O F Idris’s research while affiliated with Central Veterinary Research Laboratories, Soba and other places

Twelve of fifteen 6-9-mo-old clinically healthy Desert sheep were given single or repeated daily doses of 25 to 4000 mg cotoran/kg by drench. Cotoran poisoning was characterized by grinding of the teeth, ruminal tympany, mydriasis, dyspnea, staggering, paresis of the hind and forelimbs, and recumbency. Lesions were widespread congestion and hemorrhage, hepatic fatty change, catarrhal enteritis and degeneration of the epithelial cells of the renal proximal convoluted tubules. These were accompanied by significant increases in the activities of GOT, LDH and GGT and decreases in serum total protein and calcium.

Dans un lot de quinze chèvres de race Nubienne, six ont reçu oralement en une seule fois des doses de métolachlor (Dual 720 EC®) de 2 000 ou 500 mg/kg de poids vif. Elles sont mortes dans un délai de 1 h après l'administration du produit. Six autres ont reçu quotidiennement des doses orales de 200 ou 25 mg/kg de poids vif. Elles sont mortes ou ont été abattues entre le 8è et le 25è jour. Chez les sujets ayant reçu une dose unique du produit, les signes d'empoisonnement ont consisté en des épisodes convulsifs, de l'incoordination motrice, des tremblements, des spasmes musculaires sévères, de la raideur, une salivation intense, de la détresse respiratoire, des attitudes anormales et du décubitus. Chez les chèvres ayant reçu le métolachlor aux doses quotidiennes, les signes cliniques ont été similaires mais se sont développés lentement. L'augmentation d'activité des AST et GGT sériques, celle de la concentration en urée et la diminution de la concentration des protéines totales ont évolué en corrélation avec les changements cliniques et l'apparition des lésions.

Six out of 15 Nubian goats kids were given single oral doses of metolachlor (Dual 720 EC) at 2,000 or 500 mg/kg liveweight and died within 1 h of the dosing. Other 6 goats were given daily oral doses at 200 or 25 mg/kg and died or were slaughtered between days 8 and 25. In goats receiving single doses, the signs of poisoning were convulsive episodes, incoordination of movement, tremors, severe muscular spasms, stiffness, profuse salivation, respiratory distress, abnormal posture and recumbency. In goats receiving metolachlor at daily doses, the signs were similar, but developed slowly. Increases in the activities of serum AST and GGT and in the concentration of urea, and decreases in total protein concentration were correlated with clinical changes and lesions.

Copper sulphate was administered by the oral or intravenous route to five dromedary camels. Two camels (1 and 2) receiving copper sulphate at 200 mg per kg per day by drench died within 8 days and camel 3, receiving 100 mg per kg per day by the same route, was slaughtered on day 172. Intravenous injection of 2 mg per kg per day caused the death of camel 4 on day 95 and camel 5, treated similarly, was slaughtered on day 138. Anorexia, dullness, diarrhoea, dehydration and recumbency in camels 1 and 2 were probably clinical signs of copper toxicity. Camels 3, 4 and 5 lost weight. Jaundice was not a prominent clinical sign. The main lesions in camels 1 and 2 were fatty change and necrosis of the liver cells, dilatation and necrosis of kidney tubules, catarrhal abomasitis, enteritis and congestion of the blood vessels of the heart. In camels 3, 4 and 5 the hepatic lesions were mild, with leucocytic infiltration and gastrointestinal and heart lesions were either mild (camel 3) or absent (camels 4 and 5). Cytoplasmic copper granules in hepatic cells were generalized in distribution but more concentrated in the centrilobular zone. In the kidney these granules were confined to the cells of the proximal convoluted tubules. Copper accumulated in the liver and kidneys of all the camels and zinc accumulated in the liver and kidneys of those receiving copper sulphate intravenously. Macrocytic hypochromic anaemia developed in camels 3, 4 and 5 and haemoconcentration in camels 1 and 2. The concentration of serum copper, zinc and iron increased in animals 1, 2 and 4, and unbound iron binding capacity decreased in four camels. There was a rise in the activity of gamma GT, GOT, LDH and CPK in the serum of all the animals. Serum ALP activity, however, increased in camels 1 and 2 and decreased in camels 3, 4 and 5.

Douze chèvres nubiennes ont reçu des doses orales uniques ou répétées de chlorure de mercure à 10, 20 et 40 mg/kg de poids vif. Elles sont mortes ou ont été sacrifiées in extremis 18 heures à 18 jours après administration. Les signes majeurs de l'intoxication ont été les suivants : anorexie, écume à la bouche, détresse respiratoire, épistaxis, météorisation, diarrhée, attitudes anormales et décubitus. Les auteurs ont mis en évidence, dans le sérum, une augmentation de l'activité de la GO transaminase, des concentrations plus élevées en urée et en phosphates inorganiques, une diminution des protéines totales et de la concentration en calcium. Les principales lésions du rein ont été la dilatation et la nécrose des tubes contournés, le rétrécissement et la disparition des amas glomérulaires, la présence de quantités variables de matériaux acidophiles homogènes dans la lumière des tubes affectés. On a noté également de l'entérite, la dégénérescence ou la nécrose des cellules hépatiques, de la congestion pulmonaire, des hémorrhagies, de l'oedème et de l'emphysème. Les modifications de la formule sanguine ont révélé une anémie

Twelve Nubian goats were given single or repeated oral dosages of mercuric chloride at 10, 20 and 40 mg/kg and died or were killed in extremis at various times after dosing (18 hours-18 days). The main signs of poisoning were anorexia, frothing at the mouth, respiratory distress, epistaxis, bloat, diarrhoea, abnormal posture and recumbency. An increase in the activity of GOT and in the concentrations of urea and inorganic phosphate and a decrease in total protein and calcium concentrations in the serum were detected. The main lesions were dilatation and necrosis of the proximal convoluted tubules, shrinkage and disappearance of the glomerular tufts, varying amounts of acidophilic homogenous material in the lumens of the affected tubules of the kidney, enteritis, hepatocellular degeneration and/or necrosis and pulmonary congestion, haemorrhage, oedema and emphysema. The changes in the red blood cells indicated anaemia.

Eight Nubian goats were given Abrus precatorius seed at 2, 1 and 0.5 g/kg/day by stomach tube. Six goats receiving the plant seed at 2 and 1 g/kg died between days 2 and 5. One goat receiving Abrus seed at 0.5 g/kg/day died on day 32 and the other animal in the group was killed on day 33. The main signs of Abrus poisoning were inappetence, bloody diarrhea, dyspnea, dehydration, loss of condition and recumbency. The lesions were fatty change and necrosis of hepatocytes and renal convoluted tubules, pulmonary hemorrhage, edema and emphysema, and erosions of the abomasal and intestinal epithelium. These changes were accompanied by increases in GOT and gamma GT activities and urea, creatinine, sodium and potassium and by decreases in total protein and albumin in the serum of Abrus-poisoned goats. The blood cell changes indicated hemoconcentration.

Colloid goitre was diagnosed in adult camels in the Kordofan region of the Sudan. The disease is characterized by gross enlargement of the thyroid, histopathological follicular changes, reproductive disorders, low concentrations of circulating thyroid hormones (T3, T4) and normocytic normochromic anaemia. The possible cause of the condition is discussed and iodine supplementation is recommended.