Fusarium proliferatum

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Code: m9
Latin name: Fusarium proliferatum/F.moniliforme
Source material: Spores and mycelium
Family: Hypocreaceae
Common names: Fusarium proliferatum, Fusarium moniliforme

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Gibberella fujikuroi is the teleomorph (sexual stage) of the predominantly ascomycetous seed-borne fungus that causes bakanae (a disease that infects rice), seedling rot, grain sterility and discolouration in kernels. Infected kernels may develop a reddish discolouration due to the presence of the pathogen’s conidia. In its conidial stage it is known as Fusarium moniliforme.


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

Allergen Exposure

The genus Fusarium currently contains over 100 species. The most common of these are F. solani, F. equiseti, F. culmorum, F. oxysporum and F. chlamydosporum. As well as being a common contaminant and a well-known plant pathogen, Fusarium spp. may cause various infections in humans; the most common human pathogens are F. solani and F. oxysporum, with F. solani being the most virulent. While most species are more common in tropical and subtropical areas, some inhabit soil in cold climates. (1) Some Fusarium species have a teleomorphic state. (2) Fusarium is emerging as one of the leading causes of opportunistic mycoses.

Fusarium moniliforme, also known as Fusarium proliferatum, is a name that has been applied to any of six biological species (or mating populations) that share the teleomorph (sexual stage) Gibberella fujikuroi. (3)

F. moniliforme is a filamentous fungus/mould found in aerobiologic surveys worldwide. This mould is a common soil fungus and is widely distributed on numerous grasses and other plants, often causing plant diseases. It is a major parasite of rice, sugar cane, sorghum, bean, soybean, and is especially common on maize grains. (4) It has been shown to occur regularly on banana roots and other fruits and vegetables, e.g. tomato and watermelon. It sporulates in warm, wet weather. During winter or in dry periods, the fungus survives in the soil and on plant debris.

Certain species of Fusarium predominate in specific crops. For example, crown and root rot is one of the most important diseases of asparagus crops worldwide, and F. oxysporum f.sp. asparagi and F. proliferatum are the two species most frequently associated with this crop. (5)

Although many sources regard F. moniliforme and F. proliferatum as the same species, some sources state that F. proliferatum differs from F. moniliforme by forming chains of microconidia from both mono- and polyphialides. (5)

Fusarium spp. grow rapidly and produce woolly to cottony, flat, spreading colonies. The only slow-growing species is Fusarium dimerum. Colonies are initially white, cream or tan, becoming tinged with purple; but the eventual colour may be salmon, cinnamon, yellow, red, violet, pink, or purple. When a sclerotium (the organised mass of hyphae that remains dormant during unfavourable conditions) forms, it is usually dark blue in colour. (3) Sporodochia, when present, are tan to orange. (6)

Fusarium species (in particular F. proliferatum) are a major source of mycotoxins in food and feed as a result of these organisms contaminating agro-products, in particular cereals and especially maize. (7) Fusarium colonises a wide range of host plants besides maize, such as wheat and barley, among others, in particular in certain regions such as southern Europe. (8)

Ingestion of grains contaminated with these toxins may be carcinogenic in long-term consumption, causing oesophageal cancer in particular. Zearalenones, another group of mycotoxins, may also be produced by some Fusarium spp. growing in grains. (3)

Allergen Description

No allergens have been characterised.

A number of allergenic components of molecular weight 14, 19, 35, 45, 50 and 70 kDa have been shown to be common among three Fusarium species: F. solani, F. equiseti and F. moniliforme. (9)

From the related species F. equiseti 15 allergenic proteins have been isolated. A 65-kDa and a 25-kDa protein were found to be highly allergenic. The 65-kDa protein was shown to be a major allergen and was common among the extracts of three Fusarium species (F. equiseti, F. solani and F. moniliforme). (10)

A 45-kDa allergenic protein from the related species F. solani was shown to be shared by 11 different non- Fusarium moulds. (11) Whether a similar allergen is present in this mould was not evaluated.

A ribosomal protein P2 (Fus c 1) and a thioredoxin (Fus c 2) have been characterised from the related mould F. culmorum. Whether similar allergens are present in F. proliferatum has not yet been determined.

Potential Cross-Reactivity

At least one major allergen has been shown to be shared between members of the Fusarium species, particularly F. equiseti, F. solani and F. moniliforme (F. proliferatum), although species-specific allergens are likely. (10)

No studies have made a detailed evaluation of the cross-reactive potential of (specifically) F. proliferatum, in particular involving other moulds. However, Fusarium shares some of the same allergenic determinants as Penicillium and Aspergillus. (12)

Clinical Experience

IgE-mediated reactions

Anecdotal evidence suggests that Fusarium proliferatum may induce symptoms of asthma, allergic rhinitis and/or hypersensitivity pneumonitis in sensitised individuals. (13) However, few studies have been reported to date; it is possible that the allergy occurs more frequently than has been reported.

