Microbiology
High-yield MBBS Microbiology question bank — bacteriology, immunology, virology, mycology and parasitology, with laboratory diagnosis, at Ananthanarayan & Paniker / Jawetz depth.
12chapters144questions82High-Yield
Definition
Immunity is the ability of the body to resist infection; it is innate (inborn, non-specific) or acquired (specific, developed after exposure).
Innate (Natural) Immunity
- Present from birth; non-specific
- Barriers — skin, mucosa, cilia
- Cells — neutrophils, macrophages, NK cells
- Humoral — complement, lysozyme, interferons
- No memory; immediate response
Acquired (Adaptive) Immunity
- Develops after exposure; highly specific
- Humoral — B cells → antibodies
- Cell-mediated — T cells
- Has memory (faster secondary response)
- Active or passive; natural or artificial
Innate defence acts at once; acquired immunity is specific and remembers. Feature Innate Acquired Specificity Non-specific Specific Memory Absent Present Speed Immediate Delayed Applied
- Vaccines exploit immunological memory
- Innate defects → recurrent pyogenic infections
🔑KEY POINTS TO REMEMBER- Innate immunity: inborn, non-specific, no memory.
- Acquired: specific, humoral (B cell) + cell-mediated (T cell), with memory.
- Memory is the basis of vaccination.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Roitt’s Essential Immunology.Definition
Antibodies (immunoglobulins) are glycoproteins produced by plasma cells that bind specifically to antigens.
Structure
- Y-shaped: 2 heavy + 2 light chains
- Fab region — antigen binding (variable)
- Fc region — effector functions (constant)
- Held by disulphide bonds
Classes
- IgG — most abundant; crosses placenta; secondary response
- IgM — largest (pentamer); first in primary response
- IgA — secretions, mucosal immunity, breast milk
- IgE — allergy, parasitic infection
- IgD — B-cell receptor
Plasma cells secrete antibodies that neutralise and tag antigens. Class Key feature IgG Crosses placenta IgM First formed, pentamer IgA Secretions IgE Allergy Applied
- IgM in serum indicates recent infection
- IgG gives passive immunity to the newborn
🔑KEY POINTS TO REMEMBER- Antibody = 2 heavy + 2 light chains; Fab binds antigen, Fc mediates effector function.
- IgG most abundant and crosses placenta; IgM first in primary response.
- IgA in secretions; IgE in allergy.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Roitt’s Essential Immunology.Definition
Hypersensitivity is an exaggerated or inappropriate immune response causing tissue damage, classified by Gell and Coombs into four types.
Types
- Type I (immediate, IgE) — anaphylaxis, asthma, urticaria
- Type II (cytotoxic, IgG/IgM) — haemolytic disease, transfusion reaction
- Type III (immune complex) — serum sickness, Arthus reaction, SLE
- Type IV (delayed, T cell) — tuberculin test, contact dermatitis
Timing
- Types I–III are antibody-mediated (immediate, minutes–hours)
- Type IV is cell-mediated (delayed, 24–72 hours)
Prior sensitisation makes re-exposure damaging rather than protective. Type Mediator Example I IgE Anaphylaxis II IgG/IgM Haemolysis III Immune complex Serum sickness IV T cell Tuberculin test Applied
- Anaphylaxis → adrenaline IM
- Tuberculin (Mantoux) test is the classic Type IV reaction
🔑KEY POINTS TO REMEMBER- Four Gell and Coombs types: I IgE, II cytotoxic, III immune complex, IV delayed.
- Types I–III antibody-mediated; Type IV cell-mediated.
- Type I = anaphylaxis; Type IV = tuberculin test.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Roitt’s Essential Immunology.Definition
The complement system is a group of serum proteins activated in a cascade that mediates inflammation, opsonisation and lysis of microbes.
Pathways of Activation
- Classical — antigen-antibody complex (IgG, IgM) → C1
- Alternative — microbial surfaces directly (no antibody)
- Lectin — mannose-binding lectin
- All converge on C3
Biological Functions
- Lysis — membrane attack complex (C5b–9)
- Opsonisation — C3b
- Chemotaxis — C5a
- Anaphylatoxins — C3a, C5a (mast-cell degranulation)
All three pathways converge on C3 and end in the membrane attack complex. Component Function C3b Opsonisation C5a Chemotaxis C5b–9 Membrane attack complex Applied
- C3 deficiency → severe pyogenic infections
- C5–9 deficiency → recurrent neisserial infection
- C1 inhibitor deficiency → hereditary angioedema
🔑KEY POINTS TO REMEMBER- Three activation pathways: classical, alternative, lectin — all converge on C3.
