Projections around the globe suggest an increase in tick-vectored disease incidence and distribution, and the potential for emergence of novel tick-borne pathogens. Lyme disease is the most common reported tick-borne illness in the Unites States and is prevalent throughout much of central Europe. In recent years, the worldwide burden of Lyme disease has increased and extended into regions and countries where the disease was not previously reported. In this review, we discuss the trends for increasing Lyme disease, and examine the factors driving Lyme disease expansion, including the effect of climate change on the spread of vector Ixodid ticks and reservoir hosts; and the impacts of increased awareness on disease reporting and diagnosis. To understand the growing threat of Lyme disease, we need to study the interplay between vector, reservoir, and pathogen. In addition, we need to understand the contributions of climate conditions to changes in disease risk.

The emerging pathogen, Borrelia miyamotoi, is a relapsing fever spirochete vectored by the same species of Ixodes ticks that carry the causative agents of Lyme disease in the US, Europe, and Asia. Symptoms caused by infection with B. miyamotoi are similar to a relapsing fever infection. However, B. miyamotoi has adapted to different vectors and reservoirs, which could result in unique physiology, including immune evasion mechanisms. Lyme Borrelia utilize a combination of Ixodes-produced inhibitors and native proteins [i.e., factor H-binding proteins (FHBPs)/complement regulator-acquiring surface proteins, p43, BBK32, BGA66, BGA71, CD59-like protein] to inhibit complement, while some relapsing fever spirochetes use C4b-binding protein and likely Ornithodoros-produced inhibitors. To evade the humoral response, Borrelia utilize antigenic variation of either outer surface proteins (Osps) and the Vmp-like sequences (Vls) system (Lyme borreliae) or variable membrane proteins (Vmps, relapsing fever borreliae). B. miyamotoi possesses putative FHBPs and antigenic variation of Vmps has been demonstrated. This review summarizes and compares the common mechanisms utilized by Lyme and relapsing fever spirochetes, as well as the current state of understanding immune evasion by B. miyamotoi.

The Lyme disease spirochete, Borrelia burgdorferi, expresses RevA and numerous outer surface lipoproteins during mammalian infection. As an adhesin that promotes bacterial interaction with fibronectin, RevA is poised to interact with the extracellular matrix of the host. To further define the role(s) of RevA during mammalian infection, we created a mutant that is unable to produce RevA. The mutant was still infectious to mice, although it was significantly less well able to infect cardiac tissues. Complementation of the mutant with a wild-type revA gene restored heart infectivity to wild-type levels. Additionally, revA mutants led to increased evidence of arthritis, with increased fibrotic collagen deposition in tibiotarsal joints. The mutants also induced increased levels of the chemokine CCL2, a monocyte chemoattractant, in serum, and this increase was abolished in the complemented strain. Therefore, while revA is not absolutely essential for infection, deletion of revA had distinct effects on dissemination, arthritis severity, and host response. Borrelia burgdorferi, the causative agent of Lyme disease, is a vector-borne pathogen that successfully colonizes both ticks and a variety of vertebrate hosts. In mammals, B. burgdorferi is frequently found associated with connective tissues (1-13), and the bacterium is often detected in cartilaginous or collagen-rich tissues, such as skin and joints (6,7,9,(11)(12)(13)(14)(15)(16)(17)(18). Adhesins expressed by B. burgdorferi facilitate interactions with these tissues. B. burgdorferi expresses a plethora of outer surface proteins that interact with numerous components of the extracellular matrix (ECM), such as fibronectin, decorin, and integrins (19-23). The attachment of B. burgdorferi to the host ECM is likely critical for pathogenesis and persistence in mammals. Indeed, for many of these adhesins, deletion mutants have significant defects in infectivity, fail to disseminate widely in the host, or have other effects on disease, such as alterations in the severity of arthritis (24-27).The interactions of B. burgdorferi with fibronectin are facilitated by several distinct bacterial surface proteins, including BBK32, RevA, BB0347, and CspA (BbCRASP-1) (28-31). The redundancy in adhesins makes it difficult to dissect the role of each B. burgdorferi fibronectin binding protein in the pathogenesis of Lyme disease. For example, real-time microscopic imaging in live mice revealed a significant role for BBK32 in interactions with host vasculature, yet bbk32 mutants are still able to infect mammals (32).RevA is a 19-kDa surface protein encoded on the circular plasmid 32 (cp32) family of plasmids (33). RevA expression is elevated during mammalian infection over its expression in the tick vector, suggesting a role in pathogenesis (30,(34)(35)(36). RevA binds to fibronectin, and anti-RevA antibodies block the binding of whole B. burgdorferi bacteria to fibronectin (30). RevA is antigenic, as evidenced by the fact that both mice and human Lyme disease patients produce antibodies...

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Concentrations of hypophosphite and phosphite oxidizing bacteria were found to be high, relative to bacterial concentrations growing on phosphate, in sediment and soil during winter and summer seasons from 12 common terrestrial and aquatic sites using a most probable number method. The percent of total culturable bacterial concentrations that could use these reduced phosphorus compounds as a sole source of phosphorus were as follows: hypophosphite, 7-100%; phosphite, 10-67%; aminoethylphosphonate, 34-270%. The average MPN/g (±SEM) was as follows: phosphate, 6.19 × 10(6) (±2.40 × 10(6)); hypophosphite, 2.61 × 10(6) (±1.35 × 10(6)) phosphite, 1.91 × 10(6) (±1.02 × 10(6)); aminoethylphosphonate, 3.90 × 10(6) (± 1.95 × 10(6)). Relatively high concentrations of reduced phosphorus oxidizing bacteria were found in both pristine sites and sites with urban and agricultural disturbance. Concentrations of reduced phosphorus oxidizing bacteria in anoxic sediments and soil were equivalent. Our data indicate that reduced phosphorus oxidizing bacteria are abundant in the environment and provide strong evidence for the importance of bacterial P oxidation in nature.