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Title: A study of some factors influencing fertility and sterility in the bull
        A thesis

Author: Herbert Lester Gilman

Release date: June 17, 2024 [eBook #73852]

Language: English

Original publication: Albany: J. B. Lyon Company, Printers, 1922

Credits: Richard Tonsing, Charlene Taylor, and the Online Distributed Proofreading Team at https://www.pgdp.net (This file was produced from images generously made available by The Internet Archive/American Libraries.)


*** START OF THE PROJECT GUTENBERG EBOOK A STUDY OF SOME FACTORS INFLUENCING FERTILITY AND STERILITY IN THE BULL ***





A Study of Some Factors Influencing Fertility and Sterility in the Bull


                                A THESIS

 Presented to the Faculty of the Graduate School of Cornell University
                 for the Degree of Doctor of Philosophy

                                   BY
                 HERBERT LESTER GILMAN, D. V. M., M. S.

                           Reprinted from the
         Annual Report of the New York State Veterinary College

                                 ALBANY
                      J. B. LYON COMPANY, PRINTERS
                                  1922




A STUDY OF SOME FACTORS INFLUENCING FERTILITY AND STERILITY IN THE BULL

                           HERBERT L. GILMAN

           Veterinary Experiment Station, Cornell University


Normal reproduction is the fundamental foundation upon which the entire
cattle industry rests. For this reason, any factor capable of
interfering with it is a detriment to the industry, and a matter of
prime importance to the breeder and the veterinarian. With the relative
increase in number and value of cattle, and the fact that the profession
is depending more and more on this industry for a livelihood, these
problems are assuming greater importance. The part played by the bull
has been emphasized entirely too little, with the result that, as in
human medicine, many fail to appreciate the effects of sterility or
lowered fertility in the male. The part played by the sire in the spread
of genital infections, though discussed frequently, has received little
systematic investigation.

The bull mast be regarded as at least half the herd, not only from the
standpoint of the characters he imprints upon his progeny, but because
of his relation to the reproductive efficiency in the herd. It seems
quite probable that he does disseminate during copulation, infection
associated with the genital organs, with the result that the bull is a
very important factor in a study of the subject. Too frequently, his
ability to copulate in an apparently normal manner, is taken as a
standard of fertility. Gross changes in his genitalia, or the absence of
spermatozoa from the semen are given due consideration, while other more
obscure abnormalities are not looked for nor regarded in their proper
light. Neither fertility nor sterility are always absolute, but the
terms should be used relatively inasmuch as we may have all degrees of
infertility or impotency. All too frequently we forget the many delicate
and intricate mechanisms involved in the reproductive process, with the
result that many phases of the problem are neglected or disregarded. The
genital organs work as a unit, each part of which must function in
perfect accord with the others to the end that full fertility may
result. The physiological factors involved in the formation of the semen
are too little understood, or at best, our knowledge regarding them is
more or less hazy.

The purposes of the present work have been: (1) to summarize the work so
far done on the subject, (2) to review briefly the known facts throwing
light on the anatomy and physiology of the male genital organs, (3) to
carry our systematic studies upon the pathology and bacteriology of the
genital tract of the bull, and (4) to ascertain if possible whether the
bull is a disseminator of those infections which interfere with
reproduction in the female.

The work has been carried on for the most part from the point of view of
a laboratory man cooperating with clinicians. No attempt is made in this
paper to give detailed clinical data, methods for physical examinations,
etc. There are included many statements and some data, given in a
preliminary article on the subject. While the subject is broad in its
scope, in fact too broad for great detail, it is hoped that a start has
been made toward future and more detailed investigations.


                                HISTORY

References to, and investigations relating to, the part played by the
bull in the process of reproduction in the herd, and in the spread of
genital infections, have been limited largely to those phenomena caused
by _Bact. abortum_. Bang (1) originally called attention to the
possibility of the male transmitting the organism discovered by him, but
he reached no definite conclusion on the subject. James Law (2) writing
on contagious abortion in cows, early suspected this possibility when
stating under “casual infections,” that—“In a case which came under the
observation of the writer recently, a family cow, kept in a barn where
no abortion had previously occurred, was taken for service to a bull in
a herd where abortion was prevailing, and though she was only present at
the latter place for a few minutes, she aborted in the sixth month.”
Jansen, as quoted by Sand, reports the case of a cow from an aborting
herd having been taken into a herd that had been previously quite free
from the disease. Soon after her arrival she aborted, and later cow
after cow of the original herd aborted. The owner kept the matter a
secret, and sent his cow to a neighbor’s bull for service, with the
result that for two years abortion prevailed among cows served by this
bull. McFadyean and Stockman (3) later, in experimental work, attempted
but failed to infect cows by using a soiled bull for service. Hadley and
Lothe (4) state: “A large number of stockmen hold that the bull is an
important factor in the transmission of contagious abortion in herds. A
smaller number believe that the bull merely acts as a passive carrier of
the abortion disease and is not actively concerned in the transmission.”
In a subsequent bulletin, Hadley (5) remarks: “The abortion organisms
may enter the body ... during sexual intercourse.” In an experiment
carried on by the same author and co-workers, abortion-free virgin
heifers were mated to abortion-infected bulls, infection being evidenced
by positive reactions to the complement fixation and agglutination
tests. His results indicate, he believes, “that the bull is not so
important a factor in transmitting abortion as many believe.” The
conclusions are: “Bulls may become infected with abortion bacilli. Bulls
that reacted to the blood tests were incapable of disseminating the
abortion disease to the abortion-free heifers with which they were
mated. Bulls appear to possess a sexual or individual immunity to
abortion infection that renders them less susceptible than cows and
induces a milder form of the disease. The resistance appears to be due
to certain anatomic and physiologic differences in their sexual organs
which make them less favorable places for the growth of the abortion
germs than those of the opposite sex.”

Buck, Creech, and Ladson (6) applied the agglutination test to 325
mature bulls, of which 288 were negative and 37 positive. _Bacillus
abortus_ was isolated from five animals, of which three showed marked
lesions, two in the seminal vesicles, and one in the left testicle. They
conclude: “_B. abortus_ may involve organs of the generative apparatus
of bulls, producing chronic inflammatory changes. Of the generative
organs, the seminal vesicles appear to furnish the most favorable site
for the lodgement and propagation of abortion infection.”

Schroeder and Cotton (7) cite the case of a bull which reacted to the
abortion test and, on post mortem, _Bact. abortum_ was isolated from an
abscess of one epididymis. They state: “Our attempts to produce a
similar case of infection artificially failed, and, in agreement with
the difficulties many investigators have had to obtain incriminating
evidence against bulls, we have thus far failed to infect bulls in any
way that justifies the assumption that they are important factors in the
dissemination of abortion disease.” Further, they conclude: “Regarding
the dissemination of abortion disease by bulls, we may say, however,
that it would be foolhardy in the dim light of our present knowledge to
take liberties with reacting bulls, or bulls from infected herds, or
promiscuously used bulls.”

Cotton (8) failed to demonstrate the presence of abortion bacilli in the
genital organs of the bull used to serve aborting cows, or in the
testicles of two bull calves, one of which had been fed and the other
injected with the cultures of the abortion bacillus. He concludes that
the bull does not harbor the organisms in the testicles. Carpenter (9)
injected both _streptococci_ and _Bact. abortum_ into the scrotal sacs
of young calves, and intravenously in others. In no case was he able to
recover the organisms from any part of the genital canal, except for a
_streptococcus_ in one instance. Rettger and White (10) were unable to
obtain evidence of the presence of _Bact. abortum_ in three bulls
slaughtered after repeated reactions to the complement fixation and
agglutination tests. The three bulls had been under observation for
three years, with no conclusive evidence to indicate that they were a
source of danger to the herds in which they were a part. They believe
that the bull transmits the infection as a passive carrier.

