Poirel Laurent, Gerome Patrick, De Champs Christophe, Stephanazzi Jean, Naas Thierry, Nordmann Patrice
Service de Bactériologie-Virologie, Hôpital de Bicêtre, Assistance Publique/Hôpitaux de Paris, Faculté de Médecine Paris-Sud, 94275 Le Kremlin-Bicêtre, France.
Antimicrob Agents Chemother. 2002 Feb;46(2):566-9. doi: 10.1128/AAC.46.2.566-569.2002.
Pseudomonas aeruginosa clinical isolate CY-1, which was resistant to ceftazidime, harbored a conjugative ca. 250-kb plasmid that contained a class 1 integron with two gene cassettes encoding OXA-32, an OXA-2- type beta-lactamase, and the aminoglycoside acetyltransferase AAC(6')Ib(9). OXA-32 differed from OXA-2 by an Leu169Ile amino acid substitution (class D numbering). Site-directed mutagenesis established that Ile169 is responsible for resistance to ceftazidime but not to cefotaxime.
铜绿假单胞菌临床分离株CY-1对头孢他啶耐药,它含有一个约250kb的接合质粒,该质粒包含一个1类整合子,带有两个基因盒,分别编码OXA-32(一种OXA-2型β-内酰胺酶)和氨基糖苷乙酰转移酶AAC(6')Ib(9)。OXA-32与OXA-2在第169位氨基酸由亮氨酸突变为异亮氨酸(D类编号)。定点诱变表明,第169位异亮氨酸导致对头孢他啶耐药,但对头孢噻肟不耐药。