Difference between revisions of "Escherichia coli"
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===''Eschericia coli'' (''E. coli'') overview=== | ===''Eschericia coli'' (''E. coli'') overview=== | ||
− | + | [[File:Ecoli.jpg|200px|right]] | |
*Member of ''Enterobacteriacae'' family of Gram-negative bacilli | *Member of ''Enterobacteriacae'' family of Gram-negative bacilli | ||
− | *Facultative anaerobe | + | *'''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 | ||
*Abundant in the environment | *Abundant in the environment | ||
− | *Found in many non-specific, endogenous infections, eg. wound infections | + | *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=== | ===''E. coli'' characteristics=== | ||
− | *Oxidase negative (do not possess cytochrome C oxidase) | + | *Usually motile with flagella and fimbriae |
− | *Grow on MacConkey agar (in presence of bile salts) | + | *'''Oxidase negative''' (do not possess cytochrome C oxidase) |
− | *Reduce nitrates to | + | *Grow on '''MacConkey agar''' (in presence of bile salts), producing pink colonies |
− | *Possess a | + | *'''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 | *Epidemiological typing of ''E. coli'' uses antigen combinations, eg. O125:K12:H42 | ||
+ | |||
+ | |||
+ | ===Pathogenesis=== | ||
+ | |||
+ | *<u>Virulence factors</u> 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|'''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|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|'''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 [[:Category:Mycoplasmas|''mycoplasma'']] 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 | ||
+ | **[[Oedema Disease|'''Oedema disease of pigs''']]: | ||
+ | |||
+ | **'''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 | ||
+ | ** [[Inflammatory Bowel Disease#Histiocytic Ulcerative Colitis|Histiocytic ulcerative colitis]] in the dog and cat. | ||
+ | ** Causes [[Peritonitis - Cats and Dogs|peritonitis in dogs]] and [[Peritonitis#In pigs|peritonitis in pigs]] | ||
+ | **Found in [[Osteomyelitis|osteomyelitis]] | ||
+ | **Associated with neonatal [[Infectious Arthritis#In Cattle|polyarthritis of calves]] | ||
+ | **In [[Deep Pyoderma|deep pyoderma]] | ||
+ | **Found in [[Infectious Arthritis#In Horses|arthritis of horses]] | ||
+ | |||
+ | ==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 [[Haemorrhage#Dysentery|dysentery]] | ||
+ | |||
+ | |||
+ | *'''Enterotoxigenic ''E. coli'' (ETEC)''': | ||
+ | **General: | ||
+ | *** Contributes to [[Calf Diarrhoea, Undifferentiated Neonatal|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 | ||
+ | **Clinical signs: | ||
+ | ***The gut becomes distended with fluid and a [[Diarrhoea#Secretory Diarrhoeas|secretory diarrhoea]] which lasts several days results | ||
+ | ***Watery diarrhoea, dehydration, acidosis, death | ||
+ | **Immunity: | ||
+ | ***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)''': | ||
+ | **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|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 | ||
+ | |||
+ | ==in cattle== | ||
+ | |||
+ | |||
+ | *Neonatal polyarthritis: | ||
+ | |||
+ | **[[Escherichia coli|'''''Coliforms''''']] | ||
+ | ***Localises in joints and meninges in severe non-fatal neonatal colibacillosis | ||
+ | ***May remain as chronic arthritis in larger joints | ||
+ | |||
+ | [[Category:Enterobacteriaceae]] | ||
+ | [[Category:To_Do_-_Bacteria]] |
Latest revision as of 11:30, 20 November 2012
This article has been peer reviewed but is awaiting expert review. If you would like to help with this, please see more information about expert reviewing. |
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:
- Urogenital tract infections
- 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
- In deep pyoderma
- Found in arthritis of horses
- Watery mouth of lambs:
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
- Immunity:
- 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
in cattle
- Neonatal polyarthritis:
- Coliforms
- Localises in joints and meninges in severe non-fatal neonatal colibacillosis
- May remain as chronic arthritis in larger joints
- Coliforms