Tuberculosis and The Eye

Tuberculosis and the eye
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Official reprint from UpToDate

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Author
Section Editors
Sivakumar R Rathinam, FAMS, PhD C Fordham von Reyn, MD
Jonathan Trobe, MD
Deputy Editor
Elinor L Baron, MD, DTMH
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jul 2015. | This topic last updated: Apr 13, 2015.
INTRODUCTION Tuberculosis (TB) is an infection caused by Mycobacterium tuberculosis that can cause disease
in many organs, including the eye [1,2]. Ocular TB can involve any part of the eye and can occur with or without
evidence of systemic TB. It generally develops following hematogenous spread from a primary focus but, in rare
cases, it can also occur as a primary infection following epithelial injury. Establishing the diagnosis of TB in an
extrapulmonary focus is a clinical challenge.
Issues related to ocular TB will be reviewed here. Issues related to other aspects of TB, including ocular toxicities of
TB medications, are discussed in detail separately. (See related topics.)
EPIDEMIOLOGY Tuberculosis (TB) is an airborne communicable disease of major public health significance in
many countries. General issues related to epidemiology of TB are discussed separately. (See "Epidemiology of
tuberculosis" and "Epidemiology and pathology of extrapulmonary and miliary tuberculosis" and "Epidemiology and
molecular mechanisms of drug-resistant tuberculosis".)
Most TB disease involves the lungs. Ocular TB usually represents extrapulmonary dissemination of infection. The
incidence of ocular TB is uncertain due to difficulties in ocular sampling for microbiology and inexact diagnostic
criteria [2,3]. Prior to the era of HIV/AIDS, two prospective studies of patients with TB admitted to a sanatorium noted
ocular disease incidence of 1 to 2 percent [4,5]. Since the HIV/AIDS area, prospective surveys have noted the
following:
Among 100 patients with culture-positive TB in Spain who underwent systematic ophthalmologic evaluation,
ocular TB was identified in 18 percent of cases [6]. HIV coinfection was observed in 60 percent of patients, and
more than half of patients had no symptoms referable to the eye.
Among 109 patients with TB and HIV coinfection in Malawi who presented with fever, indirect ophthalmoscopy
demonstrated choroidal granulomas in approximately 3 percent of patients [7].
These studies suggest that routine ocular examination may be warranted for patients with suspected or proven TB,
especially if eye symptoms are present.
CLINICAL MANIFESTATIONS AND DIAGNOSIS Tuberculosis (TB) of the eye may be intraocular or it may
involve the external structures. Three manifestations of ocular TB have been described based on mode of
transmission of bacilli to the ocular tissues.
Most commonly, ocular TB develops as a result of hematogenous spread of M. tuberculosis from pulmonary or
extrapulmonary sites. The clinical manifestations consist of intraocular findings (figure 1); these include
choroiditis, chorioretinitis, choroidal granuloma optic neuritis, optic disc granuloma, subretinal abscess, orbital
cellulitis, scleritis, necrotizing scleritis, posterior scleritis, sclerokeratouveitis (picture 1), interstitial keratitis, and
anterior chamber granuloma (picture 2) [8,9].
Less commonly, ocular TB can occur as a result of direct ocular infection from an exogenous source. In such
cases, infection may involve the ocular adnexa, lacrimal gland, conjunctiva, sclera, or cornea.
In rare cases, eye involvement can occur as a result of a hypersensitivity reaction to a distant focus of infection.
Manifestations may include episcleritis, phlyctenulosis, and occlusive retinal vasculitis; the latter is similar to
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that observed in Eales' disease. (See 'Retinal TB' below and "Eales' disease".)
Intraocular TB Intraocular TB most commonly affects the uveal tract, which includes the iris and ciliary body
(anteriorly) and the choroid (posteriorly). The choroid is a vascular layer located between the sclera and the retina; it
forms the middle or vascular coat of the eye. Anatomically, tubercular uveitis may present as anterior, intermediate,
posterior, or pan uveitis
The diagnosis of intraocular TB can be challenging as the clinical manifestations are variable. Definitive diagnosis of
TB is established by isolation of bacilli from the ocular tissues, which is difficult to achieve. Therefore, a diagnosis of
tuberculosis is frequently presumed in the presence of suggestive ocular findings (such as choroidal granuloma,
broad-based posterior synechiae, retinal vasculitis with or without choroiditis, or serpiginous-like choroiditis) in
combination with systemic findings consistent with TB (such as positive acid-fast bacilli [AFB] smear and culture,
consistent radiographic findings, or a positive interferon-gamma release assay [IGRA] or tuberculin skin test [TST] in
individuals with no systemic symptoms) [9]. Clinical response to antituberculous therapy further supports a
presumed diagnosis of ocular TB. (See 'Treatment' below.)
