Crystalline Keratopathy Research Articles

Fusarium Keratitis 3 Weeks After Healed Corneal Cross-Linking

To report a case of Fusarium solani keratitis after corneal cross-linking (CXL) treatment. A 23-year-old woman presented with corneal ulcer 4 weeks following a CXL procedure. Microbiological studies revealed Fusarium species as the etiological pathogen. Fusarium species may cause infectious crystalline keratopathy after corneal CXL treatment.

Infectious Crystalline Keratopathy Caused by Streptococcus Abiotrophia defectiva

To report the first case of Streptococcus Abiotrophia defectiva-associated crystalline keratopathy. An 83-year-old woman underwent penetrating keratoplasty for pseudophakic bullous keratopathy in the OD. Ten months after surgery, the patient presented with decreased visual acuity in the OD. Slit-lamp examination showed crystalline keratopathy. Corneal scrapings were negative, and the patient was treated empirically with 2 fortified antibiotics (ciprofloxacin and vancomycin). Despite these treatments, the surface of the infiltrate increased and corneal regrafting was performed 6 weeks later. The excised prior graft was evaluated microbiologically [culture and polymerase chain reaction (PCR)] and histopathologically. In the explanted corneal graft, cultures grew Streptococcus A. defectiva, and its DNA was demonstrated by broad-range PCR (16S ribosomal DNA). A. defectiva can be a causative organism of infectious crystalline keratopathy. Risk factors may include long-term corticosteroid use and prior corneal transplantation. The present case confirms that PCR can be a useful technique in the diagnosis of deep infectious keratitis.

Zwei Fälle von schneeflockenartiger Keratitis

Patient 1 developed snowflake-like keratitis without inflammatory response in a decompensated corneal allograft. Patient 2, who had a history of repeated corneal grafting, also developed corneal opacification which initially appeared thread-like but quickly expanded. In both patients regrafting was necessary. Histological examination of the excised corneas demonstrated dense populations of Gram-positive bacteria in the interlamellar spaces. A surrounding inflammatory reaction was lacking, which is typical for infectious crystalline keratopathy (ICK).

Development of crystalline keratopathy after intravitreal injections of pegaptanib

Anti-VEGF pharmacotheraphy has recently become popular for the treatment of retinal vascular diseases due to the stabilization or even improvement of vision with these agents. Herein, we report a rare corneal complication of anti-VEGF treatment with pegaptanib (Macugen; OSI Inc. and Pfizer Inc., New York, NY, USA).

The effect of topical ocular corticosteroid administration in dogs with experimentally induced latent canine herpesvirus-1 infection

Recurrent herpes simplex virus-1 (HSV-1) ocular infection is a frequent cause of morbidity and blindness. Factors that trigger viral reactivation are poorly understood and the role of topical ocular corticosteroid administration in the development of recurrent HSV-1 ocular disease is not clear. Clinical reports and epidemiological studies suggested topical corticosteroids may reactivate latent HSV-1 and result in recrudescent ocular disease; however, experimental studies to establish this causal relationship produced inconsistent results. The previous experimental studies were performed by infecting unnatural host species with HSV-1 and aspects of viral behavior and reactivation within these animals may differ from the host for which the virus is adapted. The purpose of the study reported here was to determine if topical ocular corticosteroid administration results in viral reactivation and recrudescent ocular disease in a host-adapted pathogen animal model of HSV-1 recurrent ocular disease. Canine herpesvirus-1 (CHV-1) is a corticosteroid-sensitive alphaherpesvirus that is biologically related to HSV-1 and induces similar ocular lesions in canids during recurrent infection. A randomized, masked, placebo-controlled, crossover study was performed. Primary ocular CHV-1 infection was experimentally induced in mature specific pathogen-free beagles by topical ocular inoculation and the presence of reactivatable latency was later confirmed by administration of an immunosuppressive dosage of systemic corticosteroid to the dogs. Twelve months following experimental CHV-1 reactivation, dogs were administered either topical ocular prednisolone acetate (1.0% ophthalmic suspension, one drop in both eyes, four times daily) or placebo (artificial tear solution, one drop in both eyes, four times daily) for 28 days. After a 14 day washout period, the treatment groups were reversed and study agents administered for an additional 28 days. Ophthalmic examinations, in vivo ocular confocal microscopy, real-time quantitative CHV-1 polymerase chain reaction assays, and CHV-1 serum neutralization antibody titers were performed at regular intervals throughout the study. Viral reactivation was not detected in dogs administered topical ocular prednisolone or placebo as determined by clinical ocular disease recrudescence, in vivo ocular confocal microscopic findings, ocular viral shedding, and serologic response. Similar to other animal models of recurrent HSV-1 ocular infection, the behavior of latent CHV-1 in dogs may differ from HSV-1 in humans; however, results of the present study suggest administration of topical ocular prednisolone at the evaluated drug concentration, dosing frequency, and treatment duration is not likely to result in detectable reactivation of latent CHV-1 in experimentally infected dogs. This may be attributed to insufficient systemic absorption of locally administered corticosteroid to reactivate latent virus and produce recurrent disease. Crystalline corneal opacities that were apparently not associated with viral reactivation were detected by clinical examination and in vivo confocal microscopy in two dogs during topical ocular prednisolone administration. The crystalline keratopathy may have resulted from corneal degeneration associated with metaherpetic disease, corticosteroid administration, or a combination of both factors.

