Enteric Bacteria Flashcards
Bacteria that cause gut infections
- Shigella
- E. coli
- Salmonella
- Y enterocolitica
- Y psuedotuberculosis
- vibri0
- campylobacter
- helicobacter
- bacteroides/prevotella
- clostridium
- listeria
enterobacteriaceae
- Foodborne- Shigella, E. coli, Salmonella
- Minor foodborne- Y. enterocolitica and pseudotuberculosis
- ICU bugs- Kelsiella/Enterobacter/Serratia
- Proteus/Provdencia/Morganella
defining characteristics of enterobacteriaceae
- gram neg
- non-sporulating
- 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
T3SS/T4SS
-inject molecules to force cell to form actin bundle
virulence
- 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
salmonella
- gram neg rods
- motile
- > 2500 serovars
- food
- 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
HUS
- 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
- peds
- 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
- klebsiella/enterobacter/serratia
- proteus/providencia/morganella
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