In the 1980s, I found that the chromosomal β‐lactamase of Klebsiella pneumoniae
LEN‐1 showed a very high similarity to the R‐plasmid‐mediated penicillinase
TEM‐1 on the amino acid sequence level, and this strongly suggested the origination
of TEM‐1 from the chromosomal penicillinases of K. pneumoniae or related
bacteria. Moreover, the chromosomal K1 β‐lactamase (KOXY) of Klebsiella oxytoca
was found to belong to the class A β‐lactamases that include LEN‐1 and TEM‐1,
although KOXY can hydrolyze cefoperazone (CPZ) like the chromosomal AmpC type
cephalosporinases of various Enterobacteriaceae that can hydrolyze several
cephalosporins including CPZ. Furthermore, my collaborators and I found plural
novel serine‐type β‐lactamases, such as MOX‐1, SHV‐24, TEM‐91, CTX‐M‐64,
CMY‐9, CMY‐19, GES‐3, GES‐4, and TLA‐3, mediated by plasmids. Besides these
serine‐type β‐lactamases, we also first identified exogenously acquired metallo‐
β‐lactamases (MBLs), IMP‐1 and SMB‐1, in imipenem‐resistant Serratia marcescens,
and the IMP‐1‐producing S. marcescens TN9106 became the index case for
carbapenemase‐producing Enterobacteriaceae. I developed the sodium mercaptoacetic
acid (SMA)‐disk test for the simple identification of MBL‐producing
bacteria. We were also the first to identify a variety of plasmid‐mediated 16S
ribosomal RNA methyltransferases, RmtA, RmtB, RmtC, and NpmA, from various
Gram‐negative bacteria that showed very high levels of resistance to a wide
range of aminoglycosides. Furthermore, we first found plasmid‐mediated quinolone
efflux pump (QepA) and fosfomycin‐inactivating enzymes (FosA3 and FosK).
We also first characterized penicillin reduced susceptible Streptococcus agalactiae (PRGBS),
macrolide‐resistant Mycoplasma pneumoniae, as well as Campylobacter jejuni, and
Helicobacter pylori, together with carbapenem‐resistant Haemophilus influenzae.