Search

Purpose To describe a patient who developed concurrent acute posterior multifocal placoid pigment epitheliopathy (APMPPE) and posterior scleritis. Observations We describe a middle-aged woman that developed eye pain and photopsia. She was found to have a “T-sign” on ultrasound of the right eye and multiple, nearly confluent, ill-defined subretinal whitish lesions in both eyes. After an extensive laboratory evaluation and neuroimaging, her photopsia, pain with eye movements, and subretinal lesions began to regress on high dose systemic corticosteroids. Conclusions and Importance This is the first reported case of bilateral APMPPE and concurrent posterior scleritis. Our case highlights the importance of performing a full review of systems, specifically eliciting neurological changes, and dilated eye examination in all new uveitis cases.

Purpose: To describe new cases of sclopetaria and evaluate the risk factors, management, and visual prognosis of all reported cases in the literature. Observations: We performed a retrospective, observational case series. This study included six cases (median age 23, interquartile range 33) of sclopetaria. Additionally, literature searches were conducted in the PubMed and Cochrane Library databases to uncover risk factors associated with all published cases of sclopetaria. Main outcome measure was best corrected visual acuity (BCVA) worse than 20/20. Sixty-seven cases (71 eyes) of sclopetaria have been reported, of which 59 cases (61 eyes) met inclusion criteria in this study. Most were young (median age 19.5 years) men (51/59, 88.1%). Thirty-seven eyes were observed while 24 underwent immediate surgery including six pars plana vitrectomies and three scleral buckles. Compared to initial presentation, BCVA improved in 31/48 (64.6%) eyes, remained stable in 12/48 eyes (25.0%), and worsened in 5/48 eyes (10.4%). Ten patients (16.4%) achieved a final BCVA of 20/20 with median follow up time of seven months. In a multivariate model, location of sclopetaria in the macula, temporal retina, or immediate orbital foreign body removal predicted poor final BCVA with an area under receiver operating characteristic curve of 0.767. Conclusions and importance: Traumatic chorioretinitis sclopetaria is rare, but reports have increased dramatically over the past two decades. While pars plana vitrectomy may be required for the management of retinal detachments and non-clearing vitreous hemorrhage, close observation is appropriate in most cases. Visual prognosis is poor with most patients attaining 20/200 vision or worse. Keywords: Traumatic chorioretinitis sclopetaria, Sclopetaria, Traumatic chorioretinal rupture, Chorioretinitis proliferans, Retinitis proliferans, Traumatic proliferative chorioretinitis of Lagrange

Purpose To describe a case of congenital lymphocytic choriomeningitis virus (LCMV), a potentially severe and under-diagnosed etiology of congenital chorioretinitis. Observations A 5-month old boy presented with esotropia. Examination revealed light perception vision in the right eye and normal fixation and following behavior in the left eye, and a 50PD esotropia with full versions. The external, anterior segment, and pupil exams were normal. Fundus examination demonstrated slightly pale optic nerves, numerous geographic atrophic and hyperpigmented lesions along the vascular arcades in both eyes that extended into the fovea of the right eye. Head computed tomography (CT) imaging demonstrated bilateral cerebral volume loss with consequential ex vacuo dilation of the lateral ventricles and scattered intracranial calcifications. Serum IgG and IgM titers for toxoplasmosis, rubella, cytomegalovirus (CMV), herpes simplex virus (HSV), syphilis, and zika were all negative. Upon communication of negative TORCHS titers, the mother recalled a severe rat infestation of their home during the pregnancy. A LCMV antibody titer was then ordered and which resulted positive for IgG antibodies. Conclusions and Importance Congenital LCMV infection is an under-recognized cause of congenital chorioretinitis.

A 4-year-old-boy presented with an iris mass in the right eye in the setting of bilateral chorioretinitis and right eye anterior and posterior inflammation. Systemic workup was negative, and fine needle aspiration biopsy did not show any sign of leukemia or lymphoma. The presumed diagnosis of sarcoidosis was made, and the patient was treated with systemic steroids with good resolution of symptoms and inflammation.

A 62-year-old human immunodeficiency virus (HIV)–positive Caucasian man presented with 3 days of painless vision loss in the left eye. The right eye demonstrated optic disc edema and the left a deep, orange-yellow placoid lesion in the posterior pole. A broad differential diagnosis was entertained, including syphilis, viral retinitis, tuberculosis, primary toxoplasmosis, and endogenous infectious chorioretinitis. Syphilis serology was positive, and the patient responded to intravenous penicillin combined with prednisone.

