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| − | <big><center>[[Infectious agents and parasites|'''BACK TO INFECTIOUS AGENTS AND PARASITES''']]</center></big>
| + | #REDIRECT[[:Category:Clostridium species]] |
| − | <big><center>[[Bacteria|'''BACK TO BACTERIA''']]</center></big>
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| − | | |
| − | ===Overview===
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| − | *Organisms present in the soil, alimentary tract and faeces
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| − | *Endospores may be present in liver and may be reactivated to cause disease
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| − | *Neurotoxic clostridia, ''Clostridium tetani'' and ''Clostridium botulinum'' affect neuromuscular function but cause no tissue damage
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| − | *Histotoxic clostridia cause localised lesions in tissues and may cause toxaemia
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| − | *''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
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| − | *Obligate anaerobes
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| − | *Fermentative, catalase negative, oxidase negative
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| − | *Straight or slightly curved
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| − | *Motile by flagellae
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| − | *Require enriched media for growth
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| − | *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
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| − | *Exotoxins cause necrosis, haemolysis and death
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| − | *Collagenase, hyaluronidase and DNase enymes facilitate spread through tissues
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| − | ===Neurotoxic clostridia===
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| − | ===''Clostridium tetani''===
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| − | *Causes [[Tremors and Movement Disorders - Nervous System#Tetanus|tetanus]]
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| − | *Acute, potentially fatal intoxication affecting many species
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| − | *Horses and man particularly susceptible; carnivores fairly resistant
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| − | *Found in horse faeces
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| − | *Characteristics:
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| − | **Terminal, spherical endospores give mother cells a drumstick appearance
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| − | **Enodospores resistant to boiling and chemicals but susceptible to autoclaving
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| − | **Swarming growth and haemolytic on blood agar
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| − | **Many serotypes but all produce same neurotoxin, tetanospasmin, therefore antibodies neutralise all
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| − | *Pathogenesis:
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| − | **Endospores introduced via damaged tissues e.g. penetrating wounds
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| − | **Damaged tissue creates an anaerobic environment, allowing germination of spores
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| − | **Tetanospasmin made by bacteria replicating in damaged tissue
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| − | **Absorbed toxin affects neuromuscular junction distant from site of toxin production
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| − | **Neurotoxin binds irreversibly to ganglioside receptors on motor neurons and is transported to nerve cell body
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| − | **Toxins transported across synapse to terminals of inhibitory neurons where they block transmission of signals
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| − | **Spastic paralysis by constant tensing of muscles results
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| − | **Toxin can be blood-borne and bind to motor terminals throughout the body as well as in the CNS
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| − | *Clinical signs:
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| − | **Incubation period 5-10 days
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| − | **Stiffness, localised spasms, altered heart and respiratory rates, dysphagia, altered facial expression, lock-jaw from mastigatory muscle spasm
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| − | **Tonic muscle contraction easily stimulated
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| − | *Treatment:
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| − | **Antitoxin IV or into subarachnoid space on 3 consecutive days
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| − | **Toxoid subcutaneously to promote active immune response
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| − | **Penicillin to kill vegetative cells
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| − | **Debridement and flushing of wound with hydrogen peroxide
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| − | **Fluids, sedatives, muscle relaxants
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| − | *Control:
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| − | **Toxoid vaccine for farm animals
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| − | **Debridement of wounds in horses
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| − | ===''Clostridium botulinum''===
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| − | *Ubiquitous organism
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| − | *Oval, subterminal endospores; spores survive boiling for hours
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| − | *Causes [[Muscles - degenerative#Botulism|botulism]], a potentially fatal intoxication
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| − | *Germination of endospores, growth of bacterial cells and toxin production in anaerobic conditions e.g. decaying carcasses and vegetation
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| − | *Disease in animals consuming rotting carcasses and in herbivores through contamination of feed
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| − | *Pathogenesis:
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| − | **Intoxication on ingestion and absorbtion of toxin from GIT into the blood
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| − | **Occasionally germination of spores in wounds or GIT
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| − | **Neurotoxin carried to peripheral nervous system
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| − | **Toxin binds gangliosides irreversibly at the neuromuscular junction
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| − | **Blocks release of acetylcholine
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| − | *Clinical signs:
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| − | **Dilated pupils, dry mucus membranes, decreased salivation, tongue flacidity, dysphagia in farm animals
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| − | **Incoordination and knuckling followed by flacid paralysis and recumbency
