How does Lyme disease present after a tick bite? - briefly
Within days to weeks after attachment, most patients develop an expanding erythema migrans rash often accompanied by fever, headache, fatigue, and muscle aches. Untreated infection can advance to neurologic, cardiac, or joint manifestations.
How does Lyme disease present after a tick bite? - in detail
A tick bite that transmits Borrelia burgdorferi initiates a predictable sequence of clinical signs. The first observable manifestation typically appears within three to thirty days and consists of an expanding erythematous skin lesion, often described as a “bull’s‑eye” rash. This lesion, known as erythema migrans, measures at least five centimeters in diameter, may be warm to the touch, and can be accompanied by mild fever, chills, headache, fatigue, myalgia, and arthralgia. Absence of the rash does not exclude infection; systemic symptoms alone may be the initial clue.
Within weeks to a few months, the infection can spread through the bloodstream, producing a disseminated phase. Common presentations at this stage include:
- Multiple erythema migrans lesions on distant body sites.
- Neurological involvement: facial nerve palsy (Bell’s palsy), meningitis with neck stiffness, headache, photophobia, and peripheral neuropathy.
- Cardiac involvement: atrioventricular conduction block, myocarditis, or pericarditis, often detected by new-onset heart rhythm abnormalities.
- Musculoskeletal pain: migratory joint aches without swelling.
If untreated, the disease may progress to a late stage, emerging months to years after the bite. Late manifestations are dominated by:
- Chronic arthritis, especially in large joints such as the knee, characterized by intermittent swelling, warmth, and limited motion.
- Persistent neuroborreliosis: encephalopathy, peripheral neuropathy, or radiculopathy, sometimes accompanied by cognitive deficits and sleep disturbances.
- Less common dermatologic signs: acrodermatitis chronica atrophicans, presenting as bluish‑gray skin atrophy on distal extremities.
Laboratory confirmation frequently relies on a two‑tiered serologic approach: an initial enzyme‑linked immunosorbent assay (ELISA) followed by a confirmatory Western blot. Polymerase chain reaction (PCR) testing may be employed for synovial fluid or cerebrospinal fluid when indicated.
Prompt antibiotic therapy, typically doxycycline for early disease and intravenous ceftriaxone for neurologic or cardiac involvement, reduces the risk of progression and mitigates long‑term sequelae. Early recognition of the characteristic rash, coupled with awareness of systemic signs, is essential for timely treatment.