Dust mite allergy is an allergic condition that occurs as a reaction to the dust mite allergens that commonly live in household dust. It is also known as house dust allergy. It is sensitization and an allergic reaction to the droppings of the dust mites. The droppings are an indoor aeroallergen, which on inhalation triggers the allergic reaction. The prevalence of atopic diseases like allergic rhinitis and asthma with house dust mite being the allergen has been increasing. House dust allergy was first identified as an allergen around 1920. In 1967, Voorhorst et al. identified Dermatophagoides pteronyssinus as the causative allergen for house dust allergy. The first mite allergen identified was the cysteine protease Dermatophagoides pteronyssinus allergen I, or Der p 1 in 1980, followed by Der p 2, and homologous Dermatophagoides farinae 1 and 2.
The house dust mite (HDM or DM) is a predominant source of indoor aeroallergens. Some of the allergic diseases that have been associated with the HDM are allergic rhinoconjunctivitis, allergic asthma, and atopic eczema. The best treatment strategy for allergic rhinitis consists of allergen avoidance first, in junction with pharmacotherapy and allergen immunotherapy (AIT). The appropriate pharmacotherapy consists of antihistamines, leukotriene receptor antagonists, and inhaled or intranasal corticosteroids (ICS). All these treatments are effective and safe, but unfortunately, haven't proved to change the course of HDM related allergic diseases.
Dust mite allergy develops in childhood or adolescence, with the majority of symptoms manifesting before age 20. The dust mite's gut contains peptidase 1, which is one of the potent digestive enzymes that persist in their fecal matter and is the major inducer of the allergy. Peptidase 1 exhibits cysteine protease activity. The variants of the allergen include Der p 1 of the European house dust mite, Dermatophagoides pteronyssinus, Der f 1 of the American house dust mite Dermatophagoides farinae, Eur m 1 of the Mayne's house dust mite Euroglyphus maynei.
These allergens are found in the fecal matter of the mites. Their fecal particles are around 20 pellets per day, surrounded by a peritrophic membrane, are about the size of a pollen grain (10-35 mcg diameter), thus can be easily inhaled. The mite's exoskeleton can also contribute to allergic reactions. These allergens on inhalation cause a sensitization reaction, through epithelial leakage into the respiratory system by cleavage of the tight junctions in between the epithelial cells. This leads to increased epithelial permeability, allowing the movement of house dust mite allergens to dendritic antigen-presenting cells.
The house dust mites do not burrow under the skin and are not parasitic. Dust mites are microscopic bugs about 0.4 millimeters in length, and invisible to the naked eye. They are known to feed on the desquamated dead skin cells of humans and pets. They prefer a warm and moist environment of 70 degrees F and 70 percent humidity. Therefore, bedding, linens, carpeting, furniture linens that trap the moisture and provide the most favorable environment for the dust mites to flourish. House dust mites belong to the family Pyroglyphidae, primarily consisting of Dermatophagoides pteronyssinus, Dermatophagoides farinae, and Euroglyphus maynei.
These species constitute 80 to 90 percent of the house dust mites. The most important house dust mite is Dermatophagoides pteronyssinus. In drier areas, D. farinae is commonly found. In tropical and subtropical areas, the storage mite, that is, glycyphagid mite Blomia tropicalis (storage mite), which coexists with D. pteronyssinus, is a major source of allergen. Gylcyphagus and Lepidoglyphus may be found in rural homes.
Dust mite allergy is a prevalent form of allergy. It affects 20 million people across The United States of America. Being ubiquitous, house dust mites are found all across the world. Around 84 percent of USA households have been detected with the presence of house dust mites. In industrialized areas, like Germany, 1 out of every four people are affected by dust mite allergy. Combined, allergic rhinitis (AR) and asthma affect up to 800 million people worldwide, according to the World Health Organization (WHO).
