genospecies 2 of the A. baumannii complex was associated with greater resistance to antibiotics and higher mortality among bacteremic patients, compared with other genospecies, especially genospecies 13TU. These findings emphasize the need to focus on genospecies to better understand the pathogenesis and epidemiology of infections caused by the A. baumannii complex.
Bevacizumab may reduce intra- and postoperative hemorrhage in diabetic vitrectomy with silicone oil infusion. Increased subretinal bleeding are potential complications.
Acinetobacter spp. have emerged as important nosocomial and multidrug-resistant pathogens in the last decade. A. calcoaceticus, A. baumannii, Acinetobacter genospecies 3, and Acinetobacter genospecies 13TU are genetically closely related and are referred to as the A. calcoaceticus-A. baumannii complex (ACB complex). Distinct Acinetobacter spp. may be associated with differences in antimicrobial susceptibility, so it is important to identify Acinetobacter spp. at the species level. We developed a microsphere-based array that combines an allele-specific primer extension assay and microsphere hybridization for the identification of Acinetobacter spp. This assay can discriminate the 13 different Acinetobacter spp. in less than 8.5 h, and it has high specificity without causing cross-reactivity with 14 other common nosocomial bacterial species. The sensitivity of this assay was 100 A. baumannii cells per ml of blood, and it could discriminate multiple species in various mixture ratios. The developed assay could differentiate clinical Acinetobacter spp. isolates with a 90% identification rate. The antimicrobial susceptibility test showed that A. baumannii isolates were resistant to most antimicrobial agents other than imipenem, while the genospecies 3 and 13TU isolates were more susceptible to most antimicrobial agents, especially ciprofloxacin and ampicillinsulbactam. These results supported the idea that this assay possibly could be applied to clinical samples and provide accurate species identification, which might be helpful for clinicians when they are treating infections caused by Acinetobacter spp.
Human CMV (HCMV) is an important pathogen that causes widespread diseases in immunocompromised individuals. Among the opportunistic HCMV infections, HCMV retinitis is most common in transplant recipients and AIDS patients. It often leads to blindness if left untreated. The question as to how HCMV infection causes retinal pathogenesis remains unresolved. Here, we report that viral immediate-early gene product 2 (IE2), but not IE1, up-regulates the Fas ligand (FasL) expression in HCMV-infected human retinal pigment epithelium cells. Increased secretion of FasL from virally infected cells into cultured medium was observed upon HCMV infection. The capability of such cell-free medium to induce apoptosis of Fas (CD95)-expressing Jurkat cells further implies that Fas-FasL interaction might mediate cell death in the lesion of HCMV retinitis. To support this idea, we observed augmented soluble FasL levels in vitreous from AIDS patients with HCMV retinitis as compared with that from AIDS patients without HCMV infection. In addition, by in situ hybridization and immunohistochemistry, we detected enhanced signals of FasL, the existence of viral IE Ags and apoptotic cells at the same sites in the lesion of HCMV-infected retina. These results strongly suggest that IE2 induction of FasL expression in human retina might be an important event that takes place in the early stage of infection and finally leads to visual loss in individuals affiliated with HCMV retinitis.
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