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Allergy Panel 11, Mold Group

The Allergy Panel 11, Mold Group measures serum-specific IgE to Alternaria, Aspergillus, Cladosporium, Penicillium, Candida, and Fusarium—six clinically relevant fungal allergens. It confirms IgE-mediated mould sensitisation in patients with suspected allergic rhinitis, asthma, or ABPA, interpreted alongside exposure history, symptom timing, and total IgE to distinguish sensitisation from…

6

Biomarkers

Blood (serum)

Sample

3–5 business days

Turnaround

No

Fasting

What is the Mold Allergy Panel test?

The Allergy Panel 11, Mold Group measures serum-specific IgE antibodies to six clinically relevant fungal allergens: Alternaria alternata, Aspergillus fumigatus, Cladosporium herbarum, Penicillium chrysogenum, Candida albicans, and Fusarium proliferatum. It is a multi-allergen screen designed to confirm IgE-mediated sensitisation in patients with suspected mould allergy, offering a snapshot of the most common indoor and outdoor fungal triggers in a single panel. Practitioners order this panel to differentiate mould-driven allergic rhinitis or asthma from other causes, to evaluate patients with chronic respiratory symptoms in mould-rich environments, and to guide targeted environmental intervention. Because fungal spores are ubiquitous and patients are often polysensitised, the panel's breadth aids both diagnosis and prioritisation of remediation efforts. Results are interpreted alongside exposure history, symptom timing, and—where relevant—total IgE, eosinophil count, and imaging to distinguish isolated sensitisation from clinically significant allergy or conditions such as allergic bronchopulmonary aspergillosis.

What does the Mold Allergy Panel test measure?

1
m6 IgE(Alternaria alternata-specific IgE)
Range: <0.35 kU/L considered negative; ≥0.35 kU/L positive, with class grades 0–6 reflecting increasing antibody concentration.Optimal: <0.10 kU/L is typical for non-sensitised individuals; any detectable IgE (≥0.10 kU/L) warrants clinical correlation.kU/L / IU/mL

Alternaria alternata is one of the most clinically important allergenic moulds, ubiquitous both outdoors (on decaying vegetation) and indoors where moisture is present. Its major allergen Alt a 1 is a unique fungal protein that drives IgE-mediated sensitisation in atopic individuals. Exposure occurs primarily via inhalation of airborne spores, which peak in warm, dry weather and can trigger immediate hypersensitivity reactions in sensitised patients.

Alternaria sensitisation is strongly associated with allergic rhinitis and asthma; it is an independent risk factor for asthma severity and has been linked to life-threatening exacerbations. Detection of specific IgE confirms sensitisation and supports clinical correlation with exposure history and symptoms. The degree of sensitisation (class grade) provides some indication of reactivity, though clinical response is not strictly dose-dependent.

2
m3 IgE(Aspergillus fumigatus-specific IgE)
Range: <0.35 kU/L considered negative; ≥0.35 kU/L positive, with class grades 0–6.Optimal: <0.10 kU/L; any detectable level in a patient with asthma prompts evaluation for ABPA if other features are present.kU/L / IU/mL

Aspergillus fumigatus is a thermotolerant saprophytic mould found in soil, compost, and indoor environments. Its spores are small enough to reach the lower airways, where they can provoke IgE-mediated allergy, colonise damaged airways, or trigger allergic bronchopulmonary aspergillosis (ABPA) in susceptible hosts. IgE directed against Asp f allergens reflects Type I sensitisation.

Aspergillus-specific IgE is central to the diagnosis of ABPA, where elevated total IgE and Aspergillus-specific IgE occur alongside asthma and radiological findings. Isolated sensitisation without ABPA can contribute to allergic rhinitis, asthma exacerbations, and occupational allergy. The result must be interpreted with total IgE, eosinophil count, imaging, and lung function.

3
m2 IgE(Cladosporium herbarum-specific IgE)
Range: <0.35 kU/L negative; ≥0.35 kU/L positive, graded by concentration.Optimal: <0.10 kU/L; detectable IgE correlates with sensitisation but requires symptom and exposure correlation.kU/L / IU/mL

Cladosporium species are among the most abundant airborne moulds worldwide, thriving both outdoors on plant material and indoors in damp environments. Cladosporium herbarum produces a range of allergenic proteins; spore counts peak in late summer and autumn. IgE sensitisation develops in genetically susceptible individuals following repeated inhalation.

