bBecause of its remarkable ability to acquire antibiotic resistance and to survive in nosocomial environments, Acinetobacter baumannii has become a significant nosocomial infectious agent worldwide. Tigecycline is one of the few therapeutic options for treating infections caused by A. baumannii isolates. However, tigecycline resistance has increasingly been reported. Our aim was to assess the prevalence and characteristics of efflux-based tigecycline resistance in clinical isolates of A. baumannii collected from a hospital in China. A total of 74 A. baumannii isolates, including 64 tigecycline-nonsusceptible A. baumannii (TNAB) and 10 tigecycline-susceptible A. baumannii (TSAB) isolates, were analyzed. The majority of them were determined to be positive for adeABC, adeRS, adeIJK, and abeM, while the adeE gene was found in only one TSAB isolate. Compared with the levels in TSAB isolates, the mean expression levels of adeB, adeJ, adeG, and abeM in TNAB isolates were observed to increase 29-, 3-, 0.7-, and 1-fold, respectively. The efflux pump inhibitors (EPIs) phenyl-arginine-␤-naphthylamide (PA␤N) and carbonyl cyanide 3-chlorophenylhydrazone (CCCP) could partially reverse the resistance pattern of tigecycline. Moreover, the tetX1 gene was detected in 12 (18.8%) TNAB isolates. To our knowledge, this is the first report of the tetX1 gene being detected in A. baumannii isolates. ST208 and ST191, which both clustered into clonal complex 92 (CC92), were the predominant sequence types (STs). This study showed that the active efflux pump AdeABC appeared to play important roles in the tigecycline resistance of A. baumannii. The dissemination of TNAB isolates in our hospital is attributable mainly to the spread of CC92.

Osteomyelitis caused by nontuberculous mycobacteria (NTM) can have severe consequences and a poor prognosis. Physicians therefore need to be alert to this condition, especially in immunocompromised patients. Although the pathogenesis of NTM osteomyelitis is still unclear, studies in immunodeficient individuals have revealed close relationships between NTM osteomyelitis and defects associated with the interleukin-12–interferon-γ–tumor necrosis factor-α axis, as well as human immunodeficiency virus infection, various immunosuppressive conditions, and diabetes mellitus. Culture and species identification from tissue biopsies or surgical debridement tissue play crucial roles in diagnosing NTM osteomyelitis. Suitable imaging examinations are also important. Adequate surgical debridement and the choice of appropriate, combined antibiotics for long-term anti-mycobacterial chemotherapy, based on in vitro drug susceptibility tests, are the main therapies for these bone infections. Bacillus Calmette–Guerin vaccination might have limited prophylactic value. The use of multiple drugs and long duration of treatment mean that the therapeutic process needs to be monitored closely to detect potential side effects. Adequate duration of anti-mycobacterial chemotherapy together with regular monitoring with blood and imaging tests are key factors determining the recovery outcome in patients with NTM osteomyelitis.

BackgroundEmergence of rmtB-positive Klebsiella pneumoniae carbapenemase (KPC)-producing K. pneumoniae (KPC-KP) poses a great threat to antimicrobial treatment options.MethodsFrom January 2010 to December 2010, non-duplicate KPC-KP isolates from our hospital were screened for rmtB and multiple other resistance determinants with PCR. Subsequent studies included MIC determination, PFGE, and multilocus sequence typing. Records from patients with KPC-KP isolated were retrospectively reviewed. Comparisons of molecular and clinical characteristics between rmtB-positive and rmtB–negative isolates were systematically performed, as well as the environmental colonization study in ICU wards.ResultsA total of 84 KPC-KP strains were collected, including 48 rmtB-positive KPC-KP (RPKP) and 36 rmtB-negative KPC-KP (RNKP) isolates. All KPC-KP isolates were multidrug resistant, with colistin and tigecycline being the most active agents. Compared with RNKP, RPKP displayed a much severer resistance phenotype. Susceptibility rates for amikacin (0% for RPKP versus 88.9% for RNKP, p < 0.01), fosfomycin (8.5% for RPKP versus 88.9% for RNKP, p < 0.01), and minocycline (6.7% for RPKP versus 52.8% for RNKP, p < 0.01), were all significantly lower in RPKP strains. Isolates belonging to PFGE pulsetype A and sequence type 11 were predominant in both groups, including 39 (81.3%) RPKP and 22 (61.1%) RNKP isolates. Nevertheless, RNKP showed more complex genetic backgrounds compared with RPKP. Diverse clinical characteristics were found in both cohorts, however, no significant differences were observed between RPKP and RNKP patients.ConclusionsRPKP strains have spread widely and gradually replaced RNKP in our hospital. They seemed to show much severer resistance phenotypes compared with RNKP and had a bigger dissemination potential. Prudent use of available active agents combined with good control practices is therefore mandatory.

