On mite allergy in dogs and humans.

allergens. A described inherent difference between both species is the greater presence of endotoxin in D. farinae than in D. pteronyssinus cultures [7] . Overall, several reasons may account for these observed discrepancies between dogs and humans. They include the route of sensitization (ingestion or inhalation), shock organ (mainly skin in dogs and the lung in humans), genetic and immunologic differences and predispositions, allergen load (ingested versus inhaled), contact with intestinal and ectoparasites (much more frequent in dogs) and nutritional/ hygiene habits. Dogs tend to react with a greater frequency to chitinase and chitinase-like allergens, like group 15 and 18 mite allergens. Chitin is the second most abundant polysaccharide in nature. It is found in fungal cell walls, in the exoskeletons of crustaceans and insects and in the microfilarial sheaths of parasitic nematodes. Chitinases are induced during infection with these agents. Chitin coats provide protection for pathogens from harsh conditions inside the host. Chitin accumulation is regulated by the balance of chitin synthase-mediated biosynthesis and degradation by chitinases [8] . Chitinases catalyze the hydrolysis of N-acetylD -glucosamine 1,4 -linkages in chitin polymers. They are essential for the arthropod life cycle by aiding the digestion of the exoskeleton during moulting. Chitinases are also important for arthropod gastrointestinal epithelia, where they are needed for the maintenance of the tissue and the digestion of chitin-containing nutrients, which, for mites, include chitin-coated dung balls [9] . Chitin is an important component of the exoskeleton of arthropods and of the egg shell in nematodes. Therefore, it may be a useful target for drugs against ectoparasitic crustaceans, insects and endoparasitic nematodes. Consequently, the effect of chitin metaDust mites are the leading cause of allergy/asthma in humans. In dogs, sensitization to mite allergens seems to be more prevalent than sensitization to flea allergens. An estimated 30–80% of atopic dogs and cats have positive skin tests to dust mites and/or storage mites. In dogs, mite allergens play an important role in the pathogenesis of atopic dermatitis [1] . Atopic dermatitis may affect 3–15% of the dog population. Immediate skin test reactivity to crude mite extracts is very common in dogs with clinical manifestations of atopic dermatitis. Skin test reactions are much more frequent to D. farinae extracts (18–80%) than to D. pteronyssinus (2–22%) [2] . This occurs even in areas where D. pteronyssinus is more common than D. farinae. Group 15 and 18 allergens of Dermatophagoides spp. are the most important allergens for atopic dogs. Der f 15 (99– 109 kDa) has been shown to bind IgE in almost all atopic dogs [3] and Der f 18 (60 kDa) in 79%, in varying quantities [4] . The binding to Der f 15 is strong, and nearly all sera show specific IgE binding at a similar intensity to a complete D. farinae extract, suggesting that Der f 15 is a major allergen. In contrast, atopic dogs do not seem to recognize Der p 1, Der p 2, Der f 1 or Der f 2. These major allergens in humans are not major allergens in dogs with atopic dermatitis. Several reasons may account for this discrepancy. Key issues remain unexplored in determining the main route of sensitization in dogs as compared with humans. It is accepted that the main route of sensitization in humans is inhalation and, to a minor extent, through ingestion or contact [5] . Although dogs are also exposed to house dust mite allergens indoors, the ingestion route seems relevant as well, since it has been demonstrated that dog food is regularly contaminated with mites, especially storage mites [6] . Furthermore, there is the added peculiarity that dog-specific IgE preferably binds to D. farinae Published online: November 21, 2012