Approach

Diagnosis requires a high index of suspicion as the clinical presentation (except for ulceroglandular disease) is relatively non-specific and the disease itself is rare. Culture, polymerase chain reaction (PCR), and serological testing are all helpful in making a laboratory diagnosis. Tularaemia is a reportable disease in some countries.

Clinical presentation

Tularaemia is most common in children, although it can occur in all ages.[13]​ It is more common in spring and summer, as it is often a tick-borne disease, and this is when tick exposure is at its peak.[1]​ Infection occurs predominantly in the northern hemisphere.

Patients may present with a history of tick bite, fly bite, or direct contact with infected animals or animal skins. A history of working outdoors or lawn mowing in areas where infected animals live may also be noted.[17]

Clinical presentation depends on many factors including the subspecies of Francisella tularensis and the route of inoculation.[1]​​ All forms of tularaemia are accompanied by systemic symptoms, including chills, headache, malaise/fatigue, myalgia, anorexia, abdominal pain, and vomiting. Fever, with a pulse-temperature deficit, is seen in one half of cases, remitting only after several days, and with a high chance of relapse.[1]​​​​

Additional, more specific signs and symptoms will also be seen, depending on the type of tularaemia.[1]​​

Ulceroglandular tularaemia:

  • The most common presentation, usually reported after handling animals, or after an animal or tick bite

  • Presents with unilateral and localised tender lymphadenopathy

  • A painful ulcer where the organism was inoculated (by a tick or fly bite, or by direct contact with an infected animal) is found distal to the draining lymph nodes that are enlarged, and starts as a painful papule before ulcerating.[2]​​[3]​​[4]​​[5]​​[6]​​

Glandular tularaemia:

  • As for ulceroglandular tularaemia, except without a visible skin lesion

  • Is thought to spread via the bloodstream and lymphatic system.

Pneumonic tularaemia:

  • Spreads by airborne route

  • Presents with non-productive cough, dyspnoea, chest tightness, rales on auscultation, and pleurisy.[4]​​[7]​​[8]​​[9]​​[10]​​[11]​​

Pharyngeal tularaemia:

  • Can occur after ingestion of contaminated meat or water

  • Presents with sore throat and exudative pharyngitis or tonsillitis

  • May be accompanied by regional lymphadenopathy.

Oculoglandular tularaemia:

  • Unilateral conjunctivitis secondary to direct inoculation into the eye (e.g., from a contaminated finger)

  • Often accompanied by photophobia, vision impairment/loss, and sub-mandibular, cervical, or pre-auricular lymphadenopathy.

Typhoidal tularaemia:

  • Possibly due to septic spread of organism

  • Without skin lesions or lymphadenopathy but with diarrhoea

  • Can be accompanied by jaundice and cholestasis, and with hepatosplenomegaly in chronic presentations.

Tularaemic meningitis or brain abscess:

  • Rare presentation of tularaemia, with symptoms of acute headache, stiff neck, and Kernig's and Brudzinski's signs.[9]​​[12]

Laboratory investigations

FBC, electrolytes, LFTs, and blood culture should be evaluated in patients with suspected tularaemia. Hyponatraemia, leukocytosis, thrombocytopenia, elevated LFTs, elevated creatine kinase, myoglobinuria, and elevated erythrocyte sedimentation rate may be suggestive of tularaemia; however, the absence of any of these does not exclude the diagnosis.[16]

Serological testing using enzyme immunoassay (EIA) or immunofluorescence assay (IFA) is diagnostic for tularaemia. The clinical microbiology laboratory should be notified if tularaemia is suspected, so that proper precautions can be taken. A 4-fold rise in titre of antibodies against Francisella tularensis between acute and convalescence serums is considered diagnostic. This diagnostic increase in antibody titre usually occurs 2 to 3 weeks after onset of symptoms.[16]​ A single elevated serum antibody titre is supportive of the diagnosis; however, a single antibody titre should be confirmed by serologic tests or isolation of the organism from a clinical specimen.​[20]

Blood culture, specimen cultures, and PCR for F tularensis should be ordered on clinical presentation. Culture is optimal for diagnosis, but can be challenging as F tularensis is slow growing.[16]​ Although modern blood cultures (non-radiometric) detect bacteria, this is an insensitive test, as bacteraemia is only transient.[1]​ PCR on swab of ulcer or lymph node aspirate seems to be a more sensitive test, although experience in its use is limited.[1]​​F tularensis may also be cultured from clinical specimens (e.g., lymph node aspirate, ulcer scraping, pharyngeal swab, or respiratory specimens, depending on the type of illness) using special media.[16]​ Culture must be performed under biosafety level 3 conditions because of infection risk to laboratory personnel.

Chest x-ray is ordered in suspected cases of pneumonic tularaemia (indicated by respiratory signs and symptoms) and can show lobar or sub-segmental infiltrates or exudative pleural effusions.[4]​​[7]​​[8]​​[9]​​[10]​​[11] Infiltrates may be present in typhoidal tularaemia in the absence of respiratory symptoms.​[16]

Cerebrospinal fluid shows predominant mononuclear cells with elevated protein and low glucose in patients with tularaemic meningitis.[9]​​[12] Lumbar puncture is required only for patients who present with signs and symptoms of meningitis.

Histopathology should be ordered after initial tests; however, it is limited by the fact that caseating granulomas are not specific for tularaemia, as they can be seen with other infectious and inflammatory conditions. Despite this, it is useful to exclude other infectious and inflammatory conditions.

Current methods of antigen testing in urine have proved insensitive for the detection of F tularensis, and further investigations are needed in establishing it as a diagnostic tool.

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