PMC4998293_01
Clinical slit lamp examination of Actinomyces keratitis at the initial visit (A), after 12-week antibiotics treatments (B), after 1-week course with a new antibiotics regimen (C), and 1 month after penetrating keratoplasty (D). Red arrows indicate peripheral corneal opacity, black arrows indicate satellite infiltrates, and blue arrows indicate anterior chamber hypopyon.
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F1
Three months postoperatively, he developed peripheral corneal stromal opacities associated with a white, thin, cystic bleb, and conjunctival injection (Figure 1A). By this time, the corneal opacities had grown, and marked conjunctival injection and a moderate anterior chamber inflammatory reaction had developed (Figure 1B). His ocular conditions, however, worsened further and a peripheral epithelial defect with a diffuse peripheral whitish corneal stromal infiltrate associated with satellite infiltrates was observed (Figure 1C). Not only the size and depth of the peripheral corneal ulcer increased but also endothelium plaques and anterior chamber hypopyon were noted (Figure 1D).
Laboratory examinations of Actinomyces keratitis. Histopathologic analysis revealed filamentous, branching, gram-positive bacteria (black arrow) in the deep corneal stroma consistent with Actinomyces species with intense corneal inflammation, showing staining with hematoxylin and eosin stain (original magnification x400) (A) and acid fast stain (original magnification x400) (B). Polymerase chain reaction products from corneal specimens revealed that the causative organism in this patient was caused by 16S ribosomal deoxyribonucleic acid+, leukotoxin+, and fimbria-associated protein- Actinobacillus actinomycetemcomitans (C).
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F2
Actinomyces species (Figure 2A). Acid-fast staining was negative, suggesting Actinomyces rather than mycobacteria (Figure 2B). We performed molecular identification by PCR amplification and 16S rRNA gene sequencing analysis using deoxyribonucleic acid extracted from the corneal biopsy specimen (Figure 2C).