# Infectious Disease Exam Answers — 5th Year Medical Faculty

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## Q1. The concept of an infectious disease, patterns of development of the infectious process, its forms, periods.

**Infectious disease** = a specific reaction of the macroorganism to invasion of a pathogenic microorganism, characterized by a complex of specific clinical and pathological manifestations and a contagious (epidemic) process.

**Infectious process** = interaction of pathogen + macroorganism + environment.

**Forms:**
- Manifest (typical/atypical)
- Inapparent (subclinical)
- Latent (dormant)
- Carrier state (acute, chronic, transient)

**Periods of infectious disease:**
1. **Incubation** – from entry of pathogen to first symptoms; no clinical signs; patient may be infectious
2. **Prodromal (initial)** – non-specific symptoms (fever, malaise, headache)
3. **Peak (height)** – full clinical picture, specific syndromes appear
4. **Convalescence** – symptoms subside; may have relapse or complication
5. **Outcomes:** recovery, chronic form, carrier state, death

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## Q2. Main properties of microorganisms causing the infectious process, their variability.

**Key properties of pathogens:**
- **Pathogenicity** – potential to cause disease (species-level trait)
- **Virulence** – degree of pathogenicity of a specific strain
- **Toxigenicity** – exotoxin (proteins, highly specific, neutralized by antitoxin) vs. endotoxin (LPS of gram-negative bacteria)
- **Invasiveness** – ability to penetrate tissues
- **Adhesins** – surface molecules for host attachment
- **Aggressins** – enzymes (hyaluronidase, coagulase, neuraminidase) overcoming host defenses

**Variability:**
- Mutation (spontaneous/induced)
- Recombination, transduction, transformation
- R-plasmid transfer → antibiotic resistance
- Antigenic variability (drift/shift in influenza)
- L-form transformation → chronic infections

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## Q3. Main factors protecting the macroorganism from pathogenic infection.

**Non-specific (innate) defenses:**
- Skin and mucous membrane barriers
- Ciliary clearance (respiratory tract)
- Normal microbiota (colonization resistance)
- Phagocytosis (neutrophils, macrophages)
- Complement system (classical, alternative, lectin pathways)
- Natural killer cells
- Acute-phase proteins (CRP, fibrinogen, ferritin)
- Lysozyme, secretory IgA, defensins, lactoferrin
- Fever (elevated temperature inhibits pathogen growth)
- Inflammation

**Specific (adaptive) defenses:**
- Humoral immunity: B cells → plasma cells → antibodies (IgM, IgG, IgA, IgE)
- Cellular immunity: T-helper (CD4), cytotoxic T (CD8) cells
- Immunological memory

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## Q4. Classification of infectious diseases.

**By etiology:**
- Bacterial, viral, fungal (mycoses), protozoal, helminthic, prion

**By source of infection (reservoir):**
- Anthroponoses (humans only) – typhoid, dysentery, HIV
- Zoonoses (animals + humans) – brucellosis, rabies, plague
- Sapronoses (environment) – legionellosis, tetanus

**By transmission mechanism:**
- Fecal-oral (enteric) – cholera, typhoid, hepatitis A
- Airborne (respiratory) – influenza, measles, TB
- Contact (wound) – tetanus, rabies
- Blood (hemotransmissive) – HIV, hepatitis B/C
- Vector-borne (transmissive) – malaria, typhus, tick-borne encephalitis
- Vertical (transplacental) – rubella, CMV, toxoplasmosis

**By organ system affected:**
- Intestinal, respiratory, blood, tegumentary (skin/mucous membranes)

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## Q5. Principles of diagnostics of infectious diseases, main clinical syndromes, early diagnostics.

**Principles:**
1. Clinical (history, physical exam)
2. Epidemiological (contact, travel, occupation, vaccination history)
3. Laboratory and instrumental

**Key clinical syndromes:**
- Fever + intoxication (most infections)
- Exanthema (rash) – measles, scarlet fever, typhus
- Diarrhea/gastroenteritis – salmonellosis, cholera
- Jaundice – viral hepatitis
- Meningeal syndrome – meningitis, encephalitis
- Lymphadenopathy – mononucleosis, HIV, tularemia
- Catarrhal (respiratory) – influenza, ARI
- Hemorrhagic syndrome – viral hemorrhagic fevers, meningococcemia

**Early diagnosis:**
- Epidemiological anamnesis is key
- CBC: leukocytosis (bacterial), leukopenia + lymphocytosis (viral)
- Immediate notification for quarantine diseases

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## Q6. Role of specific research methods in diagnosis of infectious diseases.

**Bacteriological (culture):**
- Blood, stool, urine, CSF, swabs cultured on selective media
- Gold standard for bacterial infections
- Results in 24–72 hours

**Virological:**
- Cell culture, embryo inoculation
- Isolation of virus from blood, secretions

**Parasitological:**
- Thick/thin blood smear (malaria)
- Microscopy of stool (helminths, protozoa)

**Molecular (PCR):**
- Detects pathogen DNA/RNA
- High sensitivity and specificity
- Useful early, before antibodies develop (HIV, hepatitis C, herpes)
- Real-time PCR for quantification (viral load)

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## Q7. Role of serological and immunological methods in diagnosis.

**Serological tests** detect antibodies (Abs) or antigens (Ags) in patient serum:
- **ELISA** (enzyme-linked immunosorbent assay) – IgM (acute) vs. IgG (past/chronic) detection; most widely used
- **RIA** (radioimmunoassay)
- **Agglutination tests** (Widal for typhoid, Weil-Felix for rickettsia)
- **Complement fixation** (CFT)
- **Neutralization test** (virus-specific)
- **Immunofluorescence** (IFA/RNIF/ELISA) – direct or indirect
- **Western blot** – confirmatory for HIV

**Immunological:**
- T/B lymphocyte counts (CD4 in HIV)
- Interferons, cytokines (IL-6, TNF for sepsis)
- Immunoelectrophoresis

**Principles:** 4-fold rise in antibody titer in paired sera (acute + convalescent, 2–3 wks apart) = diagnostic

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## Q8. Role of biochemical and instrumental methods in infectious disease clinic.

