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Infectious uveitis: An enigma

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Ocular Infection Update

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Infectious uveitis: An enigma
Parthopratim Dutta Majumder, Avirupa Ghosh1, Jyotirmay Biswas

Abstract:
Infectious uveitis accounts for majority of the cases of uveitis in developing countries. It also
Website: encompasses an array of various microorganisms and their clinical presentations. Some of these
www.meajo.org infectious uveitic entities are familiar, while others are newly emerging in the global ophthalmic world.
Many of these entities are also a major cause of morbidity and mortality, and appropriate, timely
DOI:
management is required to save not the eye, but life of the patient. This review highlights the ocular
10.4103/meajo.
MEAJO_252_16
manifestations of various infectious uveitic entities, relevant to the ophthalmologist.
Keywords:
Acute retinal necrosis, dengue, infectious uveitis, syphilis, toxoplasmosis, tuberculosis

Introduction Ocular Toxoplasmosis

I nfectious uveitis remains an enigma for

the treating ophthalmologists. Risk of
vision‑robbing complications, higher rate
Ocular toxoplasmosis is caused by the
protozoan parasite Toxoplasma gondii.
The parasite has been reported to infect
of recurrences, absence of effective local approximately 13%–50% of the world’s
therapies, and difficulty in diagnosis are population.[10] Transmission of the disease
the major challenges in the management of can occur to human being through following
infectious uveitis. This article reviews salient routes: by ingestion of undercooked meat
features of some common infectious uveitic of an intermediate host (lamb, pork, and
entities and their management. Furthermore, beef), by inadvertent contamination of
description of infectious entity such as human hands when disposing of cat litter trays and
immunodeficiency virus (HIV)‑related eye then subsequent transfer onto food, or by
disease is beyond the scope of this article and transplacental or vertical transmission of
was not included in this write‑up. the parasite to fetus.[11] Children are usually
infected by eating dirt (pica) containing
Epidemiology of Infectious spore of the parasite. Recent report showed
Uveitis in Developing Countries that water contamination plays an important
role in the transmission of the disease in
Infectious uveitis accounts for majority of endemic areas.
the cases of uveitis in developing countries,
often up to 50% of the cases.[1] Epidemiology Ocular toxoplasmosis typically
Department of Uvea, of infectious uveitis varies considerably by manifests as a localized necrotizing
Sankara Nethralaya, geographic location around the world and retinitis. [12] Characteristic lesion can be
Chennai, Tamil Nadu, can be attributed to the differences in regional seen as a gray‑white focus of retinal necrosis
1
Department of Uvea, distribution of various microorganisms. at the edge of a preexisting pigmented
Aditya Birla Sankara
Other important factors are differences chorioretinal scar associated with severe
Nethralaya, Kolkata, India
in climatic conditions, host factor, and vitritis [Figure 1]. Visualization of white
Address for regional customs. Table 1 enlists the pattern retinal lesion hazily through a dense vitritis
correspondence: of distribution of infectious uveitis in has given the dictum “headlight in the fog”
Dr. Parthopratim Dutta developing countries. for ocular toxoplasmosis. The associated
Majumder, Department
of Uvea, Sankara iritis can be quite severe with granulomatous
This is an open access article distributed under the terms of the
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Road, Nungambakkam, License, which allows others to remix, tweak, and build upon
Chennai ‑ 600 006, the work non-commercially, as long as the author is credited How to cite this article: Majumder PD, Ghosh A,
Tamil Nadu, India. and the new creations are licensed under the identical terms. Biswas J. Infectious uveitis: An enigma. Middle East
E‑mail: drparthopratim@ Afr J Ophthalmol 2017;24:2-10.
gmail.com For reprints contact: [email protected]

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Dutta Majumder, et al.: An update on infectious uveitis

