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| enterobacteriaceae-gram stain | gram negative bacilli (rods)
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| Enterobacteriaceae-characteristics | non-spore forming, ferment glucose (make acid or acid/gas like H2S), some motile, cytochrome oxidase (-), catalase (+); able to reduce nitrates to nitrites
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| Enterobacteriaceae-motility | if motile, move by peritrichous flagella
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| enteric bacilli | bacilli of GI tract (Enterobacteriaceae + Gram-negative vibrios)
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| opportunistic pathogens, Enterobaceteriaceae | normal flora, wrong location/overabundance (E. coli)
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| frank pathogens, Enterobacteriaceae | presence in any amount=disease (Salmonella, Shigella)
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| Escherichia-diseases | UTI, gastroenteritis, meningitis, septicemia, hemorrhagic colitis
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| Shigella-disease | Bacillary dysentery
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| Salmonella-disease | Gastroenteritis, septicemia, enteric fevers (typhoid)
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| Klebsiella-disease | pneumonia, UTI
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| Yersinia-disease | Gastroenteritis, plague, zoonotic (animal to human) infection
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| biochemical identification of species | serotyping-identification by surface antigens
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| Serotyping-Antigens used | somatic cell wall antigens (O), flagellar antigens (H), capsular antigens (K)
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| MacConkey isolation-Enterobacteriaceae | yes (lactose-fermenting): E. coli, Klebsiella; no (non lactose-fermenting): Salmonella, Shigella
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| Enterobacteriaceae-lactose | coliforms (lactose fermenters-rapid, 24h fermentation) vs. non-lactose fermenters
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| Gastroenteritis | caused by coliforms & non-lactose fermenting Enterobacteriaceae
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| E. coli, lactose | most sensitive coliform; sensitive indicator of water contamination
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| virulence factors | endotoxin, capsule, phase variation, exotoxins, adhesion factors, growth factors, resistance to serum, antibiotic resistant plasmids
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| Endotoxin | virulence factor, common to all Enterobacteriaceae; lipid A part of O Ag; fncs in vascular, metabolic, pyrogenic, hematological alterations (severe Gram - infections)
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| capsule | protects against phagocytosis, obscures cell wall Ags; characteristic of Klebsiella pneumonia=mucoid colonies (non-motile, community-acquired pneumonia)
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| phase variation | alternate expression of diff forms of protein (epsecially K&H Ags and pili=2 diff genes for flagellin)
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| exotoxins | secreted toxins; 4 types: enterotoxins (heat-labile & heat-stable), cytotoxins (shiga toxin & hemolysins)
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| Enterotoxins | cause changes in ion absorption/balance of H2O transport in GI tract
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| Heat-labile enterotoxin | similar to cholera toxin in Vibrio-increases cAMP
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| Heat-stable enterotoxin | increases cGMP
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| shiga toxin | neurotoxic, enterotoxic, cytotoxic; inhibits 60S ribosomes (blocks translation)
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| hemolysins | cause lysis of blood cells, free up iron (captured by siderophores)
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| adhesion factors | pili (finbria); P&S fimbriae (both in E. coli)
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| P fimbriae | uropathogenesis (UTIs)
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| S fimbriae | neonatal sepsis, meningitis
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| phase variation | alternate expression of diff forms of protein (epsecially K&H Ags and pili=2 diff genes for flagellin)
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| exotoxins | secreted toxins; 4 types: enterotoxins (heat-labile & heat-stable), cytotoxins (shiga toxin & hemolysins)
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| Enterotoxins | cause changes in ion absorption/balance of H2O transport in GI tract
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| Heat-labile enterotoxin | similar to cholera toxin in Vibrio-increases cAMP
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| Heat-stable enterotoxin | increases cGMP
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| shiga toxin | neurotoxic, enterotoxic, cytotoxic; inhibits 60S ribosomes (blocks translation)
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| hemolysins | cause lysis of blood cells, free up iron (captured by siderophores)
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| adhesion factors | pili (finbria); P&S fimbriae (both in E. coli)
