Infectology Exam Qs

Q1 – List and brief description of the periods of pathogenesis of infectious diseases.

1. Incubation – pathogen enters host and starts multiplying; host not yet infectious if origin is infectious

2. Prodromal – causative agent multiplies; host has diffuse non-specific symptoms (fever, swelling, malaise, fatigue, pain, soreness, inflammation)

3. Acme (period of illness) – specific symptoms and signs shown; peak pathogen load = peak illness intensity

4. Acme (period of decline) – symptoms start to decline, organism more controlled; BUT immunity weakened → risk of secondary infections

5. Convalescence – gradual recovery; 4 possible outcomes: complete recovery, permanent damage, chronic condition if pathogen not eliminated, death

Q2 – List and describe the routes of transmission of infectious diseases with examples.

1. Direct contact – skin-to-skin (HSV)

2. Indirect contact – contaminated surfaces (norovirus)

3. Droplet – coughing/sneezing (influenza)

4. Airborne – aerosols inhaled (M. tuberculosis)

5. Fecal-oral – contaminated food/water (Salmonella)

6. Bloodborne – infected blood/fluids (HIV)

7. Vector-borne – mosquito bites (malaria)

8. Vertical – mother to child during pregnancy/birth/breastfeeding (HIV)

9. Zoonotic – animal to human (rabies)

10. STD – sexual contact (chlamydia)

11. Healthcare – VAP, MRSA

Q3 – Differences between the concept of “infection” and “infectious disease” and the reasons contributing to the development of infectious diseases.

• Infection – entry, presence & multiplication of a pathogen, with or without symptoms

• Infectious disease – infection that causes tissue damage + clinical symptoms

Contributing factors:

• Pathogen – virulence, toxin production

• Host – immune status, age, genetics, comorbidities, nutrition, vaccination, hygiene

• Environmental – poor sanitation, overcrowding, climate

Q4 – Diagnostic principles of infectious diseases and verification of specific infections

Principles: clinical evaluation (history + physical exam), microscopy, culture, molecular tests (PCR/NAAT), serology, antigen detection, lab tests (CBC, inflammatory markers), imaging, histopathology/biopsy, antibiotic sensitivity testing

Verification: viral → PCR or serology; bacterial → culture, microscopy PCR; fungal → culture, microscopy or PCR

Q5 – Principles of infectious disease treatment. Indications for serum, immunoglobulin, and antibiotic therapy.

Principles: early diagnosis, assess severity, empirical therapy if bacterial suspected, definitive targeted therapy, correct dose & duration, supportive care, antibiotic stewardship, source control of infection

Serum therapy – toxin-mediated diseases (diphtheria, tetanus, botulism) and anti-venom

Immunoglobulin therapy – post-exposure prophylaxis (rabies, HBV, varicella, tetanus); immunodeficiency disorders; severe infections (e.g. toxic shock); autoimmune and inflammatory disorders; replacement therapy after plasma exchange

Antibiotic therapy – confirmed bacterial infections/suspected (empirical use) (e.g. pneumonia); surgical prophylaxis

Q6 – Influenza: Incubation, Clinical Presentation, Complications

IP: 1–4 days (avg of 2 days)

Clinical: Fever, sore throat, cough, chills, myalgia, fatigue, nasal congestion

Complications:

• Primary viral pneumonia + secondary bacterial pneumonia

• Sinusitis, otitis media

• Worsening of chronic diseases (e.g. asthma)

• Systemic: myocarditis, arrhythmias, Guillain-Barré syndrome, sepsis, multi-organ failure, death

Q7 – Influenza: Treatment & Prevention (nonspecific and specific)

Treatment:

• Most cases self-limiting, Tx depends on severity and risk of complications

• Antivirals (high-risk/severe): Oseltamivir or Zanamivir — oral/inhaled, within 48hrs of symptoms

• Supportive: hydration, electrolytes, antipyretics, analgesics, rest, relief of cough

Prevention:

• Non-specific: hand hygiene, masks, avoid crowded places, isolate infected persons

• Specific: annual influenza vaccine; chemoprophylaxis (antivirals) for high-risk groups — pre/post-exposure prophylaxis

Q8 – Parainfluenza: Incubation, Clinical Presentation, Complications

IP: 2–6 days

Clinical: Fever, sore throat, barking cough, hoarseness, runny nose; croup in severe pediatric cases

Complications: Pneumonia, bronchiolitis, otitis media, secondary bacterial infections, croup

Q9 – Diphtheria: Clinical Presentation & Treatment

Caused by: Corynebacterium diphtheriae | IP: 1–3 days Transmission: Direct contact (respiratory secretions, lesions, kissing), indirect (contaminated objects), respiratory droplets

Clinical:

• Low-grade fever, sore throat

• Thick grey pseudomembrane over tonsils/pharynx or nasal mucosa

• Breathing difficulties, inspiratory stridor

• Cervical lymphadenopathy (bull neck)

• Systemic toxin effects: myocarditis (arrhythmias), peripheral neuropathy

Treatment:

• Isolation immediately

• Diphtheria Antitoxin (DAT) — ASAP, neutralizes unbound toxin; cannot reverse already-bound toxin

• Antibiotics: oral/IV erythromycin or IM penicillin G × 14 days

• Supportive: airway management (intubation/tracheostomy if needed), cardiac monitoring, IV fluids

Q10 – Legionellosis: Clinical Presentation & Treatment

Caused by: Legionella spp. | IP: 2–10 days Transmission: Inhalation of contaminated aerosols (fresh water, AC systems, humidifiers)

Clinical: Legionnaires disease: High fever, dry or productive cough, dyspnoea, chest pain, GI symptoms (diarrhoea, nausea, vomiting), neurological symptoms (headache, confusion)

Pontiac fever: mild self-limiting flu-like illness

Treatment:

• Antibiotics (first-line): fluoroquinolones (e.g. levofloxacin) or macrolides (e.g. azithromycin) — good intracellular penetration; 7–21 days

• Supportive: IV fluids, electrolytes, oxygen

Q11 – Shigellosis: Clinical Manifestations, Diagnosis, Treatment, Prevention

Caused by: Shigella spp. | IP: 1–3 days Transmission: Fecal-oral — ingestion of contaminated food or water

Clinical:

1. Mild form — watery diarrhoea, abdominal cramps, low-grade fever

2. Dysenteric form — bloody/mucous diarrhoea (inflammatory dysentery), tenesmus, high fever, severe abdominal pain, dehydration

3. Complications — dehydration, seizures, haemolytic uremic syndrome (HUS), reactive arthritis

Diagnosis: Stool culture (gold standard — confirms Shigella), PCR (rapid detection), microscopy (leukocytes + erythrocytes in stool)

Treatment: Oral rehydration solution (ORS); antibiotics in severe cases (azithromycin, ciprofloxacin, or ceftriaxone) based on local resistance patterns; avoid antimotility drugs

Prevention: Hand hygiene, safe food and water preparation, proper sanitation

Q12 – Botulism: Clinical Manifestations, Diagnosis, Treatment, Prevention

Caused by: Clostridium botulinum toxin | IP: 12–36 hours (few hours to 2 days) Transmission: Foodborne (improperly canned food, honey spores — avoid honey in infants <1 year), wound entry of spores

Clinical (cranial nerve palsies — descending):

• Symmetric descending flaccid paralysis

• Diplopia (double vision), blurred vision, ptosis

• Dysphagia, dysarthria (slurred speech)

• Respiratory paralysis in severe cases

• No fever, patient conscious

• Infants: hypotonia, poor feeding, constipation

Diagnosis: Clinical manifestations, stool culture, ELISA (toxin detection), EMG

Treatment: Botulinum antitoxin; supportive care + mechanical ventilation if needed; wound debridement (wound botulism)

Prevention: Proper food preservation, avoid improperly canned foods, avoid honey in infants <1 year, proper wound care

Q13 – Cholera: Epidemiology, Clinical Manifestations, Diagnosis, Treatment, Prevention

Caused by: Vibrio cholerae | IP: few hours to 5 days (usually 1–2 days) Transmission: Fecal-oral — contaminated water and food; common in areas with poor sanitation