Uveitis
Anterior Tubercular anterior uveitis is characterized by granulomatous keratic precipitates (picture 3), iris
granulomas (picture 4), and broad-based poster synechiae; occasionally, hypopyon may be observed (picture 2).
Cataract is a common complication. Glaucoma is not a common complication, although annular synechiae and iris
bombe can cause secondary angle closure glaucoma. Untreated chronic anterior uveitis may result in phthisis bulbi
(an atrophic, scarred globe).
Posterior Choroidal TB is the most common form of posterior uveitis. It occurs most commonly in the
presence of systemic TB and, in rare cases, it is the sole manifesting presentation of TB or the initial manifestation of
systemic infection. Choroidal TB may be unilateral or bilateral. Three funduscopic patterns have been described
(picture 5): solitary tubercle, miliary choroidal tubercles, or tuberculoma (a single large lesion that may mimic tumor
and can lead to serous retinal detachment) (picture 6) [8,9].
Tubercles appear as ill-defined, yellowish-white elevated nodules. They vary in size from a pinpoint to several
disc-diameters in size. The lesions can coalesce into larger, elevated choroidal nodules. Focal choroidal granuloma
or diffuse subretinal abscess may be observed as elevated lesions in the fundus. Ultrasonography can demonstrate
focal retinochoroidal thickening. As the lesions age, the borders become more distinct and the rim becomes
pigmented. Multifocal chorioretinitis with pigmented scars often indicates a tubercular etiology [8,9].
Patients with choroidal tubercle(s) near or at the macula present with diminished visual acuity. Patients with
choroidal tubercle(s) at sites not adjacent to the macula are asymptomatic and lesions may be identified incidentally
on screening ocular examination.
Serpiginous-like choroiditis (SLC) of presumed tubercular etiology closely mimics serpiginous choroidopathy (SC)
(picture 7). Patients with SLC are more likely to develop multifocal scattered highly pigmented lesions with vitreous
cells, in contrast with classic SC, which is characteristically less pigmented [10]. It is important to exclude TB as the
cause of serpiginous choroidopathy. Optic disc granuloma may be seen, and it can mimic a sarcoid granuloma.
Immune recovery Immune recovery uveitis (IRU) can occur among patients with HIV and TB in the setting
of immune reconstitution due to antiretroviral therapy. IRU has been described among patients with HIV and
concurrent TB, cytomegalovirus retinitis, and varicella-zoster ocular infection. Severe IRU resulting in globe rupture
has been reported in a HIV patient with coexisting tubercular uveitis (picture 4) [11]. Additional issues related to
immune reconstitution inflammatory syndrome are discussed further separately. (See "Immune reconstitution
inflammatory syndrome", section on 'IRIS associated with mycobacterial infections'.)
Retinal TB Tuberculous involvement of the retina alone is uncommon. More frequently, the retina is involved
in the setting of choroidal TB as retinochoroiditis. The diagnosis of retinal TB is usually presumptive based upon
clinical evaluation of the eye and evaluation for evidence of systemic TB infection and/or tuberculin (or IGRA)
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reactivity; biopsy of the retina is generally not possible. Exudative retinal hemorrhagic periphlebitis in a patient with
uveitis is highly suggestive of tubercular etiology. Similarly, healed periphlebitis and perivascular healed chorioretinal
scars indicate a tubercular cause (picture 2). Fundus fluorescein angiography demonstrates retinal vessel wall
staining and vascular leakage.
Eales' disease is a retinal perivasculitis affecting the peripheral retina of otherwise healthy adults. It is unclear
whether this condition occurs as a result of TB disease or whether it reflects an independent retinal hypersensitivity
reaction. In one study of 50 patients with Eales' disease or a noninfectious ocular disease, M. tuberculosis DNA was
demonstrated by polymerase chain reaction in 48 percent of patients [12]. (See "Eales' disease".)
