M207-IgG Aspergillus niger

Optimal Result: 0 - 1.9 ug/ml.

Aspergillus species are ubiquitous environmental molds that grow on organic matter and aerosolized conidia (conidia is a spore produced by various fungi at the tip of a specialized hypha).

Aspergillus is a genus of molds that includes several hundred species that grow in nutrient-depleted environments.

Humans inhale hundreds of conidia per day without adverse consequences, except for a small minority of people for whom infection with Aspergillus causes significant morbidity (=the condition of suffering from a disease or medical condition). 

The clinical manifestations of aspergillosis are determined by the host immune response to exposure with the spectrum ranging from a simple allergic response to local lung disease with mycelial balls to catastrophic systemic Aspergillus infection.

Where can they be found?

Aspergillus molds are saprophytes that thrive on decaying organic matter. They are often found as contaminants of starchy foods and other carbon-rich substrates. They are commonly found in soil and marine habitats as well as indoor environments and in drinking water.

Of the hundred species identified, only a few have been associated with pathology in humans.

Aspergillus molds continuously disseminate spores (conidia) into the environment.

How are humans exposed to Aspergillus?

Humans are constantly exposed to airborne Aspergillus spores which, once inhaled, can access the most distal airways of the lungs due to their size and durability.

What happens in the body?

In immunocompetent individuals with healthy lungs, inhaled conidia are eliminated by the neutrophils and macrophages of the innate immune system and do not lead to disease.

Illness only develops in a small proportion of patients with altered immune systems or underlying lung pathology.

Non-invasive forms of Aspergillus-induced lung disease include Allergic Bronchopulmonary Aspergillosis (ABPA) and Chronic Pulmonary Aspergillosis (CPA).

In severely immunocompromised individuals, Aspergillus infection of the respiratory system can spread to other organs in a condition referred to as Invasive Pulmonary Aspergillosis (IPA).

What does it mean if your M207-IgG Aspergillus niger result is too high?

Precipitating IgG antibodies are often present in serum of patients with hypersensitivity pneumonitis (HP) due to exposure to enviromental antigens. The serum precipitin test assists in the diagnosis of HP.

Hypersensitivity pneumonitis (HP), also referred to as extrinsic allergic alveolitis (EAA), is an inflammatory lung disease resulting from the inhalation and subsequent sensitization to a wide variety of inhaled organic dusts. HP is not mediated by IgE. It is associated with progressive pulmonary disability, irreversible lung damage, and mortality in some occupational settings.

Patients often present with intermittent chills, fever, cough, and shortness of breath that begin four to eight hours after exposure to the offending dust.

Aspergillus mold can be found in soil, foods, fresh water, and other natural sources including compost, barley, tobacco, and Esparto grass dust (stucco). These organisms grow well in decaying organic material at temperatures often attained during decomposition. Aspergillus mold can also grow on ceiling and walls where water damage has occurred.

No single laboratory test is diagnostic for hypersensitivity pneumonitis. Diagnosis is based on a complete environmental history supported by result of chest x-ray, spirometry, and in vitro immunologic tests. Identification of the causative agent is important to allow avoidance of exposure.

These antibodies may also be present in individuals not afflicted with HP. The presence of antibodies to the offending dust or antigen confirms exposure but is not diagnostic of HP, however, upon repeated or prolonged exposures, high levels of precipitating IgG antibodies are typically observed.

Aspergillus infection can also result in allergic bronchopulmonary aspergillosis (ABPA), a condition where airway colonization of individuals with asthma or cystic fibrosis results in increased inflammation and destruction of bronchial structural elements.

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