背景：耐碳青霉烯肺炎克雷伯菌（CRKP）感染是一个主要的公共卫生问题，需要施用多粘菌素E（粘菌素）作为最后一线抗生素。同时,与粘菌素耐药肺炎克雷伯菌感染相关的死亡率正在严重增加.另一方面,碳青霉烯类抗生素在促进肺炎克雷伯菌粘菌素耐药性中的重要性尚不清楚。
方法：我们报告一例肺炎克雷伯菌相关化脓性肝脓肿，其中易感肺炎克雷伯菌在亚胺培南治疗期间转化为碳青霉烯和粘菌素耐药的肺炎克雷伯菌。化脓性肝脓肿的病例是一名50岁的患有糖尿病和肝移植的男子，他被送往设拉子的阿布阿里新浪医院。分离并鉴定了负责社区获得性化脓性肝脓肿的肺炎克雷伯菌。在抗菌药物敏感性试验中，除氨苄西林外，肺炎克雷伯菌分离株对所有测试的抗生素均敏感，并被鉴定为非K1/K2经典肺炎克雷伯菌（cKp）菌株。多位点序列分型(MLST)将分离株鉴定为序列类型54(ST54)。根据病人的要求,他出院继续在另一个中心治疗。两个月后,他因发烧和进行性全身症状而再次入院。在用亚胺培南治疗期间，该菌株获得了blaOXA-48，并显示出对碳青霉烯类抗生素的抗性，并被鉴定为多药耐药（MDR）菌株。通过肉汤微量稀释法进行粘菌素的最低抑制浓度（MIC）测试，该菌株对粘菌素敏感（MIC<2µg/mL）。同时,在血琼脂上，菌落具有粘性稠度并粘附于培养基(粘性粘膜粘性菌落)。定量实时PCR和生物膜形成测定显示，CRKP菌株增加了胶囊wzi基因的表达，并产生了响应亚胺培南的粘液。最后,肺炎克雷伯菌相关化脓性肝脓肿对多种抗生素耐药，包括最后一线抗生素粘菌素和替加环素，导致败血症和死亡.
结论：根据这些信息，我们是否可以有一个理论假设，即亚胺培南是肺炎克雷伯菌对碳青霉烯类和粘菌素耐药的启动子？这需要更多的关注。
BACKGROUND: Carbapenem-resistant Klebsiella pneumoniae (CRKP) infections are a major public health problem, necessitating the administration of polymyxin E (colistin) as a last-line antibiotic. Meanwhile, the mortality rate associated with colistin-resistant K. pneumoniae infections is seriously increasing. On the other hand, importance of administration of carbapenems in promoting colistin resistance in K. pneumoniae is unknown.
METHODS: We report a
case of K. pneumoniae-related pyogenic liver abscess in which susceptible K. pneumoniae transformed into carbapenem- and colistin-resistant K. pneumoniae during treatment with imipenem. The
case of pyogenic liver abscess was a 50-year-old man with diabetes and liver transplant who was admitted to Abu Ali Sina Hospital in Shiraz. The K. pneumoniae isolate responsible for community-acquired pyogenic liver abscess was isolated and identified. The K. pneumoniae isolate was sensitive to all tested antibiotics except ampicillin in the antimicrobial susceptibility test and was identified as a non-K1/K2 classical K. pneumoniae (cKp) strain. Multilocus sequence typing (MLST) identified the isolate as sequence type 54 (ST54). Based on the patient\'s request, he was discharged to continue treatment at another center. After two months, he was readmitted due to fever and progressive constitutional symptoms. During treatment with imipenem, the strain acquired blaOXA-48 and showed resistance to carbapenems and was identified as a multidrug resistant (MDR) strain. The minimum inhibitory concentration (MIC) test for colistin was performed by broth microdilution method and the strain was sensitive to colistin (MIC < 2 µg/mL). Meanwhile, on blood agar, the colonies had a sticky consistency and adhered to the culture medium (sticky mucoviscous colonies). Quantitative real-time PCR and biofilm formation assay revealed that the CRKP strain increased capsule wzi gene expression and produced slime in response to imipenem. Finally, K. pneumoniae-related pyogenic liver abscess with resistance to a wide range of antibiotics, including the last-line antibiotics colistin and tigecycline, led to sepsis and death.
CONCLUSIONS: Based on this information, can we have a theoretical hypothesis that imipenem is a promoter of resistance to carbapenems and colistin in K. pneumoniae? This needs more attention.
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