An active transmissible virus exists in the blood of measles patients during the eruptive stage of the disease. This virus produces in rabbits after intravenous injection a specific reaction analogous in all essential features to that of the human infection. Following a definite incubation period of from 2 to 5 days the animals infected show pyrexial, leucocytic, and cutaneous alterations. Fully 90 per cent of such inoculated rabbits react in a remarkable manner. The earliest constant symptom of the infection is a rise in temperature, which on the average occurs 4 days after inoculation and most probably marks the end of the incubation period. Concomitantly with this temperature rise there is a diminution in the total number of circulating leucocytes. This decrease in the number of white blood elements may be relative or may appear in the form of a well defined leucopenia. The most striking objective signs are the coryza, conjunctival injection, enanthemata, and exanthemata. The mucous membrane lesions are similar in their physical appearance to the so called Koplik spots seen in man. They occur on the buccal side of the oral cavity ranging in number from two to eight discrete hemorrhagic areas with paler centers. They appear as a rule coincidently with the temperature rise or shortly thereafter. The exanthematous lesions though occurring only in about 40 per cent of the infected animals complete the clinical syndrome in this particular experimental host. The rash may appear as early as the 3rd and as late as the 7th day after inoculation. In its early stage it is of the macular variety, appearing as a diffuse eruption which later develops into a more papular type of lesion. At this time the cutaneous manifestations appear as slightly raised, flattened, purplish red, discrete areas in the skin of the face, neck, chest, and abdomen.

Repeated passage of the virus of measles through the rabbit seems to increase its virulence. A number of animals infected with such passage virus succumb in the fourth and subsequent generations, undoubtedly as the direct result of the action of the specific excitant, as in none of the animals was there cultural evidence of secondary intercurrent infection. In the animals dying presumably as a result of the specific virus grave nephritic changes were evident. It is a noteworthy fact that the pneumonia so common in fatal cases of human measles was not evident in any of the experimental animals. We believe this to be of considerable significance, especially in elucidating the direct etiological factor of the fatal pneumonias so often present in human measles cases. Apparently such infections in man can be explained purely on the basis of the destruction of normal defense barriers by the specific excitant of the infectious disease, and the lack of host resistance to the ordinary pyogenic microorganism.

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