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Tularemia is a zoonotic infection caused by Francisella tularensis, a fastidious, small, non-motile Gram negative intracellular coccobacillus. F. tularensis can be found throughout North America in a variety of animal hosts; including lagomorphs (rabbits and hares), aquatic rodents (muskrats, beavers, and water voles), other rodents (water and wood rats and mice), squirrels, and cats. F. tularensis can survive for weeks in contaminated water, soil, and vegetation. Airborne infections result from inhalation of dust contaminated with rodent feces that is generated during agricultural or landscaping activities.


Most human infections result from cutaneous inoculations associated with tick bites or direct contact with infected animals. Ingestion of contaminated water or the inhalation of aerosolized bacteria can also cause disease. Today, human tularemia is relatively rare. Approximately 130 cases are reported annually in the United States, which is significantly less than the peak of 2300 cases that were reported in 1939.


F. tularensis is highly infectious; as few as 10 bacteria can cause human disease through cutaneous or respiratory routes. The pathogenicity of F. tularensis is related to its capacity to evade and suppress the innate immune system while it replicates intracellularly. High infectivity and the potential for airborne transmission pose serious hazards for medical laboratory technologists. The clinical laboratory should be notified whenever tularemia is suspected so that additional safety precautions can be taken.


Tularemia can cause a wide range of symptoms in humans, depending upon the route of inoculation. After an incubation period of 2 to 6 days, the illness typically begins with the sudden onset of fever, chills, headache, and myalgias. Headache may be the dominant symptom. Pulse–temperature dissociation, which is a pulse rate that is lower than expected for a given elevation in temperature, is often present. Other manifestations of tularemia reflect the portal of entry: skin ulcers, tender lymphadenopathy, conjunctivitis, exudative pharyngitis, and pneumonia. Pneumonic tularemia can result from direct inhalation of organisms or bacteremic spread from an extrapulmonary site of infection. Common radiographic findings include unilobar or multifocal opacities, pleural effusions, and hilar adenopathy. The differential diagnosis of pneumonic tularemia includes other causes of atypical pneumonia, such as psittacosis and Q fever.


The diagnosis of tularemia is most often confirmed serologically. An increase in antibody titers by a factor of 4 or more in serum samples obtained during the acute and convalescent phases of the disease (2 to 4 weeks apart) is diagnostic. A single high titer is suggestive of recent infection, but antibody responses do not appear until the second week of illness. Beyond the 10th day of illness, serologic evidence of tularemia can be detected in more than 90% of patients, with a specificity of more than 90%. F. tularensis can also be isolated from blood, respiratory samples, and tissue biopsy specimens, but it grows slowly on routine laboratory cultures. Recovery can be expedited with the use of cysteine-enriched media. Polymerase chain reaction can provide more rapid diagnosis, but is not widely available. 

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