Infectious Uveitis

Key Points at a Glance

Highlights of This Disease Group

• Infectious uveitis accounts for approximately 16% of all uveitis cases in Japan (2002 survey) and exceeds 50% in developing countries¹⁾.
• Pathogens are broadly classified into four groups: viruses (mainly herpes family), bacteria (tuberculosis and syphilis are important), fungi, and parasites.
• The most important point in differential diagnosis is to determine whether the uveitis is infectious or non-infectious. For infectious uveitis, steroid monotherapy is generally contraindicated; misdiagnosis can lead to rapid exacerbation and fatal outcomes.
• PCR testing of intraocular fluid (aqueous humor or vitreous fluid) is essential for definitive diagnosis ¹⁹⁾, and the Goldmann-Witmer coefficient (Q value ≥6 for pathogen identification) is also useful as an adjunctive diagnostic tool ¹⁷⁾.
• Early diagnosis and initiation of pathogen-specific treatment determine visual prognosis.

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1. What is infectious uveitis?

Uveitis is a general term for intraocular inflammation. Based on etiology, it is broadly classified into exogenous (infectious) uveitis and endogenous (non-infectious) uveitis. Infectious uveitis refers to intraocular inflammation caused directly or via immune-mediated mechanisms by pathogens such as bacteria, viruses, fungi, and parasites. The annual incidence of uveitis is estimated at 17–52 per 100,000 population, and the prevalence at 38–714 per 100,000 population ^1,16).

In an epidemiological survey conducted by the Japanese Society for Ocular Inflammation in 2002 (3,060 cases), infectious uveitis accounted for approximately 16% of all cases ^1,7). Major diseases included herpetic iritis 3.6%, bacterial endophthalmitis 3.8%, acute retinal necrosis (ARN) 1.3%, ocular toxoplasmosis 1.1%, ocular toxocariasis 1.1%, CMV retinitis 0.8%, and HTLV-1-associated uveitis 1.0%. Internationally, toxoplasmosis and tuberculous uveitis are reported to account for over 50% of infectious uveitis in developing countries ^2,13), showing marked regional differences ⁸⁾.

Identifying the cause of infectious uveitis is important because the treatment strategy differs fundamentally from that of non-infectious uveitis. Non-infectious uveitis is primarily treated with immunosuppression (steroids and immunomodulatory drugs), whereas infectious uveitis requires specific treatment targeting the pathogen first, and careless steroid administration can rapidly worsen the disease.

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2. Classification

2-1. Classification by Location

Uveitis is classified into the following four types based on the primary site of inflammation (SUN Working Group classification):

Classification	Site	Representative diseases (infectious)
Anterior uveitis	Iris and ciliary body (iritis, iridocyclitis)	HSV/VZV iritis, CMV anterior uveitis, Lyme disease
Intermediate uveitis	Vitreous, pars plana	HTLV-1-associated uveitis, Lyme disease
Posterior uveitis	Retinochoroid, posterior vitreous	CMV retinitis, ocular toxoplasmosis, ocular toxocariasis
Panuveitis	Full-thickness	ARN, tuberculous, syphilitic, fungal endophthalmitis

2-2. Classification by pathogen

Infectious uveitis is classified into four groups according to the type of pathogen.

Viral

The herpesvirus family (HHV-1 to 8) is the most common, with HSV-1/2, VZV, CMV, and HTLV-1 being clinically important. Depending on the host’s immune status, various clinical presentations occur: in immunocompetent individuals, HSV/VZV cause anterior uveitis and ARN; in immunocompromised individuals, CMV retinitis and PORN are typical.

Bacterial

Major pathogens include Mycobacterium tuberculosis, Treponema pallidum (syphilis), Bartonella (cat scratch disease), and Borrelia (Lyme disease). In endogenous bacterial endophthalmitis, Gram-negative rods (e.g., Escherichia coli, Klebsiella) are common, with rapid progression and poor prognosis.

