Letters to the Journal

Infectious Crystalline Keratopathy Caused by Mycobacterium fortuitum and Pseudomonas aeruginosa

Atypical microbial keratitis refers to corneal infections caused by micro-organisms not commonly encountered in clinical practice. Unlike infections caused by common bacteria, cases of atypical microbial keratitis are often associated with worse clinical outcomes and visual prognosis. This is due to the challenges in the identification of causative organisms with standard diagnostic techniques, resulting in delays in the initiation of appropriate therapies. Furthermore, due to the comparatively lower incidence of atypical microbial keratitis, there is limited literature on effective management strategies for some of these difficult to manage corneal infections. This review highlights the current management and available evidence of atypical microbial keratitis, focusing on atypical mycobacteria keratitis, nocardia keratitis, achromobacter keratitis, and pythium keratitis. It will also describe the management of two uncommonly encountered conditions, infectious crystalline keratopathy and post-refractive infectious keratitis. This review can be used as a guide for clinicians managing patients with such challenging corneal infections.

Non-tuberculous mycobacteria are environmental, opportunistic pathogens that are increasingly being recognized as important causes of many human diseases. Among them, rapidly growing mycobacteria are the most notorious organisms causing infectious keratitis. Nontuberculous mycobacterial (NTM) keratitis commonly occurs after trauma or refractive surgery, and can masquerade as fungal, herpetic or amoebic keratitis. Therefore, the diagnosis is often delayed. Prolonged medical treatment and judicious surgical debridement are required in order to eradicate the pathogens. Combination therapy with aminoglycosides, macrolides and fluoroquinolones improves the prognosis and decreases the occurrence of drug resistance. However, regardless of the development of new diagnostic techniques and antimicrobials, NTM keratitis remains a clinical challenge for most ophthalmologists. In this article, we provide a concise introduction to the epidemiological features and clinical characteristics of NTM keratitis, and the modern diagnostic tools used for it. We also summarize the current concepts of prevention and treatment for this potentially devastating condition.

The nontuberculous (also called “atypical”) mycobacteria have become increasingly important causes of systemic as well as ocular morbidity in recent decades. All ocular tissues can become infected with these organisms, particularly in patients who are predisposed following ocular trauma, surgery, use of corticosteroids, or are immunocompromised. Because of their relative resistance to available antibiotics, multidrug parenteral therapy continues to be the mainstay of treatment of more serious ocular and adnexal infections caused by nontuberculous mycobacteria (NTM). Periocular cutaneous, adnexal, and orbital NTM infections remain rare and require surgical debridement and long-term parenteral antibiotic therapy. NTM scleritis may occur after trauma or scleral buckling and can cause chronic disease that responds only to appropriate antibiotic therapy and, in some cases, surgical debridement and explant removal. NTM infectious keratitis following trauma or refractive surgical procedures is commonly confused with other infections such as Herpes simplex keratitis and requires aggressive topical therapy and possible surgical debridement, particularly in those cases occuring after laser in situ keratomileusis. Only 18 cases of endophthalmitis due to NTM have been reported. Systemic and intraocular antibiotic therapy and multiple vitrectomies may be needed in NTM endophthalmitis; the prognosis remains poor, however. Disseminated NTM choroiditis in acquired immune deficiency syndrome patients with immune reconstitution during highly active anti-retroviral therapy is a rare infection that can present as a necrotizing chorioretinitis with dense vitritis, mimicking many other entities and needs to be recognized so that timely, life-saving treatment can be administered. Regardless of which ocular tissue is infected, all NTM ocular infections present similar challenges of recognition and of therapeutic intervention. We clarify diagnosis and delineate modern, effective therapy for these conditions.

A 63-year-old man developed infectious crystalline keratopathy (ICK) in his right eye 1 year after phacoemulsification. The white peripheral lesion was adjacent to the corneal phacoemulsification incision. Infiltrates in the form of creamy-white, midstromal branching, needle-like opacities without evidence of inflammatory cells were noted. A corneal biopsy by double lamellar flap was done and studied by 3 techniques: microbiological culture, stain, and polymerase chain reaction (PCR). Fungal and bacterial PCR were positive. A second sample was necessary to obtain a positive stain and culture. The DNA sequence analysis showed Candida parapsilosis and Staphylococcus aureus as the causal agents of the crystalline keratopathy. Treatment was started with amphotericin B 1% and cefazolin 6 times a day, and systemic voriconazole was recommended. This is the first reported case of ICK after cataract surgery. Polymerase chain reaction amplification and subsequent DNA typing were useful tools in detecting and identifying the ocular pathogens involved in this case.

To describe an outbreak of mycobacterial keratitis after laser in situ keratomileusis (LASIK), including the microbiologic investigation, clinical findings, treatment response, and outcome.

Retrospective, noncomparative, interventional case series.

Patients (n = 10) who underwent LASIK surgery between August 22 and September 4, 2000, and developed mycobacterial infection.

Patients were prospectively followed in relation to microbiologic investigation, clinical findings, treatment response, and outcome.

Most patients underwent bilateral simultaneous LASIK. Postoperative infection was signaled by the appearance of corneal infiltrates in the third postoperative week. The microbiologic workup was performed on cultures obtained either by direct scraping of the cornea or by lifting the flap. Medical therapy was instituted based on drug susceptibility testing. Surgical interventions such as corneal debridement and flap removal were performed during recurrences or when there was no satisfactory clinical response.

Cultures revealed Mycobacterium subspecies chelonae. Patients were treated with topical clarithromycin (1%), tobramycin (1.4%), and ofloxacin (0.3%). Oral clarithromycin (500 mg twice a day) was prescribed for those patients who did not respond clinically to topical treatment. Four eyes healed on this regimen. Flap removal was necessary in seven eyes.

This report highlights mycobacteria as an etiologic infectious agent after LASIK. Diagnosis can be difficult and is often delayed. The treatment mainstay is prolonged antibiotic therapy. Surgical debridement and flap removal may shorten the disease course.