Dabernat Henri, Delmas Catherine, Seguy Martine, Pelissier Roseline, Faucon Genevieve, Bennamani Safia, Pasquier Christophe
Laboratoire de Microbiologie, Centre National de Référence des Haemophilus influenzae, Toulouse, France.
Antimicrob Agents Chemother. 2002 Jul;46(7):2208-18. doi: 10.1128/AAC.46.7.2208-2218.2002.
The sequences of the ftsI gene, encoding the transpeptidase domain of penicillin binding protein (PBP) 3A and/or PBP 3B, which are involved in septal peptidoglycan synthesis, were determined for 108 clinical strains of Haemophilus influenzae with reduced susceptibility to beta-lactam antibiotics with or without beta-lactamase production and were compared to those of the ampicillin-susceptible Rd strain and ampicillin-susceptible clinical isolates. The sequences have 18 different mutation patterns and were classified into two groups on the basis of amino acid substitutions deduced from the nucleotide sequences located between bp 960 and 1618 of the ftsI gene. In group I strains (n = 7), His-517 was substituted for Arg-517. In group II strains (n = 101), Lys-526 was substituted for Asn-526. In subgroup IIa (n = 5; H. influenzae ATCC 49247), the only observed substitution was Lys-526 for Asn-526; in subgroup IIb (n = 56), Val-502 was substituted for Ala-502 (n = 13), along with several other substitutions: Asn-350 for Asp-350 (n = 15), Asn-350 for Asp-350 and Glu-490 for Gly-490 (n = 14), and Asn-350 for Asp-350 and Ser-437 for Ala-437 (n = 5). In subgroup IIc (n = 25), Thr-502 was substituted for Ala-502. In subgroup IId, Val-449 was substituted for Ile-449 (n = 15). The MICs of beta-lactam antibiotics for the 108 strains were to 8 to 16 times the MICs for susceptible strains. The strains, isolated from both adults and children, were analyzed for genetic relationship by pulsed-field gel electrophoresis and by determination of ftsI sequence phylogeny. Both analyses revealed the lack of clonality and the heterogeneity of the strains, but some clusters suggest the spread and/or persistence of a limited number of strains of the same pulsotype and pattern of amino acid substitutions. Reduced susceptibility to beta-lactam, brought about by mutations of the ftsI gene, is becoming a frequent phenomenon, affecting both strains that produce beta-lactamase and those that do not. The level of resistance remains low but opens the way to greater resistance in the future.
测定了108株对β-内酰胺类抗生素敏感性降低的流感嗜血杆菌临床菌株的ftsI基因序列,这些菌株产生或不产生β-内酰胺酶,ftsI基因编码青霉素结合蛋白(PBP)3A和/或PBP 3B的转肽酶结构域,参与隔膜肽聚糖合成,并将其与氨苄西林敏感的Rd菌株和氨苄西林敏感的临床分离株的序列进行比较。这些序列有18种不同的突变模式,并根据ftsI基因960至1618碱基之间核苷酸序列推导的氨基酸替代分为两组。在I组菌株(n = 7)中,His-517被Arg-517替代。在II组菌株(n = 101)中,Lys-526被Asn-526替代。在IIa亚组(n = 5;流感嗜血杆菌ATCC 49247)中,唯一观察到的替代是Lys-526替代Asn-526;在IIb亚组(n = 56)中,Val-502被Ala-502替代(n = 13),同时还有其他几种替代:Asn-350替代Asp-350(n = 15),Asn-350替代Asp-350且Glu-490替代Gly-490(n = 14),以及Asn-350替代Asp-350且Ser-437替代Ala-437(n = 5)。在IIc亚组(n = 25)中,Thr-502被Ala-502替代。在IId亚组中,Val-449被Ile-449替代(n = 15)。这108株菌株对β-内酰胺类抗生素的最低抑菌浓度(MIC)是敏感菌株MIC的8至16倍。通过脉冲场凝胶电泳和ftsI序列系统发育分析对从成人和儿童中分离出的这些菌株的遗传关系进行了分析。两种分析均显示这些菌株缺乏克隆性且具有异质性,但一些聚类表明相同脉冲型和氨基酸替代模式的有限数量菌株存在传播和/或持续存在。由ftsI基因突变导致的对β-内酰胺类抗生素敏感性降低正成为一种常见现象,影响产生β-内酰胺酶和不产生β-内酰胺酶的菌株。耐药水平仍然较低,但为未来更高的耐药性开辟了道路。