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Background: The increase in antimicrobial resistance includes emerging mechanisms such as 16S ribosomal RNA methylases, which confer high-level resistance to aminoglycosides. In this regard, the most predominant genes observed worldwide are rmtB and armA, but their presence in Uruguay is unknown. Objectives: We describe the genomic characterization of isolates carrying rmtB and rmtC, together with blaNDM-5 and blaNDM-1, respectively, and rmtD in our country. Methology: Five isolates from patients admitted to three hospitals were studied. Identification and antibiotic susceptibility testing were performed using the Vitek2 System. Whole Genome Sequencing was conducted, and hybrid assembly was performed with Unicycler. In silico analysis using the Center for Genomic Epidemiology’s tools was undertaken to predict antibiotic resistance determinants, plasmid incompatibility groups, and sequence types. Results: We report three K. pneumoniae ST307 isolates with an IncR plasmid carrying blaNDM-5/blaCTX-M-15/blaTEM-1B/rmtB/dfrA14/dfrA12/sul1/qacEΔ1/ermB/mphA, one K. pneumoniae ST258 harboring an IncC plasmid containing rmtC/blaNDM-1/blaCMY-6/aac(6′)-Ib/sul1, and one E. cloacae ST88 isolate with an IncFIB/II plasmid hosting rmtD, within a novel Tn21-like transposon named Tn7825, alongside blaOXA-101/sul1/tet(G)/floR, and a new variant of blaTEM assigned as blaTEM-258. One of the strains, named UH_B2, also carried an IncM1 plasmid encoding qnrE1/blaTEM-1/blaCTX-M-8 associated with ISEcp1. Conclusions: This is the first description of plasmids harboring 16S rRNA methyltransferases in Uruguay. The association and dissemination of diverse antibiotic-resistant genes underpin the health threat they represent, highlighting the lack of available antibiotics effective against multidrug-resistant microorganisms.

Pseudomonas aeruginosa is a leading cause of hospital-acquired infections worldwide. Biofilm production, antibiotic resistance, and a wide range of virulence factors contribute to their persistence in nosocomial environments. We describe an outbreak caused by a multidrug-resistant P. aeruginosa strain in an ICU. Antibiotic susceptibility was determined and blaPER-1 and qnrVC were amplified via PCR. Clonality was determined using PFGE and biofilm formation was studied with a static model. A combination of antibiotics was assessed on both planktonic cells and biofilms. WGS was performed on five isolates. All isolates were clonally related, resistant to ceftazidime, cefepime, amikacin, and ceftolozane-tazobactam, and harbored blaPER-1; 11/19 possessed qnrVC. Meropenem and ciprofloxacin reduced the biofilm biomass; however, the response to antibiotic combinations with rifampicin was different between planktonic cells and biofilms. WGS revealed that the isolates belonged to ST309 and serotype O11. blaPER-1 and qnrVC6 were associated with a tandem of ISCR1 as part of a complex class one integron, with aac(6′)-Il and ltrA as gene cassettes. The structure was associated upstream and downstream with Tn4662 and flanked by direct repeats, suggesting its horizontal mobilization capability as a composite transposon. ST309 is considered an emerging high-risk clone that should be monitored in the Americas.

Antibiotic resistance is an alarming problem throughout the world and carbapenem-resistant Pseudomonas aeruginosa has been cataloged as critical in the World Health Organization list of microorganisms in urgent need for the development of new antimicrobials. In this work, we describe two novel resistance regions responsible for conferring a multidrug resistance phenotype to two clinical isolates of P. aeruginosa (Pa873 and Pa6415) obtained from patients hospitalized in the ICU of University Hospital of Uruguay. Bacterial identification and antibiotic susceptibility tests were performed using MALDI-TOF and the Vitek 2 system, respectively. WGS was performed for both isolates using Oxford Nanopore Technologies and Illumina and processed by means of hybrid assembly. Both isolates were resistant to ceftazidime, cefepime, piperacillin–tazobactam, aztreonam, and imipenem. Strain Pa6415 also showed resistance to ciprofloxacin. Both strains displayed MICs below the susceptibility breakpoint for CAZ-AVI plus 4 mg/L of aztreonam as well as cefiderocol. Both resistance regions are flanked by the left and right inverted repeats of ISPa40 in two small regions spanning 39.3 and 35.6 kb, for Pa6415 and Pa873, respectively. The resistance region of Pa6415 includes TnaphA6, and the new Tn7516 consists of IRi, In899, qacEΔ1-sul1-ISCR1, qnrVC6-ISCR1-blaPER-1-qacEΔ1-sul1, araJ-like, IS481-like tnpA, ISPa17, and IRR. On the other hand, the resistance region of Pa873 includes Tnaph6 and the new Tn7517 (IRi, In899, qacEΔ1-sul1, ISCR1–blaPER-1–qacEΔ1-sul1, araJ-like, IS481-like tnpA, ISPa17, and IRR). It is necessary to monitor the emergence of genetic structures that threaten to invalidate the available therapeutic resources.

A nivel mundial se estima que en 2018 hubo alrededor de 10 millones de nuevos casos de tuberculosis (TBC). La detección molecular es una herramienta diagnóstica crecientemente utilizada para el diagnóstico de TBC. Los predictores de riesgo para TBC pulmonar son variados y varían de acuerdo a la población estudiada. Los objetivos del presente trabajo fueron: evaluar la performance de la detección de M. tuberculosis por la técnica Xpert® MTB/RIF para el diagnóstico de TBC pulmonar y determinar los factores predictores de presencia de esta enfermedad en pacientes asistidos en el Hospital Pasteur de Montevideo. Se realizó un estudio descriptivo, observacional y transversal. Se incluyeron 254 pacientes, 68 con TBC pulmonar. La sensibilidad de la prueba Xpert® MTB/RIF para detectar M. tuberculosis fue 100% (IC 95%: 91,2-100) y la especificidad 95,1% (IC 95%: 83,9-98,7). En el análisis multivariado se evidenció que los predictores independientes para presencia de TBC pulmonar fueron: contacto cercano con otro caso de TBC (p