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Infection and Immunity, June 2003, p. 3116-3124, Vol. 71, No. 6
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.6.3116-3124.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Relationship of plcR-Regulated Factors to BacillusEndophthalmitis Virulence

Michelle C. Callegan,1,2,3,4* Scott T. Kane,1 D. Clay Cochran,1 Michael S. Gilmore,1,2,3,4 Myriam Gominet,5 and Didier Lereclus5

Department of Ophthalmology,1 Department of Microbiology and Immunology,2 Oklahoma Center for Neuroscience, University of Oklahoma Health Sciences Center,3 Molecular Pathogenesis of Eye Infections Research Center, Dean A. McGee Eye Institute, Oklahoma City, Oklahoma,4 Unite de Biochimie Microbienne, Institut Pasteur, Paris cedex, France5

Received 11 December 2002/ Returned for modification 21 February 2003/ Accepted 10 March 2003

The explosive, destructive course of Bacillus endophthalmitis has been attributed to the production of toxins during infection. In this study we analyzed the contribution of toxins controlled by the global regulator plcR to the pathogenesis of experimental Bacillus endophthalmitis. Isogenic plcR-deficient mutants of Bacillus cereus and Bacillus thuringiensis were constructed by insertional inactivation of plcR by the kanamycin resistance cassette, aphA3. Rabbit eyes were injected intravitreally with approximately 100 CFU of wild-type B. cereus or B. thuringiensis or a plcR-deficient mutant. The evolution of endophthalmitis resulting from each plcR-deficient mutant was considerably slower than that caused by each wild-type strain. Retinal function was not eliminated until 42 h postinfection in rabbits with endophthalmitis caused by the plcR-deficient mutants, whereas wild-type infections resulted in a complete loss of retinal function within 18 h. The intraocular inflammatory cell influx and retinal destruction in plcR-deficient endophthalmitis approached the severity observed in wild-ype infections, but not until 36 h postinfection. Gross and histological examinations of eyes infected with plcR mutants demonstrated that the anterior and posterior segment changes were muted compared to the changes observed in eyes infected with the wild types. The loss of plcR-regulated factors significantly attenuated the severity of Bacillus endophthalmitis. The results therefore suggest that plcR may represent a target for which adjunct therapies could be designed for the prevention of blindness during Bacillus endophthalmitis.

* Corresponding author. Mailing address: Department of Ophthalmology DMEI 418, 608 Stanton L. Young Blvd., Oklahoma City, OK 73104. Phone: (405) 271-1084. Fax: (405) 271-8781. E-mail: michelle-callegan{at}ouhsc.edu.

Editor: D. L. Burns

Infection and Immunity, June 2003, p. 3116-3124, Vol. 71, No. 6
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.6.3116-3124.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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