Trichoderma viride

  • Allergen search puff


    Search ImmunoCAP allergens and allergen components. Note that all information is in English.

Code: m15
Latin name: Trichoderma viride
Source material: Spores and mycelium
Family: Hypocreaceae

For continuous updates:


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

Allergen Exposure

Trichoderma viride is a fungus and a bio-fungicide. T. viride is reported to be one of the most widely distributed of all soil fungi. Studies of habitats have demonstrated that this mould occurs in the extreme north, in alpine areas and in tropical regions. Its occurrence in a wide range of forests, grasslands and cultivated soils has been documented. It is commonly found on fallen timber and on tapestries, in moist dwellings and isolated in kitchens, where it grows on unglazed ceramics. It can grow on other fungi. Trichoderma can cause problems in the industrial cultivation of mushrooms, and tulip bulbs are frequently infected. Severe moisture problems may result in the growth of Trichoderma. (1)

T. viride has been used as a bio-fungicide for biological control of other fungal pathogens. (2) It is used in seed and soil treatments for suppression of various diseases caused by fungal pathogens. T. viride is a pathogen in its own right and may cause green mould rot on onions and cultivated mushrooms. (3)

T. viride produces spores asexually, by mitosis. The mycelium of T. viride can produce a variety of enzymes including cellulases and chitinases, which can degrade cellulose and chitin respectively. This fungus may often be identified by the smell of coconuts. Because of its cellulases, this mould can grow directly on wood, which is mostly composed of cellulose; and because of chitinases, on fungi, the cell walls of which are mainly composed of chitin. It parasitises the mycelia and fruiting bodies of other fungi, including cultivated mushrooms. (4) Tulip bulbs are frequently infected. Colonies are white to light green and grow in a characteristic effusion.

A closely related species, T. reesei, is used in the creation of stonewashed jeans. The cellulases produced by the fungus partially degrade the cotton material in places, making it soft and making the jeans look as if they had been washed using stones. (3)

Usukizyme is a commercial enzyme preparation from T. viride. (5)

A number of aerobiological studies have demonstrated the presence of T. viride in a variety of settings.

Trichoderma has been shown to be a prominent airborne fungus in greenhouses. Though Aspergillus/Penicillium and Botrytis showed diurnal patterns, this is not true for Trichoderma. (6)

Air-conditioned rooms have been reported to be potential reservoirs of fungi that may cause allergic problems or infections in healthy or immunocompromised individuals living in these environments. Trichoderma has been shown to be one of the relevant moulds found in this setting. (7, 8)

A number of moulds, including T. harzianum, T. polysporum, and T. viride, may be used for bio-control of pests and plant diseases, resulting in human exposure to these moulds. (9)

T. viride is often found in damp and mouldy buildings. (10) In a Cincinnati, Ohio, USA study which sought to determine if specific moulds were in significantly higher concentrations in water-damaged homes of asthmatic children compared to homes with no visible water damage, two moulds – Scopulariopsis brevicaulis and T. viride – had significantly higher concentrations in asthmatics' homes compared to control homes. (11)

The closely related species Trichoderma harzianum has also been identified in samples of urea-formaldehyde foam insulation taken from Canadian residences. Extensive or conspicuous growth has also been seen in some samples of Hormoconis resinae, Stachybotrys chartarum and T. viride. (12)

T. viride may also contaminate fresh fruit – in the field, during harvest, transport and selling at market, and in consumer homes. (13)

The giant Madagascar hissing cockroach (Gromphadorhina portentosa) is often used as an educational tool in classrooms, museums, zoos, and elsewhere. The potential existence of moulds associated with this insect was assessed by evaluating specimens obtained from laboratories, classrooms, pet stores and private homes. A total of 14 mould taxa were obtained, mostly from external surfaces and dominated by species of Rhizopus, Penicillium, Mucor, Trichoderma and Alternaria. The authors suggested that this focus of public awareness should be aimed at individuals (especially children) prone to infections and allergies who might be exposed to this insect and/or its rearing conditions. (14)

Allergen Description

No allergens have been characterised.

