Here, we presented 11 cases with colistin-resistant Pseudomonas aeruginosa infection and co-existence of OXA-48 and NDM-1 in the ST235 high-risk clone. The molecular analyses were performed by Sanger sequencing and RT–PCR. The eight patients (72.7%) had an invasive infection and three (27.3%) had colonization. The 30-day mortality rate was 87.5% (7/8). Three patients (37.5%, 3/8) received colistin therapy before isolation of P. aeruginosa. In the Multilocus sequence typing (MLST) analysis of 11 isolates, eight (72.7%) isolates belonged to P. aeruginosa ST235 clone. All isolates were NDM-1 positive, and nine isolates (81.8%) were found to be positive for both OXA-48 and NDM-1. Sequences of pmrAB and phoPQ revealed numerous insertions and deletions in all isolates. In 10 isolates pmrAB and phoPQ were found to be upregulated. In conclusion, the co-existence of OXA-48 and NDM-1 genes in colistin-resistant P. aeruginosa ST235 high-risk clone indicates the spread of carbapenemases in clinical isolates and highlights need of continuous surveillance for high-risk clones of P. aeruginosa.

The aim of this study was to determine the effect of colistin resistance and other predictors on fatality among patients with Klebsiella pneumoniae bloodstream infections (Kp-BSI) and to describe the effect of amikacin and tigecycline on the outcome in an OXA-48 dominant country. This was a retrospective study performed among patients >16 years of age in a tertiary hospital with 465 beds. All cases had ≥1 positive blood culture for K. pneumoniae 48 h after admission. Among 210 patients with Kp-BSI, the 30-day mortality rate after isolation of the microorganism was 58%. The rate of carbapenem resistance was higher (64% vs. 38%, p < 0.001) and the colistin minimum inhibitory concentration (MIC) was elevated (7 vs. 4, p < 0.029) among the patients who died. Among the colistin-resistant K. pneumoniae, the rates of OXA-48, ST101, and NDM-1 were 78%, 67%, and 35%, respectively. Amikacin was added to the treatment of 13 patients with carbapenem and colistin-resistant Kp-BSI and 77% survived (p < 0.001). Tigecycline was added to the treatment of 24 patients with carbapenem and colistin-resistant Kp-BSI, and the 30-day mortality rate was 71% (p = 0.576). In the multivariate analysis, carbapenem resistance (odds ratio (OR) 5.2, 95% confidence interval (CI) 2.47-10.9, p < 0.001) and increasing APACHE II score (OR 1.19, 95% CI 1.12-1.26, p < 0.001) were significantly associated with 30-day mortality. The addition of amikacin to the treatment regimen (OR 0.05, 95% CI 0.01-0.23, p < 0.001) was significantly beneficial. Carbapenem resistance, increasing MIC of colistin, and the lungs as the source of the infection were significantly associated with 30-day mortality. The empirical use of combined active aminoglycosides was found to be beneficial in the treatment of colistin-resistant K. pneumoniae infections.

Introduction: Ralstonia pickettii infections are rare and may be mistaken for other bacteria. This study aims to report a hospital outbreak of R. pickettii at a tertiary hospital, which was initially misidentified as Ralstonia insidiosa, along with its clinical consequences. Methodology: A bacteraemia outbreak occurred between August 14 and October 4, 2019, infecting 22 patients admitted to diverse intensive care units. All isolates were identified with the use of the automated VITEK 2 Compact system and were then subjected to a microbial identification system, matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS). Bacterial identification and genomic DNA typing was made using pulsed-field gel electrophoresis. Investigation covered all potential sources of the outbreak. Results: An index patient and five additional patients developed fever while receiving care. Blood cultures of these patients yielded R. insidiosa by the VITEK 2 Compact system. Culture isolates were then submitted to a reference centre for confirmation by the MALDI-TOF MS system, where the bacterium turned out to be R. pickettii. No pathogen was isolated in the commercial products except for three samples of unopened sterile distilled water. Despite its discontinuation, 16 new cases were identified, in which blood cultures grew R. pickettii by the MALDI-TOF MS system. Attempts to uncover the source of the outbreak failed. Clinical manifestation was confined to fever in all the patients. Conclusions: During this outbreak, R. pickettii infections ran a relatively mild course without clinical deterioration or mortality, possibly due to low virulence.

Introduction: We sought to evaluate secondary infections (SIs) in patients admitted to the intensive care unit (ICU) for COVID-19 with respect to incidence, causative pathogens, and clinical outcomes. Methodology: In this two-centre retrospective study, we analysed 146 patients (96 males, 50 females; median age, 64 years) admitted to the ICU with COVID-19 between March 26 and December 31, 2020. Inclusion criteria were an ICU admission for at least 48 hours and age beyond 18 years. Patients with and without SIs were compared and the impacts of SIs and carbapenem resistance on mortality were analysed. Results: During ICU admission, 84 episodes of SIs developed in 58 patients (39.7%). A total of 104 isolates were recovered, with Gram-negative bacteria most frequent accounting for 74%. At least one carbapenem-resistant pathogen (n = 61) was recovered in 41 patients (70.1%). In multivariate analysis, the use of ECMO and an elevated procalcitonin level were significantly associated with the development of SIs. The mortality rate and the incidence of carbapenem resistance did not differ significantly in COVID-19 patients with and without SIs (p = 0.059 and p = 0.083, respectively). Conclusions: The incidences of SIs and carbapenem resistance among COVID-19 patients were alarming, emphasizing stricter infection control measures in the ICU setting.