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| P fimbriae | uropathogenesis (UTIs)
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| S fimbriae | neonatal sepsis, meningitis
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| growth factors | include siderophores
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| resistance to serum | unknown mechanisms
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| antibiotic resistant plasmids | switch R factors back & forth; treat w/ Amp, cephalosporins, tetracycline, chloramphenicol, TMP-SXT, amonoglycosides (ototoxic); SUSCEPTIBILITY TESTING=NECESSARY FOR OPTIMAL THERAPY
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| Shiga toxin | A/B toxin; 1A:5B; destroys rRNA, disrupts prot synth
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| gastroenteritis | GI symptoms (nausea, vomiting, diarrhea, abdominal pain/discomfort)
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| diarrhea | frequent/fluid stool; inc fluid & electrolyte loss, small intestine
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| dysentery | bacteria cause sever tissue damage; inflammatory GI disorder; blood/pus in feces; also pain, fever, abdominal cramps, large intestine
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| enterocolitis | inflammation of both SI & LI mucosa
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| E. coli-major characteristics | most predominant facultative anearobic normal flora of intestinal tract; indicator of fecal contamination of food & water; can ferment lactose & make indole
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| common infections caused by E. coli | extra-intestinal & intestinal infections
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| Extra-intestinal infections caused by E. coli | UTIs, septicemia, neonatal meningitis
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| UTIs (E. coli) | most common cause cystitis (bladder infection); >10^5/mL urine=infection
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| septicemia (E. coli) | endotoxin shock
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| neonatal meningitis (E. coli) | E. coli has unique K1 capsular Ag (majority CNS infections in infants)
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| Intestinal infections caused by E. coli | enteroinvasive, enterotoxigenic, enterohemorrhagic, enteropathogenic, enteroaggregative
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| enteroinvasive E. coli | EIEC; can live in cell; shigella-like; destroy colonic epithelium; intracellular parasites following endocytosis by epithelial cells
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| enterotoxigenic E. coli | ETEC; makes 2 toxins (heat stable, ST; heat labile, LT); traveler's diarrhea-b/c of cAMP changes leading to decreased NaCl absorption, colonization pili
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| enterohemorrhagic E. coli | EHEC, shiga-like, bloody diarrhea; Hemolytic uremic syndrome (HUS)=complication in 10% young children; serotypic especially useful (O157:H7)
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| enteropathogenic E. coli | EPEC, major cause nursery outbreaks, specific serogroups; secreted factors=further epithelial colonization
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| enteroaggregative E. coli | EAEC, prolonged watery diarrhea; developing countries; adherence main virulence factor
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| invasive organisms (enter cells) | EIEC, Shigella (invade colonic epithelium cells, but don't penetrate epithelium layer; septicemia unlikely)
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| Adherent organisms | ETEC (fimbriae-attach to microvilli of small intestine epithelium), EPEC (no fimbriae, form "attaching & effacing lesion"=glue), EAEC (aggregate & adhere, pili)
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| Penetrating organisms | Salmonella (penetrates through epithelium TJs into lamina propria=risk of septicemia)
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| Sites of Infection (E. coli) | SI-ETEC, EPEC, Salmonella; LI-EIEC, EHEC, Shigella
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| Entry of Microbes | pH<1 in stomach, pH>9 near ampulla of Vater (where pancreatic secretions enter gut lumen); infective dose >10^6 cells except for Shigella (acid resistant-~200 cells=infective dose)
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| Shigella-major characteristics | cause of bacillary dysentery & occasionally secretory form of diarrhea; non-motile organisms, don't usually produce gas (differentiate from coliform bacteria)
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| 4 Shigella species | S. dysenteriae, S. flexneri, S. boydii, S. sonnei
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| Shigella-infectiveness | all species=pathogenic; cause mucosal ulcerations of ileum & colon, carry virulence plasmids & cause bacillary dysentery; organisms don't usually penetrate beyond submucosa (usually aren't in blood cultures)
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| Shigella-major virulence factor | epithelial penetration (S. dysenteriae type 1 also makes shiga toxin, inhibs prot synth)
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| Shigella transmission | fecal-to-oral route
