Escherichia coli
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BACK TO ENTEROBACTERIACEAE
BACK TO BACTERIA
BACK TO INFECTIOUS AGENTS AND PARASITES
BACK TO ENTEROBACTERIACEAE
BACK TO BACTERIA
BACK TO INFECTIOUS AGENTS AND PARASITES
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 lipopolysaccharide (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
- 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:
- Urogenital tract infections
- Most common organism infecting urinary tract
- Ascending infections of urinary tract
- Causes pyometra in the dog and cat and pyelonephritis
- Cystitis in the bitch
- Prostatitis in dogs via opportunistic infection
- Colonisation of mucosa aided by fimbriae
- Mastitis
- Opportunistic infection of mammary glands of sows and cows
- Endotoxaemia in the acute form often fatal
- Death within 24-48 hours during peracute disease
- Animals depressed with sunken eyes
- Colibacillosis:
- Avian:
- 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 mycoplasma infection or environmental stress
- Avian:
- 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
- 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 effective if administered in time
- Watery mouth of lambs:
- Affects lambs under three days old
- Lack of colostrum allows collonisation and overgrowth of E. coli in the small intestine
- Systemic invasion by E. coli
- Absorption of endotoxin leads to death
- Severe depression, anorexia, salivation and abdominal distension
- Morbidity and mortality high
- Histiocytic ulcerative colitis in the dog and cat.
- Causes peritonitis in dogs and peritonitis in pigs
- Found in osteomyelitis
- Associated with neonatal polyarthritis of calves
- Found in arthritis of horses
- Urogenital tract infections
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 fimbriae 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
- 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
- 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
- LT
- 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
- General:
- Enteropathogenic E. coli (EPEC):
- Attaching and effacing strains of E. coli
- Attach to small intestinal epithelial cells and cause necrosis of enterocytes and stunting and fusion of villi
- Possess E. coli adherence factor plasmid
- An adhesin, intimin is required for attachment to enterocytes
- Secrete signalling proteins that activate a tyrosine kinase, causing rearrangement of cytoskeletal proteins and effacement of microvilli
- Intracellular calcium levels increase and production of protein kinase C causes loss of chloride ions and water from the intestinal epithelial cells
- Diarrhoea results
- Enteroinvasive E. coli:
- Cause colisepticaemia in calves during their first week of life; occasionally in lambs, piglets and puppies
- Infection via ingestion or umbilicus; inadequate colostrum increases susceptibility
- Invade epithelial cells of small intestine by inducing endocytosis
- Traverse gut wall to lamina propria and enter lymphatics
- Resistant to complement-mediated killing
- Bacteraemia or septicaemia and endotoxaemia
- Widespread petechial haemorrhages of organs and serosa
- Abscesses, pneumonia in long term
- Death occurs in absense of treatment
- Enterohaemorrhagic E. coli:
- Possibly carried by cattle
- Produce shiga-like toxin, a vero toxin
- Plasmid-coded fimbriae important for virulence
- Intimin produced allowing intimate attachment to intestinal epithelial cells
- Strains do not product LT or ST and are not enteroinvasive
- 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
- Infrequently cause diarrhoea in calves, pigs and humans
- Important virulence factors include toxin and fimbriae