Clinical:

1. Mild — profuse rice-water diarrhoea, vomiting, dehydration

2. Severe — severe dehydration, muscle cramps, hypotension, tachycardia, hypovolemic shock

3. Complications — hypovolaemic shock, acute kidney injury, metabolic acidosis, electrolyte imbalance, death if untreated

Diagnosis: Clinical suspicion (symptoms + epidemiological history), stool culture, PCR

Treatment: Immediate oral or IV rehydration (fluid + electrolyte replacement); antibiotics: doxycycline, azithromycin; zinc for children, supportive treatment

Prevention: Safe drinking water, proper sanitation, hand hygiene, oral cholera vaccine

Q14 – Typhoid Fever: Clinical Manifestations, Diagnosis, Treatment, Prevention

Caused by: Salmonella Typhi | IP: 7–14 days average (3–60 days) Transmission: Faecal-oral — contaminated food or water

Clinical:

1. Early stage — sustained high fever, headache, malaise, abdominal pain, constipation or diarrhoea, rose spots on skin, hepatosplenomegaly

2. Severe — delirium, intestinal bleeding, intestinal perforation (complications — culture is essential)

Diagnosis: Blood culture (best in early disease), stool, urine and bone marrow culture; PCR (detects Salmonella Typhi DNA); serology (anti-O and anti-H antibodies, anti-IgM against S. Typhi)

Treatment: Antibiotics based on local resistance patterns — ceftriaxone, azithromycin, ciprofloxacin

Prevention: Vaccination (recommended for travellers in endemic areas), safe food and water, hand hygiene, proper food handling and cooking

Q15 – Campylobacteriosis and Yersiniosis: clinical manifestations, principles of diagnosis and treatment, prevention.

Campylobacter: Caused by: Campylobacter jejuni | IP: 2–5 days Transmission: Fecal-oral — undercooked poultry, unpasteurised milk, contaminated water, zoonotic (contact with infected animals)

Clinical: High-grade fever, abdominal cramps, nausea, bloody-watery diarrhoea Complications: Dehydration, reactive arthritis, Guillain-Barré syndrome

Diagnosis: Stool culture, PCR, stool microscopy

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Yersinia: Caused by: Yersinia enterocolitica | IP: 3–7 days Transmission: Fecal-oral — contaminated pork, unpasteurised milk, contaminated water

Clinical: Low-grade fever, watery diarrhoea, right lower quadrant pain (pseudoappendicitis) Complications: Reactive arthritis, erythema nodosum

Diagnosis: Stool culture, PCR, serology, imaging (ileocaecal inflammation or mesenteric lymphadenitis), lab (CBC, inflammatory markers, CRP)

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Treatment (both): Usually supportive; severe cases: azithromycin; Yersinia severe: doxycycline + aminoglycoside

Prevention (both): Proper food handling, avoid undercooked meat, pasteurise dairy, hand hygiene

Q16 – Diarrheagenic E. coli subtypes: clinical manifestations, principles of diagnosis and treatment, prevention.

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Q17 – Traveler's diarrhea – etiology, clinical manifestations, principles of diagnosis and treatment, prevention.

Definition: ≥3 unformed stools in 24 hrs + symptom of enteric disease (vomiting, cramps, fever, nausea, bloody stool)

Etiology: Most common — ETEC; also Campylobacter, Shigella, Salmonella, norovirus, Giardia. Common in: Developing countries with poor hygiene Transmission: Fecal-oral — contaminated food and water | IP: 1–3 days

Clinical: Watery diarrhoea (can become bloody), urgency to defecate, abdominal cramps, nausea, sometimes vomiting, low-grade fever

Diagnosis: Usually clinical (epidemiological history + symptoms); stool culture if severe; PCR; stool microscopy

Treatment: ORS; antibiotics if severe (azithromycin) — single dose or 3-day course; avoid antimotility drugs if fever/bloody stool

Prevention: Safe food and water, avoid raw food, hand hygiene

Q18 – Parasitic intestinal infections with the clinical picture of gastroenterocolitis: amebiasis, giardiasis, cryptosporidiosis - clinical picture, diagnostic and treatment principles, prevention.

Amebiasis (Entamoeba histolytica): Clinical: Diarrhoea (may be bloody), nausea, vomiting, abdominal pain, tenesmus; severe: liver abscess (fever + right upper quadrant pain) Diagnosis: Stool microscopy, antigen detection, PCR, serology, imaging (CT/ultrasound for liver abscess) Treatment: Metronidazole or tinidazole + luminal agent to remove cysts Prevention: Safe water, hand hygiene, proper sanitation

Giardiasis (Giardia lamblia): Clinical: Watery diarrhoea, nausea, vomiting, malabsorption, bloating, flatulence, weight loss, foul-smelling greasy stools (steatorrhoea) Diagnosis: Stool antigen test, microscopy, stool PCR Treatment: Metronidazole or tinidazole Prevention: Safe drinking water, hand hygiene, proper sanitation

Cryptosporidiosis (Cryptosporidium): Clinical: Watery diarrhoea, abdominal cramps, nausea, vomiting, low-grade fever; severe in immunocompromised Diagnosis: Stool microscopy, antigen detection, PCR Treatment: Supportive (rehydration); nitazoxanide; optimise immune function (e.g. ART in HIV); severe/immunocompromised — more aggressive management Prevention: Safe water, hand hygiene, avoid contaminated pools

Q19 – The most common blood borne diseases: VHB, VHC, HIV, epidemiology in the world and in Latvia, risk groups, possible routes of transmission.

VHB:

• Global: ~296 million affected; highly endemic in Africa, Asia, Pacific Islands

• Latvia: moderate endemicity; 2–3% of population HBsAg positive

• Risk groups: healthcare workers, IV drug users, infants of HBV+ mothers, multiple sex partners, prisoners

• Transmission: blood, sexual contact, vertical

VHC:

• Global: ~71 million affected; endemic in Eastern Europe, Central Asia, South America

• Latvia: significant — especially among IV drug users

• Risk groups: healthcare workers, IV drug users, blood receivers, prisoners, multiple sex partners (MSM)

• Transmission: blood (contaminated needles, transfusion), sexual (less efficient than HBV), vertical (rare)

HIV:

• Global: ~40 million affected; highest in sub-Saharan Africa

• Latvia: highest affected individuals in Europe; prevalence 0.5% - 0.7%; 200-300 new cases annually

• Risk groups: MSM, IV drug users, sex workers, transgender individuals, prisoners, heterosexual population

• Transmission: sexual (most common — unprotected sex), blood (needle sharing, unsafe medical practices), vertical (pregnancy, childbirth, breastfeeding — antiretroviral treatment significantly reduces risk)

Q20. Viral hepatitis B – epidemiology, clinical symptoms, and outcomes.

Epidemiology:

• Endemic: Central Asia, sub-Saharan Africa, Pacific Islands

• ~296 million affected globally

• Risk groups: healthcare workers, IV drug users, infants of HBV+ mothers, people with multiple sex partners

• Transmission: blood, sexual contact, vertical

• IP: 1–6 months (avg 3 months)

Clinical Symptoms:

• Acute: fever, jaundice, dark urine, abdominal pain, nausea/vomiting, anorexia, rash

• Chronic: often asymptomatic; fatigue, malaise, nausea, elevated liver enzymes → cirrhosis or HCC

Outcomes:

• Acute hepatitis usually resolves spontaneously

• Chronic infection → liver failure, hepatocellular carcinoma (HCC), persistent liver inflammation

Q21 – Classification & Diversity of Parasitic Diseases on the World Map

Classification by size: microparasites (unicellular) vs macroparasites (multicellular)

By host dependency: obligate, facultative

By relation to host: endoparasites, ectoparasites

3 Classes:

1. Protozoa (unicellular) — Sarcodina (ameba e.g. Entamoeba), Mastigophora (flagellates e.g. Giardia, Leishmania), Ciliophora (e.g. Balantidium), Sporozoa (e.g. Plasmodium, Toxoplasma)

