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PGIMER Entrance Microbiology Syllabus

The Microbiology syllabus for PGIMER Entrance in full: 3 chapters, 12 topics and 2 sub-topics, every one listed below, plus 57 Microbiology flashcards with answers.

3Chapters
12Topics
2Sub-topics
57Flashcards

Microbiology syllabus: all 3 chapters

Expand any chapter to see its topics and sub-topics.

  1. General and Immunology

     4 topics
    • Bacterial structure, growth and genetics
    • Sterilization and disinfection methods
    • Host defense and antigen-antibody reactions
    • Vaccines and immunization schedule

  2. Bacteriology

     4 topics
    • Gram-positive cocci and bacilli
    • Gram-negative enteric and respiratory pathogens
    • Mycobacteria and spirochetes
    • Anaerobes and zoonotic bacteria

  3. Virology, Mycology and Parasitology

     4 topics
    • DNA and RNA viruses of medical importance
    • Hepatitis viruses and HIV
    • Systemic and opportunistic fungal infections
    • Protozoa and helminths
      • Malaria and amoebiasis
      • Intestinal and tissue helminths

PGIMER Entrance Microbiology flashcards — 57 questions with answers

  1. What is the chemical composition and function of the bacterial peptidoglycan (murein) cell wall?

    A polymer of alternating N-acetylglucosamine (NAG) and N-acetylmuramic acid (NAM) cross-linked by peptide chains. It provides rigidity and shape and protects against osmotic lysis. It is the target of penicillins (inhibit transpeptidase/cross-linking) and lysozyme (cleaves NAG-NAM bond).

  2. Compare the cell wall of Gram-positive and Gram-negative bacteria.

    Gram-positive: thick peptidoglycan (multiple layers) with teichoic/lipoteichoic acids, no outer membrane, retains crystal violet (stains purple). Gram-negative: thin peptidoglycan, outer membrane containing LPS (endotoxin), periplasmic space; loses crystal violet and takes safranin counterstain (stains pink/red).

  3. What is the structure and clinical significance of bacterial lipopolysaccharide (LPS/endotoxin)?

    Found in the outer membrane of Gram-negative bacteria. Composed of lipid A (toxic/endotoxin activity), core polysaccharide, and O-antigen (somatic antigen, basis of serotyping). Lipid A triggers fever, hypotension, DIC, and septic shock via cytokine (TNF-alpha, IL-1) release; it is heat-stable and released on cell lysis.

  4. Contrast bacterial endotoxin and exotoxin.

    Endotoxin: LPS lipid A from Gram-negative cell wall, heat-stable, poorly antigenic (no toxoid), nonspecific effects (fever, shock), released on lysis. Exotoxin: secreted proteins from Gram-positive and Gram-negative bacteria, heat-labile, highly antigenic (can form toxoids/antitoxins), specific potent effects, often plasmid/phage encoded.

  5. Describe the four phases of the bacterial growth curve.

    1) Lag phase: adaptation, no division. 2) Log (exponential) phase: maximal, constant division rate; most susceptible to antibiotics. 3) Stationary phase: nutrient depletion/toxin accumulation, growth = death, spore formation begins. 4) Decline (death) phase: death exceeds growth, exponential decline.

  6. What is generation (doubling) time and the formula for number of bacteria after n generations?

    Generation time is the time required for a bacterial population to double. Number of cells N = N0 x 2^n, where N0 = initial number and n = number of generations. E. coli generation time is ~20 min; M. tuberculosis is ~18-24 hours.

  7. Name and define the three main mechanisms of bacterial genetic transfer.

    1) Transformation: uptake of naked DNA from the environment by a competent cell. 2) Transduction: transfer of bacterial DNA by a bacteriophage (generalized or specialized). 3) Conjugation: direct cell-to-cell transfer of plasmid (e.g., F factor) DNA via a sex pilus.

  8. What are bacterial spores and why are they clinically important?

    Dormant, highly resistant structures formed (mainly by Bacillus and Clostridium) under adverse conditions; contain dipicolinic acid and calcium, little water, and are metabolically inactive. They resist heat, desiccation, chemicals, and radiation. Killed only by autoclaving (121C/15 min) or sporicidal agents; basis for sterilization controls.

