Matthew R. Starr

Ocular manifestations of tick-borne diseases.

Tick-borne illnesses are a significant disease burden worldwide. Diagnosis is challenging and requires a high level of clinical suspicion. Ocular manifestations reported in association with tick-borne disease are mostly as case reports and small case series because of the relative infrequency with which they occur; however, given the global nature of health care and increase in travel in the 21st century, it is important for ophthalmologists to be aware of ocular manifestations of these diseases because early diagnosis may reduce morbidity and mortality. Here, we review of the literature of tick-borne diseases with reported ophthalmic findings. All known human tick-borne diseases are discussed, including a brief description of the causative agent, region of endemicity, vector, systemic symptoms, and any reported eye findings. When possible, we also address the strength of the evidence for these ocular associations.

The Brief Case: A “Fresh” Pair of Contact Lenses

CASE A27-year-old male presented to an emergency department in Minnesota during the summer of 2016 with 4 days of photophobia, irritation, erythema, edema, and increased lacrimation. Symptoms were present in both eyes but worse on the right. He reported decreased visual acuity in the right eye. Past medical history was significant only for myopia, for which he had been wearing soft contact lenses for many years. The patient reported that, 4 weeks prior to presentation, he swam in a lake while wearing contact lenses. Two weeks prior to presentation, he also went on a boat ride, and fresh water from the lake splashed into his eyes. Though he had worn the same pair of contact lenses during this time period, he stopped wearing them and switched to eyeglasses when his symptoms began. He retained his contact lenses in his case, however, for future possible use. The right eye had a slightly decreased visual acuity of 20/40. Ophthalmologic examination of the right eye demonstrated central corneal haze, irregular epithelium, and a few areas of punctate staining with fluorescein but no frank ulceration, which was felt to be most consistent with contact lens-associated bacterial keratitis. No abnormalities were noted in the left eye. Given these findings, treatment was initiated with topical ophthalmic moxifloxacin in the right eye only (1 drop of 0.5% ophthalmic solution 6 times a day), and he was instructed to continue avoiding lens use. He was followed daily in the ophthalmology clinic and was noted to have no improvement in his symptoms or upon his exam. He was also beginning to develop similar problems with the left eye. Two days after his initial presentation, enlarged corneal nerves were noted in both eyes. Given the history of freshwater exposure, contact lens use, and keratoneuritis upon exam (Fig. 1A), empirical treatment was initiated with hourly 0.02% chlorhexidine gluconate ophthalmic drops for possible Acanthamoeba keratitis. Cultures for freeliving amebae from his right and left contact lenses and residual contact lens solution within his lens case confirmed the presence of Acanthamoeba species, and in vivo confocal microscopy revealed characteristic Acanthamoeba cysts on the anterior stroma of the right eye (Fig. 1B) (1). Cytologic examination of the residual contact lens solution in the case was also consistent with Acanthamoeba infection (Fig. 2). The diagnosis was further confirmed using a modified version of a previously published real-time PCR assay for free-living amebae, which was positive for Acanthamoeba species in the residual contact lens solution in the case (2). Of note, there was also the following polymicrobial growth from routine bacterial cultures of his contact lenses and solution: Achromobacter xylosoxidans, Alcaligenes faecalis, Brevundimonas diminuta, Elizabethkingia meningoseptica, Mycobacterium chelonae, Pseudomonas aeruginosa, Serratia marcescens, and Staphylococcus epidermidis. Numerous bacteria were also seen on cytology preparations. The polymicrobial growth from the contact lens case may have represented normal bacterial flora of a typical contact lens case. However, for empirical Citation Tan EM, Starr MR, Henry MR, Pritt BS. 2018. The Brief Case: A “fresh” pair of contact lenses. J Clin Microbiol 56:e00790-17. https:// doi.org/10.1128/JCM.00790-17. Editor Carey-Ann D. Burnham, Washington University School of Medicine Copyright