Crystal-Storing Histiocytosis and Crystalline Keratopathy Caused by Monoclonal Gammopathy of Undetermined Significance

The purpose of this study was to report the occurrence of crystalline keratopathy and of orbital infiltrative disease resulting from crystal-storing histiocytosis (CSH) in a patient with monoclonal gammopathy of undetermined significance. The authors conducted a review of a medical record and immunohistopathologic studies. A 66-year-old man presented with a 3-year history of unilateral progressive ptosis, proptosis, and external ophthalmoplegia. Magnetic resonance imaging showed orbital fat expansion and extraocular muscle thickening with gadolinium enhancement. The patient also had bilateral crystalline keratopathy and had undergone penetrating keratoplasty in one eye. The urine and serum showed elevated levels of immunoglobulin, but the bone marrow aspirate was normal. The systemic evaluation was consistent with monoclonal gammopathy of undetermined significance. An orbital fat biopsy revealed histiocytes engorged with lambda light chain crystals. The corneal stroma also showed positive immunostaining for lambda light chains. The patient was diagnosed with orbital CSH and with lambda light chain crystalline keratopathy. CSH is characterized by the accumulation of reactive histiocytes filled with immunoglobulin crystals in various tissues and is frequently associated with systemic hyperglobulinemic states. For unknown reasons, in this patient, a systemic immunologic disorder led to lambda light chain abnormalities with histiocyte infiltration of the orbit and corneal deposition. Although CSH is rare, it should be part of the differential diagnosis of orbital infiltrative disease with or without crystalline keratopathy.

Infectious crystalline keratopathy

Abstract Purpose To provide the definition, clinical features, diagnosis and management of infectious crystalline keratopathy (ICK). Methods Personal experience, experimental study on ex‐vivo ICK and literature review Results ICK can be defined as microbial infection of the cornea in the absence of the host immune response. It can be caused by a variety of microbes including bacteria and fungi. It is characterised by corneal infiltrates in the form of branching or arborescent patterns of needles, snowflakes or fern shapes. This pattern is determined by the compactness of the corneal lamellae. Clinically there is minimal host inflammatory response although there can be areas of suppuration remote from the ICK. The epithelium is usually intact, symptoms are mild and it runs a chronic indolent course. Corneal hypoesthesia and corticosteroid use are risk factors. Diagnosis is based upon clinical examination in conjunction with careful history taking. The presence of branching crystalline deposits located in the stroma often near suture sites and following corneal surgery should raise suspicion. Intensive topical antibiotics, keratectomy of the affected site to excise lesion if possible, cessation of steroid medication or repeat corneal graft are aspects of management of ICK. Conclusion ICK is a rare but difficult to treat condition. Diagnosis is based on history and clinical features. Sample (scrape) or biopsy can be taken for culture and sensitivity of organisms involved. Treatment is difficult and surgery may be required to eliminate the infected locus. Commercial interest