**Biochemical:**
- LFTs (ALT, AST, bilirubin, ALP, GGT) → hepatitis, liver failure
- Urea, creatinine → AKI in leptospirosis, HFRS
- Electrolytes (K+, Na+) → dehydration, cholera
- Coagulation (PT, APTT, fibrinogen, D-dimers) → DIC
- CRP, procalcitonin → bacterial vs. viral infection, sepsis
- Blood glucose → altered consciousness, sepsis
- Lactate → tissue hypoperfusion in sepsis/shock

**Instrumental:**
- Chest X-ray → pneumonia, TB, plague
- Abdominal ultrasound → hepatosplenomegaly, abscess
- CT/MRI brain → encephalitis, cerebral malaria, tuberculoma
- ECG → myocarditis (diphtheria, viral)
- FGDS → colitis, esophageal candidiasis (HIV)
- Lumbar puncture (CSF analysis) → meningitis

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## Q9. Role of skin-allergic and biological tests in diagnosis.

**Skin-allergic tests** (type IV hypersensitivity – delayed):
- **Mantoux test (tuberculin test)** – PPD intradermal; induration ≥10 mm positive → TB sensitization (not disease)
- **IGRA (QuantiFERON)** – in vitro alternative
- **Tularin test** – tularemia
- **Leishmanin (Montenegro)** – leishmaniasis
- **Brucellin test (Burne)** – brucellosis
- **Toxoplasmin test** – toxoplasmosis
- **Histoplasmin, coccidioidin** – endemic mycoses

**Biological tests:**
- Inoculation of laboratory animals with patient material
- Confirm pathogenicity; used for plague, anthrax, tularemia
- Largely replaced by PCR and culture today

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## Q10. Principles of complex therapy of infectious patients.

**4 pillars:**
1. **Etiotropic** – targeting the causative agent (antibiotics, antivirals, antiparasitics)
2. **Pathogenetic** – correcting pathological processes (rehydration, detoxification, anti-DIC)
3. **Symptomatic** – alleviating symptoms (antipyretics, analgesics, antiemetics)
4. **Immunocorrective** – immunoglobulins, interferons, immunostimulants

**General principles:**
- Hospitalization for severe/quarantine cases
- Bed rest during acute phase
- Diet (table №4 for diarrhea, №5 for hepatitis)
- Adequate fluid intake
- Monitoring of vital signs and organ function
- Prevent nosocomial spread (isolation, PPE)

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## Q11. Methods of etiotropic therapy of infectious diseases.

**Antibacterials:**
- Beta-lactams (penicillins, cephalosporins, carbapenems)
- Aminoglycosides (gentamicin, amikacin)
- Fluoroquinolones (ciprofloxacin, levofloxacin)
- Tetracyclines (doxycycline) – rickettsiae, brucella, chlamydia
- Macrolides (azithromycin) – atypical pneumonia
- Glycopeptides (vancomycin) – MRSA, C. difficile

**Antivirals:**
- Acyclovir/valacyclovir – herpes simplex, VZV
- Ganciclovir – CMV
- Oseltamivir (Tamiflu) – influenza
- DAAs (sofosbuvir, NS5A inhibitors) – Hepatitis C (>95% SVR)
- Tenofovir/emtricitabine + PI or INSTI – HIV (ART)
- Entecavir, tenofovir – Hepatitis B

**Antiparasitics:**
- Chloroquine, artemisinin-based – malaria
- Metronidazole – amebiasis, giardia, anaerobes
- Pyrimethamine + sulfadiazine – toxoplasmosis
- Albendazole – helminths

**Antifungals:**
- Fluconazole – candidiasis
- Amphotericin B – severe systemic mycoses

**Key principle:** Start empirically based on likely pathogen; narrow spectrum once culture/sensitivity known.

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## Q12. Serotherapy of infectious diseases and its possible complications.

**Serotherapy** = passive immunization using ready-made antibodies from animals or humans.

**Types:**
- **Antitoxic sera** – diphtheria antitoxin (horse), botulinum antitoxin (horse), tetanus antitoxin (TAT)
- **Antimicrobial sera** – anti-plague, anti-anthrax (less used now)
- **Immunoglobulins (human)** – anti-rabies, anti-hepatitis B, anti-tetanus (TIG), anti-varicella (VZIG), intravenous immunoglobulin (IVIG)
- **Monoclonal antibodies** – newer agents

**Complications:**
- **Anaphylactic shock** – immediate (IgE-mediated); treat with epinephrine 0.1% 0.5 mL IM
- **Serum sickness** – 7–14 days after horse serum; immune complex disease; urticaria, arthralgia, fever, lymphadenopathy; treat with antihistamines, corticosteroids
- Local reactions: pain, induration at injection site

**Precautions:**
- Sensitivity test (Bezredka method) before horse serum: 0.1 mL of diluted serum SC → observe 30 min → if negative, give full dose
- Always have resuscitation ready

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## Q13. Methods of pathogenetic therapy of infectious diseases.

**Rehydration and detoxification (most important):**
- Oral rehydration: ORS (glucose-salt solution) – mild/moderate dehydration
- IV rehydration: Ringer's lactate, 0.9% NaCl, trisol – severe dehydration (cholera, gastroenteritis)
- Volume: replace deficit + ongoing losses + maintenance

**Detoxification:**
- IV colloids/crystalloids (saline, glucose)
- Hemodez, reopoliglyukin (dextran)
- Forced diuresis (furosemide after hydration)
- Plasmapheresis, hemosorption – severe toxemia

**Anti-DIC therapy:**
- Early: anticoagulants (heparin), fresh frozen plasma (FFP)
- Late (fibrinolytic stage): FFP, tranexamic acid, fibrinogen

**Corticosteroids:**
- Cerebral edema, septic shock, meningococcemia, severe toxicity
- Dexamethasone 0.4 mg/kg in bacterial meningitis (reduces hearing loss)

**Immunotherapy:**
- Interferons (IFN-alpha, IFN-beta)
- IVIG for severe bacterial infections

**Symptomatic:**
- Antipyretics (paracetamol; avoid aspirin in viral infections due to Reye syndrome risk)
- Antiemetics, antispasmodics
- O2 therapy, mechanical ventilation if needed

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## Q14. Principles of infectious disease prevention, vaccination, immunoprophylaxis.