Bulbar Conjunctival Nodule in a Patient With Rheumatoid Arthritis

A 25-year-old man with a history of rheumatoid arthritis currently taking oral methotrexate, 25 mg per week, presented with a lesion of the left bulbar conjunctiva of about 1 month’s duration. He had no other symptoms other than occasionally noticing a sensation of a foreign body in that eye and denied any changes in his vision. He had no history of contact lens use, ocular trauma, or ocular surgery. His only other medications were oral vitamin D and folic acid. He was initially treated with topical antibiotics followed by a course of oral sulindac, 200 mg twice daily, without any improvement. On examination, his visual acuity was 20/20 OD and 20/25 OS. Intraocular pressure was 16 mm Hg OD and 23 mm Hg OS. The lesion measured 6.5 × 2.5 mm and was firm, nonvascular, slightly mobile, and located on the superotemporal portion of the bulbar conjunctiva (Figure 1). It was purulent in appearance, but no material was expressed with attempted incision and drainage at the slitlamp. A culture was positive only for Propionibacterium acnes. Tests for herpes simplex, cytomegalovirus, and Epstein-Barr virus polymerase chain reactions were negative.

Acute retinal vein occlusion and cystic fibrosis

BackgroundThe ocular manifestations of cystic fibrosis typically present with surface irritation or nyctalopia due to Vitamin A deficiency, however, there have been two previous reports of patients with cystic fibrosis that developed retinal vein occlusions. These reports hypothesized that either elevated fibrinogen levels due to chronic infections or elevated homocysteine levels have predisposed patients with cystic fibrosis to develop retinal vein occlusions.Case presentationWe present a case of a 35-year-old male with cystic fibrosis complicated by chronic sinusitis with no history of organ transplantation or chronic pulmonary infections who presented with an acute branch retinal vein occlusion in his left eye with associated macular edema. Evaluation revealed an elevated fibrinogen level, while the rest of his workup was relatively unremarkable including a normal homocysteine level. His vision remained 20/20 throughout his care and he did not require treatment of his macular edema.ConclusionsPatients with cystic fibrosis are at an increased risk of developing retinal vein occlusions likely due to a variety of systemic thrombogenic factors rather than a single risk factor which had been reported previously. Elevated fibrinogen levels in these patients may not be due to chronic infections, but inherent to the cystic fibrosis.

Histoplasmosis following Systemic Immunomodulatory Therapy for Ocular Inflammation

PURPOSE Histoplasmosis is a known complication of systemic immunosuppressive therapy, particularly among patients who are receiving tumor necrosis factor α inhibitors. There are limited data on the development of disseminated or pulmonary histoplasmosis among patients who are receiving systemic immunosuppressive medication for noninfectious ocular inflammation. DESIGN Retrospective case series. METHODS We reviewed all patients with uveitis or scleritis who subsequently developed pulmonary or disseminated histoplasmosis at the Mayo Clinic in Rochester, Minnesota between September 1, 1994 and July 1, 2017, with a 3:1 age- and sex-matched control cohort who did not develop histoplasmosis. This was a single institutional study examining patients that developed histoplasmosis after the initiation of systemic immunomodulatory therapy (IMT). Patients had to develop either disseminated or pulmonary histoplasmosis while receiving systemic immunosuppressive therapy and have an ophthalmic examination at Mayo Clinic Rochester. The control group was comprised of patients who received systemic IMT for ocular inflammation but did not develop histoplasmosis. RESULTS Nine cases of histoplasmosis were identified: 2 disseminated and 7 pulmonary. Both patients with disseminated histoplasmosis were taking tumor necrosis factor α inhibitors. Seven of the 9 patients received systemic antifungal medication, including both disseminated cases. Over a median follow-up of 4.4 years, none of the patients died, and there were no recurrences of histoplasmosis. When compared to the control cohort, there was no correlation between length of time on IMT and the risk of histoplasmosis. CONCLUSIONS Ocular inflammation patients on systemic immunomodulatory therapy may develop pulmonary or disseminated histoplasmosis. Most cases require treatment with systemic antifungal medication, but it might not be necessary to stop systemic immunomodulatory medication for ocular inflammation. Ophthalmologists should be aware that patients receiving systemic immunomodulatory therapy have a higher risk of developing Histoplasma infections. Prompt diagnosis and treatment using the expertise of an infectious diseases specialist may ensure low mortality for these patients.