lyme disease lyme borreliosis is caused by the tick-borne spirochete borrelia burgdorferi

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  • Lyme disease Lyme borreliosisis caused by the tick-borne spirochete Borrelia burgdorferi

  • Lyme disease

    B. burgdorferi is transmitted by ticks of the Ixodes ricinus complex including:Ixodes scapularis in north-east and north-central USA, Ixodes pacificus on the west coast of the USA,Ixodes ricinus in Europe, Ixodes persulcatus in Asia

  • Lyme diseaseAlthough cases have occurred at all ages, individuals who are active outdoors in spring and summer months are at greatest risk

  • Lyme disease-DEFINITION

    A systemic, tick-borne disease with manifestations: dermatologic, rheumatologic, neurologic, cardiac abnormalities.

  • Lyme diseaseThe initial skin lesion, erythema migrans, is the best clinical marker (occurs in 6080% of patients)

  • Lyme disease-EM

  • Lyme diseaseThe illness usually begins in summer with a characteristic expanding skin lesion, called erythema migrans (EM), that occurs at the site of the tick bite. Within several days to weeks the spirochete may spread to many other sites, particularly to other skin sites, the nervous system, the heart, or the joints.

  • EMThe interval between tick bite and appearance of EM varies from a few days to a month (median 7 days). The lesion begins as an erythematous papule and expands over several days to achieve a median diameter of 15cm; favored sites are the groin, buttock, popliteal fossa and axillaA solitary lesion must measure at least 5cm;

  • EMThe lesions of EM are generally annular with a sharply demarcated outer border and an erythematous or bluish hue

  • Erythema migrans (EM)Skin lesion typically begining as a red macute/papule and expanding over days or weeks to form a large round lesion, often with partial central clearing The expanding EM lesion is accompanied by other acute symptoms, particularly fatigue, fever, headache, mildly stiff neck, arthralgias and myalgias.

  • Lyme disease- definition

    1. Erythema migrans present or2. At least one late manifestation and laboratory confirmation of infection

  • Laboratory confirmation

    Isolation of the spirochete from tissue or body fluid Detection of diagnostic levels of IgM or IgG antibodies to the spirochete in the serum or the CSF

  • Lyme diseaseThe antibody response to B. burgdorferi develops slowly. The specific IgM response peaks between the third and the sixth week of infection. Generally IgM antibody falls to the normal range by 6 months, but occasionally it may remain elevated for much longerThe specific IgG response develops gradually over months.

  • Erythema migrans (EM)

  • Early disseminated disease

    Within several days of the appearance of EM, many patients develop evidence of dissemination of their infection by the appearance of prominent systemic symptoms, the occurrence of multiple secondary skin lesions, or both. Malaise, fatigue, lethargy, headache, fever and chills, arthralgia and myalgia are particularly common, each occurring in one-half or more of patients.

  • Early disseminated disease

    Secondary skin lesions may occur anywhere on the body and resemble primary lesions but are usually smaller, show less expansion with time and lack indurated centers

  • Disseminated disease

    After resolution of the signs and symptoms of early disease, some patients (20% in one series) experience a long-lasting spontaneous remission.

    Most, however, subsequently develop other disease manifestations, with predominant involvement of the heart, nervous system and joints.

  • Early Disseminated diseaseNeurologic manifestations cranial neuropathy (particularly Bell's palsy), meningitis, radiculoneuropathy, myelopathyencephalopathy Neurologic symptoms generally began a few weeks after EM (median 4 weeks), although some patients presented with neurologic manifestations alone..

  • Early manifestations Cardiovascular system

    high-grade (2nd or 3rd degree) antrioventricular conduction or bundle-branch block defects generally resolves spontaneously in a few weeks or sooner, even in untreated patients.


  • Early Disseminated diseaseArthritis

    Most people who have untreated Lyme disease develop arthritis.

    Arthritis occurs in 60% of patients in the USA, at a median of 6 months after EM as disseminated disease.

  • Early Disseminated disease-Arthritismonoarticular or oligoarticular inflammatory arthritis involving large joints, particularly the knee

  • Late Lyme disease

    Late Lyme disease reserved for those patients who have symptoms that persist for longer than 1 year, generally involves persistent inflammation in the CNS, joints or skin (ACA).

  • Late (persistent) diseaseLate neurologic syndromes

    lymphocytic meningitis, peripheral neuropathy cranial neuritis, known as Garin-Bujadoux-Bannwarth (MPN-GBB) or Bannwarth's syndrome

  • Late (persistent) diseaseChronic arthritis

    Arthritis becomes chronic in 20% of patients who have untreated Lyme disease, resulting in a syndrome that is clinically indistinguishable from other forms of monoarticular or oligoarticular inflammatory arthritis. The knee is by far the most commonly affected joint.

