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274 Cards in this Set
- Front
- Back
which gram(+) rods produce spores?
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bacillus and clostridium
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which gram(+) rods are anaerobic? aerobic?
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bacillus are aerobic, clostridium are anaerobic
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club shaped morphology
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c.diphth
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loeffler's medium selects for ______
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selects for coryne. diphth
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tellurite plate test for which bacteria, mechanism and positive test result?
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tellurium salt is reduced to elemental tellurium by c.diphth. positive test = gray-black color
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metachromatic granules (Babes-Ernst granules), bacteria and which stain
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coryne. diphtheria, methylene blue
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pseudomembranes?
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coryne. diphtheria, c.diff
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clinical pictures of diphtheria?
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laryngitis, myocarditis, nerve weakness, cutaneous diphtheria (ulcerating skin lesions covered by a gray membrane, non-invasive)
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clinical pictures of listeria?
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meningitis in pregnant women, newborns, IC patients. GI from ingestion of raw milk, meat, veggies
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pathogenic factors for listeria?
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internalin binds to cadherin, listeriolysin allows escape from phagosome, actin rockets
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shows narrow zone of beta-hemolysis
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listeria
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shows double zone of hemolysis (which toxins are in each zone?)
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C.perf, alpha toxin outside and theta toxin inside
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2 bacteria that produce toxins that ADP-ribosylate, and what mechanism?
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B.cereus, diphtheria
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expresses hemolysin, DNase, hyaluronidase, collagenase?
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c.perf
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why hyperbaric O2 for c.perf?
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suppresses growth (c.perf is anaerobic) and encourages growth of new vessels in wound to improve phagocytic activity
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C.diff toxins do what to what molecule?
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toxin A and toxin B are both glucosyltransferases. they add glucose to G protein Rho GTPase. toxin B causes depolymerization of actin→loss of cell integrity and apoptosis
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clinical pictures of C.perf?
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gas gangrene (necrotizing fasciitis), alpha toxin produces gas in tissues, jaundice shock, death. food poisoning by enterotoxin action.
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C.perf normal flora of what body parts
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colon and vagina
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Naegler (egg yolk) test for which bacteria
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c.perfringens
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three superantigen enterotoxin producing bacteria?
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staph A, B.cereus, C.perf
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tennis racket
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C.tetani
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opisthotonos
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arching of back (from tetanus)
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8 antigenic types of this toxin, which are medically relevant
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botulinum (A, B, E most important)
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3 clinical pictures of botulism?
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canned food, wound botulism, infant botulism
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tetanus toxin has how many antigenic types?
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1
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anthrax toxins? what mechanisms?
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edema factor and lethal factor, both A-B. B unit is "protective antigen", forms pores in membrane allowing EF and LF to enter. EF A unit is an adenylate cyclase that ↑cAMP causing edema. LF is protease that cleaves phosphokinase activator of MAP kinase, inhibiting cell growth.
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clinical findings of anthrax?
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cutaneous anthrax: malignant pustule (painless ulcer with black eschar/scab) progressing to bacteremia. Pulmonary anthrax: RTI progressing to mediastinitis, pleural effusions, spetic shock. GI anthrax: vomiting, abd pain, bloody diarrhea
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reheated fried rice
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B.cereus
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alpha toxin
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C.perf. lecithinase activity.
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bacteria producing exotoxin A and B causing depolymerization of actin and death of enterocytes
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C.diff
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meningitis in newborns?
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listeria
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nonmotile?
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shigella
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motile?
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poly-d-glutamic acid capsule
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anthracis
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edema factor and lethal factor
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anthracis
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black eschar (painless scab with local edema)/malignant pustule, id and prognosis?
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anthracis, progress to bacteremia and death
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2 forms of food poisoning based on different toxins
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b.cereus, diarrheal by heat-labile enterotoxin, emetic by heat-stable enterotoxin
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gamma phage assay
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b.anthracis
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zoonotic viruses
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brucella x 4, c. jejuni, e.coli, francisella, pasteurella, salmonella, yersinia pestis, yersinia enterocolitica, bartonella x 2, anthrax, erysipelothrix, listeria
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V or L-shaped morphology
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c.diphth, listeria
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tumbling movement
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listeria
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blocks GABA/glycine release
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tetanospasmin
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blocks Ach release
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botulinum toxin
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protective antigen
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bacillus anthracis B-subunit
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protease that cleaves MAPK activator
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LF
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ADP-ribosylates EF2
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diphtheria toxin
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host cell receptor for diphtheria toxin
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HB-EGF (abundant on heart and nerve cells)
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elek test
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3 strips (+ control, patient's, - control) with an antitoxin strip
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lab dx of listeria?
