Twenty-one patients with syphilitic posterior uveitis were investigated retrospectively to study the disease spectrum, associations with neurosyphilis, and therapeutic implications. Ophthalmologic manifestations of syphilitic posterior uveitis are differentiated into acute and chronic uveitides. The several distinct acute uveitic syndromes are usually florid and are associated with early syphilis, with VDRL-positive syphilitic meningitis, and frequently with human immunodeficiency virus coinfection. The chronic posterior uveitides are often insidious, a manifestation of late syphilis, and associated commonly with subclinical neurosyphilis. All patients with acute cases and 54% of patients with chronic cases in our study received penicillin therapy appropriate for neurosyphilis. The frequent association of syphilitic posterior uveitis with neurosyphilis and the analogous spirochetal sequestration beyond the blood-brain and the blood-ocular barriers suggest that all patients with syphilitic posterior uveitis, irrespective of ocular disease intensity, should undergo evaluation of cerebrospinal fluid and be treated with penicillin regimens appropriate for neurosyphilis.

Objective: To evaluate patients with cytomegalovirus (CMV) retinitis treated with intravenous cidofovir for long-term outcomes.Design: Patients with CMV retinitis enrolled in a randomized, controlled clinical trial of intravenous cidofovir as treatment for retinitis were followed for long-term outcomes, including 21 patients initially enrolled in the deferral group who received cidofovir therapy after progression of retinitis.Setting: Thirteen tertiary care clinics specializing in AIDS care and ophthalmology.Participants: Fifty-eight patients with AIDS and small peripheral CMV retinitis lesions.Interventions: Cidofovir 5 mg/kg once weekly for 2 weeks followed by low-dose maintenance cidofovir therapy (3 mg/kg) in 35 patients or high-dose maintenance (5 mg/kg) in 23 patients.Main outcome measures: Time to progression of retinitis, drug toxicities.Results: Median time to progression of retinitis was 2.5 months. Median time to discontinuation of cidofovir because of intolerance was 6.6 months, and did not differ significantly between the two maintenance doses. Median time to discontinuation of cidofovir for intolerance other than probenecid reaction was 16.3 months for patients treated with low-dose maintenance and 5.0 months for patients treated with high-dose maintenance (P = 0.021). Proteinuria of 2+ or more occurred at a rate of 1.22/person year. In patients with sufficient follow-up to determine resolution of proteinuria, 89.9% of episodes resolved, and the median time to resolution was 20 days. Rates of probenecid intolerance and of cidofovir-associated uveitis were 0.35/person-year, and 0.20/person-year, respectively.

