|
|
| Line 1: |
Line 1: |
| − | {{review}}
| + | #REDIRECT[[:Category:Clostridium species]] |
| − | | |
| − | {{toplink
| |
| − | |backcolour =
| |
| − | |linkpage =Bacteria
| |
| − | |linktext =BACTERIA
| |
| − | |pagetype=Bugs
| |
| − | }}
| |
| − | <br>
| |
| − | ===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
| |
| − | | |
| − | ===Neurotoxic clostridia===
| |
| − | | |
| − | | |
| − | ===''Clostridium tetani''===
| |
| − | | |
| − | *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
| |
| − | **Endospores 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 - 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]]
| |
| − | | |
| − | | |
| − | ===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
| |