Fusarium spp.

Fusarium spp. on gypsum boardFusarium spp. on EM agarFusarium spp. on RB agarFusarium spp. - Microscopy (EM Culture)


As well as being common contaminants and well-known plant pathogens, Fusarium spp. may cause various infections in humans and are one of the emerging causes of opportunistic mycoses. They are mostly known for their production of potent mycotoxins.


Kingdom Fungi Order Hypocreales
Phylum Ascomycota Family Hypocreaceae
Class Euascomycetes Genus Fusarium

The genus Fusarium may contain hundreds of species, depending on the consulted registry; currently the genus contains 68 named species registered with the Universal Protein Resource (UniProt) agency {3318};  there are over 1300 species and strains registered with the International Mycological Association data bank (IMA- MycoBank) {3971}; these strains have been described and their specific characteristics often lie within minute differences {4275}. Fusarium roseum is the type taxon.

Many species of Fusarium have known teleomorph forms mostly included in the genera Gibberella; Gibberella fujikuroi is the perfect form of Fusarium moniliforme {3842}.

Fusarium solani is the most common Fusarium species recovered in humans and animals; F. culmorum, F. moniliforme(syn. F. proliferatum or F. verticillioides), F. napiforme have also been reported associated with infections in man.

Fusarium has often been reported with health problems associated with environmental outdoor and indoor exposure; in these cases Fusarium is mostly reported as Fusarium sp.


Fusarium species are ubiquitous and may be found in the soil, air and on plants {2972}. They are mostly known as associated with cereal crops and grain dust {2982}, rye, barley, corn, oats and buckwheat {1182}. Certain Fusarium, such asF. solani, are often associated with cereal and other specific cultures; consequently these Fusarium species are more often found in rural areas than in other settings {2964}. 

However, many Fusarium species can be found both in outdoor and indoor air {2079; 1584; 706}; the highest levels of airborne spores are found in summer, both in urban and sub-urban areas as well as coastal and inland areas {1584; 689}; occurrence may vary according to outdoor environmental factors in the immediate surroundings and levels of indoor contamination.

Fusarium species are also associated with water sources {2959; 2978}.  

More details

Fusarium species have been recovered from water system samples and their aerosolisation has been documented after running the showers {2959}.  Fusarium spp. may also be the most common taxon isolated from surfaces inside swimming pool facilities {1578}.

Aerobiological records over the different continents show that Fusarium species are regularly present in outdoor air samples even if, in most community settings, they are not observed in high concentrations {1788; 638; 2971}.  Airborne concentrations vary seasonally and constitute a small proportion of the natural aerosolised fungal flora in northern climates; although present year-round, the highest numbers of airborne Fusarium are recorded during summer {1788; 2999}. Outdoor air concentrations of Fusarium seem to be at their highest during the rainy summer season {343}. The mode of dissemination of Fusarium spores is by wet spores and water splashes, or by insects and wind once the growth has dried out.

Growth requirements

Fusarium is best known for growing on cereal crops (grain, straw, hay); many species can occasionally be found on a variety of substrates. Species of Fusarium can adapt to many nutritional circumstances although in turn, their morphological characteristics may vary greatly depending on environmental parameters {4277}. Fusarium requires wet conditions: it even grows in contaminated stagnant water such as humidifier pans. Most Fusarium species encountered in the indoor environment are slightly xerophilic and have a minimum Aw in the  0.86 to 0.91 range {3729}.

Water Activity :         F. moniliforme           Aw =87-91
F. solani :                   Aw = 87-90

Growth on building materials or indoor environment

Fusarium can be found in a small proportion of dwellings, growing on contaminated building materials {2991} and in contaminated air conditioning systems {1584}.

The occurrence of Fusarium in a dwelling is proof of humidity in the environment {1814}.

More details

In an environmental survey, positive findings of Fusarium spp. were made in 2–6% of examined US homes {2256}, with even higher values recorded in other geographical areas of North America and Europe, such as in South California (25%, with 4.5 -47 CFU/m3) {1824}, Scotland (10% of homes) {4274}, the Netherlands (9% of homes) {4314} and in 1 of the 16 homes investigated in Toronto, Canada {1817}.

Scandinavian studies showed that products most vulnerable to mould attacks were aged, water-damaged organic materials containing cellulose, such as wooden materials, jute, wallpaper and cardboard. Studies have demonstrated that certain species of Fusarium spp. are able to grow on damp building materials such as beech wood, pinewood particle board and gypsum board (715; 594).

Indoor total airborne fungal concentrations depend on sources and extent of dampness as well as type of wall and floor coverings, aeration levels, overall cleaning frequency and presence of pets (624; 2747). Other important factors such as seasonal fluctuations and outdoor environment-linked levels also largely contribute to the variability of the baseline flora {3021}.

Laboratory section

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

Fusarium species grow easily and rapidly on most media without cycloheximide.  
This genus lacks the large number of morphological characteristics that would allow to easily distinguish its numerous species. Recently, a commercially available PCR-based method was successfully tested with clinical isolates ofFusarium species and 5 ATCC isolates {3251}.

Colony, macroscopic morphology

On Sabouraud dextrose agar, at 25°C, Fusarium spp. grow rapidly and produce woolly to cottony, flat, spreading colonies. The only slow-growing species is Fusarium dimerum. From the front, the color of the colony may be white, cream, tan, salmon, cinnamon, yellow, red, violet, pink or purple. The reverse side of the colony may be colorless, tan, red, dark purple or brown.

More details

Sclerotia, (organized masses of hyphae that remain dormant during unfavourable conditions) may be observed macroscopically and are usually dark blue in color. On the other hand, sporodochia (a cushion-like mat of hyphae bearing conidiophores over its surface) are usually absent in culture. When present, they may be observed in cream to tan or orange colour, except for Fusarium solani, which gives rise to blue-green or blue sporodochia {2207; 2052}. 

On Czapek agar, at 25°C, Fusarium spp. colonies grow rapidly to 4-5 cm within 10 days. The colonies are flat, either velvety to cottony in texture, initially white or yellow often becoming pinkish or light grey in time; some species at maturity have a broad white mycelium margin and the reverse side often displays shades of pink rose to red.

Strains of Fusarium solani can grow at 37°C on Sabouraud, potato dextrose agar (PDA) and asparagine liquid media {2964}; this species can even survive at least 3 weeks in cultures at 40°C {2964}.

Microscopic morphology

The genus Fusarium can generally be identified by the typical production of hyaline, fusiform (banana-shaped), multicellular macroconidia with a foot cell at the base. In some cases, species identification is difficult and may require molecular methods (1596; 1596). Recently, a commercially available PCR-based method was tested with 21 clinical isolates ofFusarium species and 5 ATCC isolates: using sequencing identification as a gold standard, seven of nine different species were identified {3251}.

The basic elements of Fusarium spp. are hyaline septate hyphae, conidiophores, phialides, macroconidia and microconidia, observed microscopically. In addition to these basic elements, chlamydospores are also produced by some species (2207; 412; 2052).    

More details

These species are Fusarium chlamydosporumFusarium napiformeFusarium oxysporumFusarium semitectum,Fusarium solani and Fusarium sporotrichioides.

Phialides are cylindrical, with a small collaret, solitary or produced as a component of a complex branching system. Monophialides and polyphialides (in heads or in chains) may be observed.

Macroconidia (3-8 x 11-70 µm) are produced from phialides on unbranched or branched conidiophores. They are 2- or more celled, thick-walled, smooth, cylindrical or sickle- (canoe-) shaped. Macroconidia have a distinct basal foot cell and pointed distal ends. They tend to accumulate in balls or rafts.