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gram+ rods forming small, gray colonies with narrow zone of beta-hemolysis. tumbling MOTILITY (as opposed to corynebacteria)
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traveler's diarrhea and ROT
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ETEC, fecal-oral
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undercooked meat
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EHEC
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neonatal meningitis
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e.coli (also GBS)
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e.coli adhesin
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pili
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e.coli enterotoxins and mechanisms
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heat-labile toxin (LT): stimulate adenylate cyclase→PK phos ion transporters→diarrhea. heat-stable toxin (ST) stim guanylate cyclase→reduced ability to reabsorb sodium ions
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e.coli exotoxin mechanism
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A-B protein. removes adenine from 28S rRNA, CPE could lead to HUS
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UTI e.coli adhesin binding site
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gal-gal dimer, aids in ascension through urinary tract
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laboratory diagnosis of e.coli
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pink on MacConkey's. green on EMB. produces indole from try, decarboxylates lysine, uses acetate as carbon source, and is motile. EHEC does not ferment sorbitol
|
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does ETEC ferment sorbitol? does EHEC?
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ETEC sorbitol+, EHEC sorbitol-
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tx e.coli?
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UTI: ampicillin or trimethoprim. sepsis: cephalosporin (cefotaxime) w/ aminoglycoside. neonat meningitis: amp + cefotaxime. diarrhea: imodium or trimethoprim.
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contents of MacConkey's agar?
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lactose, pH indicator, crystal violet (inhibit gram+), bile salts inhibit commensals.
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lactose fermenters
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enterobacter, e.coli, klebsiella
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non-lactose fermenters
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proteus, salmonella, shigella, yersinia
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EMB agar
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selects against gram+ and differentiates lactose fermenation (green sheen by e.coli)
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TCBS agar selects for ______
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selects within vibrio because of 8.6 pH. then differentiates based on sucrose: cholera (sucrose+ = yellow) from parahaemolyticus and vulnificus (sucrose- = green)
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which vibrio grows in 1% and which in 8% NaCl
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parahaemo grows in in 8%
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CAMPY agar
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selective for campylobacter→jejuni if also susceptible to nalidixic acid and resistant to cephalothin.
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|
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is EHEC invasive? PMNs in stools?
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not invasive thus minimal PMNs
|
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methylene blue stain of fecal sample for what reason? which bacteria are positive?
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presence of neutrophils; bacteria is invasive: shigella, salmonella, campylobacter. non-invasive (rather, toxin-producing): v.cholera, e.coli, c.perf.
|
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pathogenesis for shigella? factors?
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must invade through M-cells first using outer membrane protein IPA (invasion plasmid antigens). once inside, escape vacuoles and use actin-based motility to navigate cytoplasm (like listeria). invasion of adjacent lamina propria, then basal surface of epithelials. inflammation→tight junction loosening→further pathogenesis. bloody diarrhea. also shiga toxin.
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rose spots
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salmonella typhi
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causes sequela esp. with concurrent disease i.e. osteomyelitis, pneumonia, meningitis
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salmonella septicemia
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likes to infect vascular grafts and site of previously damaged tissue (sites of infarcts, aneurysms)
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salmonella septicemia
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virulence factor
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salmonella typhi
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TSI results for salmonella?
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alkaline slant, acid butt, gas+, H2S+. salmonella typhi is exception with no gas and little H2S. alkaline b/c lactose- glucose+.
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pathogenesis for salmonella?
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fimbriae encoded on plasmids attach to microvilli. pathogen-directed endocytosis. ruffled membranes due to salmonella-induced alteration of cell signal transduction. effector molecules injected through Type III secretion encoded on pathogenicity island 1 (SPI-1). effect is to inh phagosome-lysosme fusion. multiplies in vacuole. translocates to basal side, exocytosis into lamina propria. survival/growth in macrophages. possible bacteremia. eventually inflammatory response is protective (responsible for the inflammatory diarrhea and mild fever). phase variation of h antigen.
