Is there a causal relationship between Lyme disease and amylotropic lateral sclerosis (ALS) ?

Some Lyme disease patient advocates claim that there is a causal relationship between amyotrophic lateral sclerosis (ALS) and Lyme disease, simply because some patients with ALS appear to test positive in serological tests for Lyme disease. However, the results of recent clinical studies negate the validity of such a relationship. An examination of 414 patients with ALS who also underwent validated serological tests for Lyme disease, showed that only 24 (5.8%) were seropositive for Lyme disease; furthermore, the medical record of only 4 of these seropositive patients (0.97%) confirmed previous infection by Borrelia burgdorferi(1). In another larger study conducted in the U.S., more that 4,000 patients with ALS also were tested for Lyme disease; only 30 (<1%) were found to be positive based on the results of validated ELISA and Western Blot tests (2). Such a low incidence (<1%) is comparable to the background incidence of positive tests in individuals without ALS in the population at large (3). The results of a case controlled study (4), in which 491 patients diagnosed with ALS were compared to 982 normal controls, no differences in the seroprevalence of antibodies specific for B. burfdorferi were found between ALS patients (4.1%) and controls (5.9%). All of these findings indicate that Lyme disease is rare in patients with ALS, and provide no support for a causal relationship.

It should be noted that several β-lactam antibiotics, including ceftriaxone often used to treat Lyme disease with neurological symptoms, have been shown to possess profound neuroprotective effects that are independent of their antimicrobial properties (5); such unanticipated beneficial effects might be misinterpreted to suggest the elimination of a persistent infection as a result of antibiotic therapy. Because of these neuroprotective effects, that can be rather profound in some cases, clinical trials are now underway to examine if extended ceftriaxone therapy might be beneficial in the treatment of ALS (6). This in no way implies that ALS is due to a persistent infection that requires prolonged antibiotic therapy to cure.

1. Qureshi, M, Bedlack, RS, and Cudkowicz, ME. Lyme disease serology in amyotrophic lateral sclerosis. Muscle and Nerve 40: 626-628, 2009.

2. The ALSUntangled Group. ALSUntangled update 1: investigating a bug (Lyme Disease) and a drug (Iplex) on behalf of people with ALS. Amyotrophic Lateral
Sclerosis 10: 248-250, 2009.

3. Murphree, B, Kugeler, K, and Mead, P. Surveillance for Lyme disease—United States 1992-2006. www.cdc.gov/mmwr/PDF/ss/ss5710.pdf.

4. Visser, AE, Verduyn, Lunel, FM, Veldink, JH, and van den Berg, LH. No association between Borrelia burgdorferi antibodies and amylotrophic lateral sclerosis in a case-control study. Eur. J. Neurol. Jan 24 (1): 227-230, 2017.

5. Rothstein, JD, Patel, S, Regan, MR et al. β-lactam antibiotics offer neuroprotection by increasing glutamate transporter expression. Nature 433: 73-77, 2005.

6. Clinical trials on the use of ceftriaxone in patients with ALS http://clinicaltrials.gov/ct2/results?term=ceftriaxone+and+ALS

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