Ocular manifestations of histoplasmosis are rarely described at the time of initial infection. A late sequela of subclinical histoplasmal infection, called the presumed ocular histoplasmosis syndrome,1 is common and is characterized by bilateral, multifocal chorioretinal scarring; the disease syndrome is mainly known to ophthalmologists. Small, indolent inflammatory choroidal foci may persist for many years2 and can lead to subfoveal neovascularization and loss of central vision, often decades later. Substantial epidemiologic evidence suggests a causal relationship with previous histoplasmosis.3 The literature suggests that ocular involvement may, however, be overlooked in cases of acute disseminated histoplasmosis. Clinically recognized disseminated histoplasmosis occurs in <1 in 2000 infected individuals, mainly in patients with impaired cellular immunity.4 Progressive disseminated histoplasmosis is usually fatal without treatment but responds well to amphotericin B treatment (with the notable exception of histoplasmal endocarditis).5 A rare occurrence in immunocompetent infants and children, acute disseminated histoplasmosis is occasionally observed in immunosuppressed children,5, 6 including young patients with HIV disease.7 A case with miliary multifocal choroiditis is described complicating the management of acute lymphoblastic leukemia. Case report. A 6-year-old girl presented because of spiking fever for several weeks that had failed to respond to rifampin, azithromycin and trimethoprim-sulfamethoxazole therapy. The patient had been in remission from acute lymphoblastic leukemia for 18 months, maintained with weekly intramuscular methotrexate and daily oral 6-mercaptopurine. She had fevers of 102-105°F and malaise but she was otherwise asymptomatic. There was a nontender enlargement of the liver to the umbilicus with a 3- to 4-cm palpable spleen. The chest roentgenogram was normal. Pale miliary choroidal lesions scattered in both fundi (Fig. 1), without anterior segment or vitreal inflammatory signs, were detected at an ophthalmologic consultation. Her uncorrected visual acuities were 20/30 in each eye (O.U.).Fig. 1: Scattered multifocal miliary choroiditis (arrows) in macula OD; the vitreous is clear. The appearances of both eyes were similar. Visual acuities 20/30 O.U.Investigation revealed a moderate macrocytic anemia (hemoglobin 8.0 g/dl; mean corpuscular volume 93.9 fl), low serum albumin (2.3 g/dl), normal white blood cell counts and serum biochemistry appropriate for age. Bone marrow examination showed tightly packed, noncaseating epithelioid granulomata, with rare foci of necrosis; culture and acid-fast staining for mycobacterial infections were negative. Yeastlike forms that stained with Gomori methenamine silver stain were identified within marrow granulomata. Five blood cultures and a bone marrow culture subsequently grew Histoplasma capsulatum. A urine histoplasmal antigen titer (LJ Wheat, M.D., Histoplasmosis Reference Laboratory, Indianapolis, IN) of >10 enzyme immunoassay units was detected at presentation and was still positive at 53 days. The patient received ambulatory therapy with intravenous amphotericin B 1 mg/kg daily for 4 weeks; she became afebrile on Day 7 and made an uneventful recovery. The choroidal nodules were inapparent after 3 weeks of therapy, and there was no residual scarring. The bone marrow findings reverted to normal. The patient has remained symptom-free for 22 months. Discussion. Most cases of progressive disseminated histoplasmosis in children complicate the management of hematologic malignancy, particularly Hodgkin's disease and acute and chronic lymphocytic leukemia. Usually these patients are also therapeutically immunosuppressed.4, 5 Ocular complications of progressive disseminated histoplasmosis have rarely been described during life.8-10 Our patient was immunocompromised by long term maintenance chemotherapy used in the management of acute lymphoblastic leukemia. Multifocal histoplasmic choroiditis,8 multifocal chorioretinitis9, 10 and multifocal retinitis10 may occur in patients who retain sufficient immunologic capability to localize the H. capsulatum infection. The chorioretinal lesions are generally small (<400 μm diameter), oval and creamy white with either distinct or fluffy borders. It is assumed that these lesions are granulomatous in correspondence with the bone marrow findings.9, 10 The fundal appearances must be differentiated from other causes of multifocal granulomatous posterior uveitis, such as miliary tuberculosis, sympathetic uveitis, coccidioidomycosis, sarcoidosis, disseminated cat-scratch disease and idiopathic multifocal choroiditis. In severely immunosuppressed individuals, an immune response to the infection cannot always be generated and, as a result, histoplasmal ocular involvement may sometimes not be detectable clinically.11 The diagnosis of disseminated histoplasmosis is established by biopsy of bone marrow, liver, skin or oral lesions with Gomori silver staining and culture; by blood culture (optimally using lysis centrifugation); and by Wright's stain evaluation of peripheral blood smears. Enzyme-linked immunosorbent assay testing for urinary histoplasmal antigen provides a rapid semiquantitative diagnostic test with high sensitivity.4 DNA probe techniques can also be useful.12 A 4-fold or greater rise of complement-fixing antibody to H. capsulatum is generally considered diagnostic in immunocompetent individuals. Progressive disseminated histoplasmosis should be considered as an uncommon cause of multifocal choroiditis and retinitis, but one that should be specifically looked for in an immunosuppressed febrile child. There are no previous reports describing the successful treatment of histoplasmal multifocal choroiditis as part of progressive disseminated histoplasmosis. Acknowledgments. Supported in part by an unrestricted grant from Research to Prevent Blindness (University of Missouri-Columbia). L. David Ormerod, M.D., M.Sc. Tariq U. Qamar, M.D. Kevin Toller, M.D. Michael S. Cooperstock, M.D., M.P.H. Charles W. Caldwell, M.D. Joseph Giangiacomo, M.D. Mason Eye Institute (LDO, TUQ, KT, JG); Department of Child Health (MSC); Department of Pathology (CWC); University of Missouri Health Sciences Center Columbia, MO

