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• W1968590900 abstract "InstructionsCredit can now be obtained, free for a limited time, by reading the review article in this issue and completing all activity components. Please note the instructions listed below:•Review the target audience, learning objectives and all disclosures.•Complete the pre-test online at http://www.annallergy.org (click on the CME heading).•Follow the online instructions to read the full version of the article; reflect on all content as to how it may be applicable to your practice.•Complete the post-test/evaluation and claim credit earned; at this time, you will have earned up to 1.0 AMA PRA Category 1 CreditTM. Please note that the minimum passing score on the post-test is 70%.Release Date: February 1, 2015Expiration Date: January 31, 2017Target Audience: Physicians involved in providing patient care in the field of allergy/asthma/immunologyLearning Objectives:At the conclusion of this activity, participants should be able to:•Advise patients on how to reduce exposure to fungi•Diagnose patients with fungal allergyAccreditation: The American College of Allergy, Asthma & Immunology (ACAAI) is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians.Designation: The American College of Allergy, Asthma & Immunology (ACAAI) designates this journal-based CME activity for a maximum of 1 AMA PRA Category 1 CreditTM. Physicians should claim only the credit commensurate with the extent of their participation in the activity.Planning Committee Members:Jay M. Portnoy, MD (Author)Mitchell H. Grayson, MD (CME Series Editor, Deputy Editor)Gailen D. Marshall, Jr, MD, PhD (Editor-in-Chief)Disclosure of Relevant Financial Relationships:J.M. Portnoy has served as a speaker for Thermo Fisher Scientific. M.H. Grayson has received research grants from Children’s Research Institute/Medical College of Wisconsin, Merck, National Institutes of Health (NIH), and Polyphor. G.D. Marshall has received research grants from Amgen, AstraZeneca, and National Institutes of Health (NIH). D. Jara has nothing to disclose. Reviewers and Education/Editorial staff have no relevant financial relationships to disclose. No unapproved/investigative use of a product/device is discussed.Recognition of Commercial Support: This activity has not received external commercial support.Copyright Statement: © 2014-2017 ACAAI. All rights reserved.CME Inquiries: Contact the American College of Allergy, Asthma & Immunology at [email protected] or 847-427-1200.IntroductionFungi are ubiquitous eukaryotic organisms that are members of their own kingdom. They are distinct from prokaryotes, plants, and animals. Fungi may exist as unicellular organisms, such as yeasts (eg, Candida) but more typically they have tubelike bodies, called hyphae, which range from 2 to 10 μm in diameter. Hyphae grow at their tips and frequently branch, resulting in an interconnected network called a mycelium.Fungi reproduce by making spores by asexual or sexual processes. Many of the structures that produce asexual spores are called conidia, the morphologic structure of which is often used to identify a fungus by genus and species. Fungi that lack an observable sexual stage historically were referred to as Fungi imperfecti or Deuteromycota; however, that term is no longer recognized and should no longer be used. When fungi reproduce sexually via meiosis, they produce 8 spores contained in an ascus or sack that are released when the ascus is disrupted.Fungi do not rely on photosynthesis to convert carbon dioxide into carbohydrates as plants do. Instead, they secrete digestive enzymes onto the outside world and then absorb nutrients, using oxygen from the atmosphere to obtain energy. Their byproducts consist of a complex mixture of organic compounds, some of which consist of proteins that can induce and bind to IgE in humans[1]Crameri R. Zeller S. Glaser A.G. Vilhelmsson M. Rhyner C. Cross-reactivity among fungal allergens: a clinically relevant phenomenon?.Mycoses. 2009; 52: 99-106Crossref PubMed Scopus (74) Google Scholar and others that can serve as proinflammatory compounds and irritants via non-IgE mechanisms.