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Tularemia
Last reviewed: 04.07.2025
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Tularemia (Latin: tularemia; plague-like disease, rabbit fever, minor plague, mouse disease, deer fly fever, epidemic lymphadenitis) is an acute zoonotic bacterial natural focal infectious disease with a variety of mechanisms of pathogen transmission.
Tularemia is a febrile disease caused by Francisella tularensis that resembles typhoid fever. Symptoms of tularemia include primary ulcerative lesions, regional lymphadenopathy, progressive symptoms of systemic disease, and, in some cases, atypical pneumonia. Diagnosis of tularemia is primarily based on epidemiological data and clinical presentation. Treatment of tularemia is with streptomycin, gentamicin, chloramphenicol, and doxycycline.
ICD-10 code
- A21.0. Ulceroglandular tularemia.
- A21.1. Oculoglandular tularemia.
- A21.2. Pulmonary tularemia.
- A21.3. Gastrointestinal tularemia.
- A21.8. Other forms of tularemia.
- A21.9. Tularemia, unspecified.
What causes tularemia?
Tularemia is caused by Francisella tularensis, a small, pleomorphic, nonmotile, nonspore-forming aerobic bacillus that can be acquired by ingestion, inoculation, inhalation, or contamination. Francisella tularensis can penetrate apparently intact skin, but actually enters through microlesions. Type A of the pathogen, which is highly virulent to humans, is found in rabbits and rodents. Type B of the pathogen usually causes a mild oculoglandular infection. This type is found in water and aquatic animals. Spread among animals is usually by ticks and cannibalism. Hunters, butchers, farmers, and wool handlers are most commonly infected. During the winter months, most cases are due to contact with infected wild rabbits (especially during skinning). During the summer months, infection is usually preceded by butchering infected animals or birds or by contact with infected ticks. Rarely, the disease may occur by eating undercooked infected meat, drinking contaminated water, or mowing fields in areas where the pathogen is endemic. In the western United States, alternative sources of infection include horse or moose flea bites and direct contact with hosts of these parasites. Human-to-human transmission has not been established. Laboratory workers are at high risk for infection, as the disease can be transmitted during normal handling of infected specimens. Tularemia is considered a possible agent of bioterrorism.
In cases of disseminated infection, characteristic necrotic lesions in various stages of evolution are found scattered throughout the body. These lesions can be from 1 mm to 8 cm in size, have a pale yellow color and are visually determined as primary lesions on the fingers, eyes and mouth. They can often be found in the lymph nodes, spleen, liver, kidneys and lungs. With the development of pneumonia, necrotic foci are found in the lungs. Although acute systemic intoxication can develop, toxins have not been identified in this disease.
What are the symptoms of tularemia?
Tularemia begins suddenly. It develops within 1-10 days (usually 2-4 days) after contact. Non-specific symptoms of tularemia occur: headache, chills, nausea, vomiting, fever of 39.5-40 C and acute prostration. Extreme weakness, repeated chills with profuse sweating appear. Within 24-48 hours, an inflammatory papule appears at the site of infection (finger, hand, eye, palate of the oral cavity). An inflammatory papule does not appear in the case of glandular and typhoid tularemia. The papule quickly becomes a pustule and ulcerates, resulting in the formation of a clean ulcerative crater with scanty, thin, colorless exudate. Ulcers are usually single on the hands and multiple on the eyes and in the mouth. Usually only one eye is affected. Regional lymph nodes enlarge and may become suppurated with abundant drainage. A typhoid-like condition develops by the 5th day of illness, and the patient may develop atypical pneumonia, sometimes accompanied by delirium. Although signs of consolidation are usually present, decreased breath sounds and occasional wheezes may be the only physical findings in tularemic pneumonia. A dry, nonproductive cough associated with a burning retrosternal pain develops. A nonspecific roseola-like rash may appear at any stage of the disease. Splenomegaly and perisplenitis may occur. If untreated, body temperature remains elevated for 3 to 4 weeks and gradually decreases. Mediastinitis, lung abscess, and meningitis are rare complications of tularemia.
