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Created page with '===Overview=== *Organisms present in the soil, alimentary tract and faeces *Endospores may be present in liver and may be reactivated to cause disease *Neurotoxic clostridia, ''…'
===Overview===
*Organisms present in the soil, alimentary tract and faeces
*Endospores may be present in liver and may be reactivated to cause disease
*Neurotoxic clostridia, ''Clostridium tetani'' and ''Clostridium botulinum'' affect neuromuscular function but cause no tissue damage
*Histotoxic clostridia cause localised lesions in tissues and may cause toxaemia
*''C. perfringens'' cause inflammatory lesions in the gastrointestinal tract and enterotoxaemias in sheep
===Characteristics===
*Large Gram-positive rods
*Obligate anaerobes
*Fermentative, catalase negative, oxidase negative
*Straight or slightly curved
*Motile by flagellae
*Require enriched media for growth
*Produce endospores which vary in shape and location and cause bulging of mother cell
===Pathogenesis and pathogenicity===
*Produce extracellular digestive enzymes and toxic substance known as exotoxins
*Exotoxins cause necrosis, haemolysis and death
*Collagenase, hyaluronidase and DNase enymes facilitate spread through tissues
===Diagnosis===
*Anaerobic transport medium
*Culture on blood agar enriched with yeast extract, vitamin K and haemin
*Anaerobic culture with hydrogen supplement and 5-10% carbon dioxide for 48 hours
*Colonies of ''C. perfringens'' are 5mm diameter, circular, flat and grey and surrounded by a zone of double haemolysis
*Positive cAMP test with ''Streptococci agalactiae''
*Biochemical tests
*Toxins identified in body fluids by toxin neutralisation or protection tests in lab animals
*Nagler reaction to detect alpha toxin - plate neutralisation test
*Fluorescent antibody tests for histotoxic clostridia
*ELISA, PCR for toxin detection
*Sudden death in unvaccinated farm animals may suggest ''C. perfringens'' types B, C and D
*Post mortem
*Gram positive rods present on intestinal smears suggests clostridial enterotoxaemia
===Histotoxic infections===
*Exotoxins cause local tissue necrosis and systemic effects which can be fatal - toxaemia
*''C. chauvei'' and ''C. septicum'' present in muscle as latent spores which can germinate to cause infection
*''C. novyi'' type B and ''C. haemolyticum'' have latent spores in the liver
*When inoculated into wounds, cause malignant oedema and gas gangrene
*Endospores persist in the soil
*Most ingested spores excreted in faeces, but some become dormant in tissues
*Tissue injury leads to reduced oxygen tensions allowing germination and replication of bacteria
*Exotoxins cause local necrosis
*Activated spores in the liver and muscles cause endogenous infections including blackleg, infectious necrotic hepatitis and bacillary haemoglobinuria
*Inoculation of wounds causes exogenous infections including malignant oedema and gas gangrene
===''Clostridium chauvei''===
*[[Muscles Inflammatory - Pathology#Black leg|Black leg]]:
**Acute disease of cattle and sheep
**Endogenous infection in young cattle with latent spores in muscles, activated by trauma
**Exogenous infection via wounds in sheep of any age
**Gangrenous cellulitis and myositis caused by exotoxins leads to rapid death
**Skeletal muscle damage with lameness, swelling and crepitus due to gas accumilation
**Dyspnoea due to lesions in tongue and throat muscles
**Myocardial and diaphragmatic lesions can cause sudden death
**Fluorescent antibody test for diagnosis
*Causes [[Necrosis - Pathology#Gas Gangrene|gas gangrene]], along with [[Clostridium species#Clostridium septicum|''Clostridium septicum'']]
===Clostridium septicum===
*Causes malignant oedema:
**Infection via wounds
**Cellutis with minimal gangrene and gas formation
**Tissue swelling die to oedema; coldness and discoloration of overlying skin
**Toxaemia with depression; death may be rapis if extensive lesions
*Causes braxy:
**Abomasitis of sheep
**Disease occurs during winter
**Rapidly fatal; anorexia, depression, fever
*Causes [[Necrosis - Pathology#Gas Gangrene|gas gangrene]] and [[Muscles Inflammatory - Pathology#Gas gangrene|myositis]]
===Clostridium novyi===
*Infectious necrotic hepatitis/black disease:
**Acute disease of sheep, occasionally cattle
**Hepatic necrosis caused by exotoxins of ''C. novyi'' type B in liver damaged by ''Fasciola hepatica''
**Rapid death
**Dark discoloration of skin caused by subcutaneous venous congestion
**Fluorescent antibody test diagnostic
* Causes [[Necrosis - Pathology#Gas Gangrene|gas gangrene]] and [[Muscles Inflammatory - Pathology#Gas gangrene|myositis]].