2. Helminths (multicellular worms, usually chronic) — Flatworms: trematodes (flukes e.g. Schistosoma), cestodes (tapeworms e.g. Taenia, Echinococcus, Diphyllobothrium latum); Roundworms (nematodes) e.g. Ascaris, Trichinella, Enterobius, Toxocara

3. Arthropods (ectoparasites) — Arachnids (ticks, mites), insects (lice, flies)

Distribution:

• Tropical/subtropical: malaria (sub-Saharan Africa, South Asia, S. America), Schistosomiasis (Africa, Middle East, S. America)

• Temperate: Lyme disease (N. America, Europe — ticks), Giardiasis (worldwide)

• Global: Echinococcosis (areas with sheep farming), Onchocerciasis/River Blindness (Africa, Americas)

Q22 – Diseases Caused by Protozoa: Most Common Pathogens & Clinical Profile

1. Malaria — Plasmodium falciparum/vivax → fever (tertian/quartan), chills, sweating, anaemia, jaundice, splenomegaly

2. Amoebiasis — Entamoeba histolytica → fever, bloody diarrhoea, abdominal pain, liver abscess

3. Giardiasis — Giardia lamblia → watery diarrhoea, malabsorption, bloating, flatulence, fatigue, steatorrhoea

4. Leishmaniasis — Leishmania spp. → cutaneous ulcers, fever, hepatosplenomegaly

5. Toxoplasmosis — Toxoplasma gondii → asymptomatic in immunocompetent; flu-like illness in others; severe: encephalitis, chorioretinitis, congenital defects (in immunocompromised/pregnant)

6. Trypanosomiasis — T. brucei (African sleeping sickness): fever, headache, joint pain, neurological symptoms; T. cruzi (Chagas disease): fever + swelling at infection site, chronic cardiac/digestive complications

7. Balantidiasis — Balantidium coli → diarrhoea, abdominal pain, sometimes dysentery; poor sanitation areas

Q23 – Malaria: Pathogenesis, Clinical Manifestations, Diagnosis, Treatment, Prevention

Pathogenesis: Caused by: Plasmodium spp. (P. falciparum, P. vivax, P. ovale, P. malariae) | IP: 7–30 days Transmission: Female Anopheles mosquito bite → sporozoites injected → infect liver → release merozoites → invade RBCs → cyclic rupture → fever + anaemia

Clinical:

• Flu-like: periodic fever (tertian/quartan), chills, sweating, abdominal pain, nausea, vomiting, diarrhoea

• Organ-specific (severe, esp. P. falciparum): Blood — thrombocytopenia, haemolytic anaemia; GI — nausea, diarrhoea; Liver — hepatosplenomegaly, jaundice; CNS — hallucinations, confusion, seizures, coma; multi-organ failure

Diagnosis:

• CBC: haemolytic anaemia, thrombocytopenia, leukocytopenia

• Microscopy of blood smear (Giemsa stain) — gold standard, shows presence of parasites

• RDTs detecting parasite antigens

Treatment:

1. Hospitalise, symptomatic treatment until diagnosis confirmed

2. P. falciparum: Artemisinin-based combination therapy (ACT)

3. P. vivax / P. ovale (without P. falciparum): Primaquine (targets liver-stage hypnozoites)

4. Note: Chloroquine used for sensitive strains; ACT is standard for resistant P. falciparum

Prevention: Insecticide-treated bed nets (ITNs), indoor residual spraying (IRS), avoid exposure, protective clothing, chemoprophylaxis for travellers (e.g. atovaquone–proguanil)

Q24 – Echinococcosis: Clinical Forms, Diagnosis, Treatment, Prevention

Caused by: Tapeworms (Echinococcus granulosus → cystic; E. multilocularis → alveolar) Transmission: Fecal-oral — ingestion of food/water/soil contaminated with dog feces; contact with dogs Primary hosts: Dogs and wolves | IP: variable (months–years)

Clinical forms:

1. Cystic echinococcosis (E. granulosus) — hydatid cyst in liver/lungs; right upper quadrant pain, nausea, hepatomegaly, cough, chest pain, dyspnoea; cyst rupture → anaphylactic reaction

2. Alveolar echinococcosis (E. multilocularis) — aggressive, infiltrative growth; liver damage, portal hypertension, liver failure; can metastasise; abdominal pain, weight loss, jaundice

Diagnosis: Clinical history (dog/livestock contact, endemic area), imaging (ultrasound/CT/MRI — cystic lesions, hydatid cysts, calcified walls in liver/lungs), serology (specific antibodies)

Treatment:

• Surgical removal (>10 cm cysts, complicated cases, when PAIR not possible)

• PAIR (Puncture, Aspiration, Injection, Re-aspiration) — for cysts <5 cm, uncomplicated

• Antiparasitic: Albendazole 1st line (at least 2 years with PAIR), Mebendazole 2nd line

Prevention: Regular dog deworming, control stray dog populations, avoid contact with infected animals, proper hygiene and food handling

Q25 – Name the most common human helminthiasis and describe the routes of transmission, mechanisms of pathogenesis and main clinical signs.

Transmission:

1. Ascariasis (Ascaris lumbricoides / roundworm) — ingestion of contaminated food or water

2. Hookworms — contact with contaminated soil containing larvae (skin penetration)

3. Schistosomiasis — contact with contaminated freshwater containing larvae

Pathogenesis:

• Larvae migrate through tissues → inhabit intestines or blood vessels

• Causes tissue damage and inflammation → blood loss and nutrient depletion

Clinical signs:

• Abdominal pain and diarrhoea

• Anaemia and fatigue

• Malnutrition and growth retardation

• Organ-specific signs (e.g. haematuria in schistosomiasis)

look at notes on other script

Q26 – Pneumonia Caused by Chlamydia psittaci: Reservoir, Risk Factors, Clinical, Diagnosis, Treatment

Caused by: Chlamydia psittaci

Reservoir: Birds (parrots, pigeons, ducks, chickens, poultry) — shed in droppings and respiratory secretions

Risk factors: Veterinarians, bird breeders, poultry workers, pet shop workers, bird owners, elderly, immunocompromised

Clinical: High fever, dry cough, headache, myalgia; severe: respiratory distress, ARDS, multi-organ failure, X-ray: patchy consolidation, unilateral infiltrates

Diagnosis:

• Serology: IgM + IgG — four-fold rise in titre confirms acute infection

• PCR (bacterial DNA) from sputum sample

• History of bird exposure is key!

Treatment:

• Doxycycline 100 mg × 2/day for 10–14 days (1st line)

• Macrolides (e.g. azithromycin) — 2nd line; alternative for children <8 and pregnant women

Q27 – Toxocariasis: Etiology, Transmission, Clinical, Diagnosis, Treatment, Prevention

Etiology: Caused by: Toxocara canis / Toxocara cati (roundworms of dogs/cats). Common worldwide but higher in countries with plenty stray dogs/cats | IP: 1–4 weeks

Transmission: Ingestion of eggs from contaminated soil/food/water; direct contact with infected dogs/cats

Clinical forms:

1. Visceral larva migrans (VLM) — larvae migrate through liver/lungs → fever, hepatomegaly, eosinophilia, cough, wheezing

2. Ocular larva migrans (OLM) — larvae in eye → unilateral vision loss, retinal damage, uveitis, possible blindness

3. Neurotoxocariasis — seizures, neurological symptoms

Diagnosis: Clinical history; imaging (ultrasound/MRI — granulomatous nodules in liver, pulmonary infiltrates, retinal granulomas); serology — ELISA for specific IgG antibodies

Treatment: Albendazole or mebendazole (antihelmintics); corticosteroids in VLM and OLM to prevent vision loss/severe inflammation

Prevention: Regular deworming of dogs and cats, hand hygiene, avoid soil-contaminated food, safe disposal of pet feces

Q28 – Non-Tuberculous Mycobacteria (NTM): Etiology, Risk Factors, Clinical Syndromes, Diagnosis

Etiology: Mycobacterium avium complex (MAC), M. kansasii | IP: 2–4 weeks Transmission: Fecal-oral (contaminated food/water), airborne (aerosols), open wound contact with contaminated water

Risk factors: Immunocompromised (HIV/AIDS), underlying lung disease (COPD, cystic fibrosis), organ transplant, long-term steroid use, elderly

