MIC 205 MODULES 4-7 EXAM QUESTIONS WITH VERIFIED SOLUTIONS LATEST UPDATE 2026

MIC 205 MODULES 4-7 EXAM QUESTIONS WITH VERIFIED SOLUTIONS LATEST UPDATE 2026 What is innate immunity? - Answers The body's built-in, nonspecific defense system. It responds immediately or within hours, recognizes broad microbial patterns, and does not create antigen-specific memory. What are the three broad categories of innate defenses? - Answers Physical defenses, chemical defenses, and cellular defenses. These categories overlap and work together. Why is innate immunity called nonspecific? - Answers It recognizes conserved features shared by groups of microbes, such as PAMPs, rather than one unique antigen. How quickly does innate immunity respond? - Answers Immediately or very rapidly, often within minutes to hours after exposure. Does innate immunity become stronger after repeated exposure to the same antigen? - Answers Not in the antigen-specific way adaptive immunity does; it does not generate classic B- or T-cell memory. What are the major physical barriers of innate immunity? - Answers Skin, mucous membranes, tightly joined epithelial cells, endothelial linings, and specialized barriers such as the blood-brain barrier. How does intact skin prevent infection? - Answers Keratinized, tightly packed epidermal cells form a tough barrier; the dry, salty, acidic surface inhibits many microbes; continual shedding removes attached organisms. Why does a wound increase infection risk? - Answers It bypasses the skin barrier and creates a portal of entry into susceptible tissues. How do mucous membranes protect the body? - Answers Tight epithelial junctions block entry, mucus traps microbes and debris, antimicrobial substances inhibit growth, and mechanical actions remove trapped material. What is the mucociliary escalator? - Answers Cilia move microbe-containing mucus upward and away from the lungs so it can be swallowed, coughed up, or sneezed out. List major mechanical defenses. - Answers Shedding of skin cells; mucociliary sweeping; coughing and sneezing; blinking and tears; saliva flow; peristalsis; vomiting and diarrhea; urination; and flushing by bodily fluids. How does peristalsis help prevent infection? - Answers It moves microbes and contaminated material through the gastrointestinal tract, reducing time for attachment and colonization. How do tears and urine act as defenses? - Answers They physically flush microbes away. Tears also contain lysozyme and lactoferrin; urine's mildly acidic pH inhibits many microbes. What is the role of normal microbiota in innate immunity? - Answers Resident microbes occupy attachment sites, compete for nutrients, produce inhibitory substances, and maintain local conditions that discourage pathogens. What is competitive exclusion? - Answers Normal microbiota prevent pathogen colonization by occupying binding sites and consuming nutrients the pathogen needs. How can disruption of normal microbiota cause disease? - Answers Antibiotics, illness, or environmental changes can remove protective competitors and allow opportunists such as Candida or Clostridioides difficile to overgrow. How do Lactobacillus species protect the vagina? - Answers They ferment available carbohydrates to lactic acid, lowering pH and inhibiting many transient and opportunistic microbes. How does sebum contribute to defense? - Answers It helps seal follicles and supports production of fatty acids that maintain an acidic skin surface unfavorable to many pathogens. What chemical defenses are present in saliva and mucus? - Answers Examples include lysozyme, lactoperoxidase, lactoferrin, mucins, and antimicrobial peptides. How does gastric acid protect the body? - Answers The stomach's very low pH kills or inhibits many swallowed microorganisms. How does lysozyme kill bacteria? - Answers It cleaves the NAG-NAM bond in peptidoglycan, weakening the bacterial cell wall; it is generally more effective against gram-positive bacteria. How does lactoferrin inhibit microbes? - Answers It binds and sequesters iron, depriving iron-dependent microbes of an essential nutrient. How does cerumen protect the ear canal? - Answers Earwax traps debris and contains fatty acids that help create an acidic, antimicrobial environment. What are antimicrobial peptides? - Answers Small antimicrobial molecules that commonly disrupt microbial membranes or interfere with microbial functions; examples include defensins, cathelicidins, dermcidin, histatins, cryptins, and bacteriocins. What are acute-phase proteins? - Answers Plasma proteins whose concentrations change during inflammation; examples include C-reactive protein, fibrinogen, ferritin, transferrin, serum amyloid A, and mannose-binding lectin. Give major antimicrobial functions of acute-phase proteins. - Answers They can opsonize microbes, sequester iron, activate complement, and help form clots that trap pathogens. What are the major phagocytic cells? - Answers Neutrophils, monocytes, macrophages, and dendritic cells. What is the relationship between monocytes and macrophages? - Answers Monocytes circulate in