A clinical Escherichia coli isolate (MG32) resistant to ceftazidime but susceptible to other third-generation cephalosporins was previously examined and found to harbor TEM-1 and exhibit alterations in outer membrane proteins. Reexamination of this isolate revealed the additional presence of a novel TEM-1 derivative, now designated TEM-12. Evaluation of ceftazidime and cefotaxime minimum inhibitory concentrations for isogenic derivatives demonstrated a major role for TEM-12 in the decreased susceptibility observed. This was selectively enhanced for ceftazidime resistance by the altered porins of E. coli MG32. TEM-12 appeared identical to TEM-101, an in vitro TEM derivative, in both isoelectric point (pI 5.25) and substrate profile. Hybridization and cloning of the TEM-12 determinant revealed that, unlike other TEM derivatives, TEM-12 is chromosomally encoded, not plasmid-encoded.
Bibliographical noteFunding Information:
Received 24 August 1989; revised 9 February 1990. Grant support: Health Future Foundation, Omaha. Reprints and correspondence: Dr. Christine C. Sanders, Department of Medical Microbiology, Creighton University School of Medicine, 2500 California St., Omaha, NE 68178. * Present address: Department of Infectious Diseases, the Duluth Clinic, Duluth, MN.
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