Difference between revisions of "Clostridium species"

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<big><center>[[Infectious agents and parasites|'''BACK TO INFECTIOUS AGENTS AND PARASITES''']]</center></big>
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#REDIRECT[[:Category:Clostridium species]]
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===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 ''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
 
 
 
 
 
===Neurotoxic clostridia===
 
 
 
 
 
===''Clostridium tetani''===
 
 
 
*Causes [[Tremors and Movement Disorders - Nervous System#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
 
 
 
 
 
===''Clostridium botulinum''===
 
 
 
*Ubiquitous organism
 
*Oval, subterminal endospores; spores survive boiling for hours
 
*Causes [[Muscles - degenerative#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 [[Intestines - physical disturbances#Equine dysautonomia, or grass sickness|equine grass sickness]]
 
 
 
 
 
===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#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'']]
 
 
 
 
 
===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 [[General Pathology - Necrosis#Gas Gangrene|gas gangrene]] and [[Muscles - inflammatory#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 [[General Pathology - Necrosis#Gas Gangrene|gas gangrene]] and [[Muscles - inflammatory#Gas gangrene|myositis]].
 
*May be involved in [[Bacterial skin infections#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===
 
 
 
*[[General Pathology - Necrosis#Gas Gangrene|Gas gangrene]] and [[Muscles - inflammatory#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 [[General Pathology - Necrosis#Gas Gangrene|gas gangrene]], [[Muscles - inflammatory#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
 
*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
 
*Canine haemorrhagic gastroenteritis
 
*Typhlocolotis in horses, possibly associated with [[Intestines - Fibrinous/ Haemorrhagic Enteritis#Colitis X|Colitis X]]
 
 
 
 
 
===''C. perfringens'' type B===
 
 
 
*[[Intestines - Fibrinous/ Haemorrhagic Enteritis#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
 
*Haemorrhagic enteritis and ulceration in the small intestine
 
*Fluid in the peritoneal cavity and pericardial sac due to increased capillary permeability
 
*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 plays major role in pathogenesis of the disease
 
*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
 
*[[Peritoneal cavity - inflammatory#In cattle|Peritonitis in cattle]]
 
 
 
 
 
===''C. perfringens'' type D===
 
 
 
*[[Intestines - Catarrhal Enteritis#"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
 
*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
 
 
 
 
 
===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
 

Latest revision as of 10:40, 12 May 2010