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Diffuse Bacterial Meningitis and Myelitis Secondary to a Diplococcus Organism

Published online by Cambridge University Press:  16 December 2015

Ghita Ann Wiebe ,
Sergio Fanella ,
Jens Wrogemann ,
Carrie Daymont  and
Mubeen Rafay
Ghita Ann Wiebe*
Affiliation:
Section of Child Development, Children’s Hospital Winnipeg, University of Manitoba Department of Pediatrics and Child Health, Children’s Hospital Winnipeg, University of Manitoba.
Sergio Fanella
Affiliation:
Pediatric Infectious Diseases, Children’s Hospital Winnipeg, University of Manitoba Department of Pediatrics and Child Health, Children’s Hospital Winnipeg, University of Manitoba.
Jens Wrogemann
Affiliation:
Department of Pediatric Radiology, Children’s Hospital Winnipeg, University of Manitoba Department of Pediatrics and Child Health, Children’s Hospital Winnipeg, University of Manitoba.
Carrie Daymont
Affiliation:
Children’s Hospital Research Institute of Manitoba, Children’s Hospital Winnipeg, University of Manitoba Department of Pediatrics and Child Health, Children’s Hospital Winnipeg, University of Manitoba.
Mubeen Rafay
Affiliation:
Children’s Hospital Research Institute of Manitoba, Children’s Hospital Winnipeg, University of Manitoba Section of Pediatric Neurology, Children’s Hospital Winnipeg, University of Manitoba Department of Pediatrics and Child Health, Children’s Hospital Winnipeg, University of Manitoba.
*
Correspondence to: Ghita Ann Wiebe, Section of Child Development, Department of Pediatrics and Child Health, CK253 840 Sherbrook Street, Winnipeg, MB R3A 1S1. Email: [email protected]
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Abstract

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Keywords

MeningitisPediatric Neurology
Type
Neuroimaging Highlights
Information
Canadian Journal of Neurological Sciences , Volume 43 , Issue 1 , January 2016 , pp. 192 - 194
Copyright
Copyright © The Canadian Journal of Neurological Sciences Inc. 2015 

A 16-year-old, previously healthy, female presented with a 1-week history of sore throat, fever, vomiting, and occipital headache. She also complained of generalized myalgia and lower limb weakness. There was no medication or substance use. Her immunizations were up to date, and she had no recent travel history or contact with persons from overseas. Examination in emergency revealed an unwell girl with nuchal rigidity and generalized hyperesthesia. Muscle strength in the lower extremities was graded 3-/5. In the upper extremities, strength was graded 4+/5 except distally on the right side, which was graded 4-/5 with scooping fingers and difficulty with extension of fingers, along with weak wrist flexion. Sitting was noted to be difficult. Reflexes were decreased in the lower limbs; brisk reflexes were found in the upper limbs.

Initial magnetic resonance imaging (MRI) showed extensive T2 signal changes throughout the spinal cord (Figure 1A,B). MRI of the brain did not reveal any significant intracranial abnormality. Initial differential diagnosis included demyelinating myelitis from an infectious, postinfectious, or inflammatory process. Infarction and neoplastic infiltration of the spinal cord were also considered. Her cerebrospinal fluid (CSF) had increased protein (2.29 g/L), lactate (4.2 mmol/L), cell count 840×106/L (neutrophils, 39; lymphocytes, 53; monocytes/macrophages, 8) and normal glucose (2.5 mmol/L). A CSF Gram stain revealed gram-negative diplococci versus coccobacilli (orientation of organism unclear). Blood and CSF cultures were obtained before treatment with intravenous cefotaxime and vancomycin at meningitic doses and dexamethasone (7.5 mg every 6 hours).

Figure 1 (A) MRI cervical spine sagittal T2 showing evidence of extensive high signal changes throughout the spinal cord starting in the lower medulla and involving preferentially the deep gray matter of the spinal cord. There is also swelling of the entire cervical spinal cord. (B) MRI thoracic spine sagittal T2 demonstrating evidence of extensive hyperintense signal changes in thoracic spinal cord.

Overnight, she developed progressive flaccid paralysis of extremities; cefotaxime was switched to ceftriaxone and dexamethasone was switched to daily methylprednisone (1 g for 5 days) followed by oral prednisone (1 g/kg) in tapering doses over 20 days. She demonstrated gradual improvement of her extremity weakness. Repeat MRI showed minimal interval improvement (Figure 2). CSF and blood cultures yielded negative results, as did CFS analysis using 16S RNA PCR.Reference Edwards, Rogall, Blöcker, Emde and Böttger 1 CFS, stool, and nasopharyngeal secretion viral cultures (including polio virus) revealed no causative organism. She was treated with 14 days of antibiotics for presumed bacterial meningitis resulting from either Neisseria meningitidis or Haemophilus influenzae, based on the initial CSF Gram stain. Follow-up MRI 1 month after presentation revealed improvements, with minor residual inflammation/demyelination seen within the cervical/thoracic spinal cord (Figure 3). Two months after her presentation, she was ambulating with cane assistance. A repeat MRI 9 months after presentation showed resolution of abnormal findings. Follow-up 11 months after presentation showed almost complete neurological recovery, with only mild residual bowel and bladder dysfunction.

