RESUMEN
BACKGROUND: Identification of risk factors is crucial in Foot-and-mouth disease (FMD) control especially in endemic countries. In Rwanda, almost all outbreaks of Foot-and-Mouth Disease Virus (FMDV) have started in Eastern Rwanda. Identifying the risk factors in this area will support government control efforts. This study was carried out to identify and map different risk factors for the incursion, spread and persistence of FMDV in Eastern Rwanda. Questionnaires were administered during farm visits to establish risk factors for FMD outbreaks. Descriptive statistical measures were determined and odds ratios were calculated to determine the effects of risk factors on the occurrence of FMD. Quantum Geographic Information System (QGIS) was used to produce thematic maps on the proportion of putative risk factors for FMD per village. RESULTS: Based on farmers' perceptions, 85.31% (with p < 0.01) experienced more outbreaks during the major dry season, a finding consistent with other reports in other parts of the world. Univariate analysis revealed that mixed farming (OR = 1.501, p = 0.163, CI = 95%), and natural breeding method (OR = 1.626; p = 0.21, CI = 95%) were associated with the occurrence of FMD indicating that the two risk factors could be responsible for FMD outbreaks in the farms. The occurrence of FMD in the farms was found to be significantly associated with lack of vaccination of calves younger than 12 months in herds (OR = 0.707; p = 0.046, CI = 95%). CONCLUSIONS: This is the first study to describe risk factors for persistence of FMDV in livestock systems in Rwanda. However, further studies are required to understand the role of transboundary animal movements and genotypic profiles of circulating FMDV in farming systems in Rwanda.
Asunto(s)
Enfermedades de los Bovinos/epidemiología , Fiebre Aftosa/epidemiología , Animales , Bovinos , Enfermedades de los Bovinos/etiología , Enfermedades de los Bovinos/prevención & control , Enfermedades de los Bovinos/transmisión , Industria Lechera , Brotes de Enfermedades/veterinaria , Fiebre Aftosa/etiología , Fiebre Aftosa/prevención & control , Fiebre Aftosa/transmisión , Virus de la Fiebre Aftosa , Factores de Riesgo , Rwanda/epidemiología , Estaciones del Año , Selección Artificial , Vacunas Virales/administración & dosificaciónRESUMEN
Classic galactosemia is an autosomal recessive disorder that is caused by activity deficiency of the UDP-galactose uridyl transferase (GALT). The clinical spectrum of classic galactosemia differs according to the type and number of mutations in the GALT gene. Short-term clinical symptoms such as jaundice, hepatomegaly, splenomegaly and E. coli sepsis are typically associated with classic galactosemia. These symptoms are often severe but quickly ameliorate with dietary restriction of galactose. However, long-term symptoms such as mental retardation and primary ovarian failure do not resolve irrespective of dietary intervention or the period of initial dietary intervention. There seem to be an association between deficient galactosylation of cerebrosides and classic galactosemia. Galactocerebrosides and glucocerebrosides are the primary products of the enzyme UDP-galactose:cerebroside galactosyl transferase (CGT). There has been an observation of deficient galactosylation coupled with over glucosylation in the brain tissue specimens sampled from deceased classic galactosemia patients. The plausible mechanism with which the association between GALT and CGT had not been explained before. Yet, UDP-galactose serves as the product of GALT as well as a substrate for CGT. In classic galactosemia, there is a consistent deficiency in cerebroside galactosylation. We postulate that the molecular link between defective GALT enzyme, which result in classic galactosemia; and the cerebroside galactosyl transferase, which is responsible for galactosylation of cerebrosides is dependent on the cellular concentrations of UDP-galactose. We further hypothesize that a threshold concentration of UDP-galactose exist below which the integrity of cerebroside galactosylation suffers.