Borrelia burgdorferi

Borrelia burgdorferi

Organism

A spirochete 0.2 to 0.5µm X 3-30µm that can be seen by Giemsa or Wright staining.
Microaerophilic (def).

Habitat

Found in infected ticks of the genus Ixodes, white-footed mice, and deer.

Source

The larval and nymph forms of the tick pick up the spirochete from its primary host, the white-footed mouse. Adult ticks infest the white-tailed deer.
Typically the larval form of the tick becomes infected by feeding on the mouse reservoir. As the larva molts to a nymph stage in late spring, humans can become an accidental host of the infected nymph. (The nymph stage of the tick is responsible for approximately 90% of the human Lyme disease reported.) The nymphs mature to adult ticks in late summer and the adult tick feeds on the white-tailed deer and sometimes humans.

Epidemiology

B. burgdorferi is the species that causes Lyme disease in in the U.S. and Europe.
In 1999, over 13,300 cases of Lyme disease were reported in the U.S.
Lyme disease is the most common vector-borne disease in the U.S.

Clinical Disease

After an incubation period of 3-30 days, a lesion beginning as a papule usually appears at the site of the tick bite and progressively enlarges to an area from 5cm to 50cm in diameter. The lesion, called erythema migrans, typically has a flat red border with a clearing in the center. Other early signs include fever, chills, malaise (def), severe fatigue, headache, myalagias (def), musculoskeletal pain, and lymphadenopathy (def). Early symptoms last around 4 weeks. During this time, however, the spirochetes penetrate into blood or lymph vessels and disseminate via the lymphatics and blood.
In around 80% of patients with untreated Lyme disease late manifestations appear. These can appear from within a week after initial infection to over 2 years later. The first phase of late infection, seen in 10%-15% of patients includes neurological symptoms such as encephalitis (def), meningitis (def), and peripheral nerve neoropathy (def) as well as cardiac dysfunctions such as heart block (def), myopericarditis (def), and congestive heart failure (def). The second phase is characterized by arthritis (def) and arthralgias (def) that can persist from months to years. This is the most common serious complication in untreated Lyme disease.

Pathogenicity

The spirochete appears to use outer membrane proteins to adhere to host cells. One tip of the spirochete attaches to the host cell and some form of invasin (def) apparently causes the host cell to release digestive enzymes that enable the spirochete with its corkscrewing motility to penetrate the host cell membrane. Once in the host cell the bacteria may remain dormant for years and hide from the immune system and antibiotics. Motility also helps B. burgdorferi to invade and leave blood vessels by passing between and through endothelial cells, thus enabling the spirochetes to dessiminate to other locations in the body.
Tissue destruction is mainly a result of the body's immune response to the spirochete.

Treatment

Treatment includes amoxicillin, tetracycline, cefuroxime, or ceftriaxone.* (see antibiotic table).

*Drugs may change with time.

For a more detailed article on Borrelia burgdorferi , see Lyme Disease , by John Meyerhoff, MD, Assistant Professor, Department of Internal Medicine, Johns Hopkins University School of Medicine.