Differential diagnosis Granulomatous uveitis may also be seen in patients with herpes simplex or varicellazoster infection, phacoantigenic uveitis, sarcoidosis, syphilis, leprosy, Vogt-Koyanagi-Harada disease, and
sympathetic ophthalmia. Other causes of choroidal granulomas include syphilis, sarcoidosis, and fungal lesions.
Clinical manifestations of nontuberculous mycobacterial infections also simulate TB [13].
TB of the external eye External eye structures can be involved in ocular TB including orbit, eyelid, lacrimal
gland, conjunctiva, and sclera.
Orbit Involvement of the orbit occurs most commonly in children, although rare cases have been reported in
adults [14]. Frequent findings include a draining sinus tract and/or radiographic evidence of bony destruction [15].
Eyelid Tuberculosis of the eyelid (tarsus) presents as an eyelid abscess or a chalazion-like mass.
Occasionally, spontaneous drainage of the abscess forms a draining sinus tract [16]. An apparent chalazion
(granuloma of an internal sebaceous gland leading to a localized swelling) that recurs despite surgical excision
should prompt consideration of TB.
TB of the eyelid can also develop as an extension of cutaneous TB [17]. The skin disease consists of subepithelial
nodules ("apple jelly nodules"), scaly plaques, or, rarely, erosive ulcers with destruction of facial features [18]. The
eyelid is involved as an extension of infection from the surrounding skin. (See "Cutaneous manifestations of
tuberculosis".)
Lacrimal gland TB of the lacrimal gland can present as symptomatic dacryoadenitis [19]; the presentation
may be indistinguishable clinically from bacterial infection. Failure to respond to antibiotic treatment should prompt
histopathology of the gland [20].
Conjunctiva Tuberculous infection of the conjunctiva may present as an ulcer, subconjunctival nodule,
pedunculated polyp, or tuberculoma (hard, nodular, nonulcerating mass) [21-23]. Diagnosis requires an excisional
biopsy with histopathology and culture. The number of organisms is usually small, so acid-fast bacilli may not be
observed. Phlyctenular keratoconjunctivitis is rarely seen in patients with active TB. It appears to be associated with
tuberculoprotein hypersensitivity but not with active ocular infection.
Keratoconjunctivitis Tuberculous infection of the cornea presents with pain and photophobia. Examination of
the cornea may demonstrate corneal erosion with stromal infiltration. Deep keratitis is characteristic of tubercular
infection of the cornea. The disease may be associated with anterior uveitis and/or conjunctivitis. Local lymph nodes
may also be enlarged [24,25].
Sclera Tuberculous infection of the sclera (external or fibrous coat of the eye) results from hematogenous
spread. The diagnosis can be difficult to establish and is primarily based upon evidence of scleral inflammation in a
patient with active TB at another body site (picture 8) [26,27].
LABORATORY EVALUATION Isolation of M. tuberculosis by culture is the cornerstone for diagnosis of
tuberculosis, although this is not always feasible. Even if a specimen can be obtained, it is often too small for all
procedures such as Ziehl-Neelsen staining for light microscopy or inoculation in liquid and solid media. Isolation of
M. tuberculosis by culture may take 1 to 10 weeks; however, once growth is obtained, species identification and drug
susceptibility testing are possible. Tuberculin skin testing and interferon-gamma release assays for tuberculosis (TB)
infection may support a presumed diagnosis of ocular TB if positive; however, the test result cannot be used to
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confirm the diagnosis. Conversely, a negative result for any of these tests does not rule out disease.
Biopsy specimens may be obtained for histopathological analysis either from the iris or by retinochoroidal biopsy.
However, absence of acid-fast bacilli or of caseating necrosis in the biopsy specimen does not rule out ocular TB. In
such circumstances, nucleic acid amplification (NAA) may be useful. Although no nucleic acid amplification test is
currently approved by the US Food and Drug Administration for any specimen other than respiratory tract secretions,
many laboratories use validated NAA processes to support a diagnosis of extrapulmonary TB. Diagnosis based on
detection of mycobacterial DNA through polymerase chain reaction (PCR) is becoming more widely used because of
rapid, accurate results and the ability to perform the test using a very small sample [28,29]. A positive result
indicates the presence of M. tuberculosis nucleic acid; it does not establish viability of the organism. If interpreted in
the clinical context of the case, a positive result strongly supports a diagnosis of ocular TB.