The clinical features and ophthalmologic findings of 20 patients with syphilitic posterior uveitis seen at the Detroit Medical Center from November 1993 through February 1996 were reviewed. The mean age was 58 years; 8 patients were male and 12 were female; and all patients were black. Three of 9 patients tested were HIV positive. Patients were divided into 2 groups: those with acute (8) and those with chronic (12) syphilitic posterior uveitis. Chorioretinitis was the predominant uveitic pattern (15/20). Eighteen patients presented with blurred vision. All patients had reactive serum fluorescent treponemal antibody, absorbed (FTA-ABS); 3 had nonreactive rapid plasma reagin (RPR). Mean RPR titer in the chronic uveitis group and in the acute uveitis group was 1:27.3 and 1:209.8, respectively. Seven patients had abnormal cerebrospinal fluid (CSF); CSF VDRL was reactive in 2 patients. All patients were treated with intravenous penicillin G. Eight of 14 patients seen at follow-up showed improvement of ophthalmologic findings. Syphilis should be considered in the differential diagnosis of posterior uveitis.

Dr. Lee proposes a sensible and cost-effective approach to the investigation of cases presenting with the combination of optic nerve swelling and other posterior segment inflammatory signs. A detailed history and examination will often be revealing and suggest an even more focused approach to diagnosis. The clinical picture can be complex, and consideration should be given to a number of other diagnoses, including panuveitis from any cause, herpetic and other viral retinitis, multiple sclerosis, Vogt-Koyanaga-Harada disease, sympathetic ophthalmia, a systemic or severe retinal vasculitis, birdshot chorioretinopathy, toxoplasmosis, tuberculosis, and a number of other systemic infections, including several that are AIDS-related. Lumbar puncture and neuroimaging techniques should be used selectively, but potential central nervous system involvement of newly described syndromes needs to be evaluated. Cat-scratch disease (CSD) is usually a disease of children and young adults exposed to kittens; regional lymphadenopathy should be sought. As we discussed in our recent paper (Ophthalmology 1998;105:1024–31), there are many anecdotal reports of successful CSD treatment with numerous antibiotics, but there are no controlled studies of antibiotic use in CSD neuroretinitis or CSD retinitis choroiditis. Margileth1Margileth A.M. Antibiotic therapy for cat-scratch disease clinical study of therapeutic outcome in 268 patients and a review of the literature.Pediatr Infect Dis J. 1992; 11: 474-478Crossref PubMed Scopus (273) Google Scholar evaluated 268 patients with (principally) localized lymphoidal CSD in a retrospective study of immunocompetent individuals and deduced evidence of satisfactory effectivity in only 4 of 18 antibiotics tested: rifampin, ciprofloxacin, intramuscular gentamicin, and trimethoprim-sulfamethoxazole. CSD is now known to be a common cause of Leber neuroretinitis, previously believed idiopathic, that usually resolves spontaneously without treatment. It remains to be determined by controlled trials whether there is or is not a role for ciprofloxacin therapy in disseminated intraocular CSD infections. There is some evidence that early antibiotic treatment may inhibit the bacteremic phase of CSD infection and reduce the occasional recurrence.2Wong M.T. Dolan M.J. Lattuada Jr, C.P. et al.Neuroretinitis, aseptic meningitis, and lymphadenitis associated with Bartonella (Rochalimaea) henselae infection in immunocompetent patients and patients infected with human immunodeficiency virus type 1.Clin Infect Dis. 1995; 21: 352-360Crossref PubMed Scopus (147) Google Scholar