Attempts at artificial inoculation by natural channels have failed, with
the possible exception of McFadyean, Sheather, and Minett (11) who were
able to infect the bull by the prepuce in two cases and by the mouth in
one case. The results, however, are by no means conclusive. They
conclude, nevertheless, that cattle of any age of either sex may be
infected by natural channels with the bacillus of epizootic abortion.

Schroeder (12) carried out investigations to ascertain the frequency
with which bulls react to abortion tests, and the frequency with which
lesions chargeable to abortion bacilli occur in the reproductive organs
of reacting bulls. Studies were also pursued which he states
conclusively prove that bulls with infected reproductive organs may
expel abortion bacilli with the seminal fluid. In the first two
mentioned investigations 325 bulls from a Washington abattoir were
tested, and slaughtered upon reaction. “Approximately ten per cent of
the bulls reacted, and approximately ten per cent of the reacting bulls
showed lesions of the reproductive organs from which abortion bacilli
were isolated.” The value of these studies, he emphasizes, lies not in
“that they give us a measure of the proportion of bulls that react
positively to abortion tests or the proportion of reacting bulls that
are carriers of abortion bacilli,” but in “the fact that they show that
abortion bacillus disease of the bull’s reproductive organs is not a
wholly unique affection which practically may be ignored, but an
important condition that must be taken into account in our efforts to
combat infectious abortion, since it has been proved to be associated
with contamination of the seminal fluid.” In discussing the method by
which infected bulls transmit the organisms to cattle, he believes that
leakage of semen from the penis, or vaginas of cattle after service,
contaminates the food which subsequently gains entrance to their
digestive tracts. As the result of a series of experiments, he states:
“... the results fail to justify in the least degree the assumption that
cows are infected with abortion bacilli via their vaginas or uteruses at
the time of copulation, or that the bull, through copulation, is an
agent in the spread of abortion disease.”

The work so far alluded to, has been limited to infection with, and the
transmission of, _Bact. abortum_ and the lesions associated with such
infection. The last mentioned author, however, states: “A search for
other specific causes of abortions among cattle has not been neglected,
and bureau investigators could relate at great length stories similar to
those which investigators have told about microorganisms isolated from
the products of abortions and the uteruses of cows that have aborted.
Bacilli of various kinds, different types of micrococci, and spirilla or
vibrio have been found repeatedly; but when their pathogenicity has been
tested in accordance with widely recognized and accepted and required
bacteriological standards, not one shred of evidence has been obtained
to prove them true etiological factors of bovine abortions. What role
such microorganisms may have as causes of the sequellae of infectious
abortions, and of other, possibly, independent, abnormal processes in
the reproductive organs, is far from clear and merits careful study.”
Hadley (5) mentions the fact that: “Unquestionably the male often
becomes infected with the germs that produce the various secondary
diseases in the female, which are properly classed under the more
inclusive term ‘abortion disease.’” Also, speaking of the rarity with
which the bull acquires abortion infection, he alludes to the fact that
he may act as a “mechanical carrier of various disease germs from an
infected to a healthy cow.” Carpenter (9) working on the female genital
tract, comes to the conclusion that, in all probability, the genital
organs are normally free from bacteria. Barney (13) quoting Huet finds
that bacteria may be present in the seminal vesicles of healthy animals
(horses, cattle, pigs, and laboratory animals). This, he states,
corresponds with the well recognized findings in other parts of the
genito-urinary tract, not only in animals, but in man. He (Huet) has
further found that in animals dying of acute septicemia, the specific
organism (anthrax, pneumococcus) is to be found in the vesicular
secretions. Furthermore it was definitely shown that an infection could
be transmitted to the female during the act of copulation.

Williams, W. L. (14), calls attention to the lack of veterinary
literature relating to the pathology and bacteriology of the male
genital tract, except as related to infection with _Bact. abortum_.
Infection with other types of bacteria is emphasized, the clinical
recognition of such, with the accompanying pathological changes, and of
the numerous phenomena involved in the process of reproduction in the
male. The semen and its essential germinal elements are taken up with
reference to the entire lack of study devoted to them, and some of the
abnormal changes are described. In a later contribution (15), he takes
up the part played by the bull in the dissemination of genital
infections and states: “Clinical studies now indicate with great
clearness that the bull is an active spreader of that group of genital
infections which cause sterility, abortion, and related phenomena.”

Williams, W. W. (16), studied the semen with reference to sterility,
emphasizing the importance of its examination in the diagnosis, giving
methods for collecting samples, staining of sperms, and some of the
abnormalities encountered. The work is fundamental, and should be of
great practical importance to all interested in the problem. In a later
paper (17), he brings out a more extended discussion of the question. He
concludes that the clinical examination is of vital importance, and that
the efficiency of the semen depends not only upon its physical
properties but upon the number of spermatozoa that are motile, the
degree of motility, degree of obligospermia, and the percentage of
imperfect spermatozoa, either deformed or immature. Of forty bulls
examined, he finds that twenty, or fifty per cent, showed lessened
fertility, and others, aside from this, showed minor changes in the
genital organs or semen. The same author subsequently takes up the
subject of reproduction from the viewpoint of both sexes, but
emphasizing infection in the male, and the frequency with which lowered
vitality of the germinal cells occurs. 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.”

The observations of Williams (19) in a pure bred dairy herd bring out
quite clearly the relation of the bull to the dissemination of genital
infections. The bulls in this particular herd were abnormal in many
respects, as demonstrated by pathological changes in their genital
organs, bacterial invasion of the parts, abnormalities of the semen and
spermatozoa, and the probable transmission of infection to the females.
Several of the sires from this herd furnished much of the material for
the early basic work of this investigation. Since then the tracts of
other sires have been worked upon with quite similar or identical
results.

To summarize the work already done, most investigators have considered
the bull as merely a mechanical carrier of _Bact. abortum_ infection,
though all are more or less suspicious of his ability to become an
active spreader. Schroeder, however, states that the organisms are
eliminated with the semen, but infection of the female occurs
secondarily through the digestive tract by contamination of the food
with the semen. Other investigators bring out fundamental points
demonstrating the importance of other organisms than the Bang bacillus
and call attention to the need of a more thorough study of the anatomy,
physiology, and pathology of the male genital tract.

Any study of the genital organs must of necessity rest fundamentally
upon a thorough knowledge of the anatomy and physiology of those parts.
Too few of us have stopped to consider these questions thoroughly, with
the result that our ideas on the problem are more or less vague. It is
much easier to understand why abnormal spermatozoa occur so frequently,
or changes take place in the semen with death or weakening of the
germinal elements, if we realize or stop to consider the highly
differential process of spermatogenesis, and the various structures
which contribute to the formation of the semen. We must come to realize
that each part of the genital tract is essential to the normal
functioning of the whole, and that the genital tract and reproduction
are in turn dependent upon the proper functioning of the entire body.

Walker (20) emphasizes the importance of a thorough knowledge of
physiology in stating, “Although the subject of sterility has attracted
the attention of the medical profession; and although much has been
written on its causes and treatment, it cannot be claimed that the
practical results obtained up to the present time are satisfactory, or
that when consulted for sterility, the medical man of today can hold out
to his patient much more hope of successful treatment than the medical
man of fifty years ago. Our failure in this respect is in the main due
to an ignorance of the physiology of reproduction.”

