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Summary Table

Category	Details
Risk Factors	Immunocompromised state (HIV/AIDS with CD4 < 50 for CMV), autoimmune disease (sarcoidosis, Behcet disease, Vogt-Koyanagi-Harada), exposure to cats/undercooked meat (toxoplasmosis), TB-endemic regions, unprotected sexual contact (syphilis)
Etiology	Infectious: Toxoplasma gondii (most common worldwide), CMV, tuberculosis, syphilis, Toxocara. Non-infectious: sarcoidosis, Vogt-Koyanagi-Harada (VKH), Behcet disease, birdshot chorioretinopathy, sympathetic ophthalmia
Patient Presentation	Painless blurred vision, floaters, scotomas (visual field defects). Characteristically absent: eye pain and conjunctival redness
Classic Physical Exam	Decreased visual acuity, vitreous cells and haze on slit-lamp, chorioretinal lesions on dilated fundoscopy. In toxoplasmosis: focal yellow-white necrotic lesion adjacent to an old pigmented scar ("satellite lesion"). In CMV retinitis: hemorrhagic and necrotic patches ("pizza pie" fundus)
Key Diagnostic Results	Dilated fundoscopy is the best initial step. Fluorescein angiography, OCT for structural detail. Etiology-guided labs: Toxoplasma IgG, CD4 count for CMV, chest X-ray and ACE level for sarcoidosis, RPR/FTA-ABS for syphilis, IGRA/TST for TB
Management	Toxoplasmosis: pyrimethamine + sulfadiazine + folinic acid. CMV: valganciclovir or IV ganciclovir + HAART. TB: standard anti-TB regimen. Syphilis: IV penicillin G. Non-infectious: systemic corticosteroids with or without immunosuppressive agents
Keywords	"Painless floaters and blurred vision," "headlight in the fog," "satellite lesion near pigmented scar," "pizza pie retina," "candle wax drippings," "cotton-ball lesion"

1. Pathophysiology

Posterior uveitis refers to intraocular inflammation that primarily involves the choroid (choroiditis), and often extends to the overlying retina (chorioretinitis or retinochoroiditis) and the vitreous humor (vitritis). Understanding the anatomy is the key to understanding why this condition presents the way it does: the choroid is the most vascular layer of the eye, receiving a disproportionately high percentage of ocular blood flow. This rich perfusion makes it a natural target for hematogenous seeding of infectious organisms and for immune complex deposition in systemic autoimmune conditions.

In toxoplasmic retinochoroiditis, the most common infectious cause globally, the parasite Toxoplasma gondii establishes dormant tissue cysts within the retina during primary infection. Reactivation of these cysts triggers a focal necrotizing inflammatory response, producing the characteristic white-yellow retinal lesion sitting on top of or adjacent to an old, darkly pigmented scar from a prior episode. The overlying vitreous becomes hazy with inflammatory cells, creating the classic "headlight in the fog" appearance on fundoscopy. This is why patients describe painless floaters and blurred vision: the inflammation is deep, behind the lens, and does not irritate the anterior segment the way anterior uveitis does.

In CMV retinitis, the mechanism is direct viral cytopathic destruction of retinal cells. Because CMV reactivation occurs almost exclusively in patients with profound immunosuppression (CD4 count below 50 cells/microliter), the immune system cannot mount a vigorous inflammatory response. The result is a slowly progressive, full-thickness retinal necrosis with hemorrhage rather than a brisk inflammatory infiltrate. The retina becomes friable and prone to retinal detachment, a feared complication.

In non-infectious causes such as sarcoidosis, the choroid and retinal vasculature become infiltrated by non-caseating granulomas. Periphlebitis along retinal veins produces the "candle wax dripping" pattern (taches de bougie). In Vogt-Koyanagi-Harada (VKH) disease, an autoimmune attack against melanocyte antigens in the uveal tract causes bilateral, diffuse granulomatous inflammation. Because melanocytes are also found in the skin, meninges, and inner ear, VKH presents with a multisystem syndrome: uveitis, poliosis (whitening of eyelashes and hair), vitiligo, hearing loss, and meningeal signs.