Table 1: Common causes of infectious uveitis in developing countries

Clinical entities India[2] Lebanon[3] Tunisia[4] Saudi Arabia[5] Iran[6] Iraq[7] Thailand[8] Myanmar[9]
Toxoplasmosis 2.5 8 10.1 6.9 50.9 13.8 2.8 2.9
TB 10.1 5.7 1.1 17.8 1.8 11.4 1.6 32.4
Herpetic 4.9 6.2 11.9 5.3 13.6 1.9 ‑ 2.9
ARN ‑ ‑ 0.8 ‑ 10 0.6 ‑ ‑
Syphilis 0.3 0.5 0.6 ‑ ‑ 0.6 1.1 2.9
CMV ‑ 1.9 0.6 ‑ 4.5 0.3 ‑ 3.6
Toxocariasis ‑ ‑ 1.5 ‑ 5.6 0.3 1.6 2.9
TB: Tuberculosis, ARN: Acute retinal necrosis, CMV: Cytomegalovirus

by a 25–50 mg dose daily and a 2–4 g of sulfadiazine daily

for 2 days, followed by a 500 mg to 1 g dose every 6 h as
well as 5 mg of folinic acid daily for 4–6 weeks.[17] Oral
prednisolone (1 mg/kg daily) is given from the 3rd day of
therapy and tapered over 2–6 weeks.[18] Other treatment
regimens include quadruple drug therapy (classic
regimen plus clindamycin) as well as single or combined
use of clindamycin, trimethoprim‑sulfamethoxazole,
spiramycin, minocycline, azithromycin, atovaquone, and
clarithromycin. Intravitreal clindamycin with intravitreal
corticosteroid is also used to treat ocular toxoplasmosis.
However, repeated injections are required due to shorter
half‑life of intravitreal clindamycin.[19]

Ocular Toxocariasis
Figure 1: Fundus photograph of left eye showing active chorioretinitis of ocular
toxoplasmosis at edge of a healed scar Ocular toxocariasis is caused by Toxocara canis or less
frequently by Toxocara cati. Transmission to humans
increased intraocular pressure (IOP). [12] Atypical occurs by ingestion of embryonated eggs or larvae.
presentations such as retinal vasculitis, neuroretinitis, After ingestion, the larvae migrate through the intestinal
vitritis, iritis, and papillitis may also be seen. Ocular wall, reach the bloodstream, and thus reach to various
toxoplasmosis in immunocompromised individuals organs (i.e., eye) where they induce an inflammatory
causes a severe, fulminant disease often with central reaction.[20]
nervous system involvement, which carries a poor
prognosis and may be rapidly fatal if untreated. Ocular toxocariasis is an important cause of childhood
visual morbidity. Typically, it affects one eye only,
Diagnosis of ocular toxoplasmosis is almost always bilateral cases being <40%.[21] Anterior segment clinical
clinical.[13] An acute T. gondii infection can be demonstrated findings may vary. The most common presentation is a
by detection of specific immunoglobulin M (IgM) or IgA posterior pole granuloma, a focal, whitish subretinal or
antibodies, or both, in the blood.[14] IgM usually appears intraretinal inflammatory mass usually <1‑disc diameter
in the 1st week after infection, peaks at 1 month, and with or without pigmentation, with varying degree
disappears after 9 months. The demonstration of local of overlying vitreous haze. Peripheral granulomas
synthesis of specific antibodies is a valuable diagnostic present with varying degree of pigmentary changes
tool in ocular toxoplasmosis. Intraocular production of and surrounding membranes [Figure 2]. Sometimes, the
antibody can be calculated by the Goldmann–Witmer inflammation can be diffuse leading to snow banking.
coefficient.[15] Polymerase chain reaction (PCR) and These granulomas can be connected with the optic nerve
recently, real‑time PCR have been utilized as a rapid head or posterior pole by a fibrocellular band which
and sensitive technique for the diagnosis of ocular can lead to tractional or combined retinal detachment.
toxoplasmosis. The use of intraocular antibody titer Nematode endophthalmitis is a severe manifestation
along with PCR yields higher sensitivity.[16] with diffuse inflammation which may even lead to
phthisis or panophthalmitis. Other rare manifestations
The most common treatment for ocular toxoplasmosis include optic neuritis, diffuse chorioretinitis or diffuse
consists of pyrimethamine‑sulfadiazine combination and unilateral subacute neuroretinitis, and motile subretinal
corticosteroids. This therapy consists of an initial dose of larvae.[22] The characteristic feature of ocular toxocariasis
75–100 mg of pyrimethamine daily for 2 days, followed is intraocular migration of the granuloma, continuous or

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Dutta Majumder, et al.: An update on infectious uveitis

discontinuous. Ocular complications include tractional

retinal detachment, epiretinal membrane, cystoids
macular edema, and macular hole formation.

