Tubercular serpiginous choroiditis

Abstract

Tubercular association with serpiginous choroiditis, also called 'serpiginous-like choroiditis' or 'multifocal serpiginoid choroiditis' (MSC) is reported from world over, especially from endemic countries. Though the exact mechanism is not yet clear, a direct or indirect infectious trigger by Mycobacterium tuberculosis (MTB) is believed to cause choroiditis.The link of immune mechanisms with ocular inflammation caused by MTB is emerging, and has been supported by both experimental and human data. The molecular and histopathological findings of tubercular serpiginous-like choroiditis have been demonstrated in clinicopathological reports, as well as in animal models. Young to middle-aged healthy males are more frequently affected. The choroiditis lesions of tubercular serpiginous-like choroiditis evolve as multifocal lesions, affecting the retinal periphery as well as posterior pole. They begin as discrete lesions, and spread in a serpiginoid pattern to become confluent. Fundus imaging including autofluorescence is extremely helpful in monitoring patients for response to therapy. Its diagnosis is essentially clinical. Corroborative evidence is obtained by a positive tuberculin skin test, or a positive QuantiFERON-TB Gold (Cellestis, Carnegie, Victoria, Australia) test, and/or radiological (chest X-ray or chest CT scan) evidence of TB elsewhere in the body. Systemic corticosteroids are the mainstay of therapy to control active inflammation, while ATT helps to reduce recurrence of inflammatory attacks. Immunosuppressive agents are indicated in cases with relentless progression, paradoxical worsening, or recurrent choroiditis.

Keywords: Immune mechanisms; Pathogenesis; Serpiginous choroiditis; Serpiginous-like choroiditis; Tubercular.

Fig. 1

Ultra widefield fundus photograph of an eye with tubercular serpiginouslike choroiditis

Fig. 2

Color fundus photograph showing active lesions of TB SLC (left panel). Fluorescein angiography in early phase a showing transmission hyperfluorescence in the centre of lesions (white arrows) corresponding to healed lesions and hypofluorescence along the border of lesions (red arrows) corresponding to active lesions. The late phase b shows transmission hyperfluorescence persisting in the centre of lesions (white arrows) corresponding to healed lesions and hyperfluorescence along the border of lesions (red arrows) corresponding to active lesions

Fig. 3

Color fundus photograph showing predominantly healed lesions of TB SLC (top panel) and a few subtle active lesions (white arrow). Combined fluorescein and indocyanine green angiography in early phase a shows hypofluorescence (white arrow) and hypocyanescence (red arrow) along the active lesion. Late phase b shows hyperfluorescence (white arrow) and persisting hypocyanescence (red arrow)

Fig. 4

Color fundus photograph (left panel) showing active lesions of TBSLC and fundus autofluorescence (right panel) showing stage I (acute) lesions (blue arrows), characterized by an ill-defined, diffuse halo of hyper autofluorescence along the active lesion (a). In stage II (subacute), a thin hypoautofluorescent rim (blue arrows) appears at the border of the lesion as it begins to heal, and the central hyperautofluorescence becomes prominent (b). In stage III, as the central hyper autofluorescence decreases and peripheral hypoautofluorescence increases (blue arrows), the lesion appears stippled (c). In stage IV, with complete healing of the lesion over several months, there is generalized hypo autofluorescence (blue arrows) (d)