  • Late (persistent) diseaseChronic arthritis

    Even chronic Lyme arthritis may eventually remit spontaneously. Only a minority of patients develop radiographic evidence of erosions of cartilage or bone.

  • Late (persistent) diseaseChronic skin involvement

    Chronic skin involvement (acrodermatitis chronica atrophicans) as a late manifestation of Lyme disease occurs primarily in Europe.It usually occurs on the acral portion of an extremity and is characterized by violaceous discoloration and swelling of involved skin, often at a site where EM occurred years earlier.

  • Late (persistent) diseaseChronic skin involvement

    Other clinical manifestations include: fibrotic nodules, ulnar bands, sensory disturbances, muscular weakness, myalgias, arthalgias . lichen sclerosis and atrophicus or morphea-like lesions

  • Late manifestations Nervous system

    Lymphocytic meningitis, Cranial neuritis, particularly facial palsy (may be bilateral), Radiculoneuropathy Encephalomyelitis (must be confirmed by evidence of antibody production against Borrelia burgdorferi in CSF, shown by a higher titer of antibody in the CSF than in serum)

  • Late disseminated disease-Carditis

    - congestive heart failure- dilated cardiomyopathy

  • Diagnosis Detection of a specific immune response to B. burgdorferi remains the best means of confirming the diagnosis of Lyme disease.

  • DiagnosisBoth immunofluorescence (IFA) and ELISA have been used to detect this antibody responseSerology results may be falsely positive or negative for various reasons, so the diagnosis of Lyme disease cannot be made by serologic test results alone. Immunofluorescence and ELISA may yield false-positive results because of epitopes in the test antigen preparations that cross-react with other bacteria.

  • DiagnosisSpecificity is increased by a two-step approach in which all positive ELISA results are confirmed by Western immunoblotting-to detect specific proteins in samples.

  • WESTERN BLOT CRITERIAAn IgM blot is considered positive if two of the following three bands are present: 24kDa (OspC), 39kDa (BmpA) and 41kDa (Fla)An IgG blot is considered positive if five of the following 10 bands are present: 18, 21 (OspC), 28, 30, 39 (BmpA), 41 (Fla), 45, 58, 66 and 93kDa


    When Western immunoblot is used in the first 4 weeks of illness, both IgM and IgG procedures should be performed.After the first 4 weeks of illness, IgG alone should be performed.

  • WESTERN BLOT CRITERIAMeasurement of immunoreactivity in CSF is a useful adjunct in the diagnosis of CNS Lyme disease.To have diagnostic value, a CSF index should be calculated comparing the ratios of specific antibody to total immunoglobulin in CSF and serum

  • Early disseminated disease treatment

    If antibiotic therapy is initiated early in the course of Lyme disease, EM typically resolves promptly and later stage disease is prevented

  • Early disseminated disease treatment

    Early localized limited to a single skin lesion and early disseminated disease infection with mild or no systemic symptoms: -amoxicillin (500mg q8h), -doxycycline (100mg q12h) - cefuroxime axetil (500mg q12h) for 23 weeks.

  • Early disseminated disease treatment

    Doxycycline, 100mg po, q12h for 21 days, orAmoxicillin (with or without probenecid) 500mg, q8h for 21 days, orErythromycin, 250500mg po, q6h for 21 days, orAzithromycin 500mg daily for 7 days, orCefuroxime axetil, 500mg po, q12h for 21 days

    Erythromycin and azithromycin are less effective than other choices

  • Lyme arthritistratment

    Initial treatment: Doxycyline, 100mg po, q12h for 30 days, or Amoxicillin and probenecid, 500mg each po, q6h for 30 daysIf initial treatment fails: Penicillin G, 20 106 IU iv, daily in divided doses for 14 days, or Ceftriaxone sodium, 2g iv, daily for 14 days

  • Neurologic manifestationstreatment

    For facial nerve paralysis alone: Doxycycline, 100mg po, q12h for 2130 days, or Amoxicillin, 500mg po, q8h for 2130 days

  • Lyme encephalimeningitis, radiculopathy-treatment Ceftriaxone, 2g iv, daily for 30 days, or Penicillin G, 20 106 IU iv, daily in divided doses for 30 daysPossible alternatives: Cefotaxime sodium, 2g iv, q8h for 30 days, or Doxycycline, 100mg po, q12h for 1430 days, or C

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