Diagnosis is basically clinical. Ancillary test includes

ultrasound showing the hyperechoic granuloma with
tractional band. Serological diagnosis is performed by
enzyme‑linked immunosorbent assay (ELISA) based on
the excretory‑secretory antigens of T. canis.[23] The ELISA
at a serum titer >1: 32 has 78% sensitivity for the detection
of toxocariasis. Elevated serum IgE also provides a clue
to diagnosis.

The first line of treatment is controlling the inflammation

with systemic and topical steroids. Antihelminthic
therapy with albendazole, though recommended for Figure 2: Montage photograph of an eye with peripheral granuloma in ocular
systemic toxocariasis, the role in ocular toxocariasis has toxocariasistoxocariasis
not established. Report of destroying the larva by retinal
laser photocoagulation has been reported.[24] Table 2: Clinical spectrum of ocular syphilis
Ocular structure Type of lesion/involvement
Syphilis Eyelid Chancre
Gumma
Syphilis is a systemic infection caused by the spirochete Ulcerative blepharitis
bacterium Treponema pallidum. There has been a recent Conjunctiva Chancre
reemergence of syphilis as a coinfection with HIV. Conjunctivitis
Syphilis has been found to increase the risk of HIV Cornea Interstitial keratitis
transmission. HIV infection, in turn, can alter the natural Punctate keratitis
history of syphilis, making the diagnosis of syphilis more Sclera Episcleritis
difficult. Syphilis is considered as “the great imitator” as Scleritis
it has plethora of clinical manifestations and thus mimics Iris and ciliary body Roseolae
many diseases. Papules
Gumma
Syphilis has a complex and variable course, three Pupil Argyll Robertson pupil
progressive clinical stages with chronological Optic nerve Perineuritis
overlap – primary, secondary, and tertiary syphilis. Anterior optic neuritis
Latent syphilis is characterized by positive serological Retrobulbar neuritis
tests with no clinical evidence of infection. Ocular Neuroretinitis
syphilis rarely manifests in primary stage, except as Papilledema
chancres of the eyelid and conjunctiva. The secondary Optic atrophy
stage may have ocular involvement in the form of Motility dysfunctions Cranial nerve palsies
keratitis, iris nodules, iridocyclitis, episcleritis, scleritis, Basilar meningitis
Periodic alternating nystagmus
chorioretinitis, and vitritis.[25] Ocular syphilis is more
Retina and vitreous Chorioretinitis
frequent in the late, latent, and tertiary stages. Syphilis
Necrotizing retinitis
should be suspected in any case of unexplained ocular
Retinal vasculitis
inflammation, and many a times, ocular involvement
Central retinal artery/vein occlusion
can be the only presenting feature of systemic syphilis.
Vitritis
Table 2 summarizes the spectrum of ocular involvement Exudative retinal detachment
in syphilis.

The diagnosis of syphilitic posterior uveitis requires lymph node aspirates, cerebrospinal fluid (CSF), blood,
high index of suspicion. Dark‑field microscopy involves vitreous aspirate, etc. [26] Serological testing can be
direct visualization of T. pallidum by examining exudates divided into two groups: nontreponemal tests, which
from tissue specimens with compound microscope detect nonspecific treponemal antibody (e.g., venereal
with a dark field condenser. Using specific gene target diseases research laboratory test, rapid plasma reagin
primers and probes, PCR has been reported to detect test), and treponemal tests, which detect specific
T. pallidum genomes from ulcerative lesion swabs, treponemal antibody (e.g., T. pallidum hemagglutination

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Dutta Majumder, et al.: An update on infectious uveitis

