PT - JOURNAL ARTICLE AU - Laura Balzarini AU - Chiara Mancini AU - Panagiota Mouzakiti AU - Maurizio Marvisi TI - Clinical features of a new hypersensitivity pneumonitis: Salami brusher's disease DP - 2011 Sep 01 TA - European Respiratory Journal PG - 2989 VI - 38 IP - Suppl 55 4099 - http://erj.ersjournals.com/content/38/Suppl_55/2989.short 4100 - http://erj.ersjournals.com/content/38/Suppl_55/2989.full SO - Eur Respir J2011 Sep 01; 38 AB - We observed 5 consecutive cases of hypersensitivity Pneumonitis (HP) in subjects working in a salami factory. The workers had to clean the mould growing on salami's surface by using a wire brush. The working population was of 30 female subjects, 5 of them developed a HP (17%).Two were smokers (40%) and, other two were asthmatic. All patients presented with an acute clinical manifestation with cough, high fever, dyspnea and hypoxia occurring after a short period after exposure (240±60 minutes). Three of them presented at the emergency department and a chest x-ray showed and alveolar interstitial pneumonitis and were treated as a community acquired pneumonia. Skin prick test were positive for Penicillium spp in 3 cases and for Cladosporium spp and Aspergillus spp in other 2. The results of serum immunoglobulin (Ig) G and IgA antibodies against Penicillium spp were positive in 3 patients, 2 patients were positive to Aspergillus Fumigatus. Pulmonary function test demonstrated a reduction in diffusing capacity in all 5 patients (60±15% of predicted). A bronchial hyperresponsiveness to methacoline was present in all the patients, the mean dose of methacoline causing a 20% fall in FEV1 was 3.63±4.70 mg/mL. BAL data showed a lymphocytosis 44.4±8.2%, CD4+ were 26.5±6.3%, CD8 + 53.5±8.2. Four patients had a complete recovery after chancing work, and one was treated with oral steroids for increasing dyspnea and severe interstitial involvement. Salami's brusher disease is a new type of HP, the prevalence is high in exposed subjects, and is common even in smokers. The disease has an acute clinical onset. The probable antigen is Penicillium, but Cladosporium and Aspergillus may play a key role.