Part 6

Excessive sexual use, within certain limits, probably has not, in itself, any material permanent effect upon the reproductive capacity. The frequency with which bulls used to excess break down sexually, is probably due to the devitalizing effect upon the tissues of the genital organs, this opening the way to bacterial invasion and other destructive influences. Over-use is probably not dangerous, unless continued over long periods, but at the same time it offers greater opportunity for infection to be introduced into the body from intercourse with large numbers of females. Lloyd-Jones and Hays (47) carried on very interesting experiments on the influence of excessive sexual activity of male rabbits on the properties of the semen. Their plan was to mate male rabbits in quick succession, and study the character of the semen on the first service, and every fifth service thereafter. The safe limit was twenty services in three hours. As would be expected, the volume of the semen, after the first few services, became gradually reduced in amount. “In rapidly successive services, the semen becomes less viscous and tends to lose its characteristic milky appearance until at the twentieth service, when the fluid is thin and watery.” It seemed as though there was a well marked reduction in the number of spermatozoa per cubic centimeter in the advanced services. Successive copulations also resulted in a marked decrease in the number of motile spermatozoa, together with a shorter duration of perceptible vitality. The certainty of producing impregnation at the same time became less and less. “This reduction in the per cent of effective matings when the male is sexually overworked is recognized by those engaged in animal breeding as one of the most noticeable and universal concomitants of heavy sexual service.”

In another paper, these same authors studied the effect of sexual excess upon the character of the offspring. In part, they conclude: “By no means thus far used has any inferiority of progeny from the heavy sexual service been discovered. They are fully equal if not superior to progeny from very light service of male.”

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. One bull in the department herd certainly had a severe ordeal as a calf, but as a mature bull he was highly fertile. Moderate sexual use and proper sexual hygiene probably had much to do with this. In the bull, infection of some part of the genitals, during some period of life, is very constant, however, whether or not it is productive of observable changes in his breeding efficiency. The finding of the fine connective tissue strands and tufts on the serous surface of the tail of the epididymis of practically all bulls examined, both sterile and fertile, indicates past or present infection of the scrotal sac. The vesicles and tail of the epididymis are, as stated previously, the most commonly invaded tissues of the tract. The testes are less frequently involved.

While it is difficult to obtain irreproachable proof that the bull is a disseminator of genital infections, the findings of clinicians quite clearly indicate that this is true, and laboratory methods tend to support this assumption. Williams believes that not only may the bull infect the female with organisms which interfere with the given conception, but that he often implants there organisms which interfere with future pregnancies, and even with the life of the individual in some cases. The high abortion and sterility rate following the use of certain sires, and the appearance of characteristic infections after service to certain bulls, clearly indicate that in all probability the bull does eliminate with his semen those organisms which produce lesions in his genital organs, and are capable of infecting the female. W. L. Williams (48) cites the case of a pure bred herd in which breeding had progressed satisfactorily until heifers had grown to breeding age and a second bull was obtained. “Some cows of the old herd were also assigned to the young bull which had not previously been in service. The cows bred to the old herd bull continued to breed normally. The cows and heifer’s bred to the new bull conceived with difficulty or not at all. Those which conceived mostly aborted, and those which calved had metritis and retained fetal membranes. The two first cows in which pregnancy terminated died of metritis.” I have frequently had semen samples sent in from bulls that were not only failing to get cows with calf, but following each service the females showed a severe vaginitis. W. W. Williams worked in a herd in which service to certain bulls was in each case followed by a severe vaginitis and cervicitis, only to be followed later by a characteristic salpingitis.

Vaginal smears taken before and after service, in many instances, show that in all probability bacteria, especially the streptococci, were deposited there with the semen. These results have been obtained upon several occasions, at which time the vagina was usually douched prior to each service with sterile saline solution. Streptococci and other organisms have been isolated from the vaginal samples obtained by this method. In most cases, they were absent from samples taken before service. Extraneous contamination, and error, must be taken into consideration, but the results tend to bear out clinical observations that the bull is probably a disseminator of some infections associated with the genital organs of both sexes. At any rate, organisms have been isolated repeatedly from the genital organs of the bull, of the same biological character as those which are associated with sterility, abortion, and allied phenomena in the female. In the absence of obstruction in any part of the tract, there is nothing to hinder infection from gaining access to the seminal fluid, and being excreted during ejaculation.

Hopper (18) states: “A diseased bull may manifest non-fertility or decreased potency in different ways—by repeated service to apparently normal females without conception, by a high abortion rate in females that have been apparently normal, by characteristic infections following the use of any particular sire, or by abnormalities in the breeding tract noted by rectal or physical palpation.”

