zoonoses and communicable diseases common to ... - PAHO/WHO

BOTULISM 29preformed toxins ingested with food. In wound botulism, the toxin forms by contaminationof the injured tissue. In 1976, a new clinical type, infant botulism, wasidentified. It is caused by colonization of the infant’s intestinal tract by C. botulinumand the resultant production and absorption of toxins.The species C. botulinum is very heterogeneous. The different groups (I to IV) aredifferentiated according to their ability to digest proteins and break down sugars.Group I is highly proteolytic and saccharolytic and includes all the type A strains aswell as various type B and F strains. Group II includes all the type E strains and thenonproteolytic type B and F strains that are highly saccharolytic. Group III consistsof the type C and D strains, which are not proteolytic (except that they digest gelatin).Group IV contains only type G, which is proteolytic but not saccharolytic(Sakaguchi et al., 1981; Concon, 1988).Despite the metabolic and DNA differences among them, these groups ofclostridia have until now been classified in a single species because they all producea botulinum neurotoxin that acts similarly in animal hosts (Cato et al., 1986).However, not all researchers agree with this scheme and one argument of thosefavoring a reclassification is the recent discovery of neurotoxigenic strains inClostridium baratii and C. butyricum.In effect, two cases of type E infant botulism in Rome, Italy, caused by C.butyricum (Aureli et al., 1986) have been described and another case was describedin New Mexico (USA) in a child suffering from a neurotoxigenic type F botulismproduced by a clostridium that was later identified as C. baratii (Hall et al., 1985).These clostridia were identified on the basis of their phenotype characteristics andwere later confirmed through DNA hybridization (Suen et al., 1988a). The neurotoxinisolated from C. baratii was similar in structure and amino acid sequence toC. botulinum types A, B, and E (Giménez et al., 1992). The proponents of reclassification,such as Suen et al. (1988b), have suggested renaming group IV, which containsthe single toxigenic type G, as Clostridium argentinense. Arnon (1986) agreesthat reclassification would be justified based on logical criteria and taxonomicpurity, but questions whether this would improve clinical, microbiological, and epidemiologicalknowledge.Geographic Distribution: Occurs on all continents, with a marked regional distributionthat probably reflects the presence in the soil of the microorganism and itsdifferent types of toxins.Occurrence in Man: The disease occurs more frequently in the northern hemispherethan in the southern hemisphere, and can appear sporadically and amonggroups of people who ingest the same food with the preformed toxin. From 1950 to1973, an average of 15.1 outbreaks occurred annually in the US, with 2.4 cases peroutbreak. In that period, there were only three outbreaks affecting more than 10 people,but in 1977, an outbreak of 59 cases involving type B botulinum toxin wasdescribed, caused by food eaten in a restaurant (Terranova et al., 1978). Figure 3illustrates the reported cases and deaths by year in the US during the period1960–1980 (PAHO, 1982). More than half of the cases reported since 1899 from 45states occurred in five western states. Table 1 shows the foods and type of botulinumtoxin that caused the illness. In the United States, only 4% of the outbreaks originatedin restaurants, but they represent 42% of the 308 cases occurring between1976 and 1984. The most widespread outbreak recorded in the United States