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🦠 BACTERIOLOGY (Q1-Q18)

Ans: Haemophilus ducreyi (chancroid)

Ans: Streptococcus pneumoniae

Ans: Activates adenylyl cyclase → ↑cAMP → hypersecretion (Vibrio cholerae CT)

Ans: Clostridium difficile - Toxin B (glucosylates Rho GTPase, cytotoxic); Toxin A (enterotoxin)

Ans: Haemophilus influenzae type b (epiglottitis)

Ans: Yersinia pestis (plague)

Ans: Antiphagocytic activity (resists opsonization)

Ans: Inhibiting release of Acetylcholine at NMJ (cleaves SNARE proteins)

Ans: E. coli K1 (Group B Strep also common)

Ans: Rickettsial infections (cross-reaction with Proteus OX antigens)

Ans: Klebsiella pneumoniae

Ans: Pseudomonas aeruginosa (also Staph epidermidis)

Ans: Streptococcus agalactiae (Group B Strep)

Ans: Salmonella typhi (typhoid fever)

Ans: Mycolic acid in their cell wall (resistant to decolorization with acid-alcohol)

Ans: Beta-lactam antibiotics (penicillins, cephalosporins)

Ans: Mycoplasma pneumoniae

Ans: Protective antigen (PA) + Edema factor (EF) = Edema toxin; PA + Lethal factor (LF) = Lethal toxin

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🍄 MYCOLOGY (Q19-Q24)

Ans: Cryptococcus neoformans

Ans: Branching hyphae (septate)

Ans: Sporothrix schenckii (Sporotrichosis - lymphocutaneous)

Ans: Histoplasma capsulatum

Ans: It stains polysaccharides in the fungal cell wall magenta/pink

Ans: Type I and Type III (immediate + immune complex)

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🦠 VIROLOGY (Q25-Q36)

Ans: HIV (Retrovirus) - Reverse transcriptase has RNA-dependent DNA polymerase + RNase H activity

Ans: Rabies virus - in Purkinje cells of cerebellum / hippocampal neurons (cytoplasmic inclusions)

Ans: Influenza virus

Ans: Antigenic SHIFT (reassortment of gene segments) causes pandemics

Ans: Hepatitis E virus (HEV) - mortality up to 20-25% in pregnancy

Ans: Measles (Rubeola virus)

Ans: HPV types 16 and 18 (integrate E6 and E7 oncoproteins)

Ans: CMV (Cytomegalovirus) infection

Ans: Acute HBV infection (also during "window period" when HBsAg is undetectable)

Ans: Trichomonas vaginalis (a protozoan, NOT a virus)

Ans: Converted by viral thymidine kinase to acyclovir triphosphate → inhibits viral DNA polymerase

Ans: Lack nucleic acid (composed only of misfolded PrPsc protein)

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🦟 PARASITOLOGY (Q37-Q44)

Ans: Plasmodium falciparum - infected RBCs express knobs → cytoadherence → microvascular occlusion in brain

Ans: Plasmodium falciparum

Ans: Echinococcus granulosus

Ans: Finding amastigotes (LD bodies) in bone marrow / splenic aspirate; rK39 antigen test

Ans: Ascaris lumbricoides

Ans: Entamoeba histolytica

Ans: It crosses placenta → congenital toxoplasmosis (hydrocephalus, chorioretinitis, intracranial calcifications)

Ans: Female Anopheles mosquito (sexual cycle occurs there)

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🔬 IMMUNOLOGY & GENERAL MICRO (Q45-50)

Ans: CD8+ cytotoxic T lymphocytes (CTLs)

Ans: IgA (secretory IgA = dimer + secretory component)

Ans: Deletion of chromosome 22q11 → absent thymus → T-cell deficiency

Ans: Classical pathway (C1q binds Fc region of IgG/IgM)

Ans: IL-1, IL-6, and TNF-α (all are endogenous pyrogens)

Ans: A colored product when substrate is added - the intensity is proportional to antigen concentration

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Quick Self-Assessment Guide

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🏥 NEET PG MICROBIOLOGY PYQs (2021-2025)

50 MCQs with Detailed Explanations

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🔬 BACTERIOLOGY (Q1-Q20)

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• A. Wuchereria bancrofti
• B. Brugia malayi
• C. Loa loa
• D. Onchocerca volvulus

• Brugia malayi - sheathed, 2 discrete nuclei in tail tip (with a gap between them)
• Wuchereria bancrofti - sheathed, NO nuclei in tail tip
• Loa loa - sheathed, nuclei extend all the way to the tail tip
• Mansonella - unsheathed
• Onchocerca - unsheathed, no nuclei in tail

Trick: "Brugia = two" - the two distinct nuclei at the tail is the classic differentiator.