  9. What is the difference between sterilization and disinfection?

    Sterilization: complete destruction/removal of ALL microorganisms including bacterial spores. Disinfection: destruction of vegetative pathogenic organisms on inanimate objects, but not necessarily all spores. Antisepsis is the use of chemicals (antiseptics) on living tissue.

  10. What are the standard autoclave (moist heat) operating parameters for sterilization?

    121C at 15 lb/in2 (psi) pressure for 15-20 minutes (or 134C at 30 psi for ~3 min). Moist heat kills by coagulation/denaturation of proteins. It is the most common and reliable method; Bacillus stearothermophilus spores are the biological indicator.

  11. Which biological indicator (spore) is used to test the efficacy of autoclaving versus hot-air oven?

    Autoclave (moist heat): Geobacillus (Bacillus) stearothermophilus. Hot-air oven (dry heat): Bacillus subtilis var. niger (globigii). Ethylene oxide gas: Bacillus subtilis var. niger. These spores confirm sterilization cycles.

  12. Describe dry heat sterilization parameters (hot-air oven).

    160C for 2 hours (or 170C for 1 hour, 180C for 30 min). Dry heat kills by oxidation and denaturation. Used for glassware, powders, oils, and metal instruments that withstand high temperature; not suitable for rubber or plastics.

  13. What is ethylene oxide used for and what are its limitations?

    Ethylene oxide (EtO) is a gaseous chemical (alkylating agent) used to sterilize heat-sensitive items such as plastics, catheters, endoscopes, and heart-lung machine components. It is mutagenic, carcinogenic, explosive, and requires prolonged aeration to remove toxic residue.

  14. Define pasteurization and its two main methods.

    Pasteurization is mild heating to kill non-spore-forming pathogens (e.g., M. bovis, Coxiella, Brucella) in milk without sterilizing it. Holder method: 63C for 30 min. Flash/HTST method: 72C for 15-20 seconds, then rapid cooling. Phosphatase test confirms adequacy.

  15. Name the three lines of host defense in immunity.

    1) Physical/chemical barriers: skin, mucous membranes, lysozyme, gastric acid, normal flora. 2) Innate (nonspecific) immunity: phagocytes (neutrophils, macrophages), NK cells, complement, inflammation. 3) Adaptive (specific) immunity: humoral (B cells/antibodies) and cell-mediated (T cells), with memory.

  16. Contrast innate and adaptive immunity.

    Innate: present from birth, immediate, nonspecific, no memory, same response on re-exposure (barriers, phagocytes, complement, NK cells). Adaptive: develops after exposure, specific to antigen, slower initially, possesses memory (faster/stronger secondary response), mediated by B and T lymphocytes.

  17. List the five classes of immunoglobulins and one key feature of each.

    IgG: most abundant in serum, only Ig crossing placenta, secondary response. IgM: largest (pentamer), first in primary response, best at complement fixation. IgA: secretory (dimer) in mucosa/breast milk. IgE: mediates type I hypersensitivity and antiparasitic response (binds mast cells). IgD: B-cell surface receptor.

  18. Describe the three pathways of complement activation and the common end result.

    Classical pathway: activated by antigen-antibody (IgG/IgM) complexes, starts at C1. Alternative pathway: activated by microbial surfaces (LPS), antibody-independent. Lectin pathway: mannose-binding lectin binds microbial carbohydrates. All converge on C3 cleavage and form the C5-C9 Membrane Attack Complex (MAC) causing lysis; C3a/C5a are anaphylatoxins, C3b is an opsonin.

  19. Classify the four types of hypersensitivity reactions (Gell and Coombs).

    Type I: immediate/anaphylactic, IgE-mediated (anaphylaxis, atopy). Type II: cytotoxic, IgG/IgM against cell-surface antigens (hemolytic anemia, transfusion reaction). Type III: immune-complex mediated (serum sickness, SLE, Arthus). Type IV: delayed, T-cell mediated (tuberculin/Mantoux test, contact dermatitis).

  20. Differentiate the precipitation, agglutination, and ELISA antigen-antibody reactions.

    Precipitation: soluble antigen + antibody form a visible precipitate (e.g., VDRL, immunodiffusion). Agglutination: particulate antigen + antibody form visible clumps (e.g., Widal, blood grouping). ELISA: enzyme-labeled antibody/antigen produces a colored signal, highly sensitive (e.g., HIV screening).

