Aureobasidium pullulans

Aureobasidium pullulans on gypsum boardAureobasidium pullulans on woodAureobasidium pullulans on a ceiling tileAureobasidium pullulans on EM agarAureobasidium pullulans on RB agarAureobasidium pullulans - Microscopy (EM Culture)


The genus Aureobasidium includes between 14 {3318} to 26 named species depending on the consulted registry {813; 816; 3971}. Among these, A. pullulans is the only well-known species {816}, of which two well documented varieties are associated with indoor environment and health problems:  A. pullulans var. pullulans and A. pullulans var. melanogenum{1056}. On the other hand, the fungal database of the International Mycological Association lists 6 varieties of A. pullulans{3971; 4041}.



The teleomorph stage of Aureobasidium pullulans is Discosphaerina fulvida.


Aureobasidium pullulans is an ubiquitous saprophyte mould {1056}, which is generally considered as an environmental contaminant {412; 816}. It is most common in temperate zones with numerous recordings from the British Isles and the USA, but also found in Canada, Alaska, Antarctica, Europe and Russia.

It is an ubiquitous and cosmopolitan genus found in forest soil, freshwater, aerial portions and on leaf surfaces of plants as well as on seeds (wheat), cereals(barley, oats) and some nuts such as pecans {2225; 816; 1056; 2224}. It is also found as spoilage agent on fruits (pears, grapes and tomatoes) or in fruit drinks {813; 1056}. It has been associated with the deterioration of pears and oranges in storage or in transit.

A. pullulans has also been reported as a dominant species in certain fish-ponds {2235}.  

More details

Aureobasidium is known as a primary invader of all types 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.

Aureobasidium is found in temperate-zone air, where respirable-sized conidia of A. pullulans are mostly emitted from plants {2224}, however, it has also been detected in regions without abundant plant material, even in the Artic {2224; 4041}.

In a study conducted in urban Pasadena (California, USA), peaks of hyaline unicellular Aureobasidium conidia were demonstrated to occur at night and during periods of rainfall and accounted for 90% of the total fungal count {2224}.  In this particular study, flowers, especially those of the Corymbia tree (a eucalypt), were found to be the major source of the fungus.  In rural California, recovery of A. pullulans has been correlated with cabbage and strawberry harvests {4034}.

In outdoor air of urban areas in Lithuania, researchers concluded that A. pullulans was among the most abundant fungi, with a frequency distribution of 56.7%, being the 5th most often detected fungus {2226}.

Because its growth profile is mostly yeast-like and the spores are not forcibly discharged, this fungus only becomes airborne through mechanical disruption of contaminated material or aspersion of contaminated water; it can be dispersed by wind once the mycelia have dried out.  The seasonal distribution shows a predominance of Aureobasidium pullulansfrom July to November {2227}.

Growth requirements

Aureobasidium species grow well within a wide range of temperatures, from 2 to 35 °C, with an optimum temperature of 25 °C ; some human pathogenic isolates may grow at higher temperatures {1056} while certain species are able to develop at subglacial temperatures {989; 4041}.

Aureobasidum spp. are tertiary colonisers:  A. pullulans requires high amounts of moisture to germinate and grow, i.e. an aw (available water) of 0.89-0.90 at 25°C {989; 3969}.

Water Activity :         Aw = 0.89 - 0.90  {989; 3969}.

Growth on building materials or indoor environment

Aureobasidium pullulans requires high levels of available water to grow; it is commonly found growing indoors on surfaces that are continually damp, especially in bathrooms and kitchens, on shower curtains, tile grout, window sills and frames, and also in liquid waste materials such as found in condensation pans or humidifier reservoirs {2225; 2217; 1056}. This fungus can grow on and damage interior painted surfaces; however, under certain circumstances, with a constant relative humidity of at least 75%, A. pullulans may even grow on the very surface of painted material, possibly without deteriorating it {989} .