Microconidia (2-4 x4-8 µm), on the other hand, are formed on long or short simple conidiophores. They are 1-celled (occasionally 2- or 3-celled), smooth, hyaline, ovoid to cylindrical, and arranged in balls (occasionally occurring in chains).

Chlamydospores, when present, are sparse, in pairs, clumps or chains. They are thick-walled, hyaline, intercalary or terminal (2207; 412; 2052).

Specific metabolites

Organics compounds (including VOCs)

Fusarium spp. produce various hydrocarbons, alcohols, ketones, esters and terpenes (myrcenes) in nature as well as on building materials (715; 594; 2076). They also produce other metabolites such as pyrazines, methylfurans, benzenes, limonene and products known as KAUR-like {Sunesson, 1996 607 /id} .

More details

Toxigenic strains of Fusarium produce volatile sesquiterpene hydrocarbons such as trichodiene; each of these intermediate metabolites is particular to the mycotoxin end product {3258}.

A number of organic compounds, including volatile organic compounds (VOCs), have been identified in indoor air in damp buildings contaminated by fungi: these VOCs are thought to contribute to various indoor air problems. However, most of the identified metabolites are non-reactive and found in low concentration in the indoor air {594}. 

Some species have a defined microbial volatile organic compound (mVOC) profile; mVOC production is influenced by both growth substrate and species of Fusarium. For example, experimentally grown Fusarium species show a mVOC profile which may be subject to considerable modification in response to external factors such as cultivation on different substrata {715}. These differing substrata change both the number and concentration of mVOCs  {715; 2968; 2809; 1148}, whereas other volatiles are specific for a single species (2809; 129; 1149; 2809).


Many species of Fusariumare common contaminants on various organic materials and most are recognised potential mycotoxin producers. Among the best studied mycotoxins generated by Fusarium spp. are highly potent toxins such as deoxynivalenol (DON), nivalenol (NIV), moniliformin (MON) and ochratoxin A (OTA) {1180; 2982}; many strains also produce T-2 toxin, zearalenone (ZEN) {2986} and scirpentriol toxins {1633}. DON, NIV and OTA can be found both in grain and settled dust samples, with the latter exhibiting greater concentrations {2982} suggesting the importance of inhalation exposure to these mycotoxins in occupational settings.

Some Fusarium mycotoxins have also been studied in cases of indoor building contamination {1220; 16}.  

More details

Some of the mycotoxins associated with Fusarium such as citrinine, DAS, DON sterigmatocystin and ochratoxin have been found in building materials or dust contaminated with Fusarium and other fungi.

Fusarium moniliformeF. subglutinans and F. proliferatum, all important spoilers of maize, produce fumonisins among other toxins. These mycotoxins are responsible for several animal mycotoxicoses (leuko­encephalomalacia in horses and pulmonary oedema in swines) and possibly for oesophageal cancer in humans {3247}.

T-2 toxin is a mycotoxin of type A trichothecene produced by several Fusarium species: in cereals, it ranges from trace to high concentrations in the order of one microgram per kg {2986}. This mycotoxin can affect both cell mediated and humoral immune mechanisms.

Most Fusarium toxins are associated with food and grain spoilage. In these circumstances, variation in relative air-humidity appears to play a role on the incidence of Fusarium spp. both on the amounts of fungi and on the mycotoxin content in grain {2986}.

For example, it has been observed that weather conditions at harvesting contribute to an increase in the contents ofFusarium fungi and DON and ZEN mycotoxins produced these fungi in winter wheat grain {2986}.

In a study of settled and airborne grain dust by PCR assay, the presence of F. langsethiae was associated with HT-2 and T-2 toxins in settled dust: the trichothecene levels in grain dust toxin reached detectable levels even after short exposures of 10-60 minutes {1158}. DON, T-2 and HT-2 toxins were present in most settled dust samples at levels ranging from 20 to 50 µg/kg of dust; concentrations were slightly higher in settled dust samples than in air samples.

Unsupported allegations have suggested that Fusarium toxins have been used as biological weapons {4277}.

Adverse health reactions

Health risks associated with mould exposure in water damaged buildings are well established, especially for upper and lower respiratory tract symptoms. Although Fusarium contamination seldom occurs indoors, given the numerous severe adverse health effects reported in other circumstances, such contamination must be considered as a possible contributor to various indoor air problems.   

Irritation and inflammation

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

In vitro and in vivo studies have demonstrated that Fusarium spores and spore extracts can experimentally produce eye irritation and erythema {2964}. In controlled experiments, inoculums of F. solani instilled in rabbit eyes produced a clinical reaction producing irritation and erythema {2964}.

More details

(1-->3)-Beta-D-glucans are non-specific and non-allergenic structural cell wall components present in most fungi: many authors have suggested that they play a causal role in the development of respiratory symptoms associated with indoor fungal exposure {1346}.

Allergic reactions

Airborne spores of Fusarium spp. are widespread but especially common in agricultural areas.  Fusarium airborne spores are considered common seasonal and perennial airborne allergens 2609  2971 linked to Type I allergies, hay fever and asthma {2342; 3095; 2971; 1180; 2018; 2774}.  Fusarium is among the most frequent positive dermal tests within mould allergen panels {638}.   

Fusarium solani is isolated repeatedly from patients diagnosed with allergic fungal sinusitis (AFS) {719; 1481}. Some species implicated in AFS are found to colonise the surfaces of indoor construction and finishing materials in the patients’ environments (1397; 1387).  Cases of Fusarium infectious sinusitis have also been reported in particular circumstances such as maxillary sinusitis {3272} and in transplant patients (3259). 

Allergic components and mechanism

Many extracts from species of Fusarium have been studied experimentally by various serological assays in an attempt to characterise specific fractions {2285}. In one study, up to 38 antigenic fractions were isolated and 21 were IgE binding. However these fractions are currently not available for routine testing.

In the diagnosis of Fusarium allergy, as for certain other fungi, available allergen panels for radioallergosorbent testing (RAST) {1875} seem unlikely to produce false-positive responses due to cross-reactivity because of the observed frequent significant variance in test scores from mould to mould within the same patient {1977}.

More details

Nevertheless, some components of Curvularia have been identified to cross-react with  F. solani but show negligible IgE binding properties to F. solani in Curvularia-sensitised patients {2973}. Consequently, positive reactions to Fusarium are unlikely due to Curvularia sensitisation.  Some allergenic components of spores from Fusarium vasinfectum have been shown to cross-react with raw mushroom allergens by immunoblot assay: in one case, both the skin test and the IgE test cross reacted in a patient with oral allergy symptoms to raw, but not cooked, mushrooms {2965}. 

Hypersensitivity pneumonitis

Type III hypersensitivity pneumonitis due to Fusarium is not often reported except in occupational settings related to the handling of grain or hay.  A few cases of hypersensitivity pneumonitis (HP) have been attributed to indoor contamination due to mouldy building materials {716} and contaminated air conditioners {277}. 

More details

In one study, specific IgG antibodies against fungal antigens present in a contaminated air conditioner were estimated in serum of exposed symptomatic patients: anti-Fusarium antibodies were found in 26% of these cases {277}.  In another report, a case of hypersensitivity pneumonitis (HP) caused by Fusarium napiforme found in the home environment was reported in a 17-year-old male student {716}. This case was diagnosed according to history, chest radiograph, spirometry, high-resolution chest CT and transbronchial lung biopsy.

