[Workplace-associated fever]. / Arbeitsplatzassoziiertes Fieber oder wenn es doch das Zebra ist .

INTRODUCTION: Febrile conditions often have an infectious etiology. However, there are also fevers associated with occupational exposures. A detailed occupational history can hold the key to the diagnosis. In the case of exposure to organic dusts, the development of hypersensitivity pneumonitis (HP) is possible. Thus, HP should be considered in the presence of interstitial lung disease of unclear etiology. Failure to recognize this can have dramatic consequences and, in extreme cases, lead to lung transplantation. Differentially, organic dust toxic syndrome (ODTS) must be considered. The syndrome of metal fume fever provoked by inhalation of inorganic substances is usually benign and self-limiting. The disease manifests with fever, cough, and flu-like sensations.

Hypersensitivity Pneumonitis: Challenges of a Complex Disease.

Hypersensitivity pneumonitis (HP) is a complex interstitial lung disease caused by chronic inhalation of a wide variety of antigens in susceptible and sensitized individuals, commonly associated with an occupational exposure. An impressive number of inciting antigens causing hypersensitivity pneumonitis have been found to cover a wide range of occupations. As working practices have changed over time, especially in industrialized countries, new names for occupational HP have emerged. This review emphasizes the main diagnostic issues arising from the high variability of clinical presentation and the broad spectrum of causal antigens. Furthermore, it provides an overview of current methods to unveil possible causes of hypersensitivity pneumonitis, highlights HP's current diagnostic and treatment challenges and the remaining areas of uncertainty, and presents prevention strategies.

Bird ownership and pulmonary outcomes apart from hypersensitivity pneumonitis in European older adults.

BACKGROUND: Exposure to birds has been linked with several lung pathologies and especially hypersensitivity pneumonitis, but discordant literature exist on the potential effects of this exposure on other respiratory pathologies. AIM: This study aims to examine the associations between bird ownership and asthma, lung cancer, and chronic obstructive pulmonary disease (COPD) in older European adults. METHODS: A total of 28,109 participants from the Survey of Health, Ageing, and Retirement in Europe were employed and analyzed with multivariate logistic regressions. RESULTS: No association was found with asthma or lung cancer. Bird ownership increased the odds for COPD diagnosis (OR=1.30; 95 % CI: 1.12-1.51) and more so in males (OR=1.53; 95 % CI: 1.25-1.87) after adjustment for demographic, respiratory, lifestyle, and socioeconomic factors. Male bird owners who smoke had an even more increased risk compared to non-smokers, as did those who lived in multi-person households compared to those living alone. CONCLUSION: Bird ownership may be positively associated with COPD in older European males.

Moldy Hazelnut Husk and Shell Related Hypersensitivity Pneumonitis: A Possible Novel Occupational Causative Agent.

Hypersensitivity pneumonitis (HP) is a complex immune-mediated interstitial lung disease (ILD) triggered by inhalation exposure to environmental or occupational antigens in genetically susceptible individuals. Novel exposure sources and antigens are frequently identified. However, the causative agent remains unidentified in nearly half of HP cases. Early diagnosis for nonfibrotic-HP and quitting the exposure may prevent the disease progression to fibrotic forms and related complications. Here, we present two cases of HP associated with mold exposure in hazelnut husks, leaves, and shells in hazelnut agriculture.

Recurrent episodes of febrile dyspnoea: hypersensitivity pneumonitis caused by a household ultrasonic humidifier.

Hypersensitivity pneumonitis is an immune-mediated interstitial lung disease that presents with respiratory symptoms, with or without systemic symptoms, following exposure to an identified or unidentified external factor. It can be caused by extrinsic factors including household items such as ultrasonic humidifiers.We present an intriguing case of a previously healthy 50-year-old man who displayed recurrent episodes of progressive dyspnoea and fever after repeated exposure to his household ultrasonic humidifier. He was treated with corticosteroids, followed by the removal of the humidifier, resulting in total recovery and absence of recurrence of further episodes.The clinical presentation of hypersensitivity pneumonitis can be dramatic, and the differential diagnosis is broad. The correct diagnosis is achieved by combining clinical, radiological and histopathological patterns. The key to finding the aetiology lies in a thorough history, with an important role for household investigations to identify the external factor.

Hypersensitivity pneumonitis due to metal working fluids: Detection of specific IgG antibodies to microbial antigens.

