to make copies of itself. - Examples include efavirenz (Sustiva),
rilpivirine (Edurant) and doravirine (Pifeltro).

 Nucleoside or nucleotide reverse transcriptase inhibitors (NRTIs) are faulty

versions of the building blocks that HIV needs to make copies of itself. - Examples
include abacavir (Ziagen), emtricitabine (Emtriva),) and zidovudine (Retrovir).

 Protease inhibitors (PIs) inactivate HIV protease, another protein that HIV needs
to make copies of itself. -Examples include atazanavir (Reyataz), darunavir
(Prezista) and lopinavir/ritonavir (Kaletra).

 Integrase inhibitors work by disabling a protein called integrase, which HIV uses
to insert its genetic material into CD4 T cells. - Examples include bictegravir
sodium/emtricitabine/tenofovir alafenamide fumarate (Biktarvy), raltegravir
(Isentress), dolutegravir (Tivicay) and cabotegravir (Vocabria).

 Entry or fusion inhibitors block HIV's entry into CD4 T cells. Examples include
enfuvirtide (Fuzeon) and maraviroc (Selzentry)
.