Toxic effects (mycotoxicosis)

Many strains of Fusarium are active producers of toxins under given sets of growth conditions. These fusarial toxic metabolites can cause mycotoxicosis not only in animals but also in humans following repeated ingestion of food colonised by the fungal organism {2972}. 

Fusarium toxicoses have been associated to both acute and chronic exposure to contaminated material.

Toxic effects due to ingested Fusarium include cytotoxic, nephrotoxic and tremorgenic effects as well as immunosuppressive and carcinogenic effects. These pathologies are well known to occur in man, livestock and other animals {3182; 3184; 3185}.  Consequently, concentrations of some of these toxins in livestock feed as well as in food for human consumption are strictly regulated (3189; 3190; 3191) {3191; 3190; 3189}.

More details

Immunosuppression and carcinogenetic effects have been linked to Fusarium toxins.  In fact, in vitro and in vivo studies results suggest that T-2 toxin, even at low concentrations, can induce the secretion of IL-12, TNF-alpha and IFN-gamma and may be used as a positive immuno­modulator in the human model {2958}.  

Laboratory studies have described the carcinogenicity of fumonisin B1 (FB1) in rodents and epidemiological evidence suggests an association between FB1 and cancer in humans {2963; 2305}. 

Many mycotoxicosis due to Fusarium species have been identified in veterinarian medicine including  facial eczema in sheep {2316}; alimentary toxic aleukia, has also been well studied and attributed to Fusarium mycotoxins {130}. 

Fusarium moniliformeF. subglutinans and F. proliferatum, all important spoilers of maize, produce fumonisins among other toxins. These mycotoxins are responsible for several animal mycotoxicoses (leuko­encephalomalacia in horses and pulmonary oedema in swines) and possibly for oesophageal cancer in humans {3247}.

For certain toxins, the precise mechanisms of Fusarium toxicity have been well documented at the cellular level. Such is the case of the effects of T-2 toxin on cytokine production by mice peritoneal macrophages and lymph node T-cells. T-2 toxin significantly reduces IL-1beta release in a concentration dependent manner (p<0.005, p<0.001). Conversely, Interleukin-12 and TNF-alpha production are significantly increased in response to 0.1 ng/ml, 0.01 ng/ml and even to doses as low as 0.001 ng/ml of T-2 toxin (p<0.001). However, T-2 toxin, at higher concentrations ranging from 1 ng/ml to 100 ng/ml, reduces both IL-12 (p<0.001) and TNF-alpha production (p<0.005, p<0.05). The effects of T-2 toxin on lymph node T cells also show a decrease in IL-4 and IL-10 release in a concentration-dependent manner (all with p<0.01). Lastly, T-2 toxin at concentrations between 1 ng/ml and 100 ng/ml reduces the release of both IL-2 and IFN-gamma {2958}.

Infections and colonisations

Fusarium species are saprophytic moulds and important plant pathogens. Human infections by Fusarium spp. are rare although they are increasingly recognised as agents of human mycosis in localised, focally invasive or disseminated infections. The infection is mostly superficial; deep tissue infection may occur as an opportunistic hyalohypho­mycosis, and wide dissemination can occur in immunocompromised hosts (2988; 2972). 
Infection of immunocompetent persons is rarely reported {2972}.

Fusarium is an aetiologic agent in keratitis, endophthalmitis, cutaneous infections, burn patients, mycetoma, onychomycosis, sinusitis, pulmonary disease, endocarditis, catheter infections and septic arthritis.

The clinical form of fusariosis depends largely on the immune status of the host and the portal of entry, with superficial and localised disease occurring mostly in immunocompromised subjects {1596}. The prognosis is poor and is largely determined by the degree of immunosuppression and extent of infection; there is virtually a 100% death rate among persistently neutropenic patients with disseminated disease. 

Up to 11 species of Fusarium have been documented as aetiologic agents of human infection; taxonomic identification is difficult however, as some isolates, especially the slow maturing ones, may have been attributed to the wrong species {2988}. Fusarium species frequently implicated in human infections include F. solani, F. oxysporum and F. moniliforme also termed F. verticillioides {2966; 2972}; more recently, cases of F. napiforme {2988} and F. proliferatum {730} have also been reported.   

More details

Superficial fusariosis

Onychomycosis is most commonly due to F. oxysporum or F. solani {2972; 2973} and corneal ulcers have been attributed to F. solani {2964}.  

Localised cutaneous Fusarium hyalohyphomycoses have been reported, and cutaneous manifestations of disseminated infections have also been described at later stages {3682}{1647; 1617}. These fatal infections usually occur in the setting of prolonged neutropenia.  

Among immunocompetent patients, tissue breakdown (such as caused by trauma, severe burns or foreign body) is the principle risk factor for fusariosis. Infections include keratitis, onycho­mycosis and occasionally peritonitis and cellulitis {2966}.  Localised infections also include septic arthritis, endophthalmitis, osteomyelitis, cystitis and brain abscesses {2972; 3248}. Typical skin lesions may be painful red or violaceous nodules, the center of which often becomes ulcerated and covered by a black eschar. Multiple necrotising lesions are often observed on the trunk and the extremities.

Deep-sited or disseminated fusariosis

Among immunocompromised patients, deep-sited or disseminated fusariosis are found mainly in patients with haematological malignancies: in these cases, Fusarium spp. are the second most common pathogenic mould {2966; 2972}. Risk factors for disseminated fusariosis include severe immunosuppression (neutropenia, lymphopenia, graft-versus-host disease and corticosteroids), colonisation and tissue damage. One study reported a systemic infection in a child with acute lympho­blastic leukemia caused by Fusarium proliferatum.

Most cases of disseminated infection due to Fusarium species are fatal, with mortality rates reaching 70 %.

Virulence factors

The fact that F. solani is able to grow at 37°C could represent a virulence factor.

More details

The high rate of dissemination in immunosupressed patients has been associated with the fact that some Fusariumspecies produce yeast-like structures (adventitious sporulation) which could facilitate their dissemination and growth in the blood {4280; 4281}.

Specific settings

Nosocomial infections

Fusarium spp. infections have not been thoroughly documented as true nosocomial infections. Environmental sampling in hospital settings has revealed the presence of Fusarium among the predominant fungal contamination {2409; 2978; 2987}.    Nevertheless, Fusarium is rarely isolated as a colonising or an invading fungi in nosocomial infections {2409; 1747}. In the rare instances where fusariosis appears to have been acquired in the hospital, its presence was associated with environmental exposure to Fusarium via air and water {2966} or introduced by indwelling devices.

More details

Existence of Fusariumin hospital water distribution systems may result in disseminated fusariosis in immunosuppressed patients {Squier, 2000 4282 /id}. Fusarium may also exist in soil of potted plants in hospitals. These plants constitute a hazardous mycotic reservoir for nosocomial fusariosis {396}.

In one epidemiological study conducted on 70 cases of cancer patients with fusariosis,  results failed to link the infections to the hospital environment and concluded that the most likely source of fusariosis was the external environment, such as water, rather than nosocomial sources {343}.

A second group of invasive fusariosis in immunocompromised patients with haematological malignancy treated at a same cancer center were also studied {3249}. Forty patients with disseminated and three patients with invasive lung infections were included in the analysis. All patients were immunocompromised, including three patients infected following bone marrow transplantation. In this group of patients, Fusarium was probably introduced through the subcutaneous route (33%), the sino-pulmonary route (30%) or through an unknown route (37%).

