Meningoencefalitis por herpesvirus varicelazóster como síndrome inflamatorio de reconstitución inmune. Una manifestación clínica infrecuente / VARICELLA-ZOSTER HERPESVIRUS MENINGOENCEPHALITIS AS AN INFLAMMATORY SYNDROME OF IMMUNE RECONSTITUTION. An uncommon clinical manifestation

El uso cada vez más difundido de la terapia antirretroviral de gran actividad (TARGA) en el tratamiento de los pacientes con infección por el virus de la inmunodeficiencia humana (VIH) puede dar lugar a respuestas paradojales, caracterizadas por un empeoramiento de las manifestaciones clínicas o la reactivación de ciertas infecciones oportunistas, hasta ese momento subclínicas, como el Herpes varicela-zóster (HVZ). Este cuadro clínico se conoce desde hace años como síndrome inflamatorio de reconstitución inmune (SIRI). Puede afectar a más del 30% de los pacientes seropositivos para el VIH con un tiempo de aparición promedio de 8 a 12 semanas luego del inicio o cambio de TARGA. El HZ mucocutáneo representa entre el 7% al 12% de los episodios de SIRI en estos pacientes. En este trabajo, se presenta un paciente VIH seropositivo que desarrolló un episodio de HVZ cutáneo monometamérico asociado a compromiso del sistema nervioso central bajo la forma de un síndrome meningoencefalítico

The use of highly active antiretroviral therapy (HAART) in the management of human immunodeficiency virus (HIV) infection has resulted in a paradoxical response associated with the worsening of clinical symptoms of previously subclinical infections, such as herpes varicella-zoster (HVZ). This clinical picture is named as immune reconstitution inflammatory syndrome (IRIS). It may affect up to 30% of HIV-seropositive subjects within a wide range of time after the initiation or change of HAART, but mainly after 8 to 12 weeks. Mucocutaneous HZ accounts for 7%-12% of the diseases associated with HIV infection in patients with immune reconstitution from the administration of HAART. Here we present an HIV seropositive patient that developed an episode of cutaneous metameric eruption of HVZ associated with central nervous system involvement as meningoencephalitis syndrome.

Hospitalization for acute cerebellitis in children affected by varicella: how much does it cost?

BACKGROUND: Chickenpox is a highly contagious airborne disease caused by the varicella zoster virus. It is generally benign and self-limiting, but it may be responsible of life-threatening complications. Acute cerebellitis (AC) is the most common neurological complication and is associated with prolonged hospitalization in the acute phase (HAP). AIM OF THE STUDY: To estimate the costs of AC HAP in children affected by varicella. MATERIALS AND METHODS: We retrospectively reviewed the medical records of a pediatric cohort hospitalized for chickenpox AC over a period of 15 years (from October 2003 to October 2018) and we analyzed acute care costs. For any patient the HAP has been calculated. The final value includes cost of hospital accommodation and management at the Pediatric and Infectious Diseases Unit. To this cost, the price of procedures (imaging, laboratory exams, medical and paramedical evaluations) and medical treatments was added. RESULTS: In the study period, 856 children had been hospitalized for varicella. Out of them, 65 met a diagnosis of AC and were included in the study. The hospitalization length was of 10 days (range 3-20 days). The median cost of HAP for each patient was of 5366 euro, with an average annual cost of 23,252 €. The most significant part of HAP is due to the cost of hospital accommodation and management at the Pediatric Infectious Diseases Unit, which was about € 537.78 for a single day. DISCUSSION: Although AC post-varicella is rare, its HAP cost is not negligible resulting in substantial economic burden. Vaccination would have probably prevented varicella and AC complication, avoiding hospitalization. CONCLUSIONS: Financial studies are important for evaluate the cost saving in order to influence public funding decisions. Further studies are necessary to investigate the economic burden of the disease.

Clinical management of infectious cerebral vasculitides.

A wide range of infections (virus, bacteria, parasite and fungi) may cause cerebral vasculitides. Headache, seizures, encephalopathy and stroke are common forms of presentation. Infection and inflammation of intracranial vessels may cause pathological vascular remodelling, vascular occlusion and ischemia. Vasculitis in chronic meningitis may cause ischemic infarctions, and is associated with poor outcome. Appropriate neuroimaging (CT-angiography, MR-angiography, conventional 4-vessel angiography) and laboratory testing (specific antibodies in blood and CSF, CSF culture and microscopy) and even brain biopsy are needed to quickly establish the aetiology. Enhancement of contrast, wall thickening and lumen narrowing are radiological signs pointing to an infectious vasculitis origin. Although corticosteroids and prophylactic antiplatelet therapy have been used in infectious cerebral vasculitis, there are no randomized clinical trials that have evaluated their efficacy and safety. Stable mycotic aneurysms can be treated with specific antimicrobial therapy. Endovascular therapy and intracranial surgery are reserved for ruptured aneurysms or enlarging unruptured aneurysms.

