[5][9] Prevention is by using insect repellent, wearing long pants, rapidly removing ticks, and not disturbing dead animals.

[4] Depending on the site of infection, tularemia has six characteristic clinical variants: ulceroglandular (the most common type representing 75% of all forms), glandular, oropharyngeal, pneumonic, oculoglandular, and typhoidal.

[13] Tularemia is caused by the bacteria Francisella tularensis which is typically spread by ticks, deer flies, and contact with infected animals.

[15] Francisella tularensis can live both within and outside the cells of the animal it infects, meaning it is a facultative intracellular bacterium.

Mortality in untreated (before the antibiotic era) patients has been as high as 50% in the pneumoniac and typhoidal forms of the disease, which however account for less than 10% of cases.

[18] Rodents, rabbits, and hares often serve as reservoir hosts,[19] but waterborne infection accounts for 5–10% of all tularemia in the United States,[20] including from aquatic animals such as seals.

[22] In lymph node biopsies, the typical histopathologic pattern is characterized by geographic areas of necrosis with neutrophils and necrotizing granulomas.

[23] The laboratorial isolation of F. tularensis requires special media such as buffered charcoal yeast extract agar.

The microbiologist must be informed when tularemia is suspected not only to include the special media for appropriate isolation, but also to ensure that safety precautions are taken to avoid contamination of laboratory personnel.

[25] In the United States, although records show that tularemia was never particularly common, incidence rates continued to drop over the course of the 20th century.

Between 1990 and 2000, the rate dropped to less than 1 per one million, meaning the disease is extremely rare in the United States today.

[27] In Europe, tularemia is generally rare, though outbreaks with hundreds of cases occur every few years in neighboring Finland and Sweden.

From May to October 2000, an outbreak of tularemia in Martha's Vineyard, Massachusetts, resulted in one fatality, and brought the interest of the United States Centers for Disease Control and Prevention (CDC) as a potential investigative ground for aerosolised Francisella tularensis.

For a time, Martha's Vineyard was identified as the only place in the world where documented cases of tularemia resulted from lawn mowing.

[30] However, in May 2015[31] a resident of Lafayette, Colorado, died from aerosolised F. tularensis, which was also connected to lawn mowing, highlighting this new vector of risk.

[32] In 2004, three researchers at Boston Medical Center, in Massachusetts, were accidentally infected with F. tularensis, after apparently failing to follow safety procedures.

[33] In 2005, small amounts of F. tularensis were detected in the National Mall area of Washington, D.C., the morning after an antiwar demonstration on September 24, 2005.

[31] In the summer of 2015, a popular hiking area just north of Boulder was identified as a site of animal infection and signs were posted to warn hikers.

[46][47] In the United States, practical research into using rabbit fever as a biological warfare agent took place in 1954 at Pine Bluff Arsenal, Arkansas, an extension of the Fort Detrick program.

The aerobiological stability of UL was a major concern, being sensitive to sunlight, and losing virulence over time after release.

When the 425 strain was standardized as "agent JT" (an incapacitant rather than lethal agent), the Schu S4 strain's symbol was changed again to SR.[citation needed] Both wet and dry types of F. tularensis (identified by the codes TT and ZZ) were examined during the "Red Cloud" tests, which took place from November 1966 to February 1967 in the Tanana Valley, Alaska.

[50] Cats and dogs can acquire the disease from the bite of a tick or flea that has fed on an infected host, such as a rabbit or rodent.