The basic features of Lyme disease are similar worldwide, but there are regional variations, primarily between the illness in America and that in Europe and Asia. In at least 60% to 80% of U.S. patients, Lyme disease begins with a slowly expanding skin lesion, EM, which occurs at the site of the tick bite. The skin lesion is frequently accompanied by flulike symptoms.

The Centers for Disease Control and Prevention (CDC) clinical case definition for Lyme disease includes the presence of EM or at least one objective, late manifesting sign of musculoskeletal, neurologic, or cardiovascular disease and a positive serologic test for antibodies to B. burgdorferi. Many misdiagnosed patients actually have chronic fatigue syndrome or fibromyalgia, both of which can cause similar symptoms, such as joint stiffness or pain, fatigue, and sleep disturbance.

Lyme borreliosis is a multisystem illness that primarily involves the skin, nervous system, heart, and joints (Table 1). Lyme disease usually begins during the summer months with EM and flulike symptoms and may be accompanied by right upper quadrant tenderness and a mild hepatitis (stage 1). This stage is followed weeks to months later by acute cardiac or neurologic disease in a minority of untreated individuals (stage 2) and then by arthritis and chronic neurologic disease (stage 3) in many untreated patients weeks to years after disease onset. There is considerable overlap of these stages, but Lyme disease is best characterized as an illness that evolves from early to late disease without reference to an arbitrary staging system. How ever, a patient may have one or all of the stages, and the infection may not become symptomatic until stage 2 or 3. Most affected patients have EM and 25% manifest arthritis; neuro logic manifestations and cardiac involvement are uncommon.

Table1. Clinical Features of Lyme Disease

Arthritis

 Arthralgia and myalgia are common features of early Lyme disease, but frank arthritis during EM is unusual. Arthritis is a well-described complication of Lyme disease and characteristically occurs months to years after Borrelia infection. Therefore, cases of Lyme arthritis occur during every month of the year. Lyme arthritis and parvovirus B19 arthritis can occur in the absence of other symptoms, such as the characteristic rash. Some suspected cases of Lyme arthritis might be caused by parvovirus B19, particularly those occurring during the parvo virus B19 season.

Arthritis in patients with chronic Lyme disease may be associated with a long-standing infiltration of the joints by B. burgdorferi spirochetes, along with a local inflammatory response. It may not be triggered simply by the presence of circulating immunoglobulin G (IgG) antibodies against outer surface proteins.

Cutaneous Manifestations

 Cutaneous manifestations can be demonstrated as early ECM (Fig. 1), secondary lesions (disseminated lesions and lymphocytoma), and late lesions (ACA). Except for the late lesions, cutaneous manifestations generally resolve spontaneously over weeks to months. The red papule at the site of the tick bite is most often located on the thigh, groin, or axilla. Facial EM is seen more frequently in children.

Fig1. Erythema chronicum migrans. (From Forbes BA, Sahm DF, Weissfeld AS: Bailey & Scott’s diagnostic microbiology, ed 12, St Louis, 2007, Mosby.)

Several days to weeks after the onset of EM, almost 50% of untreated patients develop secondary skin lesions. A rare early manifestation of Lyme disease is Borrelia lymphocytoma, a violaceous, tumor-like swelling or nodule at the base of the earlobe or nipple caused by a dense lymphocytic infiltrate of the dermis. This lesion occurs at the site of a tick bite and in conjunction with other symptoms; it may be confused with lymphoma.

ACA is a late skin manifestation of Lyme disease more prevalent in Europe than in the United States. Lesions display bluish red discoloration, doughy swelling, and fibrotic nodules. Eventually, striking atrophy of the skin and subcutaneous tis sues follows. Polyneuropathy coexists in 30% to 45% of patients.

Cardiac Manifestations

Lyme carditis occurs in approximately 8% of untreated patients within 1 to 2 months (range, >1 week to 7 months) after the onset of infection and may be the initial manifestation of Lyme disease. Cardiac features of Lyme disease usually result in a fluctuating degree of atrioventricular conduction defects (first-degree, second-degree, and complete block, as well as bundle branch and fascicular blocks) or tachyarrhythmias. Myopericarditis can occur, but symptomatic congestive heart failure is uncommon. Patients usually develop signs of light headedness, syncope, dyspnea, palpitations, and chest pain. Symptoms are more common in patients with more severe degrees of heart block. The carditis usually follows a self- limited and mild course, but temporary pacing may be needed in a small percentage of patients.