More details

In a rural home where two children were diagnosed with hypersensitivity pneumonitis, certain rooms were found to be heavily contaminated with Aureobasidium sp.:  indoor concentrations reached up to 659 CFU/m³, while outdoor air samples contained 70 CFU/m3 {2216}. In this instance, Aureobasidium was second only to Cladosporium in its prevalence in the indoor air. The source of the fungus was a basement covered by tarp and wood planks, in which standing water and extensive contamination were observed.

A British study revealed that commonly used pillows contain a substantial load of many species of fungi, includingAureobasidium pullulans which was present in 6 of the 10 studied samples;  the concentration of this fungus was higher in feather (5110 CFU/g) than in synthetic pillows (1926 CFU/g) {2223}.

High concentrations of Aureobasidium have also been detected in automobile air conditioning systems in Atlanta {2288; 2224}.

Laboratory section

Normal laboratory precautions should be exercised in handling cultures of this species within Biosafety Level 2 practices and containment facilities.

Colony, macroscopic morphology

A. pullulans grows moderately rapidly and matures within 7 days of incubation, at room temperature.  On potato dextrose agar (PDA), colonies measure 1 to 3 cm in diameter following incubation at 25 °C for 7 days {816}.

On malt extract agar (MEA), at 24 °C, colonies reach a diameter of 4 cm in 7 days {1056} . Colonies are at first white, pale pink, cream or yellow; at maturity, they become black and velvety, moist, yeast-like, mucoid to pasty, shiny and leathery in appearance {412; 816; 2242} . Aerial mycelium sometimes forms scanty thinly floccose fringes {1056}. The reverse often becomes black, at least in the center of the colony {412}; in some strains, the reverse may be white, light orange or apricot {415; 4041}.

Microscopic morphology

When the colony is young, moist and yeast-like unicellular budding yeast cells (blastoconidia) are the only structures observed microscopically. As the colony ages, septate hyphae (2-16 µm in diam.) become visible; they are hyaline, smooth, and thin-walled.

In older cultures, dark-brown, thick-walled hyphae may be formed; these hyphae are generally 2-10 µm wide, but may be as thick as 15-20 µm. Hyphae of some strains can differentiate to form thick-walled and large (6 x 12 µm) brown chlamydoconidia. In old mature cultures, thick-walled, one- to two-celled arthroconidia can also be produced {816} .

Aureobasidium has no distinct conidiophores.  Conidiogenous cells are located either intercalary or terminally in the hyphae.  Conidia (2-3 µm x 4-6 µm) are produced synchronously in clusters or are located along the hyphae.
These blastospores measure 7-16 µm x 3.5 µm and can in turn produce by budding short chains of 2, 3 or 4 spores.

Conidia are hyaline, smooth-walled, single-celled, ellipsoidal but of variable shape, often with an indistinct hilum (a scar at the point of attachment). Secondary smaller conidia are often produced {814; 816; 2242; 1056}.

This mould is considered a dematiaceous fungus because of its capacity to produce a dark, melanin-like pigment that accumulates in the cell wall {2228; 2225}.

Specific metabolites

Organics compounds (including VOCs)

The metabolite and specific microbial volatile organic compounds (mVOCs) profile of Aureobasidium growing indoors has not been published.

However Aureobasidium species have many industrial applications which provide insight into some of the types of metabolites produced: one species, A. pullulans, produces pullulan which is a biodegradable polysaccharide processed into fibres and used for packaging food and drug products. Different strains of A. pullulans can also produce amylase, proteinase, lipase, cellulase, xylanase, mannanase, transferases, pullulan, siderophore and single-cell protein;  the genes encoding for proteinase, lipase, cellulase, xylanase, and siderophore have been cloned and characterized {4047}.


Aureobasidium is not known to produce mycotoxins {989; 813; 2224}.

Adverse health reactions

Irritation and inflammation

No specific study on irritation or inflammation due to Aureobasidium has been published.

Allergic reactions

Historically, Aureobasidium has not been considered a major allergenic agent, however recent reports have linked the indoor and outdoor presence of Aureobasidiumto both rhinitis in children and rhinitis, asthma and sinusitis in adults {199; 3822}. Allergenicity of this fungus has been confirmed by direct in vivo (skin tests) and in vitro (serological assays) methods, epidemiological studies and by bronchial challenges {808; 1893; 2224}.     

