Aspergillus fumigatus

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Code: m3
Latin name: Aspergillus fumigatus
Source material: Spores and mycelium

Allergen Exposure

Geographical distribution
The species A. fumigatus was well-described and illustrated in the 1850s by Fresenius, working with lung material from birds dying of aspergillosis. It is a thermotolerant fungus with worldwide distribution. Due to its wide temperature range for good growth it is not limited to habitats with permanently high temperatures, even though these are obviously very frequently reported. This microorganism is one of the most prevalent airborne fungal pathogens; (1) although in comparison with other aeroallergens the concentration of spores in the air may be low, though with high localised counts. 

Aspergillus fumigatus is an opportunistic fungus causing allergic and invasive aspergillosis in humans and animals. It is unusual compared to other allergen sources in that it is both a primary and an opportunistic pathogen, as well as an important major allergen. (2) Its conidia production is prolific, so humans are continually inhaling its ubiquitous spores. The result is that exposure of the respiratory tract is almost constant. However, inhalation rarely causes adverse effects, as the conidia are usually eliminated efficiently by the innate immune system. But increasing use of immunosuppressive therapy has resulted in increasingly frequent conditions involving infection by A fumigatus.

Although the burden of invasive disease caused by A. fumigatus is substantial, the basic biology of the organism is mostly obscure. (3)

A. fumigatus is isolated from human habitats and vegetable compost heaps. It is found in soils, leaf and plant litter, decaying vegetables and roots, bird droppings, tobacco, and stored sweet potatoes. In comparison with other aeroallergens, the concentration of spores in the air may be low, though there may be high localised counts.

Unexpected exposure
Due to the nature of this allergen, nearly all exposure is unexpected.

Allergen Description

A. fumigatus secretes an array of complex biologically-active glycoprotein antigens and allergens. (4, 5, 6) Molecular characterisation has reported the presence of complex carbohydrate moieties, heat-shock proteins, and the activity of enzymes such as elastase, protease, catalase, dismutase, and cytotoxic ribonuclease. Some allergens and antigens have a multifunctional nature, which may play an important role in the pathogenesis of disease. (7)

A. fumigatus and A. niger appear to be allergenically distinct from A. versicolor, A. nidulus, and A. glaucus. (8) Extracts of A. fumigatus may also produce a toxic aflatoxin. (9)

The following allergens have been identified to date:

  • Asp f 1, an 18 kDa protein, also known as ribotoxin and mitogillin. (10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26)
  • Asp f 2, a 37 kDa protein, a fibrinogen-binding protein. (2, 3, 7, 9, 27, 28, 29, 30, 31, 32, 33, 34)
  • Asp f 3, an 18 kDa protein, also known as PMP, a peroxisomal protein. (2, 3,8, 9, 35, 36, 37)
  • Asp f 4, a 30 kDa protein. (2, 7, 9, 38, 39, 40)
  • Asp f 5, a 42 kDa protein, also known as MEP, a metalloprotease. (2, 9, 31, 41)
  • Asp f 6, a 23 kDa protein, also known as Mn-SOD, a manganese superoxide dismutase. (2, 7, 9, 31, 42, 43, 44, 45, 46, 47)
  • Asp f 7. (2, 3, 9)
  • Asp f 8, also known as ribosomal protein P2. (2, 3, 9, 39, 48)
  • Asp f 9, a glycosyl hydrolase. (2, 3, 9, 49, 50)
  • Asp f 10, also known as PEP, an aspartic protease. (2, 3, 9, 33)
  • Asp f 11, also known as cyclophilin, a cyclophilin or rotamase. (2, 3, 9, 51, 52)
  • Asp f 12, a 65 kDa protein, also known as heat shock protein P90. (2, 3, 9, 53)
  • Asp f 13,a 32-33 kDa protein, also known as oryzin, an alkaline serine protease. (2, 9, 19, 54, 55, 56)
  • Asp f 15, a serine protease. (2, 9)
  • Asp f 16. (2, 9, 42, 57)
  • Asp f 17. (2, 3, 9)
  • Asp f 18, also known as cerevisin, a vacuolar serine protease. (2, 9, 58, 59, 60, 61)
  • Asp f 22, a 47 kDa protein, also known as enolase, a glycolytic enzyme. (2, 3, 9, 62, 63, 64)
  • Asp f 23, a ribosomal protein L3. (2, 3, 65)
  • Asp f 27, also known as cyclophilin, a cyclophilin. (2, 66)
  • Asp f 28, a thioredoxin. (2, 67)
  • Asp f 29, a thioredoxin. (2, 59, 68)
  • Asp f 34, a 19.4 kDa protein, also known as PhiA. (2, 69)
  • Asp f GST, a 26 kDa protein, also known as GST, a glutathione-S-transferase. (3, 70)
  • Asp f 56kD, a 56 kDa protein, a fungal serine protease. (2)

