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
Clostridium tetani
- Causes 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 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 equine grass sickness
Histotoxic infections
- Exotoxins cause local tissue necrosis and systemic effects which can be fatal
- 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
Clostridium chauvei
- Causes gas gangrene, along with Clostridium septicum
- Infects muscles causingblack leg
Clostridium novyi
- Causes gas gangrene and myositis.
- May be involved in cutaneous lesions
Clostridium perfringens
- Causes:
- Lamb dysentery
- Colitis X.
- Pulpy kidney disease
- C. perfringens type D only.
- Peritonitis in cattle
- Dysphagia in horses
- Gas gangrene
- Myositis
Clostridium septicum
- Causes gas gangrene and myositis
Clostridium sordelli
- Causes gas gangrene and myositis
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
- C. perfringens colonies are surrounded by a zone of double haemolysis
- Biochemical tests
- Toxins identified in body fluids by toxin neutralisation or protection tests in lab animals
- Fluorescent antibody tests for histotoxic clostridia
- ELISA, PCR for toxin detection