A case of vasculitis, retinitis and macular neurosensory detachment presenting post typhoid fever
© Relhan et al.; licensee Springer. 2014
Received: 31 May 2014
Accepted: 20 August 2014
Published: 18 September 2014
Ocular and extraocular immune-mediated phenomena are known to occur following febrile illness. Vasculitis, retinitis and neurosensory detachment are not well-recognized sequelae of typhoid fever.
We report a case of vasculitis, retinitis and macular neurosensory detachment presenting post typhoid fever. A 27-year-old female presented with decreased vision in right eye with history of typhoid fever (treated adequately 6 weeks prior). Her best corrected visual acuity in right eye was 20/125, N36. Fundus showed a patch of vasculitis and retinitis superior to the disc associated with macular neurosensory detachment and disc pallor. With oral steroids, the inflammation resolved and visual acuity improved to 20/20 at 6 weeks.
Immune-mediated vasculitis and retinitis following typhoid fever may respond well to systemic steroids.
KeywordsPost typhoid retinitis Neuroretinitis Immune-mediated retinitis Post fever retinitis
Typhoid fever is caused by Salmonella typhi. It leads to enteric fever, septicemia and gastroenteritis. Salmonella can rarely affect the eye either by direct infection or rarely by immune-mediated mechanism. Hersing and Duke-Elders  reported typhoid-related uveal complications including iritis, retinal hemorrhage, choroiditis, endophthalmitis and panophthalmitis. Our group published , late-onset endogenous endophthalmitis post typhoid fever resolution. In this manuscript we report a patient who presented with retinitis and had a history of typhoid fever, beginning 6 weeks prior to presentation.
Discussion and review of literature
This case demonstrates resolution of immune-mediated retinitis following typhoid fever. A viral etiology cannot be completely ruled out. The lesions in this case were not peripheral, did not exhibit circumferential spread, did not involve the arterioles and were not associated with prominent anterior or posterior cellular reaction. Given the timing, 6 weeks following the onset of typhoid fever and significant improvement without antiviral treatment, post typhoid immune-mediated retinitis seems the most likely diagnosis.
Literature review reveals minimal data related to typhoid fever causing this type of pathology -. Anecdotal similarly reported  cases have been assumed to be due to retinal infiltration of immune origin. Pathogenesis of immune-mediated vasculitis could be attributed to post infectious immunologic effects which may lead to an immune response that reacts to self-antigens (for example, heat shock protein and myelin basic protein) or homology between retinal antigens and microbial peptides (similarity between S antigen and microbial peptides like yeasts, Escherichia coli, and hepatitis B virus) or molecular mimicry leading to autoimmunity (S antigen and interphotoreceptor retinoid binding protein - IRBP) . Diagnosis of immune-mediated retinitis is often clinical, based on past history of a febrile illness (4 to 6 weeks prior) and is supplemented by laboratory workup. Retinitis-occurring post febrile illnesses have been reported after malaria, viral fevers, Chickungunya fever and also in non-infectious immune disorders (Behcet's disease, intraocular lymphoma) ,. Management of such pathology remains controversial due to lack of published literature. Spontaneous resolution is possible. Mild cases resolve without treatment, while severe cases may need a course of corticosteroids. In our case, steroids were prescribed in view of inflammation involving the disc and macula leading to profound decrease in vision. In conclusion, though rare, one can encounter cases of non-infectious, immune-mediated retinitis after resolution of typhoid febrile illnesses that may necessitate the use of steroids in severe cases.
This paper was presented at Hyde Park Session in Andhra Pradesh Ophthalmology Conference (APOC) December 2012 at Guntur, India.
NR is doing a research fellowship at Bascom Palmer Eye Institute, Miami FL, USA. She has worked at L V Prasad Eye Institute, Hyderabad, India. AP and SJ are consultants at the Department of Vitreo-Retina, L V Prasad Eye Institute, India. TA and HWF are consultants at the Department of Ophthalmology, Bascom Palmer Eye Institute, University of Miami Miller School of Medicine, Miami, FL, USA.
We are thankful to the Uveitis Society of India (USI) and International Ocular Inflammation Society (IOIS) for funding the publication of this manuscript.
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