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*Repeated acute episodes result in progressive pulmonary fibrosis that is often prominent in the upper zones that is radiologically similar to tuberculosis. | *Repeated acute episodes result in progressive pulmonary fibrosis that is often prominent in the upper zones that is radiologically similar to tuberculosis. | ||
==Allergic | ==Allergic Aspergillus Rhinosinusitis== | ||
*The exact pathogenesis of allergic fungal rhinosinusitis is not fully understood.<ref name="pmid10488788">{{cite journal| author=Ponikau JU, Sherris DA, Kern EB, Homburger HA, Frigas E, Gaffey TA et al.| title=The diagnosis and incidence of allergic fungal sinusitis. | journal=Mayo Clin Proc | year= 1999 | volume= 74 | issue= 9 | pages= 877-84 | pmid=10488788 | doi=10.4065/74.9.877 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10488788 }} </ref> | *The exact pathogenesis of allergic fungal rhinosinusitis is not fully understood.<ref name="pmid10488788">{{cite journal| author=Ponikau JU, Sherris DA, Kern EB, Homburger HA, Frigas E, Gaffey TA et al.| title=The diagnosis and incidence of allergic fungal sinusitis. | journal=Mayo Clin Proc | year= 1999 | volume= 74 | issue= 9 | pages= 877-84 | pmid=10488788 | doi=10.4065/74.9.877 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10488788 }} </ref> | ||
*It is thought that the pathogenesis is similar to the pathogenesis of ABPA, where both type I and type III hypersensitivity responses are involved.<ref name="pmid1001063">{{cite journal| author=Safirstein BH| title=Allergic bronchopulmonary aspergillosis with obstruction of the upper respiratory tract. | journal=Chest | year= 1976 | volume= 70 | issue= 6 | pages= 788-90 | pmid=1001063 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1001063 }} </ref> However, it is not confirmed whether the reactions are systemic or local in the nose and the paranasal sinuses.<ref name="pmid15235354">{{cite journal| author=Collins M, Nair S, Smith W, Kette F, Gillis D, Wormald PJ| title=Role of local immunoglobulin E production in the pathophysiology of noninvasive fungal sinusitis. | journal=Laryngoscope | year= 2004 | volume= 114 | issue= 7 | pages= 1242-6 | pmid=15235354 | doi=10.1097/00005537-200407000-00019 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15235354 }} </ref> | *It is thought that the pathogenesis is similar to the pathogenesis of ABPA, where both type I and type III hypersensitivity responses are involved.<ref name="pmid1001063">{{cite journal| author=Safirstein BH| title=Allergic bronchopulmonary aspergillosis with obstruction of the upper respiratory tract. | journal=Chest | year= 1976 | volume= 70 | issue= 6 | pages= 788-90 | pmid=1001063 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1001063 }} </ref> However, it is not confirmed whether the reactions are systemic or local in the nose and the paranasal sinuses.<ref name="pmid15235354">{{cite journal| author=Collins M, Nair S, Smith W, Kette F, Gillis D, Wormald PJ| title=Role of local immunoglobulin E production in the pathophysiology of noninvasive fungal sinusitis. | journal=Laryngoscope | year= 2004 | volume= 114 | issue= 7 | pages= 1242-6 | pmid=15235354 | doi=10.1097/00005537-200407000-00019 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15235354 }} </ref> | ||
*Not all patients with allergic fungal rhinosinusitis have other allergies, and an alternative mechanism of disease involving T-cell mediated responses to fungi and eosinophilic chemotaxis was suggested.<ref name="pmid10488788">{{cite journal| author=Ponikau JU, Sherris DA, Kern EB, Homburger HA, Frigas E, Gaffey TA et al.| title=The diagnosis and incidence of allergic fungal sinusitis. | journal=Mayo Clin Proc | year= 1999 | volume= 74 | issue= 9 | pages= 877-84 | pmid=10488788 | doi=10.4065/74.9.877 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10488788 }} </ref> | *Not all patients with allergic fungal rhinosinusitis have other allergies, and an alternative mechanism of disease involving T-cell mediated responses to fungi and eosinophilic chemotaxis was suggested.<ref name="pmid10488788">{{cite journal| author=Ponikau JU, Sherris DA, Kern EB, Homburger HA, Frigas E, Gaffey TA et al.| title=The diagnosis and incidence of allergic fungal sinusitis. | journal=Mayo Clin Proc | year= 1999 | volume= 74 | issue= 9 | pages= 877-84 | pmid=10488788 | doi=10.4065/74.9.877 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10488788 }} </ref> | ||