- Functions: lysis (MAC), opsonisation (C3b), chemotaxis (C5a).
- Deficiencies cause pyogenic and neisserial infections.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Roitt’s Essential Immunology.Definition
Immunoprophylaxis is prevention of disease by inducing immunity through vaccines (active) or immunoglobulins (passive).
Types of Vaccine
- Live attenuated — BCG, oral polio, measles, MMR, varicella
- Killed / inactivated — injectable polio, rabies, hepatitis A, pertussis
- Toxoid — tetanus, diphtheria
- Subunit / conjugate — hepatitis B, Hib, pneumococcal, HPV
Principles
- Live vaccines give stronger, longer immunity (usually single dose)
- Killed vaccines need boosters
- Live vaccines avoided in pregnancy and immunodeficiency
- Cold chain must be maintained
Vaccination creates memory cells that respond rapidly on real exposure. Type Example Doses Live BCG, measles Usually one Killed Rabies, IPV Multiple Toxoid Tetanus With boosters Applied
- Universal Immunisation Programme schedule
- Herd immunity protects the unvaccinated
🔑KEY POINTS TO REMEMBER- Vaccine types: live attenuated, killed, toxoid, subunit/conjugate.
- Live vaccines give stronger immunity but are contraindicated in pregnancy.
- Cold chain and herd immunity are essential to programmes.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Roitt’s Essential Immunology.Definition
Active immunity is produced by the host’s own immune system; passive immunity is transferred as ready-made antibodies.
Active Immunity
- Natural — after clinical or subclinical infection
- Artificial — by vaccination
- Slow onset (days–weeks), long-lasting
- Immunological memory present
Passive Immunity
- Natural — maternal IgG across placenta, IgA in breast milk
- Artificial — antisera, immunoglobulins, antivenom
- Immediate protection, short-lived (weeks)
- No memory
Active immunity is earned and lasting; passive is borrowed and brief. Feature Active Passive Onset Slow Immediate Duration Long Short Memory Yes No Applied
- Post-exposure prophylaxis uses both (rabies, tetanus)
- Passive immunity useful in immunodeficient patients
🔑KEY POINTS TO REMEMBER- Active = host-produced, slow, long-lasting, with memory.
- Passive = transferred antibodies, immediate, short-lived, no memory.
- Both combined in rabies and tetanus post-exposure prophylaxis.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Roitt’s Essential Immunology.Definition
An antigen is a substance that is recognised by the immune system and can induce an immune response (immunogen) and react with its products.
Properties of a Good Antigen
- Foreignness — must be non-self
- High molecular weight (>10 kDa)
- Chemical complexity — proteins best
- Degradability and route of entry matter
Related Terms
- Epitope — the exact site that binds antibody
- Hapten — small molecule, immunogenic only with a carrier
- Adjuvant — enhances immune response (alum)
- Superantigen — activates many T cells (toxic shock)
Antigen must be processed and presented before lymphocytes respond. Term Meaning Epitope Antibody-binding site Hapten Needs carrier Adjuvant Boosts response Applied
- Penicillin acts as a hapten → drug allergy
- Alum used as adjuvant in vaccines
🔑KEY POINTS TO REMEMBER- Good antigens are foreign, large and chemically complex.
- Epitope = binding site; hapten needs a carrier.
- Adjuvants enhance vaccine responses.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Roitt’s Essential Immunology.Definition
Antigen–antibody reactions are specific in-vitro interactions used widely in serological diagnosis.
Main Types
- Agglutination — particulate antigen (Widal, blood grouping)
- Precipitation — soluble antigen (VDRL, immunodiffusion)
- Complement fixation — uses complement consumption
- Neutralisation — ASO test
- Labelled assays — ELISA, immunofluorescence, RIA
Characteristics
- Highly specific (lock-and-key)
- Reversible, non-covalent bonding
- Optimum proportions needed (zone phenomenon)
Specific binding produces a visible or measurable reaction used for diagnosis. Reaction Test Agglutination Widal, blood grouping Precipitation VDRL Labelled ELISA Applied
- ELISA is the mainstay of HIV screening
- Prozone phenomenon → false negative in excess antibody
🔑KEY POINTS TO REMEMBER- Types: agglutination, precipitation, complement fixation, neutralisation, labelled assays.
- Reactions are highly specific and reversible.
- ELISA is widely used (HIV screening); beware prozone effect.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Roitt’s Essential Immunology.Definition
T and B lymphocytes are the cells of acquired immunity — T cells mediate cellular immunity and B cells mediate humoral immunity.