Immunotactoid Microtubular Corneal Deposits in Bilateral Paraprotein Crystalline Keratopathy

To report an ultrastructurally distinct form of paraprotein crystalline keratopathy. Three corneas submitted from a single patient including one native cornea from each eye and a failed corneal graft from the right eye. Light microscopy, immunohistochemistry, immunofluorescence, and transmission electron microscopic examination were performed. The transmission electron microscopy showed "immunotactoid" extracellular microtubular deposits measuring >30 nm in diameter with a central lucent core. Immunotactoid keratopathy is a distinct type of paraprotein crystalline keratopathy associated with a monocolonal immunoglobulin G kappa light chain (IgGk) protein. Larger case series are needed to determine the clinical significance of this entity.

Polymicrobial Keratitis: Acanthamoeba and Infectious Crystalline Keratopathy

To report the early presentation, cause, and successful medical management of combined Acanthamoeba keratitis (AK) and infectious crystalline keratopathy (ICK). Interventional case series. Retrospective review of 111 AK patients diagnosed and managed at the University of Illinois Eye and Ear Infirmary between June 1, 2003 and November 30, 2008 for an additional diagnosis of infectious keratitis. Of 5 AK patients with microbiologic evidence of an additional bacterial keratitis during their active AK treatment, concomitant ICK developed in 3 patients. All patients were examined within 3 weeks of their AK diagnosis and were found to have characteristic signs and symptoms consistent with ICK. Bacterial culture results at the time of AK diagnosis were negative in 2 patients, but subsequent culture results were positive for Streptococcus oralis. Initial culture results demonstrated light growth of methicillin-sensitive Staphylococcus aureus in the remaining patient, who had received partial antibiotic treatment. Topical corticosteroids were used before diagnosis in 2 patients and were in use in only 1 patient after AK diagnosis. All infections resolved with medical therapy alone. One patient later required penetrating keratoplasty for visual rehabilitation. In patients with AK, ICK can develop early and without either the use of corticosteroids or a preexisting epithelial defect, inconsistent with previously suggested mechanisms and major risk factors for secondary infection. Combined AK and ICK may exhibit increased pathogenicity with the onset of severe, often new, pain and acceleration of localized tissue loss and resultant scarring. Although early recognition and aggressive medical treatment were successful in resolving the combined infections in our cases, Acanthamoeba coinfection, and perhaps endosymbiosis, should be considered in the evaluation and clinical management of AK, especially in those cases progressing atypically. Further research is needed to understand the precise mechanism of the introduction of coinfectious pathogens and their role in the pathogenicity of AK.

Laser corneal biofilm disruption for infectious crystalline keratopathy

Crystalline keratopathy can be successfully treated by the Nd:YAG laser. We present two cases of crystalline keratopathy managed this way. A 36-year-old female contact lens wearer presented with crystalline keratopathy following recent treatment with topical steroids and antibiotics for a corneal abscess. In this case crystalline keratopathy developed despite the intensive topical antibiotic treatment. A 55-year-old man with a history of acne rosacea, chronic myelomonocytic leukaemia, asthma and Crohn's disease presented with crystalline keratopathy following an episode of infectious keratitis. Treatment with the Nd:YAG laser to the area of involvement was instituted in both cases. Noticeable resolution occurred within days, with subsequent full recovery. No side-effects from the use of the Nd:YAG laser were noted. There have been only two cases previously reported using this treatment modality.