In another epidemiological investigation, invasive organ infection was documented by both culture of organ samples and histopathological examination of the affected organ {2959, Anaissie, E.J., 2001}. Eight of 20 patients with F. solaniinfections had isolates with a molecular match with either an environmental isolate or another patient isolate.

Environmental cultures yielded Fusarium sporotrichioides as well as F. solani and F. oxysporum, the latter two strains being the most frequent.    
Aerosolisation of Fusarium species was notably documented after running the showers. The hospital water distribution system was also identified as a reservoir for Fusarium species  {2959} {2978}. 
Environmental cultures yielded Fusarium sporotrichioides as well as F. solani, F. oxysporum, with the latter two strains being the most frequent. 
A total of 38 patients were identified.  The risk factors for fusariosis included relapsing underlying disease (38 patients), neutropenia (36 patients), acute myelogenous leukemia (AML) (30 patients) or therapy with adrenal corticosteroids.

The role of central venous catheters as potential portals of entry for Fusarium is possibly underestimated {3250}. One recent report confirmed an iatrogenic infection by Fusarium for which both blood cultures and catheter tip cultures grew a mould identified as  Fusarium sp. {3268}.

Occupational diseases

Type III hypersensitivity pneumonites and organic dust toxic syndrome (ODTS) (see Mycotoxicosis section) associated withFusarium spp. are known in occupational settings such as farming and grain handling. In fact, Fusarium strains may be isolated in over half of grain samples collected at different stages of grain processing {2982; 1182}. Farmers and nearby residents are hence exposed to high levels of organic dust and bioaerosols which are generally high in Fusarium spore concentration (105 -106 CFU/m³) during the wheat harvesting season. This may cause health problems in exposed individuals based on toxic or allergic reactions {2974; 1180}. Inhalation of immunomodulating mycotoxins produced byFusarium spp. commonly found in grain dust may imply health risks for grain farmers {1158; 2385}.

More details

Considerable occupational risk among farmers engaged in grain threshing due to inhalation of allergenic species of filamentous fungi and mycotoxins {1180} has been associated with the presence of Fusarium. The potential risk of mycotoxicoses to agricultural workers exposed to grain dust is particularly high when handling wheat during threshing, unloading, shuffling and other farm occupations {2984; 1181}. Thus, Fusarium spp. are among fungi that can play a significant role in allergic and non-allergic diseases in modern working environments in alimentary industries and dairy farms as well as other similar circumstances {2989}.

Such is the case of cotton and hemp processing plants {2967}: dust and Fusarium spore concentrations, among a few other moulds, have been measured as being above norm, suggesting possible occupational exposure to mycotoxic and allergenic moulds.

In one instance, Fusarium has also been linked to a significant occupational exposure in an archive storage setting {2774}.

Diagnostic tools

The diagnosis of Fusarium infection may be established from histopathological examinations, direct examination of stained clinical specimens or their culture, blood cultures or serology tests {2972}.

The characteristic clinical signs of these infections are disseminated skin nodules, fungemia and multiorgan involvement. Frequently, myalgia is also present. Skin involvement occurs in over 80% of cases of disseminated infections. These lesions are proven to be important in the early diagnosis of fusariosis as they are readily accessible for biopsy and culture {2196; 1755}.

The immediate assessment of any suspicious lesion, including a biopsy of the lesion for microbiological and histopathological examinations, will usually lead to the correct diagnosis {3253}. The diagnosis of infection by Fusarium sp. (p = 0.006) is strongly associated with a poor outcome {3254}.


In contrast to disseminated aspergillosis, disseminated fusariosis can be diagnosed by blood cultures in up to 40% of patients {2966; 3268; 1596}. 

More details

Fusarium species grow readily and rapidly in most media without cycloheximide.  Although the genus Fusarium can be identified by its typical multicellular macroconidia , species identification is difficult and may require molecular methods (1596).  

In support of a confirmed infection is i) the isolation of several colonies from the same specimen or of the same fungus from different specimens (as opposed to isolating a single colony from only one biological sample), ii) a positive direct examination of the biological material and iii) most importantly, the site of isolation and the host. For example, culture of sinus aspirates or respiratory secretions in severely immunocompromised hosts should always be considered as diagnostic of fusarial infection, as opposed to isolating Fusarium spp. from skin scrapings in an immunocompetent host.

It is difficult to establish an accurate diagnosis when an immunosuppressed patient is infected with more than one fungal species, especially when the species are morphologically very similar {3252}.


Confirmatory diagnosis of fusariosis may require histopathology. In tissue, the hyphae are similar to those of Aspergillusspecies, with hyaline and septate filaments that typically dichotomise in acute and right angles. However, adventitious sporulation may be present in tissue, and the finding of hyphae and yeast-like structures together is highly suggestive of fusariosis in the high-risk population {Nucci, 2007 1596 /id}.

In the absence of microbial growth, distinguishing fusariosis from other hyalohyphomycoses may be difficult and requires the use of in situ hybridisation in paraffin-embedded tissue specimens {3255}

The histological presentation of a deep sited infection due to Fusarium is typically that of an opportunistic fungal hyphal infection with hyaline, septate, randomly branched hyphae. The hyphal contours are regular {816}. Deep sited fusariosis histopathology reveals hyaline acute-branching septate hyphae similar to those found in aspergillosis {2966}. Cases of respiratory infections, can manifest themselves as pulmonary nodules, including the presence of cavitation {3268}.


It has been possible to detect interspecies cross-reactivity of IgG and IgE within the genus Fusarium {760; 252}. However, serological tests may still be useful when used to study the sensitisation of atopic patients to Fusarium or to measureFusarium exposure in patients with hypersensitivity pneumonitis (HP).

In a study of atopic individuals, 24.5% (n = 69) of subjects had positive intradermal tests with saline extracts of F. solani.  Results showed a positive statistical correlation between responses to cutaneous skin tests and RAST immunoenzymatic test results {4283}.

In another study, researchers found elevated levels of IgG antibodies directed against Fusarium in patients suffering from farmer’s lung disease and asymptomatic farmers with high IgG levels against other agricultural fungi; antibody levels were significantly higher in these patients compared to the control group {760}.

Fusarium, as part perennial airborne allergens, may play an important role in the pathogenesis of nasal polyposis {2609; 1975}. Polyposis is related in one way or another to allergic phenomena. Fungal sensitisation to Fusarium can be measured by IgE in vitro tests or by intradermal tests. However, in one study, patients with a clinical picture of polyposis showed sensitisation to fungal allergens, without any apparent correlation between fungal nasal colonisation and actual diagnosis {4284}.

More details

Fusarium moniliforme allergen extracts {730} are commercially available for in vitro IgE testing {3730} while allergenic extracts of Fusarium vasinfectum are available for in vivo skin testing, either as single extracts or as pooled antigens{3284}

Allergenic extracts of Fusarium are part of the American Food and Drug Administration (FDA) surveillance program and of the «Biological Product Deviation Reporting Non-Blood Product Codes» mould list {3285}.

