Salmonella Heidelberg side-step gene loss of respiratory requirements in chicken infection model.

Among the important recent observations involving anaerobic respiration was that an electron acceptor produced as a result of an inflammatory response to Salmonella Typhimurium generates a growth advantage over the competing microbiota in the lumen. In this regard, anaerobically, salmonellae can oxidize thiosulphate (S2O32-) converting it into tetrathionate (S4O62-), the process by which it is encoded by ttr gene cluster (ttrSRttrBCA). Another important pathway under aerobic or anaerobic conditions is the 1,2-propanediol-utilization mediated by the pdu gene cluster that promotes Salmonella expansion during colitis. Therefore, we sought to compare in this study, whether Salmonella Heidelberg strains lacking the ttrA, ttrApduA, and ttrACBSR genes experience a disadvantage during cecal colonization in broiler chicks. In contrast to expectations, we found that the gene loss in S. Heidelberg potentially confers an increase in fitness in the chicken infection model. These data argue that S. Heidelberg may trigger an alternative pathway involving the use of an alternative electron acceptor, conferring a growth advantage for S. Heidelberg in chicks.

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

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.

Further investigations on the epidemiology of fowl typhoid in Brazil.

Salmonella Gallinarum (SG) causes fowl typhoid (FT), a disease responsible for economic losses to the poultry industry worldwide. FT has been considered to be under control in Brazil; nevertheless, since 2012 it has frequently been identified in poultry farming of several Brazilian states. The present study was aimed at assessing (i) the pathogenicity of a SG strain recently isolated from an FT outbreak affecting chickens of both white and brown layers; (ii) the transmission of SG through eggs and hatching; (iii) the effects of antibiotic therapy on SG persistence in poultry tissues and on its vertical transmission and (iv) the genetic profiles of strains isolated over 27 years by Pulsed Field Gel Electrophoresis. Clinical signs, mortality and gross pathologies were very marked amongst brown-egg layers. In contrast, clinical manifestation of FT and mortality were barely present amongst the white-egg layers, although bacteria could be re-isolated from their tissues up to 35 days after infection. No bacteria were re-isolated from the laid eggs, so vertical transmission was not achieved, although newly hatched uninfected chicks became infected spontaneously after hatching. Antibiotic therapy was shown to be effective at reducing mortality, but was not able to clear infection or to favour SG transmission via eggs. Our pulsed field gel electrophoresis results revealed an endemic SG clone that may have been circulating in the Brazilian poultry flocks in the south and southeast regions for more than 20 years. The results suggest that the industrial incubation of SG-contaminated eggs could be one of the factors responsible for the spread of FT in Brazil.