Deletion of and in serovar Enteritidis reduced its virulence to the natural virulence of serovars Agona, Hadar and Infantis for mice but not for chickens early after infection

D. Karasova , H. Havlickova , F. Sisak , I. Rychlik

serovars Typhimurium, Enteritidis, Dublin, Choleraesuis or Gallinarum can colonise liver and spleen in particular hosts while infections with serovars Infantis, Agona, Hadar etc. are usually limited to gastrointestinal tract. Reasons for this behavior are unknown, although it has been shown that and genes exhibit a strict distribution between more and less virulent serovars and they influence virulence. However to what extent the presence or absence of these genes is associated with the increased virulence of serovars which possess them, has never been addressed experimentally. In this study we therefore first confirmed the exclusive association of and genes with the former group of serovars. In the next step we removed these two genes from . Enteritidis genome and compared the virulence of such a mutant with the virulence of . Infantis, . Agona and . Hadar for chickens and highly sensitive Balb/C mice. Single strain infection showed that the deletion of these two genes from . Enteritidis resulted in the reduction of its virulence for mice but not for chickens. Mixed infection further confirmed these observations and indicated that in mice but not in chickens the virulence of and mutant was reduced to the natural virulence of serovars Infantis, Agona and Hadar. Although and genes do not influence . Enteritidis virulence for chickens directly, they may be of an indirect effect through the increased persistence of . Enteritidis in mice and increased probability of the reintroduction of . Enteritidis into poultry flocks.

Mots clés: virulence; chicken; mouse

D. Karasova, H. Havlickova, F. Sisak, I. Rychlik. Deletion of and in serovar Enteritidis reduced its virulence to the natural virulence of serovars Agona, Hadar and Infantis for mice but not for chickens early after infection. Veterinary Microbiology, 2009, 139 (3-4), pp.304. ⟨10.1016/j.vetmic.2009.06.023⟩. ⟨hal-00526938⟩