[2]Chen J. Seviour R. Medicinal importance of fungal beta-(1→3), (1→6)-glucans.Mycol Res. 2007; 111: 635-652Crossref PubMed Scopus (456) Google ScholarAllergenic FungiThe taxonomy of fungi has been confusing, primarily because identification of species traditionally has relied on visual recognition of distinct morphologic features. This confusion was confounded by the fact that fungi can have differing morphologic features, depending on the substrate and environmental conditions in which they grow, whether they are in their sexual or asexual reproductive state, and the skill and biases of the mycologist performing the identification. Recently, a taxonomy based on molecular DNA techniques has been agreed on by experts in the field.[3]Hawksworth D.L. Crous P.W. Redhead S.A. et al.The Amsterdam declaration on fungal nomenclature.IMA Fungus. 2011; 2: 105-112Crossref PubMed Scopus (273) Google ScholarMany allergenic fungal genera are represented by 3 phyla: Zygomycota, Ascomycota, and Basidiomycota (Table 1). The largest group is the Ascomycota. On the basis of cluster analysis, a close relationship has been observed between genetic fungal taxonomy and IgE sensitization.[4]Soeria-Atmadja D. Onell A. Borga A. IgE sensitization to fungi mirrors fungal phylogenetic systematics.J Allergy Clin Immunol. 2010; 125: 1379-1386.e1Abstract Full Text Full Text PDF PubMed Scopus (34) Google Scholar The IgE-based clustering divides the Ascomycota cluster into 2 separate clusters. The first cluster includes genera in the classes Sordariomycetes, Leotiomycetes, and Eurotiomycetes and some genera from the Dothideomycetidae, whereas the second cluster contains genera from the Pleosporomycetidae, which is another subclass of the Dothideomycetidae. Genera from Saccharomycetes form a third cluster in the Ascomycota phylum. Fungi from the Zygomycota and Basidiomycota phyla form their own IgE sensitization clusters. Given these extensive cross-reactivity patterns, it might be possible to identify representative genera from each class to serve as a proxy for IgE directed to the group.Table 1Taxonomy of selected allergenic fungi[4]Soeria-Atmadja D. Onell A. Borga A. IgE sensitization to fungi mirrors fungal phylogenetic systematics.J Allergy Clin Immunol. 2010; 125: 1379-1386.e1Abstract Full Text Full Text PDF PubMed Scopus (34) Google ScholaraGenera in the same class tend to have substantial IgE cross-reactivity. Members of the Sordariomycetes, Leotiomycetes, Eurotiomycetes, and Dothideomycetidae classes also exhibit substantial cross-reactivity.PhylumClassOrderSelected generaZygomycotaZygomycetesMucoralesMucor, RhizopusAscomycotaSaccharomycetesSaccharomycetalesCandida, SaccharomycesDothideomycetesCapnodialesCladosporiumPleosporalesAlternaria, Curvularia, Bipolaris, Stemphylium, Phoma, EpicoccumDothidealesAureobasidiumEurotiomycetesEurotialesAspergillus, PenicilliumOnygenalesTrichophytonSordariomycetesHypocrealesFusarium, Trichoderma, StachybotrysSordarialesMonilia, Neurospora, Chaetomium, AcremoniumLeotiomycetesHelotialesBotrytisBasidiomycotaMicrobotryomycetesSporidiobolalesRhodotorulaUstilaginomycetesUstilaginalesUstilagoa Genera in the same class tend to have substantial IgE cross-reactivity. Members of the Sordariomycetes, Leotiomycetes, Eurotiomycetes, and Dothideomycetidae classes also exhibit substantial cross-reactivity. Open table in a new tab Major allergens have been identified for many fungal genera (Table 2). In addition to their ability to induce and bind to IgE, the biologic function for most of these allergens has been determined. A comprehensive database of fungal allergens can be found at Allergome (http://www.allergome.org/).Table 2Major allergens and their biologic activity for 4 major genera of allergenic fungiaCompiled from Allergome (http://www.allergome.org/).Genus and allergenBiologic activityAlternaria Alt a 1Unknown Alt a 2Protein initiation factor Alt a 3Heat shock protein 70 Alt a 4Thioredoxin Alt a 6Enolase Alt a 7Flavodoxin Alt a 8Mannitol dehydrogenase Alt a 10Aldehyde dehydrogenase Alt a 13Glutathione S-transferaseCladosporium Cla h 3Alcohol dehydrogenase Cla h 6Enolase Cla h 7Flavodoxin Cla h 8Mannitol dehydrogenase Cla h 9Serine protease Cla h 10Aldehyde dehydrogenase Cla h 12Heat shock protein 90Aspergillus Asp f 1Mitogillin Asp f 3Peroxisomal membrane protein Asp f 5Serine protease Asp f 6Mn superoxide dismutase Asp f 11Cyclophilin peptidyl prolyl