Xpert MTB/RIF is a nucleic acid amplification (real time PCR) assay that rapidly detects the presence of both M.
tuberculosis and rifampin resistance by PCR. This may become an important diagnostic tool for respiratory
secretions, but it has not yet been used in ocular fluids for diagnosis of ocular TB [30].
When such techniques are not possible and while awaiting culture information, the diagnosis of TB is presumptive
based on clinical eye examination and evidence of infection. (See "Diagnosis of pulmonary tuberculosis in
HIV-uninfected patients" and "Epidemiology, clinical manifestations, and diagnosis of tuberculosis in HIV-infected
patients".)
TREATMENT The approach to treatment of ocular tuberculosis (TB) is generally the same as that for pulmonary
TB. These issues are discussed in detail elsewhere. In general, where TB is considered strongly as a clinical
diagnosis, treatment should not be delayed until culture data become available. (See "Treatment of pulmonary
tuberculosis in HIV-uninfected patients" and "Treatment of pulmonary tuberculosis in the HIV-infected patient" and
"Diagnosis, treatment, and prevention of drug-resistant tuberculosis".)
The response to therapy can usually be gauged by the clinical examination and resolution of inflammation. In the
setting of choroidal TB, lesions can resolve completely with treatment. Retinal TB is managed with antituberculous
therapy together with systemic corticosteroids (prednisone 40 to 60 mg orally once daily) followed by a taper
depending on the clinical response. Development of neovascularization warrants photocoagulation of the retina.
Some favor administration of antituberculous treatment for two to four weeks without steroids, followed by
assessment for clinical improvement and subsequent determination regarding addition of steroids. However, for
cases in which a lesion is present near the macula or optic disc, administration of concomitant steroids is mandatory
to save these delicate structures from rebound inflammation that may occur with antituberculous therapy alone. In
such situations, absence of recurrence following completion of the treatment supports a clinical diagnosis.
SUMMARY
Ocular tuberculosis (TB) can involve any part of the eye and can occur with or without evidence of pulmonary
or extrapulmonary TB disease. Ocular TB usually arises after hematogenous spread from a primary focus.
(See 'Introduction' above.)
Three forms of ocular TB have been described based on mode of transmission of bacilli to the ocular tissues.
Most commonly, ocular TB develops as a result of hematogenous spread of Mycobacterium tuberculosis from
pulmonary or extrapulmonary sites. Less commonly, ocular TB can occur as a result of direct ocular infection
from an exogenous source. In rare cases, eye involvement can occur as a result of a hypersensitivity reaction
to a distant focus of infection. (See 'Clinical manifestations and diagnosis' above.)
The most common manifestation of ocular TB is intraocular disease involving the uveal tract; choroidal
tubercles are the most common clinical manifestation. (See 'Intraocular TB' above.)
A diagnosis of ocular TB is most often a clinical diagnosis, with ocular findings supported by a consistent risk
history for TB, evidence for TB elsewhere (such as the lungs), and/or a positive test for TB infection such as
the tuberculin skin test (TST) or an interferon gamma release assay (IGRA), since culture of eye tissue or fluid
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frequently is not possible. A positive TST or IGRA may support a clinical diagnosis of TB, but it does not
establish the diagnosis. Conversely, a negative test result does not rule out active TB. (See 'Laboratory
evaluation' above.)
The differential diagnosis of intraocular TB includes herpes simplex or varicella-zoster infection, phacoantigenic
uveitis, sarcoidosis, syphilis, leprosy, and sympathetic ophthalmia. Other causes of choroidal granulomas
include syphilis, sarcoidosis, and fungal lesions. (See 'Differential diagnosis' above.)
External eye structures that can be involved in ocular TB include the orbit, eyelid, lacrimal gland, conjunctiva,
and sclera. TB of these structures can occur as a result of hematogenous spread or via extension of adjacent
infection involving the skin or the sinuses. (See 'TB of the external eye' above.)
Biopsy specimens may be obtained for histopathological analysis either from the iris or by retinochoroidal
biopsy. Absence of acid-fast bacilli or of caseating necrosis in the biopsy specimen does not rule out ocular TB;
in such circumstances, nucleic acid amplification may be useful. (See 'Laboratory evaluation' above.)
The approach to treatment of ocular TB is generally the same as that for pulmonary TB. In general, for
circumstances in which TB is considered strongly as a clinical diagnosis, treatment should not be delayed until
culture data become available. The response to therapy can be gauged by the clinical examination and
resolution of objective sites of clinical involvement. Retinal TB is managed with antituberculous therapy
together with systemic corticosteroids. (See 'Treatment' above.)
