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

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BOTULISM 33<strong>and</strong> silage containing the preformed <strong>to</strong>xins (Smith, 1977). Recently, various importan<strong>to</strong>utbreaks have been recorded due <strong>to</strong> consumption of bedding silage <strong>and</strong> birddroppings. In Great Britain, 80 out of 150 stabled cattle became sick <strong>and</strong> 68 died.Type C <strong>to</strong>xin was detected in 18 of the 22 sera examined <strong>and</strong> the same <strong>to</strong>xin wasconfirmed in the remains of dead chickens found in the silage (McLoughlin et al.,1988). Similar outbreaks also occurred in Brazil <strong>and</strong> Canada because the bird beddingused <strong>to</strong> feed the cattle contained the type C <strong>to</strong>xin (Bienvenue et al., 1990;Schocken-Iturrino et al., 1990). Animal remains are usually found when botulismoutbreaks occur in cattle, especially due <strong>to</strong> silage; however, no animal remains couldbe found in the fodder in various cases in the United States <strong>and</strong> Europe.Bovine poisoning by type B is rare; outbreaks have occurred in Europe (Blood etal., 1983), the United States (Divers et al., 1986), <strong>and</strong> Brazil (Loba<strong>to</strong> et al., 1988).Botulism in sheep is due <strong>to</strong> type C <strong>and</strong> has been identified only in westernAustralia <strong>and</strong> South Africa.In horses, botulism cases are sporadic <strong>and</strong> for the most part are caused by C.botulinum type C. It has been diagnosed in various European countries, the US,Israel, Australia, <strong>and</strong> South Africa. A special form occurs in colts at 6 <strong>to</strong> 8 weeksold (“shaker foal syndrome”); it is due <strong>to</strong> the type B neuro<strong>to</strong>xin <strong>and</strong> its pathogenesisis similar <strong>to</strong> botulism in children, since apparently C. botulinum has <strong>to</strong> colonizefirst in the intestine <strong>and</strong> other sites in order <strong>to</strong> produce the neuro<strong>to</strong>xin later.Outbreaks of this form have been described in the United States <strong>and</strong> Australia(Thomas et al., 1988).Botulism in swine is rare because of the natural high resistance of this species <strong>to</strong>botulinum <strong>to</strong>xin. Outbreaks diagnosed in Senegal <strong>and</strong> Australia were caused by typeC beta <strong>and</strong> one in the United States was caused by type B.Botulism in mink can be an important problem owing <strong>to</strong> their eating habits, if theyare not vaccinated as recommended. Mink are highly susceptible <strong>to</strong> type C, whichcauses almost all the outbreaks.Botulism in fowl occurs practically worldwide <strong>and</strong> is caused principally by typeC alpha. Outbreaks of types A <strong>and</strong> E have been recorded in waterfowl. In the westernUnited States, type C is responsible for massive outbreaks in wild ducks duringthe summer <strong>and</strong> early fall. Many other species of wild fowl are susceptible <strong>to</strong> botulism<strong>and</strong> outbreaks also occur in domestic chickens <strong>and</strong> farm-bred pheasants (Smith,1977). Botulism in domestic fowl has been related <strong>to</strong> cannibalism <strong>and</strong> the ingestionof maggots in decomposing carcasses. The explanation is that the body temperatureof fowl (41°C) favors the type C <strong>to</strong>xin, which would be produced <strong>and</strong> absorbed inthe caecum, whose pH of 7.4 also favors the <strong>to</strong>xin (Castro et al., 1988).Botulism in dogs is rare <strong>and</strong> is caused primarily by ingesting bird carcasses, withtype C being responsible for the disease (Hatheway <strong>and</strong> McCroskey, 1981).The Disease in Man: (a) Botulism poisoning by foods is produced primarily bytypes A, B, <strong>and</strong> E <strong>and</strong> rarely by F or G. Outbreaks in man described as type C havenot been confirmed, as the <strong>to</strong>xin has not been found in the patients’ blood or fecesnor in foods they ate. An outbreak of type D was identified in Chad, Africa, amongpeople who had eaten raw ham (Smith, 1977). A new <strong>to</strong>xicogenic type, C. botulinumtype G, was isolated from the soil in Argentina in 1969 (Giménez <strong>and</strong> Ciccarelli,1970). The first human cases were recognized in Switzerl<strong>and</strong> (Sonnabend et al.,1981). The microorganism was isolated in au<strong>to</strong>psy specimens from four adults <strong>and</strong>

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