isomerase Asp f 12Heat shock protein 90 Asp f 18Serine protease Asp f 22Enolase Asp f 28ThioredoxinPenicillium Pen c 2Serine protease Pen c 3Peroxisomal membrane protein Pen c 13Serine protease Pen c 18Serine protease Pen c 19Heat shock protein 70 Pen c 22Enolase Pen c 24Glutathione S-transferase Pen c 30Catalasea Compiled from Allergome (http://www.allergome.org/). Open table in a new tab Exposure to FungiFungi can be found in virtually all environments in which there is a source of carbohydrate, moisture, and warmth. They serve a role as saprophytes by causing decay of plant materials. Airborne spores are typically counted using light microscopy after they are collected on adhesive-coated surfaces. The number and diversity of airborne fungi detected by this method may be underestimated. One study found that as many as 86% of genera detected by DNA sequencing were not routinely identifiable by microscopy, including some currently unrecognized aeroallergens.[5]Pashley C.H. Fairs A. Free R.C. Wardlaw A.J. DNA analysis of outdoor air reveals a high degree of fungal diversity, temporal variability, and genera not seen by spore morphology.Fungal Biol. 2012; 116: 214-224Crossref PubMed Scopus (67) Google ScholarTypical 24-hour mean outdoor spore concentrations can range from as few as 50 spores/M3 during winter to as many as 50,000 spores/M3 during summer.[6]Portnoy J. Barnes C. The National Allergy Bureau: pollen and spore reporting today.J Allergy Clin Immunol. 2004; 114: 1235-1238Abstract Full Text Full Text PDF PubMed Scopus (12) Google Scholar In temperate regions, spores in outdoor air tend to peak in the middle to late summer and decrease with the first hard frost in regions that experience cold winter seasons, although they may briefly rebound during warmer periods. Xenophilic or dry air spores, such as Cladosporium and Alternaria, peak in the afternoon hours during periods of low humidity. Hydrophilic or wet air spores, such as ascospores and basidiospores (mushrooms and puffballs), tend to peak during predawn hours, when there is high humidity. Temperature and dew point appear to be the most important meteorologic factors that affect the presence of spores.[7]Troutt C. Levetin E. Correlation of spring spore concentrations and meteorological conditions in Tulsa, Oklahoma.Int J Biometeorol. 2001; 45: 64-74Crossref PubMed Scopus (116) Google Scholar A survey of outdoor fungal genera in Tulsa, Oklahoma, identified Cladosporium, Alternaria, Epicoccum, Curvularia, Pithomyces, Drechslera, smut, ascospores, basidiospores, and others.[8]Burch M. Levetin E. Effects of meteorological conditions on spore plumes.Int J Biometeorol. 2002; 46: 107-117Crossref PubMed Scopus (153) Google ScholarEpidemics of asthma have been reported to be associated with thunderstorms and increases in airborne Alternaria. In one study, there was an increased risk of thunderstorm-related asthma (odds ratio [OR], 9.31) if one was sensitive to Alternaria, which was even greater if sensitive both to Alternaria and Cladosporium (OR, 64).[9]Pulimood T.B. Corden J.M. Bryden C. Sharples L. Nasser S.M. Epidemic asthma and the role of the fungal mold Alternaria alternata.J Allergy Clin Immunol. 2007; 120: 610-617Abstract Full Text Full Text PDF PubMed Scopus (209) Google ScholarIndoors, fungal spores usually are present in low concentrations unless sources of indoor growth are present. Lacking such growth, the indoor microbiome depends largely on dispersal from the outdoors.[10]Adams R.I. Amend A.S. Taylor J.W. Bruns T.D. A unique signal distorts the perception of species richness and composition in high-throughput sequencing surveys of microbial communities: a case study of fungi in indoor dust.Microbial Ecol. 2013; 66: 735-741Crossref PubMed Scopus (42) Google Scholar The most common taxa found in surveys of contaminated indoor environments include Penicillium, Aspergillus, Ascospores, Alternaria, Periconia, Basidiospores, Stachybotrys, and Wallemia.Fungi are adapted to varying moisture conditions. The types of fungal species present often change over time, reflecting changes in moisture as the building dries and becomes damp again. Room types most likely to have elevated spore counts include (in descending order) laundry rooms, bathrooms, basements, and bedrooms, with the lowest counts being found in living rooms, kitchens, and family/television rooms.