stellapak's version from 2015-05-14 17:58

Section 1

Question Answer
limited number o fpathogenic mechanisms used by GI pathgoens->toxin production, adhesive/aggresive to occupy microvilli, invasive-inflammation
routes of GI infection transmissionfeces, food, fluids, fingers, fomites, fornication, flies
transmission depends on#cfu required to cause disease which varies via pathogen
GI defences vs pathogenslow pH of stomach / lrge volume, proteases, bile, and IgA of small intestine / large # of natural flora of large intestine produce inhibitory substances and occupies adhesive sites

Section 2

Question Answer
cholera toxinprototype of family similar proteins able to bind cells, function as ADP ribosylaing enzyme to lock cyclase catalytic unit on (ATP to cAMP)
chlorea toxin increasescAMP leading to turn off Na absorption, incrwase Cl secretion, and reuslts in net loss of water
chlorea toxin quickly leads todehydration
organisms with chlorea like toxinLT of E coli increases cAMP / ST of E coli increase cGMP / salmonella, campylobacter, yersinia, aeromonas

Section 3

Question Answer
vibrio cholerea endemic ingulf coast in US, Africa, LA
organism lives inbrackish waters; halophilic (salt loving) but can grow in absence of salt
vibrio cholerae is ahuman pathgoen
v cholerae able toadhere-prevents organism from being washe dout
v cholerae causessecretory diarrhea, no fever, no invasion, no damaged cells, no inflammation
v cholerae levels increase inwarm months
v cholerae spreadconsumption of contaminated food/water / person to person unlikely bc need high infecitus dose and killed by acid
Abs mayshorten duration toxin secretion and decrease spread; use Cipro or AZR

Section 4

Question Answer
vibrio parahemolyticusconsumption of undercooked seafood (esp oysters) / requires salt / gastroenteritis ear round / in constrast, septicemia and wound infecitons in warm months
vibrio vulnificusespecially virulent with proteinc apsule protectign against phagocytosis and compl mediated kill / severe wound infectins and sepsis / sepsis can occur aafter oyster consumption
vibrio vlnificus esp inICH: cirrhosis, renal failure

Section 5

Question Answer
enterobacteriaceae structureG- rods, most motile except shigella, klebsiella, yersinia
lactose + enterobacteriaceaecitrobacter, serratia, E coli, enterobacter, Kleb (CSEEK)
lactose - enterobacteriaceaesalmonella, shigella, yersinia, proteus
groups of enterobacteriaceaecommensals (E coli, proteus, kleb, may be opportunistic) / virulent (shigella, salmonella yersinia) / acquired virulence (E coli)
pathogenic E coliETEC (enterotoxigenic), EPEC (enteropathgenic), EHEC (enterohemorrhagic), EAEC (enteroadhesive)

Section 6

Question Answer
ETEC causesweanling diarrhea in developign world and traveler's diarrhea
ETEC epidemiology dictated byexposure induces mucosal immunity, asymptomactic carrier states, infection requires high dose
ETEC sourcecontaminated food/water
ETEC toxinsLT (close to cholera toxin and activates adenykate cyclase o produce cAMP causing osmotic diarrhea) / ST (found in yersinia and V. cholerae and icnreases cGMP to stimulae Ct secretion and inhibht NaCL absorption / both cause secretory diarrhea
ETEC therpayABs decrease duration.severity of diarrhea
antibioticsquinolones or AZR
preventionbismuth subsalicylate

Section 7

Question Answer
EPEC causesinfant diarrhea
EPE hallmarkeffacing of microvilli and attaching cell membrane leads to activation of signal transduction
EPEC transmissionoral/fecal, hands, food, tabletops, person-person
reservoirasymptomatic kids and adults
diagnosisphenotypic culture HeLa cells; PCR
symptomsdiarrhea, somtimes vomiting
theraoyrehydration and quinolone or AZR if severe

Section 8

Question Answer
EHEC caused byE Coli O157:H7
toxinshigalike or vero-toxin / cytotoxin (Stx)+associated w HUS
many strainscan express Stx including EPEC and ETEC
Stx necessary forbloody diarrhea
HUS thought to result fromintravascular dissemination of Stx and attach Gb3 receptors renal epithelium damaging glomeruli
classicalyhemorrhage and edema transverse and asc. colon
reservoirmany animals, retail meats
transmisisionburgers, apple juice, salami, mayonasie, uncooked radish sprouts, person-person
clinicaldiarrhea, fever, cramps then bloody diarrhea / some develop HUS consisting of hemolytic anemia, oliguric RF, and thrombocytopenia
HUS more likely ifinfected with )157:H7 / very old or young, rx antimotility drigs, expresion of STx2
treatmentno antibiotics!
diagnosisculture stol on SMAC within 2d of diarrhea / non O157:H7 strains detected by Stx