Clinical syndromes:

1. Pulmonary disease (most common) — chronic cough, fever, weight loss, night sweats

2. Disseminated disease — occurs in very low CD4 count; fever, weight loss, hepatosplenomegaly

3. Skin/soft tissue infections

4. Lymphadenitis (cervical - mostly in children)

Diagnosis: CT (pulmonary nodules, bronchiectasis, cavitary lesions, infiltrates), PCR, sputum culture, AFB

Q29 – Cat Scratch Disease: Etiology, Clinical, Diagnosis, Treatment

Etiology: Caused by Bartonella henselae (gram-negative bacterial infection) | IP: 1–3 days after bite/scratch (especially kittens) Transmission: Cat scratches or bites

Clinical:

• Pustule at scratch site

• Regional lymphadenopathy near scratch site

• Fever, fatigue, malaise, headache

• Hepatosplenomegaly

Diagnosis: Clinical history; serology (IgG antibodies to B. henselae) / PCR of lymph node; biopsy in atypical cases — shows necrotizing granulomatous lymphadenitis with stellate microabscess

Treatment: Self-limiting in most cases; supportive (pain management, warm compresses); azithromycin or doxycycline in severe/immunocompromised cases

Q30 – Toxoplasmosis: Reservoir, Transmission, Risk Factors, Clinical, Diagnosis, Treatment

Reservoir: Cats (shed oocysts in feces)

Transmission: Ingestion of undercooked meat (tissue cysts), ingestion of oocysts from contaminated soil/food/water, vertical (mother → fetus — high risk to fetus)

Risk factors: Cat litter contact, raw/undercooked meat, pregnancy (risk to fetus), immunocompromised (HIV/AIDS)

Clinical:

• Immunocompetent: asymptomatic or mild flu-like illness, lymphadenopathy

• Immunocompromised/severe: encephalitis (ring-enhancing brain lesions on CT/MRI), chorioretinitis, seizures, focal neurological deficits

• Congenital: hydrocephalus, intracranial calcifications, chorioretinitis

• Other: fever, fatigue, myalgia, cervical lymphadenitis

Diagnosis:

• Serology: IgG and IgM antibodies

• PCR: detects parasite DNA in blood, amniotic fluid, CSF

• Imaging: CT/MRI — ring-enhancing brain lesions, intracranial calcifications, hydrocephalus

Treatment:

• Immunocompetent, non-pregnant: no treatment needed

• Immunocompromised/severe: Pyrimethamine + sulfadiazine + folinic acid

• Pregnant: Spiramycin only

Q31 – Specifics of the immune response against viruses.

Innate: type I interferons (IFN-α/β) inhibit replication & activate NK cells; NK cells kill infected cells via perforin/granzymes; dendritic cells/macrophages recognise viral nucleic acids, present antigens to T cells & produce cytokines

Adaptive: CD8⁺ CTLs kill infected cells via MHC I; CD4⁺ T helpers activate CD8⁺ & B cells; antibodies neutralize virus, block entry, activate complement, mediate ADCC

Immunological Memory: memory B & T cells → faster, stronger response on reinfection

Q32 – Specifics of the immune response against intracellular bacteria and fungi.

Intracellular bacteria (e.g. M. tuberculosis):

Innate – macrophage phagocytosis (bacteria often survive);

Adaptive – Th1 produces IFN-γ to activate macrophages; CD8⁺ CTLs destroy infected cells; granuloma formation contains persistent infection

Fungi (e.g. Candida):

Innate – neutrophils & macrophages phagocytose via oxidative mechanisms;

Adaptive – Th1 activates macrophages; Th17 produces IL-17, recruits neutrophils, promotes inflammation

Q33 – Specifics of the immune response against extracellular bacteria.

Innate: phagocytosis by neutrophils & macrophages (enhanced by opsonization); complement classical pathway (IgM/IgG) → C3b opsonization, inflammation, MAC lyses bacteria; cytokines TNF-α & IL-6 recruit immune cells

Adaptive: IgM activates complement; IgG promotes opsonization; IgA provides mucosal immunity; Th17 produces IL-17, recruits neutrophils and promotes inflammation

Q34 – Cytokine storm: pathogenesis, clinical and laboratory signs.

Pathogenesis: exaggerated immune response → massive macrophage & T-cell activation → excessive IL-1, IL-6, TNF-α, IFN-γ → endothelial damage, vascular permeability, coagulopathy, organ dysfunction. Triggered by: severe infections, autoimmune disease or immunotherapy.

Clinical: high persistent fever, hypotension, tachycardia, respiratory distress, multi-organ failure, shock/death

Lab: ↑ CRP, ferritin, IL-6; lymphopenia, thrombocytopenia; ↑ D-dimer, prolonged coagulation time

Management: anti-cytokine therapy + supportive care (O₂, corticosteroids, anticoagulants)

Q35 – Dynamics of antibody production in case of first and repeated contact with pathogen. Infections as triggers for autoimmune processes

Primary (1st contact): lag phase ~5–10 days; naïve B cells → plasma cells → IgM first, then IgG; lower affinity, shorter-lasting

Secondary (re-exposure): response within 1–3 days via memory B cells; mainly IgG; higher affinity, longer-lasting

Infections as triggers for autoimmune processes

• Infections can sometimes lead to autoimmune diseases. Misidentification results in tissue damage and inflammation

• Genetic predisposition

• Environmental factors (stressors and infections)

• Post-infection phenomena (e.g. strep throat → rheumatic fever)

Q36 – Features of immunological memory depending on the type of antigen.

• Protein antigens – strong memory; T-dependent (B + T helper cells); high-affinity IgG; long-lived memory B cells

• Polysaccharide antigens – weak memory; T-independent (B cells only); mainly IgM; no T-cell involvement

• Live-attenuated vaccines – long-lasting immunity by mimicking natural infections; stimulate both cellular & humoral immunity

• Inactivated vaccines – mainly humoral; require booster doses to maintain immunity

Q37 – Latent and chronic infections (pathogens and disorders of the immune response, examples).

Latent: pathogen is in dormant stage, may reactivate during immunosuppression. Examples: HSV, M. tuberculosis, EBV, CMV. Immune disorder: impaired cell-mediated immunity (↓ CD4⁺/CD8⁺), primary/secondary (e.g. HIV, transplantation, chemotherapy) immunodeficiency, loss of immune surveillance that leads to reactivation of latent pathogen.

Chronic: active infection >6 months despite active immune response; immune system unable to eliminate pathogen. Examples: HBV, HCV, HIV, H. pylori. Immune disorders: persistent immune activation, chronic inflammation, T-cell exhaustion, tissue damage/fibrosis, increased malignancy risk (e.g. HBV → hepatocellular carcinoma)

Q38 – Post-COVID syndrome.

Definition: symptoms persisting beyond 4–12 weeks after acute COVID-19

Symptoms: fatigue, myalgia, dyspnoea, persistent cough, chest pain, cognitive dysfunction, joint discomfort, anxiety/depression/sleep disturbances

Pathogenesis: immune dysregulation, persistent immune activation, chronic inflammation, persistent viral fragments, microvascular damage, endothelial dysfunction

Diagnosis: clinical evaluation, laboratory tests

Management: multidisciplinary care – pulmonary rehab, psychological support, symptom management, organ-specific care

Q39 – Laboratory diagnosis of SARS-CoV-2 infection.

• RT-PCR – gold standard; detects viral RNA; nasopharyngeal/throat swab

• Rapid Antigen tests – rapid detection of viral proteins; suitable for acute infection. faster and simpler!!

• Serology – detects IgM & IgG; not for acute diagnosis, assess exposure

• Lab markers – elevated CRP, D-dimer, IL-6; lymphopenia

Q40 – Differential diagnosis of a patient with sore throat.