assay and fluorescent treponemal antibody‑absorbed).[14] As with other forms of extrapulmonary TB, a primary
Nontreponemal tests are nonspecific and may yield false pulmonary focus is usually not found in ocular TB.[28]
positive results due to cross‑reactivity. They are usually
used as screening tests for syphilis and can be used Ocular TB has a plethora of clinical presentations.[28] A
to monitor disease activity and efficacy of treatment. brief summary of common ocular involvement in TB is
Treponemal tests use recombinant treponemal antigens highlighted in Table 3.
and unlike nontreponemal tests cannot be used to assess
disease activity and treatment outcome. These tests are The definitive diagnosis includes isolation of
primarily used to confirm the diagnosis of syphilis in a Mycobacterium tuberculosis from ocular sample, which
patient with reactive nontreponemal tests. They are more is not feasible in most of the time. Diagnosis of ocular
specific and have lower incidence of false positivity. TB in common clinical practice includes tuberculin skin
sensitivity test (TST), interferon‑gamma release assay,
The United States Center for Disease Control and and radiological evidence of pulmonary involvement
Prevention (CDC) recommends performing a lumbar with the help of X‑ray chest or high‑resolution
puncture to evaluate for neurosyphilis in all individuals computerized tomography (chest).
with ocular syphilis.[27] Furthermore, all patients with
primary and secondary syphilis should be tested for For definitive diagnosis, PCR for M. tuberculosis from
HIV infections, and in areas with high prevalence of aqueous or vitreous tap can be done. Now, the sensitivity
HIV, such patients should be retested for HIV infection and specificity have been improved using real‑time
in 3 months if first HIV test was negative. PCR and nested PCR. Histopathological evaluation for
caseating granuloma can be advised in case of enucleated
Parenteral penicillin G is the drug of choice for specimen or from retinal biopsy specimen if obtained in
treating all stages of syphilis. Syphilis is treated cases of unclear diagnosis with above tests.
according to the CDC guidelines. According to the CDC
recommendations, ocular syphilis warrants treatment Gupta et al. have proposed a classification of intraocular
like neurosyphilis even if the CSF study is normal. The TB[34] [Table 4]. The classification scheme is based on
standard regime of treatment is intravenous (IV) aqueous clinical signs, ocular and systemic investigations, and
crystalline penicillin G 18–24 million units/day for response to antitubercular therapy (ATT) over a period
10–14 days. Another recommended regimen is procaine of 4–6 weeks.
penicillin G 2.4 million units intramuscular (IM) once
daily plus probenecid 500 mg orally four times a day, ATT should be used in the presence of strong clinical
both for 10–14 days.[27] In patients with penicillin allergy suspicion and strongly positive TST (>15 mm). The
ceftriaxone 2 g daily either IM or IV for 10–14 days is a schedule is same as for other extrapulmonary TB therapy
good alternative. with four drug regimens of isoniazid, ethambutol,
rifampicin, and pyrazinamide for even 12–18 months.
Ocular Tuberculosis ATT decreases the antigen load; thus, the severity of
hypersensitivity reaction. ATT is combined with oral
Ocular tuberculosis (TB) is thought to be caused by steroids or immunosuppressive therapy in a tapering
either direct invasion of the eye by tubercle bacilli or dose over 6–12 weeks. ATT has been shown to reduce
a hypersensitivity response to the tubercular antigen. the recurrence rate of uveitis.

Table 3: Spectrum of ocular tuberculosis

Clinical signs Description
Chronic granulomatous anterior uveitis[28] Mutton fat keratic precipitates, Koeppe and Bussaca’s nodules, broad‑based posterior
synechiae
Intermediate uveitis[29] Vitritis, exudates in pars plana, peripheral vascular sheathing, peripheral
retinochoroidal granuloma
Choroidal tubercle[30] Most common, yellowish white, deep choroidal lesions, typically elevated at the
center, with fuzzy margins
Choroidal tuberculoma[31] Solitary subretinal mass with sharp and distinctive border, often associated with
hemorrhage, retinal folds and subretinal fluid surrounding it
Subretinal abscess[32] Represents extreme form of the spectrum, yellowish subretinal abscess [Figure 3],
ultrasound‑B scan shows anechoic space in mass
Serpiginous‑like choroiditis[33] Unilateral, multifocal, associated with vitreous/anterior chamber inflammation, spares
peripapillary area in early phase, pigment clumping occurs at the center of the lesions
Tubercular obliterative periphlebitis Patients have moderate vitritis, perivascular cuffing with infiltrates, extensive
peripheral capillary nonperfusion and active or healed patches of choroiditis under the
retinal vessels in cases of active bacilli inside the eye

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uveitis can occur without corneal involvement. The iris

atrophy is usually sectoral and occurs due to an occlusive
vasculitis. Usually, VZV uveitis occurs within the first
10 days of zoster, but chronic uveitis can also occur. The
characteristic skin lesions help in diagnosis, especially
involvement of the tip of nose (Hutchinson’s sign).

