Neurological manifestations of human parvovirus B19 infection

Barah, Faraj; Vallely, P. J.; Cleator, Graham M.; Kerr, Jonathan

doi:10.1002/rmv.388

Cited by 67 publications

(46 citation statements)

References 134 publications

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“…To date, an association of parvovirus infection with meningitis, encephalitis, leukoencephalopathies or peripheral neuropathies has only been described in humans infected with parvovirus B19 (3,4,25,30,54). Most frequently immunocompromised patients seem to be affected.…”

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“…The hallmark of these conditions is vacuolization in the CNS, which is most likely due to myelin alterations and/or astrocytic swelling and gliosis often associated with myelin loss. A few congenital leukodystrophies are caused by viruses that act as fetal teratogen in these cases, e.g., border disease in sheep and parvovirus B19 infections in humans (3,4,27,52). Parvovirus infection as a cause of leukoencephalopathy in the dog has not yet been described, whereas cerebellar hypoplasia represents a common sequelae of congenital parvovirus infection in the cat (32,44,50,52).…”

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Leukoencephalopathy Associated with Parvovirus Infection in Cretan Hound Puppies

Schaudien¹,

Polizopoulou

Koutinas

et al. 2010

J Clin Microbiol

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Leukoencephalopathies in dogs encompass presumably inherited conditions such as leukodystrophies, hypomyelination or spongiform degeneration, but other causes, such as virus infections and toxic or nutritional factors, might also play a contributory role. In this report, we provide evidence of parvovirus infection and replication in the brains of five 6-week-old Cretan hound puppies suffering from a puppy shaker syndrome and leukoencephalopathy. Although these puppies belonged to two different litters, they were closely related, tracing back two generations to the same sire. Histologically, a mild to moderate lymphohistiocytic meningitis, with focal lymphohistiocytic leukoencephalitis in two animals, and a mild to moderate vacuolation with myelin loss, mainly in the white matter of the cerebellum was detected. Vacuolation was also found in the corpus callosum, fimbria hippocampi, mesencephalon, capsula interna, basal ganglia, and hypothalamus.

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Leukoencephalopathy Associated with Parvovirus Infection in Cretan Hound Puppies

Schaudien¹,

Polizopoulou

Koutinas

et al. 2010

J Clin Microbiol

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“…In most of the cases, only supplem e n t a rytreatment is needed until the virus is cleare d by the immune system. If persistent symptoms occur, t reatment with intravenous immunoglobulin may be useful 12 .…”

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Isolated velopalatine paralysis associated with parvovirus B19 infection

Soares-Fernandes

Maré

2006

Arq. Neuro-Psiquiatr.

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-A case of isolated velopalatine paralysis in an 8-year-old boy is presented. The symptoms were sudden-onset of nasal speech, re g u rgitation of liquids into the nose and dysphagia. Brain MRI and cereb rospinal fluid examination were normal. Infectious serologies disclosed an antibody arrangement toward s p a rv o v i rus B19 that was typical of recent infection. In the absence of other positive data, the possibility of a correlation between the tenth nerve palsy and parvovirus infection is discussed.KEY WORDS: paralysis, vagus nerve, palate, parvovirus B19, infection, childhood. Paralisia velopalatina isolada associada a infecção por parvovírus B 19RESUMO -Apresentamos um caso de paralisia velopalatina isolada, num menino de 8 anos, que se manifestou por voz nasalada, re g u rgitação de líquidos pelo nariz e disfagia, de início súbito. A ressonância magnética encefálica e o estudo do líquido cefalo-raquidiano foram normais. O perfil serológico dos anticorpos anti-parv o v í rus B19 era típico de infecção recente. Na ausência de outros dados positivos, discute-se a possibilidade de uma correlação entre a parésia do X nervo e a infecção por parvovírus.PALAVRAS-CHAVE: paralisia, nervo vago, palato, parvovirus B19, infecção, criança.Unilateral isolated paralysis of the soft palate is uncommon. Since the first description, by Edin et al in 1976 1 , 30 cases have been re p o rted, all of them in childhood or adolescence 2 . Patients typically pre s e n t sudden onset of nasal speech and dysfagia with complete re c o v e ryin weeks or months. In four of the rep o rted cases, a concomitant viral infection was diagnosed. Implicated viruses include varicella-zoster viru s ( V Z V ) 3 , herpes simplex virus (HSV) 4 , measles viru s 5 a n d Coxsackie A9 virus 6 . Despite the increased availability of diagnostic tests, the aetiology of acquired velopalatine palsy remains largely unknown.We present a case of unilateral velopalatine palsy associated with parvovirus infection in an 8-yearold male patient. CASEA previously healthy 8-year-old boy was brought to our e m e rgency department for sudden ons et, 3 days befor e , of nasal speech, re g u rgitation of liquids into the nose and d i fficulty in swallowing. One week before, he re f e rred diarrhoea, which resolved spontaneously in two days. He denied headaches, vomits, cervical pain or visual disturbance. There was, also, no traumatic or toxic ingestion history.On examination, he had a fine general appearance. In phonation, uvula deviated to the right due to left soft hemipalate palsy (Figure). The pharyngeal reflex and the vocal c o rds were intact. The exploration of the remaining cranial nerves was normal.L a b o r a t o ryanalysis, including blood cell count, ery t h rocyte sedimentation rate, C-reactive protein, thyroid function, vitamin B12, folic acid, antinuclear, anti-double-stranded DNA, antineutrophil cytoplasmic and antihistone antibodies were normal or unremarkable.

