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Flashcards in Enteric Bacteria Deck (16)

The Enterobacteriaceae

Major Foodborne:
-E. coli

Minor Foodborne:
-Y. enterocolitica
-Y. pseudotuberculosis

ICU Bugs:


Defining characteristics of Enterobacteriaceae

-gram (-)
-straight rods
-facultative aerobes
-catalase (+)
-oxidase (-)
-glucose fermenters


Acquired gut virulence factors

-promiscuous to new DNA-
-pili for adhesions
-Type 3 Secretion Systems
1-Adhesion 2. Subversion of gut macrophage


Enterobacteriaceae antibiotic resistance

-antibiotic resistance testing must be performed for any Enterobacteriaceae infection that requires treatment
-a liquid culture of the patient isolate is spread on large agar plates
-disks of filter paper soaked in various antibiotics are placed on the plate prior to overnight incubation
-successful plating produces a solid lawn of bacteria interrupted by zones of clearing around the effective antibiotics
-measurements of the clear zones must be compared to a table to determine the most effective antibiotic


Classification of E. coli gastroenteritises

-Enterotoxigenic E coli (ETEC) is a cause of traveler's diarrhea
-Enteropathogenic E. coli (EPEC) is a cause of childhood diarrhea
-Enteroinvasive E. coli (EIEC) causes a Shigella-like dysentery
-Enterohemorrhagic E. coli (EHEC) causes hemorrhagic colitis and may progress to hemolytic-uremic syndrome (HUS)
-Enteroaggregative E. coli (EAggEC) is primarily associated with persistent diarrhea in children in developing countries
-Enteroadherent E. coli (EAEC) is a cause of childhood diarrhea and traveler's diarrhea in Mexico and North Africa


Shigella bacterium

-intestinal epithelium protected from invasion by mucus layer, tight junctions
-M cells of Peyer's patch: immunological sampling
-entry of Shigella mediated by type III secretory system and other effector proteins and cytoskeletal rearrangements
-apoptosis of macrophage
-survival of bacteria
-initiation of inflammation


Salmonella Bacteriology

-Gram (-) rods
- motile
->2500 serovars exist
-usually acquired from contaminated food
-enteric fevers (typhoid fever)
-inflammation and diarrhea, nausea and vomiting
-immune response restricts to gut, bacteremia is rare
-high infectious dose (100k bacteria)
-gastric acid is protective, antacids increase risk
-bacteria attach by fimbriae (pili) to cells lining the intestinal lumen
-salmonellae selectively attach to specialized epithelial cells (M cells) of the Peyer patches


Salmonella pathogies

-M cell attempts immunological sampling but bacterium survives
-some salmonella spp proliferate in DCs, ride to distant sites in body -> typhoid fevers


Virulence factors of Salmonella

-Ipf operon enhances adhesion to M cells
-type 3 secretion system injects M cell, enhances bacterial translocation
-SipB injected by Spi1 Type 3 sys causes macrophage apoptosis
-in S. typhi, Spi2 Type 3 sys remodels phagosomes for systemic spread
-Vi antigen: S typhi capsule for immune evasion


Enteric and Typhoid fevers

-onset: fever, malaise, diffusion, abdominal pain, constipation (sometimes diarrhea)
-3-4 week progression: dry cough, stupor, delerium, intestinal hemorrhage, bowel perforation, myocarditis, death (9-13%)
-necrosis of the infected Peyer patches causes hemorrhage/perforation
-other symptoms from toxemia
-survivors may have long-term neurological sequale or chronic carriage in gallbladder (reservoir)
-Typhoid Mary NYC c1905


Hemolytic-Uremic Syndrome (HUS)

-shigella and enterohemorrhagic E coli both routinely cause fever, dehydration, severe headache, lethargy, diarrhea progresses from watery to bloody with mucus
-in a minority of cases (1-10%) bacteria escape the gut and shiga toxin is released into the bloodstream, causing HUS: fever, dehydration, hemolysis, thrombocytopenia, uremia requiring dialysis, 5-10% mortality
-blood smear shows schistocytes (distorted, fragmented red cells) probably generated as blood passes through many small thomboses (early DIC)
-predominantly peds
-antibiotic treatment of HUS is controversial: some antibiotics may worsen the outcome


Reactive Arthritis

-autoimmune sequel in patients with HLA-B27
-triggered by infection with Shigella, Salmonella, Yersinia, Campylobacter, Chlamydia
-defined as conjunctivitis+urethritis+arthritis
-can also involve mouth, fingers, soles of feet
-treated with non-steroidal anti-inflammatories, usually resolves in 2-5 months


Non-Foodborne Enterobacteriaceae

-usually normal flora gone bad
-usually opportunistic nosocomial infections, but some community-acquired diseases exist: Klebsiella pneumonia, Serratia endocarditis in IV drug users
-all common causes of catheter-associated UTIs
-"ICU Bugs"- opportunistic and extremely antibiotic resistant. Can easily become the last straw for a patient who was already seriously ill



-can be a primary pathogen, but usually with a predisposing condition like advanced age, chronic respiratory disease, diabetes, alcoholism
-large polysaccharide capsule defends against phagocytosis, complement
-adhesins adhere to gut cells, siderophores chelate iron
-particularly in men with predisposing conditions, causes lobar pneumonia with necrosis, inflammation, and hemorrhage thick bloody sputum "currant jelly sputum" In alcoholics, mortality may be 50% in alcoholics with bacteremia approaches 100% despite treatment
-less-lethal presentations include bronchitis, UTIs, wound infection, catheter infection


Klebsiella/Enterobacter/Serratia Group Pathogenesis

-Klebsiella causes nosocomial outbreaks, among top 8 hospital-acquired infections, second only to E. coli as cause of Gram- sepsis
-K. oxytoca among top 4 pathogens in NICUs
-carbapenem-resistant K. pneumoniae is currently spreading among hospitals worldwide


Klebsiella/Enterobacter/Serratia Group Diagnosis

-begin with culture and gram stain to implicate group and enable Ab resistance testing
-K. pneumoniae polysaccharide capsule gives mucoid appearance on agar
-more specific biochemical lab tests availible, often needed
-antiobiotics as indicated begin with aminoglycoside and cephalosporin