Abstract
Pathogenic mechanisms of Leptospira interrogans, the causal agent of leptospirosis, remain largely unknown. This is mainly due to the lack of tools for genetic manipulations of pathogenic species. In this study, we characterized a mutant obtained by insertion of the transposon Himar1 into a gene encoding a putative lipoprotein, Loa22, which has a predicted OmpA domain based on sequence identity. The resulting mutant did not express Loa22 and was attenuated in virulence in the guinea pig and hamster models of leptospirosis, whereas the genetically complemented strain was restored in Loa22 expression and virulence. Our results show that Loa22 was expressed during host infection and exposed on the cell surface. Loa22 is therefore necessary for virulence of L. interrogans in the animal model and represents, to our knowledge, the first genetically defined virulence factor in Leptospira species.
Highlights
Leptospira interrogans is a spirochete responsible for leptospirosis
We recently provided evidence of gene transfer in L. interrogans, which involved the transposition of a transposon of eukaryotic origin [13]
Leptospirosis is a zoonotic disease that causes a high rate of mortality and morbidity in humans and animals throughout the world each year
Summary
Leptospira interrogans is a spirochete responsible for leptospirosis. This disease, which is considered the most geographically widespread zoonosis, has emerged as a major public health problem in developing countries [1,2,3]. Numerous mammalian species, including rodents, excrete the pathogen in their urine and serve as reservoirs for transmission. Leptospirosis imparts its greatest burden on poor rural farming and urban slum populations in developing countries [1,2,3]. More than 500,000 cases of severe leptospirosis occur each year, with a mortality rate of 5% to 20% [4]. Little is understood of Leptospira pathogenesis, which in turn has hampered the identification of new intervention strategies
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