Admittedly, Bact. abortum has little affinity for the genitalia of the bull, though Schroeder states that the bull harbors the organisms in his seminal vesicles and that they are eliminated with the semen. Other authors have occasionally isolated the organism from the vesicles, testes, or both. Schroeder’s theory that infection of the female occurs indirectly by contamination of the fodder with the semen is probably rare in occurrence. The very limited number of cases in which investigators have demonstrated the presence of the organism in the male genital organs, and the apparent immunity of the bull to the bacterium as determined by the agglutination reaction, seem to indicate that he plays a small part in the spread of this type of infection in the herd. On the other hand, it would seem that he is at times intimately associated with the spread of certain other organisms that interfere seriously with herd reproductivity.

The diagnosis of infertility and sterility rests upon a thorough physical examination of the genital organs, together with a detailed study of the semen. The history of the animal and herd involved must also be very carefully inquired into, especially the part covering the result of every service by the sire in question. Besides this, we must always consider all factors which have a bearing upon the subject, remembering the physiology of each part, and the role it plays in reproduction. Bacteria gain entrance to many parts of the tract, where they multiply and probably add toxic products to the seminal fluid, altering its biological character and resulting in partial or total destruction of the secretory tissues. The testes, epididymes, vesicles, prostate, and other parts, each contribute their essential part to the semen, abnormalities of any one of which, as a rule, result in interferences with reproduction. If the vesicles are involved, we must bear in mind just what is the part played by their secretion, and what is the probable result if their essential elements are not added to the semen. In like manner, we must consider the prostate, whose secretion stimulates the vitality of the sperms, and adds fluid bulk to the semen. Extirpation of the vesicles or prostate alone results in lowered fertility, without altering the sexual desire, while removing both glands produces total sterility. Partial or total destruction of the parenchyma of either gland produces the same effect as extirpation, in that its function is altered or entirely absent.

The semen should be examined, not only for the number of spermatozoa and the percentage of those that are motile, but for the duration and type of motion. Normal semen, when first examined under the microscope, shows a field closely packed with highly motile spermatozoa. In every study of the semen, however, we must bear in mind the temperature and other conditions under which it has been kept since emission. On the other hand, semen from bulls of lowered fertility shows changes ranging from mild disturbances such as sluggish motility and a slight decrease in the number of sperms present, to aspermia, or total lack of motion. Normal semen, when compared with abnormal specimens, as a rule presents distinct differences, either in motility, staining properties, or structure of the spermatozoa. Impotent bulls, however, may show at times few or no observable changes in their genital organs. The only assumption here is that the condition probably is of endocrine origin, or is some functional disturbance. Of oligospermia Reynolds states: “Oligospermia, with normal motility and vitality, is not absolute sterility, but is of high importance because the percentage of destruction of spermatozoa during their passage through the genital canal of the female is so enormous that the possibility of impregnation by semen which starts out with a deficient number is always poor. When the genitals of the female partner are in a condition which is even moderately hostile to the spermatozoa, impregnation by such semen becomes so unlikely as to be not even a probability.”

Motility may be lacking in a small number, its absence may be observed in a large percentage, or even in all those in the field, as in necrospermia. On the other hand, the motility may be sluggish or of abnormal types in variable percentages. Sperms with sluggish motility are always low in vitality, and have weak powers of insemination, as the motion lasts but a comparatively short time. The vitality may be but moderately lowered, so that although the sperms are highly motile when ejaculated they soon lose their power of propulsion. The type of motion is likewise an indicator of lack of vitality. The “progressive vibratile” motion described by Reynolds should proceed to a high degree for a long period before the “undulatory tactile” or bunting types of motion appear. Early appearance of these two latter types indicates in most cases a marked lack of vitality of the elements. The motion should be vigorous and lasting, for, as stated by Reynolds, “nothing is more certain than that spermatozoa of merely moderate vitality seldom impregnate a female.”

The early precipitation out of the “Boettcherchen” crystals is very characteristic of oligospermia, and impotent semen. The theory here is that crystals do not precipitate out when a fluid is actively moving, but soon do so when the fluid is motionless. The sediment which normally makes up about two-thirds of the sample is usually decreased in abnormal samples. The semen itself should be observed for unusual viscosity or a thin watery condition. Clotting should occur readily after emission, but the clot soon liquefies to some extent, allowing the spermatozoa to become more active. This clotting is, of course, to protect the delicate sperms from the hostile secretions of the vagina.

