Aureobasidium pullulans

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Code: m12
Latin name: Aureobasidium pullulans
Source material: Spores and mycelium
Family: Dothioraceae

Mould

A mould, which may result in allergy symptoms in sensitised individuals.

Allergen Exposure

The genus Aureobasidium includes 14 species and one variety. Of these, Aureobasidium pullulans is the only well-known species. (1, 2)

Aureobasidium pullulans is a ubiquitous yeast-like fungus that can be found in different environments (e.g. soil, water, air and limestone). (3) It may occur as a naturally occurring epiphyte or endophyte of a wide range of plant species (e.g. apple, grape, cucumber, green beans, cabbage) without causing any symptoms of disease. It is most common in temperate zones, with numerous recordings from the British Isles and the USA, but is also found in Canada, Alaska, Antarctica, Europe and Russia.

More than 80 fungal genera are currently recognised as being associated with allergy, and some of the most frequently occurring are Cladosporium, Penicillium, Aspergillus, Alternaria, and Aureobasidium. (4)

Aureobasidum pullulans is ubiquitous and widespread and can be found in environments with fluctuating water activities, bathrooms, food and feeds. (5) Aureobasidium is known as a primary invader of all kinds of leaves. During the summer, the spores are deposited on the leaf surface without attacking the cells. In autumn, when the leaves reach senescence, Aureobasidium begins decomposition. A. pullulans appears in the surface layers of soils, and has also been recorded on berries, grapes, citrus, wheat seeds, barley, oats, tomato and pecans. (6) It is often found in kitchens and bathrooms and can damage interior painted surfaces. A. pullulans may also result in plant disease (e.g. stigmatomycosis on cotton). It can also be found in very osmotically stressed environments, such as hypersaline waters in salterns, and in rocks and monuments. (5) Aureobasidium may also colonise hair, skin, and nails in humans. Thus, Aureobasidium pullulans is commonly considered to be a contaminant. (1)

On dextrose agar, A. pullulans produces smooth, faint pink, yeast-like colonies that are covered with a slimy mass of spores. Mature colonies change to black due to chlamydospore production. Primary conidia are hyaline, smooth, ellipsoidal, one-celled, and variable in shape and size; secondary conidia are smaller. Conidiophores are undifferentiated, intercalary or terminal, or arise as short lateral branches. Endoconidia are produced in an intercalary cell and released into a neighbouring empty cell. Hyphae are hyaline, smooth, and thin-walled, with transverse septa. The fungus grows at 10-35°C, with optimum growth at 30°C. (3) A. pullulans is notable for its phenotypic plasticity, with colony morphology being affected by a number of factors, e.g. carbon source, colony age, temperature, light and substrate, with colonies ranging from homogeneous to sectored, yeast-like to filamentous growth, and from small to large.

A. pullulans is used for the production of various enzymes, siderophores and pullulan. A. pullulans is used in the biological control of plant diseases, especially storage diseases. (3)

Hyaline conidia* emitted from yeasts and yeast-like moulds are among the most common fungal organisms detected in air samples in Asia, Australia, Europe, the Middle East and South America. (1) Most published fungal aerobiological studies have used identi?cation based on general cell or colony morphology, and all yeast-like hyaline conidia have often been pooled into the total yeast count; which results in a failure to recognise Aureobasidium as an independent mould. Reasons for failing to identify these fungi include their small size, lack of speci?c morphological characteristics, and the necessity to isolate, culture and immunologically assay with speci?c antisera. Aureobasidium spp. are likely to be included in these yeast counts, as this mould lacks a known sexual state and produces both yeast-like hyaline conidia and a ?lamentous growth form. (1) This may limit our comprehension of this mould.

* Hyaline conidia: a colourless asexual reproductive unit formed in any manner that does not involve cytoplasmic cleavage and which acts as an organ of dissemination.

Allergen Description

No proteins or allergens have been isolated to date. In a study, several allergens with high molecular weight were identified in Aureobasidium extracts: approximately 10 and 18 kDa, major bands at 35 and 45-48 kDa, and darkly stained but diffuse bands from 53-65, 80-90 and above 100 kDa. (1) The IgE-positive sera from the skin test-positive patient, as detected using immunoCAP analysis, showed a band at approximately 35 kDa and diffuse bands at 53-65 and 80 to above 100 kDa. (1)

Potential Cross-Reactivity

The potential cross-reactivity of A. pullulans is unknown.

