RESUMEN
Avian encephalomyelitis control methods were not developed until the 1950s although the disease had been discovered and described over 20 yr earlier. Inability to transmit the infection by other than intracerebral inoculation, lack of suitable immunologic methods, the unknowing use of immune chickens or embryos for experimental studies, and reliance on a highly adapted strain of virus rather than fresh field isolates were the main reasons for a general lack of progress. In the absence of supportive experimental data, at least two commercial breeding organizations turned to the use of a crude chicken brain-propagated virus for vaccination of breeder replacement flocks in the 1950s. This control procedure turned out to be practical and efficacious. Development of suitable embryo infection methods and immunologic tests and the chance finding that antibody-free flocks were essential for experimental studies led to the development of embryo-susceptibility tests to identify immune breeder flocks and formed the basis for another commercially applied control program, the testing and selection of only immune flocks for hatching purposes. The application of the new testing methods coupled with a switch from the adapted Van Roekel strain of virus to fresh field isolates for experimentation resulted in a rapid unraveling of the epizootiology and pathogenesis of the disease and also to the development of a safe and effective vaccine that was licensed for administration to breeder replacements in 1962.
Asunto(s)
Enfermedades de las Aves/prevención & control , Virus de la Encefalomielitis Aviar , Encefalomielitis/veterinaria , Infecciones por Enterovirus/veterinaria , Enfermedades de las Aves de Corral/prevención & control , Animales , Enfermedades de las Aves/historia , Embrión de Pollo , Pollos , Encefalomielitis/historia , Encefalomielitis/prevención & control , Infecciones por Enterovirus/historia , Infecciones por Enterovirus/prevención & control , Historia del Siglo XX , Enfermedades de las Aves de Corral/historia , Codorniz , Pavos , Vacunas Virales/historiaRESUMEN
OBJECTIVE: To compare the clinical course with the neuropathological findings in a patient who died of acute rabies encephalomyelitis with coexisting demyelinating lesions. DESIGN: Patient's history was extensively investigated, during her illness and after death. Details of her previous allergies, postexposure prophylaxis, early use of steroid therapy, 20-day course in an intensive care unit, and autopsy results are clinicopathologically correlated. SETTING: The intensive care unit of an 1100-bed tertiary referral center and teaching hospital. PATIENT: A 55-year-old woman, referred by her family doctor. CONCLUSIONS: Postvaccinal encephalomyelitis and rabies can run similar courses and can be misdiagnosed. On admission to the hospital, this patient was initially diagnosed as having postvaccinal disease. However, autopsy results and postmortem viral cultures disclosed a complex picture, including acute rabies and widespread perivenous demyelination. One other similar report from 1977 in the literature is reviewed. No adequate explanation of the rare coexistence of acute rabies encephalomyelitis and perivascular demyelination is available.