_Infection_ is without doubt the greatest single factor capable of producing functional and anatomic changes resulting in varying degrees of impotency and sterility. The changes produced range from the addition of the toxic products of bacterial growth to the seminal fluid, to the complete destruction of the parenchymatous tissue of one or more of the contributing sexual glands. Anatomic changes are by no means essential to the production of lowered fertility. As has been previously stated, the work on veal calves indicates that the genital organs of young bulls are normally free from bacteria. Likewise in normal adult animals, the bacterial content of the genital organs is as a rule low or negative. It is possible that a certain flora is normal for the tract at sexual maturity, as in several other organs of the body, but under the strain of sexual excess, defective diet, or other weakening influences, these organisms may become pathogenic. Streptococci and staphylococci have at times been found in apparently normal parts of the body, and at other times they are found associated with severe pathological lesions in the genital tract. The degree of pathogenicity is of course difficult to determine, except as we find the bacteria associated with abnormal conditions. Carpenter (9), however, injected streptococci into the genital tracts of female calves and produced lesions resembling very closely those from which the organisms had been isolated in adult sterile animals. Personally, I am inclined to believe that the genital organs normally are free from bacteria, or if any are there they are better able to multiply under the strain of devitalization of the tissues. Bacterial invasion, however, does take place quite frequently, but the paths of entrance of the organisms are somewhat problematical. Hematogenous origin is always possible, though it is rather difficult to definitely implicate this mode of entrance. The urethra is perhaps the easiest and most common path for the entrance of bacteria, though even here it is not possible to make definite assertions. Contiguous spread of infection from neighboring structures is very probable in some cases, particularly in pelvic peritonitis. The bacteriological results hardly bear out the theory of Williams that the organisms lie dormant in the genitalia of the animals until the advent of sexual maturity, at which time they acquire pathogenic powers. On the other hand, his clinical observations seem to indicate that this may be possible. Calves suffering from “calf infections” frequently do harbor organisms in their genital organs, but whether or not they persist there till sexual maturity is a matter of conjecture. The most logical theory seems to be that animals from herds in which genital infections are very severe, or those that have had severe attacks of scours or pneumonia, are more susceptible to those infections, due to the early lowering of their vitality.