Objective: The ability to diagnose cat-scratch disease (CSD) has been facilitated greatly by the recent isolation and characterization of Bartonella henselae (formerly genus Rochalimaea) and Afipia felis and by the subsequent development of specific enzyme-linked immunosorbent assay (ELISA) serologic tests. This study will help define the patterns of posterior segment ocular involvement in patients with confirmed CSD.Design: The study design is a retrospective case study and literature review.Participants: Two consecutive patients with acute visual loss from retinal manifestations of CSD participated.Interventions: The diagnosis was confirmed by B. henselae ELISA testing. Patients underwent extensive medical and ophthalmic investigations to exclude other causes of retinal and choroidal disease. Ophthalmic investigation included fluorescein angiography and visual field testing. One patient received antibiotic therapy with cefotaxime, then with ciprofloxacin, and was treated with oral prednisone. The other patient was improving for several weeks before oral doxycycline was given.Main Outcome Measures: The clinical syndromes observed were studied over time using visual acuity, visual field, and clinical findings. Data were collated with cases from the literature.Results: Unilateral neuroretinitis and an unusual macular retinitis developed in patient 1, as did bilateral small intraretinal white spots and a unilateral choroidal infiltrate that continued to develop while the patient received antibiotic treatment. Patient 2 had a branch arteriolar occlusion in relation to a perivascular retinal infiltrate and a few small, bilateral, intraretinal white spots. There was gradual resolution with visual improvement while the patient received the antibiotic treatment, although therapeutic efficacy could not be determined. Patient 1 also received oral corticosteroids. A detailed analysis of the literature placed these findings in context.Conclusions: An unusual, well-defined retinal opacification with features of both multiple retinal arteriolar occlusions and a low-grade retinitis was described. Several features also may occur in posterior segment CSD, including neuroretinitis, a retinal white spot syndrome, and focal choroiditis.

Eleven patients with rapidly progressive herpetic retinal necrosis (RPHRN) complicating AIDS were investigated retrospectively to study the disease spectrum, systemic involvement, and therapy. The mean CD4 cell count was 24/microL. There was a characteristic disease pattern with rapid progression, 82% bilaterality, relative resistance to intravenous antiviral therapy, and 70% retinal detachment. Varicella-zoster virus was the probable cause in 10 patients (detected by polymerase chain reaction in two eyes investigated), and herpes simplex virus was the probable cause in one. Cutaneous zoster occurred previously in 73% but was not concurrent. Seventy-three percent had central nervous system disease, possibly virus-related. RPHRN may be a local herpetic recrudescence in an immune-privileged site with transneural spread. Only four of 20 affected eyes retained useful vision. Poor ocular bioavailability, retinal ischemia, acquired drug resistance, and strain pathogenicity may underlie treatment failure. Acyclovir therapy appears relatively ineffective. Combined intravenous and intravitreal therapy with foscarnet and ganciclovir may be the best current management. Research advances are needed urgently.