A 56-year-old male hunter presented with a paracentral blind spot and floaters right eye (OD), but no ocular pain, for about 4 weeks. He noticed the problem when closing his left eye to shoot. Dilated fundus examination showed evidence of chorioretinitis, and close examination revealed a small worm in the macula. The diagnosis of diffuse unilateral subacute neuroretinitis was made. Laser photocoagulation was curative.

The use of ancillary ophthalmic imaging can aid in the timely and accurate diagnosis of West Nile neuroinvasive disease in the presence of chorioretinal involvement.

A 62-year-old man noticed difficulty shooting his rifle when looking through the mount with his left eye (OS) 1 week ago. Over the next few days he observed floaters and pericentral scotomas OS.

Purpose: To report a case of presumed bilateral chorioretinitis secondary to alendronate therapy. Observations: A 71-year-old female presented to the clinic in July 2017 with six months history of difficulty in reading along with floaters in both eyes which were more severe in the right eye. Past medical and surgical history revealed a history of hypertension, gout, hyperthyroidism, osteoporosis, and humerus fracture. She was started on alendronate three months before developing ocular symptoms. On ocular examination, best corrected visual acuity was 20/30 in the right and 20/25 in the left eye. Slit-lamp examination demonstrated normal anterior chamber examination in both eyes. Dilated fundus examination revealed geographic chorioretinal lesions around the optic nerve head in both eyes, more extensively in the right eye; and superior and temporal to the macula in the right eye. Past ocular records in February 2015 did not reveal any such findings. Fundus autofluorescence demonstrated hyper-autofluorescence in the peripapillary lesions in both eyes. The lesion adjacent to the macula in right eye displayed mixed hyper and hypo-autofluorescence. Fluorescein angiography showed combined hyper- and hypo-fluorescence compatible with window defect, staining and blockage. However, no leakage was appreciated in the macula, peripapillary, and peripheral lesions in both eyes. Optical coherence tomography scan showed septate hyporeflective intraretinal spaces in the right eye. Conclusion and importance: The index report underscore the importance of considering alendronate as an etiologic cause of chorioretinitis, especially in subjects with atypical lesions developing after alendronate therapy. We, therefore, recommend discontinuation of this medication in subjects who develop chorioretinitis after employing this medication. Keywords: Uveitis, Drug-induced, Alendronate, Chorioretinitis, Bisphosphonates

Purpose: Staphylococcus aureus bacteriemia (SAB) as critical condition for the life and occasionally involves the eyes. The aim of this report is to describe the ocular involvement with multimodal imaging. Observations: A patient admitted for evaluation of acute onset of confusion, disorientation, and generalized malaise and found to have methicillin-resistant staphylococcus aureus (MRSA)-associated endocarditis and multifocal brain abscesses was evaluated by the ophthalmology service. The patient's visual acuity was 20/20 OU without relative afferent pupillary defect and normal intraocular pressures. Bedside anterior segment examination was normal. Posterior segment examination revealed intraretinal hemorrhages and Roth spots in the posterior pole of the right eye, and two deep well-defined focal white chorioretinal infiltrates and a hemorrhagic pigment epithelium detachment in the temporal quadrant of the left eye. Multimodal imaging was utilized to document these findings and ensure adequate antibiotic therapy. Conclusion: SAB has the potential for poor visual outcomes as well as significant morbidity and mortality. Multimodal imaging of SAB-related chorioretinitis allows for accurate diagnosis as well as assessment of response to antimicrobial therapy. Keywords: Bacterial endocarditis, Brain abscess, Chorioretinitis, Methicillin-resistant staphylococcus aureus, Staphylococcus aureus bacteriemia

Purpose To describe the clinical and swept source OCT angiographic features of a patient with acute syphilitic posterior placoid chorioretinitis (ASPPC). Observations A 67-year-old man presented with acute loss of vision in the left eye. On exam, we noted a yellowish placoid lesion in the macula. Optical coherence tomography (OCT) imaging showed RPE nodularity and disruption of the inner segment-outer segment region in the left eye. Fluorescein angiography showed early hyperfluorescent and late staining within the placoid lesions. Wide field swept source OCT angiography (SS-OCTA) showed macular choriocapillaris perfusion flow deficits. Laboratory tests revealed positive 1:128 rapid plasma reagin titer and fluorescent treponemal antibody absorption (FTA-ABS) tests. OCT imaging revealed complete restoration of the IS-OS boundary layer with near complete resolution of the RPE granularity after adequate penicillin therapy. SS-OCTA showed resolution of choriocapillaris flow deficit in the left eye. Improvement in BCVA correlated with improvement in choriocapillaris perfusion. Conclusions and importance This is the first case that describes long-term SS-OCTA findings in ASPPC. SS-OCTA is a fast, safe, and easily repeatable imaging modality that offers valuable insights in our understanding of the pathophysiology and the response to treatment of ASPPC.