==Aspergilloma== | |||
*''Aspergillus fumigatus'' spores are typically inhaled and result in no clinical manifestations among healthy individuals with no prior history of lung disease. | |||
*Individuals with prior lung diseases (especially lung diseases characaterized by cavitary lesions, such as tuberculosis, sarcoidosis, fibrosis, or bronchiectasis), are at risk for developing aspergilloma.<ref name="pmid3281310">{{cite journal| author=Kibbler CC, Milkins SR, Bhamra A, Spiteri MA, Noone P, Prentice HG| title=Apparent pulmonary mycetoma following invasive aspergillosis in neutropenic patients. | journal=Thorax | year= 1988 | volume= 43 | issue= 2 | pages= 108-12 | pmid=3281310 | doi= | pmc=PMC1020751 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3281310 }} </ref><ref name="pmid6824396">{{cite journal| author=Glimp RA, Bayer AS| title=Pulmonary aspergilloma. Diagnostic and therapeutic considerations. | journal=Arch Intern Med | year= 1983 | volume= 143 | issue= 2 | pages= 303-8 | pmid=6824396 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6824396 }} </ref> | |||
*The fungus settles in a cavity and is able to grow freely. The immune system is unable to penetrate into the cavity. | |||
*As the fungus multiplies, it forms a ball, which incorporates dead tissue from the surrounding lung, mucus, inflammatory cells, epithelial cells, and other debris.<ref name="pmid3097424">{{cite journal| author=Daly RC, Pairolero PC, Piehler JM, Trastek VF, Payne WS, Bernatz PE| title=Pulmonary aspergilloma. Results of surgical treatment. | journal=J Thorac Cardiovasc Surg | year= 1986 | volume= 92 | issue= 6 | pages= 981-8 | pmid=3097424 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3097424 }} </ref> | |||
*''Aspergillus'' is also able to produce enzymes that destroy the surrounding lung parenchyma to allow for further expansion of the fungus ball.<ref name="pmid3281310">{{cite journal| author=Kibbler CC, Milkins SR, Bhamra A, Spiteri MA, Noone P, Prentice HG| title=Apparent pulmonary mycetoma following invasive aspergillosis in neutropenic patients. | journal=Thorax | year= 1988 | volume= 43 | issue= 2 | pages= 108-12 | pmid=3281310 | doi= | pmc=PMC1020751 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3281310 }} </ref> | |||
==Chronic Pulmonary Aspergillosis== | |||
===Chronic Cavitary Pulmonary Aspergillosis (CCPA)=== | |||
*Following spore inhalation, the hyphae expand in multiple cavities and may result in the formation of fungus ball(s).<ref name="pmid12975754">{{cite journal| author=Denning DW, Riniotis K, Dobrashian R, Sambatakou H| title=Chronic cavitary and fibrosing pulmonary and pleural aspergillosis: case series, proposed nomenclature change, and review. | journal=Clin Infect Dis | year= 2003 | volume= 37 Suppl 3 | issue= | pages= S265-80 | pmid=12975754 | doi=10.1086/376526 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12975754 }} </ref> | |||
===Chronic Fibrosing Pulmonary Aspergillosis (CFPA)=== | |||
*Cavitary lesions that form following spore inhalation may progress to subsequently result in pulmonary fibrosis.<ref name="pmid12975754">{{cite journal| author=Denning DW, Riniotis K, Dobrashian R, Sambatakou H| title=Chronic cavitary and fibrosing pulmonary and pleural aspergillosis: case series, proposed nomenclature change, and review. | journal=Clin Infect Dis | year= 2003 | volume= 37 Suppl 3 | issue= | pages= S265-80 | pmid=12975754 | doi=10.1086/376526 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12975754 }} </ref> | |||
*It may be considered as a complication of chronic cavitary pulmonary aspergillosis.<ref name="pmid12975754">{{cite journal| author=Denning DW, Riniotis K, Dobrashian R, Sambatakou H| title=Chronic cavitary and fibrosing pulmonary and pleural aspergillosis: case series, proposed nomenclature change, and review. | journal=Clin Infect Dis | year= 2003 | volume= 37 Suppl 3 | issue= | pages= S265-80 | pmid=12975754 | doi=10.1086/376526 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12975754 }} </ref> | |||
*Pleural involvement may be present.<ref name="pmid12975754">{{cite journal| author=Denning DW, Riniotis K, Dobrashian R, Sambatakou H| title=Chronic cavitary and fibrosing pulmonary and pleural aspergillosis: case series, proposed nomenclature change, and review. | journal=Clin Infect Dis | year= 2003 | volume= 37 Suppl 3 | issue= | pages= S265-80 | pmid=12975754 | doi=10.1086/376526 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12975754 }} </ref> | |||
