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

CLOSTRIDIAL FOOD POISONING 85lambs that receive a lot of milk are particularly likely to fall ill. The bacteria multiplyand produce beta toxin when they sporulate (Timoney et al., 1988).In hemorrhagic enteritis or “struck” caused by C. perfringens type C in adult sheepin England, the agent is found in the soil of areas of Romney Marsh and it is possiblethat most of the sheep in the region are infected. Beta toxin predominates. The soil andthe intestinal tract of healthy sheep are the reservoir for type D, which is the agent ofenterotoxemia in sheep. Epsilon toxin is the most important (Timoney et al., 1988).The intestines of 75 animals with diarrhea of unknown origin were examinedpostmortem to detect the presence of C. perfringens enterotoxins. Positive resultswere found in 8 of 37 swine, 4 of 10 sheep, 1 of 3 goats, 1 of 16 cattle, and none of9 horses (Van Baelen and Devriese, 1987).In animals, C. perfringens seems to multiply primarily in the intestine, where itsporulates and produces toxins. The types of C. perfringens (B, C, D, E) that produceenterotoxemia in animals multiply rapidly in the intestine and produce toxinswhen animals are suddenly released to rich pastures, are given too much fodder, orconsume large quantities of milk.Role of Animals in the Epidemiology of the Disease: Human food poisoning iscaused by foods contaminated by C. perfringens type A, usually foods consistingmainly of red meat or fowl. The animals themselves do not play a direct role in theepidemiology, since the etiologic agent is ubiquitous and can be found in the soil orin dust. Foods of animal origin are important as substrates for the multiplication ofthe bacteria and as vehicles for the disease. The soil and the intestines of humansand animals are the reservoir of the etiologic agent. C. perfringens type A is foundin the muscles and organs of animals a few hours after slaughter, unless they are rapidlyrefrigerated.Heat-resistant strains of C. perfringens may be found in the mesenteric lymphnodes of some animals after slaughter. Strains are isolated at a lower rate in animalsallowed to rest 24 to 48 hours before butchering.Diagnosis: The incubation period and clinical picture make it possible to distinguishclostridial food poisoning, which is afebrile, from salmonellosis, shigellosis,or colibacillosis, which produce fever. Staphylococcal intoxication usually results invomiting, while this symptom is rare with clostridial poisoning. Laboratory confirmationis based on the C. perfringens count in the implicated food and in thepatient’s stool (within 48 hours of onset of illness). The existence of 10 5 cells pergram of food and 10 6 per gram of fecal material is considered significant. Serotypingof strains from food and feces with a battery of 70 sera has provided good results inepidemiological research in Great Britain, but not in the United States, where only40% of the strains received by the Centers for Disease Control and Prevention couldbe typed. There is no proof that only certain serotypes are related to the disease(Shandera, 1983).Laboratory diagnosis of animal enterotoxemias is performed by mouse inoculationto demonstrate the presence of specific toxins. Some mice are inoculated onlywith intestinal contents and others are inoculated with both intestinal contents andantitoxin. Tests to directly detect the toxin can also be performed and are currentlypreferred. These include reverse passive latex agglutination, enzyme immunoassay,or culturing of Vero cells with neutralizing antibodies to inhibit the cytopathiceffects (Bartlett, 1990).