Diagnosis of tularemia

Step 1: History taking and clinical assessment

The onset of the disease is always acute: there is marked intoxication, chills, myalgia, and general weakness lasting from three to seven days. Against this background, regional lymphadenopathy develops — enlargement and moderate tenderness of the lymph nodes.

Special attention must be paid to the epidemiological history. The physician should specifically inquire about:

• History of staying in rural areas.
• Contact with animals (meat processing, skinning).
• Possible contact with contaminated environmental objects (hay, straw, fodder).
• Tick, horsefly, or mosquito bites (vector-borne transmission route), as well as occupational activities (hunting, agriculture).

In the ulceroglandular form, a primary affect develops at the site of the bite — a small ulcer 0.2–1.5 cm in size with elevated, thickened edges and scanty serous-hemorrhagic discharge. It is practically painless, lacks surrounding edema, and may go unnoticed by the patient. Patients often complain only that the ulcer does not heal for a long time.

The tularemic bubo enlarges gradually over 5–8 days, eventually reaching the size of a chicken egg. Initially, it has clear contours and is mildly painful, with poorly expressed perifocal inflammation. Without adequate antibiotic therapy at a later stage, suppuration occurs: the skin over the bubo acquires a purplish-bluish hue, and by the 3rd–4th week, it may spontaneously rupture with the discharge of thick, cream-like pus.

Step 2: Instrumental and laboratory diagnostics

During the peak period of the complete blood count (in approximately 40% of cases), there is leukopenia with a shift of the leukocyte formula to the left, lymphocytosis, monocytosis, eosinopenia, and an accelerated ESR. However, definitive confirmation requires specific tests.

1. Allergological diagnostics. Intradermal tularein skin test or leukocyte lysis test. Yields a positive result as early as days 3–5 of the illness.
2. Serological diagnostics (HAI, ELISA). Detection of specific antibodies begins on days 6–10 of the illness, with peak titer increases observed by weeks 4–6. A titer of 1:100 for HAI and 1:400 for ELISA is considered diagnostic.
3. Biological assay. Infection of white mice and guinea pigs with material from the patient. Considered the most sensitive method for pathogen detection, although not absolute.
4. Molecular genetic method (PCR). Detection of specific DNA in bubo aspirate or ulcer discharge.
5. Bacteriological method. Plays only an adjunctive role. Due to the extremely low concentration of the pathogen in human tissues, culture on nutrient media is rarely successful.

As an express diagnostic method, the direct immunofluorescence assay (DFA) of smears from the ulcer contents is also used.

Step 3: Differential diagnosis by clinical form

Due to the variety of clinical manifestations, tularemia is differentiated from a number of infectious and non-infectious diseases:

• Glandular form: staphylococcal and streptococcal lymphadenitis, cat-scratch disease, Hodgkin's lymphoma, mumps, and tuberculous lymphadenitis are ruled out.
• Oculoglandular / Anginoglandular form: differentiated from diphtheria, necrotizing tonsillitis (including Vincent's angina), and infectious mononucleosis. Key distinction: in tularemia, regional lymphadenitis progresses (without periadenitis), whereas the manifestations of tonsillitis simultaneously subside.
• Pulmonary form: has great clinical similarity to pulmonary tuberculosis. It is also differentiated from legionellosis and Q fever. Specific diagnostic methods and radiological findings are of decisive importance.
• Gastrointestinal form: distinguished from typhoid fever, abdominal yersiniosis, and tuberculous mesadenitis.
• Generalized form: requires the exclusion of acute brucellosis, typhoid-paratyphoid infections, and malaria.

Step 4: Formulation of diagnosis and therapy

When formulating the clinical diagnosis, it is necessary to indicate the form, severity degree, course duration, and presence of complications (e.g., relapsing course or secondary pneumonia). Important: antibiotic therapy is prescribed before receiving results of etiological confirmation, relying solely on the clinical and epidemiological picture.

The treatment course is at least 14 days. Drugs of choice include aminoglycosides (gentamicin, amikacin, streptomycin), tetracyclines (doxycycline), as well as rifampicin or chloramphenicol (especially indicated in meningitis).

Pathogenetic therapy includes detoxification with crystalloid and colloid solutions. Local treatment of ulceroglandular and glandular forms involves applying dressings with antibacterial ointments, physiotherapy (UV, UHF), and, in case of overt signs of fluctuation, surgical incision of the bubo.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Detailed antibiotic therapy regimens and drug dosage calculations
• Features of the premorbid background and immunodeficiency states worsening the prognosis
• Management tactics for severe forms: hemodynamic and respiratory support
• Surgical management and indications for incision of the tularemic bubo
• Anti-epidemic measures and hospitalization criteria

Other topics in the section "Zoonotic infections — 2024 study guide"

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