Russell James B, Houlihan Adam J
Agricultural Research Service, USDA, and Department of Microbiology, Cornell University, Wing Hall, Ithaca, NY 14853, USA.
FEMS Microbiol Rev. 2003 Apr;27(1):65-74. doi: 10.1016/S0168-6445(03)00019-6.
In recent years, there has been a debate concerning the causes of antibiotic resistance and the steps that should be taken. Beef cattle in feedlots are routinely fed a class of antibiotics known as ionophores, and these compounds increase feed efficiency by as much as 10%. Some groups have argued that ionophore resistance poses the same public health threat as conventional antibiotics, but humans are not given ionophores to combat bacterial infection. Many ruminal bacteria are ionophore-resistant, but until recently the mechanism of this resistance was not well defined. Ionophores are highly lipophilic polyethers that accumulate in cell membranes and catalyze rapid ion movement. When sensitive bacteria counteract futile ion flux with membrane ATPases and transporters, they are eventually de-energized. Aerobic bacteria and mammalian enzymes can degrade ionophores, but these pathways are oxygen-dependent and not functional in anaerobic environments like the rumen or lower GI tract. Gram-positive ruminal bacteria are in many cases more sensitive to ionophores than Gram-negative species, but this model of resistance is not always clear-cut. Some Gram-negative ruminal bacteria are initially ionophore-sensitive, and even Gram-positive bacteria can adapt. Ionophore resistance appears to be mediated by extracellular polysaccharides (glycocalyx) that exclude ionophores from the cell membrane. Because cattle not receiving ionophores have large populations of resistant bacteria, it appears that this trait is due to a physiological selection rather than a mutation per se. Genes responsible for ionophore resistance in ruminal bacteria have not been identified, but there is little evidence that ionophore resistance can be spread from one bacterium to another. Given these observations, use of ionophores in animal feed is not likely to have a significant impact on the transfer of antibiotic resistance from animals to man.
近年来，关于抗生素耐药性的成因以及应采取的措施一直存在争论。饲养场中的肉牛通常会被喂食一类名为离子载体的抗生素，这些化合物可使饲料效率提高多达10%。一些团体认为，离子载体耐药性对公众健康构成的威胁与传统抗生素相同，但人类不会使用离子载体来对抗细菌感染。许多瘤胃细菌对离子载体具有耐药性，但直到最近，这种耐药性的机制仍未得到很好的界定。离子载体是高度亲脂性的聚醚，它们积聚在细胞膜中并催化快速的离子移动。当敏感细菌通过膜ATP酶和转运蛋白抵消无效的离子通量时，它们最终会失去能量。需氧细菌和哺乳动物酶可以降解离子载体，但这些途径依赖氧气，在瘤胃或下消化道等厌氧环境中不起作用。在许多情况下，革兰氏阳性瘤胃细菌比革兰氏阴性细菌对离子载体更敏感，但这种耐药模式并不总是清晰明确的。一些革兰氏阴性瘤胃细菌最初对离子载体敏感，甚至革兰氏阳性细菌也可以适应。离子载体耐药性似乎是由细胞外多糖（糖萼）介导的，这些多糖将离子载体排除在细胞膜之外。由于未接受离子载体的牛体内有大量耐药细菌，看来这种特性是由于生理选择而非突变本身所致。瘤胃细菌中负责离子载体耐药性的基因尚未确定，但几乎没有证据表明离子载体耐药性可以从一种细菌传播到另一种细菌。基于这些观察结果，在动物饲料中使用离子载体不太可能对动物向人类的抗生素耐药性转移产生重大影响。
