NEET PG Microbiology Syllabus

Differentiate Bruton agglobulinemia, DiGeorge syndrome, and SCID as primary immunodeficiencies.

Bruton X-linked agammaglobulinemia: B-cell defect (BTK gene), absent immunoglobulins. DiGeorge syndrome: thymic aplasia (22q11 deletion), T-cell deficiency with tetany. SCID: combined T and B cell defect (e.g., adenosine deaminase deficiency).

What is the difference between hyperacute, acute, and chronic graft rejection?

Hyperacute rejection: minutes-hours, preformed antibodies (Type II). Acute rejection: days-weeks, T-cell mediated (Type IV), reversible with immunosuppression. Chronic rejection: months-years, fibrosis/vascular damage, irreversible.

Differentiate live attenuated, killed (inactivated), and toxoid vaccines with examples.

Live attenuated (BCG, OPV, MMR, varicella): weakened organism, strong/long immunity, contraindicated in immunocompromised. Killed (IPV, rabies, hepatitis A, pertussis whole cell): inactivated, needs boosters. Toxoid (tetanus, diphtheria): inactivated toxin.

At what age is the BCG vaccine given and against what does it protect?

BCG (Bacille Calmette-Guérin), a live attenuated Mycobacterium bovis vaccine, is given at birth (within the first year). It primarily protects against severe childhood TB (miliary TB and tuberculous meningitis).

What are the staphylococcal coagulase and catalase tests used to identify?

Catalase test (positive, bubbles with H2O2) differentiates Staphylococci from Streptococci. Coagulase test differentiates Staphylococcus aureus (coagulase positive) from coagulase-negative staphylococci like S. epidermidis and S. saprophyticus.

Name the major toxin-mediated diseases caused by Staphylococcus aureus.

Toxic shock syndrome (TSST-1 superantigen), scalded skin syndrome (exfoliative toxin), food poisoning (heat-stable enterotoxin, rapid onset 1-6 hrs), and bullous impetigo. It also causes abscesses, endocarditis, and osteomyelitis.

How are streptococci classified by hemolysis on blood agar?

Alpha-hemolytic (partial, green; e.g., S. pneumoniae, viridans group), beta-hemolytic (complete clearing; e.g., S. pyogenes group A, S. agalactiae group B), and gamma/non-hemolytic (e.g., Enterococcus).

What are the non-suppurative (immunologic) complications of Streptococcus pyogenes infection?

Acute rheumatic fever (follows pharyngitis, Type II/cross-reactivity, antibodies to M protein) and post-streptococcal acute glomerulonephritis (Type III immune complex, follows skin/throat infection). ASO titer is a marker of recent infection.

How are S. pneumoniae and viridans streptococci (both alpha-hemolytic) differentiated in the lab?

S. pneumoniae is optochin-sensitive and bile-soluble; viridans streptococci are optochin-resistant and bile-insoluble. S. pneumoniae is also lancet-shaped, capsulated, and Quellung-positive.

What biochemical tests are used to differentiate members of Enterobacteriaceae?

The IMViC tests (Indole, Methyl Red, Voges-Proskauer, Citrate) plus lactose fermentation. E. coli is Indole+, MR+, VP-, Citrate- and a lactose fermenter; Klebsiella is the reverse IMViC pattern with a capsule.

What are the major virulence-defined diarrheagenic E. coli pathotypes?

ETEC (traveler's diarrhea, heat-labile/stable toxins), EPEC (infantile diarrhea), EIEC (dysentery-like, invasive), EHEC/EAEC (O157:H7, Shiga-like toxin causing hemolytic uremic syndrome), and EAEC (persistent diarrhea).

How do you distinguish Vibrio cholerae morphologically and what is the mechanism of its toxin?

V. cholerae is a comma-shaped, oxidase-positive, motile Gram-negative bacillus showing darting motility. Cholera toxin (subunit A) activates adenylate cyclase, raising cAMP and causing massive secretory ('rice-water stool') diarrhea.

What stain and key features identify Mycobacterium tuberculosis?

M. tuberculosis is an acid-fast bacillus (Ziehl-Neelsen stain: red bacilli on blue background) due to mycolic acid in its cell wall. It is an obligate aerobe, slow-growing (Lowenstein-Jensen medium, ~6 weeks), with serpentine cord factor as a virulence factor.

What is the Mantoux (tuberculin) test, how is it read, and what type of hypersensitivity does it represent?

Mantoux test injects PPD intradermally; induration is read at 48-72 hours (≥10 mm generally positive). It is a Type IV delayed hypersensitivity reaction indicating prior TB exposure or BCG, not necessarily active disease.

Differentiate tuberculoid (paucibacillary) from lepromatous (multibacillary) leprosy.

Tuberculoid leprosy: strong cell-mediated immunity, few bacilli, lepromin test positive, few well-defined anesthetic patches. Lepromatous leprosy: weak CMI, abundant bacilli (highly infectious), lepromin negative, symmetric widespread lesions with leonine facies.

What organism causes syphilis, how is it detected, and what are the treponemal vs non-treponemal tests?

