Lyme Disease Content from MKSAP 15
This content has been excerpted from the latest edition of the Medical Knowledge Self-Assessment Program—MKSAP® 15. Learn more about this industry-leading educational product from the ACP.
Several diseases have a human tick vector (Table 15). Lyme disease is caused by three closely related Spirochete species classified together as Borrelia burgdorferi senso lato. In the United States, most Lyme disease is caused by B. burgdorferi senso stricto, whereas in Europe and Asia, it is most often caused by B. afzelii and B. garinii. The vector for Lyme disease is the Ixodes scapularis tick (the deer tick); the reservoirs are small mammals such as deer and mice.
Lyme disease is characterized by three stages: early, disseminated, and late. Each stage is associated with different clinical presentations, which may overlap. Most early localized Lyme disease occurs in the summer and fall and is characterized by the erythema migrans (EM) rash, an expanding erythematous patch appearing 5 to 14 days after inoculation by an infected tick. Multiple EM lesions, reflecting spirochetemia, can occur. EM may be solid, show central clearing, manifest as target lesions, and, occasionally, vesiculate or develop a necrotic center (Figure 3).
The appearance of the EM rash should not be confused with the hypersensitivity reaction that occasionally results from the tick bite itself (Table 16). The differential diagnosis of EM is limited (Table 17). The differential diagnosis of EM is limited. Patients with early Lyme disease may also have systemic symptoms including fever, myalgia, and arthralgia. In approximately 20% of patients, no EM rash is found and only systemic symptoms are present.
Early Lyme disease is usually diagnosed clinically because serologic test results are often negative at presentation and can become positive with clinical improvement. Early disseminated Lyme disease occurs weeks to months after a tick bite and may not be preceded by early-stage disease. Clinical manifestations are neurologic and cardiac. Neurologic syndromes include aseptic meningitis, cranial nerve palsies, and painful radiculopathies. Lyme carditis most often manifests as transient heart block, although severe myocarditis has been reported.
Late Lyme disease occurs months to years after the initial inoculation, may occur without the evidence of early localized or early disseminated stages, and can have rheumatologic, neurologic, or cutaneous manifestations. Lyme arthritis is characterized by a mono- or oligoarthritis most commonly involving the knees. In affected patients, the synovial fluid is inflammatory, and positive synovial fluid polymerase chain reaction test results for B. burgdorferi are diagnostic. Although arthralgia can occur in early Lyme disease, persistent diffuse arthralgia is not characteristic of late Lyme disease. Rarely, encephalitis characterized by subtle cognitive deficits may be noted. In Europe, the cutaneous disease acrodermatitis chronica atrophicans is an uncommon late manifestation.
In all patients with compatible symptoms and signs, serologic testing to confirm the diagnosis of Lyme disease is necessary except for those with typical EM.
A two-step approach should be used in the serologic diagnosis of Lyme disease. The initial serologic test is an enzyme-linked immunosorbent assay. Positive test results are confirmed with a Western blot analysis. Patients with nonspecific symptoms, such as fatigue, myalgia, or arthralgia, should not be tested. In such patients with a low pretest probability for disease, a positive enzyme-linked immunosorbent assay is most likely a false-positive result. Repeat testing to determine whether antibody titers have declined after completion of antibiotic treatment is unnecessary because seroreactivity often persists for at least months after antibiotic treatment of early infection and for years after treatment of late infection. The diagnosis of neurologic involvement requires evidence of B. burgdorferi on cerebrospinal fluid polymerase chain reaction testing (insensitive) or intrathecal production of B. Burgdorferi antibodies.
There is considerable controversy concerning post–Lyme disease syndrome, also referred to as “chronic Lyme disease.” However, despite the persistence of subjective symptoms after recommended treatment, no evidence of continued infection with B. burgdorferi exists, and treatment beyond that recommended is not beneficial and may be harmful. The notion that Lyme disease is difficult to treat has evolved because of overdiagnosis, not because patients do not respond to recommended treatment. For recommended treatment approaches, see Table 18 and Table 19.
The primary prevention is avoidance and timely removal of ticks. Transmission of B. Burgdorferi does not occur until the tick has fed for at least 36 hours. Antimicrobial prophylaxis with a single dose of doxycycline, 200 mg, after a tick bite is not recommended in most circumstances but can be considered when all four of the following are present: (1) the attached tick is Ixodes scapularis and it has been attached for at least 36 hours as determined by the degree of engorgement or the time of likely exposure; (2) prophylaxis can be given within 72 hours of tick removal; (3) the local prevalence of infected ticks is greater than 20%; and (4) doxycycline is not contraindicated.
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