To bring out some of these points, the anatomy of the tract will be
reviewed briefly, together with the physiology of reproduction, and the
various factors which should be considered in a study of the problem.


                         ANATOMY AND PHYSIOLOGY

In origin and early development the ovary and testis are identical. The
gonad and mesonephros or primitive kidney are developed from the
urogenital fold. The gonad first forms as a medio-ventral thickening of
the fold, which gradually expands until it becomes attached by a mere
stalk. At first, the gland is made up merely of a superficial epithelial
layer, and an inner epithelial mass, or epithelial nucleus. In the
process of development, large primordial germ cells migrate from the
entoderm of the future intestinal canal, and pass through the stalk to
the gonad. In the case of the male gonad, seminiferous tubules are very
difficult to make out in embryos smaller than 24 millimeters. Then they
suddenly differentiate out as solid cords of germ cells, while the
connective tissue grows in around them. These connective tissue sheaths
unite at the center of the organ to form the anlage of the mediastinum
testis. The testicular tubules unite and converge toward the hilus,
there to meet the anlage of the rete. At the mesonephric end of the
testis, the rete first appears as a collection of cells, differentiating
out from the inner epithelial mass of the gonad. These cells gradually
grow out to meet the collecting portions of the mesonephric tubules on
the one hand, and the seminiferous tubules on the other. The rete is
represented as cords of cells at first, which in forty millimeter
embryos hollow out to form tubules.

The mesonephros, or primitive kidney, early starts to degenerate
cranio-caudally,—the tubules becoming separated into a cranial and
caudal group. The collecting and secretory parts of the cranial group
separate, the collecting tubules growing out to meet the rete with which
they unite to form the efferent ductules of the epididymis. The caudal
group of tubules is vestigial and becomes the paradidymis. The
mesonephric duct becomes the vas deferens, connecting as it does with
the tubules of the epididymis, and emptying into the urethra at Müller’s
tubercle or, as it later becomes, the colliculus seminalis.

The seminal vesicles arise as hollow saccules from the dorsal wall of
the mesonephric duct just as it empties into the urethra. The prostate
develops as an outgrowth of the dorsal urethra just posterior to
Müller’s tubercle. The bulbo-urethral glands appear as solid, paired,
epithelial outgrowths from the entoderm of the urogenital sinus.

Müller’s duct, at first a solid tube growing from the anterior part of
the mesonephros, and ending at Müller’s tubercle, becomes a hollow tube,
and in the female forms the entire genital tract except for the gonad
and the lower part of the vagina. In the male, the anterior part remains
as the vestigial appendix testis, and the posterior part, as the vagina
masculina. Ellenberger states, however, that this embryonic structure is
very seldom seen in the mature bull.

The _Male Reproductive Organs_ include the penis and testes, together
with the excretory passages which connect the testes with the urethral
canal. These excretory ducts include the epididymis, vas deferens, and
seminal vesicles. Posterior to their termination in the urethra, there
are connected the ducts of the prostate gland and the bulbo-urethral or
Cowper’s glands.


TESTES: The testicles of the bull are relatively large. Varying with the
size and age of the animal they measure from fourteen to seventeen
centimeters in length, including the epididymis, and from six to eight
centimeters in diameter. Each testicle is enclosed within a serous sac,
the tunica vaginalis, whose visceral layer is very intimately fused with
the underlying covering of the organ, the tunica albuginea. The tunica
albuginea is quite thin and consists of connective tissue which is rich
in elastic fibres. Muscular tissue is not present as it is in the case
of many mammals. Inside the tunica, and closely attached to, though
separated from, the parenchyma by a thin layer of connective tissue, is
a layer of very loose connective tissue, which because of its rich
supply of blood vessels is termed the tunica vasculosa. The parenchyma
is of a yellowish gray color, and of a rather soft consistency. It is
made up of the seminiferous tubules, rete, and the connective tissue
stroma, the mediastinum testis. On section, the mediastinum appears as
the center or axis of the entire organ. It is star-shaped, and radiates
connective tissue septa out into the parenchyma to support and separate
the tubules. Ellenberger states that the testis of the bull and all
ruminants lacks a closed system of interlobular septa, because of the
feeble development of the connective tissue.

The principal blood vessels and rete tubules are found in this
structure, the function of the latter being to connect the seminiferous
tubules and the efferent tubules of the epididymis. The epithelium of
the rete is quite irregular,—consisting in places of a single layer; in
others, of two layers. At some points there are formed groups of several
cells lying over one another, with swollen homogeneous basal cells,
which sometimes form projections into the lumen.

The interstitial tissue, besides conveying the blood vessels to the
organ, contains many “interstitial cells.” These cells are relatively
sparse in the adult bull, and are comparatively delicate, slightly
granular, often shuttle-shaped, with a rather small nucleus.
Embryologically they are derived from a syncitium arising from the
mesothelium of the genital ridge, differentiating out by growth of the
cytoplasm. They contain large quantities of fat, and elaborate the
internal secretion of the testis. This secretion governs the development
of the secondary sexual characters, and has a profound influence on the
general body metabolism, and development of the skeleton. The
interstitial cells appear early in embryonic life even before there is
any differentiation of sex, and their greater relative development in
the fetus is indicative of a future male development. In very young
embryos, the growth is very rapid, followed, however, by a period of
atrophy, during which the seminiferous tubules undergo marked
development. Pende (21) states: “There seems to be an inverse relation
between the growth of the tubular and interstitial tissues, as one is
hypoplastic when the other is in full activity.” From birth to the onset
of sexual maturity, which may be called a period of rest for the
testicle, the cells are few in number. With the accentuation of the
secondary sexual characters, and the beginning of sexual life, these
cells again increase in number and activity.

The parenchyma of the testis consists for the most part of the
seminiferous tubules, which, on account of the courses they take in the
different regions, are divided into groups. The peripheral tubules are
the much-contorted tubuli contorti. These anastomose to form the much
shorter tubuli recti. These in turn anastomose frequently, uniting to
form the rete testis. The rete proceeds through the mediastinum to form
the efferent ductules which break through the tunica albuginea to form
the greater part of the head of the epididymis. The tubuli contorti are
the longer and more numerous of the tubules, for it is here that
practically all the spermatozoa are produced. The straight tubules are
relatively so short that they may be regarded more in the light of the
beginning of the system of excretory ducts.

The seminiferous tubules consist of a thin peripheral membrana propria
upon which rests the seminal epithelium, which is made up of the
essential semen forming cells, and the cells of Sertoli. The
spermatogenic cells may be divided into three groups, from within
outward: the peripheral single layer of small cuboidal spermatogonia;
one or two rows of large spermatocytes; and three to five rows of
spheroidal spermatids. The cells of Sertoli are more or less of the
syncitial type,—large in size and irregular in outline. They occur at
various intervals between the layers of spermatogenic cells, with their
bases resting upon the membrana propria. Centrally they send out
protoplasmic processes for variable distances,—some even reaching the
border of the innermost cell layers.


SPERMATOGENESIS: In this process, the primary germinal cells, the
spermatogonia, divide to form the primary spermatocytes. Maturation
consists of two cell divisions of the primary spermatocytes, and these
in turn form four spermatids. During the process, the number of
chromosomes is reduced to half the number characteristic of the species.
The spermatids then become converted into mature spermatozoa. This mode
of transformation may be seen in Plate I. In the process, the nucleus of
the spermatid forms a large part of the head: the centrosome divides,
part passing to the extremities of the neck. One centrosome becomes the
anterior, and remains attached to the head, while the other divides to
form the posterior centrosome. The latter is divided into the anterior
part, and the posterior nodule or annular ring. Besides this, the
posterior centrosome becomes elongated to form the axial filament, and
the cytoplasm forms the sheaths of the neck and tail. The spiral
filament of the connecting piece is derived from the cytoplasmic
mitochondria. At this time, a large part of the cellular cytoplasm is
cast off. Meanwhile, the spermatozoa sink their heads into the long
protoplasmic processes of the Sertoli or “nurse” cells which furnish
nutritive material for their complete development. Finally the adult
cells are cast off into the lumen. The structure of the spermatozoa, and
a discussion of the semen will be taken up later.


