Scholarship 19/25091-5 - Multiplicação, Sobrevivência - BV FAPESP
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Requirement of mgtC gene for Salmonella Gallinarum survival ability within macrophages

Grant number: 19/25091-5
Support Opportunities:Scholarships abroad - Research Internship - Doctorate
Start date: March 01, 2020
End date: October 31, 2020
Field of knowledge:Agronomical Sciences - Veterinary Medicine - Animal Pathology
Principal Investigator:Angelo Berchieri Junior
Grantee:Lucas Bocchini Rodrigues Alves
Supervisor: John Elmerdahl Olsen
Host Institution: Faculdade de Ciências Agrárias e Veterinárias (FCAV). Universidade Estadual Paulista (UNESP). Campus de Jaboticabal. Jaboticabal , SP, Brazil
Institution abroad: University of Copenhagen, Frederiksberg, Denmark  
Associated to the scholarship:18/12614-7 - Effect of the mgtC gene-deletion on Salmonella gallinarum pathogenicity in susceptible poultry, BP.DR

Abstract

Salmonella Gallinarum (SG) provokes fowl typhoid, a severe systemic infectious disease that affects gallinaceous of any age and has been considered one of the major poultry health challenges. During the typhoid-like systemic infection in mice caused by S. Typhimurium, bacteria transcribe the mgtC gene. Its function seems to be associated with bacteria replication within macrophages and the inactivation of this gene attenuates the pathogen. Thus, we hypothesize that a mgtC-lacking SG strain could have its pathogenicity altered in comparison to the wild type strain. Thus, a SG strain containing mgtC inactivation (SG mgtC) was constructed and in vivo experiments were carried out with laying hens susceptible to fowl typhoid. Both mutant and wild type (SG) strains were inoculated so bacterial counts were assessed in liver and spleen samples. Moreover, the pathogenicity and the Median Lethal Dose (LD50) of the mutant strain were evaluated, respectively. Our preliminaries results showed that bacterial counts in liver and spleen were not statistically significant between both strains and SG mgtC provoked gross lesions that were apparently less evident in comparison to SG. Moreover, the mutant strain demanded more time (P < 0.05) to cause the same mortality rates as SG and its LD50 was 22 times higher. Thus, we propose herein to evaluate the importance of mgtC gene for SG survival ability and the immune responses within macrophages to clarify the in vivo trials. (AU)

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