Fossil studies show that mites have been on earth for over 400 million years. This ancient species has been around longer than the dinosaurs! It is estimated that today there may be up to 100 million different species of mites in existence, from the depths of the ocean to the most remote desert1. The house dust mite (HDM), evolved 23 million years ago as a scavenger living in birds nests or similar habitats. Approximately 10,000 years ago this mite found its way into the human environment. It is a close relative of scabies living mainly on fungi and rotting skin scales but as a scavenger it will eat what is available2. The mite's seemingly inefficient digestive system creates up to 20 dung-pellets a day3
. The droppings, which are devoid of moisture and wrapped in a special film, contain scraps of food, debris and powerful enzymes. The enzymes, created by the mite, will continue to break down any remaining food particles; thus ensuring nourishment for the mite later4. In other words they can eat their own droppings up to three times over. The mite's microscopic dung pellets, if disturbed in an unventilated room, can remain suspended in still air for 20 minutes. During this time they can be easily inhaled by unsuspecting people5.
 The house dust mite has eight legs, each with a sucker and hooks. This ensures easy travel on clothing, blankets, soft toys and old furniture to colonise and infest suitable nest sites if the conditions are right6. The conditions needed are warm, dark and damp. Optimal growth for a mite colony occurs at a temperature of 25°C and 75% relative humidity. Below 54% humidity a mite colony will not thrive. Mites are unable to regulate their body temperature, they have no eyes, never drink and have no organised respiratory systems, yet their body weight is up to 80% water. Maturity from egg to adult may take up to 30 days in a life-span of approximately 3 months depending upon living conditions and sex of the mite. Females live longer2,3,7.
High Health Risk Factors of Dermatophagoides spp.
There are 16 known allergens of the house dust mite8. The powerful enzymes of the mite have been recorded by scientists as causing an allergic-like reaction in the absence of true allergic response9. Indeed, the major allergen Der p1 is so invasive it has been found in foetal amniotic fluid at 16-17 week gestation and in the cord blood of some babies at birth. Scientists are investigating the possibility of this phenomenon as a link to allergy10.
Possible nesting sites for the mite include carpets, padded sofas and chairs, soft toys and especially bedding. Modern homes with high temperature, high humidity and lack of ventilation have been shown to be ideal breeding grounds11. In a study in Oxfordshire, a collection of house dust, including bedding, has been found to contain micro-organisms and fungi in abundance as well as colonies of mites in various stages of life12,13. Some of these micro-organisms are known risk factors for disease14,15,16.
Genetically predisposed individuals (atopic-family, history of allergy) are most vulnerable to the mite17,18. A pathway towards sensitisation, or allergy, has recently been demonstrated by doctors in St George's Hospital Medical School. The doctors found that the major allergen Der p1, once inhaled and dissolved, causes the breakdown of the adhesion molecules binding the epithelial cells together leading to permeability of the lung and a breach of its defence system19,20. This phenomenon initiates apoptosis (cell death) leaving cells exposed to the possibility of further invasion by inhaled allergens or other micro-organisms (fungi and bacteria) 21. Potentially dangerous bacterial micro-organisms have been found living in the airways of adults with chronic asthma22. Fungi have been found as viable entities in the mite's droppings 23.
Once in the lung's epithelium the enzymes in the droppings continue to breakdown specific molecules. This may lead to exacerbation of harmful allergic response as the immune system reacts to misguided signals resulting in an over production of non-specific IgE antibodies24. It is interesting to note that the same over-production of non-specific IgE is a ploy used by certain parasites to avoid detection by the immune system25.
The immune response to this invasion has been well studied and is considered by scientists to be a cause of allergic asthma and the exacerbation of symptoms7. We must consider the house dust mite Dermatophagoides, a high risk determinant in allergic asthma and related diseases. These diseases are allergic eczema, allergic rhinitis and conjunctivitis; therefore the mite is unacceptable in the social environment of the vulnerable26,27.
Nell Nockles © Jan 2001
Up to 85% of asthmatics are allergic to the house dust mite.
National Asthma Campaign
"Evidence suggests that allergen-specific helper T (th) cell memory, which underlines expression of atopy in adulthood, is programmed during very early life. Predisposition to primary allergic sensitization per se may be related to the function of discrete gene(s) that regulate responses to microbial stimuli, particularly during early infancy, whereas a second set of genes may control tissue expression of atopic disease."