More details

In an American Midwest allergy survey performed in 100 patients diagnosed with allergic rhinitis, a prevalence of 20.5 % of Aureobasidium sensitisation (IgE) was observed among atopic individuals {1464}.  A sensitisation prevalence study conducted at an asthma and allergy center in California showed that, among 94 atopic patients, 17% had a positive skin test result against A. pullulans extracts {2224}; of these, 56% had bronchitis and/or bronchial asthma.

A similar study in Poland testing 105 asthma patients found that sensitisation to A. pullulans was associated with severity of asthma {1585}.

Furthermore, in a study monitoring teachers working in moisture-damaged school buildings, an association was established between sinusitis and elevated mould-specific IgG-levels for A. pullulans {277; 199}.

Allergic components and mechanism

Specific allergenic components of Aureobasidium pullulans have not been studied.

Hypersensitivity pneumonitis

A. pullulans hypersensitivity pneumonitis (HP) has been linked to exposure to contaminated humidifiers and air conditioning units in the workplace and in the residential environment {277; 2245; 2240} as well as linked to very damp spaces such as saunas («sauna taker’s lung»)  {813; 2224}.

More details

Aureobasidium pullulans can be a very rare cause of residential HP {4046}. HP secondary to damp residential exposure to A. pullulans has been reported in two young siblings {2216}.

In an industrial complex setting, the heating-cooling ventilation systems were found to be the source for the growth as well as the transmission vehicle of A. pullulans which was the cause of at least 115 cases of HP; in fact, a total of 152 employees had a positive precipitin test to A. pullulans {2240}.

Cases of IgG-induced sensitisation and hypersensitivity pneumonitis (humidifier lung) have been reported in a printing company where 12% of workers tested positive for antibodies against A. pullulans  {277}.  

Toxic effects (mycotoxicosis)

No human nor animal mycotoxicosis associated with Aureobasidium has been reported.

Infections and colonisations

Aureobasidium pullulans infections are rare.  Between 1996 and 2003, only 23 clinical cases had been documented in the scientific literature {2225}, many of which were associated with indwelling peritoneal dialysis catheter {2234} and other medical devices.   

Since then, it has been reported as a rare causative agent of various phaeohyphomycoses {2228; 2225; 2221} . Clinically,Aureobasidium has been reported to cause a variety of localised infections, including keratitis {2221}, pneumonia, meningitis {4016} as well as other opportunistic subcutaneous and cutaneous mycoses {2225} and septicemias {2224}. However, the pathogenicity of A. pullulans remains limited and uncommon {816; 1819}.  

A. pullulans may also be cultured from colonised sites such as skin, hair, nasal cavity and under fingernails {814; 2217; 816; 1056}.  

More details

Prior to 2000, only a few clinical cases of A. pullulans infection had been reported in the literature. In fact, in a 5-year review of 556 dematiaceous hyphomycetes fungi referred to a central mycology laboratory, 75 isolates were strains ofAureobasidium species, of which only 7 (9%) were considered to be of probable pathogenic significance; these 7Aureobasidium isolates were cultured from patients on peritoneal dialysis {2225} . Fungal infections linked to peritoneal dialysis are also often associated with underlying diseases such as diabetes mellitus {2234}.

Keratitis caused by A. pullulans is very uncommon worldwide. A study reviewing 447 cases of presumed microbial keratitis in Nepal confirmed only three cases as being caused by Aureobasidium  {2221}. Similarly, an Indian study reviewing 730 cases of eye infection {4059} reported that Aureobasidium was the causative agent in 1.6% of corneal fungal ulcers.

An unusual single case of A. pullulans keratitis was reported one month following LASIK surgery; this case was probably the result of self-infection, possibly from the contamination of a fingernail of the patient {2217} .

