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CASE REPORT  
Year : 2011  |  Volume : 4  |  Issue : 2  |  Page : 133-135
Acute disseminated encephalomyelitis subsequent to Leptospira infection


Department of Radiodiagnosis, Dayanand Medical College and Hospital, Ludhiana - 141 001, Punjab, India

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Date of Web Publication8-Oct-2011
 

   Abstract 

Acute disseminated encephalomyelitis has been rarely reported following leptospirosis. Here, we reveal an adult patient who developed the condition after Leptospira infection, which responded to intravenous steroids. Due to high prevalence of leptospirosis in developing countries, acute disseminated encephalomyelitis should be considered as a possibility in patients presenting with acute neurological disease. Increased awareness of this complication among physicians, and early diagnosis and treatment, may lessen morbidity and mortality.

Keywords: Acute Disseminated Encephalomyelitis, Leptospira, Magnetic Resonance Imaging

How to cite this article:
Singh P, Gupta AK, Saggar K, Kaur M. Acute disseminated encephalomyelitis subsequent to Leptospira infection. Ann Trop Med Public Health 2011;4:133-5

How to cite this URL:
Singh P, Gupta AK, Saggar K, Kaur M. Acute disseminated encephalomyelitis subsequent to Leptospira infection. Ann Trop Med Public Health [serial online] 2011 [cited 2018 Aug 15];4:133-5. Available from: http://www.atmph.org/text.asp?2011/4/2/133/85771

   Introduction Top


Leptospirosis is an important zoonosis caused by Leptospira interrogans. These organisms are transmitted after direct contact with urine, blood, or tissue from infected rodents. The clinical spectrum of leptospirosis varies from the mild anicteric leptospirosis to more serious Weil's syndrome, comprising icterus, renal dysfunction, and bleeding diathesis. [1] It is a disease of worldwide distribution. Leptospirosis is underreported, with 1500-2000 cases being reported globally every year. [2] Neurological symptoms seen in about 10-15% of cases are variable and remain unfamiliar and diverse. [3] Acute disseminated encephalomyelitis (ADEM) is an inflammatory demyelinating disease of central nervous system. In India, the true incidence of ADEM is unknown and is likely to be more frequent than reported because common predisposing factors are still prevalent. [4] It is rare for leptospirosis to present as a neurological disease such as ADEM. Only three cases have been reported worldwide, till date. [5],[6],[7]


   Case Report Top


A 42-year-old male, farmer by occupation, was admitted to our hospital with chief complaints of fever, altered sensorium, decreased urine output, and abdominal pain. Fever started 7 days before admission and was not associated with rigors and chills. Subsequently, patient became drowsy few hours before admission but was responding to verbal commands. There was no history of seizures. There was no icterus, cyanosis, or skin rash on physical examination. The patient was dyspneic and had pedal edema. Pupils were equal and reacting to light. Meningeal signs were negative, and fundus examination was normal. Abdominal examination was remarkable for hepatomegaly. Biochemical examination revealed thrombocytopenia (47,000), deranged renal function (serum creatinine 3.4 mg/dL), and liver function tests (asparate transaminase 100 U/L, alanine transaminase 70 U/L, total bilirubin 1.2 mg/dL, and albumin 2.9 g/dL). In view of findings of fever with hepatorenal involvement and thrombocytopenia, possibilities of leptospirosis and complicated malaria were considered. Patient was started on intravenous antibiotics (ampicillin and ceftriaxone), antimalarials, and other supportive therapy. Leptospira serology (Pan Bio IgM ELISA) came out to be positive (IGM-17.95 Pan Bio units). Malaria antigen was negative. Blood and urine cultures were negative for pyogenic organisms. Despite treatment, there was no significant neurological improvement.

During hospital course, patient complained of severe headache and developed bradycardia. To rule out possibility of intracranial hypertension, computed tomography done on day 7 of admission revealed extensive hypodensity involving white matter in bilateral cerebral hemispheres [Figure 1]. Magnetic resonance imaging (MRI) brain done on the following day depicted extensive white matter hyperintensities on T2-W and FLAIR images, predominantly involving subcortical white matter. Similar hyperintensities were also seen in bilateral internal and external capsules, basal ganglia, corpus callosum, cerebellar hemispheres, pons, and bilateral middle cerebellar peduncles [Figure 2],[Figure 3],[Figure 4]. There was no hydrocephalous. Cerebrospinal fluid examination showed 10 cells/ mm 3 (70% lymphocytes and 30% polymorphs) and proteins 81 mg/dL, with normal levels of glucose. Based on MRI and clinical findings, final diagnosis of postinfectious ADEM was made. Patient was started on intravenous steroids (methylprednisolone) for 5 days. Neurological status of patient improved gradually and was discharged in stable condition on day 18. Repeat MRI brain 1.5 months later showed complete resolution of the lesions [Figure 5]. Four months later, the patient remained asymptomatic.
Figure 1: Computed tomography image showing extensive white matter hypodensities

