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Exam (elaborations)

BMS 602 Final Exam Questions And Complete Answers

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BMS 602 Final Exam Questions And Complete Answers ...

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  • October 14, 2024
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  • 2024/2025
  • Exam (elaborations)
  • Questions & answers
  • BMS 602
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BMS 602 Final Exam Questions
And Complete Answers

What cells present antigen via MHC II? (What cells are Antigen Presenting Cells/APCs)?
- Answer Macrophages and dendritic cells (both derive from monocytes)

B-cells

All of these cells load their antigens onto MHC II proteins in the phagosome

Types of T cells - Answer CD8/Killer T cells: in response to antigen binding, secretes
chemical to kill cells infected by intracellular pathogen

CD4/Helper T cell: stimulate B-cell antibody production via cell-cell interaction. Further
defined by the types of cytokines they release.

TH0 cells are the initial response, releases cytokines and can be transferred to TH1 or
TH2

TH1 cells produce IFNgamma to activate macrophages and dendritic cells, promotes
intracellular (viral/bacterial) response and fungal response

TH2 cells stimulate antibody production, creates memory T-cells

Classes/isotypes of antibodies - Answer IgG (FIXES COMPLEMENT, most common
antibody)

IgA (ON MUCOUS MEMBRANES, doesn't fix complement)

IgM (FIXES COMPLEMENT)

IgD (receptor on B-cells)

IgE

Complement System - Answer Classical Complement Activation: Uses all components
C1-C9. ANTIBODY DEPENDENT, starts with C1 binding antibody that is bound to
bacterial surface.

Alternative Complement Activation: Free circulating C3b binds surface of bacterial cell.
Required FACTOR B, FACTOR D, C3 (a+b), C5 (a+b)

Mannose-Binding Lectin Activation: macrophage phagocytosis releases cytokines that
tells the liver to make lectin (which binds bacterial surface mannose). Uses C2, C4, C3
(convertase, a, and b), and C5

,Strep pyogenes treatment - Answer penicillin, amoxicillin, or cephalosporin

Strep pyogenes Virulence Factors - Answer Group specific carbohydrate (Lancefield
Antigen)

Fimbriae/pili

F protein (binds fibronectin to adhere to respiratory cells)

M protein (adhesion, inhibits C3b binding which inhibits opsonization)

Capsule

C5a peptidase (ScpA)

Strep toxins - Answer Streptolysin S (SLS) cytotoxin that disrupts membranes,
nonimmunogenic

Streptolysin O (SLO) cytotoxin that forms pore to lyse cell, very immunogenic (causes
beta hemolysis)

Streptococcal pyrogenic exotoxins (SpeA-D) acts as superantigen, need one of these to
be able to cause Scarlet Fever, Streptococcal Toxic Shock Like Syndrome, and
Necrotizing Fasciitis

Staph aureus treatments - Answer Flucloxacillin

For MRSA: vancomycin

Strep pyogenes diseases - Answer Pharyngitis

Scarlet Fever (untreated infection by strain that has Spe toxin): characterized by
strawberry tongue, rashes on chest and extremities

Rheumatic fever

Necrotizing fasciitis

Strep pyogenes diagnosis - Answer Rapid antigen test (tests for Lancefield A antigen by
swabbing oropharynx)

Beta hemolysis on BAP along with Gram + cocci chains

Staph aureus diagnosis - Answer Gram stain pus

Plate on MSA, look for mannitol fermentation

Catalase positive

Coagulase positive

Staph aureus toxins - Answer Alpha toxin: pore forming cytotoxin

, Beta toxin: damages membrane, causes beta hemolysis

Toxic Shock Syndrome Toxin 1 (TSST-1): SUPERANTIGEN, overstimulates CD4 T-cell
causing massive cytokine release

Exfoliative toxins (ETA and ETB or just ET toxins) cause SSSS by breaking down cell
junctions in the epidermis

Staph aureus surface proteins/virulence factors - Answer MSCRAMM binds elastin,
collagen, fibronectin to adhere to host cells

Protein A: binds the heavy chain Fc region (the bottom end) of antibodies (especially
IgG, but some IgM, E, and A) which blocks opsonization and inhibits complement
activation

Coagulase binds fibrin and converts to fibrinogen which causes clots which shields
bacteria from immune cells but makes it hard to disseminate.

Staph aureus diseases - Answer Mostly cutaneous infections, impetigo, with furuncles
and carbuncles

Toxic Shock Syndrome caused by TSST-1

Staphylococcal scalded skin syndrome (SSSS) caused by exfoliative toxin (ET toxins,
ETA and ETB) which breaks down cell junctions, causing the sloughing of epidermis.

S. aureus food poisoning (this is an intoxication, not infection)

Strep pneumoniae diseases - Answer Pneumonia

Sinusitis and otitis media (usually preceded by viral infection of URT) (otitis externa is
the one with seasonal incidence, not otitis media, but both are treated with antibiotic ear
drops)

Bronchitis

Meningitis

Bacteremia

Strep pneumoniae diagnosis - Answer Gram stain sterile tissue or fluid sample (Gram +
diplococci)

Alpha hemolysis on BAP

Urine antigen test for C-polysaccharide/teichoic acid (doesn't have a Lancefield
antigen)

Strep pneumoniae virulence factors/toxins/important surface proteins for pathogenesis
- Answer Phosphorylcholine: binds platelet active factor (PAF) receptors which allows
bacteria to be transcytosed to the basolateral side of epithelial tissue

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