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649 Cards in this Set
- Front
- Back
Exfoliatins act by
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targeting desmoglein 1a cadherin in desmosomes of stratum granulosum
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Where is Exotoxin A encoded, what controls it and what induces it?
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Chromosomally encoded, under lasR control, induced by iron restriction
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Where is Staphylokinase encoded?
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Phage
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Clostridium histo
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Gram + rods, large, pleomorphic, FORM SPORES, All but perfringens have peritrichous flagella
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Dzs caused by Fusobacterium necrophorum
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liver abscesses
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Dzs caused by Prevotella melaninogenica
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necrotizing pneumonia, periodontal disease
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How is Stenotrophomonas maltophilia spread?
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Contaminated equipment
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What Pseudomonad is important in CF and CGD patients?
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Burkholderia cepacia
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What type of flagella does Burkholderia pseudomallei have?
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Multitrichous polar flagella
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Dz caused by Burkholderia pseudomallei
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melioidosis: chronic lung dz often misdx as TB
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What is the only non-motile pseudomonad?
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Burkholderia mallei
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How do Pseudomonads respire?
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Entner Douderoff pathway (2-keto-deoxygluconate pathway). They are obligate aerobes
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Pseudomonas aeruginosa histo
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Gram negative rods, Polar flagella
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Cag pathogenicity island
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complex outer membrane protein found in most H. pylori isolates from Asia,
loosens TJs, increases likelihood that H. pylori will cause ulcer and gastric cancer |
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Vascular tropism
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something that Campylobacter fetus and Pseudomonas aeruginosa do,
attaches to vascular endothelium, causes: endocarditis, mycotic aneurysms, cellulitis and septic thrombophlebitis |
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Campylobacter fetus sx
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nonspecific fever, positive culture
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Distinguish between Campylobacter and Helicobacter pylori
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Urease test: H. pylori is +, Campylobacter is -
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STa
(STb may not be active in humans, but would increase secretion) |
heat-stable E. coli toxin, causes ETEC, plasmid encoded, 19 amino acid peptide,binds guanylate cyclase C (guanylin receptor) on brush border,INCREASES cGMP,causes Cl- secretion
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Can 1st generation beta lactam antibiotics treat Staph?
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No
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Alpha hemolysin
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Staph aureus virulence factor, most potent of its kind, mushroom structure makes pores in PM of RBCs, WBCs, Platelets (channel size is pH dependent), low MW, chromosomally encoded
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Coagulase function
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Staph aureus virulence factor, binds prothrombin to allow Fibrinogen-->Fibrin conversion.
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F protein
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Strep pyogenes virulence factor, made under high O2, low CO2 conditions in lieu of M protein, binds to fibronectin, keratinocytes, and possibly respiratory epithelial cells
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Dzs caused by Enterococcus
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UTI, esp. in older men with prostate problems, Endocarditis, Abscesses originating from intestines
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Antibody tests used to detect preceding Strep infection and level of increase required
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ASO,
Anti-DNAse B, Antihyaluronidase, Streptokinase, 4x increase over 2 weeks |
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Symptoms of GBS
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rapid onset of symmetrical limb weakness, loss of deep tendon reflexes, variable sensory loss, ascending polyneuropathy
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TSST-1
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22kD, genes located on pathogenicity island, induces production of IL-1B and TNF by monocytes, controlled by agr-quorum sensing
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Staph aureus dz by infection in blood stream
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Osteomyelitis, acute endocarditis, lung abscess, septic arthritis are caused by
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Pneumococcus virulence factors (6)
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1. Capsule (repeating oligosacch, 84 types and immunity is type-specific),
2. PDG and teichoic acid release during autolysis, 3. Pneumolysin, 4. Neuraminidase, 5. Hyaluronidase, 6. IgA1 proteases (prevent IgA-mediated immune clearance) |
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Dzs caused by Strep pyogenes
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Strep pharyngitis (throat), Skin infections (esp. erysipelas), Scarlet fever, Strep Toxic Shock Syndrome, Delayed: Rheumatic Fever, Delayed: Glomerulonephritis
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Strep pyogenes virulence factors (7)
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1. M protein, 2. Lipoteichoic acid (LTA) = fibronectin binding molecule, attached to M protein, 3. F protein, 4. Hyaluronic acid capsule, 5. C5a protease, 6. IgG and IgA binding proteins (bind Fc portions),7. Secreted virulence factors
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Hyaluronic acid capsule
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Strep pyogenes virulence factor, only 1 kind. resembles human ground substance (may help avoid immune detection).
|
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Streptokinase
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Strep pyogenes secreted virulence factor, hydrolyzes fibrin and other host proteins, antigenic (can be neutralized by Ab)
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Strep agalactiae virulence factors
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Polysacch capsule with sialic acid, C5a peptidase, Beta-hemolysin
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Beta hemolysin
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Staph aureus and Strep agalactiae virulence factor, sphingomyelinase in 20% S. aureus strains (the ones causing mastitis), toxic to monocytes, pulm. epithel and endothel but NOT PMNs, fibroblasts or lymphocytes.
inhibited by surfactant. Provokes inflamm. response, cytokine release and NO production. |
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Botulism toxin (BoNT) properties
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from Clostridium botulinum
phage encoded metalloprotease binds presynaptic peripheral cholinergic synapses at ganglia and NMJs heavy chain of toxin binds and light chain enters cell via endocytosis disrupts ACh release, leading to flaccid paralysis nonantigenic |
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dx of C. difficile infection
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endoscopy showing purulent exudates hiding necrotic intestinal tissue, toxin assay of stool (showing enterotoxin types A and B)
|
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mechanism of Enterotoxin type B
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bind receptors on intestinal epithelial cells, glucosylate Rho proteins, disrupt focal adhesions between cells, cause massive fluid secretion and acute inflammatory infiltrate
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What precipitates infection by Clostridium difficile?
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Broad-spectrum antibiotics
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Dz caused by Clostridium difficile
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Pseudomembranous colitis, Diarrhea
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Enterotoxin type A
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heat labile, cause of self-limited gastroenteritis, from Clostridium perfringens
|
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Clostridium perfringens virulence factors
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Alpha toxin (lecithinase), Enterotoxin type A
|
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Enzymes secreted by Clostridium
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collagenase, protease, hyaluronidase, lecithinase, DNAse, neuraminidase, toxins
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Normal colonization of Actinomyces israelii
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mouth and GI tract
|
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Normal colonization of Prevotella melaninogenica
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oral pharynx and GI and/or vagina
|
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Bacteroides fragilis virulence factors
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beta-lactamases, capsule (antiphagocytic and CHEMOTACTIC- can cause abscess by itself), deconjugates bile salts
|
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Bacteroides histo
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Gram - rod, nonmotile
|
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Distinguish Acinetobacter from Enterobacteriaceae
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Acinetobacter respires only, and can't reduce nitrate
|
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Distinguish Acinetobacter from Neisseria/Moraxella
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Acinetobacter is oxidase negative
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Psychrophilic def'n and example
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grows at 4 degrees Celsius, Ex. Pseudomonas fluorescens
|
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Stenotrophomonas maltophilia infects who?
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CF patients (it has low virulence)
|
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What dz does Pseudomonas aeruginosa cause in neutropenics?
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Pneumonia, bacteremia, ecthyma gangrenosum
|
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Pseudomonas aeruginosa's resistance mechanisms
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beta-lactamase, aminoglycoside inactivating enzymes, enzymes that acetylate chloramphenicol, expulsion of tetracycline, altered drug targets such as PBP (penicillin binding proteins) and gyrase
|
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What allows p. aeruginosa to cause ecthyma gangrenosum?
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Elastase
|
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Exotoxin S is... and How does it work?
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virulence factor made by 90% Pseudomonads, modifies GTP-binding proteins via ADP-ribosylation, stimulates inflammatory cytokines
|
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Exotoxin A is... and how does it work?
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an extracellular toxin of 90% Pseudomonads.
induced by iron limitation activated by unfolding enters cell by binding receptors catalyzes ADP-ribosylation of EF2 (which inhibits protein synth and kills cells -esp. during corneal infections) convergent evolution with diptheria toxin |
|
Alginate fcns
|
exopolysaccharide capsule of Pseudomonas aeruginosa, polymers of D-mannuronic and L-gluronic acid, inhibits ciliary clearance from tracheobronchial tree, antiphagocytic, adheres bacteria to each other, highly antigenic, but Abs ineffective b/c blocking Abs
|
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Are Pseudomonads fermenters?
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No.
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H. pylori tx
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Bismuth salts OR Metronidazole OR Macrolides OR Tetracyclines OR Ampicillin AND Omeprazole (direct antimicrobial and synergistic with antibiotics)
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How does Campylobacter fetus avoid complement lysis?
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S-protein capsule --> allows it to cause bacteremia
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Late onset complications of Campylobacter infection
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GBS, Reactive arthritis
|
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Campylobacter jejuni or coli sx
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Fever, Diarrhea, abdominal cramps
|
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Campylobacter and Heliobacter histo
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Gram - rods, Polar flagella, faint, curved, slender
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Anti-oxidants
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compounds that protect agains cell damage by oxygen free radicals, in some Enterobacteriaceae
|
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Cytolethal Distending toxin
|
in some E. coli and Salmonella typhi, two component DNAse (nuclear fragmentation and cell cycle arrest)
|
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HUS sx
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Hemolytic Uremic Syndrome, anemia, thrombocytopenia, renal failure, often caused by E.coli 0157:H7
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Example of invasin
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from Yersinia, just called "invasin," tightly binds beta1 integrins, rearranges the cytoskeleton and causes the uptake of Yersinia
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Klebsiella pneumoniae facts
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produces large goopy capsule in high glucose, nonmotile, causes only extra-intestinal infections, either a primary or opportunistic pathogen
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E. coli facts
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green sheen on EMB, primary pathogen or opportunistic pathogen, normal GI flora (made pathogenic by acquiring virulence factors)
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BFP
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bundle forming pili, polar, attach E. coli to epithelial cells
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P fimbriae
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on nephritogenic E. coli - bind neutral glycolipids of globoside series on human P blood group
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SPE-B
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Strep pyogenes secreted virulence factor, chromosomally encoded cysteine protease (tho some strains don't produce active protein), cleaves IL-1B into its active form and degrades fibronectin and vitronectin.