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• A. Gram-negative
• B. Gram-positive and weakly acid-fast
• C. Gram-variable
• D. Non-staining

• Nocardia is a Gram-positive, weakly acid-fast (partially acid-fast) branching filamentous bacterium
• It contains mycolic acids (shorter chain than Mycobacterium) - hence retains carbol fuchsin with 1% H2SO4 decolorizer (NOT the stronger acid-alcohol used in ZN stain)
• Modified ZN stain (using 1% H2SO4) = positive for Nocardia
• Causes nocardiosis - pulmonary (resembles TB), CNS abscesses, and cutaneous disease in immunocompromised

Key point: "Weakly acid-fast" organisms = Nocardia, Cryptosporidium, Cyclospora, Isospora, Cystoisospora

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• A. Salmonella
• B. Staphylococcus
• C. Morganella morganii / Proteus
• D. Peptostreptococcus

• Scombroid poisoning (also called histamine fish poisoning) occurs due to bacterial decarboxylation of histidine → histamine in fish
• Responsible bacteria: Morganella morganii, Proteus mirabilis, Klebsiella pneumoniae
• Note: The PrepLadder paper listed "Pseudomonas aeruginosa" but standard teaching attributes it to Morganella/Proteus
• Symptoms: flushing, urticaria, diarrhea, headache within 30 minutes of eating
• Fish involved: tuna, mackerel, mahi-mahi (dark-fleshed fish)

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• A. Ceftazidime
• B. Trimethoprim-sulfamethoxazole
• C. Temocillin
• D. Cefotetan

• Burkholderia cepacia is an opportunistic pathogen causing pneumonia in cystic fibrosis and immunocompromised patients
• It is intrinsically resistant to many antibiotics including aminoglycosides, polymyxins (colistin), and cefotetan
• It is sensitive to: TMP-SMX, ceftazidime, meropenem, chloramphenicol
• Treatment of choice: TMP-SMX or ceftazidime

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• A. Coagulase test - Staphylococcus aureus
• B. CAMP test - Streptococcus agalactiae
• C. Elek test - Corynebacterium diphtheriae
• D. Nagler reaction - Clostridium perfringens

• CAMP test (Christie, Atkins, Munch-Peterson) - Group B Strep (S. agalactiae) produces CAMP factor that synergizes with S. aureus beta-hemolysin
• This creates a characteristic arrowhead (flame-shaped) hemolysis at the junction
• S. agalactiae is the #1 cause of neonatal meningitis and sepsis in early-onset disease (0-7 days)
• Also positive CAMP: Listeria monocytogenes, Clostridium perfringens (reverse CAMP)

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• A. Sandfly
• B. Tsetse fly
• C. Triatomine bug
• D. Female Anopheles mosquito

• Clinical picture + kinetoplast-containing organisms in macrophages = Kala-azar (Visceral Leishmaniasis) caused by Leishmania donovani
• Vector = Female Phlebotomus sandfly (Phlebotomus argentipes in India)
• The kinetoplast (mitochondrial DNA mass) is the hallmark of all kinetoplastid protozoans (Leishmania, Trypanosoma)
• LD bodies (Leishman-Donovan bodies) = amastigote forms seen in macrophages
• Other associations: Tsetse fly = Trypanosoma; Triatomine = Chagas disease; Anopheles = Malaria

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• A. Enveloped ss RNA
• B. Naked ss RNA
• C. Naked ds RNA
• D. Enveloped ds RNA

• Clinical scenario = Measles (Rubeola)
• Koplik's spots (bluish-white on buccal mucosa near lower molars) are pathognomonic
• Measles virus = Paramyxovirus = Enveloped, negative-sense single-stranded RNA
• Rash spreads head to toe (centrifugal)
• Complications: pneumonia, encephalitis, SSPE (Subacute Sclerosing Panencephalitis)

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• A. Dengue
• B. Malaria
• C. Scrub typhus
• D. Typhoid

