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. 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. 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.

中文翻译：

---

耐碳青霉烯类肺炎克雷伯菌相关化脓性肝脓肿伴荚膜多糖过度生成的挑战性病例：病例报告

耐碳青霉烯类肺炎克雷伯菌 (CRKP) 感染是一个主要的公共卫生问题，需要使用多粘菌素 E（粘菌素）作为最后一线抗生素。与此同时，与耐粘菌素肺炎克雷伯菌感染相关的死亡率正在严重增加。另一方面，施用碳青霉烯类药物在促进肺炎克雷伯菌粘菌素耐药性方面的重要性尚不清楚。我们报告了一例与肺炎克雷伯菌相关的化脓性肝脓肿，其中敏感的肺炎克雷伯菌在亚胺培南治疗期间转化为耐碳青霉烯和粘菌素的肺炎克雷伯菌。化脓性肝脓肿病例是一名50岁男性，患有糖尿病并接受肝移植，住进设拉子的阿布阿里西纳医院。分离并鉴定了导致社区获得性化脓性肝脓肿的肺炎克雷伯菌分离株。在药敏试验中，肺炎克雷伯菌分离株对除氨苄西林以外的所有测试抗生素均敏感，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)。根据患者的要求，他出院到另一个中心继续治疗。两个月后，他因发烧和进行性全身症状再次入院。在亚胺培南治疗期间，该菌株获得了 blaOXA−48，并对碳青霉烯类药物表现出耐药性，被鉴定为多重耐药（MDR）菌株。采用微量肉汤稀释法对粘菌素进行最低抑菌浓度（MIC）测试，该菌株对粘菌素敏感（MIC < 2 µg/mL）。同时，在血琼脂上，菌落具有粘性并粘附在培养基上（粘性粘液菌落）。实时定量 PCR 和生物膜形成测定表明，CRKP 菌株增加了胶囊 wzi 基因的表达，并响应亚胺培南产生粘液。最后，肺炎克雷伯菌相关的化脓性肝脓肿对多种抗生素（包括最后一线抗生素粘菌素和替加环素）产生耐药性，导致败血症和死亡。基于这些信息，我们是否可以得出一个理论假设：亚胺培南是肺炎克雷伯菌对碳青霉烯类和粘菌素耐药的促进剂？这需要更多的关注。