From relative risk's website:Arthritis Rheumatol. 2014 Jun 25. doi: 10.1002/art.38756. [Epub ahead of print]
Unraveling lyme disease.
Bockenstedt LK1, Wormser GP.
http://rel-risk.blogspot.de/2014/06/unr ... eview.html
Unraveling LD- A Review
Experts from the review,
Unraveling Lyme disease. Bockenstedt LK, Wormser GP. Arthritis Rheumatol. 2014 Jun 25.
Symptoms after Lyme disease treatment
New or recurrent objective signs of Lyme disease appearing after antibiotics should prompt evaluation for reinfection or incomplete treatment. A recent study in which the causative strain of B. burgdorferi was cultured from EM lesions showed that recurrent EM after treatment was due to reinfection rather than a relapse of the prior treated infection.
About 25% of patients with EM resolve clinical disease but continue to experience fatigue, cognitive issues or joint and muscle aches at 3 months after treatment, falling to about 10% at 6 months. Post-treatment Lyme disease syndrome (PTLDS) refers to such symptoms that last for more than 6 months after a documented episode of Lyme disease and are disabling. The frequency with which PTLDS occurs is believed to be substantially less than 10%. PTLDS should not be confused with “chronic Lyme disease”. This name originally referred to late manifestations of the disease, but has been usurped as a label for clinical syndromes that may or may not be associated with previous Lyme borrelia exposure.
The reasons for persistent symptoms in some patients after treatment for Lyme disease are not known. Theories include residual damage to tissue, slow resolution of the inflammatory state, and/or a form of cytokine-induced sickness behavior due to previously high levels of circulating cytokines. Systemic inflammatory cytokines exert adverse effects on neurobehavioral function in other conditions, independent of a CNS infection. Nonspecific symptoms such as fatigue and pain are common in the general population as well.
Because no test can prove absence of Lyme borrelia infection in humans, animal models have been used to examine antibiotic efficacy. Most investigations have had methodological concerns, including suboptimal antibiotic dosing and introduction of infection in ways that did not model the inoculum size and route by which humans usually become infected (i.e., from the bite of a single Ixodes species tick).
Even so, antibiotic failures defined by the presence of cultivable spirochetes are rare and usually occur in the setting of immunodeficiency or inadequate antibiotic dosing. A recent study in mice employed two–photon intravital microscopy to examine the fate of B. burgdorferi after antibiotics. Treatment rapidly eliminated viable spirochetes but B. burgdorferi inflammatory products (antigens and DNA) could be detected for extended periods adjacent to cartilage and in certain tissues such as the entheses.
Viable spirochetes were not found, although xenodiagnosis performed by feeding uninfected ticks on the mice occasionally detected borrelia DNA. These results provide insight into the significance of borrelia DNA that can occasionally be detected in treated animals when spirochetes cannot be demonstrated by culture and in those instances in humans in which borrelia DNA may be detected after antibiotics for Lyme disease.
Four placebo-controlled trials of extended antibiotic therapy for PTLDS have been conducted. These showed either no durable benefit (n=3) or a benefit in fatigue only (n=1) with an unacceptable adverse event rate from parenteral therapy. Persistence of Lyme borrelia could not be demonstrated by culture or PCR. These trials form the basis of the recommendation to consider symptomatic treatment of PTLDS following guidelines for chronic fatigue syndrome or fibromyalgia.