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Staphylokinase
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Staph aureus virulence factor, dissolves clots by promoting plasmin activation. phage encoded
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Non-histo properties that Enterobacteriaceae share
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Oxidase negative (though they do have an electron transport chain), Facultative (can ferment glucose to pyruvate to something else), Can reduce nitrate to nitrite
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Group B Strep capsule
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polysacch, contains sialic acid (inhibits C3 binding, diminishes immune recognition), often only defense in babies is maternal anticapsular IgG
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Where is Enterococcus' hemolysin encoded?
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Plasmid
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Staph aureus virulence factor, binds prothrombin to allow Fibrinogen-->Fibrin conversion.
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Coagulase
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Sublytic concentrations induce LTB4 release and IL-8 synthesis, leading to inflammation"
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Panton Valentine Leukocidin
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MRSA mutation
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plasmid-encoded mutation in transpeptidase that's not susceptible to 2nd gen beta lactams
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Dzs caused by pneumococcus (6)
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Bacterial pneumonia (most common cause), Otitis media, Sinusitis, Bronchitis, Bacteremia, Meningitis (most common cause)
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Mechanism of Inflammation related to Pneumococcal infection
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Released teichoic acid stimulates PAF production, PDG binds CD14 on macrophages, inducing cytokine secretion.(Causes influx of fluid into alveoli, then RBCs, then neutrophils.)
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Strep pyogenes secreted virulence factors (5)
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Hyaluronidase, Streptolysin O (SLO), Streptolysin S (SLS), Streptokinase, Streptococcal Pyrogenic Exotoxins (SPE) and Related Superantigens
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Factors that predispose to Acute Rheumatic Fever (not including previous GAS infection) (8)
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Age (4-9 year old), Crowding, Winter or Spring, Economic factors (poverty, urban environment), High magnitude of Host response to GAS (high Ab titer), Family history, Previous ARF, Increased frequency of HLA-DR2 and DR4
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Infections commonly preceding GBS (by 1 month)
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Diarrheal or Upper Respiratory Infection (found in 2/3 cases): Cytomegalovirus (severe sensory deficit), EBV, Varicella Zoster Virus, Rabies vaccine (if contaminated with myelin), Mycoplasma pneumoniae, Campylobacter jejuni
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Mechanism for Staph aureusType B Enterotoxin
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Superantigen, acts at neural receptors in upper GI tract, activating the vomiting center to cause food poisoning
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Osteomyelitis, acute endocarditis, lung abscess, septic arthritis are caused by
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Staph aureus dz by infection in blood stream
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Cerebrosides
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ceramide with a sugar (usually Glu or Gal) added to the head group
|
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Motor only version of GBS, with opthalmoplegia, ataxia, and areflexia. Associated with serotype O19 of Campylobacter jejuni
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Miller-Fisher variant of GBS
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What causes the prolonged PR interval in ARF?
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Myocarditis involving the conduction system
|
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What is used to measure the progress of an ARF patient?
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Acute phase reactants
|
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What meds interfere with acute phase reactants?
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Aspirin and corticosteroids
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Typical onset of Sydenham's chorea (relative to Strep infection)
|
Gradual onset 4-8 weeks after Strep infection
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Treatment for arthritis associated with ARF
|
Aspirin and NSAIDs
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Changes that occur in a heart as a patient heals from ARF carditis
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Valves thicken and deform, Chordae shorten, Valve commissures fuse (stenosis or insufficiency)
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Winter and Spring are the peak seasons of:
|
Rheumatic Fever peaks in what seasons?
|
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Has glomerulonephritis followed skin infections of GAS?
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Yes
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Has glomerulonephritis followed pharyngeal infections of GAS?
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Yes
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Growth/Metabolic properties of Enterococcus
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PCN tolerant, metabolize esculin to a black pigment, can grow in 40% bile, can grow in 6.5% salt
|
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How does M protein facilitate the acquisition of bound plasmin for Strep pyogenes?
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M protein binds fibrinogen, that can then bind plasminogen. Streptokinase cleaves plasminogen.
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Necrotizing Fasciitis sx
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Swelling, heat and redness that moves rapidly from the initial infection site. 1 day later skin color changes red- purple - blue and large bullae form. Later skin dies and myositis may develop.
|
|
What kinds of bacteria can cause necrotizing fasciitis?
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Strep pyogenes, Staph, Clostridium, Gram Negative Enterics
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How are Beta-hemolytic Strep classified?
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By Lancefield antigen aka C carbohydrate surface antigen (A, B, D)
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Risk factors for severe pneumococcal infection
|
Debilitated health, sickle cell anemia, Hodgkin's dz, multiple myeloma, HIV, splenectomy
|
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Treatment of MRSA
|
Vancomycin, Linezolid or Synercid
|
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Examples of Beta-lactam antibiotics
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Penicillins, Cephalosporins, Monobactams, Carbapenems
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Staph aureus carriers
|
not normal flora, but colonizes nasopharynx, skin or vagina of 30% of population. Higher chance if medical personnel, diabetic, IV drug users
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Superantigen, acts at neural receptors in upper GI tract, activating the vomiting center to cause food poisoning
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Mechanism for Staph aureusType B Enterotoxin
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Dz caused by S. aureus enterotoxins
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Food poisoning (1-6 hours post-ingestion, NV & diarrhea) is caused by
|
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Scalded Skin Syndrome in newborns and Bullous Impetigo in older kids/adults are caused by
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Dz caused by Exfoliatins
|
|
Staph aureus virulence factor, most potent of its kind, mushroom structure makes pores in PM of RBCs, WBCs, Platelets (channel size is pH dependent), low MW, chromosomally encoded
|
Alpha hemolysin
|
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Staph that causes 10-20% of UTIs in sexually active women 16-35 y.o., 90% of whom have sx
|
Staph saprophyticus
|
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22kD, genes located on pathogenicity island, induces production of IL-1B and TNF by monocytes, controlled by agr-quorum sensing
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TSST-1
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Staph aureus dz by direct infection
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Folliculitis, Furuncles, Carbuncles, Abscesses, Cellulitis, Wound infections, Osteomyelitis are caused by
|
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Miller-Fisher variant of GBS
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Motor only version of GBS, with opthalmoplegia, ataxia, and areflexia. Associated with serotype O19
|
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Most common antecedent infection to GBS
|
Campylobacter jejuni (esp. serotype O19, which contains neuraminic acid aka sialic acid in the O side chain of LPS, cross reacts with peripheral nerves)
|
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Prophyllactic ARF tx (for first 5 years to prevent recurrence)
|
PCN IM monthly, Sulfadiazene qday, Erythromycin BID
|
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Tx of ARF
|
PCN, Erythromycin for PCN-allergic, Corticosteroids for acute carditis
|
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Acute phase reactants
|
Minor manifestation of ARF. A change in Erythrocyte Sed Rate (ESR), or the presence of C-reactive protein in serum, suggest inflammatory process.
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Can erythema marginatum occur in a child?
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Yes, it occurs only in children.
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Erythema Marginatum
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Uncommon Major manifestation of ARF. Evanescent (vanishing quickly) pink rash with a clear center and serpiginous (wavy) margins
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Carditis is more likely to be a symptom of ARF in what population?
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Children
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Minor manifestations for dx of ARF (Jones Criteria)
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Fever, Arthralgia, Previous RF, Acute Phase Reactants, Prolonged P-R interval
|
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Major manifestations of ARF (Jones Criteria)
|
Carditis, Polyarthritis, Sydenham's Chorea, Erythema marginatum, Subcutaneous nodules
|
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Age group most commonly stricken with Acute Rheumatic Fever (and Strep pharyngitis)
|
4-9 year olds
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Enterococcus Tx in PCN-allergic patient or PCN-resistant strains
|
Vancomycin + an aminoglycoside. But beware of VRE (Vancomycin resistant enterococci) and cross your fingers they don't spread the ability to MRSA.
|
|
Growth/Metabolic properties of Strep bovis
|
metabolize esculin to a black pigment, can grow in 40% bile
|
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Enterococcal endocarditis Tx
|
a PCN AND an aminoglycoside (ex. ampicillin and gentamycin) - synergistic effect to kill organism (since organism is isolated from host immune system)
|
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Group B Strep normal colonization
|
Normally colonizes vagina or intestines of 20-30% adult pop.
|
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Group B Strep culture results on blood agar plate
|
Beta-hemolytic, but don't produce large clear zones on blood agar plates. Produce an orange pigment.
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Strep pyogenes tx
|
PCN. For severe infections, also clindamycin to decrease protein and toxin production. For STSS, IV IgG as adjunctive therapy
|
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SPE-A
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Strep pyogenes secreted virulence factor, encoded on lysogenic phage, associated with scarlet fever, toxic shock syndrome, necrotizing fasciitis.
|
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Neuraminidase
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Pneumococcus virulence factor, unmasks cell-surface binding receptors, may contribute to hemolytic-uremic syndrome.
|
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Pneumolysin
|
Pneumococcal virulence factor, cytolysin that forms pores in eukaryotic membrane. Cytotoxic to bronchial epithelial cells, may screw up clearance mechanism, allowing bacteria to grow in lower respiratory tract. Possibly attacks macrophages and neutrophils and makes alveolar-capillary barrier leak.
|
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Agr responds ________ to H+ ions
|
positively
|
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Agr responds ________ to carbohydrates
|
negatively
|
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not normal flora, but colonizes nasopharynx, skin or vagina of 30% of population. Higher chance if medical personnel, diabetic, IV drug users
|
Staph aureus carriers
|
|
Panton-Valentine Leukocidin
|
Staph aureus virulence factor, found in 5% of strains (mostly causing abscesses), lethal to PMNs via pores.
|
|
Staph histo
|
Gram Positive Cocci growing in clusters, singly or pairs. Divide perpendicular to plane of last division. Nonmotile.
|
|
Distinguish Staph aureus from other Staph
|
Staph is coagulase positive, produces a gold pigment (carotenoids) when grown on sheep's blood agar, thermostable nuclease positive, mannitol positive,
|
|
Staph aureus subtypes
|
5 groups based on lysis patterns with 20 bacteriophages
|
|
Most common non-aureus Staph
|
Staph epidermidis
|
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Is Staph saprophyticus novobiocin sensitive or resistant?
|
novobiocin resistant
|
|
Is Staph epidermidis novobiocin sensitive or resistant?
|
sensitive
|
|
What do S. aureus, saprophyticus, and epidermidis have in their teichoic acid?
|
S. aureus - ribitol, S. saprophyticus and S. epidermidis - glycerol
|
|
Which non-aureus Staph is commonly nosocomial?
|
S. epidermidis, often from IV catheters and prosthetics, or contaminating blood cultures from needle entering skin
|
|
Distinguish Staph from Strep
|
Catalase test: drop H2O2, if O2 gas is formed, it's Staph. Catalase is a heme-containing enzyme and Strep doesn't make heme.
