Microbiology Exam 4

What is the difference between immunity and susceptibility? Why does susceptibility vary between individuals?

Immunity = ability to resist disease; susceptibility = lack of resistance. Susceptibility varies due to genetics, age, health, nutrition, and past infections.

What makes skin an effective physical barrier? Think beyond just the outer layer — what specific components contribute?

Skin has tightly packed cells, tough keratin, and a dry, slightly acidic surface that makes it hard for microbes to enter or grow.

Where is lysozyme found in the body, and what is its function? Does it count as a physical or chemical defense?

Lysozyme is in tears, saliva, sweat, and urine; it breaks down bacterial cell walls and is a chemical defense.

How does the ciliary escalator protect the respiratory tract, and what types of pathogens or particles does it help remove?

Cilia move mucus upward toward the throat to be swallowed or coughed out, removing trapped dust, bacteria, and viruses.

What is microbial antagonism, and how does the normal microbiota use it to protect the host?

When normal microbes inhibit pathogen growth by taking nutrients and space

What are the major types of white blood cells involved in nonspecific defense? What is the primary role of each one?

Neutrophils: first phagocytes.

Macrophages/monocytes: big eaters and signalers.

Dendritic cells: present antigens

NK cells: kill virus‑infected and tumor cells.

Eosinophils: attack parasites.

Basophils/mast cells: release histamine and start inflammation.

Which white blood cell is the most abundant, and why is its count clinically significant when evaluating infection?

Neutrophils are most abundant (about 60-70% of WBCs); changes in their number help show if an infection or other disease is present.

What is the role of natural killer cells? How do they recognize which cells to destroy?

NK cells kill virus‑infected and cancer cells by releasing toxic proteins. Targets cells that lack normal MHC I "self" markers.

Trace the steps of phagocytosis in the correct order. What happens at each stage from initial detection to waste removal?

Chemotaxis > Adherence > Ingestion > Phagolysosome fusion > Digestion > Waste released

What are at least three strategies pathogens use to evade or survive phagocytosis?

Using capsules or M proteins to block adherence, kill phagocytes with toxins, escape the phagosome, block phagosome‑lysosome fusion, or survive inside the phagolysosome.

What are the three complement activation pathways? Which one requires antibodies, and which ones do not?

The three pathways are classical, alternative, and lectin. The classical pathway needs antibodies; the alternative and lectin pathways do not.

What are the three major outcomes of complement activation? Describe what happens in each one.

Opsonization (coat microbes to ease phagocytosis), inflammation (increase vessel leakiness and attract phagocytes), and cytolysis (MAC punches holes and lyses cells).

What specific complement proteins form the membrane attack complex, and what does it do to a target cell?

C5b, C6, C7, C8, and C9 form the MAC, which makes pores in the membrane so fluid rushes in and the cell bursts.

What are the events of the inflammatory response, and in what order do they occur? What is the purpose of each step?

Tissue damage > chemical release > vasodilation and permeability > phagocyte migration and phagocytosis > tissue repair.

What chemical mediators trigger inflammation, and which cells release them?

Inflammation is triggered by histamine, prostaglandins, leukotrienes, and cytokines. Released primarily by mast cells, macrophages, platelets, and damaged tissue cells

What is an epitope? How is it different from the antigen itself?

An epitope is the small part of an antigen that receptors bind; the antigen is the whole molecule with many possible epitopes.

What is a hapten, and under what condition does it become capable of triggering an immune response?

A hapten is a small molecule that is only immunogenic when attached to a larger carrier protein.

What distinguishes adaptive (specific) immunity from innate (nonspecific) immunity?

Adaptive immunity is specific and has memory; innate immunity is present at birth, fast, and not specific to one microbe.

What is the difference between humoral immunity and cell-mediated immunity? Which type of lymphocyte is responsible for each?

Humoral immunity uses B cells and antibodies against free antigens; cell‑mediated immunity uses T cells against infected or abnormal cells.

For each of the five antibody classes (IgG, IgA, IgM, IgE, IgD), what is its structure and primary function or location?

IgG: monomer in blood; protects fetus/newborn.

IgA: dimer in secretions; protects mucosa.

IgM: pentamer; first made, agglutinates

IgE: monomer on mast cells/basophils; allergy and worms.

IgD: monomer on B cells; receptor.

Which antibody is most abundant in the blood? Which one crosses the placenta, and why is that clinically important?

IgG is most abundant and crosses the placenta, protecting the fetus and newborn from infection.