Clinical Experience

IgE-mediated reactions

Aureobasidium may result in adverse effects via a number of pathophysiological mechanisms including: (a) infection by the organism, (b) generation of a deleterious immune response (e.g. allergy or hypersensitivity pneumonitis), and c) toxic-irritant effects from mould metabolites (e.g. mycelial components, mycotoxins, or volatile organic compounds). (7) 

Aureobasidium has been implicated as a causative agent in allergies. (8) Positive skin tests as well as provocation test reactions to Aureobasidium are commonly observed. (Kurup et al, in 9) Previous research has shown that elevated mean concentrations of Aureobasidium in Kansas homes were associated with allergy symptoms, (10) and extracts of Aureobasidium have elicited skin reactivity in 8-12% of atopic persons in one study in the Midwest USA. (11) In a Scandinavian patient group, Aureobasidium was found to be a frequent sensitising agent. (12)

Sensitivity to A. pullulans has been significantly associated with more severe asthma, i.e. was a risk factor. In the study examining the prevalence of allergy to 15 mould allergens among 105 patients hospitalised following exacerbation of asthma, the study also reported that sensitisation to Helminthosporium was associated with an increased number of asthma exacerbations that required hospitalisation. Twenty-seven percent of the group were sensitised to A. pullulans. (13)

Similarly, in a prospective birth cohort of 405 children of asthmatic/allergic parents from metropolitan Boston, Massachusetts, high in-home fungal concentrations were measured once within the first 3 months of life as predictors of doctor-diagnosed allergic rhinitis in the first 5 years of life. Predictors of allergic rhinitis included high levels of dust-borne Aspergillus and Aureobasidium. The factors controlled for in these analyses included water damage or mildew in the building during the first year of the child's life, and any lower respiratory tract infection in the first year. (14)

In a study of 290 asthmatic patients with positive skin tests for mould allergens analysed retrospectively, tests with Alternaria alternata, A. pullulans, Penicillium notatum, Fusarium culmorum, Aspergillus fumigatus and Cladosporium herbarum showed the highest correlation with clinical allergy. (15)

A. pullulans is also a known cause of hypersensitive pneumonitis, also known as extrinsic allergic alveolitis, ‘sauna-taker’s lung’ or ‘humidifier lung’. (16) It has been isolated from air conditioning units coincident with antibodies to this organism being found in the blood of patients in Colorado, (17) New York (18) and Germany (19).This condition is characterised by dyspnoea, cough, fever, chest infiltrates, and acute inflammatory reaction. The condition can also be chronic, and lymphocyte-mediated.

A study described a 15-year-old girl and her 6-year-old brother who developed hypersensitivity pneumonitis from residential exposure to A. pullulans. Both patients lived on a horse farm and experienced fatigue, weight loss, cough, and dyspnoea. Pulmonary function tests and and serum precipitins to A. pullulans confirmed the diagnosis. Evaluation of the home revealed extensive mould contamination with A. pullulans, as well as high levels outdoors. (20)

Occupational hypersensitivity pneumonitis caused by mould contamination of an air conditioning unit has been described. Aspergillus fumigatus and A. pullulans were cultured from this unit, and serum antibodies to these organisms were identified in the patient's blood. (17)

Hypersensitivity pneumonitis, also known as allergic alveolitis, was described in a 23-year-old woman. She experienced marked hypoxemia during exercise. A broad spectrum of positive precipitating antibodies was found in the serum, mainly against Penicillium casei and A. pullulans. The source of the allergens proved to be a patch of mould of 0.5m (2) on the bedroom wall. (21)

Contaminated air conditioners are a source of antigens that may cause ‘humidifier lung’ (hypersensitivity pneumonitis) in exposed workers. In a study of 9 individuals with hypersensitivity pneumonitis, and in 3 with isolated systemic symptoms without significant changes in lung function and chest x-rays, microbiological studies demonstrated a variety of fungi and bacteria in the water supplies of humidifiers and air conditioners at the patients’ workplaces. Low concentrations of IgG antibodies against thermophilic Actinomycetes and various other fungi (such as Alternaria tenuis, A. pullulans, Penicillium notatum, Aspergilli, and fungi of the order Sphaeropsidales) was shown, and these moulds were isolated and cultured from humidifier water supplies. (19)

Similarly, in another study, specific IgG antibodies against antigens of a contaminated air conditioner were estimated in the serum of 134 workers at a printing company. Altogether, 64% of the workers investigated revealed significantly elevated levels of IgG antibodies specific for Fusarium (25%), Penicillium notatum (23%), Alternaria tenuis (13%), and A. pullulans (12%). (22)

