General information:

Agent: Borrelia burgdorferi.
Size of pathogen: 10-30 mm long, 0.2-0.3 mm wide..
Geographic distribution: World wide distribution. Most common in the northest in the USA.
Port of entry: Tick bite by Ixodes dammini in the USA and Ixodes ricinus in Europe. Deer, sheep, and cattles are the common natural hosts for ixodid ticks. Symptoms usually begin in late spring or summer.
Congenital infection: Unknown, probably not.
Number of stages: Triphasic

Clinical stages: Head

Early localized:

Illness begins most often 3 days to 1 months after a tick bite.
Manifestations: include erythema migrans, regional lymphoadenopathy, mild systemic symptoms.

Early disseminated:

Illness begins days to a week after infection. This phase is characterized by systemic dissemination to secondary skin sites, the heart, muscle, bone and joints, reticuloendothelial system, eye. Nervous system is involved in about 15% of cases.
Systemic manifestations: multiple secondary erythema migrans, severe systemic symptoms, generalized adenopathy, lymphocytoma, migratory musculoskeletal pain, and acute arthritis, carditis.
PNS: cranial neuritis, radiculitis, plexitis, mononeuritis, Guillain-Barré syndrome.
CNS: lymphocytic meningitis, encephalitis, and myelitis.

Late phase:

This phase can occur several years later.
Systemic manifestations: Acrodermatitis chronica atrophicans, chronic arthritis.
PNS: Axonopathy, neuropathy of acrodermatitis chronica atrophicans.
CNS: Progressive encephalomyelitis, encephalopathy, latent CNS borreliosis.

CSF:

Lymphomonocytic pleocytosis of 30-150 x 10⁶ cells/L. Together with the adenopathy, these findings can suggest a hematologic malignancy.
Rise in protein level and a normal or slightly lowered glucose concentration. IgM levels are particularly useful for diagnosis.

Pathology: Head

Unclear, periventricular demyelination was found on MRI scans in patients with the late phase of the disease.