CMV anterior uveitis should be considered in cases

suggestive of herpetic anterior uveitis, but not responding
to corticosteroids and high dose of acyclovir. The
characteristic finding is a nummular keratic precipitate.
CMV‑associated anterior uveitis has no corneal scars, no
posterior synechiae, no flare or fibrin, and no posterior
segment involvement.[36]

Figure 3: Fundus photograph of patient of military tuberculosis showing multiple

Diagnosis is basically clinical. Aqueous humor aspirates
choroidal tubercles may be analyzed for the local production of antibodies
directed against HSV or VZV by the ELISA method.
Table 4: Classification of ocular tuberculosis Detecting viral DNA in aqueous by PCR is confirmatory,
Confirmed IOTB (both 1and 2) but it yields positive result in only 30% of suspected
1. At least one clinical sign suggestive of IOTB herpetic anterior uveitis cases.[37]
2. Microbiological confirmation of MTB from ocular fluids/tissues
Probable IOTB (1, 2, and 3 together) Treatment is given with topical corticosteroids and
1. At least one clinical sign suggestive of IOTB (and other cycloplegics. Oral antiviral is thought to be beneficial as it
etiologies excluded) achieves therapeutic concentration in aqueous humor.[38]
2. Evidence of chest X‑ray consistent with TB infection or clinical The initial dose is 800 mg five times/day for 7–10 days
evidence of extraocular for VZV‑associated uveitis and 400 mg five times/day
TB or microbiological confirmation from sputum or extraocular sites
for 7 days for HSV‑associated uveitis.
3. At least one of the following
Documented exposure to TB Acute Retinal Necrosis
Immunological evidence TB infection
Possible IOTB (1, 2, and 3 together) (or 1 and 4) Acute retinal necrosis (ARN) generally affects healthy,
1. At least one clinical sign suggestive of IOTB (and other
immunocompetent young adults regardless of sex or
etiologies excluded)
race. It usually begins with unilateral disease. Second
2. Chest X‑ray not consistent with TB infection and no clinical
evidence of extraocular TB eye becomes involved in one‑third cases usually within
3. At least one of the following 1–6 weeks. ARN is caused by multiple members of the
Documented exposure to TB herpes virus family, mainly VZV, HSV Type 1, and
Immunological evidence TB infection Type 2, and rarely CMV and Epstein–Barr virus.
4. Evidence of chest X‑ray consistent with TB infection or clinical
evidence of extraocular TB Early symptoms are usually very minimal and patients
IOTB: Intraocular tuberculosis, TB: Tuberculosis, MTB: Mycobacterium may complain irritation, redness, photophobia, and
tuberculosis
floaters. Anterior segment examination reveals mild
to moderate anterior uveitis. The characteristic triad of
Herpetic Uveitis lesions consists of moderate to severe vitritis, confluent
necrotizing retinitis, and vasculitis. Ophthalmoscopically,
In humans, herpetic uveitis is primarily caused by three the retinal necrosis appears as well‑demarcated,
herpes viruses, herpes simplex virus (HSV), varicella multifocal patches of yellowish‑white infiltrates in the
zoster virus (VZV), and cytomegalovirus (CMV). The periphery at the level of deep retina and retinal pigment
spectrum of herpetic uveitis includes anterior uveitis, epithelium [Figure 4]. The border between the necrosis
scleral inflammation, necrotizing retinopathy, etc. and normal retina appears well‑defined, smooth, and
geographic. Over a few weeks, retinal necrosis becomes
HSV anterior uveitis usually present with corneal confluent and progresses rapidly and circumferentially
involvement. Both granulomatous and nongranulomatous toward the posterior pole. As the retinal necrosis and
anterior uveitis can occur. Both sectoral and diffuse sloughing progress, resultant debris accumulation and
iris involvement can occur because of viral‑induced inflammation of vitreous ensues often giving rise to a
endarteritis.[35] IOP rise can occur due to trabeculitis. VZV dense vitreous haze.

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Dutta Majumder, et al.: An update on infectious uveitis

vitrectomy, air‑fluid exchange, endolaser, and gas or

silicone oil tamponade, varying reports of success rate
has been published.[39]

Cytomegalovirus Retinitis
CMV is a ubiquitous double‑stranded DNA virus and
is transmitted through placental transfer, breastfeeding,
saliva, sexual contact, blood transfusions, and organ or
bone marrow transplants.

