Enterobacteriaceae I: E.coli

  1. what are the two types of infections caused by Escherichia coli
    • gastroenteritis: infections acquired exogenously or from normal microbiome thru plasmids, bacteriophage DNA (transduction)
    • non-gastroenteritis (extraintestinal infections): acquired endogenously
  2. what are the 6 types of e.coli gastroenteritis
    • entertoxigenic (ETEC)
    • enteroaggregative (EPEC)
    • shiga toxin producing (STEC)
    • enterohemorrhagic (EHEC)
    • enteroinvasive (EIEC)
  3. what are the heat stable toxins of ETEC (enterotoxigenic e.coli)
    • STa and STb
    • STa leads to increase in cellular cGMP levels and hypersecretion of fluids and reduced absorption of fluids
  4. what are the heat labile toxins of ETEC (enterotoxigenic e. coli)
    • LT-I, LT-II, LT-III
    • increases cAMP levels causing enhanced secretion of chloride and decreased absorption of sodium chloride
  5. what is the pathogenicity of enteropathogenic e.coli (EPEC)
    • bacteria attaches to epithelial cells
    • contains a cluster of 40 virulence genes in a pathogenicity island called locus of enterocyte effacement (LEE)
  6. what is LEE (locus of enterocyte effacement)
    40 virulence genes of EPEC that contains T3SS and virulence effector proteins
  7. How does EPEC cause pathogenesis
    EPEC adheres to enterocytes by adhesins and pili which forms an actin microfilament pedestal
  8. how does shiga toxin cause pathogenecity
    shiga toxin inhibits host cell protein synthesis that disrupts systemic absorption
  9. what are the non gastrointestinal E.coli infections (3)
    • UTI: caused by hemolysin HllyA, adhesins
    • neonatal meningitis: caused by K1 capsular antigen e.coli's
    • septicemia
  10. how is e.coli treated
    • strong lactose fermentation
    • antibiotic therapy (resistance to penicillins)
    • proper cooking of beef to prevent STEC
    • avoiding unnecessary catheters
    • high hygienic standards
  11. how is E.coli ID'd in lab
    • strong lactose fermentation
    • STEC strains: does not ferment sorbital, direct detection of shiga toxin from feces
  12. what are enterocytes
    intestinal absorptive cell in epithelial lining of gut
  13. peyer's patch
    lymph follicles beneath the epithelium that interact with antigens in the gut. contains peyer's patch cells
  14. what are peyer patch cells
    MQ, denderitic cells, B cells, T cells
  15. what are M cells in the gut
    • microfold cell
    • cells above Peyer's Patches that take up antigen from the gut and present them to immune cells
  16. how does Y. enterocolitica cross the gut epithelium
    • crosses by M cells or enterocytes. 
    • can mimic psuedoappendicitis and cause enterocolitis
  17. how does shigella cross the gut
    • shigella cells do not directly invade enterocytes from gut lumen
    • attaches and invades M cells before invading enterocytes
  18. how does salmonella cross the gut epithelium
    • three ways
    • 1. invasion by endocytosis by M cells, then M cells pass the bacteria to macrophages in the Peyer's patch
    • 2. bacteria enter enterocytes by endocytosis
    • 3. bacteria are directly taken up in the lumen via phagocytosis by dendritic cells that extend projections across the epithelium
  19. where do salmonella replicate in the cell
  20. what are the pathogenicity islands that regulate the attachment, engulfment, and replication of salmonella
    • pathogenicity island I (PAI I): encodes salmonella secreted invasion protein (SsP) and T3SS I that injects proteins into host cell
    • pathogenicity island II (PAI II): encodes genes for invading host immune response and T3SS II
  21. what are the host inflammatory response to salmonalla infection
    • effects mainly GI tract
    • releases prostaglandins
    • stimulates cAMP production, resulting in fluid release into gut, causing diarrhea
  22. what do typhoid strains of salmonella cause and where do they colonize
    transported by MQ to the liver, spleen, and bone marrow where they replicate and lead to development of enteric typhoid fever
  23. non typhoid strains of salmonella can colonize what reservoirs
    all animals and humans
  24. how is non typhoid strain acquired
    • ingestion of contaminated foods
    • high inoculum
