A 78 year old male was hospitalized in neurology clinic with a diagnosis of encephalopathy. On 13th day of imipenem treatment for ventilator-associated pneumonia (VAP), a new VAP episode was diagnosed based on physical examination, laboratory and radiological findings. Cefoperazone-sulbactam 2x2 gr/day IV was started empirically. In the 3rd day of treatment Acinetobacter baumannii was identified from endotracheal aspirate culture that was resistant to all other antibiotics including colistin except cefoperazone-sulbactam (intermediate) and tigecycline (MIC: 4 mg/L, intermediate) by VITEK and E-test. Tigecycline 2 x 50 mg (after loading dose of 100 mg) IV, colistin IV 2 x 150 mg and colistin inhaler 2 x 75 mg were added to the cefoperazone-sulbactam 2 x 2 gr IV. Clinical findings were improved under this combination and completed to 14 days. The patient was discharged from hospital with neurological sequel after three months. This case has been presented to emphasize that colistin resistant Acinetobacter baumannii is becoming a problem for our country.

A cinetobacter baumannii is one of the most pathogenic nosocomial infection agents because of its extreme resistance to almost all known antibiotics and host immune responses (1). The emergence of colistin-resistance in A. baumannii has been reported throughout the world (2, 3). Biofilm formation ability enhances virulence of A. baumannii by increasing survival of cells in unfavourable environmental conditions, such as underexposure of disinfectants, antibiotics or attack of immune cells (4, 5). Antibiotic-resistant phenotypes This work is licensed under a Creative Commons Attribution-Non Commercial 4.0 International License.

Introduction. Aminoglycosides are used for the treatment of carbapenemase-producing Klebsiella pneumoniae (CPK) infections. 16S rRNA methyltransferases (RMTs) confer resistance to all aminoglycosides and are often cocarried with NDM. Hypothesis/Gap Statement. There is a dart of studies looking at the aminoglycoside resistance mechanisms for invasive CPK isolates, particularly in OXA-48 endemic settings. Aim. We aimed to determine the prevalence of RMTs and their association with beta lactamases and MLSTs amongst aminoglycoside-resistant CPK bloodstream isolates in an OXA-48 endemic setting. Methodology. CPK isolates (n=181), collected as part of a multicentre cohort study, were tested for amikacin, gentamicin and tobramycin susceptibility using custom-made sensititre plates (GN2XF, Thermo Fisher Scientific). All isolates were previously subjected to whole-genome sequencing. Carbapenemases, RMTs, MLSTs and plasmid incompatibility groups were detected on the assembled genomes. Results. Of the 181 isolates, 109(60 %) were resistant to all three aminoglycosides, and 96 of 109(88 %) aminoglycoside-resistant isolates carried an RMT (85 ArmA, 10 RmtC, 4 RmtF1; three isolates cocarried ArmA and RmtC). Main clonal types associated with ArmA were ST2096 (49/85, 58 %) and ST14 (24/85, 28 %), harbouring mainly OXA-232 and OXA-48 +NDM, respectively. RmtC was cocarried with NDM (5/10) on ST395, and NDM +OXA-48 or NDM +KPC (4/10) on ST14, ST15 and ST16. All RMT producers also carried CTX-M-15, and the majority cocarried SHV-106, TEM-150 and multiple other antibiotic resistance genes. The majority of the isolates harboured a combination of IncFIB, IncH and IncL/M type plasmids. Non-NDM producing isolates remained susceptible to ceftazidime-avibactam. Conclusion. Aminoglycoside resistance amongst CPK bloodstream isolates is extremely common and mainly driven by clonal spread of ArmA carried on ST2096 and ST14, associated with OXA-232 and OXA48 +NDM carriage, respectively.

Background: We described the QTc interval prolongation and related adverse cardiac events during the administration of hydroxychloroquine (HCQ) and its combinations for treatment of COVID-19. Methods: The hospitalized patients who were infected with SARS-CoV-2 and received HCQ with initial and follow up ECGs from March 10th to May 30th were included. The critical QTc prolongation was accepted as QTc >500 ms if QRS<120ms and >550 ms if QRS >120 ms or [?]QTc levels >60 ms when compared with the initial ECG. Primary outcomes were critical QTc prolongation, ventricular tachyarrhythmia, and sudden cardiac arrest. Results: Out of 336 hospitalized patients with suspected or confirmed COVID-19, 297 received HCQ, and 94 met the inclusion criteria, and 66 cases were included in final analysis. The mean baseline QTc was 444.5 (sd= 39.5) ms. In total, 63% of the patients' QTc levels increased under HCQ treatment and critical QTc prolongation occurred in 8 cases (12%) all of whom were male. The male gender (p=0.033), DM (p=0.035) and oseltamivir use (p=0.047) were significantly associated with critical QTc prolongation. In multivariate analysis, DM (OR:5.8, %95 Cl:1.11-30.32, p:0.037), and concomitant use of oseltamivir (OR:5.3, %95 Cl:1,02-28, p:0.047) were found to be associated with critical QTc prolongation. Conclusion: Critical QTc prolongation was detected in 12% of the patients. The DM and concomitant oseltamivir use were associated with critical QTc prolongation. The use of concurrent drugs that have potential to enhance QTc interval should be kept in mind and special attention should be paid for ECG monitoring.