Occupational exposure to microbially contaminated metal working fluids (MWF) can cause hypersensitivity pneumonitis (HP). An important step in the diagnosis of HP is to identify the triggering antigen by detection of corresponding specific IgG antibodies (sIgG). As commercial sIgG tests are currently not available, protein antigens were prepared from MWF-workplace samples and from MWF-typical bacterial isolates. In 57 % of suspected HP-cases (n = 30) elevated sIgG concentrations were measured to at least one MWF-relevant antigen, of which Mycobacterium immunogenum was most prominent (88 %), followed by Pseudomonas oleovorans and Pseudomonas spec (82 % each), MWF-antigen mix and Pseudomonas alcaliphila (65 % each). Elevated sIgG concentrations to other microorganisms were measured to Micropolyspora faeni (82 %) and Aureobasidium pullulans (77 %). Correlation of sIgG values of all tested microbial antigens showed a significant relationship of MWF-antigen mixture to Pseudomonas antigens, but a low correlation to moulds. These newly prepared MWF-antigens are useful tools for the diagnosis of patients with suspected MWF-HP and are available for further investigations.

Occupational Interstitial Lung Diseases.

Occupational exposures are directly causal or partially contributory to the development of interstitial lung diseases. A detailed occupational history, relevant high-resolution computed tomography findings, and where relevant additional histopathology, are required to make a diagnosis. Treatment options are limited, and further exposure avoidance is likely to reduce disease progression.

Occupational hypersensitivity pneumonia.

Hypersensitivity pneumonitis (HP) is an immunological lung disease that affects individuals who are sensitive and susceptible to occupational and environmental exposures. While clinical and radiological findings may resemble other interstitial lung diseases, identifying the causative agents can aid in the differential diagnosis. However, this can be challenging and may result in delayed diagnosis and poor prognosis. A gold standard test for diagnosis is currently unavailable, and therefore, a multidisciplinary approach involving a clinician, radiologist, and pathologist is necessary. Avoiding exposure is the first step in treatment, with immunosuppressive therapeutics also being used. Antifibrotic agents show promise for future treatment approaches. Despite recent advancements in data and guidelines, knowledge about managing occupational HP remains limited. This review provides a summary of the epidemiological, clinical, and radiological findings, as well as diagnostic and treatment principles of occupational HP based on current literature.

Evaluation of cases with hypersensitivity pneumonia: 10 year analysis.

INTRODUCTION: The aim of this study was to examine the clinical features of hypersensitivity pneumonia (HP) cases, diagnostic methods, and related conditions in our hospital, which is a reference clinic in Turkey for chest disease. METHODS: The population of this retrospective cross-sectional study consists of all hypersensitivity pneumonia patients followed in a tertiary hospital between 2010 and 2019. The data of 78 patients were included in the analysis. Data were grouped by source of exposure (occupational, environmental, and cryptogenic) by examining the files of the patients. RESULTS: Occupational risk factors were detected in 29 (37.2%) of the cases, environmental risk factors were found in 24 (30.8%) cases, neither occupational nor environmental risk factors were detected in 25 (32%) cases, and they were evaluated as cryptogenic. The time from the onset of symptoms to diagnosis was 15.8 ± 26.6 months. The time from the onset of symptoms to diagnosis was found to be longer in the group with occupational risk factors compared with the other groups and was statistically significant (0.044). CONCLUSION: HP is a immune-mediated interstitial lung disease induced by repeated exposure to environmental and occupational antigens. Etiological agent can be detected in HP patients by detailed questioning of occupational and environmental exposure that may be associated with the onset of symptoms in cases with suspected HP.

Work-related interstitial lung disease: what is the true burden?

Interstitial lung diseases (ILDs) include a large variety of fibrotic lung conditions caused by genetic and environmental factors. Occupational exposures might also play a significant role, but the real health burden is currently unknown. Here, we aim to evaluate the role of work-related exposures in ILDs, focussing on idiopathic pulmonary fibrosis (IPF) and hypersensitivity pneumonitis (HP). We performed a focused review of the literature on work-related HP and IPF over the past 5 years. Using a meta-analytic approach, we quantified the occupational burden of IPF and HP, and estimated that occupational exposures to metal, silica and environmental tobacco smoke increased IPF risk with a pooled odds ratio of 1.7 (95% CI 1.42-2.03). The proportion of HP cases related to workplace exposure was 17% (95% CI 7-28). Our review supports the hypothesis that occupational exposures are a significant risk factor in the aetiopathogenesis of IPF and HP. We recommend that further research be performed to identify the underlying occupational factors and the maximum permitted exposure to reduce the associated IPF and HP burden.

Pediatric hypersensitivity pneumonitis: literature update and proposal of a diagnostic algorithm.

