Aspergillus niger

Aspergillus niger on gypsum boardAspergillus niger on woodAspergillus niger on a ceiling tileAspergillus niger on EM agarAspergillus niger on RB agarAspergillus niger - StereoscopyAspergillus niger - Microscopy (EM Culture)


There are over 200 named species of Aspergillus {3318}. Aspergillus niger is part of a group of species named Aspergillus section Nigriformerly known as «Aspergillus niger group »: all species of this section have black conidial heads.   

In the following text, Aspergillus niger refers to the species A. niger, unless otherwise stated.


ClassEuascomycetes (Eurotiomycetes)GenusAspergillus (section Nigri)

The section Nigri includes 15 related black-spored species that may be confused with A. niger , including A. tubingensisA. foetidusA. carbonarius and A. awamori   (3598).  The species within the Aspergillus niger groupare hyaline hyphomycetes anamorphs: some have known teleomorph forms included in the genera EupenicilliumTalaromycesHamigera andTrichocoma. The species Aspergillus niger has no known teleomorph stage.


A. niger is cosmopolitan and of very common occurrence: it grows aerobically on organic matter {2577}. This species is a common contaminant on various substrates {1056}, found in soil and litter, in compost and on decaying plant material {2577}; it can even be found in icy environments and marine environments, but usually prefers dry and warm soils {989}.  More»»

It is often isolated from house dust, soil, dried nuts, fruits and seeds as well as various types of untreated textile materials such as jute hemp and cotton bracts; hence, the often abundant presence of this species in the textile industry. A. niger can also contaminate meat and eggs, causing progressive spoilage; spices and sun-dried fruit may also contain A. niger {715}.   On the other hand, Aspergillus niger  is one of the most important microorganisms used in biotechnology {2577}, thus having enormous economic significance {2534}.

Even though it is considered an ubiquitous innocuous contaminant,  Aspergillus niger can, in special rare circumstances, cause opportunistic human diseases {509} (see Health effects section).

Growth requirements

A. niger is a mesophilic fungus: its optimal growth temperature is 20-40 °C, with good growth at 37 °C. It can survive at 60 °C {989} but, for example in fruit juices, can be killed by exposure at 63 °C for 25 minutes {2497}.

This species is xerophilic and requires a minimal Aw (available water) of 0.77 {989; 715}; this explains why A. niger is one of the most common Aspergillus species responsible for post-harvest decay of fresh fruit and is frequently isolated from nuts and sun dried products {2543}. The species can however grow very well within an environment of 90-100% relative humidity {989; 715} . For the production of the mycotoxin ochratoxin A, an Aw of at least 0.92-0.94 would however be required {2543}. It can also grow at very low pH (2.0) {989; 715}.

Water Activity :   minimumAw =   0.77    {989}

Growth on building materials or indoor environment

Aspergillus niger is prevalent in residential areas, even in urban settings, and is recovered in both indoor and outdoor air samples. A. niger can be found growing on damp building materials and in contaminated ventilation systems. It is also found as an airborne contaminant of many buildings processing vegetable matter or producing commercially A. niger metabolites.   

More details

In the outdoor air of Zagreb, A. niger was the most abundant species among airborne Aspergillus sampled, with low mean annual concentrations of 0.21-1.04 CFU/m3 {300}. Outdoor air sampling of several Lithuanian urban areas also revealed that A. niger was the most common airborne fungal species, with a prevalence of 84.25% {2226}.

In Saudi Arabia, downfall dust collected from the roofs of numerous houses and taxis revealed a high number of A. nigerspores recovered in 90% of air samples (grown on Czapek’s medium), with total counts reaching 19 600 CFU/g dry air-dust particles {930}. In air-dust particle samples collected on the rooftops of selected houses in Egypt, A. niger was recovered in concentrations of 33 to 68 CFU/mg air-dust {929}. Another investigation of air-dust particles and downfall dust from several locations in Egypt, revealed the presence of A. niger in 40-48% of samples  at concentrations of up to 158 000 CFU/g dry dust {1762}.

Aspergillus niger is also prevalent in the indoor environment. In 49 flats in Bucharest, a high percentage of samples containing A. niger  spores (concentration not given) was reported and related to positive reactions of occupants to a specific A. niger  allergen {2538}. In another study, in which air samples were collected in homes of patients allergic to fungi, A. niger was among the five most prevalent fungi and the first among the genera Aspergillus: this species was detected in 19.2% of samples, as compared to 25.3% in outdoor air samples {624}.

In the aftermath of hurricanes Katrina and Rita on the Gulf Coast of Louisiana in 2005, thousands of homes were flooded. A characterization of airborne moulds revealed a frequency of A. niger of 55% in outdoor samples and 95% in indoor air {695}, thus strongly suggesting that A. niger  grows readily on building materials after a flood.

Ventilation systems can also be contaminated by A. niger. For instance, in a study conducted in a large tertiary hospital, 74 duct dust samples were analysed for Aspergillus surveillance: A. niger  was the most prevalent Aspergillus species, with a mean concentration of 7.57 CFU/m3  {313}.  Other hospital studies have reported similar results {342; 2461}.

A. niger  is also widely distributed in certain industrial processes, especially those dealing with plant material, where it may constitute up to 99%  of total airborne fungi {2541} and thereby be a concern in cases of occupational exposure.  The same may be said of the rural indoor environment, where A. niger has been found to constitute up to 11% of total fungal spores (2373) (see Occupational settings section).

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

Colonies are fast growing on all substrates. On CZA (Czapek-Dox agar), at 25 °C, colonies reach a diameter of 4-5 cm within 7 days and 6-7 cm after 21 days {989}. The colonies consist of a compact white or yellow felt with a dense layer of brown to black conidiophores {1056}; the reverse side is cream to yellow. On malt extract agar (MEA), colonies are thinner but heavily sporulating {715}. Colonies on MEA are also thinner but densely sporulating. Poor growth is observed on creatinine sucrose dichloran agar (CREAD) medium {1056}. Colonies on PDA (potato dextrose agar) at 25 °C are initially white, quickly becoming black with conidial production. The reverse is pale yellow and growth may produce radial cracks in the agar {816}.

Microscopic morphology

Hyphae are septate and hyaline. Conidial heads are black, radiate, with a tendency to split into loose columns at maturity. Conidia are globose to subglobose, 3.5 to 5 mm in diameter; brown with warts, spines or irregular ridges. Conidiophores are long (400-3000 mm) smooth-walled, hyaline, becoming darker at the apex and ending in a globose to subglobose vesicle (50-100 mm in diameter). Phialides (7.0-9.5 x 3-4 mm) are borne on metulae; the metulae (15-25 x 4.5-6.0 mm) hyaline to brown, are often septate, {715; 812; 412; 816; 1056}.   

More details

The taxonomy of black aspergilli (Aspergillus section Nigri ) is not clear and many attempts have been made in order to find suitable taxonomic criteria.  Recognition of the several species of the section Nigri is difficult and requires considerable expertise using conventional methods based on morphological features. Newer molecular methods, or PCR assays, may be useful in identifying those species for which specific primers have been produced. These methods are both highly sensitive and specific and represent a valuable tool especially when looking to identify toxigenic strains {3587}.

However, some of the more common species can be easily distinguished by morphological criteria and dichotomous keys may be used  {464; 991} although two species of the A. niger aggregate, A. niger  and A. tubingensis, remain virtually morphologically indistinguishable from a practical standpoint.

