Ocular Immunology & Inflammation, 2015; 23(1): 14–24

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ISSN: 0927-3948 print / 1744-5078 online
DOI: 10.3109/09273948.2014.986582

REVIEW ARTICLE

Clinics of Ocular Tuberculosis

Vishali Gupta, MD1, Samir S. Shoughy, MD, FRCS2, Sarakshi Mahajan, MBBS3,
Moncef Khairallah, MD4, James T. Rosenbaum, MD5, Andre Curi, MD6, and
Khalid F. Tabbara, MD,2,7,8,9

1
Postgraduate Institute of Medical Education and Research Chandigarh, Advanced Eye Centre, India, 2The Eye
Center and The Eye Foundation for Research in Ophthalmology, Riyadh, Saudi Arabia, 3Government Medical
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College, Chandigarh, India, 4Department of Ophthalmology, Fattouma Bourguiba University Hospital, Faculty
of Medicine, University of Monastir, Monastir, Tunisia, 5Legacy Devers Eye Institute, Portland, Oregon, USA;
and Casey Eye Institute, Oregon Health & Science University, Portland, Oregon, USA, 6Research Laboratory of
Infectious Diseases in Ophthalmology, National Institute of Infectious Diseases, INI/IPEC, Oswaldo Cruz
Foundation, Rio de Janeiro, Brazil, 7The Eye Center and The Eye Foundation for Research in Ophthalmology,
Riyadh, Saudi Arabia, 8Department of Ophthalmology, College of Medicine, King Saud University, Riyadh,
Saudi Arabia, and 9The Wilmer Ophthalmological Institute of The Johns Hopkins University School of Medicine,
Baltimore, Maryland, USA
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ABSTRACT
Purpose: Ocular tuberculosis is an extrapulmonary tuberculous condition and has variable manifestations.
The purpose of this review is to describe the clinical manifestations of ocular tuberculosis affecting the anterior
and posterior segments of the eye in both immunocompetent and immunocompromised patients.
Methods: Review of literature using Pubmed database.
Results: Mycobacterium tuberculosis may lead to formation of conjunctival granuloma, nodular scleritis, and
interstitial keratitis. Lacrimal gland and orbital caseating granulomas are rare but may occur. The intraocular
structures are also a target of insult by M. tuberculosis and may cause anterior granulomatous uveitis, anterior
and posterior synechiae, secondary glaucoma, and cataract. The bacillus may involve the ciliary body, resulting
in the formation of a localized caseating granuloma. Posterior segment manifestations include vitritis, retinal
vasculitis, optic neuritis, serpiginous-like choroiditis, choroidal tubercules, subretinal neovascularization, and,
rarely, endophthalmitis.
Conclusions: The recognition of clinical signs of ocular tuberculosis is of utmost importance as it can provide
clinical pathway toward tailored investigations and decision making for initiating anti-tuberculosis therapy.
Keywords: Anterior granulomatous uveitis, intermediate uveitis, ocular tuberculosis, posterior uveitis, scleritis

Tuberculosis (TB) is a disease that primarily affects TUBERCULAR EXTERNAL

the lungs, but may also affect extrapulmonary organs,
including the eye.1 Mycobacterium tuberculosis may
affect any structure of the eye masquerading as
several infective as well as noninfective entities and
the clinical course generally tends to be insidious and
chronic. This review aims to describe the clinical
spectrum of the lesions seen in patients with ocular
TB.
EYE DISEASE
External ocular tissue involvement in TB is primarily
due to systemic dissemination of the organism
as exogenous infection is extremely rare.2,3 Ocular
surface TB may lead to a variety of clinical manifest-
ations (Table 1). TB of the eyelids may present as a
localized nodule simulating a chalazion, while

Received 4 August 2014; revised 6 November 2014; accepted 7 November 2014; published online 23 January 2015
Correspondence: Vishali Gupta, Postgraduate Institute of Medical Education and Research Chandigarh, Advanced Eye Centre, India. E-mail:
vishalisara@yahoo.co.in