Show the other 37 Microbiology flashcards

  1. What is the difference between active and passive immunization, with examples?

    Active immunity: host's own immune system makes antibodies after exposure to antigen/vaccine; slow onset, long-lasting, has memory (e.g., toxoids, live/killed vaccines). Passive immunity: preformed antibodies given directly; immediate but short-lived, no memory (e.g., antitoxins, immunoglobulins, maternal IgG, breast milk).

  2. Classify vaccines into their main types with examples.

    Live attenuated: BCG, OPV, MMR, varicella, rotavirus. Killed/inactivated: IPV (Salk), whole-cell pertussis, rabies, hepatitis A. Toxoid: diphtheria, tetanus. Subunit/conjugate: HepB (recombinant), Hib, pneumococcal, HPV. Live vaccines generally give stronger, longer immunity but are contraindicated in pregnancy/immunocompromised.

  3. List the vaccines given at birth under India's National Immunization Schedule.

    At birth: BCG (against tuberculosis), OPV-0 (oral polio zero dose), and Hepatitis B birth dose. These are given as early as possible within 24 hours (HepB) / before discharge.

  4. What vaccines does the Indian National Immunization Schedule provide at 6, 10, and 14 weeks?

    At 6, 10, and 14 weeks: OPV (1,2,3), Pentavalent vaccine (DPT + Hepatitis B + Hib) doses 1,2,3, Rotavirus vaccine (1,2,3), and fIPV (fractional inactivated polio) at 6 and 14 weeks. PCV (pneumococcal conjugate) is given at 6 and 14 weeks with a booster at 9 months in the UIP.

  5. Name a key catalase-positive, coagulase-positive Gram-positive cocci and its major virulence factors.

    Staphylococcus aureus. Catalase-positive and coagulase-positive (distinguishes it from other staphylococci). Virulence factors: protein A (binds Fc of IgG), coagulase, hemolysins, leukocidin (Panton-Valentine), TSST-1 (toxic shock), enterotoxins (food poisoning), exfoliative toxin (scalded skin syndrome).

  6. How do you distinguish Staphylococcus from Streptococcus, and S. aureus from coagulase-negative staphylococci?

    Staphylococci are catalase-positive; streptococci are catalase-negative. Among staphylococci, S. aureus is coagulase-positive, whereas S. epidermidis and S. saprophyticus are coagulase-negative. S. saprophyticus is novobiocin-resistant (UTI in young women); S. epidermidis is novobiocin-sensitive (prosthetic device infections).

  7. Classify streptococci by hemolysis on blood agar with examples.

    Alpha-hemolytic (partial, green): S. pneumoniae, viridans streptococci. Beta-hemolytic (complete clearing): Group A (S. pyogenes), Group B (S. agalactiae). Gamma (non-hemolytic): Enterococcus, S. bovis. Lancefield grouping is based on cell-wall carbohydrate antigens.

  8. What lab tests differentiate Streptococcus pyogenes, S. agalactiae, and S. pneumoniae?

    S. pyogenes (Group A): beta-hemolytic, bacitracin-sensitive, PYR-positive. S. agalactiae (Group B): beta-hemolytic, bacitracin-resistant, CAMP test-positive, hippurate hydrolysis-positive. S. pneumoniae: alpha-hemolytic, optochin-sensitive, bile-soluble, lancet-shaped diplococci.

  9. Name the major Gram-positive spore-forming bacilli and the diseases they cause.

    Bacillus anthracis: anthrax (cutaneous, pulmonary/woolsorter's, GI); non-motile, capsulated. Bacillus cereus: food poisoning (emetic from reheated rice, and diarrheal). Clostridium tetani: tetanus. C. botulinum: botulism. C. perfringens: gas gangrene/food poisoning. C. difficile: pseudomembranous colitis.

  10. Describe Corynebacterium diphtheriae morphology and its toxin's mechanism.

    Gram-positive, club-shaped (Chinese-letter/cuneiform arrangement) bacilli with metachromatic (volutin) granules stained by Albert/Neisser stain. Diphtheria toxin (phage-encoded, ADP-ribosylates EF-2 to inhibit protein synthesis) causes a grey pseudomembrane in the throat plus cardiac and neural toxicity. Grows on Loeffler's serum slope and tellurite media.