===Chronic Necrotizing Pulmonary Aspergillosis (CNPA)=== | |||
*Subacute (not chronic), progressive aspergillosis that results in tissue necrosis.<ref name="pmid12975754">{{cite journal| author=Denning DW, Riniotis K, Dobrashian R, Sambatakou H| title=Chronic cavitary and fibrosing pulmonary and pleural aspergillosis: case series, proposed nomenclature change, and review. | journal=Clin Infect Dis | year= 2003 | volume= 37 Suppl 3 | issue= | pages= S265-80 | pmid=12975754 | doi=10.1086/376526 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12975754 }} </ref> | |||
==Invasive Aspergillosis== | ==Invasive Aspergillosis== | ||
*Invasive ''Aspergillus'' infection almost always occurs in patients who are immunosuppressed with underlying lung disease, on an immunosuppressive drug therapy, or immunodeficiency. | *Invasive ''Aspergillus'' infection almost always occurs in patients who are immunosuppressed, with underlying lung disease, on an immunosuppressive drug therapy, or immunodeficiency. | ||
*Human host normally defend against inhaled spores using mucous layer, ciliary action in the respiratory tract and phagocytosis by macrophages and neutrophils. | *Human host normally defend against inhaled spores using mucous layer, ciliary action in the respiratory tract and phagocytosis by macrophages and neutrophils. | ||
*Underlying immunosuppression (eg, HIV disease, chronic granulomatous disease, pharmacologic immunosuppression) results in neutrophil dysfunction or the decreased numbers of neutrophils. Accordingly, immunosuppressed individuals are unable to mount an adequate immune response to phagocytose the organism. | *Underlying immunosuppression (eg, HIV disease, chronic granulomatous disease, pharmacologic immunosuppression) results in neutrophil dysfunction or the decreased numbers of neutrophils. Accordingly, immunosuppressed individuals are unable to mount an adequate immune response to phagocytose the organism. | ||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Christeen Henen, M.D. [2]
Allergic Bronchopulmonary Aspergillosis (ABPA)
- Allergic bronchopulmonary aspergillosis is both a type I (atopic) and type III hypersensitivity response.
Type I Hypersensitivity
- Precipitating antibodies incite a type I acute hypersensitivity reaction that results in the release of immunoglobulin E (IgE) and immunoglobulin G (IgG).
- Immunoglobulin release induces mast cell degranulation, bronchoconstriction, and increased capillary permeability.
Type III Hypersensitivity
- Immune complexes and inflammatory cells are deposited within the bronchial mucosa leading to tissue necrosis and eosinophilic infiltrate, a type III reaction.
- The subsequent damage to the bronchial wall causes (proximal) bronchiectasis. Repeated acute episodes left untreated can result in progressive pulmonary fibrosis that is often seen in the upper zones and can give rise to a similar radiological appearance to that produced by tuberculosis.
Pulmonary Tissue Destruction
- Aspergillus is not usually cleared from the airways despite the immune response.
- Proteolytic enzymes are released by the immune cells, and toxins are released by the fungi. Together these result in bronchiectasis, most pronounced in the central parts of the airways.
- Repeated acute episodes result in progressive pulmonary fibrosis that is often prominent in the upper zones that is radiologically similar to tuberculosis.
Allergic Aspergillus Rhinosinusitis
- The exact pathogenesis of allergic fungal rhinosinusitis is not fully understood.[1]
- It is thought that the pathogenesis is similar to the pathogenesis of ABPA, where both type I and type III hypersensitivity responses are involved.[2] However, it is not confirmed whether the reactions are systemic or local in the nose and the paranasal sinuses.[3]
- Not all patients with allergic fungal rhinosinusitis have other allergies, and an alternative mechanism of disease involving T-cell mediated responses to fungi and eosinophilic chemotaxis was suggested.[1]
Aspergilloma
- Aspergillus fumigatus spores are typically inhaled and result in no clinical manifestations among healthy individuals with no prior history of lung disease.