Specific metabolites

Organics compounds (including VOCs)

A. niger  produces a variety of secondary metabolites, including oxalic acid {2577} and certain volatile organic compounds such as 3-methyl-1-butanol, 1-octen-3-ol and dimethyl disulfide terpinol {598}.

Aspergillus niger  is one of the most important microorganisms used in biotechnology {2577}: in industrial fermentations, A. niger  produces various substances including enzymes such as a-amylase {989} {2534}. It produces organic acids such as oxalic acid, fumaric acid and citric acid, thus having an enormous economic significance {2534}. A. niger is classified by many countries as «generally regarded as safe» (GRAS) for food industry  {715; 2577}. 

More details

Furthermore, A. niger  produces other secondary metabolites displaying interesting biological properties such as 3-furanacetic acid, butanedioic acid, deacetylaustin, dehydroaustin,  ethanedioc acid, orlandin, oxalic acid, phenprocoumon metabolite 1, phenprocoumon metabolite 2, phenprocoumon metabolite 3, warfarin metabolite 1, warfarin metabolite 2,  warfarin metabolite 3, warfarin metabolite 4 and yanuthone  {812}.


Aspergillus niger produces many metabolites among which potent mycotoxins : austin,  fumonisin B2, gliotoxin as well as malformins including malformin C, ochratoxin  A and phthioic acid.   Two of A. niger ’s secondary metabolites, malformin C and some of the naphtho-g-quinones and naphtho-gamma-pyrones {3613}, have shown toxic effects {516}, although these substances may not typically fall within the definition of mycotoxins {715}.Certain strains of A. niger , on the other hand,produce true mycotoxins such as nigerazine B, nigragillin and ochratoxin A (OA) {2534}; this latter mycotoxin has received increasing attention because of the hazard it poses to animal and human health. OA mycotoxin is reported to be nephrotoxic, carcinogenic, teratogenic and immunosuppressive in humans as well as in animals {2589; 2534} . Most mycotoxin studies have been conducted in circumstances involving food and feed as the growing substrate although A. nigercanalso produce mycotoxins when growing on building materials {603}.   

More details

Nine of 19 isolates of A. niger from feedstuff studied by Abarca et al. produced OA in liquid cultures as well as in corn cultures {2526}. Generally, only 3-10% of the strains examined for OA production have tested positive under favourable conditions {2577}. In wine grapes, OA with levels ranging from 2 to 24.5 ng/mL have been reported, but could not be specifically linked to the presence of A. niger {2539}.

Although low-level production of aflatoxin in A. niger has been reported, this species generally does not have the ability to produce aflatoxins and previous reports may result from errors in detection methodology {2577}; moreover, fermented-products obtained by A. niger were shown to be aflatoxin-free and most industrial productions have successfully demonstrated a long history of safe use {2534}. However, A. niger was recently reported to produce the fumonisin B2, a carcinogenic mycotoxin usually produced by Fusarium verticillioides and other fusaria {1597}.

Some reports have suggested  that kojic acid could be produced by A. niger, although a review on the safety of A. nigercame to the conclusion that this is unlikely in industrial processes using this species {2577} .

Few toxic strains of A. niger are found naturally occurring in cereals: in a screening of OA-producing strains belonging to the Aspergillus and Eurotium species isolated from poultry mixed feeds and raw materials (corn, soya bean and peas), only 2 of 19 isolates of A. niger var. niger  studied produced OA in liquid cultures as well as in corn cultures {2526}.  However, the potential production of ochratoxin could be an unexpected hazard to human and animal health if such strains are used as starters in food industry.

Accensi et al. did however recover A. niger var. niger  from cereals (occurrence of 15.4%), legumes (27.8%), and mixed feed (6.1%):  a further three isolates were ochratoxin A producers {2589}. This toxin has also been identified from the mycoflora in grapes and dried vine fruits in South America {2539}. In a study of rabbit feeds, Dalcero et al. {2540} reported a percentage of A. niger ochratoxicogenic strains (var. niger  and var. awamori) ranging from 78 to 100%; in pig feeds, 61% of A. niger (var. awamori) were producers of this toxin.

The growth of A. niger on experimentally and naturally infested building materials has revealed that this species produces many secondary metabolites, including some of the aforementioned mycotoxins such as naphtho-t-pyrones, malformins and ochratoxin A {603}.

Adverse health reactions

Health risks associated with mould exposure in water-damaged buildings are well established, especially for upper and lower respiratory tract symptoms. Indoors, Aspergillus niger can be present in significant concentrations and can contribute to various indoor air problems.

Irritation and inflammation

Generally speaking, all moulds contain substances that are irritants and promote inflammation to some degree.  Some of the volatile organic compounds (VOCs) produced by moulds in the indoor setting on damp building materials are thought to contribute to various health problems, such as eye irritation, irritation of the nose and throat, lethargy and headache {594}. 

Few studies have been published on the specific inflammatory properties of A. niger.  The conidia of A. niger activate rat alveolar macrophages, causing the release of inflammatory mediators.  Based on this observation, it has been suggested that the inhalation of large numbers of A. niger conidia could lead to pulmonary inflammation {2541}.

Allergic reactions

Aspergillus niger  is linked to Type I allergies, rhinitis {3443} and asthma as well as allergic sinusitis. A study investigating 614 respiratory allergic patients reported that the frequency of positive skin test reactions to extracts of fungal spores of A. niger  was 20.4%, one of the highest prevalence levels of fungal sensitisation {162}.

An American study on the concentration of moulds in homes of asthmatic children showed that Aspergillus niger andAspergillus unguis were the primary mould species that distinguished severely asthmatic children's homes and non-asthmatic children's homes {3638}. This study suggests that A. niger is associated with allergic sensitisation in children and the presence of asthma.  A Malaysian study investigating the prevalence of skin prick test (SPT) reactivity among asthmatic patients, with and without rhinitis, showed a prevalence of 0.7% positive skin test for A. niger, among patients reacting to at least one of the common aeroallergens, thus ranking first for moulds equalling A. fumigatus {3569}.

In a study of 500 patients experiencing varying symptoms after being exposed to moulds in water-damaged buildings, Vojdani et al. detected the production of specific IgG, IgM and IgA antibodies against A. niger confirming a fungal exposure triggering an immunological response{196}.  Allergic reactions and asthma triggered by Aspergillus niger and to its components have also been reported in occupational settings (see Allergenic components and occupational sections).   

More details

Allergic fungal sinusitis may sometimes be caused by A. niger. For instance, it was one of the fungal species identified from sinus fluid in patients with allergic fungal rhinosinusitis {2558}. Chhabra et al. also reported one case (out of 11 patients with allergic fungal sinusitis) caused by A. niger  {2537}.   

Allergic bronchopulmonary aspergillosis may be caused, in rare circumstances, by A. niger {2587}. A case of allergic bronchopulmonary aspergillosis without bronchial asthma has been reported {2552}.

Allergic components and mechanism

A study of A. niger IgE-binding components revealed that serine proteinases are major allergens and may be associated with extrinsic bronchial asthma {3444}. 

Phytase is an enzyme commercially produced by A. niger and used in animal feed: it is a potentially important new occupational allergen causing specific IgE immune responses among exposed workers. Such IgE sensitisation could eventually be the cause of work related asthmatic and other respiratory symptoms {3572} {210}.  Similarly, xylanase, an enzyme of Aspergillus niger used as a baking additive, is a relevant type I-sensitizer in the baking industry {Baur, 1998 3573 /id}.