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typhoid fever
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salmonella typhi. primary asymptomatic bacteremia. secondary lasts 4-8 weeks long with fever, chills, headache, muscle pain. carriage in gall bladder by biofilm formation on gallstones.
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tx typhoid fever/septicemia/metastatic infection?
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ceftriaxone or ciprofloxacin. amp on carriers
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comma shaped
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vibrio, campylobacter, helicobacter
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sensitive to stomach acid
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salmonella, vib cholera
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salmonella that cause endocarditis?
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s.cholerasuis, s.typhimurium
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vaccines for salmonella?
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Vi capsule, live attenuated, and conjugated Vi for childrren.
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mucinase
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vibrio cholera, clears glycoprotein covering of intestinal cells for adherence.
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cholera enterotoxin
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choleragen: A-B protein. B binds to GM1 ganglioside. A-unit ADP-riboslyates adenylate cyclase, phos of membrane transporters causes watery diarrhea with NO neutrophils/RBCs. gene on CTX bacteriophage.
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cholera pili important for…
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adherence to gut, receptor for CTX bacteriophage
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rice water stool
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vib cholera
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lab dx of cholera
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lactose-, oxidase+ (distinguishes from all enterobacteria), sucrose+ so acid/acid on TSI. O1 ab
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Tcp A
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toxin coregulated pili (adheres to gut). regulated by same system that governs toxin production.
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MOT of vib parahaemolyticus?
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ingestion of raw/undercooked seafood
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distinguishing dx of vib parahaemolyticus?
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8% NaCl
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sx of vib parahaemolyticus?
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mild to severe watery diarrhea, vomiting, abd cramps, fever, lasting about 3 days.
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vib vulnificus clinical picture?
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cellulitis, bullae esp. in shellfish handlers with skin wounds. septicemia in IC people eating raw shellfish.
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liver damage predisposes to _______
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vib vulnificus
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causes guillain barre
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campylobacter jejuni
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microaerophilic (5%)
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campylobacter
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further classification of vibrio cholera?
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all vib cholera has O1. among O1 are Classical and El Tor (responsible for epidemics and higher asymptomatic carrier rates)
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reactive arthritis/reiter's syndrome
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campylobacter. large joint arthritis (knee/back) w/ relative sparing of small joints. dysuria and eye involvement as well.
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lab dx of camp. jejuni?
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failure to grow at 25% O2, oxidase+, sensitivity to nalidixic acid.
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peptic ulcers
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helicobacter pylori. risk factor for MALT lymphomas
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differences between helico and camp pylori?
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h.pylori is urease+
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MOT of c.pylori?
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domestic animals, fecal-oral. young puppy with diarrhea
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MALT lymphoma? mechanism?
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h.pylori chronic inflammation leading to B-cell prolif and eventually lymphoma
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pathogenesis of h.pylori?
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attach to mucus-secreting cells of gastric mucosa. urease creates ammonia, damaging mucus layer. neutralization of stomach acid makes better growing environment but inflames stomach. no bacteremia.
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urea breath test
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radioactive urea ingested and cleaved by urease leading to radiolabeled CO2 breath
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causes primary (asymptomatic) and secondary bacteremia
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salmonella typhi (typhoid fever)
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gal-gal dimers
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e.coli pilin binding site (UTI strains)
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red pigmented colonies
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serratia marcescens
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bacteria that has large polysacch capsule giving its colonies a mucoid appearance
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klebsiella pneumoniae
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swarming effect on agar
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PPM group (particularly proteus)
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struvite
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caused by urea producing PPM, damages urinary epithelium, obstructs urine flow, serves as "nidus" for other bacteria
|
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e.coli pathogenic factors
|
pili, capsule, endotoxin, three exotoxins (LT, ST, shiga toxin)
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GM1 ganglioside
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receptor for binding of ETEC LT and ctx toxin
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starts off as foul-smelling, watery diarrhea into bloody diarrhea
|
c.jejuni
|
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sensitive to nalidixic acid
|
c.jejuni
|
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4 characteristics of all enterobacteriaceae
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facultative anaerobes, glucose+, cytochrome oxidase-, reduce nitrates to nitrites (as part of energy production)
|
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causes reiter's syndrome complications
|
salmonella, campylobacter, yersinia
|
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toxins increase cAMP
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EF, ctx, e.coli LT, pertussis toxin, adenlyate cyclase
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location of mucin
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small intestine
|
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bacteriocin
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inhibitory substances secreted by normal flora
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O, H, and K antigens are what and help to classify what family
|
O=outer polysaccharide, H=pili, K=capsular. helps identify enterobacteriaceae
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fluoresces yellow-green under UV light
|
pyoverdin produced by pseudomonas
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biochem differences of pseudomonas from enterobacteriaceae
|
oxidase+, non-fermenter (strict aerobe)
|
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clinical pictures of pseudomonas
|
sepsis, pneumonia, UTI in IC patients, chronic LRT in patients with CF, cellulitis in burn patients, otitis externa in diabetic patients
|
|
mucoid isolates from CF patients
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pseudomonas, klebs??