CMV retinitis is the most common opportunistic

ocular infection in immunosuppressed individuals.
CMV infection progresses from the retinal vasculature
horizontally through glial cells and vertically through
Mueller cells, to result in full‑thickness necrosis. There
Figure 4: A case of tuberculous subretinal abscess
is distinction between the affected area and normal
retina, which allows us to measure the progression rate
Retinal thinning and atrophy starts at the peripheral
of CMV retinitis. The lesions in CMV retinitis spread
margins and gradually moves centrally. Meanwhile,
much more slowly than HSV or varicella‑zoster retinitis.
retinal pigment epithelium perturbation develops with
Classically, three patterns of active lesions have been
areas of clearing, forming a characteristic “Swiss‑cheese described: hemorrhagic (with a predominance of retinal
appearance.” The thin atrophic retina often contributes hemorrhage), brush fire (with a progressively expanding
to the development of retinal holes or tears. Retinal yellow‑white margin surrounding necrotic retina), and
holes, combined with vitreous traction, lead to retinal granular (with a central atrophic area surrounded by
detachment, and thus, retinal detachments in ARN punctate white granular satellite lesions).
patients have both a rhegmatogenous and tractional
component. Three drugs are approved by the Food and Drug
Administration for the treatment of CMV retinitis:
Diagnosis of ARN is usually based on the clinical ganciclovir, foscarnet, and cidofovir.[40] All three drugs
appearance and course and PCR. With the advent of act by inhibition of CMV DNA polymerase. Because
newer technique such as real‑time PCR, which helps the drugs are virostatic, not virucidal, they must be
quantitative estimation of the pathogen, aqueous or continued indefinitely in patients with persistent
vitreous specimen can be analyzed in conditions where immunosuppression. Systemic therapy is initiated
the cause of a severe uveitis may not be obvious. with 2 weeks of twice daily IV ganciclovir 5 mg/kg
or foscarnet 90 mg/kg, or once weekly IV cidofovir
IV acyclovir is the current treatment of choice for 5 mg/kg, followed by maintenance therapy consisting
ARN. Recommended therapeutic regimen consists of once daily ganciclovir 5 mg/kg or foscarnet
of 15 mg/kg/d IV acyclovir in 3 divided doses for 90–120 mg/kg, or cidofovir 5 mg/kg every 2 weeks. Oral
7–10 days, followed by oral antiviral medication, ganciclovir 1–2 g three times daily may be used instead
either acyclovir (800 mg five times a day), valacyclovir of maintenance IV ganciclovir.
(1 g three times a day), or famciclovir (500 mg three
times a day) up to 6 weeks or more. In cases with Ocular Leprosy
acyclovir‑resistant strains of HSV and VZV, ganciclovir
can be used. Corticosteroid has been used to reduce Leprosy is caused by Mycobacterium leprae and is more
the inflammatory component Topical corticosteroid common in tropical countries. The longitudinal study on
can be used to treat anterior segment inflammation. ocular leprosy found potential leprosy‑related blinding
Culbertson et al. recommended applying prophylactic pathology in 11% patients. Transmission occurs through
confluent laser photocoagulation posterior to the areas droplets from respiratory secretions as well as ulcerative
of active retinitis to create a “new artificial ora serrata.” skin lesions. Susceptibility depends on age (bimodal
A reduction in occurrence of retinal detachment to 17% distribution, <10 years and more than 60 years), sex (male
in patients with laser photocoagulation compared with sex), and low socioeconomic status. Lepromatous leprosy
67% in nonlaser‑treated patients has been reported by tends to be associated with more severe intraocular
Sternberg and its associates. Surgical management of involvement, whereas patients with tuberculoid leprosy
retinal detachment in ARN patients is often frustrating. typically present with early involvement of the motor
However, with the help of techniques such as pars plana and sensory nerves with predominantly corneal lesions.