Asp f 1
Asp f 1 is a major allergen and is produced by the mycelia of A. fumigatus. Germination of spores and growth of the fungus appear to be essential for the production of this allergen. (6) More than 80% of patients with allergic bronchopulmonary aspergillosis (ABPA) are sensitised to this allergen. (1, 24, 26, 71, 72) It is also raised in patients with cystic fibrosis with the complication of ABPA. (6) It is not present in spores, and can be used as a specific marker for the detection of germination of this fungus. (73)

Studies have demonstrated that recombinant Asp f 1 (rAsp f I/a) has similar functional characteristics when compared to the native allergen, and this has enabled serologic and clinical diagnostic exploration of the relevance of this allergen in A. fumigatus-associated diseases. (74) This has demonstrated some complex inter-relationships: for example, sensitisation to A. fumigatus in patients with atopic dermatitis is not related to the major allergen Asp f 1, in contrast to the high incidence of sensitisation to this allergen in allergic asthmatics. (75)

Early research concluded that the recombinant version of Asp f 1 (rAsp fI/a) was a highly sensitive and specific test that could be used to identify ABPA reliably in cystic fibrosis patients. (76) In a study of sera from 147 cystic fibrosis (CF) patients, specific IgE to A. fumigatus and five common inhalant allergens was measured with a radioallergosorbent test. Thirty (20%) of the patients had specific IgE to A. fumigatus, and 22 (15%) of these patients had developed total IgE levels > or = 400 IU/ml, raising the consideration of a diagnosis of ABPA. Eighty-four percent of CF sera contained specific IgG to Asp f 1, compared with 6% of sera from control patients and 20% of sera from 25 allergic children with asthma, only one of whom had specific IgE directed at A. fumigatus. (77) Extreme caution should be exercised in using Asp f 1 for in vivo skin testing, as it is a potent cytotoxin. (6)

Asp f 2
Asp f 2 is also a major allergen, with sensitisation to this allergen occurring in more than 90% of A. fumigatus-sensitised individuals. (22) Similar to Asp f 1, sensitisation may vary depending on the underlying disease: in a study of 25 patients with ABPA, 96% had IgE antibodies directed against Asp f 2, whereas none of the normal control subjects, or the subjects with allergic asthma who had positive results on the skin-prick test, had a reaction. (26)

Asp f 3
In a study evaluating recombinant Asp f 3 in patients with ABPA (n=11) or allergic asthma with A. fumigatus sensitisation (n=8) and healthy control subjects, all 11 patients with ABPA and 5 out of 8 A. fumigatus-sensitised asthmatics without ABPA exhibited a type I skin reaction. All rAsp f 3 skin-test positive subjects showed relevant rAsp f 3-specific serum IgE levels compared with intradermal skin test (IDT)-negative individuals who scored below the rAsp f 3-ImmunoCAP cut-off values of < 0.35 kU(A)/L. Therefore sensitisation to rAsp f 3 was found in 84% of asthmatics sensitised to this fungus. (32) Similar sensitisation to rAsp f 3 was demonstrated in 72% of 89 individuals sensitised to A. fumigatus. (33)

Asp f 4
In an evaluation of intracutaneous testing in 50 patients with cystic fibrosis (CF) (12 with ABPA and 21 with allergy to A. fumigatus), all patients with ABPA reacted to at least one of the two A. fumigatus allergens tested (rAsp f 4 and rAsp f 6). However, the intracutaneous tests were negative or only marginally positive in the patients with allergy to A. fumigatus, and completely negative in the control patients. The authors suggested that rAsp f 4 and rAsp f 6 can be considered specific markers for ABPA, and in particular, for early diagnosis of the disease; a clear distinction between allergic sensitisation to A. fumigatus and ABPA is essential for therapy to prevent deterioration of pulmonary function in subjects with ABPA. (78) Similar findings were reported in another study, which concluded that the IgE cut-off values for positive skin reactions to rAsp f 4 and rAsp f 6 of 0.9 and 1.2 kU(A)/L corresponded to allergen-specific serum concentrations of 2 to 3 microg/L, and allowed a sensitive, highly specific diagnosis of ABPA. (79)

