Forty-three deaths were recorded among pigs fed boiled cassava meal at a private piggery over a period of two years. There were signs of sudden death in some cases with blood exuding from the external nares, vomiting, muscular weakness and pain or reluctance to move, emaciation, and stunted growth. The necropsy lesions included skeletal and cardiac muscle degeneration and necrosis, icterus, hepatic necrosis, and oedema of the dependent parts. The deaths and clinical signs are thought to be due to a non cyanide toxic principle in cassava, possibly the coumarins (scopoletin), which is found in high levels in cassava diet even after heat treatment. Therefore, the use of proper processing technology to obtain cassava products of high quality is recommended. 1. Introduction In Nigeria, commercially reared pigs under the intensive husbandry system are kept in concrete floors and fed balanced commercially produced feeds. The use of cassava (Manihot utilisima) in form of the peels and pulp in the feeding of livestock has attracted renewed interest especially with the rising cost of commercially produced feeds [1]. Pig rations are formulated with high energy content to provide for greater growth potential in genetically improved pigs [2]. The private pig farmer fed his pigs only with peeled and boiled cassava pulp as a source of energy and to reduce cost. This paper describes the clinical signs, postmortem lesions, and histopathology of the pigs fed the cassava diet. 2. Case Report Forty-three deaths were recorded among pigs fed boiled cassava meal at a private piggery over a period of two years. A total of thirty-eight deaths occurred among the piglets less than 9 months of age, while only five deaths were reported in the adult pigs over nine months of age. The pigs were of the Landrace × Large White local crossbreeds. On examination, the clinical signs shown by the pigs varied. In acute cases the pigs were found dead without premonitory signs. These pigs were mostly 2–4 months old and in good nutritional body conditions. Blood exuded from the nose and did not clot readily or not at all. In the pigs over one year of age there was a chronic prolonged course of the disease, characterized by lack of interest in their food, progressive emaciation, and stunting; jaundice and recumbency with decubital ulcers were observed in some cases. The abdomen was distended with ascites. The pigs which exhibited clinical symptoms were treated accordingly. However, they failed to respond to treatments and ultimately died. Necropsy lesions in the acute cases showed the liver
References
[1]
F. C. Obioha and P. C. N. Anikwe, “Utilisation of ensiled and sundried cassava peels by growing swine,” Nutrition Reports International, vol. 26, no. 6, pp. 961–972, 1982.
[2]
D. T. Mortimer, “Vitamin E/selenium deficiency syndrome in pigs,” Veterinary Record, vol. 112, no. 12, pp. 278–279, 1983.
[3]
S. G. Kelly and F. J. Post, Basic Microbiology Techniques, Star Publishing Company, Belmont, Calif, USA, 3rd edition, 1989.
[4]
E. J. L. Soulsby, Helminthes, Arthropods and Protozoan of Domesticated Animals, ELBS, London, UK, 7th edition, 1982.
[5]
C. J. Nemi, Schalm's Veterinary Hematology, Lea and Febiger, Philadelphia, Pa, USA, 4th edition, 1986.
[6]
V. A. Oyenuga and E. O. Amazigbo, “A note on the hydrocyanic acid content of cassava (Manihot utilissima),” West African Journal of Biology and Chemistry, vol. 1, no. 2, pp. 39–43, 1957.
[7]
O. G. Longe and J. A. Oluyemi, “Feed value of heated and unheated cassava starch for chicks,” Zentralblatt fur Veterinarmedizin, Reihe A, vol. 27, no. 9-10, pp. 819–823, 1980.
[8]
O. L. Ekpechi, A. Dimitriadou, and R. Fraser, “Goitrogenic activity of cassava (a staple Nigerian food),” Nature, vol. 210, no. 5041, pp. 1137–1138, 1966.
[9]
C. Abuye, U. Kelbessa, and S. Wolde-Gebriel, “Health effects of cassava consumption in South Ethiopia,” East African Medical Journal, vol. 75, no. 3, pp. 166–170, 1998.
[10]
B. O. Osuntokun, “An ataxic neuropathy in Nigeria: a clinical, biochemical and electrophysiological study,” Brain, vol. 91, no. 2, pp. 215–248, 1968.
[11]
I. C. Ononogbu and I. Emole, “The effect of garri on rat plasma cholesterol,” Atherosclerosis, vol. 31, no. 1, pp. 101–104, 1978.
[12]
O. Obidoa and S. C. Obasi, “Coumarin compounds in cassava diets: 2 health implications of scopoletin in gari,” Plant Foods for Human Nutrition, vol. 41, no. 3, pp. 283–289, 1991.
[13]
S. C. Obasi, O. U. Njoku, and O. Obidoa, “Effects of single oral doses of scopoletin and aflatoxin B1 on the clotting time, serum cholesterol and phospholipid levels of chicks,” Indian Journal of Physiology and Pharmacology, vol. 38, no. 2, pp. 89–94, 1994.
[14]
S. C. Obasi and O. Obidoa, “Coumarin compound in cassava, yam, cocoyam, and maize (1) Preliminary studies on blood coagulation and binding to erythrocytes and haemoglobin,” in Proceedings of the 14th Annual Conference of the Biochemical Society of Nigeria, p. 1, 1989.
[15]
O. Obidoa and G. U. Uzoka, “Inhibition of hepatic microsomal NADPH-cytochrome C (P-450) reductase activity in gari-fed rats,” Qualitas Plantarum Plant Foods for Human Nutrition, vol. 35, no. 1, pp. 63–72, 1985.
[16]
J. A. O. Ojewole and S. K. Adesina, “Cardiovascular and neuromuscular actions of scopoletin from fruit of Tetrapleura tetrapetra,” Planta Medica, vol. 49, no. 2, pp. 99–102, 1983.
[17]
G. Feuer, “Metabolic and biological actions of coumarins,” in Progress in Medicine and Chemistry, G. P. Ellis and G. B. West, Eds., vol. 10, pp. 102–103, North-Holland Publishing Company, Amsterdam, The Netherlands, 1974.
[18]
F. C. Chilaka, E. O. Anosike, and O. Obidoa, “Effect of high and prolonged gari diets on some microsomal enzymes activities of rat liver,” Plant Foods for Human Nutrition, vol. 35, no. 2, pp. 159–164, 1985.