Influence of temperature on streptococcus agalactiae infection in Nile tilapia / Influência da temperatura na infecção de tilápias do Nilo por Streptococcus agalactiae

Environmental changes affect fish homeostasis, turning them more susceptible to diseases. In Brazil, outbreaks of Streptococcus agalactiae infection have been reported in Nile tilapia when they are outside of their thermal comfort zone. This investigation evaluated mortality rate and which were the most infected organs at temperatures that naturally occurred in southern of Brazil. Forty Nile tilapia (Oreochromis niloticus) were infected with S. agalactiae and distributed in four groups (n=10) and each group was exposed to a different temperature: G1: 24°C, G2: 26°C, G3: 28°C, and G4: 32°C. Fish were monitored for 10 days. In this period, fish that presented irreversible clinical signs were sacrificed and samples of brain, liver, and kidney were collected for bacteriological and molecular analysis. Signs compatible with a streptococcal infection were observed in all groups. Highest mortality rates occurred at 24°C and 32°C. The brain was the most affected organ with the highest percentage of isolation of S. agalactiae by both methods of diagnosis. The results suggest that, as in mammals, temperatures that are further away from the comfort zone influence fish homeostasis, increasing susceptibility to bacterial infections.

Mudanças ambientais afetam a homeostase dos peixes, tornando-os mais suscetíveis a doenças. No Brasil, têm sido relatados surtos de infecção por Streptococcus agalactiae em tilápia do Nilo, principalmente quando se encontram fora da zona de conforto térmico. No presente trabalho, foi avaliada a taxa de mortalidade e determinado quais foram os órgãos mais afetados por essa bactéria em temperaturas que ocorrem naturalmente no Sul do Brasil. Quarenta tilápias-do-nilo (Oreochromis niloticus) foram infectadas por Streptococcus agalactiae e distribuídas em quatro grupos (n = 10), cada um deles submetidos a diferentes temperaturas: G1: 24°C, G2: 26°C, G3: 28°C e G4: 32°C. Os peixes foram monitorados durante 10 dias. Os peixes com sinais clínicos irreversíveis foram sacrificados e coletadas amostras de cérebro, fígado e rins para análise bacteriológica e molecular. Foram observados sinais compatíveis com infecção estreptocócica em todos os grupos. A taxa de mortalidade mais elevada ocorreu nos grupos mantidos nas temperaturas de 24°C e 32°C. O cérebro foi o órgão mais afetado, com a maior percentagem de isolamento de S. agalactiae pelos dois métodos de diagnóstico. Os resultados sugerem que, tal como nos mamíferos, temperaturas que estão mais afastadas da zona de conforto afetam significativamente a homeostase dos peixes, aumentando a sua susceptibilidade para infecções bacterianas.

Morphological & morphometric studies on liver in rats subjected to repetitive heat stress.

Morphological and morphometric studies were conducted under light microscope on paraffin sections (H&E) of liver from controls and experimental rats subjected to repeated heat stress for 4 h/day, at 38 degrees +/- 0.5 degree C (relative humidity 65-82%) for 2-8 consecutive days. The morphometric variables were derived by intersection-point counting method, using simple square lattice test system A100. Twinning of liver cell plates and anisocytosis characterised morphological changes in rats exposed to heat twice. Following five heat exposures, rat liver showed ballooning degeneration of hepatocytes, associated with sinusoidal compression and loss of normal liver cell plate pattern. The degenerative changes in liver parenchyma were more pronounced in rats that underwent eight heat exposures. Despite hepatocytic degeneration, the numerical density of hepatocytes (Nvh) and the volume density of hepatocytes (Vvh) increased with the increase in number of heat exposures, indicating associated heat induced acceleration in hepatocytic proliferation. A successive fall, with increase in the number of heat exposures, in the sinusoidal length density (Jvs) and in the numerical density of Kupffer cells on area (Nak) revealed progressive damage to hepatic-vascular endothelium, which suggest an adverse effect on the immune status of the animals.