  • Fusarium sp.
  • Fusarium moniliforme
  • Fusarium oxysporum
  • Fusarium solani 
  • Fusarium vasinfectum
Test IgE IgG Antigens Other
Skin Tests X      
RAST-IgE X      
RAST-IgG   X    
ELISA-ELIFA   Experimental    
Complement fixation        
PCR     Experimental  


  • 16. Tuomi, T., Reijula, K., Johnsson, T., Hemminki, K., Hintikka, E. L., Lindroos, O., Kalso, S., Koukila-Kahkola, P., Mussalo-Rauhamaa, H., and Haahtela, T. (2000). Mycotoxins in crude building materials from water-damaged buildings. Appl.Environ Microbiol. 66[5], 1899-1904.
  • 129. Fischer, G. and Dott, W. (2003). Relevance of airborne fungi and their secondary metabolites for environmental, occupational and indoor hygiene. Arch Microbiol. 179[2], 75-82.
  • 130. Kuhn, D. M. and Ghannoum, M. A. (2003). Indoor mold, toxigenic fungi, and Stachybotrys chartarum: infectious disease perspective. Clin Microbiol Rev. 16[1], 144-172.
  • 252. Verma, J., Sridhara, S., Singh, B. P., and Gangal, S. V. (1995). Studies on shared antigenic/allergenic components among fungi. Allergy. 50[10], 811-816.
  • 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.
  • 343. Raad, I., Tarrand, J., Hanna, H., Albitar, M., Janssen, E., Boktour, M., Bodey, G., Mardani, M., Hachem, R., Kontoyiannis, D., Whimbey, E., and Rolston, K. (2002). Epidemiology, molecular mycology, and environmental sources of Fusarium infection in patients with cancer. Infect Control Hosp.Epidemiol. 23[9], 532-537.
  • 396. Summerbell, R. C., Krajden, S., and Kane, J. (1989). Potted plants in hospitals as reservoirs of pathogenic fungi. Mycopathologia. 106[1], 13-22.
  • 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.
  • 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.
  • 607. Sunesson, A. L., Nilsson, C. A., Andersson, B., and Blomquist, G. (1996). Volatile metabolites produced by two fungal species cultivated on building materials. Ann Occup.Hyg. 40[4], 397-410.
  • 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.
  • 638. Gonianakis, M. I., Neonakis, I. K., Gonianakis, I. M., Baritaki, M. A., Bouros, D., Potamias, G., and Kontou-Fili, K. S. (2006). Mold allergy in the Mediterranean Island of Crete, Greece: a 10-year volumetric, aerobiological study with dermal sensitization correlations. Allergy Asthma Proc. 27[5], 354-362.
  • 689. Baxter, D. M., Perkins, J. L., McGhee, C. R., and Seltzer, J. M. (2005). A regional comparison of mold spore concentrations outdoors and inside "clean" and "mold contaminated" Southern California buildings. J Occup.Environ Hyg. 2[1], 8-18.
  • 706. Hargreaves, M., Parappukkaran, S., Morawska, L., Hitchins, J., He, C., and Gilbert, D. (2003). A pilot investigation into associations between indoor airborne fungal and non-biological particle concentrations in residential houses in Brisbane, Australia. Sci Total Environ. 312[1-3], 89-101.
  • 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.
  • 716. Lee, S. K., Kim, S. S., Nahm, D. H., Park, H. S., Oh, Y. J., Park, K. J., Kim, S. O., and Kim, S. J. (2000). Hypersensitivity pneumonitis caused by Fusarium napiforme in a home environment. Allergy. 55[12], 1190-1193.
  • 719. Noble, J. A., Crow, S. A., Ahearn, D. G., and Kuhn, F. A. (1997). Allergic fungal sinusitis in the southeastern USA: involvement of a new agent Epicoccum nigrum Ehrenb. ex Schlecht. 1824. J Med Vet.Mycol. 35[6], 405-409.
  • 730. Hattori, N., Shirai, A., Sugiura, Y., Li, W., Yokoyama, K., Misawa, Y., Okuzumi, K., and Tamaki, K. (2005). Onychomycosis caused by Fusarium proliferatum. Br J Dermatol. 153[3], 647-649.
  • 760. Lappalainen, S., Pasanen, A. L., Reiman, M., and Kalliokoski, P. (1998). Serum IgG antibodies against Wallemia sebi and Fusarium species in Finnish farmers. Ann Allergy Asthma Immunol. 81[6], 585-592.
  • 816. Patterson, T. F., McGinnis, M. R., and ed. (2009). The fungi :description. Site Doctor Fungus . Mycoses Study Group.
  • 1148. Fischer, G., Muller, T., Schwalbe, R., Ostrowski, R., and Dott, W. (2000). Species-specific profiles of mycotoxins produced in cultures and associated with conidia of airborne fungi derived from biowaste. Int J Hyg.Environ Health. 203[2], 105-116.
  • 1149. Fischer, G., Muller, T., Schwalbe, R., Ostrowski, R., and Dott, W. (2000). Exposure to airborne fungi, MVOC and mycotoxins in biowaste-handling facilities. Int J Hyg.Environ Health. 203[2], 97-104.
  • 1158. Halstensen, A. S., Nordby, K. C., Eduard, W., and Klemsdal, S. S. (2006). Real-time PCR detection of toxigenic Fusarium in airborne and settled grain dust and associations with trichothecene mycotoxins. J Environ Monit. 8[12], 1235-1241.
  • 1180. Krysinska-Traczyk, E., Perkowski, J., Kostecki, M., Dutkiewicz, J., and Kiecana, I. (2003). [Filamentous fungi and mycotoxins as potential occupational risk factors among farmers harvesting various crops]. Med Pr. 54[2], 133-138.
  • 1181. Krysinska-Traczyk, E., Kiecana, I., Perkowski, J., and Dutkiewicz, J. (2001). Levels of fungi and mycotoxins in samples of grain and grain dust collected on farms in Eastern Poland. Ann Agric.Environ Med. 8[2], 269-274.
  • 1182. Land, C. J., Hult, K., Fuchs, R., Hagelberg, S., and Lundstrom, H. (1987). Tremorgenic mycotoxins from Aspergillus fumigatus as a possible occupational health problem in sawmills. Appl.Environ Microbiol. 53[4], 787-790.
  • 1220. Skaug, M. A., Eduard, W., and Stormer, F. C. (2001). Ochratoxin A in airborne dust and fungal conidia. Mycopathologia. 151[2], 93-98.
  • 1346. Douwes, J. (2005). (1-->3)-Beta-D-glucans and respiratory health: a review of the scientific evidence. Indoor Air. 15[3], 160-169.
  • 1387. Reijula, K. (1996). Buildings with moisture problems--a new challenge to occupational health care. Scand.J Work Environ Health. 22[1], 1-3.
  • 1397. Wickern, G. M. (1993). Fusarium allergic fungal sinusitis. J Allergy Clin Immunol. 92[4], 624-625.
  • 1481. Schwarze, P. E., Ovrevik, J., Lag, M., Refsnes, M., Nafstad, P., Hetland, R. B., and Dybing, E. (2006). Particulate matter properties and health effects: consistency of epidemiological and toxicological studies. Hum Exp Toxicol. 25[10], 559-579.
  • 1578. Brandi, G., Sisti, M., Paparini, A., Gianfranceschi, G., Schiavano, G. F., De, Santi M., Santoni, D., Magini, V., and Romano-Spica, V. (2007). Swimming pools and fungi: an environmental epidemiology survey in Italian indoor swimming facilities. Int J Environ Health Res. 17[3], 197-206.