The critical teaching point is that posterior uveitis is painless because the posterior segment lacks the sensory innervation density of the anterior chamber. Pain and redness point to anterior uveitis. The chief complaints of floaters (vitreous cells casting shadows on the retina) and blurred vision (macular or perimacular involvement) should immediately shift your differential toward a posterior process.

2. Classification and Clinical Manifestation

By Anatomic Pattern

Pattern	Primary Site	Clinical Appearance
Focal choroiditis	Single discrete choroidal lesion	Isolated yellow-white patch; most classic for toxoplasmosis
Multifocal choroiditis	Multiple scattered choroidal lesions	Several cream-colored spots; think sarcoidosis, TB, syphilis
Diffuse choroiditis	Widespread choroidal involvement	Thickened choroid with serous retinal detachment; classic for VKH
Chorioretinitis	Choroid primarily, retina secondarily	Lesion appears deep with overlying retinal edema
Retinochoroiditis	Retina primarily, choroid secondarily	Lesion appears superficial, white and fluffy; typical of toxoplasmosis
Retinal vasculitis	Retinal vessels	Perivascular sheathing, hemorrhage; Behcet, sarcoidosis, TB

By Etiology

Etiology	Fundoscopic Finding	Systemic Clues
Toxoplasmosis	Focal necrotizing lesion adjacent to pigmented scar ("satellite lesion"), "headlight in the fog"	Exposure to cats, undercooked meat; often reactivation in young adults
CMV retinitis	Hemorrhagic necrosis ("pizza pie" or "cottage cheese and ketchup"), full-thickness retinal whitening with scattered hemorrhages	HIV/AIDS with CD4 < 50, transplant recipients on immunosuppressives
Tuberculosis	Choroidal tubercles (small yellow-white nodules), serpiginous-like choroiditis	Cough, weight loss, night sweats; endemic area exposure
Syphilis	"Great mimicker": can produce nearly any pattern of uveitis; placoid lesion, optic neuritis, vitritis	Genital ulcer history, rash on palms and soles; any bilateral unexplained uveitis should prompt syphilis testing
Toxocara	Peripheral granuloma, posterior pole granuloma, or chronic endophthalmitis-like picture	Child with history of pica, contact with puppies, eosinophilia
Sarcoidosis	"Candle wax drippings" along retinal veins (periphlebitis), snowball and string-of-pearls vitreous opacities, choroidal granulomas	Bilateral hilar lymphadenopathy, erythema nodosum, elevated ACE, African descent female
VKH	Bilateral diffuse choroiditis, multiple serous retinal detachments, "sunset glow fundus" (late stage)	Poliosis, vitiligo, hearing loss, meningismus; more common in darker-pigmented ethnicities (Asian, Hispanic, Middle Eastern)
Behcet disease	Necrotizing retinal vasculitis, hypopyon, diffuse vitritis	Recurrent oral and genital ulcers, pathergy test positive; young male from Silk Road region
Birdshot chorioretinopathy	Scattered oval cream-colored spots radiating from the optic disc in a birdshot pattern	Strong association with HLA-A29; middle-aged Caucasian female