Treponema pallidum (a spirochete) causes syphilis, seen by dark-ground microscopy. Non-treponemal tests (VDRL, RPR) detect reagin and are used for screening/monitoring; treponemal tests (TPHA, FTA-ABS) are confirmatory and remain positive for life.

Name the toxins and clinical effects of Clostridium tetani and Clostridium botulinum.

C. tetani produces tetanospasmin, which blocks inhibitory neurotransmitters (GABA/glycine) causing spastic paralysis (lockjaw). C. botulinum produces botulinum toxin, which blocks acetylcholine release causing flaccid (descending) paralysis.

What is the typical presentation and bacterial cause of Lyme disease, and its vector?

Lyme disease is caused by the spirochete Borrelia burgdorferi, transmitted by Ixodes ticks. It presents with erythema migrans ('bull's-eye' rash), followed by arthritis, carditis, and neurologic manifestations if untreated.

Differentiate the structure and replication of DNA versus RNA viruses (Baltimore concept).

DNA viruses (e.g., herpes, hepatitis B, papilloma) usually replicate in the nucleus using host polymerases and are mostly double-stranded. RNA viruses (e.g., influenza, polio, HIV) replicate in the cytoplasm (except influenza/retrovirus) and use RNA-dependent RNA polymerase; many are single-stranded.

Which viruses cause the major viral hepatitides and how are they transmitted?

Hepatitis A and E: fecal-oral, acute, self-limiting (E dangerous in pregnancy). Hepatitis B (DNA), C, and D: blood/sexual/vertical, can become chronic and cause cirrhosis/hepatocellular carcinoma. Hepatitis D requires HBV co-infection.

What is antigenic shift versus antigenic drift in influenza virus?

Antigenic drift: small, gradual point mutations in HA/NA genes causing seasonal epidemics. Antigenic shift: sudden major reassortment of gene segments producing a new subtype, causing pandemics (e.g., H1N1).

Name the herpesvirus family members and their key associated diseases.

HSV-1 (oral/encephalitis), HSV-2 (genital), VZV (chickenpox/shingles), EBV (infectious mononucleosis, Burkitt lymphoma), CMV (congenital infection, retinitis in AIDS), HHV-8 (Kaposi sarcoma). All establish latency.

What are the classic features and lab identification of Cryptococcus neoformans?

Cryptococcus neoformans is an encapsulated yeast causing meningitis in immunocompromised (AIDS) patients; it is seen as budding yeast with a clear halo on India ink preparation, and detected by cryptococcal antigen (CrAg) latex test. It is associated with pigeon droppings.

Differentiate the dimorphic fungi and the temperature at which each form appears.

Dimorphic fungi (Histoplasma, Blastomyces, Coccidioides, Paracoccidioides, Sporothrix) grow as mold at 25°C (environment) and as yeast at 37°C (in tissue/body). Mnemonic: 'mold in the cold, yeast in the heat'.

What are the species causing human malaria and which causes the most severe (cerebral) disease?

Plasmodium falciparum (most severe, cerebral malaria, malignant tertian), P. vivax and P. ovale (benign tertian, hypnozoites cause relapse), P. malariae (quartan), and P. knowlesi. Diagnosis is by peripheral blood smear (thick and thin films).

What is the difference between the relapse caused by P. vivax/ovale and recrudescence in malaria?

Relapse (P. vivax and P. ovale) is due to dormant liver hypnozoites reactivating; it requires primaquine for radical cure. Recrudescence (P. falciparum, P. malariae) is reappearance of blood-stage parasites that were never fully cleared (no hypnozoites).

What organism causes amoebiasis, what is the infective form, and the classic complication?

Entamoeba histolytica causes amoebiasis; the infective form is the mature quadrinucleate cyst (fecal-oral). It causes amoebic dysentery (flask-shaped colonic ulcers) and amoebic liver abscess ('anchovy sauce' pus in the right lobe).

Differentiate cutaneous, mucocutaneous, and visceral leishmaniasis and the vector.

Leishmania is transmitted by the female sandfly (Phlebotomus). Cutaneous (L. tropica, oriental sore), mucocutaneous (L. braziliensis), and visceral leishmaniasis/kala-azar (L. donovani: fever, hepatosplenomegaly, pancytopenia; amastigotes seen as LD bodies).

Classify the major nematodes (roundworms) and their key transmission routes.

Intestinal nematodes: Ascaris lumbricoides and hookworm (Ancylostoma/Necator, soil-transmitted), Enterobius vermicularis (pinworm, anal autoinfection), Trichuris (whipworm). Tissue nematodes: Wuchereria bancrofti (filariasis, mosquito), Trichinella (undercooked pork).

Differentiate cestodes (tapeworms) Taenia solium and Taenia saginata and the danger of T. solium.

Taenia saginata (beef tapeworm): from undercooked beef, causes intestinal infection only. Taenia solium (pork tapeworm): from undercooked pork; ingesting eggs causes cysticercosis (including neurocysticercosis, a major cause of seizures).

Name the major trematodes (flukes) and their target organs.

Schistosoma (blood fluke: S. haematobium-bladder/hematuria, S. mansoni and japonicum-intestine/liver), Fasciola hepatica and Clonorchis sinensis (liver flukes), and Paragonimus westermani (lung fluke). Most require a snail intermediate host.