Susceptibilidad a desinfectantes de Trichomonas vaginalis y Escherichia coli presentes en fómites experimentales

Las enfermedades infecciosas provocadas por microorganismos patógenos se pueden transmitir directa o indirectamente. El protozoario Trichomonas vaginalis y la bacteria Escherichia coli son patógenos para el ser humano que pueden ser trans - mitidos por fómites. Existe una gama de productos para desinfectar, pero no existe información sobre el efecto completo de su eficacia en forma comparativa sobre bacterias o tricomonas en interacción con diferentes tipos de materiales. En este trabajo, se analizó el efecto de algunos desinfectantes sobre la viabilidad de Escherichia coli cepa 055 y Trichomonas vaginalis cepa GT-21, depositadas sobre diferentes tipos de materiales. Se diseñó un sistema in vitro con fómites experi - mentales para estudiar el efecto sobre estos patógenos. Se encontró que las tricomonas permanecen viables hasta ocho horas, y las bacterias hasta 24 horas en madera, papel, tela y plástico. Sin embargo, ambos microorganismos sobreviven solamente entre 1 y 4 horas sobre vidrio o metal. Tanto las bacterias como las tricomonas son inhibidas por los desinfec - tantes probados, siendo los más efectivos el etanol a 70% y el producto comercial Lysol ®

Plasma membrane damage repair is mediated by an acid sphingomyelinase in Entamoeba histolytica.

Entamoeba histolytica is a pathogen that during its infective process confronts the host defenses, which damages the amoebic plasma membrane (PM), resulting in the loss of viability. However, it is unknown whether amoebic trophozoites are able to repair their PM when it is damaged. Acid sphingomyelinases (aSMases) have been reported in mammalian cells to promote endocytosis and removal of PM lesions. In this work, six predicted amoebic genes encoding for aSMases were found to be transcribed in the HM1:IMSS strain, finding that the EhaSM6 gene is the most transcribed in basal growth conditions and rendered a functional protein. The secreted aSMase activity detected was stimulated by Mg+2 and inhibited by Co+2. Trophozoites that overexpress the EhaSM6 gene (HM1-SM6HA) exhibit an increase of 2-fold in the secreted aSMase activity. This transfectant trophozoites exposed to pore-forming molecules (SLO, Magainin, β-Defensin 2 and human complement) exhibited an increase from 6 to 25-fold in the secreted aSMase activity which correlated with higher amoebic viability in a Ca+2 dependent process. However, other agents that affect the PM such as hydrogen peroxide also induced an increase of secreted aSMase, but to a lesser extent. The aSMase6 enzyme is N- and C-terminal processed. Confocal and transmission electron microscopy showed that trophozoites treated with SLO presented a migration of lysosomes containing the aSMase towards the PM, inducing the formation of membrane patches and endosomes in the control strain. These cellular structures were increased in the overexpressing strain, indicating the involvement of the aSMase6 in the PM injury repair. The pore-forming molecules induced an increase in the expression of EhaSM1, 2, 5 and 6 genes, meanwhile, hydrogen peroxide induced an increase in all of them. In all the conditions evaluated, the EhaSM6 gene exhibited the highest levels of induction. Overall, these novel findings show that the aSMase6 enzyme from E. histolytica promotes the repair of the PM damaged with pore-forming molecules to prevent losing cell integrity. This novel system could act when encountered with the lytic defense systems of the host