A. niger beta-xylosidase, currently used in baking additives, is also an occupational allergen which causes sensitisation in at least 4% of symptomatic bakers and has been named  Asp-n-14  {3574}.

Hypersensitivity pneumonitis

Aspergillus Type III hypersensitivity pneumonitis is well known in occupational settings although only few cases specifically induced by A. niger have been reported {2572}.       

Toxic effects (mycotoxicosis)

Most Aspergillus species are active producers of toxins under given sets of growth conditions. Toxic effects due to ingestedAspergillus niger toxins include cytotoxicity, neurotoxicity and nephrotoxicity, although this species is not particularly noted for its toxicity.     

More details

Some species of the Aspergillus genus, including A. niger, have been reported to secrete cytotoxic factors to which neurons are the most sensitive; very low amounts of these products and short incubation times are sufficient to induce irreversible cell damage and can affect distant brain regions. This toxic activity of A. niger filtrates is likely triggered by a high molecular mass factor which can be inactivated by heat {2580}.

A. niger is also reported to produce a proteinaceous hemolysin, or niger lysin, when incubated on sheep’s blood agar; this compound was shown to cause rapid loss of viability of mouse primary cortical neuronal cells {1532}.

Infections and colonisations

Human infections by Aspergillus niger are rare.  In fact, A. niger is generally regarded as a non-pathogenic fungus; spore inhalation is common but disease in healthy subjects is quite uncommon {2574}. However, a few cases of primary cutaneous aspergillosis, onychomycosis, otomycosis, sinusitis, ocular and pulmonary infections as well as rare cases of secondary aspergillosis caused by this species have been reported {2577} . Furthermore, opportunistic infections in immunocompromised patients, leading to respiratory infections, mycotic keratitis and endocarditis have been occasionally reported.  Some cases of iatrogenic aspergillosis due to A. niger have also been reported (see Nosocomial section).        

More details

Onychomycosis (a fungal infection of the nails) is usually caused by dermatophytic fungi, but has been recognized, albeit uncommon, to be caused by Aspergillus spp. In a study of 5,221 cases of onychomycosis, 13 instances (0.2%) were found to be caused by A. niger {2535}. Tosti et al. {2584} also reported onychomycosis due to A. niger  in Italy. In Iran, a study of 1,146 patients with onychomycosis revealed that A. niger was the most frequent agent of this type of mould infection {1833}.

Otomycosis is a common infection, even in immunocompetent subjects, often caused by Aspergillus species {2553}. In investigating cases of proven fungal otitis, two independent studies (Mexico and India) found that A. niger was respectively involved in 21% and 57.5% of cases {2532} {2536}. A similar observation was made in a Turkish study in which 47% of 120 studied cases were A. niger infections {2436}. Other studies also reported that A. niger was the most common fungus involved in otomycosis {2553} {2422} {2568}.

A. niger is sometimes involved in colonisation of the sinuses, even resulting in the formation of a fungus ball or aspergilloma {2523} {2533}.

Ocular infections with Aspergillus species are associated with keratitis and sporadically with endophthalmitis; they are however rarely attributed to A. niger {2554}. An unusual black corneal ulcer due to A. niger has been reported however {2564}. Fungal endophthalmitis due to A. niger in non immunocompromised patients has also been reported following administration of presumably contaminated dextrose infusion fluid for minor eye ailments {2549}.

Invasive pulmonary aspergillosis (IPA) is an important opportunistic infection in immunosuppressed patients. A retrospective study of 72 IPA patients, for which the respiratory culture was found positive for Aspergillus species, revealed that 13 patients were positive for A. fumigatus and 2 for A. niger ; another study of 500 patients with Aspergillus respiratory colonization revealed that 80% were positive for A. fumigatus and 10% for A. niger {360}.

A case of fatal haemoptysis due to an A. niger invasive infection has been reported in a patient with cavitary lung disease {2548}.  Cases of chronic necrotizing pulmonary aspergillosis have been reported in patients with underlying cavitary lesions caused by Mycobacterium avium complex disease {172}.

A. niger was also reported to be the causative agent of pulmonary oxalosis. Pulmonary oxalosis is a rare pseudotumoral lesion which can occur following progressive lung infiltrates secondary to an A. niger saprophytic aspergilloma {2575; 2576}. A mycetoma due to A. niger in the renal collecting system and ureter, in a chronically-ill patient, has also been described {2565}.

In one case, A. niger was involved as the sole pathogen of a rare primary soft-tissue infection (lower extremity soft tissue) in a patient who ultimately died of overwhelming infection following necrotizing fasciitis {2557}.

Virulence factors

Cytotoxic properties of A. niger may contribute to the establishment of the infection even if host risk factors are stronger determinants in the Aspergillus niger infectious process {3612; 3611; 3614}.  Nevertheless, Aspergillus niger appears to be a fungal species of low virulence that requires the presence of a severely immunosuppressed host factors or severely damaged natural barriers to cause invasive disease {3599} .

More details

A  study of A. niger isolates from patients with pulmonary aspergillosis revealed that they  disrupt human respiratory epithelium cells, but without any significant slowing of ciliary beat frequency {2531}.  Cytotoxic effects and haemolysis of sheep red blood cells caused by A. niger extracts have also been reported in an experimental study {2487}.

Specific settings

Nosocomial infections

Aspergillus niger infections have been reported in the hospital setting. A. niger is frequently isolated from the hospital indoor environment, being one of the most prevalent forms of Aspergillus {401; 342; 340}. The presence of Aspergillus species in hospital air is considered a major risk factor for both invasive and allergic aspergillosis since immunocompromised patients are particularly at risk of invasive aspergillosis {526; 2448; 342}.

For hospitalized patients, even concentrations of Aspergillus spp. below 1 colony-forming unit/m3 of air are considered sufficient to cause infection {2465}.  However, the link between A. niger infections and environmental contamination has rarely been clearly demonstrated. 

More details

Hospitals are also buildings where indoor air may be contaminated by aspergilli, including A. niger {401; 340; 317}. A seven-month study at the Memorial Sloan-Kettering Cancer Center, revealed that this species accounted for 56% of air isolates but for only 17% of patient isolates {2461} . An Aspergillus surveillance protocol conducted in a large tertiary hospital with extensive indoor renovation and nearby large demolition/construction sites revealed that A. niger was the most prevalent Aspergillus in repeated air samples and 74 duct dust samples with a mean concentration of 7.57 CFU/m3{313}.  Similar studies in two other tertiary care hospitals also demonstrated that A. niger was the most commonly recovered fungus from air, with an occurrence of 39.2% in one hospital {342} while a concentration of A. nigerbetween 124 and 217 CFU/m3 was reported in the second hospital study where this species was again the most prevalent among aspergilli {2450}.

In a series of environmental samples taken in rooms of a department of Dermatology and Allergology of a Polish university hospital, A. niger was found to be one of the most common culturable airborne fungus, with a mean concentration of 16.5 CFU/m3 {2569}. High frequency of A. niger (60%) was also reported from air conditioners in intensive care units in Italian hospitals {2445}.

However very few outbreaks linked to environmental A. niger are documented in the literature {3606} {3607} {686} {344} {317}.  A pseudo-outbreak of A. niger was reported during construction of a clinical microbiology laboratory {519}.  Environmental contamination by A. niger , in a kitchenette located in a bone marrow transplantation unit, was also reported as the source of aspergilli infections in some patients {523}.