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| − | **Paralysis of respiratory muscles leads to death
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| − | **Flacid paralysis of legs and wings in birds
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| − | *Diagnosis:
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| − | **Mouse inoculation with infected serum
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| − | **Toxin detection by PCR, ELISA
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| − | **Toxin neutralisation tests in mice
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| − | *Treatment: polyvalent antiserum neutralises unbound toxin
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| − | *Toxoid vaccine used in endemic regions
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| − | *Implicated in [[Intestines - physical disturbances#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
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| − | *''C. chauvei'' and ''C. septicum'' present in muscle as latent spores which can germinate to cause infection
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| − | *''C. novyi'' type B and ''C. haemolyticum'' have latent spores in the liver
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| − | *When inoculated into wounds, cause malignant oedema and gas gangrene
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| − | *Endospores persist in the soil
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| − | *Most ingested spores excreted in faeces, but some become dormant in tissues
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| − | *Tissue injury leads to reduced oxygen tensions allowing germination and replication of bacteria
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| − | *Exotoxins cause local necrosis
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| − | *Activated spores in the liver and muscles cause endogenous infections including blackleg, infectious necrotic hepatitis and bacillary haemoglobinuria
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| − | *Inoculation of wounds causes exogenous infections including malignant oedema and gas gangrene
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| − | ===''Clostridium chauvei''===
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| − | *[[Muscles - inflammatory#Black leg|Black leg]]:
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| − | **Acute disease of cattle and sheep
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| − | **Endogenous infection in young cattle with latent spores in muscles, activated by trauma
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| − | **Exogenous infection via wounds in sheep of any age
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| − | **Gangrenous cellulitis and myositis caused by exotoxins leads to rapid death
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| − | **Skeletal muscle damage with lameness, swelling and crepitus due to gas accumilation
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| − | **Dyspnoea due to lesions in tongue and throat muscles
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| − | **Myocardial and diaphragmatic lesions can cause sudden death
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| − | **Fluorescent antibody test for diagnosis
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| − | *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:
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| − | **Infection via wounds
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| − | **Cellutis with minimal gangrene and gas formation
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| − | **Tissue swelling die to oedema; coldness and discoloration of overlying skin
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| − | **Toxaemia with depression; death may be rapis if extensive lesions
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| − | *Causes braxy:
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| − | **Abomasitis of sheep
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| − | **Disease occurs during winter
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| − | **Rapidly fatal; anorexia, depression, fever
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| − | *Causes [[General Pathology - Necrosis#Gas Gangrene|gas gangrene]] and [[Muscles - inflammatory#Gas gangrene|myositis]]
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| − | ===Clostridium novyi===
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| − | *Infectious necrotic hepatitis/black disease:
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| − | **Acute disease of sheep, occasionally cattle
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| − | **Hepatic necrosis caused by exotoxins of ''C. novyi'' type B in liver damaged by ''Fasciola hepatica''
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| − | **Rapid death
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| − | **Dark discoloration of skin caused by subcutaneous venous congestion
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| − | **Fluorescent antibody test diagnostic
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| − | * Causes [[General Pathology - Necrosis#Gas Gangrene|gas gangrene]] and [[Muscles - inflammatory#Gas gangrene|myositis]].
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| − | *May be involved in [[Bacterial skin infections#Systemic bacterial infections|cutaneous lesions]]
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| − | *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
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| − | **Extensive bacterial invasion of damaged muscle
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| − | **Gas production causing subcutaneous crepitus
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| − | **Similar manifestations as malignant oedema
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| − | ===''Clostridium haemolyticum''===
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| − | *Causes bacillary haemoglobinuria in cattle, occasionally sheep
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| − | *Endogenous infection - endospores dormant in liver
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| − | *Fluke migration allows germination
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| − | *Beta toxin causes intravascular haemolysis and hepatic necrosis
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| − | *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#Gas gangrene|myositis]] and abomasitis (lambs)
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| − | ===Treatment of histotoxic infections===
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| − | *Early penicillin
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| − | *Vaccination with bacterin or toxoid at 3 months and booster after 3 weeks, then annually
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| − | ===Diagnosis===
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| − | *Anaerobic transport medium
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| − | *Culture on blood agar enriched with yeast extract, vitamin K and haemin
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| − | *Anaerobic culture with hydrogen supplement and 5-10% carbon dioxide for 48 hours
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| − | *Colonies of ''C. perfringens'' are 5mm diameter, circular, flat and grey
