Department of Respiratory Medicine, Allergy and Clinical Immunology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Department of Respiratory Medicine, Allergy and Clinical Immunology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan; Department of Respiratory Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan.
J Infect Chemother. 2019 Dec;25(12):995-1000. doi: 10.1016/j.jiac.2019.05.028. Epub 2019 Jun 22.
Although fluoroquinolones are considered as alternative therapies of pulmonary Mycobacterium avium complex (MAC) disease, the association between fluoroquinolone resistance and MAC genotypes in clinical isolates from individuals not previously treated for MAC infection is not fully clear.
Totals of 154 M. avium isolates and 35 Mycobacterium intracellulare isolates were obtained from treatment-naïve patients with pulmonary MAC disease at the diagnosis of MAC infection at 8 hospitals in Japan. Their susceptibilities of moxifloxacin were determined by broth microdilution methods. Moxifloxacin-resistant isolates were examined for mutations of gyrA and gyrB. Variable numbers of tandem repeats (VNTR) assay was performed using 15 M. avium VNTR loci and 16 M. intracellulare VNTR loci.
Moxifloxacin susceptibility was categorized as resistant and intermediate for 6.5% and 16.9%, respectively, of M. avium isolates and 8.6% and 17.1% of M. intracellulare isolates. Although the isolates of both species had amino acid substitutions of Thr 96 and Thr 522 at the sites corresponding to Ser 95 in the M. tuberculosis GyrA and Gly 520 in the M. tuberculosis GyrB, respectively, these substitutions were observed irrespective of susceptibility and did not confer resistance. The VNTR assays showed revealed three clusters among M. avium isolates and two clusters among M. intracellulare isolates. No significant differences in moxifloxacin resistance were observed among these clusters.
Although resistance or intermediate resistance to moxifloxacin was observed in approximately one-fourth of M. avium and M. intracellulare isolates, this resistance was not associated with mutations in gyrA and gyrB or with VNTR genotypes.
氟喹诺酮类药物被认为是治疗肺部鸟分枝杆菌复合群(MAC)疾病的替代疗法,但是在未曾接受 MAC 感染治疗的个体的临床分离株中,氟喹诺酮类药物耐药性与 MAC 基因型之间的关系尚不完全清楚。
从日本 8 家医院诊断为 MAC 感染的初治肺部 MAC 疾病患者中获得了 154 株鸟分枝杆菌和 35 株胞内分枝杆菌。通过肉汤微量稀释法测定它们对莫西沙星的敏感性。对莫西沙星耐药株进行了 gyrA 和 gyrB 突变检测。使用 15 个鸟分枝杆菌 VNTR 基因座和 16 个胞内分枝杆菌 VNTR 基因座进行可变数目串联重复(VNTR)分析。
莫西沙星敏感性分别为 6.5%和 16.9%的鸟分枝杆菌和胞内分枝杆菌的耐药和中介,而 8.6%和 17.1%的敏感和中介。尽管这两种物种的分离株在相应于结核分枝杆菌 GyrA 中的 Ser95 的 Thr96 和 Thr522 位点以及结核分枝杆菌 GyrB 中的 Gly520 处具有氨基酸取代,但这些取代与敏感性无关,并且不会导致耐药性。VNTR 分析显示,鸟分枝杆菌分离株中有 3 个簇,胞内分枝杆菌分离株中有 2 个簇。这些簇之间未观察到莫西沙星耐药性的显著差异。
尽管大约四分之一的鸟分枝杆菌和胞内分枝杆菌分离株对莫西沙星表现出耐药或中介耐药,但这种耐药性与 gyrA 和 gyrB 突变或 VNTR 基因型无关。