Poster Presentation MedVetPATHOGENS 2018

Comparative study of the pathogenesis of Mycobacterium bovis and Mycobacterium tuberculosis in a murine model. (#81)

Santiago Uranga 1 2 , Elena Mata 1 2 , Carlos Martin 1 2 , Nacho Auilo 1 2
  1. Universidad de Zaragoza. Q-5018001-G, Zaragoza, ZARAGOZA, Spain
  2. CIBER Enfermedades Respiratorias, Instituto de Salud Carlos III, Madrid

 

INTRODUCTION

Mycobacterium bovis, the causative of bovine tuberculosis, represents a problem in livestock production mainly in Africa but also in some countries of Europe, as well as a growing threat to humans due to the associated zoonosis. Therefore, the understanding of its pathogenesis is crucial for the development of an effective vaccine.

 It has been observed that M. bovis is more virulent than Mycobacterium tuberculosis in several animal models 1, 2. However, more information is needed to establish the differences between both species, and to advance, as it is being done in the case of human tuberculosis, towards a possible prophylaxis for cattle.

 

OBJECTIVE:

To compare, in a murine model, the pathogenesis of both M. bovis and M. tuberculosis, analysing the bacterial distribution along with the associated tissue damage.

 

METHODS

The virulence and in vivo dissemination of two different strains, the H37Rv strain of M. tuberculosis and the reference strain AF2122 of M. bovis, have been studied. Mice were infected intranasally 3, and the histopathology of the infected lungs and bacterial replication in different organs, including lungs, spleen, liver and kidneys, was evaluated. GPF-expressing strains were also used to rate the infectivity and to characterise the populations of infected cells through the fluorescence of the pulmonary immune cells.

 

CONCLUSIONS

M. bovis has been found to have a larger dissemination in organs compared to M. tuberculosis, in addition to a greater ability to infect host cells in vivo. Hence, M. bovis shows an increased capacity to cause pathology.

 Further studies are necessary to determine the genomic origin behind these phenotypic differences between the two members of M. tuberculosis complex.

 

 

1 Dunn PL, North RJ. . IAI. 1995 Sep;63(9):3428-37.

2 Nedeltchev GG, et al.  IAI. 2009 Feb;77(2):598-603.

3 Uranga S, et al. J Vis Exp. 2016 Sep 19;(115).