Interpretive Summary: Impact of Brachyspira hyodysenteriae on intestinal amino acid digestibility and endogenous amino acid losses in pigs
By: Dr. Caitlin Vonderohe
Brachyspira hyodysenteriae is the primary cause of swine dysentery. Swine dysentery is a significant disease in international swine production, resulting in mortality of 30% and morbidity approaching 90%. It causes bloody diarrhea and necrosis in the cecum and colon. The small intestine is largely unaffected, but B. hyodysentaeriae has been shown to affect immunologic processes in the small intestine. Additionally, multiple pathogens have been shown to affect weight gain, feed intake, and feed efficiency due to rerouting nutrients away from muscle development to power the immune system. Amino acid digestibility can also be affected by enteric and systemic pathogens, primarily due to basal endogenous losses. A recent article by Schweer et al., published in the Journal of Animal Science, entitled “Impact of Brachyspira hypodysenteriaie on intestinal amino acid digestibility and endogenous amino acid losses in pigs” hypothesized that swine dysentery infection would increase endogenous losses and decrease amino acid digestibility.
A total of 32 gilts were surgically fitted with T-cannulas in the distal ileum. 21 of these were inoculated with Brachyspira hyodysentariae, and 11 served as negative controls. Rectal swabs were taken prior to the study to ensure that all pigs were negative for B. hyo. After inoculation, pigs were fed a nitrogen-free diet to measure basal endogenous losses for eight days and a complete diet throughout the rest of the study period. Ileal and fecal contents were collected and analyzed to estimate nitrogen, amino acid, and energy digestibility. Pigs were harvested at day 14 or 15-post infection and internal organs were examined for lesions associated with prior PRRSV or enteric disease.
Pigs infected with Brachyspira hyodysenteriae had 3% decreased dry matter digestibility, 8% nitrogen digestibility and 4% decreased digestibility compared to B.hyo. negative pigs on days 9-11 post infection, at the height of clinical disease. This reduction in digestibility may be due to increased passage rate of digesta through the intestine and colon, as the primary clinical sign of B. hyodysentariae is diarrhea. On days 12-13 post infection, a period associated with fewer clinical signs of B.hyo, there were no differences between infected and non-infected pigs in ileal digestibility of dry matter, nitrogen, total amino acid and gross energy. This was not surprising to investigators because B.hyo tends to affect the colon and cecum rather than the ileum. Interestingly, glycine digestibility was increased in B.hyo. infected pigs which may be a von of the immune response, or enterocyte metabolism.
The investigators expected an increased in basal endogenous losses of nitrogen and amino acids. However, B.hyo infection resulted in a 55% reduction in endogenous proline losses, and a tendency for less arginine, tryptophan and glycine loss. During the mucohemorrhagic phase of swine dysentery, endogenous nitrogen losses were increased, but this was not statistically significant. More expectedly, B.hyo infection reduced hind-gut disappearance of dry matter, nitrogen and energy, which was likely due to mucohemorrhagic diarrhea and altered microbial populations.
Overall, the diarrhea associated with infection with swine dysentery reduced total tract nutrient digestibility compared to the controls, but B.hyo infection did not affect amino acid digestibility. Additionally, decreased nutrient disappearance in the hind-gut may reflect nutrient retention, resulting in slower rates of growth and poor performance during Brachyspira hyodysentariae challenges.
To view the full article, visit the Journal of Animal Science.