Patrick G Holt et al. Primary Sensitization to Inhaled Allergens; Am J Respir. Crit. Care Med. 2000; 162 : 591-594 References: 1. D.E. Walter. Mites: Ecology, Evolution and Behavior.1999, ISBN 08199 375
2. Colloff. M. Differences between the allergen repertoires of house dust mites and stored products mites; Clin.Immunol. 1993; 16:2
3. Arlian L. Biology and Ecology of House Dust Mite, Dermatophagoides spp. and Euroglyphus spp.; Immun. and Aller. Clin of NAm.;Aug 1989: 339-355.
4. Oh H et al. Ultrastructure of house dust mite, Dermatophagoides farinae and D.pteronyssinus. Jpn. J. Sanit. Zool., 1986; 37 No 3
5.Who's been sleeping in your pillow? (Video) University of Southampton, Teaching and Support Media Services.
6. Mollet JA, Robinson. Dispersal of American house dust mites (acari : pyroglyphidae) in a residence. J. Medical Ent. 1996; 33:
No.5, 844-847
7. Chapman M D. Environmental Allergen Monitoring and Control ,Allergy: 1998; 53: 48-53
8. Thomas W R and W Smith. Towards defining the full spectrum of important house dust mite allergens. Clin.& Exp, Allergy
1999; 29; 1583-1587
9. Machado D.C. et al. Potential allergens stimulate the release of mediators of the allergic response from cells of the mast cell
lineage in the absence of sensitization with antigen specific IgE. Eur. J Immunol. 1996; 26; 2972-2980
10. Warner J O et al. Detection of House-Dust Mite Allergen in amniotic Fluid and Umbilial-Cord Blood, Lancet, 2000; 356:
Issue 9245: 1900 1903
11. Platts-Mills T A E, J A Woodfolk. Dust Mites and Asthma. Allergy and Asthma; 1997; 52 A. B. Kay Editor
12. D B Hay et al. How relevant are house dust mite fungal interactions in laboratory culture to the natural dust system? Exp. &
Applied Acar. 1992; 16: 37-47.
13. Hay David B. Ecology of the House Dust Mite, 1991 Linacre College, Oxford University (unpublished, British Library,
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14. Pepys J. Hypersensitivity disease of the lung due to fungi and other organic dust: 1969; Monogr. Allergy: 4: 44.
15. Banerjee B et al. Immunological characterization of Asp f2, a major allergen from Aspergillus fumigatus associated with
allergic bronchopulmonary aspergillosis. Infect. Immunol. 1998: Nov 66 (ll): 5175-5182
16. Eaton T.et al. Allergic bronochopulmonary aspergillosis in the asthma clinic. Chest; July 2000, 66.
17. Holgate Stephen. The cellular and mediator basis of asthma in relation to natural history. The Lancet. 1997; 350: Sup. 5-9
18. Young R P et al. House dust mite sensitivity: interaction of genetics and allergen dosage. Clin.& Exp. Allergy, 1992; 22:
205-211
19. Robinson et al. Class specific inhibition of house dust mite proteinases which cleave cell adhesion, induce cell death and which
increase the permeability of the lung epithelium. Brit. J. Pharma , 1998; 124: 1048-1059.
20. Wan H.et al. Der p1 facilitates transepithelial allergen delivery by disruption of tight junctions. J Clin. Invest: July 1999; 104: 1
21. Holt P et al. A contiguous network of dendritic antigen-presenting cells within the respiratory epithelium. Int.Arch. Allergy App.
Immunol. 1990; 91: 155-159
22. Kraft M et al. Detection of Mycoplasma pneumoniae in the airways of adults with chronic asthma. Am. J Respir. Crit. Care
Med. 1998; 158: 998 -1001
23. Lustgraaf.B v d. Ecological relationships between xerophilic fungi and house dust mites (Acarida: Pyroglyphidae).
Oecologia: (Berl.) 1978; 33: 351-359
24. Hewitt CRA. Brown AP, Hart BJ & Pritchard DI. A major house dust mite allergen disrupts the immunoglobulin E network by
selectively cleaving CD23: innate protection by antiproteases', J. Exp Med. 1995, 182: 1537-1544
25. Pritchard DI. Immunity to helminths: is too much IgE parasite- rather than host protective? Parasite Immunology, 1993: 15: 5-9
26. Bruijnzeel-Koomen, Madde & Kapp. Atopic Dermatitis,1997. Allergy and Asthma: Chapter 101, A B. Kay Editor
27. Olsson S. & Van Hage-Hamsten. Allergens from house dust and storage mites, similarities and differences with emphasis on the
storage mite, Lepidoglyphus destructor. Clin & Exp Allergy 2000; 30: 912-919.
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