Nocardia subretinal abscess is a rare complication of nocardiosis with typically poor visual outcomes. We present a case of a large submacular abscess that responded favorably to early, frequent intravitreal amikacin along with systemic antibiotic therapy. Keywords: Nocardia, Subretinal abscess, Chorioretinitis, Pseudohypopyon, Amikacin

Purpose To report a novel clinical sign in patients with intraocular tuberculosis. The current study is an observational consecutive case series of patients diagnosed with intraocular tuberculosis managed at a tertiary eye care centre from June 1, 2012 to December 31, 2015. Observations The diagnosis of intraocular tuberculosis was made in 6 patients based on ocular features suggestive of tuberculosis along with a positive tuberculin skin testing and chest X-ray consistent with tuberculosis. All patients presented with decreased visual acuity ranging from 20/25 to 20/400, anterior chamber reaction, vitritis, multifocal choroiditis and vasculitis. All patients had an area of active chorioretinitis within the zone of pre-existing chorioretinal atrophy, apart from various other signs suggestive of intraocular inflammation. All patients were started on anti-tubercular therapy for a period of 9 months alone or in combination with oral corticosteroids tapered over 3–4 months. A prompt response to the treatment with resolution of chorioretinitis within the chorioretinal atrophy occurred in all patients. In addition, there was resolution of vitritis and improvement in the visual acuity ranging from 20/20 to 20/40 at last follow-up. Conclusions and importance and Importance: Active chorioretinitis within an area of chorioretinal atrophy is a novel clinical sign that may indicate intraocular tuberculosis.

Multiple evanescent white dot syndrome (MEWDS) is an acute-onset chorioretinal inflammatory disease. This disorder is characterized by unilateral multiple gray-white dots of the posterior pole in young healthy women. Symptoms include blurred vision, photopsia, and visual field (VF) defects. Although the etiology of MEWDS is still unknown, most patients have spontaneous improvement in vision and fundus appearance within a period of weeks. Herein, we report a typical case of MEWDS, and describe the spontaneous resolution of photoreceptor damage during the entire course, demonstrated by serial optical coherence tomography (OCT). The OCT is a sensitive and noninvasive tool for the diagnosis and serial microstructure evaluation of patients with MEWDS.

Infectious processes of the eye require prompt attention in order to prevent long-term sequelae, of which irreversible vision loss is the most concerning. Microbes may enter the eye directly through inadvertent inoculation, spread of a contiguous infectious process, or endogenously through the bloodstream. All components of the human optical system may be affected by a broad spectrum of infectious pathogens either as an isolated infectious process or become secondarily affected by a systemic infection. Infectious processes of periocular structures may also affect vision if not identified and treated.

Ocular toxoplasmosis is a common cause of posterior uveitis and chorioretinitis throughout the world. Despite its prevalence, pathogenesis of ocular toxoplasmosis is not well understood, nor is there consensus as to the best treatment. This chapter reviews the clinical features and epidemiology of ocular toxoplasmosis, our current understanding of disease pathogenesis as gleaned from experimental models and clinical research, as well as diagnosis and clinical management of ocular toxoplasmosis.

Toxoplasma gondii causes a variety of clinical diseases in humans. The parasite is typically asymptomatic in immune-competent individuals but can cause serious, even fatal, disease in congenitally infected children. Due to T. gondii’s ability to persist as bradyzoites for the life of the host, toxoplasmosis frequently presents as an opportunistic infection of the immune compromised, including AIDS patients. This comprehensive chapter discusses the diagnosis, treatment, and clinical manifestations of human toxoplasmosis.

Toxoplasma gondii is an important zoonotic parasite with a worldwide distribution. Felids are the definitive hosts and, upon primary infection, they shed millions of oocysts into the environment. These oocysts are infectious to a wide range of warm-blooded animals, and these intermediate hosts develop tissue cysts. Humans can be infected through oocysts, or by consumption of raw or undercooked meat containing tissue cysts. If a woman is infected for the first time during pregnancy, the parasite can be transmitted transplacentally, which may result in death of the fetus, or a baby born with nervous system abnormalities or chorioretinitis. Moreover, all people infected with T. gondii are at risk of developing ocular toxoplasmosis, and immunocompromised individuals are at risk for disseminated toxoplasmosis. Prevention strategies are usually aimed at pregnant women and are based on health education or early detection and treatment. Insight into the relative attribution of the different sources of infection and the possible intervention measures associated with these sources will aid the development of more effective prevention strategies that also will protect the general population.

