Virulence factor profiles and antimicrobial susceptibilities of ocular bacillus isolates.

Bacillus causes one of the most rapidly blinding intraocular infections: endophthalmitis. In this study, Bacillus spp. were isolated from ocular infection cases, taxonomically characterized by riboprint analysis, and screened for the presence of putative virulence factors. The ability of these isolates to kill retinal and corneal cells was examined, as were antibiotic susceptibility profiles. The majority of isolates belonged to the B. cereus taxonomic group of microorganisms and were identified as B. cereus (53%) or B. thuringiensis (26%). Toxins were identified in most B. thuringiensis and B. cereus isolates. Most B. cereus and B. thuringiensis killed corneal and retinal cells within 6 h. All isolates were susceptible to most antibiotics tested, with quinolones and vancomycin being the most potent. These findings represent the first report of B. thuringiensis as an important ocular pathogen, demonstrates the potential ocular toxicity of B. cereus and B. thuringiensis isolates, and identifies antibiotics whose efficacy against Bacillus were superior to those used clinically.

Bacillus endophthalmitis: roles of bacterial toxins and motility during infection.

PURPOSE: Bacillus endophthalmitis is a highly explosive infection of the eye that commonly results in rapid inflammation and vision loss, if not loss of the eye itself, within a few days. Quorum-sensing-controlled toxins are essential to virulence during infection. Another unique characteristic of this disease is the ability of Bacillus to replicate rapidly and migrate to all parts of the eye. This study was conducted to determine the combined roles of toxins and motility during Bacillus endophthalmitis. METHODS: Rabbit eyes were injected intravitreally with approximately 100 cfu of wild type, nonmotile, or nonmotile/quorum-sensing-deficient Bacillus thuringiensis. Infection courses were analyzed by biomicroscopy, histology, electroretinography, and quantitation of bacteria and inflammatory cells. RESULTS: Infection with wild type B. thuringiensis resulted in complete retinal function loss by 18 hours after infection, whereas nonmotile B. thuringiensis infections required 30 hours to achieve a reduction of >90% in retinal function. Further attenuation of infection resulted from infection with the nonmotile/quorum-sensing-deficient B. thuringiensis strain, with approximately 90% retinal function loss occurring at 36 hours. Overall, the nonmotile and nonmotile/quorum-sensing-deficient mutants were significantly less virulent than wild-type B. thuringiensis. CONCLUSIONS: The results demonstrate that, in addition to quorum-sensing-controlled toxin production, bacterial migration within the eye contributed to the rapidly fulminant and destructive course of Bacillus endophthalmitis. Motility and quorum-sensing may therefore represent possible targets for the development of therapies designed to attenuate the devastating effects of Bacillus in the eye during endophthalmitis.

Contribution of membrane-damaging toxins to Bacillus endophthalmitis pathogenesis.

Membrane-damaging toxins are thought to be responsible for the explosive clinical course of Bacillus endophthalmitis. This study analyzed the contribution of phosphatidylinositol-specific phospholipase C (PI-PLC) and phosphatidylcholine-specific phospholipase C (PC-PLC) to the pathogenesis of experimental Bacillus endophthalmitis. Isogenic mutants were constructed by insertion of lacZ into Bacillus thuringiensis genes encoding PI-PLC (plcA) and PC-PLC (plcB). Rabbit eyes were injected intravitreally with 2 log(10) CFU of strain BT407 (wild type), the PI-PLC mutant (BTplcA::lacZ), or the PC-PLC mutant (BTplcB::lacZ). The rates of decrease in retinal responses of eyes infected with the isogenic mutants were similar to that of wild type, with all infections resulting in elimination of retinal function by 18 h. Strain BT407 caused a significant increase in the latency of retinal responses at 6 h, but strains BTplcA::lacZ and BTplcB::lacZ did not. All strains elicited significant inflammatory cell influx into the anterior chamber by 12 h. Histologically, eyes infected with each strain were indistinguishable throughout the infection course. In this model, neither PI-PLC nor PC-PLC had an effect on the course or severity of experimental Bacillus endophthalmitis. Alterations in retinal responses early in infection may mark the beginnings of specific photoreceptor or glial cell dysfunction.

Molecular mechanisms of Bacillus endophthalmitis pathogenesis.

Bacillus endophthalmitis is one of the most devastating intraocular infections, frequently resulting in significant vision loss, if not loss of the eye itself, in only a few days. This review summarizes recent research focused on characterizing the interactions between Bacillus and the host response during endophthalmitis. Analyses of the contribution of Bacillus toxins and cell wall components, and the behavior of the organism during progressive disease are discussed. A better understanding of the host/pathogen interactions occurring during endophthalmitis is critical for the development of novel therapeutic agents designed to impede the progression of infection and protect vision.