Effects of diet on fecal occult blood testing in healthy dogs.

Six dogs were fed each of nine diets to evaluate the effects of diet on fecal occult blood test results. The diets represented a range of different type (i.e. canned, dry or semi-moist), protein and vegetable constituents, and fiber contents. Each diet was fed twice daily for five consecutive days; fecal samples were collected twice daily on days 4 and 5. An o-tolidine test kit and a guaiac paper test kit for fecal occult blood were used. Two hundred and sixteen fecal samples were analyzed (24 samples/diet). When using the guaiac test the following positive results were obtained from fecal samples from dogs consuming a canned meat- and vegetable-based diet (24/24 samples); a canned meat-based diet (24/24 samples); a dry corn and poultry-based diet (9/24 samples); a dry corn, wheat, and meat meal diet (4/24 samples), a canned poultry-based diet (1/24 sample) and a semi-moist soybean meal-based diet (2/24 samples). A total of 64 samples were positive using the guaiac test. Using the o-tolidine test, no samples were positive. The difference between the number of positive results with each test kit was highly significant (p < 0.001). Results indicate that 1) diet affects the specificity of guaiac test fecal occult blood results in the dog and 2) positive o-tolidine test results were not caused by diets fed in the study.     

Response of susceptible and resistant peach-potato aphids Myzus persicae (Sulz.) to insecticides in leaf-dip bioassays

The response of susceptible (S), moderately resistant (R₁) and strongly resistant (R₂) peach-potato aphids, Myzus persicae (Sulz.) to organophosphorus, carbamate and pyrethroid insecticides was tested by a leaf-dip bioassay. The aphids were placed on potato leaves (dipped in insecticide solutions 1–2 or 24 h before infestation) and their mortality examined 48 h later. R₁ aphids were virtually susceptible to most of the carbamates, demephion and acephate, but were slightly to moderately resistant (2.1–9.4 times) to permethrin, cypermethrin and (S)-α-cyano-3-phenoxybenzyl (1R)-cis-3-(2,2-dibromovinyl)-2,2-dimethylcyclopropanecarboxylate (I), (NRDC 161), to 5,6,7,8-tetrahydro-2-methylquinolin-4-yl dimethylcarbamate (II), (Hoechst 25 682) and demeton-S-methyl. R₂ aphids resisted more strongly or very strongly (between 65 and 1280 times) the pyrethroids, demeton-S-methyl (×94), II (×83) and demephion (×9), and were slightly to moderately (2–5 times) resistant to acephate, pirimicarb, ethiofencarb and 2-(dimethylcarbamoyloxyimino)-3-methoxyimino-N,N- dimethylbutyramide (III), (DPX 3853). Both resistant strains were susceptible to nitrilacarb [4,4-dimethyl-5-(methylcarbamoyloxyimino)pentanenitrile] complex (1:1) with zinc chloride (IV), (AC 85 258). The implications of these results in terms of practical aphid control are discussed.     

Lack of effect of selenium supplementation on the incidence of weak calves in dairy herds

A double blind controlled trial was carried out on four commercial dairy herds, to investigate the effect of one 50 mg injection of selenium, 10 days before parturition, on the incidence of weak calves. Although the treatment marginally increased the selenium status of treated calves it did not decrease the incidence of the weak calf syndrome.     

Influence of fiber form in a complete mixed ration on incidence of left displaced abomasum in postpartum dairy cows.

During the fall of 1982, increased incidence of left displaced abomasum (LDA) was seen in a group of cows fed a complete pelleted ration (3/16 inch) at the university's dairy center during the early postpartum period. Of these, 17.4% developed LDA when fed this experimental ration, whereas only 1.6% of the remaining cows in the herd developed LDA. The latter cows (as a control) were fed loose alfalfa hay, sorghum silage, and an 18% crude protein mix. Most of the fiber in the experimental diet or pelleted diet was alfalfa hay (30% as-fed basis) that was ground through a quarter-inch screen for incorporation into the pellet. Another 10% of the dietary fiber was contributed by cottonseed hulls. Thus, increased incidence of LDA may be associated with short length of the dietary fiber in the pelleted form.     

Histopathologic and ultrastructural myocardial alterations in calves deficient in vitamin E and selenium and fed polyunsaturated fatty acids.

We developed an experimental model of nutritional degenerative myopathy in ruminant cattle. Fourteen experimental calves were fed a diet low in vitamin E and selenium for 127 to 137 days. Six of these calves were then euthanatized. After 127 days, a dietary additive of linseed oil that had been treated to protect it against ruminal hydrogenation was added to the low vitamin E and selenium diet of the eight remaining calves as a source of polyunsaturated fatty acids. Six of these animals were euthanatized after 6 to 11 days of polyunsaturated fatty acid feeding; the other two died after 6 and 8 days. Macroscopic myocardial alterations were seen in five polyunsaturated fatty acid-fed calves but not in any other experimental calf. Microscopic lesions, comprising multifocal or diffuse cardiocyte degeneration and necrosis, were seen in atrial and ventricular myocardium of all experimental calves. These changes were more severe in polyunsaturated fatty acid-fed calves than in animals that did not receive polyunsaturates. Ultrastructurally, sublethally damaged cardiocytes had lysed contractile material; vacuolated sarcoplasm; altered mitochondria, sarcoplasmic myelin figures, and lipofuscin granules; and multiple nuclei. Necrotic cardiocytes had contracted myofibrils, pyknotic nuclei, mineralized mitochondria, and plasmalemmal disruption; the external lamina remained largely intact. Necrosis was followed by macrophage invasion and phagocytosis of necrotic debris. Repair of the lesions was by deposition of collagen and elastin fibers. No alterations were seen in the hearts of control calves fed vitamin E and selenium-supplemented diet. The induced myocardial lesions are similar to those of spontaneous nutritional degenerative myopathy in ruminant cattle.