Allergen expression from spores of 11 moulds, including T. viride, showed that for 9 of them, between 5.7% and 92% of spores released allergens before germination. However, spores of Penicillium and Trichoderma did not release detectable allergens. (15)

Potential Cross-Reactivity

No studies have evaluated the clinical cross-reactive potential of T. viride.

An endo-1,4-beta-xylanase has been isolated from a commercial preparation of T. viride, with a molecular weight of 22 kDa. The xylanase was a true xylanase but without cellulase activity. Compared with a xylanase from Schizophyllum commune, strong evidence for homology was found. The clinical relevance of this was not determined. (16)

Clinical Experience

IgE-mediated reactions

Anecdotal evidence suggests that T. viride may induce symptoms of asthma and hypersensitivity pneumonitis (HP) in sensitised individuals. (17) However, few studies have been reported to date; it is possible that the allergy occurs more frequently than has been reported.

The closely related genus member T. citrinoviride may play a role in the aetiology of adult-onset asthma, or serve as an indicator of other causal factors. (18)

A 54-year-old woman presented with dyspnoea, cough, chest pain, and fever. A diagnosis of HP was made by a combination of clinical, radiologic, physiologic, and immunologic studies. T. viride was isolated in cultures of water samples from an ultrasonic humidifier installed in the patient's home a year earlier. Precipitating immunoglobulin G antibodies to T viride were detected in the patient's serum by enzyme-linked immunosorbent assay. The patient remained symptom-free after the humidifier was removed from her home. (17)

A 34-year-old sawmill maintenance engineer developed a dry cough associated with widespread wheezes and crackles in his lungs, which worsened with the development of work-related lethargy, fever, breathlessness, and a marked loss in weight. Serum precipitins were identified to extracts of sawdust, wood chips, and bark from the sawmill, as well as eight species of mould. Specific IgG-binding inhibition studies suggested that a common epitope present on the genus-related T. koningii might be responsible for the cross-reactivity of the patient's serum with the wood and fungal extracts. (19)

The related mould T. longibrachiatum has resulted in allergic fungal sinusitis in a patient with a history of atopy and asthma. (20)

In an American study of IgE antibodies against mould, antibodies to Trichoderma were as frequent as those to Aureobasidium and Fusarium. (21)

In a study in Sao Paulo, Brazil, evaluating sensitisation to 42 airborne fungi in 201 patients with asthma and/or allergic rhinitis using skin specific IgE tests, 19 were shown to be sensitised to Trichoderma, 15 to Alternaria, 15 to Aspergillus, 23 to Aureobasidium, 37 to Candida, 15 to Chaetomium, 19 to Epicoccum, 17 to Mucor, 20 to Phoma, and 14 to Rhizopus. (22)

The enzyme cellulose, derived from T. viride, has been reported to result in sensitisation in mould-allergic individuals. In a study evaluating IgE antibody reactivity to commercially available fungal enzymes, 17 commercial fungal enzymes were used as antigens in the evaluation of 20 subjects with symptoms of respiratory allergies and skin test reactivity to 2 or more fungal allergens. The most reactive fungal enzymes were invertase (baker’s yeast, Saccharomyces cerevisiae), cellulase (T. viride), and glucoside (brewer’s yeast, S. cerevisiae). (23)

Trichoderma viride may result in hypersensitivity reactions in occupational settings.

Allergic alveolitis due to inhalation of wood dust or fungi has been described in wood-workers. (24)

In a study evaluating workers occupationally exposed to fungal enzymes in 2 animal feed factories in order to determine if the sensitisation originated from the enzymes or was caused by the microorganism used to produce the enzymes, 8 of 86 (9%) workers analysed tested positive and were more frequently sensitised to phytase from Trichoderma and Peniophora. No cross-reactions were observed between Trichoderma and Peniophora sp. phytases. (25)

A number of studies have alluded to the prevalence of sensitisation to T. viride in various communities.

