Fig. 12.1
Slit lamp anterior segment photographs of both eyes. From a 45-year-old woman who presented with complaints of discomfort and photophobia 6 weeks following the resolution of chikungunya fever. The photograph shows pigmented keratic precipitates in the inferior cornea of the right eye (a) and pigmented and stellate keratic precipitates in the left eye (b), with 1+ cells and 2+ flare in the anterior chamber of both eyes (Mahendradas et al. [33])
Chikungunya retinitis occurs several weeks after the primary illness, which is characterized by minimal vitritis, retinitis, and retinal hemorrhages with retinal edema (Figures), whereas in acute retinal necrosis, multifocal retinitis lesions with severe vitritis are seen primarily in the retinal periphery [24, 28]. Although chikungunya retinitis may morphologically mimic the herpetic viral retinitis, the history of fever, skin rash, and joint pains prior to the onset of the visual symptoms is helpful in the clinical diagnosis, particularly in endemic regions [24, 35]. Optic neuritis can present with sudden decrease in vision secondary to chikungunya virus infection and prompt visual recovery after immediate administration of systemic steroid therapy [25, 32] (Fig. 12.2).
Fig. 12.2
Ocular involvements in chikungunya infection. (a) Fundus photograph of the left eye showing confluent area of retinal whitening suggestive of retinitis. Fundus fluorescence in angiography reveals (b) early hypofluorescence in the posterior pole and (c) late hyperfluorescence in the posterior pole. (d) Spectral domain optical coherence tomography (SD OCT) revealed increased reflectivity in the nerve fiber layer zone corresponding to the areas of retinitis with after shadowing and fluid-filled spaces in the outer retina with serous retinal detachment. (e) Fundus photograph showing resolving retinitis lesion 2 weeks after initiation of systemic steroid therapy. (f) SD OCT showing decreased area of hyper-reflectivity in the inner retina with resolving retinal detachment. (g) Fundus photograph after 4 months, showing complete resolution of retinitis. (h) SD OCT showing resolution of retinitis with thinning of the inner retinal layers nasal to the fovea (Mahendradas et al. [28])
12.6 Diagnosis
Laboratory investigations such as virus isolation, serological tests, and molecular techniques are used to diagnose chikungunya infection [34]. Real-time polymerase chain reaction (RT-PCR) and virus isolation are useful during the initial viremic phase of illness, whereas antibody demonstration from the serum is of use in the later phases of the disease [34]. RT-PCR assay that quantifies viral load in clinical samples can be used as an indicator of active infection [36]. More recently, RT-PCR with real-time loop-mediated isothermal amplification (RT-LAMP) has been developed for rapid diagnosis of chikungunya infection [37].
Enzyme-linked immunosorbent assay (ELISA), indirect immunofluorescent method, and immunochromatographic test (ICT) may be used to detect chikungunya IgM and IgG antibodies in the serum [28].
12.7 Differential Diagnosis
Chikungunya clinically resembles dengue and can be differentiated by the absence of dengue IgM and IgG antibodies in the serum and also by normal platelet count [12]. The differential diagnosis also includes rickettsiosis, herpes, cytomegalovirus, human immunodeficiency virus, syphilis, West Nile virus, tuberculosis, and sarcoidosis.
12.8 Treatment
There is no specific antiviral drug available for the treatment of chikungunya virus infection [12, 20]. There is no commercial vaccine against chikungunya virus infection even though a lot of research is happening to prepare the vaccine. Symptomatic treatment of the acute stage of the disease is with antipyretics and analgesics such as nonsteroidal anti-inflammatory drugs (NSAIDs) [38]. Chronic arthritis due to chikungunya infection has been treated with corticosteroids, with chloroquine phosphate [39], disease-modifying antirheumatic drugs (DMARDS), and even tumor necrosis factor blockers [40].
Anterior uveitis has been treated with topical steroids and cycloplegic agents [24]. The associated ocular hypertension has been managed with topical beta-blockers and oral or topical carbonic anhydrase inhibitors. Systemic steroids have been required to control the inflammation in posterior uveitis, panuveitis, and optic neuritis [24–26, 30–32]. Preventive measures against mosquito bite continue to be the mainstay for control of chikungunya disease [28].
12.9 Prognosis
Prognosis of chikungunya infection is good in most patients. However, severe cases may result in persistent arthralgia, especially in patients who are elderly or debilitated.
Ocular involvement usually has a good prognosis except in some cases of optic neuritis, and retinitis occur due to foveal ischemia and optic atrophy [17, 31, 32].
Conclusion
Ocular manifestations of chikungunya infection can be present at the time of fever or may manifest after few weeks. Anterior uveitis, retinitis, and optic neuritis are the commonest manifestations. In the absence of a specific antiviral regimen, the treatment of ocular disease is supportive. The development of specific antiviral therapy and vaccination against chikungunya are the fields under research [28].
Core Messages
Chikungunya should be considered in the differential diagnosis of viral anterior uveitis, optic neuritis, or multifocal retinitis in patients living in or returning from specific endemic regions.
Chikungunya infection is diagnosed by RT-PCR from the ocular fluids and serum or by the demonstration of IgM antibodies in the serum.
In the absence of special antiviral regimen, the treatment of ocular disease is symptomatic and supportive with topical and systemic steroid therapy.
References
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Lumsden WH (1955) An epidemic of virus disease in Southern Province, Tanganyika Territory, in 1952–53; II. General description and epidemiology. Trans Royal Society Trop Med Hyg 49:33–57CrossRef
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