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

34 BACTERIOSESan 18-week-old child. In addition, the presence of the toxin could be confirmed inthe blood serum of three of these persons who died suddenly at home. The symptomswere similar to those of classic botulism. Nine additional cases of sudden andunexpected death were described (Sonnabend et al., 1985).The incubation period is usually from 18 to 36 hours, but the illness can show upwithin a few hours or as long as eight days after ingestion of the contaminated food.The clinical signs of the different types vary little, although the mortality rate seemsto be higher for type A. The disease is afebrile, and gastrointestinal symptoms, suchas nausea, vomiting, and abdominal pain, precede neurological symptoms.Neurological manifestations are always symmetrical, with weakness or descendingparalysis. Diplopia, dysarthria, and dysphagia are common. Consciousness and sensibilityremain intact until death. The immediate cause of death is usually respiratoryfailure. The mortality rate in botulinum poisonings is high. The highest rate isrecorded in patients with short incubation periods, i.e., those who have ingested ahigh dose of the toxin. In the United States, the fatality rate has been reduced from60% in 1899–1949 to 15.7% in 1970–1977, by means of early and proper treatment.In patients who survive, complete recovery, especially of ocular movement, maytake as long as six to eight months.Treatment should be initiated as soon as possible through administration of thetrivalent botulinum antitoxin (A, B, and E). The patient must be hospitalized inintensive care in order to anticipate and treat respiratory distress, which is the immediatecause of death (Benenson, 1990).(b) Infant botulism is an intestinal infection caused by the ingestion of C. botulinumspores, which change in the intestine into the vegetative form, multiply, andproduce toxins. Of 96 cases studied (Morris et al., 1983) in the United States,excluding California, 41 were caused by C. botulinum type A, 53 by type B, one bytype F, and another by type B together with F. Type A appeared almost exclusivelyin the western states, while type B predominated in the East. This distribution is similarto that of the spores in the environment (see the section on source of poisoningor infection and mode of transmission). In addition, two cases in Italy due to type Eproduced by Clostridium butyricum and one case in New Mexico (USA) due to typeF produced by Clostridium baratii have been described; i.e., by two species otherthan C. botulinum (see section on etiology). The case of a girl under age 6 monthswith paroxystic dyspnea due to C. botulinum type C toxin was also described. Thechild survived the illness, but may have been left with a cerebral lesion probablycaused by hypoxia (Oguma et al., 1990). Sonnabend et al. (1985) had previouslyidentified the bacteria and C toxin in the colon of a child who died suddenly inSwitzerland.The fact that C. botulinum primarily colonizes the caecum and colon, and that96% of patients with infant botulism are under 6 months of age led to research onthe characteristics of the intestinal microflora that allow the clostridium to multiply.Using a normal mouse as a model, it was established that the microflora in adultsprevent the establishment of C. botulinum; however, if adult “germ-free” mice areused, the clostridium multiplies in their intestines. The same thing happens to conventionalmice from 7 to 13 days old, which are very susceptible. In addition, breastfedinfants have feces with a lower pH (5.1–5.4) than those fed with formula (pH5.9–8.0). This difference may be significant, because the multiplication of C. botulinumdeclines as pH falls and ceases below 4.6. In addition, breast-feeding has the