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| Shigella: dysentery | incubation period of 1-4 days followed by sudden onset of abdominal cramps, diarrhea, fever; blood & mucus often in stool; diagnosis by isolation of organism on selective media
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| Salmonella-general characteristics | 3 species; motile; do not ferment lactose or sucrose; produce H2S
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| Salmonella-pathogenic species | S. typhi, S. choleraesuis, S. enteritidis (turkeys & chickens)
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| Salmonella-infections | enteric (typhoid) fever, septicemia, acute gastroenteritis (classic enteric fever)
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| Typhoid fever-general | caused by S. typhi, incubation 7-14 days
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| Typhoid fever-symptoms | malaise, anorexia, headache=first symptoms, then fever (bacteria spread through body via lymphatics)
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| S. typhi--location | first week=blood; later weeks=stool, urine (grows well in biliary tract--chronic carrier state)
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| S. typhi--phagocytic mononuclear cells | can survive inside them
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| Salmonella-septicemia | caused by S. choleraesuis; high intermittant fever, suppurative focal lesions
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| Salmonella-gastroenteritis | most common; symptoms=8-48h after consumption infected food
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| Salmonella, gastroenteritis-sources | meats & poultry often contaminated
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| Salmonella, gastroenteritis-symptoms | 1st: headache, chills, abdominal pain; 2nd: vomiting, nausea, diarrhea (SI & LI), fever
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| Salmonella, gastroenteritis-diagnosis | based on recovery of organism from blood (stools); Widal test for specific agglutinins
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| Typhoid fever, septicemia-treatment | chloramphenicol (Amp, trimethoprim-sulfamethoxazole=alternatives); must continue at least 2 wks (survival inside phagocytic cells can cause relapse)
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| gastroenteritis-treatment | antibiotics not indicated (thought to prolong carrier state)
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| Klebsiella pneumoniae-general characteristics | nonmotile, encapsulated, lactose fermenter; polysaccharide capsule (mucoid appearance of colonies)
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| K. pneumoniae, diseases | 2nd leading cause UTIs, impt cause acute pneumonia
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| K. pneumoniae, virulence | capsule (inhibits phagocytosis); possible enterotoxin
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| Yersinia-general characteristics | Y. pestis, Y. enterocolitica, Y. pseudotuberculosis; animal pathogens, bubonic plague, other Yersinia infections=self-limiting (more later)
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| rare species Enterobacteriaceae | Enterobacter, Serratia, Citrobacter, Proteus, Morganella, Providencia
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| Enterobacter | motile; Klebsiella-like colonies; less virulent than K.
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| Serratia | some produce red colonies, opportunistic infections (nosocomial, multiresistance)
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| Citrobacter | opportunistic; normal intestinal flora, like Salmonella but doesn't cause enterocolitis/enteric fever
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| Proteus, Morganella, Providencia | opportunistic; normal intestinal flora; Proteus=UTIs in elderly men
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| Enterobacteriaceae treatment | antimicrobial therapy (contraindicated for Salmonella gastroenteritis)
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| Enterobacteriaceae-resistance | chromosomal & plasma-encoded R factors=resistance; susceptibility testing=crucial; usually resistant to penicillin G/erythromycin, often susceptible to B lactams, tetracycline, polypeptide antibiotics
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| Salmonella gastroenteritis-primary therapy | fluid & electrolyte replacement, control of nausea
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| see chart page 9 | (blank)
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| Genus Vibrio, general characteristics | Gram-negative curved rods, facultative anaerobes, ferment carbs, cytochrome oxidase (+), highly motile-single polar flagellum; species=halophilic (salt-loving), associated w/ marine envts
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| V. cholerae O1, O139 | cholera (epidemic)
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| V. cholerae non-O1, non-O139 | gastroenteritis
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| V. parahaemolyticus | gastroenteritis (wound infections, bacteremia rarely)
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| V. vulnificus | wound infections, bacteremia
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| V. alginolyticus | wound infections, external otitis
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| V. damsela | wound infections, bacteremia