EPIDIDYMIS: The epididymis is divided into three parts: the head, body
and tail. The head is made up principally of the lobules formed by the
much-coiled efferent ductules proceeding from the rete. The ductules,
about twelve in number in the bull, unite to form the body, which
remains coiled and runs along the postero-medial part of the testicle to
which it is more or less closely attached. To quote Ellenberger (23):
“The transition from the rete into the ductules is gradual, as the
characteristic epithelium of the latter (ductules) begins in cavities
without walls, and at first, gradually form a wall which is well marked
out as a thin ring of interstitial tissue.... The epithelium of the
ductules is in sharp contrast to the rete in that it has a
single-layered ciliated columnar epithelium, in which here and there one
finds round basal cells. The dark and light columnar cells alternate;
the cilia are often cemented together, and form cone-shaped, homogeneous
appearing protuberances. The secretory activity is quite clearly
observable. In the light cells one finds secretory globules,
accumulating in rows, sometimes above, other times below, arches of
cells. The secretory droplets pass from the cells into the lumen, and
often lie in irregular layers on the epithelium; also the basal cells
appear swollen and shoved out between the cylindrical cells.” At the
lower extremity of the testicle, the tail is formed, which is globular
in shape, and more or less loosely attached to the testicle. Here the
ductules anastomose freely, gradually become less coiled, and end in the
single excretory tube, the vas deferens. The epithelium at the tail part
is more or less of the pseudo-stratified columnar, ciliated variety.
Outside this is a membrana propria, a circular muscular layer, and a
connective tissue coat. The secretory activity is very marked here and
one finds much secretion in the lumen, Courrier (24), working on the
bat, suggests that the glandular activity is conditioned by the
secretion from the interstitial (endocrine) gland. The action of the
secretion is to dilute the large mass of spermatozoa present, nourish
them to some extent and also stimulate them to active motility. Stigler
(25) states that the properties of the sperms are modified in the
epididymis; the motility, the ability to resist heat, and other
properties are augmented, at least in the case of the guinea pig, rat,
and mouse. Some authors state that the sperms first become motile when
in contact with the prostatic secretion, but I have repeatedly examined
the contents of the tail of the epididymis of the bull, rabbit, and
guinea pig, finding full motility in each case, though the duration is
not nearly as long as when the sperms are ejaculated in the semen.


The VAS DEFERENS is quite narrow (2 mm.) and runs from the tail of the
epididymis to the verumontanum, or colliculus seminalis, where it
empties into the urethra in common with the duct of the vesicle. At
first it is lined by epithelium similar to that of the vas epididymis,
but this changes over into a peculiar low stratified type. Ellenberger
describes it as follows: “The epithelium shows a very pronounced basal
coat. The overlying cell zone shows more (at the most, three) rows lying
over each other of elongated nuclei, while an outline of cell form is
not ordinarily noticeable, so that it may be spoken of as a syncitium,
and at the same time as a many layered epithelium.” The mucosa forms
low, broad folds into the lumen. The tunica propria is a thin connective
tissue layer. The submucosa consists of thin connective tissue. Three
muscular coats are present: an inner thin longitudinal layer, middle
circular layer, and an outer longitudinal layer. All are more or less
intimately blended, and are surrounded by the adventitia, made up of
connective tissue, elastic fibres and scattered longitudinal muscle
cells of the internal cremaster muscle. Near the dorsal surface of the
bladder, the ducts come in close apposition, and for ten to twelve
centimeters dilate to form the ampullae. Here the mucous membrane
becomes much plicated, forming long folds which anastomose freely. The
function of the vas is to convey the spermatozoa and secretions from the
epididymis to the urethra. Disselhorst (26) believes the ampulla acts as
a seminal reservoir and states that he has found spermatozoa stored up
in the little pockets in the walls of this structure in animals during
the rutting time. He suggests, further, that there is a relation between
the state of development of the ampulla and the time occupied by
copulation. When the organ is small or absent, as in dogs, cats, and
boars, the coition is a slow process, but when the ampulla is large and
well developed, as in horses and sheep, the coitus requires a relatively
short time. Inasmuch as coitus is so rapid in the bull, and the ampulla
is so well developed, it seems as though this function is very probable.


The SEMINAL VESICLES are very compact glandular structures lying on
either side of the median line, on the dorsal side of the bladder, and
ventral to the rectum. In the mature bull they measure ten to twelve
centimeters in length, four centimeters in width, and about two and
one-half to three centimeters in thickness. The glands are distinctly
lobulated, quite tortuous, and are often asymmetrical in size and shape.
They converge posteriorly, to empty into the urethra at the colliculus
seminalis with the ampulla, in a slightly oval slit in the mucosa.
Microscopically, the gland is of the anastomosing tubular type, with
very poorly developed excretory ducts to the glandular cavities.
Posteriorly one finds centrally a few sinus-like narrow excretory
passages, which open into the somewhat larger collecting and excretory
duct. The epithelium is of the simple columnar type and produces a
relatively large amount of secretion. The gland cavities are surrounded
by a membrana propria, over which is a relatively thick layer of smooth
muscle. Outside this is a connective tissue covering which sends
trabeculae or septa in between the lobules. The secretion of the seminal
vesicles is a tenacious albuminous fluid with a slightly yellowish
tinge, all or part of which appears in the ejaculate in the form of
swollen sago-like grains which are soon dissolved following ejaculation
and the liquefaction of the semen. The proteid compounds belong to the
group of histones. The secretion is liquid when warm and coagulates when
cold. Some say that the filling of the vesicles serves to excite sexual
feeling, but this is doubtful in view of the fact that in some animals
the sexual desire exists before the vesicles are filled. Likewise,
Steinach found that rats, whose seminal vesicles had been removed, still
retained their desire for copulation. The function of the secretion is
to furnish much of the volume to the semen, and in some way it has a
distinct bearing on fertility, inasmuch as extirpation of the organs in
rats leads to lowered fertility. The vesicles of the bull are in no
sense a store-house for spermatozoa, as is usually understood. Repeated
examinations in a large number of bulls have led to the finding of
spermatozoa there only in very rare instances. That they serve as a
resorption place for sperms that are not ejaculated is also very
unlikely. Normally, one sees on smear of the vesicles, occasional cells,
leucocytes, lecithin granules, sago bodies, and rarely a few degenerated
spermatozoa.


The COLLICULUS SEMINALIS is a rounded or cone-shaped eminence in the
posterior urethra, upon which the ducts of the seminal vesicles and vasa
deferentia open. The ducts open separately at the bottom of two narrow
slits, one on each side of the mound, there being no distinct
ejaculatory duct as in man. The function of the colliculus or
verumontanum is not definitely known. It is generally believed that the
structure is made up of blood spaces which become engorged during
erection, causing a blockage of the posterior urethra, which prevents
regurgitation of the semen. Rytina (27), however, demonstrated that the
structure is not composed of any unusual number of blood vessels or
spaces, and that removal of the organ was not followed by regurgitation
of the semen into the bladder during ejaculation. He believes, and quite
logically, that its function is to afford a prominence upon which the
ducts may empty. The mixture of the thick gelatinous semen with the thin
prostatic secretion must occur at the moment of ejaculation and must be
perfectly homogeneous, otherwise large numbers of the organisms remain
in the thick gelatinous portion of the fluid. The eminence serves this
purpose in that the prostatic ducts which converge toward it, may eject
their secretion toward the eminence, producing an admixture more evenly
and quickly.


