224 Journal of Neurosciences in Rural Practice | May - August 2012 | Vol 3 | Issue 2

Letters to the Editor

of RPLS is rapid clinical and imaging resolution with appropriate treatment.

The treatment is to control the blood pressure, discontinue or decrease the dose of offending agents (immunosuppressive, cytotoxic), and treat seizures with anticonvulsants. Prognosis of RPLS is good. Most patients recover completely with prompt treatment, within hours to days. Imaging findings may persist for weeks. Resolutions of imaging findings have been reported within eight days to seventeen months after the first abnormal results.[1] It can lead to posterior circulation infarction or hemorrhage if not treated promptly.

The RPLS is often not suspected by clinicians. The common precipitant is acute elevation of blood pressure, such as in eclampsia, as was evident in our patient. As this diagnosis has important therapeutic and prognostic implications, clinicians as well as radiologists should be aware of the spectrum of imaging findings in RPLS. The clinical signs and findings on neuroimaging in patients with the reversible posterior leukoencephalopathy syndrome are consistent enough that this entity should be promptly recognized, as it is reversible and readily treated by controlling the blood pressure.

Sujeet Raina, DM Mahesh1, G Rajendra1, Narvir S Chauhan2

Departments of Medicine, and 2Radiology, Dr. RPGMC, Tanda, Kangra, 1Department of Medicine, IGMC, Shimla,

Himachal Pradesh, India

Address for correspondence: Dr. Sujeet Raina,

B-1, Type-IV Quarters, Dr. RPGMC Campus, Tanda, Kangra - 176 001, Himachal Pradesh, India.

E-mail: sujeetrashmishera@yahoo.co.in

References1. Hinchey J, Chaves C, Appignani B, Breen J, Pao L, Wang A, et al.

A reversible posterior leukoencephalopathy syndrome. N Engl J Med 1996;334:494-500.

2. Mukherjee P, McKinstry RC. Reversible posterior leukoencephalopathy syndrome: Evaluation with diffusion-tensor MR imaging. Radiology 2001;219:756-65.

3. Javed MA, Sial MS, Lingawi S,Alfi A, Lubbad E. Etiology of posterior reversible encephalopathy syndrome(PRES). Pak J Med Sci 2005;21:149-54.

4. Covarrubias DJ, Luetmer PH, Campeau NG. Posterior Reversible Encephalopathy Syndrome: Prognostic Utility of Quantitative Diffusion Weighted MR images. Am J Neuroradiol 2002;23:1038-48.

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DOI: 10.4103/0976-3147.98262

Leptospirosis presenting as neuroretinitis

Sir,We report a 25-years-old man, presented with sudden onset of reduced vision of the left eye for 1 week duration. Initially, it was a central field loss, which had then progressively involved the whole visual field. It was associated with floaters but was painless with no eye redness, itchiness or discharge. The left eye had normal function. There were no other constitutional symptoms like fever, body ache, jaundice etc. He denied any contact with animals. Past medical history was insignificant. However, he often indulged in swimming in the river during his current posting.

On examination, the best corrected visual acuity was 6/24 OD and 6/6 OS. The right eye had decreased color vision with presence of RAPD. Bulbar and palpebral conjunctival hyperemias were absent. Visual field testing revealed a centrocecal scotoma and cells were present in the vitreous of the right eye on slit lamp examination. Fundoscopic examination revealed a hyperemic optic disc with blurring of margin with macular edema and hard exudates in star shaped arrangement [Figure 1] without any evidence of vasculitis or retinal hemorrhage. Optical coherence tomography (OCT) revealed subretinal and intraretinal fluid in the macula. The left eye findings were normal. General physical and systemic examinations were normal. There were no features of systemic leptospirosis such as fever, conjunctival suffusion, jaundice and hepatosplenomegaly.

The clinical findings of optic disc edema, coupled with subretinal fluid and a macular star, were consistent with a diagnosis of neuroretinitis. On investigation, there was mild leucocytosis with neutrophilia and ESR of 5 mm at the end of 1st hour. Blood biochemistry, urine examination was normal. A systemic workup revealed a positive leptospira IgG titer in serum 11.0 U/mL (positive > 9), leptospira IgM 25 U/mL (positive > 20). Other tests such as Mantoux test, ANA, VDRL, HIV, serologic tests for hepatitis B and C, toxoplasmosis, cysticercosis were negative. CT scan of head and thorax revealed no abnormalities. VEP demonstrated a prolonged latency in the right eye.

He was treated as a case of leptospirosis with neuroretinitis, with intravenous ampicilin 1 g IV 6 hourly and oral doxycycline 100 mg orally twice daily for

Published online: 2019-11-13

Journal of Neurosciences in Rural Practice | May - August 2012 | Vol 3 | Issue 2 225

Letters to the Editor

VA to 6/6 OD with normal color vision; however, the disc swelling and macular star persisted with mild vascular sheathing [Figure 2]. Last follow-up at 5 months revealed normal vision and optic disc with few retinal pigment epithelial changes [Figure 3] and normal OCT.

Neuroretinitis is thought to be a result of an infectious or immune mediated process that may be precipitated by a number of bacterial, viral and parasitic agents.[1-3] The hallmark of neuroretinitis is optic disc edema with a macular star, which develops approximately 9 - 12 days after an onset and starts to disappear after 1 month, but can take 6 - 12 months for total resolution.[4]

Leptospirosis remains under-diagnosed despite its widespread prevalence due to various reasons.[4] Ocular findings in leptospirosis have been reported in 3 to 92%. Conjunctival hyperemia with engorged vessels is the most characteristic finding. Uveitis occurs in 10% of patients, from 2 weeks to 1 year after an initial infection with a good prognosis.[5]

Leptospirosis presenting as neuroretinitis without systemic manifestations has not been reported in Indian literature previously. Hence, the knowledge of this condition and institution of prompt treatment may result in full visual recovery. Treatment with anti-microbial agents (Amoxycillin, Doxycycline etc) is indicated in systemic leptospirosis. However, steroids are the mainstay of treatment for uveitis.[2]

Although neuroretinitis is the disease of varied etiology, and the extent of diagnostic workup should be determined by detailed history and examination.[4] It is a potentially treatable condition with a favorable outcome.

