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Some of the first advances and developments in the understanding of fungal infections of the lung occurred in the early 1950s during the emergence of resectional surgery for the therapy of tuberculosis. With the advent of pulmonary resection as a therapy for tuberculosis, it became apparent that some of the patients thought to be afflicted with tuberculosis on the basis of their chest radiographic findings were, in fact, suffering from invasive and pathogenic fungal infections.[1] The first major non-surgical therapy for pulmonary fungal infections came with the isolation of amphotericin B from a soil actinomycete.[2]
Serious pulmonary fungal infection represents a relatively small proportion of pulmonary fungal infections in general. The vast majority of patients present with minimal symptoms that rapidly subside and have no sequela. An even larger number of patients develop primary fungal infections of a subclinical nature that is evidenced only by conversion of skin tests or serology.
With the increased use of immunosuppression for a growing number of autoimmune conditions, immunosuppression for organ transplantation, the widespread use of chemotherapy, and the spread of human immunodeficiency virus (HIV), there is an ever-increasing experience with fungal infections due to secondary or opportunistic pathogens in immunocompromised patients. Of all transplant patients, those with lung or heart-lung transplants are particularly vulnerable for fungal infection due to multiple reasons including: high level of immune suppression required, decreased mucociliary clearance and impaired lymphatics due to the transplant, and continuous environmental exposure of the allograft to pathogens. Additionally, immunocompromised patients may present with pulmonary infections due to a combination of fungal, bacterial and viral pathogens. Although they form a small minority of patients, it is in immunocompromised patients that we see the most serious manifestations of mycotic infections of the lung.
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Some of the first advances and developments in the understanding of fungal infections of the lung occurred in the early 1950s during the emergence of resectional surgery for the therapy of tuberculosis. With the advent of pulmonary resection as a therapy for tuberculosis, it became apparent that some of the patients thought to be afflicted with tuberculosis on the basis of their chest radiographic findings were, in fact, suffering from invasive and pathogenic fungal infections.[1] The first major non-surgical therapy for pulmonary fungal infections came with the isolation of amphotericin B from a soil actinomycete.[2]
Serious pulmonary fungal infection represents a relatively small proportion of pulmonary fungal infections in general. The vast majority of patients present with minimal symptoms that rapidly subside and have no sequela. An even larger number of patients develop primary fungal infections of a subclinical nature that is evidenced only by conversion of skin tests or serology.
With the increased use of immunosuppression for a growing number of autoimmune conditions, immunosuppression for organ transplantation, the widespread use of chemotherapy, and the spread of human immunodeficiency virus (HIV), there is an ever-increasing experience with fungal infections due to secondary or opportunistic pathogens in immunocompromised patients. Of all transplant patients, those with lung or heart-lung transplants are particularly vulnerable for fungal infection due to multiple reasons including: high level of immune suppression required, decreased mucociliary clearance and impaired lymphatics due to the transplant, and continuous environmental exposure of the allograft to pathogens. Additionally, immunocompromised patients may present with pulmonary infections due to a combination of fungal, bacterial and viral pathogens. Although they form a small minority of patients, it is in immunocompromised patients that we see the most serious manifestations of mycotic infections of the lung.
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