Invasive aspergillosis, including A. niger infection, may in fact be an important clinical problem in bone marrow transplantation recipients {2555; 523}. A. niger was identified in the aetiology of septic shock in neutropenic patients with cancer {2561}.

In a study of 18 patients with haematological malignancies who had positive cultures for Aspergillus species, only one had definite aspergillemia, along with 5 probable aspergillemia (one associated with A. niger ) {2560}.

An Aspergillus aortitis following cardiac surgery attributed to A. niger has beenreported {2542}. Cases of endocarditis following open heart surgery, caused by A. niger have also been reported, suggesting that surgery and prosthesis relatedA. niger infections are possible even in immunocompetent patients {2586}; {2562}.

The study of a burn care unit revealed that A. niger was the most frequent isolate both in patients and their environment {1839}. Other underlying conditions affecting the integrity of the epitheliums may also represent a predisposing condition for invasive A. niger aspergillosis: such risk factors include diabetes mellitus {2579} and  tuberculosis {2585}.

Occupational diseases

Many studies have assessed occupational exposure to A. niger  in both industrial and rural settings, but few have studied the health risks associated with this exposure.  Allergic reactions, occupational asthma and Type III hypersensitivity pneumonitis due to Aspergillus niger have been occasionally reported in occupational settings.

Allergic and immunotoxic properties of A. niger could be involved in certain allergic reactions in some industrial processing plants; for example, A. niger was associated with allergic alveolitis in a tea packing factory {2573} and with occupational asthma in pharmacy workers, bakers {2541}, workers using powdered phytase (an additive to animal feed) from Aspergillus niger  {210} as well as in a greenhouse worker {2544} and in a worker of a sugar beet processing facility {2588}.   

More details

A case of occupational asthma due to exposure to A. niger ,used in the production of citric acid, has been described; 8 other workers had been sensitized to A. niger (positive skin prick test) and remained asymptomatic {2583}; in these cases, sensitisation had occurred as a consequence of exposure to free aerosolized antigen {2578}.  The extensive use of A. niger in the industrial production of compounds such as citric acid and enzymes exposes workers to high concentrations of conidia or proteinaceous fractions resulting in possible sensitisation and various types of airway allergies {715}. 

This species may be found in biotechnology plants using this fungus in fermentation process, such as citric acid production, where very high counts of A. niger spores have been reported {2578}.

Many studies have shown A. niger to be widely prevalent in certain agricultural processes, especially those using plant material. In a large potato processing plant, air samples collected for the determination of concentrations of microorganisms revealed that fungi accounted for 1.2 to 26.9% of the total count, with A. niger being the dominant species constituting99.8% of total airborne fungi {2541}, hence leading the authors to express concern regarding this potential sensitisation exposure in potato processing plants. Similarly, workers in beet sugar refineries may be exposed to a high concentration of fungal spores, including A. niger {2556}. In cotton samples provided from many areas of the world, A. niger represented the most frequently identified species (9 samples out of 13) and may represent a source of occupational health problems for cotton workers {700}.

A. niger is a contaminant of agricultural material, especially in grain raw material (grain before and after treatment) and can be recovered in the air from both mills and bakeries {1883}; it has been cultured from aerosol samples in a rural bakery of India, at concentrations up to 420 CFU/m3 {2401}. This species was also found in almonds, peanuts, hazelnuts, pistachios and sunflower seeds destined for human consumption {2498}.

In large rural indoor cattle shed, A. niger was the third most abundant airborne fungal contaminant, contributing between 8.28 and 11.26 % of total fungal spores (concentration up to 326 CFU/m3) {2373}.

A. niger has been isolated from cultures of greenhouse roses and has been reported as the source of hypersensitivity pneumonitis in one case {2572}. Flournay et al. {2546} reported that A. niger was the third most prevalent species isolated from rose thorns.  Indeed, rose plants are notoriously susceptible to fungal diseases and may act as important vehicles in the transmission of pathogenic microorganisms via punctures penetrating the skin.

Diagnostic tools


Even in autopsy-confirmed cases of invasive septate mould infection, the culture yield of mould is low {3600}. In the case of common moulds such as A. niger, in order to be considered as indicative of infection, A. niger must be recovered from normally sterile sites or found in multiple samples.  One must interpret a positive A. niger culture with caution so as not to confuse the latter with an environmental contamination of the sample.


Histopathological visualization of typical septate hyphae growing within the affected tissue may confirm the presence of a mycosis; species identification of the aetiologic agent may be obtained by culture methods.   The histological presentation of a deep sited infection due to A. niger is typically that of an opportunistic fungal hyphal infection and cannot be distinguished from other aspergillosis. 


Serodiagnosis of A. niger infection may contribute to the diagnosis of invasive infections although some degree of cross-reactivity has been observed {3526; 3532}.

Skin TestsX   
RAST-IgG Experimental  
Complement fixation    

More details

The common commercially available allergen preparations of A. niger for use in vivo and/or in vitro are either sold as single species extracts or within Aspergillus mixes or environmental mould mixes {2758} {581} {3284} {Immuno Mycologics, 2003 3874 /id}.  

Aspergillus niger  antigens are part of the American  Food and Drug Administration (FDA) surveillance program and part of the Biological Product Deviation Reports mould list {3285}.

  • GJ08 - Aspergillus amsterdami
  • GJ09 - Aspergillus clavatus
  • GJ10 - Aspergillus flavipes
  • GJ11 - Aspergillus flavus
  • GJ12 - Aspergillus fumigatus
  • GJ13 - Aspergillus glaucus
  • GJ14 - Aspergillus nidulans
  • GJ15 - Aspergillus niger  
  • GJ16 - Aspergillus ochraceus
  • GJ17 - Aspergillus restrictus
  • GJ18 - Aspergillus sydowi
  • GJ19 - Aspergillus terreus
  • GJ20 - Aspergillus ustus
  • GJ21 - Aspergillus versicolor


