Isolates of similar pulsotypes could appear after 15 months and caused urosepsis in another resident of the same LTCF. The bacterium may have persisted in the environment and caused opportunistic infection. As LTCF residents are usually vulnerable to infections, surveillance of multidrug-resistant organisms and infection control intervention that have been established in acute-care hospitals to control infections by resistant organisms are apparently as essential in LTCFs.

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Enterobacter cloacae is one of the most common carbapenem-resistant Enterobacteriaceae (CRE) global wide. Resistance to tigecycline, one of the few therapeutic options for CRE infections, in carbapenem-resistant E. cloacae is of clinical significance. Fourteen E. cloacae clinical isolates (EC1-EC14) co-resistant to tigecycline and carbapenems were studied. Two tigecycline-susceptible/carbapenem-resistant isolates (TS1-TS2) were used for comparison. Genotyping by pulsed-field gel electrophoresis and multilocus sequence typing identified seven pulsotypes and three sequence types (STs). All three STs belonged to the published international clones. Polymerase chain reaction (PCR) and sequence analysis revealed the coexistence of bla and bla in 11 EC isolates from five pulsotypes/two STs. Reverse transcription PCR demonstrated overexpression of the chromosomal AmpC-like β-lactamase in seven EC isolates (four pulsotypes/two STs) and TS1 (pulsotype F/ST78). Reduced expression of outer membrane protein C (OmpC) was found in three EC isolates (all pulsotype C/ST204), whereas reduced expression of OmpF was found in nine EC isolates (three pulsotypes/two STs) and TS2 (pulsotype G/ST114). Overexpression of the efflux pump AcrB was found in all EC isolates although three showed borderline significance. Multiple mechanisms jointly contributed to the observed co-resistance to tigecycline and carbapenems. Some international clones have infiltrated into Taiwan and acquired various resistance traits independently.

IntroductionWe describe an immunocompromised patient with Tsukamurella tyrosinosolvens bacteremia and coinfection of Mycobacterium bovis pneumonia.Case DescriptionA 75-year-old male was admitted to our hospital complaining of persistent fever with general malaise. His medical history showed that he had diabetes mellitus (HbA1C 9.2%). A chest computed tomography (CT) showed left upper lung consolidation . Two sets of blood culture at admission finally showed Tsukamurella tyrosinosolvens. Moreover, three transbronchoscopy washing specimen cultures revealed Mycobacterium bovis.Discussion and EvaluationThe organism Tsukamurella tyrosinosolvens was identified using conventional biochemical identification methods, PCR-restriction DNA fragment analysis, and 16S rRNA gene sequencing. The clinical mycobacterial isolates were identified to the species level by combining Polymerase Chain Reaction (PCR) with an oligonucleotide microarray to detect the M. bovis amplicons.ConclusionAccording to our literature review, our patient’s case was the first of a coinfection with Tsukamurella tyrosinosolvens and Mycobacterium bovis. Prolonged antibiotic treatment and underlying disease control are necessary for this type of patient.

Enterobacter cloacae (E. cloacae) is one of the most frequently isolated and virulent human pathogens in its genus, and is increasingly significant as an intensive care unit (ICU)-acquired pathogen (1,2). This microorganism can cause a wide variety of infections, including bacteremia, soft tissue and ophthalmic infections (1), pneumonia (2), endocarditis (3), urinary tract infections (4), central nervous system infections (5), and osteomyelitis (6). Two cases of necrotizing pneumonia caused by E. cloacae were also reported (7,8). E. cloacae has emerged as a nosocomial pathogen from intensive care patients, especially who are on mechanical ventilation (9). However, no cases of E. cloacae-induced complicated necrotizing pneumonia with lung abscess, empyema, pyopneumothorax, and tension pneumothorax occurring simultaneously in an ICU has been reported. This paper reports an intractable case of ICU-acquired E. cloacae as the cause of fatal complicated necrotizing pneumonia. Ceftazidime or piperacillin-tazobactam is usually used empirically to treat ICU-acquired pneumonia. However, the increasing prevalence of extended-spectrum-beta-lactamaseproducing E. cloacae is becoming a concern, not only for infection therapy and empirical use of antibiotics but also for infection control programs (10). This case also highlights the importance of choosing appropriate empirical antimicrobial therapy for E. cloacae-induced complicated necrotizing pneumonia in ICUs. Summary A 58-year-old man with a history of diabetes mellitus and end-stage renal disease acquired pneumonia with acute respiratory failure during his stay in an intensive care unit (ICU). Empirical antimicrobial therapy with ceftazidime and vancomycin was initiated, and imipenem replaced ceftazidime 2 days later due to the patient's pulmonary condition failed to improve. However, within 5 days, pulmonary consolidation rapidly progressed to necrotizing pneumonia complicated by lung abscess, empyema, pyopneumothorax, and tension pneumothorax, leading to the patient's death. After the patient had died, all bacterial isolates from cultures of pleural effusion, blood, and tracheal aspirate were identified as Enterobacter cloacae (E. cloacae), which was susceptible to imipenem but resistant to ceftazidime. E. cloacae should be considered in the differential diagnosis of complicated necrotizing pneumonia with lung abscess, empyema, pyopneumothorax, and tension pneumothorax. Carbapenem therapy should be immediately initiated until the pathogen in such rapidly progressive ICU-acquired pneumonia is confirmed. Increased awareness among physicians regarding E. cloacaeinduced complicated necrotizing pneumonia acquired in ICUs could enable earlier detection and appropriate antimicrobial therapy for this invasive disease.