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 damaaged tissues e.g. penetrating wounds
  • Anaerobic conditions in the 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 to terminals of inhibitory neurons where they block transmission of signals
  • Spastic paralysis 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

• The toxin also causes botulism
• Toxin produced in decaying organic matter absorbed from GIT into the blood and affects neuromuscular junction
• Implicated in equine grass sickness

Clostridium chauvei

• Causes gas gangrene, along with Clostridium septicum.
• Infects muscles giving black leg myositis

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