Output list
Conference paper
Brachyspiral colitis: An evolving problem
Published 2014
Proceedings of the 23rd International Pig Veterinary Society (IPVS) Congress, 08/06/2014–11/06/2014, Cancun, Mexico
The name “Brachyspiral colitis” recently was introduced into the literature on swine diseases to describe the situation where colitis, diarrhea and/or dysentery occur in pigs infected with one or more pathogenic Brachyspira species (Hampson, 2012). The term was created to emphasise an increasing understanding of the diversity of anaerobic intestinal spirochetes in the genus Brachyspira and the fact that a number of different species may have a role in inducing inflammation in the large intestine. Until only a few years ago most veterinarians would have felt comfortable with the concept of there being two pathogenic Brachyspira species capable of causing disease in pigs, each associated with a distinct named disease. The first was the strongly hemolytic Brachyspira hyodysenteriae causing swine dysentery, a severe mucohemorrhagic colitis seen mainly in grower and finisher pigs. The second was the weakly hemolytic Brachyspira pilosicoli causing porcine intestinal spirochetosis (porcine colonic spirochetosis), a milder form of colitis seen mainly in weaner and grower pigs. Other weakly hemolytic species colonising pigs generally were thought of as being commensals. Now it is known that there are at least three strongly hemolytic pathogenic Brachyspira species that may infect swine and cause a swine dysentery-like disease; furthermore, there is increasing evidence that one or more of the other weakly hemolytic species besides B. pilosicoli also have pathogenic potential in swine and other species. Specifically, the weakly hemolytic Brachyspira murdochii is increasingly being implicated as an occasional cause of mild colitis in pigs (Jensen et al., 2000; Weissenböck et al., 2005; Komarek et al., 2009; Osorio et al., 2013). It is also clear that individual pigs on different farms may be colonised with more than one Brachyspira species and/or strains that may contribute towards causing disease symptoms. In and interesting parallel, the ceca and colon of adult chickens and other poultry species may be colonised by a number of Brachyspira species that can induce inflammation, wet feces and reduced egg production. This disease complex (most commonly is associated with B. intermedia and/or B. pilosicoli) currently is known as “Avian Intestinal “Spirochetosis” (Hampson, 2013), but for clarity and consistency with the revised disease nomenclature in pigs it might be better if it was to be called “Brachyspiral typhlitis”.
Conference paper
Published 2013
Manipulating Pig Production XIV. Proceedings of the 14th Australasian Pig Science Association (APSA) Biennial Conference, 24/11/2013–27/11/2013, Melbourne, Australia
The recommended standardised ileal digestible (SID) ratio of tryptophan to lysine (Trp:Lys) is 0.16 for 7-11 kg pigs (NRC, 2012). However, Simongiovanni et al. (2012) showed the requirement for dietary Trp increases during inflammatory states, such as in the post-weaning period, suggesting that NRC (2012) recommendations might be insufficient. This study hypothesised that weaner pigs kept in commercial conditions will show a positive response to increased Trp:Lys ratios above the NRC (2012) recommendations.
Conference paper
Colonic antibody responses in pigs with swine dysentery
Published 2009
Manipulating Pig Production XII. Proceedings of the 12th Australasian Pig Science Association (APSA) Biennial Conference, 22/11/2009–25/11/2009, Werribee, Australia
Swine dysentery (SD) is a mucohaemorrhagic colitis of pigs resulting from infection of the large intestine with the anaerobic intestinal spirochaete Brachyspira hyodysenteriae. The infection has been reported to result in the development of specific IgG, IgA and IgM antibodies in serum and the production of secretory IgA in the gut mucosa (Rees et al., 1989). The hypothesis tested in this experiment was that colonic antibody levels can be used as a diagnostic tool to assist the diagnosis of SD. The experimental design involved testing samples from non-infected pigs to define appropriate cut-off values for the assays, and then using these in assays of serum and colonic samples from pigs that had been experimentally exposed to B. hyodysenteriae.
Conference paper
Published 2009
Manipulating Pig Production XII. Proceedings of the 12th Australasian Pig Science Association (APSA) Biennial Conference, 22/11/2009–25/11/2009, Werribee, Australia
Swine dysentery (SD) is a contagious mucohaemorrhagic diarrhoeal disease with severe impacts on production efficiency in grower/finisher pigs. The causative agent of SD is the intestinal spirochaete Brachyspira hyodysenteriae that induces inflammation and necrosis of the caecum and colon (Hampson et al., 2006). Recently, Thomsen et al. (2007) found that an organic diet containing sweet lupins and dried chicory root completely prevented SD following experimental challenge with B. hyodysenteriae. However, based on the study by Thomsen et al. (2007) it wasn't possible to determine whether the dietary protection against SD was due to the galactans supplied by the sweet lupins or inulin from the dried chicory roots or if both carbohydrate sources are needed. It was hypothesised that diets (barley and triticale based) containing galactans (as lupins) and fructans (as inulin) could prevent the occurrence of swine dysentery (SD) after experimental infection with B. hyodysenteriae.
