The Inadvertent Pathogen: Borrelia burgdorferi and Lyme Disease

Abstract

Borrelia burgdorferi, the organism causing Lyme disease, infects humans via tick bites. The European tick vector is different from the North American tick vector. Humans are inadvertent hosts for the ticks which normally feed on wild animals. Following infection with Borrelia burgdorferi, the symptoms range from none to very severe, the latter including arthritis, neurological disorders, and carditis. Arthritis is caused by release of peptidoglycan cell wall components that stimulate inflammation but the causes of the other symptoms are not known. Tick larvae acquire Borrelia during their first blood meal. The bacterium over-winters in the tick midgut with the aid of its OspA protein. The first blood meal the following Spring cause the bacterium to stop making OspA and now make the OspC protein. This permits the bacterium to move to the salivary glands and be injected into a new host. Borrelia avoids the immune system of its mammalian hosts using the vls (variable major protein-like sequence) system to create highly diverse epitopes of the outer membrane VlsE lipoprotein. The genome of Borrelia is small but very complex as each strain has thirteen to twenty-one plasmids. The majority of genes facilitating life in the tick vector and the mammalian host are found on the plasmids. The genes responsible for many of the symptoms of Lyme disease have not been identified but, given the differing symptoms between Europe and North America, probably are located on one or more plasmids.