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| V. cholerae, colonization | non-invasive, colonizes small intestine; disease due to heat-labile enterotoxin (like E. coli); species subdivided based on LPS O Ags; low salt tolerance=unique among Vibrios (grows only in 0-1% NaCl)
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| V. cholerae, epidemiology | humans=major reservoir; shellfish also possible; cholera=endemic to S. Asia, outbreaks can become worldwide
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| V. cholerae, pathogenesis | incubation 8-72h after ingestion contaminated food/water, colonizes SI by adhering to mucosal cell layer; non-invasive=doesn't damage intestinal tract
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| V. cholerae, A1 subunit | typical AB toxin, inc cAMP production=net flow fluid & electrolytes
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| V. cholerae, clinical symptoms | can be attributed to production of choleragen; nausea, vomiting, abdominal cramping, diarrhea (mucus but no blood, inflammatory cells)
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| V. cholerae, fluid loss | can exceed 20L/day; avg=10L/day
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| cholera toxin, bio effects (O1, O139) | hypersecretion of electrolytes & water
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| toxin coregulated pilus (O1, O139) | adherence to mucosal cells
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| accessory cholera enterotoxin (O1, O139) | increases intestinal fluid secretion
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| zonnula occludens toxin (O1, O139) | increases intestinal permeability
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| colonization factor (O1, O139) | adhesion factor
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| neuraminidase (O1, O139) | increase toxin receptors
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| diagnosis of cholera | isolate/ID V. cholerae from stool specimens on selective medium; serotyping against LPS O-Ag
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| cholera treatment | rapid replacement lost fluids & electrolytes (reverse condition); medication: doxycycline (shortens shedding period, reduces fluid loss)
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| cholera infection | healthy ppl-ingest 10^8 bacteria to develop disease, partially protected by native flora; gastric acid=impt barrier
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| cholera immunity | natural infection=long-lasting immunity to O1 but not to O139; vaccine=short-lived protection, not recommended
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| vibrio species primarily associated w/ gastroenteritis | V. cholerae non-O1, non-O139
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| V. cholerae non-O1, non-O139 | different LPS O Ags; 1/2 V. cholerae strains in US; don't make cholergen but make related enterotoxins; mild form gastroenteritis, not normally treated
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| V. parahaemolyticus-general characteristics | marine organism, halophilic; causes gastroenteritis, related to consumption of raw seafood
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| V. parahaemolyticus-pathogenic strains | make thermostable direct hemolysin (TDH)
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| TDH | enterotoxin, induces chloride ion secretion in epithelial cells; invasion of intestinal tract; symptoms similar to cholera, less severe
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| V. parahaemolyticus-symptoms | may persist for 72h or more; no treatment usually; 5-72h incubation time; 50% of those exposed get disease; cause wound infections
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| Vibrio vulnificus-general | primarily associated w/ wound infections/bacteremia
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| V. vulnificus-invasiveness | invades through GI tract after ingestion contaminated seafood--septicemia; patients w/ hepatic cirrhosis=most vulnerable; causes rapidly progressive wound infections
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| V. vulnificus-wound infections | characterized by initial swelling, erythema, pain; then development of vesicles/bullae, eventual tissue necrosis
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| V. vulnificus-treatment | antibiotics & surgical drainage; death rate from bacteremia approaches 50% w/o antimicrobial therapy (tetracycline)
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| V. vulnificus infection severity | most sever in patients w/ hepatic disease, hematopoietic disease, chronic renal failure, immunosuppressed patients
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| V. vulnificus-virulence factors | serum resistance, antiphagocytic capsule, polysaccharide, cytolysin, collagenase, protease, siderophore
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| V. alginolyticus | normal flora of marine life; wound infection; virulence factor=collagenase
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| V. damsela | marine-associated wound infections; Texas Gulf Coast; cytolysin-mediated infection; looks like Strep necrotizing fasciitis
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| Neisseria | N. gonorrhoeae, N. meningitidis
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| N. gonorrhoeae, incidence | highly populated urban centers; women become reservoirs (are asymptomatic)