|
|
Virulent factor of Staph epidermidis
|
"Slime" aka biofilm. Viscous, exopolysaccharide, allows it to cling to hospital equipment and is more difficult for host to clear.
|
|
Bacteremia
|
presence of viable bacteria in blood (positive blood cultures)
|
|
presence of viable bacteria in blood (positive blood cultures)
|
Bacteremia
|
|
Septicemia
|
bacteremia with symptoms of systemic response (tachycardia, hypotension)
|
|
bacteremia with symptoms of systemic response (tachycardia, hypotension)
|
Septicemia
|
|
Most Gram Positives adhere via...
|
protein-protein interactions
|
|
Most Gram Negatives adhere via...
|
cell surface appendages interacting with cell surface sugars
|
|
Staph aureus virulence factors (11)
|
1. Microcapsule
2. Binding proteins (fibronectin, fibrinogen, vitronectin, collagen type II) 3. Clumping factor 4. Coagulase 5. Hemolysins (alpha, beta, gamma, delta) 6. Leukocidins 7. Penicillinase/beta-lactamase 8. Enzymes to tunnel through tissue (Staphylokinase, Hyaluronidase, Lipase) 9. Exotosins (Exfoliatin A&B, Enterotoxins, TSST-1) 10. Release of PDG from cell wall 11. Protein A |
|
Staph aureus binding proteins
|
Fibronectin, Fibrinogen, Vitronectin, Collagen type II.
|
|
Protein A
|
Staph aureus virulence factor, 42 kD, usually linked to PDG, binds Fc of IgG and prevents opsonization/phagocytosis
|
|
Staph aureus virulence factor, 42 kD, usually linked to PDG, binds Fc of IgG and prevents opsonization/phagocytosis
|
Protein A
|
|
Staph aureus virulence factor, sphingomyelinase in 20% S. aureus strains (the ones causing mastitis), toxic to monocytes, but NOT PMNs, fibroblasts or lymphocytes
|
Beta hemolysin
|
|
Staph aureus virulence factor, dissolves clots by promoting plasmin activation. phage encoded
|
Staphylokinase
|
|
Hyaluronidase
|
Staph aureus virulence factor, drills through proteoglycans in connective tissue
|
|
Staph aureus virulence factor, drills through proteoglycans in connective tissue
|
Hyaluronidase
|
|
Lipase
|
Staph aureus virulence factor, dissolves fats and oils, helps disseminate the bacteria
|
|
Staph aureus virulence factor, dissolves fats and oils, helps disseminate the bacteria
|
Lipase
|
|
Superantigen
|
A molecule that promotes TH cell and APC (MHCII) attachment regardless of Ag, leading to cytokine release (and thus fever, hypotension, shock, skin lesions, multiorgan faulure, and possibly death)
|
|
A molecule that promotes TH cell and APC (MHCII) attachment regardless of Ag, leading to cytokine release (and thus fever, hypotension, shock, skin lesions, multiorgan faulure, and possibly death)
|
Superantigen
|
|
Dz caused by Exfoliatins
|
Scalded Skin Syndrome in newborns and Bullous Impetigo in older kids/adults are caused by
|
|
Food poisoning (1-6 hours post-ingestion, NV & diarrhea) is caused by
|
Dz caused by S. aureus enterotoxins
|
|
Sx of toxic shock syndrome
|
fever, desquamative skin rash, hypoTN, multisystem involvement, possibly death
|
|
fever, desquamative skin rash, hypoTN, multisystem involvement, possibly death
|
Sx of toxic shock syndrome
|
|
Toxin-mediated Staph aureus dz
|
Scalded Skin syndrome, Bullous impetigo, Gastroenteritis/food poisoning, Toxic Shock Syndrome are caused by
|
|
Scalded Skin syndrome, Bullous impetigo, Gastroenteritis/food poisoning, Toxic Shock Syndrome are caused by
|
Toxin-mediated Staph aureus dz
|
|
Folliculitis, Furuncles, Carbuncles, Abscesses, Cellulitis, Wound infections, Osteomyelitis are caused by
|
Staph aureus dz by direct infection
|
|
Agr is expressed in ______ phase, and causes
|
expressed in stationary phase, and causes upreg. of toxins (alpha, beta hemolysins, serpin, PLC, exotoxin B, C, TSST-1) and downreg. of surface proteins (fibronectin BP, protein A, independent fibrinogen BP, beta-lactamase, collagen)
|
|
Quorum Sensing mechanism
|
bacteria secrete RAP (RNAIII-activating protein). When a certain concentration threshold is reached (sensed by 2 component system), TRAP (target of RAP) gets phosphorylated, activating it to make RNAIII, which regulates txn of Agr genes.
|
|
A global regulator
|
A genetic element that controls the transcription of many independent genes (ex. Agr - accessory gene regulator)
|
|
Penicillins, Cephalosporins, Monobactams, Carbapenems
|
Examples of Beta-lactam antibiotics
|
|
Can 1st generation beta lactam antibiotics treat Strep?
|
Yes
|
|
Can 2nd generation beta lactam antibiotics treat Staph?
|
Yes
|
|
Can 2nd generation beta lactam antibiotics treat Strep?
|
Yes
|
|
Quorum Sensing definition
|
The ability to sense the number of similar organisms in the vicinity.
|
|
Coagulase Test
|
Incubate 1-4 hours in rabbit plasma at 37 degrees, watch for clot (positive test)
|
|
Alpha hemolytic
|
RBCs intact, hemoglobin converted to biliverdin, green color
|
|
Beta hemolytic
|
Complete RBC lysis, clear blood agar plate
|
|
Gamma hemolysis
|
no hemolysis
|
|
Strep histo
|
Gram positive cocci in chains, pairs or singly
|
|
P disk
|
Optochin, distinguish between Strep pneumoniae (sensitive) and other alpha hemolytic Strep
|
|
A disk
|
Bacitracin, distinguish between Strep pyogenes (sensitive) and other beta hemolytic Strep
|
|
Distinguish between Strep pyogenes and other beta hemolytic Strep
|
A disk (bacitracin)
|
|
Distinguish between Strep pneumoniae and other alpha hemolytic Strep
|
P disk (optochin)
|
|
Most autolytic of the Strep
|
Pneumococcus. When its autolysin (muramidase) is activated, bacterium destroys itself. In stationary phase, this happens naturally.
|
|
Method of transmission of pneumococcus
|
Person-to-person only.
|
|
Most common cause of bacterial pneumonia in adults
|
Pneumococcus
|
|
Most common cause of meningitis in children and adults
|
Pneumococcus
|
|
Pneumovax contents and indications
|
23 types of pneumococcal capsule antigens. Indicated for adults >65 y.o., or those with underlying conditions
|
|
Most important Pneumococcus virulence factor
|
Capsule
|
|
Children less than 18 mo. old do not raise a good response (only a T-independent response) to a pure oligosacch vaccine. How can we elicit a protective response?
|
Conjugate the oligosacch. to a protein, and a T-dependent response will be raised.
|
|
Treatment of pneumococcal infections
|
Test for resistance to beta lactams, but generally PCN.
|
|
Viridans Strep that forms plaque
|
S. mutans
|
|
Dzs caused by Viridans Strep
|
Endocarditis (usually on previously damaged heart valves), Caries (via lactic acid production and trapping within plaque and tartar)
|
|
Lancefield Antigen D
|
Now recognized as glycerol teichoic acid, and genus is called Enterococcus
|
|
Most virulent beta-hemolytic Strep
|
Strep pyogenes, Group A
|
|
Does Strep pyogenes infect animals?
|
No
|
|
Necrotizing fasciitis tx
|
surgically excise fascia, rapid antibiotic therapy. Despite best efforts, mortality >50%.
|
|
Fournier's gangrene
|
Necrotizing Fasciitis of male genital and perineal areas
|
|
Most important virulence factor of Strep pyogenes
|
M protein
|
|
C5a protease
|
Strep pyogenes and agalactiae virulence factor, cleaves C5a and inhibits neutrophil chemotaxis
|
|
Which terminal (C or N) of M protein is attached to PDG?
|
C - this terminal shows little variability, whereas the N terminal shows some variability.
|
|
How does M protein prevent phagocytosis?
|
By inhibiting C3b deposition.
|
|
Can we get repeat infections of Strep pyogenes?
|
Yes, because the N terminal of its M protein is what elicits Abs, and the N terminal shows wide variability.
|
|
How many types of M protein are there?
|
More than 80!
|
|
What molecule does M protein mimic?
|
Human coiled-coil alpha helical structure
|
|
Streptolysin O (SLO)
|
###############################################################################################################################################################################################################################################################
|
|
Streptolysin S
|
Strep pyogenes secreted virulence factor, nonantigenic, oxygen stable, very potent cytotoxin (ex. necrotizing fasciitis), structurally similar to other Gram positive bacteriocin, causes beta hemolysis.
|
|
Streptococcal Pyrogenic Exotoxins (SPE) - formerly erythrogenic toxins
|
Strep pyogenes secreted virulence factor, ex. SPE-A, SPE-C, SPE-B
|
|
Strep pyogenes secreted virulence factor, encoded on lysogenic phage, associated with scarlet fever, toxic shock syndrome, necrotizing fasciitis.
|
SPE-A
|
|
Strep pyogenes secreted virulence factor, chromosomally encoded cysteine protease (tho some strains don't produce active protein), cleaves IL-1B into its active form and degrades fibronectin and vitronectin.
|
SPE-B
|
|
Mode of mother-baby Group B Strep transmission
|
Colonization in vagina EITHER infects amniotic fluid through placental membranes, then is aspirated, and works its way into the bloodstream, OR acquired during passage through birth canal.
|
|
Dzs caused by Group B Strep in newborns
|
Pneumonia and Septicemia (RDS and fever in first few days of life, esp for low birth weight or premature water breaking), Bacteremia and Meningitis (usually Capsule type III, can cross BBB via brain capillary cells)
|
|
CAMP test
|
Test used to ID Group B Strep (Strep agalactiae). Single streak Staph aureus across plate of sheep blood agar, then streak potential Group B Strep perpendicularly (but not crossing the line). If an arrowhead lysis pattern forms pointing to Staph aureus line, it is Strep agalactiae.
|
|
Subtypes of Group B Strep
|
Based on surface polysacch capsular Ags (I, II, III ... VI)
|
|
Group B Strep tx
|
PCN, ampicillin or CEPH
|
|
Group C Strep hemolysis pattern, dzs
|
beta-hemolytic, uncommon infective agent, syndromes similar to Group A (cellulitis, lymphangitis)
|
|
Are enterococcus alpha-hemolytic?