  • 1584. Basilico, Mde L., Chiericatti, C., Aringoli, E. E., Althaus, R. L., and Basilico, J. C. (2007). Influence of environmental factors on airborne fungi in houses of Santa Fe City, Argentina. Sci Total Environ. 376[1-3], 143-150.
  • 1596. Nucci, M. and Anaissie, E. (2007). Fusarium infections in immunocompromised patients. Clin Microbiol Rev. 20[4], 695-704.
  • 1617. Perez-Perez, L., Pereiro, M., Jr., Sanchez-Aguilar, D., and Toribio, J. (2007). Ulcerous lesions disclosing cutaneous infection with Fusarium solani. Acta Derm.Venereol. 87[5], 422-424.
  • 1633. Schollenberger, M., Drochner, W., and Muller, H. M. (2007). Fusarium toxins of the scirpentriol subgroup: a review. Mycopathologia. 164[3], 101-118.
  • 1647. Chi, C. C. and Wang, S. H. (2007). Disseminated cutaneous Fusarium moniliforme infections in a leukemic child. Int J Dermatol. 46[5], 487-489.
  • 1747. Tomsikova, A. (2002). Causative agents of nosocomial mycoses. Folia Microbiol (Praha). 47[2], 105-112.
  • 1755. Guarro, J., Soler, L., and Rinaldi, M. G. (1995). Pathogenicity and antifungal susceptibility of Chaetomium species. Eur J Clin Microbiol Infect Dis. 14[7], 613-618.
  • 1788. Gioulekas, D., Damialis, A., Papakosta, D., Spieksma, F., Giouleka, P., and Patakas, D. (2004). Allergenic fungi spore records (15 years) and sensitization in patients with respiratory allergy in Thessaloniki-Greece. J Investig.Allergol.Clin Immunol. 14[3], 225-231.
  • 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.
  • 1817. Tarlo, S. M., Fradkin, A., and Tobin, R. S. (1988). Skin testing with extracts of fungal species derived from the homes of allergy clinic patients in Toronto, Canada. Clin Allergy. 18[1], 45-52.
  • 1824. Kozak, P. P., Gallup, J., Cummins, L. H., and Gillman, S. A. (1979). Factors of importance in determining the prevalence of indoor molds. Ann Allergy. 43[2], 88-94.
  • 1875. Forastiere, F., Balmes, J., Scarinci, M., and Tager, I. B. (1998). Occupation, asthma, and chronic respiratory symptoms in a community sample of older women. Am J Respir Crit Care Med. 157[6 Pt 1], 1864-1870.
  • 1975. Asero, R. and Bottazzi, G. (2001). Nasal polyposis: a study of its association with airborne allergen hypersensitivity. Ann Allergy Asthma Immunol. 86[3], 283-285.
  • 1977. King, W. P. (1989). Clinical significance of molds newly available for radioallergosorbent testing. Otolaryngol.Head Neck Surg. 101[1], 1-4.
  • 2018. Lopez, L. R., Noriega, Y., and Losno, R. (1988). Immediate skin test reactivity to common aeroallergens in patients with respiratory allergies: a comparative analysis of allergen-induced skin reactions and their histamine controls. J Allergy Clin Immunol. 81[6], 1143-1148.
  • 2052. Sutton, D. A., Timm, W. D., Morgan-Jones, G., and Rinaldi, M. G. (1999). Human phaeohyphomycotic osteomyelitis caused by the coelomycete Phomopsis saccardo 1905: criteria for identification, case history, and therapy. J Clin Microbiol. 37[3], 807-811.
  • 2076. Claeson, A. S., Sandstrom, M., and Sunesson, A. L. (2007). Volatile organic compounds (VOCs) emitted from materials collected from buildings affected by microorganisms. J Environ Monit. 9[3], 240-245.
  • 2079. Aydogdu, H. and Asan, A. (2008). Airborne fungi in child day care centers in Edirne City, Turkey. Environ Monit.Assess. .
  • 2196. Guarro, J. and Gene, J. (1992). Fusarium infections. Criteria for the identification of the responsible species. Mycoses. 35[5-6], 109-114.
  • 2207. de Hoog, G. and Guarro, J. (1995). Atlas of clinical fungi. Baarn, Centraalbureau voor Schimmelcultures.
  • 2256. Lumpkins, E. D., Sr., Corbit, S. L., and Tiedeman, G. M. (1973). Airborne fungi survey. 1. Culture-plate survey of the home environment. Ann Allergy. 31[8], 361-370.
  • 2285. Horner, W. E., Helbling, A., Salvaggio, J. E., and Lehrer, S. B. (1995). Fungal allergens. Clin Microbiol Rev 8[2], 161-179.
  • 2305. Lemmer, E. R., de la Motte, Hall P., Omori, N., Omori, M., Shephard, E. G., Gelderblom, W. C., Cruse, J. P., Barnard, R. A., Marasas, W. F., Kirsch, R. E., and Thorgeirsson, S. S. (1999). Histopathology and gene expression changes in rat liver during feeding of fumonisin B1, a carcinogenic mycotoxin produced by Fusarium moniliforme. Carcinogenesis. 20[5], 817-824.
  • 2316. Marasas, W. F., Adelaar, T. F., Kellerman, T. S., Minne, J. A., Van, Rensburg, I, and Burroughs, G. W. (1972). First report of facial eczema in sheep in South Africa. Onderstepoort J Vet.Res. 39[2], 107-112.
  • 2342. Burge, H. A. (1985). Fungus allergens. Clin Rev Allergy. 3[3], 319-329.
  • 2385. Halstensen, A. S., Nordby, K. C., Klemsdal, S. S., Elen, O., Clasen, P. E., and Eduard, W. (2006). Toxigenic Fusarium spp. as determinants of trichothecene mycotoxins in settled grain dust. J Occup Environ Hyg. 3[12], 651-659.
  • 2409. Chakrabarti, A., Nayak, N., Kumar, P. S., Talwar, P., Chari, P. S., and Panigrahi, D. (1992). Surveillance of nosocomial fungal infections in a burn care unit. Infection. 20[3], 132-135.
  • 2609. Asero, R. and Bottazzi, G. (2000). Hypersensitivity to molds in patients with nasal polyposis: A clinical study. J Allergy Clin Immunol. 105[1 Pt 1], 186-188.
  • 2747. Dharmage, S., Bailey, M., Raven, J., Mitakakis, T., Thien, F., Forbes, A., Guest, D., Abramson, M., and Walters, E. H. (1999). Prevalence and residential determinants of fungi within homes in Melbourne, Australia. Clin Exp Allergy. 29[11], 1481-1489.
  • 2774. Zielinska-Jankiewicz, K., Kozajda, A., Piotrowska, M., and Szadkowska-Stanczyk, I. (2008). Microbiological contamination with moulds in work environment in libraries and archive storage facilities. Ann Agric Environ Med. 15[1], 71-78.
  • 2809. Fischer, G., Schwalbe, R., Moller, M., Ostrowski, R., and Dott, W. (1999). Species-specific production of microbial volatile organic compounds (MVOC) by airborne fungi from a compost facility. Chemosphere. 39[5], 795-810.
  • 2958. Ahmadi, K. and Riazipour, M. (2008). Effects of T-2 toxin on cytokine production by mice peritoneal macrophages and lymph node T-cells. Iran J Immunol. 5[3], 177-180.
