RESUMO
Salmonella enterica serotypes are 99% responsible for salmonellosis in human and animals, especially Salmonella enterica serovar Albany that has been identified in chicken carcass representing a risk for human and animal health. Salmonella enterica serovar Albany was isolated from the feces of a male ocelot (Leopardus pardalis), at the zoo in Culiacan, Sinaloa, Mexico, and from raw chicken (feline's diet). The pulsed-field gel electrophoresis pattern (PFGE) generated by Xba I enzyme was identical in both isolates, indicating that the source of infection was the raw chicken. Five months after having isolated the bacteria from the feces, a post mortem study was carried out on the feline. Macroscopically, severe hemorrhagic enterocolitis and renal fibrosis was observed and microscopically, there was evidence of severe mononuclear lymphocytic infiltration in the ileum, as well as necrosis of intestinal villi and crypts, besides severe multifocal interstitial nephritis and fibrosis in both kidneys. The invA gene was amplified from intestinal samples confirming an infection by Salmonella. The microbiologic, molecular and histopathology diagnoses suggest that death of the feline was caused by ingestion of raw chicken contaminated with Salmonella enterica serovar Albany. This clinical case highlights the importance of persistent fecal Salmonella shedding animals and describes the molecular epidemiological relationships of isolates from feces and food, which allowed to find the primary source of infection.
Los serotipos de Salmonella especie enterica son los responsables del 99% de las salmonelosis en humanos y animales, en particular, Salmonella enterica serovariedad Albany se ha identificado en canales de pollo, por lo que representa un riesgo para la salud humana y animal. Se aisló Salmonella enterica serovariedad Albany a partir de heces de un ocelote macho (Leopardus pardalis), cautivo en el zoológico de Culiacán, Sinaloa, México, y de pollo crudo (alimento del felino). El patrón por electroforesis en campo pulsado (PFGE) con la enzima Xba I fue idéntico en ambos aislados, lo que indica que la fuente de infección fue el pollo crudo. Cinco meses después de haber aislado las bacterias de las heces, se realizó estudio post mortem del felino anteriormente mencionado, y se observó macroscópicamente: enterocolitis hemorrágica severa y fibrosis renal; y microscópicamente: necrosis de vellosidades y de criptas e infiltrado mononuclear linfocitario severo en íleon, además nefritis intersticial severa multifocal y fibrosis en riñón. A partir de muestras intestinales se amplificó el gen invA que confirma la infección por Salmonella. Los diagnósticos microbiológico, molecular e histopatológico sugieren que la muerte del felino se debió a la infección causada por la ingesta de pollo crudo contaminado con Salmonella enterica serovariedad Albany. Este caso clínico confirma la importancia que tienen los animales que excretan Salmonella vía fecal y describe la relación epidemiológica-molecular de los aislamientos obtenidos de heces y alimento, lo que permitió esclarecer la fuente primaria de infección.
RESUMO
Background. Several factors inhibit cellular immune response by deactivating macrophages, but very few, such as those described here, prevent macrophage activation. Methods. Ascites liquid from 12-day-old BALB/c mice bearing 5178Y lymphoma tumors was collected, and cell-free ascites liquid (CFAL) was separated from lymphoblasts. The supernatant (SI) was obtained from the homogenized and centrifuged lymphoblasts Then, macrophage cultures contaning 0.2 X 10 a the sixth cells from lymphoma-bearing or hearthly mice were added to 10 µL of CFAL or S1, plus 5 µg of lipopolysaccharides (LPS)/mL, 40 U interferon-ç or a blend of both. Macrophages were incubated with CFAL or S1 prior to or after adding the activators to investigate whether any of the previously mentioned lymphoma fraction inhibited macrophage activation or whether they deactivated them. The effect of CFAL or S1 was estimated as the diminution of the amount of nitric ixide released by the experimental macrophage cultures with respect to controls (activated macrophages treated with none of the lymphoma fractions). Results. LPS, IFN-ç, and the LPS/ç blend activated macrophages from both lymphomabearing and healthy mice. None of the lymphoma fractions deactivated macrophages. CFAL, but not S1, inhibited the macrophage activation, i.e., the percentage of inhibition of nitric oxide releasing 76.7 percent in macrophages from healthy and lymphomabearing mice, respectively. In addition, CFAL was unable to inhibit macrophage-activation effect of IFN-ç or the LPS/IFN-ç blend. Conclusions. Mouse L5178Y Lymphoma releases a factor that in vitro inhibits the macrophage activation induced by LPS, but not by IFN-ç controls