ABSTRACT
Introducción: La COVID-19, infección causada por el SARS-CoV-2, ocasiona daños a diferentes órganos y sistemas, como el sistema nervioso central. Entre las alteraciones neurológicas se describe la "niebla mental" como manifestación neurocognitiva frecuente en el síndrome post-COVID-19, con un impacto negativo en la calidad de vida de los pacientes. Se revisaron 104 artículos publicados desde junio 2020 a octubre del 2022, en las bases de datos Pubmed, Medline, Lilacs y Cumed. Objetivo: Actualizar conocimientos sobre las manifestaciones neurocognitivas de "niebla mental" en el síndrome post-COVID-19. Desarrollo: Se describen alteraciones neurocognitivas de "niebla mental", trastornos de atención, concentración y memoria, asociados a otros síntomas neurológicos, como cefalea, insomnio, anosmia, ageusia, ansiedad, depresión, y otros síntomas persistentes, que caracterizan al síndrome post-COVID-19. Se hace referencia a elementos de la etiopatogenia, resaltando la respuesta inmune sistémica exagerada, generada por la liberación de citoquinas, aspectos a tener presentes para la conducta diagnóstica y terapéutica de los pacientes post-COVID-19. Conclusiones: Los síntomas neurocognitivos de "niebla mental", constituyen las alteraciones neurológicas frecuentes del síndrome post-COVID-19, son variados, con combinación de diferentes síntomas en cada enfermo, más frecuentes en mujeres y en pacientes que presentaron enfermedad grave.
Introduction: COVID-19, infection caused by SARS-CoV-2, causes damage to different organs and systems, such as the central nervous system. Among the neurological alterations, brain fog is described as a frequent neurocognitive manifestation in post-COVID-19 syndrome, with a negative impact on patients' quality of life; 104 articles published were reviewed from June 2020 to October 2022, in Pubmed, Medline, Lilacs and Cumed databases. Objective: To update knowledge on the neurocognitive manifestations of brain fog in post-COVID-19 syndrome. Development: Neurocognitive alterations of mental fog, attention, concentration and memory disorders, associated with other neurological symptoms, such as headache, insomnia, anosmia, ageusia, anxiety, depression, and other persistent symptoms, which characterize post-COVID-19 syndrome, are described. Reference is made to elements of the etiopathogenesis, highlighting the exaggerated systemic immune response, generated by the release of cytokines, aspects to keep in mind for the diagnostic and therapeutic conduct of post-COVID-19 patients. Conclusions: The neurocognitive symptoms of brain fog are frequent neurological alterations of post-COVID-19 syndrome, they are varied, with a combination of different symptoms in each patient, more frequent in women and in patients who presented severe disease.
ABSTRACT
Infection by the opportunistic pathogen Pseudomonas aeruginosa is a leading cause of morbidity and mortality seen in cystic fibrosis (CF) patients. This is mainly due to the genotypic and phenotypic changes of the bacteria that cause conversion from a typical nonmucoid to a mucoid form in the CF lung. Mucoid conversion is indicative of overproduction of a capsule-like polysaccharide called alginate. The alginate-overproducing (Alg(+)) mucoid phenotype seen in the CF isolates is extremely unstable. Low oxygen tension growth of mucoid variants readily selects for nonmucoid variants. The switching off mechanism has been mapped to the algT/U locus, and the molecular basis for this conversion was partially attributed to mutations in the algT/U gene itself. To further characterize molecular changes resulting in the unstable phenotype, an isogenic PAO1 derivative that is constitutively Alg(+) due to the replacement of the mucA with mucA22 (PDO300) was used. The mucA22 allele is common in mucoid CF isolates. Thirty-four spontaneous nonmucoid variants, or sap (suppressor of alginate production) mutants, of PDO300 were isolated under low oxygen tension. About 40% of the sap mutants were rescued by a plasmid carrying algT/U (Group A). The remaining sap mutants were not (Group B). The members of Group B fall into two subsets: one similar to PAO1, and another comparable to PDO300. Sequence analysis of the algT/U and mucA genes in Group A shows that mucA22 is intact, whereas algT/U contains mutations. Genetic complementation and sequencing of one Group B sap mutant, sap22, revealed that the nonmucoid phenotype was due to the presence of a mutation in PA3257. PA3257 encodes a putative periplasmic protease. Mutation of PA3257 resulted in decreased algT/U expression. Thus, inhibition of algT/U is a primary mechanism for alginate synthesis suppression.