3. Diagnostic Workup

Test	Role	When to Order
Dilated fundoscopic examination	Best initial test for all suspected posterior uveitis	Always the first step
Fluorescein angiography (FA)	Characterizes vascular leakage, vasculitis pattern, ischemia	When retinal vasculitis or neovascularization is suspected
Optical coherence tomography (OCT)	Detects macular edema, subretinal fluid, choroidal thickening	To evaluate structural damage and monitor treatment
Toxoplasma IgG serology	Screening for toxoplasmosis (high seroprevalence limits utility; negative IgG effectively rules it out)	Focal retinochoroiditis with satellite lesion
CD4 count + CMV PCR (aqueous/vitreous)	Confirm CMV retinitis	Any retinitis in an immunocompromised patient
Chest X-ray	Screen for sarcoidosis (bilateral hilar lymphadenopathy) and TB (apical infiltrates, cavitary lesion)	Virtually all cases of unexplained posterior uveitis
Serum ACE level, lysozyme	Supportive of sarcoidosis	When sarcoidosis is in the differential
RPR/VDRL and FTA-ABS/TP-PA	Syphilis screening and confirmation	Every case of unexplained uveitis (syphilis is a great mimicker)
IGRA or TST	TB screening	Endemic area, choroidal tubercles, serpiginous-like choroiditis
HLA-A29 testing	Supportive of birdshot chorioretinopathy	Bilateral birdshot-pattern lesions
Aqueous or vitreous tap with PCR	Gold standard for confirming infectious etiology (toxoplasma, CMV, HSV, VZV, TB)	Atypical presentations, diagnostic uncertainty, immunocompromised host

The diagnostic approach to posterior uveitis follows a principle of pattern recognition on fundoscopy first, then etiology-directed laboratory testing.

Step 1 is always a dilated fundoscopic examination. The morphology of the lesion, its location, laterality, and the presence or absence of vitreous haze or retinal hemorrhage will narrow the differential dramatically. A focal white lesion with a pigmented scar strongly suggests toxoplasmosis. Hemorrhagic necrosis in an immunosuppressed patient points to CMV. Multiple serous retinal detachments bilaterally raise concern for VKH.

Step 2 involves baseline laboratory screening that should be ordered for nearly every patient with posterior uveitis of unclear etiology. This panel typically includes a chest X-ray (to evaluate for sarcoidosis and TB simultaneously), RPR/VDRL with confirmatory FTA-ABS (syphilis must be excluded in every case of bilateral or atypical uveitis), a complete blood count, IGRA or tuberculin skin test, and serum ACE level. The rationale for this broad screening is that syphilis, TB, and sarcoidosis can each mimic nearly any form of uveitis, and missing them has serious consequences.

Step 3 is directed testing based on the clinical picture. If the presentation is classic for toxoplasmosis (immunocompetent patient, focal lesion with adjacent scar, unilateral), the diagnosis is usually clinical, and serologic confirmation with Toxoplasma IgG is supportive but not required. A negative IgG, however, is valuable because it essentially excludes toxoplasmosis. For CMV retinitis, the combination of a characteristic fundoscopic appearance in a patient with a CD4 count below 50 is often sufficient, but PCR of aqueous or vitreous humor is the gold standard confirmatory test when there is doubt.

Fluorescein angiography is not a first-line screening tool but becomes important when retinal vasculitis is suspected (as in Behcet, sarcoidosis, or TB), when ischemic complications need to be evaluated, or when cystoid macular edema requires documentation. OCT has become increasingly central for detecting and monitoring macular edema, a common cause of vision loss in posterior uveitis regardless of etiology.

A key exam principle: never forget to test for syphilis. Syphilitic uveitis can present as anterior, intermediate, posterior, or panuveitis, and it is one of the few causes of uveitis that is fully curable with appropriate antibiotic therapy. Missing syphilis is considered a diagnostic failure.