• Key features pointing to Dengue: thrombocytopenia (platelets < 1 lakh), petechial rash, arthralgia ("breakbone fever"), prolonged bleeding time (platelet dysfunction) but normal clotting time (coagulation factors intact)
• Scrub typhus would have eschar and maculopapular rash
• Malaria = paroxysmal fever with splenomegaly, parasites on blood smear
• Dengue vector = Aedes aegypti mosquito (day-biting)
• Diagnosis: NS1 antigen (first 5 days), IgM antibody (after day 5)

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• A. Oral candidiasis
• B. Hairy leukoplakia
• C. Lichen planus
• D. Diphtheria

• Budding yeasts + pseudohyphae = Candida albicans
• Oral thrush is the most common oral manifestation in HIV patients (CD4 < 200)
• Hairy leukoplakia (EBV) shows white corrugated plaques on lateral tongue - NOT pseudohyphae
• Candida: forms germ tubes at 37°C (positive germ tube test = C. albicans)
• Treatment: Fluconazole (systemic); Nystatin (topical/"swish and swallow")

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• A. Aedes aegypti
• B. Culex mosquito
• C. Anopheles mosquito
• D. Phlebotomus papatasii

• Zika virus = Flavivirus, transmitted by Aedes aegypti (also Aedes albopictus)
• Also transmitted: sexual contact, blood transfusion, mother to fetus (congenital)
• Causes: microcephaly in newborns, Guillain-Barre syndrome in adults
• Same vector (Aedes): Dengue, Chikungunya, Yellow fever, Zika
• Anopheles = Malaria; Culex = West Nile, JE, Filaria; Phlebotomus = Leishmaniasis, Sandfly fever

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• A. Candida albicans
• B. Histoplasma capsulatum
• C. Cryptococcus neoformans
• D. Aspergillus fumigatus

• Dimorphic fungi = mould at room temp (25°C), yeast at body temp (37°C) - "mnemonic: BOMBS" = Blastomyces, cOccidioides, Mucor/Microsporum (exception), Blastomyces, Sporothrix
• Histoplasma capsulatum: endemic in Ohio River valley (USA) and parts of India
• Associated with bird/bat droppings (caves, pigeon roosts)
• Mimics TB - calcified granulomas, weight loss
• Key: Cryptococcus is NOT dimorphic (always yeast); Aspergillus = always mould

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• A. Bacterial meningitis
• B. Viral meningitis
• C. Tuberculous meningitis
• D. Fungal meningitis

• Viral (aseptic) meningitis: most common causes = Enteroviruses (Coxsackievirus, Echovirus)
• Normal glucose + lymphocytic pleocytosis + clear CSF = viral meningitis

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• A. PCR
• B. CD4 count
• C. Western blot
• D. p24 antigen detection

• ELISA = screening test (high sensitivity, may have false positives)
• Western blot = traditional confirmatory test (detects antibodies to specific HIV proteins: gp120, gp41, p24)
• Western blot positive if 2 of 3 bands (p24, gp41, gp120/160) are reactive
• Modern approach: 4th-generation HIV test (Ag/Ab combination) → if positive → HIV-1/2 differentiation assay → if indeterminate → RNA PCR
• CD4 count is NOT a diagnostic test - it guides treatment and staging

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• A. Immunity to HBV
• B. Past infection
• C. High infectivity / active viral replication
• D. Window period

• HBsAg = active infection (present or chronic carrier)
• Anti-HBs = immunity (from vaccine OR past infection)
• HBeAg = active viral replication, HIGH INFECTIVITY
• Anti-HBe = low infectivity, viral replication decreasing
• HBcAg = NOT found in serum (intracellular)
• Anti-HBc IgM = acute infection / window period
• Anti-HBc IgG = past exposure

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• A. Klebsiella pneumoniae
• B. Mycoplasma pneumoniae
• C. Streptococcus pneumoniae
• D. Legionella pneumophila

• "Walking pneumonia" = Mycoplasma pneumoniae
• Clinically mild but X-ray looks severe (radiological-clinical dissociation)
• Cold agglutinin test positive (IgM antibodies against I antigens on RBCs) - positive in 50% of cases
• No cell wall → Gram stain negative, beta-lactam resistant
• Treatment: Macrolides (azithromycin) or Doxycycline (NOT penicillin)
• Other atypical organisms: Legionella, Chlamydophila pneumoniae, Chlamydophila psittaci

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• A. Inhibiting protein synthesis
• B. Blocking acetylcholine release at NMJ
• C. Inhibiting inhibitory neurotransmitter (GABA/glycine) release
• D. Causing demyelination

