122. General characteristics of diseases caused by Escherichia coli. Flashcards

1
Q

Etiology of E coli?

A

Etiology:

  • E. coli (Enterobacteriaeceae family)
  • Gr(-), lactose (+)
  • Antigens:
  • O: LPS (181), endotoxin, cell wall antigens (NOT a virulence factor)
  • K: polysaccharide (60), capsule antigen
  • H: protein (53), flagella antigen
  • F: protein (30) - F1-F18, F41, frimbra antigens - species specific
  • Normal inhabitant of LI, normal flora, vitamin production
  • Pathogenicity: mainly saprophyte (gut flora), some are facultative pathogenic strains
  • Virulence factors:
  • capsule, endotoxin (LPS, same as cell wall antigens, released when the bacteria breakdown),
  • adhesins (frimbrae), toxins, invasive ability (normally cannot invade host cells, some strains can),
  • ability of survival in blood
  • Adhesins (endotoxin): fimbria -
  • human (F2, F3 in newborn children),
  • calves (F5, F17, F41),
  • pigs (F4 -mostly, F6, F18),
  • urogenital (F7-16),
  • outer membrane protein of bacteria help with attachment,
  • attach to the surface of GI epithelia and damage cells
  • Intimin: produced by host cells, but initiated by bacteria
  • Fibronectine receptors
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2
Q

Toxins of E Coli?

A

Toxins:

  • Enterotoxins: produced in gut
  • LT: increased cAMP, large molecule, act on AC enzyme of host
  • ST: increased cGMP, smaller, dehydration (normally enterocytes absorb water from gut, but damaged from toxins - enterocytes excrete fluid instead = causing diarrhea),
  • metabolic acidosis
  • Cytotoxins:
  • Verotoxins: SLT/VT1/VT2 - inhibition of protein synthesis (endothel damage > edema
  • > hemorrhagic, necrosis)
  • Cytotoxic necrotic factor (CNF): human strains
  • Cytolethal distending toxin (CDT): human strains, urogenital, extra-intestinal
  • Alpha-hemolysin: pore-forming toxin
  • Invasive ability
  • Survival in blood (siderophors): septicemia strain (replicate and spread in blood)
  • Genetic variability
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3
Q

Pathotypes of E.coli ?

A

Pathotypes of E. coli- Enteric

  • Enterotoxigenic ETEC
  • produces enterotoxins, fimbria - causes diarrhea in suckling animals,
  • newborn children, travellers,
  • purely toxic effect that causes diarrhea (NO inflammation)
  • Enteropathogenic EPEC
  • adhesion from intimin, damage mainly microvilli (decreased absorption)
  • causing dyspepsia of newborns
  • Enterohemorrhagic/Verotoxigenic EHEC/VTEC
  • bind with intimin,
  • produce verotoxins (damage endothelial cells) -
  • causing hemorrhagic colitis/diarrhea,
  • hemolytic-uremic syndrome, purely toxic
  • effect that causes diarrhea (NO inflammation)
  • Enteroinvasive EIEC
  • more in humans, dysentery-like
  • Enteroadhesive-aggregative EAEC
  • mild enteritis in humans
  • Combined types: EHEC/EAEC Germany 2011 (O:104:H4)
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4
Q

Extra-intestinal of Ecoli?

A

Extra-intestinal

  • Urogenital: adhesin (F7-16), toxins (CNF, CDT, alpha-hemolysin)
  • Septicemia, meningitis: newborn children, old people, immune compromised
  • Colicin-V plasmid, alpha-hemolysin
  • Can survive in blood and spread
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5
Q

Diseases of animals caused by E coli ?

A

Diseases of animals caused by E. coli

  • Enteric
  • Calves: ETEC, VTEC
  • Piglets: ETEC, VTEC, EPEC
  • Rabbit: EPEC
  • Dog, cat: ETEC, VTEC, EPEC
  • Septicemic: calves, poultry
  • Urinary tract infection, mastitis: cows, sows (MMA)
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6
Q

Epidemiology of E coli?

A

Epidemiology

  • Infection: bacteria replicate in gut (fast, 4X within 1 hr)
  • Faeces (high amount), feed/water contaminated with feces, egg
  • (poultry: germinative - infected eggs > infected chickens, can also survive on eggshells)
  • Predisposing factors:
  • insufficient hygiene,
  • insufficient feeding of pregnant cows/weak calves,
  • insufficient colostrum,
  • overcrowding,
  • environment/stable (low temperature, high humidity),
  • nutritional deficiencies
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7
Q

Pathogenesis of E Coli?

A

Pathogenesis:

  • Infection PO: asymptomatic presence in the gut + predisposing factors
  • Replicate in gut: production of enterotoxins (act in gut - diarrhea),
  • verotoxins (more generalized effects - hemorrhages, edema)
  • Septicemia: endotoxin effect, spread in blood and affect different organs
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8
Q

Diagnosis of Ecoli ?

A

Diagnosis:

  • epidemiology, clinical signs, PM
  • Bacteriology:
  • Isolation/identification: pure culture (samples from guts, parenchymal organs)
  • Identification of serotype (O, K, H, F): certain serotypes produce certain diseases
  • Identification of virulence factors:
  • adhesins (agglutination, PCR),
  • toxins (isolated gut test - inoculate bacteria into the gut, PCR)
  • Examination of AB susceptibility
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9
Q

Treatment of E coli?

A

Treatment

  • Enteric diseases: AB that acts in the gut, not necessary absorbed
  • Per os AB: polymyxins, quinolones, aminoglycosides, broad spectrum beta-lactam (amox, cephalosporines)
  • Rehydration: fluid therapy
  • Septicemia: parenteral, generally too late when see signs caused by endotoxins released when the bacteria die
  • Mastitis: quinolones, aminoglycosides
  • AB resistance
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10
Q

Prevention of E Coli?

A

• Prevention

  • Predisposing factors: correct feeding of pregnants, good nutrition and management, hygiene!
  • Specific prevention
  • Colostrum: received in time, quality (10% of their weight, presence of appropriate AB),
  • quantity
  • Vaccination: mainly in case of neonatal diseases (vaccination in pregnant animals)
  • Probiotics (Gr+): Lactobacillus, Enterococcus, Bifidobacterium - colonize the gut, gut flora will shift to Gr+
  • Prebiotics: feed additives
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