Asunto(s)
Capnocytophaga/aislamiento & purificación , Infecciones por Bacterias Gramnegativas/diagnóstico , Meningitis Bacterianas/diagnóstico , Meningitis Bacterianas/microbiología , Antibacterianos/uso terapéutico , Secuencia de Bases , Capnocytophaga/genética , Ceftriaxona/uso terapéutico , Infecciones por Bacterias Gramnegativas/tratamiento farmacológico , Humanos , Masculino , Meningitis Bacterianas/tratamiento farmacológico , Persona de Mediana Edad , Datos de Secuencia Molecular , Reacción en Cadena de la Polimerasa , ARN Ribosómico 16S/genéticaRESUMEN
Transmissible spongiform encephalopathies (TSE) are dementing diseases and have been known to affect humans for over 90 years. The most common of these is the sporadic form of Creutzfeldt-Jakob disease (sCJD), followed by its familial (fCJD) and an iatrogenic (iCJD) form. 1996 a variant of CJD (vCJD) has been described in the UK, of which so far 131 cases have been observed worldwide. Specific biochemical and neuropathological signatures allow to distinguish between vCJD and sCJD and lead to the hypothesis that vCJD is due to transmission of BSE prions to humans. Although promising therapeutical approaches are being investigated, human TSE remain untreatable entities. Thus preventive measures are essential. In Switzerland the population has been exposed to BSE prions, too, but no case of vCJD as described in the UK has been observed until now. Since 2001, however, a so far unexplained increase of sCJD cases is being observed.
Asunto(s)
Encéfalo/patología , Enfermedades por Prión/transmisión , Zoonosis , Animales , Bovinos , Síndrome de Creutzfeldt-Jakob/epidemiología , Síndrome de Creutzfeldt-Jakob/terapia , Síndrome de Creutzfeldt-Jakob/transmisión , Encefalopatía Espongiforme Bovina/epidemiología , Encefalopatía Espongiforme Bovina/terapia , Encefalopatía Espongiforme Bovina/transmisión , Humanos , Enfermedades por Prión/epidemiología , Enfermedades por Prión/terapia , Suiza/epidemiologíaRESUMEN
Transmissible spongiform encephalopathies are degenerative disorders affecting the central nervous system (CNS) occurring in a variety of species. The causative agent is thought to be composed of an abnormal form of the host encoded prion protein (PrPC), termed PrPSc. The conformational change of PrPC into PrPSc can occur spontaneously, however, it can also be induced by PrPSc. Prion diseases such as bovine spongiform encephalopathy (BSE), scrapie and variant Creutzfeldt-Jakob-Disease (vCJD) are most likely caused by peripheral uptake of prions. The process by which prions proceed to the CNS following peripheral uptake is referred to as neuroinvasion. Infection with prions is thought to occur in two phases: After ingestion prions first replicate in lymphatic tissue and then gain access to the CNS via peripheral nerves. Studies looking at the biochemical and clinical characteristics of BSE and vCJD demonstrated that BSE is most likely responsible for vCJD in humans.
Asunto(s)
Enfermedades por Prión/etiología , Priones/fisiología , Zoonosis , Animales , Humanos , Enfermedades por Prión/transmisión , Factores de RiesgoRESUMEN
To determine whether systemic immunization against Helicobacter pylori could be achieved with an adjuvant approved for human use, the efficacy of vaccination with Helicobacter antigen in combination with aluminum hydroxide (AlOH) was evaluated in a murine model of Helicobacter infection. Immunization with antigen and AlOH induced interleukin-5-secreting, antigen-specific T cells, and immunization with antigen and complete Freund's adjuvant induced interferon-gamma-secreting, antigen-specific T cells, as determined by ELISPOT assay. Both immune responses conferred protection after challenge with either H. pylori or H. felis, as confirmed by the complete absence of any bacteria, as assessed by both histology and culture of gastric biopsy samples. Protection was antibody independent, as demonstrated with antibody-deficient muMT mice (immunoglobulin-gene knockout mice), and CD4(+) spleen T cells from immunized mice were sufficient to transfer protective immunity to otherwise immunodeficient rag1(-/-) recipients. These results suggest an alternative and potentially more expeditious strategy for development of a human-use H. pylori vaccine.