• Tetanospasmin (tetanus toxin) is a zinc metalloprotease that cleaves synaptobrevin (VAMP) - a SNARE protein
• It blocks release of GABA and glycine from Renshaw cells (inhibitory interneurons) in spinal cord
• Result: Unopposed excitatory input → spastic paralysis, muscle rigidity, risus sardonicus, trismus
• Contrast with Botulinum toxin: also cleaves SNARE proteins but inhibits ACh release at NMJ → flaccid paralysis
• "Tetanus = Tonic (spastic); Botulism = Bot (not moving/flaccid)"

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• A. Leptospira interrogans
• B. Rickettsia
• C. Treponema pallidum
• D. Borrelia burgdorferi

• Weil-Felix test = agglutination test using Proteus vulgaris (OX2, OX19, OXK antigens)
• Based on cross-reactivity between Proteus O antigens and Rickettsial antigens
• OX19 + OX2 positive: R. typhi, R. rickettsii (typhus group + spotted fever group)
• OXK positive: Orientia tsutsugamushi (Scrub typhus)
• All negative in Q fever (Coxiella burnetii) - which is why Q fever is the "exception"

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• A. Moraxella lacunata
• B. Haemophilus influenzae
• C. Adenovirus type 32
• D. Coxsackievirus B

• Angular blepharoconjunctivitis (inflammation at the corners/angles of the eye) = Moraxella lacunata
• Also known as Diplobacillus of Morax-Axenfeld
• The angular involvement is due to maceration of skin at lid margins
• Loeffler's medium (originally for diphtheria) also grows Moraxella
• Compare: Haemophilus aegyptius = "pink eye" epidemic conjunctivitis in children

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• A. Chlamydia trachomatis
• B. Neisseria gonorrhoeae
• C. Staphylococcus aureus
• D. Herpes simplex virus

• Developing countries: N. gonorrhoeae - hyperacute purulent conjunctivitis within 24-48 hours of birth
• Developed countries: Chlamydia trachomatis (serovars D-K) - subacute onset at 5-14 days
• Prevention: Crede's prophylaxis (1% silver nitrate drops) → now replaced by erythromycin/tetracycline eye ointment
• Treatment: Gonorrhea = ceftriaxone; Chlamydia = erythromycin

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• A. R. rickettsii - Weil Felix OX19+
• B. Orientia tsutsugamushi - Weil Felix OXK+
• C. Borrelia burgdorferi - ELISA
• D. Leptospira - MAT

• Eschar at the site of chigger bite + fever + rash = Scrub typhus (Orientia tsutsugamushi)
• Weil-Felix: OXK positive (OX2 and OX19 negative)
• Vector = Trombiculid mite (chigger)
• Endemic in "tsutsugamushi triangle" - Asia Pacific
• Treatment: Doxycycline (drug of choice); Azithromycin in pregnancy

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🦠 VIROLOGY (Q21-Q32)

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• A. HSV
• B. CMV
• C. EBV
• D. Adenovirus

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• A. Inhibits viral RNA polymerase
• B. Inhibits viral thymidine kinase only
• C. Converted by viral thymidine kinase → triphosphate → inhibits viral DNA polymerase
• D. Blocks viral attachment to host cell

• Acyclovir is a guanosine analogue (prodrug)
• Step 1: Viral thymidine kinase (TK) phosphorylates acyclovir → acyclovir monophosphate (selective step - why it's selectively toxic to infected cells)
• Step 2: Cellular kinases → acyclovir triphosphate
• Step 3: Acyclovir-TP acts as: (a) competitive inhibitor of viral DNA polymerase, (b) chain terminator
• Resistance: mutation in TK gene (most common) or DNA polymerase gene
• Active against: HSV-1, HSV-2, VZV (high dose), CMV (low activity - use ganciclovir for CMV)

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• A. RNA-dependent RNA polymerase + DNA-dependent DNA polymerase
• B. RNA-dependent DNA polymerase + RNase H activity
• C. DNA-dependent RNA polymerase + helicase
• D. Integrase + protease activity

• HIV reverse transcriptase (RT) has two activities:
  1. RNA-dependent DNA polymerase: converts viral RNA → DNA strand (creates RNA:DNA hybrid)
  2. RNase H: degrades the RNA template of the hybrid, leaving single-stranded DNA
  3. DNA-dependent DNA polymerase: creates the second DNA strand → dsDNA
• RT is the target of NRTIs (tenofovir, emtricitabine) and NNRTIs (efavirenz, nevirapine)
• RT lacks proofreading → high mutation rate → rapid drug resistance

