Aspergillosis pathophysiology: Difference between revisions
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*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. | *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. | *Repeated acute episodes result in progressive pulmonary fibrosis that is often prominent in the upper zones that is radiologically similar to tuberculosis. | ||
==Allergic Fungal 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> | |||
*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> | |||
==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 | *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. | ||
==Aspergilloma== | ==Aspergilloma== | ||
The most common place affected by aspergillomas is the lung. Aspergillus fumigatus, the most common species, is typically inhaled as small (2 to 3 micrometer) spores which do not affect people without underlying lung or immune system disease. However, people who have pre-existing lung problems, especially the cavities typically caused by tuberculosis, are at risk for developing aspergillomata. The fungus settles in a cavity and is able to grow free from interference because 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, and other debris.[2] | The most common place affected by aspergillomas is the lung. Aspergillus fumigatus, the most common species, is typically inhaled as small (2 to 3 micrometer) spores which do not affect people without underlying lung or immune system disease. However, people who have pre-existing lung problems, especially the cavities typically caused by tuberculosis, are at risk for developing aspergillomata. The fungus settles in a cavity and is able to grow free from interference because 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, and other debris.[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 Fungal 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]
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.
Aspergilloma
The most common place affected by aspergillomas is the lung. Aspergillus fumigatus, the most common species, is typically inhaled as small (2 to 3 micrometer) spores which do not affect people without underlying lung or immune system disease. However, people who have pre-existing lung problems, especially the cavities typically caused by tuberculosis, are at risk for developing aspergillomata. The fungus settles in a cavity and is able to grow free from interference because 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, and other debris.[2]
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.