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Clostridium spp. are anaerobic spore-forming organisms that are
able to survive well in the environment. Their normal habitats are
soil, water and the intestinal tract of humans and animals. Only a
few of the 80 species are human pathogens. Toxin production is
the main pathogenicity mechanism.
Clostridium difficile
Pseudomembranous colitis, an acute inflammatory diarrhoeal
disease, is an important cause of morbidity and mortality in
hospitals.
Epidemiology and pathogenesis
The frequency of Clostridium difficile carriage increases with duration
of hospital stay. When the gut microflora is disturbed by
antibiotics overgrowth can occur. Enterotoxins A and B and
binary toxin production cause tissue damage and fluid diarrhoea.
Some strains that are fluoroquinolone resistant and have evidence
of enhanced toxin production are associated with more severe
disease and extensive hospital outbreaks.
Clinical features
- History of previous antibiotic exposure.
- Three or more loose/unformed stools per day.
- Possible development of abdominal pain.
- Pseudomembranes seen on sigmoidoscopy on the mucosal
surface of the rectum and sigmoid colon.
- Possible complications of toxic megacolon, bowel perforation
and systemic toxicity, which are associated with high mortality.
Diagnosis
- Detection of toxin or glutamate dehydrogenase (GDH) by
enzyme immunoassay (EIA).
- Detection of toxin genes by nucleic acid amplification test
(NAAT).
- Typing - generally by ribotyping, but multilocus variablenumber
tandem repeat analysis is superseding this.
Treatment and prevention
- Stop the inciting (antibiotic) agent.
- Treat with oral metronidazole for 10 days.
- Oral vancomycin plus intravenous metronidazole for severe
cases and treatment failures.
- Relapse occurs in up to 25% of patients.
- Rapid and strict isolation is essential.
- Enhanced ward cleaning and attention to hand hygiene are
essential (Awareness may be raised by 'SIGHT' - Suspect Isolate
Gloves and aprons Hand hygiene Toxin test).
Botulism
Clostridium botulinum is found in the environment and can contaminate
wounds and food. Of the seven serotypes, A, B and E are
most commonly associated with human disease.
Epidemiology and pathogenesis
Incomplete heat treatment of contaminated food in canning or
bottling processes allows this organism to survive and produce
toxin. Botulinum toxin, a neurotoxin, inhibits the release of neurotransmitters. Clinically, there are three forms of the disease: food
intoxication, wound botulism and infant botulism.
Clinical features
- Rapid onset - within 6 h of ingestion.
- Descending flaccid paralysis, beginning with the cranial nerves.
- Dysphagia and blurred vision, followed by more general
paralysis.
- Sensory function is normal.
- Infants appear floppy and listless, constipated and have generalized
muscle weakness.
Diagnosis is based on the clinical features and a history of ingestion
of suspect food. Toxin may be detected in food, faeces and
serum by EIA. Botulinum neurotoxin genes can be detected by
NAAT.
Treatment and prevention
Treatment is with specific antitoxin and ventilatory support. Ventilator-
associated pneumonia is an important complication. The
disease is prevented by adequate process control in the foodprocessing
industry and home preservation.
Gas gangrene
Clostridium perfringens is the organism most commonly associated
with gas gangrene, but C. septicum, C. novyi, C. histolyticum and
C. sordellii can also be implicated. C. perfringens is capsulate and
produces a range of toxins, of which lecithinase C (a-toxin) is the
most important.
Epidemiology and pathogenesis
- At-risk wounds are those where devitalized tissue is contaminated
by environmental spores.
- Spores germinate and organisms multiply in the ischaemic
conditions.
- Toxin is released.
- Toxin-mediated tissue damage creates more anaerobic conditions
and progression is rapid.
- Infections can be mixed with other organisms especially in drug
users.
Clinical features
- Onset within 3 days of injury.
- Pain in the wound.
- Tenseness of the skin, which develops an underlying blue discoloration,
foul smell and crepitus.
- Toxaemia producing circulatory shock.
Diagnosis
The diagnosis is made clinically and treatment must not wait for
laboratory confirmation, which is rarely available.
Treatment and prevention
Treatment depends on debridement of devitalized tissue and intravenous
antibiotics. Hyperbaric oxygen may also be beneficial. The
condition is prevented by good management of potentially infected,
devitalized wounds.
Clostridium perfringens food poisoning
This condition is typically associated with meals containing meat
that are cooled slowly and subsequently reheated. Surviving
clostridia release toxin in the stomach when they form spores; this
leads to nausea, vomiting and diarrhoea. An EIA to detect toxin
in faeces is available. Rarely, gut infection with clostridia causes
severe enteritis.