A 29-year-old man presented to Emergency Department with chest pain and non-productive-cough. His symptoms had been ongoing for 2 months and were accompanied by night sweat, weight loss (approximately 5 kg in 3 months), but no fever. He was previously a fit and well warehouse worker with no past medical history. He was not taking any regular medications and there was no known allergy. He was an active smoker of 20 cigarettes/day for 4 years and admitted to previous cannabinoids use. He denied any family history for respiratory disease. He did admit to an ongoing mould exposure in his dwelling. An initial chest x-ray showed evidence of para-hilar left upper lobe consolidation with indistinct margins, compatible with inflammatory thickening.  He was sent home for a presumed respiratory tract infection with antibiotic therapy of levofloxacin with a plan for follow-up Interval chest x-ray. After 7 days the symptoms did not resolve and follow-up chest x-ray after antibiotic therapy was unchanged, so we proceeded to a thorax CT scan with IV contrast. The CT (Figure 1) showed a marked progression of number, density and dimension of the already present cystic alteration on previous HRTC scan, with evidence of consolidation in the anterior segment of the left upper lobe. He was therefore referred to our respiratory team for further inpatients work-up.

Physical examination and findings:
On admission physical examination the patient appeared in no acute distress. Vital signs revealed a temperature of 36.5°C, peripheral pulse of 68 beats/minute, respiratory rate of 16/min and blood pressure of 130/80 mmHg and oxygen saturation of 98% on room air. Respiratory examination revealed scattered bilateral crackles in absence of wheezes or rubs. Cardiac and abdominal examinations were unremarkable. Laboratory examination of peripheral blood highlighted a borderline increase in inflammatory markers: C-reactive protein was 0,75 mg/dL and procalcitonin was negative; the remaining admission blood exams were unremarkable.

Diagnostic studies:
Following up from the CT thorax findings, further imaging was arranged as an impatient in the form of PET scan (Figure 2). There was significant uptake from the opacification in the left upper lobe (SUV 13.83) and from mediastinal lymph nodes in the aortopulmonary region (SUV 4.46), paratracheal (SUV 4), sub-carinal (SUV 5.34) e hilar regions bilaterally (SUV 4.82). PET alterations were suggestive for lymphoproliferative disease or a granulomatous disease. Consequently, a lung tissue biopsy of the apical portion of the left lung in video assisted thoracoscopy was arranged. The histological exam evidenced: inflammatory reactive infiltrate characterised by giant cell foreign body-like cellular components and an exuberant reaction identifying an inflammatory pseudotumor. The cultural tests and research were all negative. In addition, the patient underwent an endobronchial ultrasound with transbronchial needle aspiration (EBUS TBNA) in order to biopsy mediastinal lymph nodes which was not conclusive, highlighting lymphocytes aggregation with some bronchial epithelial cells. Contextually to EBUS a bronchoalveolar lavage (BAL) was performed; the cultures from the lavage were negative and tuberculosis infection was again excluded.  Another HRTC Thorax scan was performed with evidence of new appearance of opacities in the right lung.

Diagnosis:
The case was therefore discussed with a Multidisciplinary Team (MDT) composed of respiratory physician, thoracic surgeon, radiologist and pathologist; the MDT agreed the next step would be a lung segment biopsy during Video Assisted Thoracoscopy (VATS). This time the histology exam was conclusive for Hypersensitivity Pneumonitis (HP). In hindsight the upper lung lobes localisation of disease, the referred exposure to moulds and the chest CT scan lesions’ tendency to evolve, all support the diagnostic hypothesis of an unusual form of hypersensitivity pneumonitis.