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| uninfected woman + infected male | 50-70% infected, 30-60% asymptomatic
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| uninfected man + infected woman | 20-30% infected; 80% typical acute urethritis (2-5% asymptomatic)
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| N. gonorrhoeae, pathogenic mechanisms | virulence factors, antigenic/phase variation, pathophysiology
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| N. gonorrhoeae, virulence factors | pilus, Por I, Opa, Rmp, LOS
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| N. gonorrhoea, pilus | initial attachment to nonciliated cells; interferes w/ neutrophil killing
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| N. gonorrhoeae, Por I | protein I; antigenically stable; porin proteins; form pores in outer mem; used for serotype classification; prevents phagolysosome fusion in neutrophils
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| N. gonorrhoeae, Opa | protein II, mediates firm attachment to eukaryotic cells (conjunctival cells, epithelial cells, neutrophils)
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| N. gonorrhoeae, Rmp | Protein III; reduction-modifiable protein; protects other surface antigens (Por, LOS) from bacteriocidal antibodies
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| N. gonorrhoeae, LOS | lipooligosaccharide; endotoxin activity; cause release of TNF-alpha; lipid A + core oligosaccharide; diff LOS's=diff levels of gonorrhea resistance
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| N. gonorrhoeae, Antigenic variation | change in composition/structure of a molecule; Pili, Opa protein, LOS undergo this type of variation
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| N. gonorrhoeae, Phase variation | reversible loss/gain of a molecule or of a defined structure (on/off switch--presence/absence of pili)
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| N. gonorrhoeae, Mechanisms to account for variation | transcription, homologous recombination, error in replication
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| N. gonorrhoeae, transcriptional variation | modulation of gene expression
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| N. gonorrhoeae, homologous recombination | (1) b/w silent and expressed genes at diff positions in the genome (2) b/w copies of pilin genes taken up by cell during transformation & expressed gene
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| N. gonorrhoeae, error in replication | slipped-strand synthesis: addition of an extra base pair during replication (shift in reading frame)
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| N. gonorrhoeae, antigenic/phase variation importance for virulence | promote adhesion to mucosal surfaces; allow bacterium to attach to new & different cell types; confer ability to evade host immune system
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| N. gonorrhoeae, pathophysiology (route of infection) | deposition --> mucosal attachment (distant)-pili --> attachment (close)-Opa --> epithelial penetration-Opa --> transport through the cell in phagosomes (through submucosa) --> egestion into the submucosa & blood stream invasion
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| N. gonorrhoeae, host response | strong neutrophil response, sloughing off of epithelium, development of submucosal microabscesses; classical exudate in males (contains host inflammatory cells like PMNs, epithelial cells, & gonococci)
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| N. gonorrhoeae, host response in untreated infections | neutrophils gradually replaced by macrophages & lymphocytes; abnormal infiltration persists for several weeks (can no longer be IDed histologically)
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| N. gonorrhoeae, clinical manifestations | asymptomatic carrier; local infection; invasion restricted to sex organs; invasion of the blood stream; disseminated gonococcal infection
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| N. gonorrhoeae, clinical manifestations, asymptomatic carrier | women: up to 50%; men: 15%
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| N. gonorrhoeae, clinical manifestations, local infection | men: acute urethritis (inc period 2-10d, discharge & dysuria; mucoid-->overtly purulent; untreated resolves spontaneously); women: cervicitis/urethritis + inc vaginal discharge, intermenstrual bleeding; incubation period up to 10d
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| N. gonorrhoeae, clinical manifestations; invasion restricted to sex organs | men: epididymitis; women: PID (1/2 PID infections=concurrent chlamydia+gonorrhea)-symptoms=fever, lower abdominal pain; spread of organisms along fallopian tubes-into pelvic cavity=peritonitis
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| N. gonorrhoeae, clinical manifestations, invasion of blood stream | endocarditis, osteomyelitis, meningitis, arthritis-dermatic syndrome, perihepatitis (Fitz-Hugh-Curtis syndrome, conjunctivitis (ophthalmia neonatorum)
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| N. gonorrhoeae, clinical manifestations, disseminated gonococcal infection (DGI) | 1-2% of patients progress to DGI (bacteremic); sensitive to ABs, rapidly suppressed by antibiotic therapy; flulike-localized/disseminated skin lesions; joint pain
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| N. gonorrhoeae, gram stain | for diagnosis gonococcal urethritis in men (intracellular PMN=gram-neg diplococci=sensitive)