An evaluation was made of a large Phadia repository of human blood serum from which a subset of 668 unique samples, each with recorded IgE antibody concentrations against 17 separate fungal species, but devoid of clinical history; of these, 333 tested positive for F. proliferatum. (14)

A number of studies have documented the prevalence of sensitisation to a member or members of the Fusarium species, without specifying the specific species involved.

In a study of 100 Thai individuals (diagnosed with allergic rhinitis by history and clinical presentation) who underwent a skin-prick test with 30 aeroallergens, 26% were sensitised to Fusarium spp. (14)

In an evaluation in Sao Paulo, Brazil, of the sensitisation profile of 201 patients with asthma and/or allergic rhinitis to 42 airborne fungi using skin-specific IgE tests, 18 were shown to be sensitised to Fusarium spp. (15)

In an another South American study, conducted in Mexico City, the most frequent inhalable fungal aeroallergens positive on skin-prick test at an allergy clinic were Candida and Fusarium, with a predominance in the dry season. (16) In an earlier retrospective review of 247 clinical files of patients in Monclova, Coah, Mexico, specific IgE testing found that patients were highly sensitive to house dust (13.5%), Russian thistle (7.1%), pigweed (5.4%), Bermuda grass (4.9%), pecan (4.8%), ragweed mix (4.8%), rye grass (4.8%), and other pollen (32.4%). The most common moulds were Candida (3.2%), Alternaria (2.7%), Rhizopus (3.6%), Penicillium (2.1%), Fusarium (2.1%), and other moulds (8.7%). (17)

The aim of a Finnish study was to determine the prevalence of IgE-mediated sensitisation to microbes common in a work environment in an adult population in Finland. Specific IgE-antibodies were determined to 33 fungi and 11 bacteria in around 300 serum samples. In all, 6.1% of the study population had IgE-antibodies >0.70 kU/l to one or several microbes; additionally, 10.2% had IgE levels in the range 0.35 to 0.69 kU/l, suggesting possible sensitisation. For a number of moulds – including Fusarium spp. – IgE levels were significantly higher among blue-collar workers. (18)

Nasal provocation testing with moulds on 150 children with perennial rhinitis, reported that 13.3% experienced positive challenges to Fusarium. (19) Skin-prick tests in some patients clinically allergic to Alternaria were shown to result in immediate positive responses to Fusarium extract. (20) As Fusarium shares some of the same allergenic determinants as Penicillium and Aspergillus (13, 17) it is possible that a number of the positive results found are as a result of cross-reactivity with these moulds.

Importantly, a study of patients with atopic dermatitis described many developing specific IgE antibodies to a number of fungi. Although in selected patients fungi may trigger an IgE-mediated reaction that may contribute to the exacerbation of eczema, one-half of the patients produced IgE antibodies to fungal (glyco)proteins without a significant histamine release or skin test response. This was possibly because of nonspecific interaction with carbohydrate moieties on IgE and poor biologic activity of IgE antibodies directed to cross-reactive carbohydrate determinants of fungal glycoproteins. The authors suggested that caution is warranted when interpreting results in order to show the clinical relevance of serologic fungal IgE antibodies.

Allergic bronchopulmonary mycosis to Fusarium vasinfectum was described in a 12-year-old boy with asthma and 6 years of recurrent episodes of pneumonia, but with normal serum immunoglobulin concentrations. Skin-prick reactivity was positive for Fusarium, Cladosporium, Helminthosporium and Aspergillus fumigatus. (21) Whether F. proliferatum can produce a similar clinical disease is not known. (22)

Fusarium species have been isolated from about 3% of patients with onychomycoses in the Swiss population. F. oxysporum was the most frequently isolated species, accounting for 54% of the isolates. F. proliferatum and 4 taxons belonging to the F. solani species complex were identified with an appreciable frequency, ranging from 4 to 14%. (23)

Other reactions

In humans, Fusarium species can cause mycotoxicosis following ingestion of food that has been colonised by the fungal organism. Fusarium generally affects immune-compromised individuals, with infection of immune-competent persons rarely reported. Fusarium species can cause disease that is localised, focally invasive or disseminated. Localised infection includes cutaneous and subcutaneous infection, septic arthritis, endophthalmitis, osteomyelitis, onychomycosis, cystitis, otitis, sinusitis, arthritis, osteomyelitis, and brain abscess. (24) Infections due to Fusarium spp. are collectively referred to as fusariosis. The species most commonly involved – and the most virulent Fusarium spp. – is F. solani; however F. oxysporum and F. moniliforme (F. proliferatum) may be responsible. (25)

Trauma is the major predisposing factor for development of cutaneous infections due to Fusarium strains.

Compiled by Dr Harris Steinman.