|
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pseudomonas is normal flora of _____
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colon, skin (moist areas), URT in hospitalized patients
|
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can grow in antiseptics and low nutrient environments (distilled, tap water)
|
pseudomonas
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pseudomonas virulence factors
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endotoxin, exotoxin A, elastase, proteases, pyocyanin, sec III system
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exotoxin A action and mechanism
|
tissue necrosis by ADP-ribosylation of EF2 (same as diphtheria toxin)
|
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damages cilia and mucosal cells in resp tract
|
pyocyanin
|
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pseudomonas sec system and purpose
|
sec III, injects toxins (namely ExoS) directly into cell
|
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Exo S
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ADP-ribosylates a Ras protein, damaging cytoskeleton
|
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ecthyma gangrenosum
|
bacteremic pseudomonas spreading to skin, causing black, necrotic lesions (sign of high mortality)
|
|
underchlorinated pools/hot tubs
|
pseudomonas
|
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puncture wounds in shoe soles causing osteochondritis
|
pseudomonas
|
|
dirty contact lenses causing corneal infection
|
pseudomonas
|
|
biochem dx of pse. aeruginosa
|
lactose-, oxidase+, metallic sheen on TSI agar with blue-green pigment on ordinary agar (and fruity aroma)
|
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tx for pseudomonas
|
high resistance, so antipseudomonal penicillin + aminoglycoside
|
|
common agent of acute epiglottitis
|
hib
|
|
polyribitol phosphate capsule
|
haemophilus influenza
|
|
IgA protease
|
hib
|
|
only toxin produced by haemophilus influenza
|
endotoxin
|
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most common cause of meningitis in children 2 months to 5 years old until vaccine development
|
hib
|
|
epidemiological concern with hib vaccine success?
|
appearance of nonencapsulated strains including aegyptius, ducreyi, aphrophilus
|
|
hib conjugate vaccine target, mechanism?
|
capsular PRP antigen, activates TI-2
|
|
name 4 species of haemophilus, diseases caused, and growth factors
|
influenzae causing URT/sepsis in children and pneumonia in adults (X and V), aegyptius causing acute purulent conjunctivitis (X and V), ducreyi causing STD chancroid disease (X), aphrophilus causing subacute endocarditis with heart valve damage (neither X/V)
|
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septic arthritis, cellulitis, sepsis
|
haemophilus influenza
|
|
lab dx of haemophilus?
|
chocolate agar with X and V or tests to detect capsule
|
|
tx for haemophilus
|
high resistance (beta-lactamase), ceftriaxone
|
|
morphology of bordetella
|
coccobacillary, encapsulated gram- rod
|
|
attacks ciliated epithelium leading to severe coughing episodes
|
bordetella p.
|
|
path. factors for bord. p?
|
filamentous hemagglutinin (adhesin), pertussis toxin (ADP-ribsolyte Gi protein), adenylate cyclase, tracheal cytotoxin (bacterial peptidoglycan fragment, induces NO production to kill ciliated cells)
|
|
produces lymphocytosis in pertussis. how?