Infectious crystalline keratopathy and its management

Infectious crystalline keratopathy and its management

Infectious crystalline keratopathy and its management

Abstract Purpose Infectious crystalline keratopathy (ICK) is defined as microbial infection of the cornea in the absence of the host inflammatory response. It presents as slowly progressive crystalline opacities resembling needles, snowflakes or ferns and are filamentous or branching in pattern within the cornea stroma. Methods Pathogenesis: Streptococcus viridans is the most common cause of ICK but a range of fungi and bacteria have been isolated from cases of ICK. They are located within the corneal stroma within the interlamellar planes. The pattern of spread of bacteria within corneal tissue is determined by the compactness of the corneal stroma. Another common feature is reduced corneal sensation, abrogating the triple response reflex at the limbus and hence the lack of the host response. The diagnosis of ICK is made on history and examination as microbiological diagnosis by culture of scrapes is difficult. Histology of biopsy specimen confirms diagnosis. Results Medical treatment with broad spectrum topical anti‐microbial agents is initiated. Any concomitant use of topical steroids should be discontinued. If no resolution of infection occurs, surgery in the form of lamellar or penetrating keratoplasty or superficial keratectomy is required. The successful use of excimer laser therapeutic keratectomy and Nd:YAG laser in the treatment of ICK has been demonstrated in single case reports but these techniques need further evaluation. Conclusion The diagnosis of ICK is largely clinical. It is difficult to treat medically often requiring surgical intervention. Poor corenal sensation and steroid use are important predisposing factors.

Borrelia-associated Crystalline Keratopathy With Intracorneal Detection of Borrelia garinii by Electron Microscopy and Polymerase Chain Reaction

First report of a patient with Borrelia-associated crystalline keratopathy with intracorneal evidence of Borrelia garinii by polymerase chain reaction (PCR) and electron microscopy (EM). Report of a 67-year-old patient with medical history of recurrent iridocyclitis and arthritis presented with a bilateral, progressive, asymmetric crystalline keratopathy, which was particularly pronounced in the peripheral temporal superior cornea. After penetrating keratoplasty, crystalline keratopathy with stromal haziness recurred. Corneal regrafting was performed. The corneal specimen from the penetrating keratoplasty was examined by light and EM as well as by PCR. In the explanted corneal graft, as well as retrospectively in the corneal specimen from the first keratoplasty, spirochetelike bodies and fragments were detected by light and EM. Borrelia burgdorferi sensu lato DNA was demonstrated by broad-range (16S rDNA) PCR. A more precise identification as Borrelia garinii serotype 5 was possible by analyses of the flaB and ospA gene sequences. Borrelia-specific serological tests showed borderline titers in immunofluorescence and weak reaction in immunoblot, respectively. This case illustrates that borreliae must be considered as a cause of crystalline keratopathy; Borrelia-specific serological tests can be false negative; explanted cornea specimens of etiologically unclear crystalline keratopathy should be analyzed by EM or PCR for detection of pathogens; and prolonged antibiotic treatment might be effective to prevent progression or recurrence of the disease.

Phosphate and electrolyte content of topical steroid drops and potential clinical implications

The ocular surface is constantly bathed by tears, which provide nutrition and protection to the ocular surface epithelium. The milieu of the ocular surface, including the fluids and electrolytes are...

Gemella haemolysans Infectious Crystalline Keratopathy

Purpose To report a case of infectious crystalline keratopathy caused by Gemella haemolysans. Methods Observational case report. A 65-year-old woman underwent penetrating keratoplasty for contact lens-related Acanthamoeba keratitis and developed a nonhealing epithelial defect. Despite continued prophylaxis with topical gatifloxacin, small superficial stromal opacities were noted and cultured 6 months after penetrating keratoplasty. The opacities coalesced into a fine, crystalline keratopathy in the superficial stroma with persistent overlying epithelial defect. Results Culture results from corneal scraping showed more than 100 colonies of G. haemolysans. Topical vancomycin was instituted, with complete resolution of the crystalline keratopathy and epithelial defect over the next 2 months. Conclusions G. haemolysans can be a causative organism of infectious crystalline keratopathy. This infection can arise in a postkeratoplasty patient despite prophylaxis with a fourth-generation fluoroquinolone.