ACKNOWLEDGMENT The editorial staff at UpToDate would like to acknowledge Dr. Michele Trucksis, who
contributed to an earlier version of this topic review.
Use of UpToDate is subject to the Subscription and License Agreement.
REFERENCES
1. Thompson MJ, Albert DM. Ocular tuberculosis. Arch Ophthalmol 2005; 123:844.
2. Yeh S, Sen HN, Colyer M, et al. Update on ocular tuberculosis. Curr Opin Ophthalmol 2012; 23:551.
3. Helm CJ, Holland GN. Ocular tuberculosis. Surv Ophthalmol 1993; 38:229.
4. Donahue HC. Ophthalmologic experience in a tuberculosis sanatorium. Am J Ophthalmol 1967; 64:742.
5. Goldenburg M, Fabricant ND. The eye in the tuberculous patient. Trans Sect Ophthalmol Am Med Assn 1930;
135:8.
6. Bouza E, Merino P, Muoz P, et al. Ocular tuberculosis. A prospective study in a general hospital. Medicine
(Baltimore) 1997; 76:53.
7. Beare NA, Kublin JG, Lewis DK, et al. Ocular disease in patients with tuberculosis and HIV presenting with
fever in Africa. Br J Ophthalmol 2002; 86:1076.
8. Vasconcelos-Santos DV, Rao PK, Davies JB, et al. Clinical features of tuberculous serpiginouslike choroiditis
in contrast to classic serpiginous choroiditis. Arch Ophthalmol 2010; 128:853.
9. Gupta A, Bansal R, Gupta V, et al. Ocular signs predictive of tubercular uveitis. Am J Ophthalmol 2010;
149:562.
10. Gupta V, Gupta A, Arora S, et al. Presumed tubercular serpiginouslike choroiditis: clinical presentations and
management. Ophthalmology 2003; 110:1744.
11. Rathinam SR, Lalitha P. Paradoxical worsening of ocular tuberculosis in HIV patients after antiretroviral
therapy. Eye (Lond) 2007; 21:667.
12. Madhavan HN, Therese KL, Gunisha P, et al. Polymerase chain reaction for detection of Mycobacterium
tuberculosis in epiretinal membrane in Eales' disease. Invest Ophthalmol Vis Sci 2000; 41:822.
13. Griffith DE, Aksamit T, Brown-Elliott BA, et al. An official ATS/IDSA statement: diagnosis, treatment, and
prevention of nontuberculous mycobacterial diseases. Am J Respir Crit Care Med 2007; 175:367.
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14. Pillai S, Malone TJ, Abad JC. Orbital tuberculosis. Ophthal Plast Reconstr Surg 1995; 11:27.
15. Sen DK. Tuberculosis of the orbit and lacrimal gland: a clinical study of 14 cases. J Pediatr Ophthalmol
Strabismus 1980; 17:232.
16. Raina UK, Jain S, Monga S, et al. Tubercular preseptal cellulitis in children: a presenting feature of underlying
systemic tuberculosis. Ophthalmology 2004; 111:291.
17. Mohan K, Prasad P, Banerjee AK, Dhir SP. Tubercular tarsitis. Indian J Ophthalmol 1985; 33:115.
18. Dinning WJ, Marston S. Cutaneous and ocular tuberculosis: a review. J R Soc Med 1985; 78:576.
19. Madhukar K, Bhide M, Prasad CE. Tuberculosis of the lacrimal gland. J Trop Med Hyg 1991; 94:150.
20. Panda A, Singhal V. Tuberculosis of lacrimal gland. Indian J Pediatr 1989; 56:531.
21. Cook CD, Hainsworth M. Tuberculosis of the conjunctiva occurring in association with a neighbouring lupus
vulgaris lesion. Br J Ophthalmol 1990; 74:315.
22. Singh I, Chaudhary U, Arora B. Tuberculoma of the conjunctiva. J Indian Med Assoc 1989; 87:265.
23. Fernandes M, Vemuganti GK, Pasricha G, et al. Unilateral tuberculous conjunctivitis with tarsal necrosis. Arch
Ophthalmol 2003; 121:1475.
