MM 337-342; ID 1327-1335
 

SYNONYM:     Lyme Arthritis
 

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:

Lyme disease is treatable with a variety of antibiotics; the most efficaceous are doxycycline, amoxicillin; ceftriaxone, cefuroxime, and clarithrimycin.
 

PREVENTION:

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.