Parenteral chemotherapy of helminthosis of sheep and cattle.
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It has been suggested that the larvae of the pig nematode Ascaris suum is a possible cause of rejection of lambs' livers in the abattoir. However, this assertion was not substantiated in an experimental study in which lambs were dosed with infective A suum eggs. This produced, at the worst, small trivial lesions (up to 2 mm diameter) which would probably have been missed at meat inspection under commercial conditions. No evidence of ascarid lesions was observed in the livers of 5873 lambs and hoggs slaughtered between June and August. The most important causes of rejection were lesions caused by Cysticercus tenuicollis and migrating Fasciola hepatica, and these accounted for 90 and 8 per cent, respectively, of 1337 livers rejected either totally or partially by the meat inspectors.
The efficacy of the oxfendazole pulse release bolus system for the control of parasitic gastroenteritis and parasitic bronchitis in first-season grazing calves was evaluated in Belgium. Twenty-two calves were allocated to two groups. The calves in one group received a bolus at the time of turn out, while the other group remained untreated. The efficacy of the bolus was assessed by comparison of faecal worm egg counts, plasma pepsinogen concentrations, the antibody response to Ostertagia, Cooperia and Dictyocaulus species total plasma protein and albumin concentrations, and weight gains throughout the grazing season and the housing period. The oxfendazole pulse release bolus provided good control of parasitic gastroenteritis dominated by ostertagia. The effects of parasitic gastritis were greatly reduced as shown by the significantly lower values of serum pepsinogen and ostertagia antibody titres. The use of the bolus further reduced the adverse effects of parasitism as indicated by better liveweight gains and normal total plasma protein and albumin concentrations whereas in the untreated control group hypoproteinaemia and hypoalbuminaemia were observed. Most animals exhibited clinical signs of parasitic bronchitis at the end of the grazing season, and the bolus may not adequately control parasitic bronchitis in all cases at all times.
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Five pregnant queens were inoculated orally with Toxoplasma gondii tissue cysts. Twenty-two live and three dead kittens were born 16 to 31 days after inoculation. Four kittens were eaten by queens and, thus, were not available for histologic examination. Twenty-one kittens that died or were euthanatized on day 2 (two kittens), 4 (one kitten), 5 (five kittens), 6 (five kittens), 7 (one kitten), 8 (four kittens), 16 (two kittens), and 29 (one kitten) after birth were studied histologically. T gondii was detected by bioassay and was seen in histologic sections of tissues from all 21 kittens. The histologic lesions associated with neonatal toxoplasmosis were widely disseminated infiltrates of macrophages and neutrophils often accompanied by necrosis; lymphocytes and plasma cells were occasionally present. The most consistent lesions were proliferative interstitial pneumonia (21/21); necrotizing hepatitis (20/21); myocarditis (21/21); skeletal myositis (21/21); glossal myositis (19/19); nonsuppurative encephalitis affecting the cerebrum (18/18), brain stem (15/15), and spinal cord (9/9); uveitis (19/19); necrotizing adrenal adenitis (18/18); and interstitial nephritis (16/21). Placental lesions (2/2) consisted of grossly visible areas of necrosis and mineralization.
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Schistosome egg-induced lesions in congenitally athymic mice differed from those found in normal heterozygous controls. Heterozygote liver granulomas were chareacterized by poorly phagocytic epithelioid macrophages, and were rich in eosinophils and fibroblasts, with peripheral lymphocytes and plasma cells. Hepatic lesions in nude mice were much smaller and lacked epithelioid macrophages, with lesions about mature eggs, typically consisting of monocytes and macrophages filled with pigment, occasional neutrophils, and rarely one or more eosinophils or giant cells. While heterozygote granulomas damaged liver cells mainly by encroachment or by their vascular effects, in the nudes hepatocytes bordering the lesions showed microvesicular cytoplasmic damage and either hydropic degeneration or focal acidophilic necrosis of individual liver cells. In heterozygotes, immunofluorescent-stainable schistosome egg antigen (SEA) was concentrated in the granuloma center. In nude mice, SEA, was distributed throughout the infiltrates and in and around hepatocytes adjacent to egg lesions corresponding to the observed pattern of hepatocyte necrosis. We conclude that, in contrast to heterozygotes, nude mice lack hypersensitivity granulomas and fail to sequester toxic egg products, this resulting in zonal hepatocellular damage. Alternative explanations include the possibility of a latent hepatitis virus being activated by the schistosome infection; however, several cogent arguments are presented against that alternative.
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