|
No
|
|
Distinguish between Strep bovis and Enterococcus
|
Strep bovis canNOT grow in high salt (6.5%)
|
|
Cause of Acute Rheumatic Fever
|
Previous Strep pyogenes (GAS) pharyngitis
|
|
Average time between Strep pharyngitis and onset of Acute Rheumatic Fever
|
2 weeks
|
|
Most common cause of acquired heart disease
|
Acute Rheumatic Fever
|
|
Has Acute Rheumatic Fever followed skin infections of GAS?
|
No
|
|
Can we prevent primary or secondary attacks of Acute Rheumatic Fever?
|
Yes, by prophyllactically treating Strep pyogenes pharyngeal infections.
|
|
Rheumatic Fever peaks in what seasons?
|
Winter and Spring are the peak seasons of:
|
|
Chance of developing ARF with a low Ab titer
|
<1%
|
|
Chance of developing ARF with a high Ab titer
|
3%
|
|
Which MHC Class II alleles predispose to ARF?
|
HLA-DR2 and DR4
|
|
Probability of ARF following Strep throat in a person who has a hx of ARF
|
30-50%
|
|
What is the structure of M protein?
|
alpha helical coiled structure (common in human tissue - myosin, collagen, tropomyosin)
|
|
True/False: Abs to M proteins conserved region cross-react with human proteins
|
True
|
|
True/False: Abs to the variable regions of M protein cross-react with human proteins
|
Usually no, but yes in the case of M19 and human sarcolemmal protein
|
|
Dx of ARF
|
2 major criteria, or 1 major and 2 minor criteria, if supported by evidence of GAS infection
|
|
What constitutes evidence of a preceding Strep infection in the dx of ARF?
|
One of the following: Increased ASO (antistreptolysin O) titer or increase in other Ab titers, Hx of recent case of scarlet fever, Positive GAS throat culture
|
|
The most severe manifestation of ARF
|
Carditis (because the heart damage is permanent)
|
|
Do patients with ARF usually have symptoms referable to the heart?
|
The majority do not.
|
|
Which valves are most frequently involved in endocarditis?
|
Mitral>Aortic>Tricuspid>>>>>Pulmonic
|
|
Which layers of heart muscle does ARF's carditis usually affect?
|
All of them (pancarditis)
|
|
What is MacCallan's patch and what dz is it associated with?
|
In ARF carditis, a rough and thickened area in the left atrium above the base of the post. leaflet of the mitral valve.
|
|
Arthritis associated with ARF is more likely to be worse in what population?
|
Older, elderly
|
|
most commonly recognized sympton of ARF
|
arthritis
|
|
Does ARF arthiritis leave permanent damage?
|
No
|
|
Another name for Sydenham's chorea
|
St. Vitus' dance
|
|
Sydenham's chorea
|
Major manifestation of ARF, characterized by sudden, aimless, irregular movement accompanied by muscular weakness and emotional instability. Disappears during sleep.
|
|
Does Sydenham's chorea continue throughout the night?
|
No, it disappears with sleep.
|
|
Where does erythema marginatum occur?
|
Trunk or proximal extremities, never face
|
|
Can erythema marginatum occur in an adult?
|
No
|
|
Subcutaneous nodules
|
Major manifestation of ARF, also seen in Rheumatoid Arthritis. Pea-sized painless swellings over bony prominences. Only seen with severe carditis.
|
|
True/False: Subcutaneous Nodules are pathognomic for ARF
|
False- they also occur in RA
|
|
True/False: Ashoff bodies are pathognomic for RHD
|
True
|
|
Can subcutaneous nodules occur as the only symptom of ARF?
|
No, they are only seen with severe carditis (and with RA)
|
|
ARF Subcutaneous nodule histo
|
Spindle shaped interstitial aggregate of large mononuclear cells surrounding an area of fibinous necrosis (Aschoff body)
|
|
Typical location of Aschoff body
|
Heart, though possibly through the body, incl. subcutaneous nodules
|
|
Tx of Group A Strep pharyngitis to prevent ARF
|
10 day tx with PCN (Effective even if delayed after symptom onset), Doesn't work with 5 day PCN or 10 day sulfa
|
|
Guillan Barre Syndrome (GBS)
|
acute polyneuropathy that can lead to motor and sensory deficits
|
|
Can GBS hit a 1 year old?
|
No, it doesn't occur in children <3 yrs old
|
|
ceramide with a sugar (usually Glu or Gal) added to the head group
|
Cerebrosides
|
|
Ganglioside
|
ceramide that has multiple sugars added to the head group
|
|
ceramide that has multiple sugars added to the head group
|
Ganglioside
|
|
Biopsies from GBS patients show C3 or Ab bound to...
|
Schwann cells
|
|
Currently, do people think Chlamydia causes atherosclerosis or ACS?
|
No.
|
|
Function of Staph aureus binding proteins
|
Bind/adhere to ECM proteins, important for arthritis
|
|
Pneumococcus histo
|
lancet shaped diplococci
|
|
% of population normally infected by Pneumococcus
|
20-40% normally colonized in nasopharynx
|
|
Sublytic concentrations of Panton-Valentine leukocidin induce
|
LTB4 release and IL-8 synthesis, leading to inflammation
|
|
Enterobacteriaceae histo
|
Gram negative rods, peritrichous flagella (except Klebsiella and Shigella), no spores
|
|
Outer membrane antigens of Enterobacteriaceae
|
H - flagella, O - somatic antigen (oligosacch side chain of LPS), K - acidic polysacch capsule, Pili (Type 1 or 2) or P fimbriae, X adhesins, BFP
|
|
K antigen (Vi) functions
|
Enterobacteriaceae Outer Membrane Antigen - acidic polysacch capsule. Vi is the Salmonella typhi capsule.- Evasion of phagocytosis and complement- Adhesion to GI/GU epithelia (ex. E. coli K1 capsule adheres to GU?)
|
|
Salmonella H Antigen
|
Two different flagella, switch between them.
|
|
Receptor that senses LPS, systemic symptoms that follow
|
TLR4, fever and shock
|
|
Type 1 pili
|
mannose sensitive (bind at same site as D-mannose), important for colonization of GI tract, on Enterobacteriaceae
|
|
Type 2 pili
|
mannose-resistant pili, cause dz outside normal niche
|
|
X adhesins
|
on nephritogenic E. coli - bind to different globosides
|
|
3 strains of Enterobacteriaceae that are clinically significant from wherever they are isolated
|
Shigella, Salmonella and Yersinia
|
|
Highly pathogenic strains of Enterobacteriaceae (6)
|
Escherichia, Shigella, Proteus, Salmonella, Klebsiella, Yersinia
|
|
selective media
|
made with substances that inhibit the growth of unwanted organisms
|
|
differential media
|
allows strains to be distinguished based on a metabolic property
|
|
Normal enteric bacteria are capable of fermenting
|
lactose
|
|
Differential media for lactose fermentation
|
EMB and MacConkey agar. Suppress Gram + growth also.
|
|
EMB agar
|
Eosin Methylene Blue agar, Eosin inhibits Gram + growth, Lactose fermentation produces acid that colors the colony (methylene blue), Peptone fermentation leaves the colony clear
|
|
MacConkey agar
|
Bile inhibits Gram + growth, Lactose fermentation produces acid that colors the colony. Peptone fermentation leaves colonies clear
|
|
Pyruvate breakdown pathways of Enterobacteriaceae
|
Mixed acid pathway (products = formic acid, acetic acid, lactic acid, succinic acid -->methyl red test), 2,3 -butanediol pathway (products = butanediol, ethanol, acid -->Voges-Proskauer test detects acetoin)
|
|
Enterobacteriaceae that use the Mixed Acid pathway
|
E. coli, Citrobacter
|
|
Enterobacteriaceae that use the 2,3 - butanediol pathway
|
Klebsiella, Enterobacter, Serratia
|
|
Enterobacteriaceae lactose fermenters
|
E. coli, Citrobacter, Klebsiella, Enterobacter
|
|
Nonmotile Enterobacteriaceae
|
Klebsiella, Shigella
|
|
Enterobacteriaceae Primary Pathogens (capable of causing dz in anyone)
|
Shigella, Salmonella, Yersinia, Klebsiella pneumoniae, Escherichia coli
|
|
Enterobacteriaceae Opportunistic pathogens (only cause dz in certain hosts)
|
Escherichia coli, Klebsiella pneumoniae, Proteus, Serratia, Enterobacter, Morganella, Providencia, Citrobacter
|
|
Enterobacteriaceae that are both Primary and Opportunistic pathogens
|
Escherichia coli, Klebsiella pneumoniae
|
|
Invasiveness
|
either the ability to enter and survive inside host cells or the ability to invade systemically from an epithelial surface
|
|
Pathogenicity Island
|
a contiguous set of virulence genes that has been transferred from one bacterial species to another
|
|
2 component regulators
|
mechanism for sensing environment and respond. A membrane component, under certain conditions, phosphorylates a TF that expresses virulence genes
|
|
Example of 2 component regulator
|
Salmonella PhoP/PhoQ, senses low Mg2+ in phagosome and allows survival inside a cell
|
|
Type III secretion system
|
Used by Gram - bacteria to secrete host-destructive proteins into host cells in response to host cell contact, O2 tension, Ca2+, nutrient availability
|
|
Examples of Type III secretion systems
|
###############################################################################################################################################################################################################################################################
|
|
E. coli functions in GI
|
synthesizes Vitamin K, deconjugates bile salts and sex hormones, occupies receptors (protects against enteropathogen colonization), produces colicins, stimulates eptihel. cells to synth anti-microbial peptides
|
|
Shigella facts
|
nonmotile, does not make H2S, primary pathogen, but usually only in colon, ONLY in humans, most virulence factors are plasmid encoded (but Shiga toxin chromosomally encoded, shared via phage with EHEC and EIEC)
|
|
Salmonella facts
|
all make H2S except S. typhi, primary pathogen, S. typhi and S. paratyphi are ONLY in humans (the others are zoonotic)
|
|
Proteus: culture, dist. dz
|
swarms on blood agar plates, "ripples" on EMB plates, causes alkaline (pH>8) urine in UTIs (due to urease), opportunistic pathogen
|
|
Adhesins
|
macromolecule on cell envelope that helps adhere to host cells
|
|
Examples of adhesins
|
type 1 and 2 pili, F protein of Strep pyogenes, Filamentous hemagglutinin of Bordetella
|
|
Invasins
|
proteins that act locally to aid in the invasion of the host cell
|
|
Capsule type K1
|
E. coli's capsule, heavily sialylated (prevents activation of alternative complement pathway by binding factor H)
|
|
Toxin
|
poisonous substance produced by a microorganism
|
|
Toxin causing ETEC
|
LT (heat-labile) toxin, ST (heat-stable) toxin
|
|
Toxin causing EHEC
|
Shiga toxin
|
|
Toxin causing EIEC
|
Shiga toxin
|
|
Toxin causing Dysentery
|
Shiga toxin
|
|
ETEC, sx
|
Enterotoxigenic E. coli: traveler's diarrhea. decreased Na+ and Cl- reabsorption, increased Cl- and HCO3- secretion, Water diarrhea "rice water" resembling cholera
|
|
EHEC, sx
|
Enterohemorrhagic E. coli, inhibition of 60s ribosome inside intestinal epithelial cells kills them. Bloody diarrhea with severe ab cramps = "hemorrhagic colitis"
|
|
EIEC, sx
|
Enteroinvasive E. coli, inflammatory reaction- fever, bloody diarrhea with WBCs, resembles Shigellosis
|
|
LT
|
heat-labile toxin of E. coli, causing ETEC, plasmid-encoded, mechanism similar to cholera toxin, two-components (A and B, where B binds and A ADP ribosylates Galpha, destroying GTPase activity), causes continual secretion of Cl-, Na+ and H2O
|
|
Shiga toxin
|
employed by Shigella dysenterie, EHEC and EIEC, chromosomally encoded in Shigella, phage encoded in E. coli, two component cytotoxin, cleaves adenosine residue in 23S rRNA part of 60s ribosome (inhibits proteins synth-->death)
|
|
RTX = hemolysin
|
in some invasive E. coli, pore-forming protein, secreted by ABC transporter (ATP dependent), kills RBCs and phagocytic cells (increases virulence 100x)
|
|
Iron transporters
|
in some Enterobacteriaceae, Siderophores compete with iron binding proteins, then transport iron-siderophore complexes inside the cell by outer membrane receptors
|
|
Iron-binding proteins normally in human tissues and mucosal surfaces
|
Transferrin, lactoferrin, ferritin, myoglobin, hemoglobin.
