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Leptospirosis is an emerging disease with an annual occurrence of over 1 million human cases worldwide. PathogenicLeptospira bacteria are maintained in zoonotic cycles involving a diverse array of mammals, with the capacity to survive outside the host in aquatic environments. Survival in the diverse environments encountered byLeptospira likely requires various adaptive mechanisms. Little is known aboutLeptospira outer membrane modification systems, which may contribute to the capacity of these bacteria to successfully inhabit and colonize diverse environments and animal hosts.Leptospira bacteria carry two genes annotated as UDP-3-O -[3-hydroxymyristoyl] glucosamineN -acyltransferase genes (la0512 and la4326 [lpxD1 andlpxD2 ]) that in other bacteria are involved in the early steps of biosynthesis of lipid A, the membrane lipid anchor of lipopolysaccharide. Inactivation of only one of these genes, la0512/lpxD1 , imparted sensitivity to the host physiological temperature (37°C) and rendered the bacteria avirulent in an animal infection model. Polymyxin B sensitivity assays revealed compromised outer membrane integrity in thelpxD1 mutant at host physiological temperature, but structural analysis of lipid A in the mutant revealed only minor changes in the lipid A moiety compared to that found in the wild-type strain. In accordance with this, anin trans complementation restored the phenotypes to a level comparable to that of the wild-type strain. These results suggest that the gene annotated aslpxD1 inLeptospira interrogans plays an important role in temperature adaptation and virulence in the animal infection model.

Leptospira interrogans lpxD Homologue Is Required for Thermal Acclimatization and Virulence