Asp f 6
Similarly, Asp f 6 has been shown to be recognised by IgE from ABPA patients but not from A. fumigatus-sensitised individuals, which result can be used to differentiate between these two groups of allergic patients. A. fumigatus colonises its environment by the formation of hyphae. Hyphae are found in the lungs of ABPA patients, but not in patients suffering from atopic asthma. Asp f 6 is specifically expressed in hyphae, which might explain why an IgE response to Asp f 6 is specific for ABPA patients. (41)

Asp f 9
Seventy percent of the patients with ABPA were shown to have high levels of serum-specific IgE to Asp f 16, whereas patients with allergic asthma, Aspergillus skin test-positive asthmatics without clinical evidence of ABPA, and normal controls did not show Asp f 16-specific IgE binding. (46)

Asp f 12
Asp f 12 belongs to the heat shock protein 90 (Hsp 90) family. Recombinant Asp f 12 has been shown to react with serum IgE and IgG antibodies from patients with ABPA. (47) Hsps are considered to be important for stress response during inflammation. (6)

Asp f 16
Seventy percent of the patients with ABPA were shown to have high levels of serum IgE antibodies to Asp f 16, whereas patients with allergic asthma, Aspergillus skin test-positive asthmatics without clinical evidence of ABPA, and normal controls failed to show Asp f 16-specific IgE binding by ELISA. (44)

Asp f 18
Asp f 18 was shown to react with IgE antibodies in 79% of the Aspergillus-sensitised individuals, and may be considered a major allergen of A. fumigatus. (52)

Asp f 23
Specific IgE directed at Asp f 23 was demonstrated in 26.7% of 30 individuals with ABPA. (61)

Asp f 34
Asp f 34 appears to be a fungal cell-wall component, and shows sequence homology to phiA, an essential protein for the formation of conidia in the genus Aspergillus. About 94% of ABPA and 46% of A. fumigatus-sensitised individuals tested were shown to have Asp f 34-specific serum IgE. Eight patients with anti-Asp f 34 serum IgE tested reacted positively in SPT, whereas four A. fumigatus-sensitised individuals without Asp f 34-specific IgE and eight healthy controls scored negatively. (63)

Asp f 56kD
IgE against Asp f 56kD was detected in 75.5% of 12 A. fumigatus-allergic patients. It also exhibited IgG and IgE immunobinding, with antibodies present in the sera of allergic bronchopulmonary aspergillosis patients. (2)

Specific IgE to a recently-isolated allergen, Asp f AfCalAp, a laminin-binding protein, was demonstrated in the sera of 2 out of 7 patients with ABPA. (80)

A number of studies have evaluated the diagnostic use of Aspergillus allergens, and recombinant allergens, in the diagnosis of Aspergillus-caused diseases. Studies have demonstrated a heterogenous pattern of sensitisation to Aspergillus allergens.

Studies have specifically tried to address whether IgE responses to Aspergillus allergens, in particular purified recombinant forms, may differentiate ABPA from atopic CF patients. A study evaluated serum IgE reactivity to seven recombinant purified allergens and to a crude extract of Aspergillus in 15 patients with ABPA, and 23 Aspergillus skin test-positive (ST+) and 19 Aspergillus skin test-negative (ST-) CF patients. Four of the ABPA CF patients were studied before and after developing ABPA. The ABPA patients had significantly increased IgE reactivity to Asp f 2, Asp f 3, Asp f 4, Asp f 6, and Asp f 16 compared with the Asperigillus ST+ and ST- non-ABPA CF patients. In ABPA patients studied during periods of remission, the IgE reactivity to Asp f 3 and f 4 remained significantly elevated compared with Aspergillus ST+ non-ABPA patients. The IgE responses, when considered to be either positive or negative to Asp f 3 and f 4, significantly differentiated ABPA from Aspergillus ST+ and ST- non-ABPA CF patients.