[11]Portnoy J. Flappan S. Barnes C. A procedure for evaluation of the indoor environment.Aerobiologia. 2001; 17: 43-48Crossref Scopus (24) Google Scholar The total biomass of indoor fungi in such buildings is likely to be underestimated because most airborne fungal material is present in the form of mycelial fragments that cannot be easily be recognized as being fungal in origin.[12]Reponen T. Seo S.C. Grimsley F. Lee T. Crawford C. Grinshpun S.A. Fungal fragments in moldy houses: a field study in homes in New Orleans and Southern Ohio.Atmos Environ. 2007; 41: 8140-8149Crossref Scopus (71) Google ScholarThe National Survey of Lead and Allergens in Housing was a population-based study that measured indoor allergens in US homes. Of the surveyed homes, 51.5% had at least 6 detectable allergens, and 45.8% had at least 3 allergens that exceeded increased levels. An increased allergen level was defined as 7 μg/g of Alt a 1 for Alternaria alternata. The most commonly found allergens detected at increased levels were cat, dog, and Alternaria. Children with high allergen exposure had increased odds of having asthma symptoms.[13]Salo P.M. Arbes Jr., S.J. Crockett P.W. Thorne P.S. Cohn R.D. Zeldin D.C. Exposure to multiple indoor allergens in US homes and its relationship to asthma.J Allergy Clin Immunol. 2008; 121: 678-684.e2Abstract Full Text Full Text PDF PubMed Scopus (155) Google ScholarFungal ConstituentsAccording to allergen databases (http://www.meduniwien.ac.at/allergens/allfam/), 189 fungal species are thought to produce allergens, and these consist of 61 protein families that contain approximately 132 allergens.[14]Radauer C. Bublin M. Wagner S. Mari A. Breiteneder H. Allergens are distributed into few protein families and possess a restricted number of biochemical functions.J Allergy Clin Immunol. 2008; 121: 847-852.e7Abstract Full Text Full Text PDF PubMed Scopus (378) Google Scholar Some allergens from the genera Alternaria, Aspergillus, and Cladosporium are well characterized, and some have even been purified.[15]Kurup V.P. Fungal allergens.Curr Allergy Asthma Rep. 2003; 3: 416-423Crossref PubMed Scopus (55) Google Scholar On the basis of genomewide studies of several species, fungi appear to share a highly conserved set of allergen orthologues. These allergens include enolases, heat shock proteins, cyclophilins, proteases, redoxins, and disulphide isomerases. Other allergens include peroxisomal membrane proteins, acid ribosomal proteins, and alcohol dehydrogenases.[16]Bowyer P. Fraczek M. Denning D.W. Comparative genomics of fungal allergens and epitopes shows widespread distribution of closely related allergen and epitope orthologues.BMC Genomics. 2006; 7: 251Crossref PubMed Scopus (66) Google ScholarFungi also produce a number of other nonvolatile metabolites, including ergosterol, β-glucans, and mycotoxins. Because ergosterol is nearly unique to fungi, its measurement has been used to estimate fungal load in house dust.[17]Choi H. Byrne S. Larsen L.S. et al.Residential culturable fungi, (1-3, 1-6)-beta-d-glucan, and ergosterol concentrations in dust are not associated with asthma, rhinitis, or eczema diagnoses in children.Indoor Air. 2014; 24: 158-170Crossref PubMed Scopus (34) Google Scholar Airborne ergosterol correlates with airborne glucan; however, it is more highly correlated with the presence of visible mold.β-Glucans are polysaccharides found in the outer cell membrane of fungi, higher plants, and some bacteria.[18]Cherid H. Foto M. Miller J.D. Performance of two different Limulus amebocyte lysate assays for the quantitation of fungal glucan.J Occup Environ Hyg. 2011; 8: 540-543Crossref PubMed Scopus (12) Google Scholar The cell walls of grasses and fungi contain β-1,3-d-glucan, sometimes in mixtures with other glucans. Studies in humans suggest that there is a dose-response relationship between exposure to airborne fungal glucan and respiratory symptoms, itching skin, hoarseness, and fatigue.[19]Douwes J. (1→3)-Beta-D-glucans and respiratory health: a review of the scientific evidence.Indoor Air. 2005; 15: 160-169Crossref PubMed Scopus (175) Google Scholar Exposure to glucans has also been associated with an increased prevalence of atopy and a decrease in forced expiratory volume.