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micro block 2, week1
micro flashcards
| Question | Answer |
|---|---|
| enterobacteriaceae-gram stain | gram negative bacilli (rods) |
| 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 |
| Enterobacteriaceae-motility | if motile, move by peritrichous flagella |
| enteric bacilli | bacilli of GI tract (Enterobacteriaceae + Gram-negative vibrios) |
| opportunistic pathogens, Enterobaceteriaceae | normal flora, wrong location/overabundance (E. coli) |
| frank pathogens, Enterobacteriaceae | presence in any amount=disease (Salmonella, Shigella) |
| Escherichia-diseases | UTI, gastroenteritis, meningitis, septicemia, hemorrhagic colitis |
| Shigella-disease | Bacillary dysentery |
| Salmonella-disease | Gastroenteritis, septicemia, enteric fevers (typhoid) |
| Klebsiella-disease | pneumonia, UTI |
| Yersinia-disease | Gastroenteritis, plague, zoonotic (animal to human) infection |
| biochemical identification of species | serotyping-identification by surface antigens |
| Serotyping-Antigens used | somatic cell wall antigens (O), flagellar antigens (H), capsular antigens (K) |
| MacConkey isolation-Enterobacteriaceae | yes (lactose-fermenting): E. coli, Klebsiella; no (non lactose-fermenting): Salmonella, Shigella |
| Enterobacteriaceae-lactose | coliforms (lactose fermenters-rapid, 24h fermentation) vs. non-lactose fermenters |
| Gastroenteritis | caused by coliforms & non-lactose fermenting Enterobacteriaceae |
| E. coli, lactose | most sensitive coliform; sensitive indicator of water contamination |
| virulence factors | endotoxin, capsule, phase variation, exotoxins, adhesion factors, growth factors, resistance to serum, antibiotic resistant plasmids |
| Endotoxin | virulence factor, common to all Enterobacteriaceae; lipid A part of O Ag; fncs in vascular, metabolic, pyrogenic, hematological alterations (severe Gram - infections) |
| capsule | protects against phagocytosis, obscures cell wall Ags; characteristic of Klebsiella pneumonia=mucoid colonies (non-motile, community-acquired pneumonia) |
| phase variation | alternate expression of diff forms of protein (epsecially K&H Ags and pili=2 diff genes for flagellin) |
| exotoxins | secreted toxins; 4 types: enterotoxins (heat-labile & heat-stable), cytotoxins (shiga toxin & hemolysins) |
| Enterotoxins | cause changes in ion absorption/balance of H2O transport in GI tract |
| Heat-labile enterotoxin | similar to cholera toxin in Vibrio-increases cAMP |
| Heat-stable enterotoxin | increases cGMP |
| shiga toxin | neurotoxic, enterotoxic, cytotoxic; inhibits 60S ribosomes (blocks translation) |
| hemolysins | cause lysis of blood cells, free up iron (captured by siderophores) |
| adhesion factors | pili (finbria); P&S fimbriae (both in E. coli) |
| P fimbriae | uropathogenesis (UTIs) |
| S fimbriae | neonatal sepsis, meningitis |
| phase variation | alternate expression of diff forms of protein (epsecially K&H Ags and pili=2 diff genes for flagellin) |
| exotoxins | secreted toxins; 4 types: enterotoxins (heat-labile & heat-stable), cytotoxins (shiga toxin & hemolysins) |
| Enterotoxins | cause changes in ion absorption/balance of H2O transport in GI tract |
| Heat-labile enterotoxin | similar to cholera toxin in Vibrio-increases cAMP |
| Heat-stable enterotoxin | increases cGMP |
| shiga toxin | neurotoxic, enterotoxic, cytotoxic; inhibits 60S ribosomes (blocks translation) |
| hemolysins | cause lysis of blood cells, free up iron (captured by siderophores) |
| adhesion factors | pili (finbria); P&S fimbriae (both in E. coli) |
| P fimbriae | uropathogenesis (UTIs) |
| S fimbriae | neonatal sepsis, meningitis |
| growth factors | include siderophores |
| resistance to serum | unknown mechanisms |
| antibiotic resistant plasmids | switch R factors back & forth; treat w/ Amp, cephalosporins, tetracycline, chloramphenicol, TMP-SXT, amonoglycosides (ototoxic); SUSCEPTIBILITY TESTING=NECESSARY FOR OPTIMAL THERAPY |
| Shiga toxin | A/B toxin; 1A:5B; destroys rRNA, disrupts prot synth |
| gastroenteritis | GI symptoms (nausea, vomiting, diarrhea, abdominal pain/discomfort) |
| diarrhea | frequent/fluid stool; inc fluid & electrolyte loss, small intestine |
| dysentery | bacteria cause sever tissue damage; inflammatory GI disorder; blood/pus in feces; also pain, fever, abdominal cramps, large intestine |
| enterocolitis | inflammation of both SI & LI mucosa |
| 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 |
| common infections caused by E. coli | extra-intestinal & intestinal infections |
| Extra-intestinal infections caused by E. coli | UTIs, septicemia, neonatal meningitis |
| UTIs (E. coli) | most common cause cystitis (bladder infection); >10^5/mL urine=infection |