In an evaluation of the prevalence of sensitisation to common indoor fungal species in an atopic population in West Virginia in the USA, 102 patients with symptoms consistent with allergic rhinitis or asthma were evaluated for IgE reactivity to a panel of skin-prick test reagents, including six additional fungi that are common indoor contaminants. Overall, 21 out of 102 patients (21%) with asthma or allergic rhinitis were skin-test-positive to at least one fungal extract. Of the patients with a positive SPT to fungi, 12 out of 21 (58%) showed sensitivity to one or more of the newly-tested species; most notably T. viride (8%), Chaetomium globosum (7%), Paecilomyces variotii (7%), and Acremonium strictum (6%). Immunoblotting revealed specific IgE against a number of protein bands belonging to these fungal species. The authors suggested that cross-reactivity with other fungi may partially explain the results. (26)

In a study in Connecticut in the USA, sensitisation to 30 airborne fungi was conducted using skin-specific IgE tests on 100 patients with asthma and/or allergic rhinitis . Of the group, 43 were shown to be sensitised to Trichoderma viride, 42 to Alternaria alternata, 53 to Aspergillus fumigatus, 51 to Aspergillus niger, 52 to Aspergillus terreus, 62 to Pullularia pullulans (now known as Aureobasidium pullulans), 45 to Botrytis cinerea, 39 to Candida albicans, 45 to Cephalosporium acremonium (Acremonium kiliense), 50 to Epicoccum purpurascens, 49 to Coprinus micaceus, 5 to Agaricus campestris, 50 to Ustilago maydis, and 68 to Penicillium notatum. (27)

Similarly, in a study in Sao Paulo, Brazil, evaluating sensitisation to 42 airborne fungi in 201 patients with asthma and/or allergic rhinitis using skin-specific IgE tests, 19 were shown to be sensitised to Trichoderma, 15 to Alternaria, 15 to Aspergillus, 23 to Aureobasidium, 37 to Candida, 15 to Chaetomium, 19 to Epicoccum, 17 to Mucor, 20 to Phoma, and 14 to Rhizopus. (22)

From a large Phadia (Sweden) repository of human blood serum, a subset was compiled to include the maximal numbers of individual blood sera that had been consistently tested across the largest panel of fungal allergen preparations. Only those individuals with at least 1 positive test (>0.35 kUA/L) were considered. The compiled dataset included 668 unique samples, each with recorded IgE antibody concentrations against 17 separate fungal species, but devoid of clinical history. Of these, 222 were positive for T. viride. (28)

In a Finnish study with the aim of assessing the prevalence of IgE-mediated sensitisation in an adult population and common to a work environment, specific IgE-antibodies were determined to 33 fungi and 11 bacteria in almost 300 serum samples. Approximately 6% 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 0.35-0.69 kU/l, suggesting possible sensitisation. IgE to a number of moulds, including the closely-related Trichoderma citrinoviride, was significantly higher among blue-collar workers. (29) In an earlier study of 121 Finnish suspected mould-allergic children with asthma, 40.5% were positive for a mould screen: the allergens most frequently positive were Cladosporium (28%), Candida (28%), Helminthosporium (26%) and Botrytis cinerea (24%). The 14th most prevalent mould sensitisation was to Trichoderma (12%). (30)

Other reactions

Trichoderma species are recognised to be pathogenic in immunosuppressed hosts, and in particular, for peritoneal dialysis-associated peritonitis and infections in immunocompromised patients with a hematologic malignancy or having undergone solid organ transplantation. T. longibrachiatum was the most common species involved in these infections. (31) However, T. viride was shown to be responsible for fungal peritonitis in a patient with renal failure secondary to amyloidosis and undergoing continuous ambulatory peritoneal dialysis. (32) A liver transplant recipient developed infection of a perihepatic haematoma due to T. viride. Although the death of the patient was not directly related to the fungal infection, abundant quantities of this pathogen were recovered in the haematoma at post-mortem examination, despite previous treatment. (33)

T. viride was reported to be responsible for pulmonary infection in a 54-year-old female who had received chemotherapy for acute myeloid leukemia. (31) Pulmonary mycoma caused by T. viride has been reported. (34)

Trichoderma has been shown to cause onychomycosis. (35)

In a report of two cases of acute eosinophilic pneumonia in which the patients presented with an acute febrile illness, dry cough, severe hypoxemia and diffuse pulmonary infiltrates, precipitating antibodies against Trichosporon cutaneum and T. viride were found in the patients' sera. Provocation tests were positive. (36) A review of 22 cases of acute eosinophilic pneumonia previously reported in Japan showed 3 that were positive for Trichosporon cutaneum, T. viride and Aspergillus species. (37)


Compiled by Dr Harris Steinman.


