Lyme disease is caused by the bacterial spirochete B. burgdorferi, which is transmitted to humans through tick bites. The disease typically begins with a skin rash and is followed by fever, joint pain, and other flu-like symptoms. If diagnosed early, Lyme disease can be successfully treated with antibiotics; however, up to 25% of patients experience arthritis-like symptoms after treatment. The cause of this condition, termed antibiotic refractory Lyme arthritis, is currently unknown. In the current issue of the JCI, researchers led by Dr. Linda Bockenstedt at Yale University reported on a fluorescent form of B. burgdorferi spirochetes used to determine what happens to the bacteria during and after antibiotic treatment. Using a special type of microscopy to examine the joints and cartilage in living mice, the researchers found that the number of spirochetes diminished quickly during antibiotic treatment and that live spirochetes were entirely eradicated by the time the treatment was completed. Despite being unable to detect live spirochetes after treatment, the researchers detected a fluorescent signal in the joints of the infected mice, which they attributed to bacterial debris. This debris could not cause an infection, but was still be detected by antibodies and elicited an inflammatory immune response. In a related commentary, Alan Barbour of the University of California Irvine notes the important ramifications of discovering non-viable and non-transmissible bacterial remnants following antibiotic treatment and the implications for antibiotic-refractory Lyme arthritis. Further studies will be required to determine if B. burgdorferi debris can cause arthritis in humans, as mice do not develop chronic Lyme arthritis.
TITLE:
Spirochete antigens persist near cartilage after murine Lyme borreliosis therapy
AUTHOR CONTACT:
Linda K. Bockenstedt
Yale University School Of Medicine, New Haven, CT, USA
Phone: 203-785-2453; Fax: 203-785-7053; E-mail: linda.bockenstedt@yale.edu
ACCOMPANYING COMMENTARY
TITLE:
Remains of infection
AUTHOR CONTACT:
Alan G. Barbour
University of California Irvine, Irvine, CA, USA
Phone: 949-824-5626; Fax: ; E-mail: abarbour@uci.edu
Journal
Journal of Clinical Investigation