Background: Although vaccination has been proved to be a safe, efficacious, and cost-effective intervention, immunisation rates remain suboptimal in many European countries, resulting in poor control of many vaccine-preventable diseases.
Safe and effective vaccines against varicella zoster virus (VZV), the aetiological agent of varicella and shingles, have been available in Europe for the last 5-10 years. The USA has had a universal childhood vaccination policy since 1995 and this has resulted in a dramatic decrease in the incidence, morbidity and mortality related to varicella. The economic and medical burden of VZV has led to discussions regarding both the desirability and feasibility of a similar routine immunisation policy for all European children. This article examines the epidemiology of varicella in Europe and how the data emerging from the USA can be used to achieve adequate prevention of the disease. It looks into the current evidence of the health economic evaluation of universal varicella vaccination and explores the concerns surrounding such a policy, including the postulated impact on the incidence of zoster. In conclusion, the Society of Independent European Vaccination Experts (SIEVE) recommends that the immunisation of susceptible adolescents needs to be urgently implemented, in addition to the current recommendations targeting high-risk patients, their close contacts with a negative history of varicella and seronegative health-care workers. A universal policy, optimally incorporating a two-dose schedule, will be needed to finally reduce the burden of disease of varicella from a societal point of view. The SIEVE recommends the implementation of such a policy as soon as financially and practically possible.
The need for a rotavirus vaccine in any particular country depends primarily on the number of hospitalized cases. Since only limited data are available for Germany, we undertook a retrospective hospital‐based analysis in order to gather further information. From 1987 through 1996, a total of 3618 inpatients were hospitalized with a diagnosis of gastroenteritis (ICD 9). In 892 (25%) of them the causative organism wasa rotavirus. During the same period, 1886 (out of 8383; 22%) stool speciment tested in the hospital laboratory were obtained from rotavirus‐positive inpatients. In 49.2% the infection was community‐acquired, and in the remainder of nosocomial origin. Infants under 4 months of age(n=709; 38%) predominated among both the nosocomial and community‐acquired infections. Premature neonates made up 26% of the nosocomial, but only 2% of the community‐acquired cases of diarrhoea. The winter peak (January) was most pronounced in the age group 4‐12 months, but in those more than 1 y old the peak came a month later. The median hospitalization time for community‐acquired cases was 4 d (mean 5.9 d).The mortality was 0.1%. Rotavirus infection must therefore be regarded as a considerable burden, particularly with regard to infants and young children. Furthermore, the morbidity due to nosocomial infection with the rotavirus, analysed here in a long‐term observational study, is unexpectedly high. □Hospital‐based study, nosocomial infection, rotavirus
Mutations of the Janus kinase 3 (JAK3) have been previously described to cause an autosomal recessive variant of severe combined immunodeficiency (SCID) usually characterized by the near absence of T and NK cells, but preserved numbers of B lymphocytes (T-B+SCID). We now report a family whose JAK3 mutations are associated with the persistence of circulating T cells, resulting in previously undescribed clinical presentations, ranging from a nearly unaffected 18-year-old subject to an 8-year-old sibling with a severe lymphoproliferative disorder. Both siblings were found to be compound heterozygotes for the same deleterious JAK3 mutations: an A96G initiation start site mutation, resulting in a dysfunctional, truncated protein product and a G2775(+3)C mutation in the splice donor site sequence of intron 18, resulting in a splicing defect and a predicted premature stop. These mutations were compatible with minimal amounts of functional JAK3 expression, leading to defective cytokine-dependent signaling. Activated T cells in these patients failed to express Fas ligand (FasL) in response to IL-2, which may explain the accumulation of T cells with an activated phenotype and a skewed T cell receptor (TcR) Vbeta family distribution. We speculate that residual JAK3 activity accounted for the maturation of thymocytes, but was insufficient to sustain IL-2-mediated homeostasis of peripheral T cells via Fas/FasL interactions. These data demonstrate that the clinical spectrum of JAK3 deficiency is quite broad and includes immunodeficient patients with accumulation of activated T cells, and indicate an essential role for JAK3 in the homeostasis of peripheral T cells in humans.
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