RESUMEN
Nosocomial infections are acquired during hospital treatment or in a hospital environment. One such infecting agent, Escherichia coli, harbours many virulence genes that enable it to become pathogenic, causing damage to the host. The mechanism of the E. coli virulence factors provenance to cause infection in host environments is not clearly elucidated. We investigated the virulence and pathogenicity of E. coli affected by the host environment. For this, blood (n = 78) and faecal (n = 83) E. coli isolates were collected from patients with and without sepsis, respectively, who had been admitted to the intensive care unit. The E. coli genomic DNA was isolated; the phylogenetic grouping was conducted by triplex PCR. The occurrence of nine virulence genes among the all the isolates was confirmed by gene-specific PCR. The prevalence of E. coli in blood isolates was more in phylogenetic groups B2 and D compared to groups A and B1. However, in faecal isolates, there was no significant difference. The prevalence of adhesin and toxin (papG, sfa, afa, cnf1, hlyA) genes was higher in blood compared to faecal E. coli isolates. However, the prevalence of aer, traT and PAI was similar as well as higher among both of these groups. These observations indicate a role of external environment (hospital setting) on host susceptibility (development of infection) in the faecal E. coli isolates, thereby making the patient prone to a sepsis condition.
RESUMEN
The prevalence of the tcpC in the blood Escherichia coli isolates collected from the sepsis patients admitted to the intensive care unit was investigated for the first time. The blood and faecal samples were collected from sepsis and nonsepsis patients, respectively. The prevalence of the tcpC and phylogroups was confirmed by gene-specific PCR. The occurrence of the tcpC in the blood E. coli isolates from sepsis patients was significantly higher than the faecal isolates. The higher prevalence of blood E. coli isolates among the pathogenic groups (B2, D) compared to the commensal groups (A, B1) suggests tcpC as a prospective new virulence marker for sepsis.
RESUMEN
Innate and adaptive immunity play a significant role in urogenital infections. Innate immunity is provided by the epithelial cells and mucus lining along with acidic pH, which forms a strong physical barrier against the pathogens in female reproductive tract. Cells of innate immune system, antimicrobial peptides, cytokines, chemokines and adaptive immunity in the reproductive tract are evolved during infection, and a pro-inflammatory response is generated to fight against the invading pathogen Trichomonas vaginalis, a primary urogenital protozoa, the etiological agent of human trichomoniasis, a curable sexually transmitted infection. The involvement of the urogenital tract by other protozoal infections such as P. falciparum, Trypanosoma, Leishmania, Toxoplasma, Entamoeba histolytica and Acanthamoeba infection is rarely reported. Trichomonas induce pro-inflammatory and immunosuppressive responses in infected subjects. Multifactorial pathogenic mechanisms including parasite adherence, cysteine proteases, lipophosphoglycan, free radical, cytokine generation and Toll-like receptors appear to interplay with the induction of local and systemic immune responses that ultimately determine the outcome of the infection. However, the involvement of urogenital pathogen-specific immune mechanisms and effect of normal local resident flora on the outcome (symptomatic vs. asymptomatic) of infection are poorly understood. Moreover, immune interactions in trichomoniasis subjects co-infected with bacterial and viral pathogens need to be elucidated.
