Atlas of pathophysiology, 2 Edition

Part II - Disorders

Skin Disorders

Lyme disease

A multisystemic disorder, Lyme disease is caused by the spirochete Borrelia burgdorferi, which is carried by the minute tick Ixodes dammini (also known as I. scapularis) or another tick in the Ixodidae family. It commonly begins in the summer months with a papule that becomes red and warm but isn't painful. This classic skin lesion is called erythema migrans. Weeks or months later, cardiac or neurologic abnormalities sometimes develop, possibly followed by arthritis of the large joints.

Causes

B. burgdorferi

Pathophysiology

Lyme disease begins when a tick injects spirochete-laden saliva into the bloodstream or deposits fecal matter on the skin. After incubating for 3 to 32 days, the spirochetes migrate out to the skin, causing erythema migrans. Then they disseminate to other skin sites or organs by the bloodstream or lymph system. The spirochetes' life cycle isn't completely clear. They may survive for years in the joints, or they may trigger an inflammatory response in the host and then die.

Signs and symptoms

Prodrome

·   Malaise

·   Fatigue

·   Headache

·   Fever

·   Lethargy

·   Chills

·   Arthralgia

·   Myalgia

·   Anorexia

·   Sore throat

·   Nausea

·   Vomiting

·   Abdominal pain

·   Photophobia

Stage I

·   Initial red macule or papule that enlarges within days, forming an expanding annular lesion with a well-defined red border and central clearing (erythema migrans) with an average maximum diameter of 15 to 20 cm; center of lesion may become vesicular, indurated, or necrotic, or concentric rings may occur (when occurring on the face, neck, or scalp, only a linear streak may be noted)

·   Multiple tick bites producing multiple erythema migrans lesions

·   Erythema migrans lesions most commonly occurring in the proximal extremities, especially the axillae and groin

·   As erythema migrans lesion evolves, possible development of postinflammatory erythema or hyperpigmentation, alopecia, or desquamation

·   Additionally, a malar rash, diffuse urticaria, or subcutaneous nodules possible

Stage II

·   Low-grade fever in adults, high persistent fever in children; adenopathy

·   Neurologic involvement occurs in up to 20% of untreated cases—meningitis, encephalitic signs (poor concentration, memory, and sleep, or irritability), cranial neuritis, radiculoneuropathy, and myelitis

·   Cardiac involvement in up to 10% of untreated cases—atrioventricular block, myopericarditis, left ventricular dysfunction

·   Migratory pain in joints, bursae, tendons, bones, or muscles

Stage III

·   Fever and adenopathy

·   Arthritis

·   Chronic neurologic involvement

Diagnostic test results

·   Assays for anti–B. burgdorferi show evidence of previous or current infection.

·   Enzyme-linked immunosorbent technology or indirect immunofluorescence microscopy shows immunoglobulin (Ig) M levels that peak 3 to 6 weeks after infection; IgG antibodies detected several weeks after infection may continue to develop for several months and generally persist for years.

·   Positive Western blot assay shows serologic evidence of past or current infection with B. burgdorferi.

·   Lumbar puncture with analysis of cerebrospinal fluid reveals antibodies to B. burgdorferi.

Treatment

·   Antibiotics, such as doxycycline, tetracycline, cefuroxime, ceftriaxone, and penicillin

·   Anti-inflammatory medications such as ibuprofen

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LYME DISEASE ORGANISM AND LESION

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