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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

Clostridium novyi

Clostridium perfringens

Clostridium septicum

Clostridium sordelli


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