blood; after entering tissues, many differentiate into macrophages or dendritic cells. Name examples of tissue macrophages. - Answers Microglia in the CNS, Kupffer cells in the liver, alveolar macrophages in the lungs, and peritoneal macrophages in the abdominal cavity. What are PAMPs and PRRs? - Answers PAMPs are conserved microbial structures such as LPS, peptidoglycan, flagellin, or viral nucleic acids. PRRs are host receptors that detect them. What are Toll-like receptors? - Answers A major family of PRRs on cell surfaces or internal membranes that activate inflammatory, antimicrobial, and antiviral gene expression after recognizing PAMPs. What happens after a macrophage PRR binds a PAMP? - Answers The macrophage increases phagocytosis and intracellular killing and releases cytokines or interferons that recruit and activate other defenses. What is chemotaxis? - Answers Directed movement of immune cells toward higher concentrations of chemical attractants released by microbes, damaged tissues, complement, or cytokines. What is extravasation or diapedesis? - Answers The process by which leukocytes adhere to vascular endothelium, squeeze between endothelial cells, and enter infected tissue. List the steps of phagocytosis. - Answers Chemotaxis and recognition → attachment → engulfment by pseudopods → phagosome formation → fusion with lysosomes → phagolysosome killing and digestion → disposal of residual material; APCs may also present antigen. What is a phagosome? - Answers A membrane-bound vesicle formed after a phagocyte engulfs a microbe or particle. What is a phagolysosome? - Answers A digestive compartment formed when a phagosome fuses with lysosomes. How are microbes killed inside a phagolysosome? - Answers Low pH, lysozyme, proteases, phospholipases, defensins, reactive oxygen species, and reactive nitrogen species damage and digest them. What is the respiratory burst? - Answers A rapid increase in oxygen consumption by activated phagocytes used to generate antimicrobial reactive oxygen species. What is opsonization? - Answers Coating a pathogen with molecules such as C3b or antibodies so phagocytes bind, engulf, and destroy it more efficiently. What is the complement system? - Answers More than 30 plasma proteins that circulate as inactive precursors and activate in a cascade to promote opsonization, inflammation, chemotaxis, and lysis. What are the three complement pathways? - Answers Alternative, lectin, and classical pathways. What triggers the alternative complement pathway? - Answers Spontaneous C3 activation followed by stabilization of C3b on a microbial surface; antibody is not required. What triggers the lectin complement pathway? - Answers Mannose-binding lectin or similar molecules bind microbial carbohydrates; antibody is not required. What triggers the classical complement pathway? - Answers Antibody bound to antigen activates the C1 complex, linking adaptive immunity to complement. Where do all complement pathways converge? - Answers At formation of a C3 convertase, which cleaves C3 into C3a and C3b and leads to downstream C5 activation and MAC formation. What are the four major outcomes of complement activation? - Answers Opsonization, inflammation, chemotaxis/leukocyte recruitment, and cytolysis through the membrane attack complex. What are the roles of C3a and C5a? - Answers They are anaphylatoxins that promote inflammation and mast-cell degranulation; C5a is also a powerful chemoattractant. What is the role of C3b? - Answers It binds microbial surfaces, acts as an opsonin, and helps form downstream complement convertases. What is the membrane attack complex? - Answers A pore-forming complex made from C5b and C6-C9 that can lyse susceptible cells, especially gram-negative bacteria. Why is the MAC less effective against gram-positive bacteria? - Answers Their thick peptidoglycan wall prevents the MAC from reaching and disrupting the cytoplasmic membrane. What is inflammation? - Answers A coordinated response to infection or injury that increases blood flow and permeability, recruits leukocytes and antimicrobial molecules, removes damaged material, and begins repair. What are the five cardinal signs of inflammation? - Answers Redness, heat, swelling, pain, and loss or alteration of function. What causes redness and heat in inflammation? - Answers Vasodilation increases blood flow to the affected tissue. What causes swelling in inflammation? - Answers Increased vascular permeability allows plasma fluid and proteins to enter tissues, producing edema. What causes inflammatory pain? - Answers Edema pressure and mediators such as bradykinin and prostaglandins stimulate pain receptors. What does histamine do? - Answers Promotes vasodilation, increased vascular permeability, smooth-muscle effects, and increased mucus secretion. What do leukotrienes, prostaglandins, and bradykinin do? - Answers Leukotrienes cause strong prolonged inflammation; prostaglandins promote inflammation, pain, and fever; bradykinin increases permeability, vasodilation, edema, and pain. How does inflammation help control infection? - Answers It