- Individuals with prior lung diseases (especially lung diseases characaterized by cavitary lesions, such as tuberculosis, sarcoidosis, fibrosis, or bronchiectasis), are at risk for developing aspergilloma.[4][5]
- The fungus settles in a cavity and is able to grow freely. The immune system is unable to penetrate into the cavity.
- As the fungus multiplies, it forms a ball, which incorporates dead tissue from the surrounding lung, mucus, inflammatory cells, epithelial cells, and other debris.[6]
- Aspergillus is also able to produce enzymes that destroy the surrounding lung parenchyma to allow for further expansion of the fungus ball.[4]
Chronic Pulmonary Aspergillosis
Chronic Cavitary Pulmonary Aspergillosis (CCPA)
- Following spore inhalation, the hyphae expand in multiple cavities and may result in the formation of fungus ball(s).[7]
Chronic Fibrosing Pulmonary Aspergillosis (CFPA)
- Cavitary lesions that form following spore inhalation may progress to subsequently result in pulmonary fibrosis.[7]
- It may be considered as a complication of chronic cavitary pulmonary aspergillosis.[7]
- Pleural involvement may be present.[7]
Chronic Necrotizing Pulmonary Aspergillosis (CNPA)
- Subacute (not chronic), progressive aspergillosis that results in tissue necrosis.[7]
Invasive Aspergillosis
- Invasive Aspergillus infection almost always occurs in patients who are immunosuppressed, with underlying lung disease, on an immunosuppressive drug therapy, or immunodeficiency.
- Human host normally defend against inhaled spores using mucous layer, ciliary action in the respiratory tract and phagocytosis by macrophages and neutrophils.
- Underlying immunosuppression (eg, HIV disease, chronic granulomatous disease, pharmacologic immunosuppression) results in neutrophil dysfunction or the decreased numbers of neutrophils. Accordingly, immunosuppressed individuals are unable to mount an adequate immune response to phagocytose the organism.
References
- ↑ 1.0 1.1 Ponikau JU, Sherris DA, Kern EB, Homburger HA, Frigas E, Gaffey TA; et al. (1999). "The diagnosis and incidence of allergic fungal sinusitis". Mayo Clin Proc. 74 (9): 877–84. doi:10.4065/74.9.877. PMID 10488788.
- ↑ Safirstein BH (1976). "Allergic bronchopulmonary aspergillosis with obstruction of the upper respiratory tract". Chest. 70 (6): 788–90. PMID 1001063.
- ↑ Collins M, Nair S, Smith W, Kette F, Gillis D, Wormald PJ (2004). "Role of local immunoglobulin E production in the pathophysiology of noninvasive fungal sinusitis". Laryngoscope. 114 (7): 1242–6. doi:10.1097/00005537-200407000-00019. PMID 15235354.
- ↑ 4.0 4.1 Kibbler CC, Milkins SR, Bhamra A, Spiteri MA, Noone P, Prentice HG (1988). "Apparent pulmonary mycetoma following invasive aspergillosis in neutropenic patients". Thorax. 43 (2): 108–12. PMC 1020751. PMID 3281310.
- ↑ Glimp RA, Bayer AS (1983). "Pulmonary aspergilloma. Diagnostic and therapeutic considerations". Arch Intern Med. 143 (2): 303–8. PMID 6824396.
- ↑ Daly RC, Pairolero PC, Piehler JM, Trastek VF, Payne WS, Bernatz PE (1986). "Pulmonary aspergilloma. Results of surgical treatment". J Thorac Cardiovasc Surg. 92 (6): 981–8. PMID 3097424.
- ↑ 7.0 7.1 7.2 7.3 7.4 Denning DW, Riniotis K, Dobrashian R, Sambatakou H (2003). "Chronic cavitary and fibrosing pulmonary and pleural aspergillosis: case series, proposed nomenclature change, and review". Clin Infect Dis. 37 Suppl 3: S265–80. doi:10.1086/376526. PMID 12975754.