There are similarities between Lyme disease pathology and conditions such as Systemic Lupus erythematosus (SLE) and Lupus profundus which can complicate diagnosis of both conditions. Lyme disease may resemble mild cerebritis with lymphocytes and plasma cells in the leptomeninges as found in SLE, along with a similarity between lymphoplasmacytic panniculitis in Lyme disease and lupus profundis due to the interraction between plasma cells and blood vessels. The chronic inflammation that occurs in Lyme disease also leads to vascular thickening in many cases along with scleroderma-like collagen expansion, and this can create a similar type of degeneration in the synovia as found in the vessels of lupus spleens.
Cutaneous disorders are also a feature of chronic Lyme disease infection, with acrodermatitis chronic atrophicans (ACA) a major feature in elderly European populations where the disease is endemic. Sclerodermoid-like reactions, lichen sclerosis et atrophicus, eosinophilic fasciitis-like lesions of the extremities, and subcuticular fibrous nodules have all been associated with the presence of spirochaetes. The specific nature of these cutaneous conditions and their incidence appears to vary according to the species of infectious Borrelia bacteria, with ACA less common in North American Lyme disease patients.
Autoimmunity and Lyme Disease Pathology
Long-term chronic manifestations of Lyme disease are increasingly thought to be due to induced autoimmune conditions rather than acute pro-inflammatory action by the infection, although experimental support for this theory is lacking in most cases with the exception of a small group of patients with persistent arthritis symptoms following Lyme disease infection. These patients were found to have immune reactivity to outer surface protein A (OspA) of Borrelia burgdorferi, and the human leukocyte function-associated antigen-1 (hLFA-1) indicating a possible initiating bacterial antigen and a cross-reactive autoantigen which would explain the development of Lyme disease-related treatment-resistant arthritis. Research published in April 2011 has however found that the enzyme 5-lipoxygenase (5-LO), which catalyzes the conversion of arachidonic acid into the leukotrienes and was previously suspected of involvement in the development of arthritis is in fact not a causative agent and is unlikely to be a useful therapeutic target. Deficiency of the enzyme does however appear to lead to earlier manifestations of the condition and an inability to resolve the arthritis in the longer-term.
The variety of pro-inflammatory and immunomodulatory-immunosuppressive features of Lyme disease are still only beginning to be understood and have significant consequences for the success of any treatments. Whilst antibiotic treatment appears appropriate for acute and early stage Lyme disease, later manifestations may require immunosuppresive treatment to combat autoimmune-related Lyme disease pathology.
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Lyme Disease, Comorbid Tick-Borne Diseases, and Neuropsychiatric Disorders
By Robert C. Bransfield, MD | December 1, 2007, Psychiatric Times. Vol. 24 No. 14, http://j.mp/j0DEB5