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