Toxoplasma gondii, an Apicomplexan, is a pathogic protozoan that can infect the central nervous system. Infection during pregnancy can result in a congenial infection with severe neurological sequelae. In immunocompromised individuals reactivation of latent neurological foci can result in encephalitis. Immunocompetent individuals infected with T. gondii are typically asymptomatic and maintain this infection for life. However, recent studies suggest that these asymptomatic infections may have effects on behavior and other physiological processes. Toxoplasma gondii infects approximately one-third of the world population, making it one of the most successful parasitic organisms. Cats and other felidae serve as the definite host producing oocysts, an environmentally resistant life cycle stage found in cat feces, which can transmit the infection when ingested orally. A wide variety of warm-blooded animals, including humans, can serve as the intermediate host in which tissue cysts (containing bradyzoites) develop. Transmission also occurs due to ingestion of the tissue cysts. There are three predominant clonal lineages, termed Types I, II and III, and an association with higher pathogenicity with the Type I strains in humans has emerged. This chapter presents a review of the biology of this infection including the life cycle, transmission, epidemiology, parasite strains, and the host immune response. The major clinical outcomes of congenital infection, chorioretinitis and encephalitis, and the possible association of infection of toxoplasmosis with neuropsychiatric disorders such as schizophrenia, are reviewed.

Publisher Summary Even though ocular toxoplasmosis is the most common etiology of posterior uveitis in the United States and the world, it remains a poorly understood disease. For instance, there is limited understanding as to why macular lesions are common in congenitally infected individuals, limited understanding regarding the details of ocular recurrences, and there is no agreement on best treatment. There is no regimen that can eliminate the bradyzoite stage of infection; therefore, once an individual is infected by Toxoplasma gondii the retina is randomly undetectably seeded, resulting in a chance for local recurrences in the future. There is irreversible damage to the involved retina where a recurrence occurs. If a recurrence occurs within the central macula, the consequence is severe visual morbidity. Toxoplasma gondii is one of the most common parasitic infections in the world, with as many as one-third of all humans being infected. Currently, there is considerable controversy concerning the treatment of ocular toxoplasmosis. Some clinicians reserve treatment for active disease unless there is imminent threat to a patient's vision.

Publisher Summary Investigations into bradyzoite biology and the differentiation of tachyzoites into bradyzoites have been accelerated by the development of in vitro techniques to study and produce bradyzoites, as well as by the genetic tools that exist for the manipulation of T. gondii. T. gondii is a ubiquitous protozoan parasite of mammals and birds. It belongs to the phylum Apicomplexa, which includes other important pathogens such as Plasmodium, Eimeria, Cyclospora, Babesia, and Cryptosporidium. Toxoplasma gondii has three infectious stages: tachyzoites, bradyzoites, and sporozoites. Infection is acquired either by ingestion of under cooked meat harboring tissue cysts or by the ingestion of food contaminated with oocysts. Bradyzoites contained in cysts are refractory to most chemotherapeutic agents used for treatment of toxoplasmosis, and tissue cysts are produced in any animal capable of being infected with T. gondii. The persistence and reactivation of bradyzoite forms is a major cause of disease in humans. In most individuals, acute infection with T. gondii is asymptomatic or causes mild symptoms similar to a self-limited mononucleosis-like syndrome. If an immunologically naive pregnant woman is infected, transmission of this parasite to the fetus can occur with the development of a congenital infection that can result in a fetopathy and a relapsing chorioretinitis.

Lymphocytic choriomeningitis virus (LCMV) is an arenavirus that is a natural pathogen of mice but can be transmitted to humans. Human infection with LCMV is frequently asymptomatic, but it may be associated with aseptic meningitis or, more rarely, meningoencephalitis. The meningitis is thought to be immunopathological, resulting from recruitment of antiviral CD8 + T cells to sites of LCMV replication in the meninges where they trigger an influx of myelomonocytic cells that cause vascular damage leading to edema. Congenital LCMV infection is an often unrecognized cause of chorioretinitis, hydrocephalus, microcephaly, or macrocephaly and mental retardation.