Fungal

Candida, Aspergillus, and Cryptococcus cause endogenous infections in immunocompromised hosts (e.g., central venous catheter, immunosuppression, HIV infection). Endophthalmitis following candidemia is particularly problematic.

Parasitic

Ocular toxoplasmosis (Toxoplasma gondii) and ocular toxocariasis (Toxocara canis/cati) are representative diseases. Toxoplasmosis can reactivate even after adult-acquired infection, causing lymphadenopathy and acquired retinochoroiditis.

2-3. Classification by route of infection

Classification	Route of infection	Representative diseases
Endogenous	Hematogenous dissemination (other organs → eye)	Bacterial endophthalmitis, fungal endophthalmitis, tuberculosis, syphilis, CMV retinitis
Exogenous	Direct invasion (trauma/surgery)	Postoperative infectious endophthalmitis, post-traumatic endophthalmitis

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3. Overview of Viral Uveitis

Uveitis involving viruses in the inflammation of the uvea, retina, and vitreous is called viral uveitis. Human herpesviruses (HHV) have a strong affinity for retinal tissue and cause various ocular diseases. Viral uveitis is characterized by diverse clinical presentations depending on the host’s immune status, driven by direct viral toxicity and inflammation triggered by immune responses. Comprehensive detection using PCR of intraocular fluids has greatly improved diagnostic rates.

3-1. Herpesvirus Pathogens and Ocular Manifestations

Virus	Ocular manifestations in immunocompetent patients	Ocular manifestations in immunocompromised patients
HSV-1/2 (HHV-1/2)	Herpetic iridocyclitis, ARN	PORN (rare)
VZV (HHV-3)	Herpes zoster ophthalmicus, herpetic iridocyclitis, ARN	PORN
CMV (HHV-5)	Corneal endotheliitis, CMV anterior uveitis	CMV retinitis, immune recovery uveitis (IRU)
EBV (HHV-4)	Mild uveitis (rare)	ARN-like lesions (rare)
HTLV-1	Intermediate to panuveitis (veil-like vitreous opacities)	Same as left (severe)
Rubella virus	Association with Fuchs heterochromic iridocyclitis	─

3-2. Acute retinal necrosis (ARN)

ARN presents as acute iridocyclitis with pigmented keratic precipitates and is a necrotizing retinitis in which yellowish-white granular lesions in the peripheral fundus rapidly coalesce and expand. VZV is the most common cause (often severe cases), followed by HSV-1/2. Rhegmatogenous retinal detachment with retinal tears occurs at a high rate (approximately 75%), and visual prognosis is poor¹⁸⁾.

Japanese Ocular Inflammation Society ARN Diagnostic Criteria (Definite diagnosis group):

• Initial ocular findings: ① anterior chamber cells or mutton-fat KP, ② one or more yellow-white lesions (peripheral), ③ retinal arteritis, ④ optic disc hyperemia, ⑤ inflammatory vitreous opacities, ⑥ elevated intraocular pressure; ① and ② are essential.
• Progression items: one or more of rapid circumferential expansion, retinal tear/retinal detachment, vascular occlusion, optic atrophy, response to anti-herpetic drugs.
• Intraocular fluid test: PCR of aqueous humor or vitreous fluid positive for HSV-1, HSV-2, or VZV.

The clinical diagnostic group (not requiring intraocular fluid test) can be diagnosed when initial findings ① and ② are present, plus two items from ③ to ⑥ and one progression item.

Zhu W, et al. Atypical presentation of acute retinal necrosis mimicking Vogt-Koyanagi-Harada disease leading to misdiagnosis: a case report. Front Med (Lausanne). 2024. Figure 2. PMCID: PMC11620890. License: CC BY.