• Viral: adenovirus, EBV, rhinovirus, influenza, SARS-CoV-2

• Bacterial: Streptococcus pyogenes (GAS), C. diphtheriae, Mycoplasma pneumoniae, N. gonorrhoeae, H. influenzae

• Non-infectious: allergic pharyngitis, GERD, smoking/chemical irritation, dry air, voice strain

Diagnostic approach: throat swab (culture or rapid antigen test), blood tests (CRP, ESR), serology

Q41. Viral hepatitis A: epidemiology, clinical presentation, diagnosis, treatment and prophylaxis

Epidemiology:

• Fecal-oral route; contaminated food/water

• Endemic in developing countries (poor sanitation); parts of Africa

• IP: 2–6 weeks (avg ~1 month)

Clinical Presentation:

• Fever, jaundice, dark urine, pale stools, nausea/vomiting, anorexia, fatigue, hepatomegaly

Diagnosis:

• Antigen testing: HAV Ag in serum

• Serology: Anti-HAV IgM → acute infection; Anti-HAV IgG → past infection

• Labs: Elevated ALT, AST, bilirubin

Treatment:

• Supportive: hydration, rest

• Avoid hepatotoxic substances (alcohol)

Prophylaxis:

• HAV vaccination - 2 dose

• Post-exposure immunoglobulin for non-immune close contacts

• Proper sanitation, hand hygiene, safe food/water

Q42. Viral hepatitis B: epidemiology, clinical presentation, diagnosis and treatment.

Epidemiology:

• Blood, sexual contact, vertical transmission

• ~296 million globally; IP 1–6 months (avg 3 months)

Clinical Presentation:

• Acute: fever, jaundice, dark urine, fatigue, anorexia, nausea/vomiting, hepatomegaly

• Chronic (>6 months): often asymptomatic → can progress to cirrhosis, HCC

Diagnosis:

• Antigen testing: HBsAg → current infection (acute or chronic), HBeAg → higher infectivity

• Serology (antibody testing): Anti-HBc IgM → acute; Anti-HBc IgG → past; Anti-HBs → immunity

• Molecular testing: HBV DNA (PCR) → viral load

• Labs: Elevated ALT, AST

Treatment:

• Acute: supportive care

• Chronic: antivirals – pegylated interferon-alpha-2a, tenofovir, or entecavir

Q43. Viral hepatitis B: specific and non-specific prophylaxis.

Specific:

• HBV vaccination

• Post-exposure prophylaxis: HBIG + HBV vaccine

• Perinatal prophylaxis: infants of HBsAg+ mothers → HBIG + HBV vaccine within 12 hours of birth

Non-specific:

• Avoid sharing needles/razors

• Safe sex practices

• Screening of blood and blood products for high risk groups

Q44. Acute viral hepatitis C: epidemiology, clinical presentation, diagnosis, treatment, and possible outcomes.

Epidemiology:

• Blood (contaminated needles, transfusion), sexual (rare), vertical (rare)

• ~58 million globally; endemic Eastern Europe, Central Asia, South America

• IP: 2–12 weeks (avg 1.5–2 months)

Clinical Presentation:

• Fever, jaundice, dark urine, fatigue, anorexia, nausea/vomiting, hepatomegaly

• Sometimes asymptomatic

Diagnosis:

• Serology: Anti-HCV IgM → acute; Anti-HCV IgG → past/chronic

• Molecular testing: HCV RNA (PCR) → active infection

• Labs: Elevated ALT, AST

Treatment:

• Direct-acting antivirals (DAAs) e.g. sofosbuvir (12 weeks)

Outcomes:

• Can resolve spontaneously or progress to chronic → cirrhosis, HCC

Q45. Chronic viral hepatitis C: diagnosis and treatment.

Diagnosis:

1. Serology: Anti-HCV IgG → past/chronic infection

2. PCR: HCV RNA present >6 months

3. Genotype testing to determine specific HCV strain

4. Liver biopsy or elastography → assess fibrosis

5. Labs: Elevated ALT, AST

Treatment:

• Direct-acting antivirals (DAAs) e.g. sofosbuvir (12 weeks)

Q46. Viral hepatitis E: epidemiology, clinical presentation, diagnosis, treatment, and prophylaxis

Epidemiology:

• Fecal-oral route; contaminated food/water

• Common in developing countries (Africa, Asia); poor sanitation

• Higher mortality in pregnant women

• IP: 2–8 weeks (avg 1–1.5 months)

Clinical Presentation:

• Same as HAV: jaundice, fatigue, dark urine, nausea, anorexia, hepatomegaly

Diagnosis:

• Anti-HEV IgM or IgG (serology)

• HEV RNA via PCR

• Elevated ALT, AST

Treatment:

• Supportive care

• Ribavirin for chronic cases

Prophylaxis:

• Proper sanitation and hand hygiene

• Safe drinking water

• Avoid undercooked food

• HEV vaccine (available in some countries)

Q47. Viral hepatitis D: epidemiology, clinical presentation, diagnosis, treatment, and prophylaxis

Epidemiology:

• Blood, sexual, vertical transmission

• Risk groups: same as HBV + IV drug users especially

• Endemic: Middle East, Mediterranean, Central Asia

• Occurs as:

  • Co-infection (HDV + HBV simultaneously)

  • Superinfection (HDV in a patient with chronic HBV)

Clinical Presentation:

• Co-infection: acute hepatitis (fever, jaundice, dark urine) – similar to HBV

• Superinfection: cirrhosis, liver failure (more severe)

Diagnosis:

• Anti-HDV IgM + IgG + HBsAg or Anti-HBc IgM (serology)

• HBsAg (antigen detection)

• HDV RNA (PCR)

• Labs: Elevated ALT, AST

Treatment:

• Pegylated interferon-alpha for chronic HDV

• New: Bulevirtide – for chronic HDV in patients who also have HBV

Prophylaxis:

• HBV vaccination (prevents HDV as it requires HBV)

• Screening of blood and blood products for high risk groups

• Safe injection practices

Q48. Hemorrhagic fevers – etiology, pathogenetic principles

Etiology (RNA viruses):

• Filoviridae: Ebola, Marburg

• Arenaviridae: Lassa

• Flaviviridae: Dengue, Yellow fever

• Bunyaviridae: Hantavirus, Crimean-Congo hemorrhagic fever

• Reservoirs: bats, rodents, non-human primates, arthropods (mosquitoes, ticks)

• Transmission: bodily fluids, zoonotic exposure, vector bites, contaminated materials

Pathogenetic Principles:

• After infection, virus replicates in macrophages and endothelial cells →

• Massive cytokine release

• Increased vascular permeability + endothelial dysfunction → vascular leakage

• Hypotension → shock

• Direct cellular damage

• Impaired adaptive immune response

• Activation of coagulation cascade → consumption of clotting factors → thrombocytopenia + DIC → multi-organ failure

Q49. Ebola virus infection – epidemiology, clinical symptoms, and diagnostic principles

Epidemiology:

• Zoonotic; natural reservoir: fruit bats

• Endemic: sub-Saharan Africa

• Spread via bodily fluids of infected persons

• IP: 2–21 days

Clinical Symptoms:

• Early: high fever, headache, myalgia, sore throat, fatigue, diarrhea, vomiting, abdominal pain

• Severe: hemorrhagic manifestations (bleeding), shock, multi-organ failure

Lab Findings:

• Thrombocytopenia, leukopenia, elevated ALT/AST

Diagnostics:

• RT-PCR – detects viral RNA

• Antigen detection immunoassay

• Serology – Ebola-specific antibodies

• Labs: CBC, liver tests

Q50. Ebola virus infection – principles of treatment and prevention

Treatment:

• Antivirals: monoclonal antibodies – Inmazeb, Ebanga

• Supportive: rehydration, electrolytes, oxygen

Prevention:

• Vaccination: rVSV-ZEBOV (for high-risk or post-exposure)

• Infection control: PPE, strict hygiene, isolation of suspected cases, contact tracing

• Public education

Q51. Yellow fever – epidemiology, clinical picture, and principles of prevention

Epidemiology:

• Tropical Africa and South America

• Transmitted by Aedes aegypti and Haemagogus mosquitoes

• Reservoir: non-human primates

• IP: 3–6 days

Clinical Picture:

• Early: high fever, headache, myalgia, back pain, nausea/vomiting

• Severe: jaundice, hemorrhage (bleeding), shock, multi-organ failure

Prevention:

• Live-attenuated yellow fever vaccine (long-lasting protection)

