Oral Presentation The Prato Conference on the Pathogenesis of Bacterial Infections of Animals 2016

A preliminary investigation into the origin of the weakly haemolytic phenotype encountered in Brachyspira hyodysenteriae strains (#36)

Tom La 1 , Nyree D Phillips 1 , Judith Rohde 2 , David J Hampson 1
  1. School of Veterinary and Life Sciences, Murdoch University, Murdoch, WA, Australia
  2. Institute for Microbiology, University of Veterinary Medicine, Hannover, Germany


Brachyspira hyodysenteriae is the classical agent of swine dysentery. An important property that is used in its initial identification is its characteristic strong beta-haemolysis, and this activity also is thought to be an important virulence factor. Recently strains of B. hyodysenteriae that are weakly haemolytic have been reported. This study aimed to identify potential causes of the weakly haemolytic phenotype.

Weakly haemolytic B. hyodysenteriae from four German pig herds were subjected to whole genomic sequencing on an Illumina MiSeq. Three herds showed no signs of disease whilst the other herd had diarrhoea of unknown aetiology in fattening pigs. Each genome sequence was searched using the BlastN function of Geneious R9 software. In silico multilocus sequence typing was undertaken, and seven haemolysin-associated genes and adjacent genomic regions were examined and compared with the genomic sequence of the reference strain WA1.

Isolates from the four herds had different unrelated sequence types. The seven haemolysin-associated genes were identified in all isolates, and the nucleotide and translated amino acid sequences generally were well conserved. The greatest dissimilarity was in the haemolysin III gene, which had nucleotide similarities to WA1 of 89.8-91% and amino acid similarities of 95.6%.

There were no obvious disruptions in potential promoter regions up to 50bp upstream from the coding sequence for the genes in all strains, apart from one that had a five-nucleotide insertion in the -10 promoter element for the hlyA gene.

The disruption in the promotor region for hlyA in one strain may explain its lack of strong haemolysis, but there were no other obvious reasons for weak haemolysis in the other strains. Potentially other genes may be involved in promoting haemolysis, including those involved in secretory pathways, and these require further investigation. Transcriptional analysis of the known genes also is required.