Figure 2 Repeat MRI cervical spine sagittal T2 done 5 days after presentation and treatment. Evidence of slightly less cord swelling and less signal abnormality is noted in the cervicothoracic spinal cord.

Figure 3 MRI cervical and upper thoracic spine sagittal T2 done 1 month after the patient’s presentation reveals resolution of cord swelling and evidence of only minor residual hyperintense signal abnormalities.

Comment

Meningitis presenting with diffuse myelopathy is rare. Proposed mechanisms of spinal cord damage include infarction, autoimmune-mediated infectious/postinfectious inflammatory myelopathy, direct infection, vasculitis, and hypoxia.Reference Khan, Altafullah and Ishaq 2 - Reference Rathore, Gill and Malik 6 , Reference Kastenbauer, Winkler, Fesl, Schiel, Ostermann and Yousry 8

Myelitis, an inflammation of the spinal cord, is a rare complication of meningococcal meningitis that usually occurs during treatment or as a late complication.Reference Khan, Altafullah and Ishaq 2 - Reference Kastenbauer, Winkler, Fesl, Schiel, Ostermann and Yousry 8 The thoracic cord and conus medullaris are most commonly affected.Reference Bhojo, Akhter, Bakshi and Wasay 4 Symptoms may evolve over hours or days, with lower extremity flaccidity, bowel and bladder dysfunction, and a reduced sensory level.Reference Roos 7 Reported MRI findings include intramedullary signal on T2-weighted images, cord swelling, leptomeningeal and intramedullary contrast enhancement.Reference Bhojo, Akhter, Bakshi and Wasay 4 - Reference Choudhary, Kumar, Ahlawat, Kapil, Yasir and Gaurav 5 , Reference Kastenbauer, Winkler, Fesl, Schiel, Ostermann and Yousry 8 Enhancement of the cauda equina and lumbosacral nerve roots is also documented.Reference Kastenbauer, Winkler, Fesl, Schiel, Ostermann and Yousry 8

Overall prognosis is guarded, with residual deficits including bowel/bladder dysfunction and ambulation difficulties. It is difficult to determine the contribution of steroids in neurological recovery.Reference Ibrahim, Elalamy, Doiphode, Mobyaed and Darweesh 3 , Reference Choudhary, Kumar, Ahlawat, Kapil, Yasir and Gaurav 5 - Reference Rathore, Gill and Malik 6 , Reference Kastenbauer, Winkler, Fesl, Schiel, Ostermann and Yousry 8 Since 1996, The Canadian Pediatric Surveillance Program has maintained a protocol to identify and investigate acute flaccid paralysis in children.Reference Desai 9 , 10

In our patient, CSF pleocytosis and biochemical analysis with positive Gram stain confirms an infectious etiology. Possibilities for cultures being negative include artifact on Gram stain or accumulation of the stain. Another possibility is that there was failure of the polymerase chain reaction because of a dead organism. Either direct infectious or infectious immune-mediated mechanisms are suspected for this diffuse myelitis. This rare presentation highlights considerations for an acute infectious diffuse myelopathy in patients that present with acute-onset progressive extremity weakness.

Disclosures

Ghita Ann Wiebe, Mubeen Rafay, Sergio Fanella, Jens Wrogemann, and Carrie Daymont have nothing to disclose.

There was no financial support or conflict of interest identified.

References

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2. Khan, J, Altafullah, I, Ishaq, M. Spinal cord dysfunction complicating meningococcal meningitis. Postgrad Med J. 1990;66:302-303.CrossRefGoogle ScholarPubMed
3. Ibrahim, WH, Elalamy, OR, Doiphode, SH, Mobyaed, H, Darweesh, A. Acute myelopathy with sudden paraplegia as the sole manifestation of meningococcal meningitis. Libyan J Med. 2010;8:4862-4864.CrossRefGoogle Scholar
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Figure 0

Figure 1 (A) MRI cervical spine sagittal T2 showing evidence of extensive high signal changes throughout the spinal cord starting in the lower medulla and involving preferentially the deep gray matter of the spinal cord. There is also swelling of the entire cervical spinal cord. (B) MRI thoracic spine sagittal T2 demonstrating evidence of extensive hyperintense signal changes in thoracic spinal cord.

Figure 1

Figure 2 Repeat MRI cervical spine sagittal T2 done 5 days after presentation and treatment. Evidence of slightly less cord swelling and less signal abnormality is noted in the cervicothoracic spinal cord.

Figure 2

Figure 3 MRI cervical and upper thoracic spine sagittal T2 done 1 month after the patient’s presentation reveals resolution of cord swelling and evidence of only minor residual hyperintense signal abnormalities.