**Prevention levels:**
- **Primary** – preventing disease (vaccination, hygiene, safe sex, vector control)
- **Secondary** – early detection and treatment
- **Tertiary** – preventing complications

**Types of immunoprophylaxis:**
- **Active immunization (vaccines):**
  - Live attenuated: BCG, OPV, MMR, yellow fever, varicella → long-lasting immunity
  - Killed/inactivated: IPV, influenza (injectable), hepatitis A → safe in immunocompromised
  - Toxoids: diphtheria (DT), tetanus → against exotoxins
  - Subunit/recombinant: hepatitis B, HPV, acellular pertussis
  - mRNA: COVID-19

- **Passive immunization:**
  - Immunoglobulins (human): rapid protection, short-lived (3–4 weeks)
  - Used for post-exposure prophylaxis: rabies, hepatitis B, tetanus, varicella

**Russian national vaccination calendar:**
- BCG (day 3–7), HBV (birth, 1, 6 months), DPT (3, 4.5, 6 months), MMR (12 months), etc.

**Non-specific prevention:**
- Sanitation, vector control, quarantine, food safety, disinfection

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## Q15. Organizational structure of medical care for infectious patients.

**Outpatient level:**
- Polyclinic: initial diagnosis, mild cases managed at home
- Mandatory reporting (Form 058/u) to sanitary-epidemiological service (Rospotrebnadzor) within 12 hours

**Inpatient level – Infectious Disease Hospital (Инфекционная больница):**
- Box wards (Melzer boxes) – individual rooms with separate entrance/exit, laminar flow; for highly contagious patients
- Semi-box/ward system for less contagious
- Separate departments by pathogen type (intestinal, respiratory, etc.)
- ICU for severe cases
- Disinfection zone, sanitary checkpoint at entry

**Structure:**
- Reception/admissions (sanitary filter) – history, examination, preliminary diagnosis, disinfection
- Clinical departments
- Bacteriology/Virology laboratory
- Disinfection department
- Emergency department

**Discharge criteria:**
- Clinical recovery + bacteriological clearance (culture-negative for typhoid, cholera, dysentery)
- Following epidemiological regulations

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## Q16. Early detection, hospitalization and discharge rules, rehabilitation of convalescents.

**Early detection:**
- Active: screening (blood donors, pregnant women, food workers)
- Passive: patient presentation to clinic
- Emergency notification within 12 h for Group I (plague, cholera, VHFs) or 24 h for Group II diseases

**Hospitalization indications:**
- Clinical: severe course, complications, need for parenteral therapy
- Epidemiological: quarantine diseases, food workers, children's institution staff, housing conditions

**Isolation periods (examples):**
- Typhoid: until 2 negative stool cultures (not before day 21 from onset)
- Dysentery: 3 days after clinical recovery + negative stool culture
- Diphtheria: 2 negative cultures
- Hepatitis A: until clinical/biochemical recovery (minimum 28 days)

**Discharge:**
- Certificate of recovery
- Referral to polyclinic for follow-up (dispensarization)

**Rehabilitation/dispensarization:**
- Typhoid: observation 3 months, monthly stool cultures
- Hepatitis B/C: 12 months in hepatology
- Brucellosis: 2 years
- Meningococcal infection: 2 years (neurologist)

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## Q17. Physician's tactics with acute respiratory infections (ARI). Specimen collection.

**Physician's tactics:**
- Epidemiological history (contact, travel – especially for influenza, COVID-19, SARS)
- If "unusual" ARI (severe, unusual epidemiology, atypical course) → suspect dangerous infection
- For highly pathogenic (H5N1, SARS, COVID-19): immediately contact chief physician, call Rospotrebnadzor, isolate patient, use PPE (FFP3 mask, gown, gloves, goggles)

**Specimen collection:**
- **Nasopharyngeal swab** – for influenza, COVID-19, adenovirus (PCR)
- **Nasopharyngeal washings** – flu rapid antigen test
- **Sputum** – bacteriological culture, AFB smear for TB
- **Blood** – culture (sepsis), CBC, paired serology
- **Broncho-alveolar lavage** – atypical pneumonia, PCP (in HIV)
- From corpse: lung tissue, tracheal contents → must inform Rospotrebnadzor

**Transport:** Cold chain (2–8°C), special containers, labeled with clinical data, sent to virological reference lab

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## Q18. Infectious-toxic shock (ITS) – pathogenesis, stages, clinic.

**Pathogenesis:**
Massive release of bacterial toxins (endotoxin/exotoxin) → activation of macrophages, cytokine storm (TNF-α, IL-1, IL-6) → vasodilation, increased vascular permeability → distributive shock → organ hypoperfusion → MODS

**Stages (Bone classification):**

| Stage | BP | Features |
|-------|-----|---------|
| Stage I (warm shock) | Normal or ↑ | Hyperdynamic; skin warm, flushed; tachycardia; fever; urine output decreased |
| Stage II (cold shock) | ↓ (90–60 mmHg) | Hypodynamic; skin cold, pale, clammy; oliguria; mental changes |
| Stage III (irreversible) | <60 mmHg | Anuria, coma, DIC, MODS; often fatal |

**Clinic:** High fever → sudden chills → skin flushing/pallor → tachycardia → hypotension → confusion → oliguria/anuria → hemorrhagic manifestations (DIC)

Most commonly: meningococcemia, salmonellosis, typhoid, gram-negative sepsis, leptospirosis

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## Q19. Treatment of ITS (stages of care).

**Pre-hospital:**
- IV access (2 large-bore lines)
- Bolus crystalloids (0.9% NaCl or Ringer's lactate) 10–20 mL/kg over 15–30 min
- Oxygen
- Antibiotics ASAP (do not delay for cultures >45 min)
- Corticosteroids: prednisolone 60–120 mg IV or dexamethasone 8–16 mg IV

**Hospital (ICU):**
- Aggressive fluid resuscitation: 30 mL/kg crystalloids in first 3 hours (Surviving Sepsis Campaign)
- Vasopressors: norepinephrine (first choice) if MAP <65 mmHg despite fluids; target MAP ≥65
- Broad-spectrum antibiotics (within 1 hour): e.g., ceftriaxone 2 g + metronidazole ± vancomycin
- Corticosteroids: hydrocortisone 200 mg/day IV if vasopressor-refractory shock
- Correct metabolic acidosis, electrolytes
- Heparin for DIC (early phase), FFP
- Organ support: mechanical ventilation (ARDS), RRT (AKI)
- Monitoring: hourly urine output, CVP, SpO2, lactate clearance

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## Q20. DIC Syndrome in infectious diseases – pathogenesis, clinical features, diagnostics.

