Lyme borreliosis

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Related to Lyme borreliosis: Borrelia burgdorferi, Lyme neuroborreliosis


infection with spirochetes of the genus Borrelia.
Lyme borreliosis a general term encompassing several different diseases that are caused by Borrelia burgdorferi and have similar manifestations, including Lyme disease, acrodermatitis chronica atrophicans, and erythema chronicum migrans.
Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition. © 2003 by Saunders, an imprint of Elsevier, Inc. All rights reserved.

Lyme dis·ease

Avoid the incorrect phrase Lyme's disease.
A subacute inflammatory disorder caused by infection with Borrelia burgdorferi, a nonpyogenic spirochete transmitted by Ixodes scapularis, the deer tick, in the eastern U.S. and I. pacificus, the western black-legged tick, in the western U.S. The characteristic skin lesion, erythema chronicum migrans, is usually preceded or accompanied by fever, malaise, fatigue, headache, and stiff neck. Neurologic, cardiac, or articular manifestations may occur weeks to months later. Tick nymphs are thought to be responsible for about 90% of transmission to human beings. Nymphs and larvae feed especially on the white-footed mouse, Peromyscus leucopus, while the preferred host of adults is the white-tailed deer, Odocoileus virginianus. Infected reservoir animals and ticks do not become ill. Residual articular or neurologic symptoms, which may persist for months or years after the initial infection, presumably reflect an immune response to the organism. Variations in clinical features or severity from one patient to another may be due to inborn variations in immune response, perhaps linked to the human lymphocytic antigen (HLA) system.
Synonym(s): Lyme borreliosis
[Lyme, CT, where first observed]

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.

Farlex Partner Medical Dictionary © Farlex 2012

Lyme disease

An 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
Stage I
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.
Stage II
Cardiovascular–myocarditis, pericarditis, transient atrioventricular block, ventricular dysfunction; neurologic—Bell’s palsy, meningoencephalitis, optic atrophy, polyneuritis symptoms.
Stage III
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.
Segen's Medical Dictionary. © 2012 Farlex, Inc. All rights reserved.

Lyme borreliosis

Collins Dictionary of Medicine © Robert M. Youngson 2004, 2005

Lyme borreliosis

Another name for Lyme disease.
Mentioned in: Lyme Disease
Gale Encyclopedia of Medicine. Copyright 2008 The Gale Group, Inc. All rights reserved.

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?

A. Lyme disease is transmitted through the bite of a tick. Once the dog starts to be affected by the bacteria, Lyme Disease can progress from a mild discomfort to the stage where a dog will be in such joint and muscle pain it will refuse to move; it is not uncommon for an owner to have to carry a sick dog into the animal hospital. Over the span of two or three days a dog can progress from normal to completely unable to walk due to generalized joint pain. In addition to joint damage, the bacteria can affect the dog's heart muscle and nerve tissue. If the disease is diagnosed in time, treatment can cure the dog before permanent joint or nerve damage occurs. Certain antibiotics, such as the Tetracyclines, are very helpful in eliminating the disease. The earlier the antibiotic is started in the course of the disease, the better the patient's chances of a complete recovery.

Q. lyme disease, how long do the effects last? How often do they come back? What helps?

A. Lyme disease affects different areas of the body in varying degrees as it progresses. The site where the tick bites the body is where the bacteria enter through the skin. Initially, the disease affects the skin, causing an expanding reddish rash often associated with "flu-like" symptoms. Later, it can produce abnormalities in the joints, heart, and nervous system. Lyme disease is medically described in three phases as: (1) early localized disease with skin inflammation; (2) early disseminated disease with heart and nervous system involvement, including palsies and meningitis; and (3) late disease featuring motor and sensory nerve damage and brain inflammation and arthritis. It takes weeks to months after the initial redness of the skin for its effects to spread throughout the body. Lyme disease can be treated with antibiotics. Lyme disease can be prevented by using tick avoidance techniques.
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?

A. I did test positive for Lyme disease on the ELISA test.

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.

More discussions about Lyme borreliosis
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References in periodicals archive ?
Safety and immunogenicity of a novel multivalent OspA vaccine against Lyme borreliosis in healthy adults: A double-blind, randomised, dose-escalation phase 1/2 trial.
Conclusions: The risk of contracting Lyme borreliosis in Trabzon is high, and necessary measures need to be taken to avoid the spread of disease.
The expanding clinical spectrum of ocular lyme borreliosis. Ophthalmology.
Simultaneous human granulocytic ehrlichiosis and Lyme borreliosis. N Engl J Med 1997; 337: 27-30.
[26.] Wilske B., Fingerle V., Schulte-Spechtel U.: Microbiological and serological diagnosis of Lyme borreliosis. FEMS Immunol.
However, most of what is known about Lyme borreliosis is based upon human clinical studies, and experimental studies in laboratory rodents.
coli, Clostridium difficile infections, multi-drug resistant tuberculosis, Acinetobacter infections, infections due to NDM-1 (New Delhi metallo-beta-lactamase) producers, the Exserohilum rostratum incident, mucormycosis, Lyme borreliosis, Plasmodium knowlesi, measles, pertussis, and Buruli ulcer.
Lyme Borreliosis (LB) is a complex multisystemic infection that involves the skin, joints, nervous system, eyes, and heart, caused by spirochetes of the Borrelia burgdorferi (Bb) sensu lato complex, which are transmitted primarily by Ixodid ticks.
Recent evidence has shown that the presence or absence of chronic Lyme borreliosis may be objectively adjudicated by tissue examinations which demonstrate or which fail to show pathogenic microbes in patients who have received a full course of antibiotics [78].
Ruzicka, "Lyme borreliosis," The Lancet Infectious Diseases, vol.
Lyme borreliosis is a multiorgan disease transmitted by ticks of the genus Ixodes that carry the spirochete Borrelia burgdorferi [1].