Mary B. Kirkbride
Oklahoma State Department of Health
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Featured researches published by Mary B. Kirkbride.
Experimental Biology and Medicine | 1924
Mary B. Kirkbride; Mary W. Wheeler
With toxins prepared in this laboratory from a strain of a scarlet fever streptococcus received from Doctor Dochez, no skin reactions were induced in rats, mice, guinea-pigs, kittens, chickens, pigeons, monkeys, sheep or a calf. Questionable reactions were obtained in two young pigs with undiluted toxin and also in four rabbits out of eighteen, the remaining fourteen giving no reactions. Definite skin reactions, however, have been induced in white goats. All fourteen goats tested gave reactions to the toxin, but individual goats appeared to vary in susceptibility. With ten, definite reactions were obtained with 0.2 cc. of a 1:500 dilution of a toxin which gives a reaction in a 1:1000 dilution in a susceptible human being. Four other goats gave reactions to lower dilutions, varying from 1:50 to 1:250. The reactions in goats reached a maximum in 18 to 24 hours and at this stage were usually quite similar to those observed in human beings. In the more susceptible goats according to the potency of the material tested, these reactions varied in degree from slightly reddish areas, 1.5-2 cm. in diameter with no swelling, to large reddish areas from 3-5 cm. in diameter with considerable swelling. All reactions, even the most severe, faded in 48 to 72 hours. With some goats, the darker color of the skin made the readings difficult. Toxin heated for one hour at 100° C. and uninoculated broth gave no reaction nor was any obtained with toxin neutralized with scarlet fever antitoxic serum, but normal horse serum, even in low dilutions did not neutralize the toxin. Toxins from another strain of streptococcus from scarlet fever, which gave no reaction in susceptible human beings in a 1:250 dilution, also induced no reaction in goats, in the same dilution.
Experimental Biology and Medicine | 1915
Mary B. Kirkbride
For the purpose of ascertaining to what extent conditions of hypersusceptibility determine the character of pneumococcus lesions of the lung, series of experiments were made with a moderately virulent strain, and with an extremely virulent strain in its virulent state and after artificial attenuation. Rabbits were inoculated intravenously for purposes of sensitization with .1-15 c.c. pneumococcus filtrates or dead cells and then after two weeks injected tracheally with 1. c.c. live cultures. The animals surviving 48 hours were killed. Microscopic sections were made of all lungs. In these experiments with attempted active sensitization none of the animals developed symptoms resembling anaphylactic shock nor was the lung involvement definitely increased in any series of previously treated rabbits. Tracheal injection of the moderately virulent organisms, however, caused marked lesions in both sensitized and unsensitized control rabbits. In experiments with attempted passive sensitization, mixtures of 1 c.c. virulent or attenuated live cultures and .1 c.c. or .5 c.c. sera from normal or immunized rabbits when injected tracheally failed to incite uniformly extensive lesions in any series of animals though the proportion developing diffuse involvement was greater than in the previous experiments with active sensitization. Sudden paroxysms, similar to those of fatal anaphylactic shock were observed about twenty-four hours after tracheal injection in practically all the animals of two or three experiments. But these paroxysms were not associated with extensive lesions of the lung because in a number of the rabbits no characteristic exudative pneumonias were found, although the lungs were almost invariably deeply conjested. While a hypersensitive state probably takes some part in the inception of the infection, these experiments indicate that the subsequent exudative lobar involvement is essentially a progressive and cumulative process.
Journal of Immunology | 1927
Mary B. Kirkbride; Mary W. Wheeler
Journal of Immunology | 1926
Mary B. Kirkbride; Mary W. Wheeler
JAMA | 1926
Augustus B. Wadsworth; Mary B. Kirkbride; Mary W. Wheeler
The Journal of Infectious Diseases | 1930
Mary B. Kirkbride; Mary W. Wheeler; Cutler D. West
American Journal of Epidemiology | 1936
Mary B. Kirkbride; Jessie L. Hendry; Philip P. Murdick
Journal of Immunology | 1928
Mary B. Kirkbride; Mary W. Wheeler; Jessie L. Hendry
American Journal of Epidemiology | 1934
Mary B. Kirkbride; Sophia M. Cohen
JAMA | 1927
Mary B. Kirkbride; Mary W. Wheeler