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A longitudinal study of the role of Dichelobacter nodosus and Fusobacterium necrophorum load in initiation and severity of footrot in sheep

Footrot is an infectious bacterial disease of sheep that causes lameness. The causal agent is Dichelobacter nodosus. There is debate regarding the role of Fusobacterium necrophorum in disease initiation. This research used an observational longitudinal study of footrot, together with quantitative PC...

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Detalles Bibliográficos
Autores principales: Witcomb, Luci A., Green, Laura E., Kaler, Jasmeet, Ul-Hassan, Atiya, Calvo-Bado, Leo A., Medley, Graham F., Grogono-Thomas, Rose, Wellington, Elizabeth M.H.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier Scientific Publishing 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4029074/
https://www.ncbi.nlm.nih.gov/pubmed/24703249
http://dx.doi.org/10.1016/j.prevetmed.2014.03.004
Descripción
Sumario:Footrot is an infectious bacterial disease of sheep that causes lameness. The causal agent is Dichelobacter nodosus. There is debate regarding the role of Fusobacterium necrophorum in disease initiation. This research used an observational longitudinal study of footrot, together with quantitative PCR (qPCR) of bacterial load of D. nodosus and F. necrophorum, to elucidate the roles of each species in the development of disease. All feet of 18 a priori selected sheep were monitored for five weeks assessing disease severity (healthy, interdigital dermatitis (ID) and severe footrot (SFR)) and bacterial load. A multinomial model was used to analyse these data. Key unadjusted results were that D. nodosus was detected more frequently on feet with ID, whereas F. necrophorum was detected more frequently on feet with SFR. In the multinomial model, ID was associated with increasing log(10) load of D. nodosus the week of observation (OR = 1.28 (95% CI = 1.08–1.53)) and the week prior to development of ID (OR = 1.20 (95% CI = 1.01–1.42). There was no association between log(10) load(2) of F. necrophorum and presence of ID (OR = 0.99 (95% CI = 0.96–1.02))). SFR was associated with increasing log(10) load of D. nodosus the week before disease onset (OR = 1.42 (95% CI = 1.02–1.96)) but not once SFR had occurred. SFR was positively associated with log(10) load(2) of F. necrophorum once disease was present (OR = 1.06 (95% CI = 1.01–1.11)). In summary, there was an increased risk of increasing D. nodosus load the week prior to development of ID and SFR and during an episode of ID. In contrast, F. necrophorum load was not associated with ID before or during an episode, and was only associated with SFR once present. These results contribute to our understanding of the epidemiology of footrot and highlight that D. nodosus load plays the primary role in disease initiation and progression, with F. necrophorum load playing a secondary role. Further studies in more flocks and climates would be useful to confirm these findings. This study identifies that D. nodosus load is highest during ID. This supports previous epidemiological findings, which demonstrate that controlling ID is the most effective management strategy to prevent new cases of ID and SFR.