Descripción de la micobiota de los tubos endotraqueales de pacientes de unidades de cuidados intensivos en Bogotá, Colombia / Description of the colonizing mycobiota of endotracheal tubes from patients admitted to two intensive care units in Bogotá, Colombia

Introducción. La colonización por microorganismos patógenos de los dispositivos médicos usados en las unidades de cuidados intensivos es un factor de riesgo para el aumento de infecciones asociadas con la atención en salud y, por lo tanto, al de la morbilidad y la mortalidad de los pacientes intubados. En Colombia, no se ha descrito la colonización por hongos de los tubos endotraqueales, con lo cual se podrían considerar nuevas opciones terapéuticas para el beneficio de los pacientes. Objetivo. Describir los hongos que colonizan los tubos endotraqueales de los pacientes en unidades de cuidados intensivos, junto con su perfil de sensibilidad a los antifúngicos. Materiales y métodos. Se realizó un estudio observacional, descriptivo, en dos centros hospitalarios durante 12 meses. Se recolectaron tubos endotraqueales de pacientes de las unidades de cuidados intensivos. Estos fueron procesados para cultivar e identificar hongos, y para establecer su perfil de sensibilidad a los antifúngicos. Resultados. Se analizaron 121 tubos endotraqueales obtenidos de 113 pacientes. De estos, el 41,32 % se encontró colonizado por los hongos Candida albicans (64,61 %), C. no-albicans (30,77 %), Cryptococcus spp. (3,08 %) o mohos (1,54 %). Todos los hongos evaluados presentaron una gran sensibilidad a los antifúngicos, con un promedio del 91 %. Conclusión. Se encontró colonización fúngica en los tubos endotraqueales de pacientes con asistencia respiratoria mecánica. El perfil de sensibilidad en estos pacientes fue favorable. Se requiere un estudio clínico para correlacionar los microorganismos colonizadores y su capacidad de generar infección.

Introduction. Medical device colonization by pathogenic microorganisms is a risk factor for increasing infections associated with health care and, consequently, the morbidity and mortality of intubated patients. In Colombia, fungal colonization of endotracheal tubes has not been described, and this information could lead to new therapeutic options for the benefit of patients. Objective. To describe the colonizing fungi of the endotracheal tubes from patients in the intensive care unit, along with its antifungal sensitivity profile. Materials and methods. We conducted a descriptive, observational study in two health centers for 12 months. Endotracheal tubes were collected from patients in intensive care units. Samples were processed for culture, fungi identification, and antifungal sensitivity profile assessment. Results. A total of 121 endotracheal tubes, obtained from 113 patients, were analyzed: 41.32 % of the tubes were colonized by Candida albicans (64.62%), C. non-albicans (30.77%), Cryptococcus spp. (3.08%) or molds (1.54%). All fungi evaluated showed a high sensitivity to antifungals, with a mean of 91%. Conclusion. Fungal colonization was found in the endotracheal tubes of patients under invasive mechanical ventilation. The antifungal sensitivity profile in these patients was favorable. A clinical study is required to find possible correlations between the colonizing microorganisms and infectivity.

Prevalence of SARS-CoV-2 infection and SARS-CoV-2-specific antibody detection among healthcare workers and hospital staff of a university hospital in Colombia.

Objective: The aim of this study was to determine current and previous SARS-COV-2 infection, and describe risk factors associated with seropositivity, among HCWs and hospital staff between June and October of 2020. Methodology: Data from the day of enrollment for a prospective cohort study were analyzed to determine point prevalence and seroprevalence of SARS-CoV-2 infection in HCWs and hospital staff of a university hospital in Colombia. Respiratory samples were collected to perform RT-PCR tests, along with blood samples to measure SARS-CoV-2 IgM and IgG antibodies. Data on nosocomial and community risk factors for infection were also collected and analyzed. Findings: 420 HCWs and hospital staff members were included. The seroprevalence at baseline was 23.2%, of which 10.7% had only IgM antibodies, 0.7% had IgG, and 11.7% had IgM and IgG. The prevalence of acute SARS-CoV-2 infection was 1.9%. Being a nurse assistant was significantly associated with seropositivity when compared with all other job duties (PR 2.39, 95% CI 1.27-3.65, p = 0.01). Conclusions: Overall SARS-CoV-2 prevalence was 1.9% and seroprevalence was 23.15%. Nurse assistants, medical doctors or students, and laboratory workers had a higher possibility of being SARS-CoV-2 seropositive.

MAPK-dependent degradation of G protein-coupled receptor kinase 2.

G protein-coupled receptor kinase 2 (GRK2) is a key modulator of G protein-coupled receptors (GPCR). Altered expression of GRK2 has been described to occur during pathological conditions characterized by impaired GPCR signaling. We have reported recently that GRK2 is rapidly degraded by the proteasome pathway and that beta-arrestin function and Src-mediated phosphorylation are involved in targeting GRK2 for proteolysis. In this report, we show that phosphorylation of GRK2 by MAPK also triggers GRK2 turnover by the proteasome pathway. Modulation of MAPK activation alters the degradation of transfected or endogenous GRK2, and a GRK2 mutant that mimics phosphorylation by MAPK shows an enhanced degradation rate, thus indicating a direct effect of MAPK on GRK2 turnover. Interestingly, MAPK-mediated modulation of wild-type GRK2 stability requires beta-arrestin function and is facilitated by previous phosphorylation of GRK2 on tyrosine residues by c-Src. Consistent with an important physiological role, interfering with this GRK2 degradation process results in altered GPCR responsiveness. Our data suggest that both c-Src and MAPK-mediated phosphorylation would contribute to modulate GRK2 degradation, and put forward the existence of new feedback mechanisms connecting MAPK cascades and GPCR signaling.