14

TABLE 1. Clinical manifestations of tubercular external
eye disease.
1. Eyelids Localized mass
2. Lacrimal gland Granuloma
Localized mass
3. Conjunctivae Conjunctival granuloma
Conjunctival ulceration
Hypertrophied papillary lesions
4. Sclera Focal non-necrotizing scleritis
Focal necrotizing scleritis
Nodular scleritis
Diffuse scleritis
Scleromalacia
Sclerokeratitis
Sclerouveitis
5. Cornea Interstitial keratitis
Disciform keratitis
Phlyctenulosis
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Corneal edema
tubercular affection of the orbit and lacrimal gland
may lead to formation of localized granuloma.2
Orbital TB is rare form of extrapulmonary TB and
forms an important differential diagnosis of orbital
mass lesions. It may reach the ocular tissue by
hematogenous route or spread directly from the
paranasal sinuses.3 Orbital TB usually spreads from
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the paranasal sinuses and may present as classical
periostitis, orbital soft tissue tuberculoma, or a cold
abscess with or without bony involvement and tuber-
culous dacryoadenitis. The ocular adnexa, including
the nasolacrimal system and the overlying skin, may
also be involved.4 Diagnosis is usually by biopsy and
supported by ancillary investigations like the tubercu-
lin skin test, imaging, interferon gamma release assay,
and molecular diagnostic techniques, such as the
polymerase chain reaction (PCR).4,5
TB of the conjunctiva may give rise to conjunctival
ulceration, conjunctival nodular lesions, or hypertro-
phied papillary lesion.6 Phlyctenular
keratoconjunctivitis is a delayed hypersensitivity
response in the cornea or conjunctiva to a variety of
antigens, including mycobacterial, staphylococcal, or
parasitic antigens.7 Phlyctenulosis in ocular TB is a
localized hypersensitivity reaction to the antigens of
M. tuberculosis that presents as a nodule at the limbus
or on the conjunctiva. Clinically, the lesions appear as
a localized elevated nodule at the limbus or at
conjunctiva with leash of blood vessels.7,8
TB may affect the cornea, leading to interstitial
keratitis that may be seen as an isolated finding or in
association with scleritis and uveitis. This association
is probably related to the presence of tubercular
antigen in aqueous humor.9 TB affecting the cornea
may also present as disciform keratitis.10
The association between scleritis and infectious
disease may be higher than earlier reports. In a recent
study including 500 patients with scleritis, 9.4% had
an underlying infectious cause and TB accounted for
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Clinics of Ocular Tuberculosis 15
10.6% of these cases.11 Scleral involvement in TB is
usually anterior.11 Involvement of the posterior sclera
is extremely rare and may present as infective isolated
posterior scleritis or posterior scleral tuberculoma.12,13
TB may also affect the episclera causing nodular
episcleritis.14 Tuberculous scleritis may result from
either a direct invasion of the sclera by M. tuberculosis
or an immune-mediated reaction to circulating myco-
bacterial anigens.15,16 Anterior tuberculous scleritis
may be localized or diffuse; most of the lesions are
nodular and localized with slight elevation of the
sclera.2 The lesions may remain focal and non-
necrotizing or may undergo scleral necrosis leading
to scleromalacia.2 If not properly treated, the lesions
may progress leading to scleral perforation. Diffuse
scleritis may occur in patients with TB but is less
common than localized nodular scleritis.2 Scleritis
may be associated with adjacent keratitis or uveitis
leading to a condition known as tuberculous
sclerokeratitis.
Scleral involvement in TB may occur in isolation or
affect the adjacent peripheral corneal stroma and iris,
causing sclerokeratitis and uveitis, respectively.2
Sclerokeratitis can be seen with peripheral stromal
inflammation in association with adjacent localized
scleritis that responds to anti-TB treatment (Figures 1,
2). Severe anterior granulomatous uveitis with pos-
terior synechiae may accompany anterior scleritis in
patients with ocular TB.17 Rarely, tuberculous scler-
ouveitis may masquerade as an ocular tumor and may
be associated with necrotizing scleritis and scleral
