Infectious Inflammatory Diseases


3


Infectious Inflammatory Diseases


ENDOPHTHALMITIS


Meera D. Sivalingam, MD and Sunir J. Garg, MD, FACS



Signs and Symptoms


Decreased vision, eye pain, red eye, floaters


Exam Findings




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Figure 3-1. External photo showing subacute post-operative endophthalmitis with mild conjunctival injection, keratic precipitates, and hypopyon.




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Figure 3-2. Color fundus photo of the right eye in the setting of methicillinsusceptible Staphylococcus aureus endogenous endophthalmitis showing vitritis, diffuse chorioretinitis, and retinal hemorrhages.




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Figure 3-3. B-scan showing vitreous debris (arrows) and dense vitritis in an eye with post-operative endophthalmitis.


Testing



Differential Diagnosis


Acute noninfectious uveitis, sterile endophthalmitis, neoplastic conditions including retinoblastoma and lymphoma, retinochoroidal infection


Management



OCULAR TOXOPLASMOSIS


Nikolas J. S. London, MD



  • Ubiquitous parasite/protozoa (Toxoplasma gondii), endemic in tropical environments. In North America, definitive host is the domestic cat.
  • Most common etiology of posterior uveitis in immunocompetent patients
  • Congenital (transplacental) infections typically involve the macula and may be bilateral; acquired (postnatal) infections are typically extramacular and unilateral


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Figure 3-4. Color fundus photograph of the left eye shows a creamy yellow-white area of retinitis nasal to the optic disc and associated vasculitis with peri-arterial Kyrieleis plaques.


Signs and Symptoms


Systemic: acute infection is often asymptomatic, but may present with fever, malaise, sore throat, and/or lymphadenopathy in 10% to 20% of adults with acquired toxoplasmosis; Ocular: prominent blurred vision and floaters, often painless unless there is significant anterior uveitis


Exam Findings




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Figure 3-5. FA of the same eye seen in Figure 3-4 shows hyperfluorescence in the area of retinitis, adjacent perivascular staining and mild leakage, and optic disc staining.


Testing



Differential Diagnosis


Necrotizing herpetic retinitis, syphilis, ocular tuberculosis, endogenous endophthalmitis, ocular lymphoma


Management


Treatment may not be necessary in all cases.



  • Treatment criteria: macular or juxtapapillary lesion, lesions that threaten a large vessel, prominent hemorrhage, visual acuity impaired by 2 or more lines attributable to inflammation; immunocompromised patient
  • Bactrim DS (trimethoprim-sulfamethoxazole) 800 mg/160 mg double-strength twice a day by mouth; pyrimethamine (100 mg loading dose followed by 25 to 50 mg once a day) and sulfadiazine (1 g 4 times a day) for 4 to 6 weeks. Give with folic acid (3 to 5 mg twice a week) to prevent leukopenia and thrombocytopenia; clindamycin 300 mg every 6 hours for 3 or more weeks; atovaquone 750 mg 4 times a day for 3 months.
  • Topical cycloplegic and corticosteroid for significant anterior segment inflammation
  • Systemic corticosteroids are often unnecessary unless threatening macula. If used, start 24 to 48 hours after initiation of antibiotics and taper prior to stopping antibiotics.

PRESUMED OCULAR HISTOPLASMOSIS SYNDROME


Katherine E. Talcott, MD



  • Characterized by atrophic chorioretinal scars, peripapillary atrophy, and absence of intraocular inflammation that can lead to a choroidal neovascular membrane (CNV)
  • May be due to infection with yeast form of Histoplasma capsulatum, a fungus endemic to the Ohio and Mississippi river valleys
  • May also represent an inflammatory reaction triggered by certain organisms, including H. capsulatum, as disease is linked to human leukocyte antigen (HLA) haplotypes DRw2 and B7

Signs and Symptoms


Painless vision loss, metamorphopsia, and central/paracentral scotomas, due to CNV; often asymptomatic without CNV


Exam Findings


Characteristic (often bilateral) findings include: (1) discrete, atrophic or “punched-out” choroidal scars in macula or periphery, smaller in size than optic disc; confluent mid-peripheral scars in a linear or curvilinear pattern may be present (Figure 3-6A), (2) peripapillary atrophy, (3) absence of intraocular inflammation. Findings may be accompanied by a CNV (risk is 25% in patients with macular scars) that can progress to disciform scarring with subretinal fibrovascular tissue.