The study concluded that IgE reactivity to a panel of purified Aspergillus allergens, especially to Asp f 3 and Asp f 4, differentiates ABPA from atopic Aspergillus ST+ non-ABPA CF patients, and that serial determinations of IgE reactivity to individual purified Aspergillus allergens, especially Asp f 3, demonstrate that increases in IgE reactivity may provide improved distinction between stages of flares and remission compared with changes in IgE reactivity to a crude Aspergillus extract. (81)

Similarly, an earlier study demonstrated the differential IgE responses to the allergens in A. fumigatus-sensitised CF patients, with or without ABPA, and CF controls without sensitisation to A. fumigatus. rAsp f 1 and rAsp f 3 were recognised by sera from A. fumigatus-sensitised CF-patients with or without ABPA. rAsp f 6 and rAsp f 4 were recognised exclusively by IgE from the sera of CF patients with ABPA. The authors concluded that Asp f 4 and Asp f 6 represented specific markers for ABPA and allowed a sensitive, fully-specific diagnosis of the disease, and that the data suggested distinct IgE responses to colonisation of the bronchial tree in CF patients with ABPA or A. fumigatus allergy. (46)

Other studies have demonstrated similar variability and markers. In a study of recombinant Asp f 1, f 2, f 3, f 4, and f 6 in the sera of ABPA patients, A. fumigatus skin-prick test-positive asthmatics, and normal controls (all from the USA and Switzerland), all the recombinant allergens showed IgE antibody binding with sera from patients with ABPA, whereas only (and fewer) asthmatics and normal sera showed significant binding. Recombinant Asp f 2, f 4, and f 6 together reacted with all the ABPA patients studied, leading the authors to conclude that Asp f 2, f 4, and f 6 can be used in the serodiagnosis of ABPA. IgE antibody binding to Asp f 1 and f 3 was not specific. (82)

An observational, cross-sectional study of 65 Brazilian patients (aged from 12 to 81 years) with asthma sensitised to A. fumigatus (positive skin tests) demonstrated that serum IgE specific for Asp f (IgEm3) could be detected in 40% of patients. Only 19 of these 65 patients had IgE against at least one recombinant, recombinant Asp f1, f2, f3, f4, and f6. ABPA was diagnosed by classical criteria in six patients (9.2%); and of these, only two had serum IgE specific for the recombinant allergens. One had low levels of specific IgE only against rAsp f 3. (83)

Potential Cross-Reactivity

Mala f 2 and Mala f 3, from Malassezia furfur, a common allergen in atopic dermatitis, have sequence homology with two peroxisomal membrane proteins of Candida boidinii and Asp f 3. (84, 85)

Mala s 11 from Malassezia furfur has a high degree of amino acid sequence homology to manganese superoxide dismutase (MnSOD) from Homo sapiens (50%) and A. fumigatus (Asp f 6) (56%). (86) The clinical relevance of this cross-reactivity was not determined, except that MnSODs from other organisms (including humans) are recognised by IgE antibodies from individuals sensitised to Asp f 6. (37)

Asp f 12, a heat shock protein belonging to the hsp 90 family, is homologous with other members of the hsp 90 family of heat shock proteins in human beings and other organisms. (47) The clinical relevance of this needs to be determined.

Pen ch 13, an alkaline serine protease allergen from P. chrysogenum, is cross-reactive with Pen c 13 of Penicillium citrinum and Asp f 13, suggesting that atopic patients sensitised primarily by either of these prevalent fungal species may develop allergic symptoms by exposure to other environmental fungi, due to cross-reacting IgE antibodies against this protease. (87) Asp f 13 has also been shown to have a 42-49% identity with two proteases from P. cyclopium and T. Album, and with the Pen c 1 allergen from P. citrinum. (48)

Asp f 16 has been shown to have extensive sequence homology to Asp f 9 at the N-terminal region of the protein. (46) 

Asp f 18, a major allergen of Aspergillus-sensitised individuals, a vacuolar serine proteinase, shows IgE cross-reactivity with P. notatum and P. oxalicum. (58) 

Extensive cross-reactivity has been reported to occur between the enolases of Cladosporium herbarum, Alternaria alternata, Saccharomyces cerevisiae, Candida albicans and A. fumigatus. (88) S. cerevisiae (Baker's yeast) enolase has been shown to exhibit high cross-reactivity with other fungal enolases, in particular with C. herbarum, A. alternata, C. Albicans and Asp f 22. (64) The enolase from Rhodotorula mucilaginosa has a high sequence identity with enolase allergens from C. albicans (85%), S. cerevisiae (76%), P. citrinum (76%), A. fumigatus (76%), C. herbarum (76.5%), and A. alternata (74%). However, the authors point out that although enolases are highly conserved allergens among different fungal species, most of the allergic patients examined in this study differed in their IgE reactivity to the 5 different fungal enolases tested. (62)