4. Management and Treatment

Etiology	First-Line	Duration	Key Notes
Toxoplasmosis	Pyrimethamine 25-50 mg/day + sulfadiazine 1 g QID + folinic acid (leucovorin) 5-10 mg/day	4 to 6 weeks	Folinic acid prevents bone marrow suppression from pyrimethamine. Alternative: TMP-SMX. Add corticosteroids only 24-48 hours after starting antimicrobials, never before
CMV retinitis	Valganciclovir 900 mg PO BID (induction) then 900 mg PO daily (maintenance), OR IV ganciclovir 5 mg/kg BID	Induction: 14-21 days; maintenance until immune reconstitution (CD4 > 100 for 3-6 months on HAART)	Foscarnet is second-line (nephrotoxic). Intravitreal ganciclovir for sight-threatening lesions. Must initiate/optimize HAART
Ocular syphilis	IV aqueous crystalline penicillin G 18-24 million units/day (3-4 million units q4h)	10 to 14 days	Treat as neurosyphilis regardless of CSF findings. Penicillin allergy: desensitize, do not substitute
Ocular TB	Standard 4-drug anti-TB regimen: isoniazid + rifampicin + pyrazinamide + ethambutol	2 months intensive + 4 months continuation (or longer per guideline)	Systemic corticosteroids added concurrently to control inflammation. Paradoxical worsening may occur with treatment initiation
Sarcoidosis	Oral prednisone 1 mg/kg/day, taper over weeks to months	Chronic; guided by response	Steroid-sparing agents (methotrexate, azathioprine, mycophenolate) for chronic or recurrent disease
VKH	High-dose systemic corticosteroids: IV methylprednisolone 1 g/day for 3 days, then oral prednisone taper over 6+ months	Prolonged taper essential; early immunosuppression recommended	Rapid initiation prevents chronic recurrent disease. Steroid-sparing agents (azathioprine, cyclosporine, mycophenolate) started early
Behcet disease	Systemic corticosteroids + azathioprine or cyclosporine; anti-TNF agents (infliximab, adalimumab) for refractory disease	Long-term immunosuppression	Isolated topical therapy is insufficient. Interferon-alpha is an alternative

The single most important management principle in posterior uveitis is: identify and treat the underlying etiology before giving corticosteroids for infectious causes. Administering steroids to a patient with untreated infectious posterior uveitis (especially CMV or toxoplasmosis) can worsen the infection catastrophically. This is a frequent exam trap.

For toxoplasmosis, the classic "triple therapy" is pyrimethamine plus sulfadiazine plus folinic acid (leucovorin). It is critical to understand that folinic acid (not folic acid) is used to prevent pyrimethamine-induced bone marrow toxicity without interfering with the drug's antiparasitic mechanism. After 24 to 48 hours of effective antimicrobial coverage, an oral corticosteroid (prednisone 0.5-1 mg/kg/day) may be added to limit inflammatory tissue destruction. Self-limited episodes in immunocompetent patients with lesions away from the macula and optic disc may sometimes be observed without treatment, but vision-threatening lesions always warrant therapy.

For CMV retinitis, the immediate priorities are antiviral therapy and immune reconstitution. Valganciclovir is the preferred oral agent for both induction and maintenance. Ganciclovir's principal toxicity is myelosuppression (neutropenia, thrombocytopenia), which requires monitoring of the complete blood count. Foscarnet is the alternative for ganciclovir-resistant CMV or when myelosuppression is prohibitive, but foscarnet carries its own risk of nephrotoxicity and electrolyte disturbances (hypocalcemia, hypomagnesemia). Immune reconstitution with HAART is the definitive long-term strategy; maintenance antiviral therapy can be discontinued once the CD4 count has been sustained above 100 cells/microliter for 3 to 6 months.

For non-infectious posterior uveitis (sarcoidosis, VKH, Behcet, birdshot), the cornerstone of treatment is immunosuppression. Systemic corticosteroids are the initial agents, but most patients require steroid-sparing immunosuppressive therapy to avoid long-term corticosteroid complications (cataracts, glaucoma, osteoporosis, hyperglycemia). Methotrexate, azathioprine, mycophenolate mofetil, and cyclosporine are all used as second-line agents. Biologic agents such as infliximab and adalimumab (anti-TNF) have become increasingly important, particularly in Behcet disease and refractory cases.

A crucial point for VKH: early and aggressive treatment with systemic corticosteroids is associated with better visual outcomes. Delayed or inadequate therapy leads to chronic recurrent inflammation, "sunset glow fundus" depigmentation, subretinal fibrosis, and permanent vision loss.