  1. Nelson PE, Dignani MC, Anaissie EJ. Taxonomy, biology, and clinical aspects of Fusarium species. Clin Microbiol Rev 1994;7(4):479-504.
  2. Larone DH. 1995. Medically Important Fungi - A Guide to Identification, 3rd ed. ASM Press, Washington, D.C.
  3. Leslie JF. Introductory biology of Fusarium moniliforme. Adv Exp Med Biol 1996;392:153-64.
  4. Pitt JI, Hocking AD, Bhudhasamai K, Miscamble BF, Wheeler KA, Tanboon-Ek P. The normal mycoflora of commodities from Thailand. 2. Beans, rice, small grains and other commodities. Int J Food Microbiol. 1994;23(1):35-43.
  5. Rubio-Pérez E, Molinero-Ruiz ML, Melero-Vara JM, Basallote-Ureba MJ. Selection of potential antagonists against asparagus crown and root rot caused by Fusarium spp. Commun Agric Appl Biol Sci 2008;73(2):203-6.
  6. Doctorfungus.org. Fusarium proliferatum. http://www.doctorfungus.org/thefungi/Fusarium_proliferatum.php. Accessed 30 April 2011.
  7. Scott PM. Recent research on fumonisins: a review. Food Addit Contam Part A Chem Anal Control Expo Risk Assess 2011;15:1-7.
  8. Jurado M, Marín P, Callejas C, Moretti A, Vázquez C, González-Jaén MT. Genetic variability and Fumonisin production by Fusarium proliferatum. Food Microbiol 2010;27(1):50-7.
  9. Horner WE, Helbling A, Salvaggio JE, Lehrer SB. Fungal allergens. Clin Microbiol Rev 1995;8(2):161-79.
  10. Verma J, Sridhara S, Rai D, Gangal SV. Isolation and immunobiochemical characterization of a major allergen (65 kDa) from Fusarium equiseti. Allergy 1998;53(3):311-5.
  11. Verma J, Sridhara S, Singh BP, Gangal SV. Studies on shared antigenic/allergenic components among fungi. Allergy 1995;50(10):811-6.
  12. Verma J, Gangal SV. Studies on Fusarium solani. Cross-reactivity among Fusarium species. Allergy 1994;49(5):330-6.
  13. Pumhirun P, Towiwat P, Mahakit P. Aeroallergen sensitivity of Thai patients with allergic rhinitis. Asian Pac J Allergy Immunol 1997;15(4):183-5.
  14. Soeria-Atmadja D, Onell A, Borga A. IgE sensitization to fungi mirrors fungal phylogenetic systematics. J Allergy Clin Immunol 2010;125(6):1379-86.
  15. Mohovic J, Gambale W, Croce J. Cutaneous positivity in patients with respiratory allergies to 42 allergenic extracts of airborne fungi isolated in Sao Paulo, Brazil. Allergol Immunopathol (Madr) 1988;16(6):397-402.
  16. Enríquez Palomec O, Hernández Chávez L, Sarrazola Sanjuan DM, Segura Méndez NH, Hernández Colín DD, Martínez-Cairo S. Aeroallergens, skin tests and allergic diseases in 1091 patients. [Spanish] Rev Alerg Mex 1997;44(3):63-6.
  17. Ramos Morin CJ, Canseco Gonzalez C. Hypersensitivity to common allergens in the central region of Coahuila [Spanish]. Rev Alerg Mex 1993;40(6):150-4.
  18. Pennanen S, Putus T, Reiman M. IgE antibodies against environmental molds, yeast and bacteria in an adult population. (Poster) 2nd Int Symp Molecular Allergol, Rome, Italy 2007; 22-24 April.
  19. Al Doory Y, Domson J. Eds. Mould Allergy. Lea & Febiger 1984;150.
  20. Frankland AW. Fusarium: A neglected mould. Grana 1983;22:167-170.
  21. Saini SK, Boas SR, Jerath A, Roberts M, Greenberger PA. Allergic bronchopulmonary mycosis to Fusarium vasinfectum in a child. Ann Allergy Asthma Immunol 1998;80(5):377-80.
  22. Nissen D, Petersen LJ, Esch R, Svejgaard E, Skov PS, Poulsen LK, Nolte H. IgE-sensitization to cellular and culture filtrates of fungal extracts in patients with atopic dermatitis. Ann Allergy Asthma Immunol 1998;81(3):247-55.
  23. Ninet B, Jan I, Bontems O, Léchenne B, Jousson O, Lew D, Schrenzel J, Panizzon RG, Monod M. Molecular identification of Fusarium species in onychomycoses. Dermatology 2005;210(1):21-5.
  24. Romano C, Caposciutti P, Ghilardi A, Miracco C, Fimiani M. A case of primary localized cutaneous infection due to Fusarium oxysporum. Mycopathologia 2010;170(1):39-46.
  25. Gupta AK, Baran R, Summerbell RC. Fusarium infections of the skin. Curr Opin Infect Dis 2000;13(2):121-8.



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