Difference between revisions of "Escherichia coli"
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− | + | <big><center>[[Enterobacteriaceae|'''BACK TO ENTEROBACTERIACEAE''']]</center></big> | |
+ | <big><center>[[Bacteria|'''BACK TO BACTERIA''']]</center></big> | ||
+ | <big><center>[[Infectious agents and parasites|'''BACK TO INFECTIOUS AGENTS AND PARASITES''']]</center></big> | ||
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+ | * [[Intestines - Inflammatory Bowel Disease And Related Conditions#Histiocytic Ulcerative Colitis|Histiocytic ulcerative colitis]] in the dog and cat. | ||
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+ | * Causes [[Peritoneal cavity - inflammatory#In dogs|peritonitis in dogs]] and [[Peritoneal cavity - inflammatory#In pigs|peritonitis in pigs]] | ||
+ | * In [[Bones - inflammatory#Osteomyelitis|osteomyelitis]] | ||
+ | *In neonatal [[Joints - inflammatory#In Cattle|polyarthritis of calves]] | ||
+ | *In [[Joints - inflammatory#In Horses|arthritis of horses]] | ||
===''Eschericia coli'' (''E. coli'') overview=== | ===''Eschericia coli'' (''E. coli'') overview=== | ||
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*Member of ''Enterobacteriacae'' family of Gram-negative bacilli | *Member of ''Enterobacteriacae'' family of Gram-negative bacilli | ||
− | * | + | *Facultative anaerobe |
*One of predominant bacterial species in colonic flora | *One of predominant bacterial species in colonic flora | ||
*Colonisation of intestinal tract from environmental sources shortly after birth | *Colonisation of intestinal tract from environmental sources shortly after birth | ||
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*Most strains have low virulence | *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 | *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 | ||
− | * | + | *Also an enteropathogen, causing neonatal diarrhoea in young animals and enteric colibacillosis |
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*Pathogenic strains possess virulence factors allowing colonisation of mucosal surfaces | *Pathogenic strains possess virulence factors allowing colonisation of mucosal surfaces | ||
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*Usually motile with flagella and fimbriae | *Usually motile with flagella and fimbriae | ||
− | * | + | *Oxidase negative (do not possess cytochrome C oxidase) |
− | *Grow on | + | *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 | + | *Reduce nitrates to nitrits and ferment glucose to produce acid and gas |
− | *Possess a | + | *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 | *Epidemiological typing of ''E. coli'' uses antigen combinations, eg. O125:K12:H42 | ||
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===Pathogenesis=== | ===Pathogenesis=== | ||
− | * | + | *Virulence factors include capsules, endotoxin, enterotoxins and colonisation factors |
*Capsular polysaccharides produced by some strains prevent phagocytosis and interfere with complement | *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 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 | *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== | + | ===Extra-intestinal infection=== |
*Soft tissue infections in adult animals | *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: | *Pathogenesis: | ||
**Produces an alpha-haemolysin which may be cytotoxic | **Produces an alpha-haemolysin which may be cytotoxic | ||
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**May enter blood to cause septicaemia | **May enter blood to cause septicaemia | ||
*Clinical infections: | *Clinical infections: | ||
− | ** | + | **Avian [[Intestines - Catarrhal Enteritis#Colibacillosis|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: | |
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***Systemic disease in young calves, piglets, foals, lambs | ***Systemic disease in young calves, piglets, foals, lambs | ||
***Penetration of intestinal mucosa and entrance into the blood | ***Penetration of intestinal mucosa and entrance into the blood | ||
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***Virulence related to adhesive properties, complement resistance and ability for iron aquisition | ***Virulence related to adhesive properties, complement resistance and ability for iron aquisition | ||
***Ammonia, dust, viral infections and temperature changes enhance likelihood of disease | ***Ammonia, dust, viral infections and temperature changes enhance likelihood of disease | ||
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− | + | ===Intestinal disease=== | |
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− | ==Intestinal | ||
*''E. coli'' is part of the flora of the large intestine, but is not usually found in the small intestine | *''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 | *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 | + | *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 | |
− | * | + | *''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): | |
− | + | ** Contributes to [[Intestines - Catarrhal Enteritis#Undifferentiated Neonatal Calf Diarrhoea|undifferentiated neonatal calf diarrhoea]], a mixed viral enteritis in calves | |
− | + | **Causes scours in pigs and calves | |
− | + | **'Traveller's diarrhoea' in humans | |
− | + | **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 | |
− | + | **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 | |
− | + | **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 | |
− | **** | + | **The gut becomes distended with fluid and a [[Intestines - diarrhoea#Secretory Diarrhoeas|secretory diarrhoea]] which lasts several days results |
− | ** | + | **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): | |
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**Possess ''E. coli'' adherence factor plasmid | **Possess ''E. coli'' adherence factor plasmid | ||
− | **An adhesin, intimin is required for | + | **An adhesin, intimin is required for attchment to enterocytes |
− | ** | + | **Cause attching and effacing lesions in the gut |
− | + | *Enteroinvasive ''E. coli'' | |
− | + | **Dysentry-like strains | |
− | + | **Invade epithelial cells by inducing endocytosis | |
− | + | **Traverse gut wall to lamina propria | |
− | * | + | *Enterohaemorrhagic ''E. coli'': |
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− | **Invade epithelial cells | ||
− | **Traverse gut wall to lamina propria | ||
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**Possibly carried by cattle | **Possibly carried by cattle | ||
**Produce shiga-like toxin, a vero toxin | **Produce shiga-like toxin, a vero toxin | ||
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**Attaching and effacing lesions, unrelated to toxin production | **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 | **''E. coli'' O157:H7 causes haemorrhagic collitis-haemolytic uraemic syndrome in humans | ||
+ | *Enteroaggretative ''E. coli'': | ||
+ | *Oedema disease of pigs: | ||
+ | **Associated with oedema disease toxin-producing strains of ''E. coli'' | ||
+ | **Verotoxin released in the small intestine and carried in the bloodstream | ||
+ | **Haemolysin production | ||
− | * | + | *Haemorrhagic gastroenteritis: |
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− | + | *Watery mouth of lambs: | |
− | + | **Lack of colostrum allows collonisation and overgrowth of ''E. coli'' in the small intestine | |
+ | **Absorption of endotoxin leads to death |
Revision as of 11:56, 24 December 2007
- 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
- Also an enteropathogen, causing neonatal diarrhoea in young animals and enteric colibacillosis
- 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 nitrits 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
- Avian colibacillosis:
Intestinal disease
- 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
- 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
- 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):
- Contributes to undifferentiated neonatal calf diarrhoea, a mixed viral enteritis in calves
- Causes scours in pigs and calves
- 'Traveller's diarrhoea' in humans
- 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
- 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
- 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
- The gut becomes distended with fluid and a secretory diarrhoea which lasts several days results
- 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 attchment to enterocytes
- Cause attching and effacing lesions in the gut
- 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
- Enteroaggretative E. coli:
- Oedema disease of pigs:
- Associated with oedema disease toxin-producing strains of E. coli
- Verotoxin released in the small intestine and carried in the bloodstream
- Haemolysin production
- 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