Reply to “Mobilization of bla_BKC-1 by ISKpn23?”

REPLY

We read with great interest the letter by Partridge (1) in response to the article reporting the new class A carbapenemase BKC-1 (2). Partridge has found the probable DR sequences of ISKpn23, which are located upstream of ISKpn23 and downstream of the bla_BKC-1 gene. The author suggests that this element was responsible for bla_BKC-1 and aph(3)-VI expression.

In our previous study, we showed that the BL21 clone harboring only bla_BKC-1 exhibited very low carbapenem MICs (0.12 to 0.5 μg/ml) compared to those of the T3 transformant strain (MICs, 8 to 64 μg/ml), which carries the entire plasmid (p60136). We agree with Partridge that the presence of ISKpn23 may have driven the expression of bla_BKC-1. The level of variation in carbapenem MICs was too high to be justified only by the distinct machineries of the recipient strains. To confirm this hypothesis, we are currently working on the construction of laboratory derivative strains carrying the identical genetic background of bla_BKC-1, except for the deletion of ISKpn23.

Partridge has also demonstrated curiosity about the mobilization of bla_BKC-1, since ISKpn23 belongs to the IS1380 family, as does ISEcp1. ISEcp1 has been shown to mobilize the bla_CTX-M-19 gene. It was also responsible for transferring the bla_CTX-M-2 gene from the Kluyvera ascorbata chromosome to plasmids (3). We also agree with Partridge that it will be interesting to see how successful bla_BKC-1 will become, in comparison with bla_CTX-M genes associated with ISEcp1. So far, the frequency of bla_BKC-1 seems to be very low. Recently, we found only two K. pneumoniae strains harboring bla_BKC-1 among the 635 investigated Klebsiella species clinical isolates (4). The spread of an epidemic clone rather than the spread or mobilization of bla_BKC-1 by ISKpn23 was detected among the studied K. pneumoniae isolates.