Foodborne botulism cause

Botulism is a neuroparalytic, primarily foodborne illness first described in 1897 (GDC, 1998). The disease is caused by a toxin produced by the anaerobic bacterium Clostridium botulinum. Although botulism is rare, it can kill rapidly and foodborne botulism is a public health emergency carrying significant risk for widespread disease and death, as potentially preventable deaths may occur if the source of botulism is not discovered and eliminated. There are classically four major types of botulism foodborne botulism, infantile botulism, wound botulism, and intestinal botulism. 

Human foodborne botulism outbreaks have typically been linked to the consumption of toxin-contaminated home-prepared or home-preserved foods (Maselli, 1998). The vast majority of foodborne botulism cases are attributed to toxin types A, B, or E. Maselli (1998) reports that type B is the most prevalent (52%) in the United States, followed by type A (34%) and type E (12%), while the CDC (1998) suggests 37.6% of all foodborne botulism outbreaks since 1950 were caused by type A, 13.7% by type B, 15.1% by type E, 0.7% by type F, and 32.9% were unidenhfied with respect to toxin type. Outbreaks of type F and G botulism are rare (Sonnabend et al., 1981 Maselli, 1998 Richardson et al., 2004), and only anecdotal reports of isolated type Cl and D botulism cases can be found in the published literature (e.g., Lamanna, 1959). 

All botulin neurotoxins act in a similar way. They only differ in the amino-acid sequence of some protein parts (Prabakaran et al., 2001). Botulism symptoms are provoked both by oral ingestion and parenteral injection. Botulin toxin is not inactivated by enzymes present in the gastrointestinal tracts. Foodborne BoNT penetrates the intestinal barrier, presumably due to transcytosis. It is then transported to neuromuscular junctions within the bloodstream and blocks the secretion of the neurotransmitter acetylcholine. This results in muscle limpness and palsy caused by selective hydrolysis of soluble A-ethylmalemide-sensitive factor activating (SNARE) proteins which participate in fusion of synaptic vesicles with presynaptic plasma membrane. SNARE proteins include vesicle-associated membrane protein (VAMP), synaptobrevin, syntaxin, and synaptosomal associated protein of 25 kDa (SNAP-25). Their degradation is responsible for neuromuscular palsy due to blocks in acetylcholine transmission from synaptic terminals. In humans, palsy caused by BoNT/A lasts four to six months. 

Since inhalation bomlism does not occur in nature, aU outbreaks must be considered as suspicious. Prudence would dictate that each should be treated as a criminal or terrorist attack, unless other causes are found (Arnon et al., 2001). From the limited human and animal data currently available, inhalation bomlism does not have a unique presentation rather, the signs and symptoms resemble those of other forms of botulism. The latent period is comparable with that of foodborne bomlism without the early G1 signs (Adler, 2006). 

In addition to disease caused by direct infection, some foodborne diseases are caused by the presence of a toxin in the food that was produced by a microbe in the food. For example, the bacterium StaphykKoccus aureus can grow in some foods and produce a toxin that causes intense vomiting. The rare but deadly disease botulism occurs when the bacterium Clostridium botulinum grows and produces a powerful paralytic toxin in foods. These toxins can produce illness even if the microbes that produced them are no longer there. 

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