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−===Overview===
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−*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
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−===Characteristics===
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−*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
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−===Pathogenesis and pathogenicity===
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−*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
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−===Diagnosis===
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−*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 ''Sreptococci 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
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−===Neurotoxic clostridia===
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−===''Clostridium tetani''===
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−*Causes [[Tremors and Movement Disorders (Nervous System) - Pathology#Tetanus|tetanus]]
−*Acute, potentially fatal intoxication affecting many species
−*Horses and man particularly susceptible; carnivores fairly resistant
−*Found in horse faeces
−*Characteristics:
−**Terminal, spherical endospores give mother cells a drumstick appearance
−**Enodospores resistant to boiling and chemicals but susceptible to autoclaving
−**Swarming growth and haemolytic on blood agar
−**Many serotypes but all produce same neurotoxin, tetanospasmin, therefore antibodies neutralise all
−*Pathogenesis:
−**Endospores introduced via damaged tissues e.g. penetrating wounds
−**Damaged tissue creates an anaerobic environment, allowing germination of spores
−**Tetanospasmin made by bacteria replicating in damaged tissue
−**Absorbed toxin affects neuromuscular junction distant from site of toxin production
−**Neurotoxin binds irreversibly to ganglioside receptors on motor neurons and is transported to nerve cell body
−**Toxins transported across synapse to terminals of inhibitory neurons where they block transmission of signals
−**Spastic paralysis by constant tensing of muscles results
−**Toxin can be blood-borne and bind to motor terminals throughout the body as well as in the CNS
−*Clinical signs:
−**Incubation period 5-10 days
−**Stiffness, localised spasms, altered heart and respiratory rates, dysphagia, altered facial expression, lock-jaw from mastigatory muscle spasm
−**Tonic muscle contraction easily stimulated
−*Treatment:
−**Antitoxin IV or into subarachnoid space on 3 consecutive days
−**Toxoid subcutaneously to promote active immune response
−**Penicillin to kill vegetative cells
−**Debridement and flushing of wound with hydrogen peroxide
−**Fluids, sedatives, muscle relaxants
−*Control:
−**Toxoid vaccine for farm animals
−**Debridement of wounds in horses
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−===''Clostridium botulinum''===
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−*Ubiquitous organism
−*Oval, subterminal endospores; spores survive boiling for hours
−*Causes [[Muscles Degenerative - Pathology#Botulism|botulism]], a potentially fatal intoxication
−*Germination of endospores, growth of bacterial cells and toxin production in anaerobic conditions e.g. decaying carcasses and vegetation
−*Disease in animals consuming rotting carcasses and in herbivores through contamination of feed
−*Pathogenesis:
−**Intoxication on ingestion and absorbtion of toxin from GIT into the blood
−**Occasionally germination of spores in wounds or GIT
−**Neurotoxin carried to peripheral nervous system
−**Toxin binds gangliosides irreversibly at the neuromuscular junction
−**Blocks release of acetylcholine
−*Clinical signs:
−**Dilated pupils, dry mucus membranes, decreased salivation, tongue flacidity, dysphagia in farm animals
−**Incoordination and knuckling followed by flacid paralysis and recumbency
−**Paralysis of respiratory muscles leads to death
−**Flacid paralysis of legs and wings in birds
−*Diagnosis:
−**Mouse inoculation with infected serum
−**Toxin detection by PCR, ELISA
−**Toxin neutralisation tests in mice
−*Treatment: polyvalent antiserum neutralises unbound toxin
−*Toxoid vaccine used in endemic regions
−*Implicated in [[Intestine Physical Disturbances - Pathology#Equine dysautonomia, or grass sickness|equine grass sickness]]
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−===Histotoxic infections===
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−*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
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−===''Clostridium chauvei''===
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−*[[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 [[General Pathology - Necrosis#Gas Gangrene|gas gangrene]], along with [[Clostridium species#Clostridium septicum|''Clostridium septicum'']]
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−===Clostridium septicum===
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−*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 [[General Pathology - Necrosis#Gas Gangrene|gas gangrene]] and [[Muscles Inflammatory - Pathology#Gas gangrene|myositis]]
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−===Clostridium novyi===
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−*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 [[General Pathology - Necrosis#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
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−===''Clostridium perfringens'' type A===
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−*[[General Pathology - Necrosis#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
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−===''Clostridium haemolyticum''===
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−*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
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−===Clostridium sordelli===
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−*Causes [[General Pathology - Necrosis#Gas Gangrene|gas gangrene]], [[Muscles Inflammatory - Pathology#Gas gangrene|myositis]] and abomasitis (lambs)
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−===Treatment of histotoxic infections===
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−*Early penicillin
−*Vaccination with bacterin or toxoid at 3 months and booster after 3 weeks, then annually
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−===Enteropathogenic and enterotoxaemic clostridia===
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−*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
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−===''C. perfringens'' type A===
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−*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]]
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−===''C. perfringens'' type B===
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−*[[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
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−===''C. perfringens'' type C===
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−*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
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−===''C. perfringens'' type D===
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−*[[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
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−===''C. perfringens'' type E===
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−*Enteritis in rabbits, haemorrhagic enteritis in calves
−*ALpha and iota toxins
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−===Treatment and control of enterotoxaemic infections===
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−*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
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−===''C. piliforme''===
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−*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
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−===''C. difficile''===
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−*Dogs with chronic diarrhoea
−*New born foals with haemorrhagic enterocolitis
−*Possibly associated with acute colitis in adult horses following antibiotic therapy or grain overload
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−===''C. colinum''===
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−*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
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−===''C. spiroforme''===
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−*Spontaneous and antibiotic-induced enteritis in rabbits
−*Enterotoxaemia, fatal within 48 hours
−*Oral antibiotics upset the intestinal flora, allowing overgrowth of clostridia
#REDIRECT[[:Category:Clostridium species]]
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