Hepatic profile of Gallus gallus Linnaeus, 1758 experimentally infected by Plasmodium juxtanucleare Versiani & Gomes, 1941.

One of the species that causes avian malaria is Plasmodium juxtanucleare. It is commonly found in poultry, especially when the birds receive food free of coccidiostats. Since industrial and organic poultry breeding is increasing in the world and few studies have been conducted examining the clinical parameters of both healthy and infected birds, this work evaluated whether the infection caused by P. juxtanucleare in Gallus gallus provokes alterations in the birds' hepatic profile. We analyzed the activity of ALT and AST and carried out histological analyses of liver sections of infected fowls by intracelomic inoculation with infected blood from a donor fowl with a parasite load of around 7%. The infected birds' parasite load was evaluated during 45 days by means of blood smears. There was a positive correlation between the increase in parasite load and higher ALT activity in the infected fowls, but there was no significant variation of the AST activity between the control and infected groups, possibly because of the non-specificity of this enzyme as an indicator of hepatic lesion. The results show that infection caused by P. juxtanucleare in G. gallus provokes hepatic alterations, indicated by the increase in the ALT enzyme activity and by the inflammatory infiltrates found in the liver sections of the infected fowls.

An avian pathogenic Escherichia coli isolate induces caspase 3/7 activation in J774 macrophages.

Avian pathogenic Escherichia coli (APEC) strains, the etiological agent of colibacillosis in poultry, must resist the attack of incoming macrophages in order to cause disease. In this work, we show that an APEC strain (APEC17) remained viable inside J774 macrophages for at least 8 h and was cytotoxic to them 6-8 h after infection. APEC17 induced caspase 3/7 activation, the central caspases in apoptosis, in infected macrophages already at 2h after infection. Both cytotoxicity and caspase 3/7 activation were reduced when cells were infected with heat-killed APEC17, showing that bacteria must be viable to induce apoptosis. Our findings using APEC17 suggest that APEC may escape destruction by triggering macrophage apoptotic death.

Nitric oxide synthase expression in the endothelium of pulmonary arterioles in normal and pulmonary hypertensive chickens subjected to chronic hypobaric hypoxia.

To determine whether or not exposure to chronic hypoxia and subsequent development of pulmonary hypertension syndrome (PHS) induce alterations in endothelial nitric oxide (NO) production in broiler's pulmonary vascular bed of broilers, we studied the expression of nitric oxide synthase enzyme in pulmonary endothelial cells by a nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase histochemical staining reaction. For this purpose, 60 broilers of three different ages (17, 30, and 42 days) were used. The animals were distributed in two groups: a) 30 healthy (nonhypertensive) broilers and b) 30 chicks with PHS. All broilers in group b had fewer NADPH-diaphorase-positive endothelial cells in arterioles than did the nonhypertensive broilers. These differences were highly significant (P < 0.01). These results demonstrate for, the first time in broilers, that hypoxia-induced pulmonary hypertension is associated with a decrease of endothelial-derived NO expression in pulmonary vessels.

Enzimas de funçäo hepática na aflatoxicose aguda experimental em frangos de corte / Hepatic enzimes function in experimental acute enzimes aflatoxicosis en broilers

Com o objetivo de avaliar a funçäo hepática de aves experimentalmente intoxicadas por aflatoxina, com e sem uso de bentonita sódica, foram utilizados 40 (quarenta) frangos de corte, machos, linhagem Ross, divididos em 4 (quatro) grupos de 10 (dez) animais, sendo que cada grupo foi submetido a um tratamento: T1 - controle (raçäo sem aflatoxina ou bentonita), T2 - raçäo com 5ppm de aflatoxina, T3 - raçäo com 5ppm de aflatoxina e 0,5 porcento de bentonita sódica e T4 - raçäo com 0,5 porcento de bentonita sódica. Todos estes tratamentos foram aplicados do 1§ ao 42§ dia de vida das aves. Aos 21, 35 e 42 dias de idade, foram analizados os níveis séricos das enzimas aspartato aminotransferase (AST), alanina aminotransferase (ALT), lactato desidrogenase (LDH) e gama glutamiltransferase (GGT). A análise da variância mostrou que houve interaçäo entre os tratamentos e datas de colheita de material, para as seguintes variáveis: AST, LDH e GGT. Para estas, foi aplicado o teste de Tukey, comparando-se as médias de cada tratamento em cada data. Observou-se que as enzimas AST, ALT e GGT näo apresentaram diferenças significativas entre tratamentos, porém, nos tratamentos 1 e 2, a AST apresentou um aumento linear (p<0,05) ao longo de todo o experimento, sendo este mais acentuado no tratamento 2. A enzima ALT näo apresentou nenhuma variaçäo para qualquer tratamento por todo o período. A GGT, nos tratamentos 2 e 3, sofreu aumento linear (p<0,05) dos níveis ao longo do experimento. Os níveis da enzima LDH, aos 21 dias, foram mais elevados (p<0,05) nos tratamentos 2 e 3 em relaçäo aos tratamentos 1 e 4. A análise dos resultados permitiu concluir que é possível detectar hepatotoxicidade provocada pela aflatoxina, através do monitoramento dos níveis das enzimas AST e GGT no soro das aves com faixa etária entre 21 e 42 dias e pela avaliaçäo dos níveis de LDH aos 21 dias de idade; sendo que o uso da bentonita na raçäo com aflatoxinas näo modifica o comportamento destas enzimas.