Type:
Whole Allergen
Whole Allergen
m15 Trichoderma viride
m15 Trichoderma viride Scientific Information
Display Name:
Trichoderma viride
Route of Exposure:
Inhalation
Family:
Hypocreaceae
Species:
viride
Latin Name:
Trichoderma viride
Other Names:
Hypocrea rufa; green mold of narcissus
Summary
Trichoderma viride (Hypocrea rufa) is a ubiquitous mold of the Order Hypocreales, mostly found in plant materials and soil worldwide. It shows a variety of phenotypes and interactions with plants, other fungi and life forms. The particles causing allergic reactions are spores found in the environment.
Hypersensitivity pneumonitis (HP) and asthma are the main clinical presentations of T. viride allergy; molds of the Trichoderma genus are also able to cause opportunistic disease. Cross reactivity with other molds, especially if taxonomically close, may occur.
Allergen
Nature
The Genus Trichoderma is a group of common filamentous fungi showing a wide range of phenotypes and interactions with other life forms (1). Trichoderma viride is the anamorph (asexual form) of the fungus Hypocrea rufa (teleomorph, the asexual form) (1, 2). T. viride can grow on a wide variety of substrates, including wood (from many plant species), soil, leaf litter, peat, bark, water-damaged buildings (2) and other moldy, damp buildings (3). It was isolated in 22% of surface-derived water samples, and frequently found throughout the water systems (4).
Most Trichoderma tipically produce copious large amounts of green conidia, organized in pustules (1-5 mm) or “lawns” when cultured in vitro. Pustules appear cottony, with individual fertile branches and conidiophores protruding beyond the surface. In cultures of T. viride, conidia often formed at the surface of a pustule and reached a deep-dark green color after a week. Various types of conidia are produced, though warted (i.e. presenting warts on the surface)(5), is the most common; size also varies, with a wide range of 3–5.5 by 2.8–5 μm. Optimal growth temperature was 25°C (2). T. viride colonies may have a coconut-like odor (5).
There is considerable overlap between peak fungal activity season and other allergens such as grass and weed pollens, often masking the pathology caused by fungal spores in multi-sensitized people (6). Trichoderma spp contributed on average to 0.23% of the total mold spores caught during a study spanning a 2-year period (7).
Trichoderma viride may prove to be a bio-control agent against plant pathogens (8), though it is not believed to produce antibiotics (5).
Taxonomy
Taxonomic tree of Trichoderma genus (9) |
|
|---|---|
Domain |
Eukaryota |
Kingdom |
Fungi |
Phylum |
Ascomycota |
Subphylum |
Pezizomycotina |
Class |
Sordariomycetes |
Order |
Hypocreales |
Family |
Hypocreaceae |
Genus |
Trichoderma |
Taxonomic tree of Trichoderma genus (9) |
|---|
Tissue
Spores release detectable amounts of allergens following germination (6, 7, 10). T. viride spores were more likely to be found in dust samples than air (11).
Epidemiology
Worldwide distribution
Allergic disease caused by Trichoderma viride has been described in several countries around the world, including India (7), USA (11, 12), Spain (13), and Sweden (14).
Risk factors
Occupational health risks may be present for workers handling fungal enzymes in the animal feed industry, specifically phytase produced by Trichoderma spp. (15) and cellulase (16). Water-damaged, moldy homes may present a higher risk of developing asthma due to T. viride sensitization (11).
Environmental Characteristics
Worldwide distribution
T. viride has been identified worldwide (2, 17).
Route of Exposure
Main
Inhalation of spores, which appeared at higher concentration in dust than air samples (11), are able to reach the lung alveoli (3).
Detection
Main methods
Personal volumetric petri plate sampler (7)
Measures
The concentrations of Trichoderma spp spores ranged between 1–15 CFU/m3 (7).
Clinical Relevance
In a study of patients with pre-existing allergies, 35% showed positive reactions to a Trichoderma viridae cellulase, showing evidence of sensitization in the workplace (16).
T. viride spores are able to reach the alveoli, and in an in vitro study were found to trigger histamine release from bronchoalveolar lavage (BAL) cells (3).
In a 54-year old patient who presented with dyspnea, cough, chest pain and fever, T. viride caused hypersensitivity pneumonitis (HP). T. viride was cultured from the patient’s humidifier, and specific precipitating IgG were present in the patient’s serum (13).
Asthma
Trichoderma viride was amongst the molds that showed significantly higher concentrations in the homes of asthmatic children, compared with control homes (11).
Other diseases
T. viride is able to cause opportunistic lung infections in immunocompromised patients (18).
Other topics
A closely related fungal species, T. longibrachiatum, was the causative agent of allergic fungal sinusitis (AFS) in a 52-year old atopic and asthmatic patient who complained of headaches, nasal congestion and sinus pressure (19). Research into IgG reactivity to fungal agents showed that another Trichoderma species related to T. viride, T. citrinoviride could be a causative agent of adult-onset asthma (20).
Diagnostics Sensitization
The presence of allergen-specific antibodies is usually determined by skin prick tests (SPTs) and serology for IgE (6, 7). Radioallergosorbent Assays (RAST) may also be used to determine the ability of IgE to bind specific allergens (21). In a study of 102 patients reporting symptoms of allergic rhinitis or asthma, between 4–8% had a positive SPT result to T. viride antigen preparations (the difference was attributed by differing manufacturing process of the extracts) (12). In another study of 150, SPT reactions to Trichoderma viride allergens in patients with respiratory allergies varied in positivity, with 30% of patients showing mild to moderately positive reactions, 8.7% showing moderately positive reactions and 3.3% showing highly positive skin reactions (7). In the same study, the serum of SPT+ (positive) patients was tested by ELISA for the presence of IgE specific for the fungal antigens that caused the positive skin reactions. This showed 16.7% concordance for T. viride antigens when comparing the skin-prick tests and the ELISA in vitro immunoassay (7). A study using RAST to determine the IgE specificity of serum from patients with respiratory allergies showed that 7 of 20 patients had IgE for a T. viride cellulase (21).
Prevention and Therapy
Allergen immunotherapy
Immunotherapy is currently not recommended for patients allergic to molds, due to complexities of the allergens and patient co-allergies (6).
Prevention strategies
Avoidance is difficult to achieve (6), due to the wide range of environments in which T. viride can be found (2, 17).
Molecular Aspects
Cross-reactivity
Cross-reactivity has been demonstrated to other molds. In a study carried out on 668 serum samples from patients who had previously recorded at least one IgE positivity to fungal antigens, associations were observed between the patterns of IgE sensitization and fungal phylogenetic relationships. Using a panel of 17 fungal extracts including T. viride, some samples were only positive to one fungal species, whereas many were multi-sensitized. The results suggest that the associations are likely due to antigen cross-reactivity between fungal species, not uncommon in more closely related species (14).
Compiled By
Author: RubyDuke Communications
Reviewer: Dr. Christian Fischer
Last reviewed:January 2022
References
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