  1. Ebbehøj NE, Hansen MØ, Sigsgaard T, Larsen L. Building-related symptoms and molds: a two-step intervention study. Indoor Air 2002;12(4):273-7.
  2. Turóczi G, Fekete C, Kerényi Z, Nagy R, Pomázi A, Hornok L. Biological and molecular characterisation of potential biocontrol strains of Trichoderma. J Basic Microbiol 1996;36(1):63-72.
  3. Tom Volk's Fungus of the Month. Accessed 10 February 2011.
  4. Trichoderma viride. Accessed 10 February 2011.
  5. Omumasaba CA, Yoshida N, Ogawa K. Purification and characterization of a chitinase from Trichoderma viride. J Gen Appl Microbiol 2001;47(2):53-61.
  6. Li DW, LaMondia J. Airborne fungi associated with ornamental plant propagation in greenhouses. Aerobiologia 2010;26(1):15-28.
  7. Khan A, Karuppayil S, Manoharachary C, Kunwar I, Waghray S. Isolation, identification and testing for allergenicity of fungi from air-conditioned indoor environments. Aerobiologia 2009;25(2):119-23.
  8. Bagy MM, Gohar YM. Mycoflora of air-conditioners dust from Riyadh, Saudi Arabia. J Basic Microbiol 1988;28(9-10):571-7.
  9. Madsen AM, Hansen VM, Meyling NV, Eilenberg J. Human exposure to airborne fungi from genera used as biocontrol agents in plant production. Ann Agric Environ Med 2007;14(1):5-24.
  10. Larsen FO, Clementsen P, Hansen M, Maltbaek N, Gravesen S, Skov PS, Norn S. The indoor microfungus Trichoderma viride potentiates histamine release from human bronchoalveolar cells. APMIS 1996;104(9):673-9.
  11. Vesper SJ, McKinstry C, Yang C, Haugland RA, Kercsmar CM, Yike I, Schluchter MD, Kirchner HL, Sobolewski J, Allan TM, Dearborn DG. Specific molds associated with asthma in water-damaged homes. J Occup Environ Med 2006;48(8):852-8.
  12. Bissett J. Fungi associated with urea-formaldehyde foam insulation in Canada. Mycopathologia 1987;99(1):47-56.
  13. Tournas VH, Katsoudas E. Mould and yeast flora in fresh berries, grapes and citrus fruits. Int J Food Microbiol 2005;105(1):11-7.
  14. Yoder JA, Glenn BD, Benoit JB, Zettler LW. The giant Madagascar hissing-cockroach (Gromphadorhina portentosa) as a source of antagonistic moulds: concerns arising from its use in a public setting. Mycoses 2008;51(2):95-8.
  15. Green BJ, Mitakakis TZ, Tovey ER. Allergen detection from 11 fungal species before and after germination. J Allergy Clin Immunol 2003;111(2):285-9.
  16. Ujiie M, Roy C, Yaguchi M. Low-molecular-weight xylanase from Trichoderma viride. Appl Environ Microbiol 1991;57(6):1860-2.
  17. Enríquez-Matas A, Quirce S, Cubero N, Sastre J, Melchor R. Hypersensitivity pneumonitis caused by Trichoderma viride. [Spanish] Arch Bronconeumol 2009;45(6):304-5.
  18. Jaakkola MS, Laitinen S, Piipari R, Uitti J, Nordman H, Haapala AM, Jaakkola JJ. Immunoglobulin G antibodies against indoor dampness-related microbes and adult-onset asthma: a population-based incident case-control study. Clin Exp Immunol 2002;129(1):107-12.
  19. Halpin DM, Graneek BJ, Turner-Warwick M, Newman Taylor AJ. Extrinsic allergic alveolitis and asthma in a sawmill worker: case report and review of the literature. Occup Environ Med 1994;51(3):160-4.