|
|
Mechanisms for bacteria to obtain iron
|
1. stealing from transferrin/lactoferrin, 2. use broken down heme, 3. siderophores (ex. Enterobacteriaceae)
|
|
Culture properties shared by Campylobacter and Helicobacter
|
Fastidious and slow growing (requires specific conditions), Microaerophilic (5-10% oxyygen), Capnophilic (4-8% CO2), Peptone fermentation, CAN'T ferment carbohydrates, Oxidase +
|
|
Distinguish between Campylobacter jejuni and coli and all other species
|
Campylobacter jejuni and coli grow optimally at 42 degrees Celsius, resistance to cephalotoxin, sensitive to nalidixic acid, sensitive to complement lysis, (opposite for all others, including C. fetus)
|
|
Oxidase test
|
Add phenylethylene diamine dye, if it turns black, it contains cytochrome c oxidase in its electron transport chain
|
|
Dzs caused by Campylobacter jejuni and coli
|
Enteritis/diarrhea
|
|
Dzs caused by Campylobacter fetus
|
systemic infections in immunodeficient patients, abortions in sheep and cattle
|
|
Normal location of Campylobacter
|
GI flora of animals, esp. pigs and birds
|
|
Campylobacter transmission
|
contact with animals, eating contaminated food (esp. chicken b/c no air chilling involved in processing) or drinking contaminated water. NOT person to person
|
|
Does Campylobacter have a carrier state?
|
No
|
|
Who gets Campylobacter infections?
|
In developing countries, children get LOTS of infections. In developed countries, adults get it, and a severe case of it.
|
|
Who dies from Campylobacter infections?
|
Children and elderly
|
|
What meds increase chances of Campylobacter infection?
|
Antacids (anything that decreases gastric acid, because Campylobacters are sensitive to gastric acid).
|
|
What kind of diarrhea do Campylobacter jejuni and coli cause?
|
Bloody diarrhea of the jejunum, ileum and colon.
|
|
Time course of Campylobacter jejuni/coli infection (if sx)
|
First fever and HA, Then small amount of blood in diarrhea by 2nd/3rd day, end by 4-5 days
|
|
What is the gold standard for dx of Campylobacter diarrhea?
|
Culture (though this is difficult since it's microaerophilic and capnophilic!)
|
|
Campylobacter jejuni/coli tx
|
If any (self-limited), erythromycin and fluoroquinolones, because intrinsically resistant to trimethoprim and most beta lactams.
|
|
Mech for Campylobacter epithelial cell killing
|
cytotoxin = DNAse, breaks DNA and cell-cycle arrests
|
|
Normal colonization of Campylobacter fetus
|
GI flora of cattle and sheep
|
|
Best stain to visulaize H. pylori
|
Silver stain
|
|
What % of people have H. pylori?
|
50%
|
|
When is H. pylori acquired?
|
Usually childhood, lasts a lifetime.
|
|
Is H. pylori zoonotic?
|
No
|
|
Where does H. pylori reside?
|
Near but NOT INSIDE gastric epithelial cells and ectopic gastric mucosa (duodenal ulcers).
|
|
Can H.pylori occur without gastritis?
|
No, but the gastritis can be asx.
|
|
Dzs caused by H. pylori
|
Duodenal ulcer (#1), Gastric ulcer (#2 to aspirin), Gastric cancer, MALT lymphoma, chronic/acute antral/corpus gastritis
|
|
Antral gastritis is precursor to
|
duodenal ulcers
|
|
Corpus gastritis is precursor to
|
either gastric ulcers, gastric metaplasia and non-cardia gastric cancer
|
|
Is GERD associated with H. pylori?
|
No
|
|
True/False: H.pylori's genome is one of the most conserved known.
|
False, it is one of the most variable! Antibiotic resistance is common.
|
|
H. pylori virulence factors
|
surface urease, epithelial cell adhesins, Cag pathogenicity island (60% of strains), Vac (same strains as Cag+)
|
|
urease and how does it act as a virulence factor?
|
enzyme that splits urea into ammonia, on surface of H. pylori, protects from acid stress (urea channel is open at low pH, closes at neutral pH)
|
|
Cytokines/chemokines produced by H.pylori-infected tissue
|
IL-8 (attracts neutros, initiates TH1 inflammatory response), IL-1 (gastritis, gastric atrophy, gastric cancer)
|
|
Vac
|
vacuolating cytotoxin of H. pylori that disrupts cellular organelles
|
|
What type of ulcer is preventative of gastric cancer?
|
Duodenal ulcer
|
|
Gastric cancer is caused by
|
chronic inflammation due to H. pylori
|
|
H. pylori treatment can cure what cancer?
|
MALT lymphomas
|
|
Can duodenal ulcers be cured by antacids? Do they recur?
|
Yes, yes
|
|
Can duodenal ulcers be killed by anti-H.pylori meds? Do they recur?
|
Yes, No :)
|
|
CLO test
|
test for urease activity (cleaves urea to liberate ammonia) on antral biopsy obtained during endoscopy, dx for H. pylori infection
|
|
What dx H. pylori?
|
Urease positive by CLO test of antral biopsy obtained during endoscopy OR serology/urea breath test/stool antigen testing
|
|
Urea breath test
|
give patient labeled carbon isotope of urea by mouth, if H. pylori is present, tagged CO2 can be detected in breath samples
|
|
How long do anti-H.pylori IgG Abs persist after infection is eradicated?
|
6 months
|
|
H. pylori cure rates
|
90% on multiple drugs and prolonged therapy
|
|
Distinguish Pseudomonas from Enterobacteriaceae
|
Pseudomonas has polar flagella, Enterobacteriaceae have peritrichous flagella. Pseudomonas is oxidase positive, Pseudomonas can't ferment
|
|
Stenotrophomonas maltophilia properties
|
non-fermentative but oxidase negative Gram negative rod. Sensitive only to co-trimoxazole and tigecycline
|
|
Can Pseudomonas aeruginosa survive in anaerobic conditions?
|
Yes! Although it is an obligate respirer, it can use nitrate as a terminal electron acceptor.
|
|
Can Pseudomonads grow on minimal media?
|
Yes, they are nutritionally versatile.
|
|
Why is Pseudomonas aeruginosa so scary?
|
It's resistant to nearly everything and takes advantage of immunocompromised and burn patients.
|
|
Is Pseudomonas aeruginosa normal flora?
|
Yes, it is a minor component of bowel flora (but cannot ferment lactose, so it may come up on EMB and MacConkey agar).
|
|
Pseudomonas aeruginosa culture
|
hemolytic on BAP, extra-cellular pigments diffuse into agar, nutritionally versatile
|
|
Distinguish between Pseudomonas species
|
temperature tolerance and biochemical tests
|
|
Pseudomonas aeruginosa virulence factors
|
capsule: Alginate
binding proteins (fimbriae, pyochelin siderophore) Secreted toxins (endotoxin, exotoxin A and S, pyocins) Pigments (fluorescein, phenazines) Enzymes and Proteases (gelatinase, collagenase, lecithinase, neutral and alkaline protease, elastase, PLC, cytotoxin) |
|
Regulation of Pseudomonas aeruginosa virulence factors
|
Las R coordinates proteases, elastase and Exotoxin A, quorum sensing- When Las I is plentiful, it induces LasR
|
|
Do all Pseudomonas aeruginosa strains make Alginate constituitively?
|
No, only those strains associated with CF patients
|
|
Psuedomodad pigment fcn
|
toxic to WBC, antibiotic
|
|
When does Pseudomonad pigment production increase?
|
minimal media, low iron
|
|
Fluorescein (aka ___), properties
|
aka pyoverdin, yellow-green pigment, fluoresces with UV light
|
|
Phenazine pigments and colors
|
pyocyanin = blue green, pyorubin = rust brown, alpha-oxyphenazine = colorless, breakdown product of pyocyanin
|
|
Differences between Pseudomonas endotoxin and Enterobacteriaceae endotoxin
|
Pseudomonas endotoxin produces O side chains that are not attached to the core, and have Ca2+ pyrophosphate links that help make the outer membrane impenetrable (sometimes even to antibiotics)
|
|
Pyocins are...
