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we know that resistant strains (MDR, XDR, PDR) have arisen in single incidents around the globe but why are these bacteria not common and not spreading quickly as humans keep using antibiotics and killing the non-resistant strains which these Amr strains have to compete for resources. One might say that they ARE spreading but my question is why is the increase in population so slow. compare it with malaria parasite 'plasmodium' which despite being a higher organism with slower reproduction cycle kills so many.

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Natural selection is environment-dependent. A mutation that makes an individual more fit in one context, might make it less fit in a different context.

The mutations that make bacteria more fit in an environment where they're exposed to antibiotics generally make them less fit in a "natural" environment where they don't have to deal with antibiotics. That means that MDR bacteria are often out-competed by their less-resistant competitors, unless they're in the "right" environment for them, such as a hospital or an infected, antibiotic-treated patient.

Some references:

  • Barnett M, Busby SR, Mitchison DA. Tubercle bacilli resistant to isoniazid: virulence and response to treatment with isoniazid in guinea-pigs and mice. Br J Exp Pathol 1953; 34:568–81.
  • urgos M, Deriemer K, Small PM, Hopewell PC, Daley CL. Effect of drug resistance on the generation of secondary cases of tuberculosis. J Infect Dis 2003; 118:1878–84.
  • Davies AP, Billington OJ, Bannister BA, Weir WR, McHugh TD, Gillespie SH. Comparison of fitness of two isolates of Mycobacterium tuberculosis, one of which had developed multi-drug resistance during the course of treatment. J Infect 2000; 41:184–7.
  • Gagneux S, Long CD, Small PM, Van T, Schoolnik GK, Bohannan BJM. The competitive cost of antibiotic resistance in Mycobacterium tuberculosis. Science 2006; 312:1944–6.
  • Li Z, Kelley C, Collins F, Rouse D, Morris S. Expression of katG in Mycobacterium tuberculosis is associated with its growth and persistence in mice and guinea pigs. J Infect Dis 1998; 177:1030–5.
  • Middlebrook G, Cohn M. Some observations on the pathogenicity of isoniazid-resistant variants of tubercle bacilli author. Science 1953; 118:297–9.
  • van Soolingen D, Borgdorff MW, de Haas PE et al. Molecular epidemiology of tuberculosis in the Netherlands: a nationwide study from 1993 through 1997. J Infect Dis 1999; 180:726–36.
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    $\begingroup$ In addition, the M. tuberculosis complex, except for M. canetti, had lost the ability to do horizontal gene transfer. Resistances thus arise by point mutations or indels, a comparatively slower route than in other species of bacteria. $\endgroup$ – Eliane B. Jul 9 '18 at 16:20

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