Type:
Whole Allergen
Whole Allergen
m13 Phoma betae
m13 Phoma betae Scientific Information
Display Name:
Phoma betae
Route of Exposure:
Inhalation
Family:
Neocamarosporiaceae
Species:
betae
Latin Name:
Neocamarosporium betae (obsolete: Phoma betae)
Other Names:
Pleospora betae, beet black rot fungus
Summary
Neocamarosporium betae (previously known as Phoma betae) is a ubiquitous mold of the Order Pleosporales, found in soil and decaying plant materials worldwide. It is a well-known plant pathogen, causing mostly root and leaf damage. The main particles causing sensitization are airborne spores.
Hypersensitivity pneumonitis (HP), allergic rhinitis (seasonal allergy) and asthma are the main clinical presentations of P. betae allergy. This fungus is also able to cause opportunistic disease in humans. Cross reactivity with other molds, especially if taxonomically close, may occur.
Allergen
Nature
Neocamarosporium betae (reclassified from Phoma betae/Pleospora betae to the current name) is a ubiquitous mold, found in soil and crops, and an agent of Phoma leaf spot and root decay primarily in Beta vulgaris, but other plants can also be affected (1, 2). Phoma spp. are plant pathogens, but can also cause opportunistic disease in animals and humans (3). Species of the Genus Phoma are crop and food contaminants; their presence was found on a variety of produce including (but not limited to) potatoes, nuts, bananas, tomatoes, sorghum and maize (3). Foods grown close to the ground are more likely to have higher contamination (3). Phoma spp can also be found in water systems (4).
Phoma betae colonies have an olive-brown colored mycelium, showing patches of white-grey to greenish-brown. The pycnidia structures are globose to subglobose in shape, 100–350 μm in diameter, producing conidia (a type of spore) by proliferation and subsequently extruding them. The conidia are unicellular and hyaline (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 people multi-sensitized (6). Spores of P. betae have been detected between the months of July and September (7).
Taxonomy
Taxonomic tree of Neocamarosporium genus (8, 9) |
|
|---|---|
Domain |
Eukaryota |
Kingdom |
Fungi |
Phylum |
Ascomycota |
Subphylum |
Pezizomycotina |
Class |
Dothideomycetes |
Order |
Pleosporales |
Family |
Neocamarosporiaceae |
Genus |
Neocamarosporium |
Taxonomic tree of Neocamarosporium genus (8, 9) |
|---|
Tissue
Airborne parts of the mold (spores) are the tissues that cause sensitization and allergy symptoms (6, 7).
Epidemiology
Worldwide distribution
Allergic conditions associated with P. betae have been described in many parts of the world, including North America (10), Hungary (11), and England (7). Allergic conditions attributed to P. betae sensitization ranged between 6-16% of patients with pre-existing allergies (7, 12)
Risk factors
Working in a museum may pose a risk factor due to higher exposure to molds and other microorganisms (12).
Environmental Characteristics
Worldwide distribution
Phoma spp. are present in a multitude of environments worldwide, within the soil, air, water systems, both natural and artificial (2-4, 7).
Route of Exposure
Main
Inhalation of allergenic mold parts (7, 10).
Detection
Main methods
A Hirst spore trap can be used to sample air throughout a 24 hour period to collect fungal spores (7).
Clinical Relevance
The allergic conditions that may be caused by Phoma betae can vary. Acute eosinophilic pneumonia (AEP) is a disorder caused by diffuse lung damage with accumulation of eosinophils within alveolar and interstitial spaces, usually leading to rapid respiratory failure. It is thought that AEP may be an allergic reaction to specific antigens, which causes rapid accumulation of eosinophils. P. betae can be a cause of AEP as shown by a case report in which a 20-year-old man developed acute pneumonia symptoms of fever, tachycardia, crackles and wheezes at auscultation. Hypersensitivity testing was positive for P. betae IgE (10).
Asthma in children has been associated with environmental exposure to P. betae following Skin Prick Tests (SPTs) (11).
Seasonal respiratory symptoms consistent with hay fever, which did not coincide with the release of grass pollens, were attributed to P. betae in 6.8% of patients included in a study carried out in London, England (7).
Occupational exposure and sensitization to P. betae has been reported. In a study testing for mold allergies in museum employees, 85% of patients reported at least one symptom of allergy (ranging from cough, dyspnea, wheezing, rhinitis, conjunctivitis and skin symptoms); 16% of patients had positive SPT to P. betae (12).
Diagnostics Sensitization
The presence of allergen-specific antibodies is determined by skin prick tests (SPTs) and serology for IgE (10-12).
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 often not possible, as P. betae is a very common contaminant mold of decaying plant material (8, 11).
Molecular Aspects
Cross-reactivity
Cross-reactivity has been demonstrated to other molds. 83% of patients with positive IgE reaction to P. betae were also positive to Alternaria alternata (11). In another study, the serum of 10 patients diagnosed with allergic fungal sinusitis (AFS) was used to determine whether IgE specific to other fungi (including P. betae) were present. All of the AFS patients showed a degree of cross reactivity to 6 other fungi (13). In a study carried out on 668 serum samples from patients which 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 P. betae, 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:February 2022
References
- Vaghefi N, Silva A, Koenick LB, Pethybridge SJ. Genome Resource for Neocamarosporium betae (syn. Pleospora betae), the Cause of Phoma Leaf Spot and Root Rot on Beta vulgaris. Molecular Plant-Microbe Interactions®. 2019;32(7):787-9.
- Bassimba DDM, Mira JL, Vicent A. First Report of Leaf Spot of Spinach Caused by Pleospora betae in Spain. Plant Dis. 2014;98(11):1583.
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- Buisseret PD. Seasonal allergic symptoms due to fungal spores. Br Med J. 1976;2(6034):507-8.
- Valenzuela-Lopez N, Cano-Lira JF, Guarro J, Sutton DA, Wiederhold N, Crous PW, et al. Coelomycetous Dothideomycetes with emphasis on the families Cucurbitariaceae and Didymellaceae. Studies in Mycology. 2018;90:1-69.
- Uniprot.org. Taxonomy - Neocamarosporium betae (Beet black rot fungus) (Pleospora betae) 2021 [cited 2021 23.11.21]. Available from: https://www.uniprot.org/taxonomy/1979465.
- McElligott M, Carrington J, Huebert C. Acute Eosinophilic Pneumonia Following Marijuana Inhalation. CHEST. 2017;152(4):A426.
- Szánthó A, Osváth P, Horváth Z, Novák EK, Kujalek E. Study of mold allergy in asthmatic children in Hungary. J Investig Allergol Clin Immunol. 1992;2(2):84-90.
- Wiszniewska M, Walusiak-Skorupa J, Pannenko I, Draniak M, Palczynski C. Occupational exposure and sensitization to fungi among museum workers. Occup Med (Lond). 2009;59(4):237-42.
- Hutcheson PS, Schubert MS, Slavin RG. IgE immunoblot reactivity in allergic fungal sinusitis. Journal of Allergy and Clinical Immunology. 2005;115(2):S53.
- Soeria-Atmadja D, Onell A, Borgå A. IgE sensitization to fungi mirrors fungal phylogenetic systematics. J Allergy Clin Immunol. 2010;125(6):1379-86.e1.