Fundus photograph and OCT of acute retinal necrosis (ARN). Peripheral yellow-white necrotic retinal lesions, hemorrhage, vascular sheathing, and optic disc edema are seen, corresponding to the initial ocular findings of ARN diagnostic criteria. Corresponds to the clinical findings of peripheral necrotizing retinitis discussed in the section “Acute Retinal Necrosis (ARN).“

3-3. CMV retinitis

CMV is an opportunistic infection that occurs in immunocompromised patients, primarily those with AIDS, and is most common in AIDS patients whose CD4-positive T-cell count has dropped to 50–100/µL ²⁰⁾. There are three clinical types: (1) peripheral granular type (fan-shaped lesions with white granules), (2) posterior polar vasculitis type (hemorrhage and edema), and (3) frosted branch angiitis type (perivascular whitening of large vessels), which often coexist. Immune recovery uveitis (IRU) following immune recovery is an important complication ¹⁵⁾, and ophthalmic management after initiation of antiretroviral therapy is necessary.

3-4. HTLV-1-associated uveitis (HAU)

HAU occurs in approximately 0.1% of HTLV-1 carriers and is more common in regions such as Kyushu and Okinawa ¹²⁾. Characteristic findings include white granular keratic precipitates, iris nodules, vitreous opacities that are veil-like, stringy, or granular, and white granular deposits around retinal vessels. Hyperthyroidism is frequently associated. Visual prognosis is relatively good, but recurrence may occur after steroid tapering or discontinuation.

3-5. Rubella virus and Fuchs heterochromic iridocyclitis

Fuchs heterochromic iridocyclitis (characterized by the triad of heterochromia, iridocyclitis, and cataract) has been suggested to be associated with rubella virus. In congenital rubella syndrome, transplacental infection within the first three months of pregnancy leads to retinochoroiditis with a salt-and-pepper fundus appearance.

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4. Overview of Bacterial Uveitis

4-1. Tuberculous Uveitis

Intraocular inflammation caused by Mycobacterium tuberculosis involves two mechanisms: direct infection and immune-mediated (hypersensitivity reaction). The clinical forms are diverse, including choroidal granulomas (tubercles), serous retinal detachment, shotgun choroiditis, vasculitis, and panuveitis.

IGRA (QuantiFERON®-TB Gold Plus or T-SPOT®.TB) is useful for diagnosis. Note that the tuberculin skin test may be negative in elderly patients and those with impaired cell-mediated immunity such as AIDS. Regarding visual prognosis in tuberculous uveitis, it has been reported that best-corrected visual acuity falls below 3/60 in about one-third of cases ³⁾. The diagnostic criteria for tuberculous uveitis proposed by the SUN Working Group (2021) include: (1) anterior uveitis with iris nodules, (2) serpiginous-like choroiditis, (3) choroidal nodules (tuberculomas), (4) multifocal choroiditis in cases of active systemic tuberculosis, and (5) occlusive retinal vasculitis ⁵⁾. In India and Indonesia, approximately 22.9–48.0% of infectious uveitis cases are attributed to tuberculosis ^3,14), highlighting its particular importance in high tuberculosis prevalence regions.

Caution

If misdiagnosed as non-infectious uveitis and treated with steroids, immunosuppressants, or biologics, it may not only worsen ocular symptoms but also trigger severe systemic tuberculosis. Before initiating biologics, always reassess the possibility of tuberculous uveitis.

4-2. Syphilitic Uveitis

Intraocular inflammation caused by Treponema pallidum is known as the “great mimicker” and can present as anterior, posterior, or panuveitis. In recent years, a global resurgence has been observed, particularly among men who have sex with men (MSM), and HIV-coinfected individuals have approximately twice the risk of ocular syphilis⁴⁾. Worldwide, an estimated 5.7 to 6 million new syphilis infections (ages 15–49) are reported annually⁴⁾, and ocular involvement occurs in about 1–1.5% of syphilis patients^4,10).

Diagnosis is made by serological tests (TPHA, RPR/VDRL), interpreted using a combination of treponemal and non-treponemal methods. Treatment follows neurosyphilis guidelines: intravenous benzylpenicillin G (Aqacillin®) 24 million units/day for 10–14 days is first-line, with intravenous ceftriaxone as an alternative. Be alert for the Jarisch-Herxheimer reaction (fever and inflammation exacerbation within 24 hours of treatment).

