On the genetic basis of equine allergic diseases: II. Insect bite dermal hypersensitivity

Summary The horses studied were of the Swiss Warmblood breed and most were ELA‐typed to assess a possible association of dermal hypersensitivy to insect bites with the major histocompatibility complex. Firstly, the occurrence of the condition was examined in 304 half‐siblings sired by six stallions (A to F). Fourteen cases of dermal hypersensitivity were recognized and all were in the 153 offspring of Stallions C, E and F. Most animals of this group were also investigated for chronic hypersensitivity bronchitis: none of the sires displayed clinical signs of dermal hypersensitivity, but Stallions D, E and F were affected by chronic bronchitis. Among the animals investigated for both conditions only one horse showed coincidence of the two diseases as can be expected when the diseases are not correlated. The frequency of manifest dermal hypersensitivity and/or chronic hypersensitivity bronchitis varied in the half‐sibling groups of individual sires. These findings suggest that the allergic conditions are independent entities. Secondly, the occurrence of dermal hypersensitivity was studied in three generations of horses at a stud at which Stallion C had exerted a particularly strong influence. A total of 302 animals, all born and raised at this stud, were surveyed over a period of 12 years. The descendants of Stallion C showed a significantly higher incidence (P<0.01) of dermal hypersensitivity (two daughters out of 19; eight second generation offspring out of 103; one third generation offspring out of 85) than did the controls of the same age classes but unrelated to Stallion C at the same stud (0 out of 95). In this group the predisposition was not associated with the ELA antigens of Stallion C. Thirdly, the pedigrees and the ELA‐haplotypes of eight affected half‐siblings by Stallion F were studied more closely. The predisposition in these horses was associated with the paternal haplotype A3,W23. Four multiple‐case families were studied separately. One sire (G) produced nine affected offspring out of 22 out of four clinically healthy dams. The dams, however, were descendants from Stallion C and they produced four unaffected foals by other sires. The paternal ELA‐haplotype, A15,W23, segregated (with one exception) coupled with the predisposition to the affection. Stallion G and the dams were born, raised and kept at the same stud as their offspring. Based on these findings, we suggest that certain animals can transfer hereditary susceptibility for dermal hypersensitivity due to insect bites to their offspring. In different families the ELA class II specificity W23 segregated with the susceptibility. A gene or genes of the major histocompatibility complex appeared to play a role in some families as well as a gene or genes outside the MHC. Therefore we suggest that insect bite dermal hypersensitivity is a multifactorial disease, including hereditary and environmental factors in its pathogenesis.