| septicemia (E. coli) | endotoxin shock |
| neonatal meningitis (E. coli) | E. coli has unique K1 capsular Ag (majority CNS infections in infants) |
| Intestinal infections caused by E. coli | enteroinvasive, enterotoxigenic, enterohemorrhagic, enteropathogenic, enteroaggregative |
| enteroinvasive E. coli | EIEC; can live in cell; shigella-like; destroy colonic epithelium; intracellular parasites following endocytosis by epithelial cells |
| 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 |
| enterohemorrhagic E. coli | EHEC, shiga-like, bloody diarrhea; Hemolytic uremic syndrome (HUS)=complication in 10% young children; serotypic especially useful (O157:H7) |
| enteropathogenic E. coli | EPEC, major cause nursery outbreaks, specific serogroups; secreted factors=further epithelial colonization |
| enteroaggregative E. coli | EAEC, prolonged watery diarrhea; developing countries; adherence main virulence factor |
| invasive organisms (enter cells) | EIEC, Shigella (invade colonic epithelium cells, but don't penetrate epithelium layer; septicemia unlikely) |
| Adherent organisms | ETEC (fimbriae-attach to microvilli of small intestine epithelium), EPEC (no fimbriae, form "attaching & effacing lesion"=glue), EAEC (aggregate & adhere, pili) |
| Penetrating organisms | Salmonella (penetrates through epithelium TJs into lamina propria=risk of septicemia) |
| Sites of Infection (E. coli) | SI-ETEC, EPEC, Salmonella; LI-EIEC, EHEC, Shigella |
| 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) |
| Shigella-major characteristics | cause of bacillary dysentery & occasionally secretory form of diarrhea; non-motile organisms, don't usually produce gas (differentiate from coliform bacteria) |
| 4 Shigella species | S. dysenteriae, S. flexneri, S. boydii, S. sonnei |
| 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) |
| Shigella-major virulence factor | epithelial penetration (S. dysenteriae type 1 also makes shiga toxin, inhibs prot synth) |
| Shigella transmission | fecal-to-oral route |
| 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 |
| Salmonella-general characteristics | 3 species; motile; do not ferment lactose or sucrose; produce H2S |
| Salmonella-pathogenic species | S. typhi, S. choleraesuis, S. enteritidis (turkeys & chickens) |
| Salmonella-infections | enteric (typhoid) fever, septicemia, acute gastroenteritis (classic enteric fever) |
| Typhoid fever-general | caused by S. typhi, incubation 7-14 days |
| Typhoid fever-symptoms | malaise, anorexia, headache=first symptoms, then fever (bacteria spread through body via lymphatics) |
| S. typhi--location | first week=blood; later weeks=stool, urine (grows well in biliary tract--chronic carrier state) |
| S. typhi--phagocytic mononuclear cells | can survive inside them |
| Salmonella-septicemia | caused by S. choleraesuis; high intermittant fever, suppurative focal lesions |
| Salmonella-gastroenteritis | most common; symptoms=8-48h after consumption infected food |
| Salmonella, gastroenteritis-sources | meats & poultry often contaminated |
| Salmonella, gastroenteritis-symptoms | 1st: headache, chills, abdominal pain; 2nd: vomiting, nausea, diarrhea (SI & LI), fever |
| Salmonella, gastroenteritis-diagnosis | based on recovery of organism from blood (stools); Widal test for specific agglutinins |
| Typhoid fever, septicemia-treatment | chloramphenicol (Amp, trimethoprim-sulfamethoxazole=alternatives); must continue at least 2 wks (survival inside phagocytic cells can cause relapse) |
| gastroenteritis-treatment | antibiotics not indicated (thought to prolong carrier state) |
| Klebsiella pneumoniae-general characteristics | nonmotile, encapsulated, lactose fermenter; polysaccharide capsule (mucoid appearance of colonies) |
| K. pneumoniae, diseases | 2nd leading cause UTIs, impt cause acute pneumonia |
| K. pneumoniae, virulence | capsule (inhibits phagocytosis); possible enterotoxin |
| Yersinia-general characteristics | Y. pestis, Y. enterocolitica, Y. pseudotuberculosis; animal pathogens, bubonic plague, other Yersinia infections=self-limiting (more later) |
| rare species Enterobacteriaceae | Enterobacter, Serratia, Citrobacter, Proteus, Morganella, Providencia |
| Enterobacter | motile; Klebsiella-like colonies; less virulent than K. |
| Serratia | some produce red colonies, opportunistic infections (nosocomial, multiresistance) |
| Citrobacter | opportunistic; normal intestinal flora, like Salmonella but doesn't cause enterocolitis/enteric fever |
| Proteus, Morganella, Providencia | opportunistic; normal intestinal flora; Proteus=UTIs in elderly men |
| Enterobacteriaceae treatment | antimicrobial therapy (contraindicated for Salmonella gastroenteritis) |
| 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 |