[20]Thorn J. Rylander R. Airways inflammation and glucan in a rowhouse area.Am J Respir Crit Care Med. 1998; 157: 1798-1803Crossref PubMed Scopus (115) Google ScholarMycotoxins are low-molecular-weight organic chemicals produced by fungi to better compete for nutrient resources by eliminating growth of other microorganisms in the immediate environment. A person must be exposed to a sufficient concentration for a sufficient amount of time to experience a toxic effect. Because of agricultural exposure, human health effects of mycotoxins have been extensively studied.[21]Miller J. Mycotoxins.in: Jorgenson S. Encyclopedia of Environmental Management. Taylor & Francis, New York, NY2013: 1696-1699Google Scholar These effects include T-2 toxin from Fusarium, trichothecene mycotoxins from Stachybotrys, mitogillin from Aspergillus, and others. Most mycotoxins are rapidly metabolized and eliminated within hours after ingestion in farm animals and humans. Although commercial fungal extracts are not routinely assayed for mycotoxins, they are dialyzed, which should remove mycotoxins if they are present in the source material.Volatile metabolites are often revered to as microbial volatile organic compounds. Such volatile compounds have a distinctive musty or moldy odor that can serve as reliable indications of mold growth. This odor often is transferred to clothes, leading individuals who live in moldy houses to smell musty. Occupants of moldy houses frequently become adapted to the smell and may be unaware of its presence. The direct health risk of microbial volatile organic compounds is unclear; however, they could act as an irritants in susceptible individuals.[22]Gunschera J. Fuhrmann F. Salthammer T. Schulze A. Uhde E. Formation and emission of chloroanisoles as indoor pollutants.Environ Sci Pollut Res Int. 2004; 11: 147-151Crossref PubMed Scopus (43) Google ScholarFungal SensitivityPatients with a clinical history of fungal allergy develop symptoms when exposed to environments likely to have high fungal exposure. Examples of questions to ask patients suspected of having fungal allergy include whether symptoms are worse in old homes or buildings, basements, or other damp environments, after rain storms, and during raking or mowing the lawn.[23]Horner W.E. Barnes C. Codina R. Levetin E. Guide for interpreting reports from inspections/investigations of indoor mold.J Allergy Clin Immunol. 2008; 121: 592-597.e7Abstract Full Text Full Text PDF PubMed Scopus (27) Google ScholarTests for Fungus SensitizationSensitization to fungi can be detected using prick24Escudero A.I. Sanchez-Guerrero I.M. Mora A.M. et al.Cost-effectiveness of various methods of diagnosing hypersensitivity to Alternaria.Allergol Immunopathol (Madr). 1993; 21: 153-157PubMed Google Scholar, 25Fernandez C. Bevilacqua E. Fernandez N. et al.Asthma related to Alternaria sensitization: an analysis of skin-test and serum-specific IgE efficiency based on the bronchial provocation test.Clin Exp Allergy. 2011; 41: 649-656Crossref PubMed Scopus (30) Google Scholar and intradermal[24]Escudero A.I. Sanchez-Guerrero I.M. Mora A.M. et al.Cost-effectiveness of various methods of diagnosing hypersensitivity to Alternaria.Allergol Immunopathol (Madr). 1993; 21: 153-157PubMed Google Scholar skin tests with fungal extracts or in vitro tests for specific IgE antibodies.24Escudero A.I. Sanchez-Guerrero I.M. Mora A.M. et al.Cost-effectiveness of various methods of diagnosing hypersensitivity to Alternaria.Allergol Immunopathol (Madr). 1993; 21: 153-157PubMed Google Scholar, 25Fernandez C. Bevilacqua E. Fernandez N. et al.Asthma related to Alternaria sensitization: an analysis of skin-test and serum-specific IgE efficiency based on the bronchial provocation test.Clin Exp Allergy. 2011; 41: 649-656Crossref PubMed Scopus (30) Google Scholar, 26Williams P.B. Dolen W.K. Koepke J.W. Selner J.C. Comparison of skin testing and three in vitro assays for specific IgE in the clinical evaluation of immediate hypersensitivity.Ann Allergy. 