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 Table of Contents 
Year : 2019  |  Volume : 8  |  Issue : 1  |  Page : 292-295  

An interesting case of acute disseminated encephalomyelitis following E. coli infection

1 Department of Medicine, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, Tamil Nadu, India
2 Department of Paediatrics, Government Villupuram Medical College, Villupuram, Tamil Nadu, India
3 Health Centre, Central University of Tamil Nadu, Thiruvarur, Tamil Nadu, India

Date of Web Publication31-Jan-2019

Correspondence Address:
Prem Davis
Health Centre, Central University of Tamil Nadu, Thiruvarur - 610 005, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jfmpc.jfmpc_402_18

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Acute disseminated encephalomyelitis (ADEM) is a rare inflammatory demyelinating disease of central nervous system (CNS), characterized by multifocal white matter involvement with neurological deficits and accompanied by encephalopathy. ADEM is thought to be caused by autoimmune etiology. CNS autoantigens are produced by molecular mimicry triggered by an environmental stimulus, mostly infection (viral/bacterial) or post vaccination, in genetically susceptible individuals. ADEM is sometimes referred to as post/para-infectious or post-immunization ADEM. ADEM is characterized by multifocal neurological signs and occasionally it rapidly progresses to coma. Magnetic resonance imaging (MRI) is used to confirm the diagnosis. The treatment is based on intravenous high-dose methylprednisolone, which usually leads to a rapid improvement. Recently, the use of intravenous immunoglobulins and plasma exchange (PLEX) has also been suggested. We report a case of a 6-year-old girl who was admitted for urinary tract infection but developed neurological complications which was treated successfully.

Keywords: Acute disseminated encephalomyelitis, Escherichia coli, high-dose methylprednisolone, magnetic resonance imaging

How to cite this article:
Balamurugesan K, Ponprabha R, Davis P. An interesting case of acute disseminated encephalomyelitis following E. coli infection. J Family Med Prim Care 2019;8:292-5

How to cite this URL:
Balamurugesan K, Ponprabha R, Davis P. An interesting case of acute disseminated encephalomyelitis following E. coli infection. J Family Med Prim Care [serial online] 2019 [cited 2021 Jul 25];8:292-5. Available from: https://www.jfmpc.com/text.asp?2019/8/1/292/251181

  Introduction Top

Acute disseminated encephalomyelitis (ADEM) is the disease of central nervous system (CNS) characterized by the inflammatory demyelination with multifocal white matter involvement and neurological deficits.[1] The worldwide annual incidence is 0.07–0.4 per 100,000 population per year but the true incidence of ADEM in India is unknown and this is mostly because of the underreporting of the cases. ADEM is more common among young adults and children and it does not show any predilection for sex or ethnicity.[2] The autoimmune etiology is being proposed in the majority of the cases that usually develops after the acute viral or bacterial infection, vaccination, or organ transplantation.[3],[4] Though there are many bacterial and viral pathogens that leads to ADEM, the development of ADEM due to  Escherichia More Details coli (E. coli) has never been reported till now. Therefore, we report a case of para-infectious encephalomyelitis (ADEM) following urosepsis due to E. coli.

  Case History Top

A 6-year-old female child, born to nonconsanguineous parents was brought to the hospital with 2 weeks history of dysuria, 7 days of fever, and lethargy for a day. At admission she had hypotension and was in sick-looking state but was conscious, oriented without any evidence of focal neurological deficit. Her hypotension was treated with intravenous fluids and was started on empirical cefotaxime, considering as urinary tract infection.

