Treatment of bacterial keratitis remains almost entirely dependent on topical antimicrobials. In spite of their efficacy, clinical outcome remains unpredictable, and other forms of treatment are needed.
Staphylococcus aureus is a prominent cause of keratitis and not uncommonly is associated with poor outcomes and recurrent disease.
1 Use of a bacterial marker to differentiate patients at presentation into those who are likely to have good or poor outcomes would be helpful in stratifying patients and modifying treatment. Not all strains of
S. aureus associated with keratitis are the same, and various strains may contain genetic loci that encode virulence factors. One such locus encodes Panton-Valentine leukocidin (PVL), an exotoxin comprising LukF-PV and LukS-PV protein subunits encoded by genes on a bacteriophage lysogenized within the
S. aureus chromosome. The PVL subunits assemble into cytolytic pore-forming octamers on susceptible cells.
Zaidi et al.
2 used a murine and tissue culture model to investigate the effects of PVL. Because different strains of
S. aureus may carry different virulence factors, they used several strains including meticillin resistant and sensitive strains. In addition, because low levels of PVL stimulate an immune response that may affect outcome, they included strains overproducing PVL. They found that inactivation of PVL caused reduced pathology and bacterial counts, while stains overproducing PVL caused increased bacterial burdens.
2 They also noted that PVL was associated with increased clinical morbidity and cellular disease.
2 This is consistent with the increased morbidity recently reported in patients with
S. aureus PVL-positive keratitis.
3 Importantly, they found that although there was inconsistency between strains, topical antibody to PVL resulted in reduced bacterial levels and disease.
2 Topical application of antibody to PVL, therefore, needs to be considered as a potential treatment for patients with
S. aureus keratitis and is worthy of human trials.