  • 2959. Anaissie, E. J., Kuchar, R. T., Rex, J. H., Francesconi, A., Kasai, M., Muller, F. M., Lozano-Chiu, M., Summerbell, R. C., Dignani, M. C., Chanock, S. J., and Walsh, T. J. (2001). Fusariosis associated with pathogenic fusarium species colonization of a hospital water system: a new paradigm for the epidemiology of opportunistic mold infections. Clin Infect.Dis. 33[11], 1871-1878.
  • 2963. Carlson, D. B., Williams, D. E., Spitsbergen, J. M., Ross, P. F., Bacon, C. W., Meredith, F. I., and Riley, R. T. (2001). Fumonisin B1 promotes aflatoxin B1 and N-methyl-N'-nitro-nitrosoguanidine-initiated liver tumors in rainbow trout. Toxicol Appl Pharmacol. 172[1], 29-36.
  • 2964. Cuero, R. G. (1980). Ecological distribution of Fusarium solani and its opportunistic action related to mycotic keratitis in Cali, Colombia. J Clin Microbiol. 12[3], 455-461.
  • 2965. Dauby, P. A., Whisman, B. A., and Hagan, L. (2002). Cross-reactivity between raw mushroom and molds in a patient with oral allergy syndrome. Ann Allergy Asthma Immunol. 89[3], 319-321.
  • 2966. Dignani, M. C. and Anaissie, E. (2004). Human fusariosis. Clin Microbiol Infect. 10 Suppl 1:67-75., 67-75.
  • 2967. Dimitrov, M., Ivanova-Dzhubrilova, S., Nikolcheva, M., and Drenska, E. (1990). [The mycotoxicological and dust contamination of the air in plants for the preliminary processing of cotton and hemp]. Probl.Khig. 15:121-7., 121-127.
  • 2968. 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.
  • 2971. Green, B. J., O'meara, T., Sercombe, J., and Tovey, E. (2006). Measurement of personal exposure to outdoor aeromycota in northern New South Wales, Australia. Ann Agric Environ Med. 13[2], 225-234.
  • 2972. Gupta, A. K., Baran, R., and Summerbell, R. C. (2000). Fusarium infections of the skin. Curr Opin Infect.Dis. 13[2], 121-128.
  • 2973. Gupta, R., Singh, B. P., Sridhara, S., Gaur, S. N., Kumar, R., Chaudhary, V. K., and Arora, N. (2002). Allergenic cross-reactivity of Curvularia lunata with other airborne fungal species. Allergy. 57[7], 636-640.
  • 2974. Hameed, A. A. and Khodr, M. I. (2001). Suspended particulates and bioaerosols emitted from an agricultural non-point source. J Environ Monit. 3[2], 206-209.
  • 2978. Kauffmann-Lacroix, C., Bousseau, A., Dalle, F., Brenier-Pinchart, M. P., Delhaes, L., Machouart, M., Gari-Toussaint, M., Datry, A., Lacroix, C., Hennequin, C., Toubas, D., and Morin, O. (2008). [Prevention of fungal infections related to the water supply in French hospitals: proposal for standardization of methods]. Presse Med. 37[5 Pt 1], 751-759.
  • 2982. Krysinska-Traczyk, E., Perkowski, J., and Dutkiewicz, J. (2007). Levels of fungi and mycotoxins in the samples of grain and grain dust collected from five various cereal crops in eastern Poland. Ann Agric Environ Med. 14[1], 159-167.
  • 2984. Krysinska-Traczyk, E. (2000). [Microflora of the farming work environment as an occupational risk factor]. Med Pr. 51[4], 351-355.
  • 2986. Mankeviciene, A., Butkute, B., Dabkevicius, Z., and Suproniene, S. (2007). Fusarium mycotoxins in Lithuanian cereals from the 2004-2005 harvests. Ann Agric Environ Med. 14[1], 103-107.
  • 2987. Martins-Diniz, J. N., da Silva, R. A., Miranda, E. T., and Mendes-Giannini, M. J. (2005). [Monitoring of airborne fungus and yeast species in a hospital unit]. Rev Saude Publica. 39[3], 398-405.
  • 2988. Melcher, G. P., McGough, D. A., Fothergill, A. W., Norris, C., and Rinaldi, M. G. (1993). Disseminated hyalohyphomycosis caused by a novel human pathogen, Fusarium napiforme. J Clin Microbiol. 31[6], 1461-1467.
  • 2989. Palmas, F., Cosentino, S., and Cardia, P. (1989). Fungal air-borne spores as health risk factors among workers in alimentary industries. Eur J Epidemiol. 5[2], 239-243.
  • 2991. Pieckova, E. and Jesenska, Z. (1999). Microscopic fungi in dwellings and their health implications in humans. Ann Agric Environ Med. 6[1], 1-11.
  • 2999. Trautmann, C., Gabrio, T., Dill, I., and Weidner, U. (2005). [Background concentrations of molds in house dust. Determination of mold concentrations in dwellings without known mold infestations in three parts of Germany]. Bundesgesundheitsblatt.Gesundheitsforschung.Gesundheitsschutz. 48[1], 29-35.
  • 3021. Dassonville, C., Demattei, C., Detaint, B., Barral, S., Bex-Capelle, V., and Momas, I. (2008). Assessment and predictors determination of indoor airborne fungal concentrations in Paris newborn babies' homes. Environ Res. 108[1], 80-85.
  • 3095. Foundation for Allergy Research in Europe. (1984). Atlas of moulds in Europe causing respiratory allergy. Knud Wilken-Jensen et Suzanne Gravesen. -110. Danemark, ASK Publising.
  • 3182. Bryden, W. L. (2007). Mycotoxins in the food chain: human health implications. Asia.Pac.J Clin.Nutr. 16 Suppl 1:95-101., 95-101.
  • 3184. Heberer, T., Lahrssen-Wiederholt, M., Schafft, H., Abraham, K., Pzyrembel, H., Henning, K. J., Schauzu, M., Braeunig, J., Goetz, M., Niemann, L., Gundert-Remy, U., Luch, A., Appel, B., Banasiak, U., Bol, G. F., Lampen, A., Wittkowski, R., and Hensel, A. (2007). Zero tolerances in food and animal feed -- are there any scientific alternatives? A European point of view on an international controversy. Toxicol.Lett. 175[1-3], 118-135.
  • 3185. Kendra, D. F. and Dyer, R. B. (2007). Opportunities for biotechnology and policy regarding mycotoxin issues in international trade. Int.J Food.Microbiol. %20;119[1-2], 147-151.
  • 3189. van Egmond, H. P., Schothorst, R. C., and Jonker, M. A. (2007). Regulations relating to mycotoxins in food: perspectives in a global and European context. Anal.Bioanal.Chem. 389[1], 147-157.
  • 3190. van Egmond, H. P. (2002). Worldwide regulations for mycotoxins. Adv.Exp.Med Biol. 504:257-69., 257-269.
  • 3191. van Egmond, H. P. (1993). Rationale for regulatory programmes for mycotoxins in human foods and animal feeds. Food.Addit.Contam. 10[1], 29-36.
  • 3247. Marasas, W. F. O. (1996). Fumonisins: history, world-wide occurence and impact. Jackson, L. et al. Fumonisins in food. 1-27. New York, Plenum Press.
  • 3248. Richardson, S. E., Bannatyne, R. M., Summerbell, R. C., Milliken, J., Gold, R., and Weitzman, S. S. (1988). Disseminated fusarial infection in the immunocompromised host. Rev.Infect.Dis. 10[6], 1171-1181.
  • 3249. Boutati, E. I. and Anaissie, E. J. (1997). Fusarium, a significant emerging pathogen in patients with hematologic malignancy: ten years' experience at a cancer center and implications for management. Blood. 90[3], 999-1008.