Aureobasidium pullulans invasive infections or septicaemia have been reported in immunocompromised patients {2224}, in cancer patients {2237; 2242}, in severely traumatised patients {2228} and in organ transplant recipients {2231}. A lethalA. pullulans fungemia with invasive infection was reported in a 4-month-old infant {2225} .

Aureobasidium mansoni was reported to cause nosocomial meningitis in a paediatric patient {4016}.  

Virulence factors

No particular virulence factors have been reported.

Specific settings

Nosocomial infections

Although immunocompromised individuals are at greater risk of opportunistic fungal infections, the risk for such patients from environmental exposure to high concentrations of airborne Aureobasidium conidia is not known {2224}.

Aureobasidium nosocomial infections have been reported, most of which were transmitted iatrogenically.   A paediatric case of Aureobasidium mansoni nosocomial meningitis has been described {4016}. 

More details

Because of an affinity of A. pullulans for certain medical devices, patients in continuous peritoneal dialysis are at greater risk for nosocomial infection caused by this fungus {2225; 2232; 1819}. Fungal infections linked to peritoneal dialysis are often exacerbated by other underlying diseases such as diabetes mellitus {2234}.

In hospitals settings, A. pullulans has demonstrated an affinity for synthetic materials and surgically implanted devices, as confirmed by the relatively frequent isolation of the organism from peritoneal dialysis catheters and central venous lines. Moreover, Aureobasidium  is difficult to eradicate with standard disinfection procedures {2225} .

Occupational diseases

No occupational infections, in the strict sense of the term, due to Aureobasidium have been reported.

No particular outbreaks due to exposure to Aureobasidium sp. have been reported associated with an exposure specific to a particular occupation except, perhaps, in the case of hypersensitivity pneumonitis (HP) in wood processing workers {4013}. Moreover, cases of HP have been reported in the workplace associated with contaminated HVAC systems {277; 2240}. 

More details

In an industrial complex, the heating-cooling ventilation systems were found to serve as the vehicle for growth and transmission of A. pullulans which was the cause of at least 115 cases of HP (a total of 152 employees had positive precipitin to A. pullulans) {2240}.

IgG-induced sensitisation and hypersensitivity pneumonitis (humidifier lung) was reported in a printing company where 12% of workers tested positive for antibodies against A. pullulans  {277}. 

Diagnostic tools


A number of fungi of low virulence, such as A. pullulans, are often considered contaminants when isolated from healthy hosts; its isolation from clinical specimens is generally considered as a contaminant {2228}. Thus, the isolation ofAureobasidium in a clinical specimen requires cautious evaluation.    

More details

It is important to note that A. pullulans has been found in the nasal mucus of both healthy individuals as well as in chronic rhinosinusitis patients; its prevalence of 5.2% is however far below Aspergillus and Penicillium species, both totalling 40% of fungal genera identified {2227}.


Aureobasidium, as in the case of other agents of phaeohyphomycosis, appears as dark-walled, short, septate hyphae in hematoxylin-eosin (H&E) stained sections. If pigment production is not prominent, the use of Fontana-Masson silver stain may be advantageous {4080}.


Aureobasidium pullulans allergen extracts are available commercially and specific testing may be useful in the diagnosis ofAureobasidium sensitisation {808}.  Allergen extracts are available for both in vitro (RAST) and in vivo (intradermal) testing {4073; 3284; 581}.

Aureobasidium pullulans antigen extracts are available commercially for in vitro IgG testing; specific testing may be useful in the diagnosis of Aureobasidium pneumonitis. 

More details

No Aureobasidium allergens or antigens are registered with the «Biological Product Deviation Reporting»  surveillance program of the American Federal Drug Administration (FDA, 2008 register) {3285}.

It should be emphasized that since Aureobasidium pullulans has been considered as a poorly allergenic fungus, its extracts are not normally included in allergen screening sets. Notwithstanding, the results of the few clinical or epidemiological studies that have added Aureobasidium to the sensitisation panels confirm the importance of this fungus as an allergen and indicate the value of its inclusion as well as others to basic allergen panels {4058; 1814}. 

