Borrellia burgdorferi - MegaMicro

Taxonomy: Bacteria, spirochete

Staining: Weakly stains Gram negative, not typically classified based on gram staining.

Morphology/structure: Slender and helical, with a double membrane and flexible cell wall. It is highly motile due to flagella structure contained within the periplasmic space; motility is key for virulence of this organism and allows it to be especially invasive. Contains variable surface proteins (i.e. OspA/OspC).

Pathology/Infection: B. burgdorfei live in midgut of unfed nymphal ticks. Bacteria become active during “blood meal” and switch gene expression from OspA (quiescent) to OspC (infectious). The active microbes then penetrate the midgut and gradually migrate to salivary glands where they are passed to the host (mouse/human) in saliva. Process takes approximately 48 to 72 hours.

Tick Life cycle: Enzootic; Hard tick (Ixodes scapularis) larvae feed on infected mice (Peromyscus leucopus reservoir) and mature to nymph stage. The disease carrying nymphs can feed on uninfected mice to create a new biological reservoir. Adult feeds and lives on Deer until replete female drops to ground and lays eggs. Humans and dogs are incidental or dead-end hosts.

Clinical Manifestations/Disease Patterns: Infection in Human causes Lyme disease. Lyme disease progression can be divided into the following stages –

Early disease: Erythema migrans (>80% cases) often with systemic symptoms (fever, headaches, myalgias, etc.)

Early disseminated disease: Skin (erythema migrans), musculoskeletal (esp. arthritis in children), neurologic (esp. aseptic meningitis and facial nerve palsy), and/or cardiac manifestations (conduction abnormalities) are possible.

Late disease: Recurrent arthritis of large joints (possibly autoimmune), peripheral neuropathies and/or encephalopathy is possible.

Epidemiology: Lyme disease is the most prevalent arthropod-borne disease in the US, with 30,000 new cases each year and an estimated 300,000 cases total per year. Cases arise mainly in the northeastern, mid-Atlantic, and upper mid-western US.

Diagnosis: Diagnosis is typically based on erythema migrans lesions because most patients are seronegative at presentation (false negative). Other forms of disease where erythema migrans lesions aren’t present require clinical manifestations and laboratory confirmation (ELISA + Western blot or C6 peptide test) to confirm diagnosis. Microbes can be recovered and cultured from lesions, but special expertise and growth medium are required for culture so this is rarely done clinically.