**Pathogenesis:**
Infection → endotoxin/exotoxin → activation of coagulation cascade (tissue factor pathway) → widespread microthrombi (thrombotic phase) → consumption of clotting factors (fibrinogen, platelets, factors V, VIII) → hemorrhagic phase → organ ischemia

**Clinical features:**
- **Phase I (hypercoagulation):** skin mottling, acrocyanosis, thrombosis, organ dysfunction
- **Phase II (consumption coagulopathy):** bleeding from injection sites, mucous membranes, GI, hematuria; petechiae/ecchymoses
- **Phase III (fibrinolysis):** massive hemorrhage, shock

**Associated infections:** meningococcemia, sepsis, leptospirosis, typhus, viral hemorrhagic fevers, plague

**Diagnostics:**
- Platelet count ↓ (<100,000)
- PT/APTT prolonged
- Fibrinogen ↓ (<1 g/L in severe)
- D-dimer ↑ (fibrin degradation products)
- Schistocytes on blood smear (microangiopathy)
- ISTH DIC score: platelets + PT + fibrinogen + D-dimer → score ≥5 = overt DIC

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## Q21. Treatment and prevention of DIC in infectious patients.

**Treatment by phase:**

**Phase I (hypercoagulation):**
- Treat underlying infection (antibiotics)
- Unfractionated heparin 5000–10,000 U IV bolus → 500–1000 U/h infusion (monitor APTT ×1.5–2.5)
- Fresh frozen plasma (FFP) 10–15 mL/kg – replaces all clotting factors
- Antiplatelet agents if needed

**Phase II (consumption):**
- Discontinue/reduce heparin
- FFP 15–20 mL/kg
- Cryoprecipitate (fibrinogen + factor VIII) if fibrinogen <1 g/L
- Platelet transfusion if <20,000 or active bleeding
- Antithrombin III concentrate

**Phase III (fibrinolysis/hemorrhage):**
- Tranexamic acid (antifibrinolytic) 10–15 mg/kg IV
- FFP, cryoprecipitate, platelets
- Corticosteroids for vascular stabilization
- No heparin in this phase

**Prevention:**
- Prompt treatment of infection
- Avoid triggers (hypothermia, acidosis, hypoxia)
- Monitoring of coagulation in high-risk patients (sepsis, meningococcemia)

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## Q22. Dehydration shock – pathogenesis, stages, clinical features, treatment.

**Pathogenesis:**
Massive fluid and electrolyte loss (vomiting/diarrhea) → intravascular volume depletion → decreased cardiac output → compensatory vasoconstriction → tissue hypoperfusion → lactic acidosis → MODS
Classic cause: Cholera (rice-water stools, up to 20 L/day)

**Stages (Russian classification of dehydration):**

| Degree | Fluid Loss (body weight) | Clinic |
|--------|--------------------------|--------|
| I | 1–3% | Thirst, slight dry mucosae, normal BP |
| II | 4–6% | Dry skin, sunken eyes, tachycardia, BP normal or ↓, oliguria, muscle cramps |
| III | 7–9% | Severe dehydration, hypotension, acrocyanosis, anuria, aphonia |
| IV (algid) | >10% | Cold skin, anuria, asphyxia, hypotension, coma, DIC |

**Treatment:**
- Degree I–II: oral rehydration (ORS – WHO formula: NaCl 3.5g, KCl 1.5g, NaHCO3 2.5g, glucose 20g per 1L)
- Degree III–IV: IV rehydration
  - **Trisol** (NaCl 5g + KCl 1g + NaHCO3 4g per 1L water) – standard Russian solution
  - **Quartasol, Acesol, Ringer's lactate**
  - Primary rehydration: replace calculated deficit in 1–2 hours; then compensatory rehydration matching ongoing losses
- Monitor: BP, pulse, urine output, electrolytes, acid-base balance

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## Q23. Acute Renal Failure (ARF) in infectious diseases.

**Causes in infections:**
- Direct renal involvement: leptospirosis (tubular), HFRS (hantavirus – hemorrhagic fever with renal syndrome), malaria
- Indirect: shock (sepsis, dehydration, ITS), DIC, myoglobinuria (tetanus, diphtheria), nephrotoxic antibiotics (aminoglycosides)

**Stages:**
1. **Oliguric** – urine output <400 mL/day; rising creatinine/urea; hyperkalemia; fluid overload
2. **Polyuric** – urine output increases (often >3 L/day); risk of hypokalemia, dehydration
3. **Recovery** – gradual return of concentrating ability (months)

**Clinical features:**
- Oliguria/anuria, edema, hypertension
- Uremic symptoms: nausea, drowsiness, asterixis
- Hyperkalemia → cardiac arrhythmias
- Metabolic acidosis

**Diagnosis:**
- Creatinine ↑, urea ↑, GFR ↓
- Urine: low specific gravity, proteinuria, casts (granular in ATN)
- Ultrasound: normal/enlarged kidneys (acute vs. chronic)

**Indications for hemodialysis (AEIOU):**
- **A**cidosis (pH <7.1)
- **E**lectrolytes (K+ >6.5 mmol/L)
- **I**ntoxication (uremic symptoms, toxic ingestion)
- **O**verload (refractory pulmonary edema)
- **U**remia (urea >30 mmol/L, symptoms)

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## Q24. Acute hepatic encephalopathy – mechanisms, clinical features, diagnosis, treatment.

**Mechanism:**
Massive hepatocyte necrosis (fulminant viral hepatitis B, B+D, drug toxicity) → failure to detoxify ammonia → ammonia crosses BBB → glutamine accumulation in astrocytes → cerebral edema + neurotransmitter imbalance (false neurotransmitters, GABA agonists)

**Clinical stages (West Haven criteria):**

| Stage | Features |
|-------|----------|
| I | Mild confusion, sleep-wake reversal, euphoria/anxiety |
| II | Drowsiness, disorientation, asterixis (liver flap) |
| III | Stupor, responds to stimuli, marked asterixis |
| IV | Coma, no response to stimuli |

**Other signs:** Fetor hepaticus (sweet-musty breath), jaundice, bleeding tendency (PT ↑ ↑), shrinking liver

**Diagnostics:**
- Ammonia ↑ (arterial >200 μmol/L = severe)
- Bilirubin ↑↑ (>200 μmol/L in severe)
- ALT/AST ↑↑ initially, then ↓ (liver destruction)
- PT/INR markedly prolonged
- EEG: triphasic waves
- CT/MRI: cerebral edema

**Treatment:**
- ICU, avoid sedatives
- Lactulose 30–45 mL orally TID (reduces NH3 absorption)
- Rifaximin 550 mg BD (reduces ammonia-producing gut bacteria)
- Protein restriction (moderate, not severe)
- Correct hypoglycemia (10% glucose)
- FFP, vitamin K for coagulopathy
- Manage cerebral edema: elevate head 30°, mannitol 20%, avoid fluid overload
- Liver transplantation (definitive for fulminant hepatic failure)

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## Q25. Viral Hepatitis A and E.