Cladosporium is a common trigger of seasonal allergic rhinitis and can exacerbate asthma. Cross-reactivity with other fungi is limited, so specific IgE helps pinpoint the relevant allergen in polysensitised patients. Clinical relevance is confirmed by symptom timing aligned with outdoor spore seasons or indoor mould exposure.

4
m1 IgE(Penicillium chrysogenum-specific IgE)
Range: <0.35 kU/L negative; ≥0.35 kU/L positive, class-graded.Optimal: <0.10 kU/L; any elevation warrants environmental and symptom correlation.kU/L / IU/mL

Penicillium chrysogenum (formerly Penicillium notatum) is a cosmopolitan mould found on decaying food, damp walls, and in poorly ventilated indoor spaces. Its spores are readily aerosolised and inhaled. The genus produces multiple allergens, some shared across Penicillium species, that elicit IgE responses in atopic individuals.

Penicillium sensitisation contributes to perennial allergic rhinitis, asthma, and exacerbations in damp indoor environments. It is less strongly associated with severe asthma than Alternaria or Aspergillus but remains clinically relevant in patients with mould-rich exposures. Specific IgE confirms sensitisation and guides environmental control measures.

5
m5 IgE(Candida albicans-specific IgE)
Range: <0.35 kU/L negative; ≥0.35 kU/L positive, class-graded.Optimal: <0.10 kU/L; detectable IgE is common in atopy and requires careful clinical correlation.kU/L / IU/mL

Candida albicans is a commensal yeast of human mucosa (gut, oropharynx, vagina) and a facultative pathogen. Unlike environmental moulds, exposure is primarily endogenous. IgE to Candida allergens can develop in atopic individuals, though its clinical relevance in respiratory allergy is less clear than for dermatological or mucosal disease. Cross-reactivity with other fungi has been described.

Candida-specific IgE is occasionally positive in polysensitised atopic patients but does not typically drive isolated respiratory allergy. Elevated IgE may correlate with chronic mucocutaneous candidiasis or atopic dermatitis in some patients. Interpretation requires clinical context; many positive results reflect cross-reactivity or asymptomatic sensitisation rather than causative allergy.

6
m9 IgE(Fusarium proliferatum-specific IgE)
Range: <0.35 kU/L negative; ≥0.35 kU/L positive, class-graded.Optimal: <0.10 kU/L; any detectable level warrants symptom and exposure history review.kU/L / IU/mL

Fusarium species are soilborne moulds and plant pathogens, also found indoors in water-damaged buildings and on shower curtains. Fusarium proliferatum is a representative allergen source within the genus. Spores become airborne and can be inhaled; allergen proteins provoke IgE production in susceptible individuals.

Fusarium sensitisation is less prevalent than Alternaria or Cladosporium but is relevant in patients with water-damage exposure or occupational agricultural contact. Specific IgE supports the diagnosis of mould-induced allergic rhinitis or asthma when symptoms correlate with exposure. Clinical significance increases when multiple mould IgE are elevated.

Why is the Mold Allergy Panel test ordered?

  • Evaluation of persistent allergic rhinitis, conjunctivitis, or asthma in patients reporting symptom exacerbation in damp, mouldy, or poorly ventilated indoor environments
  • Investigation of seasonal respiratory symptoms peaking in late summer or autumn, consistent with outdoor mould spore seasons (Alternaria, Cladosporium)
  • Diagnostic work-up of suspected allergic bronchopulmonary aspergillosis (ABPA) in patients with asthma, central bronchiectasis, and elevated total IgE
  • Assessment of occupational or hobby-related mould exposure (agriculture, greenhouse work, composting, water-damage restoration) with new-onset respiratory symptoms
  • Screening of polysensitised atopic patients to identify contributory fungal allergens and direct environmental control measures
  • Unexplained asthma exacerbations or corticosteroid-dependent asthma where fungal sensitisation—particularly Alternaria—is a known severity marker
  • Follow-up confirmation after positive skin-prick testing or when skin testing is contraindicated (active dermatitis, antihistamine use, dermatographism)

Sample collection and turnaround

Sample type

Blood (serum)

Fasting required

No

Collection method

Venipuncture at patient service centre

Turnaround

3–5 business days

Collection notes

Phlebotomy via Quest draw site; no special preparation required. Antihistamines do not need to be withheld. Avoid haemolysis during collection; grossly haemolysed specimens may require recollection.

Specimen requirements

Minimum 1.0 mL serum (gel separator acceptable). Separate from cells and refrigerate or freeze if processing is delayed; specific IgE is stable refrigerated for several days and frozen for months.