What is an antibody titer, and what does a rising titer tell you about a patient's immune status?

An antibody titer is the level of antibody in blood; a rising titer means an active immune response to a recent or current infection.

What are the possible outcomes when an antibody binds to an antigen? Describe each one.

Agglutination (clumping), opsonization (better phagocytosis), neutralization (blocks toxins/attachment), complement activation (inflammation/lysis), and ADCC (cells kill tagged target).

What is clonal selection, and what two types of cells are produced as a result?

An antigen activates only B cells with matching receptors; they form plasma cells (secrete antibodies) and memory cells.

How does the primary antibody response differ from the secondary antibody response in terms of speed, magnitude, and antibody class produced?

Primary: slow, low level, IgM first then IgG. Secondary: faster, higher level, mostly IgG due to memory cells.

What is the role of memory cells in long-term immunity, and how do vaccines take advantage of this?

Memory cells give quick, strong responses to repeat exposure; vaccines create these cells without causing disease.

What is the difference between a CD4+ T helper cell and a CD8+ cytotoxic T cell? What does each one do?

CD4+ T helper cells release cytokines and help B cells and other cells; CD8+ cytotoxic T cells directly kill infected or cancer cells.

What is the role of MHC class I molecules? What is the role of MHC class II molecules? Which cells display each type?

MHC I shows internal antigens to CD8+ cells and is on almost all nucleated cells; MHC II shows external antigens to CD4+ helpers and is on APCs (dendritic cells, macrophages, B cells).

What is the difference between a T-dependent and a T-independent antigen? Why does this distinction matter for vaccine design, especially in infants?

T‑dependent antigens need T helper help and give strong, long‑lasting responses; T‑independent antigens activate B cells alone but give weaker responses, important in infant vaccine design.

For each of the four types of acquired immunity (natural active, natural passive, artificial active, artificial passive), give a specific example and explain how immunity is obtained in each case.

Natural active: infection and recovery (measles). Natural passive: antibodies via placenta or breast milk. Artificial active: vaccination (MMR). Artificial passive: injected antibodies (antivenom).

For each major vaccine type (live attenuated, killed/inactivated, toxoid, subunit, mRNA), describe how it works and what kind of immune response it produces.

Live attenuated: weakened live microbe; strong, long-lasting antibody and T‑cell responses. Killed/inactivated: dead microbe; mainly antibody, needs boosters. Toxoid: inactivated toxin; antitoxin antibodies. Subunit: pieces of microbe; safe, antibody responses (often with adjuvant). mRNA: mRNA makes antigen in host cells; antibodies and memory without whole pathogen.

Why does a live attenuated vaccine generally produce stronger, longer-lasting immunity than a killed vaccine?

Because weakened microbes replicate, they mimic real infection, strongly stimulating both antibodies and T cells with fewer doses.

Why would a live attenuated vaccine be contraindicated for an immunocompromised patient?

Their weak immune system might not control even the weakened microbe, so it could cause serious disease.

How does an mRNA vaccine produce immunity without containing any part of the actual pathogen?

The mRNA makes antigen protein in your cells; your immune system reacts and forms memory with no whole pathogen present.

What are the four types of hypersensitivity reactions? For each one, identify the immune mechanism involved and give at least one clinical example.

Type I: IgE‑mediated immediate allergy (hay fever, food allergy, anaphylaxis).

Type II: IgG/IgM against cell surfaces with complement or ADCC (transfusion reaction, HDN).

Type III: immune complexes in tissues (glomerulonephritis, RA, lupus).

Type IV: T‑cell mediated delayed (PPD test, contact dermatitis, Type 1 diabetes, MS).

What is the role of IgE in Type I hypersensitivity? What cells does it bind to, and what happens upon re-exposure to the allergen?

IgE binds mast cells and basophils; re‑exposure causes allergen to cross‑link IgE, leading to degranulation and mediator release.

Why does anaphylactic shock require immediate administration of epinephrine? What physiological events make it life-threatening?

Systemic mediator release causes airway narrowing and a big blood pressure drop with shock; epinephrine opens airways and slows mediator release.

How does Type II hypersensitivity differ from Type I? What kind of immune component is involved in Type II reactions?

Type I is IgE allergy; Type II uses IgG or IgM binding to cell antigens plus complement or cytotoxic cells to lyse cells.

What is hemolytic disease of the newborn (HDN)? Under what specific conditions does it occur, and why is the second pregnancy more dangerous than the first?