Asp f 27, a cyclophilin, may exhibit cross-reactivity with other cyclophilins such as Mala s 6 from Malassezia sympodialis. (66)

Asp f glutathione-S-transferase has been demonstrated to be cross-reactive in other fungal extracts containing this allergen, e.g. A. alternata, C. herbarum, Curvularia lunata, and Epicoccum purpurascens. (64)

Clinical Experience

IgE-mediated reactions
Aspergillus fumigatus is one of the most prevalent airborne fungal pathogens, and the etiological agent in 80% of Aspergillus-related diseases. Inhalation of conidia and mycelium of A. fumigatus can lead to benign colonisation of the lung by several diseases, the severity of which depends on the host's immune response: as a result of the complexity in the antigenic structure of A. fumigatus, the varying immune responses of different hosts lead to a wide spectrum of clinical conditions such as hypersensitivity, pneumonitis, allergic rhinitis, IgE-mediated asthma, allergic bronchopulmonary aspergillosis (ABPA), aspergilloma, and invasive aspergillosis in immune-compromised patients and in individuals with cystic fibrosis. (1, 6, 89, 90, 91, 92, 93)

Other species that have been associated with aspergillosis include A.flavus, A. nidulans, A. niger, A. terreus, A. oryzae and A.ochraceous. (6)

Other uncommon conditions associated with Aspergillus disease may occur. Disseminated intravascular coagulation (DIC) is a rarely-described finding in invasive pulmonary aspergillosis. (94) Systemic Aspergillus presenting with visual symptoms has been reported. (95) Osteomyelitis has been described. (96)

About 15-20% of allergic asthmatics suffer from Aspergillus-induced allergies. ABPA is an immunologically complex allergic disorder in which type I and type III hypersensitivity reactions are involved in pathogenesis. ABPA may occur as a complication of asthma or cystic fibrosis (CF). (97) ABPA is clinically characterised by episodic bronchial obstruction; positive immediate skin reactivity; elevated total immunoglobulin E (IgE), specific IgG, and IgE antibodies; peripheral and pulmonary eosinophilia; central bronchiectasis; and expectoration of brown plugs. (13) High levels of specific IgE and IgG antibodies in these patients are of diagnostic value. (3) Indeed, specific IgE antibody against A. fumigatus may be high and demonstrated in over 80% of cases with confirmed clinical ABPA. (98) Although not common, ABPA may occur at any age, as illustrated by a report of ABPA with hilar adenopathy in a 42-month-old boy. (99) In an Indian study, over a period of 2 years, of consecutive patients with asthma presenting to a north Indian chest clinic and screened with an Aspergillus skin test, of 564 patients, 223 patients (39.5%) were found to be positive, and ABPA was diagnosed in 126 patients (27.2%). (100)

A. fumigatus has also been implicated as an important causative agent in allergic fungal sinusitis. (9) Other diseases, such as extrinsic allergic alveolitis (hypersensitivity pneumonitis) and Farmer's Lung, have been reported to be linked to this mould. (101, 102, 103)

In a Japanese study of 94 asthmatic patients (mean age 12 years) determining sensitisation to A. restrictus, A. fumigatus, A. alternata and house dust with skin- and serum-specific IgE tests, positive reactions were demonstrated in 8 (8.5%), 8 (8.5%), 15 (16.0%) and 69 (73.4%) patients respectively. Twenty-two (23.4%) were shown to have serum-specific IgE directed at A. fumigatus. (104) Similarly, in a study in Sao Paulo, Brazil, evaluating sensitisation in 201 patients with asthma and/or allergic rhinitis to 42 airborne fungi using skin-specific IgE tests, 15 were shown to be sensitised to Alternaria, 15 to Aspergillus, 23 to Aureobasidium, 37 to Candida, 15 to Chaetomium, and 19 were shown to be sensitised to Epicoccum. (105)

In a study conducted in Kolkata Metropolis, India, skin-prick tests were performed on 1079 allergic patients between the ages of 5 and 50 years using a variety of 16 common aero-allergens, of which approximately 22% were sensitised to A. fumigatus. (106) Similarly, in another recent Indian report of the results of 2880 skin prick tests with 60 allergens performed on 48 patients with nasobronchial allergy, A. fumigatus was found to be a common sensitiser. (107)