Ye Z, et al. Syphilis and the Eye: Clinical Features, Diagnostic Challenges, and Evolving Therapeutic Paradigms. Pathogens. 2025. Figure 1. PMCID: PMC12472546. License: CC BY.

Fundus, FAF, OCT, and fluorescein angiography of syphilitic posterior uveitis (ASPPC). Yellow-white placoid lesions at the posterior pole, outer retinal disruption, and optic disc hyperfluorescence are observed. Corresponds to posterior placoid chorioretinitis (ASPPC) discussed in the “Syphilitic Uveitis” section.

4-3. Cat Scratch Disease (Bartonella Infection)

Infection caused by Bartonella henselae, with a history of cat contact being an important interview item. Fundus findings include optic neuritis (macular star sign), macular stellate whitish spots, and serous retinal detachment, often presenting as posterior uveitis. Diagnosis is made by measuring anti-Bartonella henselae antibody titers, and antibiotic treatment with azithromycin, doxycycline, or rifampicin is administered.

4-4. Lyme Disease

An infectious disease caused by Borrelia spirochetes transmitted by ticks, with various ocular manifestations (uveitis, retinal vasculitis, optic neuritis, keratitis, etc.) appearing in stages 2 to 3. Erythema migrans is a characteristic rash in stage 1, and a history of tick bite is a diagnostic clue. Diagnosis is made by elevated serum IgM antibody titers via ELISA, and treatment is with penicillin or tetracycline antibiotics. Differentiation from syphilis and sarcoidosis is necessary.

4-5. Hansen’s Disease (Leprosy)

A chronic granulomatous infection caused by Mycobacterium leprae, with ocular involvement reported in 70-80% of cases (30-40% in recent new patients). Chronic granulomatous anterior uveitis is predominant, with characteristic findings including iris pearls, iris atrophy, small pupil, and tent-shaped peripheral anterior synechiae. Multidrug therapy (rifampicin, dapsone, clofazimine) is used, and steroid eye drops are added when uveitis is present.

4-6. Endogenous Bacterial Endophthalmitis

Endogenous bacterial endophthalmitis, in which infection spreads hematogenously to the eye from other organ infections (e.g., liver abscess, endocarditis, pneumonia), is primarily caused by Gram-negative bacilli (e.g., Klebsiella, Escherichia coli) and has an extremely poor prognosis. It progresses more rapidly than exogenous (postoperative) Gram-positive coccal infection, and systemic search for and treatment of the infection source are essential.

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5. Overview of Fungal Uveitis

Fungal endophthalmitis is mostly endogenous, with Candida spp. being the most common, and Aspergillus and Cryptococcus are also important pathogens.

Main risk factors:

• Central venous nutrition (IVH) and indwelling catheters
• Long-term broad-spectrum antibiotic use
• Immunosuppression (HIV infection, organ transplantation, malignancy, chemotherapy)
• Diabetes mellitus
• Intravenous drug use

Fungal endophthalmitis is characterized by white spherical or cotton-like vitreous opacities (“clumped opacities”) and progresses more slowly than bacterial endophthalmitis. Early stages may be asymptomatic or present only with mild floaters, making them easy to overlook. As it progresses, redness, eye pain, and panuveitis appear. 30% of endogenous fungal endophthalmitis occurs in both eyes⁸⁾.

Diagnosis is made by blood/catheter tip culture, β-D-glucan, Candida antigen measurement, and vitreous culture. Treatment is based on a combination of antifungal drugs (voriconazole, amphotericin B, fluconazole) and vitrectomy.

Tip

Unlike Behçet’s disease (where white clumps disappear relatively early), fungal endophthalmitis presents with white clumpy vitreous opacities that do not disappear and gradually enlarge, which is a key differentiating feature.

