Abstract
Despite leadership by dedicated lay organization and patient-based advocacy groups, the way forward for prospective candidates for disulfiram treatment has been difficult. This article provides the background, overview of disulfiram, in particular its intended use in post-treatment Lyme disease syndrome after a standard of care course of antibiotics fails to alleviate symptoms of tick borne disease. A series of recommendations are offered to guide patients and clinicians.
Highlights
Borrelia (B.) burgdorferi sensu lato is the causative agent of Lyme disease worldwide, while the genus, B. burgdorferi sensu stricto is the causal infectious agent of the North American disease transmitted by the bite of hard-shelled Ixodes scapularis ticks
The recurrence or emergence of systemic and nervous system symptoms after a standard of care course of therapy may occur with an enduring positive or indeterminate two-tier Lyme serology or other biomarkers in the cerebrospinal fluid (CSF), and abnormal findings in neuroimaging, electrodiagnostic and autonomic studies correlative with central, peripheral and autonomic nervous system (CNS, PNS and ANS) symptoms and signs [8] [9] have led to reconsideration of post-treatment Lyme disease syndromes (PTLDS)
It is not well understood why some patients experience PTLDS, the varied presentation no doubt incorporates at least four etiopathogenic mechanisms, singly or in combination in affected cases including persistent but difficult to detect infection [10], host-induced immunity targeting non-viable spirochetes or their remnants [11], a triggered immune response that lasts well after the infection similar to Group A beta hemolytic streptococcus (GABHS) infection in rheumatic heart disease and pediatric autoimmune neuropsychiatric disorder (PANDAS) [12] [13]; and as some might argue, causes unrelated to infection or immunity [14]
Summary
Borrelia (B.) burgdorferi sensu lato is the causative agent of Lyme disease worldwide, while the genus, B. burgdorferi sensu stricto is the causal infectious agent of the North American disease transmitted by the bite of hard-shelled Ixodes scapularis ticks. The recurrence or emergence of systemic and nervous system symptoms after a standard of care course of therapy may occur with an enduring positive or indeterminate two-tier Lyme serology or other biomarkers in the cerebrospinal fluid (CSF), and abnormal findings in neuroimaging, electrodiagnostic and autonomic studies correlative with central, peripheral and autonomic nervous system (CNS, PNS and ANS) symptoms and signs [8] [9] have led to reconsideration of post-treatment Lyme disease syndromes (PTLDS) It is not well understood why some patients experience PTLDS, the varied presentation no doubt incorporates at least four etiopathogenic mechanisms, singly or in combination in affected cases including persistent but difficult to detect infection [10], host-induced immunity targeting non-viable spirochetes or their remnants [11], a triggered immune response that lasts well after the infection similar to Group A beta hemolytic streptococcus (GABHS) infection in rheumatic heart disease and pediatric autoimmune neuropsychiatric disorder (PANDAS) [12] [13]; and as some might argue, causes unrelated to infection or immunity [14]. The antibiotic treatment of patients with PTLDS has been stymied by negative randomized placebo-controlled trials that fail to show significant, sustained benefit of antibiotic retreatment [15] [16], yet this may be related in part to the antibiotic regimens used, the limitations of current antibody-based assays, polymerase chain reaction (PCR), and culture techniques to determine successful eradication of B. burgdorferi
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