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Micro/Immuno Part 2 > Enteric Bacteria > Flashcards

Flashcards in Enteric Bacteria Deck (23):

Bacteria that cause gut infections

-E. coli
-Y enterocolitica
-Y psuedotuberculosis




-Foodborne- Shigella, E. coli, Salmonella
-Minor foodborne- Y. enterocolitica and pseudotuberculosis
-ICU bugs- Kelsiella/Enterobacter/Serratia


defining characteristics of enterobacteriaceae

-gram neg
-straight rods
-facultative aerobes
-catalse pos, oxidase neg
-glucose fermenters


common characteristics

-promiscuous to new DNA-acquired gut virulence factors
-pili for adhesion then secrete exotoxin-ETEC
-T3SS for adhesion, subverting gut macrophage
-antibiotic resistance



-inject molecules to force cell to form actin bundle



-adhesion and inject toxin
-secretion systems-for actin bundles/ deliver toxin
-actin based cell to cell motility


shigella bacteria

-bacteria taken up in Peyer's patch (M cell)
-macrophage engulfs but can't kill
-bacteria escapes and gets into the gut via the outside which is much easier to penetrate
-mediated by T3SS
-also mediated by cytoskeletal rearrangements
-yersenia has same mechanism ins addition to local and systemic dissemination


antimicrobial sensitivity assay

-grown lawn of bacteria on large agar plate
-place paper disks soaked in antibiotic
-measure diameter and compare to a chart to see if it's effective



-gram neg rods
->2500 serovars
-enterocolitis and enteric fevers (typhoid not typhus)


salmonella pathogenesis

-inflammation and diarrhea, nausea and vomiting
-immune response restricts to gut, bacteremia is rare
-high ID (need a lot)
-gastric acid is protective, antacids increase risk
-bacteria attach by fimbriae to cells lining lumen
-salmonellae selectively attach to specialized epithelial cells-M cells


salmonella mechanism

-same as Shigella with addition of trojan horses that disseminate and get triggered to form infection elsewhere (in typhoid- not in regular GI illness)


virulence of salmonella

-Ipf operon enhances adhesion to M cells
-T3SS injects M cell, enhances bacterial translocation
-SipB injected by Spi1 type 3 causes macrophage apoptosis
-in S typhi, spi2 type 3 sys remodels phagosomes for systemic spread
-Vi antigen-s typhi capsule for immune evasion


salmonella pathogenesis 2

-usually s typhi or paratyphi
-human restricted fecal oral
-high ID
-invades peyers patches of distal ilieum and enters macrophages
-rides in macrophages through lymphatics, invading major organs
-once critical density is reached, bacteria induce macrophage apoptosis and escape into bloodstream


Typhoid fever

-onset-fever, malaise, diffuse abd pain, constipation (sometimes diarrhea)
-3-4 week progression: dry cough, stupod, delerium, intestinal hemhorrage, bowel perforation, myocarditis, death (9-13%)
-necrosis in the infected Peyer's patches causes hemorrhage/perforation
-other symptoms from toxemia
-survivors may have long term neurological sequale or chronic carrier in gallbladder
-typhoid Mary, NYC, 1905



-complication of enteric infection
-hemolytic uremic syndrome
-shigella and enterohemorrhagic e coli both routinely cause fever, dehydration, severe headache, lethargy, diarrhea progresses from watery to bloody with mucus
-in minority of cases 1-10% bacteria escape the gut and shiga toxin released into the bloodstream, causing HUS
-fever, dehydration, hemolysis, thrombocytopenia, uremia requiring dialysis, 5-10% mortality
-shiga toxin interferes with complement and almost causes DIC- loss of balance between breakdown and synthesis of clots
-blood smear has schistocytes-generated as blood passes through some thromboses
-antibiotics are controversial


reactive arthritis

-used to be Reiter's Syndrome
-AI sequel of bacterial infection in patients positive for HLA-B27
-common trigger infections are Shigella, Salmonella, Yersinia, Chlamydia
-conjunctivitis, urethritis, arthritis
-can't see, can't pee, can't climb a tree
-treated with NSAIDs


ICU bugs



non foodborne enterobacteriaceae

-normal flora gone bad
-opportunistic nosocomial infections, some community acquired diseases exist: Klebsiella pneumonia, serratia endocarditis in IV drug users
-all common causes of catheter associated UTIs
-ICU bugs are opportunistic and extremely antibiotic resistant- can be last straw


K pneumoniae

-can be primary pathogen, but usually with a predisposing position like age, chronic resp disease, diabetes, alcoholism
-large polysaccharide capsule defends against phagocytosis, complement
-adhesins adhere to gut cells, siderophores chelate iron
-alcoholic men
-lobar pneumonia with necrosis, inflammation and hemorrhage, currant jelly sputum
-50% mortality in alcoholics, approaches 100 in alcoholics with bacteremia
-less lethal presentations include bronchitis, UTI, wound or catheter infection


spread of Klebsiella group

-causes nosocomial outbreaks, among top 8 HAI, second only to e coli as cause of gram neg sepsis
-k. oxytoca among top 4 pathogens in NICUs
-carbapenem resistant k pneumoniae is currently spreading among hospitals worldwide


klebsiella group diagnosis

-culture and gram stain and enable Ab resistance testing
-capsule is mucoid on agar
-more specific biochemical tests available and often needed


klebsiella group trt

-antibiotics indicated
-us Ab testing
-begin with aminoglycoside and cephalosporin


klebsiella group prevention

-prompt removal or relocation of catheters
-maintenance of resp therapy devices
-minimization of hospital stays
-regular scrubdowns of ICU and patients