|
pertussis toxin. inhibits transduction by chemokine receptors → lymphocytes cannot enter lymphoid tissue
|
|
whooping cough lasting 1-4 weeks in children, months in adults
|
bordetella pertussis
|
|
isolate from nasopharyngeal swabs during paroxysmal stage, grow on Bordet-Gengou medium
|
bordetella pertussis (Bordet-Gengou contains high % of blood to inactivate inhibitors)
|
|
highest period of risk for spread of bord.p?
|
catarrhal stage (prodromal symptoms)
|
|
toxin that inhibits neutrophil activation and chemokine signaling. also acts as T lymphocyte mitogen
|
pertussis toxin. ADP-ribosylation of Gi
|
|
toxin internalized by PMNs disrupting PMN oxidative funciton. needs which activator?
|
adenylate cyclase, requires calmodulin
|
|
BvgA, BvgS responsive to what factors? belongs to which bacteria?
|
environmental signals like Mg, sulfate ion conc., temperature. bord.p
|
|
name 5 2-component regulatory systems
|
sarA/agr, VanS/VanR, PilS/PilR, PhoP/PhoQ
|
|
components of aPertussis vaccine?
|
Fha, pertussis toxoid, fimbriae, pertactin
|
|
name the events in formation of legionella phagosome
|
pseudopod coiling, surround by smooth vesicles from vacuolar membrane, surround by mitoch., assc. of ribosomes, multiplication and then rupture
|
|
requires iron and cysteine to grow
|
legionella
|
|
hot tubs and other water sources
|
legionella
|
|
only virulence factor from legionella
|
endotoxin
|
|
do secondary cases of legionella occur?
|
no
|
|
mental confusion, nonbloody diarrhea, proteinuria, hematuria, hyponatremia
|
legionella
|
|
charcoal-yeast agar
|
medium supplemented with iron and cysteine (selects for legionella)
|
|
tx legionella
|
erythromycin
|
|
pseudomonas iron scavenger, competes with transferrin
|
siderophore
|
|
purpose of elastase, exotoxinA in pseudomonas
|
damages tissue, releasing iron
|
|
response to low phosphate in pseudomonas
|
phospholipaseC
|
|
causes pulmonary infection in CF patients, why?
|
pseudomonas, core polysaccharide adheres to chloride channel protein in CF patients
|
|
pseudomonas virulence factors
|
core polysachh of LPS, glycocalyx (alginate biofilm)
|
|
pseudomonas pigment, damages cilia/mucosal cells
|
pyocyanin
|
|
cellulitis in burn patients
|
pseudomonas
|
|
malignant otitis externa in diabetics
|
pseudomonas
|
|
able to grow in distilled water and disinfectants
|
pseudomonas
|
|
blue-green color in agar
|
pseudomonas
|
|
turns pus in a wound blue
|
pyocyanin produced by pseudomonas
|
|
fluoresces yellow-green under UV light
|
pyoverdin produced by pseudomonas
|
|
biochem differences of pseudomonas from enterobacteriaceae
|
oxidase+, non-fermenter (strict aerobe)
|
|
clinical pictures of pseudomonas
|
sepsis, pneumonia, UTI in IC patients, chronic LRT in patients with CF, cellulitis in burn patients, otitis externa in diabetic patients
|
|
mucoid isolates from CF patients
|
pseudomonas, klebs??
|
|
pseudomonas is normal flora of _____
|
colon, skin (moist areas), URT in hospitalized patients
|
|
can grow in antiseptics and low nutrient environments (distilled, tap water)
|
pseudomonas
|
|
pseudomonas virulence factors
|
endotoxin, exotoxin A, elastase, proteases, pyocyanin, sec III system
|
|
exotoxin A action and mechanism
|
tissue necrosis by ADP-ribosylation of EF2 (same as diphtheria toxin)
|
|
damages cilia and mucosal cells in resp tract
|
pyocyanin
|
|
pseudomonas sec system and purpose
|
sec III, injects toxins (namely ExoS) directly into cell
|
|
Exo S
|
ADP-ribosylates a Ras protein, damaging cytoskeleton
|
|
ecthyma gangrenosum
|
bacteremic pseudomonas spreading to skin, causing black, necrotic lesions (sign of high mortality)
|
|
underchlorinated pools/hot tubs
|
pseudomonas
|
|
puncture wounds in shoe soles causing osteochondritis
|
pseudomonas
|
|
dirty contact lenses causing corneal infection
|
pseudomonas
|
|
biochem dx of pse. aeruginosa
|
lactose-, oxidase+, metallic sheen on TSI agar with blue-green pigment on ordinary agar (and fruity aroma)
|
|
tx for pseudomonas
|
high resistance, so antipseudomonal penicillin + aminoglycoside
|
|
myelitis
|
spinal cord tissue
|
|
entryways into CNS
|
circulation, olfactory nerve, peripheral nerves, choroid plexus
|
|
bacterial meningitis in infants (<2 months)
|
GBS, E.coli (K1), listeria
|
|
causes of bacterial meningitis in childhood (CA)
|
meningococcus, pneumococcus, hib
|
|
bacterial meningitis in adults (CA)
|
meningococcus, pneumococcus, listeria
|
|
nosocomial bacterial meningitis
|
e.coli, pseudomonas, klebs, streps, staphA, staphE
|
|
what do GBS and K1 e.coli have in common?
