A 59 year old male presented to our hospital 1 week after experiencing diminution of vision in the right eye. He gave a history of typhoid fever 4 weeks prior to presentation for which Widal test was performed to confirm diagnosis. The test results showed significant titres for 'O' antigen (>1:80) and 'H' antigen (>1:160) and negative for 'AH' and 'BH' antigens. He was subsequently started on oral Ofloxacin 400 mg twice daily for 2 weeks following which fever subsided. There was no known history of diabetes mellitus or hypertension. On ocular examination his best corrected visual acuity was 2/60 in the right eye and 6/6 in left eye. Anterior segment findings were unremarkable with IOP being within normal range for both eyes. Fundus examination of right eye showed white fluffy lesions along the superior and inferior arcades with superficial haemorrhages in around the macula with a macular star suggestive of retinitis (Fig. 1a). Left eye fundus showed few dispersed retinitis lesions with superficial haemorrhage along the superior arcade with intact foveal reflex (Fig. 1b). On optical coherence tomography of right eye underlying macular serous retinal detachment was noted (Fig. 2a). Blood tests were done to rule out VDRL and HIV status. X-cyton analysis of the anterior chamber aspirate was negative for organisms like Mycobacterial Tuberculosis, Toxoplasma Gondii, Hepes Simplex Virus, Cytomegalovirus and Varicella Zoster Virus. After analysis of the reports diagnosis of post typhoid retinitis in both eyes was made. Patient was started on oral prednisolone 1 mg/kg body weight which was tapered over 2 months along with monitoring of systemic and ocular health. Patient came for follow up every 2 weeks for 3 months. Every visit fundus photo was documented. After 2 months of initiating treatment there was an improvement in the BCVA in right eye to 6/6 which was maintained on further visits. Fundus examination revealed resolving lesions in both eyes (Fig. 3a, b) and OCT of the right eye showed resolution of the serous detachment (Fig. 2b).   
Retinitis is characterized by confluent areas of retinal whitening which progresses along the retinal blood vessels, often associated with intraretinal hemorrhages and hard exudates. A significant number of retinitis cases are thought to be idiopathic in etiology but a small proportion of cases are infectious in etiology such as Toxoplasma gondii (toxoplasmosis), Leptospira spp. (leptospirosis), Mycobacterium tuberculosis (tuberculosis) and other viral and fungal etiologies. Non infectious causes of retinitis include sarcoidosis, Behcet's disease. Infectious causes are usually unilateral and may be associated with mild vitritis. Patients can present with Neuroretinitis like picture with optic disc edema and macular hard exudates. The macular star becomes prominent over first 3 weeks with neuroretinitis resolving over 6-8 weeks. Leakage from the optic nerve head can lead to retinal swelling, exudation and edema, whereas retinal venous occlusion due to vasculitis results in intraretinal haemorrhage, cotton wool spots and retinal and optic nerve head edema. It was postulated that microbial pathogens may be responsible for immune mediated ocular and systemic pathology through postinfectious immunological effects. These may be due to molecular mimicry eliciting an immune response that cross react with self antigens. Even though active infection is an unusual cause of retinal vasculitis, it is possible that many idiopathic and systemic disease associated cases are precipitated by previous encounters with microbes bearing DNA sequence homologous to retinal and vascular autoantigens. Similarity between S-antigen and peptides derived from yeast, E. coli, and Hepatitis B virus was found and there was an ability of these microbial peptides to elicit an immune response post infection. Immune mediated retinitis is a clinical diagnosis most often when there is past history of infection few weeks or days prior to the onset of ocular manifestations. In this case, treatment with oral steroids was initiated due to inflammation of the retina, especially the macula which caused decrease in vision. By taking into consideration the time of onset of ocular presentation, previous history of typhoid fever and the response to oral steroids; the most likely diagnosis was post typhoid fever immune mediated retinitis with macular neurosensory detachment in the right eye and retinitis in left eye. In our case as the disc edema was not prominent, neuroretinitis was not considered as the diagnosis. Similar case reports by Relhan et al. and Laul et al. showed immune mediated response post typhoid fever presenting with neuroretinitis, vasculitis and macular detachment. Successful treatment with steroids was seen in them. Fusco et al. reported a case of bilateral chorioretinitis and stellate maculopathy post typhoid fever. However, in our case Xcyton analysis was done to rule out possible infectious retinitis before initiating steroid therapy, as it could exacerbate non immune mediated retinitis. Xcyton multiplex PCR analysis even though has the advantage of increasing the diagnostic yield it has certain disadvantages like false positive and negative results due to cross reactivity and preferential amplification, negative internal control if there is high amount of a particular target causing exhaustion of reagents and high cost.