Mechanism
Clinical manifestation
Immune reaction to tubercular antigens
Phlyctenulosis
Interstitial keratitis
Tissue invasion by Mycobacterium tuberculosis
Nodular scleritis
Conjunctival Tuberculosis
M. tuberculosis may affect any structure of the eye or adnexa. Tuberculous affliction of the conjunctiva may present as an ulcer, subconjunctival nodule, pedunculated polyp, or tuberculoma . The symptomatology includes features of chronic conjunctivitis like itching, discomfort, redness, mucopurulent discharge, inflamed edematous lids, preauricular/cervical swelling, and rarely fever [5]. The initial diagnosis is often missed due to the nonspecific findings and similar presentations with other diseases affecting the eye. This often leads to delayed diagnosis and incorrect treatment administered to the patient thereby increasing ocular morbidity and prolonging therapy [6].
Phlyctenular Keratoconjunctivitis
Phlyctenular keratoconjunctivitis (PKC) is seen due to a variety of distinct conditions with TB being the commonest in India. In the Western world, this has been supplanted by Staphylococcus aureus as the most common causative antigen [7]. Phlycten is derived from the Greek word, phlyctaena, which means blister. The name is a misnomer because the lesion is actually a solid nodule instead of a fluid-filled bubble that can be single or multiple [8]. These nodules are referred to as phlyctenules and represent a localized hypersensitivity reaction to the mycobacterial antigens [9].
Clinical Presentation
Phlyctenules are usually localized to the limbus in the exposed interpalpebral region and occur more commonly in children [10]. Conjunctival lesions may cause only mild to moderate irritation of the eye or may be asymptomatic in many cases, while the corneal lesions may be associated with severe pain, photophobia, and blepharospasm [10]. It has also been seen that the nodules due to TB may have more light sensitivity than those associated with staphylococcus [11].
Phlyctenular conjunctivitis can present in three forms: simple, necrotizing, and military (Table 12.2). The usual presentation is a localized, elevated, gelatinous pinkish-gray nodular limbal lesion with a soft necrotic center and marked injection of the surrounding conjunctival vessels (Fig. 12.1). With progression, the lesions may show some degree of ulceration and staining with fluorescein but later on get epithelized. In few cases, there may be a very large phlycten associated with necrosis and ulceration which fails to epithelize and may lead to severe conjunctivitis. In some cases, multiple nodules may be present along the corneal limbus in a disorganized manner or may be arranged linearly along the limbus in the form of a ring.
Table 12.2
Clinical presentations of phlyctenular keratoconjunctivitis
Type | Clinical features |
|---|---|
Simple | Most common Isolated limbal nodule |
Necrotizing | Large phlycten with necrosis and ulceration |
Miliary | Multiple phlyctens arranged linearly at limbus |
Fig. 12.1
Clinical presentation of phlyctenular conjunctivitis. (a) Limbal location of a phlyctenule. (b) Presence of a localized, elevated, gelatinous pinkish-gray nodule with a soft necrotic center and marked injection of the surrounding conjunctival vessels
Corneal phlyctenules also begin at the limbus, and unlike conjunctival phlyctenules, they frequently ulcerate and develop neovascularization. In some instances, the phlyctenule will migrate across the corneal surface due to recurrent episodes of inflammation and be associated with cervical lymphadenopathy. These “marching phlyctenules” demonstrate an elevated leading edge with a trailing leash of vessels. Corneal phlyctenulosis may leave corneal scars upon healing leading to permanent visual loss. In very rare instances, corneal perforation may occur [12].
Diagnosis
The diagnosis of PKC is mainly clinical. One should have a strong suspicion for PKC especially in recurrent episodes and failure of remission. Chest radiographs, purified protein derivative skin testing, or QuantiFERON Gold testing should be done for patients with a history of travel to endemic regions or symptoms suggestive of tuberculosis infection. Active multiplying bacilli are not found in these cases since it is a hypersensitivity reaction , and hence an excision biopsy to isolate the offending microorganism is of no use.
Histologically, scrapings can be taken from the affected eye which show predominantly helper T cells, cytotoxic T lymphocytes, monocytes, and Langerhans cells. The presence of antigen-presenting cells, monocytes, and T cells and conspicuously absence of bacilli support the rationale that PKC is likely due to a delayed cell-mediated reaction [13].
Differential Diagnosis
The nodules of phlyctenular conjunctivitis may be confused with other causes of nodules on the ocular surface such as nodular episcleritis, Salzmann’s nodular degeneration, and inflamed pinguecula or pterygium. Long-standing recurrent episodes of conjunctivitis may be similar to that seen in acne rosacea keratitis, trachoma, and vernal keratoconjunctivitis. Cases where ulceration of the phlycten is seen may be misdiagnosed as infectious corneal ulcer, ulcer associated with spring catarrh, and peripheral ulcerative keratitis due to other causes.
Treatment
The rationale of management for PKC is the reduction of inflammatory response, and hence the mainstay of treatment is topical steroids. Surface-acting steroids such as fluorometholone may be used in mild cases. However, severe cases require topical prednisolone acetate 1% eye drops or dexamethasone/betamethasone for achieving remission. In eyes with multiple recurrences or those developing steroid dependence, topical cyclosporine A is added, and steroids are tapered off [14]. The retinal examination, slit lamp examination, and intraocular pressure measurement should be done periodically to rule out steroid-induced glaucoma and cataract in view of prolonged use of steroids.
In cases with corneal ulceration, topical fourth-generation fluoroquinolones are added along with cycloplegics in the form of atropine 1% eye drops twice a day. Corneal scrapings should be taken to rule out secondary superadded infection.
In addition to treating the inflammatory response, it is important to treat the underlying etiology, that is, to decrease the source of antigens responsible for the inflammation. In patients with suspected TB on chest radiography, tuberculin skin test, or PCR, full-dose antitubercular treatment (ATT) is given to eliminate the focus of antigenic load [15]. Close contacts should also be evaluated and treated accordingly.
In rare instances of corneal perforation , surgical treatment in the form of corneal gluing, amniotic membrane grafting, or corneal patch grafts may be required.
Other Forms of Tubercular Conjunctivitis
Based on the morphological characteristics, the other manifestations of TB-related conjunctivitis that can be seen are hypertrophic, granulomatous, and pedunculated mass and tuberculomas . Upper palpebral conjunctiva is the most common site of involvement followed by bulbar conjunctiva and fornix. Unilateral presentations are more common than bilateral. These cases may have presence of live mycobacteria in the ocular tissues. The definitive diagnosis can be made by demonstration of bacilli in the histopathology specimens [16]. However, they may be missed on small biopsy tissues available after excision. Further, the chances of detection of mycobacteria on microscopic examination are less than on cultures. These bacteria show a slow growth on the Lowenstein-Jensen media and should be examined periodically for a minimum of 8 weeks before reporting negative results. The presence of granulomatous inflammation with caseation in the biopsied specimen strongly suggests the diagnosis of conjunctival TB. In case of negative results, nested PCR may be performed which shows amplification of the Mycobacterium tuberculosis genome and increases the detection rates [17].
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