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流感病毒加剧细菌对幼雪貂的毒性:可能在婴儿猝死综合征中起作用。

Exacerbation of bacterial toxicity to infant ferrets by influenza virus: possible role in sudden infant death syndrome.

作者信息

Jakeman K J, Rushton D I, Smith H, Sweet C

机构信息

Microbial Molecular Genetics and Cell Biology Research Group, School of Biological Sciences, University of Birmingham, United Kingdom.

出版信息

J Infect Dis. 1991 Jan;163(1):35-40. doi: 10.1093/infdis/163.1.35.

Abstract

Of several toxins examined, only staphylococcal alpha and gamma toxin, endotoxin, and diphtheria toxins were lethal for 5-day-old ferrets. Their toxicities were enhanced in animals infected at 1 day old with influenza virus, from 3-fold with staphylococcal gamma toxin through 14-fold for staphylococcal alpha toxin, 84-fold for endotoxin, and 219-fold for diphtheria toxin. No increased viral replication occurred in any tissue; thus the effects of the toxins were exacerbated by the infection, not vice versa. Neonates died suddenly without clinical symptoms as in human babies dying from the sudden infant death syndrome (SIDS). Pathologic examination showed inflammation in the upper respiratory tract, lung edema and collapse, and early bronchopneumonia in the toxin- and influenza virus-treated animals but not in those treated with toxin or virus alone. Thus, bacterial toxins could play a role in SIDS, this being more likely with a concomitant influenza virus infection.

摘要

在检测的几种毒素中,只有葡萄球菌α毒素、γ毒素、内毒素和白喉毒素对5日龄雪貂具有致死性。在1日龄感染流感病毒的动物中,它们的毒性增强,葡萄球菌γ毒素增强了3倍,葡萄球菌α毒素增强了14倍,内毒素增强了84倍,白喉毒素增强了219倍。任何组织中均未出现病毒复制增加的情况;因此,毒素的作用因感染而加剧,而非相反。新生儿突然死亡,无临床症状,如同死于婴儿猝死综合征(SIDS)的人类婴儿一样。病理检查显示,在毒素和流感病毒处理的动物中,上呼吸道有炎症、肺水肿和肺萎陷,以及早期支气管肺炎,但单独用毒素或病毒处理的动物中未出现这些情况。因此,细菌毒素可能在SIDS中起作用,伴随流感病毒感染时这种可能性更大。

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