Acknowledgment

The authors thank Dr. Monalisa Bhoktiari, MD and Dr. Rahul Jain, MD for helping in preparation and writing of this manuscript.

Lakshya J Basumatary, Subhra Das1, Marami Das, Munindra Goswami, Ashok K Kayal

Departments of Neurology, and 1Ophthalmology, Gauhati Medical College and Hospital,

Guwahati, Assam, India

Address for correspondence:Dr. Ashok K. Kayal,

Department of Neurology, Gauhati Medical College and Hospital, Indrapur,

Guwahati – 781 032, Assam, India.E-mail: akkayal.gmcneuro@gmail.com

Figure 1: Neuroretinitis showing (a) swelling of disc with (b) retinal edema and (c) macular star

Figure 2: Partial resolution of (e) disc edema with (f) few hard exudates in macular area

Figure 3: Fundus revealing (g) mild sheathing of vessels over the disc and (h) complete resolution of retinal and macular edema with few (i) retinal pigment epithelial changes

2 weeks, based on recommendation by CDC, Atlanta. Oral prednisolone was started at a dose of 1 mg/kg body weight for 2 weeks, with gradual taper over 2 weeks. Follow-up at 1 and 3 months showed an improvement of

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References

1. Narayan SK, Kaliaperumal S, Srinivasan R. Neuroretinitis, a great mimicker. Ann Indian Acad Neurol 2008;11:109-13.

2. Rathinam SR. Ocular manifestations of leptospirosis. J Postgrad Med 2005;51:189-94.

3. Walse FB, Hoyt WF. Neuroretinitis. In: Clinical neuroopthalmology. 3rd ed. Baltimore, Md: Williams and Wilkins Co; 1982. p. 234-5

4. Gass JD. Diseases of the optic nerve that may simulate macular disease. Trans Am Acad Ophthalmol Otolaryngol 1977;83:766-9.

5. Bernard N, Moshe H. Human leptospirosis associated with eye complications. Isr Med J 1963;22:182.

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DOI: 10.4103/0976-3147.98264

Commentary

Leptospirosis is a zoonotic infection that is caused by Leptospira interrogans, a spirochete. The organism is motile, gram-negative aerobic and slow growing. Numerous animal populations can serve as carriers, but rodents, cattle, dogs and pigs appear to be the predominant animal hosts in many countries.[1,2] Humans are infected through direct contact with infected animals or an exposure to fresh water or soil, contaminated by urine of the carrier.[1,3]

The occurrence of leptospirosis is associated with socio-economic status, occupation, association with animals, recreational activity, climate and rainfall. Heavy rain and flooding will cause leaching of leptospira from soil into the water. Because of the occurrence of recent large outbreaks following the occurrence of severe floods, leptospirosis is a re-emerging infection.[1]

The pathogenesis of leptospirosis is not well-understood. The pathogenic mechanism can be classified into direct effect of the organism during bacteremic phase, and the host’s response to an infection in the immunological phase. After entering the body, the organism invade the blood stream resulting in a bacteremia, disseminating into various organs such as the kidney, liver, lungs, heart and central nervous system. The organism disrupts the endothelial cell membranes of small vessels, leading to organ hemorrhage and ischemia.[2]

Fever, chills and rigor, myalgia, headache and proteinuria characterize an acute bacteremic phase of leptospirosis. [4] Hepatic involvement results in jaundice[2], and other systemic manifestations include pulmonary hemorrhage, acalculous cholecystitis, myocarditis and pancreatitis. [1] Symptom resolution may coincide with an immune phase and antibody production. Severe headache, meningism and lymphocytic meningitis may occur during this immune phase.[2]

Ocular involvement in leptospirosis may occur during both the systemic bacteremic and immunological phases. Ocular manifestations in an acute phase include conjunctival congestion without discharge, chemosis or subconjunctival hemorrhage.[5] Jaundice and limbal congestion is a pathognomonic of severe systemic leptospirosis.[2] Uveitis is an important complication of the late immunological phase, and hypopyon may occur when an inflammation is severe. Other ocular immunological manifestations include interstitial keratitis, hyperemic disc, membranous vitreous opacities, perivasculitis without vascular occlusion, retinal hemorrhage and neuroretinitis.[5]

Neuroretinitis is a type of optic neuropathy with which there is an inflammation of the retina and optic nerve, and classically characterized by the presence of optic disc edema accompanied by serous retinal detachment, extending to the macular area with formation of a partial or complete macular star. Neuroretinitis is a rare ocular manifestation of leptospirosis.[6] Infection like syphilis, tuberculosis, cat-scratch disease, lyme disease, toxoplasmosis, hepatitis B, mumps, measles and cycticercosis can be presented with neuroretinitis.[6]

Leptospirosis remains a diagnostic challenge since it often presents as non-specific febrile event. Ocular manifestation with neuroretinitis alone without systemic manifestation makes the diagnosis of leptospirosis more challenging.

The authors report a case of leptospirosis presenting as neuroretinitis alone without systemic manifestation of leptospirosis.[7] However, with the serological test, they were able to confirm the diagnosis and managed successfully.

Embong ZunainaDepartment of Ophthalmology, School of Medical Sciences,

Universiti Sains Malaysia, 16150, Kubang Kerian, Kelantan, Malaysia