Biomedical subjects
Publications and source records attributed to S P Sharma.
Quantitative measurements of glycogen in aging bruchids showed there was a considerable decrease (> 50%) with age except on the fifth day when an increase was observed, followed by a decrease on the sixth day. The variations in glycogen content with age suggests that glycogen serves as one of the energy sources responsible for the maintenance of metabolism in the process of aging in bruchids.
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The distribution of Toxoplasma gondii in blood and other tissues of nine adult sheep experimentally infected with T. gondii oocysts was studied by inoculation of mice with ovine tissues. Parasitemia was detected in five sheep 6 to 11 days after inoculation (DAI) and lasting usually for 1 to 2 days. Toxoplasma gondii was isolated from numerous internal organs of five sheep killed between 7 and 28 DAI and from eight organs of a sheep killed 64 DAI. Of the three sheep killed 117, 118, and 119 DAI, T. gondii was isolated only from brain, heart, diaphragm, skeletal muscle, and intestine. Skeletal muscle was infected in all sheep. More mice became infected after inoculation with chronically infected tissues digested in 1% trypsin than undigested tissues. Results indicate that skeletal muscle and brain should be used for parasitological surveys in sheep.
One cow elk (approx 4 months pregnant) and one calf elk were each inoculated intraruminally with 10(5) infective oocysts of Toxoplasma gondii. Both animals were seronegative when inoculated, but became seropositive to T gondii. Sabin-Feldman dye test antibody titers in relation to day postinoculation were as follows: 1:1024, 1:1024, and 1:2048 (days 28, 69, and 73) for the calf; 1:2048, 1:128, and 1:128 (days 34, 69, and 73) for the cow; and 1:2546 (73 days after inoculation of the cow) for the fetus. Indirect hemagglutination antibody titers were not detected in sera of the cow or her fetus and remained low (1:64 or lower) in calf sera. Both the cow and the calf remained asymptomatic until necropsy 73 days after they were inoculated. Toxoplasma was isolated in mice and cats after they were inoculated with brain, spinal cord, heart, diaphragm, liver, pancreas, cervical lymph nodes, and intestines of the infected calf; with brain, heart, diaphragm, and skeletal muscles of the infected cow; and with brain, heart, cervical lymph nodes, and spleen of the fetus.
Toxoplasma gondii was demonstrated by mouse inoculation in semen of three of three goats orally inoculated with 10(4) oocysts of the GT-1 strain of T gondii. From goats 1 and 3, T gondii was first detected in semen 7 days after inoculation (DAI) and 12 DAI from goat 2. Excretion continued over a period of 52 days from goat 1 and 16 days from goat 2. Goat 3 had excreted T gondii for 5 days when its was killed 14 DAI.
Thirteen goats (9 does and 4 bucks) were each inoculated orally with 10,000 infective Toxoplasma gondii oocysts. Three does and one buck were used as noninoculated controls. In 2 to 4 days after inoculation (DAI), inoculated goats became dull, pyrectic (40 to 41 C), and anorectic. Three goats died (10, 10, and 14 DAI) and two goats were killed (7 and 32 DAI) because they were moribund; also, 3 does aborted, 2 had weak kids, and 2 had dead fetuses. Toxoplasma was isolated from the placenta of three goats, and the fetal tissues of four goats. The control goats remained asymptomatic. The distribution of T gondii in blood and other tissues was studied by inoculation of mice with caprine tissues. Parasitemia was detected in 7 of 7 goats--beginning 4 DAI in 1 goat, 5 DAI in 5 goats, and 8 DAI in 1 goat. The parasitemia lasted 3 to 10 days. Toxoplasma was isolated from the milk of 2 goats at 12 and 14 DAI. Toxoplasma was isolated from 15 or more tissues of 5 goats killed 7 to 35 DAI and from 10 tissues of 2 goats killed 69 and 95 DAI.
The effect of fenbendazole therapy was studied in 9 dogs with pulmonary paragonimiasis induced by inoculation of metacercariae (25/dog) of Paragonimus kellicotti. At 42 to 47 days after 6 dogs were inoculated, they were given fenbendazole in 2 divided doses totaling 50 mg (4 dogs) or 100 mg (2 dogs)/kg of body weight each day for 10 to 14 days. Three dogs were not treated. The passage of Paragonimus eggs in the feces ceased after 3 days at the high dosage and after 3 to 8 days at the low dosage. All dogs were euthanatized and necropsied on day 14. Live flukes were not recovered from the lungs of any treated dog, but 15, 19, and 23 live flukes were recovered from the untreated dogs.
Toxoplasmosis was diagnosed at necropsy in a 4-week-old pig from a litter of 16 born to a clinically normal sow. Multifocal acute necrosis of blood vessels and parenchyma was found in the small intestine, mesenteric lymph nodes, liver, lungs, and brain. Numerous tachyzoites, ultrastructurally indistinguishable from Toxoplasma gondii, were found in lesions. The affected pig and seven other littermates died after diarrhea had developed within 1 to 2 weeks of birth. The most likely source of infection was oocysts from cats on the farm.
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The formation of lipofuscin pigment in the anterior horn cells of the cervical spinal cord has shown in the fetuses and neonates under the extrinsic influence of maternal protein deprivation during the gestation period in the squirrel monkeys.
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The nucleolar changes in the dorsal root ganglion cells of the squirrel monkey, Saimiri sciureus, have been investigated by the use of histological and histochemical methods in the healthy neonates (born to mothers maintained on 25% protein diet during gestation) and young adults, and compared with those observed in the protein-malnourished neonates (born to mothers maintained on a 8% protein diet during gestation). Also studied were young adults maintained on a high protein diet (25% protein) as well as on a low protein diet (2% protein content) for a period of 15 weeks. Whereas in the healthy animals (neonates and young adults) only a few cells show nucleolar budding and finally their extrusion into the cytoplasm, the protein-malnourished animals show a significantly enhanced nucleolar activity in the form of increased size (3-4 times the original) and active budding either from one focal point or at several places on the body of the nucleolus. In the neurons which show chromatolytic changes, these extrusions migrate to the nuclear membrane, wherefrom they pass on to the cytoplasm through an evagination of the nuclear envelope. Such a migration appears to occur by a focal dissolution of the nuclear membrane. It appears that, under conditions of severe malnutrition and advanced chromatolytic changes in the neuronal cytoplasm, the nucleolar material provides a compensatory mechanism for the increased cytoplasmic catabolism and loss of ribonucleoprotein material in order to facilitate additional protein synthesis for cell survival.