Disease relevance of Lyme Disease

• Parvovirus B19 as the cause of a syndrome resembling Lyme arthritis in adults [1].
• BORRELIA: burgdorferi, the causative agent of Lyme disease (LD), expresses two surface-exposed decorin-binding adhesins, DbpA and DbpB [2].
• A spirochete (IDS) isolated from Ixodes dammini ticks has been implicated as the etiologic agent of Lyme disease [3].
• OBJECTIVE: To compare the efficacy of cefuroxime axetil and doxycycline in the treatment of patients with Lyme disease associated with erythema migrans [4].
• The various manifestations of Lyme disease can usually be treated successfully with oral doxycycline or amoxicillin, except for objective neurologic manifestations, which seem to require intravenous therapy [5].

High impact information on Lyme Disease

• Single-dose doxycycline for the prevention of Lyme disease [6].
• In cases of suspected Lyme disease, culture of skin lesions, polymerase-chain-reaction testing, or serologic testing was done [7].
• Successful parenteral penicillin therapy of established Lyme arthritis [8].
• In a double-blind placebo-controlled trial carried out from 1980 to 1982, 20 patients with established Lyme arthritis were assigned treatment with 2.4 million U of intramuscular benzathine penicillin weekly for three weeks (total, 7.2 million U) and 20 patients received saline [8].
• Individuals with treatment-resistant Lyme arthritis, but not other forms of arthritis, generated responses to OspA, hLFA-1, and their highly related peptide epitopes [9].

Chemical compound and disease context of Lyme Disease

• We conclude that binding of a single spirochetal peptide to certain DRB molecules is a marker for antibiotic-refractory Lyme arthritis and might play a role in the pathogenesis of the disease [10].
• Treatment of long-standing Lyme disease with ceftriaxone [11].
• Pulsed high-dose cefotaxime therapy in refractory Lyme borreliosis [12].
• Treatment of late Lyme borreliosis with cefoperazone and sulbactam [13].
• For patients with early Lyme disease, tetracycline appears to be the most effective drug, then penicillin, and finally erythromycin [14].

Biological context of Lyme Disease

• We studied the frequencies of HLA-DRB1-DQA1-DQB1 haplotypes in 121 patients with antibiotic-refractory or antibiotic-responsive Lyme arthritis and correlated these frequencies with in vitro binding of the OspA(163-175) peptide to 14 DRB molecules [10].
• We examined the antibody responses of Lyme disease patients to IDS lysate components in order to further understand the pathogenesis of this disease [3].
• Chronic Lyme arthritis. Clinical and immunogenetic differentiation from rheumatoid arthritis [15].
• The finding of reactive Lyme serology in an MS patient with no suggestive features of the infection is unlikely to indicate neurological Lyme disease [16].
• Molecular mimicry in Lyme arthritis demonstrated at the single cell level: LFA-1 alpha L is a partial agonist for outer surface protein A-reactive T cells [17].

Anatomical context of Lyme Disease

• Balance of synovial fluid IL-1 beta and IL-1 receptor antagonist and recovery from Lyme arthritis [18].
• In this paper, we show that the morphology of the Lyme disease spirochete Borrelia burgdorferi is the result of a complex interaction between the cell cylinder and the internal periplasmic flagella [19].
• These results suggest that chemokine-mediated recruitment of neutrophils into the infected joint is a key requirement for the development of experimental Lyme arthritis [20].
• That this IL 1 is produced by Lyme disease spirochete-stimulated macrophages may explain some of the clinical manifestations of Lyme disease [21].
• Bb2Bb3 regulation of murine Lyme arthritis is distinct from Ncf1 and independent of the phagocyte nicotinamide adenine dinucleotide phosphate oxidase [22].

Gene context of Lyme Disease

• The preferential induction by B. burgdorferi of IL-1 beta over IL-1ra is an example of excess agonist over antagonist synthesis induced by a microbial pathogen, and may contribute to the destructive lesion of Lyme arthritis [23].
• Borrelia burgdorferi, the causative agent of Lyme disease, is a potent inducer of interleukin-1 beta (IL-1 beta), a cytokine implicated in the pathogenesis of inflammatory arthritis [18].
• To assess the role of Ncf1 in Lyme arthritis, we introgressed Bb2Bb3 from severely arthritic C3H/He mice onto mildly arthritic C57BL/6 mice [22].
• Murine Lyme arthritis development mediated by p38 mitogen-activated protein kinase activity [24].
• These data indicate that TLR2 facilitates the inflammatory events associated with Lyme arthritis [25].
• Patients with antibiotic-refractory Lyme arthritis have high synovial fluid levels of proinflammatory chemokines and cytokines, especially CXCL9 and IFNgamma, throughout the illness [26].

Analytical, diagnostic and therapeutic context of Lyme Disease

• In another assessment of functional significance, the flagella-less mutant was equal if not superior to flagella-bearing, isogenic isolates when examined in an enzyme-linked immunosorbent assay for anti-B. burgdorferi antibodies in the sera of Lyme disease patients [27].
• In contrast to the findings with Lyme disease sera, sera from controls showed little reactivity with IDS components in either the western blots or a derivative solid-phase radioimmunoassay [3].
• PCR results in the UOA patients were compared with the results in cohorts of patients with definite rheumatoid arthritis (RA), Lyme arthritis, and Chlamydia-induced arthritis (CIA) [28].
• PURPOSE: To compare the safety and efficacy of azithromycin, amoxicillin/probenecid, and doxycycline for the treatment of early Lyme disease, to identify risk factors for treatment failure, and to describe the serologic response in treated patients [29].
• Despite longer and more frequent parenteral therapy, late Lyme disease frequently required retreatment, owing to poor clinical response (p less than .05) [30].

References