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| − | *''C. perfringens'' colonies are surrounded by a zone of double haemolysis
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| − | *Positive cAMP test with ''Sreptococci agalactiae''
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| − | *Biochemical tests
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| − | *Toxins identified in body fluids by toxin neutralisation or protection tests in lab animals
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| − | *Nagler reaction to detect alpha toxin - plate neutralisation test
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| − | *Fluorescent antibody tests for histotoxic clostridia
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| − | *ELISA, PCR for toxin detection
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| − | ===Enteropathogenic and enterotoxaemic clostridia===
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| − | *General:
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| − | **''Clostridium perfringens'' types B, C and D
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| − | **Found in soil, feaces and intestinal tract
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| − | **Survive in soil as spores
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| − | **Husbandry, changes in diet and environment predispose to proliferation in the intestine
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| − | *Pathogenesis and pathogenicity:
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| − | **Clostridial replication and overgrowth in the interstinal tract of sheep
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| − | **Production of potent exotoxins which cause local and systemic effects of enterotoxaemia
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| − | **Type of toxins produced determine clinical syndrome
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| − | **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
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| − | **Canine haemorrhagic gastroenteritis
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| − | **Typhlocolotis in horses, possibly associated with [[Intestines - Fibrinous/ Haemorrhagic Enteritis#Colitis X|Colitis X]]
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| − | *''C. perfringens'' type B:
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| − | **[[Intestines - Fibrinous/ Haemorrhagic Enteritis#Lamb Dysentery (Enterotoxaemia with Blood)|Lamb dysentery]]
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| − | **Up to 30% morbidity and high mortality
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| − | **Affects lambs in first week of life
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| − | **Abdominal distension, pain, bloody faeces, sudden death
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| − | **Bacterial overgrowth in the intestine of the lamb due to immature bacterial flora
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| − | **Lack of proteases in the immature gut prevents cleavage of the beta toxin, allowing it to cause disease
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| − | **Haemorrhagic enteritis and ulceration in the small intestine
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| − | **Fluid in the peritoneal cavity and pericardial sac due to increased capillary permeability
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| − | **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'
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| − | **Sudden death or terminal convulsions in sheep at pasture
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| − | **Beta toxin plays major role in pathogenesis of the disease
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| − | **Post mortem: jejunal ulceration; hyperaemia in small intestine; fluid accumulation in peritoneal cavity; congestion of peritoneal vessels; petechial haemorrhages
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| − | **Haemorrhagic enteritis in piglets
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| − | ***Peracute enterotoxaemia often of entire litter with mortality rates 80%
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| − | ***Infection from sow's faeces
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| − | ***Death within 24 hours in young piglets
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| − | ***Chronic disease in older piglets
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| − | ***Dullness, anorexia, bloody faeces, perianal hyperaemia
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| − | ***Post mortem: necrosis of terminal small intestinal mucosa, caecum and colon and blood-stained contents; serosanguinous fluid in pleural and peritoneal cavities
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| − | **Necrotic enteritis in chickens:
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| − | ***Broilers under 12 weeks
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| − | ***Acute enterotoxaemia, sudden onset and high mortality
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| − | ***Necrosis of small intestine
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| − | ***Predisposing factors include diet changes, coccidial infection and intestinal hypomotility
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| − | **Acute enterotoxaemia with haemorrhagic enteritis in calves, lambs, foals
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| − | **[[Peritoneal cavity - inflammatory#In cattle|Peritonitis in cattle]]
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| − | *''C. perfringens'' type D:
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| − | **[[Intestines - Catarrhal Enteritis#"Pulpy Kidney" Disease|Pulpy kidney disease]] in well-fed 3-10 week-old lambs
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| − | **Follows overeating high grain diet or luchious pasture
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| − | **Starch from partially digested food enterering the intestine from the rumen allows rapid clostridial proliferation
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| − | **Epsilon toxin activated by proteolytic enzymes causes toxaemia
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| − | **Lambs found dead or with opisthotonos, convulsions, coma in acute phases
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| − | **Blindness and head pressing in subacute disease; bloat in later stages
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| − | **Hyperglycaemia, glycosuria
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| − | **Post mortem: hyperaemia in intestine; fluid in pericardial sac; kidney autolysis with pulpy cortical softening (acute death)
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| − | **Subacute death causes symmetrical encephalomalacia and haemorrhage in basal ganglia and midbrain
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| − | **Enterotoxaemia in kids and adult goats
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| − | ** [[Respiratory system - clinical signs#Dysphagia|Dysphagia in horses]]
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| − | *''C. perfringens'' type E:
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| − | **Enteritis in rabbits, haemorrhagic enteritis in calves
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