*May be involved in [[Bacterial skin infections - Pathology#Systemic bacterial infections|cutaneous lesions]]
*Causes big head in rams - oedema of subcutaneous tissues of the head, neck and cranial thorax; necrotising lethal alpha toxin
===''Clostridium perfringens'' type A===
*[[Necrosis - Pathology#Gas Gangrene|Gas gangrene]] and [[Muscles Inflammatory - Pathology#Gas gangrene|myositis]]
**Extensive bacterial invasion of damaged muscle
**Gas production causing subcutaneous crepitus
**Similar manifestations as malignant oedema
===''Clostridium haemolyticum''===
*Causes bacillary haemoglobinuria in cattle, occasionally sheep
*Endogenous infection - endospores dormant in liver
*Fluke migration allows germination
*Beta toxin causes intravascular haemolysis and hepatic necrosis
*Haemoglobinuria due to destruction of red blood cells
===Clostridium sordelli===
*Causes [[Necrosis - Pathology#Gas Gangrene|gas gangrene]], [[Muscles Inflammatory - Pathology#Gas gangrene|myositis]] and abomasitis (lambs)
===Treatment of histotoxic infections===
*Early penicillin
*Vaccination with bacterin or toxoid at 3 months and booster after 3 weeks, then annually
===Enteropathogenic and enterotoxaemic clostridia===
*General:
**''Clostridium perfringens'' types B, C and D
**Found in soil, feaces and intestinal tract
**Survive in soil as spores
**Husbandry, changes in diet and environment predispose to proliferation in the intestine
**Abrupt changes to rich diets and intestinal hypomotility due to overeating
*Pathogenesis and pathogenicity:
**Clostridial replication and overgrowth in the interstinal tract of sheep
**Production of potent exotoxins which cause local and systemic effects of enterotoxaemia
**Type of toxins produced determine clinical syndrome
**Haemolysins, collagenases and hyaluronidases also produced
===''C. perfringens'' type A===
*Necrotising enterocolitis in pigs and necrotic enteritis in chickens (alpha toxin with lecithinase activity)
*Canine haemorrhagic gastroenteritis (cytotoxic enterotoxin)
*Typhlocolotis in horses, possibly associated with [[Intestines Fibrinous/Haemorrhagic Enteritis - Pathology#Colitis X|Colitis X]]
===''C. perfringens'' type B===
*[[Intestines Fibrinous/Haemorrhagic Enteritis - Pathology#Lamb Dysentery (Enterotoxaemia with Blood)|Lamb dysentery]]
*Up to 30% morbidity and high mortality
*Affects lambs in first week of life
*Abdominal distension, pain, bloody faeces, sudden death
*Bacterial overgrowth in the intestine of the lamb due to immature bacterial flora
*Lack of proteases in the immature gut prevents cleavage of the beta toxin, allowing it to cause disease
*Also alpha and epsilon toxins
*Haemorrhagic enteritis and ulceration in the small intestine
*Fluid in the peritoneal cavity and pericardial sac due to increased capillary permeability (beta toxin)
*Fatal haemorrhagic enteritis in newborn foals, calves and adult goats
===''C. perfringens'' type C===
*Acute enterotoxaemia in adult sheep, 'struck'
*Sudden death or terminal convulsions in sheep at pasture
*Beta toxin (lethal, necrotising) plays major role in pathogenesis of the disease - increases intestinal and capillary permeability
*Also alpha toxin (lecithinase)
*Post mortem: jejunal ulceration; hyperaemia in small intestine; fluid accumulation in peritoneal cavity; congestion of peritoneal vessels; petechial haemorrhages
*Haemorrhagic enteritis in piglets
**Peracute enterotoxaemia often of entire litter with mortality rates 80%
**Infection from sow's faeces
**Death within 24 hours in young piglets
**Chronic disease in older piglets
**Dullness, anorexia, bloody faeces, perianal hyperaemia
**Post mortem: necrosis of terminal small intestinal mucosa, caecum and colon and blood-stained contents; serosanguinous fluid in pleural and peritoneal cavities
*Necrotic enteritis in chickens:
**Broilers under 12 weeks
**Acute enterotoxaemia, sudden onset and high mortality
**Necrosis of small intestine
**Predisposing factors include diet changes, coccidial infection and intestinal hypomotility
*Acute enterotoxaemia with haemorrhagic enteritis in calves, lambs, foals, goats
*[[Peritoneal Cavity Inflammatory - Pathology#In cattle|Peritonitis in cattle]] - sudden death in feedlot cattle
===''C. perfringens'' type D===
*[[Intestines Catarrhal Enteritis - Pathology#"Pulpy Kidney" Disease|Pulpy kidney disease]] in well-fed 3-10 week-old lambs
*Follows overeating high grain diet or luchious pasture
*Starch from partially digested food enterering the intestine from the rumen allows rapid clostridial proliferation
*Epsilon toxin activated by proteolytic enzymes causes toxaemia
*Epsilon toxin increases intestinal and capillary permeability; also alpha toxin
*Lambs found dead or with opisthotonos, convulsions, coma in acute phases
*Blindness and head pressing in subacute disease; bloat in later stages
*Hyperglycaemia, glycosuria
*Post mortem: hyperaemia in intestine; fluid in pericardial sac; kidney autolysis with pulpy cortical softening (acute death)
*Subacute death causes symmetrical encephalomalacia and haemorrhage in basal ganglia and midbrain
*Enterotoxaemia in kids and adult goats
===''C. perfringens'' type E===
*Enteritis in rabbits, haemorrhagic enteritis in calves
*ALpha and iota toxins
===Treatment and control of enterotoxaemic infections===
*Hyperimmune serum
*Vaccination - vaccinate ewes with toxoid 6 weeks before lambing to allow passive protection of lambs
*Vaccination of lambs with toxoid before 2 months of age to protect against pulpy kidney
*Avoid sudden dietary changes
===''C. piliforme''===
*Spore-forming filamentous Gram negative intracellular pathogen
*Only grows in tissue culture or embryonated eggs
*Causes Tyzzer's disease - severe hepatic necrosis
*Sporadic disease in foals, calves, dogs, cats
*Foals under 6 weeks, found dead or comatose
*Incubation period up to 1 week
*Depression, anorexia, fever, jaundice, diarrhoea
*Hepatomegaly and necrosis on post mortem
*Diagnosis: Warthin-Starry silver impregnation technique demonstrates organisms in hepatocytes
===''C. difficile''===
*Dogs with chronic diarrhoea
*New born foals with haemorrhagic enterocolitis
*Possibly associated with acute colitis in adult horses following antibiotic therapy or grain overload
===''C. colinum''===
*Enteritis in poulty and game birds
*Shed in faeces of clinically affected and carrier birds
*Intestinal ulceration and hepatic necrosis
*Therapeutic antibiotics in drinking water
===''C. spiroforme''===
*Spontaneous and antibiotic-induced enteritis in rabbits
*Enterotoxaemia, fatal within 48 hours
*Oral antibiotics upset the intestinal flora, allowing overgrowth of clostridia[[Category:Bacteria]][[Category:Gram_positive_bacteria]]
*Organisms present in the soil, alimentary tract and faeces
*Endospores may be present in liver and may be reactivated to cause disease
*Neurotoxic clostridia, ''Clostridium tetani'' and ''Clostridium botulinum'' affect neuromuscular function but cause no tissue damage
*Histotoxic clostridia cause localised lesions in tissues and may cause toxaemia
*''C. perfringens'' cause inflammatory lesions in the gastrointestinal tract and enterotoxaemias in sheep
===Characteristics===
*Large Gram-positive rods
*Obligate anaerobes
*Fermentative, catalase negative, oxidase negative
*Straight or slightly curved
*Motile by flagellae
*Require enriched media for growth