With treatment, the mortality rate is almost 0. Without treatment, the mortality rate is 6%. Death in tularemia is usually the result of superimposed infection, pneumonia, meningitis, or peritonitis. In cases of inadequate treatment, relapses of the disease may occur.
Types of tularemia
- Ulceroglandular (87%) - Primary lesions are located on the hands and fingers.
- Typhoid (8%) - A systemic disease characterized by abdominal pain and fever.
- Oculoglandular (3%) - Inflammation of the lymph nodes on one side, most likely caused by inoculation of the pathogen into the eye, from infected fingers or a hand.
- Glandular (2%) - Regional lymphadenitis in the absence of a primary lesion. Often cervical adenopathy, suggesting oral infection.
Diagnosis of tularemia
The diagnosis of tularemia should be suspected in patients with a history of exposure to rabbits or wild rodents or tick bites. The acute onset of symptoms and the characteristic primary lesion are important considerations. Patients should have blood cultures and diagnostic specimens (eg, sputum, lesion fluid) and antibody titers obtained at 2-week intervals during the acute and convalescent periods. A 4-fold increase or a titer greater than 1/128 are diagnostic. Serum from patients with brucellosis may cross-react with Francisella tularensis antigens, but titers are usually much lower. Fluorescent antibody staining is used in some laboratories. Leukocytosis is common, but the white blood cell count may be normal, with only an increase in the proportion of polymorphonuclear neutrophils.
Because Francisella tularensis is highly infectious, specimens and culture media suspected of having tularemia should be examined with extreme caution and, if possible, should be performed in a class B or C laboratory.
[ How is tularemia treated?
Tularemia is treated with streptomycin 0.5 g intramuscularly every 12 hours (in case of bioterrorism - 1 g every 12 hours) until the temperature is normalized. Then 0.5 g once a day for 5 days. In children, the dose is 10-15 mg / kg intramuscularly every 12 hours for 10 days. Gentamicin at a dose of 1-2 mg / kg intramuscularly or intravenously 3 times a day is also effective. Chloramphenicol (there is no oral form in the US) or doxycycline 100 mg orally every 12 hours can be prescribed until the temperature is normalized, but relapses of the disease may occur with these drugs, and these drugs do not always prevent suppuration of the lymph nodes.
Moist saline dressings are good for treating primary skin lesions and can also relieve the severity of lymphangitis and lymphadenitis. Surgical drainage of large abscesses is rarely used in cases where antibiotic treatment of tularemia is delayed. In ocular tularemia, warm saline compresses and dark glasses can provide some relief. In acute cases, 2% homatropine 1-2 drops every 4 hours can relieve symptoms of tularemia. Severe headache usually responds to oral opioids (eg, oxycodone or hydroxycodone with acetaminophen).
How is tularemia prevented?
Tularemia is prevented by wearing tick-resistant clothing and insect repellents. A thorough inspection for ticks should be carried out after returning from endemic areas. Ticks should be removed promptly. Protective clothing such as rubber gloves and face masks should be used when handling rabbits and rodents, especially in endemic areas, as Francisella tularensis may be present in animal and tick feces and in animal fur. Wild poultry should be thoroughly cooked before consumption. Water that may be contaminated should be decontaminated before consumption. Vaccination against tularemia is used.
What is the prognosis for tularemia?
Tularemia has a favorable prognosis in common forms of the disease, but a serious prognosis in pulmonary and generalized forms. Mortality does not exceed 0.5-1% (according to American authors, 5-10%).
During the recovery period, prolonged subfebrile condition and asthenic syndrome are typical; residual phenomena (enlarged lymph nodes, changes in the lungs) may persist. In a number of patients, work capacity is restored slowly, which requires a medical and labor examination.