Conference paper
Published 2009
Manipulating Pig Production XII. Proceedings of the 12th Australasian Pig Science Association (APSA) Biennial Conference, 22/11/2009–25/11/2009, Werribee, Australia
Post-weaning diarrhoea (PWD) reduces production efficiency through increased morbidity and mortality and poorer efficiency of growth (Halas et al., 2007). Dietary proteins that are not digested and absorbed in the small intestine are fermented by the intestinal micro biota to produce a number of potentially toxic epithelial irritants such as ammonia, which are thought to increase the incidence of PWD. Limiting the amount of protein available for microbial fermentation has been proposed as a strategy to reduce the risk of PWD in weaner pigs without using in-feed antibiotics (Halas et al., 2007). In this experiment, we hypothesised that feeding a lower protein diet for a short period of time after weaning would reduce PWD by reducing the amount of protein entering the hindgut from the small intestine, thereby reducing protein fermentation in the colon.
Conference presentation
Conservation and metabolic functional significance of overlapping gene in the bacterial genomes
Published 2008
The 20th Annual Meeting and International Conference of the Thai Society for Biotechnology, 14/10/2008–17/10/2008, Maha Sarakham, Thailand
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Conference presentation
Comparison of Brachyspira central metabolism pathways
Published 2008
19th International Conference on Genome Informatics (GIW2008), 01/12/2008–03/12/2008, Gold Coast, QLD
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Conference paper
Published 2007
Manipulating Pig Production XI. Proceedings of the 11th Australasian Pig Science Association (APSA) Biennial Conference, 25/10/2007–28/10/2007, Brisbane, Australia
Post-weaning diarrhoea (PWD), a condition associated with proliferation of B-haemolytic strains of Escherichia coli in the small and large intestine, often occurs after weaning. Once attached to the small intestinal epithelium, these strains of E. coli can disrupt digestive and absorptive functions of the enterocytes by releasing both heat labile toxins (LT) and heat stable toxins (ST; variants STa and STb ) that are responsible for hypersecretory diarrhoea (Pluske et al., 2002). Numerous dietary strategies have been attempted to ameliorate the losses associated with PWD. Of these, feeding a lower-protein diet with supplementation of essential amino acids has been suggested because by-products of protein fermentation, such as ammonia and amines, are implicated in the aetiology of the condition (Aumaitre et al., 1995). However feeding a lower-protein diet after weaning is associated with reductions in performance (Nyachoti et al., 2006). In this study, we hypothesized that feeding a low protein diet for a short period of time after weaning would reduce PWD by reducing protein fermentation in the LI .
Conference paper
Published 2007
2nd International Symposium on Energy and Protein Metabolism and Nutrition (ISEP), 09/09/2007–13/09/2007, Vichy, France
Conference paper
Published 2007
Manipulating Pig Production XI. Proceedings of the 11th Australasian Pig Science Association (APSA) Biennial Conference, 25/10/2007–28/10/2007, Brisbane, Australia
Gastrointestinal disturbances can cause large economic losses in the pig industry. Diseases and conditions of the gastrointestinal tract (GIT) that can cause economic loss have generally been controlled by the use of dietary (and or in the water) antimicrobial compounds, such as antibiotic feed additives and (or) minerals such as zinc and copper. However the implementation of legislation in some parts of the world, for example the European Union, and a growing sentiment worldwide to reduce the use of dietary antimicrobial compounds, has caused a reassessment of measures to influence GIT 'health' and caused enormous interest in alternative means to control diseases and conditions of the GIT. There are now available a wide array of products and strategies available to the pig industry that influence 'gut health'. The products in the market place are characterised predominately not only by their (claimed) different modes of action, but also by the variation in responses seen when offered to pigs, and not only in the post-weaning period. This variation is presumably a consequence of the many different conditions of management that pigs are under, that in turn influences factors such as composition of the microbiota and mucosal immunity. Other strategies, such as the manipulation of particle size and changing the protein content of a diet, might also be adopted to influence the expression of enteric pathogens and the expression of disease. Ultimately, the cost-benefit of adopting such practices to influence gastrointestinal 'health' requires consideration.