Varicella-zoster virus infections of the central nervous system ­ Prognosis, diagnostics and treatment.

Both varicella and herpes zoster that are caused by varicella-zoster virus (VZV), are associated with central nervous system disease. Since the introduction of polymerase chain reaction, the opportunity to detect the virus in cerebrospinal fluid (CSF) has improved dramatically. As a result VZV is diagnosed as one of the most common viruses causing CNS disease and it has become evident that this disease includes a wide spectrum of different CNS manifestations. The most evaluated CNS manifestations are encephalitis which is associated with both varicella and herpes zoster and, cerebellitis which occurs predominantly in children with varicella. Other manifestations have been less widely investigated. The incidence of cerebrovascular disease caused by VZV has been only scarcely studied and, in addition, some data indicate that vasculitis might also be involved in other VZV CNS manifestations such as herpes zoster-associated encephalitis. For this reason, VZV CNS infection must be suspected in several CNS syndromes and diagnostics should be based on CSF analysis for detection of VZV DNA by PCR and/or intrathecal antibody production. The prognosis is reported as favourable in children but few follow-up studies are available. Moreover, in adults, the prognosis is reported to be good in overall terms, but later studies indicate more serious neurological sequelae including cognition. Despite considerable mortality and morbidity, so far also in vaccinating countries, few treatment studies are available. Further treatment studies including assessments of neurological and cognitive sequelae, are warranted.

Psychiatric aspects of herpes simplex encephalitis, tick-borne encephalitis and herpes zoster encephalitis among immunocompetent patients.

The psychopathological symptoms occurring in the course of diseases associated with infections are often initially isolated and non-characteristic, and may cause diagnostic difficulties. Moreover, such disorders tend to be less responsive to psychiatric management. Among possible causes such as trauma, neoplasm and vascular changes, inflammatory changes of the brain as a result of a viral infection should also be considered. There were 452 registered cases of viral encephalitis in Poland in 2010, and although not very prevalent they remain a severe and life-threatening condition. What is more, the frequently occurring neurological and psychiatric complications of viral encephalitis often result in permanent disabilities, causing a significant decrease in the quality of life. This article presents the three types of encephalitis that are most prevalent among immunocompetent patients in Poland, i.e. herpes simplex encephalitis (HSE), tick-borne encephalitis (TBE) and herpes zoster encephalitis (HZE). The psychopathology of the acute phase of the infection, the residual symptoms, features apparent in imaging studies and some neuropathological aspects are also presented. The paper also focuses on psychiatric aspects of the diagnostics and treatment of the described conditions. The clinical pictures of these infections are quite specific, although they cover a wide range of symptoms, and these characteristic features are described. The aim of this review is also to show the significance of thorough diagnostics and a multidisciplinary approach to patients with viral CNS infections.

Varicella zoster virus vasculopathies: diverse clinical manifestations, laboratory features, pathogenesis, and treatment.

Vasculopathies caused by varicella zoster virus (VZV) are indicative of a productive virus infection in cerebral arteries after either reactivation of VZV (shingles) or primary infection (chickenpox). VZV vasculopathy can cause ischaemic infarction of the brain and spinal cord, as well as aneurysm, subarachnoid and cerebral haemorrhage, carotid dissection, and, rarely, peripheral arterial disease. VZV vasculopathy in immunocompetent or immunocompromised individuals can be unifocal or multifocal with deep-seated and superficial infarctions. Lesions at the grey-white matter junction on brain imaging are a clue to diagnosis. Involvement of both large and small arteries is more common than that of either alone. Most patients have a mononuclear cerebrospinal fluid pleocytosis, often with red blood cells. Cerebrospinal fluid pleocytosis and rash are absent in about a third of cases. Anti-VZV IgG antibody in the cerebrospinal fluid is found more frequently than VZV DNA. In recent years, the number of recognised VZV vasculopathies has grown, and accurate diagnosis is important for the effective treatment of these disorders.