**HAV:**
- RNA picornavirus; fecal-oral transmission; water/food-borne outbreaks
- Incubation: 15–50 days (avg 28 days)
- **Self-limiting** – no chronic form; complete recovery in >99%
- At-risk: children, travellers, poor sanitation areas

**HEV:**
- RNA hepevirus; fecal-oral; contaminated water (endemic in India, Central Asia, Africa)
- Incubation: 15–60 days
- **High mortality in pregnancy (20–25%)** in genotype 1/2
- Genotype 3/4: zoonotic (pigs); can cause chronic hepatitis in immunocompromised

**Both: Clinical features (icteric form):**
- Preicteric: 5–7 days; fever, malaise, nausea, right upper quadrant pain, dark urine
- Icteric: jaundice appears; fever subsides; hepatomegaly; pruritus; pale stools
- Recovery: 2–4 weeks

**Atypical forms:** Anicteric (most common), cholestatic, fulminant (rare)

**Diagnosis:**
- Anti-HAV IgM (acute HAV), anti-HAV IgG (past/immune)
- Anti-HEV IgM; HEV RNA by PCR
- LFTs: ALT ↑↑ (>10× ULN in acute), bilirubin ↑↑ (conjugated dominant)

**Treatment:** Supportive (rest, diet №5, no alcohol, avoid hepatotoxic drugs)
**Vaccine:** HAV – inactivated vaccine (2 doses); HEV – recombinant vaccine (HEV 239, approved in China)

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## Q26. Viral Hepatitis B.

**Etiology:** HBV – partially double-stranded DNA hepadnavirus; highly infectious (100× more than HIV)

**Antigens:**
- HBsAg (surface) – marker of infection (acute + chronic)
- HBeAg – marker of active replication/high infectivity
- HBcAg – core antigen (not detectable in serum)
- HBV DNA – best marker of replication

**Epidemiology:** Blood, sexual contact, vertical (perinatal) transmission
**Incubation:** 60–180 days

**Outcomes:**
- Acute: 90–95% adults recover; 5–10% → chronic
- Neonates: 90% → chronic
- Chronic → cirrhosis (20%) → HCC (hepatocellular carcinoma)

**Serology interpretation:**

| HBsAg | Anti-HBs | Anti-HBc IgM | Anti-HBc IgG | Interpretation |
|-------|----------|--------------|--------------|----------------|
| + | – | + | – | Acute HBV |
| – | + | – | + | Past infection / immune |
| – | + | – | – | Vaccinated |
| + | – | – | + | Chronic HBV |

**Treatment:**
- Acute: supportive; no antivirals unless fulminant
- Chronic: entecavir 0.5 mg/day or tenofovir (TDF/TAF) – lifelong; goal: suppress HBV DNA, prevent cirrhosis/HCC
- Pegylated IFN-alpha (48 wks) – finite course option; less tolerated

**Prevention:** HBV vaccine (3 doses, 0-1-6 months); HBIG for post-exposure prophylaxis (newborns + needlestick)

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## Q27. Viral Hepatitis D.

**Etiology:** HDV (delta agent) – defective RNA virus; requires HBsAg for assembly; can only infect those with HBV

**Types of infection:**
- **Coinfection** (HBV + HDV simultaneously): usually self-limiting; low risk of chronicity; higher risk of fulminant hepatitis
- **Superinfection** (HDV in chronic HBV carrier): rapid progression to cirrhosis; >90% become chronically co-infected; worst prognosis

**Epidemiology:** Blood and sexual transmission (same as HBV); endemic in Mediterranean, Eastern Europe, Central Asia, South America (Amazonia)

**Clinical:** More severe than HBV alone; biphasic pattern in coinfection; rapid cirrhosis in superinfection

**Diagnosis:**
- Anti-HDV total/IgM antibodies
- HDV RNA (PCR) – most sensitive
- HBsAg must be positive

**Treatment:**
- Pegylated IFN-alpha (48–72 weeks) – only approved therapy; 25% SVR
- Bulevirtide (Hepcludex) – new entry inhibitor (blocks NTCP receptor); approved in Europe 2020
- HBV suppression with nucleos(t)ide analogs (controls HBV but not HDV replication directly)

**Prevention:** HBV vaccination prevents HDV (since HDV needs HBV)

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## Q28. Viral Hepatitis C.

**Etiology:** HCV – RNA flavivirus; 7 genotypes (1–7); genotype 1 most common globally, most prevalent in Russia

**Epidemiology:** Blood-borne (IV drug use, transfusions pre-screening, medical procedures); sexual/vertical – less efficient than HBV

**Incubation:** 15–180 days (avg 7 weeks)

**Stages:**
- Acute: 80% asymptomatic; 20% jaundice
- Chronic (75–85% of acute cases): silent; decompensated cirrhosis in 20% after 20 years; HCC risk

**Clinical:** Often discovered incidentally via elevated ALT or screening; "silent killer"

**Diagnosis:**
- Anti-HCV antibodies (ELISA) – screening; positive 8–12 weeks after exposure
- HCV RNA (PCR) – confirms active infection; appears within 1–2 weeks
- HCV genotype – guides treatment
- Liver biopsy/elastography (FibroScan) – assess fibrosis

**Treatment (DAAs – Direct-Acting Antivirals):**
- Sofosbuvir/ledipasvir (Harvoni), Sofosbuvir/velpatasvir (Epclusa) – pangenotypic
- 8–12 weeks course; SVR (sustained virological response = cure) >95–98%
- SVR = HCV RNA undetectable 12 weeks after treatment end

**Prevention:** No vaccine; needle exchange programs, blood screening

---

## Q29. Early diagnosis of viral hepatitis. Prehospital management.

**Early (preicteric) signs to detect:**
- Flu-like prodrome (fatigue, anorexia, nausea, RUQ discomfort) before jaundice
- Dark urine (bilirubinuria) appears before clinical jaundice – key early sign
- Pale stools (acholia)
- ALT elevation precedes jaundice by 5–10 days

**Early diagnostic markers:**
- ALT/AST ↑ (often 10–100× ULN) – most sensitive early marker
- Bilirubin ↑ (conjugated)
- Thymol turbidity test (protein fraction changes)
- Urinary bilirubin (dipstick)

