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以carbapenem治療產SHV-5之克雷伯式肺炎桿菌肺炎後衍生carbapenem之抗藥性

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以carbapenem治療產SHV-5之克雷伯式肺炎桿菌肺炎後衍生carbapenem之抗藥性

Emergence of Carbapenem Resistance for SHV-5-producing Klebsiella pneumoniae after Carbapenem Therapy

A 71 year-old diabetic woman presented at the hospital on October 19, 2012 due to short of breath. Laboratory data showed white cell count, 5,900/uL; hemoglobin, 7.6 g/dL; BUN, 40 mg/dL; creatinine 2.4 mg/dL; CPK120 IU/L; CK-MB5.4 ng/dL and troponin I, 1.51 ng/mL. Echocardiography suggested posterior wall hypokinesis. The cardiac catheterization revealed segmental stenosis over right coronary artery. Blood cultures on October 25 yielded Salmonella group B. Ceftriaxone was given for 2 weeks. Acute coma occurred on October 30 and MRI of the brain revealed recent multiple cerebral and cerebellar embolic infarcts. Then aspiration pneumonia occurred on November 5 and Acinetobacter baumannii and KP were isolated from the sputum. Ertapenem and sulbactam for KP and A. baumannii, respectibely, were given for 2 weeks followed by a week of imipenem and sulbactam. But, blood cultures on November 30 and December 2 yielded carbapenem-resistant K. pneumoniae(CRKP), designed KP 341. The central venous catheter tip culture also yielded CRKP. Transesophageal echocardiography did not find any vegetation. MICs of KP 341 were > 32 ug/mL for ertapenem and 4 ug/mL for imipenem, meropenem and doripenem. PCR and DNA sequencing revealed genetic mutation of both outer membrane porin genes of OmpK35 and OmpK36. PCR was used to screen bla genes on plasmid for TEM, SHV, CTX-M, DHA-1, CMY-1 and cabapenemase genes (such as KPC, VIM, IMP, NDM-1, and OXA-48) and only identified blaSHV-5. In conclusion, prolonged carbapenem use may be associated with OmpK35 and OmpK36 mutation on KP and led to high level resistance to ertapenem as well as low-level resistance to imipenem, meropenem and doripenem.

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