*Produce endospores which vary in shape and location and cause bulging of mother cell
===Pathogenesis and pathogenicity===
*Produce extracellular digestive enzymes and toxic substance known as exotoxins
*Exotoxins cause necrosis, haemolysis and death
*Collagenase, hyaluronidase and DNase enymes facilitate spread through tissues
===Diagnosis===
*Anaerobic transport medium
*Culture on blood agar enriched with yeast extract, vitamin K and haemin
*Anaerobic culture with hydrogen supplement and 5-10% carbon dioxide for 48 hours
*Colonies of ''C. perfringens'' are 5mm diameter, circular, flat and grey and surrounded by a zone of double haemolysis
*Positive cAMP test with ''Streptococci agalactiae''
*Biochemical tests
*Toxins identified in body fluids by toxin neutralisation or protection tests in lab animals
*Nagler reaction to detect alpha toxin - plate neutralisation test
*Fluorescent antibody tests for histotoxic clostridia
*ELISA, PCR for toxin detection
*Sudden death in unvaccinated farm animals may suggest ''C. perfringens'' types B, C and D
*Post mortem
*Gram positive rods present on intestinal smears suggests clostridial enterotoxaemia
===Histotoxic infections===
*Exotoxins cause local tissue necrosis and systemic effects which can be fatal - toxaemia
*''C. chauvei'' and ''C. septicum'' present in muscle as latent spores which can germinate to cause infection
*''C. novyi'' type B and ''C. haemolyticum'' have latent spores in the liver
*When inoculated into wounds, cause malignant oedema and gas gangrene
*Endospores persist in the soil
*Most ingested spores excreted in faeces, but some become dormant in tissues
*Tissue injury leads to reduced oxygen tensions allowing germination and replication of bacteria
*Exotoxins cause local necrosis
*Activated spores in the liver and muscles cause endogenous infections including blackleg, infectious necrotic hepatitis and bacillary haemoglobinuria
*Inoculation of wounds causes exogenous infections including malignant oedema and gas gangrene
===''Clostridium chauvei''===
*[[Muscles Inflammatory - Pathology#Black leg|Black leg]]:
**Acute disease of cattle and sheep
**Endogenous infection in young cattle with latent spores in muscles, activated by trauma
**Exogenous infection via wounds in sheep of any age
**Gangrenous cellulitis and myositis caused by exotoxins leads to rapid death
**Skeletal muscle damage with lameness, swelling and crepitus due to gas accumilation
**Dyspnoea due to lesions in tongue and throat muscles
**Myocardial and diaphragmatic lesions can cause sudden death
**Fluorescent antibody test for diagnosis
*Causes [[Necrosis - Pathology#Gas Gangrene|gas gangrene]], along with [[Clostridium species#Clostridium septicum|''Clostridium septicum'']]
===Clostridium septicum===
*Causes malignant oedema:
**Infection via wounds
**Cellutis with minimal gangrene and gas formation
**Tissue swelling die to oedema; coldness and discoloration of overlying skin
**Toxaemia with depression; death may be rapis if extensive lesions
*Causes braxy:
**Abomasitis of sheep
**Disease occurs during winter
**Rapidly fatal; anorexia, depression, fever
*Causes [[Necrosis - Pathology#Gas Gangrene|gas gangrene]] and [[Muscles Inflammatory - Pathology#Gas gangrene|myositis]]
===Clostridium novyi===
*Infectious necrotic hepatitis/black disease:
**Acute disease of sheep, occasionally cattle
**Hepatic necrosis caused by exotoxins of ''C. novyi'' type B in liver damaged by ''Fasciola hepatica''
**Rapid death
**Dark discoloration of skin caused by subcutaneous venous congestion
**Fluorescent antibody test diagnostic
* Causes [[Necrosis - Pathology#Gas Gangrene|gas gangrene]] and [[Muscles Inflammatory - Pathology#Gas gangrene|myositis]].