The same can be said of diseases mediated by IgG immune responses: some cases of hypersensitivity pneumonitis have been attributed to Aureobasidium {836; 2224}. The use of antigen extracts could contribute to the diagnosis of certain under-diagnosed respiratory problems.

Skin TestsX   
RAST-IgG Experimental  
Complement fixation    


  • 199. Patovirta, R. L., Reiman, M., Husman, T., Haverinen, U., Toivola, M., and Nevalainen, A. (2003). Mould specific IgG antibodies connected with sinusitis in teachers of mould damaged school: a two-year follow-up study. Int J Occup.Med Environ Health. 16[3], 221-230.
  • 277. Baur, X., Richter, G., Pethran, A., Czuppon, A. B., and Schwaiblmair, M. (1992). Increased prevalence of IgG-induced sensitization and hypersensitivity pneumonitis (humidifier lung) in nonsmokers exposed to aerosols of a contaminated air conditioner. Respiration. 59[4], 211-214.
  • 412. Larone, D H. (1987). Medically important fungi. A guide to identification. 2nd edition, -230 p. New York - Amsterdam - London, Elsevier Science Publishing Co., Inc.
  • 415. St-Germain, G and Summerbell, R. (1996). Champignons filamenteux d'intérêt médical. Caractéristiques et idenfication. -314 p. Belmont, Star Publishing Company.
  • 417. Matsson, P, Hamilton, R G, Adkinson, N F, Esch, R, Homburger, H, Maxim, P, and Williams, B. (1997). Evaluation methods and analytical performance characteristics of immunological assays for human immunoglobulin E (IgE) antibodies of defined allergen specificities; approved guideline. [17, no. 24], -81 p. Wayne, The National Committee for Clinical Labora
  • 581. Pharmacia Diagnostics AB. (2007). Allergy & autoimmunity. Diagnostics product catalogue 2007. internet , 1-48. Pharmacia.
  • 808. Al-Doory, Y and Domson, JF. (1984). Mould allergy. Lea & Febiger.
  • 813. EMLAB. (2007). Environmental Microbiology Laboratory, Inc. (EMLab): An index of some commonly encountered fungal genera.
  • 814. Ellis, D. (2007). Mycology online. University of Adelaide . School of molecular & biomedical science. The University of Adelaide.
  • 816. Patterson, T. F., McGinnis, M. R., and ed. (2009). The fungi :description. Site Doctor Fungus . Mycoses Study Group.
  • 989. Centre de recherche sur la conservation des documents graphiques. (2007). Moisissures et biens culturels. Ministère de la culture et de la Communication, France .
  • 1056. Samson, RA, Hoekstra, ES, and Frisvad, JC. (2004). Introduction to food and airbone fungi. 7th, -389 p. Baarn, Centralalbureau voor Schimmellcultures, Institute of the Royal Netherlands Academy of Arts and Sciences.
  • 1464. Corey, J. P., Kaiseruddin, S., and Gungor, A. (1997). Prevalence of mold-specific immunoglobulins in a Midwestern allergy practice. Otolaryngol.Head Neck Surg. 117[5], 516-520.
  • 1585. Niedoszytko, M., Chelminska, M., Jassem, E., and Czestochowska, E. (2007). Association between sensitization to Aureobasidium pullulans (Pullularia sp) and severity of asthma. Ann Allergy Asthma Immunol. 98[2], 153-156.
  • 1814. Su, H. J., Rotnitzky, A., Burge, H. A., and Spengler, J. D. (1992). Examination of fungi in domestic interiors by using factor analysis: correlations and associations with home factors. Appl Environ Microbiol. 58[1], 181-186.
  • 1819. Pritchard, R. C. and Muir, D. B. (1987). Black fungi: a survey of dematiaceous hyphomycetes from clinical specimens identified over a five year period in a reference laboratory. Pathology. 19[3], 281-284.