|
bacteriocins that kill other Pseudomonads
|
|
Evidence for convergent evolution of Exotoxin A and diptheria toxin
|
not related immunologically and lack sequence homology, use different receptors, Exotoxin A activated by unfolding, diptheria toxin by cleavage, Diptheria toxin production localized to the throat
|
|
Pseudomonas enzymes and proteases
|
Gelatinase, Collagenase, Lecithinase, Neutral and alkaline protease, Elastase, PLC, Cytotoxin
|
|
Elastase
|
Pseudomonas enzyme
one of the nastiest in terms of damaging our bodies accounts for "vascular tropism" of Psuedomonas allows P. aeruginosa to cause ecthyma gangrenosum destroys blood vessel linings, implicated in hemorrhagic and necrotic lesions of the lung and skin |
|
Is Pseudomonas aeruginosa a primary pathogen?
|
No, it only causes dz in ppl with damaged defenses.
|
|
What dz does Pseudomonas aeruginosa cause in chronic lung dz patients?
|
Pneumonia, esp. after intubation
|
|
What dz can Pseudomonas aeruginosa cause in hospitalized pts?
|
UTI
|
|
What dz can Pseudomonas aeruginosa cause in IV drug users?
|
endocarditis
|
|
What dz can Pseudomonas aeruginosa cause in burn victims?
|
Infection of their burns
|
|
What dz can Pseudomonas aeruginosa cause in puncture wound patients?
|
Osteochondritis (#1 cause) or osteomyelitis.
|
|
What dz can Pseudomonas aeruginosa cause in CF patients and how?
|
Infection of the respiratory tract with inhibited ciliary clearance. Blocking Abs are made against alginate capsule, Only normal epithel cells (not CF cells) have the receptor to take up Pseudomonas and kill it.
|
|
Ecthyma gangrenosum
|
necrotic skin lesion in neutropenics caused by Pseudomonas aeruginosa, infection can progress to bloodstream, where elastase destroys vessel (vascular tropism) causing clotting, obstruction and necrosis.
|
|
infection can progress to bloodstream, where elastase destroys vessel (vascular tropism) causing clotting, obstruction and necrosis"
|
Ecthyma gangrenosum
|
|
What dz can Pseudomonas aeruginosa cause in contact lens-wearers?
|
Corneal infections
|
|
What dz can Pseudomonas aeruginosa cause in hot tub users?
|
What causes Hot tub folliculitis?
|
|
What causes Hot tub folliculitis?
|
What dz can Pseudomonas aeruginosa cause in hot tub users?
|
|
What causes external otitis?
|
Pseudomonas aeruginosa
|
|
What can external otitis lead to?
|
Osteomyelitis of the skull and involvement of cranial nerves (only in diabetics)
|
|
Malignant otitis externa
|
A Pseudomonas aeruginosa-mediated external otitis that progressed to osteomyelitis of the skull and cranial nerve involvement.
|
|
Burkholderias are in the same genus as
|
Pseudomonads
|
|
Dz caused by Burkholderia mallei
|
Glanders
|
|
Glanders is a dz obtained from..
|
Horses
|
|
Pneumonia, necrosis of mucous membranes, skin and lymphatics is called
|
glanders
|
|
Where is Burkholderia pseudomallei found?
|
tropical soil of Southeast Asia
|
|
When do meloidosis sx occur?
|
Burkholderia psuedomallei is dormant for years, then sx appear under stress
|
|
Burkholderia cepacia tx
|
piperacillin, 3rd gen CEPH, sometimes only polymyxins
|
|
What type of flagella does Burkholderia cepacia have?
|
Multitrichous polar flagella
|
|
Stenotrophomonas maltophilia tx
|
Trimethoprim/sulfamethoxazole (TMP/SMX)
|
|
Psuedomonas fluorescens transmission
|
infected blood transfusions and medications
|
|
Acinetobacter histo
|
Gram - (tho can be mistaken for + since it has a tendency to retain crystal violet), rods in log phase, coccobaccilary in stationary phase
|
|
Is Acinetobacter a primary pathogen?
|
No, it is an opportunistic, nosocomial pathogen.
|
|
Normal colonization of Acinetobacter
|
soil and water, skin and distal urethra of healthy ppl., (only Gram - part of normal skin flora)
|
|
Major Acinetobacter pathogen
|
Acinetobacter baumanii complex (80% of infections)
|
|
What type of flagella does Acinetobacter have?
|
None! It's nonmotile.
|
|
Acinetobacter virulence factors
|
Capsule (can give mucoid appearance, may predispose C' deficient people to infection), LPS, Bacteriocins
|
|
Acinetobacter resistance mechs
|
beta-lactamases, alterations of PCN-binding proteins and gyrase, loss of porins, efflux pump
|
|
Risk factors for Acinetobacter infection
|
severe illness, immunocompromised state, ICU extended stay, previous admin of 3rd gen CEPH, intubation, ventilator use, indwelling urinary catheter, neurosurgery
|
|
What color are Acinetobacter colonies?
|
Colorless, but may be mucoid
|
|
Are Acinetobacter nutritionally versatile?
|
Yes
|
|
Dzs caused by Acinetobacter
|
Pneumonia, Meningitis, Bacteremia, UTIs, wound infections, cellulitis
|
|
What pathogen causes nosocomial pneumonia associated with ventilators?
|
Acinetobacter
|
|
What % of patients with Acinetobacter bacteremia get septic shock?
|
30%
|
|
Enzymes that detox superoxide ion
|
superoxide dismutase, peroxidases, catalase
|
|
obligate anaerobes are normal inhabitants of..
|
mouth, vagina and intestines
|
|
dz caused by obligate anaerobes tends to involve
|
tissue injury and compromised vasculature
|
|
host defenses against anaerobic infection
|
increased redox potential (major), phagocytes (minor)
|
|
Anaerobic infection tx
|
metronidazole (must be reduced to become a DNA synthesis inhibitor)
|
|
What is the most prevalent bacteria in stool, AND cause of anaerobic infections?
|
Bacteroides, Bacteroides fragilis
|
|
What are the fermentation products of Bacteroides?
|
Acetate, propionate, succinate
|
|
Dz caused by Bacteroides fragilis
|
Diverticulitis, Septic abortion, Septic thrombosis, GI infections
|
|
Normal colonization of Bacteroides fragilis
|
Lower GI and vagina
|
|
Can Bacteroides fragilis grow in O2?
|
No, but it can survive O2 exposure.
|
|
What does Bacteroides fragilis produce?
|
Vitamin K
|
|
Prevotella melaninogenica histo
|
Gram - rod, grows black
|
|
Prevotella melaninogenica virulence factors
|
capsule, collagenase, leukocyte inhibitory factor, 10-25% are PCN-resistant
|
|
Fusobacterium histo
|
Gram - rods, pale-staining, slender with tapered ends
|
|
How does Bacteroides LPS compare to Enterobacteriaceae LPS?
|
Bacteroides' is much less virulent
|
|
Normal colonization of fusobacterium
|
oral cavity, GI and vagina
|
|
Fusobacterium virulence factors
|
very potent LPS, NO CAPSULE, necrophorum: hemolysin and leukocidin
|
|
What is the fermentation product of Fusobacterium?
|
butyric acid
|
|
Fusobacterium necrophorum histo
|
Gram - rods, broad, rounded ends with bulges in the middle of cells
|
|
Fusobacterium nucleatum histo
|
Gram - rod, thin pointed ends
|
|
Dz caused by Fusobacterium nucleatum
|
pulmonary infections
|
|
Normal colonization of Peptostreptococci
|
mouth and intestine
|
|
Dz caused by Peptostreptococci
|
Abscesses in brain, liver, breast and lung
|
|
Peptostreptococci histo
|
Gram + cocci, short chains, pairs or singly
|
|
Distinguish Actinomyces israelii and Nocardia (identical histo)
|
Nocardia is acid-fast, Actinomyces is anaerobic, Actinomyces is PCN sensitive
|
|
Dz caused by Actinomyces israelii
|
Actinomycosis: chronic eroding abscesses all over the body and burrowing through with NO regard for tissue planes
|
|
Normal colonization of Clostridium
|
GI tract, soil
|
|
Dz caused by Clostridium perfringens
|
Gas gangrene, Soft tissue infections, Food poisoning
|
|
Will Clostridium perfringens form spores on aritficial culture media?
|
No
|
|
Clostridium perfringens culture
|
double zone of hemolysis
|
|
Gas gangrene
|
caused by Clostridium perfringens, rapid infection of injured muscle, gas forms inside muscle tissue
|
|
What kind of spore does Clostridium perfringens make?
|
Subterminal spore
|
|
Alpha toxin
|
lecithinase, Ca2+ dependent PLC, strain A makes the most, causes lysis of RBCs and other cells, from Clostridium perfringens
|
|
What kind of spore does Clostridium difficile have?
|
Subterminal spore
|
|
C. difficile tx
|
oral vancomycin, metronidazole, STOP ANTIBIOTIC
|
|
Exotoxin A properties
|
from Pseudomonas aeruginosa (in low iron setting), chromosomally encoded, controlled by LasR, catalyzes ADP ribosylation of EF2, blocking host protein synth, activated by unfolding, convergent evolution with diptheria toxin
|
|
Tetanus toxin (aka tetanospasmin) properties
|
from Clostridium tetani
plasmid encoded metalloprotease reaches spinal cord and brains stem via retrograde axonal transport blocks neurotransmission by cleaving neuroexocytosis proteins inhibits inhibitory neurons Doesn't develop enough of an immune response to cause immunity |
|
Dz caused by Clostridium botulinum
|
Adult botulism (flaccid paralysis), Floppy baby syndrome, Wound botulism (usually drug associated)
|
|
Where is SPE-B encoded?
|
chromosomally encoded
|
|
Where is SPE-A encoded?
|
Lysogenic phage
|
|
Where is Shiga toxin encoded?
|
Chromosomally encoded in Shigella, phage encoded in E. coli
|
|
Where is BoNT encoded?
|
Phage
|
|
Where is ST encoded?
|
Plasmid
|
|
What shape is the EB of C. trachomatosis? C. psittaci? C pneumoniae?
|
round, round, pear-shaped
|
|
Who is the primary host of C. psittaci?
|
birds
|
|
Dz caused by C. psittaci
|
acute pneumoniae, endocarditis
|
|
Dz caused by C. pneumoniae
|
pneumonia, pharyngitis, bronchitis
|
|
Who is the primary host of C. trachomatis?
|
Humans
|
|
Why are Chlamydia considered parasites?
|
They can't make their own ATP so they are energy parasites and live intracellularly.
