Evaluation of pathogenicity of Salmonella Gallinarum strains harbouring deletions in genes whose orthologues are conserved pseudogenes in S. Pullorum

Author(s)

Alves Batista, Diego Felipe ^[1] ; de Freitas Neto, Oliveiro Caetano ^{[2, 1]} ; de Almeida, Adriana Maria ^[1] ; Maboni, Grazieli ^[3] ; de Carvalho, Tatiane Furtado ^[4] ; de Carvalho, Thaynara Parente ^[4] ; Barrow, Paul Andrew ^[3] ; Berchieri Junior, Angelo ^[1]

Affiliation

^[1] Sao Paulo State Univ Unesp, Sch Agr & Vet Sci, Post Grad Program Agr & Livestock Microbiol, Dept Vet Pathol, Campus Jaboticabal, Sao Paulo - Brazil

^[2] Univ Fed Paraiba, Dept Vet Sci, Areia, Paraiba - Brazil

^[3] Univ Nottingham, Sch Vet Med & Sci, Loughborough, Leics - England

^[4] Fed Univ Minas Gerais UFMG, Sch Vet, Dept Vet Clin & Surg, Belo Horizonte, MG - Brazil

• Document type: Journal article
• Source: PLoS One; v. 13, n. 7 JUL 20 2018.
• Web of Science Citations: 0

Abstract

The diseases caused by Salmonella Gallinarum and S. Pullorum in chickens known as fowl typhoid and pullorum disease, respectively, pose a great threat to the poultry industry mainly in developing countries, since they have already been controlled in the developed ones. These bacteria are very similar at the genomic level but develop distinct host-pathogen relationships with chickens. Therefore, a deep understanding of the molecular mechanisms whereby S. Gallinarum and S. Pullorum interact with the host could lead to the development of new approaches to control and, perhaps, eradicate both diseases from the chicken flocks worldwide. Based on our previous study, it was hypothesised that metabolism-related pseudogenes, fixed in S. Pullorum genomes, could play a role in the distinct host-pathogen interaction with susceptible chickens. To test this idea, three genes (idnT, idnO and ccmH) of S. Gallinarum str. 287/91, which are pseudogenes on the S. Pullorum chromosomes, were inactivated by mutations. These genetically engineered strains grew well on the solid media without any colony morphology difference. In addition, similar growth curves were obtained by cultivation in M9 minimal medium containing D-gluconate as the sole carbon source. Infection of chickens with idnTO mutants led to increased numbers of bacteria in the livers and spleens at 5 days post-infection, but with slightly decreased heterophil infiltration in the spleens when compared to the wild-type strain. On the other hand, no significant phenotypic change was caused by mutation to ccmH genes. Apart from the above-mentioned alterations, all S. Gallinarum strains provoked similar infections, since mortality, clinical signs, macroscopic alterations and immune response were similar to the infected chickens. Therefore, according to the model applied to this study, mutation to the idnTO and ccmH genes showed minor impact on the fowl typhoid pathogenesis and so they may be relics from the ancestor genome. Our data hints at a more complex mechanism driving the distinct host-pathogen interaction of S. Gallinarum/Pullorum with chickens than differential inactivation of a few genes. (AU)

• FAPESP's process: 13/22920-4 - Pathogenicity evaluation of mutant strains from Salmonella Gallinarum biovar Gallinarum for genes related to metabolism naturally defectives in Salmonella Gallinarum biovar Pullorum
• Grantee: Diego Felipe Alves Batista
• Support Opportunities: Scholarships in Brazil - Doctorate
• FAPESP's process: 13/26127-7 - Factors involved in the pathogenesis of fowl typhoid
• Grantee: Angelo Berchieri Junior
• Support Opportunities: Regular Research Grants