|
sialic acid capsules
|
|
cat scratch disease
|
bartonella henselae
|
|
bacillary angiomatosis
|
bartonella henselae, bartonella quintana
|
|
trench fever
|
bartonella quintana
|
|
human body louse
|
bartonella quintana
|
|
cat reservoir
|
bartonella henselae
|
|
undulating fever? why?
|
brucella. localizes in small granulomas in lymphoid tissue, then periodically release into blood
|
|
name 4 brucellas and their reservoirs
|
melitensis (goats/sheep), abortus (cattle), suis (swine), canis (dogs)
|
|
adenopathy of nodes surrounding site of entry
|
francisella tularensis
|
|
infected rabbits, ticks/mites/lice
|
francisella tularensis
|
|
yersinia virulence factors
|
yad adhesin, yops, Fra1 protein capsule, pla protease (plasminogen activation), LPS, iron-acquisition systems, endotoxin, V and W antigens
|
|
Yersinia pla purpose?
|
degrades fibrin clots, and c3b/c5a
|
|
name two epidemiologic forms of yersinia p.
|
urban, sylvatic
|
|
bipolar staining
|
yersinia pestis, pasteurella
|
|
yops purpose?
|
inhibit phagocytosis and cytokine production. i.e. YopJ protease cleaves two proteins required for TNF synthesis
|
|
giemsa/wayson stain
|
plague
|
|
tx plague
|
streptomycin/tetracycline
|
|
cat and dog bites? sutures?
|
pasteurella
|
|
tx pasteurella
|
penG
|
|
erysipelothrix reservoir
|
meat/fish, causes eryseipelas
|
|
notable distinguishing characteristics of mycobacteria
|
obligate aerobes, non-motile, non-spore forming, non-toxin producing, acid fast, grows extremely slowly, resistent to chemicals (acids/bases) and dehydration, niacin+, catalase+
|
|
Lowenstein-Jensen medium
|
contains complex nutrients (egg yolk) and malachite green dye (inhibits normal flora in sputum)
|
|
components of mycobacteria cell wall
|
mycolic acid (long chain FA), wax D, phosphatides (play role in caseation necrosis)
|
|
correlated to high virulence in tuberculosis
|
production of cord factor and cell wall component called phthiocerol dimycocerosate
|
|
antibiotic genes on M. tuberculosis located where?
|
chromosome
|
|
mechanism of KatG mutation
|
mutates catalase-peroxidase that activates INH
|
|
definition of MDR?