perforation.18
Tuberculous Anterior and Intermediate
Uveitis
Intraocular inflammations secondary to TB are rare but
TB infection is common worldwide, especially in
developing countries and in immigrant populations
and immunocompromised patients in developed
nations.19 Patients with anterior uveitis secondary to
TB present with unilateral or bilateral symptoms of
redness, photophobia, and floaters. In bilateral cases,
the disease is usually asymmetric.2 Patients may
present with anterior uveitis alone or may have other
associated clinical manifestations, such as chronic
conjunctivitis, phylectenosis, keratitis, or scleritis.2–7
Anterior uveitis is characterized by large mutton-
fat keratic precipitates (KPs), which can be few or
diffuse over the corneal endothelium (Figure 3). The
KPs may appear moderate to large in size and may
affect the corneal endothelium, leading to edema of
the lower half of the cornea. The mutton-fat KPs may
decrease in size and number after treatment with
topical steroids. Activity of anterior uveitis in patients
with ocular TB may show episodes of exacerbation
with fibrin in the anterior chamber.2 Hypopyon
 16 V. Gupta et al.
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FIGURE 1. A 31 year-old female who developed redness of the
left eye 9 months after receiving therapy for pulmonary
tuberculosis. Figure shows tuberculous nodular scleritis with
adjacent keratitis (Sclerokeratitis).
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FIGURE 2. Color photograph same eye as in Figure 1 shows the
resolution of tuberculous sclerokeratitis 3 months after anti-
tuberculous therapy.
uveitis is a rare manifestation of intraocular tubercu-
losis.20,21 Aggressive anterior uveitis may be accom-
panied by granulomatous nodules of the iris pupillary
border (Koeppe) or on the iris surface (Busacca
nodules).22 Localized nodules may form at the angle
of the anterior chambers that may lead to anterior
synechiae.2 Posterior synechiae may form and tend to
be broad-based.23 Anterior pupillary membranes with
neovascularization of the iris may occur. Cataract is a
common complication of chronic uveitis and may
occur at the site of posterior synechiae. The prolonged
use of topical corticosteroids may increase the inci-
dence of cataract.24
Intermediate Uveitis
Intermediate uveitis (IU) was defined by the
Standardization of Uveitis Nomenclature (SUN) work-
ing group as a form of uveitis where the vitreous is the
FIGURE 3. Anterior segment photograph showing granuloma-
tous uveitis with mutton fat keratic precipitates.
major site of inflammation.25 IU may be initiated by a
trabecular antigen, leading to a clinical picture of
vasculitis with presence of vitreous cells.26 IU asso-
ciated with TB tends to be particularly nonspecific in
terms of its clinical presentation. Patients generally
present with a low-grade, smoldering, chronic uveitis,
vitritis, snowball opacities, peripheral vascular sheath-
ing, and peripheral retinochoroidal granuloma.27
Snow banking is usually described in IU due to
autoimmune etiology but it has also been reported in
tubercular IU.28 In a series reported from a tertiary care
referral institute in India, TB was the most common
underlying etiology of IU seen in 57/122 (46.7%) of
patients. Addition of anti-tuberculosis treatment (ATT)
in these patients reduced the rate of recurrences to
11.9% (5 out of 42) compared to 46.7% (7 out of 15) in
patients who did not receive any ATT.29
Posterior and Panuveitis
Posterior uveitis is the most common clinical presen-
tation of ocular TB, followed by panuveitis with
granulomatous anterior uveitis.27 Tubercular posterior
segment involvement may occur as a consequence of
tissue invasion by M. tuberculosis or immune-
mediated disease.27 The main site of ocular TB is the
choroid, where the high oxygen tension may promote
organism growth. Other main posterior segment
changes include retinal vasculitis, which may occur
with or without associated choroiditis, and optic
nerve involvement.27,30–32
Choroidal TB
TB-associated choroiditis is usually characterized by a
multifocal pattern, with chorioretinal lesions variable
in shape, number, size, and location. There may or
Ocular Immunology & Inflammation

