Patogénesis molecular, epidemiología y diagnóstico de Escherichia coli enteropatógena

Abstract

Enteropathogenic Escherichia coli (EPEC) is a leading cause of diarrhea in infants less than two years of age in developing countries. To induce diarrhea EPEC uses several virulence factors acting on a still unknown and mysterious mechanism. The hallmark of EPEC infection is a histological intestinal alteration known as the attaching and effacing (A/E) lesion. The bacterium attaches intimately to the enterocyte and induces assembly of cytoskeleton intracellular actin on the cellular surface. Rearrangements of the actin cytoskeleton form a pedestal-like structure where bacterium tightly cups the cells, leading to degeneration of brush border microvilli. Although the mechanism of EPEC-induced pedestal formation has been dissected in detail, the overall mechanism of diarrhea is still obscure. It is believed that EPEC-mediated secretory diarrhea is related to a) intestinal microvilli effacement, b) massive loss of intracellular ions into the intestinal milieu and c) secretion of an EPEC enterotoxin. Epidemiological studies conducted in developing countries have shown that EPEC is one of the main bacteria frequently isolated from children with diarrhea, causing high morbidity and mortality rates. The microbiological diagnosis of EPEC-induced disease is performed with analytic methodologies different from those used by the standard microbiology laboratory, the most relevant being: a) serotypification, b) the adherence assay, c) FAS test, and d) the specific detection of virulence-involved genes (bfpA and eae genes) using molecular biology techniques. The purpose of this review is to update the most recent findings regarding the molecular pathogenesis of EPEC, its epidemiology in Mexico as well as other developing countries, and also the developed methodology for the diagnosis of EPEC infection.

Surveillance of Diarrheagenic Escherichia coli Strains Isolated from Diarrhea Cases from Children, Adults and Elderly at Northwest of Mexico

“…Strains were classified as typical if they carried the intimin eae gene, and bfp A, whereas atypical strains encodes eae but not bfp A (Vidal et al, 2007). Our studies revealed that atypical EPEC strains ( n = 36) were significantly more prevalent ( p < 0.001) than typical strains ( n = 17).…”

Frecuencia, susceptibilidad antimicrobiana y patrón de adherencia de Salmonella enterica aislada de carne de pollo, res y cerdo de la Ciudad de México

“…El efecto "in vivo" a nivel intestinal es muy semejante a lo observado "in vitro" con células HEp-2, ya que estas células re-arreglan sus filamentos de actina facilitando la penetración inducida por Salmonella, en forma similar a como ocurre en el hospedero infectado 42 y porque la bacteria reconoce los receptores de manosa a los que se adhiere de la misma forma que en los enterocitos 43 . Este proceso, de manera semejante a otras enterobacterias como sucede con Escherichia coli enteropatógena, permite la acumulación de la actina del citoesqueleto en la región apical de la célula, hasta formar una estructura de tipo "pedestal" y causar la eliminación de las microvellosidades intestinales 44 . Althouse y cols.…”

Mecanismos de virulencia de Escherichia coli enteropatógena

“…La bacteria entra en contacto con la célula mediante un flagelo y el pili tipo IV (BFP: bundle-forming pilus), que tienen como función la auto-agregación bacteriana y la adherencia a la célula mediante la formación de microcolonias 17,18 26 . Estas proteínas efectoras contribuyen al daño celular mediante la formación de conductos o filamentos (EspA, EscF) 27 y poros para la translocación de proteínas en la membrana del enterocito (EspB, EspD) 28 , cambios del potencial de membrana de la mitocondria (proteína asociada a la mitocondria Map: mitochondria-associated protein), formación transitoria de filopodios mediante la activación de GTPasas 29, 30 , reorganización y pérdida de la nucleolina para bloquear el proceso del ARNr (EspF) 31 y la alteración de los microtúbulos en algunas células epiteliales (EspG) 32 (Figura 1).…”