Biomedical subjects

C Novoa

Publications and source records attributed to C Novoa.

9 recordsLinked to original sources

PubMed1996

Use of polymerase chain reaction in the diagnosis of tuberculosis in cats and dogs.

Samples from four dogs and four cats suspected of having tuberculosis were processed for histopathology, bacterial culture and polymerase chain reaction (PCR). A simple, rapid method for the extraction of DNA from tissue samples was used in two PCR assays designed to confirm the diagnosis of tuberculosis. The PCR assays detected all the culture-positive samples from these animals and no false positive results were obtained. The PCR technique was successful for the direct detection of organisms from the Mycobacterium tuberculosis complex and reduced the time needed for a diagnosis to two days.

Animals↗

PubMed1990

Amyloidosis in adrenal glands of hamsters experimentally infected with Leishmania infantum.

Thirty 10-week-old hamsters were inoculated intraperitoneally with leishmania infantum amastigotes and were serially killed after 15, 30, 45, 60, 75 and 89-90 days. The adrenal glands of each of them were examined by means of light and electron microscopy. The cortex and medulla of the adrenal gland showed a progressive deposition of amyloid, selectively identified by both optical and ultrastructural techniques. It has been suggested that adrenal amyloidosis during visceral leishmaniasis is directly related to a stimulation of the phagocitary mononuclear system due to the persistence of the antigenic stimulation of the parasite. In addition to these deposits, the presence of inflammatory infiltrates containing lymphocytes, plasmocytes and macrophages with leishmanias confirmed the establishment of leishmaniasis. The deposition of the amyloid fibrils finally leads to the partial destruction of the adrenal parenchyma.

Adrenal Gland Diseases↗

PubMed1988

Structural and ultrastructural hepatic changes in experimental canine leishmaniasis.

Six 4 month-old beagles were inoculated with Leishmania donovani infantum, three of them intraperitoneally (Group A) and the other three intravenously (Group B). The animals from Group A were killed 109, 433 and 592 days after inoculation and animals from Group B 109, 171 and 334 after inoculation. The liver of each of them was examined by means of light and electron microscopy. The lesions observed in both groups were very similar, but developed more rapidly in Group B. A chronic hepatitis appeared due to infection, characterized by the presence of multiple intralobular granulomas and portal inflammatory infiltrates consisting of lymphocytes, plasmocytes and macrophages with a variable number of amastigotes. The Kupffer cells were hyperplastic and contained parasites in their cytoplasm. Gradually the hepatocytes developed a progressive cellular swelling, which during the end-stages of the process showed itself with severe nuclear degeneration, disintegration of cytoplasmic organelles, enlargement of the cytoplasmic matrix and disruption of the plasma membranes, leading to cytolysis.

Animals↗

PubMed1986

Intestinal amyloidosis in hamsters with visceral leishmaniasis.

Thirty hamsters about 10 weeks old were inoculated intraperitoneally with Leishmania donovani amastigotes and were serially killed after 15, 30, 45, 60, 75 and 85-90 days. Both the small and large intestines were examined grossly, and the histopathology was assessed by light and electron microscopy. The lamina propria and the submucosa of the whole length of the intestinal tract showed a progressive deposition of amyloid, selectively identified by optical and ultrastructural techniques. The presence of amyloid fibrils in the cytoplasm of plasma cells suggests that appearance of intestinal amyloidosis during visceral leishmaniasis may be the result of a pathological dysfunction of these cells. In addition to these deposits, the presence of inflammatory infiltrates containing lymphocytes, plasmocytes and macrophages confirmed the establishment of leishmaniasis. In the end-stages of the infection both vacuolar degeneration of the epithelial cells lining the lumen of the intestine and a moderate hyperplasia of lymphatic nodules was observed.

Amyloidosis↗

PubMed1979