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6. Overview of Parasitic Uveitis

6-1. Ocular Toxoplasmosis

Toxoplasma gondii (an intracellular parasitic protozoan) is estimated to infect about one-third of the world’s population, and the antibody positivity rate in Japanese adults is reported to be 20–30% ¹¹⁾. Felids are the definitive hosts, and infection occurs through oral ingestion of oocysts from cat feces or consumption of undercooked meat.

Ocular toxoplasmosis accounts for approximately 1% of the causes of uveitis ¹¹⁾. The fundus findings in acquired infection are peripheral, poorly demarcated white to milky-white exudative chorioretinitis, and “satellite lesions” adjacent to old scarred lesions are characteristic findings upon recurrence. It is accompanied by anterior chamber inflammation and vitreous opacities (“headlights in the fog”). In congenital infection, scarred lesions with central gray-white fibrous proliferation and pigmentation are seen in both maculae.

Diagnosis is primarily based on characteristic ocular findings and measurement of serum antibody titers (IgG, IgM). Intraocular fluid testing using the Q value (Goldmann-Witmer coefficient) or PCR is also useful. Treatment involves oral administration of spiramycin acetate ester (acetylspiramycin) or clindamycin 1.2 g/day for 4 to 6 weeks, combined with steroids 0.5 mg/kg/day to control exudative lesions.

Miyagaki M, et al. Ocular Toxoplasmosis: Advances in Toxoplasma gondii Biology, Clinical Manifestations, Diagnostics, and Therapy. Pathogens. 2024. Figure 2. PMCID: PMC11509995. License: CC BY.

Fundus photograph of ocular toxoplasmosis. Recurrent image showing an old chorioretinal scar with pigmentation in the posterior pole and a white satellite lesion nearby. Corresponds to the satellite lesion discussed in the section “Ocular Toxoplasmosis”.

6-2. Ocular Toxocariasis

This is a larval migration disease caused by the dog roundworm (Toxocara canis) or cat roundworm (Toxocara cati), and is often unilateral. There are three types: endophthalmitis type, posterior pole mass type, and peripheral mass type (most common), which can cause severe vitreous opacities and retinal detachment. Diagnosis is made by serum antibody testing (e.g., Toxocara CHECK® ELISA) and characteristic ocular findings. Treatment includes oral anthelmintics (diethylcarbamazine), oral steroids, and may involve cryocoagulation, laser photocoagulation, or vitrectomy.

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7. Diagnostic Strategy

7-1. Key Points in History Taking

Systematic history taking is essential for the diagnosis of infectious uveitis:

• Age and sex: CMV retinitis is common in AIDS patients (mostly men in their 20s-40s), HAU in residents of Kyushu and Okinawa
• Region and travel history: Travel to areas with high tuberculosis prevalence (e.g., Southeast Asia, Africa)
• Animal contact history: Cats (Toxoplasma, Bartonella), Dogs (Toxocara)
• Dietary history: Raw meat or raw fish consumption (Toxoplasma)
• Sexual history and HIV testing history: Syphilis, CMV
• Immunosuppressed state: HIV, malignancy, organ transplant, immunosuppressant use
• IVH or catheter history: Fungal endophthalmitis
• History of herpes zoster or herpes labialis: VZV or HSV iritis

7-2. Differentiation by Ocular Findings

Finding	Suspected Infectious Disease
Mutton-fat KP	HSV/VZV iritis, ARN, tuberculous uveitis
Anterior uveitis with high intraocular pressure (≥25 mmHg)	HSV/VZV iritis, CMV anterior uveitis
Peripheral confluent white necrotic lesions	ARN (VZV/HSV)
White infiltrates with posterior pole hemorrhage	CMV retinitis (vasculitic type)
Massive vitreous opacities (progressive)	Fungal endophthalmitis
Veil-like or string-like vitreous opacities	HTLV-1-associated uveitis
Old scar + satellite lesions	Ocular toxoplasmosis
Peripheral white mass + vitreous strands	Ocular toxocariasis
Granulomatous iritis + choroidal granuloma	Tuberculous uveitis, syphilitic
Optic neuritis + macular star	Cat scratch disease (Bartonella)