Neurologic Manifestations

Neurologic abnormalities occur in approximately 15% of untreated patients. These are usually observed 2 to 8 weeks after disease onset and may include aseptic meningitis, cranial nerve palsies, peripheral radiculoneuritis, and peripheral neuropathy. The predominant symptoms of Lyme meningitis are severe headache and mild neck stiffness, which may fluctuate for weeks after a post-EM latent period.

Months to years after the initial infection with B. burgdorferi, patients with Lyme disease may have chronic encephalopathy, polyneuropathy or, less often, leukoencephalitis. The appearance of mild encephalopathy has been seen 1 month to 14 years after the onset of disease. Encephalopathy is characterized by memory loss, mood changes, or sleep disturbances. In addition, increased cerebrospinal fluid (CSF) protein levels and evidence of intrathecal production of antibody to B. burgdorferi may occur. Chronic neurologic manifestations can also include polyneuropathy with radicular pain or distal paresthesias, fatigue, headache, hearing loss, and verbal memory impairment. These chronic neurologic abnormalities usually improve with antibiotic therapy.

Ocular manifestations may occur in Lyme disease and include cranial nerve palsies, optic neuritis, panophthalmitis with loss of vision, and choroiditis with retinal detachment.

Pregnancy

Transplacental transmission of B. burgdorferi with fetal infection has been confirmed. A uniform pattern of congenital mal formations has not been identified in maternal-fetal transmission of Lyme disease.

In observed cases cited, infants succumbed shortly after birth. The mothers acquired infection during the first trimester and received inadequate or no treatment.

Immunologic Manifestations

 Cellular immune responses to B. burgdorferi antigens begin concurrent with early clinical illness. An increase in spontaneous suppressor cell activity and reduction in natural killer (NK) cell activity have been noted. Mononuclear cell, antigen specific responses develop during spirochetal dissemination and humoral (antibody) immune responses soon follow.

Serodiagnostic tests are insensitive during the first several weeks of infection. In the United States, approximately 20% to 30% of Lyme patients have positive responses, usually of the IgM isotype, during this period, but by convalescence 2 to 4 weeks later, about 70% to 80% have seroreactivity even after antibiotic treatment. After about 1 month, most patients with an active infection have IgG antibody responses. After antibiotic treatment, antibody titers slowly fall, but IgG and even IgM responses may persist for many years after treatment. An IgM response cannot be interpreted as a manifestation of recent infection or reinfection unless the appropriate clinical characteristics are present. Antibodies formed include cryoglobulins, immune complexes, antibodies specific for B. burgdorferi, and anticardiolipin antibodies. Elevated titers of IgM are noted in early disease. Immunoblot analysis demonstrates that IgM antibodies form initially against the flagellar 41-kilodalton (kDa) polypeptide, but react later to additional cell wall anti gens. An overlapping IgG response to these antigens develops in some individuals. These antigen-specific cellular and humoral responses are not known to eradicate infection in early disease or participate in disease pathogenesis.

Specific IgM or IgG antibodies against B. burgdorferi are usually not detectable in a patient’s serum unless symptoms have been present for at least 2 to 4 weeks. In cases of Lyme arthritis, tests for serum antinuclear antibodies (ANAs) and rheumatoid factor (RF) and Venereal Disease Research Laboratory (VDRL) test results are generally negative. However, anti–B. burgdorferi antibodies of the IgG type should be present in the serum of patients with Lyme arthritis.

Outer surface protein A antibodies develop late in the course of human Lyme infection and then only in a subset of patients. A temporal association may exist between the onset of chronic Lyme arthritis in four patients who were HLA-DR4 positive and the development of antibodies to the outer surface protein.

Persistent organisms and spirochetal antigen deposits elicit a vigorous immune reaction, as manifested by a tissue-rich plasma cell and lymphocytic exudate containing abundant T cells, predominantly of the helper subset, plus IgD-bearing B cells. B. burgdorferi antigens elicit a strong immune reaction that intensifies with chronicity of arthritis and stimulates macrophages to secrete interleukin-1 (IL-1). IL-1 is capable of stimulating synovial cells and fibroblasts to secrete collage nase and prostaglandin E2; levels of both are elevated in Lyme synovial fluid and can cause erosion of joint cartilage and bone.

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