**Prehospital management:**
- Bed rest
- Diet №5 (restrict fats, fried food, alcohol, hepatotoxic drugs)
- Oral rehydration
- Symptomatic: antiemetics, hepatoprotectors (ursodeoxycholic acid – controversial)
- Refer to hospital: fulminant course, pregnancy, elderly, immunocompromised, hepatitis B/C with complications
- Epidemiological measures: identify contacts, notify Rospotrebnadzor (HAV/HEV = acute notification)

---

## Q30. Laboratory diagnostics of viral hepatitis.

**Non-specific (functional liver tests):**
- ALT, AST (cytolysis syndrome) – ↑↑ in acute hepatitis
- Bilirubin (total, conjugated/unconjugated)
- ALP, GGT (cholestasis)
- Albumin, PT/INR (synthetic function – ↓ in severe)
- Thymol turbidity ↑

**Specific markers:**

| Hepatitis | Acute | Chronic/Past | Replication |
|-----------|-------|-------------|------------|
| HAV | Anti-HAV IgM | Anti-HAV IgG | – |
| HBV | HBsAg + Anti-HBc IgM | HBsAg + Anti-HBc IgG | HBeAg, HBV DNA |
| HCV | Anti-HCV IgM/IgG | Anti-HCV IgG | HCV RNA (PCR) |
| HDV | Anti-HDV IgM | Anti-HDV IgG | HDV RNA |
| HEV | Anti-HEV IgM | Anti-HEV IgG | HEV RNA |

**Additional:**
- Ultrasound: hepatomegaly, splenomegaly, altered echogenicity
- Liver biopsy / FibroScan (FibroTest): fibrosis staging
- AFP ↑ → HCC screening (HBV/HCV cirrhosis)

---

## Q31. Principles of treatment, clinical examination of viral hepatitis convalescents, preventive measures.

**Treatment principles:**
- Hepatitis A/E: supportive (bed rest, diet №5, no alcohol, no hepatotoxics)
- Hepatitis B acute: supportive; if fulminant → antivirals (entecavir)
- Hepatitis B chronic: entecavir or tenofovir (lifelong or until HBsAg seroconversion)
- Hepatitis C: DAAs (sofosbuvir-based) 8–12 weeks; >95% cure
- Hepatitis D: pegIFN-alpha; bulevirtide

**Clinical examination (dispensarization):**
- HAV convalescents: 3 months follow-up; LFTs at 1 and 3 months
- HBV: 12 months observation; LFTs + HBsAg every 3 months; if HBsAg persists >6 months → chronic
- HCV: SVR assessment at 12 weeks post-treatment; annual ultrasound if cirrhosis
- HBV/HCV cirrhosis: 6-monthly AFP + ultrasound for HCC surveillance

**Prevention:**
- HAV: vaccine (2 doses), sanitation, hand hygiene
- HBV: vaccine (universal infant immunization), HBIG for newborns of HBsAg+ mothers, safe sex, universal precautions
- HCV: no vaccine; harm reduction (needle programs), blood screening, universal precautions
- HEV: safe water, no vaccine widely available (except China)

---

## Q32. Typhoid Fever – etiology, pathogenesis, pathological anatomy, clinical presentation, diagnosis, treatment, discharge guidelines.

**Etiology:** Salmonella enterica serovar Typhi (gram-negative, facultative anaerobe)

**Pathogenesis:** Fecal-oral → colonizes Peyer's patches (ileum) → bacteremia (1st week) → seeding liver, spleen, gallbladder, bone marrow → lymph node hyperplasia → necrosis of Peyer's patches → ulceration (3rd week) → healing (4th week)

**Pathological anatomy (Peyer's patches stages):**
1. Medullary swelling (week 1)
2. Necrosis (week 2)
3. Ulcer formation (week 3) – risk of bleeding/perforation
4. Clean ulcer (week 4)
5. Healing (week 5)

**Clinical (4 weeks classic course):**
- Fever: stepwise rise (Wunderlich curve) to 39–40°C by end of week 1
- Relative bradycardia (pulse-temperature dissociation)
- Headache, adynamia, anorexia
- Roseolar rash (rose spots) on abdomen/trunk – appears day 8–10; sparse (5–20 elements); blanches on pressure
- "Typhoid tongue" – coated center, red edges/tip
- Hepatosplenomegaly
- Constipation typical (diarrhea "pea soup" stools later)

**Complications:** Intestinal bleeding (week 3–4), intestinal perforation (peritonitis), hepatitis, myocarditis, pneumonia, nephritis

**Diagnosis:**
- Blood culture (bacteremia) – weeks 1–2 (most sensitive early)
- Bone marrow culture – most sensitive overall
- Stool culture – week 2 onward
- Urine culture – week 2 onward
- Widal test (agglutination): O-antibodies (active disease) + H-antibodies (past/vaccine); requires 4-fold rise in paired sera; less specific
- PCR available
- CBC: leukopenia, eosinopenia, relative lymphocytosis; ESR normal

**Treatment:**
- Fluoroquinolones (ciprofloxacin 500 mg BD × 10–14 days) – 1st choice
- Ceftriaxone 2g IV OD × 14 days (for MDR strains)
- Chloramphenicol, ampicillin (historical, resistance common)
- Azithromycin (500 mg × 7 days) for uncomplicated

**Discharge:** Not before day 21 of illness + 2 negative stool cultures (3–5 days apart) + negative urine culture

---

## Q33. Salmonellosis – etiology, epidemiology, pathogenesis, clinical forms, diagnosis, treatment.

**Etiology:** Salmonella enteritidis, S. typhimurium, and 2500+ other serovars (not S. Typhi)

**Epidemiology:** Zoonosis; contaminated poultry, eggs, dairy, meat; fecal-oral; outbreaks in food establishments

**Pathogenesis:** Ingestion of large dose → colonize small intestine → produce enterotoxin + endotoxin → inflammation, secretory diarrhea → may invade and bacteremia

**Clinical forms:**
1. **Gastrointestinal (most common – 96%):**
   - Gastritis, gastroenteritis, gastroenterocolitis
   - Onset 6–72 hours after exposure
   - Nausea, vomiting, fever (38–39°C), watery diarrhea (not bloody usually)
   - No tenesmus (vs. dysentery)
2. **Typhoid-like** – fever, headache, hepatosplenomegaly; no Peyer's patches changes
3. **Septic (bacteremic)** – high fever, chills, pyemic foci (osteomyelitis, meningitis); mainly immunocompromised
4. **Carrier** – asymptomatic, transient (>1 month = chronic)