PROSTATE: The bull possesses what Ellenberger calls a diffuse prostate.
That is, there is no distinct glandular body as in man. It is composed
principally of a glandular sheath around the urethral wall. Just
posterior to the neck of the bladder, and in front of the urethral
muscle, there is formed a slight dorsal transverse elevation, extending
downward on the sides. This is what might be termed the body. The
greater part of the gland is “disseminate” in form, being a sheath of
glandular tissue embedded in the urethral wall. Dorsally it is about ten
to twelve millimeters thick, and ventrally about two millimeters. The
gland is a branched tubular structure, the interlobular tissue of which
contains much unstriped muscle. The lobules are lined by a columnar type
of epithelium. The ducts, about thirty to forty in number, open into the
urethra in two rows posterior to the colliculus. The secretion is a
thin, slightly turbid fluid, of a faintly alkaline reaction. Its
function is to dilute the semen, stimulate the motility of the
spermatozoa and nourish them.

Fish (28) believes that the activating property of the secretion is due
to enzymes, because boiling deprives the fluid of its power to
accelerate the motility of the spermatozoa. Serrlach and Pares, quoted
by Marshall (29), working on dogs, have adduced evidence indicating that
the prostate is an internal secretory gland which controls the
testicular functions, and regulates the process of ejaculation. It is
stated that if the prostate is removed, spermatozoa are no longer
produced in the testis, and that the secretory activity of the accessory
genital glands ceases. These changes, however, can be prevented by the
administration of extracts of the prostate. The fact that the prostate
elaborates a secretion having a definite relation to the testis, has
been verified by other authors.


COWPER’S GLANDS (Bulbo-Urethral): These glands are paired, oval
structures about one and one-half by two and one-half centimeters in
size, situated on either side of the dorsal pelvic part of the urethra
close to the ischial arch. They are deeply embedded, with the bulbus
urethae, in the bulbo-cavernosus muscle, thereby being inaccessible to
palpation. In general, they are of a well developed anastomosing tubular
type. The connective tissue stroma is relatively thin, and thickens only
in between the larger lobules, where one finds the larger collecting
ducts. Each gland opens by a single duct. The epithelium is of the
simple cuboidal type. Little is known of the function of its secretion,
though Kingsbury (30) regards it in the light of a mating gland; that
is, it lubricates the genital passages during coitus, as does its
homologous structure in the female, Bartholin’s gland.

Ellenberger describes the urethra, slit ventrally, as presenting the
following picture: “The colliculus seminalis distinctly appears as a
process or offshoot of the crista urethralis of the Trigonium Vesicae.
At the summit, and at the bottom of the two slits, open laterally the
ducts of the vesicles, and medially the ductus deferens.... From the
caudal slope of the colliculus go two distinct mucous membrane folds
which run through the entire pelvic urethra, near together, somewhat
diverging, and then coming together, so that they form an elongated,
narrow oval. At their caudal union, the excretory ducts of the
bulbo-urethral glands open side by side. At the point of departure of
the folds from the colliculus, arises a niche-shaped opening, between
both folds, and likewise lateral to each fold. In these niches open the
ducts of the prostate. The openings of the disseminate prostate lie in
rows as in the horse, but form not less than six rows. There is one row
medial to each fold, and two lateral. Mullet mentions only the medial
rows. These rows extend to the opening of the ducts of Cowper’s glands.
The stratum glandulare (disseminate prostate) is very easy to recognize
with the naked eye.”


SEMEN: The semen is the mixed product of the testicles, their excretory
passages, and the accessory sexual glands, a fact which complicates its
study considerably. The freshly ejaculated fluid is cloudy, tenacious,
more or less coagulable, and is rich in albumen. It is weakly alkaline
in reaction, and contains eighty to ninety per cent of water. Of the
solid constituents, there is forty per cent of ash, of which
three-fourths is calcium phosphate. Besides the spermatozoa, the semen
frequently contains epithelial cells, leucocytes, concentric amyloid
concretions, and lecithin bodies. When cold, the characteristic
phosphoric acid salts are precipitated. The fluid content is the product
of the tubules of the testicles, their excretory ducts, and the
accessory sexual glands. The characteristic odor of the semen is
supplied by a slimy nucleoalbumen “spermin” which forms the spermatic
crystals, and is furnished by the prostatic secretion.

During ejaculation the spermatozoa and secretions added by the testicle
and epididymis are probably carried to the ampulla by peristaltic
muscular action, in the earlier stages of the orgasm. At the height of
the orgasm, the ampulla is emptied into the posterior urethra in common
with the secretion of the contracting vesicles, here to be admixed with
the thin prostatic secretion. The entire mixture is then propelled, and
ejaculation produced by strong muscular contractions of the entire
urethra. As was stated before, the semen is the product of the
testicles, the excretory ducts, and the accessory sexual glands. The
testes furnish the essential germinal elements, the sperms, and some of
the fluid content. Then is added the product of the epididymis, vas, and
ampulla, which stimulates the spermatozoa to active motility, nourishes
the organisms, and adds somewhat to the fluid bulk of the secretion.

Stigler (25) states: “During its sojourn in the epididymis, the
properties of the spermatozoa are modified; the motility, ability to
resist heat, and other properties are augmented, at least in the case of
the guinea pig, rat, and mouse.” To the secretion is then added the
product of the vesicles, which contributes markedly to its fluid
content, nourishes the sperms, and supplies the ferment which induces
clotting of the semen when ejaculated. This is very important because
the clot formed in the vagina protects the delicate spermatozoa from the
hostile acid vaginal secretion. The prostate likewise adds bulk and
nourishing substances, besides stimulating the spermatozoa to fuller and
more lasting motility. The addition of the spermin is perhaps
unimportant. The function of the secretion of the Cowper’s glands, which
is added at this time, is problematical. It does, however, have a
diluting action on the semen. Perhaps its secretion is poured out prior
to ejaculation so as to lubricate the canal and prepare the way for the
semen.

Fish (28) has demonstrated by means of darkfield illumination, the
presence of numerous minute particles or ultraparticles in this fluid.
Their character and significance are matters of conjecture, but it would
seem as though they were not identical with the “chylomicrons” or fat
particles found in the blood by Gage. Perhaps further researches will
reveal some intimate connection between the number present in a field,
and the relative potency of the animal.