Hypersensitivity pneumonitis (HP) is a rare disease in childhood with the prevalence of 4 cases per 1 million children and an incidence of 2 cases per year. The average age of diagnosis at pediatric age is approximately 10 years. The pathogenesis of HP is characterized by an immunological reaction caused by recurrent exposure to triggering environmental agents (mostly bird antigens in children). The clinical picture of HP is complex and variable in children, often presenting in subacute forms with cough and exertion dyspnea. A diagnosis of HP should be considered in patients with an identified exposure to a triggering antigen, respiratory symptoms, and radiologic signs of interstitial lung disease. Blood tests and pulmonary function tests (PFT) support the diagnosis. Bronchoscopy (with bronchoalveolar lavage and tissue biopsy) may be needed in unclear cases. Antigen provocation test is rarely required. Of note, the persistence of symptoms despite various treatment regimens may support HP diagnosis. The avoidance of single/multiple triggers is crucial for effective treatment. No evidence- based guidelines for treatment are available; in particular, the role of systemic glucocorticoids in children is unclear. With adequate antigen avoidance, the prognosis in children with HP is generally favorable.

Hypersensitivity pneumonitis in a slaughterhouse worker: A case report.

This case report describes a 60-year-old male, who presented to the Respiratory Outpatient Unit due to dyspnea on exertion and persistent dry cough, worsened during the preceding 6 months. He was nonsmoker with an otherwise unremarkable medical history and had been working in a sheep/goat slaughterhouse for the last 25 years. He recalled a number of episodes of flu-like symptoms in the past that subsided without any specific treatment. Given the compatible occupational history, the radiologic pattern in chest High-Resolution Computed Tomography and the Bronchoalveolar Lavage subpopulation analysis, hypersensitivity pneumonitis was diagnosed, and the patient was advised to leave temporarily his current occupational activity. Four weeks later, clinical and functional improvement was observed. A permanent job change was subsequently suggested, and sustained improvement was confirmed during his follow-up at 3 months.

Lung fibrosis in autoimmune diseases and hypersensitivity: how to separate these from idiopathic pulmonary fibrosis.

Lung involvement in autoimmune diseases (AID) is uncommon, but may precede other organ manifestations. A diagnostic problem is chronicity presenting with lung fibrosis. A new category of interstitial pneumonia with autoimmune features for patients with clinical symptoms of AID and presenting with usual interstitial pneumonia (UIP) enables antifibrotic treatment for these patients. Hypersensitivity pneumonia (HP) and other forms of lung fibrosis were not included into this category. As these diseases based on adverse immune reactions often present with unspecific clinical symptoms, a specified pathological diagnosis will assist the clinical evaluation. We aimed to establish etiology-relevant differences of patterns associated with AID or HP combined with lung fibrosis. We retrospectively evaluated 51 cases of AID, and 29 cases of HP with lung fibrosis, and compared these to 24 cases of idiopathic pulmonary fibrosis (UIP/IPF). Subacute AID and HP most often presented with organizing pneumonia (OP), whereas chronicity was associated with UIP. Unspecified fibrosis was seen in a few cases, whereas NSIP pattern was rare. In 9 cases, the underlying etiology could not be defined. Statistically significant features differentiating chronic AID or HP from UIP/IPF are lymphocytic infiltrations into myofibroblastic/fibroblastic foci. Other features significantly associated with AID and HP were granulomas, isolated Langhans giant cells, and protein deposits, but seen in only a minority of cases. A combination of UIP with one of these features enabled a specific etiology-based diagnosis. Besides the antifibrotic drug regimen, additional therapies might be considered.

Hypersensitivity pneumonitis: Current concepts in pathogenesis, diagnosis, and treatment.

Hypersensitivity pneumonitis is an immune-mediated interstitial lung disease caused by an aberrant response to an inhaled exposure, which results in mostly T cell-mediated inflammation, granuloma formation, and fibrosis in some cases. HP is diagnosed by exposure identification, HRCT findings of ground-glass opacities, centrilobular nodules, and mosaic attenuation, with traction bronchiectasis and honeycombing in fibrotic cases. Additional testing including serum IgG testing for the presence of antigen exposure, bronchoalveolar lavage lymphocytosis, and lung biopsy demonstrating granulomas, inflammation, and fibrosis, increases the diagnostic confidence. Treatment for HP includes avoidance of the implicated exposure, immunosuppression, and anti-fibrotic therapy in select cases. This narrative review presents the recent literature in the understanding of the immunopathological mechanisms, diagnosis, and treatment of HP.