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Related to Lyme borreliosis: Borrelia burgdorferi, Lyme neuroborreliosis
Lyme dis·easeAvoid the incorrect phrase Lyme's disease.
About 18,000 cases of Lyme disease are confirmed annually in the U.S. The largest proportion of cases occur in people aged 5-9 years and 50-59 years. States with the highest incidence are Connecticut, Rhode Island, and New Jersey. Lyme disease is generally benign and self-limited even without treatment. Antibody studies in endemic areas suggest that as many as 50% of people who contract the infection never show symptoms. The case fatality rate is virtually zero. The diagnosis is essentially clinical. Serologic tests for antibody to Borellia burgdorferi are notoriously poor in both sensitivity and specificity. In nonendemic areas, false positive test results statistically outnumber true positives. Because IgM antibody appears and peaks relatively late, one half of patients are seronegative during the first month following appearance of the rash. Antibiotic treatment administered early can alter or prevent the expected acute immune response. IgG antibody persists for months or years after infection and hence affords no help in diagnosing acute disease. Given the nonspecific and variable clinical picture and the unreliability of laboratory diagnostic measures, it is inevitable that many cases of Lyme disease are missed, and that, conversely, the diagnosis is often wrongly made. The drug of choice is doxycycline administered orally for several weeks. Amoxicillin is the standard alternative for children and pregnant patients. Recovery does not confer immunity to future attacks. In fact, in highly endemic areas, the reinfection rate may be as high as 20%. Infectious disease authorities do not recommend antibiotic prophylaxis after a tick bite, even in endemic areas, nor do they countenance treatment of asymptomatic people who have serologic evidence of past infection. A vaccine consisting of lipidated outer surface protein A (OspA) of B. burgdorferi synthesized by a nonvirulent strain of recombinant Escherichia coli induces formation of antibody that enters a feeding tick and binds any spirochetes present, preventing their mobilization. However, because of low demand the vaccine was withdrawn from the market by the manufacturer in 2002.
Lyme diseaseAn infection by Borrelia burgdorferi, acquired from tick bites. Lyme disease symptoms may resemble an anxiety disorder and include fatigue, concentration difficulties and/or joint pain; the clinical findings may be mediated by IL-1.
25–30,000 cases occurred in the US in 2010, making it the most common zoonosis in the US, especially along the Eastern seaboard; B burgdorferi has also been found in Northern Europe and Australia.
Deer tick (Ixodes dammini), Eastern USA—up to 60% carry the spirochete; white-footed mouse tick (I pacificus), Western US—±1% carry the spirochete; wood tick (I ricinus), Europe; Lone Star tick (Amblyomma americanum); and rarely in deerflies and horseflies.
Deer mice, field mice.
Nonspecific findings include increased ESR, IgM cryoglobulins, decreased C3 and C4, increased IgG and IgM antibody titers to B burgdorferi; definitive diagnosis requires identification of IgG antibodies to B recurrentis by the “Western” tick (immunoblot).
60% of untreated subjects develop recurring arthritis—chronic Lyme arthritis—lasting up to years after infection.
May be positive in patients who are also infected with Ehrlichia spp, which may be due to a co-infection with the same tick bite; PCR for human granulocytic ehrlichiosis is required to confirm the latter infection.
1 month of doxycycline or amoxicillin or 2 weeks of IV ceftriaxone or penicillin.
Osp A vaccine.
Lyme disease stages
Erythema chronicum migrans–rash stage, associated with wood tick bites and confined to Northern Europe until 1970 when the first US cases were described, presenting as a solitary reddish papule and plaque with centrifugal expansion (up to 20 cm), peripheral induration and central clearing, persistis for months to years; potentially pruritic with IgM and C3 deposition in vessels; first described in 1910 by Afzelius.
Cardiovascular–myocarditis, pericarditis, transient atrioventricular block, ventricular dysfunction; neurologic—Bell’s palsy, meningoencephalitis, optic atrophy, polyneuritis symptoms.
Lyme disease may be accompanied by headache, stiff neck, fever and malaise that is subsequently manifest as migratory polyarthritis, intermittent oligoarthritis, chronic arthritis of the knees, chronic meningoencephalitis, cranial or peripheral neuropathy, migratory musculoskeletal pains or cardiac abnormalities.
Lyme borreliosisSee LYME DISEASE.
Patient discussion about Lyme borreliosis
Q. what is lyme disease my dog can't seem to get rid of it - anything other than antibiotics for treatment?
Q. lyme disease, how long do the effects last? How often do they come back? What helps?
Hope this helps.
Q. What to do for early Lyme that's not responding to treatment? I came down with Lyme disease three months ago with a bulls-eye rash. Even though it was supposedly a recent case, I already was having Bell's palsy, memory loss, trouble thinking of words, joint arthritis, severe bone pain, and fatigue. I took 100mg doxycycline 2x a day, as my doctor prescribed, for 3 weeks, but still felt bad, so I took it for 3 more weeks. When I stopped after 6 weeks, all my symptoms came back and I kept getting worse. I finally convinced my doctors to give me a refill, and I've been taking the same prescription since then. Any time when I'm late on a dose or eat something with magnesium, I get very sick again. I'm not getting better, I'm merely suppressing the Lyme disease, and it comes back whenever I stop the antibiotics. What can I do to actually get rid of it? Higher dose doxycycline? Another antibiotic? Two antibiotics at once? IV antibiotics? Supplements? (I'm biased against this, but) Rife machines?
I think it is just disseminated (I've been having Bell's palsy), so maybe I need 400mg doxy/day (200mg 2x a day) in order to reach the proper concentrations to inhibit B. burgdorferi in the CSF.