Enteric Bacteria Flashcards
1
Q
Bacteria that cause gut infections
A
- Shigella
- E. coli
- Salmonella
- Y enterocolitica
- Y psuedotuberculosis
- vibri0
- campylobacter
- helicobacter
- bacteroides/prevotella
- clostridium
- listeria
2
Q
enterobacteriaceae
A
- Foodborne- Shigella, E. coli, Salmonella
- Minor foodborne- Y. enterocolitica and pseudotuberculosis
- ICU bugs- Kelsiella/Enterobacter/Serratia
- Proteus/Provdencia/Morganella
3
Q
defining characteristics of enterobacteriaceae
A
- gram neg
- non-sporulating
- straight rods
- facultative aerobes
- catalse pos, oxidase neg
- glucose fermenters
4
Q
common characteristics
A
- promiscuous to new DNA-acquired gut virulence factors
- pili for adhesion then secrete exotoxin-ETEC
- T3SS for adhesion, subverting gut macrophage
- antibiotic resistance
5
Q
T3SS/T4SS
A
-inject molecules to force cell to form actin bundle
6
Q
virulence
A
- adhesion and inject toxin
- secretion systems-for actin bundles/ deliver toxin
- actin based cell to cell motility
7
Q
shigella bacteria
A
- 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
8
Q
antimicrobial sensitivity assay
A
- 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
9
Q
salmonella
A
- gram neg rods
- motile
- > 2500 serovars
- food
- enterocolitis and enteric fevers (typhoid not typhus)
10
Q
salmonella pathogenesis
A
- 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
11
Q
salmonella mechanism
A
-same as Shigella with addition of trojan horses that disseminate and get triggered to form infection elsewhere (in typhoid- not in regular GI illness)
12
Q
virulence of salmonella
A
- 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
13
Q
salmonella pathogenesis 2
A
- 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
14
Q
Typhoid fever
A
- 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
15
Q
HUS
A
- 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