|
resistant to at least INH and rifampin
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acute inflammatory response in the lungs at site of initial infection, M. tuberculosis
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exudative lesion
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GI tuberculosis associated with ________
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cow's milk
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M. tuberculosis mechanism of survival in phagosomes
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inhibition of: phagosome-lysosome fusion, oxidative burst, acidification of phagosome, inhibitory cytokine responses
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protein inhibiting phagosome-lysosome fusion
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exported reptitive protein
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giant cells containing tubercle bacilli surrounded by epithelioid cells
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granulomatous lesion
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Langhan's giant cells
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contain tubercle bacilli
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tubercle
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granuloma surrounded by fibrous tissue that has undergone central caseation necrosis. heals by fibrosis and calcification
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Ghon complex
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single parenchymal lesion and caseation resulting in calcified bronchial lymph nodes (visible on X-ray)
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miliary tuberculosis
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dissemination of tuberculosis, causing hepatosplenomegaly, organ dysfunction, adrenal insufficiency, meningitis, osteomyelitis. IC patients predisposed. millet seed x-ray of lungs
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point mutations responsible for tuberculosis drug resistances
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antibiotic receptors, drug activator molecules (KatG)
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immunity involved in M. tuberculosis infection
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cellular (macrophages and Th1 helper T cells)
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NRAMP protein
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located in membrane of phagosome in macrophages, mutations = high rate of tuberculosis
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scrofula
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mycobacterial cervical adenitis (swollen but nontender)
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non-respiratory forms of tuberculosis
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GI, renal, oropharyngeal
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erythema nodosum
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tender lymph nodes along leg representing active cell-mediated immunity response. tuberculosis and leprae.
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auramine-rhodamine stain
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makes mycobacteria fluoresce yellow-orange
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common acid-fast stain for mycobacteria
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Kinyoun's acid-fast stain with carbolfuchsin
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niacin test
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M. tuberculosis lacks niacin ribonucleotide enzyme so free niacin react with cyanogen bromide to form yellow compound.
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BACTEC medium
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medium with radioactive metabolites. more sensitive for mycobacteria.
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luciferase assay
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detects presence of ATP with flashes of light
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IFN-gamma release assay or Quantiferon-TB
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expose blood cells to tub. antigen and measure IFN-gamma release.
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BCG vaccine significance
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can result in false positive in PPD. contains attenuated M.bovis Calmette-Guerin. Suppresses tuberculosis disease but not infection.
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optimal growing temperature for M.leprae and significance?
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30degC, grows on skin and superficial nerves.
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MOT for leprosy?
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nasal secretions, skin lesions
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site of replication for leprosy?
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skin histiocytes, endothelial cells, Schwann cells
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forms granulomas
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brucella, francisella, mycobacteria tuberculosis, tuberculoid leprosy
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tuberculoid leprosy characteristics
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infection limited by CMI. few acid-fast bacilli seen. granulomas. lepromin skin test+
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lepromatous leprosy characteristics
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poor CMI response. large numbers of organisms in skin/mucous membranes. foamy histiocytes rather than granulomas. negative lepromin.
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disfiguring appearance of leprosy is from what?
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skin anesthesia, resorption of bone, thickening/folding of skin due to infiltration
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foam cells
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lipid-laden macrophages. tuberculoid leprosy
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tx leprosy
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dapsone
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very small, walless bacteria with sterols in membrane
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mycoplasma
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fried egg colony
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mycoplasma
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SP4 blood agar
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contains several lipids including sterols that allow mycoplasma growth
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shape of mycoplasma? why?
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pleomorphic, lack cell wall, very flexible membrane
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rod-shaped with tapered tip containing proteins? what do the proteins do?
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mycoplasma pneumoniae. proteins serve as attachment point to resp epithelium.
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pathogenesis of m. pneumoniae?
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inhibits ciliary motion, necrosis of epithelium
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m. pneumonia produces what molecule?
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hydrogen peroxide
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cold agglutinins
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autoantibodies produced during infection by m.pneumoniae against RBCs, brain, lung, liver cells. can be used in serologic testing; agglutinates cells at 4degC but not 37degC
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most common type of atypical pneumonia
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mycoplasma pneumoniae
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extrapulmonary manifestations of m.pneumoniae
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stevens-johnson syndrome, erythema multiforme, raynaud's, cardiac arrythmia, arthralgia, hemolytic anemia, GBS
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main lab dx
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serologic testing. cold agglutinin titer of 1:128 or higher but half patients will have false negatives. false positives during flu and adenovirus infections. ab titer in complement fixation test.
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what can you NOT treat m.pneumoniae with? why?
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penicillin, cephalosporins (no cell wall)
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tx for m.pneumoniae and m.hominis?
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tetracycline for both pneumoniae and hominis; erythromycin for m.pneumoniae
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diseases caused by m.hominis and ureaplasma?
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hominis: pelvic inflammatory disease. ureaplasma: urethritis. both cause inflammation of chorioamniotis and postpartum fever and are isolated from fetal CSF (transferred during pregnancy and/or childbirth)
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