Escherichia coli

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• Histiocytic ulcerative colitis in the dog and cat.

• Causes peritonitis in dogs and peritonitis in pigs
• In osteomyelitis
• In neonatal polyarthritis of calves
• In arthritis of horses

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
  • 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
  • ST activates guanylate cyclase in enteric epithelial cells, stimulating fluid secretion
• 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:
  • 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