Most antibiotic use in humans is to reduce the magnitude and term of morbidity of acute, community-acquired infections in immune competent patients, rather than to save lives. Thanks to phagocytic leucocytes and other host defenses, the vast majority of these infections are self-limiting. Nevertheless, there has been a negligible amount of consideration of the contribution of phagocytosis and other host defenses in the research for, and the design of, antibiotic treatment regimens, which hyper-emphasizes antibiotics as if they were the sole mechanism responsible for the clearance of infections. Here, we critically review this approach and its limitations. With the aid of a heuristic mathematical model, we postulate that if the rate of phagocytosis is great enough, for acute, normally self-limiting infections, then (i) antibiotics with different pharmacodynamic properties would be similarly effective, (ii) low doses of antibiotics can be as effective as high doses, and (iii) neither phenotypic nor inherited antibiotic resistance generated during therapy are likely to lead to treatment failure.

在人类中，大多数抗生素的使用是为了减少免疫能力强的患者的急性，社区获得性感染的发病率和发病率，而不是挽救生命。由于吞噬性白细胞和其他宿主防御，这些感染中的绝大多数是自限性的。然而，在研究和设计抗生素治疗方案的过程中，对吞噬作用和其他宿主防御的贡献的考虑微不足道，过分强调了抗生素，就好像它们是清除细菌的唯一机制一样。感染。在这里，我们严格审查这种方法及其局限性。借助启发式数学模型，我们假设如果吞噬作用的速度足够快，那么对于急性的，通常是自限性的感染，