• Vector control: eliminate breeding sites, insect repellents, protective clothing

Q52. Dengue fever – clinical forms, their symptoms, and principles of therapy

Caused by: Dengue virus; transmitted by Aedes aegypti; tropical/subtropical regions; IP 2–7 days

Clinical Forms:

1. Dengue Fever (DF): high fever, severe headache, retro-orbital pain, myalgia, arthralgia, rash, petechiae possible

2. Dengue Hemorrhagic Fever (DHF): increased vascular permeability, thrombocytopenia, mucosal bleeding, plasma leakage, persistent vomiting, rising hematocrit + falling platelets

3. Dengue Shock Syndrome (DSS): severe plasma leakage, severe bleeding, hypotension, circulatory shock, multi-organ failure

Treatment:

• Supportive: fluids, fever management, electrolytes

• AVOID NSAIDs and aspirin (bleeding risk)

Q53. Hanta virus infection – renal syndrome, stages and typical symptoms, diagnostic principles

Caused by: Hantavirus; reservoir: rodents; transmission: airborne – inhalation of aerosolized rodent excreta (urine, feces, saliva)

Stages:

1. Febrile phase: high fever, headache, myalgia, back pain, malaise, nausea/vomiting

2. Hypotensive phase: hypotension, petechiae, possible shock due to vascular leakage

3. Oliguric phase: reduced urine output, acute renal failure, petechiae, elevated creatinine/urea, hematuria, proteinuria

4. Diuretic phase: increased urine output (polyuria) – renal function recovering

5. Convalescent phase: gradual recovery, possible persistent fatigue

Symptoms

Diagnostics:

• Serology: hantavirus-specific IgM + IgG

• PCR: viral RNA

• Labs: elevated creatinine/urea, thrombocytopenia, proteinuria, hematuria

• Imaging: chest X-ray (pulmonary edema)

Q54. Hanta virus infection – cardiopulmonary syndrome, stages and typical symptoms, diagnostic principles

Stages:

1. Prodromal (febrile) phase: fever, myalgia, headache, fatigue, back pain, nausea/vomiting, malaise

2. Cardiopulmonary phase: non-cardiogenic pulmonary edema, respiratory distress, hypotension/shock, cough

3. Convalescent phase: gradual pulmonary/cardiac recovery; fatigue may persist

Typical Symptoms:

• Fever, cough, shortness of breath, tachypnoea, hypoxia, signs of pulmonary edema

Diagnostic Principles:

• Serology: hantavirus-specific IgM + IgG

• RT-PCR: viral RNA in blood/tissue

• Chest X-ray: pulmonary edema, interstitial infiltrates

• Labs: thrombocytopenia, leukocytosis, elevated hematocrit, elevated lactate, hemoconcentration

Q55. Clinical manifestations and diagnosis of pulmonary TB.

Caused by: Mycobacterium tuberculosis

Clinical Manifestations:

• Persistent productive cough >2 weeks (often with sputum)

• Fever, night sweats, weight loss, fatigue, chest pain, dyspnea

• Hemoptysis (advanced stage)

• Cavitary lesions

Diagnosis:

• Sputum microscopy: Ziehl-Neelsen staining (Acid fact bacilli (AFB)

• Sputum culture: Löwenstein-Jensen medium / liquid MGIT

• PCR/NAAT on sputum (also detects rifampin resistance – Xpert MTB/RIF)

• Chest X-ray: shows infiltrates, cavitary lesions, consolidations

• Tuberculosis Skin Test or IGRA (latent infection)

• Bronchoscopy or CT (further assessment)

Q56. Peripheral lymph node tuberculosis: clinical manifestation and diagnosis.

Clinical Manifestations:

• Painless lymph node enlargement

• Firm nodes → can become fluctuant over time → formation of sinus tracts + discharge (advanced)

• Fever, night sweats, weight loss

Diagnosis:

• FNAC (fine-needle aspiration): granulomatous inflammation with caseous necrosis

• Excisional biopsy: caseating granulomas + AFB (histopathology)

• Culture or NAAT/PCR (aspirate/biopsy sample)

• Sputum smear microscopy

• Tuberculosis Skin Test or IGRA

• X-ray to rule out pulmonary TB

Q57. Pleural tuberculosis: clinical manifestation and diagnosis.

Clinical Manifestations:

• Low-grade fever, pleuritic chest pain (worsens with breathing/coughing), dyspnoea, non-productive cough

• Decreased breath sounds + chest expansion on affected side

• Dullness on percussion

• Systemic: anorexia, fatigue, night sweats, weight loss

Diagnosis:

• Chest X-ray / CT / Ultrasound: pleural effusion, pleural thickening

• Thoracentesis (pleural fluid analysis/pleural biopsy): exudative fluid, elevated protein + lymphocytes + ADA, low glucose – GOLD STANDARD. Biopsy shows caseating granulomas + AFB

• Culture or PCR for confirmation

Q58. Miliary tuberculosis: characteristics of pathogenesis, clinical and radiological manifestation, principles of diagnosis.

Pathogenesis:

• Hematogenous dissemination of M. tuberculosis from a primary focus → multiple small granulomas in lungs, liver, spleen, etc.

• More common in immunocompromised individuals; can lead to TB meningitis

Clinical Manifestations:

• Systemic: Fever, night sweats, weight loss, anorexia, fatigue

• Respiratory: Cough, dyspnoea

• Organ specific: Hepatomegaly, splenomegaly

• Neurological symptoms if CNS involved. can lead to TB meningitis

Radiological Manifestations:

• Chest X-ray: diffuse bilateral fine miliary nodules

• CT: same miliary nodules with higher sensitivity/precision (diffuse tiny nodules)

Diagnosis:

1. Clinical suspicion

2. Microbiological: sputum smear + culture, blood culture, bone marrow biopsy

3. NAAT/PCR for confirmation

4. Imaging: X-ray, CT

Q59. Microbiological diagnosis of tuberculosis.

1. Microscopy: Sputum with Ziehl-Neelsen staining → detects AFB (rapid but low sensitivity; needs 5,000–10,000 bacilli/mL)

2. Culture (Gold Standard):

   • Solid: Löwenstein-Jensen medium (3–8 weeks)

   • Liquid: MGIT (1–3 weeks, faster, more sensitive)

   • Allows colony morphology + DST

3. Molecular (NAATs):

   • Xpert MTB/RIF or Xpert Ultra: detects M. tuberculosis DNA + rifampin resistance in <2 hours; WHO recommended initial test

   • Line Probe Assays (LPAs): for first and second-line drug resistance

4. Drug Susceptibility Testing (DST): phenotypic (culture-based) or genotypic (molecular); performed on positive cultures

Specimen collection: Based on site of disease – sputum, BAL, pleural fluid, CSF, urine, tissue biopsies

Q60. Diagnostic algorithm of tuberculosis.

1. Clinical suspicion: fever, cough, night sweats, weight loss, contact with TB patient

2. Radiological: chest X-ray (initial imaging)

3. Microbiological:

   • Sputum microscopy (AFB) – minimum 2–3 samples

   • NAAT/PCR – Xpert MTB/RIF — confirmation + drug resistance detection

   • Culture

4. Latent infection detection: TST or IGRA

5. Imaging: X-ray, CT

Q61. Criteria for determining infectiousness of TB patient.

1. Respiratory symptoms: persistent cough >2 weeks with sputum

2. Positive sputum smear: AFB present

3. Radiological findings: cavitary lesions on chest X-ray

4. Positive microbiological confirmation: PCR/NAAT positive

5. Non-adherent to treatment (patients are usually non-infectious after 2 weeks of proper treatment)

Q62. Definition of HAI. HAI risk factors. The most common HAI clinical syndromes (syndrome, brief description).