worldwide was estimated at a staggering 10.4 million, with a significant percentage (10%) resulting from concomitant HIV-TB coinfections. [1] Given the closely knitted association between TB infections and poor sanitation/poverty, it thus comes with no surprise that an overwhelming majority of disease burden (60%) is actually shouldered by countries from the developing world (Figure 1). [1] TB infections are compounded by the emergence of multidrug resistance (MDR). In spite of the tremendous amount of resources and research dollars that have been devoted to TB research, TB diagnostics and treatment outcomes still remain startlingly poor. TB remains worryingly underreported, under-diagnosed and undertreated. A 4.3 million gap was reported between incident and notified TB cases, chiefly in developing countries; majority of TB infections remain latent and unreported, and only 30% of new incident TB cases were subjected to drug susceptibility testing. [1] The Xpert Mycobacterium Tuberculosis (MTB)/RIF assay remains the only available WHOrecommended rapid diagnostic platform for detection of TB and drug (rifampicin) resistance. Treatment success rates are highly variable, ranging from 28% (extensively drug-resistant strains) to 83% (garden strains) of TB. The rate of decline in TB incidence has remained stagnant at 1.5% annually over the past decade, far lagging behind the 5% projected by the WHO's End TB Strategy. Against such a backdrop, TB remains firmly entrenched among the top 10 causes of death worldwide. [2] To this end, the WHO has since 2015, adopted the End TB Strategy in an effort to stem this burgeoning epidemic. Major diagnostic and treatment gaps in TB management still remain, and these need to be addressed to effectively curtail TB spread and its impact on global health. Pathogenesis of TB InfectionsMTB is the infectious agent responsible for TB infections. It originates from the family Mycobacteriaceae and is an obligate bacteria chiefly spread via air droplets.

BackgroundSeveral studies have suggested a relationship between hepatitis B virus (HBV) basal core promoter/pre-core mutations and HBV-induced acute-on-chronic liver failure (ACLF). Therefore, we evaluated this potential relationship using a meta-analysis.MethodsChinese or English studies from 1966 to January 31, 2014 were included in the analysis. A random or fixed-effects model was used to merge the odds ratios (ORs).ResultsWe identified 31 case–control studies containing a total population of 1995 ACLF and 3822 chronic hepatitis B (CHB) patients. Several mutations were significantly correlated with ACLF: T1753V (1.889, 95 % confidence interval (CI) [1.357–2.631]), A1762T (2.696 [2.265–3.207]), G1764A (3.005 [2.077–4.347]), A1762T/G1764A (2.379 [1.519–3.727]), C1766T (1.849 [1.403–2.437]), T1768A (2.440 [1.405–3.494]), A1846T (3.163 [2.157–4.639]), G1896A (2.181 [1.800–2.642]), G1899A (3.569 [2.906–4.385]) and G1896A/A1762T/G1764A (1.575 [1.172–2.116]). Additionally, HBeAg-negative status was also statistically significant for the progression to ACLF (OR = 2.813, 95 % CI = 2.240–3.533, p < 0.001). However, there was no association between ACLF development and HBV genotype.ConclusionsThe HBV basal core promoter/pre-core mutations T1753V, A1762T, G1764A, C1766T, T1768A, A1846T, G1896A and G1899A, and an HBeAg-negative status correlate with an increased risk of HBV-ACLF.Electronic supplementary materialThe online version of this article (doi:10.1186/s12985-015-0313-5) contains supplementary material, which is available to authorized users.