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• The prevalence of carbapenem-resistant Acinetobacter baumannii (CR-AB) varied among countries. • Of 232 CR-AB isolates, 224 (96.6%) harbored at least one carbapenemase gene. • Of the 226 carbapenemase genes detected, bla OXA-23 was the most dominant (94.7%). • CR-AB showed varied resistance rates for minocycline, colistin, and tigecycline. This study aimed to investigate the geographic distribution of carbapenem-resistant Acinetobacter baumannii (CR-AB) isolates in the Asia-Pacific region. We collected A. baumannii isolates using the Antimicrobial Testing Leadership and Surveillance program from 2012 to 2019. The minimum inhibitory concentrations (MICs) of the isolates were determined using the broth microdilution method. The major carbapenemase genes were identified using multiplex polymerase chain reaction assays for the isolates collected between 2012 and 2014. CR-AB was defined as isolates with meropenem MICs ≥8 mg/l. In total, 2674 A. baumannii isolates were collected from 13 countries, of which 1918 (71.7%) were CR-AB. The carbapenem resistance rates among A. baumannii isolates were as low as 2.8% and 6.5% in Japan and Australia, respectively, but as high as 88% and 87.2% in South Korea and India, respectively. Of the 232 CR-AB isolates that underwent carbapenemase gene screening, 224 (96.6%) harbored at least one carbapenemase gene. A total of 226 carbapenemase genes were detected, with bla OXA-23 (94.7%, 214/226) being the most dominant, followed by bla OXA-72 (2.7%, 6/226), bla OXA-58 (2.2%, 5/226), and bla NDM-1 (0.4%, 1/226). CR-AB isolates had >80% resistance to amikacin, ampicillin/sulbactam, cefepime, ceftazidime, ciprofloxacin, levofloxacin, and piperacillin/tazobactam. The rates of CR-AB resistance to minocycline and colistin were 7.2% (31/429) and 1.7% (23/1368). For cefoperazone/sulbactam and tigecycline, 50.2% (527/1049) and 93.3% (1789/1918) of CR-AB isolates had an MIC ≤16 mg/l and ≤2 mg/l, respectively. The prevalence of carbapenem resistance in A. baumannii showed significant differences among countries in the Asia-Pacific region, and the treatment options were limited. [ABSTRACT FROM AUTHOR]

• Tigecycline treatment causes a significant decrease in fibrinogen levels. • Tigecycline exposure is highly predictive of hypofibrinogenemia. • Serum concentration at the 6 hours after the dosing (C 1/2) ≥ 0.645 mg/l with best predictive performance may be the optimal toxicity threshold. This study aimed to determine the thresholds of serum concentration as a predictor of tigecycline (TGC)-induced hypofibrinogenemia (HF) in critically ill patients. A retrospective cohort study was conducted in intensive care unit patients treated with TGC. The clinical data and serum concentration were extracted from the patients' electronic medical records. Patients were divided into an HF group and a normal group according to fibrinogen value. The receiver operating characteristic curves and logistic regression were used to derive serum concentration thresholds and quantify the association between exposure thresholds and HF while adjusting for confounders. In total, 100 patients were included. The receiver operating characteristic curves analysis showed that TGC concentration parameters were strongly predictive of HF. Adjusting for duration of TGC, serum concentration at the 6 hours after the dosing (C 1/2) ≥ 0.645 mg/l, area under the concentration-time curve over a 24-hour period (AUC 0-24) ≥ 20.76 mg·h/l, and serum concentration of 30 minutes before next dose (C min) ≥ 0.455 mg/l were associated with a three- to five-fold increased risk of TGC-induced HF in logistic regression. The findings from this study provide evidence that TGC exposure is highly predictive of HF, with an approximately three- to five-fold increased risk. Serum concentration at the 6 hours after the dosing (C 1/2) ≥ 0.645 mg/l with best area under the receiver operating characteristic curve and negative predictive value appears to be the most appropriate toxicity threshold. [Display omitted] [ABSTRACT FROM AUTHOR]

• This is the first multicenter retrospective study about tigecycline drug-induced liver injury (DILI). • The prevalence of tigecycline DILI in the study population was 10.3%. • Abnormal baseline alanine aminotransferase, intensive care unit admission, and treatment length were risk factors. We conducted this multicenter retrospective study to evaluate the prevalence, clinical patterns, and risk factors for tigecycline-induced liver injury, which is a type of drug-induced liver injury (DILI). Inpatients receiving intravenous tigecycline for ≥7 days were included. Patient information was collected to assess possible DILIs. The pattern and severity of tigecycline DILI were evaluated. A multivariable logistic regression model was used to identify the independent risk factors associated with tigecycline DILI. A total of 986 patients were identified and 397 patients were included in this study. The prevalence of tigecycline DILI was 10.3% (95% confidence interval [CI] = 7.51–13.7%). The most common type of tigecycline DILI was cholestatic, with mild severity observed in most cases. Abnormal baseline alanine aminotransferase levels (odds ratio [OR] = 3.11, 95% CI = 1.55–6.24, P = 0.001), intensive care unit admission (OR = 2.63, 95% CI = 1.32–5.36, P = 0.006), and treatment length (in weeks) (OR = 1.25, 95% CI = 1.05–1.49, P = 0.011) were independent risk factors for tigecycline DILI. Our results indicate that the prevalence of tigecycline DILI is high, and that the patients at risk should receive special attention. [Display omitted] [ABSTRACT FROM AUTHOR]

