Discussion 



Pheasant botulism differs clinically from chicken botulism. Loose feathers and prolapse of the third eyelid 

 observed in chickens are not clinical features of pheasant botulism. Flaccid paralysis is the predominant clinical sign. 

 Two facets of pheasant botulism may be used to make a diagnosis. First, a source of botulinum toxin must be 

 established. Dead fly-blown pheasant carcasses have been reported to be the predominant source of toxin (6). Spores 

 of C. botulinum are swallowed while pheasants are picking up grit. Subsequent unrelated deaths may initiate an 

 outbreak of botulism under proper environmental conditions. Anaerobic conditions exist in dead birds facilitating 

 C. botulinum growth and toxin production. Maggots aid in maintaining a suitable pH in the carcass allowing 

 continued growth and toxin production. Botulinum toxin does not affect maggots (8). Maggots are thought to 

 concentrate botulinum toxins (6), but this has not been proven experimentally. Pheasants apparently find fly-blown 

 carcasses in the weeds and ingest the larvae. The presence of C. botulinum and its toxin in the carcasses can be 

 determined by culturing the organism or by macerating the larvae and injecting mice. 



The second and most difficult step in the diagnosis of pheasant botulism is finding the toxin in serum or 

 parenchymatous organs of affected birds. Several pheasants may be needed to demonstrate the presence of toxin in 

 serum. Blood samples should be obtained from birds as soon as possible after clinical signs are noted. Serum toxin 

 titers apparently decline rapidly, frequently preventing a laboratory diagnosis. The decline in serum toxin titers in 

 experimental animals is not due to toxin excretion (7). In rats botulinum toxins leave the serum and are so firmly 

 bound to neuromuscular junctions that antitoxin will not remove them (4). During reinnervation the nerve sprouts 

 and grows around the old neuromuscular junction (2). This firm neuromuscular binding has also been reported to 

 account for the accumulation of toxin in mink and mice (5). Undetectable levels of toxin in the mink feed have been 

 shown experimentally to cause clinical botulism without detectable serum levels (5). Therefore, failure to find toxin 

 in serum may indicate the titers are too low to detect (since botulism is a cumulative toxin) or the toxin has 

 disappeared from serum prior to collection. Several attempts may be necessary to make a definitive diagnosis. 



REFERENCES 



1. Dowell, V. R. and Hawkins, T. M. Laboratory Methods in Anaerobic Bacteriology. U.S. National 

 Communicable Disease Center, Atlanta, Ga. (1968). 



2. Duchen, L. W. An Electron Microscopic Study of the Changes Induced by Botulinum Toxin in the 

 Motor-End-Plates of Slow and Fast Skeletal Muscle Fibres of the Mouse. J. Neurol. Sci., 14, (1971): 47-60. 



3. Gross, W. B. and Smith, L. DS. Experimental Botulism in Gallinaceous Birds. Avian Diseases, 15, (1971): 

 716-722. 



4. Lamanna, C. Critical Comment on Research Needs in Botulism: Ecology, Nature, and Action of Toxin. 

 Proceedings of the First U.S.-Japan Conference on Toxic Micro-Organisms. Edited by M. Herzberg, U.S. 

 Government Printing Office, Washington, D.C., (1970): 230-235. 



5. Loftsgard, G., Yndestad, M., and Helgebostad, A. Cumulative Effect of Repeated Doses of Clostridium 

 botulinum Toxin in Mice and Mink. Can. Vet. J., 11, (1970): 227-231. 



6. Shave, H. J. Progressive Pathologic Signs of Botulism in Pheasants. Journal of Wildlife Diseases, 6, (1970): 

 402-403. 



7. Smith, L. DS., Davis, J. W., and Libke, K. G. Experimentally Induced Botulism in Weanling Pigs. Am. J. Vet. 

 Res., 32, (1971): 1327-1330. 



8. Wagenaar, R. 0., Dack, G. M., and Mayer, D. P. Studies on Mink Food Experimentally Inoculated with 

 Toxin-Free Spores of Clostridium botulinum Types A, B, C, and E. Am. J. Vet. Res., 14 (1953): 479-483. 



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