Lyme Disease (Lyme Borreliosis)
Basics
Lyme disease, or Lyme borreliosis (LB), is a systemic infection caused by the spirochete Borrelia burgdorferi, which is transmitted by the bite of a tick.
B. burgdorferi is the most common cause of LB in North America, and is most commonly associated with joint disease.
In Europe, several Borrelia species are implicated in human disease; Borrelia afzelii is typically associated with skin disease and Borrelia garinii with neurologic symptoms.
The tick has to be attached for 24 hours for the organism to be transmitted.
Once in the skin, the spirochete may stay localized at the site of inoculation, or it may disseminate via the blood and lymphatics. Hematogenous dissemination can occur within days or weeks of the initial infection. The organism can travel to other parts of the skin, the heart, the joints, the central nervous system, and other parts of the body.
The tick vector of Lyme disease, Ixodes dammini, is found in the northeastern and midwestern United States where most cases are reported. Ixodes scapularis in the southeastern United States, Ixodes pacificus on the Pacific coast, and Ixodes ricinus, the sheep tick, in Europe are also vectors. Because the disease depends on deer, mice, ticks, and bacteria, it is limited geographically to the areas where all these organisms are present.
LB can occur in any season, although it is most prevalent during the warmer months from May through September during the nymphal stage of the tick. The ticks cling to vegetation (not trees) in grassland, marshland, and woodland habitats. They transfer to animals and humans via brushing up against the vegetation.
Description of Lesions
Initially, the LB lesion is a red macule or papule at the site of a tick bite. The bite itself usually goes unnoticed (only 15% of patients report a tick bite). The rash appears approximately 2 to 30 days after infection.
The lesion expands to form an annular erythematous lesion, erythema migrans (EM), which is the classic lesion of LB (Fig. 29.7). The lesion measures from 4 to 70 cm in diameter, generally with central clearing.
The center of the lesion, which corresponds to the putative site of the tick bite, may become darker, vesicular, hemorrhagic, or necrotic (Fig. 29.8).
Lesions may be confluent (not annular), and concentric rings may form.
Multiple lesions occur in approximately 20% of patients, likely a result of bacteremia (Figs. 29.9 and 29.10). The presence of multiple lesions of erythema migrans indicates early disseminated disease. These secondary lesions tend to be more uniform in morphology than the primary lesion.
Distribution of Lesions
Because secondary lesions spread hematogenously, they are less restricted than primary lesions in terms of location.
Late Lyme disease refers to symptoms, primarily rheumatologic and neurologic in nature, that occur months to years after initial infection.
It is not unusual for patients to first present with late extracutaneous symptoms without ever having had an initial EM lesion or other overt symptoms of early Lyme disease. This may occur because the patient was asymptomatic or because early disease was not recognized by the patient or correctly diagnosed by the health care provider.
The signs and symptoms of intermediate, chronic, and late Lyme disease include the following:
Arthritis in one or more large joints, nervous system problems that may include pain, paresthesias, Bell palsy, headaches, memory loss, and cardiac dysrhythmias.
Rarely, a lesion of lymphocytoma cutis may develop, usually occurring on the earlobe or nipple. These lesions are bluish-red nodules.
Acrodermatitis chronica atrophicans (ACA) is a manifestation of chronic LB that begins as an inflammatory eruption marked by edema and erythema, usually on the distal extremities. Later, atrophy occurs, and thin cigarette-paper skin is seen. Because of the loss of subcutaneous fat, underlying venous structures are more visible, and the skin becomes thin, atrophic, and xerotic.
Both lymphocytoma cutis and ACA are late cutaneous presentations of borreliosis and are very rare findings in the United States. They are seen primarily in Europe where the clinical differences probably result from the different antigenic strains of Borrelia.
Laboratory Testing
Serologic testing, using enzyme-linked immunosorbent assay (ELISA) and Western blot analyses for B. burgdorferi, is notoriously unreliable.
At the early presenting stage of LB, serologic testing has been reported to be positive in only 25% of infected patients. After 4 to 6 weeks, approximately 75% of these patients test positive, even after antibiotic therapy.
Patients with past LB and those who have been vaccinated may be persistently seropositive.
The poor reputation of serologic testing is derived somewhat from the many false-negative test results of patients treated very early in the course of the disease and from the many misdiagnosed cases of supposed LB.
In endemic areas, seropositivity may exist in as much as 50% of residents.
The U.S. Centers for Disease Control and Prevention currently recommends a two-step testing procedure consisting of a screening ELISA or immunofluorescent assay followed by a confirmatory Western immunoblot test on any samples with positive or equivocal results on ELISA.
Other diagnostic measures, such as polymerase chain reaction and cultures for B. burgdorferi have had some success; however, these techniques are time consuming and expensive. The Borrelia organism is fastidious, and culture of skin biopsy specimens is not readily available.
Differential DiagnosisDifferential Diagnosis Tinea Corporis (see Discussion in Chapter 18: Superficial Fungal Infections) Acute Urticaria (see Discussion in Chapter 27: Diseases of Cutaneous Vasculature) Erythema Multiforme (see Discussion in Chapter 27: Diseases of Cutaneous Vasculature) |
Tick Recognition
Tick Removal
Treatment of Erythema Migrans (Early Lyme Borreliosis)
Prevention
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SEE PATIENT HANDOUT Lyme Disease AND Lyme Disease: Prevention IN THE COMPANION eBOOK EDITION. |