We found that the two mouse strains with a functional tlr4 gene (C3H/HeN and C57BL/6) developed clinical and molecular signs of leptospirosis less pronounced but not significantly different than tlr4 hyporesponsive C3H/HeJ, as quantified by weight loss, survival curves, presence of Leptospira 16S rRNA in blood and urine and burden of viable spirochetes in kidney as compared to the respective uninfected controls. This evidence concerns the gene TLR4 and leptospirosis.