· This is usually caused in humans by types A, B, E, and rarely F. The initial phase of the disease is often so subtle as to go unnoticed or misdiagnosed. Type A botulism generally causes a more severe illness, and is more likely to require intubation than either type B or E botulism. In general, the earlier the onset of symptoms, the more serious the disease and the more protracted the course. Even a small taste of contaminated food may result in illness.
· Nausea, vomiting, thirst, abdominal pain. Abdominal cramps may be an early symptom of foodborne botu-lism. Marked abdominal distension with absent bowel sounds may be present due to paralytic ileus.
· Constipation; refusal to feed and diarrhoea have been reported in a few cases of paediatric botulism.
· Ptosis, difficulty with visual accommodation, photo-phobia, mydriasis, and diplopia (due to ocular paresis). Strabismus and nystagmus have also been reported. The triad of extraocular muscle palsy, pupillary dysfunction, and ptosis is said to be predictive of illness severity (i.e. the development of respiratory failure). Early onset of neurological symptoms, particularly ocular, generally indicates a more severe infection and worse prognosis.
· Dizziness: Postural dizziness is a relatively frequent symptom resulting from cholinergic blockade.
· Dry mouth,* soreness of throat due to drying of pharynx, dryness of lacrimal secretions.
· Dysphonia, dysarthria, dysphagia.
· Bilaterally symmetrical descending motor paralysis, beginning with abducens (VI) or oculomotor (III) nerve palsy, and progressing to respiratory insufficiency. The risk of ventilatory failure is greatest within the first two days of hospitalisation. Respiratory arrest may develop suddenly in patients with apparently adequate respira-tory reserve; absent signs and symptoms of respiratory insufficiency are not necessarily indicative of normal lung function. Respiratory failure can also develop insid-iously, and may be difficult to diagnose. Many patients experience dyspnoea of varying degree for a year or more after recovery from botulism, despite essentially normal pulmonary function. The cause of dyspnoea may be a residual defect of respiratory muscles.
· Urinary retention (especially in Type E botulism): due to cholinergic blockade.
· Mental status, sensory examination, reflexes, body temperature, and pulse are all usually normal.
· Cardiac arrest may occur in patients with respiratory failure. It is not known whether arrest is secondary to hypoxia or due to a direct effect of botulinum toxin on the myocardium.
· A syndrome of inappropriate secretion of antidiuretic hormone has been reported in some cases of botulism. Most of these patients were on a ventilator when this occurred.
· Toxicoinfectious Botulism: There are a few reports ofgastrointestinal colonisation by C. botulinum spores in adults resulting in cases of adult infectious botulism (the in vivo toxin that is produced is similar to that of infant botulism). Several factors are associated with this form of botulism: GIT abnormalities (e.g. achlorhydria), antibiotic therapy disrupting the normal GI flora, a history of abdominal surgery (e.g. gastrectomy), etc.
· A detailed list of symptoms and signs is mentioned in Table 33.2. Mortality is estimated to be less than 10%with symptomatic and supportive care.
· Differential Diagnosis: The common conditionsconfused with botulism are presented in Table 33.3, along with clues to help resolve a given case that may appear perplexing. The condition that is most often confounding is Guillain Barre´ syndrome, especially the Miller Fisher variant (Table 33.4).
· Treatment: Supportive measures.
This is a rare, life-threatening complication of trauma which occurs after spores of Cl. botulinum have germinated in a wound and produced botulinum toxin resulting in flaccid paralysis. It can also result from intravenous drug abuse. Of late, cocaine and heroin (especially “black tar heroin” which is often injected subcutaneously) have been increasingly associated with cases of wound botulism. Deep wounds, crush injury, or compound fracture treated with open reduction are invariably the type of trauma predisposing to wound botulism. Incubation period varies from 4 to 18 days.
–– Fever (usually associated with sinusitis, abscess, or tissue infection which acts as the focus of infection).
–– Absence of GI manifestations.
–– Cranial nerve palsies resulting in ptosis, diplopia, poor accommodation, ophthalmoplegia, dysphagia, dysphonia, and dysarthria.
–– Other neurological features such as descending flaccid paralysis, shortness of breath, and respira-tory failure.
· Infant botulism is said to be the commonest form of botulism. Since 1976, when the first case was reported till 2005, more than 2000 hospitalisations have been documented. Of these, 95% occurred in the USA, and 99% were due to botulinum neurotoxin type A or B. Most cases involved infants of 1 to 3 months age (range 1 month to 1 year).
· It is postulated that infant botulism is the result of inges-tion of Cl. botulinum organisms with subsequent in vivo production of toxin, followed by gut absorption. Some investigators suggest that bacterial growth associated with breastfeeding may favour Bifibobacterium devel-opment, instead of bacteria known to inhibit Cl. botu-linum (i.e., Coliforme, Enterococcus, and Bacteroides species). Of all the food items associated with infant botulism, honey is said to be the commonest food source contaminated with Cl. botulinum spores.
Clinical features of infant botulism include constipation, feeding difficulty, feeble crying, and a “floppy” baby with decreased muscle tone, particularly of the neck and limbs. Loss of facial grimacing, ophthalmoplegia, diminished gag reflex, dysphagia, poor anal sphincter tone, and respiratory failure have also been reported.
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