Definition: Infections acquired ≥48 hours after hospitalization OR within 2 days after discharge; not present at admission

Risk Factors:

• Invasive devices (urinary catheters, central venous catheters, ventilators)

• Prolonged hospitalization (especially ICU)

• Immunosuppression, chronic diseases (DM)

• Surgical procedures

• Antibiotic use

• Advanced age, poor nutritional status

• Poor hand hygiene and infection control

Common Clinical Syndromes:

1. CAUTI – catheter-associated urinary tract infection

2. CLABSI – central line-associated bloodstream infection

3. VAP – ventilator-associated pneumonia - pts on medical venticaltion

4. SSI – surgical site infections

5. CDI – Clostridioides difficile infection (antibiotic-associated diarrhea)

Q63. Gr- agents in HAI – ESBL+, KPE+, Acinetobacter baumannii, Pseudomonas aeruginosa (clinical presentation, diagnosis, treatment).

Clinical Presentation (all):

• VAP, bloodstream infections, UTIs (catheter-associated), surgical site/wound infections

Diagnosis:

• Microbiological culture (blood, urine, sputum, wound)

• Antimicrobial susceptibility testing (AST)

• PCR for resistance genes (e.g. ESBL genes: CTX-M, TEM, SHV; KPC genes)

Treatment:

1. ESBL+ (e.g. E. coli, Klebsiella): Carbapenems (meropenem) – 1st line; newer: ceftazidime-avibactam, meropenem-vaborbactam

2. KPE+ (Klebsiella carbapenemase): Combination – ceftazidime-avibactam, colistin ± tigecycline ± aminoglycosides

3. Acinetobacter baumannii (often carbapenem-resistant): Colistin-based regimens; colistin + tigecycline; cefiderocol as newer option

4. Pseudomonas aeruginosa (often multi-drug resistant): Anti-pseudomonal beta-lactams – piperacillin-tazobactam, cefepime, meropenem; often combined with aminoglycoside or fluoroquinolone; ceftazidime-avibactam for resistant strains

Q64. MRSA, clinical picture, diagnosis, treatment, prevention.

Gram+ cocci in clusters; resistant to methicillin and other beta-lactams

Clinical Picture:

• Skin/soft tissue infections: abscess, cellulitis

• Wound infections

• Pneumonia

• Bloodstream infections

• Invasive infections: endocarditis

Diagnosis:

• Culture from infected site (blood, sputum, wound)

• Antimicrobial susceptibility testing

• PCR: detection of mecA gene → confirms methicillin resistance

Treatment:

1. 1st line: Vancomycin or daptomycin

2. 2nd line: Linezolid or clindamycin

3. Topical mupirocin (localized skin/decolonization)

Prevention:

• Strict hand hygiene

• Contact precautions, gowns

• Isolation + screening of high-risk patients

• Decolonization of carriers

• Antibiotic stewardship

Q65. Ways of transmission of hospital-acquired infection, preventive measures (isolation, screening, transmission prevention, antibiotic management). Personal protective equipment.

Transmission:

1. Direct contact – physical contact with infected person

2. Indirect contact – contaminated surfaces/objects/medical equipment

3. Droplet transmission – respiratory droplets

4. Airborne transmission – aerosols

Preventive Measures:

• Proper hand hygiene

• Isolation + screening of infected persons

• Sterilization of medical equipment; proper cleaning of hospital surfaces

• PPE: gloves, masks, gowns, eye protection

• Rational antibiotic use (stewardship)

Q66. Nosocomial sepsis, screening scales, diagnosis, and treatment.

Definition: Sepsis developing >48 hours after hospital admission; caused by HAI pathogens (Gram- ESBL, KPE, Pseudomonas, Acinetobacter; Gram+ MRSA, Enterococci; Candida spp.)

Screening Scales:

1. SIRS: need at lest 2: temp abnormality (>38, <36), HR >90, RR >20, WBC abnormality (>12,000 or <4,000) – less specific

2. SOFA: organ dysfunction score (respiratory, cardiovascular, renal, liver, coagulation, CNS); increase ≥2 = sepsis

3. qSOFA: ≥2 of – RR ≥22, SBP ≤100 mmHg, altered mental status

4. NEWS (National Early Warning Score) for general ward patients

Diagnosis:

• Clinical evaluation: fever/hypothermia, tachycardia, tachypnea, hypotension, altered mental status, reduced urine output, organ dysfunction signs

• Blood cultures (positive – hospital pathogen)

• Labs: elevated CRP, lactate, procalcitonin; leukocytosis/leukopenia; thrombocytopenia

• Imaging: chest X-ray, ultrasound, CT - pneumonia, pleura effusion, infiltrates

Treatment:

• Empiric broad-spectrum antibiotics (cover Gram+ and Gram-) like doxycycline, penecillin or amoxicillin

• Hemodynamic support: IV fluids + vasopressors for shock

• Removal of infected devices (e.g. catheters)

• Monitor: lactate, organ function, urine output

• De-escalate based on culture results

Q67. Hospital and ventilator-associated pneumonia, diagnosis, treatment.

HAP: Pneumonia occurring ≥48h after hospitalization VAP: Pneumonia occurring ≥48h after ventilator use

Diagnosis:

• Clinical signs: cough, fever, purulent sputum, leukocytosis, dyspnea, hypoxia, crackles on auscultation

• Imaging: chest X-ray – progressive infiltrates

• Microbiological: culture of respiratory secretions (sputum); blood cultures (note: blood cultures negative in pneumonia)

Treatment: note: MDR = multi-drug resistance

• Low MDR risk: monotherapy (just vancomycin)

• High MDR risk (e.g. recent antibiotics >5 days, hospital stay >5 days, high local resistance): combination therapy

  • MRSA coverage: Vancomycin or linezolid PLUS

  • Anti-pseudomonal beta-lactam: piperacillin-tazobactam, meropenem, or cefepime

• De-escalate after 48–72h based on cultures

• Supportive: oxygen, hydration, rest

Q68. Vascular catheter-related infection, diagnosis, treatment.

Definition: Bloodstream infection from intravascular catheter; pathogens colonize and form biofilm on catheter surface

Diagnosis:

• Clinical signs: fever + erythema, tenderness, or purulence at catheter insertion site

• Blood cultures from both the catheter AND a peripheral vein (microbiological confirmation)

Treatment:

• Empiric antibiotics: Vancomycin (Gram+) + piperacillin-tazobactam (Gram-) – broad spectrum

• Removal of infected catheter

• Targeted/definitive therapy based on culture results

Q69. Catheter-associated urinary tract infection, diagnosis, treatment.

Definition: UTI occurring ≥48h after urinary catheter insertion/removal; biofilm formation on catheter

Diagnosis:

• Clinical signs: fever, suprapubic tenderness, costovertebral angle tenderness, altered mental status, dysuria, cloudy/foul-smelling urine

• Urine analysis: pyuria + bacteriuria

• Urine culture: ≥10³ CFU/mL

• CBC, CRP, IL-6 etc.

Treatment:

• Removal or replacement of catheter

• Empiric antibiotics based on local resistance patterns (cover E. coli, Klebsiella, Pseudomonas – e.g. ciprofloxacin, ceftriaxone, or piperacillin-tazobactam); 7–14 days

• Definitive: based on urine culture + sensitivity

• Supportive: hydration, rest, monitoring

Q70. Describe the objectives of epidemiological surveillance of infectious diseases.

1. Early detection of outbreaks + monitoring of incident/outbreak situations

2. Epidemiological data collection

3. Data analysis to identify high-risk populations and pathogen spread patterns

4. Antibiotic resistance monitoring

5. Planning of public health interventions (vaccination programs, quarantine)

6. Evaluation of intervention effectiveness

7. Healthcare resource allocation

8. Communication and reporting to healthcare system and public

Q71. Explain the rationale and relevance of the One Health approach.

Rationale: Recognizes that human, animal, and environmental health are interconnected; many infectious diseases are zoonotic → requires collaboration between medical, veterinary, and environmental disciplines

Relevance:

1. Many human infectious diseases originate in animals

2. Prevents/controls zoonotic diseases through coordinated surveillance

3. Supports antimicrobial resistance (AMR) control through coordinated antibiotic use

4. Improves pandemic preparedness and response

5. Improves global health through interdisciplinary cooperation

Q72. Explain the reasons and criteria for using the infectious disease case definitions.