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Figure 2: T2-W image showing white matter hyperintensities involving predominantly subcortical white matter. Hyperintensities are also seen involving internal and external capsules, basal ganglia, and copus callosum

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Figure 3: T2-W image showing distribution of hyperintensities. Predominant involvement of subcortical white matter with sparing of deep white matter is evident

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Figure 4: T2-W image showing hyperintensities involving brainstem, middle cerebellar peduncles, and cerebellum

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Figure 5: Follow-up MRI after 1.5 months showing complete resolution of all the lesions

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   Discussion Top


The patient presented with altered sensorium following a 7-day history of fever and a raised antileptospiral antibody titer. The cerebrospinal fluid examination including culture excluded an intracranial infection. The MR imaging depicted a demyelinating process. The presence of hyperintensities on T2-W and FLAIR images in subcortical white matter, pons, cerebellum, basal ganglia, and brainstem with a history of prior infection and complete disappearance of lesions in the follow up MRI after 1.5 months confirmed the diagnosis of ADEM. Central nervous system manifestations of leptospira may include aseptic meningitis, encephalitis, Guillain-Barre syndrome, cerebellar ataxia, tremor, rigidity, and intracerebral bleed. [2] ADEM following Leptospira is rare. In a study of 40 Indian patients of neuroleptospirosis, no patient had ADEM. [2] MRI is the procedure of choice to define the neurological involvement in ADEM, and it usually demonstrates diffuse and asymmetrical lesions of increased signal on T2-W images and decreased signal on T1 W images, as were seen in our patient. The outcome of the disease is usually good and many patients present a complete recovery. [8] The initial MRI showed multiple lesions involving the corpus callosum. The follow-up scan after 1.5 months showed resolution of all lesions, and no new lesions were demonstrable, thus favoring diagnosis of a monophasic illness like ADEM over multiple sclerosis.

In developing countries such as India, leptospirosis is often underdiagnosed because of variable clinical manifestations, leading to considerable morbidity and mortality. The diagnosis is missed because of atypical presentations, particularly when coupled with neurological manifestations. [9] Hence, it is essential to be mindful of unusual manifestations of leptospirosis such as ADEM. Early treatment in such cases will be rewarding.

 
   References Top

1.Farr RW. Leptospirosis. Clin Infect Dis 1995;21:1-6.  Back to cited text no. 1
[PUBMED]  [FULLTEXT]  
2.Panicker JN, Mammachan R, Jayakumar RV. Primary neuroleptospirosis. Postgrad Med J 2001;77:589-90.  Back to cited text no. 2
[PUBMED]  [FULLTEXT]  
3.Mathew T, Satishchandra P, Mahadevan A, Nagarathna S, Yasha TC, Chandramukhi A, et al. Neuroleptospirosis - revisited: Experience from a tertiary care neurological centre from south India. Indian J Med Res 2006;124:155-62.  Back to cited text no. 3
[PUBMED]  Medknow Journal  
4.Murthy JM. Acute disseminated encephalomyelitis. Neurol India 2002;50:238-43.  Back to cited text no. 4
[PUBMED]  Medknow Journal  
5.Alonso-Valle H, Muñoz R, Hernández JL, Matorras P. Acute disseminated encephalomyelitis following Leptospira infection. Eur Neurol 2001;46:104-5.  Back to cited text no. 5
    
6.Chandra SR, Kalpana D, Anilkumar TV, Kabeer KA, Chithra P, Bhaskaran R. Acute disseminated encephalomyelitis following leptospirosis. J Assoc Physicians India 2004;52:327-9.  Back to cited text no. 6
[PUBMED]    
7.Lelis SS, Fonseca LF, Xavier CC, Horta MB, Cordeiro SS. Acute disseminated encephalomyelitis after leptospirosis. Pediatr Neurol 2009;40:471-3.  Back to cited text no. 7
[PUBMED]  [FULLTEXT]  
8.Singh S, Alexander M, Korah IP. Acute disseminated encephalomyelitis: MR imaging features. AJR Am J Roentgenol 1999;173:1101-7.  Back to cited text no. 8
[PUBMED]  [FULLTEXT]  
9.Kamath SA, Joshi SR. Re-emerging of infections in urban India-focus leptospirosis. J Assoc Physicians India 2003;51:24.  Back to cited text no. 9
    

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Correspondence Address:
Paramdeep Singh
Department of Radiodiagnosis, Dayanand Medical College and Hospital, Ludhiana - 141 001, Punjab
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1755-6783.85771

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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]

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2 æMini-boomerang signæ: Reversible corpus callosal signal change in neuroleptospirosis
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