Background: Cytomegalovirus (CMV) retinitis is a common infection and a major cause of visual loss in patients with the acquired immunodeficiency syndrome (AIDS). Objective: To evaluate intravenous cidofovir as a treatment for CMV retinitis. Design: Two-stage, multicenter, phase II/III, randomized, controlled clinical trial. Setting: Ophthalmology and AIDS services at tertiary care medical centers. Patients: 64 patients with AIDS and previously untreated, small, peripheral CMV retinitis lesions (that is, patients at low risk for loss of visual acuity). Intervention: Patients were randomly assigned to one of three groups: the deferral group, in which treatment was deferred until retinitis progressed; the low-dose cidofovir group, which received cidofovir, 5 mg/kg of body weight once weekly for 2 weeks, then maintenance therapy with cidofovir, 3 mg/kg once every 2 weeks; or the high-dose cidofovir group, which received cidofovir, 5 mg/kg once weekly for 2 weeks, then maintenance therapy with cidofovir, 5 mg/kg once every 2 weeks. To minimize nephrotoxicity, cidofovir was administered with hydration and probenecid. Measurements: Progression of retinitis, evaluated in a masked manner by a fundus photograph reading center; the amount of retinal area involved by CMV; the loss of visual acuity; and morbidity. Results: Median time to progression was 64 days in the low-dose cidofovir group and 21 days in the deferral group (P = 0.052, log-rank test). The median time to progression was not reached in the high-dose cidofovir group but was 20 days in the deferral group (P = 0.009, log-rank test). Analysis of the rates of increase in the retinal area affected by CMV confirmed the data on time to progression. The three groups had similar rates of visual loss. Proteinuria of 2+ or more occurred at rates of 2.6 per person-year in the deferral group, 2.8 per person-year in the low-dose cidofovir group (P > 0.2), and 6.8 per person-year in the high-dose cidofovir group (P = 0.135). No patient developed 4+ proteinuria, but two cidofovir recipients developed persistent elevations of serum creatinine levels at more than 177 mu mol/L (2.0 mg/dL). Reactions to probenecid occurred at a rate of 0.70 per person-year. Conclusions: Intravenous cidofovir, high- or low-dose, effectively slowed the progression of CMV retinitis. Concomitant probenecid and hydration therapy, intermittent dosing, and monitoring for proteinuria seemed to minimize but not eliminate the risk for nephrotoxicity.

Although the pathogenesis in most cases of intermediate uveitis is unknown, a small minority of cases is associated with a variety of specific inflammatory etiologies: sarcoidosis; multiple sclerosis; Lyme disease; syphilis; ocular lymphoma; and as a rare manifestation of Behçet's disease and AIDS. A 61-year-old woman developed pars planitis after cataract surgery. A vitrectomy was performed after ten months when a white capsular plaque and an hypopyon developed. Propionibacterium acnes was isolated. The intermediate uveitis was not controlled until later removal of the intraocular lens and capsular remnants. Chronic propionibacterial endophthalmitis may be a cause of intermediate uveitis.

BACKGROUND:There is an increasing association between ocular-central nervous system (CNS) lymphoma and the acquired immunodeficiency syndrome (AIDS). In this population, the disease generally occurs in a younger age group. The origin of these B-cell neoplasms remains unknown.METHOD:Case study of a 26-year-old AIDS patient with an incidental finding of localized retinal vasculitis and local vitritis. Disease progression and the failure of antiviral therapy led to early diagnostic vitrectomy with vitreal and retinal biopsy. Cerebrospinal fluid (CSF) evaluation, head magnetic resonance imaging (MRI), and brain biopsy were performed.RESULTS:The diagnosis of ocular non-Hodgkin lymphoma was made by vitreous cytology. Serial sectioning of a retinal biopsy showed no retinal neoplastic infiltration, only perivascular inflammatory cells. CSF was normal. MRI showed multicentric brain mass lesions that enhanced with intravenous contrast. Brain biopsy revealed an immunoblastic, angiocentric, B-cell non-Hodgkin lymphoma. The patient died within two months, despite cerebral and ocular irradiation.CONCLUSIONS:The segmentally localized retinal vasculitis-vitritis and absence of retinal infiltration suggested early primary involvement of the vitreous. Coarse perivascular sheathing is characteristic of the mixed retinal vasculitis in this disease. The diagnosis of ocular-CNS lymphoma must be considered in patients with AIDS, however young, with unexplained posterior segment inflammatory disease or subretinal masses.

