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ALL / Infectious Diseases
Clostridia
Clostridia
Clostridia are Gram-positive, spore-forming, obligate anaerobic bacilli. Their clinical importance is largely due to potent exotoxin production.Pathophysiology
- many clostridial toxins are exotoxins that cause disease by disrupting neurotransmission or cell membranes
- tetanus and botulinum toxins are proteases that cleave SNARE proteins, preventing neurotransmitter vesicle release
C. perfringens
- produces alpha-toxin (lecithinase/phospholipase)
- causes myonecrosis (gas gangrene) and haemolysis
- features: rapidly progressive severe pain, oedema, haemorrhagic bullae, skin discolouration and crepitus
- may also cause food poisoning via a heat-labile enterotoxin
C. botulinum
- classically associated with improperly canned food; infant botulism is linked to honey
- toxin blocks acetylcholine release at the neuromuscular junction, causing a descending flaccid paralysis
- typical features: diplopia, dysarthria, dysphagia and dyspnoea
- treat with antitoxin
C. difficile
- causes antibiotic-associated diarrhoea and pseudomembranous colitis, especially after broad-spectrum antibiotics; risk is increased by PPI use
- toxin A is an enterotoxin; toxin B is a cytotoxin causing actin depolymerisation
- diagnosis: stool toxin assay/PCR
- management: stop the precipitating antibiotic where possible; oral vancomycin or fidaxomicin
C. tetani
- tetanospasmin blocks release of inhibitory neurotransmitters (glycine and GABA) from Renshaw cells in the spinal cord, causing spastic paralysis
- features: trismus, risus sardonicus and opisthotonos
- prevention: tetanus vaccination
- treatment: human tetanus immunoglobulin, wound debridement, antibiotics and diazepam for spasms
+PassMedicine Notes
Clostridia are Gram-positive, spore-forming, obligate anaerobic bacilli. Their clinical importance is largely due to potent exotoxin production.
Pathophysiology- many clostridial toxins are exotoxins that cause disease by disrupting neurotransmission or cell membranes
- tetanus and botulinum toxins are proteases that cleave SNARE proteins, preventing neurotransmitter vesicle release
- produces alpha-toxin (lecithinase/phospholipase)
- causes myonecrosis (gas gangrene) and haemolysis
- features: rapidly progressive severe pain, oedema, haemorrhagic bullae, skin discolouration and crepitus
- may also cause food poisoning via a heat-labile enterotoxin
- classically associated with improperly canned food; infant botulism is linked to honey
- toxin blocks acetylcholine release at the neuromuscular junction, causing a descending flaccid paralysis
- typical features: diplopia, dysarthria, dysphagia and dyspnoea
- treat with antitoxin
- causes antibiotic-associated diarrhoea and pseudomembranous colitis, especially after broad-spectrum antibiotics; risk is increased by PPI use
- toxin A is an enterotoxin; toxin B is a cytotoxin causing actin depolymerisation
- diagnosis: stool toxin assay/PCR
- management: stop the precipitating antibiotic where possible; oral vancomycin or fidaxomicin
- tetanospasmin blocks release of inhibitory neurotransmitters (glycine and GABA) from Renshaw cells in the spinal cord, causing spastic paralysis
- features: trismus, risus sardonicus and opisthotonos
- prevention: tetanus vaccination
- treatment: human tetanus immunoglobulin, wound debridement, antibiotics and diazepam for spasms
