Acute demyelinating disorder by parvovirus B19

Parvovirus B19 is an airborne virus that belongs to the Parvoviridae family and which is principally responsible for fifth disease and arthralgia, as well as aplastic crisis.¹ Although neurological manifestations of this disease are rare, an increase has recently been reported in cases of meningoencephalitis, encephalitis and encephalopathy in which parvovirus B19 was confirmed as the causal agent.² Even so, cases of demyelinating diseases are still anecdotal, which is why we are reporting a case of a young female patient with transverse myelitis attributed to this viral infection.

A 30-year-old female patient, with no significant pathological history, was admitted to hospital owing to symptoms of weakness and abnormal tactile perception in the lower limbs. The patient reported that two weeks prior to admission, she had attended an outpatient clinic owing to an unquantified rise in temperature, arthralgia, adenopathies in the bilateral cervical, axillary and inguinal region and a morbilliform rash on her face, thorax, abdomen and upper and lower limbs, with a predominance on the palms of her hands and soles of her feet, with a tendency towards nocturnal exacerbation. She received symptomatic treatment, with apparent resolution of the acute symptoms. However, three weeks after her initial symptoms, she rapidly and progressively developed paraesthesia at medial level of the left lower limb, which subsequently progressed bilaterally to the side of the thigh and which hindered walking, particular climbing stairs.

Physical examination upon admission showed the patient to be awake, oriented and afebrile. Mobile and painful adenopathies measuring approximately 3 cm could be felt in the occipital and posterolateral cervical region; mobile and painful adenopathies of around 3 cm in the anterior axillary line, and mobile and painful adenopathies of around 2 cm in the fixed left anterior inguinal region. Neurological examination showed a bilateral 3/5 reduction of strength in the lower limbs; 3/5 ipsilateral hyperreflexia in right knee-jerk reflex and 4/5 in right Achilles reflex, 2/5 in contralateral reflexes; numbness to touch, painful and throbbing in the outer region of the thigh and the right leg (level L1–L2).

Clinical chemistry findings showed: leukocytes 9.6 × 10³/mm³, neutrophils 67.3%, lymphocytes 22.8%, basophils 2%, red blood cells 4.7 × 10⁶/mm³, haemoglobin 14.6 g/dl, haematocrit 43.6%, platelets 390 × 10³/mm³. C-reactive protein 0.10 mg/dl, procalcitonin 0.02 ng/ml and negative anti-nuclear antibodies (<1/80). A serological examination was performed which revealed rubella IgG+, cytomegalovirus IgG+, herpes virus i and ii IgG−, and parvovirus B19 IgG+ (>50.0 IU/ml) and IgM+ (>200.0 IU/ml), thus confirming parvovirus B19 infection. In light of the patient's neurological symptomatology, a lumber puncture was performed with an analysis of the cerebrospinal fluid (CSF), which presented a clear cytochemistry, glucose 58 mg/dl, mononuclear cells 100 cells/μl, proteins 431 mg/dl, the bacteriological analysis was negative. To corroborate the serological finding, a real-time polymerase chain reaction in the CSF for parvovirus 19 was ordered, which was positive.

In parallel, an MRI of the lumbar spine was performed, with coronal, sagittal and axial views, with mapping techniques T1 and T2, including STIR, prior and subsequent to the intravenous administration of contrast agent, which showed thickening of the right neural root L1-L2 without abnormal uptake of contrast (Fig. 1).

Fig. 1.

MRI of lumbar spine in the sagittal view showing thickening of right L1–L2 neural root.

With these results, a diagnosis of acute post-infectious transverse myelitis by parvovirus B19 was established, and immunosuppressive treatment was initiated with five doses of IV methylprednisolone (1 g/24 h), and oral prednisone (40 mg/24 h), tapering the dose by 5 mg every five days until 20 mg and maintaining this dose for a further 30 days. The patient recovered 5/5 strength and sensitivity within one week.

Transverse myelitis is a rare disorder, with a global incidence of 4–8 cases per 1,000,000 people per year^3,4 and with 1–4 cases per 100,000 population reported in the western literature.⁴ It is characterised by sensory dysfunction (neuropathic pain, hyperalgesia, allodynia, paraesthesia and hypoesthesia), motor or autonomic dysfunction attributable to the spinal cord; bilateral (not necessarily symmetrical) signs and/or symptoms, a clearly defined sensory level, exclusion of extra-axial compressive aetiology in the neuroimaging study, inflammation of the spinal cord indicated by pleocytosis in the cerebrospinal fluid or increase in the IgG index or increase in the uptake of gadolinium in the MRI study, and progression up to a clinical deficit nadir between 4 h and 21 days after the onset of symptoms.^3,5,6 Our case exhibited motor and sensory dysfunction, taking the form of a bilateral reduction of strength in the lower limbs and numbness at level L1–L2, which got progressively worse over a period of three weeks; inflammation of the spinal cord indicated by pleocytosis and exclusion of extra-axial compressive aetiology in the neuroimaging study, meeting the aforesaid criteria for transverse myelitis.

Acute transverse myelitis may result from autoimmune processes,⁴ after vaccination⁷ or in the majority of cases subsequent to infectious viral processes, the most commonly reported of which include cytomegalovirus, herpes virus, Epstein–Barr virus and varicella zoster.^8,9 A systematic review conducted in Europe, which evaluated the neurological signs of 129 cases due to infection by parvovirus B19, documented only two cases of transverse myelitis and one case of parainfectious myelitis associated with parvovirus B19, confirmed serologically by the presence of de IgG and IgM in the CSF of patients between 1970 and 2012.^2,10,11 Susuki et al. published the case of a nine-year-old boy diagnosed with acute transverse myelitis associated with parvovirus B19 confirmed serologically by the presence of DNA in serum and cerebrospinal fluid.¹² A search of the PubMed database has revealed no further cases to date.

Parvovirus B19 is a single-stranded DNA virus, with tropism towards bone marrow erythroblasts in humans, which are its sole hosts.¹ In immunocompetent adults, the principal clinical signs of parvovirus B19 infection identified in the study conducted in France by Parra et al. included fever (65%), arthralgia (62%), maculopapular rash on the trunk, limbs and face (47%), myalgia (38%), adenopathies (38%), diffuse oedema of the hands (32%), pruritus (16%) and paraesthesia (4%).¹³ Owing to an outbreak of parvovirus B19 in a paediatric hospital in the area, we focused our case on a viral aetiology. As a result, as part of the viruses to be investigated, antibodies for parvovirus B19 were requested, which turned out to be positive in serum and in CSF.

In conclusion, acute demyelinating disorders due to parvovirus B19 constitute a rare clinical manifestation in infection by this disease. Our patient exhibited all the clinical criteria for transverse myelitis, even though the MRI report showed thickening of the neural root, which rules out a compressive aetiology. It is important to bear in mind that the diagnosis of transverse myelitis is based on clinical findings. Moreover, in our case there was evidence of inflammation of the spinal cord caused by pleocytosis with a predominance of mononuclear cells in the CSF. Finally, the symptoms responded favourably to the intravenous and oral administration of corticosteroids.