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Background: Objective outcome measures capable of tracking different aspects of functional recovery in dogs with acute intervertebral disc herniation are needed to optimize physical rehabilitation protocols. Normal, pre-injury distribution of body weight in this population is unknown. The aims of this study were to quantify static weight distribution (SWD) using digital scales and to establish the feasibility of different scale methods in neurologically normal, mature, chondrodystrophic small breed dogs predisposed to intervertebral disc herniation. Results: Twenty-five healthy, mature dogs were enrolled with a mean age of 4.6 years (SD 2.7) and a mean total body weight of 11.5 kg (SD 3.6). SWD for the thoracic and pelvic limbs and between individual limbs was acquired in triplicate and expressed as a percentage of total body weight using commercially available digital scales in four combinations: two bathroom, two kitchen (with thoracic and pelvic limbs combined), four bathroom and four kitchen (with limbs measured individually). SWD was also obtained using a pressure sensing walkway for comparison to scale data. Feasibility for each method was determined and coefficients of variation were used to calculate inter-trial variability. Mean SWD values were compared between methods using an ANOVA. The two bathroom scales method had the highest feasibility and lowest inter-trial variability and resulted in mean thoracic and pelvic limb SWD of 63 % (SD 3 %) and 37 % (SD 3 %), respectively. Thoracic limb mean SWD was higher for the PSW compared to any of the scale methods (p < 0.0001). Conclusions: SWD in a population of healthy chondrodystrophic dogs was simple to obtain using inexpensive and readily available digital scales. This study generated SWD data for subsequent comparison to dogs recovering from acute intervertebral disc herniation. [ABSTRACT FROM AUTHOR]

Salmonella Enteritidis (SE) is one of the most common causes of bacterial food-borne illnesses in the world. Despite the SE’s ability to colonize and infect a wide-range of host, the most common source of infection continues to be the consumption of contaminated shell eggs and egg-based products. To date, the role of the source of SE infection has not been studied as it relates to SE pathogenesis and resulting disease. Using a streptomycin-treated mouse model of human colitis, this study examined the virulence of SE grown in egg yolk and Luria Bertani (LB) broth, and mouse feces collected from mice experimentally infected with SEE1 (SEE1 passed through mice). Primary observations revealed that the mice infected with SE grown in egg yolk displayed greater illness and disease markers than those infected with SE passed through mice or grown in LB broth. Furthermore, the SE grown in egg yolk achieved higher rates of colonization in the mouse intestines and extra-intestinal organs of infected mice than the SE from LB broth or mouse feces. Our results here indicate that the source of SE infection may contribute to the overall pathogenesis of SE in a second host. These results also suggest that reservoir-pathogen dynamics may be critical for SE’s ability to establish colonization and priming for virulence potential. [ABSTRACT FROM AUTHOR]