Department of Clinical Microbiology, Christian Medical College, Vellore, India.
Department of Internal Medicine, Christian Medical College, Vellore, India.
Indian J Med Res. 2019 Feb;149(2):185-191. doi: 10.4103/ijmr.IJMR_2086_17.
BACKGROUND & OBJECTIVES: The escalation in carbapenem resistance among Enterobacteriaceae has resulted in a lack of effective therapeutic alternatives. Older antimicrobials, fosfomycin, nitrofurantoin and colistin for urinary tract infections (UTIs) caused by carbapenem-resistant Enterobacteriaceae (CRE) may be effective treatment options. The objectives of this study were to evaluate the utility of fosfomycin, nitrofurantoin and colistin in treating UTI caused by CRE and molecular characterization of the plasmid-mediated carbapenem resistance mechanisms.
Consecutive, non-duplicate isolates of CR Escherichia coli and Klebsiella spp. from urine cultures were included (n=150). Minimum inhibitory concentrations (MIC) were determined by E-test (fosfomycin and nitrofurantoin) and broth microdilution (colistin). Efficacy ratios were derived by dividing susceptibility breakpoints by observed MIC values of the drugs for the isolates. Isolates were screened for genes coding for carbapenemases using multiplex PCR. Fosfomycin, nitrofurantoin and colistin-resistant isolates were screened for plasmid-borne resistance genes fos A3, oqx AB and mcr-1, respectively using PCR.
Among E. coli, 98.9, 56 and 95 per cent isolates were susceptible to fosfomycin, nitrofurantoin and colistin, respectively, while 94 and 85 per cent of Klebsiella spp. were susceptible to fosfomycin and colistin, respectively. The efficacy ratios indicated fosfomycin as the drug of choice for UTI caused by CR E. coli and Klebsiella spp., followed by colistin. The bla gene was most common, followed by bla. Plasmid-borne genes encoding resistance to fosfomycin, nitrofurantoin and colistin were absent.
INTERPRETATION & CONCLUSIONS: With increasing resistance against the current treatment options, older drugs may emerge as effective options. Molecular screening of resistant isolates is essential to prevent the spread of plasmid-borne resistance against these drugs.
肠杆菌科的碳青霉烯类耐药性不断升级，导致治疗选择有限。对于由碳青霉烯类耐药肠杆菌科（CRE）引起的尿路感染（UTI），较老的抗生素如磷霉素、呋喃妥因和黏菌素可能是有效的治疗选择。本研究的目的是评估磷霉素、呋喃妥因和黏菌素治疗 CRE 引起的 UTI 的效用，并对质粒介导的碳青霉烯类耐药机制进行分子特征分析。
连续收集尿液培养物中耐碳青霉烯类的大肠埃希菌和克雷伯菌的非重复分离株（n=150）。采用 E 试验（磷霉素和呋喃妥因）和肉汤微量稀释法（黏菌素）测定最小抑菌浓度（MIC）。通过将药物的药敏折点除以观察到的分离株的 MIC 值，计算疗效比值。使用多重 PCR 筛选编码碳青霉烯酶的基因。使用 PCR 筛选磷霉素、呋喃妥因和黏菌素耐药分离株中的质粒携带的耐药基因 fosA3、oqxAB 和 mcr-1。
在大肠埃希菌中，98.9%、56%和 95%的分离株分别对磷霉素、呋喃妥因和黏菌素敏感，而 94%和 85%的克雷伯菌对磷霉素和黏菌素敏感。疗效比值表明，磷霉素是治疗 CR 大肠埃希菌和克雷伯菌引起的 UTI 的首选药物，其次是黏菌素。bla 基因最常见，其次是 bla。未发现编码对磷霉素、呋喃妥因和黏菌素耐药的质粒携带基因。
随着对现有治疗方案的耐药性不断增加，较老的药物可能成为有效的选择。对耐药分离株进行分子筛选对于防止这些药物的质粒携带耐药性传播至关重要。
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