Pulmonary tularaemia. / Pulmonal tularemi.

BACKGROUND: The diagnosis of pulmonary tularaemia can be challenging. We present a case illustrating how pulmonary tularaemia may be an important radiological differential diagnosis to lung cancer. CASE PRESENTATION: A man in his fifties presented with several weeks of dry cough, weight loss and profuse night sweats. The physical examination was normal. A chest computer tomography showed evidence of lymphadenopathy and two consolidated lung masses. The lung masses and lymph nodes showed signs of necrosis. The radiological findings were described as suspicious of lung cancer. A detailed history revealed that he had chopped wood prior to symptom onset. He tested positive for Francisella tularensis IgM and IgG, confirming the diagnosis of pulmonary tularaemia. INTERPRETATION: The radiological findings in pulmonary tularaemia may mimic lung cancer. Serology is an easy way to confirm the diagnosis, if faced with clinical or radiological suspicion of pulmonary tularaemia.

Pulmonary tularaemia: a differential diagnosis to lung cancer.

BACKGROUND: Pulmonary manifestations of tularaemia are reported to be infrequent in previous publications. During 2016, we noticed an increase in the number of hospitalised patients with pulmonary tularaemia in Eastern Norway. We aimed to investigate primary pulmonary tularaemia in Eastern Norway in terms of symptoms, radiological and microbiological findings, incidence and risk exposure. METHODS: A retrospective analysis of consecutive primary pulmonary tularaemia cases from 2016 until 2018 was conducted. RESULTS: From 1 September, 2016 until 31 December, 2018, 22 patients were diagnosed with primary pulmonary tularaemia at Innlandet Hospital Trust, representing 48% of all reported tularaemia cases in the region. A peak annual incidence of 3.4 in 100 000 was found in 2017.All 22 patients lived in, or had recently visited, rural areas. Eighteen patients reported risk exposure for tularaemia, such as wood chopping, outdoor activities and farming prior to symptom onset. All patients experienced fever, and 19 patients had respiratory symptoms. Ten patients were in spontaneous recovery at diagnosis.All patients had a chest computed tomography scan. Overall, 19 patients had pulmonary lesions and 18 had enlarged intrathoracic lymph nodes. The computed tomography images were described as suspicious of malignancy in 17 patients. CONCLUSION: Pulmonary manifestations in tularaemia occurred more frequently in our region than expected from previous reports. Although all patients had symptoms consistent with infection, the majority were primarily investigated considering lung cancer due to the radiology report. In endemic areas, pulmonary tularaemia may be an important differential diagnosis to lung cancer.

Delayed leukocytosis after hard strength and endurance exercise: aspects of regulatory mechanisms.

BACKGROUND: During infections, polymorphonuclear neutrophilic granulocytes (PMN) are mobilized from their bone marrow stores, travel with blood to the affected tissue, and kill invading microbes there. The signal(s) from the inflammatory site to the marrow are unknown, even though a number of humoral factors that can mobilize PMN, are well known. We have employed a standardized, non-infectious human model to elucidate relevant PMN mobilizers. Well-trained athletes performed a 60-min strenuous strength workout of leg muscles. Blood samples were drawn before, during and just after exercise, and then repeatedly during the following day. Cortisol, GH, ACTH, complement factors, high-sensitive CRP (muCRP), IL-6, G-CSF, IL-8 (CXCL8) and MIP-1beta (CCL4) were measured in blood samples. PMN chemotaxins in test plasma was assessed with a micropore membrane technique. RESULTS: About 5 hr after the workout, blood granulocytosis peaked to about 150% of baseline. Plasma levels of GH increased significantly 30 min into and 5 min after the exercise, but no increase was recorded for the other hormones. No significant correlation was found between concentrations of stress hormones and the subjects' later occurring PMN increases above their individual baselines. Plasma G-CSF increased significantly - but within the normal range - 65 min after the workout. IL-6 increased very slightly within the normal range, and the chemokines IL-8 and MIP-1beta did not increase consistently. However, we found a significant increase of hitherto non-identified PMN-chemotactic activity in plasma 35, 50, and 60 min after the exercise. No systemic complement activation was detected, and (mu)CRP was within the reference range at rest, 5 h and 23 h after the exercise. After endurance exercise, similar findings were made, except for a cortisol response, especially from non-elite runners. CONCLUSION: Apparently, a multitude of humoral factors can - directly or indirectly - mobilize PMN from marrow to blood; some of the factors are, others are not known to be, chemotactic. Under different conditions, different selections of these mobilizers may be used. In the late granulocytosis after heavy, long-lasting exercise a number of factors thought capable of mimicking the granulocytosis of infectious diseases were apparently irrelevant.