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• A. HAV
• B. HBV
• C. HCV
• D. HEV

• HEV = Hepevirus, positive-sense ssRNA, non-enveloped
• Transmission: feco-oral (contaminated water, major outbreaks in developing countries)
• Mortality in general: 1-2%; In pregnancy (3rd trimester): 15-25% (highest risk)
• No chronic infection in immunocompetent (exception: immunocompromised can get chronic HEV)
• No vaccine available in India (vaccine available in China - Hecolin)
• Compare: HAV also feco-oral but does NOT cause severe disease in pregnancy

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• A. Types 6 and 11
• B. Types 16 and 18
• C. Types 31 and 33 only
• D. All HPV types equally

• Low-risk HPV (condylomata, genital warts): types 6 and 11
• High-risk HPV (cervical carcinoma): types 16 and 18 (cause 70% of cervical cancers)
  • HPV 16 → squamous cell carcinoma
  • HPV 18 → adenocarcinoma of cervix
• HPV E6 protein: degrades p53 (tumor suppressor)
• HPV E7 protein: inactivates Rb protein
• Vaccine: Gardasil (4-valent: 6,11,16,18) or Gardasil 9 (9-valent)

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• A. Period between infection and onset of symptoms
• B. Period when the patient is non-infectious
• C. Period when HBsAg is negative but anti-HBc IgM is positive
• D. Period when p24 antigen disappears and before anti-HIV antibodies appear

• Window period in HIV = seronegative period (~3-12 weeks after infection)
• p24 antigen appears first (2-4 weeks) then declines → antibodies appear after 3-12 weeks
• During window period: HIV RNA/PCR is detectable (can diagnose)
• 4th generation HIV test detects both p24 Ag AND antibodies - reduces window period
• HBV window period: HBsAg has cleared but anti-HBs not yet detectable; anti-HBc IgM is the only positive marker

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• A. Cannot replicate
• B. Lack nucleic acid
• C. Are killed by autoclaving
• D. Do not infect humans

• Prions = Proteinaceous Infectious Particles (PrP)
• Composed only of misfolded protein (PrPsc = scrapie form)
• No nucleic acid (no DNA/RNA)
• Normal cellular protein PrPc (alpha helix) gets misfolded into PrPsc (beta sheet) - propagating cascade
• Causes: Creutzfeldt-Jakob disease (CJD), kuru, fatal familial insomnia, Gerstmann-Straussler-Scheinker (GSS)
• Resistant to: heat, UV, ionizing radiation, formalin, DNase, RNase (because no nucleic acid!)
• Sterilized by: Prolonged autoclaving (134°C for 18 min) or 1N NaOH

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• A. Point mutations in HA gene
• B. Reassortment of genome segments between two influenza strains
• C. Deletion of neuraminidase gene
• D. Increased virulence of existing strain

• Influenza has 8 segmented RNA genome
• Antigenic drift = minor changes due to point mutations in HA/NA → seasonal epidemics
• Antigenic shift = major change due to genetic reassortment when two strains infect same cell (e.g., pig acts as "mixing vessel") → entirely new HA/NA combination → population has no immunity → PANDEMIC
• Influenza A undergoes both shift and drift
• Influenza B: only drift (no animal reservoir for reassortment)
• Example: H1N1 (2009 swine flu pandemic) = antigenic shift

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• A. Chickenpox
• B. Measles (Rubeola)
• C. Rubella
• D. Roseola infantum

• Koplik's spots = salt-grain-like bluish-white spots on the buccal mucosa near the lower molar teeth - appear 1-2 days before rash
• Appear before the rash (prodromal phase: 3 C's - Coryza, Cough, Conjunctivitis)
• Measles = Paramyxovirus (morbillivirus genus), ssRNA, enveloped
• Rash = centrifugal (head → feet), maculopapular, fades in same direction
• Complications: Pneumonia (#1 cause of death), otitis media, encephalitis, SSPE

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• A. Hippocampal cells and Purkinje cells in rabies
• B. Liver cells in yellow fever
• C. Neurons in polio
• D. Macrophages in measles