  20. Tang P, Mohan S, Sigler L, Witterick I, Summerbell R, Campbell I, Mazzulli T. Allergic fungal sinusitis associated with Trichoderma longibrachiatum. J Clin Microbiol 2003;41(11):5333-6.
  21. Karlsson-Borgå Å, Jonsson P, Rolfsen W. Specific IgE antibodies to 16 widespread mold genera in patients with suspected mold allergy. Ann Allergy 1989;63(12):521-6.
  22. 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.
  23. Horner WE, Armstrong M, El-Dahr J, McCants M, Reese G, Kobernick AK, Lehrer SB. Prevalence of IgE reactivities in mold-allergic subjects to commercially available fungal enzymes. Allergy Asthma Proc 2008;29(6):629-35.
  24. Al Doory Y, Domson J. Eds. Mould Allergy. Lea & Febiger 1984;150.
  25. Caballero ML, Gomez M, Gonzalez-Munoz M, Reinoso L, Rodriguez-Perez R, Alday E, Moneo I. Occupational sensitization to fungal enzymes used in animal feed industry. Int Arch Allergy Immunol 2007;144(3):231-9.
  26. Beezhold DH, Green BJ, Blachere FM, Schmechel D, Weissman DN, Velickoff D, Hogan MB, Wilson NW. Prevalence of allergic sensitization to indoor fungi in West Virginia. Allergy Asthma Proc 2008;29(1):29-34.
  27. Santilli J, Rockwell WJ, Collins RP. Individual patterns of immediate skin reactivity to mold extracts. Ann Allergy 1990;65:454-8.
  28. Soeria-Atmadja D, Onell A, Borga A. IgE sensitization to fungi mirrors fungal phylogenetic systematics. J Allergy Clin Immunol 2010;125(6):1379-86.
  29. 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;April 22-24.
  30. Koivikko A, Viander M, Lanner A. Use of the extended Phadebas RAST panel in the diagnosis of mould allergy in asthmatic children. Allergy 1991;46:85-91.
  31. De Miguel D, Gómez P, González R, García-Suárez J, Cuadros JA, Bañas MH, Romanyk J, Burgaleta C. Nonfatal pulmonary Trichoderma viride infection in an adult patient with acute myeloid leukemia: report of one case and review of the literature. Diagn Microbiol Infect Dis 2005;53(1):33-7.
  32. Loeppky CB, Sprouse RF, Carlson JV, Everett ED. Trichoderma viride peritonitis. South Med J 1983;76(6):798-9.
  33. Jacobs F, Byl B, Bourgeois N, Coremans-Pelseneer J, Florquin S, Depré G, Van de Stadt J, Adler M, Gelin M, Thys JP. Trichoderma viride infection in a liver transplant recipient. Mycoses 1992;35(11-12):301-3.
  34. Escudero Gil MR, Pino Corral E, Muñóz Muñóz R. Pulmonary mycoma cause by Trichoderma viride. [Spanish] Actas Dermosifiliogr 1976;67(9-10):673-80.
  35. Hilmioglu-Polat S, Metin DY, Inci R, Dereli T, Kilinç I, Tümbay E. Non-dermatophytic molds as agents of onychomycosis in Izmir, Turkey - a prospective study. Mycopathologia 2005;160(2):125-8.
  36. Imokawa S, Sato A, Taniguchi M, Imamura M, Shirai T, Suda T, Iwata M, Gemma H. Two cases of acute eosinophilic pneumonia with precipitating antibody against Trichosporon cutaneum and Trichoderma viride. [Japanese] Nihon Kyobu Shikkan Gakkai Zasshi 1993;31(3):352-9.
  37. Mouri M, Nambu Y, Horii H, Kobayashi Y, Yamanouchi K, Sakurai S, Toga H, Ohya N. Case report and review of literature on seasonal distribution and pathogenesis of acute eosinophilic pneumonia in Japan. [Japanese] Nihon Kyobu Shikkan Gakkai Zasshi 1993;31(12):1578-84.



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