  11. What are the key features distinguishing the Enterobacteriaceae family?

    Gram-negative bacilli that ferment glucose, reduce nitrates to nitrites, are oxidase-negative, and are facultative anaerobes. Includes E. coli, Klebsiella, Salmonella, Shigella, Proteus, Enterobacter. Lactose fermentation on MacConkey separates lactose fermenters (pink, e.g., E. coli, Klebsiella) from non-fermenters (pale, e.g., Salmonella, Shigella).

  12. Differentiate the four major diarrheagenic E. coli pathotypes.

    ETEC (enterotoxigenic): traveler's diarrhea via heat-labile/heat-stable toxins. EPEC (enteropathogenic): infantile diarrhea, attaching/effacing lesions. EHEC/STEC (e.g., O157:H7): bloody diarrhea, Shiga-like toxin, hemolytic uremic syndrome. EIEC (enteroinvasive): dysentery-like, invades colon similar to Shigella.

  13. Describe the laboratory diagnosis and pathogenesis of typhoid fever (Salmonella Typhi).

    Salmonella Typhi is a non-lactose-fermenting, H2S-producing, motile Gram-negative bacillus. Blood culture is positive in week 1, stool/urine culture in weeks 2-3. Widal test detects O and H agglutinins (rising titer). Vi antigen confers virulence. It causes enteric fever via invasion of Peyer's patches and intracellular survival in macrophages.

  14. What are the distinguishing features of Vibrio cholerae and its toxin?

    Curved (comma-shaped), Gram-negative, oxidase-positive, motile (single polar flagellum) bacillus showing darting motility; grows on TCBS agar as yellow colonies. Cholera toxin ADP-ribosylates Gs protein, raising cAMP, causing massive secretory ('rice-water stool') diarrhea. Serogroups O1 and O139 cause epidemics.

  15. Describe the key features of Pseudomonas aeruginosa.

    Gram-negative, oxidase-positive, non-lactose-fermenting, obligate aerobe producing blue-green pigment (pyocyanin) and fluorescein, with a grape/fruity odor. Causes burn-wound infections, hospital-acquired pneumonia, UTIs, otitis externa, and infections in cystic fibrosis/neutropenic patients. Often multidrug-resistant.

  16. What are the main respiratory Gram-negative pathogens and their key features?

    Haemophilus influenzae: requires factors X (hemin) and V (NAD), satellitism around S. aureus; type b causes meningitis/epiglottitis. Bordetella pertussis: whooping cough, Bordet-Gengou medium, pertussis toxin. Legionella pneumophila: atypical pneumonia from water sources, BCYE medium, silver stain. Klebsiella pneumoniae: lobar pneumonia (red-currant jelly sputum).

  17. Describe Neisseria meningitidis and N. gonorrhoeae and how they are distinguished.

    Both are Gram-negative, oxidase-positive, kidney-shaped diplococci. N. meningitidis: capsulated, causes meningitis/meningococcemia, ferments maltose AND glucose, has a vaccine. N. gonorrhoeae: causes gonorrhea/PID/ophthalmia neonatorum, ferments glucose ONLY, no useful capsule vaccine, often intracellular in neutrophils.

  18. Why is Mycobacterium tuberculosis described as acid-fast, and how is it stained?

    Its cell wall is rich in mycolic acids (long-chain lipids) that resist decolorization by acid-alcohol after staining. Demonstrated by Ziehl-Neelsen (carbol fuchsin, acid-alcohol decolorizer, methylene blue counterstain) showing red bacilli, or by auramine-rhodamine fluorescent stain. It is a slow-growing obligate aerobe.

  19. Which media and key tests are used for Mycobacterium tuberculosis diagnosis?

    Culture on Lowenstein-Jensen (LJ) medium (egg-based, takes 3-6 weeks; rough, tough, buff colonies) or liquid MGIT. Niacin test positive and nitrate reduction positive (differentiates from M. bovis). Rapid molecular tests: CBNAAT/GeneXpert (detects DNA + rifampicin resistance). Tuberculin (Mantoux) is a type IV hypersensitivity test.

  20. Differentiate tuberculoid and lepromatous leprosy (Mycobacterium leprae).

    Tuberculoid (paucibacillary): strong cell-mediated immunity, few bacilli, few well-defined anesthetic lesions, lepromin test positive. Lepromatous (multibacillary): weak CMI, abundant bacilli (globi/foam cells), numerous symmetrical lesions, leonine facies, lepromin test negative. M. leprae cannot be cultured in vitro (grown in armadillo/mouse footpad).