HDN occurs when an Rh− mother has an Rh+ fetus; she is sensitized in the first Rh+ pregnancy, and in a later Rh+ pregnancy her anti‑Rh IgG crosses the placenta and destroys fetal RBCs.

How does RhoGAM prevent HDN? When should it be administered, and why does timing matter?

RhoGAM anti‑Rh antibodies destroy fetal Rh+ RBCs in the mother so she doesn’t become sensitized; it is given around 28 weeks and after delivery, before her immune system can make antibodies

Why is a tuberculin skin test (PPD) classified as a Type IV hypersensitivity reaction? What type of immune cell drives this response?

It is delayed (read at 48-72 hours) and driven by TH1 T cells that release cytokines and recruit macrophages.

What is the difference between a primary and secondary immunodeficiency? Give an example of each.

Primary one is genetic and present at birth (e.g., SCID). Secondary one is acquired later (e.g., HIV).

What is autoimmunity? What has gone wrong in the immune system when autoimmune disease develops?

Autoimmunity is when the immune system attacks the body's own tissues because self-tolerance fails and self looks foreign.

For each autoimmune disease discussed in class (lupus, rheumatoid arthritis, Type 1 diabetes, multiple sclerosis), what tissue or cell type is being attacked?

Lupus: many organs/tissues. Rheumatoid arthritis: joints. Type 1 diabetes: pancreatic beta cells. Multiple sclerosis: myelin sheath around CNS nerves.

What is the difference between phenotypic and genotypic methods of microbial identification? Give an example of each.

Phenotypic methods look at what the microbe looks like and how it acts (for example, Gram stain or sugar fermentation tests), while genotypic methods look directly at its DNA or RNA (for example, PCR).

2. What biochemical characteristics can be used to identify bacteria? Why are these useful for distinguishing species?

Things like which sugars they can ferment, what enzymes they make, whether they produce gas, and what antibiotics they are sensitive to are used, because different species have different metabolic abilities.

3. What is the fundamental principle behind all serological tests?

They all rely on the specific binding between an antigen and its matching antibody to show whether a certain pathogen or antibody is present.

4. How does a latex agglutination test work, and what does a positive result look like?

Latex beads are coated with antigen or antibody, and if the matching partner is in the sample, the beads clump together; a positive result is seen as visible clumps.

5. What is the difference between a direct ELISA and an indirect ELISA? What does each one detect, and what is added to the well first in each case?

Direct ELISA detects antigen and starts by coating the well with antibody; indirect ELISA detects patient antibody and starts by coating the well with antigen.

In the complement fixation test, what does the presence or absence of hemolysis tell you about the patient's antibody status?

No hemolysis means the patient has the antibody, while hemolysis (red/pink color) means the patient does not have the antibody.

7. In a Western blot, how are proteins separated, and what does the test ultimately detect?

Proteins are separated by size using gel electrophoresis, and the test detects specific proteins that bind to antibodies (for example, antibodies to HIV proteins).

8. How is an indirect ELISA used as a screening test, and why is a confirmatory test such as a Western blot needed before a final diagnosis is made?

Indirect ELISA is used first to quickly screen for antibodies, but because it can give false positives, a more specific test like a Western blot is needed to confirm the result.

9. For a suspected infection, what factors determine which specimen collection method is most appropriate? How would the location of the infection in the body guide your choice of specimen type?

You choose the specimen based on where the infection is: for example, lung infection → sputum, urinary infection → urine, bloodstream infection → blood, meningitis → cerebrospinal fluid, throat infection → throat swab, wound infection → wound swab.

10. Which type of tests is most appropriate when results are needed within minutes? Which methods would be unsuitable for those situations?

Latex agglutination, rapid ELISA kits, or fluorescent antibody tests are best; slow methods like culture, full biochemical panels, and complex molecular tests are not suitable.

11. When accuracy and confirmation are more important than speed, which diagnostic methods would be most appropriate, and why might a clinician choose to run more than one test before making a final diagnosis?

Culture with full identification, PCR/gene tests, and confirmatory immunologic tests like Western blot or complement fixation are best; using more than one test helps avoid false results and gives stronger proof before deciding on treatment.

12. How do you interpret a differential white blood cell count? What would a very low neutrophil count suggest, and what clinical risks does it create?

You look at the percentages of each white cell type; a very low neutrophil count means neutropenia, which puts the patient at high risk for serious bacterial infections.

13. When a patient tests positive on a screening test for an infectious disease, what is the next step and why?

You follow up with a more specific confirmatory test (like a Western blot) to make sure the result is real and not a false positive before diagnosing the disease.