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After a period of localized skin infection at the site of inoculation, B burgdorferi infection may spread hematogenously to various target organs. Disseminated Lyme disease occurs 1 to 4 months after an infected tick bite and can include cutaneous, rheumatic, neurologic, and cardiac manifestations.” Clinical acumen is required at this stage of illness, because involvement of any of these organ systems may be the first indication of disseminated infection.
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The principal cutaneous manifestation of disseminated infection is multiple erythema migrans lesions remote from the original tick bite. These secondary lesions are similar to primary erythema migrans but show less expansion and may be evanescent. B burgdorferi has been cultured from biopsy specimens of secondary skin lesions.
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The classic rheumatic manifestation is intermittent large-joint arthritis, which presents most often as acute monarthritis of the knee. Attacks of arthritis appear suddenly with the development of large effusions. White cell counts in joint fluid usually range from 10,000 to 50,000/mm3 with polymorphonuclear cells predominating. Attacks resolve in a few days to weeks but are recurrent. This pattern of intermittent inflammatory arthritis affecting one or more large joints most closely mimics reactive arthritis.
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Neurologic complications may present as isolated peripheral neuropathy of the seventh cranial nerve, lymphocytic aseptic meningitis, radiculoneuropathy, or the triad of cranial neuropathy, meningitis, and radiculoneuropathy, which is unique to B burgdorferi infection. Any neurologic manifestation occurring in isolation, however, may present a diagnostic challenge. Idiopathic Bell’s palsy is clinically indistinguishable from palsy that occurs in Lyme disease. Viral meningitis resembles Lyme meningitis except that the latter has a relapsing course. Most patients with neurologic Lyme disease, however, have had erythema migrans, even if it was minor and considered insignificant by the patient. Therefore, a high index of suspicion and careful history taking, perhaps with photographic examples of erythema migrans to assist the patient, may aid in diagnosis.
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Cardiac involvement presents with palpitations or syncope, or both, resulting from variable atrioventricular block, which is usually transient but sometimes high-grade and requires temporary cardiac pacing. Symptomatic involvement of pericardium, impairment of contractility, or both, can occur but are distinctly unusual? Acute rheumatic fever may present similarly, but symptomatic heart block is unusual with rheumatic fever, and valvular heart disease is not a manifestation of Lyme disease.
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Rarely, cases involving inflammation of muscle, tendons, subcutaneous tissues, eye structures, spleen, liver, and bone have been reported. Comprehensive reviews of these clinical manifestations are readily available in standard textbooks.
With such a variety of multi-system manifestations occurring over time, disseminated Lyme disease poses a challenging differential diagnosis. A history of erythema migrans strongly suggests that such disseminated features are caused by B burgdorferi infection. However, since erythema migrans is usually recognized and treated effectively, patients presenting with disseminated Lyme disease may have no previous history of erythema migrans because the skin lesions either were absent or went unrecognized by the patient. Fortunately, the vast majority of patients are seropositive by the time disseminated infection develops.