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The spirochete Treponema pallidum subsp. pallidum is the causative agent of syphilis, a chronic, sexually transmitted infection characterized by multiple symptomatic and asymptomatic stages. Although several other species in the genus are able to cause or contribute to disease, T. pallidum differs in that it is able to rapidly disseminate via the bloodstream to tissue sites distant from the site of initial infection. It is also the only Treponema species able to cross both the blood-brain and placental barriers. Previously, the T. pallidum proteins, Tp0750 and Tp0751 (also called pallilysin), were shown to degrade host proteins central to blood coagulation and basement membrane integrity, suggesting a role for these proteins in T. pallidum dissemination and tissue invasion. In the present study, we characterized Tp0750 and Tp0751 sequence variation in a diversity of pathogenic and nonpathogenic treponemes. We also determined the proteolytic potential of the orthologs from the less invasive species Treponema denticola and Treponema phagedenis. These analyses showed high levels of sequence similarity among Tp0750 orthologs from pathogenic species. For pallilysin, lower levels of sequence conservation were observed between this protein and orthologs from other treponemes, except for the ortholog from the highly invasive rabbit venereal syphilis-causing Treponema paraluiscuniculi. In vitro host component binding and degradation assays demonstrated that pallilysin and Tp0750 orthologs from the less invasive treponemes tested were not capable of binding or degrading host proteins. The results show that pallilysin and Tp0750 host protein binding and degradative capability is positively correlated with treponemal invasiveness., (Copyright © 2015, American Society for Microbiology. All Rights Reserved.)

Leptospira interrogans serovar Bratislava infection occurs in multiple domestic and wildlife species and is associated with poor reproductive performance in swine and horses. We present the complete genome assembly of strain PigK151 comprising two chromosomes, CI (4.457 Mbp) and CII (358 kbp)., (Copyright © 2015 Alt et al.)

Pathogenic Leptospira has the capacity to infect a broad range of mammalian hosts. Leptospirosis may appear as an acute, potentially fatal infection in accidental hosts, or progress into a chronic, largely asymptomatic infection in natural maintenance hosts. The course that Leptospira infection follows is dependent upon poorly understood factors, but is heavily influenced by both the host species and bacterial serovar involved in infection. Recognition of pathogen-associated molecular patterns (PAMPs) by a variety of host pattern recognition receptors (PRRs) activates the host immune system. The outcome of this response may result in bacterial clearance, limited bacterial colonization of a few target organs, principally the kidney, or induction of sepsis as the host succumbs to infection and dies. This chapter describes current knowledge of how the host recognizes Leptospira and responds to infection using innate and acquired immune responses. Aspects of immune-mediated pathology and pathogen strategies to evade the host immune response are also addressed.