Difference between revisions of "Escherichia coli"

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***This causes irreversible activation of adenylate cyclase in target cells
 
***This causes irreversible activation of adenylate cyclase in target cells
 
***This raises the cAMP level and causes hypersecretion of water and chloride ions into the lumen of the small intestine and inhibits reabsorption of sodium
 
***This raises the cAMP level and causes hypersecretion of water and chloride ions into the lumen of the small intestine and inhibits reabsorption of sodium
 +
***ST activates guanylate cyclase in enteric epithelial cells, stimulating fluid secretion
 
**Clinical signs:
 
**Clinical signs:
 
***The gut becomes distended with fluid and a [[Intestines - diarrhoea#Secretory Diarrhoeas|secretory diarrhoea]] which lasts several days results
 
***The gut becomes distended with fluid and a [[Intestines - diarrhoea#Secretory Diarrhoeas|secretory diarrhoea]] which lasts several days results
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***Parenteral vaccination of pigs and cattle protects offspring from scours via antibody production in the colostrum (passive immunity)
 
***Parenteral vaccination of pigs and cattle protects offspring from scours via antibody production in the colostrum (passive immunity)
 
***ST is not immunogenic; it is small, with only 19 amino acids
 
***ST is not immunogenic; it is small, with only 19 amino acids
***ST activates guanylate cyclase in enteric epithelial cells, stimulating fluid secretion
 
 
*Enteropathogenic ''E. coli'' (EPEC):
 
*Enteropathogenic ''E. coli'' (EPEC):
 
**Possess ''E. coli'' adherence factor plasmid
 
**Possess ''E. coli'' adherence factor plasmid
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**Cause attching and effacing lesions in the gut, with necrosis of enterocytes and stunting and fusion of villi
 
**Cause attching and effacing lesions in the gut, with necrosis of enterocytes and stunting and fusion of villi
 
*Enteroinvasive ''E. coli'':
 
*Enteroinvasive ''E. coli'':
 +
**Bacteraemia and septicaemia
 
**Dysentry-like strains
 
**Dysentry-like strains
 
**Invade epithelial cells by inducing endocytosis  
 
**Invade epithelial cells by inducing endocytosis  

Revision as of 20:01, 8 February 2008

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Eschericia coli (E. coli) overview

  • Member of Enterobacteriacae family of Gram-negative bacilli
  • Facultative anaerobe
  • One of predominant bacterial species in colonic flora
  • Colonisation of intestinal tract from environmental sources shortly after birth
  • Abundant in the environment
  • Most strains have low virulence
  • Found in many non-specific, endogenous infections, eg. wound infections, upper respiratory tract infections, infections of the urinary tract, mammary glands and uterus and septicaemia
  • An enteropathogen, causing neonatal diarrhoea in young animals and enteric colibacillosis
  • Enterotoxigenic E. coli is the most common cause of diarrhoea in calves, lambs and pigs
  • Pathogenic strains possess virulence factors allowing colonisation of mucosal surfaces


E. coli characteristics

  • Usually motile with flagella and fimbriae
  • Oxidase negative (do not possess cytochrome C oxidase)
  • Grow on MacConkey agar (in presence of bile salts), producing pink colonies
  • Haemolytic activity on blood agar characteristic of certain strains
  • Lactose fermenter
  • Reduce nitrates to nitrites and ferment glucose to produce acid and gas
  • Possess a lipolysaccharide (O) antigen, a flagellate (H) antigen, polysaccharide capsule (K) antigens and fimbrial (F) antigens
  • Epidemiological typing of E. coli uses antigen combinations, eg. O125:K12:H42


Pathogenesis

  • Virulence factors include capsules, endotoxin, enterotoxins and colonisation factors
  • Capsular polysaccharides produced by some strains prevent phagocytosis and interfere with complement
  • Endotoxin is a lipolysaccharide component of the cell wall of Gram-negative bacteria, composed of lipid A, a core polysaccharide and various side chains
  • Endotoxin is realeased when bacteria die, and causes endothelial damage leading to disseminated intravascular coagulation and endotoxic shock; it is also a pyrogen
  • Enterotoxins, verotoxins and cytotoxic necrotising factors produced by many pathogenic E. coli; these produce cell damage at their site of action
  • Alpha-haemolysin may increase iron availability for invading organisms
  • Siderophores are made by certain pathogenic strains, and are responsible for iron aquisition; they include aerobactin and enterobactin