Each portion of the tract furnishes some essential element to the mixed
product which is so remarkably adapted both as a vehicle for the
ejaculation of the spermatozoa, and as a fluid in which their motility
is initiated and maintained. Any derangement of one part is fraught with
danger to the existence of viable spermatozoa, and the continuation of
full fertility on the part of the animal. The physiology of each
contributing gland must be borne in mind at all times. Walker (31)
investigated the fertility of the semen of the dog, taken from various
parts of the tract. His results were: (1) semen from the testicle and
head of the epididymis showed no motility, (2) semen from the tail of
the epididymis showed some motility in the more fluid contents of the
preparations, (3) semen from the vas deferens appeared about the same,
(4) a mixture of epididymis semen and prostatic secretion showed active
motility, and (5) likewise in a mixture of epididymis semen, though only
in those places where the fluids had become well mixed. My observations,
however, differ in one respect with regard to the bull, as I have found
full motility of the spermatozoa from the epididymis, but it is not so
lasting as when augmented by the addition of the prostatic fluid.
Boettcher (32) concludes: “that the secretion of the accessory male
genital organs possesses a protective colloid, which (1) hinders the
spermatozoid action of the vaginal secretion, at least until the sperms
have time to reach the interior of the uterus which is an alkaline
reaction, (2) that it makes the ejaculate more voluminous, so that by
cohabitation, a very good part of the vagina becomes moistened, and the
spermatozoa become distributed over the greater part of the vaginal
mucosa. This distribution is rendered necessary because some of the
fluid flows from the vagina following coitus. In this manner the
opportunity is given for a part of the ejaculate containing the
spermatozoa to be brought easier to the external os, and (3) it happens
that because of its content of sodium chloride the life of the
spermatozoa is stimulated and prolonged.” A fuller discussion of the
essential physiology of the various parts of the tract on the semen
content, and fertility, will be taken up later. The changes in
biochemical content, reaction, and the result of the addition of
bacterial products will also be more fully discussed.


SPERMATOZOA: The history of the discovery of spermatozoa is very
interesting, and for that reason a brief outline will be given. The
“semen threads” were first observed in the year 1667, by Ham, a student
of Leeuwenhoek at Leyden. The discovery was announced, confirmed by
findings in the dog and rabbit, and discussed by the latter author under
the title: Observationes Anthonii L. de natis e semine genitali
animaculis (Upon the formation of young from procreative material). The
sperms were taken to be animals on account of their motility, and their
significance remained questionable if not unknown. Spallanzani, quoted
by Marshall (29), was the first to show that the filtered fluid was
impotent, and that spermatozoa in the semen were essential to
fertilization. Kolliker, in 1841, discovered that the sperms arise from
the cells of the testis, and Barry in 1843, observed the conjugation of
sperm and ovum in the rabbit. This led to a clear understanding of the
function of these important germinal elements.

The spermatozoa are the male procreative cells, and are characterized by
the possession of a head containing the chromosomes necessary for
fertilization, and a tail capable of propelling the organism on its way
to meet the ovum. The length of the entire sperm, including the head, is
seventy-five to eighty microns. The head is nine and five-tenths microns
long, and five and five-tenths microns wide. It may be divided into two
principal parts, the head and tail. The head, for the larger part, is
made up of the nucleus, and may be differentiated by staining reactions
into a darker staining posterior part, an anterior lighter part, and
often a still lighter area between the two. On the anterior part is a
sharpened edge, the acrosome, which serves to perforate the ovum. The
whole is surrounded by a very definite limiting membrane which often
becomes obscured under abnormal conditions. The tail may be divided into
three parts: connecting piece, principal part, and terminal filament.
The connecting piece, the essential motile apparatus, is the thickest
and strongest part, and joins the tail proper to the head. It consists
of the central axial filament, a spiral filament around this, and an
outer mitochondrial covering. Anteriorly it is limited by the anterior
portion of the posterior chromosome, and posteriorly by the annular
chromosome. The anterior chromosome is directly connected with the head,
there appearing a light break here at the neck where separation
frequently occurs. This neck serves as a joint for the motion. The axial
filament, therefore, does not reach the head, but extends back from the
anterior part of the posterior chromosome. The principal part consists
merely of the axial filament, and a thin outer covering, while the end
piece is quite thin and is made up solely of the uncovered axial
filament. The finer structures are seen only when special staining
reactions are used, and then only when the sperms are obtained directly
from the testicle. The function of the sperms is of course primarily
that of fertilization. Numerous observers have, however, thought that
they might have some other definite, though unknown, use.

An editorial in the Journal of the American Medical Association (33)
raises several important questions regarding this obscure phenomenon.
The fact that an enormous number of spermatozoa are produced, and only
one, or at most, a few perform the function of fertilization, raises the
question as to what becomes of the remainder. It is stated: “Zoologists
have found that in some of the invertebrates the spermatozoa invade the
entire body of the female, and in some species they reach the ovum by
penetrating the cuticle from outside and migrating to their goal.
Studies on rodents show that the sperms invade the epithelium of the
generative mucosa and underlying connective tissue. These tissues seemed
to be stimulated to growth, suggesting that this may influence the
uterine mucosa in its preparation for receiving and embedding the egg,
and in forming the decidua.” It has been shown that the sperms contain a
specific protein capable of producing antibodies in the blood plasma, by
citing the fact that rabbits develop a distinct Aberhalden reaction for
testicular proteins shortly after cohabitation. One very important
observation showed that by immunizing female rabbits with sperms they
were rendered sterile for some time, although after a few months they
again became capable of impregnation. The question raised is: “... if
the spermatozoa invade the female tissues and cause the formation of
specific antibodies which are capable of preventing fertilization, may
not such a process participate in the problem of sterility?” This very
problem seems to be a factor in explaining why some couples who are not
fertile to each other subsequently are both fertile when they cohabit
with other individuals.

_Motility_: After clinical observation of the motility of the
spermatozoa of the bull, I find that it differs little or none from the
types as observed by Reynolds (34) in his work on human spermatozoa. His
observations are so accurate and well described that they will be given
in his words. “All normal motions appear to be consecutive phases.
Initial motion, i. e., motion as seen in fresh semen under favorable
conditions, consists of a lashing of the after part of the tail from
side to side which is so rapid as to constitute vibration. It produces
rapid forward motion in a practically straight line, the head, middle
piece, and forward portion of the tail maintaining their position in the
line of motion with practically no swaying from side to side. The action
of the flagellum is so rapid that it is quite impossible to follow its
individual movements. Spermatozoa swimming in this manner head against
the current and usually cross the field of observation in about five
seconds in the absence of currents or obstacles. This type of motion
will be described throughout the paper as ‘progressive vibratile’
motion. Progressive vibratile motion is normally succeeded after a
variable length of time by what I regard as the second phase of normal
motion.

“The second normal motion differs from the first not only in its
character but in markedly reduced speed. The tail movement alters to a
long stroke from side to side and almost the whole length of the tail
partakes in the stroke. This is, moreover, accompanied by swaying of the
head and middle piece through an arc which is always considerable and
may even equal ninety degrees. The general outline of the spermatozoa,
from being practically straight with almost non-detectable sharp, quick,
small arc vibration of the after-tail, has become an S in outline, with
large, slow, plainly perceptible undulations traveling gradually
backward throughout the length of the spermatozoon. Speed has been lost
and direction seems to be more specifically determined by the
surroundings. Individuals at this stage show a pronounced choice of
direction and go up to objects in the medium, from which they later make
off as though the movement were determined by tactile reaction to some
extent. This type of motion has, therefore, been named ‘undulatory
tactile’ in contradistinction to ‘progressive vibratile.’

“The third type of normal motion succeeds the second and consists in a
tendency on the part of the spermatozoon to push itself against or into
any small masses of cells, or sometimes other materials, which it may
find in the neighborhood, bunting itself into any small cove that can be
found, and maintaining a slight burrowing motion by a lashing tail
movement of the vibratile type not unlike the movements of the caudal
fin of a fish. The movement of the flagellum in this third type is
unlike the second type in that it is vibratile rather than lashing, but
is slower than the vibratile motion of the first type and less limited
to the afterpart of the tail. These spermatozoa are apparently not
caught in the debris or unable to move off. From time to time, they back
out of such a cove and seek another mooring place.

“This ‘stationary hunting’ motion is less universal than the other two.
Many individual spermatozoa fail to attain it. It seems probable that
only the most vigorous individuals ever reach this stair”. It has not
been encountered in unmixed semen or in any artificial mediums. It has
been observed only when the spermatozoon is in the secretions of the
female genital tract. It is most frequent when the spermatozoon is in
contact with a nest of epithelial cells....

