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micro block 2, week1

micro flashcards

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