What can affect Mold Allergy Panel results?

reducesRecent or current corticosteroid or immunosuppressive therapy

Systemic immunosuppression can lower total and specific IgE synthesis, potentially yielding false-negative results; inhaled corticosteroids have minimal effect on serum IgE.

variableAntihistamine use

Antihistamines do not interfere with serum IgE measurement (unlike skin-prick tests), so the panel can be performed while a patient is on symptomatic therapy.

variableTotal IgE concentration

Very high total IgE (>1,000–2,000 kU/L) can cause assay competition or non-specific binding, occasionally suppressing detection of specific IgE; correlation with total IgE and clinical context is essential.

elevatesAge and atopic status

Sensitisation prevalence increases through childhood and adolescence in atopic individuals; infants and very young children may not yet have developed detectable specific IgE despite exposure.

variableCross-reactivity among fungal allergens

Some fungal proteins share epitopes, so polysensitisation can reflect true multiple exposures or cross-reactive IgE; component-resolved diagnostics (where available) can clarify primary sensitisation.

variableSample haemolysis or lipemia

Grossly haemolysed or lipaemic specimens may interfere with immunoassay performance; laboratories will flag and may request recollection if interference is suspected.

What do Mold Allergy Panel results mean?

Elevated

Specific IgE ≥0.35 kU/L to one or more moulds confirms sensitisation. Alternaria and Aspergillus elevations are of particular concern: Alternaria sensitisation is an independent risk factor for asthma severity and life-threatening exacerbations, while Aspergillus IgE raises suspicion for ABPA when total IgE is also elevated and imaging or pulmonary function is abnormal. Multiple positive results suggest polysensitisation and often correlate with perennial symptoms. Clinical relevance is confirmed by temporal or geographic correlation between exposure and symptoms; not all sensitisation is symptomatic.

Normal

Specific IgE <0.35 kU/L is classified as negative by most laboratories, though detectable values between 0.10 and 0.34 kU/L represent borderline sensitisation that may be clinically relevant in highly exposed or symptomatic patients. Negative serology does not exclude allergy if symptom-exposure correlation is strong; consider skin-prick testing or empirical environmental intervention.

Reduced

Specific IgE <0.10 kU/L across all moulds makes IgE-mediated mould allergy unlikely, though it does not exclude non-IgE inflammatory responses (e.g. hypersensitivity pneumonitis) or allergy to moulds not included in the panel. Very low or undetectable IgE in a patient with high clinical suspicion may reflect early sensitisation, immunosuppression, or non-allergic disease.

Note: Results must be correlated with exposure history, symptom timing, and—where relevant—total IgE, eosinophil count, and imaging. The degree of IgE elevation (class grade) provides a rough indicator of sensitisation intensity but does not predict symptom severity in a linear fashion. Cross-reactivity is common, so positive results to multiple moulds may overestimate the number of independent sensitisations. In suspected ABPA, Aspergillus-specific IgE should be interpreted alongside total IgE (typically >1,000 kU/L), peripheral eosinophilia, radiological findings, and precipitating antibodies (IgG). The panel does not cover all allergenic moulds; rare or regional species require individual testing.

Frequently asked questions

The panel measures specific IgE to six moulds: Alternaria alternata, Aspergillus fumigatus, Cladosporium herbarum, Penicillium chrysogenum, Candida albicans, and Fusarium proliferatum—the most clinically relevant indoor and outdoor fungal allergens.

How to access the Mold Allergy Panel test

The Mold Allergy Panel reference page is free and open to all practitioners. Create a free practitioner account to see pricing, save tests to your list, and generate requisition forms. Verification takes 1–2 business days.

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About this page

Published: October 7, 2026

Last reviewed: October 7, 2026

References:
  1. Agarwal R, et al. Allergic bronchopulmonary aspergillosis: review of literature and proposal of new diagnostic and classification criteria. Clin Exp Allergy. (2013)
  2. Denning DW, et al. The link between fungi and severe asthma: a summary of the evidence. Eur Respir J. (2006)
  3. Zureik M, et al. Sensitisation to airborne moulds and severity of asthma: cross-sectional study from European Community respiratory health survey. BMJ. (2002)
  4. Simon-Nobbe B, et al. The spectrum of fungal allergy. Int Arch Allergy Immunol. (2008)
  5. EAACI guidelines on allergen immunodiagnosis: IgE-mediated allergy to fungal allergens (verify citation). (2020)

This content is for licensed healthcare practitioners only and does not constitute medical advice. Clinical decisions should be based on the full clinical picture and not on any single test result.