7-3. Systemic examination

Examination	Target disease
Serum TPHA・RPR/VDRL	Syphilitic uveitis
IGRA (QuantiFERON・T-SPOT)	Tuberculous uveitis
CMV antigenemia (C7-HRP method)・CMV-PCR	CMV retinitis
Anti-HTLV-1 antibody	HTLV-1-associated uveitis
Anti-HIV antibody / CD4 count	CMV / PORN / ocular syphilis
β-D-glucan / Candida antigen	Fungal endophthalmitis
Anti-Toxoplasma IgG/IgM	Ocular toxoplasmosis
Anti-Toxocara antibody (ELISA)	Ocular toxocariasis
Anti-Bartonella henselae antibody	Cat scratch disease
Blood culture and echocardiography	Endogenous bacterial endophthalmitis

7-4. Intraocular fluid testing (aqueous humor and vitreous humor)

Testing using intraocular fluid is the most important definitive method for diagnosing infectious uveitis, and specimens are obtained by anterior chamber paracentesis (aqueous humor collection) or vitrectomy (vitreous humor collection)⁹⁾.

PCR method

DNA is extracted from aqueous humor or vitreous humor, and DNA of each pathogen is detected by PCR. Multiplex real-time PCR allows comprehensive detection of multiple viruses from a small sample volume and is particularly useful for differential diagnosis of ARN¹⁹⁾.

Infectious uveitis kit (advanced medical care): Can simultaneously detect HSV-1/2, VZV, CMV, EBV, HHV-6/7, HTLV-1, Toxoplasma gondii DNA, etc., and is used for diagnosing co-infections with multiple pathogens and refractory cases. However, note that PCR may not detect CMV retinitis in the early stage (before anterior chamber inflammatory cells appear).

Goldmann-Witmer ratio (Q value, antibody ratio)

This method detects the presence of pathogen-specific antibody production within the eye and is calculated using the following formula:

Q value = (Intraocular fluid virus antibody titer ÷ Intraocular fluid IgG level) ÷ (Serum virus antibody titer ÷ Serum IgG level)

• Q value >1: Possible local antibody production within the eye
• Q value ≥6: Significant local antibody production confirmed, allowing identification of the virus as the causative agent

Note that the Q value may be underestimated within the first 10 days of onset because intraocular antibody production is insufficient. Etiological diagnosis cannot be made based solely on serum antibody titers (most adults are seropositive due to past infection)⁶⁾.

Intraocular fluid PCR usage flow

眼内炎症患者
  ├─ ウイルス性疑い（高眼圧・前房炎症・壊死性網膜炎）
  │     → 前房水PCR（HSV/VZV/CMV）+ Q値 ← 第一選択
  │         ─ 前房水で陰性かつ壊死性病変 → 硝子体液PCR
  │         ─ 免疫不全者 → マルチプレックスPCR（先進医療）
  ├─ 寄生虫疑い（衛星病巣・周辺部腫瘤）
  │     → 眼内液Q値（Toxoplasma）または眼内液PCR
  ├─ 真菌疑い（塊状混濁・リスク因子あり）
  │     → 硝子体液培養 + β-D-グルカン（血液）
  └─ 細菌疑い（急速進行・IVH歴）
        → 硝子体液グラム染色・培養（至急）

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8. Principles of treatment

Corticosteroid monotherapy is generally contraindicated

Using corticosteroids alone for infectious uveitis may cause rapid worsening of inflammation. For infectious cases, specific treatment (antiviral, antibacterial, antifungal, antiparasitic) must precede or accompany corticosteroid therapy. Systemic corticosteroid administration should not be initiated without ruling out infection.