1992; 68: 35-45PubMed Google Scholar Fungal extracts currently are unstandardized in part due to variability among manufacturers and even between batches from the same manufacturer. The performance characteristics of diagnostic tests are not known with the exception of Alternaria, which has been studied in several clinical trials that used either nasal[24]Escudero A.I. Sanchez-Guerrero I.M. Mora A.M. et al.Cost-effectiveness of various methods of diagnosing hypersensitivity to Alternaria.Allergol Immunopathol (Madr). 1993; 21: 153-157PubMed Google Scholar or bronchial[25]Fernandez C. Bevilacqua E. Fernandez N. et al.Asthma related to Alternaria sensitization: an analysis of skin-test and serum-specific IgE efficiency based on the bronchial provocation test.Clin Exp Allergy. 2011; 41: 649-656Crossref PubMed Scopus (30) Google Scholar provocation as the criterion standard for rhinitis and asthma, respectively (Table 3). In these studies, skin prick tests for Alternaria had high positive likelihood ratios and low negative likelihood ratios, indicating that the test effectively discriminated between patients with and without sensitivity for rhinitis and asthma. Intradermal tests had positive likelihood ratios near 1, indicating that for patients with negative skin prick test results, such tests did not provide useful information. In vitro tests had high positive likelihood ratios, but the negative likelihood ratio was not very low, indicating that the test is good at detecting sensitive patients but not so good at ruling out nonallergic ones.Table 3Performance characteristics of skin prick test, intradermal skin test when skin prick test result is negative, and in vitro tests for specific IgE to AlternariaTestLR+LR−SensitivitySpecificityStandardReferenceSkin prick test11.750.0595.291.9Nasal[24]Escudero A.I. Sanchez-Guerrero I.M. Mora A.M. et al.Cost-effectiveness of various methods of diagnosing hypersensitivity to Alternaria.Allergol Immunopathol (Madr). 1993; 21: 153-157PubMed Google Scholar9.450.0297.889.7Bronchial[25]Fernandez C. Bevilacqua E. Fernandez N. et al.Asthma related to Alternaria sensitization: an analysis of skin-test and serum-specific IgE efficiency based on the bronchial provocation test.Clin Exp Allergy. 2011; 41: 649-656Crossref PubMed Scopus (30) Google ScholarIntradermal test (negative skin prick test result)1.040.041003.8Bronchial[25]Fernandez C. Bevilacqua E. Fernandez N. et al.Asthma related to Alternaria sensitization: an analysis of skin-test and serum-specific IgE efficiency based on the bronchial provocation test.Clin Exp Allergy. 2011; 41: 649-656Crossref PubMed Scopus (30) Google ScholarIn vitro test140.4655.896Nasal[24]Escudero A.I. Sanchez-Guerrero I.M. Mora A.M. et al.Cost-effectiveness of various methods of diagnosing hypersensitivity to Alternaria.Allergol Immunopathol (Madr). 1993; 21: 153-157PubMed Google Scholar150.281.194.6Nasal[26]Williams P.B. Dolen W.K. Koepke J.W. Selner J.C. Comparison of skin testing and three in vitro assays for specific IgE in the clinical evaluation of immediate hypersensitivity.Ann Allergy. 1992; 68: 35-45PubMed Google Scholar2.310.7635.876Bronchial[24]Escudero A.I. Sanchez-Guerrero I.M. Mora A.M. et al.Cost-effectiveness of various methods of diagnosing hypersensitivity to Alternaria.Allergol Immunopathol (Madr). 1993; 21: 153-157PubMed Google ScholarAbbreviations: LR+, positive likelihood ratio; LR−, negative likelihood ratio. Open table in a new tab A recent study compared percentages of positive fungal skin prick test results with ImmunoCAP. Skin prick testing detected 100% of patients who were sensitized to only one of Alternaria, Candida, or Trichophyton, whereas ImmunoCAP detected 89%, 75%, and 61%, respectively. When multiply fungus-sensitized patients were evaluated, the in vitro tests generally detected a higher percentage of patients than did the skin prick tests.[27]Mari A. Schneider P. Wally V. Breitenbach M. Simon-Nobbe B. Sensitization to fungi: epidemiology, comparative skin tests, and IgE reactivity of fungal extracts.Clin Exp Allergy. 2003; 33: 1429-1438Crossref PubMed Scopus (185) Google ScholarFungi TestsIn one study, the most common skin prick test–positive genera among 3,248 patients with any allergy were Alternaria (12.6%) and Candida (8.5%). When only patients with a positive skin test result to a fungus were considered (19% of allergic patients), the most common positive test results were for Alternaria (66.1%), Candida (13.1%), Cladosporium (13.1%), Aspergillus (12.6%), and Trichophyton (10.2%). In patients who were sensitized to only 1 or 2 fungi, the most common genera consistently reactive were Alternaria and Candida. Multiply fungus-sensitized patients reacted in descending order to Alternaria, Candida, Cladosporium, Aspergillus, Saccharomyces, Penicillium, and Trychophyton.