Extra-intestinal infection

  • Soft tissue infections in adult animals
  • Most common organism infecting urinary tract
  • Causes pyometra in the dog and cat and pyelonephritis
  • Acute mastitis in lactating animals
  • Pathogenesis:
    • Produces an alpha-haemolysin which may be cytotoxic
    • Iron aquisition system
    • K antigens prevent phagocytosis or mimic host antigens and resist complement
    • Fimbriae permit adhesion to mucosal surfaces
    • May enter blood to cause septicaemia
  • Clinical infections:
    • Avian colibacillosis:
      • Septicaemia in newly-hatched chickens
      • Infection enters via faecal contamination of the egg surface or via the ovary of the hen
      • Infection enters via the respiratory tract
      • A bacteraemia develops
      • Acute colisepticaemia, subacute fibrinopurulent serositis or chronic granulomatous disease of the viscera
      • Occurs in older birds via inhalation of E. coli in dust; respiratory infection spreads to the blood to cause acute colisepticaemia
      • Airsacculitis, pericarditis and perihepatitis during acute phase
      • Often secondary to virus or mycoplamsa infection or environmental stress
    • Colisepticaemia:
      • Systemic disease in young calves, piglets, foals, lambs
      • Penetration of intestinal mucosa and entrance into the blood
      • Invasive strains survive the host defences
      • Virulence related to adhesive properties, complement resistance and ability for iron aquisition
      • Ammonia, dust, viral infections and temperature changes enhance likelihood of disease


Intestinal infection

  • E. coli is part of the flora of the large intestine, but is not usually found in the small intestine
  • Some strains possess fimbrae which attach the bacteria to the small intestinal epithelium of particular animal species
  • E. coli may cause diarrhoea via attaching and effacing lesions, where bacteria adhere intimately to the enterocyte, and cause localised effacement of the brush border microvilli; the epithelial erosion causes dysentery
  • Enterotoxigenic E. coli (ETEC):
    • General:
      • Contributes to undifferentiated neonatal calf diarrhoea, a mixed viral enteritis in calves, also known as enteric colibacillosis
      • Causes scours in pigs, calves and lambs
      • 'Traveller's diarrhoea' in humans
    • Pathogenesis:
      • Oral infection, intestinal colonisation and toxin production
      • Fimbrial antigen or colonisation factor antigens (CFAs)determine species specificity
      • Fimbrial adhesins allow bacteria to attach to mucosal surfacesin the small intestine and lower urinary tract; this prevents expulsion by peristalsis and flushing of urine
      • K88 (F4) is associated with adhesion to the small intestinal mucosa of pigs
      • K99 (F5) associated with adhesion in pigs and cattle (these fimbrial adhesins were originally thought to be capsular (K) antigens)
      • The fimbrae are encoded by plasmids
      • These strains carry a plasmid which encodes an enterotoxin
      • Two types of enterotoxin: heat-labile (LT) and heat-stable (ST) toxins
      • The plasmids which produce these toxins are responsible for the pathogenicity of these strains
      • LT is an oligometric toxin composed of an enzymatically-active A subunit (30KDa; 2 fragments - A1 and A2) and 5 identical B subunits (12KDa) forming the binding portion (B oligomer)
      • It attaches to the brush border of the epithelial cells of the small intestine
      • LT causes ADP-ribosylation of the stimulatory subunit of guanine nucleotide binding proteins of the adenylate cyclase complex in eukaryotic cell membranes
      • This causes irreversible activation of adenylate cyclase in target cells
      • This raises the cAMP level and causes hypersecretion of water and chloride ions into the lumen of the small intestine and inhibits reabsorption of sodium
      • ST activates guanylate cyclase in enteric epithelial cells, stimulating fluid secretion
    • Clinical signs:
      • The gut becomes distended with fluid and a secretory diarrhoea which lasts several days results
      • Watery diarrhoea, dehydration, acidosis, death
    • Immunuty:
      • LT is antigenic
      • Immunity is developed via production of antibody to LT protein and fimbrial antigen
      • Parenteral vaccination of pigs and cattle protects offspring from scours via antibody production in the colostrum (passive immunity)
      • ST is not immunogenic; it is small, with only 19 amino acids
  • Enteropathogenic E. coli (EPEC):
    • Possess E. coli adherence factor plasmid
    • An adhesin, intimin is required for attachment to enterocytes
    • Cause attching and effacing lesions in the gut, with necrosis of enterocytes and stunting and fusion of villi
  • Enteroinvasive E. coli:
    • Bacteraemia and septicaemia
    • Dysentry-like strains
    • Invade epithelial cells by inducing endocytosis
    • Traverse gut wall to lamina propria
  • Enterohaemorrhagic E. coli:
    • Possibly carried by cattle
    • Produce shiga-like toxin, a vero toxin
    • Attaching and effacing lesions, unrelated to toxin production
    • Disseminated intravascular coagulation and thrombus formation
    • E. coli O157:H7 causes haemorrhagic collitis-haemolytic uraemic syndrome in humans
  • Cytotoxin necrotising factor-producing E. coli


  • Oedema disease of pigs:
    • Acute, frequently fatal enterotoxaemia of weaned pigs
    • Associated with particular haemolytic serotypes of E. coli
    • Verotoxin (Shiga toxin II e) released in the small intestine and carried in the bloodstream
    • Haemolysin production
    • Subcutaneous and subserosal oedema
    • Peracute disease affecting particulary healthy piglets
    • Mortality rate 30%-90%
    • Antimicrobial treatment effectic if administered in time
  • Haemorrhagic gastroenteritis:
  • Watery mouth of lambs:
    • Lack of colostrum allows collonisation and overgrowth of E. coli in the small intestine
    • Absorption of endotoxin leads to death