8-1. Specific treatment by pathogen

Pathogen	First-line treatment	Notes
HSV (ARN, iritis)	ACV 10 mg/kg ×3 times IV for 2 weeks → VACV 1,000 mg ×3 times/day oral	Combine with steroid eye drops and IV for anti-inflammation
VZV (ARN, iritis)	ACV 10-15 mg/kg x3 IV + VACV oral	PORN follows CMV treatment
CMV (retinitis)	GCV 5 mg/kg x2 IV for 2-3 weeks (induction) → VGCV 900 mg x2/day oral (maintenance)	Immune recovery is the curative treatment
CMV (anterior uveitis)	GCV gel 0.15% eye drops (73% of specialists choose as first-line) ± oral VGCV	For chronic course, consider 12-month maintenance therapy (73% of specialists choose GCV gel 0.15%) 2)
Tuberculosis	INH, RFP, PZA, EMB (standard 6-month regimen)	Corticosteroids used as appropriate
Syphilis	Benzylpenicillin G 24 million units/day IV for 10–14 days	Watch for Jarisch-Herxheimer reaction
Fungal (Candida)	Voriconazole or amphotericin B ± vitrectomy	Monitor with β-D-glucan index
Toxoplasma	Acetylspiramycin + steroid or clindamycin	Caution in pregnancy (use spiramycin)
Toxocara	Diethylcarbamazine + steroid	Consider laser/vitrectomy
Lyme disease	Amoxicillin or doxycycline for 3 weeks	Add steroid eye drops for ocular involvement
Leprosy	MDT (rifampicin, DDS, clofazimine)	Steroids needed during leprosy reaction

8-2. Appropriate Use of Steroids

When using steroids for infectious uveitis, anti-pathogen treatment must precede or be given concurrently. The role of steroids is to reduce secondary tissue damage caused by inflammation, and they are used in combination with appropriate pathogen treatment for many infectious uveitis conditions such as ARN, toxoplasmosis, tuberculous uveitis, and Hansen’s disease uveitis.

On the other hand, for CMV retinitis (a pure opportunistic infection), treatment of the underlying disease (AIDS) to improve immune function is the curative therapy, and steroids are generally not used.

8-3. Mydriatics and Intraocular Pressure Management

To prevent posterior synechiae, tropicamide-phenylephrine eye drops (1–6 times/day) are used for anterior segment inflammation. For elevated intraocular pressure (characteristic of HSV/VZV iritis and CMV anterior uveitis), intraocular pressure-lowering drugs such as carbonic anhydrase inhibitors and beta-blockers are selected, but prostaglandin-related drugs carry a risk of exacerbating inflammation and should be used with caution.

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9. Risk Matrix by Immunosuppressive Condition

Background	Pathogens Requiring Special Attention	Priority Tests
HIV infection (CD4 <50/µL)	CMV (retinitis, ARN, PORN), fungi (Cryptococcus), syphilis	Intraocular fluid PCR (multiplex), CMV antigen, β-D-glucan
After solid organ transplant / immunosuppressant use	CMV, fungi (Aspergillus, Candida), EBV	CMV-PCR, β-D-glucan, blood culture
Malignancy / after chemotherapy	Fungi (Candida, Aspergillus), CMV	β-D-glucan, blood culture
Long-term IVH / catheter placement	Candida endophthalmitis	β-D-glucan / blood culture (ophthalmology consultation mandatory)
High tuberculosis risk (travel / contact history)	Tuberculosis (choroidal granuloma / vasculitis type)	IGRA / chest CT
MSM (men who have sex with men) / HIV+	Syphilis (ocular syphilis approx. 1–1.5%), CMV	TPHA, RPR, HIV testing
Immunocompetent (middle-aged and older)	HSV/VZV iridocyclitis, ARN	Anterior chamber PCR, Q value
Childhood/pet contact history	Toxocara/Toxoplasma	Serum antibody (ELISA)

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10. Frequently Asked Questions

Q If infectious uveitis is suspected, at what point should intraocular fluid testing be performed?