  • 162. Guneser, S., Atici, A., Koksal, F., and Yaman, A. (1994). Mold allergy in Adana, Turkey. Allergol.Immunopathol.(Madr.). 22[2], 52-54.
  • 172. Kobashi, Y., Fukuda, M., Yoshida, K., Miyashita, N., Niki, Y., and Oka, M. (2006). Chronic necrotizing pulmonary aspergillosis as a complication of pulmonary Mycobacterium avium complex disease. Respirology. 11[6], 809-813.
  • 196. Vojdani, A., Thrasher, J. D., Madison, R. A., Gray, M. R., Heuser, G., and Campbell, A. W. (2003). Antibodies to molds and satratoxin in individuals exposed in water-damaged buildings. Arch Environ Health. 58[7], 421-432.
  • 210. Baur, X., Melching-Kollmuss, S., Koops, F., Strassburger, K., and Zober, A. (2002). IgE-mediated allergy to phytase -- a new animal feed additive. Allergy. 57[10], 943-945.
  • 300. Kosalec, I., Klaric, M. S., and Pepeljnjak, S. (2005). Verruculogen production in airborne and clinical isolates of Aspergillus fumigatus Fres. Acta Pharm. 55[4], 357-364.
  • 313. Curtis, L., Cali, S., Conroy, L., Baker, K., Ou, C. H., Hershow, R., Norlock-Cruz, F., and Scheff, P. (2005). Aspergillus surveillance project at a large tertiary-care hospital. J Hosp.Infect. 59[3], 188-196.
  • 317. Petrova, N. A. and Kliasova, G. A. (2005). [Possible sources of aspergilla infection in a hematological hospital]. Ter.Arkh. 77[7], 71-77.
  • 340. Petrova, N. A., Kliasova, G. A., and Funygina, L. P. (2003). [Prevalence of mycelial fungi in hematological hospital]. Ter.Arkh. 75[7], 58-63.
  • 342. Panagopoulou, P., Filioti, J., Petrikkos, G., Giakouppi, P., Anatoliotaki, M., Farmaki, E., Kanta, A., Apostolakou, H., Avlami, A., Samonis, G., and Roilides, E. (2002). Environmental surveillance of filamentous fungi in three tertiary care hospitals in Greece. J Hosp.Infect. 52[3], 185-191.
  • 344. Hahn, T., Cummings, K. M., Michalek, A. M., Lipman, B. J., Segal, B. H., and McCarthy, P. L., Jr. (2002). Efficacy of high-efficiency particulate air filtration in preventing aspergillosis in immunocompromised patients with hematologic malignancies. Infect Control Hosp.Epidemiol. 23[9], 525-531.
  • 360. Pegues, C. F., Daar, E. S., and Murthy, A. R. (2001). The epidemiology of invasive pulmonary aspergillosis at a large teaching hospital. Infect Control Hosp.Epidemiol. 22[6], 370-374.
  • 401. Mallea, M., Renard, M., and Charpin, J. (1983). [Fungal flora in a hospital milieu]. Pathol.Biol.(Paris). 31[3], 177-181.
  • 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.
  • 464. Abarca, M. L., Accensi, F., Cano, J., and Cabanes, F. J. (2004). Taxonomy and significance of black aspergilli. Antonie Van Leeuwenhoek. 86[1], 33-49.
  • 509. Heinemann, S., Symoens, F., Gordts, B., Jannes, H., and Nolard, N. (2004). Environmental investigations and molecular typing of Aspergillus flavus during an outbreak of postoperative infections. J Hosp.Infect. 57[2], 149-155.
  • 516. Nogler, M., Lass-Florl, C., Ogon, M., Mayr, E., Bach, C., and Wimmer, C. (2001). Environmental and body contamination through aerosols produced by high-speed cutters in lumbar spine surgery. Spine. 26[19], 2156-2159.
  • 519. Laurel, V. L., Meier, P. A., Astorga, A., Dolan, D., Brockett, R., and Rinaldi, M. G. (1999). Pseudoepidemic of Aspergillus niger infections traced to specimen contamination in the microbiology laboratory. J Clin Microbiol. 37[5], 1612-1616.
  • 523. Loudon, K. W., Coke, A. P., Burnie, J. P., Shaw, A. J., Oppenheim, B. A., and Morris, C. Q. (1996). Kitchens as a source of Aspergillus niger infection. J Hosp.Infect. 32[3], 191-198.
  • 526. Arnow, P. M., Sadigh, M., Costas, C., Weil, D., and Chudy, R. (1991). Endemic and epidemic aspergillosis associated with in-hospital replication of Aspergillus organisms. J Infect Dis. 164[5], 998-1002.
  • 581. Pharmacia Diagnostics AB. (2007). Allergy & autoimmunity. Diagnostics product catalogue 2007. internet , 1-48. Pharmacia.
  • 594. Claeson, A. S., Levin, J. O., Blomquist, G., and Sunesson, A. L. (2002). Volatile metabolites from microorganisms grown on humid building materials and synthetic media. J Environ Monit. 4[5], 667-672.
  • 598. Gao, P., Korley, F., Martin, J., and Chen, B. T. (2002). Determination of unique microbial volatile organic compounds produced by five Aspergillus species commonly found in problem buildings. AIHA.J (Fairfax., Va.). 63[2], 135-140.
  • 603. Nielsen, K. F., Gravesen, S., Nielsen, P. A., Andersen, B., Thrane, U., and Frisvad, J. C. (1999). Production of mycotoxins on artificially and naturally infested building materials. Mycopathologia. 145[1], 43-56.
  • 624. de Ana, S. G., Torres-Rodriguez, J. M., Ramirez, E. A., Garcia, S. M., and Belmonte-Soler, J. (2006). Seasonal distribution of Alternaria, Aspergillus, Cladosporium and Penicillium species isolated in homes of fungal allergic patients. J Investig.Allergol.Clin Immunol. 16[6], 357-363.
  • 686. Loo, V. G., Bertrand, C., Dixon, C., Vitye, D., DeSalis, B., McLean, A. P., Brox, A., and Robson, H. G. (1996). Control of construction-associated nosocomial aspergillosis in an antiquated hematology unit. Infect Control Hosp.Epidemiol. 17[6], 360-364.
  • 695. Rao, C. Y., Riggs, M. A., Chew, G. L., Muilenberg, M. L., Thorne, P. S., Sickle, D. V., Dunn, K. H., and Brown, C. (2007). Characterizing airborne molds, endotoxins and glucans in homes in New Orleans after Hurricanes Katrina and Rita. Appl.Environ Microbiol. .
  • 700. Lane, S. R. and Sewell, R. D. (2006). The fungal profile of cotton lint from diverse sources and implications for occupational health. J Occup Environ Hyg. 3[9], 508-512.
  • 715. Fiedler, K., Schutz, E., and Geh, S. (2001). Detection of microbial volatile organic compounds (MVOCs) produced by moulds on various materials. Int J Hyg.Environ Health. 204[2-3], 111-121.
  • 812. Fungal Research Trust. (2007). The Aspergillus Web-Site. . 2007.
  • 816. Patterson, T. F., McGinnis, M. R., and ed. (2009). The fungi :description. Site Doctor Fungus . Mycoses Study Group.
  • 929. Abdel-Hafez, S. I., Shoreit, A. A., Abdel-Hafez, A. I., and el Maghraby, O. M. (1986). Mycoflora and mycotoxin-producing fungi of air-dust particles from Egypt. Mycopathologia. 93[1], 25-32.
  • 930. Abdel-Hafez, S. I. and Shoreit, A. A. (1985). Mycotoxins producing fungi and mycoflora of air-dust from Taif, Saudi Arabia. Mycopathologia. 92[2], 65-71.
