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PubMed2026

Rashless varicella-zoster virus encephalitis diagnosed by metagenomic next-generation sequencing: two case reports.

BACKGROUND: Varicella-zoster virus (VZV) can cause a range of central nervous system (CNS) infections, but early diagnosis is difficult when typical skin rash is absent. Rashless VZV encephalitis may present with nonspecific clinical, cerebrospinal fluid (CSF), and neuroimaging findings and can mimic autoimmune encephalitis, primary central nervous system lymphoma, or other disorders. We report two cases of rashless VZV encephalitis diagnosed by CSF metagenomic next-generation sequencing (mNGS), with subsequent neurological complications. CASE PRESENTATION: Case 1 was a 68-year-old man admitted with fever, seizures, and impaired consciousness. Brain magnetic resonance imaging (MRI) showed multifocal abnormal signals. CSF analysis revealed marked pleocytosis and elevated protein levels, and CSF cytology showed suspected atypical lymphocytes, leading to early consideration of autoimmune encephalitis and primary central nervous system lymphoma. CSF mNGS detected VZV, and rashless VZV encephalitis was diagnosed. The patient improved after intravenous acyclovir combined with a short course of dexamethasone. On day 45 after disease onset, follow-up MRI showed a new acute cerebral infarction adjacent to the posterior horn of the left lateral ventricle. Recurrent CSF pleocytosis and persistent protein elevation suggested possible VZV-associated vasculopathy. After repeated antiviral treatment, he improved again, and no recurrence was observed during more than 3 years of follow-up. Case 2 was a 74-year-old man admitted with fever, low back pain, vomiting, and impaired consciousness. Brain MRI showed multifocal abnormal signals, and CSF analysis revealed marked inflammatory changes. CSF mNGS detected VZV, supporting the etiological diagnosis of rashless VZV encephalitis. The patient improved after intravenous acyclovir combined with a short course of dexamethasone. On day 14 after disease onset, he developed urinary retention, impaired defecation sensation, and bilateral lower-limb weakness, suggesting possible lumbosacral nerve root or cauda equina involvement. Suspected VZV-related Elsberg syndrome was considered. His urinary and bowel dysfunction recovered at 2 months after disease onset. CONCLUSIONS: Rashless VZV encephalitis may be diagnostically challenging because early clinical, CSF, and neuroimaging findings are nonspecific. CSF mNGS can support etiological diagnosis, and careful follow-up is needed to detect delayed vascular and lumbosacral nerve root complications.

Humans↗
PubMed1978

[The virostatic effect of adenine-arabinoside monophosphate. Experimental findings and preliminary clinical experiences].

Adenine arabinoside (Ara-A), a synthetic nucleoside, is an antiviral agent, which is effective against poxviruses and viruses of the herpes group. The monophosphate (Ara-AMP) has the great advantage of better solubility, compared to the parent compound. Experimental studies show the outstanding effect of Ara-AMP on the encephalitis by vaccinia-virus in white mice. Even after immunesuppression by total body irradiation, the survival rate of the Ara-AMP treated animals was significantly higher compared to the untreated controls. In experimental vaccinia-virus infections in rabbits, who had undergone total body irradiation. Ara-AMP has a favourable influence upon the course of the disease and the prognosis. Some clinical observations in children with immunesuppression, who suffered from generalized zoster of varicella-infections, are reported. Furthermore in cases of viral encephalitis Ara-AMP was successful. Controlled studies of a greater number of patients on the therapeutic value of Ara-AMP in infections with DNS-viruses are needed.

Adenosine Monophosphate↗
PubMed1975

Treatment of varicella-zoster virus infections with adenine arabinoside.

Twenty-three patients with complicated varicella-zoster virus infections were treated with adenine arabinoside. Of 14 patients with herpes zoster, 13 had malignancy treated with irradiation and cytotoxic agents or steroids. Although the duration of active vesicle formation in these patients ranged from two to 14 days before therapy, no new lesions appeared after the fourth day of treatment with adenine arabinoside. Zoster encephalitis developed in one patient on the third day of treatment, and severe postherpetic neuralgia was seen in three patients. Of nine treated patients with primary varicella, six improved, including five with evidence of varicella pneumonia. Two of the three patients with varicella who died were immunosuppressed and had progressive viral pneumonia with persistently high titers of virus in vesicular fluid; the third pateint was a child with Reye's syndrome. Double-blind controlled studies will be necessary to demonstrate the efficacy of adenine arabinoside in the treatment of infections with varicella-zoster virus.

Adult↗
PubMed1976

Vidarabine therapy for severe herpesvirus infections. An unusual syndrome of chronic varicella and transient immunologic deficiency.