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| N. gonorrhoeae, cultures | use in addition to gram stain; culture on AB medium and on nonselective (like chocolate agar) b/c some strains sensitive to vancomycin
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| N. gonorrhoeae, presumptive ID | gram neg diplococci growing as mucoidy colonies; oxidase pos
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| N. gonorrhoeae, definitive ID | biochem characterization, primarily sugar fermentation (also can use monoclonal Abs & DNA hybridization)
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| N. gonorrhoeae, treatment | ceftriaxone/spectinomycin + doxycycline (for infections complicated by Chlamydia)
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| N. gonorrhoeae, treatment for neonates | 1% silver nitrate
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| N. gonorrhoeae, prevention & control | common in sexually promiscuous individuals; chemopropylaxis (preventative medicine)=ineffective; monitor incidence & AB resistance
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| N. meningitidis-dissemination | throughout leptomeninges, brain, spinal cord
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| N. meningitidis-epidemiology | predominantly pediatric; 80% of cases in kids <5 yrs
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| N. meningitidis-disease development | virulence of infecting strain; host susceptibility, environmental influences (epidemics in crowded envts)
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| N. meningitidis, antigenic components for serotyping | 13 serogroups based on polysaccharide capsules (A-cause of epidemics; B-most common in US; others= C-endemic,Y-pulmonary,W-bacteremia)
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| N. meningitidis, fatality rate | high despite AB intervention (5-15%)
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| N. meningitidis, pathogenic mechanisms | exclusively human pathogen (either normal flora or acute disease)
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| N. meningitidis outcome-4 factors of dependence | (1) if bacteria are able to colonize nasopharynx-mediated by pilus (2) if specific group- & serotype-spcfc Abs are present (3) if systemic spread happens w/o Ab-mediated phagocytosis (4) if toxic effects expressed (mediated by LOS endotoxin)
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| N. meningitidis-clinical manifestations | mucous membrane carriage/infection-->blood stream invasion (meningococcemia); (transient bacteremia-->chronic meningococcemia-->acute invation-->fulminant meningococcemia
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| N. meningitidis, transient bacteremia | 1-2d; no sequelae
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| N. meningitidis, chronic meningococcemia | 2-19d; transient episodes bacteremia w/ arthritis/pustular dermatitis; low-grade fever; petechial skin lesions
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| N. meningitidis, acute invasion | several days upper resp tract symptoms, then: abrupt fever onset, headach (worst ever), stiff neck, stupor, coma, vomiting; dvlpmnt of petechial skin lesions; meningitis/pericarditis/arthritis/conjunctivitis
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| N. meningitidis, fulminant | intravascular coagulation, circulatory collapse, death in a few hours (AB therapy can worsen illness-endotoxin release; use steriods to suppress inflamm response)
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| N. meningitidis, lab diagnosis | hardest in infants, can't talk; abnormal CSF (high leukocyte count, low glucose level)
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| N. meningitidis, presumptive identification | culture specimens from blood, CSF, petechial skin lesion, gram neg diplococci in PMNs, oxidase positive
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| N. meningitidis, definitive diagnosis | biochem tests: sugar fermentation; fluorescent Ab staining
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| N. meningitidis, newer techniques | latex particle agglutination (LPA) using CSF/urine specimens
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| N. meningitidis, treatment | Penicillin G; chemoprophylaxis for househould/intimate contacts; sulfonamide/rifampin; immunoprophylaxis (capsules from serogroups)
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| N. meningitidis, prevention and control | unlikely to eradicate carrier pool; breast feed infants for 1st 6 mo; chemoprophylactic trtmnt (rifampin) for people w/ significant exposure; immunoprophylaxis
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| N. meningitidis vs. N. gonorrhoeae | N. gonorrhoeae only ferments glucose (G=G); N. meningitidis ferments glucose and maltos (M=M)
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| see chart, p. 14 | (blank)
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To hide a column, click on the column name.
To hide the entire table, click on the "Hide All" button.
You may also shuffle the rows of the table by clicking on the "Shuffle" button.
Or sort by any of the columns using the down arrow next to any column heading.
If you know all the data on any row, you can temporarily remove it by tapping the trash can to the right of the row.
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