Introduction:Pseudomonas aeruginosa, an important pathogen globally, presents several resistance mechanisms. This study aimed to investigate the presence of bla GES in clinical isolates of Pseudomonas aeruginosa obtained from various clinical specimens from patients admitted to three different hospitals in Recife, Brazil. The Guiana extended spectrum beta-lactamase (GES) enzymes are responsible for conferring broad spectrum resistance to beta-lactam drugs, including the carbapenems. Methods: A total of 100 carbapenem-resistant P. aeruginosa isolates underwent polymerase chain reaction (PCR) testing to identify bla GES, bla KPC, bla SPM-1, bla IMP , and bla VIM . Additionally, PCR products positive for bla GES were sequenced. The clonal profi les of these same isolates were then determined by means of enterobacterial repetitive intergenic consensus (ERIC)-PCR analysis. Results: PCR analysis revealed that four isolates harbored bla GES ; DNA sequencing showed that two harbored bla GES-1 and two bla . Beta-lactamase genes bla SPM-1 , bla IMP , bla VIM , and bla KPC were investigated; none of these genes was detected. Automated susceptibility testing methods (Vitek®2, bioMérieux) showed that the bla GES-1 -positive isolates were only susceptible to polymyxin B. The patterns obtained with ERIC-PCR methods showed clonal relationship between the two isolates that harbored bla , whereas different clonal profi les were found in the isolates harboring bla GES-1. Conclusions: We detected the presence of bacterial isolates positive for two different variants of the enzyme GES in three different hospitals from Recife, Brazil. These enzymes have a great capacity for dissemination among Gram-negative bacteria and confer broad-spectrum resistance to betalactam antibiotics and to the carbapenems.
Primrose syndrome (PRIMS), a rare genetic disorder with several clinical findings including intellectual disability, macrocephaly, typical facial features, and muscle wasting, is caused by heterozygous variants in the ZBTB20 gene. We report the cases of two males diagnosed with PRIMS at different ages, emphasizing the likely progressive nature of the disorder, as well as the differences and similarities of presentation during infancy and adulthood. Patient 1 is a 2-year-old American male with a medical history marked by impaired hearing, developmental delays, and fainting spells. Patient 2 is a 28-year-old Brazilian male, who presents with a phenotype similar to that seen
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