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M C Boxaca

Publications and source records attributed to M C Boxaca.

At least 37 records · Page 2Linked to original sources
PubMed1982

[Development of a cytological method to detect pregnancy in guinea pigs].

Diagnosis of guinea pig pregnancy by the inhibition hemagglutination test used to detect chorionic gonadotrophin in urine showed to be unreliable after the 57% false positive and 3% false negative results obtained over 79 urine samples tested. On the other hand, by comparing the cell morphology of about 60 vaginal smears taken from 20 non-pregnant guinea pigs, stained by a Papanicolaou modified technique, the 4 estrous cycle stages were characterized. The subsequent study of many vaginal smears taken from 15 pregnant guinea pigs showed no pathognomic cells but a picture where 60-70% proestrus and 40-30% diestrus cells appeared. This proestrus-diestrus (Pd) picture was accepted as typical for pregnancy, because it showed up in every pregnant guinea pig lasting all the gestation period, changing only after delivery or abortion. Fecundation does not change the estrous cycle sequence which, as it was proved, progressed normally until it reached this Pd picture. Therefore, the persistence of a Pd picture during +/- 6 days should be considered as diagnosis for pregnancy; when estrus has been detected a Pd picture 12-14 days post estrus as prognosis, and at 16-19 days post-estrus as diagnosis for pregnancy. This cytologic assay proved to be reliable. Besides, once cell characterization has been performed, the staining procedure can be substituted by a direct observation of wet specimen, saving time without loosing accuracy.

Animals↗
PubMed1975

Experimental biology and pathogenesis of Junin virus infection in animals and man.

A fatal disease resembling Argentine haemorrhagic fever of man has been produced in guinea-pigs and mice by inoculation with Junin virus. Infected guinea-pigs show macroscopic and microscopic haemorrhagic lesions, marked bone marrow changes, decreased leukocytes and platelets in the peripheral blood, and impairment of immunological response. This response permits differentiation between pathogenic (XJ) and attenuated (XJ Cl(3)) strains. Guinea-pigs inoculated with the XJ Cl(3) strain develop an inapparent infection accompanied by slight haematological changes, the appearance of antibody, and protection against challenge with the pathogenic strain. The attenuated strain has been used successfully as an immunizing antigen in 636 human volunteers. Guinea-pigs infected with Tacaribe virus show cross-protection against Junin virus, with the presence of heterologous neutralizing antibodies. Suckling mice infected with Junin virus develop a typical viral encephalitis; the pathogenicity of the virus decreases with increasing age of the mice. Experiments with thymectomized mice and with mice treated with antithymocyte serum suggest that the pathogenicity of Junin virus in this host is related to the integrity of the thymus-dependent immune system. There is evidence that humoral antibodies do not play any role in the development of the encephalitic lesions but rather protect mice against Junin virus infection. A recent serological survey among laboratory workers and inhabitants of the endemic area has demonstrated the presence of inapparent infection with Junin virus.

Animals↗
PubMedDate not supplied

[Experimental Junin virus infection in the mouse: rototype of the disease].

As previously postulated, the pathological changes which develop in 1-4 day old mice after intracerebral inoculation of 1-1000 DL50 of Junín virus prototype strain (XJ), was designated as experimental hemorrhagic fever of the mouse EHFm. In this paper, virus distribution, hematological alterations, interferon and circulating antibody responses are described. A mortality of 93.45% occurred between 9 and 20 days post-infection (p.i.), with 81.6% of death occurring between 11 and 18 days p.i. This last period can be considered to be the critical period of the disease. The study of virus distribution shows that the brain, where the virus was inoculated, was the only place where virus could be detected 48 hs, p.i. Four days p.i., the titer in the brain increased remarkably and virus was detected in the blood. Virus, within the same values, could be isolated up to the 10th. day. Invasion of liver and spleen occurred on the 10th. and 15th. days p.i., respectively (Fig. 1). The onset of clinical symptoms coincided with widespread disemination of the virus. CF antibodies were found only 15 days p.i., with a titer of 1/64. Neutralizing antibodies remained below detection levels during the whole experiment (Fig. 1). Surviving mice (6.3%) had high circulating antibody titers 40 days p.i. This result would indicate that the morobidity of EHFm is aproximately 100% (Table 1). Poor interferon response was registered in all the organs examined, indicating a low intereron producing ability for Junin virus6. Total leukocytes and lymphocyte counts showed a slight tendecy to drop, although the values were within normal range during the first ten days (Table 2, Fig 1). On day 14 p.i., a statistically significant decrease (p less than 0.001) was found. This leuko-lymphopaenia continued until death of the animals. It is expected that the data presente here would contribute to a better understanding of the Junin virus infection in the newborn mouse, the experimental animal used.

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