35 



McGinnis, 1959; Genest, I960). Papular, ves i culo-papu 1 ar , urticarial, 

 or a combination of these primary lesions will develop at the bite site, 

 the extent and severity of which is thought to be due to an allergic 

 mechanism (Frazier, 1969). Contact with living mites may not be 

 necessary to produce symptoms as both body parts and excretory products 

 of the mites have inherent toxic properties (Chandler, 19^9). 



Several non-poultry-related cases of northern fowl mite dermatitis 

 have resulted from mites entering buildings via window air conditioners 

 (Cahn and Shechter, 1958; McGinnis, 1959; Genest, I960. In all of the 

 cases, abandoned birds' nests were found in or near air conditioner 

 air intakes. Affected persons were advised to remove mites by bathing 

 after which all symptomology disappeared in 2k hours. Fumigation of the 

 buildings and air conditioners, and removal of birds' nests from the 

 air conditioners eliminated the mite populations. 

 Disease transmission 



When it was found that the chicken mite, Dermonyssus gallinae , 

 could transmit the virus of St. Louis encephalitis directly and trans- 

 ovarily (Smith et al., 19^5, 19^6, 19^7), the question arose as to 

 whether or not the northern fowl mite possessed the same capability. 

 Collections of northern fowl mites from wild birds yielded mixtures of 

 viruses containing not only St. Louis encephalitis virus, but also the 

 virus of western equine encephalitis (Reeves et al., 19^*7; Hammon et a!., 

 19^3; Bisseru, 1967). The importance of the mite as a vector or reser- 

 voir for either virus later proved questionable (Reeves et al., 1955). 

 Subsequent studies have shown the northern fowl mite to be a very poor 

 transmittor of western equine encephalitis (Chamberlain and S i kes , 1955) 