Section 9

Question Answer
invasive enteric pathogens causestructural damage to large intestine, invasion or damage to mucosa causes bloody diarrhea or dysentery
dysenteryfreq stools of small volume with gross pus +/- blood
classic causes of dysenteryshigella or entamoeba which invade intestinal epithelium and cause inflammatory leukocyte rx in lamina propria which release inflammatory mediators/vasc abn results in blood
bloody diarrheainvasionof gut mucosa seen; nontypphoid salmonella, campylobacter, yersini

Section 10

Question Answer
shigella dysenteriaedevloping coutnries, most severe
shigella sonneimost common US, mildest
other shigella speciesflexneri and boydii
shigella is highly host adapted: infect only humans
shigella infecitus doselow bc resistant to acid
spreaddirect contact, sex, food, water
endemic disease inmale homosexuals
mechanisminvade colonic mucosa, multiply intracellular and spread fr cell to cell leading to mucosal ulcers and inflammation (Dysentery)
cytotoxinonly S. dysenteriae has shiga toxin / others have less virulent cytotoxins
shiga toxinhighly specific enzyme reversibly inactivates 60S ribosomal subunit->cessation of protein synthesis
disease symptomsranges from mild watery diarrhea to dysentery
fecal sampleleukocutes indicates invasion
culturelactose- bacillus
ID DNA probe/PCR
therayantibodies reduce duration and period of infectivity but resistance common

Section 11

Question Answer
salmonella strains distinguished byO (somatic), H (flagellar) and K (capsular) Ags
S typhi1 serotype / host is humans
S. cholerasuis1 serotype / host is pigs
E. enteritides2000 serotypes / host is humans/animals
clinicaltyphoid fever, focal infection of vascular endothelium (choleraesuis) or osteo (S. typhimurium HbSS), diarrhea
infecitous dosehigh
vehiclesS typhi is infected humans / others are food, water, zoonosis
most common in USS. typhimurium

Section 12

Question Answer
S. typhi invadesacross mucosa and is sequestered in mononuclear cells in regional Inn
initialbactermemia spread to liver and spleen where they multiple in macrophages
as intracellular number reaches thershold->released and continuous bacteremia results=clinical disease of daily high fevers and gall bladder invasion (carrier state), kidney, reinvasion fo gut (inflammation)
isolate organism fromblood, stool, urine
notadherent to endothelium-->rarely endocarditis / in contrast to choleraesuis and enteritidis which adhere aviduly often cause IE, intravasucalr infections
treatmentquinolones, AMP, CEF, bactrim

Section 13

Question Answer
diarrhea causing salmonella multiple inlamina propria
inducefluid secretion by increasing cAMP and relase of PG
salmonella oftennters bloodstream and normally rapidly killed in blood by phagocytes
condtions thatimpair function of the phagocytic system enhance suscpetibility to salmonella bacteremia (HbSS, AIDS, leukemia)
Dxnonlactose fermenter, biochemical proprties
therapyno antibiotics for S enteritidis nl host / always treat ICH and bacteremia esp cholerasuis and S dublin and adults >50 with atherosclerosis
S typhi drugsAMP, CEF(ceftriaxone) bactrim
carrier drugsAMP+probenecid, Bactrim

Section 14

Question Answer
Yersinia speciesY. enterocolitica and Y pseudotuberculosis primary enteric pathgoens
all yersinia plasmids with virulence genes
Yersina resistphagocytosis
infectionszoonostic: humans incidental hosts
spread throughcontaminated foods esp milk, meat, water (belgian chocolates!!!_
common inscandinavian and othe reuropeanc ountries
_ related diseaseblood transfusion bc organism can grow t 4C
incubation1-10 days
symptomsdiarrhea, fever, abdominal pain / chronic disease can develop
mainly infectsterminal ileum
if mesenteric lymph nodes invovledmimics appendecitis
treatcipro 3rd gen ceph, bactrim

Section 15

Question Answer
H. pylori sturcturesprial, G- rod with corkscrew motility and urease production
H pylro associated withgastritis, peptic ulcers, duodenal, gastric carcinoma, mucosa-assocayed lymphoid tissue (MALT) associated lymphoma
H pylori blocksacid secretion and produces urease to neutralzie acid
motile bacteria canpass through gastric mucosa and cause epithelial damage
H pylori stimulatesinflammatory response
primary sourcehumans
highest rate colonizationpoor sanitiation
colonixation in US increasesiwth age
colonization protects vsesophageal reflux
lab testantibodies via ELISA
test of choicetiter
stainwarthr-starry silver
biopsy specimenurease actiivty
breath test forurease
treatmentcombo of proton pump inhib+tetra_MET_bismuth o amox, clarithro