The presence of immature and deformed types of sperms represents some disturbance of spermatogenesis, but it is difficult to explain the significance of these forms. They are seldom seen in normal samples, and undoubtedly none are capable of producing impregnation. In the case of minor abnormalities of staining reactions, the sperms are probably deficient in nuclear material or otherwise altered so that probably they are incapable of reaching and uniting with the ovum. When impregnation does occur in these cases, weak offspring undoubtedly result in many instances.

The work has by no means progressed to the point where one may, by an examination of the semen, determine the degree of impotency with great accuracy, or even whether the animal may be restored to sexual health by proper hygienic and therapeutic treatment. Relatively, the greater the changes in the semen and spermatozoa, the less the chances of impregnation. Infertility to any marked degree, is, however, usually accompanied by corresponding changes in the seminal fluid and its germinal elements.

Examination of the semen is, and probably always will be, simply an aid in reaching a diagnosis. While abnormalities of the semen and spermatozoa are associated with sterility or infertility, it is unwise to lay too much emphasis upon this method of diagnosis alone, especially with regard to the making of a definite prognosis. When large numbers of abnormal spermatozoa are present in the semen, we are safe in saying that the animal is, at the time, of lowered degree of fertility. One should be very cautious, however, in foretelling how long the condition will last, or if the animal may in time be restored to full fertility. Sterility, due to organic disturbances, probably seldom yields to treatment, but when it is due to functional disorders resulting from defective diet or lack of exercise, the condition is frequently remedied by overcoming the cause. Lack of exercise and overfeeding seem to be etiological factors in a fair percentage of cases.

Besides abnormalities of the male genital tract, we must always consider the numerous factors in the female that may kill or weaken the sperms. Impediments to successful coitus may be present in the form of vaginal constrictions, abnormally short or small vagina, or other deformities. Hostile exudates, mechanical obstructions, and other factors may interrupt the progress of the sperms at any point in the tract.

Although little is known definitely regarding disorders of the endocrines in the bull and their relation to reproduction, the work in human medicine and experimental researches upon laboratory animals warrant thoughtful consideration of these factors which are by no means insignificant. In the future, these glands will no doubt receive more and more attention in their relation to the genital organs and reproduction.

CONCLUSIONS

1. The genital organs of the bull quite frequently undergo pathological changes, due to infection with the same varieties of microorganisms associated with genital infections in the female.

2. In all probability, these microorganisms are frequently eliminated with the semen and infect the female during copulation.

3. Past or present infection in the genital organs of all the bulls so far examined was evidenced by the presence of the fine connective tissue tufts and strands upon the tunica vaginalis, particularly that part covering the tail of the epididymis.

4. Lowered sexual capacity is, as a rule, accompanied by demonstrable changes in the semen.

5. A study of impotency and sterility includes not only a thorough study of the genital organs, but also those extrinsic factors which govern reproduction either directly or indirectly.

6. A thorough knowledge of the anatomy and physiology of the male genital organs is fundamental to a clear understanding of the problem.

I am much indebted to Drs. W. L. and W. W. Williams for some of the material, and for helpful cooperation in the early part of the work; to Drs. C. M. Carpenter and R. R. Birch for many helpful suggestions; and to Dr. J. N. Frost and others who so kindly co-operated by placing at my disposal samples of semen and some of the genital tracts.

BACTERIOLOGY OF THE GENITAL TRACTS OF NORMAL YOUNG CALVES Group I ══════╤══════════════════╤══════════════════╤════════════╤════════════ NUMBER│Right sem. vesicle│Left sem. vesicle │Right testis│Left testis ──────┼──────────────────┼──────────────────┼────────────┼──────────── 1│ │ │ │ ──────┼──────────────────┼──────────────────┼────────────┼──────────── 2│ │ │ │ ──────┼──────────────────┼──────────────────┼────────────┼──────────── 3│ │ │ │ ──────┼──────────────────┼──────────────────┼────────────┼──────────── 4│ │ │ │ ──────┼──────────────────┼──────────────────┼────────────┼──────────── 5│ │ Staph. albus. │ │ ──────┼──────────────────┼──────────────────┼────────────┼──────────── 6│ │ │ │ ──────┼──────────────────┼──────────────────┼────────────┼──────────── 7│ │ │ │ ──────┼──────────────────┼──────────────────┼────────────┼──────────── 8│ │ │ │ ──────┼──────────────────┼──────────────────┼────────────┼──────────── 9│ Staph. albus. │ Staph. albus. │ │ ──────┼──────────────────┼──────────────────┼────────────┼──────────── 10│ │ │ │ ──────┼──────────────────┼──────────────────┼────────────┼──────────── 11│ │ │ │ ──────┼──────────────────┼──────────────────┼────────────┼──────────── 12│ │ │ │ ──────┼──────────────────┼──────────────────┼────────────┼──────────── 13│ │ │ │ ──────┼──────────────────┼──────────────────┼────────────┼──────────── 14│ │ │ │ ══════╧══════════════════╧══════════════════╧════════════╧════════════

