Download Lyme`s Disease

Unit 4
Part 2 Lyme Disease
Terry Kotrla, MS, MT(ASCP)BB
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
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Causative Organism
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Borrelia burgdorferi
Loosely coiled
spirochete
8-20 micrometers
Isolated from blood,
CSF, skin lesions and
joint fluid.
Vector
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Ixodes scapularis ticks are much smaller than common
dog and cattle ticks
Below adult female, adult male, nymph, and larva on a
centimeter scale.
Humans acquire disease from bite of nymphal or adult
tick.
Vector
Tick reservoir is the white footed mouse,
white tail deer and dusky footed wood rat.
 For infection to occur tick must remain
attached 24-48 hours.
 Peek feeding is late spring, early summer
and fall.
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Lyme Disease Symptoms
The Lyme disease bacterium can infect
several parts of the body, producing
different symptoms at different times.
 Not all patients with Lyme disease will
have all symptoms, and many of the
symptoms can occur with other diseases
as well.
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Three Stages of Disease
1.
2.
3.
Localized rash – erythema chronicum
migrans
Dissemination to multiple organ systems
Chronic disseminated stage often with
arthritic symptoms
Stage 1 Localized Rash
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First sign of infection usually a circular rash called erythema migrans or
EM.
Rash occurs in approximately 70-80% of infected persons.
Begins at the site of a tick bite after a delay of 3-30 days.
Distinctive feature of the rash is that it gradually expands over a period of
several days, reaching up to 12 inches (30 cm) across.
Center of the rash may clear as it enlarges, resulting in a bull's-eye
appearance.
May be warm but is not usually painful.
Some patients develop additional EM lesions in other areas of the body
after several days.
Patients also experience symptoms of fatigue, chills, fever, headache, and
muscle and joint aches, and swollen lymph nodes. In some cases, these
may be the only symptoms of infection.
Localized Rash
Stage 2 Dissemination
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Untreated, the infection may spread to other parts of the
body within a few days to weeks after appearance of
rash, producing an array of discrete symptoms.
Neurologic
 Bell’s Palsy-loss of muscle tone on one or both sides
of the face.
 Severe headaches and neck stiffness
Musculoskeletal manifestations may include migratory
joint, bone and muscle pains.
Late disseminated Lyme disease is intermittent swelling
and pain of one or a few joints.
Cardiac include carditis and arrhythmia.
Symptoms usually resolve without treatment.
Stage 3 Chronic Disseminated
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After several months 60% will develop chronic
arthritis, severe joint pain and swelling.
5% of untreated develop neurological
symtpoms.
 Shooting
pains, numbness or tingling in the hands or
feet.
 problems with concentration and short term memory.
Prognosis
Lyme disease morbidity may be severe,
chronic, and disabling.
 Rarely, if ever, fatal
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Diagnosis
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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 test first, 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.
Diagnosis
Serological tests are often falsely negative
during early weeks.
 Antibodies to antigens of B. burgdorferi
can be detected by IFA, ELISA and
Western Blot.
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Immune Response
IgM antibodies develop against flagellar
antigens.
 Antibody production peaks between 3 and
4th weeks of infection.
 IgG lags, not detectable until 4 to 6 weeks
after erythema migrans.
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Serology
Patients with early disseminated or latestage 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.
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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.
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Western Blot
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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.
Lane 1, monoclonal antibodies defining selected antigens to B. burgdorferi Lane 2,
human serum (IgG) reactive with the 10 antigens scored in the currently recommended
criteria for blot scoring; lines indicate other calibrating antibodies. Molecular masses are
in kilodaltons.
Treatment
Single dose doxycycline shortly after tick
bite.
 Lyme disease give doxycycline followed by
amoxacillin
 Neuroborreliosis requires IV antibiotic
therapy.
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Reference
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http://www.cdc.gov/ncidod/dvbid/lyme/index.htm