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63 Cards in this Set

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  • Back
Mechanism of Staphylococcal Toxic Shock Syndrome Toxin 1 (TSST-1)?
Binds beta chain of TCR nonspecifically --> 20% of all T cells activated --> cytokine storm, systemic inflammation, shock
What percentage of staph aureus strains produce TSST-1?
<10%
Function of Staphylococcal coagulase?
forms complex w/prothrombin: STAPHYLOTHROMBIN that converts/polymerizes fibrinogen into fibrin clots.
Which Staphylococcal enzymes function in the degradation of skin?
lipases
glycerol ester hydrolases
Function of Staphylococcal alpha-toxin?
forms trans-membrane pores that allow egress of vital molecules
Function of Staphylococcal Panton-Valentine Leukocidin (PVL)?
effective at lysing PMNs in vitro.
may indicate especially invasive S. aureus strain.
Function of Staphylococcal gamma-toxin?
lyses PMNs in vitro
What is a furuncle and where does it develop?
-well defined abscess containing pus enclosed by a fibrin capsule
-forms in the skin, often in a hair follicle or sebaceous/sweat gland
-result of tissue destruction by alpha toxin
What disease results from spread of furuncles?
multiple furuncles may coalesce into a carbuncle

disseminated deep tissue infections result in cellulitis
Which abx are used for tx of Staph saprophyticus UTI's?
fluoroquinolones
What % of UTI's are caused by Staph Saprophyticus?
10-20%
2nd most common cause of UTI's in young women
Dx methods for S. aureus infections?
Cx overnight growth of catalase positive, coagulase positive GPC in clusters on BA

Blood cultures usually negative for deep abscesses other than endocarditis, osteomyelitis, and arthritis (muscle/bone stuff).
Pathogenesis of Staphylococcal food poisoning?
only toxins (not cells) necessary for sickness.

enterotoxins A through E
heat-stable (not necessarily destroyed by cooking!)

+ serotonin release in GI tract --> vomiting
Pathogenesis of STSS?
caused by TSST-1 or enterotoxins B or C, superantigens

High fever, vomiting, diarrhea, sore throat, muscle pain -> in 48 hrs can progress to shock due to massive T cell activation, cytokine storm
Pathogenesis of bullous impetigo?
superifcial skin infection by S. aureus, usually young children

production of exfoliatin results in fluid-filled, red, itchy blisters filled w/bacteria.

blisters break and scab over w/yellow crust.
pathogenesis of scalded skin syndrome?
redness, skin peeling off in sheets due to production of exfoliatin at site of infection (may not be clinically apparent) and beyond

most common in <5 y/o

face, armpit, groin affected first; may spread over entire body
Which adhesion factors does Staph aureus employ?
Fibronectin Binding Proteins: FnbpA, FnbpB

Collagen Binding Proteins
What is the functions of Staph aureus Protein A?
Binds Fc portion of antibodies to inhibit their ability to trigger phagocytosis.
How does Staph aureus evade the immune system?
-capsule (inhibit phagocytosis)
-exopolysaccharide --> biofilm formation, resists phagocytosis
-protein A production
What abx are Staphylococci resistant to, and why are they resistant?
resistant to classical PENICILLINS

PENICILLINASE or BETA-LACTAMASE enzyme allows degradation of beta-lactam abx.
What is the mechanism of Staphylococcus' methicillin resistance?
Pbp2a (Penicillin Binding Protein 2a) has low beta-lactam affinity --> retains transpeptidase activity and can still make cell wall in presence of methicillin

beta-lactams normally bind PBP and block its transpeptidase activity. PBP2a is mutant.
Function of Staphylococcal exfoliatin?
ser protease
disrupts desmosomes (cell junctions)
Function of Staphylococcal hyaluronidase?
hydrolyzes connective tissue
(hyaluronic acid is a component of connective tissue.)
Function of Staphylococcal enterotoxin?
+ serotonin release in GI tract --> vomiting
Toxins produced by Bordetella pertussis?
TCT (tracheal cytotoxin)
PT (pertussis toxin)
ACT (adenylate cyclase toxin)
List all the AB subunit toxins we've discussed.
Pertussis Toxin
Diphtheria Toxin
Botulinum Toxin
Cholera Toxin
Anthrax Toxin
Tetanus Toxin
Which of the Rickettsiae and Chalmydiaciae can be cultured on a plate in lab?
Bartonella spp.
Which two bacteria cause meningitis following hematogenous spread after a respiratory infection?
N. meningitidis
H. influenzae
What mutations cause Pseudomonas aeruginosa to exhibit increased biofilm formation?
MUCOID: mucA mutation --> increased Alginate production

WRINKLY: WspF mutation --> increased cdGMP production --> increased pel, psl gene expression
What is unique about the structure of Mycoplasma pneumoniae?
no peptidoglycan cell wall!

