Excerpts have been reprinted with permission from the APHA’s Control of Communicable Diseases Manual (CCDM). Please refer to the CCDM for more complete information.
FORMERLY INFANT BOTULISM ICD-9 005.1; ICD-10 A05
1. Identification – Human botulism is a serious but relatively rare intoxication caused by potent preformed toxins produced by Clostridium botulinum. Of the 7 recognized types of Clostridium botulinum, types A, B, E, rarely F and possibly G cause human botulism.
There are 3 forms of botulism: foodborne (the classic form), wound, and intestinal (infant and adult) botulism. The site of toxin production differs for each form but all share the flaccid paralysis that results from botulinum neurotoxin. The name "intestinal botulism" is now used instead of infant botulism.
Foodborne botulism is a severe intoxication resulting from ingestion of preformed toxin present in contaminated food. The characteristic early symptoms and signs are marked fatigue, weakness and vertigo, usually followed by blurred vision, dry mouth, and difficulty in swallowing and speaking. Vomiting, diarrhea, constipation and abdominal swelling may occur. Neurological symptoms always descend through the body: shoulders are first affected, then upper arms, lower arms, thighs, calves, etc. Paralysis of breathing muscles can cause loss of breathing and death unless assistance with breathing (mechanical ventilation) is provided. There is no fever and no loss of consciousness. Similar symptoms usually appear in individuals who shared the same food. Most cases recover, if diagnosed and treated promptly, including early administration of antitoxin and intensive respiratory care. The case-fatality rate in the USA is 5%-10%. Recovery may take months.
Intestinal (infant) botulism is rare; it affects children below 1 and (rarely) adults with altered GI anatomy and microflora. Ingested spores germinate and produce bacteria that reproduce in the gut and release toxin. In most-adults and children over 6 months, germination would not happen- because natural defences prevent germination and growth of Clostridium botulinum. Clinical symptoms in infants include constipation, loss of appetite, weakness, an altered cry, and a striking loss of head control. Infant botulism has in some cases been associated with ingestion of honey contaminated with botulism spores, and mothers are warned not to feed raw honey to their infants … The case fatality rate of hospitalized cases is less than 1%; it is much higher without access to hospitals with paediatric intensive care units.
Wound botulism, a rare disease, occurs when spores get into an open wound and reproduce in an anaerobic environment. Symptoms are similar to the foodborne form, but may take up to 2 weeks to appear.
Diagnosis of foodborne botulism is made by demonstration of botulinum toxin in serum, stool, gastric aspirate or incriminated food; or through culture of C. botulinum from gastric aspirate or stool in a clinical case … The diagnosis may be accepted in a person with the clinical syndrome who had consumed a food item incriminated in a laboratory-confirmed case. Toxin in serum or positive wound culture confirms the diagnosis of wound botulism. Electromyography with rapid repetitive stimulation can corroborate the clinical diagnosis for all forms of botulism …
2. Infectious agent – … Clostridium botulinum, a spore-forming obligate anaerobic bacillus. A few nanograms of the toxin can cause illness. Most human outbreaks are due to types A, B, E and rarely F … Type E outbreaks are usually related to Clostridium botulinum fish, seafood and meat from marine mammals.
Toxin is produced in improperly processed, canned, low acid or alkaline foods, and in pasteurized and lightly cured foods held without refrigeration, especially in airtight packaging. Toxin is destroyed by boiling (e.g. 80°C/176°F for 10 minutes or longer); inactivation of spores requires much higher temperatures. Type E toxin can be produced slowly at temperatures as low as 3°C (37.4°F), lower than that of ordinary refrigeration …
3. Occurrence – Worldwide; sporadic cases, family and general outbreaks occur where food is prepared or preserved by methods that do not destroy spores and permit toxin formation. Cases rarely result from commercially processed products; outbreaks have occurred from contamination through cans damaged after processing.
4. Reservoir – Spores, ubiquitous in soil worldwide … also found in marine sediments and in the intestinal tract of animals, including fish.
5. Mode of transmission – Foodborne botulism occurs when C. botulinum is allowed to grow and produce toxin in food which is then eaten without sufficient heating or post-production cooking to inactivate the toxin …
Inhalation botulism, following inhalation of the toxin (aerosol), has occurred in laboratory workers. In these cases, neurological symptoms may be the same as in foodborne botulism, but the incubation period may be longer.
Waterborne botulism could theoretically also result from the ingestion of the preformed toxin. Since water treatment processes inactivate the toxin, the risk is considered low.
Wound botulism often results from contamination of wounds by ground-in soil or gravel or from improperly treated open fractures. It has been reported among chronic drug abusers (primarily in dermal abscesses from subcutaneous injection of heroin and also from sinusitis in cocaine "sniffers").
Intestinal botulism arises from ingestion of spores that germinate in the colon, rather than through ingestion of preformed toxin …
6. Incubation period – Neurological symptoms of foodborne botulism usually appear within 12-36 hours, sometimes several days after eating contaminated food. The shorter the incubation period, the more severe the disease and the higher the case-fatality rate …
7. Period of communicability – Despite excretion of C. botulinum toxin and organisms at high levels (about 106 organisms/gram) in the feces of intestinal botulism patients weeks to months after onset of illness, no instance of secondary person-to-person transmission has been documented. Foodborne botulism patients typically excrete the toxin for shorter periods.