Report all suspected cases of tularemia immediately to Public Health - Seattle & King County by calling 206-296-4774.

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	Epidemiology
	Microbiology
	Clinical presentation
	Diagnosis
	Infection control
	Treatment
	Prophylaxis
	Web resources

• The natural reservoirs for Francisella tularensis, the causative agent of tularemia, are small and medium-sized mammals, including rabbits, hares, squirrels, and rodents.
• Humans, other mammalian species (e.g., cats, dogs, cattle), and some species of birds, fish, and amphibians are incidental hosts.
• Infection results from:
  • the bite of infective arthropod vectors (e.g., tick, mosquitoes, biting flies).
  • handling infectious animal tissues or fluids.
  • direct contact with or ingestion of contaminated water, food, or soil.
  • inhalation of infectious aerosols.
• The infectious dose is low: Inhalation of 10 to 50 organisms can produce disease.
• Disease occurs naturally in the south-central and western United States and northern and central Europe.
  • Most infections occur in rural areas during the summer.
  • Cases in the winter can occur in hunters, trappers, and butchers.
• There is no known person-to-person transmission.

Tularemia and Bioterrorism

• Aerosolization is thought to be the most likely mode of dissemination of F. tularensis in a biological attack.
• Pneumonic, oculoglandular, glandular, ulceroglandular and oropharyngeal tularemia are possible clinical presentations.

• F. tularensis is a small, non-motile, non-spore-forming, pleomorphic, aerobic, gram-negative coccobacillus.
• There are two major subspecies or biovars:
  • Type A, responsible for most cases in North America, is highly infectious and virulent.
  • Type B, prevalent in Europe and Asia, causes milder disease.
• F. tularensis is resistant to freezing temperatures but sensitive to heat and disinfectants.

• The incubation period is two to 10 days (range, one to 14 days).
• Non-specific, constitutional symptoms can occur with any form of tularemia: fever, chills, malaise, fatigue, myalgia, arthralgia, headache, sore throat.
• Case-fatality rate is less than 5% with treatment.

Ulceroglandular Tularemia:

• Is the most common naturally occurring form (75-85% of cases) of tularemia.
• A tender erythematous papule develops at the site of inoculation before, or concurrent with, constitutional symptoms.
• The papule enlarges over 48 hours to 1-2 cm, becoming a tender, indurated, vesiculated lesion that subsequently ulcerates and may or may not develop an eschar.
• Tender regional lymphadenopathy accompanies the lesion.
• Other skin lesions (e.g., erythema nodosum, maculopapular rash, urticaria) may also be noted.

Glandular Tularemia:

• Presents the same as ulceroglandular but without an ulcer.

Pneumonic Tularemia:

• Can be primary due to inhalation of infectious particles or secondary to hemotogenous spread.
• Characterized by an abrupt onset of constitutional and respiratory symptoms, including a non- to slightly productive cough, pleural chest pain, and dyspnea.
• Nausea, vomiting, and diarrhea may occur.
• Illness may be rapidly progressive and severe or may be indolent with progressive weakness and weight loss over several weeks to months.
• Lung abscesses, empyema, fibrosis, granulomatous pleuritis, ARDS, sepsis, meningitis, and pericarditis are possible complications.

Oculoglandular Tularemia:

• After direct contamination of the eye, superficial ulceration of the conjunctiva may develop along with granulomatous nodules over time.
  
• Chemosis, vasculitis, and regional lymphadenitis can occur.
• Organisms spread from the conjunctiva to the preauricular, submandibular, or cervical lymph nodes where focal necrosis may occur.

Oropharyngeal Tularemia:

• In addition to constitutional symptoms, presenting features include exudative pharyngitis or tonsillitis, ulceration of the pharynx, tonsils, or soft palate, or stomatitis.
• A pharyngeal membrane suggestive of diphtheria may develop, but unlike diphtheria, the membrane does not bleed when removed.
• Cervical or retropharyngeal adenopathy may develop.

Typhoidal Tularemia:

• Presents as a febrile systemic illness without anatomic localization of infection.
• Constitutional symptoms, watery, non-bloody diarrhea, vomiting, and abdominal pain may be prominent.
• Sepsis, rhabdomyolysis, renal failure, secondary pneumonia, and involvment of other organs via hematogenous spread are potential complications.

• Diagnostic tests include Gram stain, immunohistochemical stain, and culture of secretions, exudates, biopsy specimens, or blood.
• Rapid diagnostic tests include direct fluorescent antibody stain, PCR, and antigen detection, and are performed by designated public health labs.
• The lab should be notified at the time of specimen submission that tularemia is suspected.
• Chest radiograph findings in pneumonic tularemia may be minimal early in disease, progressing to peribronchial infiltrates, pleural effusions, hilar lymphadenopathy, and bronchopneumonia; cavitations and cardiomegaly may also develop.
• White blood cells, hepatic enzymes, and bilirubin may be elevated.

• Person-to-person transmission has not been documented; standard precautions are adequate.

• Streptomycin and gentamicin are considered the first-line therapies and should be given for 10 days.
• Refer to www.bt.cdc.gov for current treatment and prophylaxis guidelines

• In the setting of a biological attack, antibiotic prophylaxis with ciprofloxacin or doxycycline may be recommeded for those with a suspected or known exposure to F. tularensis, as determined by public health officials, for 14 days post-exposure.

• Centers for Disease Control and Prevention
  
  
• Infectious Disease Society of America
  
  
• Center for Biosecurity of UPMC
  
  
• Bioterrorism preparedness training modules
  
  
• Washington State Department of Health