“The three types of normal motion are not only distinctive but are
always consecutive, i. e., the second follows the first after a period
which is apparently determined both by initial vitality and by the
favorable or unfavorable character of the medium, while the third has
been observed to occur only in individuals which have already developed
the second. They apparently constitute a normal cycle.

“This cycle is open to the theoretical explanation that these types of
motion are directly adapted to the function of the spermatozoon; thus,
the progressive vibratile motion which is characteristic of the earliest
period of its existence appears especially suitable for its prolonged
journey through the cervix and uterus to the fundus and tube. This is
supported by the fact that during this motion it always heads directly
against any existing current, and that during this stage of its journey
it must under natural conditions be continuously exposed to the faint
outward ciliary currents of the mucous membrane of these passages.

“The undulatory tactile motion which succeeds the progressive vibratile
would then be well adapted to the later stage in which the spermatozoon
has reached the tube, where its success in conjugation is dependent on
its finding the ovum rather than on further progress.

“The stationary bunting type of motion is that which would be demanded
by the passage of the spermatozoon through the egg membrane which has
been so often observed in the lower animals. This very plausible
explanation is, however, necessarily theoretical and must always remain
so, as the conditions which surround the specimen on the field of the
microscope vary in so many respects from those in which it accomplishes
conjugation in the course of nature; but the practical importance of the
study of types of motion is not affected by their explanation.”

The duration of motility is a variable factor, dependent entirely upon
the environment in which the spermatozoa are placed. Within the body
they usually survive at least a week. One author describes a case in
which he found living sperms in a woman who stated that coition had not
been experienced for three and one-half weeks. It has been stated with
regard to human sperms, that their motion should continue or be capable
of being re-established for twelve hours. Cary (35) states, “first, that
in their proper medium and at the body temperature the viability of the
sperm cells may extend over a period of a few days; second, that their
prolonged vitality is probably dependent upon the normal lime salts of
the prostatic fluid; third, that the sustaining power of the seminal
fluid is increased by its union with the normal secretion of the female
genital tract.” After death of the male animal they retain their
motility in the genital tract for twenty-four to forty-eight hours.

Wolf (36) worked on this problem in rabbits, and summarizes as follows:
“The motility of rabbit spermatozoa can be preserved for at least nine
days by placing the juice of the epididymis in the Tyrode solution which
had been buffered and to which glucose had been added. The solution is
adjusted to a pH of about 7.4. Oxygen is passed in and a suitable amount
of sodium bicarbonate added. The preparation must be kept at a
temperature near the freezing point of water.” Under ordinary conditions
motility persists outside the body only a few hours after ejaculation,
but if the semen is kept quite cool till the time of examination on a
warm stage, motility should be capable of being restored in at least a
fair percentage of the sperms for twenty-four to forty-eight hours. The
cells are more sensitive to heat than to cold, and even to dilute acids
more than to alkalies.

Henle (quoted by Ellenberger) states that a spermatozoon under favorable
conditions travels at the rate of twenty-seven millimeters in seven and
one-half minutes, which makes three and five-tenths millimeters per
minute. This is about sixty times the entire length of the spermatozoon,
and twenty-one centimeters in an hour. Forward motion is also more
pronounced when the swim is against the current, such as is produced by
the cilia of the oviduct. It has been demonstrated that feebly motile
sperms become very actively motile when placed on the mucosa of a fresh
Fallopian tube.


                               TECHNIQUE

The material used in the work came from abattoir animals, bull calves
and adult bulls raised in the department herd, and sires upon which
clinical observations had been made by various veterinarians in the
field. Semen samples, many of which were sent in, were collected as
often as possible after the method described by Williams (16). The
genital organs were removed with as little chance of contamination as
possible, and taken or sent to the laboratory where the examinations
were made soon after arrival.

All cultures were made by searing the surface carefully, tearing out a
small portion of the tissue with sterile forceps, and placing it upon
the media. In most cases, however, where fluids were present, tubes were
inoculated with the material which had been drawn off with a sterile
pipette. As stated by Carpenter (9), in his work on the female genital
tract, the organisms usually live in the depths of the tissue. The media
used principally were glucose glycerin agar (glucose 1 per cent,
glycerin 3 per cent); plain agar, both with a pH value of 7.4, and
Loeffler’s blood serum. Small amounts of sterile blood serum or
defibrinated blood were added to most of the agar slants to insure
better growths of streptococci when present. All tubes, to which the
serum had been added, were incubated for forty-eight hours before
inoculation to insure absolute sterility.

After inoculation, the agar tubes were sealed with sealing wax to give a
partial oxygen tension which was quite necessary in isolating the
streptococci. The growth of other organisms was by no means hindered by
the procedure, for one tube from each organ was often left unsealed.
Incubation was at 37° C, and the routine method of examining the tubes
was identical with the method of Carpenter (9).

Whenever possible, a sample of blood was obtained from the animal either
before, or at the time of slaughter, for agglutination with _Bact.
abortum_ antigen. Extracts from the seminal vesicles, testes, and
epididymes were injected into the guinea pigs and examined at the end of
four to six weeks for the presence of _Bact. abortum_.

Sections of all organs were fixed as soon as possible in either Zenker’s
or Helly’s fluid. Hematoxylin and eosin were used as routine tissue
stains. Eosin and methylene blue, and Mallory’s connective tissue stain
were, however, frequently utilized for special staining reactions.

The motility of the spermatozoa is best observed about half an hour
after ejaculation, when the thick tenacious clot has started to liquefy.
A drop of the fluid is placed upon a warmed slide, preferably one with a
slight depression in it, and observation made with high or low powered
objectives. The semen may be examined whole, or diluted with
physiological saline solution. In the latter case, the sperms have a
greater opportunity for freedom of motion in the absence of the thick
viscid coagulate. A small vial of saline solution may be carried in
one’s pocket where it will be kept warm, and a drop of this placed upon
the glass slide. If the clot of semen is merely touched to this drop on
the slide, plenty of spermatozoa will be deposited for an examination.
This method is very satisfactory for the observation of motility, but
needless to say, the undiluted semen must be used for the determination
of the number of sperms present. If necessary, the specimen may be
covered with a cover glass and the oil immersion objective used. While a
warmed slide is quite sufficient to enable one to detect the presence of
motility, the field soon cools and the sperms gradually become less
motile. If possible, it is best to use a small electrically heated stage
warmer, which keeps the field at a constant body temperature, so that
the duration of the motion may be observed for hours if warmed
physiological saline solution is added as the fluid evaporates.

Stained preparations are best made with _thin_ smears on the glass
slides. This is conveniently done by placing a drop of the semen on a
slide and smearing it over the surface with the edge of another slide. A
fairly thin and even field is thus obtained. A still better method is to
first dilute the semen with physiological saline solution, so as to
obtain fewer sperms in the field. After drying the preparation in air,
fixation may be produced by drawing the slide through a gas flame
several times, by immersion in equal parts of alcohol and ether, or even
by the use of tissue fixers such as Helly’s or Zenker’s fluids. For
ordinary staining, heat fixation is the quickest, and at the same time
is quite satisfactory. After the slide is cooled, or washed, to remove
the fixing solutions, it should be placed for a few minutes in a
_freshly_ prepared solution (1 per cent) of chlorazene, as recommended
by Williams, to remove the mucus and proteid material which otherwise
blur the field. Other authors (38) have recommended diluting the semen
with about twenty volumes of a 0.12 per cent sodium carbonate solution
in 0.8 per cent sodium chloride. From this liquid the cells should be
centrifuged for several minutes, removed with a pipette, and smeared on
the slide. Following this, the slide should be thoroughly washed,
preferably for ten minutes in running water, after which it is ready for
staining. Numerous methods have been used for this procedure, but the
sperms are more or less erratic in their reactions to the dyes, and one
must be very careful to use the same method in all samples, in order to
obtain uniform results. For quick staining, to bring out gross
abnormalities of structure, and number of sperms present, one may use
Gram’s stain, or a light stain with any of the aniline dyes, such as
fuchsin. To bring out the finer structure, particularly of the head,
more careful technic must be employed.

