Is SCV generation a survival strategy of bacteria?

Most of the SCVs are reported to be hemin, menadione, thymidine or thiamine auxotrophs. It is argued that SCV generation is a survival strategy of bacteria to resist adverse conditions, especially antibiotic therapy. Thus, in the presence of aminoglycoside antibiotics, only SCVs may survive whereas the normal wild type population gets killed by the antibiotic. However, once the antibiotic is removed, SCVs can revert to normal wild type and cause re-infection.

However, if the formation of SCV is a survival strategy, why do high frequencies of hemin-deficient mutants occur among the Enterobacteriacae family? It is documented that Enterobacteriacae lacks the ability to take up hemin (Sasarman et al. 1968). To revert to the normal wild type, it needs a second independent mutation that helps it take up hemin (Roggenkamp et al. 1998). However, the frequency of this second mutation is very low (Roggenkamp et al. 1998). This would mean that the hemin-deficient mutants of Enterobacteriacae will remain as SCVs even in the presence of hemin, thus offering them no growth advantages. If reversion is not possible, how it can be argued that SCVs are responsible for chronic infections?

Similarly, if the reversion to normal wild type is not possible, what is the fate of those Enterobacteriacae SCVs inside the body?

Next- A switching mechanism between the normal bacterial population and SCVs

Sasarman et al. (1968). Hemin-deficient mutants of Escherichia coli K-12. J Bacteriol 96(2), 570-2.

Roggenkamp et al. (1998). Chronic prosthetic hip infection caused by a small-colony variant of Escherichia coli. J Clin Microbiol 36(9), 2530-4.