F tularensis is endemic throughout the Northern Hemisphere, although prevalence varies by country. Three subtypes cause the majority of disease: Subspecies tularensis type A1 occurs primarily in the central United States; tularensis type A2 occurs in the western United States; and subspecies holarctica (type B) is dispersed throughout the Northern Hemisphere. Lagomorphs (rabbits and hares) and rodents are the primary reservoir (including squirrels in urban areas), although arthropods such as ticks and deer flies can harbor the bacterium. Transmission to humans occurs primarily by direct contact with a contaminated animal, a bite from an infected arthropod, or inhalation of aerosolized bacteria. Tularemia has six major clinical forms: ulceroglandular, glandular, oculoglandular, pharyngeal, pneumonic, and typhoidal. The first three present with regional lymphadenopathy from intradermal inoculation (with or without an ulcerative skin lesion) or inoculation of the eye (resulting in severe conjunctivitis). Pharyngeal tularemia occurs with ingestion of contaminated food or water, causing severe, ulcerative pharyngitis. Primary pneumonic tularemia is acquired by inhalation of organisms, although pneumonic disease can also be secondary to hematogenous spread with any form of the disease. Last, typhoidal tularemia is characterized by a nonspecific febrile illness not fitting the aforementioned forms of disease, although up to 45% of patients will have lung opacities. Characteristic parenchymal abnormalities include bilateral lower zone patchy opacities, denser lobar consolidation, or a diffuse miliary pattern. Despite its virulence, human-to-human transmission of F tularensis has not been observed, and no special patient isolation precautions are required.