|
|
Life Cycle of Chlamydia
|
Elementary body (EB) passed extracellularly to new host cell, prevents fusion with lysosome, binary fisses with nucleus, replicates as Reticulate body (RB) and makes more EBs.
|
|
Chlamydia histo
|
Gram - (but no PDG), doesn't grow on culture unless inoculated into cells
|
|
Dz caused by Chlamydia trachomatis
|
Blindness (trachoma), Urethritis, Cervicitis, Salpingitis
|
|
Dx of Chlamydia trachomatis
|
direct fluorescent monoclonal anti-MOMP or anti-LPS Ab staining of genital exudates, OR nucleic acid hybridization techniques for asx female genital infections
|
|
Dx of Chlamydia psittaci and Lymphogranuloma Venereum (LGV)
|
complement fixation test to look for genus-specific LPS
|
|
Chlamydia trachomatis tx
|
long-acting azithromycin, >10 day macrolide or tetracycline
|
|
How are Chlamydia's biovars divided?
|
Based on target host cells
|
|
mech of Chlamydia trachomatis biovar trachoma
|
infects squamocolumnar epithelial cells of the eye and GU tract, causes conjunctivitis
|
|
Mech of Chlamydia trachomatis biovar lymphogranuloma venereum (LGV)
|
infects inguinal lymph nodes to cause LGV
|
|
What are serovars?
|
Subdivisions of biovars, equivalent to strains, based on different major outer membrane proteins (MOMP).
|
|
Which Chlamydia serovars cause chronic conjunctivitis?
|
A, B and C
|
|
Which Chlamydia serovars cause oculogenital dz?
|
D, E, F, G
|
|
Which Chlamydia serovars cause LGV?
|
L1, L2, L3
|
|
What is the leading cause of preventable blindness?
|
Trachoma caused by Chlamydia trachomatis
|
|
How is C. trachomatis spread?
|
common house fly and person to person
|
|
Pathology of trachoma
|
chronic follicular conjunctivitis due to Chlamydia trachomatis, progresses to scarring, eyelashes turn in and cause corneal scarring
|
|
Consequences of recurrent Chylamydia trachomatis infections in women's genitals
|
tubal scarring, ectopic pregnancy, infertility
|
|
Dz caused by Ureaplasma urealyticum
|
genitourinary infections (urethritis, epididymitis)
|
|
Dz caused by Mycoplasma hominis
|
genitourinary tract and nongenital infections (pyelonephritis, PID, post partum fever)
|
|
What surrounds the cytoplasm of Mycoplasma?
|
No PDG, just a 3 layered membrane
|
|
Can Mycoplasma grow on minimal media?
|
No, they have complex nutritional requirements and are dependent on external sources for nucleotides, AAs, fatty acids and sterols
|
|
What does Mycoplasma have in its membrane?
|
Sterols
|
|
Mycoplasma histo
|
Gram -, on artificial media, grow into "fried egg" colonies (hemadsorb and hemolyse RBCs)
|
|
Does PCN clear Mycoplasma infections?
|
No. They have no PDG cell wall and are inherently resistant to beta-lactam ABX
|
|
Dz caused by Mycoplasma pneumoniae
|
"walking" pneumonia
|
|
Mycoplasma pneumoniae transmission
|
droplets to the upper respiratory tract
|
|
If you find cold agglutinins in a pneumonia patients serum, what bacteria would you suspect?
|
Mycoplasma pneumoniae (though this test is not sensitive or specific)
|
|
Can you get recurrent infections of Chlamydia?
|
Yes, in fact, you will.
|
|
Can you get recurrent infections of Mycoplasma?
|
No, because there is no antigenic variation
|
|
Mycoplasma pneumonia tx
|
Erythromycin and doxycycline
|
|
Mech of Mycoplasma pneumoniae invasion
|
uses P1 adhesin to bind sialic acid on host respiratory tract cells, damages mucosa with hydrogen peroxide and superoxide, causes ciliastasis and epithelial necrosis
|
|
Extrapulmonary infestations of Mycoplasma pneumoniae
|
myocarditis, pericarditis, encephalitis, neuropathies, rashes, tender joints and muscles, polyarthritis
|
|
dx of Mycoplasma pneumoniae
|
Complement Fixation Test (measures early IgM and IgG), ELISA (measures IgM and IgG to P1 adhesin), Ag Capture Enzyme Immunoassay (Ag-EIA), PCR (detects genomic DNA)
|
|
Dz caused by Hib
|
meningitis, pneumonia, epiglottitis, septicemia
|
|
Dz caused NtHi
|
bronchitis/pneumonia, otitis media, sinusitis
|
|
Who gets H. flu infections?
|
Children <5 y.o. who have not been immunized
|
|
What does H. flu require for growth?
|
Media with X (hematin) and V (NAD)
|
|
H. flu histo
|
Gram - coccobacilli (small), pleomorphic rods
|
|
Does H. flu grow on chocolate agar?
|
Yes
|
|
Dz caused by H. ducreyi
|
Chancroid (STD)
|
|
What strain should you cross-streak on a blood agar plate to allow H. flu growth?
|
Staph aureus, to provide NAD (V factor)
|
|
H. flu virulence factors (5)
|
Capsule (PRP), IgA1 protease, LPS, Iron-acquiring outer membrane proteins, Pili/adhesins
|
|
H. flu capsule comp, types, most pathogenic, antigenic?
|
composed of polymers of PRP (polyribosyl ribitol phosphate), 6 serotypes, type b most pathogenic, antigenic (Abs are bacteriocidal) - only after child is 18months old
|
|
Hib vaccine, time course
|
PRP polymer conjugated to protein (to provoke a protective T-dependent response), 1st dose at 2 months, booster dose at 12-15 months
|
|
Hib vaccine Abs cross react with
|
E. coli K100
|
|
Dz caused by Bordetella pertussis
|
Whooping cough, Pertussis
|
|
Dz caused by Bordetella parapertussis
|
parapertussis (mild to severe respiratory disease)
|
|
Which is smaller, H. flu or B. pertussis?
|
B. pertussis is smaller.
|
|
Is H. flu PCN sensitive?
|
Usually yes but some strains have beta-lactamases
|
|
Bordetella pertussis histo
|
Gram - coccobacilli (small), Pleomorphic rods, "Bisected pearls" on Bordet-Gengou agar
|
|
Bordet-Gengou agar
|
will grow Bordetella pertussis, made of potato infusion, glucose, glycerol, peptones and 15-30% blood
|
|
Dist. H. flu and B. pertussis
|
Grow in anaerobic conditions, H. flu is a facultative anaerobe, B. pertussis is a strict aerobe
|
|
Bordetella pertussis transmission
|
droplets of resp. tract
|
|
Dz course of Pertussis
|
biphasic, catarrhal: colonization of resp. epithelium with local damage, paroxysmal: systemic intoxication, intense coughing, vomiting and convulsions
|
|
Is B. pertussis antigenic
|
Yes, survivors are immune
|
|
bvg controls what?
|
Bordetella virulence gene locus, controls Pertussis toxin, Adenylate cyclase/hemolysin, Pertactin, Filamentous hemagglutinin (FHA)
|
|
B. pertussis virulence factors
|
Filamentous hemagglutinin (FHA), Pertactin, Pili, Adenylate cyclase/hemolysin, Tracheal cytotoxin, Pertussis toxin, LOS (lipooligosaccharide)
|
|
Pertactin
|
69 kD outer membrane protein, Bordetella pertussis virulence factor
|
|
Tracheal cytotoxin
|
Bordetella pertussis virulence factor, tetrapeptide derived from PDG, causes ciliostasis, inhibits DNA synth and cell death
|
|
Pertussis toxin
|
Bordetella pertussis virulence factor, ADP ribosylates Gi, blocks its inhibition of AC, increased cAMP, inhibition of chemotaxis, and function of neutros, macrophages and lymphocytes
|
|
ABX only effective against Pertussis in what phase?
|
Catarrhal
|
|
Development of Pertussis vaccine
|
1st vaccine caused side effects, 2nd one was acellular but req'd 5 doses, recent one is 1 dose
|
|
Neisseria histo
|
Gram - cocci (diplococci), kidney bean shaped
|
|
What types of agar can you culture Neisseria on?
|
Chocolate agar, Thayer-martin
|
|
Why can you culture Neisseria on chocolate agar?
|
The heating released Hb, which binds FFAs. Neisseria cannot tolerate FFAs in media.
|
|
What temperature can you NOT grow Neisseria?
|
22 degrees
|
|
What is Thayer-Martin media?
|
chocolate agar plus vancomycin (to kill Gram +), colistin (to kill non-Neisseria Gram -), trimethoprim (broad spectrum antibiotic), nystatin (to kill yeast)
|
|
Are Neisseria susceptible to heat, cold or drying?
|
Yes to all 3
|
|
What % CO2 does Neisseria prefer?
|
4-8% CO2 (capnophilic)
|
|
Does Neisseria have cytochrome c?
|
Yes, oxidase +
|
|
What morphologically resembles Neisseria?
|
Moraxella, Acinetobacter, Veillonella
|
|
Is Neisseria gonorrhoeae glucose positive?
|
Yes
|
|
Is Neisseria gonorrhoeae maltose positive?
|
No
|
|
Is Neisseria meningitidis glucose positive?
|
Yes
|
|
Is Neisseria meningitidis maltose positive?
|
Yes
|
|
Dist. Neisseria gonorrhoeae and meningitidis
|
Neisseria meningitidis is maltose positive
|
|
Are Neisseria autolytic?
|
Yes, Neisseria is highly autolytic in stationary phase
|
|
Which Neisseria strain has a capsule, Class 4 surface protein, and porin serotyping Class 1, 2, etc.
|
Meningitis
|
|
Which Neisseria strain has antigenic pili and LOS, Rmp surface protein, and porins PorA and PorB
|
Gonorrhoeae
|
|
Neisseria virulence factors
|
IgA protease, pili, steals iron from transferrin, lactoferrin and Hb, LOS, porins
|
|
Neisseria meningitidis capsule
|
made mostly of sialic acid, antigenic
|
|
Rmp
|
Neisseria gonorrhoeae surface protein, elicits IgG blocking Ab response
|
|
Class 4 surface protein
|
Neisseria meningitidis virulence factor, elicits IgA blocking Abs
|
|
What kind of blocking Abs does each strain of Neisseria elicit?
|
N. meningitidis class 4 surface protein elicits IgA blocking Abs, N. gonorrhoeae Rmp elicits IgG blocking Abs
|
|
What kind of Ab is elicited by N. gonorrhoeae's LOS?
|
IgM
|
|
What does each of the Neisseria strains use for adherence?
