Microbiology of Lyme disease
), not to be confused with the single species Borrelia burgdorferi sensu stricto (s.s.), a member of the complex, which is responsible for nearly all cases of Lyme disease in North America.
The primary reason for the long delays when diagnosing Lyme disease is their greater strain diversity than previously estimated.
genospecies suspected of causing illness, but not confirmed by culture, include B. japonica, B. tanukii, and B. turdae (Japan); B. sinica (China); and B. andersonii (US).
Lyme disease is most endemic in the Northern Hemisphere temperate regions of the US,[22][23] but sporadic cases have been described in other areas of the world.
[25] In Europe, cases of B. burgdorferi s.l.-infected ticks are found predominantly in Norway, Netherlands, Germany, France, Italy, Slovenia, and Poland, but have been isolated in almost every country on the continent.
Ticks carrying B. burgdorferi s.l., as well as canine and human tick-borne diseases, have been reported widely in Brazil, but the subspecies of Borrelia has not yet been defined.
[31][32][33] In Western and sub-Saharan Africa, tick-borne relapsing fever has been recognized for over a century, since it was first isolated by the British physicians Joseph Everett Dutton and John Lancelot Todd in 1905.
[citation needed] Hard ticks have a variety of life histories with respect to optimizing their chance of contact with an appropriate host to ensure survival.
[39] One of the most striking features of B. burgdorferi as compared with other bacteria is its unusual genome, which is far more complex than that of its spirochetal cousin Treponema pallidum, the agent of syphilis.
[citation needed] Chemical analysis of the external membrane of B. burgdorferi revealed the presence of 46% proteins, 51% lipids, and 3% carbohydrates.
[43] B. burgdorferi is a highly specialized, motile, two-membrane, flat-waved spirochete, ranging from about 9 to 32 micrometers (μm) in length.
Like other spirochetes, such as Treponema pallidum (the agent of syphilis), B. burgdorferi has an axial filament composed of flagella that run lengthways between its cell wall and outer membrane.
This structure allows the spirochete to move efficiently in a corkscrew fashion through viscous media, such as connective tissue.
In some in vitro experiments, round bodies seemed to be formed in response to adverse conditions, such as a culture medium containing no serum or antimicrobial drugs.
[50][51][52] Advocates of the "chronic Lyme disease" theory sometimes propose that the formation of round bodies is a way that B. burgdorferi could survive standard antibiotic treatment protocols.
However, a 2014 review found that there was currently no clear evidence for this, and noted that samples from patients diagnosed with chronic Lyme disease following antibiotic treatment usually showed no round bodies (and indeed often no spirochaetes), suggesting that their symptoms might be due to something other than surviving B. burgdorferi bacteria.
Simultaneous with the disappearance of OspA, the spirochete population in the midgut begins to express an OspC and migrates to the salivary gland.
[61] In infected ticks feeding on a mammalian host, OspC may also be necessary to allow B. burgdorferi to invade and attach to the salivary gland after leaving the gut, although not all studies agree on such a role for the protein.
[62][63] OspC attaches to the tick salivary protein Salp15, which protects the spirochete from complement and impairs the function of dendritic cells.
[69] The presence of multiple Erp proteins was proposed to be important in allowing B. burgdorferi to evade killing by the alternative complement pathway of a broad range of potential animal hosts, as individual Erp proteins exhibited different binding patterns to the complement regulator factor H from different animals.
[70] However, the presence of factor H was recently demonstrated to be not necessary to enable B. burgdorferi to infect mice, suggesting that the Erp proteins have an additional function.
[72] Like the Borrelia that causes relapsing fever, B. burgdorferi has the ability to vary its surface proteins in response to immune attack.