• Negri bodies = eosinophilic, cytoplasmic inclusions in rabies
• Found in: Hippocampus (Ammon's horn) and Purkinje cells of cerebellum
• Composed of viral nucleocapsid + matrix protein
• Rabies = Rhabdovirus, bullet-shaped, ssRNA, enveloped
• Travels via retrograde axoplasmic transport to CNS
• Post-exposure prophylaxis: wound cleaning + RIG (rabies immunoglobulin) + vaccine series

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• A. Block viral fusion with host cell
• B. Competitive inhibition of reverse transcriptase + chain termination
• C. Inhibit viral protease
• D. Block integrase enzyme

• NRTIs (Nucleoside/Nucleotide RT Inhibitors): require phosphorylation → incorporated into DNA chain → chain termination (lack 3'-OH group)
• Examples: Zidovudine (AZT), Tenofovir, Lamivudine, Emtricitabine, Abacavir
• NNRTIs (Non-nucleoside): bind allosteric site of RT → conformational change → inhibit RT non-competitively
• Examples: Efavirenz, Nevirapine, Rilpivirine
• Standard 1st line ART: TDF + 3TC/FTC + EFV (or DTG)

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• A. Dengue
• B. Zika
• C. Chikungunya
• D. West Nile virus

• Zika virus (Flavivirus) causes congenital Zika syndrome when a pregnant woman is infected
• Features: microcephaly, ventriculomegaly, intracranial calcifications, eye abnormalities, arthrogryposis
• Also causes Guillain-Barre syndrome in adults
• Transmission: Aedes mosquito, sexual contact (unique among arboviruses), vertical
• PCR of amniotic fluid/maternal serum or IgM in newborn CSF for diagnosis

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🍄 MYCOLOGY (Q33-Q38)

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• A. Candida albicans
• B. Cryptococcus neoformans
• C. Histoplasma capsulatum
• D. Aspergillus fumigatus

• India ink (nigrosin) preparation = negative staining technique - dark background with clear halo around yeast
• The clear halo = polysaccharide capsule of Cryptococcus
• Cryptococcus neoformans: found in pigeon droppings, causes meningoencephalitis in immunocompromised (HIV, CD4 < 100)
• CSF findings: increased opening pressure, few WBCs, India ink +ve
• Latex agglutination test detects cryptococcal antigen (more sensitive than India ink)
• Treatment: Amphotericin B + Flucytosine (induction) → Fluconazole (maintenance)

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• A. Type I only
• B. Type III only
• C. Type I and Type III
• D. Type IV only

• ABPA = caused by Aspergillus fumigatus in atopic individuals (asthma, cystic fibrosis)
• Type I (IgE-mediated, immediate): early bronchospasm
• Type III (immune complex): tissue damage, central bronchiectasis
• Diagnostic criteria: asthma + eosinophilia + elevated total IgE + Aspergillus-specific IgE/IgG + central bronchiectasis + fleeting infiltrates on CXR
• Treatment: Corticosteroids + Itraconazole

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• A. Blastomyces dermatitidis
• B. Sporothrix schenckii
• C. Coccidioides immitis
• D. Paracoccidioides brasiliensis

• Sporothrix schenckii = classic "rose-thorn/rose gardener disease" or "gardener's disease"
• Primary inoculation → nodule at injury site → lymphocutaneous spread (chain of nodules along lymphatics)
• Dimorphic: mould at 25°C, yeast at 37°C
• Diagnosis: Culture (gold standard), asteroid bodies in tissue
• Treatment: Itraconazole (drug of choice); Potassium iodide (older treatment)

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• A. Budding yeast cells
• B. Branching septate hyphae
• C. Rhizoids
• D. Spherules

• KOH (10-20%) mount = dissolves keratin, reveals fungal elements
• Dermatophytes (Tinea infections): show septate, branching hyphae (arthrospores in Tinea capitis)
• Dermatophytes = Trichophyton, Microsporum, Epidermophyton
• Identify by: colony morphology + Sabouraud's dextrose agar + microconidia/macroconidia morphology
• Wood's lamp: Microsporum canis shows green-yellow fluorescence

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• A. Fluconazole alone
• B. Amphotericin B + Flucytosine (induction) → Fluconazole (maintenance)
• C. Voriconazole
• D. Itraconazole

• Induction phase (2 weeks): Amphotericin B (liposomal preferred) + Flucytosine (5-FC)
• Consolidation (8 weeks): Fluconazole 400 mg/day
• Maintenance (lifelong until CD4 > 200): Fluconazole 200 mg/day
• Flucytosine mechanism: converted to 5-fluorouracil → inhibits thymidylate synthase → blocks DNA synthesis
• Lumber puncture drainage (repeated) important for raised ICP management