24. Aclimandos WA, Kerr-Muir M. Tuberculous keratoconjunctivitis. Br J Ophthalmol 1992; 76:175.
25. Sheu SJ, Shyu JS, Chen LM, et al. Ocular manifestations of tuberculosis. Ophthalmology 2001; 108:1580.
26. Saini JS, Sharma A, Pillai P. Scleral tuberculosis. Trop Geogr Med 1988; 40:350.
27. Nanda M, Pflugfelder SC, Holland S. Mycobacterium tuberculosis scleritis. Am J Ophthalmol 1989; 108:736.
28. Wroblewski KJ, Hidayat AA, Neafie RC, et al. Ocular tuberculosis: a clinicopathologic and molecular study.
Ophthalmology 2011; 118:772.
29. Vasconcelos-Santos DV, Zierhut M, Rao NA. Strengths and weaknesses of diagnostic tools for tuberculous
uveitis. Ocul Immunol Inflamm 2009; 17:351.
30. World Health Organiation. Nucleic Acid Amplification Technology for Rapid and Simultaneous Detection of
Tuberculosis and Rifampicin Resistance: Xpert MTB/RIF System. Policy Statement http://whqlibdoc.who.int
/publications/2011/9789241501545_eng.pdf (Accessed on March 04, 2013).
Topic 7999 Version 12.0
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GRAPHICS
Eye anatomy in cross section
Graphic 57690 Version 4.0
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Sclerokeratitis due to ocular tuberculosis
(A) Recurrent sclerokeratitis resulting in multiple corneal peripheral scars. The

patient also has active scleritis. (B) Chest computed tomography (CT) revealed
enlarged lymph nodes with necrosis involving pretracheal, paratracheal, and
subcarinal groups, with the largest lymph node measuring 1.89 x 1.35 cm.
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Anterior chamber granuloma due to ocular tuberculosis
(A) Anterior chamber granuloma with granulomatous keratic precipitates and

hypopyon. Aspiration of the granuloma demonstrated acid-fast bacilli in ZiehlNeelsen stain. (B) Following antituberculous treatment, the posterior segment
demonstrates healed pigmented scars along the vasculature.
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Anterior uveitis due to ocular tuberculosis
(A) Granulomatous keratic precipitates and posterior synechiae in 12-year-old girl.

(B) Fundus examination shows neuroretinitis in the right eye. (C) Fundus
examination shows optic neuritis in the left eye.
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Iris granuloma due to tuberculosis followed by immune recovery

tuberculous uveitis
(A) Right eye of an HIV patient with coexisting tubercular uveitis showing iris granuloma and
hypopyon. Anterior chamber aspiration revealed acid-fast bacilli, confirming the diagnosis of
tuberculosis. (B) Severe form of immune recovery uveitis resulting in perforation of the right
eye following highly active antiretroviral therapy and antitubercular treatment. Iris is seen
prolapsed through the perforation site at the limbus.
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Posterior uveitis due to ocular tuberculosis
(A) A 35-year-old woman presented with massive subretinal abscess and optic
nerve granuloma with neovascularisation in her left eye. Her mantoux test was
necrotic positive, and ultrasonography demonstrated thickened choroid. (B)
Interval improvement was observed after one month of antituberculous therapy.
(C) Resolution of funduscopici findings and choroidal thickening was observed
after three months of antituberculous therapy.
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Tuberculoma of the eye
Raised yellowish choriodal lesion with surrounding serous elevation of

the neurosensory retina, intraretinal exudation, and macular star.
Retinal vessels are seen over the lesion and appear normal.
Reproduced with permission from: Cangemi FE, Friedman R, Josephberg R.
Opthalmology 1980; 87:252.
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Serpiginous-like choroiditis due to ocular tuberculosis
Highly pigmented serpiginous-like choroiditis in a patient with pulmonary

tuberculosis.
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Scleral tuberculosis
Multinodular scleral mass in the left eye.

Reproduced with permission from: Saini JS, Sharma A, Pillai P. Trop Geogr
Med 1988; 40:350.
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Disclosures
Disclosures: Sivakumar R Rathinam, FAMS, PhD Nothing to disclose. C Fordham von Reyn, MD Nothing to disclose. Jonathan Trobe,
MD Nothing to disclose. Elinor L Baron, MD, DTMH Nothing to disclose.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a
multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content is
required of all authors and must conform to UpToDate standards of evidence.
Conflict of interest policy
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Tuberculosis and The Eye

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