That hay fever is a form of hypersensibility to pollen proteins is conceded by everyone. The mechanism of this form of hypersensibility, likewise the phenomenon of its desensitization with pollen extract (phylactically or prophylactically administered) are still mooted questions.
Cooke, Flood, Coca's (1) definition of hay fever as a “clinical symptomatic expression of local hypersensitiveness” cannot hold. The skin and conjunctional reactions in hay fever subjects are certainly extranasal. Sewall's (2) criticism that no local manifestation of hypersensibility can occur without the background of a general hypersensibility is amply justified.
Up to now animal experiments to produce clinical hay fever have not been successful. Koessler (3) reports passive anaphylaxis in guinea-pigs. Cooke, Flood and Coca (4) and myself2 have failed to produce active or passive anaphylaxis with pollen extracts. My experiments to produce a passive anaphylaxis were made with patients' blood out of season. It is possible that Koessler's experiments were made in season.
Read before the annual meeting of the American Association of Immunologists, Philadelphia, March 29, 1918.