Her investigations revealed neutrophilic leukocytosis with plenty of pus cells in urine. She was euglycemic and her renal, hepatic parameters were within the normal range. Urine culture grew E. coli sensitive to cefotaxime and amikacin. Injection amikacin was added along with cefotaxime. On the second and third day of hospitalization she remained afebrile, conscious but complaining of myalgia. On the fourth day she remained conscious but developed neurological symptoms such as difficulty in walking, diminished vision, ataxia with broad-based gait. On examination she had involvement of the pyramidal tract (hypertonia, brisk reflexes in all four limbs with positive Babinski sign, and ankle clonus), cerebellum (ataxia with broad-based gait) with intact sensory system. Ophthalmological evaluation revealed decreased visual acuity of 6/18 with normal fundus. Immunological markers of inflammation such as antinuclear antibody, C-reactive protein were negative. CT brain and lumbar puncture was done immediately and the reports are shown in [Table 1].
Table 1: CT brain and CSF analysis

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Neurology opinion was obtained. On the basis of history, examination, cerebrospinal fluid (CSF) analysis, possibility of ADEM was considered and MRI brain was suggested. MRI brain showed nonenhancing hyperintense foci in left thalamus as in [Figure 1] and [Figure 2] and left cerebellar white matter on T2-weighted fluid-attenuated inversion recovery (FLAIR) as in [Figure 3], suggestive of ADEM. Possible differential diagnoses considered were the first attack of multiple sclerosis, cerebrovascular accident, meningoencephalitis, and vasculitis.
Figure 1: MRI brain T2-weighted image showing Lt thalamic hyperintensity

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Figure 2: MRI brain sagittal section showing Lt thalamic hyperintensity

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Figure 3: MRI brain showing Lt cerebellar hyperintensity

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The diagnosis was made according to the guidelines given by International Pediatric Multiple Sclerosis Study Group. The patient was started on intravenous methylprednisolone 20 mg/kg for 5 days, followed by oral steroid for 4 weeks along with other supportive measures. The patient had dramatic improvement and had complete recovery without any residual sequelae.

  Discussion Top

ADEM is a rare disease characterized by an immune-mediated inflammatory demyelination of the CNS, which predominately affects the white matter of the brain and spinal cord.[1] The ADEM is characterized by the development of acute onset encephalopathy with multifocal neurological deficits.[3],[5] The ADEM usually develops following the acute viral etiology, especially exanthematous disease, bacterial as well as due to vaccination and rarely after the immune sera.[3],[4] Approximately 50–75% of the ADEM is due to postinfectious cause, following measles, mumps, coronavirus, coxsackie B, dengue virus, Epstein-Barr virus, hepatitis A and C virus, Borrelia burgdorferi, Chlamydia, Legionella, Mycoplasma pneumoniae, Rickettsia rickettsi, Streptococci, Plasmodium vivax.[6],[7] Nearly 5% of the ADEM occurs following the vaccination. The vaccines that are associated with the development of ADEM are hepatitis B, Japanese B encephalitis, measles, mumps, pertussis, polio, rubella, tetanus, rabies (Semple vaccine).[8] There are two proposed concepts for the development of ADEM. The first one is the inflammatory cascade concept which is by the direct invasion of the neurotropic pathogens into the CNS. The second concept is the molecular mimicry between the pathogen and myelin proteins of the host.[9] The ADEM is characterized by the onset of fever, malaise, myalgia, headache, and vomiting but encephalopathy is the hallmark feature of the ADEM, which ranges from simple confusion to coma. Within a period of 4–13 days after the infection or vaccination, the neurological signs and symptoms will develop.[10],[11] In addition to encephalopathy, other neurological signs such as hemiparesis, cranial nerve palsies, paraparesis, meningismus, ataxia, and optic neuritis may occur.[12],[13] The diagnosis of the ADEM is mainly based on the clinical and radiological features. CT brain is usually normal. Cranial MRI is the imaging study of choice. T2 and FLAIR images show patchy areas of increased intensity in the white matter regions. Deep gray matter structures such as thalami, basal ganglia are often involved.[14] The CSF examination shows nonspecific changes such as increased pressure, lymphocytic pleocytosis, and raised protein. Increased amount of IgG specific for myelin protein can be noted.[14] The clinical and radiological features that distinguish ADEM from the first attack of multiple sclerosis is given in [Table 2].
Table 2: Clinical and radiological features that may distinguish ADEM from first attack of multiple sclerosis (MS)