  • 1893. Karlsson-Borga, A., Jonsson, P., and Rolfsen, W. (1989). Specific IgE antibodies to 16 widespread mold genera in patients with suspected mold allergy. Ann Allergy. 63[6 Pt 1], 521-526.
  • 2216. Temprano, J., Becker, B. A., Hutcheson, P. S., Knutsen, A. P., Dixit, A., and Slavin, R. G. (2007). Hypersensitivity pneumonitis secondary to residential exposure to Aureobasidium pullulans in 2 siblings. Ann Allergy Asthma Immunol. 99[6], 562-566.
  • 2217. Maverick, K. J. and Conners, M. S. (2007). Aureobasidium pullulans fungal keratitis following LASEK. J Refract.Surg. 23[7], 727-729.
  • 2221. Panda, A., Das, H., Deb, M., Khanal, B., and Kumar, S. (2006). Aureobasidium pullulans keratitis. Clin Experiment Ophthalmol. 34[3], 260-264.
  • 2223. Woodcock, A. A., Steel, N., Moore, C. B., Howard, S. J., Custovic, A., and Denning, D. W. (2006). Fungal contamination of bedding. Allergy. 61[1], 140-142.
  • 2224. Taylor, P. E., Esch, R., Flagan, R. C., House, J., Tran, L., and Glovsky, M. M. (2006). Identification and possible disease mechanisms of an under-recognized fungus, Aureobasidium pullulans. Int Arch Allergy Immunol. 139[1], 45-52.
  • 2225. Hawkes, M., Rennie, R., Sand, C., and Vaudry, W. (2005). Aureobasidium pullulans infection: fungemia in an infant and a review of human cases. Diagn.Microbiol Infect Dis. 51[3], 209-213.
  • 2226. Lugauskas, A., Sveistyte, L., and Ulevicius, V. (2003). Concentration and species diversity of airborne fungi near busy streets in Lithuanian urban areas. Ann Agric Environ Med. 10[2], 233-239.
  • 2227. Buzina, W., Braun, H., Freudenschuss, K., Lackner, A., Habermann, W., and Stammberger, H. (2003). Fungal biodiversity--as found in nasal mucus. Med Mycol. 41[2], 149-161.
  • 2228. Bolignano, G. and Criseo, G. (2003). Disseminated nosocomial fungal infection by Aureobasidium pullulans var. melanigenum: a case report. J Clin Microbiol. 41[9], 4483-4485.
  • 2231. Tan, H. P., Wahlstrom, H. E., Zamora, J. U., and Hassanein, T. (1997). Aureobasidium pneumonia in a post liver transplant recipient: a case report. Hepatogastroenterology. 44[16], 1215-1218.
  • 2232. Ibanez, Perez R., Chacon, J., Fidalgo, A., Martin, J., Paraiso, V., and Munoz-Bellido, J. L. (1997). Peritonitis by Aureobasidium pullulans in continuous ambulatory peritoneal dialysis. Nephrol.Dial.Transplant. 12[7], 1544-1545.
  • 2234. Caporale, N. E., Calegari, L., Perez, D., and Gezuele, E. (1996). Peritoneal catheter colonization and peritonitis with Aureobasidium pullulans. Perit.Dial.Int. 16[1], 97-98.
  • 2235. Slavikova, E. and Vadkertiova, R. (1995). Yeasts and yeast-like organisms isolated from fish-pond waters. Acta Microbiol Pol. 44[2], 181-189.
  • 2237. Girardi, L. S., Malowitz, R., Tortora, G. T., and Spitzer, E. D. (1993). Aureobasidium pullulans septicemia. Clin Infect Dis. 16[2], 338-339.
  • 2240. Woodard, E. D., Friedlander, B., Lesher, R. J., Font, W., Kinsey, R., and Hearne, F. T. (1988). Outbreak of hypersensitivity pneumonitis in an industrial setting. JAMA. 259[13], 1965-1969.
  • 2242. Salkin, I. F., Martinez, J. A., and Kemna, M. E. (1986). Opportunistic infection of the spleen caused by Aureobasidium pullulans. J Clin Microbiol. 23[5], 828-831.
  • 2245. Storms, W. W. (1978). Occupational hypersensitivity lung disease. J Occup Med. 20[12], 823-824.