Infectious Crystalline Keratopathy Caused by Serratia marcescens

To report the case of a 70-year-old woman with Serratia infectious crystalline keratopathy. Case report. This is a report of a 70-year-old woman with a history of chronic open-angle glaucoma and trachoma with lagophthalmos, entropion, and trichiasis in both eyes who developed crystalline keratopathy after penetrating keratoplasty and cataract extraction in the right eye followed up with treatment with long-term topical steroids. Ten months after the initial penetrating keratoplasty and cataract extraction, the patient had decreased visual acuity, intense pain, and tearing in the right eye. Corneal cultures showed Serratia marcescens. Topical steroids were discontinued, and treatment with tobramycin and vancomycin ophthalmic solution every hour was initiated. Despite 1 week of aggressive therapy, there was an increase in corneal infiltrate, epithelial defects, and melting, which eventually involved the peripheral recipient cornea. Therapeutic penetrating keratoplasty, debridement of the peripheral cornea, and amniotic membrane transplantation were performed. Antibiotic agents were used postoperatively. There has been no evidence of recurrent infection. The best-corrected visual acuity improved to 6/15 at the 6-month follow-up period after the second intervention. S. marcescens may cause infectious crystalline keratopathy after penetrating keratoplasty in patients treated with long-term topical steroids. Therapeutic penetrating keratoplasty, surgical debridement, and amniotic membrane transplantation may be necessary when the clinical response to intensive medical treatment is inadequate.

Infectious Crystalline Keratopathy Caused by Gemella haemolysans

To report a novel case of infectious crystalline keratopathy after penetrating keratoplasty caused by Gemella haemolysans. Observational case report. Patient notes and literature review. A 51-year-old woman presented with the clinical picture of infectious crystalline keratopathy 18 months after a second penetrating keratoplasty was performed for corneal decompensation secondary to recurrent herpes simplex infection. Corneal biopsy yielded a heavy growth of G. haemolysans. Initial treatment was made up of frequent topical vancomycin 0.5% and was later changed to topical cefuroxime 5% and ofloxacin 0.3%. Snellen visual acuity after complete resolution of the keratitis was 6/60 as a result of a residual corneal scar. Gemella haemolysans may be an etiologic agent in infectious crystalline keratopathy. A corneal biopsy may be diagnostic but may also promote healing by allowing direct access of antibiotics to deep-seated infected tissue and by altering the growth environment of the organism.

Gemella haemolysans Infectious Crystalline Keratopathy

To report a case of infectious crystalline keratopathy caused by Gemella haemolysans. Observational case report. A 65-year-old woman underwent penetrating keratoplasty for contact lens-related Acanthamoeba keratitis and developed a nonhealing epithelial defect. Despite continued prophylaxis with topical gatifloxacin, small superficial stromal opacities were noted and cultured 6 months after penetrating keratoplasty. The opacities coalesced into a fine, crystalline keratopathy in the superficial stroma with persistent overlying epithelial defect. Culture results from corneal scraping showed more than 100 colonies of G. haemolysans. Topical vancomycin was instituted, with complete resolution of the crystalline keratopathy and epithelial defect over the next 2 months. G. haemolysans can be a causative organism of infectious crystalline keratopathy. This infection can arise in a postkeratoplasty patient despite prophylaxis with a fourth-generation fluoroquinolone.

Detection of Streptococcus Species by Polymerase Chain Reaction in Infectious Crystalline Keratopathy

Investigation of a positive polymerase chain reaction (PCR) for Streptococcus species from an excised cornea of a patient with infectious crystalline keratopathy. Samples microdissected from corneal intrastromal aggregates present in infectious crystalline keratopathy were subjected to PCR for 3 primer pairs respectively specific for Streptococcus, Staphylococcus, and several kinds of fungi. The PCR detected DNA from Streptococcus but not from Staphylococcus or fungi. Direct sequencing of the PCR products showed that the PCR products had the highest identity (99.8%) with Streptococcus mitis and Streptococcus gordoni, indicating that these species were the most probable causes of infectious crystalline keratopathy in this patient. Our findings suggest that PCR provides a good adjunct technique in the diagnosis of corneal infection.

Corneal injury by wild taro

We report a case of crystalline keratopathy caused by Alocasia macrorrhiza. The diagnosis was made based on the observation of needle-like crystals in the corneal stroma following injury to that eye. The condition resolved in 3 months with the disappearance of the crystals confirmed by follow-up confocal microscopy.