Gurung Sushma, Kafle Sonali, Dhungel Binod, Adhikari Nabaraj, Thapa Shrestha Upendra, Adhikari Bipin, Banjara Megha Raj, Rijal Komal Raj, Ghimire Prakash
Central Department of Microbiology, Tribhuvan University, Kirtipur, Kathmandu, Nepal.
Alka Hospital, Lalitpur, Nepal.
Infect Drug Resist. 2020 Jul 14;13:2311-2321. doi: 10.2147/IDR.S259967. eCollection 2020.
Resistance to carbapenem in Gram-negative bacteria is attributable to their ability to produce carbapenemase enzymes. The main objective of this study was to detect the presence of genes in carbapenem-resistant uropathogenic and isolated from urine samples from patients attending Alka Hospital, Jawalakhel, Lalitpur, Nepal.
A total of 1013 mid-stream urine samples were collected from patients with suspected urinary tract infection (UTI) between April and September 2018. The identified isolates underwent antibiotic susceptibility testing using the modified Kirby-Bauer disc-diffusion method. Phenotypic carbapenemase production was confirmed by the modified Hodge test, and the gene was detected using conventional polymerase chain reaction.
Out of 1013 urine samples, 15.2% (154/1013) had bacterial growth. Among the isolates, 91.5% (141/154) were Gram-negative bacteria, and was the most common bacterial isolate (62.9%; 97/154), followed by 15.6% (24/154). Among 121 bacterial isolates (97 isolates and 24 isolates), 70.3% (52/121) were multidrug-resistant and 29.7% (22/121) were multidrug-resistant . In addition, 9.1% (11/121) were carbapenem resistant (both imipenem and meropenem resistant). Development of multidrug resistance and development of carbapenem resistance were significantly associated (<0.05). Of the 11 carbapenem-resistant isolates, only seven were carbapenemase producers; of these, 28.6% (2/7) were , 72.4% (5/7) were and 42.8% (3/7) had the gene. Of the three bacterial isolates with the gene, 33.3% (1/3) were and 66.7% (2/3) were
One in ten isolates of and were carbapenem resistant. Among carbapenem-resistant isolates, one-third of and two-thirds of had the gene. OXA-48 serves as a potential agent to map the distribution of resistance among clinical isolates.
革兰氏阴性菌对碳青霉烯类药物的耐药性归因于它们产生碳青霉烯酶的能力。本研究的主要目的是检测耐碳青霉烯类的尿路致病性细菌中的基因，这些细菌是从尼泊尔拉利特布尔贾瓦拉赫尔阿尔卡医院患者的尿液样本中分离出来的。
2018年4月至9月期间，从疑似尿路感染（UTI）患者中总共收集了1013份中段尿样本。对鉴定出的分离株使用改良的 Kirby-Bauer 纸片扩散法进行抗生素敏感性测试。通过改良 Hodge 试验确认表型碳青霉烯酶的产生，并使用常规聚合酶链反应检测基因。
在1013份尿液样本中，15.2%（154/1013）有细菌生长。在分离株中，91.5%（141/154）是革兰氏阴性菌，大肠杆菌是最常见的细菌分离株（62.9%；97/154），其次是肺炎克雷伯菌15.6%（24/154）。在121株细菌分离株（97株大肠杆菌分离株和24株肺炎克雷伯菌分离株）中，70.3%（52/121）对多种药物耐药，29.7%（22/121）对多种药物耐药。此外，9.1%（11/121）对碳青霉烯类耐药（对亚胺培南和美罗培南均耐药）。多重耐药的发生与碳青霉烯类耐药的发生显著相关（<0.05）。在11株耐碳青霉烯类分离株中，只有7株是碳青霉烯酶产生菌；其中，28.6%（2/7）是KPC型，72.4%（5/7）是NDM型，42.8%（3/7）有OXA-48基因。在3株有OXA-48基因的细菌分离株中，33.3%（1/3）是大肠杆菌，66.7%（2/3）是肺炎克雷伯菌。
十分之一的大肠杆菌和肺炎克雷伯菌分离株对碳青霉烯类耐药。在耐碳青霉烯类分离株中，三分之一的大肠杆菌和三分之二的肺炎克雷伯菌有OXA-48基因。OXA-48可作为一种潜在工具来描绘临床分离株中耐药性的分布情况。