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• A. Lipids in cell membrane
• B. Polysaccharides/glycogen in fungal cell wall
• C. Nucleic acid
• D. Protein moieties

• PAS stain: Periodic acid oxidizes adjacent hydroxyl groups of polysaccharides → aldehydes → react with Schiff's reagent → magenta/pink color
• Stains: fungi (pink), glycogen, mucin, basement membrane
• Other fungal stains: GMS (Gomori Methenamine Silver) = black/brown fungi on green background (most sensitive)
• India ink = Cryptococcus capsule
• Calcofluor white = fluorescent stain (UV) for all fungi

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🔬 PARASITOLOGY (Q39-Q44)

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• A. P. vivax
• B. P. malariae
• C. P. falciparum
• D. P. ovale

• P. falciparum causes cerebral malaria due to:
  • Cytoadherence: infected RBCs express PfEMP1 (knobs) → bind ICAM-1 on brain capillary endothelium → microvascular occlusion
  • Rosetting: infected RBCs bind uninfected RBCs
  • Sequestration in brain, placenta, lungs
• Also: invades ALL ages of RBCs (other species are size-specific), causes hyperparasitemia
• Banana-shaped gametocytes = P. falciparum
• Treatment: Artesunate IV (severe malaria)

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• A. Humans
• B. Female Anopheles mosquito
• C. Male Anopheles mosquito
• D. Culex mosquito

• Definitive host = where sexual reproduction occurs
• Intermediate host = where asexual reproduction occurs
• In malaria: Female Anopheles = DEFINITIVE host (gametocytes → sporogony)
• Humans = INTERMEDIATE host (asexual schizogony in liver and RBCs)
• Note: Female mosquito (NOT male) because only females take blood meals

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• A. Shigella dysenteriae
• B. Entamoeba histolytica
• C. Balantidium coli
• D. Campylobacter jejuni

• E. histolytica causes amoebic dysentery - undermines the mucosa to form characteristic flask-shaped (bottle-shaped) ulcers with narrow neck and broad base
• Trophozoites contain ingested RBCs (erythrophagocytosis) - pathognomonic
• Extra-intestinal: amoebic liver abscess ("anchovy sauce" aspirate - chocolate brown)
• Cysts: 4 nuclei (mature) - infective form
• Serology: indirect hemagglutination (IHA) for liver abscess diagnosis

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• A. Hydrops fetalis
• B. Hydrocephalus, chorioretinitis, intracranial calcifications (classic triad)
• C. Limb hypoplasia
• D. Deafness

• Congenital toxoplasmosis classic triad: Hydrocephalus + Chorioretinitis + Intracranial calcifications (periventricular)
• Toxoplasma gondii: definitive host = cats; intermediate = humans, rodents
• Transmission: ingestion of oocysts from cat feces, undercooked meat (bradyzoites)
• First trimester infection = most severe; 3rd trimester = subclinical but can reactivate
• Treatment: Pyrimethamine + Sulfadiazine + Leucovorin (folinic acid)
• Screening: IgG avidity test (low avidity = recent infection)

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• A. Taenia solium
• B. Ascaris lumbricoides
• C. Wuchereria bancrofti
• D. Strongyloides stercoralis

• Loffler's syndrome = transient pulmonary eosinophilia due to larval migration through lungs
• Most classically associated with Ascaris lumbricoides (also Hookworm, Strongyloides)
• Migration path: small intestine → portal blood → liver → heart → lungs → bronchi → trachea → swallowed → intestine (Ascaris)
• Features: cough, wheeze, fever, eosinophilia, fleeting X-ray shadows
• Adult worms in intestine: malnutrition, intestinal obstruction (in heavy infection)

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• A. Taenia solium
• B. Taenia saginata
• C. Echinococcus granulosus
• D. Echinococcus multilocularis

• Hydatid cyst (Cystic Echinococcosis) = larval stage of Echinococcus granulosus
• Definitive host = dog; Intermediate host = sheep, humans
• Humans ingest eggs from dog feces → larvae → cyst in liver (MC), lung, bone
• Cyst layers: Pericyst (host-derived) + Ectocyst (laminated) + Endocyst (germinal layer)
• "Daughter cysts" inside = pathognomonic on imaging
• Diagnosis: Casoni test (outdated), Serology (ELISA/IHA), CT scan (water lily sign)
• Treatment: PAIR (Puncture, Aspiration, Injection of scolicidal agent, Re-aspiration) + Albendazole