5. Differential Diagnosis and Distractors

Differential	Why It Is Similar	Key Discriminator
Anterior uveitis (iritis)	Both are forms of uveitis causing visual disturbance	Anterior uveitis presents with pain, photophobia, and redness (ciliary flush); posterior uveitis is painless with floaters and blurred vision without significant redness
Endophthalmitis	Both cause decreased vision, vitritis, and may show hypopyon	Endophthalmitis follows recent eye surgery or penetrating trauma and progresses rapidly with severe pain; posterior uveitis has an insidious onset without surgical history
Primary intraocular lymphoma (masquerade syndrome)	Presents with vitreous cells, blurred vision, and poor response to steroids, mimicking chronic posterior uveitis	Suspect when uveitis in an elderly patient is refractory to corticosteroids. Diagnosis requires vitreous biopsy with cytology showing atypical lymphoid cells. Often associated with CNS lymphoma
Retinal detachment	Both cause floaters and visual field defects	Retinal detachment classically presents with a curtain or shadow descending over the visual field, flashes of light (photopsia), and shows retinal elevation on fundoscopy without inflammatory cells in the vitreous
Acute retinal necrosis (ARN)	Causes necrotizing retinitis with vitritis, similar to toxoplasmic or CMV retinitis	ARN is caused by HSV or VZV in immunocompetent patients, progresses rapidly and circumferentially, and shows prominent arteritis (unlike CMV which typically spares arterioles). Pain may be present
Toxoplasmosis vs. CMV retinitis	Both cause necrotizing retinitis with vitreous haze	Toxoplasmosis shows a focal lesion with an adjacent pigmented scar and prominent vitritis in an immunocompetent host. CMV retinitis shows hemorrhagic necrosis with minimal vitritis in severely immunocompromised patients (CD4 < 50)
Central serous chorioretinopathy (CSR)	Both can cause serous retinal detachment and blurred vision	CSR affects young stressed males, is unilateral, shows a single area of serous detachment with a "smokestack" pattern on FA, and has no vitreous cells or choroidal inflammation

6. Traps and High-Yield Pearls

The most common way students lose points on posterior uveitis questions is by giving corticosteroids before ruling out or treating an infectious etiology. A vignette describing a patient with a focal retinal lesion, floaters, and blurred vision who is started on corticosteroids alone without antimicrobial coverage is testing whether you recognize that steroids will worsen untreated toxoplasmosis, CMV, TB, or syphilis. The correct sequence is always: confirm or strongly suspect the etiology, initiate targeted antimicrobial therapy, and only then consider adding corticosteroids as adjunctive anti-inflammatory treatment.

A second common trap involves CMV retinitis and the CD4 threshold. If the vignette describes a patient with HIV and a CD4 count of 200 who has retinal findings, students may reflexively select CMV. However, CMV retinitis overwhelmingly occurs at CD4 counts below 50 cells/microliter. At a CD4 of 200, toxoplasmosis, syphilis, or TB-associated posterior uveitis are far more likely.

A third pitfall is confusing folinic acid (leucovorin) with folic acid in the toxoplasmosis regimen. Pyrimethamine works by inhibiting dihydrofolate reductase in the parasite. Folinic acid bypasses this block in human cells to prevent bone marrow suppression without reducing the drug's efficacy against Toxoplasma. Folic acid, on the other hand, would be converted through the same blocked pathway and is therefore ineffective as rescue therapy. This distinction is a favorite test question.

Fourth, always remember that syphilis can mimic any form of uveitis. Any exam question presenting bilateral, atypical, or treatment-refractory uveitis where syphilis testing was not performed is likely testing whether you would order RPR/FTA-ABS. The principle is: test for syphilis in every unexplained uveitis case, because it is one of the few infectious causes that is completely curable.

Finally, the core competency being tested in posterior uveitis questions is threefold: (1) recognizing that painless floaters and blurred vision without redness or pain points to a posterior (not anterior) process, (2) matching the fundoscopic pattern and patient immune status to the correct etiology, and (3) sequencing the management correctly by treating infection before inflammation.

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