may not be associated vitritis, which is usually mild or
moderate. The disease is often insidious, frequently
bilateral, affecting predominantly young to middle-
aged males.27,30–35 There may or may not be active
concomitant systemic TB.
Choroidal Tubercles
The primary lesion in TB choroiditis is represented by
choroidal tubercles, which are foci of granuloma in
the choroid that indicate a hematogenous dissemin-
ation of the tubercular bacilli. Choroidal tubercles
appear as multiple ill-defined, round-to-oval, grayish
white or yellowish deep lesions, measuring between
0.2 and 3 mm27,30–36 (Figure 4). They predominantly
involve the posterior pole and may have overlying
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serous retinal detachment. Nearly 30% of patients
with disseminated TB or tubercular meningitis may
exhibit small choroidal tubercles, also called miliary
choroidal lesions. On fluorescein angiography (FA),
active choroidal tubercles show early hypofluores-
cence and late staining (Figures 4B, C). On indocya-
nine green angiography (ICGA), choroidal lesions are
more extensive and show hypofluorescence during
the early and intermediate phases, progressing to a
hypofluorescent center with surrounding hyperfluor-
escent edges during the late phase of the angio-
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gram.27,30–33,36
FIGURE 4. (A) Fundus photograph of the right eye of a 49 year-old male patient with tubercular meningitis shows in the posterior
fundus multiple tubercles, some of which are confluent. Fluorescein angiography shows early hypofluorescence (B) and late staining
of choroidal lesions with retinal vasculitis and optic disc staining (C).
! 2015 Informa Healthcare USA, Inc.
Clinics of Ocular Tuberculosis 17
Active choroidal tubercules gradually heal, leading
to well-demarcated atrophic areas with variable
pigmentation.
Choroidal Tuberculomas
Choroidal granuloma is described as a large, solitary,
elevated yellowish subretinal mass that may mimic
a tumor. It is usually unilateral, commonly seen in
the posterior fundus, measuring 4–14 mm, usually
associated with an overlying exudative retinal
detachment27,31,33,37 (Figure 5). Solitary choroidal
tuberculoma is usually associated with systemic
disseminated TB. On FA, choroidal tuberculomas
show early hypofluorescence and late hyperfluores-
cence. ICGA reveals a hypofluorescent lesion
throughout the angiogram phases larger than seen
on FA.38
OCT is useful in confirming the presence of
exudative retinal detachment. It may also reveal a
distinctive feature of attachment between the retinal
pigment epithelial–choriocapillaris layer and the
neurosensory retina over the granuloma (‘‘contact’’
sign).39,40 Ultrasonography shows a moderate to low
internal reflectivity mass that is not specific to TB
origin.27,41
 18 V. Gupta et al.
Subretinal abscess may develop as a result of
progressive, liquefied caseation necrosis with rapid
multiplication of bacilli and tissue destruction.27,34,42
The subretinal abscesses are more yellowish in color,
have overlying retinal hemorrhages, and have a
tendency to develop retinal angiomatous proliferation
over a period of time.27
Serpiginous-like Choroiditis
Patients, particularly from TB-endemic regions, may
present with a relentless choroiditis that may simulate
acute posterior multifocal placoid pigment epithelio-
pathy or mainly serpiginous choroiditis. This has been
referred as to serpiginous-like choroiditis (SLC), also
called multifocal serpiginoid choroiditis.43 SLC is
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believed to be caused by immune reaction to TB
antigens, and may have three morphological clinical
patterns. The first is characterized by the initial
appearance of noncontiguous, round, multifocal
lesions that show a progressive, wave-like enlarge-
ment and become confluent.36,43 The second pattern
initially presents as a disseminated plaque-like chor-
oiditis with amoeboidal spread (Figure 6). The asso-