recruits phagocytes and antimicrobial proteins, dilutes toxins, helps contain infection, removes damaged cells, and initiates repair. How can inflammation harm the host? - Answers Excessive or chronic inflammation can damage healthy tissue, obstruct airways, cause shock or organ failure, and produce scarring or granulomas. What is fever? - Answers A regulated increase in the hypothalamic temperature set point, usually caused when pyrogenic cytokines stimulate prostaglandin production. What is the difference between exogenous and endogenous pyrogens? - Answers Exogenous pyrogens come from microbes, such as LPS; endogenous pyrogens are host cytokines such as IL-1, IL-6, and TNF. How can moderate fever help control infection? - Answers It may slow some pathogens, enhance immune activity and interferon effects, and reduce availability of nutrients such as iron. What are risks of very high or prolonged fever? - Answers Dehydration, increased metabolic demand, confusion, seizures in susceptible children, tissue injury, and severe physiologic stress. What do natural killer cells do? - Answers They recognize stressed, abnormal, or virus-infected cells, especially cells with reduced MHC I, and induce apoptosis using perforin and granzymes. What is adaptive immunity? - Answers A specific defense system mediated by B and T lymphocytes that develops after antigen exposure, undergoes clonal expansion, and produces immunologic memory. What are the defining characteristics of adaptive immunity? - Answers Specificity, receptor diversity, self-tolerance, clonal expansion, specialized effector functions, contraction after infection, and memory. What are the two arms of adaptive immunity? - Answers Humoral immunity mediated by B cells and antibodies, and cell-mediated immunity mediated mainly by T cells. What does humoral immunity primarily fight? - Answers Extracellular microbes, toxins, and pathogens in body fluids before they enter host cells. What does cell-mediated immunity primarily fight? - Answers Intracellular pathogens and abnormal host cells, including virus-infected and tumor cells. Where do B cells mature? - Answers Primarily in bone marrow, followed by final maturation in secondary lymphoid tissues such as the spleen. Where do T cells mature? - Answers T-cell precursors arise in bone marrow but mature and undergo selection in the thymus. What is clonal selection? - Answers Antigen activates only lymphocytes whose receptors specifically bind that antigen. What is clonal expansion? - Answers Rapid proliferation of an activated lymphocyte into many cells with the same antigen specificity. What are the outcomes of lymphocyte activation? - Answers Effector cells that fight the current infection and memory cells that respond rapidly during future exposure. How is a B cell activated by a T-dependent antigen? - Answers BCR binds antigen → B cell internalizes and presents peptide on MHC II → matching helper T cell provides CD40L-CD40 costimulation and cytokines → clonal expansion and differentiation. What are the outcomes of T-dependent B-cell activation? - Answers Plasma cells, antibody secretion, class switching, affinity maturation, and memory B cells. What is T-independent B-cell activation? - Answers Strong BCR cross-linking by repetitive nonprotein antigens without helper T-cell support; it mainly produces IgM, little class switching, limited affinity maturation, and weak memory. What is a plasma cell? - Answers A differentiated effector B cell specialized for high-level antibody secretion. What is a memory B cell? - Answers A long-lived antigen-specific B cell that responds rapidly and strongly after re-exposure. What is antibody class switching? - Answers A cytokine-directed change in the heavy-chain constant region that changes IgM to IgG, IgA, or IgE while preserving antigen specificity. What is affinity maturation? - Answers Selection of B-cell clones that produce progressively higher-affinity antibodies during a T-dependent response. What three signals activate a naïve T cell? - Answers TCR recognition of peptide-MHC; costimulation such as B7-CD28; and cytokines that direct proliferation and differentiation. What happens if a T cell receives antigen recognition without costimulation? - Answers It may become anergic, undergo apoptosis, or remain unresponsive, helping prevent inappropriate activation. How are CD4 helper T cells activated? - Answers An APC presents extracellular-derived peptide on MHC II, and the matching CD4 T cell receives TCR, costimulatory, and cytokine signals. How are CD8 cytotoxic T cells activated? - Answers A matching CD8 T cell recognizes peptide on MHC I and receives costimulation and cytokines, often with helper T-cell support. What is the main role of helper T cells? - Answers They coordinate immunity by activating B cells, macrophages, cytotoxic T cells, and other leukocytes through cytokines and cell-contact signals. What is the role of helper T cells in B-cell activation? - Answers They recognize antigen presented by B cells on MHC II and provide CD40L-CD40 signaling plus cytokines that drive