  21. Name the major spirochetes and the diseases they cause.

    Treponema pallidum: syphilis. Borrelia burgdorferi: Lyme disease; Borrelia recurrentis: relapsing fever. Leptospira interrogans: leptospirosis (Weil's disease). Spirochetes are thin, helical, motile (axial filaments/endoflagella) bacteria, mostly not seen on Gram stain and visualized by dark-field microscopy or silver staining.

  22. List the serological tests for syphilis and classify them.

    Non-treponemal (cardiolipin, screening, become negative after treatment): VDRL and RPR. Treponemal (specific, confirmatory, remain positive for life): TPHA, FTA-ABS, TP-PA. Dark-field microscopy demonstrates motile T. pallidum from primary chancre. Biological false-positive VDRL occurs in SLE, pregnancy, leprosy.

  23. Name the major Gram-positive and Gram-negative anaerobes of medical importance.

    Gram-positive anaerobes: Clostridium (tetani, botulinum, perfringens, difficile), Actinomyces, Peptostreptococcus. Gram-negative anaerobes: Bacteroides fragilis (most common in intra-abdominal abscesses), Fusobacterium, Prevotella. Anaerobic infections are often polymicrobial, foul-smelling, with gas/abscess formation.

  24. Describe the mechanism of action of tetanus and botulinum toxins.

    Both are neurotoxins. Tetanospasmin (C. tetani) blocks release of inhibitory neurotransmitters (GABA/glycine) at spinal inhibitory neurons, causing spastic paralysis (lockjaw, risus sardonicus, opisthotonus). Botulinum toxin (C. botulinum) blocks acetylcholine release at the neuromuscular junction, causing flaccid (descending) paralysis.

  25. Name important zoonotic bacteria and their animal reservoirs/transmission.

    Brucella (brucellosis): cattle/goats, unpasteurized milk. Yersinia pestis (plague): rodents via flea bite. Bacillus anthracis (anthrax): herbivores, animal products. Francisella tularensis (tularemia): rabbits/ticks. Leptospira: rodent urine in water. Coxiella burnetii (Q fever): cattle, inhalation. Rickettsia: ticks/lice/mites.

  26. Classify medically important DNA viruses by their families.

    Herpesviridae (HSV-1/2, VZV, CMV, EBV, HHV-8): dsDNA, enveloped, latency. Hepadnaviridae (HBV): partial dsDNA. Adenoviridae: dsDNA, naked. Papovaviridae/Papillomaviridae (HPV): dsDNA, naked. Poxviridae (smallpox): largest, dsDNA. Parvoviridae (B19): ssDNA, naked (smallest DNA virus).

  27. Classify medically important RNA viruses with key examples.

    Picornaviridae (polio, hepatitis A, rhino, coxsackie): ssRNA naked. Orthomyxoviridae (influenza): segmented ssRNA, antigenic shift/drift. Paramyxoviridae (measles, mumps, RSV, parainfluenza). Togaviridae (rubella). Flaviviridae (dengue, yellow fever, JE, hepatitis C). Rhabdoviridae (rabies, bullet-shaped). Retroviridae (HIV, reverse transcriptase).

  28. What is the difference between antigenic drift and antigenic shift in influenza?

    Antigenic drift: minor, gradual point mutations in hemagglutinin (HA)/neuraminidase (NA) genes causing seasonal epidemics. Antigenic shift: major, abrupt change from reassortment of genome segments (e.g., from animal strains) producing a new subtype, which can cause pandemics because of lack of population immunity.

  29. Distinguish the serological markers of hepatitis B infection (HBsAg, anti-HBs, HBeAg, anti-HBc, HBV DNA).

    HBsAg: active infection (acute or chronic). Anti-HBs: immunity (recovery or vaccination). HBeAg: high infectivity/active replication. Anti-HBe: low infectivity. IgM anti-HBc: recent/acute infection (also the marker in the 'window period'). Anti-HBc IgG: past or chronic infection. HBV DNA: direct measure of viral load.

  30. Compare the five hepatitis viruses by genome and transmission route.

    HAV: ssRNA (Picornavirus), fecal-oral, no chronicity. HBV: DNA (Hepadnavirus), blood/sexual/perinatal, can become chronic, has vaccine. HCV: ssRNA (Flavivirus), blood-borne, high chronicity, no vaccine. HDV: defective RNA, needs HBV coat, blood-borne. HEV: ssRNA, fecal-oral, severe in pregnancy, no chronicity.