To investigate the prevalence of ESBL-producing Enterobacteriaceae from blood specimens sent to Microbiology Laboratory RSUP H. Adam Malik and its antibiotic susceptibility pattern to various antibiotics We conducted a retrospective study on blood specimens sent to Microbiology Laboratory RSUP H. Adam Malik, January 2019 - March 2021. The Vitek-2 compact system (bioMerieux®) performed identification and susceptibility testing with Advanced Expert System (AES). In addition, ESBL phenotypic screening was performed with the VITEK 2 compact, which compared the proportion of decreased bacterial growth to cefepime, cefotaxime, and ceftazidime, alone and in the presence of clavulanic acid. We found 1040 isolates from positive blood culture. A total of 333 (32,0%) isolates of Enterobactericeae were identified. From those isolates, there are 60,7% isolates were ESBL-producing Enterobactericeae , consisted of 121 (59,9%) Klebsiella pneumoniae , 76 (37,6%) Escherichia coli , 3(1,5%) isolat Klebsiella oxytoca and 2 (1%). ESBL-producing K.pneumoniae were susceptible to ertapenem (99,2%), meropenem (97,5%), amikacin (95,9%), tigecycline (90,9%), piperacillin-tazobactam (78,5%), cephalosporin (0-60,3%), trimethoprim-sulfamethoxazole (31,4%), ciprofloxacin (25,6%), gentamicin (20,7%), ampicillin sulbactam (19%), aztreonam (4,1%), amoxicillin (0%). ESBL - producing E coli were susceptible to meropenem, ertapenem, amikacin (100%), tigecycline (98,7%), piperacillin-tazobactam (88,2%), gentamicin (53,9%), cephalosporin (0% - 55,3%), ampicillin sulbactam (38,2%), trimethoprim-sulfamethoxazole (22,4%), ciprofloxacin (14,5%), aztreonam (11,8%),amoxicillin(0%). The prevalence of ESBL-producing Enterobacteriaceae from blood specimens, is high and most isolates highly sensitive toward tigecycline, amikacin, meropenem and ertapenem. [ABSTRACT FROM AUTHOR]

Tigecycline is a broad-spectrum antibiotic usually used as a last resort for infections caused by multidrug-resistant and extensively drug-resistant Gram-negative bacteria, such as Enterobacterales and Acinetobacter spp. The evolvement of antimicrobial resistance has led to the increased demand for tigecycline. However, data comparing the efficacy and safety of high (HD) versus standard doses (SD) of tigecycline are limited. Therefore, this study aimed to compare the clinical and microbiological outcomes of these doses in hospitalized patients. This was a retrospective cohort multicenter study. Adult patients admitted between January 2018 and October 2020 who received tigecycline as monotherapy or in combination with other antibiotics for at least 3 days with a microbiologically documented infection were included. Clinical cure was the primary endpoint. Secondary endpoints included microbiological cure, mortality and length of stay. Of 292 patients, 77 were in the HD group while 215 were in the SD group. Baseline characteristics were similar, except for the duration of tigecycline therapy, which was 3 days longer in the HD group (P = 0.007), and source of infection (P <0.0001). Most patients in the HD group had either respiratory (54.5%), skin and soft tissue infections (SSTIs; 22.1%), or more than one site of infections (23.4%). On the other hand, most patients in the SD group had either respiratory (40.4%) or skin and soft tissue infections (40.8%), While microbiological cure was higher in the HD group (16.9% vs. 10.8%; P =0.005), clinical cure rates were lower in the HD group (24.7% vs. 39.1%; P = 0.02). Mortality rate was higher in the HD group at 63.6% compared with 39.1% in the SD group (P <0.0001). Notably, most isolates from patients in the HD group had intermediate susceptibility to tigecycline (51.3%), whereas isolates were mostly susceptible in the SD group (47.9%; P <0.0001). HD regimen of tigecycline in this study was not superior to SD. The less favorable outcomes could be attributed to the lower susceptibility to tigecycline in the HD group. More studies are needed to assess the impact of HD in patients with susceptible isolates. [ABSTRACT FROM AUTHOR]