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The Pediatric Forum |

Facial Palsy in Lyme Disease—Reply

Anita L. Belman, MD; P. K. Coyle, MD; Thomas Preston, PhD; Roger Grimson, PhD; Douglas Postels, MD; Leslie Reynolds, MD
Arch Pediatr Adolesc Med. 1998;152(9):929. doi:.
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The patients in our study were evaluated between 1988 and 1996.1(p1225) As we stated in our article1(p1227) confirmatory Western blot was not a standard of care practice for our patients, since it was not until August 1995 that the Centers for Disease Control and Prevention (CDC) recommended these studies and published criteria for interpretation.2 However, all of the children lived in an endemic Lyme disease area, had tick exposure, and developed new onset facial nerve palsy in the spring, summer, or fall. Other causes (mass lesions, varicella-zoster [Ramsey-Hunt], Epstein-Barr virus, and other rheumatologic disorders) were ruled out. These children were considered to have Lyme disease–associated facial nerve palsy (cranial neurities with detectable serum anti–B burgdorferi antibodies) according to the 1990 Lyme Disease National Surveillance Case Definition criteria of the CDC. We agree with Sood's comment regarding false-positive (and although he did not mention it, false-negative) results using ELISA of total antibodies to B burgdorferi. In fact we discussed this in our article.1(p1227) Of course, the false-positive rate in high endemic areas is much less than in nonendemic regions. The ELISA performed by Stony Brook University Hospital, Stony Brook, NY, is also considered to be one of the most reliable available. The diagnosis of Lyme disease is made on clinical and epidemiologic features based on the development of abnormal symptoms and signs consistent with B burgdorferi infection, failure to establish an alternative diagnosis, endemic area exposure as well as tick exposure. The CDC recommends laboratory confirmation for clinical syndromes other than physician-documented erythema migrans (EM). The most convincing laboratory support would be direct detection of the organism by culture. However, B burgdorferi culture requires the use of special (Barbour-Stoenner-Kelly) medium, which must be maintained for weeks for organisms to be detected, and unfortunately even then the yield is low. Polymerase chain reaction to detect B burgdorferi nuclei acid is a promising technique but now PCR assays remain experimental since they are not standardized for routine use on clinical samples. They also require meticulous detail to avoid contamination and false-positive results. Thus, serological tests to detect antibodies to the organism have been developed and are widely used. Both false-positive and false-negative results may occur.3 False-positive reactions may occur with other bacterial or viral infections, high autoantibody titers, or hypergammaglobulinemia. Furthermore, as we pointed out (page 1227) ELISA does not differentiate between active B burgdorferi infection and prior exposure, nor does Western blot. False-positive results may also occur, eg, in patients with rheumatoid arthritis where multiple antigen cross reactivity on Western blot has been noted.3 Serum IgM immunoblot assays during the acute phase of the infection followed by documentation of seroconversion by IgG immunoblot in the convalescent period is confirmatory as discussed by Sood. However it is possible that antibiotic therapy in early infection may blunt the immunologic response, thus in this scenario, seroconversion would not be demonstrated.

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