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The clinical and pathological spectrum of the disease is dependent on the host s immune response to M leprae and re ects the relative balance between Th1 (helper) and Th2 (suppressor) T cells (Table 15 2)1 4 The tuberculoid form de nes one end of the
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LYME DISEASE
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Lyme disease is caused by infection with Borrelia burgdorferi, a spirochete, transmitted by ticks The deer tick, Ixodes dammini, is responsible for the disease in
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Figure 15 2 Borderline leprosy A patient with borderline leprosy has multiple skin lesions with hypopigmented center with raised erythematous borders on the back (A) and on the leg (B) (With permission from Amato AA, Dumitru D Acquired Neuropathies In Dumitru D, Amato AA, Swartz MJ (eds) Electrodiagnostic Medicine, 2nd edn Philadelphia: Hanley & Belfus, 2002, Fig 23 8, p 973)
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most cases Ticks acquire the spirochetes by feeding on infected host (eg, deer) and then transmits the spirochetes to the next hosts (eg, humans) at a latter feed It takes approximately 12 24 hours of tick attachment to transfer the spirochetes to the next host There are three recognized stages of Lyme disease: (1) early infection with localized erythema migrans, (2) disseminated infection, and (3) late-stage infection Within 1 month of a tick bite, erythematous circular region appears around the area of the original tick bite and gradually expands, with the center of the lesion becoming clear creating a bull s eye appearance The rash resolves spontaneously after approximately a month Importantly, not all patients with Lyme disease develop erythema migrans The second stage of the illness is marked by dissemination of the spirochetes throughout the body, and patients develop systemic symptoms including fever, chills, localized adenopathy, fatigue, myalgias, headache, neck and back pain, and additional skin lesions about the body Cardiac involvement may lead to pericarditis and heart block In ammatory arthritis of large and small joints may also occur
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Neurological complications may develop during the second and third stages of infection (Table 15 3)9 17 Facial neuropathy is most common and is bilateral in about half of cases, which is rare for idiopathic Bell s palsy Involvement of nerves is frequently asymmetric The presentation with a polyradiculoneuropathy may resemble GBS The late stage of infection is characterized by further destructive in ammatory changes in the joints The distal extremities develop a bluish discoloration of the skin (acrodermatitis chronica atrophicans) Spirochetes may be readily cultured from biopsy of these sites Approximately 50% of patients have numbness, paresthesia, weakness, and cramps in the distal extremities, and proprioception and vibration are reduced as are muscle stretch re exes
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Immuno uorescent or enzyme-linked immunoabsorbent assay may detect antibodies directed against the
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NEUROPATHIES ASSOCIATED WITH INFECTIONS
Figure 15 3 Borderline leprosy Sural nerve biopsy perivascular and diffuse endoneurial in ammation consisting of lymphocytes and macrophages, paraf n section stained with trichrome (A) Fite stain reveals red staining bacilli (the so-called red snappers ) sometimes in clusters in the endoneurium and within Schwann cells (B) Electron microscopy reveals electron-dense bacilli with surrounding clear halos within the cytoplasm of a Schwann cell surrounding a myelinated axon (C) and on higher power within a Schwann cell surrounding unmyelinated axons (D)
spirochete False-positive reactions are not uncommon, and, therefore, Western blot analysis should be performed to con rm a positive enzyme-linked immunoabsorbent assay Examination of the cerebrospinal
TABLE 15 3 NEUROPATHIES ASSOCIATED WITH LYME DISEASE
Encephalitis/meningitis Myelitis Cranial neuropathies (eg, facial nerve palsy) Peripheral neuropathy Mononeuropathies Multiple mononeuropathies Radiculopathy Plexopathy In ammatory myopathy
uid (CSF) should demonstrate lymphocytic pleocytosis and increased protein in patients with polyradiculitis, cranial neuropathies, and central nervous system involvement Electrodiagnostic studies are suggestive of a primary axonopathy Patients with mononeuropathy or mononeuropathy multiplex NCS reveal reduced compound muscle action potential (CMAP) and sensory nerve action potential (SNAP) amplitudes9,13 18 H-re exes may be absent Those with facial nerve palsies have reduced facial nerve CMAPs and abnormal blink re exes11 The electrophysiological abnormalities are often asymmetric18,19 Needle EMG reveals increased insertional and spontaneous activity in the form of brillation potentials and positive sharp waves and decreased recruitment of neurogenic-appearing motor unit action
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