  • 989. Centre de recherche sur la conservation des documents graphiques. (2007). Moisissures et biens culturels. Ministère de la culture et de la Communication, France .
  • 991. Pitt, J. I. (1989). Recent developments in the study of Penicillium and Aspergillus systematics. J.Appl.Bact.Symp. Suppi. 37S45S.
  • 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.
  • 1532. Donohue, M., Wei, W., Wu, J., Zawia, N. H., Hud, N., De, Jesus, V, Schmechel, D., Hettick, J. M., Beezhold, D. H., and Vesper, S. (2006). Characterization of nigerlysin, hemolysin produced by Aspergillus niger, and effect on mouse neuronal cells in vitro. Toxicology. 219[1-3], 150-155.
  • 1597. Frisvad, J. C., Smedsgaard, J., Samson, R. A., Larsen, T. O., and Thrane, U. (2007). Fumonisin B2 Production by Aspergillus niger. J Agric Food Chem. 55[23], 9727-9732.
  • 1762. Abdel-Hafez, S. I., Moubasher, A. H., and Barakat, A. (1990). Keratinophilic fungi and other moulds associated with air-dust particles from Egypt. Folia Microbiol (Praha). 35[4], 311-325.
  • 1833. Hilmioglu-Polat, S., Metin, D. Y., Inci, R., Dereli, T., Kilinc, I., and Tumbay, E. (2005). Non-dermatophytic molds as agents of onychomycosis in Izmir, Turkey - a prospective study. Mycopathologia. 160[2], 125-128.
  • 1839. Mousa, H. A., Al-Bader, S. M., and Hassan, D. A. (1999). Correlation between fungi isolated from burn wounds and burn care units. Burns. 25[2], 145-147.
  • 1867.  (2003). The truth about mold. Most experts say there's more fear than fact to "toxic mold." But that doesn't mean that indoor mold can't cause health problems. Harv.Health Lett. 28[3], 1-3.
  • 1883. Lugauskas, A., Raila, A., Railiene, M., and Raudoniene, V. (2006). Toxic micromycetes in grain raw material during its processing. Ann Agric Environ Med. 13[1], 147-161.
  • 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.
  • 2373. Adhikari, A., Sen, M. M., Gupta-Bhattacharya, S., and Chanda, S. (2004). Volumetric assessment of airborne fungi in two sections of a rural indoor dairy cattle shed. Environ Int. 29[8], 1071-1078.
  • 2401. Adhikari, A., Sen, M. M., Gupta-Bhattacharya, S., and Chanda, S. (2000). Incidence of allergenically significant fungal aerosol in a rural bakery of West Bengal, India. Mycopathologia. 149[1], 35-45.
  • 2422. Fasunla, J., Ibekwe, T., and Onakoya, P. (2008). Otomycosis in western Nigeria. Mycoses. 51[1], 67-70.
  • 2436. Kaya, A. D. and Kiraz, N. (2007). In vitro susceptibilities of Aspergillus spp. causing otomycosis to amphotericin B, voriconazole and itraconazole. Mycoses. 50[6], 447-450.
  • 2445. Mobin, M. and do Amparo, Salmito M. (2006). [Fungus microbiota in air conditioners in intensive care units in Teresina, Piaui]. Rev Soc Bras.Med Trop. 39[6], 556-559.
  • 2448. Niessen, L. (2008). PCR-based diagnosis and quantification of mycotoxin-producing fungi. Adv Food Nutr Res. 54:81-138., 81-138.
  • 2450. Panagopoulou, P., Filioti, J., Farmaki, E., Maloukou, A., and Roilides, E. (2007). Filamentous fungi in a tertiary care hospital: environmental surveillance and susceptibility to antifungal drugs. Infect Control Hosp Epidemiol. 28[1], 60-67.
  • 2461. Schmitt, H. J., Blevins, A., Sobeck, K., and Armstrong, D. (1990). Aspergillus species from hospital air and from patients. Mycoses. 33[11-12], 539-541.
  • 2465. Vonberg, R. P. and Gastmeier, P. (2006). Nosocomial aspergillosis in outbreak settings. J Hosp Infect. 63[3], 246-254.
  • 2487. Budzko, D. B. and Negroni, R. (1975). Hemolytic, cytotoxic and complement inactivating properties of extracts of different species of Aspergillus. Mycopathologia. 57[1], 23-26.
  • 2497. Jesenska, Z., Pieckova, E., and Bernat, D. (1993). Heat resistance of fungi from soil. Int J Food Microbiol. 19[3], 187-192.
  • 2498. Jimenez, M., Mateo, R., Querol, A., Huerta, T., and Hernandez, E. (1991). Mycotoxins and mycotoxigenic moulds in nuts and sunflower seeds for human consumption. Mycopathologia. 115[2], 121-127.
  • 2523. Willinger, B., Obradovic, A., Selitsch, B., Beck-Mannagetta, J., Buzina, W., Braun, H., Apfalter, P., Hirschl, A. M., Makristathis, A., and Rotter, M. (2003). Detection and identification of fungi from fungus balls of the maxillary sinus by molecular techniques. J Clin Microbiol. 41[2], 581-585.
  • 2526. Abarca, M. L., Bragulat, M. R., Castella, G., and Cabanes, F. J. (1994). Ochratoxin A production by strains of Aspergillus niger var. niger. Appl Environ Microbiol. 60[7], 2650-2652.
  • 2531. Amitani, R., Murayama, T., Nawada, R., Lee, W. J., Niimi, A., Suzuki, K., Tanaka, E., and Kuze, F. (1995). Aspergillus culture filtrates and sputum sols from patients with pulmonary aspergillosis cause damage to human respiratory ciliated epithelium in vitro. Eur Respir J. 8[10], 1681-1687.
  • 2532. Araiza, J., Canseco, P., and Bonifaz, A. (2006). Otomycosis: clinical and mycological study of 97 cases. Rev Laryngol.Otol.Rhinol.(Bord.). 127[4], 251-254.
  • 2533. Arnaud, M. V., Moraes, M. A., and Nobrega, P. (1994). [2 cases of paranasal aspergilloma due to Aspergillus niger]. Rev Soc Bras.Med Trop. 27[1], 43.
  • 2534. Blumenthal, C. Z. (2004). Production of toxic metabolites in Aspergillus niger, Aspergillus oryzae, and Trichoderma reesei: justification of mycotoxin testing in food grade enzyme preparations derived from the three fungi. Regul Toxicol.Pharmacol. 39[2], 214-228.
  • 2535. Bonifaz, A., Cruz-Aguilar, P., and Ponce, R. M. (2007). Onychomycosis by molds. Report of 78 cases. Eur J Dermatol. 17[1], 70-72.
  • 2536. Chander, J., Maini, S., Subrahmanyan, S., and Handa, A. (1996). Otomycosis--a clinico-mycological study and efficacy of mercurochrome in its treatment. Mycopathologia. 135[1], 9-12.
  • 2537. Chhabra, A., Handa, K. K., Chakrabarti, A., Mann, S. B., and Panda, N. (1996). Allergic fungal sinusitis: clinicopathological characteristics. Mycoses. 39[11-12], 437-441.
  • 2538. Chirila, M., Nicolau, C., and Florescu, L. (1990). Houses and allergic respiratory syndromes. Med Interne. 28[4], 341-346.
  • 2539. Chulze, S. N., Magnoli, C. E., and Dalcero, A. M. (2006). Occurrence of ochratoxin A in wine and ochratoxigenic mycoflora in grapes and dried vine fruits in South America. Int J Food Microbiol. 111 Suppl 1:S5-9. Epub;%2006 May 22., S5-S9.
  • 2540. Dalcero, A., Magnoli, C., Hallak, C., Chiacchiera, S. M., Palacio, G., and Rosa, C. A. (2002). Detection of ochratoxin A in animal feeds and capacity to produce this mycotoxin by Aspergillus section Nigri in Argentina. Food Addit.Contam. 19[11], 1065-1072.
