Seronegative Lyme Disease

Raymond J. Dattwyler, David J. Volkman, Benjamin J. Luft, John Halperin, Josephine Thomas, Marc G. Golightly

Research output: Contribution to journalArticle

294 Citations (Scopus)

Abstract

The diagnosis of Lyme disease often depends on the measurement of serum antibodies to Borrelia burgdorferi, the spirochete that causes this disorder. Although prompt treatment with antibiotics may abrogate the antibody response to the infection, symptoms persist in some patients. We studied 17 patients who had presented with acute Lyme disease and received prompt treatment with oral antibiotics, but in whom chronic Lyme disease subsequently developed. Although these patients had clinically active disease, none had diagnostic levels of antibodies to B. burgdorferi on either a standard enzyme-linked immunosorbent assay or immunofluorescence assay. On Western blot analysis, the level of immunoglobulin reactivity against B. burgdorferi in serum from these patients was no greater than that in serum from normal controls. The patients had a vigorous T-cell proliferative response to whole B. burgdorferi, with a mean (±SEM) stimulation index of 17.8±3.3, similar to that (15.8±3.2) in 18 patients with chronic Lyme disease who had detectable antibodies. The T-cell response of both groups was greater than that of a control group of healthy subjects (3.1+0.5; P<0.001). We conclude that the presence of chronic Lyme disease cannot be excluded by the absence of antibodies against B. burgdorferi and that a specific T-cell blastogenic response to B. burgdorferi is evidence of infection in sero-negative patients with clinical indications of chronic Lyme disease. (N Engl J Med 1988; 319:1441–6.)

Original languageEnglish (US)
Pages (from-to)1441-1446
Number of pages6
JournalNew England Journal of Medicine
Volume319
Issue number22
DOIs
StatePublished - Dec 1 1988
Externally publishedYes

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Lyme Disease
Borrelia burgdorferi
Chronic Disease
Antibodies
T-Lymphocytes
Serum
Anti-Bacterial Agents
Spirochaetales
Acute Disease
Infection
Antibody Formation
Fluorescent Antibody Technique
Immunoglobulins
Healthy Volunteers
Western Blotting
Enzyme-Linked Immunosorbent Assay
Control Groups
Therapeutics

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

Dattwyler, R. J., Volkman, D. J., Luft, B. J., Halperin, J., Thomas, J., & Golightly, M. G. (1988). Seronegative Lyme Disease. New England Journal of Medicine, 319(22), 1441-1446. https://doi.org/10.1056/NEJM198812013192203
Dattwyler, Raymond J. ; Volkman, David J. ; Luft, Benjamin J. ; Halperin, John ; Thomas, Josephine ; Golightly, Marc G. / Seronegative Lyme Disease. In: New England Journal of Medicine. 1988 ; Vol. 319, No. 22. pp. 1441-1446.
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Dattwyler, RJ, Volkman, DJ, Luft, BJ, Halperin, J, Thomas, J & Golightly, MG 1988, 'Seronegative Lyme Disease', New England Journal of Medicine, vol. 319, no. 22, pp. 1441-1446. https://doi.org/10.1056/NEJM198812013192203

Seronegative Lyme Disease. / Dattwyler, Raymond J.; Volkman, David J.; Luft, Benjamin J.; Halperin, John; Thomas, Josephine; Golightly, Marc G.

In: New England Journal of Medicine, Vol. 319, No. 22, 01.12.1988, p. 1441-1446.

Research output: Contribution to journalArticle

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AU - Dattwyler, Raymond J.

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AU - Golightly, Marc G.

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N2 - The diagnosis of Lyme disease often depends on the measurement of serum antibodies to Borrelia burgdorferi, the spirochete that causes this disorder. Although prompt treatment with antibiotics may abrogate the antibody response to the infection, symptoms persist in some patients. We studied 17 patients who had presented with acute Lyme disease and received prompt treatment with oral antibiotics, but in whom chronic Lyme disease subsequently developed. Although these patients had clinically active disease, none had diagnostic levels of antibodies to B. burgdorferi on either a standard enzyme-linked immunosorbent assay or immunofluorescence assay. On Western blot analysis, the level of immunoglobulin reactivity against B. burgdorferi in serum from these patients was no greater than that in serum from normal controls. The patients had a vigorous T-cell proliferative response to whole B. burgdorferi, with a mean (±SEM) stimulation index of 17.8±3.3, similar to that (15.8±3.2) in 18 patients with chronic Lyme disease who had detectable antibodies. The T-cell response of both groups was greater than that of a control group of healthy subjects (3.1+0.5; P<0.001). We conclude that the presence of chronic Lyme disease cannot be excluded by the absence of antibodies against B. burgdorferi and that a specific T-cell blastogenic response to B. burgdorferi is evidence of infection in sero-negative patients with clinical indications of chronic Lyme disease. (N Engl J Med 1988; 319:1441–6.)

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Dattwyler RJ, Volkman DJ, Luft BJ, Halperin J, Thomas J, Golightly MG. Seronegative Lyme Disease. New England Journal of Medicine. 1988 Dec 1;319(22):1441-1446. https://doi.org/10.1056/NEJM198812013192203