**Diagnosis:**
- Stool culture (main method) – from early diarrhea
- Blood culture – in septic/typhoid-like forms
- Serology (RNGA) – diagnostic if >1:200, 4-fold rise
- PCR

**Treatment:**
- Mild/moderate GI: rehydration (oral), no antibiotics needed
- Severe GI/systemic: ciprofloxacin 500 mg BD × 5–7 days
- Septic form: ceftriaxone IV × 14 days
- Rehydration: oral (ORS) or IV (trisol, Ringer's)

---

## Q34. Cholera – etiology, epidemiology, pathogenesis, clinical, diagnosis, treatment.

**Etiology:** Vibrio cholerae O1 (biotypes: classical, El Tor) and O139; comma-shaped gram-negative rod; highly acid-labile

**Epidemiology:** Fecal-oral; contaminated water (main); 7 pandemics; endemic in South Asia; El Tor pandemic ongoing since 1961

**Pathogenesis:** Ingestion → colonize small intestine → produce CT (choleragen = cholera toxin, AB5 structure) → CT activates adenylate cyclase via Gs protein → ↑cAMP → hypersecretion of Cl⁻ and water; Na⁺ absorption blocked → massive watery secretory diarrhea (up to 20 L/day); no mucosal invasion; no fever initially

**Clinical features:**
- Sudden watery diarrhea ("rice-water stools") – no blood, no odor
- Vomiting (no nausea)
- No fever or low-grade
- Rapid severe dehydration: muscle cramps (K+ loss), dry skin, sunken eyes/fontanelle, husky voice → aphonia → oliguria → algid stage (hypothermia, circulatory collapse, coma)

**Diagnosis:**
- Dark-field microscopy (motile vibrios in stool) – rapid
- Stool culture on TCBS agar (selective)
- Agglutination with specific antisera
- PCR
- Quarantine disease – immediate reporting

**Treatment:**
- **Rehydration = cornerstone:**
  - Degree I–II: oral (ORS)
  - Degree III–IV: IV Trisol, Quartasol; primary rehydration rapid (within 2 hours)
- Antibiotics: doxycycline 300 mg single dose or tetracycline; ciprofloxacin 1g single dose – reduce duration/shedding
- **No antidiarrheal agents (loperamide contraindicated)**
- Strict isolation, contact tracing, chemoprophylaxis of contacts (doxycycline)

---

## Q35. Food poisoning (Bacterial toxicoses) – etiology, pathogenesis, clinical, diagnosis, treatment.

**Etiology:**
- **Staphylococcal toxicosis** (S. aureus enterotoxin A–F, heat-stable)
- **Botulism** (Clostridium botulinum neurotoxin, types A–G)
- **Bacillus cereus** toxin (emetic or diarrheal type)

**Food Poisoning (non-toxicosis – PTI = Pищевая токсикоинфекция):**
- Caused by: Salmonella, E. coli (ETEC), Proteus, Klebsiella, Enterobacter, Clostridium perfringens
- Live bacteria ingested → multiply → produce toxins in gut

**Staphylococcal toxicosis:**
- Incubation: 1–6 hours (most rapid)
- Violent nausea/vomiting, abdominal pain, ± diarrhea
- No fever (toxin, not invasion)
- Short duration (12–24 hours)

**PTI in general:**
- Incubation: 6–24 hours
- Acute onset: nausea, vomiting, watery diarrhea, abdominal cramps, fever
- May cause dehydration

**Diagnosis:** Epidemiological (group outbreak + specific food); culture of food/stool/vomitus; toxin detection (ELISA)

**Treatment:**
- **Gastric lavage** if vomiting not complete (early, <6 hours)
- **Rehydration** (oral or IV depending on severity)
- Enterosobents (activated charcoal, smectite)
- No antibiotics for mild PTI (self-limiting)
- Antibiotics for severe/systemic: ciprofloxacin
- Botulism: antitoxin (polyvalent A+B+E horse serum antitoxin) + ICU

---

## Q36. Botulism – etiology, epidemiology, pathogenesis, clinical, diagnosis, treatment.

**Etiology:** Clostridium botulinum – spore-forming, anaerobic gram-positive rod; produces botulinum neurotoxin (types A, B, E most common in humans); most potent biological toxin known

**Epidemiology:** Food-borne (home-canned foods, smoked fish, mushrooms); wound botulism (IV drug use); infant botulism (honey, spores); no person-to-person transmission

**Pathogenesis:** Toxin absorbed in upper GI → bloodstream → peripheral cholinergic nerve terminals → irreversibly blocks ACh release at NMJ → flaccid paralysis (descending, bilateral, symmetric)

**Clinical (triad):**
1. Descending flaccid paralysis (cranial nerves first → respiratory muscles)
2. Autonomic dysfunction (dry mouth, constipation, urinary retention, fixed dilated pupils)
3. No fever, consciousness preserved, no sensory loss

**Cranial nerve signs first:** diplopia, ptosis, dysarthria, dysphagia → respiratory failure

**Diagnosis:**
- Clinical (descending paralysis + autonomic signs + food history)
- Mouse bioassay (gold standard – detect toxin in serum/food/stool in mice)
- ELISA for toxin
- EMG: decremental response at high-frequency stimulation (vs. Eaton-Lambert: incremental)

**Treatment:**
- **Equine trivalent antitoxin (A+B+E) – earliest possible** (neutralizes unbound toxin)
- ICU: respiratory support (mechanical ventilation if FVC <30%)
- Enteric decontamination: activated charcoal, laxatives (if ingestion <12 hrs)
- No antibiotics (unless wound botulism – penicillin)
- Supportive care: NG feeding, catheterization, eye care

---

## Q37. Dysentery (Shigellosis) – etiology, epidemiology, pathogenesis, clinical, diagnosis, treatment.

**Etiology:** Shigella dysenteriae (most severe), S. flexneri (most common globally), S. sonnei (mildest), S. boydii; gram-negative non-motile rods; very low infectious dose (10–100 organisms)

**Epidemiology:** Fecal-oral; person-to-person (dirty hands), food, water; mainly affects children; no animal reservoir

**Pathogenesis:** Shigella invades colonocytes of distal colon → intracellular multiplication → cell-to-cell spread → colonic mucosa inflammation, ulceration → bloody mucous diarrhea; Shiga toxin (S. dysenteriae) → HUS (hemolytic uremic syndrome)