  • 2541. Dutkiewicz, J., Krysinska-Traczyk, E., Skorska, C., Cholewa, G., and Sitkowska, J. (2002). Exposure to airborne microorganisms and endotoxin in a potato processing plant. Ann Agric Environ Med. 9[2], 225-235.
  • 2542. Duygu, H., Nalbantgil, S., Ozerkan, F., Kirilmaz, B., and Yagdi, T. (2006). Aspergillus niger aortitis after aortic valve replacement diagnosed by transesophageal echocardiography. Echocardiography. 23[5], 405-406.
  • 2543. Esteban, A., Abarca, M. L., Bragulat, M. R., and Cabanes, F. J. (2006). Effect of water activity on ochratoxin A production by Aspergillus niger aggregate species. Int J Food Microbiol. 108[2], 188-195.
  • 2544. Farruggia, E. and Bellia, M. (2001). [Occupational allergic asthma in greenhouses. Report of a clinical case]. Med Lav. 92[3], 203-205.
  • 2546. Flournoy, D. J., Mullins, J. B., and McNeal, R. J. (2000). Isolation of fungi from rose bush thorns. J Okla.State Med Assoc. 93[7], 271-274.
  • 2547. George, D. L., McLeod, R., and Weinstein, R. A. (1991). Contaminated commercial charcoal as a source of fungi in the respiratory tract. Infect Control Hosp Epidemiol. 12[12], 732-734.
  • 2548. Gifford, A. H., Lahey, T., and Fordham Von, Reyn C. (2006). Fatal hemoptysis from invasive Aspergillus niger in a patient with cavitary lung disease and Mycobacterium avium complex infection. Med Mycol. 44[6], 557-560.
  • 2549. Gupta, A., Gupta, V., Dogra, M. R., Chakrabarti, A., Ray, P., Ram, J., and Patnaik, B. (2000). Fungal endophthalmitis after a single intravenous administration of presumably contaminated dextrose infusion fluid. Retina. 20[3], 262-268.
  • 2551. Ho, I. C., Milan, D. J., Mansour, M. C., Mela, T., Guy, M. L., Ruskin, J. N., and Ellinor, P. T. (2006). Fungal infection of implantable cardioverter-defibrillators: case series of five patients managed over 22 years. Heart Rhythm. 3[8], 919-923.
  • 2552. Hoshino, H., Tagaki, S., Kon, H., Shibusa, T., Takabatake, H., Fujita, A., Sekine, K., and Abe, S. (1999). Allergic bronchopulmonary aspergillosis due to Aspergillus niger without bronchial asthma. Respiration. 66[4], 369-372.
  • 2553. Hueso, Gutierrez P., Jimenez, Alvarez S., Gil-Carcedo, Sanudo E., Gil-Carcedo Garcia, L. M., Ramos, Sanchez C., and Vallejo Valdezate, L. A. (2005). [Presumption diagnosis: otomycosis. A 451 patients study]. Acta Otorrinolaringol.Esp. 56[5], 181-186.
  • 2554. Jager, M. J., Chodosh, J., Huang, A. J., Alfonso, E. C., Culbertson, W. W., and Forster, R. K. (1994). Aspergillus niger as an unusual cause of scleritis and endophthalmitis. Br J Ophthalmol. 78[7], 584-586.
  • 2555. Jantunen, E., Piilonen, A., Volin, L., Parkkali, T., Koukila-Kahkola, P., Ruutu, T., and Ruutu, P. (2000). Diagnostic aspects of invasive Aspergillus infections in allogeneic BMT recipients. Bone Marrow Transplant. 25[8], 867-871.
  • 2556. Jensen, P. A., Todd, W. F., Hart, M. E., Mickelsen, R. L., and O'Brien, D. M. (1993). Evaluation and control of worker exposure to fungi in a beet sugar refinery. Am Ind Hyg Assoc J. 54[12], 742-748.
  • 2557. Johnson, M. A., Lyle, G., Hanly, M., and Yeh, K. A. (1998). Aspergillus: a rare primary organism in soft-tissue infections. Am Surg. 64[2], 122-126.
  • 2558. Karpovich-Tate, N., Dewey, F. M., Smith, E. J., Lund, V. J., Gurr, P. A., and Gurr, S. J. (2000). Detection of fungi in sinus fluid of patients with allergic fungal rhinosinusitis. Acta Otolaryngol. 120[2], 296-302.
  • 2560. Kontoyiannis, D. P., Sumoza, D., Tarrand, J., Bodey, G. P., Storey, R., and Raad, I. I. (2000). Significance of aspergillemia in patients with cancer: a 10-year study. Clin Infect Dis. 31[1], 188-189.
  • 2561. Krcmery, V., Jr., Fuchsberger, P., Trupl, J., Blahova, M., Danisovicova, A., Svec, J., and Drgona, L. (1993). Fungal pathogens in etiology of septic shock in neutropenic patients with cancer (short communication). Zentralbl.Bakteriol. 278[4], 562-565.
  • 2562. Kreiss, Y., Vered, Z., Keller, N., Kochva, I., Sidi, Y., and Gur, H. (2000). Aspergillus niger endocarditis in an immunocompetent patient: an unusual course. Postgrad Med J. 76[892], 105-106.
  • 2564. Kumar, M., Arora, R., Sanga, L., and Sota, L. D. (1997). Black corneal ulcer. Cornea. 16[5], 590-591.
  • 2565. Lang, E. K. (2005). Myceliatomas (Aspergillus niger) in the renal collecting system and ureters. J Urol. 174[5], 2014.
  • 2568. Loh, K. S., Tan, K. K., Kumarasinghe, G., Leong, H. K., and Yeoh, K. H. (1998). Otitis externa--the clinical pattern in a tertiary institution in Singapore. Ann Acad Med Singapore. 27[2], 215-218.
  • 2569. Lukaszuk, C., Krajewska-Kulak, E., Baran, E., Szepietowski, J., Bialynicki-Birula, R., Kulak, W., Rolka, H., and Oksiejczuk, E. (2007). Analysis of the incidence of fungal pathogens in air of the Department of Dermatology, Venereology and Allergology of Medical University in Wroclaw. Adv Med Sci. 52 Suppl 1:15-7., 15-17.
  • 2572. Miyazaki, H., Gemma, H., Uemura, K., Ono, T., Masuda, M., Sano, T., Sato, M., Koshimizu, N., Suda, T., and Chida, K. (2004). [Hypersensitivity pneumonitis induced by Aspergillus niger--a case report]. Nihon Kokyuki.Gakkai Zasshi. 42[7], 676-681.
  • 2573. Muller, J., Halweg, H., Podsiadlo, B., and Radwan, L. (1991). [Symptoms and functional disorders of the respiratory system caused by exposure to tea dust]. Pneumonol.Alergol.Pol. 59[5-6], 210-217.
  • 2574. Paula, J. S., Bryk, A., Jr., Lauretti, Filho A., and Romao, E. (2006). Secondary glaucoma associated with bilateral Aspergillus niger endophthalmitis in an HIV-positive patient: case report. Arq Bras.Oftalmol. 69[3], 395-397.
  • 2575. Procop, G. W. and Johnston, W. W. (1997). Diagnostic value of conidia associated with pulmonary oxalosis: evidence of an Aspergillus niger infection. Diagn.Cytopathol. 17[4], 292-294.
  • 2576. Roehrl, M. H., Croft, W. J., Liao, Q., Wang, J. Y., and Kradin, R. L. (2007). Hemorrhagic pulmonary oxalosis secondary to a noninvasive Aspergillus niger fungus ball. Virchows Arch. 451[6], 1067-1073.
  • 2577. Schuster, E., Dunn-Coleman, N., Frisvad, J. C., and Van Dijck, P. W. (2002). On the safety of Aspergillus niger--a review. Appl Microbiol Biotechnol. 59[4-5], 426-435.
  • 2578. Seaton, A. and Wales, D. (1994). Clinical reactions to Aspergillus niger in a biotechnology plant: an eight year follow up. Occup Environ Med. 51[1], 54-56.