Reasons:

1. Ensures consistency in diagnosis and reporting

2. Facilitates comparison of data across regions and time periods

3. Enables early detection and tracing of outbreaks

4. Improves accuracy of epidemiological surveillance and public health decision-making

Criteria:

1. Clinical presentation

2. Laboratory confirmation

3. Epidemiological linkage (exposure history/contact with confirmed case)

4. Standardized definitions from WHO

Q73. What is bioterrorism? Briefly describe the current actualities and dangers in the world.

Definition: Intentional release of biological agents (bacteria, viruses, toxins) to cause illness, death, or fear. Agents may be naturally occurring or modified to increase harmful effects.

Dangers:

• High potential for large-scale harm and panic

• Difficult to detect and respond to early

• Rapid spread

• Risk of social and economic disruption

Q74. What are the most dangerous toxins, viruses, and microorganisms in the context of bioterrorism? Please list the Group A biological agents of the CDC ABC classification.

Group A = highest lethality, aerosol transmission potential, lack of public immunity

Bacteria

• Bacillus anthracis (anthrax)

• Yersinia pestis (plague)

• Francisella tularensis (tularemia)

Viruses

• Variola virus (smallpox)

• Filoviruses: Ebola, Marburg (hemorrhagic fevers)

Toxins

• Clostridium botulinum toxin (botulism)

Q75. What signs could indicate a bioterrorism attack?

• Unusual clustering of cases in a specific geographic area

• Sudden increase in cases of a rare or eradicated disease

• Unusual clinical presentation and unexplained severe illness

• High mortality and morbidity rates (especially in healthy populations)

• Detection of unusual antimicrobial resistance patterns or genetically modified organisms

Q76. What should government institutions and epidemiologists do to detect a bioterrorism threat and attack in time?

• Develop early warning and epidemiological surveillance systems

• Develop rapid reporting systems (e.g. hotlines)

• Mandate reporting of unusual or high-risk infections to health authorities

• Train HCWs and laboratories to recognize unusual disease patterns

• Collaborate with national and international public health organizations

• Collaborate between healthcare, veterinary, environmental, military, and security specialists

Q77. Please briefly describe the main aspects of the actions of health care professionals in the event of a bioterrorism threat and attack.

• Early detection and isolation of affected individuals

• Immediate notification to public health authorities (e.g. Ministry of Health)

• Laboratory confirmation of the infection

• Administration of appropriate treatment and prophylaxis to exposed individuals

• Rapid application of infection control measures (decontamination, disinfection)

• Give instructions and information to the public

• Psychological support to staff and patients

Q78. Describe what is meant by sensitivity and specificity of methods.

Sensitivity: A test's ability to correctly identify those who have the disease (true positives). High sensitivity = few false negatives → good for ruling OUT disease.

Specificity: A test's ability to correctly identify those who do NOT have the disease (true negatives). High specificity = few false positives → good for ruling IN disease.

Q79. Name the modifiable factors of the pre-analytical stage that affect the testing results.

Sample Collection: Correct patient ID & labelling; correct collection tubes; proper technique and blood draw site; avoid contamination

Sample Handling & Transport: Proper storage temperature; timely serum/plasma separation; timely transport; avoid haemolysis; avoid repeated freeze-thaw cycles

Patient Preparation: Correct fasting/non-fasting status; no interfering medications; proper hydration; avoid stress factors

Q80. Laboratory diagnosis algorithm of HIV infection.

1. Initial Screening: 4th generation ELISA — detects HIV antibodies + p24 antigen (rapid & fast)

2. Confirmatory test: HIV-1/HIV-2 antibody differentiation immunoassay if screening positive → confirms & differentiates HIV-1 from HIV-2

3. Additional testing: HIV RNA PCR — if screening positive but confirmatory negative → detects acute/early HIV infection

4. Monitoring post-diagnosis: CD4+ count (immune function); HIV RNA (viral load/treatment efficacy)

Q81. Viral hepatitis (HAV, HBV, HCV) laboratory diagnostic screening tests.

HAV:

• Antigen detection: HAV Ag in serum → current infection

• Serology: Anti-HAV IgM → acute infection | Anti-HAV IgG → past infection

• Labs: AST, ALT, Bilirubin FOR ALL

HBV

• Antigen detection: HBsAg → current infection (acute or chronic); HBcAg - highly infectious

• Serology: Anti-HBs → immunity

• Anti-HBc IgM → acute | Anti-HBc IgG → previous infection

• PCR: HBV DNA (PCR)

HCV

• Serology: Anti-HCV IgM → current | Anti-HCV IgG → past infection

• PCR: HCV RNA

Q82. Laboratory diagnosis and differential diagnosis of acute viral gastroenterocolitis.

Lab Diagnosis (Viral)

• PCR — detects norovirus, rotavirus, adenovirus

• Antigen detection — rotavirus & adenovirus mainly

• Stool sample testing

Differential Diagnosis

Bacterial: Stool culture to rule out Salmonella, Shigella, Campylobacter, pathogenic E. coli
Parasitic: Stool microscopy or antigen tests (Giardia lamblia, Cryptosporidium)

Q83. Laboratory diagnostic tests for cardiovascular diseases.

Myocardial Infarction Markers

• Cardiac troponin I and troponin T

• Creatine kinase-MB (CK-MB)

• Myoglobin

Heart Failure Markers

• BNP (B-type natriuretic peptide)

• NT-proBNP

Cardiovascular Risk Markers

Lipid profile: total cholesterol, LDL, HDL, triglycerides; CRP

Q84. Diabetes: laboratory diagnostic tests.

1. FPG (Fasting Plasma Glucose): ≥126 mg/dL (7.0 mmol/L) after ≥8h fasting

2. HbA1c (glycated haemoglobin): ≥6.5% → reflects avg blood glucose over past 2–3 months

3. OGTT (oral glucose tolerance test): 2h plasma glucose ≥200 mg/dL (11.1 mmol/L)

4. Random plasma glucose: ≥200 mg/dL with hyperglycemia symptoms

5. Urinalysis: Glucosuria, possible ketonuria (esp. Type 1)

6. C-peptide;

7. Autoantibodies;

8. Microalbuminuria

Q85. Laboratory diagnosis of diseases of the skin and its derivatives.

1. Microscopy: Gram staining (bacterial); KOH prep (fungal); direct microscopy (parasites); Tzanck smear (herpes virus)

2. Cultures: Bacterial, viral, fungal

3. PCR: Viral, bacterial, fungal DNA/RNA

4. Skin biopsy: Inflammatory, autoimmune, infectious, neoplastic diseases

5. Serology/immunology: Autoimmune antibodies; direct immunofluorescence (autoimmune diseases)

Q86. Objectives of medicine laboratory quality controls, internal and external quality controls.

Objectives of QC

Ensure accuracy, reliability, reproducibility; detect & prevent errors; maintain precision; ensure patient safety & correct clinical decisions; ensure compatibility between labs & over time

Internal Quality Control (IQC)

• Monitor day-to-day performance

• Use control samples with known values

• Calibration & maintenance of equipment

• Detect random and systemic errors before reporting

External Quality Assessment (EQA)

• Compare results with other laboratories

• Evaluate laboratory performance and accuracy

• Participate in proficiency testing programs

• Ensure standardisation and harmonisation between labs

Q87. Risk groups of biological agents.

CDC classifies based on: pathogenicity, mode of transmission, availability of preventive measures → determines Biosafety Level (BSL)

Risk Group 1 (RG1) Not associated with disease in healthy adult humans. Minimal risk.
Examples: non-pathogenic E. coli strains, Bacillus subtilis

Risk Group 2 (RG2) Can cause human disease but unlikely to be serious laboratory or community hazard. Effective treatments usually available.
Examples: Salmonella spp., Staphylococcus aureus, Hepatitis A virus, Toxoplasma gondii

Risk Group 3 (RG3) Cause serious/potentially lethal disease through inhalation. Significant lab risk; may spread to community. Treatments often available.
Examples: Mycobacterium tuberculosis, Bacillus anthracis, Yersinia pestis, HIV, SARS-CoV-2

Risk Group 4 (RG4) Likely to cause life-threatening disease; high aerosol transmission risk. No effective treatments or vaccines usually available. High community risk.
Examples: Ebola virus, Marburg virus, Crimean-Congo HF virus, Smallpox virus