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“…In the present case, histological features associated with B19 virus infection were at first typical of ulcerative colitis and then, in the small bowel, were characterized by villous atrophy with increased intraepithelial lymphocytes and a reactive inflammatory infiltrate of the mucosa. On the other hand, an etiological role for B19 virus in the encephalitis (bulbar syndrome) observed in the initial phase of the disease cannot be directly assessed because of the lack of virological testing but can be hypothesized because of the temporal coincidence and clinical evolution (1). The observation that our patient was positive for HLA class II antigen alleles DRB1*07 and DQB1*02 agrees with previous findings which suggest a role for patient genotype in clinical manifestation of B19 virus infection.…”

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Parvovirus B19 Infection Localized in the Intestinal Mucosa and Associated with Severe Inflammatory Bowel Disease

Pironi¹,

Bonvicini²,

Gionchetti³

et al. 2009

J Clin Microbiol

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Infection by human parvovirus B19 is widespread and can be associated with a wide range of different pathologies and clinical manifestations. We provide the first evidence of localization of an active parvovirus B19 infection in the intestinal mucosa and its association with a severe inflammatory bowel disease, characterized by duodenal villous atrophy with increased intraepithelial lymphocytes and inflammatory infiltrates in the colonic mucosa. Virus in the intestinal mucosa was detected in cells of the inflammatory infiltrate, identified as T lymphocytes and selectively localized in sites of active tissue degeneration. CASE REPORTIn February 2004, a diagnosis of extensive ulcerative colitis in a 52-year-old Caucasian man was made. Treatment with oral methylprednisolone (20 to 60 mg/day) resulted in improvement of the condition.In June 2004, he presented with a subacute bulbar syndrome. Spinal fluid analysis showed increased white blood cells. No specific infection was detected, and, as neoplastic and autoimmune diseases were excluded, an unrecognized infective etiology was hypothesized. Treatment with acyclovir was begun, along with corticosteroid maintenance (methylprednisolone, 20 to 60 mg/ day). Encephalitis healed within 2 months.In August 2004, ulcerative colitis was not responsive to medical treatment (methylprednisolone, 40 to 60 mg/day). A total colectomy with temporary ileostomy was performed, and corticosteroid treatment was stopped.In January 2005, bloody diarrhea with an ileostomy output of 5,000 to 6,000 ml/day, severe malabsorption, and systemic inflammatory reaction appeared. Ileoscopy revealed a diffuse superficial ulceration of the ileum. Histology showed a reactive inflammatory infiltrate with eosinophils as well as an increased number of intraepithelial lymphocytes associated with degenerative changes of the epithelial lining. A diagnosis of aspecific enteritis was made. Treatment with intravenous methylprednisolone (60 mg/day), oral fasting, and total parenteral nutrition were started.In March 2005, histology of the ileum showed ulcerative enteritis with focal pseudomembranes. Treatment with oral azathioprine, 50 to 100 mg/day, was started.In May 2005, ileostomy output was 3,000 to 4,000 ml/day and histology of the ileum was unchanged. Upper endoscopy showed a granular duodenal mucosa with severe villous atrophy, crypt hyperplasia, and inflammatory infiltrate with plasma cells, and more than 25 intraepithelial lymphocytes per 100 enterocytes were observed. Autoimmune enteropathy was excluded by a search for serum enterocyte autoantibodies, and intestinal lymphoma was excluded by immunohistochemistry. Serum chromogranin A concentration was normal. Tests for antitransglutaminase and antigliadin antibodies were negative. Serum immunoglobulin A (IgA) concentration was normal. HLA typing for celiac disease indicated that DQA1*0501 was absent, DQB1*0201 was present, and DQB1*0302 was absent; that for chronic inflammatory bowel disease indicated that DRB1*07 was present.Infections by Salmonella, B...

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Neurological manifestations of human parvovirus B19 infection

Cited by 67 publications

References 134 publications

Leukoencephalopathy Associated with Parvovirus Infection in Cretan Hound Puppies

Leukoencephalopathy Associated with Parvovirus Infection in Cretan Hound Puppies

Isolated velopalatine paralysis associated with parvovirus B19 infection

Parvovirus B19 Infection Localized in the Intestinal Mucosa and Associated with Severe Inflammatory Bowel Disease

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