Detecting Mutations in the Mycobacterium tuberculosis Pyrazinamidase Gene pncA to Improve Infection Control and Decrease Drug Resistance Rates in Human Immunodeficiency Virus Coinfection.
Detecting Mutations in the Mycobacterium tuberculosis Pyrazinamidase Gene pncA to Improve Infection Control and Decrease Drug Resistance Rates in Human Immunodeficiency Virus Coinfection.
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DOI：
10.4269/ajtmh.15-0711
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发表时间：
2016-12-07
期刊：
影响因子：
--
通讯作者：
Zimic M
中科院分区：
文献类型：
--
作者：
Dudley MZ;Sheen P;Gilman RH;Ticona E;Friedland JS;Kirwan DE;Caviedes L;Rodriguez R;Cabrera LZ;Coronel J;Grandjean L;Moore DAJ;Evans CA;Huaroto L;Chávez-Pérez V;Zimic M
在照顾人类免疫缺陷病毒（HIV）阳性患者的环境中，医院感染控制措施对于结核病（TB）控制战略至关重要，因为这些患者患结核病的风险较高。吡嗪酰胺（PZA）是一种有效灭菌顽固结核分枝杆菌的强效药物。然而，与烟酰胺酶/吡嗪酰胺酶编码基因pncA突变相关的PZA耐药正在增加。对从秘鲁利马4个地点获得的794株患者分离株进行了spoligo分型和耐药试验。在其中一个地点，Dos de Mayo医院（HDM）的HIV病房，这是一个在研究期间开放的HIV/TB合并感染患者的隔离病房，作为感染控制干预措施：比较了干预前后的循环基因型和耐药性。所有其他hiv阴性门诊患者的站点：将这些站点的基因型和耐药率与HDM进行比较。HDM患者多药耐药、Wayne法测定的PZA耐药、两种最常见的基因型（拉丁美洲-地中海(LAM)-9分支的spoligotype international type [SIT] 42和T1分支的SIT 53）以及两种最常见的pncA突变（G145A和A403C）具有高度的一致性。这些关联在社区分离株中不存在。感染控制干预与SIT 42或SIT 53基因型引起的结核病减少58-92%相关（优势比[or] = 0.420, P = 0.003）；耐多药结核病（OR = 0.349, P < 0.001）；耐pza结核（OR = 0.076, P < 0.001）。总之，pncA突变分型、耐药检测和孢子寡分型有助于确定院内结核暴发，并在实施感染控制措施后证明其得到解决。
Hospital infection control measures are crucial to tuberculosis (TB) control strategies within settings caring for human immunodeficiency virus (HIV)–positive patients, as these patients are at heightened risk of developing TB. Pyrazinamide (PZA) is a potent drug that effectively sterilizes persistent Mycobacterium tuberculosis bacilli. However, PZA resistance associated with mutations in the nicotinamidase/pyrazinamidase coding gene, pncA, is increasing. A total of 794 patient isolates obtained from four sites in Lima, Peru, underwent spoligotyping and drug resistance testing. In one of these sites, the HIV unit of Hospital Dos de Mayo (HDM), an isolation ward for HIV/TB coinfected patients opened during the study as an infection control intervention: circulating genotypes and drug resistance pre- and postintervention were compared. All other sites cared for HIV-negative outpatients: genotypes and drug resistance rates from these sites were compared with those from HDM. HDM patients showed high concordance between multidrug resistance, PZA resistance according to the Wayne method, the two most common genotypes (spoligotype international type [SIT] 42 of the Latino American-Mediterranean (LAM)-9 clade and SIT 53 of the T1 clade), and the two most common pncA mutations (G145A and A403C). These associations were absent among community isolates. The infection control intervention was associated with 58–92% reductions in TB caused by SIT 42 or SIT 53 genotypes (odds ratio [OR] = 0.420, P = 0.003); multidrug-resistant TB (OR = 0.349, P < 0.001); and PZA-resistant TB (OR = 0.076, P < 0.001). In conclusion, pncA mutation typing, with resistance testing and spoligotyping, was useful in identifying a nosocomial TB outbreak and demonstrating its resolution after implementation of infection control measures.
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