Frank M. Boyd

Effect of Dietary Fats on Infection by Escherichia coli in Chicks.

Ross and Adamson (1) reported that chicks deficient in essential fatty acids (EFA) developed aspergillosis more readily than those fed a diet containing corn oil. Hopkins et al (2) reported that chicks fed an EFA-dencient diet developed a respiratory disease while those which received the diet supplemented with soybean oil did not. The causative agent of the disease was not identified. Nagai et al (3) showed that EFA-deficient mice were susceptible to bacterial infections but added linoleate conferred protection. Dubos(4) reported peanut oil increased survival of tuberculosis-infected mice, while Hedgecock(5) found olive oil to be ineffective against that agent compared with coconut oil. The experiments reported here were conducted to determine if the EFA-deficient chick is more susceptible to E. colt infection than chicks given diets supplemented with various oils of widely varying fatty acid content and to determine the comparative activity of purified fatty acids. Experimental. White Plymouth Rock chicks from flocks of the Poultry Disease Research Center were selected at random and placed in wire-floored electrically heated batteries. All chicks were fed the prescribed ration from the time of hatching. The basal ration was a casein-gelatin-cerelose diet described by Edwards(6). Supplementary oils: coconut, corn, menhaden and linseed, were added at the rate of 2%. The fatty acid composition of these oils as determined by gas-liquid chroma tography is shown in Table 1(7). Methyl oleate (18:1) or methyl linoleate (18:2) were added at the 1% level, approximately the amount present in the corn oil diet. The methyl oleate was prepared from olive oil by low temperature crystallization(8) and the methyl linoleate by the urea adduct method (9). The methyl oleate was 98% pure, containing traces of myristic acid, palmitic acid and palmitoleic acid.

Action of lithocholic acid in the germ-free chick.

Feeding of lithocholic acid to chicks and hens caused a rise in their serum cholesterol in work of Edwards(1) and Edwards et al. (2). When this compound was fed to mice or rats it caused a depression in serum cholesterol in the work of Beher et al.(3), Howe et al.(4) and Portman and Bruno (5). Recently Howe and Bosshardt(6) demonstrated that in the presence of a mixture of succinyl-sulfathiazole and oxytetracycline in the diet of mice, lithocholic acid no longer had a serum cholesterol-depressing effect while hyodeoxycholic acid was still effective. They interpreted these findings to mean that lithocholic acid was active by virtue of conversion to an unidentified compound under the influence of the intestinal bacteria. The investigation reported here was carried out to determine if the cholesterol elevating action of lithocholic acid in the chick might also be due to some other compound produced from lithocholic acid in the chickens gastrointestinal tract. Experimental. Four plastic canopy germ-free isolators (American Sterilizer Co.) were used for the experiment. The isolators were sterilized by spraying with 30% beta-propiolactone solution; each air filter (Fiber-glass 50) was sterilized with 1 ml methyl bromide; water bottles, cages and other equipment were autoclaved; feed was sterilized with ethylene oxide. Eggs of Single Comb White Leghorns were obtained from a local hatchery after 18 days of incubation. The eggs were washed in detergent and passed through 2% HgCl2 solution into the isolators. Twelve eggs were placed in each isolator. After hatching, 6 chicks were placed in each of 2 wire cages in each isolator. The basal ration was fed to the chicks in one cage and the lithocholic ration to the chicks in the other cage. Cultures were taken daily for 3 days and each 3 days thereafter.