T Lymphocytes
- Mature in the thymus
- Helper (CD4) — coordinate the immune response
- Cytotoxic (CD8) — kill virus-infected and tumour cells
- Regulatory T cells — suppress responses
- Mediate cell-mediated immunity and delayed hypersensitivity
B Lymphocytes
- Mature in bone marrow
- Differentiate into plasma cells → antibodies
- Form memory B cells
- Mediate humoral immunity
T cells attack directly; B cells work through antibodies. Feature T cell B cell Maturation Thymus Bone marrow Product Cytokines Antibodies Immunity Cellular Humoral Applied
- HIV destroys CD4 T cells → immunodeficiency
- CD4 count monitors HIV progression
🔑KEY POINTS TO REMEMBER- T cells mature in thymus (CD4 helper, CD8 cytotoxic) — cellular immunity.
- B cells mature in bone marrow → plasma cells → antibodies.
- HIV depletes CD4 cells.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Roitt’s Essential Immunology.Definition
The major histocompatibility complex (MHC), called HLA in humans, is a set of cell-surface molecules that present antigen to T cells.
Classes
- Class I (HLA-A, B, C) — on all nucleated cells; present to CD8 cells
- Class II (HLA-DP, DQ, DR) — on antigen-presenting cells; present to CD4 cells
- Class III — complement components
Significance
- Genes on chromosome 6; highly polymorphic
- Determines transplant compatibility (tissue typing)
- Disease associations — HLA-B27 (ankylosing spondylitis), HLA-DR (autoimmune disease)
MHC molecules display antigen fragments so T cells can recognise them. Class Found on Presents to I All nucleated cells CD8 II APCs CD4 Applied
- HLA matching in organ and marrow transplantation
- HLA-B27 in ankylosing spondylitis
🔑KEY POINTS TO REMEMBER- MHC (HLA) presents antigen to T cells; genes on chromosome 6.
- Class I → CD8 cells; Class II → CD4 cells.
- Basis of transplant matching and disease associations (HLA-B27).
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Roitt’s Essential Immunology.Definition
Interferons are cytokines produced by host cells in response to viral infection, conferring resistance on neighbouring cells.
Types & Sources
- IFN-α — leucocytes; IFN-β — fibroblasts (both antiviral)
- IFN-γ — T cells and NK cells (mainly immunomodulatory)
- Species-specific but not virus-specific
Actions & Uses
- Induce antiviral proteins → block viral replication
- Activate NK cells and macrophages
- Antitumour and immunomodulatory effects
- Therapeutic: hepatitis B and C, multiple sclerosis (IFN-β), some malignancies
Infected cells warn their neighbours, which then resist the virus. Type Source Main role IFN-α Leucocytes Antiviral IFN-β Fibroblasts Antiviral IFN-γ T / NK cells Immunomodulatory Applied
- Interferon therapy in chronic viral hepatitis
- Adverse: flu-like symptoms, marrow suppression
🔑KEY POINTS TO REMEMBER- Interferons are antiviral cytokines: α, β (antiviral), γ (immunomodulatory).
- Species-specific but not virus-specific.
- Used in chronic hepatitis and multiple sclerosis.
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Roitt’s Essential Immunology.Definition
Monoclonal antibodies are identical antibodies produced by a single clone of plasma cells, directed against a single epitope.
Production (hybridoma technique)
- Immunise mouse → harvest spleen B cells
- Fuse with myeloma cells → hybridoma
- Select in HAT medium, clone the desired cell
- Immortal cell line secreting identical antibody
Uses
- Diagnostic — ELISA, immunohistochemistry, blood grouping, pregnancy tests
- Therapeutic — rituximab, trastuzumab (cancer), infliximab (rheumatoid arthritis)
- Transplant rejection (basiliximab)
Fusing a B cell with a myeloma gives an immortal antibody factory. Use Example Cancer Trastuzumab Autoimmune Infliximab Diagnosis ELISA reagents Applied
- Named with the suffix -mab
- Humanised antibodies reduce hypersensitivity
🔑KEY POINTS TO REMEMBER- Monoclonal antibodies come from one clone — single epitope specificity.
- Made by the hybridoma technique (B cell + myeloma).
- Used diagnostically and therapeutically (-mab drugs).
📚SOURCES: Textbook of Microbiology (Ananthanarayan & Paniker); Jawetz, Melnick & Adelberg’s Medical Microbiology; Roitt’s Essential Immunology.