ciation of discrete lesions and plaque-like lesions in
the same patient characterize the third pattern of
SLC.36,43 On FA, active choroidal lesions show initial
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hypofluorescence, followed by hyperfluorescence in
the late stages (Figure 6). On ICGA, the active lesions
appear hypofluorescent during the early and late
phases. SD-OCT reveals outer retinal disruption and
increased outer retinal and choroidal reflectivity in the
involved areas.43,44
In TB-associated SLC, fundus autofluorescence
shows hypoautofluorescence patches related to retinal
pigment epithelium defects that are multiple and
discrete with an irregular geographic or serpentine
pattern or like pieces of a puzzle. The early phase of
the disease shows hyperautofluorescnce of the active
edge that corresponds to active edge seen on fluores-
cein angiography. As the lesions start healing, they
FIGURE 5. Fundus photograph of the right eye showing
tubercular granuloma in the posterior pole.
show mixed autofluorescence and become more
and more hypoautofluorescent as they heal. The
completely healed lesions become totally hypofluor-
escent.43–45
Unlike typical SC, tubercular SLC is seen at a
younger age, usually accompanied with vitreous
inflammatory reaction, and may be unilateral or
bilateral. Coexistence in the same patient of
active and healed choroidal lesions, involving the
posterior pole and periphery, usually sparing the
juxtapapillary area, also characterizes tubercular
SLC.46,47 In contrast with the lesions of SC, SLC
lesions show marked progression under corticoster-
oids and immunosuppressive treatment, and improve
well on ATT.43–47
Retinal Vasculitis
Tuberculous retinal vasculitis involves more com-
monly veins than arteries.48 Active vasculitis typically
presents as severe perivenular cuffing with thick
exudates, usually associated with retinal hemorrhages
(Figure 7A), active or healed focal choroiditis lesions,
and moderate vitritis.31–33,48 Healed periphlebitis
manifests with gliotic perivenular sheathing and
abnormal vascular anastomoses. FA in active retinal
vasculitis shows staining and leakage from the vessel
walls, mainly from the veins, and papillitis31–33,48
(Figure 7B). There also may be focal or diffuse retinal
capillary leakage. Tubercular retinal vasculitis is
typically occlusive in nature. It may cause branch
retinal vein occlusion, extensive peripheral capillary
nonperfusion, branch retinal/central artery occlusion,
and retinal or optic disc neovascularization, with
sequelae such as vitreous hemorrhage, traction retinal
detachment, iris neovascularization, and neovascular
glaucoma.31–33,48–52
Macular edema also may complicate tubercu-
lar retinal vasculitis.53 OCT is useful in evaluating
macular edema and any associated serous retinal
detachment.54
The term Eales disease has been traditionally
used to describe a specific entity, mainly seen in
young adults from endemic areas and characterized
by periphlebitis, retinal capillary nonperfusion,
neovascularization, recurrent vitreous hemorrhages,
and tractional membrane formation, in the absence
of associated signs of intraocular inflammation.55,56
It has been postulated that Eales disease could
result from cell-mediated immunological damage to
retinal vessels triggered by a sequestered tubercu-
loprotein in an inactive form.57 The association
between TB and retinal vasculitis is supported by
the identification by PCR-based assays of
M. tuberculosis DNA from the aqueous vitreous,
and epiretinal membranes of patients with Eales
disease.58–60
Ocular Immunology & Inflammation
 Clinics of Ocular Tuberculosis 19
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FIGURE 6. Fundus photography (Top right and left) and fluorescein angiography (Middle and bottom) in a 35 year-old female patient
with presumed ocular tuberculosis shows active serpiginous-like choroiditis in the right eye and inactive serpiginous-like choroiditis
in the left eye.