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The International Pediatric Multiple Sclerosis Study Group gave a diagnostic criterion to diagnose ADEM in children,[15] as shown in [Table 3]. This criterion is very helpful to distinguish ADEM from other clinically isolated syndromes. The treatment options available for the ADEM are corticosteroids, plasma exchange, and intravenous immunoglobulins. High dose of intravenous corticosteroids is widely accepted as the first line of treatment, especially the methylprednisolone with a dose of 20–30 mg/kg per day with a maximum dose of 1 g per day should be given for 3–5 days followed by oral prednisolone for 3–6 weeks. Other modalities of treatment include intravenous immunoglobulin at a dose of 2 g/kg over 2–5 days and plasma exchange are very useful in case of steroid nonresponders.[1],[11] The long-term prognosis of the ADEM is good. About 60–90% of the patients recovered without any neurological deficit in an average period of 1–6 months.[10],[11]
Table 3: Diagnostic criteria given by International Pediatric Multiple Sclerosis Study Group

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Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Wender M. Acute disseminated encephalomyelitis (ADEM). J Neuroimmunol 2011;231:92-99.  Back to cited text no. 1
Lotze TE, Chadwick DJ. Acute disseminated encephalomyelitis in children: Pathogenesis, clinical features, and diagnosis. UpToDate 2009.  Back to cited text no. 2
Tenembaum S, Chitnis T, Ness J, Hahn JS. Acute disseminated encephalomyelitis. Neurology 2007;68(Suppl 2):S23-36.  Back to cited text no. 3
Weng WC, Peng SS, Lee WT, Fan PC, Chien YH, Du JC, et al. Acute disseminated encephalomyelitis in children: One medical center experience. Acta Paediatr Taiwan 47:67-71.  Back to cited text no. 4
Rust RS. Multiple sclerosis, acute disseminated encephalomyelitis and related conditions. Semin Neurol 2000;7:66-90.  Back to cited text no. 5
Menge T, Hemmer B, Nessler S, Wiendl H, Neuhaus O, Hartung HP. Acute disseminated encephalomyelitis an update. Arch Neurol 2005;62:1673-80.  Back to cited text no. 6
Sidhu J, Maheshwari A, Gupta R, Devgan V. Acute disseminated encephalomyelitis after plasmodium vivax infection: Case report and review of literature. Pediatr Rep 2015;7:5859.  Back to cited text no. 7
Hemachudha T, Griffin DE, Giffels JJ, Johnson RT, Moser AB, Phanuphak P. Myelin basic protein as an encephalitogen in encephalomyelitis and polyneuritis following rabies vaccinations. N Engl J Med 1987;316:369-74.  Back to cited text no. 8
Fujinami RS, Oldstone MB. Amino acid homology between the encephalitogenic site of myelin basic protein and virus: Mechanism of autoimmunity. Science 1985;230:1043-5.  Back to cited text no. 9
Murthy SN, Faden HS, Cohen ME, Bakshi R. Acute disseminated encephalomyelitis in children. Pediatrics 2002;110:e21.  Back to cited text no. 10
Hynson JL, Kormberg AJ, Coleman LT, Shield L, Harvey AS, Kean MJ. Clinical and neuroradiologic features of acute disseminated encephalomyelitis in children. Neurology 2001;56:1308-12.  Back to cited text no. 11
Murthy JMK, Yangala R, Meena AK, Reddy JJ. Clinical, electrophysiological and magnetic resonance imaging study of acute disseminated encephalomyelitis. J Assoc Physicians India 1999;47:280-3.  Back to cited text no. 12
Schwarz S, Mohr A, Knauth M, Wildemann B, Storch-Hagenlocher B. Acute disseminated encephalomyelitis: A follow-up study of 40 adult patients. Neurology 2001;56:1313-8.  Back to cited text no. 13
Garg RK. Acute disseminated encephalomyelitis. Postgrad Med J 2003;79:11-7.  Back to cited text no. 14
Krupp LB, Banwell B, Tenembaum S; International Pediatric MS Study Group. Consensus definitions proposed for pediatric multiple sclerosis and related disorders. Neurology 2007;68:S7-12.  Back to cited text no. 15


  [Figure 1], [Figure 2], [Figure 3]

  [Table 1], [Table 2], [Table 3]


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