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ETIOLOGICAL AGENT:
Borrelia burgdorferi, a unicellular, loosely coiled, left-handed helix. It is 30 um in length with seven turns of the coil. It is 0.18 um in diameter which allows it to pass through most bacteriological filters. It is Gram- and microaerophilic.
VECTOR:
Ixodes dammini, the deer tick
OVERVIEW:
Lyme disease is transmitted via the bite of a tick which injects a spirochete into the blood stream. It is manifested by recurrent bouts of arthritis or arthralgia associated with erythema chronicum migrans skin lesions.
PATHOLOGY:
The resulting pathology is due to two effects:
1. Immune complexes accumulate
in the joints. This attracts neutrophils which release a variety
of enzymes which attack the antigen - antibody complexes. These enzymes
also attack the
joint and erode bone and cartilage to cause arthritis-like symptoms.
2. The O-antigen (lipopolysaccharide)
of Borrelia stimulates macrophages to secrete
interleukin-1. Interleukin-1 stimulates the production of collagenase and
prostaglandin.
Collagenase degrades collagen, the primary component of the connective
tissue of joints;
the degradation leads to the pattern of erosion seen in severe cases of
Lyme disease.
Prostaglandins promote pain.
CLINICAL SYMPTOMS:
There are three stages of the disease:
1. Rash stage, Two to 30
days after an individual is bitten, the erythema chronicum migrans
rash occurs. It is a large bull's eye rash which expands radially from
the site of the tick bite
and is noticeably swollen at its center. This single lesion may be up to
50 centimeters in
diameter. Secondary skin lesions may occur at various sites on the body
but they lack the
swollen center of the primary lesion. The rash is frequently accompanied
by profound
fatigue, fever, chills, headache and backache.
2. Neurological stage. This
stage is marked by neurological complication and migratory
musculoskeletal pain. About 15% of patients will develop more severe complications
including meningitis, inflamed nerve roots in the neck and Bell's palsy,
a paralysis of the 7th
cranial nerve. At this stage some patients develop cardiac difficulties
lasting from three three
days to six weeks. These patients experience palpitations, dizziness or
shortness of breath
associated with irregular electrical impulses to the heart (atrioventricular
block).
3. Arthritis stage. Joint
problems characteristic of rheumatoid arthritis occur within several
months to two years after the rash. These recurrent attacks of arthritis
last a few days to a
few weeks and primarily affect the knees and other large joints. During
the third stage,
a small percentage of patients also suffer from somnolence, loss
of memory, mood
swings, and an inability to concentrate.
DIAGNOSIS:
This is mainly a disease of children in the 4-14 year old age range. Thus it is most frequently diagnosed as juvenile arthritis. The presumptive diagnosis of Lyme disease is based on recognition of the typical erythema chronicum migrans skin lesions and an association between neurologic, cardiac, and rheumatic abnormalities. Definitive diagnosis can be achieved with an enzyme-linked immunobinding assay for the qualitative simultaneous detection of IgG and IgM antibodies to Borrelia burgdorferi.
TREATMENT:
Penicillin V, 15mg/kg body weight per day, po, as four equal portions. Patients allergic to penicillin can be treated with tetracycline. Phenoxymethyl penicillin, Penicillin G, Amoxicillin or Doxycycline may also be useful.
There is a vaccine for the prevention of Lyme disease which is a recombinant outer surface protein A (rOspA) vaccine (LYME rix). The rOspA protein is expressed in Escherichia coli. It is given to people between 15-70 years old via intramuscular injections at one month after the first injection and 12 months after the first injection. It has a 76% efficacy rate after 3 doses.
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