*May be involved in [[Bacterial skin infections - Pathology#Systemic bacterial infections|cutaneous lesions]]
*Causes big head in rams - oedema of subcutaneous tissues of the head, neck and cranial thorax; necrotising lethal alpha toxin
===''Clostridium perfringens'' type A===
*[[Necrosis - Pathology#Gas Gangrene|Gas gangrene]] and [[Muscles Inflammatory - Pathology#Gas gangrene|myositis]]
**Extensive bacterial invasion of damaged muscle
**Gas production causing subcutaneous crepitus
**Similar manifestations as malignant oedema
===''Clostridium haemolyticum''===
*Causes bacillary haemoglobinuria in cattle, occasionally sheep
*Endogenous infection - endospores dormant in liver
*Fluke migration allows germination
*Beta toxin causes intravascular haemolysis and hepatic necrosis
*Haemoglobinuria due to destruction of red blood cells
===Clostridium sordelli===
*Causes [[Necrosis - Pathology#Gas Gangrene|gas gangrene]], [[Muscles Inflammatory - Pathology#Gas gangrene|myositis]] and abomasitis (lambs)
===Treatment of histotoxic infections===
*Early penicillin
*Vaccination with bacterin or toxoid at 3 months and booster after 3 weeks, then annually
===Enteropathogenic and enterotoxaemic clostridia===
*General:
**''Clostridium perfringens'' types B, C and D
**Found in soil, feaces and intestinal tract
**Survive in soil as spores
**Husbandry, changes in diet and environment predispose to proliferation in the intestine
**Abrupt changes to rich diets and intestinal hypomotility due to overeating
*Pathogenesis and pathogenicity:
**Clostridial replication and overgrowth in the interstinal tract of sheep
**Production of potent exotoxins which cause local and systemic effects of enterotoxaemia
**Type of toxins produced determine clinical syndrome
**Haemolysins, collagenases and hyaluronidases also produced
===''C. perfringens'' type A===
*Necrotising enterocolitis in pigs and necrotic enteritis in chickens (alpha toxin with lecithinase activity)
*Canine haemorrhagic gastroenteritis (cytotoxic enterotoxin)
*Typhlocolotis in horses, possibly associated with [[Intestines Fibrinous/Haemorrhagic Enteritis - Pathology#Colitis X|Colitis X]]
===''C. perfringens'' type B===
*[[Intestines Fibrinous/Haemorrhagic Enteritis - Pathology#Lamb Dysentery (Enterotoxaemia with Blood)|Lamb dysentery]]
*Up to 30% morbidity and high mortality
*Affects lambs in first week of life
*Abdominal distension, pain, bloody faeces, sudden death
*Bacterial overgrowth in the intestine of the lamb due to immature bacterial flora
*Lack of proteases in the immature gut prevents cleavage of the beta toxin, allowing it to cause disease
*Also alpha and epsilon toxins
*Haemorrhagic enteritis and ulceration in the small intestine
*Fluid in the peritoneal cavity and pericardial sac due to increased capillary permeability (beta toxin)
*Fatal haemorrhagic enteritis in newborn foals, calves and adult goats
===''C. perfringens'' type C===
*Acute enterotoxaemia in adult sheep, 'struck'
*Sudden death or terminal convulsions in sheep at pasture
*Beta toxin (lethal, necrotising) plays major role in pathogenesis of the disease - increases intestinal and capillary permeability
*Also alpha toxin (lecithinase)
*Post mortem: jejunal ulceration; hyperaemia in small intestine; fluid accumulation in peritoneal cavity; congestion of peritoneal vessels; petechial haemorrhages