FIGURE 7. (A) Fundus photograph of the left eye of a 55 year-old female patient with presumed ocular tuberculosis shows
perivascular exudates, retinal hemorrhages, and retinal edema. (B) Late-phase fluorescein angiogram shows retinal vascular staining,
blocked fluorescence by retinal hemorrhages, and areas of peripheral capillary nonperfusion.

! 2015 Informa Healthcare USA, Inc.

 20 V. Gupta et al.
Optic Nerve Involvement
Optic nerve involvement is a common complication of
TB. It may result from direct mycobacterial infection,
by contiguous spread from the choroid or hematogen-
ous dissemination, or from a hypersensitivity to the
infectious agent. Clinical presentation forms include
papillitis, optic neuritis, neuroretinitis, optic nerve
tubercle, retrobulbar neuritis, compressive optic neur-
opathy, anterior ischemic optic neuropathy, optic
atrophy, and optico chiasmatic arachnoiditis.12,27,61–67
In a recent multicenter study on tuberculous optic
neuropathy, papillitis (51.6%), neuroretinitis (14.5%),
and optic nerve tubercle (11.3%) were found to be the
most common clinical presentations.67 Uveitis, mostly
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posterior uveitis or panuveitis, is a common finding
in patients with tubercular optic neuropathy, found in
almost 90% of cases.67 TB also should be considered in
the differential diagnosis of apparently isolated
papillitis or neuroretinitis. In such cases, ICGA may
show subclinical choroidal involvement.64 Tubercular
choroidal lesions may develop as well later in the
course of optic neuropathy.65 Unilateral optic disc
swelling may be secondary to tubercular posterior
scleritis.66 Papilledema and, in advanced cases, bilat-
eral optic atrophy usually result from central nervous
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system TB, particularly tubercular meningitis (hydro-
cephalus), opticochiasmatic arachnoiditis, and opto-
chiasmatic tuberculoma.27,61,62
Endophthalmitis and Panophthalmitis
Endophthalmitis and panophthalmitis have been
rarely described as manifestations of ocular TB.
They are often characterized by acute onset and
rapid progression. The anterior chamber and vitreous
reaction is typically severe.27,68–70 Clinical presenta-
tion may mimic ocular tumors, particularly retino-
blastoma in children.68–70 Panophthalmitis may lead
to scleral perforation. Microbiological detection of
M. tuberculosis is often made after culture or PCR on
vitrectomy specimen or histopathological examination
of enucleated eye.68–70 The most probable mechanism
seems to be hematogenous spread.27,68–70 However, a
case of tubercular endophthalmitis following cataract
surgery has been reported with presumptive exogen-
ous acquisition during surgery.71
OCULAR TUBERCULOSIS IN
NONENDEMIC AREAS
The purpose of a laboratory test such as a skin test or
an interferon gamma release assay to determine
exposure to TB is to estimate the likelihood that a
patient has TB. Interpreting the test depends not only
on the actual result; the interpretation also depends
greatly on what is known as the pre-test likelihood
that a patient has ocular TB.72 If you as the treating
physician estimate that the pre-test likelihood for
ocular tuberculosis is low, say 1%, a positive skin test
still means that the patient is unlikely to have ocular
tuberculosis. On the other hand, if you estimate that a
patient has a high likelihood of having ocular TB, say
50%, a positive skin test would increase that likeli-
hood even further and it would induce most phys-
icians to initiate a trial of ATT.
TB is a rare disease in North America. In 2013, the
incidence of TB in the United Sates was 3 per
100,000.73 The incidence within the United States for
non-U.S.-born patients was about 13 times greater.73
The most common site for TB is the lung. In a review
of TB at Boston City Hospital from 1968 to 1977, fewer
than 5% of patients had extrapulmonary TB. None of
these patients had ocular disease. If one extrapolates
from the incidence rate noted above, the incidence of
extrapulmonary TB must be approximately 1.5 per
million. Only a tiny fraction of those with extrapul-
monary TB have ocular involvement. Thus, ocular TB
is a rare presentation of a rare disease, rare at least in
nonendemic countries. The treatment of TB with a
four-drug regimen involves potential adverse effects
from the medications as well as cost. In the average
United States uveitis clinic, it would be wrong to
screen every patient with either a QuantiFERON test
or a TB skin test and then to treat every patient with a
positive result with a four-drug regimen. Although
this approach would allow treatment of most patients
with ocular TB, it would also expose many to undue
risk and expense.
Two recent studies shed some light on the fre-
quency of ocular TB in U.S. uveitis clinics. An
esteemed group from the University of Illinois,
Chicago, reviewed its experience for a 16-year
period ending in 2010.74 This is a busy referral
center that evaluated 3606 patients with uveitis
during this time. It concluded that 14 patients with
ocular TB and 3 with atypical mycobacteria in the eye
were evaluated in that period, about 1 newly
diagnosed patient with ocular TB per year. This
calculates as 1 patient with ocular TB for every 258
patients with uveitis. While this percentage is low, the
diagnosis is obviously vital not to overlook. The delay
in diagnosis for most of the patients in this series was
nearly 2 years and this delay was associated with
irreversible damage.
A quite different experience was reported from a
group evaluating patients at a county hospital in Los
Angeles. This talented group found 6 patients with
probable or definite TB from a series of 142 consecu-
tive patients,75 1 patient with ocular TB for every 24
uveitis patients in the clinic. The Los Angeles clinic,
however, differs from many uveitis clinics in North
America in that a high percentage of patients attend-
ing the clinic are not born in the United States.
Ocular Immunology & Inflammation