Up to two-thirds of children with asthma and up to 1/2 of adults who have asthma also suffer from allergies. Of these patients who suffer from asthma and allergies, about 40%-85% of them are allergic to the HDM, this trend is observed all over America, Europe, south-east Asia, and Australia. Around 5 to 30 percent of the general population show house dust mite sensitivity to skin test reactivity.
Ninety-seven percent of people with dust mite allergy are sensitized to the allergen Der p 1. Der p 11 has been most frequently associated with atopic dermatitis. 70 percent of the people with dust mite allergy have been recently found to be sensitized to Der p 23 allergen. To date, 24 allergens associated with house dust mite have been identified.
IgE mediated sensitization is responsible for the pathogenesis of dust mite allergy. This a Type 1 hypersensitivity reaction in which the CD4 + and T helper cells stimulate the B cells to produce IgE antibodies specific to the antigen, which is the house dust mite allergen. The IgE binds onto the FceRI receptors on mast cells and blood basophil cells. The mast cells and basophil cells now get sensitized to the allergen-specific IgE antibodies. On subsequent exposure to the same allergens, there is crosslinking of the bound IgE sensitized cells, leading to their degranulation. The inflammatory mediators are released, causing the clinical manifestation of the dust mite allergy. Sensitizations to the dust mite allergens occur quite early in life and lead to a progression from allergic rhinitis to asthma. This is known as the allergic march. It is a significant risk factor for the development of asthma.
When the house dust mite fecal pellets are inhaled, they contact the airway epithelium and become hydrated and discharge their allergenic contents onto a mucosal barrier. For interaction with dendritic antigen-presenting cells, potential allergens must cross this protective epithelium. The tight junctions are the route for their entry. The allergens, predominantly, Der p 1 disrupt these tight junctions by either of the following two processes:
Two major groups of allergens from mites of the genus Dermatophagoides have been identified.
The common house dust mites and their allergens are listed as follows:
Der p 1, being the major cause of dust mite allergy, is responsible for triggering the IgE binding levels of 80 to 90 percent. It targets CD23 and CD25, which cleaves these receptors from the surface of the active B and T cells, respectively, triggering the further release of IgE. Der p 1 catalytically inactivates the alpha antitrypsin, thus making the lower respiratory tract vulnerable to damage by proteinases, promoting airway inflammation and asthma. There is a quantitative relationship between house dust mite allergen exposure and the development of sensitization and, consequently, asthma. Studies have shown that 2 micrograms of Der p 1 per one gram of house dust, that is 100 house dust mites per one gram house dust, potentially lead to sensitization and development of asthma. 10 micrograms of Der p 1 per one gram of house dust that is 500 house dust mites per one gram of house dust lead to acute asthma in individuals who are allergic to house dust mites.
Asthma usually develops as a result of combined environmental and genetic factors. Dust mite allergy leads to the development of atopic asthma, which is a predisposition to the development of hypersensitivity Type 1 reactions.
House dust mite allergy plays a role in the development or exacerbation of atopic dermatitis. The house dust mite allergens activate the pattern activation receptors that include toll-like receptor 1, toll-like receptor 6, and toll-like receptor 9 and nucleotide-binding oligomerization domain 2. This leads to a release of innate proallergic cytokines, namely interleukin-25 and interleukin-33, in epidermal keratinocytes, causing the activation of the innate immune system in the keratinocytes.
Dust mite allergy leads to perennial allergic rhinitis; that is, the symptoms of dust mite allergies occur throughout the year. Symptoms are more likely to occur while sleeping at night and early in the morning on waking up because the dust mites inhabit the pillows, bedcovers, mattresses, and blankets. Common dust mite allergy symptoms include:
If dust mite allergy triggers asthma, the following may also present:
The following risk factors predispose an individual to develop dust mite allergy:
The development of allergies to certain foods like shellfish or mollusks can also occur as a result of cross-reactivity.
Present symptoms, past medical history of allergic manifestations, home environment, and circumstances prompt the clinician to carry out further tests for the diagnosis of dust mite allergy.
