The Infectious Diseases Society of America (IDSA) asserts that Borrelia burgdorferi (the tick-transmitted spirochete that causes Lyme disease) readily succumbs to antibiotic treatment. Microbiologists who have studied the organism disagree. It survives assaults from drugs and the immune system by hiding in biofilms and by changing form (See Townsend Letter, July 2009; 312:30–31). Norwegian researchers øystein Brorson and Sverre-Henning Brorson say: “B.burgdorferi has the ability to convert (and reconvert) to cystic forms both in vivo and in vitro” when exposed to the antibiotics ceftriaxone, doxycyclin, ciprofloxacin, and vancomycin. When the environment is safe for growth, the bacteria returns to its motile form.
Recent studies involving the use of the new antibiotic tigecycline show the difficulty of finding a treatment for Borrelia. In vitrolaboratory tests found that tigecycline inhibited and destroyed the cyst and motile forms of B. burgdorferi. Unfortunately, in vitroresearch does not always match the results of in vivo research. Researchers at University of California-Davis tested this antibiotic on mice with different stages of Borrelia infection (1 week, 3 weeks, or 4 months) in a controlled study. Three months after treatment, infection status was evaluated by culture, quantitative OspA (outer surface protein A) real-time polymerase chain reaction (PCR), and subcutaneous transplantation of joint and heart tissue into other mice. Not surprisingly, tissue from the saline-treated control mice were culture- and PCR-positive for Borrelia. Some tissues from the antibiotic-treated mice were also PCR-positive, although the DNA markers were greatly reduced compared with the controls. Antibiotic treatment at the 1-week stage appeared to be more effective than treatment that began at the later stages.
All of the antibiotic-treated mice were culture-negative. Even though the spirochetes could not be cultured, mice that received transplants from the antibiotic-treated mice developed spirochetal DNA in multiple tissues. Moreover, ticks that fed on the antibiotic-treated mice acquired Borrelia and were then able to transmit the infection to other mice. Clearly, negative cultures do not mean that Borrelia is absent. The researchers conclude: “… antibiotic treatment [with tigecycline] is unable to clear persisting spirochetes, which remain viable and infectious, but are nondividing or slowly dividing.”
Unfortunately, tigecycline is not the only failure. The UC-Davis researchers state: “Treatment failures have been documented with nearly every type of antimicrobial drug, based upon clinical relapse, culture, or PCR.” Studies such as this one support the view that the IDSA’s treatment guidelines are inadequate. They also show how challenging this infection is.
Barthold SW, Hodzic E, Imai DM, Feng S, et al. Ineffectiveness of tigecycline against persistent Borrelia burgdorferi [abstract]. Antimicrob Agents Chemother. February 2010;54(2):643–651.Available at: www.ncbi.nlm.nih.gov/pubmed/19995919.
Brorson ø, Brorson S-H. An in vitro study of the susceptibility of mobile and cystic forms of Borrelia burgdorferi to tinidazole. Int Microbiol. 2004;7:139–142. Available at www.im.microbios.org. Accessed April 21, 2010.
Brorson ø, Brorson SH, Scythes J, MacAllister J, et al. Destruction of spirochete Borrelia burgdorferi round-body propagules (RBs) by the antibiotic tigecycline [abstract]. Proc Natl Acad Sci U.S.A. November 3, 2009;106(44):18656-61. Available at: www.ncbi.nlm.nih.gov/pubmed/19843691. Accessed April 21, 2010.
Johnson L. LYMEPOLICYWONK: Barthold and Luft – persistence and integrity in science [blog]. December 15, 2009. www.lymedisease.org/news/lymepolicywonk/290.html. Accessed April 27, 2010.