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Tularemia advisories and resources for King County health care providers

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

Epidemiology

  • 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.

Microbiology

  • 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.

Clinical presentation

  • 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.

Diagnosis

  • 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.

Infection control

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

Treatment

  • 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

Prophylaxis

  • 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.

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