  • 2579. Siraj, C. A., Krishnan, J., Nair, R. R., and Girija, A. S. (2005). Invasive aspergillosis producing painful ophthalmoplegia. J Assoc Physicians India. 53:901-2., 901-902.
  • 2580. Speth, C., Rambach, G., Lass-Florl, C., Wurzner, R., Gasque, P., Mohsenipour, I., and Dierich, M. P. (2000). Culture supernatants of patient-derived Aspergillus isolates have toxic and lytic activity towards neurons and glial cells. FEMS Immunol.Med Microbiol. 29[4], 303-313.
  • 2583. Topping, M. D., Scarisbrick, D. A., Luczynska, C. M., Clarke, E. C., and Seaton, A. (1985). Clinical and immunological reactions to Aspergillus niger among workers at a biotechnology plant. Br J Ind Med. 42[5], 312-318.
  • 2584. Tosti, A. and Piraccini, B. M. (1998). Proximal subungual onychomycosis due to Aspergillus niger: report of two cases. Br J Dermatol. 139[1], 156-157.
  • 2585. Viggiani, P. and Besozzi, G. (2006). AmBisome treatment of pulmonary aspergillosis in a patient with tuberculosis. Acta Biomed. 77 Suppl 4:31-3., 31-33.
  • 2586. Vivas, C. (1998). Endocarditis caused by Aspergillus niger: case report. Clin Infect Dis. 27[5], 1322-1323.
  • 2587. Wardlaw, A. and Geddes, D. M. (1992). Allergic bronchopulmonary aspergillosis: a review. J R Soc Med. 85[12], 747-751.
  • 2588. Rosenman, K. D., Hart, M., and Ownby, D. R. (1992). Occupational asthma in a beet sugar processing plant. Chest 101[6], 1720-1722.
  • 2589. Accensi, F., Abarca, M. L., and Cabanes, F. J. (2004). Occurrence of Aspergillus species in mixed feeds and component raw materials and their ability to produce ochratoxin A. Food Microbiology 21, 623-627.
  • 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.
  • 3443. Shah, A. and Sircar, M. (1991). Sensitization to Aspergillus antigens in perennial rhinitis. Asian.Pac.J Allergy.Immunol. 9[2], 137-139.
  • 3444. Shen, H. D., Tam, M. F., Chou, H., and Han, S. H. (1999). The importance of serine proteinases as aeroallergens associated with asthma. Int.Arch.Allergy.Immunol. 119[4], 259-264.
  • 3526. Coleman, R. M. and Kaufman, L. (1972). Use of the immunodiffusion test in the serodiagnosis of aspergillosis. Appl.Microbiol. 23[2], 301-308.
  • 3532. Froudist, J. H., Harnett, G. B., and McAleer, R. (1989). Comparison of immunodiffusion and enzyme linked immunosorbent assay for antibodies to four Aspergillus species. J Clin.Pathol. 42[11], 1215-1221.
  • 3538. Battilani, P., Logrieco, A., and Magan, N. (2006). Black aspergilli and ochratoxin A in grapes and wine. Introductory note. Int.J Food.Microbiol. 111 Suppl 1:S1. Epub;%2006 May;%19., S1.
  • 3569. Liam, C. K., Loo, K. L., Wong, C. M., Lim, K. H., and Lee, T. C. (2002). Skin prick test reactivity to common aeroallergens in asthmatic patients with and without rhinitis. Respirology. 7[4], 345-350.
  • 3572. Doekes, G., Kamminga, N., Helwegen, L., and Heederik, D. (1999). Occupational IgE sensitisation to phytase, a phosphatase derived from Aspergillus niger. Occup.Environ.Med. 56[7], 454-459.
  • 3573. Baur, X., Sander, I., Posch, A., and Raulf-Heimsoth, M. (1998). Baker's asthma due to the enzyme xylanase -- a new occupational allergen. Clin.Exp.Allergy. 28[12], 1591-1593.
  • 3574. Sander, I., Raulf-Heimsoth, M., Siethoff, C., Lohaus, C., Meyer, H. E., and Baur, X. (1998). Allergy to Aspergillus-derived enzymes in the baking industry: identification of beta-xylosidase from Aspergillus niger as a new allergen (Asp n 14). J Allergy.Clin.Immunol. 102[2], 256-264.
  • 3587. Gonzalez-Salgado, A., Patino, B., Vazquez, C., and Gonzalez-Jaen, M. T. (2005). Discrimination of Aspergillus niger and other Aspergillus species belonging to section Nigri by PCR assays. FEMS.Microbiol.Lett. 245[2], 353-361.
  • 3598. Klich, MA. (2002). Identification of common Aspergillus species. Ultrecht, Pays-Bas, Centraalbureau voor Schimmelcultures.
  • 3599. Xavier, M. O., Sales, Mda P., Camargo, Jde J., Pasqualotto, A. C., and Severo, L. C. (2008). Aspergillus niger causing tracheobronchitis and invasive pulmonary aspergillosis in a lung transplant recipient: case report. Rev.Soc.Bras.Med Trop. 41[2], 200-201.
  • 3600. Tarrand, J. J., Lichterfeld, M., Warraich, I., Luna, M., Han, X. Y., May, G. S., and Kontoyiannis, D. P. (2003). Diagnosis of invasive septate mold infections. A correlation of microbiological culture and histologic or cytologic examination. Am.J Clin.Pathol. 119[6], 854-858.
  • 3606. Grossman, M. E., Fithian, E. C., Behrens, C., Bissinger, J., Fracaro, M., and Neu, H. C. (1985). Primary cutaneous aspergillosis in six leukemic children. J Am.Acad.Dermatol. 12[2 Pt 1], 313-318.
  • 3607. Opal, S. M., Asp, A. A., Cannady, P. B., Jr., Morse, P. L., Burton, L. J., and Hammer, P. G. (1986). Efficacy of infection control measures during a nosocomial outbreak of disseminated aspergillosis associated with hospital construction. J Infect.Dis. 153[3], 634-637.
  • 3611. Benedetto, N., Sabatini, P., Galdiero, E., and Romano, Carratelli C. (1992). Cytotoxic activity and IL-1 production in mice infected with Aspergillus niger. Microbiologica. 15[3], 243-248.
  • 3612. Benedetto, N., Sabatini, P., Sellitto, C., and Romano, Carratelli C. (1988). Interleukin-2 and increased natural killer activity in mice experimentally infected with Aspergillus niger. Microbiologica. 11[4], 339-345.
  • 3613. Bouras, N., Mathieu, F., Coppel, Y., and Lebrihi, A. (2005). Aurasperone F--a new member of the naphtho-gamma-pyrone class isolated from a cultured microfungus, Aspergillus niger C-433. Nat.Prod.Res. 19[7], 653-659.
  • 3614. Romano, Carratelli C., Benedetto, N., and Sabatini, P. (1986). Modification of the T, K and NK cell population in experimental infection of mice with Aspergillus niger. Microbiologica. 9[4], 461-469.
  • 3638. Vesper, S., McKinstry, C., Haugland, R., Neas, L., Hudgens, E., Heidenfelder, B., and Gallagher, J. (2008). Higher Environmental Relative Moldiness Index (ERMIsm) values measured in Detroit homes of severely asthmatic children. Sci.Total.Environ. 394[1], 192-196.
  • 3864. Immuno Mycologics, Inc. (2003). Aspergillus detection systems : immunodiffusion & complement fixation for antibody detection. 2008.
  • 3874. Immuno Mycologics, Inc. (2003). Online product catalog.
  • 3875. Immuno Mycologics, Inc. (2007). Protocol: fungal antigens, positive controls and immunodiffusion plates for use in the immunodiffusion (ID) test. -7. Immuno Mycologics,Inc. 2009.