Human herpesvirus-6 infection-associated acute encephalopathy without skin rash

Yamamoto, Shigeo; Takahashi, Satoru; Tanaka, Ryosuke; Okayama, Akie; Araki, Akiko; Katano, Harutaka; Tanaka‐Taya, Keiko; Azuma, Hiroshi

doi:10.1016/j.braindev.2014.12.005

Cited by 9 publications

(13 citation statements)

References 12 publications

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“…Human herpesvirus 6 (HHV-6), and less often HHV-7, may cause encephalitis and their reactivation may be an important cause of encephalitis in transplant patients. 23 24 25 HHV-6 and HHV-7 are diagnosed by PCR, although this may not be positive initially. 26 There are no approved treatments, but ganciclovir, foscarnet, and cidofovir have been used.…”

Section: Exclusion Of Infectious Causesmentioning

confidence: 99%

The Diagnosis and Treatment of Autoimmune Encephalitis

2016

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Autoimmune encephalitis causes subacute deficits of memory and cognition, often followed by suppressed level of consciousness or coma. A careful history and examination may show early clues to particular autoimmune causes, such as neuromyotonia, hyperekplexia, psychosis, dystonia, or the presence of particular tumors. Ancillary testing with MRI and EEG may be helpful for excluding other causes, managing seizures, and, rarely, for identifying characteristic findings. Appropriate autoantibody testing can confirm specific diagnoses, although this is often done in parallel with exclusion of infectious and other causes. Autoimmune encephalitis may be divided into several groups of diseases: those with pathogenic antibodies to cell surface proteins, those with antibodies to intracellular synaptic proteins, T-cell diseases associated with antibodies to intracellular antigens, and those associated with other autoimmune disorders. Many forms of autoimmune encephalitis are paraneoplastic, and each of these conveys a distinct risk profile for various tumors. Tumor screening and, if necessary, treatment is essential to proper management. Most forms of autoimmune encephalitis respond to immune therapies, although powerful immune suppression for weeks or months may be needed in difficult cases. Autoimmune encephalitis may relapse, so follow-up care is important.

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Section: Exclusion Of Infectious Causesmentioning

confidence: 99%

The Diagnosis and Treatment of Autoimmune Encephalitis

2016

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“…Amoxicillin (Mardivirin et al 2010 ), carbamazepine, and sodium valproate (Mardivirin et al 2009 ) have been shown to activate HHV-6 in vitro ; thus, they might facilitate the development of encephalopathy. Hydrocortisone is a strong enhancer of HHV-6 replication (Arbuckle et al 2010 ), and prednisolone derivates given to suppress skin rash might contribute to higher CSF viral load (Hill et al 2015a , b ), but in children with CNS diseases, prednisolone therapy (Kawamura et al 2013 ; Pohl-Koppe et al 2001 ) helps protect the BBB (Kawamura et al 2013 ; Steiner et al 2010 ; Venancio et al 2014 ; Yamamoto et al 2015 ).…”

Section: Epidemiology and Risk Factorsmentioning

confidence: 99%

Roseolovirus-associated encephalitis in immunocompetent and immunocompromised individuals

et al. 2016

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The roseoloviruses, human herpesvirus (HHV)-6A, HHV-6B, and HHV-7, can cause severe encephalitis or encephalopathy. In immunocompetent children, primary HHV-6B infection is occasionally accompanied by diverse clinical forms of encephalitis. Roseolovirus coinfections with heterologous viruses and delayed primary HHV-7 infection in immunocompetent adults result in very severe neurological and generalized symptoms. Recovery from neurological sequelae is slow and sometimes incomplete. In immunocompromised patients with underlying hematological malignancies and transplantation, frequent single or simultaneous reactivation of roseoloviruses elicit severe, lethal organ dysfunctions, including damages in the limbic system, brain stem, and hippocampus. Most cases have been due to HHV-6B with HHV-6A accounting for 2–3%. The most severe manifestation of HHV-6B reactivation is post-transplantation limbic encephalitis. Seizures, cognitive problems, and abnormal EEG are common. Major risk factors for HHV-6B-associated encephalitis include unrelated cord blood cell transplantation and repeated hematopoietic stem cell transplantation. Rare genetic disorders, male gender, certain HLA constellation, and immune tolerance to replicating HHV-6 in persons carrying chromosomally integrated HHV-6 might also predispose an individual to roseolovirus-associated brain damage. At this time, little is known about the risk factors for HHV-7-associated encephalitis. Intrathecal glial cell destruction due to virus replication, overexpression of proinflammatory cytokines, and viral mimicry of chemokines all contribute to brain dysfunction. High virus load in the cerebrospinal fluid, hippocampal astrogliosis, and viral protein expression in HHV-6B-associated cases and multiple microscopic neuronal degeneration in HHV-7-associated cases are typical laboratory findings. Early empirical therapy with ganciclovir or foscarnet might save the life of a patient with roseolovirus-associated encephalitis.

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“…Primary HHV-6 infection is a common benign and self-limiting illness of infancy [7]. However, primary HHV-6 infection can cause acute encephalopathy without exanthema [8]. HHV-6 is sometimes the etiological agent of febrile seizures [5].…”

Section: Discussionmentioning

confidence: 99%

“…Direct detection of HHV-6 by PCR in blood of patient with primary infection is also possible during the febrile phase of illness [3]. When the patient shows no skin rash, the etiological diagnosis is possible only by examining the blood [8]. Reactivation or reinfection with HHV-6 may also occur in an individual who is already seropositive [3].…”

Section: Discussionmentioning

confidence: 99%

“…A careful review of the literature revealed no similar case of exanthema subitum; however, thrombocytopenia is reported to be a complication of exanthema subitum [7]. Patient with acute encephalopathy with primary HHV-6 infection with no skin rash has also been described [8]. Many infectious diseases can cause acute febrile illness associated with thrombocytopenia and leukopenia.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Human Herpesvirus 6 Infection Presenting as an Acute Febrile Illness Associated with Thrombocytopenia and Leukopenia

Arnež

Avšič–Županc

Uršič

et al. 2016

Case Reports in Pediatrics

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We present an infant with acute fever, thrombocytopenia, and leukopenia, coming from an endemic region for tick-borne encephalitis, human granulocytic anaplasmosis, and hantavirus infection. The primary human herpesvirus 6 infection was diagnosed by seroconversion of specific IgM and IgG and by identification of viral DNA in the acute patient's serum. The patient did not show skin rash suggestive of exanthema subitum during the course of illness.

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Human herpesvirus-6 infection-associated acute encephalopathy without skin rash

Cited by 9 publications

References 12 publications

The Diagnosis and Treatment of Autoimmune Encephalitis

The Diagnosis and Treatment of Autoimmune Encephalitis

Roseolovirus-associated encephalitis in immunocompetent and immunocompromised individuals

Human Herpesvirus 6 Infection Presenting as an Acute Febrile Illness Associated with Thrombocytopenia and Leukopenia

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