Lyme Disease

September 16, 2011

Lyme disease is an infection caused by a bacterium, Borrelia burgdorferi, which is carried around in the adult deer tick, Ixodes dammini. It begins as a slowly expanding skin rash and is associated with a tick bite or potential exposure to ticks. The Centers for Disease Control and Prevention (CDC) began surveillance for Lyme disease in 1982 and the Council of State and Territorial Epidemiologists (CSTE) designated Lyme disease as a nationally notable disease in January 1991. Currently all 50 states and the District of Columbia have reporting requirements.

THE VECTOR

Lyme disease is transmitted to humans through the bite of infected Ixodes ticks. Ticks feed by inserting their mouths into the skin of unsuspecting prey, and slowly ingesting host blood. The preferred host of nymphal Ixodes tick is the white-footed mouse. The preferred habitat for the adult tick is the white-tailed deer. These ticks do not look like the common dog or wood tick, they are much smaller, about 0.2 mm.

Even in endemic regions only 15% of ticks are infected with B. burgdorferi (the causative agent of Lyme disease). The vast majority of infection and disease onset occur between May and November, peaking in June and July, when the nymphal stage tick is prepared to feed. For infection to occur, an infected tick needs to remain attached for 36-48 hours. Identification of the tick bite and recognition of symptoms are key to early diagnosis. There is no evidence of any person-toperson transmission (respiratory or via body fluids), or of any other vectors (flies, fleas, mosquitoes) transmitting the disease.

THE DISEASE

Lyme disease is a zoonotic (coming from animals), multisystem, multistage disease with the typical sign of an early expanding skin lesion erythema migrans (EM) present in 90% or more of patients. If unrecognized or untreated, a patient may present weeks to months later with neurologic, cardiac, and/or joint abnormalities. Tissue damage occurs not as a direct result of spirochetal infection, but rather from a nonspecific immune response to infection.

Early Symptoms—Localized Disease

Within 3 days to about 1 month after being infected, 90% of patients experience EM. Erythema begins as a small red macular or papular lesion at the site of the tick bite. As the bacteria migrate outward, the area enlarges and eventually a “clearing” of the central aspect of the lesion occurs (the “bull’s-eye” lesion). The leading edge, though infected, remains flat and without scaling. It may be warm, but is not usually painful, thus often missed. As borrelia infection continues, it will enter the bloodstream and disseminate.

Early Symptoms—Disseminated Disease

When the bacteria disseminate, one quarter of patients experience multiple secondary annular skin lesions. Both EM and the secondary skin lesions may fade, but often reoccur. Systemic flu-like symptoms including headache, fatigue, fever, chills, myalgia (muscle pain), and/or arthralgia (joint pains) may present as well, or alone. Few patients may also present with excruciating headache, neck pain, and/or stiffness that resolves in hours, without neurological deficit, and normal cerebrol spinal fluid (CSF) assessment.

Late Disease (Weeks to Months)

Sixty percent of untreated patients experience arthritis, which is classically intermittent, asymmetric with pain, and swelling in large joints, often the knee. Arthritic episodes may last weeks to months, subside, and reoccur with decreasing frequency over several years. Fatigue is common but fever is rare. Ten percent of patients become chronic through the stimulation of an immune response against cartilage and bone similar to that found in rheumatoid arthritis. Fifteen percent of patients experience neurologic symptoms including meningitis, encephalitis, radiculoneuropathy (spinal nerve/nerve root manifestations), and/or facial nerve palsies. These central nervous system symptoms present with abnormal CSF, but patients do not have classic meningitis. Symptoms last for months but usually resolve. Eight percent of patients with late symptoms will develop cardiac involvement: A-V block, mild left ventricular dysfunction, or rarely cardiomegaly (enlarged heart). No murmurs are associated and symptoms are brief (days to weeks), but may also reoccur.

Very late sequelae may include the chronic skin lesions, acrodermatitis chronica atrophicans, which are firm red patches that atrophy, often on the hands, elbows, or knees. Neuropsychological effects, although rare, may include mild memory dysfunction, subtle mood changes, chronic fatigue, spinal cord inflammation, and sensory neuropathy.

DIAGNOSIS

Clinical symptoms with history of tick bite are sufficient for the diagnosis and treatment of Lyme disease. Early Lyme disease is based on the clinical presentation and there is no need for laboratory testing. Culture is definitive but very difficult, thus not used. Antibody titers (a measurement of antibodies the body produces in response to a specific infection) can prove helpful in diagnosis of patients with nonspecific symptoms. Caution in indiscriminant testing may result in false positives and confusion. Testing is best done to confirm the clinical suspicion, not just to search for a diagnosis.

LYME DISEASE AND PREGNANCY

Though an early report linked Lyme disease with adverse outcomes, a later prospective study of about 2,000 pregnant women refuted the evidence, and concluded that maternal infection of Lyme disease was not associated with fetal mortality, decreased birthweight, premature delivery, or congenital malformations. If a pregnant woman, however, becomes infected, it is recommended that she receive prompt treatment to eliminate disease and prevent future manifestations. There have been no known cases of fetal infection from mothers who contracted the disease and were treated.

TREATMENT

Early, nonspecific symptoms in an endemic area are an indication to treat. Successful treatment can occur even with late symptoms, but will be most rapid when identified early. As some symptoms may not clear for 3 months after completion of antibiotics and it is difficult to prove successful elimination of B. burgdorferi from the system, the determination of end point for treatment may be difficult! Current guidelines should guide all treatments. Doxycycline, amoxicillin, and cefuroxime axetil are currently the preferred drugs. With late symptoms, intravenous antibiotics are advised. Approximately 10% of patients experience a Jarisch-Herxheimer reaction (temporary worsening of symptoms with the initiation of treatment), headache, musculoskeletal pain, and/or fatigue depending on the severity of their disease.

PROPHYLAXIS AND PREVENTION

Prevention is the key step in avoiding infection.

  1. When possible, avoid tick habitats, especially during spring and summer. Ixodes prefers a moist shaded environment: areas of leaf litter and forests or areas of low-growing vegetation.
  2. Minimize exposed skin when venturing into infested areas: Wear light-colored clothes (to see ticks better), tuck pants into socks, and wear long sleeved shirts.
  3. Insect repellants containing DEET are very effective when applied to clothing and exposed skin. DEET can be used safely on children but follow product directions.
  4. Perform tick checks regularly and remove attached ticks. If embedded ticks are found, remove them using fine-tipped tweezers. Grab the tick as close to the skin as possible and with a firm steady motion pull the animal away. Do not worry if mouthparts are left behind, they do not transmit disease and human immunity can usually handle the remnants. Next, clean the area thoroughly with an antiseptic, and report any signs of EM or Lyme disease.

There is no indication for prophylactic treatment of asymptomatic patients after tick bite, but if symptoms arise (EM or nonspecific), medical attention and treatment are indicated. As of February 2002, the LYMErix™ Lyme disease vaccine was no longer manufactured, primarily due to concerns that the vaccine itself induced chronic arthritis in certain patients. There is ongoing research into new vaccines.

SEE ALSO: Arthritis, Rheumatoid arthritis

Suggested Reading

  • Malawista, S. E. (2000). Lyme disease. Cecil textbook of medicine (pp. 1757-1761). Philadelphia: W.B. Saunders.
  • Strobino, B. A., Williams, C. L., Abid, S., Chalson, R., & Spierling, P. (1993). Lyme disease and pregnancy outcome: A prospective study of two thousand prenatal patients. American Journal of Obstetrics and Gynecology, 169, 367-374.

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