Objective: To evaluate the the efficacy and safety of an intravenous human monoclonal antibody to cytomegalovirus (CMV), MSL-109, as adjuvant treatment for CMV retinitis.Methods: Two hundred nine patients with acquired immunodeficiency syndrome and active CMV retinitis were enrolled in a multicenter, phase 2/3, randomized, placebo-controlled clinical trial. Patients received adjuvant treatment with MSL-109, 60 mg intravenously every 2 weeks, or placebo. Randomization was stratified on the basis of whether patients had untreated or relapsed retinitis. Primary drug therapy for CMV retinitis was determined by the treating physician.Results: The rates of retinitis progression, as evaluated in a masked fashion, were 3.04/person-year in the MSL-109-treated group and 3.05/person-year in the placebo-treated group (P=.98; Wald test); the median times to progression were 67 days in the MSL-109-treated group and 65 days in the placebo-treated group. No differences between the 2 groups were noted in the rates of increase in retinal area involved by CMV, visual field loss, or visual acuity outcomes. The mortality rate in the MSL-109-treated group was 0.68/person-year, and in the placebo-treated group, 0.31/person-year (P=.01). The mortality difference was not explained by differences in baseline variables or in concurrent antiretroviral therapy. Among patients with newly diagnosed retinitis, mortality rates were similar (MSL-109, 0.41/person-year; placebo, 0.42/person-year; P=.95), whereas among patients with relapsed retinitis the MSL-109-treated group had a greater mortality rate (MSL-109, 0.83/person-year, placebo, 0.24/person-year; P=.003). However, the mortality rate in the placebo-treated patients with relapsed CMV retinitis was lower than that in the placebo-treated patients with newly diagnosed CMV retinitis and lower than that in other trials of patients with relapsed CMV retinitis.Conclusions: Intravenous MSL-109, 60 mg every 2 weeks, appeared to be ineffective adjuvant therapy for CMV retinitis. The mortality rate was higher in the MSL-109-treated group, but the reasons for this difference remain uncertain.

PURPOSE:Progressive multifocal leukoencephalopathy (PML) is increasingly described as a late complication of the acquired immune deficiency syndrome (AIDS). The purpose of this study is to evaluate retrospectively the ophthalmologic, clinical, and investigational aspects of AIDS-associated PML.METHODS:The authors evaluated ten patients in whom ophthalmologic manifestations developed in the course of AIDS-associated PML. Findings at clinical examination and their progression over time, neuroimaging correlates, the results of pathologic investigation, and visual outcomes were reviewed.RESULTS:Progressive multifocal leukoencephalopathy was the AIDS-defining illness in six of ten patients. Homonymous visual field defects were the presenting symptom in three patients and detected in six patients overall. Occipital blindness developed in one patient. Cerebellar signs and brain stem nuclear and supranuclear palsies also were common. Confluent white matter lesions with increased intensity on T2-weighted magnetic resonance imaging were supratentorial in seven patients and infratentorial in three patients. With incomplete data, the median survival time was 3 months from PML onset. Histopathologic confirmation of PML diagnosis was available for nine of the ten patients.CONCLUSIONS:The development of progressive retrochiasmal visual field defects, supranuclear and nuclear cranial nerve palsies, or nystagmus ataxia in the relatively young patient should alert the ophthalmologist to the possibility of PML, particularly in the presence of long-tract central nervous system signs or dementia. Progressive multifocal leukoencephalopathy will often be human immunodeficiency virus associated. Human immunodeficiency virus encephalopathy, cerebral toxoplasmosis, lymphoma, and infarction need to be discriminated. Effective therapy is required urgently for this devastating disease.

