近日,，美國研究者發(fā)現(xiàn),，在動物飼料中添加抗生素會產(chǎn)生令人憂慮的效果：藥物會刺激動物腸道內(nèi)的病毒在腸道細菌間轉(zhuǎn)移基因。如此一來,，令腸道細菌對抗生素產(chǎn)生耐藥性的基因就會被大量轉(zhuǎn)移,。科學(xué)家在專業(yè)期刊《微生物學(xué)》(Microbiology)上撰文警告稱,，激活這些病毒會導(dǎo)致耐藥性在細菌間大幅擴散,。
人們早就知道，如果給豬或家禽喂食抗生素,，那么這些動物的腸道細菌會大量產(chǎn)生耐藥性,。而現(xiàn)在研究者發(fā)現(xiàn)，特定病毒在耐藥性的擴散過程中發(fā)揮著重要作用,。大部分遺傳信息并不是在細菌間直接傳遞的,，而是借助于噬菌體。
噬菌體在休眠階段只是細菌遺傳物質(zhì)中的一小段脫氧核糖核酸,。然而,，一旦受到刺激，它們就會突變成真正的病毒：這些病毒會在細菌細胞內(nèi)爆炸性地復(fù)制,，然后大量沖出細胞,，最終沖入其他細菌細胞內(nèi)，將遺傳信息注入這些細菌的遺傳物質(zhì),。
研究者稱,，他們現(xiàn)在首次研究了抗生素對這種噬菌體的影響。研究表明,，藥物促進了病毒的激活過程,。研究者發(fā)現(xiàn)，與未服用抗生素的豬相比,，服用了抗生素的豬的腸道內(nèi)被釋放出的噬菌體要多得多,。
“這一發(fā)現(xiàn)很有意義，因為人們知道噬菌體會轉(zhuǎn)移耐藥性基因”,，希瑟·艾倫說,。她是論文的第一作者，任職于美國農(nóng)業(yè)部動物疾病中心,。一旦噬菌體的活動致使耐藥性基因在細菌間廣泛傳播,，那么這些基因被轉(zhuǎn)移給人類病原體的危險也就增加了——例如在家禽和家畜的腸道內(nèi)。（生物谷Bioon.com）
doi:10.1128/mBio.00260-11
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Antibiotics in Feed Induce Prophages in Swine Fecal Microbiomes
Heather K. Allena, Torey Loofta, Darrell O. Baylesb, Samuel Humphreya, Uri Y. Levinea, David Altb, and Thaddeus B. Stantona
Antibiotics are a cost-effective tool for improving feed efficiency and preventing disease in agricultural animals, but the full scope of their collateral effects is not understood. Antibiotics have been shown to mediate gene transfer by inducing prophages in certain bacterial strains; therefore, one collateral effect could be prophage induction in the gut microbiome at large. Here we used metagenomics to evaluate the effect of two antibiotics in feed (carbadox and ASP250 [chlortetracycline, sulfamethazine, and penicillin]) on swine intestinal phage metagenomes (viromes). We also monitored the bacterial communities using 16S rRNA gene sequencing. ASP250, but not carbadox, caused significant population shifts in both the phage and bacterial communities. Antibiotic resistance genes, such as multidrug resistance efflux pumps, were identified in the viromes, but in-feed antibiotics caused no significant changes in their abundance. The abundance of phage integrase-encoding genes was significantly increased in the viromes of medicated swine over that in the viromes of nonmedicated swine, demonstrating the induction of prophages with antibiotic treatment. Phage-bacterium population dynamics were also examined. We observed a decrease in the relative abundance of Streptococcus bacteria (prey) when Streptococcus phages (predators) were abundant, supporting the “kill-the-winner” ecological model of population dynamics in the swine fecal microbiome. The data show that gut ecosystem dynamics are influenced by phages and that prophage induction is a collateral effect of in-feed antibiotics.
