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"A refratariedade das galinhas ao T. (S.) cruzi, ocorre desde o nascimento e não é eliminada pela bursectomia hormonal. Noventa e oito pintos de 1 a 15 dias de vida (normais ou tratados com testosterona) inoculados com o T. (S.) cruzi foram negativos. Deste modo, dificilmente a refratariedade poderia ser interpretada como decorrência de um "anticorpo natural", uma vez que a bursectomia provoca uma queda na produção de anticorpos e das gamaglobulinas. Em cerca de 50% de ovos embrionados (normais ou tratados com o hormônio) foram vistos flagelados do 4º ao 12º dia de inoculação, observando-se ninhos de amastigotos em alguns embriões. Os pintos nascidos dos mesmos grupos dos ovos examinados e positivos, foram sistematicamente negativos pelo exame do sangue. Um deles sacrificado horas depois de nascido, mostrou amastigotos no coração, mas esses parasitos pareciam degenerados. Provavelmente, se alguns chegam a evoluir para tripomastigotos, estes são destruídos á medida que as células hospedeiras se rompem, e assim jamais são encontrados no sangue circulante. It has already been shown that the refractory state of chickens toward "T. (S.) cruzi" appears early at time of hatch. Fifty-four normal newly hatched and inoculated chicks were negative. it has also been verified that this refractory state persists even after hormonal bursectomy (eggs being injected with 2.5 mg of testosterone). Forty-four bursectomized and inoculated newly hatched chicks were negative. If we consider the fact that bursectomy causes a deficiency in the production of antibodies and gammaglobulins, the refractory state seems not to occur on account of a "natural antibody". Inoculations of "T. (S.) cruzi" made in 153 eggs (normal or treated with testosterone) produced infections of variable intensity in about 50% of them. Although chicks newly hatched from the same groups were always negative. As we have some embryos to be positive until the 21st day of incubation it seems probable that some of those not previously examined and from which these chicks were hatched might have been positive too. Nevertheless, all of them have not parasithemia. So, something happens near the time of hatch that turns the organisms of birds an unfavorable environment to the parasites. The most impressive idea is that in several of the positive embryos the parasites found were remainders of the inoculum and resulting of the infection of the chorioallantoic membrane and its surrounding blood vessels. However there is no doubt that in some embryos invasion of tissues by the parasites definetely occured with amastigote multiplication forms specially in the heart and liver. These amastigotes could persist for sometime after hatching but it seems that they degenerated and only excepcionally could accomplish its evolution to trypomastigote forms. And even when this happened the flagellates were destroyed as soon as the host cells burst. Probably that is the reason why they were not met in the peripheral blood. Parasithemia of the embryos results mainly of extracellular multiplication. Epimastigotes in binary division are very frequent

memórias do instituto oswaldo cruz

A refratariedade das aves ao "Trypanosoma (Schizotrypanum) cruzi" II - refratariedade das galinhas desde o nascimento; persistência da refratariedade após Bursectomia; infecções em ovos embrionados