| Salmonella gastroenteritis-primary therapy | fluid & electrolyte replacement, control of nausea |
| see chart page 9 | (blank) |
| 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 |
| V. cholerae O1, O139 | cholera (epidemic) |
| V. cholerae non-O1, non-O139 | gastroenteritis |
| V. parahaemolyticus | gastroenteritis (wound infections, bacteremia rarely) |
| V. vulnificus | wound infections, bacteremia |
| V. alginolyticus | wound infections, external otitis |
| V. damsela | wound infections, bacteremia |
| 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) |
| V. cholerae, epidemiology | humans=major reservoir; shellfish also possible; cholera=endemic to S. Asia, outbreaks can become worldwide |
| 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 |
| V. cholerae, A1 subunit | typical AB toxin, inc cAMP production=net flow fluid & electrolytes |
| V. cholerae, clinical symptoms | can be attributed to production of choleragen; nausea, vomiting, abdominal cramping, diarrhea (mucus but no blood, inflammatory cells) |
| V. cholerae, fluid loss | can exceed 20L/day; avg=10L/day |
| cholera toxin, bio effects (O1, O139) | hypersecretion of electrolytes & water |
| toxin coregulated pilus (O1, O139) | adherence to mucosal cells |
| accessory cholera enterotoxin (O1, O139) | increases intestinal fluid secretion |
| zonnula occludens toxin (O1, O139) | increases intestinal permeability |
| colonization factor (O1, O139) | adhesion factor |
| neuraminidase (O1, O139) | increase toxin receptors |
| diagnosis of cholera | isolate/ID V. cholerae from stool specimens on selective medium; serotyping against LPS O-Ag |
| cholera treatment | rapid replacement lost fluids & electrolytes (reverse condition); medication: doxycycline (shortens shedding period, reduces fluid loss) |
| cholera infection | healthy ppl-ingest 10^8 bacteria to develop disease, partially protected by native flora; gastric acid=impt barrier |
| cholera immunity | natural infection=long-lasting immunity to O1 but not to O139; vaccine=short-lived protection, not recommended |
| vibrio species primarily associated w/ gastroenteritis | V. cholerae non-O1, non-O139 |
| 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 |
| V. parahaemolyticus-general characteristics | marine organism, halophilic; causes gastroenteritis, related to consumption of raw seafood |
| V. parahaemolyticus-pathogenic strains | make thermostable direct hemolysin (TDH) |
| TDH | enterotoxin, induces chloride ion secretion in epithelial cells; invasion of intestinal tract; symptoms similar to cholera, less severe |
| 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 |
| Vibrio vulnificus-general | primarily associated w/ wound infections/bacteremia |
| V. vulnificus-invasiveness | invades through GI tract after ingestion contaminated seafood--septicemia; patients w/ hepatic cirrhosis=most vulnerable; causes rapidly progressive wound infections |
| V. vulnificus-wound infections | characterized by initial swelling, erythema, pain; then development of vesicles/bullae, eventual tissue necrosis |
| V. vulnificus-treatment | antibiotics & surgical drainage; death rate from bacteremia approaches 50% w/o antimicrobial therapy (tetracycline) |
| V. vulnificus infection severity | most sever in patients w/ hepatic disease, hematopoietic disease, chronic renal failure, immunosuppressed patients |
| V. vulnificus-virulence factors | serum resistance, antiphagocytic capsule, polysaccharide, cytolysin, collagenase, protease, siderophore |
| V. alginolyticus | normal flora of marine life; wound infection; virulence factor=collagenase |
| V. damsela | marine-associated wound infections; Texas Gulf Coast; cytolysin-mediated infection; looks like Strep necrotizing fasciitis |
| Neisseria | N. gonorrhoeae, N. meningitidis |
| N. gonorrhoeae, incidence | highly populated urban centers; women become reservoirs (are asymptomatic) |
| uninfected woman + infected male | 50-70% infected, 30-60% asymptomatic |
| uninfected man + infected woman | 20-30% infected; 80% typical acute urethritis (2-5% asymptomatic) |
| N. gonorrhoeae, pathogenic mechanisms | virulence factors, antigenic/phase variation, pathophysiology |
| N. gonorrhoeae, virulence factors | pilus, Por I, Opa, Rmp, LOS |
| N. gonorrhoea, pilus | initial attachment to nonciliated cells; interferes w/ neutrophil killing |
| N. gonorrhoeae, Por I | protein I; antigenically stable; porin proteins; form pores in outer mem; used for serotype classification; prevents phagolysosome fusion in neutrophils |
| N. gonorrhoeae, Opa | protein II, mediates firm attachment to eukaryotic cells (conjunctival cells, epithelial cells, neutrophils) |
