Establishment of Pneumocystis carinii infection in a rat population.
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Biomedical subjects
Publications and source records attributed to M Chinchilla.
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An avirulent T. gondii strain isolated from a owl (Glaucidium brasilianum) produces randomly distributed cysts in the brain of mice which can survive to inocula as high as 1000 oocysts. Cysts appeared for the first time after 15 days of infection. Regarding to humoral immunity development due to our TCR-2 strain, detectable antibodies were found after 12 days of infection.
In an experimental model the anti--Toxoplasma effect of watermelon and cantaloupe seeds, together with sulfadiazine (Sd7.5 and Sd15) given by oral route, were studied. Combination of any of these seeds with the drug was able to increase the survival time and cure some tachyzoite infected mice. The effect was produced either by peeled or complete seeds and more significant results were obtained when Sd7.5 and 10(3) tachyzoite inoculum was used in the model. Some Toxoplasma oocyst infected mice were cured with the seeds alone (75% for watermelon, 37,5 or 50% for cantaloupe. Body weight variations are independent of the treatment with Sd alone or in combination with watermelon or cantaloupe seeds.
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An in vitro model for studying the protection of mouse myocardial cells against Trypanosoma cruzi was developed. It was demonstrated that immune mouse lymphocytes stimulated with a specific antigen elicited a mediator which protected myocardial cells from newborn mice against T. cruzi infection. The substance responsible for this activity was sensitive to acid (pH 2) treatment.
Cysts of Tritrichomonas muris are reported. The morphology of this evolution stage is described under light and electron microscopy. The biologic and epidemiologic importance of this finding is discussed.
An electron microscope model was used to study the effect of rat peritoneal macrophages on Toxoplasma gondii. 10(7) tachyzoites were injected i.p. in 30 days-old rats. After 1, 2, 4, 8 and 24 h peritoneal exudate was withdrawn and infected phagocytic cells were prepared for electronic microscope studies. Toxoplasma organisms inside of rat macrophages showed remarkable lesions such as vacuolization and organisms were totally lysed inside of macrophages of more than 8 h infection rats. The results confirm at molecular level, the importance of rat macrophages in the natural adaptation of this rodent to T. gondii.
Lymphocytes from mice immunized against Toxoplasma gondii protected T. gondii-infected macrophage and kidney cell cultures. After contact with antigens, supernatants of such immune lymphocytes, also contained a factor protective for T. gondii-infected macrophages and kidney cells. Supernatants were protective only when the lymphocytes and kidneys cells were isogeneic. Protection was specific in that supernatants from only T. gondii-immune, but not Besnoitia jellisoni-immune, lymphocytes provided protection against toxoplasmosis. Sixteen to 24 h were required for an appreciable amount of protective factor to be secreted; a similar absorption time was necessary for kidney cells to be protected. Peritoneal lymphocyte lysates, prepared as transfer factor, contained protective substances with a potency similar to that of lymphocyte supernatants, which were also strain restricted in their effect.
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White rats were found to be resistant to 3 x 10(7) Toxoplasma gondii organisms (RH strain) inoculated either sc or ip. That resistance was age-dependent since survival time of 1- or 5-day-old rats inoculated with 10(4) or 10(6) tachyzoites was lower as compared with those 10 or 15 days old. Organisms kept in contact with a lysate of white rat complete peritoneal exudate showed reduced capacity to infect mice. Peritoneal exudate of 5-day-old rats showed a stronger effect than that of 1, 2, 3, or 4 day-infected animals. After 10 days the anti-toxoplasma effect diminished and it almost disappeared after 15 days of infection. Apparently age and macrophage activity are very important factors in the natural adaptability of the white rat to Toxoplasma gondii.
Groups of "immunized" and "non-immunized" hamsters were inoculated weekly with 2, 10 or 20 mg of cortisone acetate per 100 gr of body weight and infected with Leishmania mexicana or L. braziliensis. Doses of 10 and 20 mg of cortisone were excessive, since the animals died with bacterial infections before they developed leishmaniasis. Inflammation and necrosis were more evident in animals inoculated with cortisone and L. mexicana. Furthermore, this strain caused lesions in lymphatic ganglia of immunosuppressed animals, but was not observed in those inoculated with L. braziliensis. There was no difference between the pathological findings in nonimmune and immune hamsters. These results could indicate that passive immunization with dead antigen is not effective.
Antigen-treated lymphocytes from immune hamsters specifically protected not only macrophages, but also cultured fibroblasts and kidney cells infected with Toxoplasma gondii or Besnoitia jellisoni. Macrophages were not necessary for the protection of fibroblasts and kidney cells. A mediator that inhibited the intracellular proliferation of these microbes was obtained from immune lymphocytes in contact with specific antigen. Again, macrophages were not necessary for the elaboration of this mediator or its activity in kidney cells or fibroblasts. The mediator was microbe and host specific, had a molecular weight between 4,000 and 5,000, was resistant to heating at 56 degrees C for 30 min, and was sensitive to chymotrypsin, but resistant to ribonuclease and deoxyribonuclease. A single injection of Besnoitia mediator afforded better protection to hamsters infected with Besnoitia than did antibody. Whereas antibody lysed extracellular organisms, the microbe-specific mediators conferred immunity not only on macrophages, but also on other cells of the body, apparently the first such demonstration.
A positive dye test for Toxoplasma antibodies was observed in 5% of 100 mice (Mus musculus) and 30.4% of 23 rats (Rattus norvegicus and R. rattus). The parasite was isolated from two mice. The animals were captured in several urban localities in the metropolitan area of San José, Costa Rica. The number of positive animals found appears to be enough to infect cats, whose principal source of infections are the Toxoplasma cysts in the rodents. Therefore it is apparent that domestic mice and rats, besides the felines play an important role in the epidemiology of Toxoplasmosis in Costa Rica. Additional studies showed that the presence of Eimeria falciformis, a common coccidian in domestic mice, did not inhibit the Toxoplasma infections in these rodents.
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Toxoplasma oocysts in cat feces were marked with a tracer amount of strontium-85 (85-SR), and were superficially buried simulating the natural disposal of feces by cats. Oocyst infectivity in Costa Rica was followed qualitatively and persisted for 1 year in three shaded sites, two moist, and one relatively dry site. Oocyst infectivity was quantitated in the Kansas deposit over a period of 18 months, including two winters. After initial mixing in soil, the level of infectivity remained fairly stable. Infectivity was recovered, probably from the surface on one Musca, several isopods, and earthworms. These data on persistence of Toxoplasma oocysts in soil support the concept that Toxoplasma infectivity in nature may be increased logarithmically by cats.
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The effects of a modified natural porcine surfactant (Curosurf) on phagocytosis and killing of Cryptococcus neoformans by alveolar macrophages and on the production of superoxide anions were investigated in vitro. Attachment and ingestion were evaluated separately by a fluorescent quenching technique. The nitroblue tetrazolium reduction test was used as an indirect measurement of superoxide anion production. Killing was assessed by a colony-forming assay. Surfactant induced increased ingestion of C. neoformans, unopsonized as well as opsonized with fresh serum or anticryptococcal polyclonal IgG. Surfactant had, however, no effect on the attachment or killing of unopsonized or opsonized C. neoformans by the alveolar macrophages. In addition, the enhancement of the oxidative metabolism of the macrophages after stimulation with opsonized yeast was impaired, although the killing was not affected. This study indicates that in vitro Curosurf can influence the alveolar macrophage defence against C. neoformans by enhancing its ingestion and by interacting with the superoxide anions release from alveolar macrophages stimulated with fresh serum or anticryptococcal polyclonal IgG opsonized yeast cells.