**Clinical:**
- **Prodrome (1–2 days):** Fever, headache, abdominal pain
- **Colitis syndrome:** Tenesmus (painful straining), frequent small stools (up to 20–30/day) with blood and mucus ("rectal spitting"), severe lower abdominal cramps, palpable sigmoid colon
- Dehydration less common than cholera (colon, not small intestine)

**Forms:** Mild, moderate, severe; toxic (ITS, convulsions in children)

**Complications:** HUS (S. dysenteriae type 1), rectal prolapse, perforation (rare)

**Diagnosis:**
- Stool culture (main) – culture on Ploskirev's or MacConkey agar; positive in 50–70%
- Colonoscopy: catarrhal → fibrinous → ulcerative colitis changes
- CBC: leukocytosis, neutrophilia; ESR ↑
- Serology: RNGA ≥1:200 (diagnostic); 4-fold rise

**Treatment:**
- Mild: rehydration only
- Moderate-severe: **ciprofloxacin** 500 mg BD × 5 days (1st choice); azithromycin for resistant strains
- Children: azithromycin; avoid fluoroquinolones <18 yrs when possible
- Ceftriaxone for severe/HUS-associated
- **No antidiarrheal agents (loperamide contraindicated)** – worsens invasive colitis
- Rehydration (mainly oral)

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## Q38. Escherichia coli Intestinal Infections.

**Classification of pathogenic E. coli:**

| Type | Mechanism | Disease |
|------|-----------|---------|
| ETEC | Heat-labile/stable toxin (↑cAMP/cGMP) | Traveler's diarrhea, watery diarrhea |
| EPEC | Attaches + effaces | Infant diarrhea |
| EIEC | Invasive (like Shigella) | Dysentery-like |
| EHEC (O157:H7) | Shiga toxin 1+2 | Bloody diarrhea + HUS |
| EAEC | Aggregative adhesion | Persistent diarrhea |

**ETEC** – most common cause of traveler's diarrhea; watery, profuse; self-limiting

**EHEC O157:H7:**
- Undercooked beef, unpasteurized dairy; outbreak source
- Bloody diarrhea (colitis) → HUS in 5–10% (children, elderly): microangiopathic hemolytic anemia + thrombocytopenia + AKI
- **Do NOT give antibiotics** (↑ toxin release → ↑ HUS risk)
- **Do NOT give antidiarrheals**
- Supportive care, dialysis for HUS

**Diagnosis:** Stool culture; EHEC: sorbitol-MacConkey agar (O157 is sorbitol-negative); Shiga toxin ELISA; PCR

**Treatment (general):** Rehydration; antibiotics only for ETEC/EIEC (ciprofloxacin 3–5 days); azithromycin for traveler's diarrhea

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## Q39. Yersinioses – etiology, epidemiology, pathogenesis, clinical forms, diagnosis, treatment.

**Two species:**
1. **Yersinia enterocolitica** – intestinal yersiniosis
2. **Yersinia pseudotuberculosis** – pseudotuberculosis (Far East scarlatina)

**Epidemiology:** Zoonosis (pigs, rodents, cattle); contaminated food (pork, vegetables, milk); fecal-oral; no person-to-person; Y. pseudotuberculosis – vegetables, water

**Pathogenesis:** Colonize ileum/cecum → invade Peyer's patches → mesenteric lymphadenitis → possible bacteremia and dissemination → immune complex complications

**Y. enterocolitica clinical forms:**
- Gastroenteritis (most common): fever, diarrhea (±blood), abdominal pain
- Pseudoappendicitis: severe RIF pain (mimics appendicitis); mesenteric lymphadenitis
- Terminal ileitis
- Septicemia (immunocompromised, iron overload)
- Post-infectious: reactive arthritis (HLA-B27), erythema nodosum, uveitis

**Y. pseudotuberculosis (Far East scarlatina):**
- Fever, scarlatiniform rash (palms/soles), "strawberry tongue," arthralgia
- Mesenteric lymphadenitis, hepatosplenomegaly

**Diagnosis:**
- Stool/blood culture (cold enrichment helps: CIN agar)
- RNGA serology: ≥1:200 diagnostic
- CBC: leukocytosis, ↑ESR
- PCR

**Treatment:**
- Mild GI: supportive
- Moderate-severe: ciprofloxacin 500 mg BD × 7–10 days OR doxycycline × 10 days
- Septicemia: ceftriaxone + doxycycline or ciprofloxacin × 14 days

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## Q40. Amebiasis – etiology, epidemiology, pathogenesis, clinical forms, diagnosis, treatment.

**Etiology:** Entamoeba histolytica; exists as trophozoite (invasive, large, hematophagous – "E. histolytica magna") and cyst (4-nucleate, infective form)

**Epidemiology:** Fecal-oral; contaminated water/food; endemic in tropics (India, Africa, Mexico); 50 million infections/year; 100,000 deaths/year

**Pathogenesis:** Cysts ingested → excyst in colon → trophozoites invade colonic mucosa → flask-shaped ulcers (undermined edges) → may invade portal vein → liver abscess (and rarely other organs)

**Clinical forms:**
1. **Intestinal amebiasis (amebic colitis):**
   - Gradual onset; bloody mucous diarrhea with little fever
   - Tenesmus, abdominal pain (mainly RIF + right flank)
   - No systemic toxicity (unlike shigellosis)
   - Chronic form with alternating diarrhea/constipation

2. **Amebic liver abscess:**
   - Fever (hectic), RUQ pain (radiates to right shoulder), tender hepatomegaly
   - No diarrhea (50% have no gut symptoms)
   - Ultrasound: single abscess in right lobe
   - Risk of rupture into pleura/peritoneum

3. **Extraintestinal** (lung, brain, skin) – rare

**Diagnosis:**
- Stool microscopy: motile hematophagous trophozoites (gold standard for colitis)
- Stool antigen test (ELISA for E. histolytica)
- PCR (most sensitive)
- Serology (anti-amebic IgG): positive in >94% of liver abscess
- Colonoscopy: flask-shaped ulcers (ameboma)
- Ultrasound/CT: liver abscess

**Treatment:**
- Intestinal/invasive: **metronidazole** 750 mg TID × 10 days (or tinidazole 2g/day × 3 days)
- Then luminal agent (to eliminate cysts): **paromomycin** 500 mg TID × 7 days (or diloxanide furoate)
- Liver abscess: metronidazole ± drainage (if large >5 cm, risk of rupture)
- Asymptomatic cyst passer: paromomycin alone

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