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🛡️ IMMUNOLOGY (Q45-Q50)

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• A. CD4+ helper T cells
• B. CD8+ cytotoxic T lymphocytes
• C. B cells
• D. Natural Killer cells

• MHC Class I - expressed on ALL nucleated cells (not RBCs)
  • Presents endogenous antigens (viral proteins, intracellular pathogens)
  • Recognized by CD8+ CTL (cytotoxic T lymphocytes)
• MHC Class II - expressed on APCs (dendritic cells, macrophages, B cells)
  • Presents exogenous antigens (extracellular bacteria)
  • Recognized by CD4+ Helper T cells
• Memory trick: "CD8 × 8 = Class 1" or "Eight, eight = Class I; Four, Four = Class II"

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• A. Pentameric structure
• B. Dimeric structure with secretory component
• C. Monomeric form with high affinity
• D. Ability to activate complement

• Secretory IgA = dimer (2 IgA molecules) + J chain + secretory component (poly-Ig receptor remnant)
• Secretory component protects IgA from proteolytic digestion in mucosa
• Found in: saliva, tears, colostrum, bronchial secretions, gut lumen
• Prevents pathogen adherence to mucosal epithelium (first line of defense)
• Serum IgA = monomer; IgM = pentamer (J chain present, most efficient at agglutination and complement activation)

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• A. 22q11 deletion - absent thymus - B cell deficiency
• B. 22q11 deletion - absent thymus - T cell deficiency
• C. Deletion chromosome 7 - absent thymus
• D. X-linked - absent B cells

• DiGeorge syndrome = deletion of chromosome 22q11 (velocardiofacial syndrome)
• Failure of 3rd and 4th pharyngeal pouches development → absent thymus + absent parathyroids
• Results in: T cell deficiency + hypocalcemia (tetany)
• Features: Cardiac defects (conotruncal), Abnormal facies, Thymic hypoplasia, Cleft palate, Hypocalcemia = CATCH-22
• Immunodeficiency: recurrent viral, fungal infections (T cell deficient), normal B cells
• Normal/↑ B cells, ↓ T cells

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• A. Alternative pathway
• B. Classical pathway
• C. Lectin pathway
• D. Both alternative and lectin

• Classical pathway: triggered by antigen-antibody complex (IgG or IgM) → C1q binds Fc region → C1r, C1s activated → C4b2a (C3 convertase)
• Lectin pathway: Mannose-binding lectin (MBL) binds mannose on microbial surface
• Alternative pathway: spontaneous C3 hydrolysis, triggered by bacteria, fungi, endotoxin (no antibody needed)
• All three pathways converge at C3 → C5b-9 = Membrane Attack Complex (MAC)
• C1q is the KEY initiation molecule of classical pathway

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• A. Anti-inflammatory cytokines
• B. Endogenous pyrogens
• C. Growth factors
• D. Anti-viral interferons

• Endogenous pyrogens: IL-1β, IL-6, TNF-α, IL-17, IFN-γ
• Produced by macrophages in response to LPS (exogenous pyrogen)
• Act on hypothalamic thermoregulatory center → ↑PGE2 (via COX-2) → raises temperature set-point → fever
• Antipyretics (aspirin, paracetamol) inhibit COX → block PGE2 production → reduce fever
• IL-1 also: activates T cells, stimulates acute phase proteins, bone resorption
• TNF-α: cachexia ("cachectin"), shock in sepsis

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• A. Amount of antibody added
• B. Amount of substrate added
• C. Concentration of antigen (or antibody) in the sample
• D. Enzyme concentration only

• ELISA (Enzyme-Linked Immunosorbent Assay):
  1. Antigen coated on plate
  2. Patient serum added → antibodies bind antigen
  3. Enzyme-linked secondary antibody added
  4. Substrate added → colored product (optical density)
  5. Intensity of color ∝ amount of antibody (antigen) in sample
• Types: Direct, Indirect (most common for serology), Sandwich (for antigen detection), Competitive
• Indirect ELISA = used for HIV diagnosis (detects anti-HIV antibodies)
• Sandwich ELISA = detects antigen (e.g., HBsAg, NS1 in dengue)

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📊 Score Tracker

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🎯 Most Repeated Topics in NEET PG Micro (2021-2025)