How does a tick bite cause Lyme disease? - briefly
During feeding, an infected tick injects the bacterium Borrelia burgdorferi into the skin, where it enters the bloodstream and disseminates to tissues, initiating Lyme disease.
How does a tick bite cause Lyme disease? - in detail
A tick of the Ixodes genus attaches to the skin, inserts its hypostome, and creates a sealed feeding cavity. During the blood meal the arthropod secretes saliva that contains anticoagulants, anti‑inflammatory agents, and immunomodulatory proteins. These compounds suppress the host’s immediate defensive responses, allowing the parasite to remain attached for several days.
The bacterium Borrelia burgdorferi resides in the tick’s midgut. When the tick has been attached for roughly 36‑48 hours, the spirochetes migrate from the gut to the salivary glands. This movement is triggered by the tick’s prolonged feeding and the altered environment within its body. Once in the salivary glands, the bacteria are released into the host’s dermal tissue through the saliva.
Key steps in the infection process:
- Attachment and feeding – the tick secures itself with its mouthparts and begins ingesting blood.
- Salivary injection – saliva delivers anticoagulant and immune‑modulating factors, creating a microenvironment favorable to pathogen survival.
- Spirochete migration – B. burgdorferi moves to the salivary glands after the tick has fed for more than a day.
- Transmission – bacteria are introduced into the host’s skin alongside saliva.
- Local colonization – spirochetes proliferate at the bite site, often forming a characteristic erythema migrans lesion.
- Systemic dissemination – through the bloodstream and lymphatic system, the pathogen reaches joints, heart tissue, and the nervous system, leading to the clinical manifestations of Lyme disease.
The pathogen’s outer surface proteins (e.g., OspA, OspC) adapt to the changing environments of the tick and the mammalian host, facilitating adherence to host cells and evasion of immune detection. The initial immune response is often delayed because tick saliva interferes with complement activation and cytokine signaling, granting the spirochetes time to establish infection before adaptive immunity can respond effectively.
Early removal of the tick, preferably within 24 hours, markedly reduces the probability of bacterial transfer because the spirochetes have not yet migrated to the salivary glands. If removal occurs after the critical window, prophylactic antibiotic treatment is recommended to prevent disease progression.