A large pan-European study, demonstrating sensitisation patterns using skin-prick tests for different inhalant allergens in patients across Europe, found the sensitisation rate for Aspergillus to vary from country to country: Austria (Vienna) - 0.5; Belgium (Ghent) - 2.4; Denmark (Odense) - 4.8; Finland (Helsinki) - 2.5; France (Montpellier) - 4.3; Germany (Berlin/Munich) - 6.2; Greece (Athens) - 10.3; Hungary (Budapest) - 2.5; Italy (Genoa/Palermo) - 0.4; The Netherlands (Amsterdam) - 4.6; Poland (Lodz) - 4.8; Portugal (Coimbra) - 6.9; Switzerland (Zurich) - 2.1; United Kingdom (London) - 7.9. (108) Similar results were suggested in a second publication. (109)

In a Japanese study evaluating the prevalence of allergic rhinitis in subjects between 20 and 49 years of age, Cedar pollen and mites were predominant allergen sources. Two percent were sensitised to A. fumigatus. (110)

In a Thai study of patients with allergic rhinitis, of 434 patients, 277 (63.8%) were skin-prick test-positive. Skin-prick tests for Aspergillus were positive in 2.2%. (111)

A Turkish study, to determine whether or not first-degree relatives with respiratory allergies are more likely to be skin test-positive to the same allergen extracts as unrelated patients, tested by skin test for 35 common aeroallergens in 264 pairs of genetically related subjects and 264 pairs of age- and sex-matched (but unrelated) subjects, and found sensitisation for Aspergillus mix in 3.4%. (112)

Clearly the frequency of sensitisation may vary, not only in different population groups but also depending on locality. A Mongolian screening study of 9453 subjects aged 10 to 60 years, of which a subsample of 869 subjects underwent clinical examination (including skin-prick tests), reported the frequency of sensitisation to A. fumigatus in Ulaanbaatar city to be 1.8%, compared to 0.3% for patients from rural towns and villages. (113)

Importantly, even young children may be sensitised, as demonstrated in an egg-allergy study of 2-year-olds; of 1942 children, 3 (0.2%) were sensitised to A. fumigatus. (114)

A Danish study evaluating sensitisation to three common species of moulds (C. herbarum, A. alternaria, A. fumigatus) and other common inhalation allergens in 677 asthmatic patients using skin- and serum-specific IgE tests, found that 10% of patients were SPT positive and 5% serum-specific IgE positive to at least one mould species. (115)

In a study evaluating specific IgG antibodies against antigens of a contaminated air conditioner in the sera of 134 workers at a printing company, 64% of the workers had significantly elevated levels of IgG antibodies to these antigens, as compared to a nonexposed control group: Fusarium 25%, Penicillium notatum 23%, Alternaria tenuis 13%, Aureobasidium pullulans 12%, Sphaeropsidales species 9%, Micropolyspora faeni 3%, A. fumigatus 2% and Thermoactionomyces vulgaris 2%. The authors concluded that these findings indicated that crude water extracts from contaminated air conditioners are the best choice as antigen sources for the diagnosis of “humidifier lung” in exposed workers. (116)

Importantly, ABPA, allergic Aspergillus sinusitis, and aspergilloma can occur simultaneously in the same patient. (117)

Individuals working in laboratories (in particular, medical research laboratories) may also be exposed to this mould, as demonstrated by a report of 4 workers in medical research laboratories, located in the basement level of a University facility equipped with a humidified air conditioning system, who complained of cough and/or asthma and/or rhinitis during their normal working activities. A. fumigatus and Penicillium notatum were found in some laboratories. Specific IgE sensitisation to A. fumigatus was found in 8 atopic and in 6 non-atopic workers, while P. notatum was found in 7 atopic and 4 non-atopic subjects. The presence of aspergillosis or allergic bronchial aspergillosis in the sensitised subjects was excluded. (118)

In Spain, esparto fibre is often used, which may result in clinical chest disease. In a report of 5 plaster workers from the same family who developed cough, dyspnoea, malaise, and fever after exposure to the esparto fibre used in their work, precipitating antibodies against an esparto extract were found in the sera of all patients. However, specific IgG antibodies against A. fumigatus were also detected, and the mould was identified in the esparto fibre samples. (119) This mould has also been shown to be present in air samples from barns. (120)

Patients with bird fancier’s disease, although primarily sensitised to avian sera and avian droppings, may be significantly and more frequently sensitised to other allergens such as A. fumigatus. (121)

Immunotherapy research against this mould is still in its infancy. (6, 122, 123)

Compiled by Dr Harris Steinman,


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Updated 2010



As in all diagnostic testing, the diagnosis is made by the physican based on both test results and the patient history.