| N. gonorrhoeae, Rmp | Protein III; reduction-modifiable protein; protects other surface antigens (Por, LOS) from bacteriocidal antibodies |
| N. gonorrhoeae, LOS | lipooligosaccharide; endotoxin activity; cause release of TNF-alpha; lipid A + core oligosaccharide; diff LOS's=diff levels of gonorrhea resistance |
| N. gonorrhoeae, Antigenic variation | change in composition/structure of a molecule; Pili, Opa protein, LOS undergo this type of variation |
| N. gonorrhoeae, Phase variation | reversible loss/gain of a molecule or of a defined structure (on/off switch--presence/absence of pili) |
| N. gonorrhoeae, Mechanisms to account for variation | transcription, homologous recombination, error in replication |
| N. gonorrhoeae, transcriptional variation | modulation of gene expression |
| 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 |
| N. gonorrhoeae, error in replication | slipped-strand synthesis: addition of an extra base pair during replication (shift in reading frame) |
| 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 |
| 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 |
| 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) |
| 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) |
| N. gonorrhoeae, clinical manifestations | asymptomatic carrier; local infection; invasion restricted to sex organs; invasion of the blood stream; disseminated gonococcal infection |
| N. gonorrhoeae, clinical manifestations, asymptomatic carrier | women: up to 50%; men: 15% |
| 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 |
| 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 |
| N. gonorrhoeae, clinical manifestations, invasion of blood stream | endocarditis, osteomyelitis, meningitis, arthritis-dermatic syndrome, perihepatitis (Fitz-Hugh-Curtis syndrome, conjunctivitis (ophthalmia neonatorum) |
| 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 |
| N. gonorrhoeae, gram stain | for diagnosis gonococcal urethritis in men (intracellular PMN=gram-neg diplococci=sensitive) |
| 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 |
| N. gonorrhoeae, presumptive ID | gram neg diplococci growing as mucoidy colonies; oxidase pos |
| N. gonorrhoeae, definitive ID | biochem characterization, primarily sugar fermentation (also can use monoclonal Abs & DNA hybridization) |
| N. gonorrhoeae, treatment | ceftriaxone/spectinomycin + doxycycline (for infections complicated by Chlamydia) |
| N. gonorrhoeae, treatment for neonates | 1% silver nitrate |
| N. gonorrhoeae, prevention & control | common in sexually promiscuous individuals; chemopropylaxis (preventative medicine)=ineffective; monitor incidence & AB resistance |
| N. meningitidis-dissemination | throughout leptomeninges, brain, spinal cord |
| N. meningitidis-epidemiology | predominantly pediatric; 80% of cases in kids <5 yrs |
| N. meningitidis-disease development | virulence of infecting strain; host susceptibility, environmental influences (epidemics in crowded envts) |
| 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) |
| N. meningitidis, fatality rate | high despite AB intervention (5-15%) |
| N. meningitidis, pathogenic mechanisms | exclusively human pathogen (either normal flora or acute disease) |
| 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) |
| N. meningitidis-clinical manifestations | mucous membrane carriage/infection-->blood stream invasion (meningococcemia); (transient bacteremia-->chronic meningococcemia-->acute invation-->fulminant meningococcemia |
| N. meningitidis, transient bacteremia | 1-2d; no sequelae |
| N. meningitidis, chronic meningococcemia | 2-19d; transient episodes bacteremia w/ arthritis/pustular dermatitis; low-grade fever; petechial skin lesions |
| 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 |
| 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) |
| N. meningitidis, lab diagnosis | hardest in infants, can't talk; abnormal CSF (high leukocyte count, low glucose level) |
| N. meningitidis, presumptive identification | culture specimens from blood, CSF, petechial skin lesion, gram neg diplococci in PMNs, oxidase positive |
| N. meningitidis, definitive diagnosis | biochem tests: sugar fermentation; fluorescent Ab staining |
| N. meningitidis, newer techniques | latex particle agglutination (LPA) using CSF/urine specimens |
| N. meningitidis, treatment | Penicillin G; chemoprophylaxis for househould/intimate contacts; sulfonamide/rifampin; immunoprophylaxis (capsules from serogroups) |
| 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 |
| N. meningitidis vs. N. gonorrhoeae | N. gonorrhoeae only ferments glucose (G=G); N. meningitidis ferments glucose and maltos (M=M) |
| see chart, p. 14 | (blank) |
Created by:
gmuallem
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