  • 2288. Simmons, R. B., Noble, J. A., Rose, L., Price, D. L., Crow, S. A., and Ahearn, D. G. (1997). Fungal colonization of automobile air conditionning systems. Journal of Industrial Microbiology & Biotechnology 19, 150-153.
  • 2758. Kurup, V. P., Shen, H. D., and Vijay, H. (2002). Immunobiology of fungal allergens. Int Arch Allergy Immunol. 129[3], 181-188.
  • 3284. Hollister-Stier Laboratories. (2009). Allergenic extracts : Molds. Hollister-Stier Laboratories .
  • 3285. Federal Drug Administration (FDA). (2008). Biological products deviation reporting (BPDR). Non-blood product codes. 3-29-2009.
  • 3318. UniProt Consortium. (2009). Taxonomy : fungi metazoa group. Site de UniProt . 4-6-2009.
  • 3729. Flannigan, B., Samson, R. A., and Miller, J. D. (2002). Microorganisms in home and indoor work environments: diversity, health impacts, investigation and control. -504 p. CRC Press.
  • 3822. Stark, P. C., Celedon, J. C., Chew, G. L., Ryan, L. M., Burge, H. A., Muilenberg, M. L., and Gold, D. R. (2005). Fungal levels in the home and allergic rhinitis by 5 years of age. Environ.Health Perspect. 113[10], 1405-1409.
  • 3969. Grant, C., Hunter, C. A., Flannigan, B., and Bravery, A. F. (1989). The moisture requirements of moulds isolated from domestic dwellings . International Biodeterioration 25, 259-284.
  • 3971. Robert, V., Stegehuis, G., and Stalpers, J. (2005). The MycoBank engine and related databases. International Mycological Association . International Mycological Association. 9-9-2009.
  • 4013. Lacey, J. and Dutkiewicz, J. (1994). Bioaerosols and occupational lung disease. Journal of Aerosol Science 25[8], 1371-1404.
  • 4016. Huttova, M., Kralinsky, K., Horn, J., Marinova, I., Iligova, K., Fric, J., Spanik, S., Filka, J., Uher, J., Kurak, J., and Krcmery, V., Jr. (1998). Prospective study of nosocomial fungal meningitis in children--report of 10 cases. Scand.J Infect.Dis. 30[5], 485-487.
  • 4034. Sneller, M. R., Roby, R. R., and Thurmond, L. M. (1979). Incidence of fungal spores at the homes of allergic patients in an agricultural community. III. Associations with local crops. Ann.Allergy. 43[6], 352-355.
  • 4041. Zalar, P., Gostincar, C., de Hoog, G. S., Ursic, V., Sudhadham, M., and Gunde-Cimerman, N. (2008). Redefinition of Aureobasidium pullulans and its varieties. Stud.Mycol. 61:21-38., 21-38.
  • 4046. Flannigan, B., McCabe, E. M., and McGarry, F. (1991). Allergenic and toxigenic micro-organisms in houses. Soc.Appl.Bacteriol.Symp.Ser. 20:61S-73S., 61S-73S.
  • 4047. Chi, Z., Wang, F., Chi, Z., Yue, L., Liu, G., and Zhang, T. (2009). Bioproducts from Aureobasidium pullulans, a biotechnologically important yeast. Appl.Microbiol.Biotechnol. 82[5], 793-804.
  • 4058. Palmas, Francesca, Meloni, Valeria, and Fadda, Maria. (1997). Fungi allergic pathologies: correlation between allergological tests and presence of fungi in the upper respiratory tract. Aerobiologia 13[1], 17-22.
  • 4059. Chander, J. and Sharma, A. (1994). Prevalence of fungal corneal ulcers in northern India. Infection. 22[3], 207-209.
  • 4073. Greer Laboratories. (2009). Product catalog 2009. Site de Greerlabs . 9-30-2009.
  • 4080. Collier, L. (1998). Topley & Wilson 's Microbiology and Microbial Infections. Collier, L, Balows, A., and Sussman, M. 9th edition[6 vols]. Edward Arnold.