proliferation, plasma-cell formation, class switching, affinity maturation, and memory. What is the main role of cytotoxic T cells? - Answers They recognize specific peptide-MHC I complexes on infected or abnormal cells and induce apoptosis. How do perforin and granzymes kill a target cell? - Answers Perforin facilitates access to the cytoplasm, and granzymes activate caspases that trigger apoptosis. Compare helper and cytotoxic T cells. - Answers Helper T cells are usually CD4+, recognize MHC II, and coordinate responses. Cytotoxic T cells are usually CD8+, recognize MHC I, and directly kill infected or abnormal cells. Both are antigen specific, clonally expand, and form memory. Compare MHC I and MHC II. - Answers MHC I is on nearly all nucleated cells, presents intracellular peptides, and activates CD8 cells. MHC II is mainly on professional APCs, presents extracellular-derived peptides, and activates CD4 cells. What are professional antigen-presenting cells? - Answers Dendritic cells, macrophages, and B cells; dendritic cells are especially important for activating naïve T cells. What is an antigen? - Answers A molecule specifically recognized by antibodies, BCRs, or TCRs; the exact recognized region is an epitope. What is an antibody? - Answers An antigen-specific immunoglobulin secreted by plasma cells; variable regions bind antigen and the constant region determines isotype and effector function. Name three major outcomes of antigen-antibody interaction. - Answers Neutralization; agglutination or precipitation; and opsonization. Antibodies can also activate complement and support antibody-dependent cellular cytotoxicity. What is neutralization? - Answers Antibodies block microbial adhesins, viral attachment sites, or toxin active sites. What is agglutination? - Answers Antibodies cross-link cells or particles into clumps, limiting spread and improving phagocytic removal. What is precipitation? - Answers Antibodies cross-link soluble antigens into larger insoluble complexes that phagocytes can remove. How do antibodies promote opsonization? - Answers Fab regions bind antigen while Fc regions bind Fc receptors on phagocytes, strengthening engulfment. How do antibodies activate complement? - Answers Antigen-bound IgM or certain IgG molecules bind C1 and initiate the classical pathway. Compare innate and adaptive immunity. - Answers Innate immunity is rapid, broadly specific, germline encoded, and lacks antigen-specific memory. Adaptive immunity is slower initially, highly specific, uses diverse BCRs/TCRs, undergoes clonal expansion, and creates memory. Both use cells, cytokines, and coordinated effector mechanisms. How do innate and adaptive immunity cooperate? - Answers Innate defenses contain infection and provide antigen presentation, costimulation, inflammation, and cytokines that activate adaptive responses. Adaptive antibodies and T cells then strengthen complement, phagocytosis, macrophage activation, and targeted killing. Give a flow chart of innate-adaptive cross-talk. - Answers Barrier breach → PRRs detect PAMPs → phagocytosis and inflammation → dendritic cell processes antigen and enters lymph node → peptide-MHC plus costimulation activates T cells → helper T cells activate B cells, macrophages, and CD8 cells → antibodies, complement, and cytotoxic T cells clear infection → memory B and T cells remain. How does inflammation help activate adaptive immunity? - Answers It recruits leukocytes, activates dendritic cells, increases costimulatory molecule expression, and promotes APC migration to lymph nodes. How do antibodies strengthen innate defenses? - Answers They opsonize pathogens, activate classical complement, neutralize toxins and viruses, and can direct NK cells to antibody-coated targets. How do helper T cells strengthen innate defenses? - Answers Their cytokines activate macrophages and recruit or stimulate neutrophils and other innate leukocytes. What is the principle of immunization? - Answers Safe exposure to antigen stimulates a primary adaptive response and memory cells, allowing a faster and stronger response during later exposure. What occurs during a primary antibody response? - Answers There is a lag while B and helper T cells activate and expand; IgM appears first, then class-switched antibodies such as IgG; antibody levels are lower and memory cells form. What occurs during a secondary antibody response? - Answers Memory cells produce a shorter lag, much higher antibody levels, mainly class-switched antibody, greater affinity, and longer-lasting protection. Compare primary and secondary antibody responses. - Answers Primary: slower, lower peak, IgM first, lower average affinity, shorter duration. Secondary: faster, higher peak, mainly class-switched antibody, higher affinity, longer duration. What important application relies on the secondary response? - Answers Vaccination and booster doses: the first dose primes memory, and later doses trigger rapid high-level protection. What is active immunity? - Answers Protection produced by the person's own B and T cells; slower to develop but usually longer