[27]Mari A. Schneider P. Wally V. Breitenbach M. Simon-Nobbe B. Sensitization to fungi: epidemiology, comparative skin tests, and IgE reactivity of fungal extracts.Clin Exp Allergy. 2003; 33: 1429-1438Crossref PubMed Scopus (185) Google ScholarThis finding suggests that a limited number of skin tests with Alternaria, Candida, Cladosporium, Aspergillus, and Trichophyton could be used to identify patients with fungal sensitization because most will react to one of these. Because Candida and Trichophyton are not aeroallergens, their use in this context would be as markers for fungal sensitization and not to diagnose Candida or Trichophyton hypersensitivity disorders. A more extensive panel of fungi could be tested for if it is important to identify the specific sensitization pattern. This might be the case if immunotherapy is being considered or if evidence of an association between exposure and fungus-induced symptoms in a patient's environment is being sought.Health Effects of FungiExposure to airborne fungi is associated with morbidity in patients who have respiratory disorders, including rhinitis and asthma. Other conditions, such as atopic dermatitis, can be exacerbated by cutaneous fungi, such as Malassezia species. Several other diseases are known to be caused or triggered by exposure to fungi, including allergic bronchopulmonary mycosis, allergic fungal sinusitis, and hypersensitivity pneumonitis. Candida hypersensitivity is controversial because the syndrome is poorly defined and the association between Candida exposure and the condition has not been demonstrated.Because fungi can cause adverse health effects via IgE- or non–IgE-mediated mechanisms,[2]Chen J. Seviour R. Medicinal importance of fungal beta-(1→3), (1→6)-glucans.Mycol Res. 2007; 111: 635-652Crossref PubMed Scopus (456) Google Scholar it is not necessary for a person to be allergic to fungi to experience symptoms after exposure. Prevention of health effects due to fungal exposure can be separated into primary (exposures that cause development of asthma in young children), secondary (exposure that leads to morbidity in individuals who already have asthma), and tertiary (medications used to treat symptoms that already are present) prevention. This review will not address tertiary prevention.Primary PreventionPrimary prevention is based on the assumption that exposure to fungi increases the risk of developing an adverse health effect (eg, sensitization and asthma) and that reducing exposure can reduce that risk. Studies on the association between increased fungal exposure and increased risk of developing asthma generally are observational, which cannot be used to infer causality. Studies to prove causality would need to randomly assign children to live in an environment with various amounts of fungal exposure and then observe for subsequent health effects. Although this has been done for dust mites,[28]Arshad S.H. Bojarskas J. Tsitoura S. et al.Prevention of sensitization to house dust mite by allergen avoidance in school age children: a randomized controlled study.Clin Exp Allergy. 2002; 32: 843-849Crossref PubMed Scopus (54) Google Scholar such studies have not been performed for fungi.A comprehensive review found sufficient evidence to conclude that there is an association between indoor dampness (defined as sufficient water activity on indoor substrates to support fungal growth), fungal exposure, and increased risk of developing asthma in allergic and nonallergic individuals.[29]Mendell M.J. Mirer A.G. Cheung K. Tong M. Douwes J. Respiratory and allergic health effects of dampness, mold, and dampness-relate" @default.
• W1968590900 created "2016-06-24" @default.
• W1968590900 creator A5023501914 @default.
• W1968590900 creator A5036900631 @default.
• W1968590900 date "2015-02-01" @default.
• W1968590900 modified "2023-10-16" @default.
• W1968590900 title "Mold allergy revisited" @default.
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