Biomedical subjects
Kristien Verheyen
Publications and source records attributed to Kristien Verheyen.
Exercise distance and speed affect the risk of fracture in racehorses.
In order to gain insight into those training regimens that can minimise the risk of fracture in athletic populations, we conducted a large epidemiological study in racehorses. Thoroughbred racehorses provide a suitable model for studying fracture development and exercise-related risk factors in physically active populations. They represent a homogeneous population, undertaking intensive exercise programmes that are sufficiently heterogeneous to determine those factors that influence injury risk. Daily exercise information was recorded for a cohort of 1178 thoroughbreds that were monitored for up to 2 years. A total of 148 exercise-induced fractures occurred in the study population. Results from a nested case-control study showed a strong interactive effect of exercise distances at different speeds on fracture risk. Horses that exceeded 44 km at canter (< or =14 m/s) and 6 km at gallop (>14 m/s) in a 30-day period were at particularly increased risk of fracture. These distances equate to ca. 7700 bone loading cycles at canter and 880 loading cycles at gallop. Fifty-six fractures occurred in the subset of study horses that were followed since entering training as yearlings, when skeletally immature (n = 335). Cohort analysis of this data set showed that, in previously untrained bones, accumulation of canter exercise increased the risk of fracture (P < or = 0.01), whereas accumulation of high-speed gallop exercise had a protective effect (P < 0.01). However, increasing distances at canter and gallop in short time periods (up to one month) were associated with an increasing fracture risk. All training exercise involves a balance between the risk of fracture inherent in exposure to loading and the beneficial effect that loading has by stimulating bone cells to produce a more robust architecture. Results from our study provide important epidemiological evidence of the effects of physical exercise on bone adaptation and injury risk and can be used to inform the design of safer exercise regimens in physically active populations.
Back problems and lameness in horses.
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Streptococcus equi with truncated M-proteins isolated from outwardly healthy horses.
The M-protein genes of Streptococcus equi isolated from 17 outwardly healthy horses after 4 strangles outbreaks had ended, including a quarantined animal, were compared with those of S. equi isolates from 167 active cases of strangles across 4 countries. The healthy horses included 16 persistent S. equi carriers, at least one from each of the four outbreaks. These carriers, despite being outwardly healthy, had empyema of the guttural pouch(es), an enlargement of the equine Eustachian tube. A persistent carrier from two of these outbreaks, the quarantined animal and a healthy animal with normal guttural pouches, from which S. equi was isolated only once, were colonized by variant S. equi with truncated M-protein genes (24% of outwardly healthy animals with S. equi). The truncated M-protein genes had in-frame deletions in slightly different positions between the signal sequence and the central repeat region, equivalent to approximately 20% of the mature expressed protein. Immunoblotting with antibody to recombinant M-protein confirmed that the variants expressed a truncated form of the M-protein. In contrast to the outwardly healthy S. equi carriers, only 1/167 of S. equi isolates from strangles cases possessed a truncated M-protein gene (<1%; Fisher's exact test, P=0.0002). Compared with isolates from healthy horses with a truncated M-protein, much more of the N terminus of the truncated M-protein was retained in the variant S. equi from a strangles case. Variant S. equi from outwardly healthy animals were more susceptible to phagocytosis by neutrophils in vitro than typical isolates. This is the first report of detection of S. equi with a truncated M-protein. The distribution of the variants between strangles cases and carriers suggests that the 80% of the M-protein retained in the variants may contribute to colonization whilst the deleted portion of the gene may be needed for full virulence.