  31. Describe the structure and replication of HIV.

    HIV is an enveloped retrovirus with two copies of ssRNA, reverse transcriptase, integrase, and protease enzymes; envelope glycoproteins gp120 (binds CD4 and CCR5/CXCR4 co-receptor) and gp41 (fusion). It infects CD4+ T cells and macrophages, reverse-transcribes RNA into DNA that integrates into the host genome (provirus), progressively depleting CD4 cells and causing AIDS.

  32. What are the laboratory tests used to diagnose and monitor HIV infection?

    Screening: ELISA for anti-HIV antibodies (and 4th-generation p24 antigen/antibody combo). Confirmation: Western blot or a second different antibody assay. Early/window-period diagnosis and infant diagnosis: HIV RNA PCR (viral load). Monitoring: CD4 count (immune status; AIDS-defining when below 200 cells/uL) and viral load (treatment response).

  33. Name the major systemic (dimorphic) fungi and the diseases they cause.

    Dimorphic fungi (mould in environment at 25C, yeast in tissue at 37C): Histoplasma capsulatum (histoplasmosis, intracellular in macrophages), Blastomyces dermatitidis (blastomycosis), Coccidioides immitis (spherules, coccidioidomycosis), Paracoccidioides, and Sporothrix schenckii (rose-gardener's, subcutaneous).

  34. List the major opportunistic fungal infections and the typical host risk factors.

    Candida albicans (germ tube positive; thrush, candidemia) in diabetics/immunosuppressed/catheters. Aspergillus fumigatus (invasive aspergillosis, aspergilloma; acute-angle septate hyphae) in neutropenia. Cryptococcus neoformans (capsulated yeast, India ink, meningitis) in HIV/AIDS. Mucor/Rhizopus (mucormycosis, broad aseptate hyphae) in diabetic ketoacidosis. Pneumocystis jirovecii pneumonia in AIDS.

  35. What is the difference between intestinal and tissue (extraintestinal) amoebiasis caused by Entamoeba histolytica?

    Entamoeba histolytica is transmitted by the fecal-oral route (cyst is infective form, trophozoite is invasive). Intestinal amoebiasis causes amoebic dysentery with flask-shaped colonic ulcers. Extraintestinal/tissue spread (via portal vein) causes amoebic liver abscess ('anchovy sauce' pus). Diagnosed by stool microscopy, serology, and antigen detection.

  36. Differentiate the four Plasmodium species causing human malaria.

    P. falciparum: most severe (cerebral malaria, blackwater fever), malignant tertian, multiple ring forms/banana-shaped gametocytes, no relapse. P. vivax and P. ovale: benign tertian (48-hr cycle), form hypnozoites causing relapses. P. malariae: quartan (72-hr cycle), can cause nephrotic syndrome. Diagnosis by thick and thin blood smears (Giemsa) or rapid antigen tests.

  37. Name important intestinal helminths and a key diagnostic/clinical feature of each.

    Ascaris lumbricoides: largest roundworm, Loeffler's syndrome from larval migration. Ancylostoma/Necator (hookworm): iron-deficiency anemia, skin penetration. Enterobius vermicularis (pinworm): perianal itching, diagnosed by cellophane (NIH) swab. Trichuris trichiura (whipworm): rectal prolapse. Strongyloides stercoralis: autoinfection, hyperinfection in immunosuppressed. Taenia (tapeworm): from undercooked pork/beef; T. solium causes cysticercosis.

PGIMER Entrance Microbiology FAQ

What is in the PGIMER Entrance Microbiology syllabus?

PGIMER Entrance Microbiology is split into 3 chapters: General and Immunology, Bacteriology and Virology, Mycology and Parasitology. Together they contain 12 topics and 2 sub-topics.

How many chapters are in PGIMER Entrance Microbiology?

3 chapters, containing 12 topics and 2 sub-topics. The largest chapter is General and Immunology, with 4 topics.

Are there flashcards for PGIMER Entrance Microbiology?

Yes — a 57-card Microbiology deck, printed in full in the flashcards section of this page and available in the Examius app with spaced repetition. The free plan covers one exam of your choice, including its flashcards; Examius Pro, a one-time purchase, unlocks every other exam and deck.