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Patient can present with nodular episcleritis, diffuse Table 5: Ocular manifestations of few common
scleritis, or episcleritis which is an immune reaction. emerging infectious entities
This diffuse variety usually has associated iridocyclitis Clinical entity Clinical manifestations
and keratitis. Other findings include iris pearls, ocular Dengue Subconjunctival hemorrhage
hypotony, diffuse choroiditis, focal retinal pigment Iritis, iridocyclitis
epithelial alterations. Diagnosis is clinical with PCR or Intermediate uveitis
histopathology having a supportive role. Management Maculopathy, foveolitis
Retinal vascular occlusions
is basically with multidrug therapy, with corticosteroids
Retinitis, chorioretinitis, neuroretinitis
and cycloplegics. Clofazimine 100 mg TDS is also helpful.
Panuveitis
Chikungunya Conjunctivitis
Emerging Infections
Keratitis
Episcleritis
With tremendous advancements in the field of
Anterior uveitis
microbiological diagnostics, various newer infectious
Retinitis, choroiditis, neuroretinitis
agents have been detected worldwide in the last few
Exudative retinal detachment
decades. Salient clinical manifestations of few common
Panuveitis
emerging infectious uveitic entities are enlisted in
West Nile virus Choroiditis, chorioretinitis
Table 5.
Vitritis
Optic neuritis
Dengue virus is a mosquito‑borne single‑positive
Rift‑valley fever Macular/paramacular retinitis
stranded RNA virus of the family Flaviviridae. Dengue Retinal hemorrhage
fever is an important cause of morbidity and mortality Vitritis
in humans. Common ocular manifestations of dengue Disc edema
virus include focal chorioretinitis with macular edema, Rickettsioses Retinitis with vitritis
foveolitis, and periphlebitis. In addition, patients can Retinal vasculitis
have vitritis, anterior uveitis, intermediate uveitis, and Optic disc edema
uncommonly, optic neuritis or papillitis.[41] Foveolitis has Optic neuritis
been described as discrete, well‑defined, yellow‑orange
subretinal lesions with striae in the fovea. Diagnosis is
done by history, clinical examination, and supportive
evidence of dengue fever by serology. Most patients
improve spontaneously though some may require
corticosteroid therapy. Usually, patients retain a central
visual scotoma. Chikungunya virus, an alphavirus of the
family Togaviridae with a single‑stranded RNA genome,
can present with conjunctivitis, nongranulomatous
anterior uveitis, as well as granulomatous uveitis, keratitis
with dendritic lesions.[42] Posterior segment involvement
can manifest as retinitis, choroiditis, neuroretinitis,
and optic neuritis. Retinitis in chikungunya retinitis
usually involves posterior pole and may present with
minimal vitritis, retinal hemorrhages, retinal edema, and
associated retinal vessel involvement with cotton wool
spots [Figure 5]. West Nile virus is prevalent in Africa,
Europe, Australia, and Asia. It usually presents with a Figure 5: Montage photograph of a case acute retinal necrosis. Note the area of
confluent necrotizing retinitis
bilateral or rarely unilateral multifocal chorioretinitis
with vitritis. The distribution of chorioretinal lesions is
usually in linear arrays or scattered. Other manifestations usually bilateral and ocular symptoms start 2–3 weeks
include occlusive retinal vasculitis and optic neuritis.[43,44] after constitutional symptoms. Diagnosis is clinical
In both chikungunya and West Nile virus, diagnosis with typical inoculation papule, supported by positive
is clinical with supporting evidence by ELISA.[45] Both ELISA or immunofluorescent assay for B. henselae. Many
of them have a self‑limiting course with usually good physicians elect not to treat mild to moderate systemic cat
visual recovery. Supportive treatment is given with scratch disease in the immunocompetent host. However,
oral and topical steroids. Cat scratch disease caused by in more severe disease, a 10–14‑day course of doxycycline,
Bartonella henselae usually presents with neuroretinitis, erythromycin, trimethoprim‑sulfamethoxazole, rifampin,
multifocal choroiditis, or vasculitis.[46] Condition is or IM gentamicin is often administered.

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Dutta Majumder, et al.: An update on infectious uveitis

Diagnosis and management of infectious etiology remain Corticosteroids as adjuvant therapy for ocular toxoplasmosis.
a real challenge to the ophthalmologists. Diagnosis Cochrane Database Syst Rev 2013;(4):CD007417.
19. Baharivand N, Mahdavifard A, Fouladi RF. Intravitreal
of infectious uveitis requires high index of suspicion. clindamycin plus dexamethasone versus classic oral therapy in
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There are no conflicts of interest. Read RW, et al. Ocular toxocariasis: Epidemiologic, anatomic,
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