lasting and associated with memory. What is passive immunity? - Answers Immediate temporary protection from transferred preformed antibodies; no memory is formed. What is naturally acquired active immunity? - Answers Immunity after natural infection, such as recovery from chickenpox. What is naturally acquired passive immunity? - Answers Maternal antibody transfer, such as IgG through the placenta and IgA in breast milk. What is artificially acquired active immunity? - Answers Immunity produced by vaccination, which activates the recipient's own adaptive immune system. What is artificially acquired passive immunity? - Answers Administration of preformed antibodies, such as antivenom, rabies immune globulin, or monoclonal antibody prophylaxis. Compare the four forms of acquired immunity. - Answers Natural active: infection, memory, long-lasting. Natural passive: maternal antibody, immediate, temporary. Artificial active: vaccine, memory, often long-lasting. Artificial passive: injected antibody, immediate, temporary. What is a live attenuated vaccine? - Answers A vaccine containing a weakened living pathogen that can replicate to a limited extent without normally causing disease in an immunocompetent person. What are advantages of live attenuated vaccines? - Answers They mimic natural infection, stimulate strong humoral and cell-mediated immunity, often last longer, and may require fewer doses. What are disadvantages of live attenuated vaccines? - Answers They may be unsafe in severe immunocompromise or pregnancy, require careful storage, and carry a very small risk of reversion or vaccine-associated disease. Give examples of live attenuated vaccines. - Answers MMR, varicella, rotavirus, intranasal influenza, and yellow fever. What is an inactivated vaccine? - Answers A vaccine containing killed whole pathogens that cannot replicate. What are advantages of inactivated vaccines? - Answers They cannot revert, cannot replicate, are generally safer for immunocompromised people, and are often relatively stable. What are disadvantages of inactivated vaccines? - Answers They usually produce weaker cell-mediated immunity and may require adjuvants, multiple doses, and boosters. Give examples of inactivated vaccines. - Answers Inactivated polio, hepatitis A, rabies, and injected inactivated influenza vaccines. Compare live attenuated and inactivated vaccines. - Answers Live vaccines replicate and usually produce stronger, longer humoral and cellular immunity but have more restrictions. Inactivated vaccines cannot replicate and are safer but usually need repeated doses or boosters. What is infection? - Answers Successful colonization of a host by a microorganism; it may remain asymptomatic or progress to disease. What is disease? - Answers Damage or impairment of normal body structure or function that produces signs, symptoms, or both. What requirements must be met for infection to become established? - Answers The microbe must encounter the host, enter through an appropriate portal, adhere, obtain nutrients, multiply, evade or withstand defenses, and often invade or damage tissue; dose and host susceptibility also matter. What are the four main stages of pathogenesis? - Answers Exposure, adhesion/colonization, invasion, and infection; many pathogens then exit the host for transmission. What is a portal of entry? - Answers An anatomical route through which a pathogen enters, such as respiratory, gastrointestinal, genitourinary, skin, placental, or parenteral routes. Why does exposure not always lead to infection? - Answers The organism may lack the correct portal, adhesins, infectious dose, nutrients, or virulence factors, or it may be removed by barriers, microbiota, and immunity. What is an infectious dose? - Answers The number of organisms required to establish infection in a defined proportion of exposed hosts. What is virulence? - Answers The relative degree of pathogenicity or severity of disease caused by a microorganism. What is a virulence factor? - Answers A microbial structure, product, or strategy that promotes adhesion, invasion, immune evasion, nutrient acquisition, host damage, or transmission. What is a primary pathogen? - Answers A microbe capable of causing disease in an otherwise healthy host. What is an opportunistic pathogen? - Answers A microbe that mainly causes disease when barriers, microbiota, immunity, or anatomy are compromised or when it enters an unusual site. How do pili and fimbriae contribute to disease? - Answers They carry adhesins that bind host receptors, allowing attachment, colonization, resistance to mechanical removal, and sometimes biofilm formation. What is an adhesin? - Answers A microbial surface protein or glycoprotein that binds a specific host receptor. How does receptor specificity affect tropism? - Answers A pathogen efficiently infects only cells or tissues that display receptors recognized by its adhesins. How do capsules increase virulence? - Answers They aid attachment and biofilms and inhibit phagocytosis by masking the surface, reducing opsonization, and making engulfment more difficult.