Intraspecific classification
The causative agent belongs to the species Francisella tularensis. Within the species, four subspecies are distinguished, differing in geographical distribution, biochemical properties, and degree of virulence. Clinically, two of them are most significant:
- Subsp. tularensis (Nearctic subspecies): Circulates in North America. It is characterized by high aggressiveness—it causes severe forms of infection in humans and is lethal to rabbits. A characteristic biochemical feature is the ability to ferment glycerol.
- Subsp. holarctica (Halaerctic subspecies): Found in Europe and Asia. It is characterized by moderate virulence: the disease proceeds in a moderately severe form, and the microbe is not lethal to rabbits.
Morphology and cultural characteristics
The bacteria are small, non-motile, Gram-negative rods prone to forming a capsule and equipped with type IV pili. They do not form spores.
Microorganisms are extremely fastidious regarding cultivation conditions and are strict aerobes. They grow at 35–37 °C in an atmosphere with 5% CO₂ for 2–5 days. Growth requires complex nutrient media containing cysteine, hemin, and egg yolk, or the use of chicken embryo yolk sacs. They form small, milky-white colonies. The saccharolytic activity of the bacteria is weakly expressed, and proteolytic properties are completely absent.
Pathogenicity factors and mechanism of infection development
A key feature of Francisella tularensis is its ability to survive inside macrophages (incomplete phagocytosis). The bacterium blocks lysis within the phagolysosome, penetrates the host cell cytoplasm, and actively multiplies there. This process is facilitated by the capsule and lipopolysaccharide (LPS), which possess anti-phagocytic activity. At the same time, the endotoxin (LPS) itself has an anomalous structure and reduced toxicity compared to other Gram-negative microbes.
The incubation period lasts 3–7 days. Pathogenesis begins with the formation of a primary inflammatory lesion at the site of bacterial entry. Then, the causative agent reaches regional lymph nodes via the lymphatic route, causing their inflammation—a bubo is formed. The localization of lesions (bubonic, oculoglandular, ulceroglandular or generalized septic form) depends entirely on the portal of entry of the infection. Without etiotropic treatment, mortality reaches 60%.
Epidemiology
Tularemia is widely distributed globally. The natural reservoir consists of lagomorphs and rodents (especially water voles). Human infection occurs via several routes:
- Vector-borne: through the bites of infected mosquitoes, horseflies, and ticks.
- Contact: when the causative agent gets onto mucous membranes or damaged skin.
- Alimentary and waterborne: through food and water contaminated with rodent excreta.
- Aerosol: by inhaling infected aerosol or dust.
Due to its ability to spread via airborne dust, its minuscule infectious dose, and high virulence, the Nearctic subspecies of the bacterium is considered a potential biological weapon agent.
Principles of microbiological diagnostics
Direct inoculation of clinical material is rarely successful. The main method for isolating the culture is the biological test—infecting white mice or guinea pigs with material from the patient (bubo aspirate, blood) followed by isolating the bacteria from the animals' organs. Important: such studies are permitted only in specialized high-security laboratories (for working with dangerous infectious diseases).
In routine practice, the diagnosis is confirmed by serological methods (IFAT, ELISA, HIAT, agglutination test), taking into account possible cross-reactivity with Brucella antigens. Allergic diagnostics is also used—a skin test with tularin to assess the development of delayed-type hypersensitivity (DTH).
Briefly: answers to topical questions
What forms of tularemia are distinguished depending on the portal of entry of the infection?
Depending on the route of penetration and the portal of entry of the infection, several clinical forms of tularemia are distinguished. These include:
- Bubonic — includes ulceroglandular, oculoglandular, glandular, and abdominal forms.
- Generalized — also known as the septic form.
- Pulmonary — distinguished as an independent form of the disease.
The localization of internal organ lesions directly depends on how the microbe enters the body. In all the listed forms, the disease has an acute onset and is accompanied by a pronounced general toxic syndrome (chills, fever, headache, and muscle pain).
The clinical triad of tularemia is easy to remember using the rule of three "F"s: Fever, Lymphadenopathy (bubo development), and Focus (the form of the disease strictly depends on the site of microbial entry).
Class and exam questions
Can one contract tularemia from an infected person?
No. One of the most important epidemiological features of this infection is the complete absence of transmission from person to person.
Why F. tularensis is considered a potential biological weapon?
The bacterium is capable of entering the body via the aerosol route, possesses high virulence, and has an extremely low infectious dose (10–50 cells are sufficient for disease development).
How does the pathogen survive in the external environment?
The microbe exhibits pronounced psychrophilicity: at low temperatures and high humidity, the bacteria remain viable for 8–10 months. However, they are instantly killed by boiling and are sensitive to ultraviolet light.
Is there a vaccine against tularemia?
Yes, for specific prophylaxis according to epidemiological indications, a live vaccine is used, created by B.Ya. Elbert and N.A. Haysky based on the attenuated strain No. 15 of the subspecies holarctica.
What else to study on this topic
- Molecular mechanisms of incomplete phagocytosis during tularemia infection
- Differential diagnosis of cross-serological reactions between Francisella and Brucella
- Specifics of immunological changes and the formation of delayed-type hypersensitivity
- Features of antibiotic therapy: choosing between aminoglycosides, macrolides, and fluoroquinolones
- Safety rules and workflows for dangerous infectious diseases when isolating the pathogen culture
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