Acute Lyme Disease Research Articles

Circulating Borrelia burgdotferi in Patients with Acute Lyme Disease: Results of Blood Cultures and Serum DNA Analysis

To determine the usefulness of blood culture and polymerase chain reaction (PCR) analysis in detecting circulating Borrelia burgdorferi or its DNA, blood and serum from untreated patients with acute Lyme disease were examined. None of the cultures of blood or serum from the 7 patients tested demonstrated spirochetes. Similarly, all patient serum samples, assayed in two laboratories, were negative for B. burgdorferi DNA using PCR amplification. These results suggest that in patients with acute Lyme disease, spirochetes, spirochete DNA, or both circulate early, only intermittently, or at low levels and that neither culture nor PCR testing of blood or serum, as currently done, appears likely to prove generally useful in the diagnosis of Lyme disease.

The 93-kilodalton protein of Borrelia burgdorferi: an immunodominant protoplasmic cylinder antigen.

Using immunoblots, we identified proteins of Borrelia burgdorferi recognized by sera from 62 patients with either acute or chronic Lyme disease. In all groups studied, the 41-kDa flagellar protein and a relatively minor 93-kDa protein (p93) were the most commonly recognized antigens in patients with acute and chronic disease due to B. burgdorferi. A murine monoclonal antibody (MAb 181.1) was developed against p93, and the antigen was detected by immunoblot analysis in four European and American strains of B. burgdorferi. On two-dimensional gel electrophoresis, p93 had an apparent pI of 6.8. Immunoelectronmicroscopy with MAb 181.1 demonstrated that p93 is located within the protoplasmic cylinder compartment of the organism. The gene encoding p93 was retrieved from a phage expression library. The derived amino acid sequence of p93 confirmed chemical characterization of the antigen, including its amino-terminal peptide sequence. The derived amino acid sequence predicted it to be predominantly alpha helical. A prominent antigenic domain located at the carboxy portion of the protein was recognized by human and rabbit polyclonal antisera and human (MAb D4) and mouse (MAb 181.1) MAbs.

Autoimmunity associated with infection: leprosy, acute rheumatic fever and lyme disease

Autoimmunity associated with infection: leprosy, acute rheumatic fever and lyme disease

Autoimmunity associated with infection: leprosy, acute rheumatic fever and Lyme disease

This review examines the links between autoimmunity and three common infectious diseases. These disorders are associated with a variety of clinical and serological autoimmune phenomena. In addition they might conceivably trigger autoimmune diseases themselves. Mechanisms that may be responsible for these links, including molecular mimicry, are explored.

Cardiovascular manifestations of Lyme disease

Although the cardiac manifestations of Lyme disease may be diverse, in general they are treatable with currently available therapies. A high index of suspicion is required to make a diagnosis, especially for patients who may lack a suggestive history of tick exposure or residence in an endemic region. Lyme disease-related heart block may require pacemaker insertion and supportive care. The efficacy of antibiotics in the therapy of acute and chronic cardiac Lyme disease will require further study. Serologic testing and cardiac histopathology are the most precise methods of diagnosis. There is a need to develop more sensitive and specific diagnostic tests for Lyme disease and for Lyme carditis in particular.

California Serogroup Virus Infections in the Ryazan Region of the USSR

Serum samples from 60 people diagnosed in the summer of 1989 as having acute respiratory infections, meningitis or meningoencephalitis, acute pneumonia, Lyme disease, or other illnesses were tested by neutralization and hemagglutination-inhibition with Tahyna, Inkoo, and snowshoe hare viruses of the California serogroup (family Bunyaviridae, genus Bunyavirus). Demonstration of a diagnostic increase in antibody titers between paired serum samples from seven people showed that their illnesses were probably caused by Inkoo or Tahyna viruses. The clinical pictures were less specific. One patient had signs of meningoencephalitis, three had signs of meningitis, and three had influenza-like illnesses. These observations and other results suggest that California serogroup viruses are widespread in Russia and may account for an unexpectedly large number of presently undiagnosed febrile illnesses, some with central nervous system involvement.

Cross-reactivity of nonspecific treponemal antibody in serologic tests for Lyme disease

Serum samples obtained from 59 persons who had acute necrotizing ulcerative gingivitis, periodontitis, syphilis, or Lyme disease were tested against Treponema phagedenis biotype Reiter, Treponema denticola, Treponema vincentii, and Treponema scoliodontum by indirect fluorescent-antibody staining methods. Although there were positive reactions for sera representing each of these study groups and for 20 (13%) of 156 samples collected from the general population (premarital screening for syphilis), titration endpoints were relatively low (less than or equal to 1:256). Serum samples from 18 persons who had gingivitis or periodontitis but no history of Lyme borreliosis were tested by enzyme-linked immunosorbent assay for antibodies to Borrelia burgdorferi. Of these, five (28%) had immunoglobulin M antibody and four (22%) contained immunoglobulin G antibodies to this spirochete. Adsorption with either sorbent commercially prepared from T. phagedenis biotype Reiter or with washed, whole cells of T. phagedenis biotype Reiter reduced cross-reactivity in the enzyme-linked immunosorbent assay for Lyme borreliosis.

Seronegative Lyme Disease

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 less than 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 seronegative patients with clinical indications of chronic Lyme disease.

Septal panniculitis as a manifestation of lyme disease

A 22-year-old woman presented with fever, chills, photophobia, and headaches, followed by a centrally clearing erythematous skin eruption, migratory polyarthralgias, conjunctivitis, and subsequently, tender, nodular skin lesions. Antibodies to Borrelia burgdorferi were consistent with acute Lyme disease. Skin biopsy revealed acute septal panniculitis. This dermatologic manifestation has not been previously described in Lyme disease.