BACKGROUND:The poor results of laser photocoagulation in patients with age-related macular degeneration who have subfoveal neovascular membranes, as reported by the Macular Photocoagulation Study Group, have posed the question as to whether the surgical removal of the neovascular membranes by subfoveal surgery might provide superior functional results, possibly in subgroups of patients.METHODS:The authors' first ten patients treated by subfoveal surgery were followed prospectively. Follow-up of a mean duration of 2 years is presented, with particular emphasis on visual and anatomic outcomes. Preoperative subfoveal choroidal neovascular membranes and postoperative retinal pigment epithelial defects were measured using digitized planimetry.RESULTS:Initial visual acuities were equal to or less than 20/400, with a mean duration of visual loss of 8 months. The mean choroidal neovascular membrane size was 7 disc areas. Eight of ten patients improved one to two lines of Snellen visual acuity postoperatively. One patient achieved visual acuity of 20/60 at 15 months before declining because of recurrent neovascularization. Surgically induced retinal pigment epithelial defects were invariable; the mean defect was 14 standard disc areas in size. Choriocapillaris atrophy and focal losses of deeper choroidal tissue also occurred. Surgical complications were frequent but responded to routine management. The authors observe a 2-year recurrence rate of 40%. Recurrences often are atypical, fibrous, and poorly vascularized.CONCLUSIONS:Although substantial visual improvements are common, long-term reading vision has not been achieved. Retinal pigment epithelial incorporation into late subfoveal membranes remains a major limiting factor. The role of early surgery and the role of surgery for patient subgroups need to be compared directly with the results of foveal laser treatment, using several visual outcomes.

BACKGROUND:Climatic or chronic actinic keratopathy is an important corneal degeneration occurring after prolonged climatic exposure. The advanced stages of disease are confined generally to tropical or arid localities (including the Arctic) with high levels of sunlight. After many years of disease evolution, the advent of stage 3 keratopathy often presages a rapid downhill course. The instability of advanced climatic keratopathy has received little attention.METHODS:Eighteen patients with advanced climatic keratopathy are described from the Transvaal region in South Africa and from Saudi Arabia. Patients with rapid disease progression, spontaneous sterile ulceration, and secondary microbial keratitis are described.RESULTS:The rapid progression characteristic of stage 3 climatic keratopathy is illustrated. Severe, focal, sterile ulceration of the devitalized corneal degeneration may be common. Secondary infection may occur, leading to rapid dissolution of the climatic keratopathy material. Corneal perforation may ensue. The occurrence of yellow or brown fragments of the climatic keratopathy within or adjacent to the corneal inflammatory infiltrate indicates the predisposing cause of the infection, as usually also with examination of the opposite eye.CONCLUSIONS:These observations emphasize the inherent instability of advanced climatic keratopathy, which frequently takes a relentless downhill course. In rural populations of the developing world, climatic keratopathy is an important cause of blindness. Disease pathogenesis, treatment, and prevention deserve greater study.

Purpose: This study, comprising 60 patients with coagulase-negative staphylococcal endophthalmitis which occurred after cataract surgery, was designed to define the variation in disease presentation and visual outcome and to evaluate statistically the role of the primary surgery and its management.Methods: An intensive evaluation of microbiological, inpatient, outpatient, and cataract surgery charts was made retrospectively using a standardized protocol. The predictive value of surgical, iatrogenic, and clinical factors was analyzed for their influence on defined aspects of the disease pattern and of the visual results using multiple regression models, via a stepwise technique.Results: There was commonly a significant asymptomatic latent period after cataract surgery. The median diagnostic delay was 7 days; 22% of patients presented after 2 weeks and 12% after 1 month. Symptoms progressed longer than 3 days in 25% of patients. Ten percent had no pain. Clinical variation proved largely unrelated to cataract surgery events and postoperative management; bacterial factors were implicated. Good visual outcome was associated statistically with intensive topical corticosteroid in the symptomatic period, but was negatively associated with operative subconjunctival corticosteroid.Conclusions: The clinical variation in cases of postoperative coagulase-negative staphylococcal endophthalmitis poses particular problems for diagnosis in the outpatient setting. Surgical and perioperative events (except corticosteroid use) probably can be disregarded in studies of endophthalmitis management.