Six patients with severe herpesvirus infections were successfully treated with vidarabine. One patient had a previously undescribed syndrome of chronic cutaneous varicella infection of eight months' duration, associated with transient but complete duppression of lymphocyte response to conconavalin A. Other diagnoses were severe varicella pneumonia, progressive cytomegalovirus pneumonia associated with acute lymphocytic leukemia, herpes simplex encephalitis, severe zoster associated with stage IV lymphoma, and disseminated herpes simplex in a patient receiving high doses of steroids. All patients showed cessation of new lesions or abrupt clinical improvement between days 2 and 4 after initiation of therapy, and all were cured of their clinical infection. Dramatic improvement in all of our patients and the minimal toxicity observed make vidarabine suitable for use in severe herpesvirus infections.

Adolescent↗
PubMed1975

Prophylaxis of varicella in children with neoplastic disease: comparative results with zoster immune plasma and gamma globulin.

The incidence and severity of varicella following a close family contact were evaluated in children with neoplastic diseases who received prophylaxis either with commerical gamma globulin or with zoster immune plasma, as compared to patients who did not receive any prophylaxis. In the untreated group, all 14 patients developed varicella, complicated by 1 case of encephalitis and 2 cases of fatal pneumonia. In the group of 17 patients who received 0.6-1.2 ml/kg body weight of gamma globulin, 16 developed varicella, complicated by pneumonia in 2 cases, with 1 death. In the third group of 27 patients who received 10 ml/kg body weight of zoster immune plasma (ZIP), obtained from healthy adults convalescing from herpes zoster, there were only 8 cases of varicella, all very mild. Thus, prophylaxis with ZIP significantly reduced the incidence of clinical varicella (p less than 0.01) and attenuated the severity of its course.

Antineoplastic Agents↗
PubMed1978

[Severe generalized courses of zoster due to cellular immunologic defects. Importance of an absolute or relative T-cell deficiency].

Four patients with chronic lymphatic leukaemia, M. Hodgkin and metastatic breast carcinoma developed particularly severe generalised herpes zoster, with complications of herpes zoster pneumonia, signs of encephalitis and phrenic nerve paresis. Virus specific complement-fixing antibodies increased regularly or delayed, without strict correlation to the clinical course. However, in all these cases there was a relative or absolute deficiency of T-lymphocytes in the peripheral blood, as a result of the underlying illness and of treatment with cytostatic agents. Because of the vital role of cell-mediated immunity in the control of the varicella-zoster virus (VZV), the observed T-cell deficiency seems to be an important pre-condition for the development of severe generalised herpes zoster.

Adult↗
PubMedDate not supplied

Acute facial palsy. Some clinical and virological observations.

A prospective clinical and virological study on 44 patients with acute, peripheral facial paralysis was carried out in consecutive cases during one year. In 9 cases varicella-zoster infections were serologically established. In 5 additional patients an associated varicella-zoster, or herpes simplex, infection was possible. Of the 9 confirmed cases, 6 were clinically diagnosed as zoster oticus, whereas on clinical grounds, 3 were regarded as Bell's palsy. No evidence was obtained of associated enterovirus, mumps, measles, cytomegalovirus, tick-borne encephalitis virus, para-influenza virus, mononucleosis or Mycoplasma pneumoniae infection.

Acute Disease↗
PubMed1977

Effect of a novel adenosine deaminase inhibitor (co-vidarabine, co-V) upon the antiviral activity in vitro and in vivo of vidarabine (Vira-Atm) for DNA virus replication.

A new potent inhibitor of adenosine deaminase (co-vidarabine) was used in combination studies with adenine arabinoside (vidarabine, Vira-ATM) to protect this purine nucleoside from enzymatic deamination to the more weakly active metabolite, hypoxanthine arabinoside. Comparing the combination to vidarabine alone, a significant increase (10-fold) of the antiviral activity of the combined drugs was observed against herpes and vaccinia viruses in tissue culture and subcutaneously, against cranial herpesvirus infections in mice. Several other investigators have also recently reported several-fold enhancement of vidarabine activity by newly described deaminase inhibitors. They observed that plaque formation by several large DNA-containing viruses (herpes, vaccinia, varicella zoster) and an RNA-containing oncogenic virus was markedly prevented by the combination compared to vidarabine alone. In animals, enhanced protection (increased survivors) and/or highly significant increase in the life span of dying mice treated with the 2-drug combination, was also observed compared to vidarabine administered singly. These observations in animals clearly indicate that combination studies with vidarabine (Vira-ATM) and co-vidarabine (deaminase inhibitor) deserve serious consideration as future therapy for systemic virus infections in man including herpesvirus encephalitis.

Adenosine Deaminase Inhibitors↗