Primary lung abscess caused by Staphylococcus lugdunensis.

Staphylococcus lugdunensis, a strain of coagulase-negative staphylococci, is part of the normal flora of human skin but can cause multiple infections at various sites. This microorganism has emerged as a major human pathogen. However, no study has reported primary lung abscess caused by S. lugdunensis. A 54-year-old alcoholic man without relevant past medical history was admitted because of primary lung abscesses. Empirical amoxicillin/clavulanate therapy was initially administered; however, the patient had persistent pleuritic chest pain and fever. He subsequently underwent resection of the lung abscess and removal of exudative pleural effusion on the fourth hospital day. Histopathologic examination confirmed the diagnosis of lung abscess, and colonies of gram-positive bacteria were identified. The culture specimen from the abscess was positive for S. lugdunensis, which was susceptible to amoxicillin/clavulanate, cefazolin, ciprofloxacin, clindamycin, erythromycin, oxacillin, teicoplanin, tetracycline, and vancomycin. Following resection and 3 weeks of amoxicillin/clavulanate therapy, the patient eventually recovered well without relapse. This case report is the first to describe S. lugdunensis as a cause of primary lung abscess; this microorganism should be considered a potential monomicrobial pathogen in primary lung abscess.

Intensive care unit-acquired complicated necrotizing pneumonia caused by Enterobacter cloacae: A case report.

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 patients 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. cloacae-induced complicated necrotizing pneumonia acquired in ICUs could enable earlier detection and appropriate antimicrobial therapy for this invasive disease.

Laboratory investigation of a suspected outbreak caused by Providencia stuartii with intermediate resistance to imipenem at a long-term care facility.

BACKGROUND: Providencia stuartii survives well in natural environment and often causes opportunistic infection in residents of long-term care facilities (LTCFs). Clinical isolates of P. stuartii are usually resistant to multiple antibiotics. The bacterium is also naturally resistant to colistin and tigecycline. Treatment of infections caused by carbapenem-resistant P. stuartii is challenging. METHODS: During a 15-month period in 2013-2014, four isolates (P1, P2, and P3B/P3U) of P. stuartii showing intermediate resistance to imipenem were identified at a regional hospital in southern Taiwan. They were identified from three patients (P1-P3) transferred from the same LTCF for the treatment of the infection. Pulsed-field gel electrophoresis was used to genotype the isolates. Resistance genes/plasmids and outer membrane proteins were investigated by polymerase chain reaction and sequence analysis. RESULTS: Isolates P1 and P3B/P3U demonstrated similar pulsotypes. All isolates were found to have resistance genes (blaCMY-2, qnrD1, aac(6')-Ib-cr) carried on nonconjugative IncA/C plasmids of different sizes. A single point mutation was identified in the chromosomal gyrA (Ser83Ile) and parC (Ser84Ile) genes of all isolates. Various point mutations and insertion/deletion changes were found in their major outer membrane protein gene ompPst1. CONCLUSIONS: 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.

A Snapshot of Co-Resistance to Carbapenems and Tigecycline in Clinical Isolates of Enterobacter cloacae.

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 blaSHV-12 and blaIMP-8 in 11 EC isolates from five pulsotypes/two STs. Reverse transcription PCR demonstrated overexpression of the chromosomal AmpC-like ß-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.

Tsukamurella tyrosinosolvens bacteremia with coinfection of Mycobacterium bovis pneumonia: case report and literature review.

INTRODUCTION: We describe an immunocompromised patient with Tsukamurella tyrosinosolvens bacteremia and coinfection of Mycobacterium bovis pneumonia. CASE DESCRIPTION: A 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 EVALUATION: The 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. CONCLUSION: According 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.

Prototheca wickerhamii cutaneous and systemic infections.

Prototheca wickerhamii, an environmental alga, rarely causes human infections. We present a case of Prototheca wickerhamii cutaneous and systemic infections in an 85-year-old male with adrenal insufficiency. This organism was identified by morphological features and microbiological tests. The patient was successfully treated with ketoconazole.

Clinical characteristics, antimicrobial susceptibilities, and outcomes of patients with Chryseobacterium indologenes bacteremia in an intensive care unit.

Ten patients with intensive care unit (ICU)-acquired Chryseobacterium indologenes bacteremia between January 2004 and December 2008 were studied. The primary site of infection was unknown for 80% of the cases. The known primary sites of infection were empyema (10%) and catheter-related bacteremia (10%). Eight patients (80%) had polymicrobial bacteremia, spent more than 21 days in the ICU, and received more than 14 days of broad-spectrum antibiotic therapy prior to the onset of C. indologenes bacteremia. All isolates were 100% susceptible to minocycline and trimethoprim/sulfamethoxazole. Vancomycin, imipenem, piperacillin/tazobactam, ciprofloxacin, and levofloxacin exhibited 0%, 10%, 20%, 30%, and 30%, respectively, susceptibility against this pathogen. All isolates were 100% resistant to ceftazidime, cefepime, meropenem, piperacillin, and amikacin. The 14-day mortality rate was 40%. Our findings suggest that this pathogen should be included among the causes of ICU-acquired bacteremia, especially in patients with a prolonged stay in an ICU or who had received long-term broad-spectrum antibiotic therapy. Extended-spectrum penicillins, third- and fourth-generation cephalosporins, and quinolones had very little or no effect against this pathogen. Therefore, choosing an appropriate antibiotic therapy for this pathogen is very difficult.