eared for large effusions in right pleural and resulted in a restrictive ventilatory dysfunction. And the WBC count was 15.8 × 10^9^/L with 93.8% granulocytes and 3.8% lymphocytes. After discharging more than 1,100 ml dark-red colored effusions in right pleural, the patient condition obviously improved. And microbiological culture of the pleural effusion sample was still negative. Until June 3rd, the patient had almost completely recovered with most parameters of routine blood tests being near normal (6.3 × 10^9^/L WBC with 71.3% granulocytes and 16.0% lymphocytes). Thus antibiotic treatment was stopped. Unexpectedly, at 10:40 PM, on June 8th, the patient experienced acute pneumonia including high temperature (39.0°C), red foamy bloody sputum, breathing difficulty and low oxygen saturation, immediately followed by respiratory distress syndrome. The patient was rapidly transferred to the ICU. At 9 PM on June 9th, despite combination therapy of ganciclovir, imipenem/cilastatin, tigecycline, and hemofiltration, the patient deteriorated and finally died of multiple organ failure caused by severe pneumonia and septic shock at 11:45 PM, June 10th. Subsequent routine microbiological culture of blood sample successfully isolated *K. pneumoniae* strain named *Kp562*.

The protocol for this study was approved by Ethics Committee of Ruijin Hospital, Shanghai JiaoTong University School of Medicine. The combination of routine PFGE and MLST typing revealed that the two isolates shared highly similar PFGE profiles as *K. pneumoniae* ST86 (**Figure [2A](#F2){ref-type="fig"}**). Via PCR targeting *wzx* gene of capsule serovar K1, K2,([@B13]) and aerobactin, *allS, kfu, magA*, and *rmpA* ([@B7]). The detailed PCR conditions listed in Supplementary Table [S1](#SM1){ref-type="supplementary-material"}. The two strains were confirmed as serotype K2 and Aerobactin-*kfu-rmpA* positive but *magA-allS* negative (**Figure [2B](#F2){ref-type="fig"}**). The two isolates grew as positive hypermucoviscous phenotype (HV) with a mucoviscous s