*Haemorrhagic enteritis in piglets
**Peracute enterotoxaemia often of entire litter with mortality rates 80%
**Infection from sow's faeces
**Death within 24 hours in young piglets
**Chronic disease in older piglets
**Dullness, anorexia, bloody faeces, perianal hyperaemia
**Post mortem: necrosis of terminal small intestinal mucosa, caecum and colon and blood-stained contents; serosanguinous fluid in pleural and peritoneal cavities
*Necrotic enteritis in chickens:
**Broilers under 12 weeks
**Acute enterotoxaemia, sudden onset and high mortality
**Necrosis of small intestine
**Predisposing factors include diet changes, coccidial infection and intestinal hypomotility
*Acute enterotoxaemia with haemorrhagic enteritis in calves, lambs, foals, goats
*[[Peritoneal Cavity Inflammatory - Pathology#In cattle|Peritonitis in cattle]] - sudden death in feedlot cattle
===''C. perfringens'' type D===
*[[Intestines Catarrhal Enteritis - Pathology#"Pulpy Kidney" Disease|Pulpy kidney disease]] in well-fed 3-10 week-old lambs
*Follows overeating high grain diet or luchious pasture
*Starch from partially digested food enterering the intestine from the rumen allows rapid clostridial proliferation
*Epsilon toxin activated by proteolytic enzymes causes toxaemia
*Epsilon toxin increases intestinal and capillary permeability; also alpha toxin
*Lambs found dead or with opisthotonos, convulsions, coma in acute phases
*Blindness and head pressing in subacute disease; bloat in later stages
*Hyperglycaemia, glycosuria
*Post mortem: hyperaemia in intestine; fluid in pericardial sac; kidney autolysis with pulpy cortical softening (acute death)
*Subacute death causes symmetrical encephalomalacia and haemorrhage in basal ganglia and midbrain
*Enterotoxaemia in kids and adult goats
===''C. perfringens'' type E===
*Enteritis in rabbits, haemorrhagic enteritis in calves
*ALpha and iota toxins
===Treatment and control of enterotoxaemic infections===
*Hyperimmune serum
*Vaccination - vaccinate ewes with toxoid 6 weeks before lambing to allow passive protection of lambs
*Vaccination of lambs with toxoid before 2 months of age to protect against pulpy kidney
*Avoid sudden dietary changes
===''C. piliforme''===
*Spore-forming filamentous Gram negative intracellular pathogen
*Only grows in tissue culture or embryonated eggs
*Causes Tyzzer's disease - severe hepatic necrosis
*Sporadic disease in foals, calves, dogs, cats
*Foals under 6 weeks, found dead or comatose
*Incubation period up to 1 week
*Depression, anorexia, fever, jaundice, diarrhoea
*Hepatomegaly and necrosis on post mortem
*Diagnosis: Warthin-Starry silver impregnation technique demonstrates organisms in hepatocytes
===''C. difficile''===
*Dogs with chronic diarrhoea
*New born foals with haemorrhagic enterocolitis
*Possibly associated with acute colitis in adult horses following antibiotic therapy or grain overload
===''C. colinum''===
*Enteritis in poulty and game birds
*Shed in faeces of clinically affected and carrier birds
*Intestinal ulceration and hepatic necrosis
*Therapeutic antibiotics in drinking water
===''C. spiroforme''===
*Spontaneous and antibiotic-induced enteritis in rabbits
*Enterotoxaemia, fatal within 48 hours
*Oral antibiotics upset the intestinal flora, allowing overgrowth of clostridia[[Category:Bacteria]][[Category:Gram_positive_bacteria]]