cell wall is sterols stolen from host.
Function of Mycoplasma pneumoniae's terminal organelle?
Adhesion to host cell (ciliated resp. epithelium)

P1 protein = adhesin, trafficks to terminal organelle and binds host glycopeptides

Also contains actin for coordinating cytoskeletal activities.
What causes Q fever?
Coxiella burnetii
What causes Rocky Mountain Spotted Fever?
Rickettsia rickettsii

transmitted by ixodes ticks
How do GC and MC evade host immunity?
-IgA protease
-pili phase variation
-vary Opa, Por types
-Sialic acid attachment to LOS may block AB binding
How does Treponema pallidum evade host immunity?
Vary surface Ag with TprK gene
How do Borrelia recurrentis and hermesii evade host immunity?
~30 vlp/vsp alleles moved from linear plasmid to another plasmid for expression.

serovar switching in population concurrent with fever spikes.
What are the two vectors and species that cause relapsing fever?
TICK (saliva/feces) Borrelia hermesii.

LOUSE (hemolymph--only if crushed!): B. recurrentis
How does Corynebacterium diphtheriae regulate diphtheria toxin production?
DtxR gene: repressor turned OFF in low Fe2+ environments (ex. human) --> Dtx expressed.
Which toxins are phage-encoded?
Diphtheria toxin
Botulinum toxin
Pseudomonas cytotoxins
S. aureus: enterotoxin, exfoliatin
Which diseases are transmitted by ticks?
Lyme Disease (B. burgdorferi)
Rocky Mountain Spotted Fever (R. rickettsii)
Relapsing Fever (B. hermesii)
Human Monocytic Ehrlichiosis (E. chaffeensis)
Human Granulocytic Ehrlichiosis (Anaplasma phagocytophilum)
Which diseases are transmitted by lice?
Relapsing Fever (Borrelia recurrentis)
Trench Fever (Bartonella quintana)
Typhus group fevers (Rickettsiae)
What is the main killer of whooping cough pts?
dehydration, malnutrition, anoxic brain damage
How does Bordetella pertussis regulate TCT, ACT, PT production?
2-component regulatory system: Bvg genes
Attack rate of Bordetella pertussis/whooping cough in unimmunized population?
>95%
How does Pertussis Toxin work?
ADP-ribosylates a Gprotein --> ++host cAMP --> alter lymphocyte homing and function.
Which bug has Elementary Bodies and Reticulate Bodies?
Chlamydia trachomatis
What serovars of C. trachomatis cause Trachoma?
A B Ba C
What serovars of C. trachomatis cause STD?
D-K, L1, L2, L3
What serovars of C. trachomatis cause LGV?
L1, L2, L3
Describe stages of LGV.
Genital lesion

Suppurative inguinal lymphadenopathy, fever, headache, chills

Fibrotic changes (formation of xs connective tissue), multiple draining fistulas
Describe stages of Lyme Disease.
ECM-target lesion at tick bite. (must be attached for >24hr)

Neurologic/cardiac abnormalities, headache, neck and muscle pain, conjunctivitis (weeks after ECM)

Arthritis (months-years after ECM)
Describe stages of Syphilis.
genital chancre, painless indurated lesion; localized lymphadenopathy

1-3mos later: general lymphadenopathy, rash (foci are where treponemes are proliferating)

2-50yr later: latency OR benign gummatous lesions OR cardiovascular/neurological complications
Which diseases are zoonoses?
Leptospirosis
Psittacine Fever/Parrot Fever
Rickettsiae and Chlamydiaciae diseases (Rocky Mtn, Cat scratch, Trench, Q Fevers; HGE, HME)
What determines whether C. trachomatis causes Trachoma vs. STD/LGV?
-serotype
-route of infection: eyes/fomites (trachoma) vs. sexual contact (LGV/STD)
Function of metronidazole?
disrupt DNA helix --> no replication
Function of linezolid?
bind 50S ribosomal subunit --> no translation initiation
Function of tetracyclines?
bind 30S ribosomal subunit --> charged tRNA cannot enter
Function of quinolones, fluoroquinolones?
attacks gm- DNA gyrase, gm+ topoisomerase IV --> no DNA replication/repair
Function of vancomycin?
binds NAG/NAM peptide tails --> PBP cannot form crossbridges.
Function of Macrolides?
binds 50S ribosomal subunit --> no protein synthesis
Function of aminoglycoside abx?
binds 30S ribosomal subunit --> misread or truncate proteins
Which abx disrupt cell wall synthesis?
penicillins
cephalosporins
imipinem
vancomycin (glycopeptides)
Function of rifampin?
binds beta subunit of RNA pol --> no transcription.