A. pullulans has been responsible for hypersensitivity pneumonitis even in young children. A 14-year-old girl developed hypersensitivity pneumonitis which was associated with indoor hydroponics (a method of growing plants using mineral nutrient solutions, in water, without soil). Water samples from the hydroponics revealed A. pullulans as the dominant fungal micro-organism, and the diagnosis was supported by the existence of serum precipitating antibodies against A. pullulans, lymphocytic alveolitis on bronchoalveolar lavage (BAL) fluid, a corresponding reaction on a lung biopsy, and the sustained absence of clinical symptoms following the removal of hydroponics from the home. (23)

A boy with unknown fever and without respiratory symptoms subsequently developed progressive dyspnoea, and was then diagnosed with hypersensitivity pneumonitis. The precipitated antibody test was positive for A. pullulans. (24)

A number of studies have elucidated the frequency of sensitisation to A. pullulans in various settings.

An American mould study performed in patients’ homes reported finding Aureobasidium in 6%, compared to Chaetomyces (18%), Acrosporium (15%), Stachybotrys (39%), Aspergillus (55%), Acremonium (6%), Scopulariopsis (9%), Rhodotorula (9%), Cladosporium (30%), Penicillium (30%), Epicoccum (6%), Phoma (3%), and Alternaria (6%). (7)

In a study in Connecticut, USA, evaluating sensitisation in 100 patients with asthma and/or allergic rhinitis to 30 airborne fungi using skin-specific IgE tests, 42 were shown to be sensitised to Alternaria alternata, 53 to Aspergillus fumigatus, 51 to Aspergillus niger, 52 to Aspergillus terreus, 62 to A. pullulans, 45 to Botrytis cinerea, 39 to Candida albicans, 45 to Cephalosporium acremonium (Acremonium kiliense), 50 to Epicoccum purpurascens, 49 to Coprinus micaceus, 5 to Agaricus campestris, 50 to Ustilago maydis, 43 to Trichoderma viride, and 68 were shown to be sensitised to Penicillium notatum. (25)

In Chicago, USA, in a study of a subgroup of 39 allergic rhinitis patients whose history was strongly suggestive of mould allergy, 44% were positive to a panel of mould tested. Of this group, the results were: Alternaria (n=18), Helminthosporium (n=15), Aspergillus (n=14), Stemphylium (n=12), Candida (n=12), Phoma (n=12), Curvularia (n=11), Botrytis (n=11), Epicoccum (n=10), Trichoderma (n=9), Penicillium (n=9), Aureobasidium (n=8), Cladosporium (n=8) and Mucor (n=8). (26)

In Sao Paulo, Brazil, an evaluation of sensitisation in 201 patients with asthma and/or allergic rhinitis to 42 airborne fungi using skin-specific IgE tests found that 15 were sensitised to Alternaria, 15 to Aspergillus, 23 to Aureobasidium, 37 to Candida, 15 to Chaetomium, 19 to Epicoccum, 17 to Mucor, 20 to Phoma, 19 to Trichoderma, and 14 to Rhizopus. (27)

In a study conducted in Pasadena in the USA, allergy patients were skin and serum tested, 17% (16/94) of atopic individuals (bronchitis and/or bronchial asthma) were skin-prick test-positive for A. pullulans extract. (1)

From a large Phadia repository of human blood serum, a subset of 668 unique samples, each with at least one raised serum-specific IgE for 17 separate fungal species, but devoid of clinical history, found serum-specific IgE for A. pullulans in 331. (4)

Considering that A. pullulans may be found in occupational settings, occupational rhinitis and asthma could be expected to occur as a result of exposure to this mould.

A. pullulans in cooling lubricant was found to be a cause of hypersensitivity pneumonitis in a hard metal grinder. (28, 29)

A. pullulans spores were recovered in the homes of asthmatics and found to have some correlation to the cabbage harvest as well as to the harvest of strawberries in the region, and with symptoms of asthma and occupational asthma. (30)

Other reactions

A. pullulans is a causal agent of phaeohyphomycosis, occasionally found in men and animals. This mould is also responsible for a range of opportunistic fungal infections including fungemia (septicaemia), systemic infections and abscesses in different viscera, including meningitis and/or cerebral abscesses. (31, 32, 33, 34, 35) A. pullulans may cause keratomycosis, pulmonary mycosis with sepsis and other opportunistic infections, as well as cutaneous mycoses such as eumycotic dermatitis. (1) A. pullulans fungemia has been described in an infant. (36)

A. pullulans may result in septicaemia in immune-competent individuals, but is more commonly associated with immune-compromised or immunosuppressed individuals, as described in a number of reports.