Testing



  • FA: window defects of hyperfluorescence in areas of atrophy; CNV can be identified by leakage of fluorescein dye (Figure 3-6B)


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Figure 3-6. (A) Fundus photograph of left eye showing multiple chorioretinal scars and peripapillary atrophy consistent with presumed ocular histoplasmosis syndrome. (B) FA demonstrates window defects. (C) OCT shows subretinal hyperreflective material (arrow) but no subretinal fluid. (D) Repeat OCT 1 month later shows new intraretinal edema (arrowhead), subretinal fluid (*), and enlargement of the subretinal hyperreflective material (arrow), consistent with a CNV. (Reprinted with permission from Sundeep K. Kasi, MD.)



Differential Diagnosis


Multifocal choroiditis with panuveitis, multiple evanescent white dot syndrome (MEWDS), myopic degeneration, punctate inner choroidopathy, sarcoidosis, serpiginous choroiditis, choroidal rupture with choroidal neovascularization, age-related macular degeneration


Management


Monitor for development of CNV; anti-vascular endothelial growth factor injections are the primary treatment for CNV


CANDIDA CHORIORETINITIS


Joshua H. Uhr, MD and Sunir J. Garg, MD, FACS



  • Ocular candidiasis is uncommon, with recent studies reporting rates as low as 1% in those with candidemia. Occurs in patients with candidemia via hematogenous spread to the choroid and retina through capillaries, with potential breakthrough into the vitreous.
  • Usually endogenous but can be exogenous (eg, trauma). Risk factors for ocular candidiasis: infection with Candida albicans (vs non-albicans Candida species); multiple positive blood cultures; immunosuppression, either due to illness or medications

Signs and Symptoms


May be asymptomatic due to an indolent course; blurred vision, pain, photophobia


Exam Findings



Testing


OCT has 2 patterns:



  • Chorioretinal infiltration: eruption from choroid through the retinal pigment epithelium (RPE) with progression through the retinal layers (Figure 3-7B)
  • Retinovascular infiltration without choroidal involvement: fungal “emboli” leading to focal vasculitis, nerve fiber layer infarction

Differential Diagnosis



  • Infectious (bacterial endophthalmitis, acute retinal necrosis, toxoplasmosis chorioretinitis, tuberculosis); inflammatory (intermediate/posterior uveitis, sarcoidosis, Behçet’s disease, Vogt-Koyanagi-Harada disease); neoplastic (retinoblastoma, intraocular lymphoma, leukemic infiltrate)

Management



  • Systemic antifungal therapy: consider in patients with chorioretinitis (no vitritis) that does not involve the macula

    • Oral fluconazole (if susceptible) 800 mg (12 mg/kg) loading dose, then 400 to 800 mg (6 to 12 mg/kg) once a day
    • Intravenous voriconazole 400 mg (6 mg/kg) every 12 hours for 2 doses, then 300 mg (4 mg/kg) every 12 hours


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Figure 3-7. (A) Localized deep white chorioretinal lesions, characteristic of Candida chorioretinitis, without vitritis. (B) Enhanced-depth imaging OCT of the same eye shows a focal sub-RPE infiltrate with RPE breakthrough (arrow). (Reprinted with permission from Sonia Mehta, MD.)



  • Intravitreal antifungal therapy: use in conjunction with systemic antifungals if macula is threatened or vitritis is present

    • Amphotericin B deoxycholate 5 to 10 μg/0.1 mL or voriconazole 100 μg/0.1 mL

  • Surgery (eg, PPV): may be necessary in recalcitrant cases or to obtain specimen for diagnostic testing
  • Treatment course is usually 4 to 6 weeks or until all lesions have resolved on serial funduscopic examinations
  • In patients with candidemia without ocular involvement, a repeat exam should be performed every 2 weeks

SYPHILITIC CHORIORETINITIS


Douglas R. Matsunaga, MD and Sonia Mehta, MD



  • Syphilis is a sexually transmitted infection caused by the spirochete Treponema pallidum that may involve almost any structure in the eye.
  • Most common ocular presentations: panuveitis and posterior uveitis with chorioretinitis
  • Manifestation of secondary syphilis
  • May be unilateral or bilateral and may or may not present with systemic symptoms

Signs and Symptoms


Decreased vision, floaters


Exam Findings


One or more placoid, yellow, outer retinal lesions (Figure 3-8A); may have associated anterior uveitis, vitritis, retinal vasculitis, serous/exudative retinal detachment (RD) or papillitis



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Figure 3-8. (A) Color fundus photograph showing an outer retinal yellow placoid syphilitic lesion. (B) FA in venous phase showing hyperfluorescence of the lesion with scattered hypofluorescent spots. (C) OCT of syphilitic lesion showing areas of retinal pigment epithelial nodularity (arrow), subretinal fluid (*), and scattered punctate hyperreflective spots in the choroid (arrowhead).

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Nov 28, 2021 | Posted by in OPHTHALMOLOGY | Comments Off on Infectious Inflammatory Diseases

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