Infectious Inflammatory Diseases
Meera D. Sivalingam, MD and Sunir J. Garg, MD, FACS
- Inflammation of vitreous and aqueous, typically due to an infection
- Exogenous: most common type, categorized depending upon underlying cause
- Acute post-operative: within 6 weeks of surgery, incidence after cataract surgery reported between 0.13% and 0.7% a year, incidence following pars plana vitrectomy (PPV) reported between 0.02% and 0.15%
- Subacute post-operative: weeks to months after surgery, common pathogens include Propionibacterium acnes, Staphylococcus, fungi
- Filtering bleb associated: may occur months to years after surgery, incidence between 0.12% and 1.2%
- Post-trauma: days to weeks after penetrating trauma
- Post-intravitreal injection: days after injection, reported incidence ranges in the literature but is approximately 0.05%
- Post-trauma: days to weeks after penetrating trauma
- Acute post-operative: within 6 weeks of surgery, incidence after cataract surgery reported between 0.13% and 0.7% a year, incidence following pars plana vitrectomy (PPV) reported between 0.02% and 0.15%
- Endogenous
- Bacterial: hematogenous seeding of the eye from bacteremia; 40% of cases occur in patients with endocarditis commonly caused by Streptococcus and Staphylococcus species; may occur in patients with urinary tract infections commonly caused by Escherichia coli; associated with intravenous drug abuse due to transient bacteremia commonly from Bacillus cereus
- Yeast: typically Candida species; found in patients who are immunocompromised, on long-term antibiotic treatment, or have indwelling catheters
- Fungal: rare in North America; may be exogenous or endogenous; Aspergillus and Fusarium are the most common pathogens; occurs in immunocompromised patients with persistent fungemia
- Bacterial: hematogenous seeding of the eye from bacteremia; 40% of cases occur in patients with endocarditis commonly caused by Streptococcus and Staphylococcus species; may occur in patients with urinary tract infections commonly caused by Escherichia coli; associated with intravenous drug abuse due to transient bacteremia commonly from Bacillus cereus
Signs and Symptoms
Decreased vision, eye pain, red eye, floaters
Exam Findings
- Anterior segment: eyelid edema, conjunctival injection, corneal edema, anterior chamber cell, hypopyon, severe anterior chamber reaction with fibrin1 (Figure 3-1)
- Posterior segment: vitreous cell, vitreous debris, decreased red reflex, retinal hemorrhages, retinal vascular sheathing, choroidal detachment (Figure 3-2)
- Pathogen dependent, ranges from focal chorioretinitis with low-grade vitritis to panophthalmitis
Testing
- Rule out wound/bleb leak, exposed suture
- B-scan if posterior view is limited: may reveal vitritis, choroidal thickening (Figure 3-3)
- Complete medical workup in endogenous infection
Differential Diagnosis
Acute noninfectious uveitis, sterile endophthalmitis, neoplastic conditions including retinoblastoma and lymphoma, retinochoroidal infection
Management
- Bacterial: Vitreous (or anterior chamber) tap sent for gram stain/culture with injection of intravitreal antibiotics. If endogenous, patients should undergo systemic workup to identify the source of infection and receive appropriate systemic antibiotics.
- Common intravitreal injection preparations: vancomycin (1 mg/0.1 ml) and ceftazidime (2.25 mg/0.1 ml); consider amikacin (0.4 mg/0.1 ml) instead of ceftazidime if allergic to penicillin/cephalosporins
- Endophthalmitis Vitrectomy Study (EVS): evaluated role of PPV and intravenous antibiotics in management of post-cataract surgery bacterial endophthalmitis and found the following:
- Systemic antibiotics did not improve visual outcomes
- Hand motion or better vision: no difference in outcomes between immediate tap and inject vs PPV
- Light perception vision: improved visual outcomes with immediate PPV
- Fungal and yeast: intravitreal voriconazole (0.1 mg/0.1 ml) or amphotericin (5 mcg/0.1 ml); vitrectomy with intravitreal injection
- Common intravitreal injection preparations: vancomycin (1 mg/0.1 ml) and ceftazidime (2.25 mg/0.1 ml); consider amikacin (0.4 mg/0.1 ml) instead of ceftazidime if allergic to penicillin/cephalosporins
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
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
- Creamy-yellow, circular area of retinitis with secondary involvement of choroid and sclera which is often adjacent to a chorioretinal scar (Figure 3-4), prominent vitritis (“headlight-in-fog” appearance), vasculitis with possible peri-arterial exudates (Kyrieleis plaques), potential vascular occlusion; potential elevated intraocular pressure (IOP)
Testing
- Fluorescein angiography (FA): leakage in area of active lesion, perivascular staining and leakage, optic disc leakage (Figure 3-5)
- Serology for toxoplasmosis antibodies IgG and IgM. IgM indicative of acute infection and does not appear after repeated exposures. IgM does not cross the placental barrier while IgG does. IgG is indicative of previous exposure.
- Polymerase chain reaction (PCR) testing of ocular fluid (vitreous and/or aqueous) can be helpful in challenging cases
- Magnetic resonance imaging (MRI) scan of the brain in immunocompromised patients to assess central nervous system involvement
- Polymerase chain reaction (PCR) testing of ocular fluid (vitreous and/or aqueous) can be helpful in challenging cases
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)
- Indocyanine green angiography: early hypercyanescence may reveal disorganized choriocapillaris in cases of CNV
- Optical coherence tomography (OCT): shows location and extent of CNV; useful for monitoring disease activity and response to therapy (Figures 3-6C and 3-6D)
- Fundus autofluorescence: small, non-pigmented chorioretinal scars appear hypoautofluorescent
- Histoplasmin skin antigen testing: not necessary for diagnosis or routinely performed but can help identify prior exposure to H. capsulatum
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
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
- Chorioretinitis: focal, deep, yellow-white lesions without vitritis (Figure 3-7A)
- Endophthalmitis: vitritis and “fluff balls” in vitreous; may have hypopyon, scleritis, and optic nerve involvement
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
- Oral fluconazole (if susceptible) 800 mg (12 mg/kg) loading dose, then 400 to 800 mg (6 to 12 mg/kg) once a day
- 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
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