BACTERIOLOGY OF THE GENITAL TRACTS OF MATURE FERTILE BULLS Group II ══════════╤══════════════╤══════════════╤══════════════╤══════════════ NUMBER │ 1 │ 2 │ 3 │ 4 ──────────┼──────────────┼──────────────┼──────────────┼────────────── Right │ │ │ │ seminal │ │ │ │ vesicle │ │ │ │ ──────────┼──────────────┼──────────────┼──────────────┼────────────── Left │ │ │ │ seminal │ │ │ │ vesicle │ │ │ │ ──────────┼──────────────┼──────────────┼──────────────┼────────────── Prostate │ │ │ │ ──────────┼──────────────┼──────────────┼──────────────┼────────────── Cowper’s │ │ │ │ ──────────┼──────────────┼──────────────┼──────────────┼────────────── Right │ │ │ │ testis │ │ │ │ ──────────┼──────────────┼──────────────┼──────────────┼────────────── Left │ │ │ │ testis │ │ │ │ ──────────┼──────────────┼──────────────┼──────────────┼────────────── Right │ │ │ │ epid. │ │ │ │ ──────────┼──────────────┼──────────────┼──────────────┼────────────── Left epid.│ │Streptococcus │ │ │ │ viridans. │ │ ──────────┼──────────────┼──────────────┼──────────────┼────────────── Right │ │ │ │ scrotal │ │ │ │ sac │ │ │ │ ──────────┼──────────────┼──────────────┼──────────────┼────────────── Left │ │Streptococcus │ │ scrotal │ │ viridans. │ │ sac │ │ │ │ ══════════╧══════════════╧══════════════╧══════════════╧══════════════

BACTERIOLOGY OF THE GENITAL TRACTS OF ABATTOIR BULLS Group III

══════╤═══════╤═══════╤════════╤════════╤════════ NUMBER│ Right │ Left │Prostate│Cowper’s│ Right │seminal│seminal│ │ │ testis │vesicle│vesicle│ │ │ ──────┼───────┼───────┼────────┼────────┼──────── 1│ │ │ │ │ ──────┼───────┼───────┼────────┼────────┼──────── 2│ │Staph. │ │ │ │ │ alb. │ │ │ │ │ │ │ │ │ │ │ │ │ ──────┼───────┼───────┼────────┼────────┼──────── 3│ │ │ │ │ │ │ │ │ │ ──────┼───────┼───────┼────────┼────────┼──────── 4│Staph. │Staph. │ │ │ │ alb. │ alb. │ │ │ │Strep. │Strep. │ │ │ │ vir. │ vir. │ │ │ ──────┼───────┼───────┼────────┼────────┼──────── 5│ │ │ │ │ ──────┼───────┼───────┼────────┼────────┼──────── 6│ │ │ │ │ ──────┼───────┼───────┼────────┼────────┼──────── 7│ │ │ │ │Bact. │ │ │ │ │ abort. ──────┼───────┼───────┼────────┼────────┼──────── 8│Staph. │Staph. │ │ │ │ alb. │ alb. │ │ │ │Strep. │ │ │ │ │ hem. │ │ │ │ ──────┼───────┼───────┼────────┼────────┼──────── 9│ │ │ │ │ ──────┼───────┼───────┼────────┼────────┼──────── 10│Staph. │ │ │ │ │ alb. │ │ │ │ ──────┼───────┼───────┼────────┼────────┼──────── 11│ │ │ │ │ ──────┼───────┼───────┼────────┼────────┼──────── 12│Staph. │ │ │ │Staph. │ alb. │ │ │ │ alb. ──────┼───────┼───────┼────────┼────────┼──────── 13│ │ │Staph. │ │ │ │ │ alb. │ │ ──────┼───────┼───────┼────────┼────────┼──────── 14│ │ │ │Staph. │ │ │ │ │ alb. │ ──────┼───────┼───────┼────────┼────────┼──────── 15│Staph. │Staph. │ │ │ │ alb. │ alb. │ │ │ ──────┼───────┼───────┼────────┼────────┼──────── 16│ │ │ │ │ ══════╧═══════╧═══════╧════════╧════════╧════════