There are a variety of risk factors for the development
of TB in the United States. These risk factors include a
history of homelessness, a history of HIV, a history of
incarceration, a history of previously living in an area
endemic for TB, a history of immunosuppression, or a
history of having been born outside the United States.
A failure of the inflammation to improve on standard
therapy such as topical or oral corticosteroids should
also alert the clinician to the possibility of TB. While
ocular TB was far more common in Los Angeles than
it was in Chicago, all the California patients had a risk
factor for TB.
The dilemma of not wishing to treat all uveitis
patients with either a positive TB skin test or positive
QuantiFERON test for TB but also not wishing to miss
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a treatable diagnosis can be addressed by not request-
ing the test indiscriminately. Rather than ordering a
QuantiFERON Gold test as part of the initial screening
on all attendees in the uveitis clinic, the test should be
ordered selectively. Anyone with a known diagnosis,
such as ankylosing spondylitis or Vogt-Koyanagi-
Harada syndrome, does not need a test to determine
TB exposure unless prolonged immunosuppression or
treatment with a biologic drug is anticipated. Anyone
with inflammation that resolves promptly does not
need a TB skin test. But anyone in the subset of patients
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with uveitis of unknown etiology and a risk factor for
TB or the subset with disease that is not responding to
conventional therapy becomes a good candidate for
screening. Many but not all of these patients will have
granulomatous inflammation and/or occlusive retinal
vasculitis.
Ocular TB in the United States remains a feared
diagnosis, feared by patients because of its ability to
cause irreversible visual loss, but also feared by
specialists who recognize it as a treatable cause of
uveitis. Not wishing to overlook the opportunity to
diagnose a treatable disease is an important goal. But
it is also important to reduce medical costs by
ordering lab tests appropriately, to avoid exposing
patients to unnecessary risk by treating for an unlikely
diagnosis, and to spare patients from the anxiety that
results by mentioning a diagnosis that is unlikely.
TUBERCULOSIS IN
IMMUNODEFICIENCY PATIENTS
TB is one of the most common infectious diseases in
immunodeficient host but the ocular involvement is
quite uncommon. Morinelli et al.76 reported 470 eyes
of 235 consecutive autopsies of patients with AIDS,
where they found 18 cases of infectious choroiditis of
distinct etiology, including M. tuberculosis.
Choroidal tubercles are the most common finding
reported in HIV patients with ocular TB and includes
the development of choroidal tubercles.77–80 Babu
et al.80 reviewed 766 consecutive cases of HIV/AIDS
! 2015 Informa Healthcare USA, Inc.
Clinics of Ocular Tuberculosis 21
FIGURE 8. Choroidal tubercle (arrow) in a HIV patient with
ocular tuberculosis.
in India and found 15 (1.95%) presenting with ocular
TB. Ocular manifestations included choroidal granu-
loma, subretinal masses, panophthalmitis, and con-
junctival TB. All patients presented with simultaneous
