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Lyme Disease
Dr. Peter Dobie
Introduction


Lyme disease was named in 1977 when arthritis was
observed in a cluster of children in and around
Lyme, CN



Conditions suggested that this was an infectious
disease probably transmitted by an arthropod



Further investigation revealed that Lyme disease is
caused by the bacterium
Causative Organism


Borrelia burgdorferi



Loosely coiled
spirochete



8-20 micrometers
Ticks that cause Lyme
disease

Lone Star Tick

Black-legged Tick

Rocky Mountain Tick
Three Stages of Disease


Localized rash – erythema chronicum migrans



Dissemination to multiple organ systems



Chronic disseminated stage often with arthritic
symptoms
Localized Rash
Dissemination


Signs of early disseminated infection usually occur
days to weeks after the appearance of a solitary
erythema migrans lesion



Neurologic – Bell’s Palsy



Musculoskeletal
manifestations
migratory joint and muscle pains



Late disseminated Lyme disease is intermittent
swelling and pain of one or a few joints.

may

include
Chronic Disseminated


Chronic arthritis



Chronic axonal polyneuropathy



Lyme
disease
morbidity
severe, chronic, and disabling.



Rarely, if ever, fatal

may

be
Diagnosis


Diagnosed clinically, confirmed serologically.



Often appropriate to treat patients with early
disease solely on the basis of objective signs and a
known exposure.



CDC recommends testing initially with a sensitive
first test, ELISA or an IFA test, followed by testing
with the more specific Western immunoblot (WB)
test to corroborate equivocal or positive results
obtained with the first test.
Serology


Patients with early disseminated or late-stage
disease usually have strong serological reactivity



Antibodies often persist for months or years
following successfully treated or untreated
infection.



Seroreactivity alone cannot be used as a marker of
active disease
Problems with Serology


IFA false positive may occur if patient has
syphilis, relapsing fever or RA.



IFA interpretation highly subjective



EIA lacks sensitivity in early disease.



EIA false positives with syphilis, other
treponemes, IM and autoimmune disease.
Western Blot


Must be used if the Lyme IgG/IgM antibody
serology is equivocal or positive



"Osp" refers to outer surface protein of the
bacteria.



"kDa" is the abbreviation for "kilodalton," which is
used for molecular weight designations.



Lyme antibodies of importance are against the
following molecular weights of the B. burgdorferi
antigens: 23-25 kDa (Osp C); 31 kDa (Osp A); 34
kDa (Osp B); 39 kDa; 41 kDa; and 83-93 kDa7.
Treatment


Single dose doxycycline shortly after
tick bite.



Lyme disease give doxycycline followed
by amoxacillin



Neuroborreliosis requires IV antibiotic
therapy.
Address: SUITE 3A, EDGECLIFF COURT, 2 NEW McLean
ST, EDGECLIFF, NSW 2027
Email: info@drpeterdobie.com
Telephone: 02 9362 0493
Fax: 02 9363 0767

Dr. Peter Dobie

Thank You

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Lyme Disease

  • 2. Introduction  Lyme disease was named in 1977 when arthritis was observed in a cluster of children in and around Lyme, CN  Conditions suggested that this was an infectious disease probably transmitted by an arthropod  Further investigation revealed that Lyme disease is caused by the bacterium
  • 3. Causative Organism  Borrelia burgdorferi  Loosely coiled spirochete  8-20 micrometers
  • 4. Ticks that cause Lyme disease Lone Star Tick Black-legged Tick Rocky Mountain Tick
  • 5. Three Stages of Disease  Localized rash – erythema chronicum migrans  Dissemination to multiple organ systems  Chronic disseminated stage often with arthritic symptoms
  • 7. Dissemination  Signs of early disseminated infection usually occur days to weeks after the appearance of a solitary erythema migrans lesion  Neurologic – Bell’s Palsy  Musculoskeletal manifestations migratory joint and muscle pains  Late disseminated Lyme disease is intermittent swelling and pain of one or a few joints. may include
  • 8. Chronic Disseminated  Chronic arthritis  Chronic axonal polyneuropathy  Lyme disease morbidity severe, chronic, and disabling.  Rarely, if ever, fatal may be
  • 9. Diagnosis  Diagnosed clinically, confirmed serologically.  Often appropriate to treat patients with early disease solely on the basis of objective signs and a known exposure.  CDC recommends testing initially with a sensitive first test, ELISA or an IFA test, followed by testing with the more specific Western immunoblot (WB) test to corroborate equivocal or positive results obtained with the first test.
  • 10. Serology  Patients with early disseminated or late-stage disease usually have strong serological reactivity  Antibodies often persist for months or years following successfully treated or untreated infection.  Seroreactivity alone cannot be used as a marker of active disease
  • 11. Problems with Serology  IFA false positive may occur if patient has syphilis, relapsing fever or RA.  IFA interpretation highly subjective  EIA lacks sensitivity in early disease.  EIA false positives with syphilis, other treponemes, IM and autoimmune disease.
  • 12. Western Blot  Must be used if the Lyme IgG/IgM antibody serology is equivocal or positive  "Osp" refers to outer surface protein of the bacteria.  "kDa" is the abbreviation for "kilodalton," which is used for molecular weight designations.  Lyme antibodies of importance are against the following molecular weights of the B. burgdorferi antigens: 23-25 kDa (Osp C); 31 kDa (Osp A); 34 kDa (Osp B); 39 kDa; 41 kDa; and 83-93 kDa7.
  • 13. Treatment  Single dose doxycycline shortly after tick bite.  Lyme disease give doxycycline followed by amoxacillin  Neuroborreliosis requires IV antibiotic therapy.
  • 14. Address: SUITE 3A, EDGECLIFF COURT, 2 NEW McLean ST, EDGECLIFF, NSW 2027 Email: info@drpeterdobie.com Telephone: 02 9362 0493 Fax: 02 9363 0767 Dr. Peter Dobie Thank You