726 Diseases of the Genital Organs 



from the exterior. The bacteria causing death and macera- 

 tion are apparently identical, and I consider it logical to as- 

 sume that, as a rule, the destiny of an embryonic cadaver is 

 largely fixed by the nature of the infection causing its death. 

 In swine there are plenty of bacteria incarcerated within the 

 gravid uterus. They regularly cause necrosis with varying 

 degrees of maceration or desiccation of each fetal sac at its 

 poles. The same bacteria logically have power to cause solu- 

 tion of a necrotic embryo. So in the ewe the uterus regu- 

 larly contains necrosis-producing bacteria which produce 

 necrosis of the tips of the embryonic sac, and it would be 

 very difficult to understand why the same bacteria may not 

 cause maceration of a necrotic embryo. As the evidence 

 now stands, it appears that the death of the fetus and its 

 maceration are generally referable to the activities 

 of the same organism or group of organisms. As in 

 cattle, so in sheep, the infection already exists in the cervix 

 or uterus at the moment of coitus, or is introduced as a 

 component part of the semen during coitus. A little later 

 the cervical canal, if healthy, is sealed and invasion thereby 

 inhibited. 



In the outbreak of genital disease of ewes studied by Car- 

 penter and me, the history of the herd points strongly to 

 the rams as the essential source of the infections and to 

 coitus as the date of invasion. As related, a Tunis ram 

 broke into the inclosure and copulated successfully with 

 some ewes. These remained apparently healthy and pro- 

 duced vigorous lambs. When the Shropshire rams were 

 placed with the ewes, the disease began with those which 

 were still non-pregnant. Those ewes bred to the Shropshire 

 rams began aborting eight or ten weeks before the Tunis 

 lambs were born. There was abundant time for a contagion 

 to spread rapidly by ordinary contact from an aborting ewe 

 to a healthy pregnant one, but this failed to occur. The out- 

 break also suggests that the infection, as a highly destruc- 

 tive force, developed in what may be termed a spontaneous 

 manner. That is, the infection existed during the prior 

 breeding season in low virulence, depressing the reproduc- 