pulmonary TB. In this study too choroidal granuloma
was the most common ocular manifestation, occurring
in 10 patients (52.63%). In these 10 patients the
diagnosis of ocular TB was made based on clinical
suspicion, systemic findings, and clinical response to
ATT therapy. Five patients had the diagnosis proven
by histopathology and/or PCR. In a recent report,
Mehta et al.81 reviewed 47 HIV/MDR-TB co-infected
patients and found choroidal granulomas as the most
common finding. All patients were visually asymp-
tomatic. The authors suggested that all patients with
TB or suspected to have TB should be routinely seen
by ophthalmologist.81 Curi et al.,82 too, reported 17
patients with choroidal granulomas in a Brazilian
cohort of HIV patients and all these patients were
asymptomatic. The number of choroidal lesions
ranged from 1 to 4 and no patient presented with
vitritis or anterior segment involvement. The authors
considered a single small, yellowish choroidal lesion
as the typical finding of ocular TB among HIV
positive patients (Figure 8).
In a recent study of 1000 consecutive HIV-positive
patients, ocular TB was found in 26 patients (3.8%).
Although TB is the most common systemic infection
related to HIV in India, ocular TB is rare. Ocular TB was
found to have no correlation with the CD4+ count
range.83 In a prospective study by Beare et al.84 a
choroidal granuloma was found in 2.8% patients with
TB admitted with fever in Malawi, Africa. However, in
a prospective cross-sectional study Mehta and Gilada85
found a very high correlation between pulmonary TB
and the presence of ocular tuberculosis. They reported
23.5% patients with ocular TB in 17 patients with
clinical and radiological evidence of pulmonary
 22 V. Gupta et al.
tuberculosis. In this study all patients with ocular TB
showed evidence of abdominal tuberculosis.
There is still a lack of consensus about the
diagnostic criteria of ocular TB in immnocompetent
patients. The diagnostic criteria proposed by Gupta
et al.27 take into consideration the clinical presentation
along with corroborative or definitive evidence of
intraocular TB and therapeutic response to ATT. In
immunodeficient individuals, the majority of the
cases are presumed, where patients with HIV
having a disseminated disease present with choroidal
tubercles that are presumed to be TB. There are no
well-established clinical diagnostic criteria for intrao-
cular TB.
Ocul Immunol Inflamm Downloaded from informahealthcare.com by University of Laval on 01/25/15
SUMMARY AND CONCLUSIONS
In conclusion, ocular TB has protean manifestations
and can involve any structure of the eye, producing
various clinical manifestations. Development of these
lesions is rare in HIV-positive patients where chor-
oidal granuloma is the most common ocular finding,
usually without any ocular symptom. The investiga-
tions should be interpreted along with clinical signs as
only those patients with high pre-test probability and
For personal use only.
clinical suspicion of the ocular disease would merit
treatment.
DECLARATION OF INTEREST
The authors report no conflicts of interest. The authors
alone are responsible for the content and writing of
the paper.
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