Lyme Arthritis Presentation and Treatment

Lyme Arthritis is a feature of Lyme disease is caused by the spirochete Borrelia burgdorferi, a type of bacteria and is transmitted by the tick Ixodes dammini (deer tick) or a related tick.

Arthritis is the presenting manifestation in the majority of cases.

The infection is endemic in certain areas of North America. The disease characteristically develops in the summer and autumn-periods when the ticks are very active.

Recently, inflammatory arthritis after Lyme disease has been identified and is a distinct clinical entity than arthritis associated with Lyme disease. It needs to be identified as its treatment is more like autoimmune disorders.

Lyme disease is endemic in North America, Europe, and Asia. It is the most common vector-borne illness in the United States.

Lyme disease is reported primarily in whites, although it occurs in individuals of all races.

No strong preponderance of Lyme disease is noted in either sex.

Pathophysiology

B burgdorferi colonizes Ixodes ticks which is responsible for transmission to humans. Out of four stages of ticks [egg, larva, nymph, and adult], only three -larva, nymph, and adult require bloodmeal. Ticks can acquire B burgdorferi from feeding on an infected animal host during any of these three stages.

However, only the nymphal and adult stages can transmit B burgdorferi.

Nymphs are responsible for 90% of transmission.

The disease is spread to humans when there is a bite from an infected tick especially during the time of the year when nymphs are seeking blood which is usually summers.

The bloodmeal needs to trigger the Borrelia reproduction to reach a large enough number. Therefore nymphs must feed 36-48 hours and adults 48-72 hours to transmit B burgdorferi.

Pathogenesis of Lyme disease

Once the spirochete is in the skin it may either get destroyed by host or remain viable in skin [produces erythema migrans], or it may disseminate through the lymphatics or blood.

Preferred sites of lodging are the skin, heart, central nervous system, joints, and eyes but any part of the body can be affected.

Stage 1 is Primary disease or early localized infection and occurs within 30 days of the tick bite. It is characterized by erythema migrans [an expanding rash]) at the site of the tick bite 7-14 days after the tick is removed. Fever, chills, fatigue, headache, neck stiffness, muscle, and joint pains.

Stage 2 is early disseminated disease and occurs weeks to months after the bite. Muscle pains, joint pains and neural symptoms are most common.

Intermittent inflammatory arthritis begins as a migratory polyarticular and evolves over 1-2 days into a monoarticular arthritis.

Cranial neuropathy, meningitis and encephalopathy are main neural manifestations.

Diplopia secondary to a cranial neuropathy or Bell palsy may occur.

Skin manifestations may persist.

Stage 3 or chronic Lyme disease happens months to years after an infection involving musculoskeletal and neurologic systems are most commonly affected.

Lyme arthritis which is said to be the hallmark of stage 3 involves large joints mainly.

Knee is involved in 90% of cases.

Neurologic abnormalities of stage 3 Lyme disease occur both in the central and peripheral nervous system.

Usual manifestations are subacute encephalopathy, chronic progressive encephalomyelitis, and neuropathies

The symptoms of Lyme disease are probably due to B burgdorferi induced immune response.

Clinical Features

The early symptoms are generally mild and can be easily overlooked. An expanding rash 2-20 inches is usually the first to appear in 80-90% cases.

The rash generally begins at the site of the bite and may be solid red or central spot surrounded by a margin of clear skin and ringed by an expanding red rash (bull’s-eye rash). The rash appears about after 1 to 2 weeks and persists for about 3 to 5 weeks. Preferred places for tick bites are armpits, groin, posterior side knee and nape of neck. The rash usually stats at these places.

Multiple rashes may occur.

Mild joint pains, fever, chills etc might occur along with the rash for some time.

With the further spread, severe fatigue, neck pain, stiff neck, tingling or numbness in the extremities [peripheral nervous system involvement] or facial palsy (cranial nerves) can occur.

Weeks, months or even years later, potentially debilitating symptoms of late-stage disease show up.

These include severe headaches, painful arthritis, and swelling of joints, cardiac abnormalities, and cognitive disorders due to central nervous involvement.

The arthritis is pauciarticular, usually affecting one or a few large joints.

The knee is the most common site and is involved in over 90 percent of cases. Other joints that can be affected are the elbow, hip, ankle, shoulder, sternoclavicular, and interphalangeal.

Arthritis follows the skin rash or prodromal systemic symptoms usually within a few months (Range- One week to 12 months).

The synovitis manifests itself as joint swelling, increased local heat, joint tenderness, and pain on extremes of motion. When the knee, hip, or ankle is involved, the patient is able to bear weight and walk on the affected lower limb with an antalgic limp.

The typical pattern of synovitis is brief and intermittent. If untreated, however, it becomes chronic.

Other clinical features of Lyme disease are meningitis or neurologic disease in the form of nerve palsy such as Bell’s, and cardiac involvement, particularly conduction defect.

Fifty percent of untreated persons experience intermittent episodes of monarthritis or oligoarthritis involving the knee and/or other large joints. The symptoms wax and wane without treatment over months, and each year 10 to 20 percent of patients report a loss of joint symptoms.

Twenty percent of untreated persons develop a pattern of waxing and waning arthralgias. Ten percent of patients develop chronic inflammatory synovitis resulting in erosive lesions and destruction of the joint.

Diagnosis

Elevated titers of I&M and I&G antibodies against Ixodes dammini will establish the diagnosis of Lyme disease.

A nonspecific finding is the elevation of the erythrocyte sedimentation rate. In its initial stages, Lyme disease should be differentiated from the monarticular or pauciarticular form of juvenile rheumatoid arthritis.

This may be difficult but the following differences can help to delineate.

The attacks of Lyme arthritis are usually brief and self-limited, but that of juvenile rheumatoid arthritis is unremitting for at least six weeks.
Chronic iridocyclitis does not occur in Lyme arthritis.

It is advisable to carry out serologic tests to rule out Lyme disease when one is working on JRA.

For confirmation of Lyme disease The serological laboratory tests most widely available and employed are the Western blot and ELISA.

The sensitive ELISA test is performed first, and if it is positive or equivocal, then the more specific Western blot is run.

Polymerase chain reaction (PCR) tests for Lyme disease have also been developed to detect the genetic material (DNA) of the Lyme disease spirochete. PCR tests are susceptible to false-positive results from a poor laboratory technique

Pyogenic septic arthritis is another entity to be differentiated from Lyme disease.

In pyogenic arthritis, the affected joint is acutely painful, red, and hot, and the patient is unable to bear weight on the lower limbs if the knee or hip is involved. In septic arthritis, joint fluid cultures are positive in 70 percent of cases.

Synovial fluid analysis is ordinarily not of great assistance in differentiating the two because in both conditions the leukocyte count is elevated with neutrophilia. The erythrocyte sedimentation rate is elevated in both.

In case of doubt, arthritis should be treated as if septic while serologic tests for Lyme disease are sent which should be available within one to two weeks.

Treatment of Lyme Arthritis

Joint is given rest. Antibiotics are the primary treatment

Oral administration of doxycycline is widely recommended as the first choice [ contraindicated in children younger than eight years of age and women who are pregnant or breastfeeding]. Alternatives to doxycycline are amoxycillin, cefuroxime axetil, and azithromycin.

Intravenous administration of ceftriaxone is recommended as the first choice in disseminated cases.