  25. who are the patients at risk from non typhoid salmonella
    • ppl that eat contaminated foods
    • patients with reduced gastric acid levels
  26. how is typhoid strains of salmonella acquired
    • contaminated foods
    • fecal-oral spread in children
    • low inoculum
  27. what are the two significant salmonella strains
    • salmonella typhi 
    • salmonella paratyphi
  28. what are the pathogenesis of s. typhi and s. paratyphi
    • typhoid fever/ paratyphoid fever
    • colonizes gall bladder, may be asymptomatic
  29. what are the clinical diseases of salmonella
    • gastroenteritis: non blood diarrhea
    • septicemia: seen in s. typhi, paratyphi, and choleraesuis
    • enteric fever: s. typhi produces typhoid fever
    • asymptomatic colonization in gall bladder (s. typhi and s. paratyphi)
  30. how is salmonella ID'd in lab
    isolation from stool
  31. how is salmonella treated
    • antibiotic treatment not recommended for enteritis
    • S. typhi and S. paratyphi should be treated with antibiotics
    • proper cooking of food
    • vaccines
  32. what are the 4 clinical species of shigella
    • shigella dysenteriae: produces shiga toxin
    • shigella flexneri: infectous in developing countries
    • shigella sonnei: infections in developed countries
    • shigella boydii: not commonly isolated
  33. how does shigella cause pathogenesis
    • invade inside host cells of the colon
    • secrete virulence effector proteins IpaA, IpaB, IpaCm and IpaD by T3SS
    • resists phagocytosis by inducing apoptosis
  34. what molecule is released by shigella during apoptosis and how does it cause damage to colon
    IL-18 which attracts polymorphonuclear leukocytes (PMNs) that destabilize integrity of intestinal wall, allowing for more shigella cells to cross the epithelial barrier and reach deeper tissues
  35. describe the shiga toxin
    • A-B enterotoxin 
    • disrupts protein synthesis by cleaving ribosome
    • toxin activity primarily damages epithelium
  36. what is the reservoir for shigella
    only humans
  37. how is shigellosis transmitted
    • low inoculum
    • transmitted person to person, fecal-oral in low sanitary and personal hygiene standards
    • occurs mainly in day care centers, nurseries,
  38. what is shigellosis and symptoms
    • enterocolitis, a pediatric disease
    • profuse watery diarrhea
    • cramps
    • tenesmus (straining to defecate)
    • pus and blood in stool
    • can progress to severe shigella dysenteriae
    • symptoms occur 1-3 days after ingestion
  39. what is the sample to analyze shigella cases
  40. how is shigella treated
    antibiotic therapy
  41. klebsiella significant physiology
    • capsule
    • mucoid colonies
  42. what disease does klebsiella pneumoniae and klebsiella oxytoca cause
    • necrotic destruction of alveolar spaces
    • cavitation
    • production of blood tinged sputum
  43. what does klebsiella granulomatis cause
    • granuloma inguinale
    • transmitted by sex or nonsexual trauma to genitalia
  44. what disease does klebsiella rhinoscleromatis cause
    granulomatous disease of nose
  45. what disease does klebsiella ozaenae cause
    chronic atrophic rhinitis
  46. what disease does proteus mirabils cause
    • UTI
    • infections in bladder or kidney
    • produces large quantities of urease which increases pH of urine and kidney stones
  47. are proteus species motile
    yes they swarm
  48. what is the clinical significance of enterobacter
    • nosocomial infections affecting neonates or immunocompromised pts
    • can colonize any body site
    • linked to surgical wounds or pts who stay in ICUs
  49. what is the clinical significance of citrobacter
    • nosocomial infections
    • affecting neonates and immunocompromised patients
    • causes meningitis and brain abscess in neonates
    • UTI
  50. what is the clinical significance of morganella
    • nosocomial
    • UTI
    • wound infections
  51. what is the clinical signficance of serratia
    • nosocomial
    • colonizes urinary and respiratory tracts
  52. what are the tests used to detect shiga toxin or shiga toxin genes
    • immunoassays 
    • molecular probes
Card Set
Enterobacteriaceae I: E.coli
e.coli, salmonella, shigella