|Cell Wall: Gram Negative||Shape: Spirochete|
- The natural reservoir of B. burgdorferi are rodents and transmission to humans occurs through blood meals of the Ixodes tick vector. Disease is observed throughout the world but mostly in temperate areas where Ixodes ticks are more common.
- Following initial inoculation into the skin by the Ixodes tick, B. burgdorferi disseminates lympho-hematogenously throughout the body. Like Syphilis, Lyme Disease progresses chronologically through three stages typified by a localized phase, disseminated phase, and a late phase. In notable contrast to Syphilis, Lyme Disease does not possess a significant latent phase.
- Localized Infection
- Localized infection manifests within 0.5-4 weeks after inoculation and appears as a characteristic skin lesion termed Erythema Migrans. Erythema Migrans appears as an erythamatous macule at the site of inoculation whose outer border slowly expands as a red ring. As the lesion grows, the central portion clears or becomes blue.
- Disseminated Phase
- Skin: Multiple, but smaller Erythema Migrans-like lesions over the entire body
- Meningitis: Is associated with a CSF pleocytosis composed largely of lymphocytes
- CNS: Neurological impairments, peripheral neuropathies, along with Bell's Palsy due to impairment of CN VII may occur
- Heart: Occurs in a small minority of patients and mostly manifests as heart block at the level of the AV Node but may include signs of myocarditis.
- Joints: Manifests as a migratory arthralgia
- Late phase
- Nearly half untreated patients that display the disseminated phase develop late phase symptomology
- Joints: Manifests as a intermittent, repeated attacks of arthritis especially of large joints such as the knee
- CNS: A small minority of patients may develop a subtle encephalopathy characterized by mild changes in memory and mood
- Doxycycline or Amoxicillin: Treatment can result in precipitation of a Jarisch-Herxheimer Reaction.