  • 3250. Velasco, E., Martins, C. A., and Nucci, M. (1995). Successful treatment of catheter-related fusarial infection in immunocompromised children. Eur.J Clin.Microbiol.Infect.Dis. 14[8], 697-699.
  • 3251. Healy, M., Reece, K., Walton, D., Huong, J., Frye, S., Raad, I. I., and Kontoyiannis, D. P. (2005). Use of the Diversi Lab System for species and strain differentiation of Fusarium species isolates. J Clin.Microbiol. 43[10], 5278-5280.
  • 3252. Guarro, J., Nucci, M., Akiti, T., and Gene, J. (2000). Mixed infection caused by two species of Fusarium in a human immunodeficiency virus-positive patient. J Clin.Microbiol. 38[9], 3460-3462.
  • 3253. Nucci, M., Pulcheri, W., Spector, N., Maiolino, A., Caiuby, M. J., Maceira, J., and Oliveira, H. P. (1992). Cutaneous involvement of systemic fungal infections in neutropenic patients. Haematologica. 77[6], 522-523.
  • 3254. Nucci, M., Pulcheri, W., Spector, N., Bueno, A. P., Bacha, P. C., Caiuby, M. J., Derossi, A., Costa, R., Morais, J. C., and de Oliveira, H. P. (1995). Fungal infections in neutropenic patients. A 8-year prospective study. Rev.Inst.Med Trop.Sao.Paulo. 37[5], 397-406.
  • 3255. Hayden, R. T., Isotalo, P. A., Parrett, T., Wolk, D. M., Qian, X., Roberts, G. D., and Lloyd, R. V. (2003). In situ hybridization for the differentiation of Aspergillus, Fusarium, and Pseudallescheria species in tissue section. Diagn.Mol.Pathol. 12[1], 21-26.
  • 3258. Demyttenaere, J. C., Morina, R. M., De, Kimpe N., and Sandra, P. (2004). Use of headspace solid-phase microextraction and headspace sorptive extraction for the detection of the volatile metabolites produced by toxigenic Fusarium species. J Chromatogr.A. %20;1027[1-2], 147-154.
  • 3259. Drakos, P. E., Nagler, A., Or, R., Naparstek, E., Kapelushnik, J., Engelhard, D., Rahav, G., Ne'emean, D., and Slavin, S. (1993). Invasive fungal sinusitis in patients undergoing bone marrow transplantation. Bone.Marrow.Transplant. 12[3], 203-208.
  • 3268. Madariaga, M. G. and Kohl, S. (2006). Disseminated fusariosis presenting with pulmonary nodules following a line infection. Braz.J Infect.Dis. 10[6], 419.
  • 3271. Perry, L. P., Iwata, M., Tazelaar, H. D., Colby, T. V., and Yousem, S. A. (1998). Pulmonary mycotoxicosis: a clinicopathologic study of three cases. Mod.Pathol. 11[5], 432-436.
  • 3272. Pino, Rivero, V, Trinidad, Ruiz G., Keituqwa, Yanez T., Marcos, Garcia M., Pardo, Romero G., Gonzalez, Palomino A., Alvarez, Dominguez J., and Blasco, Huelva A. (2004). [Maxillary sinusitis by Fusarium sp. Report of a case and literature review]. An.Otorrinolaringol.Ibero.Am. 31[4], 341-347.
  • 3282. Von, Essen S., Robbins, R. A., Thompson, A. B., and Rennard, S. I. (1990). Organic dust toxic syndrome: an acute febrile reaction to organic dust exposure distinct from hypersensitivity pneumonitis. J Toxicol.Clin.Toxicol. 28[4], 389-420.
  • 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.
  • 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.
  • 3682. Mays, S. R., Bogle, M. A., and Bodey, G. P. (2006). Cutaneous fungal infections in the oncology patient: recognition and management. Am.J Clin.Dermatol. 7[1], 31-43.
  • 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.
  • 3730. Pharmacia Diagnostics AB. (2009). Allergy & autoimmunity. Diagnostics product catalogue 2009. internet , 1-48. Pharmacia.
  • 3842. Kendrick, B. and Murase, G. (2003). Anamorph-teleomorph dabase. CBS. Centraalbureau voor Schimmelcultures. 2009.
  • 3872. Chabasse, D., Bouchara, J.-P., de Gentile, L., Brun, S., Cimon, B., and Penn, P. (2002). Les moisissures d'intérêt médical. Cahier de formation : biologie médicale. -159. Paris, Bioforma.
  • 3971. Robert, V., Stegehuis, G., and Stalpers, J. (2005). The MycoBank engine and related databases. International Mycological Association . International Mycological Association. 9-9-2009.
  • 4274. Hunter, C. A., Grant, C., Flannigan, B., and Bravery, A. F. (1988). Mould in buildings: the air spora of domestic dwellings. International Biodeterioration 24[2], 81-101.
  • 4275. Christensen, C. M. (1975). Mould, mushrooms and mycotoxins. Minneapolis, University of Minnesota Press.
  • 4277. Leslie, J. F., Summerell, B. A., and Bullock, S. (2006). The Fusarium laboratory manual. Ames, Iowa, Blackwell.
  • 4278. Mirocha, C. J., Pawlosky, R. A., Chatterjee, K., Watson, S., and Hayes, W. (1983). Analysis for Fusarium toxins in various samples implicated in biological warfare in Southeast Asia. J Assoc.Off.Anal.Chem. 66[6], 1485-1499.
  • 4280. Cocuroccia, B., Gaido, J., Gubinelli, E., Annessi, G., and Girolomoni, G. (2003). Localized cutaneous hyalohyphomycosis caused by a Fusarium species infection in a renal transplant patient. J Clin.Microbiol. 41[2], 905-907.
  • 4281. Thomas, P. A. (2003). Current perspectives on ophthalmic mycoses. Clin.Microbiol.Rev. 16[4], 730-797.
  • 4282. Squier, C., Yu, V. L., and Stout, J. E. (2000). Waterborne Nosocomial Infections. Curr.Infect.Dis.Rep. 2[6], 490-496.
  • 4283. O'Neil, C. E., McCants, M. L., Salvaggio, J. E., and Lehrer, S. B. (1986). Fusarium solani: prevalence of skin reactivity and antigenic allergenic analysis. J Allergy.Clin.Immunol. 77[6], 842-849.
  • 4284. Munoz-Del-Castillo, F., Jurado-Ramos, A., Soler, R., Fernandez-Conde, B. L., Barasona, M. J., Cantillo, E., Moreno, C., and Guerra, F. (2009). Fungal sensitization in nasal polyposis. J Investig.Allergol.Clin.Immunol. 19[1], 6-12.
  • 4314. Reenen-Hoekstra, van E. S., Samson, R. A., Verhoeff, A. P., van Wijnen, J. H., and Brunekreef, B. (1991). Detection and identification of moulds in Dutch houses and non-industrial working environments. Grana 30, 418-423.
  • 4316. Ammari, L. K., Puck, J. M., and McGowan, K. L. (1993). Catheter-related Fusarium solani fungemia and pulmonary infection in a patient with leukemia in remission. Clin.Infect.Dis. 16[1], 148-150.
  • 4317. Kiehn, T. E., Nelson, P. E., Bernard, E. M., Edwards, F. F., Koziner, B., and Armstrong, D. (1985). Catheter-associated fungemia caused by Fusarium chlamydosporum in a patient with lymphocytic lymphoma. J Clin.Microbiol. 21[4], 501-504.
  • 4318. Raad, I. and Hachem, R. (1995). Treatment of central venous catheter-related fungemia due to Fusarium oxysporum. Clin.Infect.Dis. 20[3], 709-711.