|
N. meningitidis uses class 5 OM proteins (host cells and leuks), N. gonorrhoeae uses Opa "opacity" protein
|
|
Opa protein
|
"opacity proteins" from N. gonorrhoeae - makes colony opaque, antigenic variation, colonies lacking opa tend to be disseminated (DGI- disseminated gonococcal infections)
|
|
Where is cholera toxin encoded?
|
Lysogenic phage
|
|
Vibrio cholerae histo
|
Gram - rod, short, curved, motile
|
|
Mechanism of cholera toxin
|
enters via 5 B and 1 A subunit, ADP ribosylates G-alpha, blocking GTPase activity, INCREASE cAMP, Cl- leaves cell
|
|
Where are ST and LT encoded?
|
Plasmid
|
|
Mechanism of E. coli LT
|
enters cell via 5 B and 1 A subunit, ADP-ribosylates G-alpha, blocks GTPase activity, INCREASE cAMP, Cl- leaves the cell
|
|
Why is LT's effect smaller than Cholera toxin, despite 80% homology and identical mechanisms?
|
LT toxin is not secreted, and must be cleaved by host cell proteases to be activated
|
|
What causes traveler's diarrhea?
|
LT toxin of E. coli (ETEC)
|
|
Why do infants get more severe diarrhea with ST than adults?
|
They have more guanylin receptors.
|
|
Mech of Pertussis toxin
|
Identical to cholera toxin and LT , (ADP ribosylates G-alpha subunit, INCREASE cAMP), BUT it also secretes it's own AC (adenylate cyclase)
|
|
Where is pertussis toxin encoded?
|
Chromosomally encoded
|
|
How is the expression of pertussis toxin controlled?
|
bvg
|
|
Where is diptheria toxin encoded?
|
Lysogenic phage
|
|
What toxins are produced in response to iron restriction?
|
Exotoxin A (P. aeruginosa), Diptheria toxin (Corynebacterium diptheriae)
|
|
Mechanism of Diptheria toxin
|
Identical to Exotoxin A, enters cell by B and A subunits, catalyzes ADP-ribosylation of EF2, blocking protein synthesis
|
|
Dz caused by C. diptheria
|
throat infection- post. pharynx necrosis, heart failure (if absorbed systemically), wound infections
|
|
Dz caused by Neisseria meningitidis
|
Meningitis, Meningococcemia, Waterhouse-Friederichsen syndrome, Pneumonia (rare)
|
|
Risk factors for Neisseria meningitidis infection
|
Age (6-24 months and 10-20 years), Overcrowding, Winter or early Spring, C6, 7, 8 or MB-lectin deficiency
|
|
How is Neisseria meningitidis transmitted?
|
Nasal droplets
|
|
Neisseria meningitidis dx?
|
Gram stain of CSF, Culture of CSF, blood or skin lesions
|
|
Can serum kill Neisseria meningitidis?
|
No, because IgA blocking Ab to Class 4 surface protein, Sialic acid on capsule/LOS
|
|
Neisseria meningitidis vaccine
|
1) MPSV4 - 3-5yr. immunity to all strains except B (because not immunogenic), 2) MCV4 - should last longer
|
|
Neisseria meningitidis tx
|
high dose IV PCN or CEPH, Prophyllaxis with rifampin, adjunctive therapy with rBPI21
|
|
rBPI21
|
fragment of natural proteins from PMNs that bind LOS and kills Neisseria meningitidis, adjunctive therapy
|
|
Neisseria meningitidis Meningitis sx
|
brain damage (due to cytokines), potentially neuro deficits, SKIN LESIONS (petechiae-->necrotic, due to LOS)
|
|
Meningococcemia sx
|
low grade fever, skin lesions, arthritis, due to Neisseria meningitidis
|
|
Waterhouse-Friderichsen syndrome
|
bilateral hemorrhagic destruction of the adrenal glands, fulminating DIC, shock, due to Neisseria meningitidis
|
|
Dz caused by Neisseria gonorrhoeae
|
Men: urethritis, epididymitis, Women: cervicitis, salpingitis, PID
|
|
Risk factors for Neisseria gonorrhoeae infection
|
sexually active young adults, age 15-30yrs, C6, 7, 8 deficiency
|
|
All women with Gonorrhea show sx
|
No, only about 50% do!
|
|
All men with Gonorrhea show sx
|
Just about, 90% of urethritis has sx
|
|
Neisseria gonorrhoeae dx
|
men: Gram stain showing Neisseria gonorrhoeae in PMNs, women: culture of cervical pus
|
|
What Ab can kill Neisseria gonorrhoeae?
|
IgM
|
|
What Ab can kill Neisseria meningitidis?
|
IgG to capsule
|
|
Neisseria gonorrhoeae tx
|
Cephtriaxone (injectable CEPH), Cefixime PO, Quinolone if PCN-resistant due to plasmid beta-lactamase
|
|
Quellung reaction
|
method to type Pneumococcal capsule, mix unknown pnuemococcus with Abs against known capsule type, if swells --> + test, correct capsule type
|
|
Ziehl-Neelsen stain
|
Acid Fast stain (for Mycobacterium), HOT carbol fuscin, HCl and EtOH decolorize, methylene blue counterstain
|
|
Why doesn't Mycobacterium stain with Gram's stain?
|
It is acid-fast, cell envelope has mycolic acid, lipids and waxes
|
|
Kinyoun modification of Ziehl-Neelsen stain
|
dissolve carbol fuscin in phenol (no need for heat), Carbol fuscin in phenol, HCl and EtOH decolorize, methylene blue counterstain
|
|
Modified acid fast stain
|
Dist. Nocardia and Actinomyces: HOT carbol fuscin, sulfuric acid decolorize, methylene blue counterstain
|
|
What organism(s) have a long doubling time (and therefore a long log phase)?
|
Mycobacterium TB
|
|
What organism(s) have a short doubling time (and therefore a short log phase)?
|
E. coli
|
|
What organism(s) have a long stationary phase?
|
Staph aureus
|
|
What organism(s) have a short stationary phase?
|
Pneumococcus, Neisseria
|
|
Aerobactin
|
E. coli's siderophore
|
|
How does Bacteroides get iron?
|
from heme (once it's broken down)
|
|
Fermentation product of Streptococcus
|
lactic acid
|
|
Fermentation product of E. coli
|
mixed acids
|
|
Fermentation product of Clostridium
|
Butyric acid
|
|
What does E. coli have that Shigella doesn't
|
"peritrichous flagella
|
|
What must a cell have in order to respire?
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Electron transport chain and final electron acceptor (O2 or nitrate...)
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What uses fumarate as a terminal electron acceptor?
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Bacillus fragilis
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Island (as in pathogenicity island)
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Operon and additional genes
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Operon
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cluster of genes encoding enzymes in the same pathway
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episome
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nonessential DNA, either integrated in chromosome or free in cytoplasm (ex. F plasmid)
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Are insertion sequences capable of self-replication?
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No
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Do transposons require sequence homology?
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No
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Which strains are natural transformers?
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Pneumococcus, Neisseria, H. pylori, H. influenzae
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Superantigens
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TSST-1, Enterotoxin, Exfoliatins, SPEs
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Which bacteria cannot be cultured?
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Mycobacterium leprosae
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Where can Mycobacterium leprosae be grown?
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armadillos or mouse footpads
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What is optimal temp for Mycobacterium leprosae?
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lower than core body temp, grows best by surviving in macrophages and Schwann cells in skin and superficial nerves
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Where does Mycobacterium leprosae grow best in the infected body?
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In macrophages and Schwann cells in skin and superficial nerves
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What cell wall component is specific to Mycobacterium leprosae?
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PGL-1, M. leprae-specific phenolic glycolipid
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What cell wall component do Mycobacterium leprosae and tuberculosis share?
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LAM (lipoarabinomannan)
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What's Hansen's dz?
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Leprosy
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Incubation period for leprosy
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5-7 years
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How is M. leprosae transmitted?
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Household contact, maybe mosquito or bed bug bite
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What % of ppl infected with M.leprosae develop the dz?
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10%
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States with highest M. leprosae rates
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CA, TX, NY, HI (immigrants from endemic areas)
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Endemic leprosy areas
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India, China, Brazil, Nigeria
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|
Tuberculoid leprosy aka
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Paucibacillary dz (since few of the bacilli are found in skin cultures)
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Treatment for leprosy
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Dapsone, Rifampin with or without clofazimine
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Role of IFN-gamma in lepromatous granulomas
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secreted by CD4 cells to stimulate macrophages to contain M. leprae growth
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Role of IL-2 in lepromatous granulomas
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secreted by CD4 cells to recruit more CD4 cells
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Are CD8 cells present in a lepromatous granuloma?
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Yes, on the periphery
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Tuberculoid leprosy sx
|
anesthetic skin plaques, asymmetric peripheral nerve trunk involvement
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Which form of leprosy has a poor cell-mediated response?
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Lepromatous
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What is the role of CD8 cells in lepromatous leprosy?
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secrete cytokines that ENHANCE bacterial growth and inhibit CD4 function and expansion
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Which form of leprosy produces well-formed granulomas?
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Tuberculoid
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What is the role of IL-4 in lepromatous leprosy infection?
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secreted by CD8 cells, suppresses CD4 cell proliferation and function
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Lepromatous leprosy sx
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symmetric skin nodules, plaques, leonine (lion-like) facies, loss of eyelashes and body hair, loss of digits secondary to trauma, and testicular dysfcn (infertility)
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Which dz causes leonine facies?
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Lepromatous leprosy
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Where is Mycobacterium ulcerans endemic?
|
wetlands of tropical and subtropical Africa, Western Pacific, Asia and South America
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How is Mycobacterium ulcerans transmitted?
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Unknown
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What is the 3rd most common mycobacterial infection in immunocompromised ppl?
|
Buruli ulcer (m. ulcerans)
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What causes Buruli ulcer?
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M. ulcerans
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How long does it take a Buruli ulcer to develop?
|
1-2 months
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name the organism:single, small, painless, subq nodule on a limb expands to 15cm ulcerated nodule over months, with whole limb edema
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M. ulcerans
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What is a Buruli ulcer?
|
single, small, painless, subq nodule on a limb expands to 15cm ulcerated nodule over months, with whole limb edema
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Does a Buruli ulcer yield inflammatory infiltrate/pus?
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No!
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Tx for Buruli ulcer
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No antibiotics, wide surgical debridement (stop before greater disfiguring/deformity!)
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Which mycobacteria species are not in the Runyon grouping?
|
M. leprae and M. ulcerans
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