In vivo techniques
In vitro techniques
Diagnosis of asthma. Over time dust mite allergy culminates into asthma or may lead to exacerbation of asthma.
The quantification of dust mite allergens from the house can be done through immunochemical assays, namely, RAST inhibition technique, sandwich radio or enzyme immunoassays, or MAb assays. However, their use is limited due to the requirement of trained laboratory personal and sophisticated equipment.
The most effective intervention for dust mite allergy is primary prevention, that is allergen avoidance. This can be achieved by reducing the levels of mite allergens.
Measures for allergen avoidance in the bedroom
Measures for allergen avoidance in the whole house
Over the counter medications. These provide symptomatic relief to the allergic manifestations.
Nonpharmacological measures. These are safe, effective, and convenient modalities to help manage symptoms of dust mite allergy. Their use as an adjunctive helps to reduce the use of pharmacological drugs.
HDM allergen immunotherapy (AIT). This is also known as desensitization. AIT has been in use for achieving clinical tolerance to allergens through the administration of allergen extracts to the sensitized individual. It is effective in the treatment of Type I allergic diseases induced by IgE in terms of alleviating the clinical manifestations of allergic rhinitis and asthma, reducing the use of symptom-relieving medication, and improving the quality of life. It provides an effective improvement in clinical symptoms, reduces the need for rescue medications, improves lung function, and brings about intrinsic disease-modifying effects such that the allergic inception of asthma and new sensitizations can be completely or partially abrogated. The effects persist for years after therapy discontinuation. The following forms of immunotherapy are available:
Treatment of asthma. It depends on the severity of asthma. Short-term relief is provided through short-acting beta-agonists (SABA). The long term relief is provided by anticholinergics, long-acting beta-agonists (LABA), and low dose inhaled corticosteroids. Oral corticosteroids are used in acute exacerbations of asthma. Leukotriene antagonists and mast cell stabilizers may be useful.
Other than dust mites, house dust allergy can be caused by the following allergen sources:
Dust mite allergy can be confused with non-allergic forms of rhinitis. These include the following:
Minimizing or avoiding the dust mite allergens leads to fewer allergic reactions. However, house dust mite allergy leads to a decreased quality of life in the long run. This can be explained by the following:
The cost-benefit analysis demonstrates that immunotherapy is more cost-effective in the long term as compared with symptomatic treatment.
Persistent exposure to dust mite allergens for a sensitized individual lead to the following complications:
Education involving the patient, their families, and the public, in general, is necessary to ensure the best patient outcomes. The potential severity of dust mite allergy is often underestimated, leading to failure to seek medical therapy. The annual direct medical costs due to dust mite allergy might be substantial, however loss of work productivity leads to higher indirect costs, mainly due to asthmatic symptoms. It is a frequent cause of increased office visits. Handouts, internet sources, and media can help to spread awareness regarding the potential sources of dust mite allergens and the interventions that can be done for allergen avoidance. Proper education on the technique of using nasal sprays and sublingual immunotherapy must be emphasized.
Dust mite allergy is a frequently underdiagnosed, misdiagnosed, and mistreated condition. It leads to detrimental effects on health and life quality as well as increased societal costs. The primary responsibility of diagnosing the condition, educating the patient and their family, management of symptoms to achieve an improved quality of life lies in the hands of primary clinicians. It is vital to consult the interprofessional team of immunologists, otolaryngologists, pulmonologists, primary clinicians, and the patients themselves. Nurses and pharmacists play a significant role in the education of the public as well as ensuring long term benefits to the patients and their families.
The social worker helps to assess the house to look for allergen sources and provides suggestions and resources that can help to remove the allergens. With the vast array of in-vivo and in-vitro diagnostic tests available for dust mite allergy, the role of the laboratory and the laboratory personnel cannot be underestimated. The outcome of dust mite allergy depends on the ability to identify dust mites as the source of the allergic manifestations. However, to improve outcomes, prompt consultation with an interprofessional group of specialists combined with the individual's self-motivation is recommended.
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