A

When it is difficult to differentiate between infectious and non-infectious uveitis based on clinical findings alone, or when serological tests are negative despite suspicion of infection, anterior chamber paracentesis is actively considered. In particular, when necrotizing retinitis (ARN, PORN, CMV retinitis) is suspected, intraocular fluid PCR is performed as early as possible because early definitive diagnosis directly affects treatment choice and prognosis. Multiplex PCR is useful for cases that are PCR-negative in the early stage or refractory cases.

Q How should patients with infectious uveitis who have been treated with steroids be managed?

A

First, intraocular fluid PCR for pathogen identification should be performed promptly, and specific antimicrobial therapy should be initiated as soon as the pathogen is identified. Since abrupt discontinuation of steroids may cause rebound inflammation, the dose should be carefully tapered after starting anti-pathogen treatment. In particular, when steroids have been administered alone for tuberculous uveitis, the risk of reactivation and dissemination of latent tuberculosis is increased, so systemic evaluation (chest CT, IGRA) should be performed urgently in collaboration with a respiratory physician.

Q Can recurrence of ocular toxoplasmosis be prevented?

A

After treatment, Toxoplasma remains as drug-resistant cysts within atrophic scarred lesions. Recurrence occurs in approximately 5–30% of cases, triggered by immunosuppression or pregnancy. For patients with frequent recurrences, long-term prophylactic treatment with trimethoprim-sulfamethoxazole may be considered. During pregnancy, if a Toxoplasma antibody-negative pregnant woman has a primary infection, there is a risk of vertical transmission to the fetus (approximately 40%), so she should be advised to avoid contact with cat feces, soil, and consumption of raw meat.

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11. Related Articles

Viral Uveitis

壊死性ヘルペス性網膜炎（ARN・PORN） 急性網膜壊死と進行性外層網膜壊死：VZV/HSVによる壊死性網膜炎の診断基準と治療

CMV網膜炎 免疫不全患者に発症するサイトメガロウイルス網膜炎の診断・治療・免疫回復ぶどう膜炎

CMV前部ぶどう膜炎 免疫正常者にも発症するCMVによる高眼圧性前部ぶどう膜炎

単純ヘルペスぶどう膜炎 HSVによる前部ぶどう膜炎：前房水PCRによる診断とアシクロビル治療

帯状疱疹ぶどう膜炎 VZVの再活性化による前部ぶどう膜炎：眼部帯状疱疹と高眼圧の管理

HTLV-1関連ぶどう膜炎 九州・沖縄に多いHTLV-1キャリアに発症するベール状硝子体混濁を特徴とするぶどう膜炎

風疹ウイルス関連ぶどう膜炎 Fuchs虹彩異色性虹彩毛様体炎と先天風疹症候群の眼病変

Bacterial and Other Infectious Uveitis

梅毒性ぶどう膜炎 近年再増加する梅毒による多彩なぶどう膜炎：神経梅毒に準じたペニシリン療法

結核性ぶどう膜炎 IGRAと脈絡膜肉芽腫による診断・抗結核療法の実際

ライム病ぶどう膜炎 マダニ媒介ボレリア感染による多彩な眼病変

猫ひっかき病（バルトネラ） ネコ接触歴と神経乳頭炎・黄斑部星状白斑が特徴

ハンセン病の眼合併症 らい菌による肉芽腫性虹彩毛様体炎：虹彩真珠と多剤併用療法

内因性細菌性眼内炎 血行性散布による急速進行性眼内炎：感染源検索と早期治療

真菌性眼内炎 カンジダを中心とした内因性真菌眼内炎：易感染性宿主での管理

眼トキソプラズマ症 衛星病巣と霧中のヘッドライト：後天感染・先天感染の診断と治療

眼トキソカラ症 回虫幼虫移行症による眼内炎・後極部/周辺部腫瘤型の管理

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References

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