Type E toxin (associated with fish products): Pacific Northwest/Alaska/Great Lakes area
Wound Botulism Outbreak (reported in JAMA, 1998): associated with black-tar heroin injection (usually due to skin-popping with associated SQ or IM infections)
Etiology
Clostridium botulinum
Anaerobic Gram positive, spore-forming rod
Found in soil and water
Botulinum Neurotoxin (types A through G) is the most potent bacterial toxin known
Toxin is inactivated by 100°C x 10 min (routine home cooking)
Spores are inactivated only by 120°C (steam or pressure cooking)
Physiology
Botulinum Neurotoxin
One of the most powerful known toxins: about one microgram is lethal to humans.
It acts by blocking nerve function and leads to respiratory and musculoskeletal paralysis.
In all cases illness is caused by the toxin made by Clostridium botulinum, not by the bacterium itself.
The pattern of damage occurs because the toxin affects nerves that are firing more often
In peripheral nervous system, toxin exhibits irreversible presynaptic inhibition (interference with calcium release) of Ach release at neuromuscular junction
Sprouting of new terminals -> cure
Pathogenesis by Clinical Syndrome
Food-Borne Botulism: contaminated food ingestion (especially anaerobically preserved home-canned foods, like vegetables, fruit, condiments/ less common with meats, fish)
Certain type of C. Botulinum with proteolytic activity can spoil food/ others leave food appearance unchanged
Wound Dotulism (rare): spores in wound -> germination into vegetative organisms -> toxin produced in wound
Reported with soil contamination of wounds/ IVDA/ post-C-section
May even occur when antibiotics were given to prevent wound infection
Infant Botulism: due to ingestion of spores -> germination into vegetative organism -> toxin production in intestine
Reported to occur with spore-contaminated honey (avoid feeding honey to infants <12 months old)
Resistance may occur with development of normal intestinal flora
Adult Infant Botulism: similar to mechanism in infant botulism, except cases occur in older children and adults
Diagnosis
CBC: normal
ESR: normal
LP: normal
PFT’s: restriction
Decreased VC (due to muscle weakness, de-creased lung compli-ance, and decreased CW compliance):
Decreased TLC, MVV
Increased RV (due to inability to overcome recoil of chest wall outward at volume less than FRC)
Serum Assay for Botulinum Toxin (in mice): definitive (may be negative in infant and wound cases), but takes 24-86 hrs to complete
Detection in gastric fluid/stool is suggestive (intestinal carriage is rare)
Wound C/S: suggestive if positive
Tensilon Test: may be weakly positive
Clinical
Food-borne Botulism
Incubation: 18-36 hrs (range: hrs-several days)
Variable Symptoms: range from mild illness to death within 24 hrs
Symmetric (usually) Descending Paralysis:
Cranial Nerve Weakness (diplopia/dysarthria/dysphagia/dizziness/dry mouth/dry sore throat/ptosis/decreased gag/fixed or dilated pupils): seen in 50% of cases -> progresses to neck/extermities/thorax
Absence of Sensory Findings: distinguishes Botulism from GBS
Organisms and toxin may be found in stools for prolonged periods
May occur after surgery, with GI disease
Treatment
Ventilatory Support: indicated for cases with FVC <30% predicted
MIP: predicts need for vent support
Trivalent (type A/B/E) Equine Anti-Toxin: test for sensitivity to horse serum -> give 2 vials IV ASAP (may be repeated in 2-4 hrs)
Not beneficial in infant Botulism cases
Neutralizes circulating toxin in serum
Human Botulism Ig: experimental for infant cases
GI Decontamination: to purge GI tract of toxin
Antibiotics (to eliminate organism): unproven
PCN: high-dose
Wound Debridement: for wound cases
Guanidine: unproven (may be useful for ocular muscles)
Prognosis
7.5% mortality currently
Type A disease is more severe/ higher mortality in cases >60 y/o
Residual decreased exercise tolerance and autonomic dysfunction (may persist for years after recovery even when PFT’s normalized): tachypnea/dyspnea/rapid shallow breathing/ decreased VO2max
References
Werner SB, Passaro D, McGee J, et al. Wound botulism in California, 1951-1998: recent epidemic in heroin injectors. Clin Infect Dis 2000; 31:1018-1024
Sandrock CE, Murin S. Clinical predictors of respiratory failure and long-term outcome in black tar heroin-associated wound botulism. Chest 2001; 120:562-566
Shapiro RL, Hatheway C, Swerdlow DL. Botulism in the United States: a clinical and epidemiologic review. Ann Intern Med 1998; 129:221-228
Passaro DJ, Werner SB, McGee J, et al. Wound botulism associated with black tar heroin among injecting drug users. JAMA 1998; 280:1479-1480
