Identification of a VapA virulence factor functional homolog in Rhodococcus equi isolates housing the pVAPB plasmid.
Authors: Willingham-Lane Jennifer M, Coulson Garry B, Hondalus Mary K
Journal: PloS one
Summary
Rhodococcus equi causes serious pyogranulomatous disease in foals and immunocompromised individuals by replicating within macrophages, a process historically attributed to the VapA virulence factor present on pVAPA-type plasmids found predominantly in equine isolates. Using targeted gene deletion and complementation approaches, Willingham-Lane and colleagues identified VapK1 and VapK2 proteins encoded on pVAPB-type plasmids (naturally found in porcine strains) as functional homologs of VapA, demonstrating that either protein alone is sufficient to restore intracellular replication capacity to a VapA-deficient equine strain within macrophages. Deletion of both vapK genes rendered transconjugant strains completely unable to replicate within equine macrophages, confirming their essential role in bacterial survival equivalent to that of VapA. These findings broaden our understanding of R. equi pathogenesis beyond the classical VapA paradigm and suggest that virulence potential varies across plasmid types through functionally redundant mechanisms. For equine practitioners, this work implies that isolates lacking VapA may still pose significant infection risk if harbouring alternative virulence determinants, potentially influencing diagnostic interpretation and antimicrobial selection strategies in foal pneumonia cases.
Read the full abstract on PubMed
Practical Takeaways
- •R. equi strains from non-equine sources (pigs, humans) can still cause severe disease in foals through alternative virulence mechanisms (VapK), complicating prevention and control strategies
- •Understanding that multiple plasmid types and virulence factors drive R. equi pathogenesis may inform development of more comprehensive diagnostic and therapeutic approaches for foal pneumonia
- •Cross-species transmission potential of R. equi with functional virulence factors warrants attention to biosecurity and source management in facilities with mixed animal populations
Key Findings
- •VapK1 and VapK2 proteins on pVAPB-type plasmids are functionally equivalent to VapA in enabling intracellular replication within macrophages
- •vapK1 or vapK2 deletion in pVAPB R. equi strains eliminates the ability to replicate in equine macrophages
- •VapK proteins can complement a VapA-deficient R. equi strain and restore macrophage replication capacity
- •pVAPB-type plasmids from pig-origin R. equi strains can function as virulence determinants in equine macrophages