In immunocompetent patients, A. pullulans has been reported to have resulted in extensive skin infection, (37) and persistent, neutrophilic, chronic septal panniculitis. (38)

The first record of A. pullulans as an opportunistic pulmonary infection was reported in a 46-year-old man who had undergone an orthotopic liver transplant in 1988. The patient had been living in the California desert for two months prior to admission and presented with ventilator-dependent acute respiratory failure and haemodialysis-dependent acute renal failure. Imaging studies revealed severe bilateral infiltrates, and bronchoalveolar lavage (BAL) and brushings grew A. pullulans. (39)

Subsequent to this, a number of other reports of A. pullulans affecting immune-supressed or compromised hosts have been recorded. Peritonitis from A. pullulans was reported in a patient undergoing continuous ambulatory peritoneal dialysis, (40) and similarly, peritoneal catheter colonisation and subsequent peritonitis. (41)

Disseminated A. pullulans fungal infection was described in a severely traumatised patient. (42) A. pullulans was responsible for catheter-related sepsis and septicaemia in a chronically ill child. (43) Similar cases have been described elsewhere. (44)

Chromoblastomycosis produced by A. pullulans in an immunosuppressed patient was reported. (45)

A 32-year-old woman presented during pregnancy with a two-month history of painless subcutaneous nodules. Excision biopsy of one lesion showed dematiaceous fungal elements. Three weeks into the puerperium, she developed generalised seizures attributed to systemic fungal infection with Aureobasidium spp. (46)

Sinus mould infections have been reported, and an association between sinusitis and elevated mould-specific IgG levels for a number of fungi (including Aspergillus fumigatus, Aspergillus versicolor, Aureobasidium pullulans, Chaetomium globosum, etc.) has been reported. (47)

‘Toxic mould syndrome’ is a controversial diagnosis associated with exposure to mould-contaminated environments. Mould metabolites may be irritants and may be involved in ‘sick building syndrome.’ A study's objective was to characterise the clinical features and possible aetiology of symptoms in patients with chief complaints related to mould exposure. It attributed 5 patients with positive SPT or intra-cutaneous test reactions to A. pullulans. NOTEREF _Ref301170610 \f  (33)

A 23-year-old patient being treated for the inflammatory complication of leprosy (erythema nodosum leprosum) presented with a 60-day complaint of daily fever, hoarseness, odynophagia and weight loss. Laboratory tests showed pancytopenia with severe neutropenia, cervical adenomegaly and solid contrast uptake lesions in the oropharyngeal region. A. pullulans was found to be the responsible organism. (31)

Subcutaneous mycosis and fungemia was described in a post-allogeneic bone marrow transplant patient, (48) and similarly, the former in a renal transplant recipient. (49)

A. pullulans infection appears to be particularly common in ophthalmology.

Primary or secondary infection of the eyes have been described, as demonstrated by a report of a 52-year-old woman after treatment of a corneal ulcer that was unresponsive to conventional therapy. Aureobasidium was identified as the infectious organism. (50) A retrospective analysis of cases of corneal ulcer (keratomycosis) reported that of 200 fungal organisms isolated, 25 were identified as A. pullulans. (51) A. pullulans scleritis following keratoplasty has been described. (52)

Fungal corneal ulcer is reported to be common in India. A 6-year study from Northern India revealed that fungi were detected in 8.4% of 730 patients investigated. Although Aspergillus spp. was the most common causative agent, accounting for 40.1% of the isolates, other common organisms included Fusarium sp. (16.4%), Curvularia sp. (8.2%), and Candida albicans (8.2%). In this series, A. pullulans was only responsible for one isolate (1.6%). (53)

A 32-year-old male, with an asymptomatic radiolucency first identified 3 years after the removal of an impacted mandibular right third molar 16 years previously, was found to have an intra-osseous cavity filled with a black, homogeneous, gelatinous substance thought to be foreign material, but which was diagnosed histologically as containing black yeasts. The yeast isolate was identified as an Aureobasidium species, but different from typical A. pullulans. (54)

Cases of phaeohyphomycosis caused by Aureobasidium pullulans, Exophiala jeanselmei, and other moulds have been reported. (55)

A study reported that 23% of 915 chronic wounds were positive for fungal species, of which one of the most abundant fungi was Aureobasidium. (56)

Recently authors have cautioned against the diagnostic pitfall of an incorrect diagnosis of A. pullulans resulting from contamination of bronchial aspirates mimicking cryptococcosis. (57)

Compiled by Dr Harris Steinman.

References

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