The switching mechanism between the wild type and small colony variants as proposed by Massey et al. (2001) is not convincing

Massey et al. (2001) proposed that small colony variants (SCVs) could emerge by switching from the wild type and vice versa. They found that SCVs of S. aureus could be isolated after just 30 min of exposure to gentamicin. Their number increased as the exposure time increased and reached a maximum by 14 h, but subsequently declined due to the emergence and overgrowth of gentamicin-resistant wild type bacteria. The authors hypothesized that the increase in the frequency of SCVs after gentamicin treatment for the first 14 h was either due to the very short generation time of SCVs or due to the switching from wild type to SCVs. 

To test which of the above hypotheses was responsible for the increase in SCV numbers, the mean generation time of SCVs and the wild type population was compared. The former hypothesis was ruled out since the actual mean generation time was found to be much higher than the wild type. Since the first hypothesis was wrong, they studied whether the increase in the frequency of SCVs was due to their presence in the inoculum. For this purpose, they reduced the initial inoculum size of bacteria by 100-fold and calculated the percentage of SCVs. They found that the proportion of SCVs at 24 h increased when the initial inoculum size was reduced. They calculated that, if the emergence of SCVs actually depended on the initial inoculum, their number should have reduced at 24 h at low inoculum. Since they found an increased percentage of SCVs, it was concluded that the emergence of SCVs was not dependent on its initial numbers, but was due to the switching from the wild type bacteria.

However, the increase in the number of SCVs at a low inoculum size may not be due to the switching of wild type bacteria. Until 14 h (in the above experiment), the increase in the population of SCVs could be due to the selective killing of normal bacteria along with the gradual multiplication of SCVs. But, at a high inoculum size, antibiotics may not kill all normal bacteria. Some bacteria may escape killing and may remain dormant for a short period of time but later may undergo adaptation and re-grow and overcome the SCV population. On the other hand, at a low inoculum size, most of the normal bacteria get killed and thus the percentage of SCVs may increase. The switching mechanism proposed by Massey et al. (2001) could have resulted from the selective and complete killing of normal bacteria at a lower inoculum size, resulting in the selective multiplication and the increase in the number of SCVs.

The fundamental flaw with the above article is that they could find only two hypotheses for their results and assumed that if one of them is wrong, other should be correct. What, if there are more than two reasons or explanations for their results?

Massey, R. C., Buckling, A., and Peacock, S. J. (2001). Phenotypic switching of antibiotic resistance circumvents permanent costs in Staphylococcus aureus. Curr Biol 11(22), 1810-4.