Carnett and others (38) recommend the following: “The method of staining
by iron-hematoxylin, particularly when supplemented by a cytoplasm
stain, has proved, on the whole, the most satisfactory, and possesses
the additional advantage of being absolutely permanent, a quality that
few anilines can boast. The method consisted of treating the fixed
object—and here the fixing agent was heat—with a two per cent solution
of iron-alum for from two to four hours. The excess of iron-alum was
then _completely_ removed by pure water, and the object treated with a
solution of hematoxylin (one per cent aqueous) for twelve hours or
longer. The cells by this time were perfectly black. However, a 1 per
cent solution of iron-alum removed the stain from the cytoplasm, leaving
the chromatin of the head, the centrosome, and the axial filament a
brilliant blue-black. Care must be taken that the preparation is not
over-decolorized. After decolorization a saturated aqueous solution of
eosin was added for from one to three minutes. This stained the
protoplasmic envelope pink, and, unless the envelope is overstained, the
view of the inner structures is not impaired in the least.”

Williams (17) recommends using two staining solutions, one of alcoholic
eosin and fuchsin, the other a diluted methylene blue. The results
obtained are, however, more or less erratic, due to the unstable
character of the former stain, and the ease with which one may over or
under stain. Many beautiful specimens may, nevertheless, be obtained by
this method. I have frequently used a fairly quick method, though one
not satisfactory in all cases, which consists of staining for five or
six minutes in a saturated aqueous solution of fuchsin, washing in
water, and counterstaining for a few seconds in a strong solution of
methylene blue. A quite satisfactory method is to stain from two to five
minutes in a saturated aqueous solution of methyl green, with the
application of gentle heat. The heat may be applied by warming the slide
over a gas flame as it steams, or by placing the jar containing the
stain in a hot water bath. The slide is then washed thoroughly and
counterstained for five minutes in a strong aqueous solution of eosin.
This is a fairly reliable method, and many excellent preparations may be
obtained by its use. The nucleus is stained green, the anterior part of
the head and all of the tail pink. So far, I have found this a very
reliable stain for routine work.


                               PATHOLOGY

In the genital tracts that I have studied, a complete pathological and
bacteriological examination was made wherever possible, but in many of
the abattoir animals, and certain others, gross and microscopical
examinations only could be made. The genital organs of one hundred and
ninety-six males have been examined, and the gross or microscopical
changes, or both, determined. The abattoir animals were from a large
slaughter house, and a small local plant.

Of the tracts, the pathology of which was studied, two were from aborted
fetuses; seven from apparently normal young calves; four from mature
fertile bulls; and sixteen from mature infertile or sterile sires. The
remainder (167) of those examined were from abattoir animals. Besides
these, three specimens of seminal vesicles, and seven of testes were
studied.

The tracts of the aborted fetuses and veal calves were apparently
normal, both on gross and microscopic examination of the vesicles and
testes. On gross examination, the tracts of the mature fertile bulls
were normal, except for the presence of many fine connective tissue
tufts and strands upon the serous covering of the tails of the
epididymes, and adjacent portion of the parietal layer of the tunica
vaginalis. Microscopic sections of all parts were apparently normal. The
more important pathological changes in the tracts of the sixteen sterile
or infertile bulls are given in the appended chart. The tracts are
numbered the same as in Group VI of the report of the bacteriological
findings; that is, any particular number in either table refers to the
same animal. References are made throughout the text to some cases which
appear in this group of animals. Prostate and Cowper’s glands are not
included in the chart as they were not examined in some, and were
negative in the others. Fibrous tufts and strands were present on the
covering of the epididymes in each animal.

The study of sections from the abattoir animals, as well as those from
the sterile or infertile bulls, forms the basis for the following
observations upon the pathology of the male genital tract. The tracts
secured from the abattoir were studied for the most part on the basis of
the organ rather than on that of the animal. For example, all sections
of testes were placed in the same bottle of fixer, and the same plan
followed for the other organs.


TESTES: The testes seldom presented gross alterations of structure
except for abscess formation, which, according to Williams, occurs more
frequently in the bull than in any of the other domesticated animals. He
also states that arrest in development by which the organs remain soft,
flaccid, and somewhat smaller than normal is not uncommon. One very
interesting specimen, which typifies abscess formation, came from a bull
with a history revealing that one testis had become much enlarged, hot,
and painful. These symptoms developed very rapidly. Anorexia was well
marked. Local applications were used for several weeks, but at the end
of two months the condition was so little improved that unilateral
castration was performed. The general condition of the animal soon
improved, but after a year of service he was so uncertain compared to
what he had been, that he was sent to the butcher. It was impossible to
obtain the other testicle for study, though it undoubtedly was abnormal.
The testicle removed was considerably enlarged, measuring twenty by ten
and one-half centimeters. The tunica albuginea presented a thickness of
six millimeters, and was made up of firm sclerotic tissue. The
epididymis was not recognizable in the mass. Testicular tissue was
almost entirely gone. The only remains, of what appeared to have been
parenchyma, was an elongated irregular area at one side of the organ.
This tissue consisted of a whitish opalescent material, speckled with
varying sized abscesses. This organ is pictured in Fig. 3. The remainder
of the organ consisted of a thick yellowish caseous mass. _Streptococcus
viridans_ was recovered from the outer portion of the organ, and guinea
pig inoculations failed to demonstrate _Bact. abortum_.

Microscopically, changes are quite common and varied in character. In
the seminiferous tubules, the changes range from a slight desquamation
of the germinal epithelium to atrophy and complete degeneration of the
entire tubule, as was the case in the left testis of Bull 1. In the mild
cases, spermatogenesis occurs apparently in a normal manner up to the
spermatid stage, at which point many of the cells degenerate and slough
off. These appear in the seminal fluid, associated with the few sperms
that reach maturity. This sloughing and degeneration may be localized in
a few of the tubules, or it may be widespread over the entire organ.
Likewise, the changes may involve not only the more mature cells, but
they may be so severe as to cause almost total degeneration and
desquamation of the seminal epithelium, as in Fig. 15. These defects in
spermatogenesis are of course evidenced in the semen by the presence of
immature, or abnormal types of sperms. With cessation of spermatogenesis
or degeneration of the epithelium of the entire gland, no sperms are
formed. Not infrequently one finds numerous tubules, or even the entire
testis in which the germinal epithelium is intact, but there is little
or no evidence of mitosis, as in some tubules of Bull 6. The cells are
several layers deep as in the normal condition, but they are not
dividing. This condition is shown in Fig. 13.

In the more chronic forms, the tubules become atrophied, and frequently
disappear entirely. The membrana propria may become thickened, due to
excessive connective tissue formation, or infiltration with serum or
exudate. On the other hand, a distinct atrophy may occur. The stroma of
the organ not infrequently is thickened by inflammatory exudates, or by
a noticeable increase in the connective tissue. In some testes, the
connective tissue is so much increased that the tubules rapidly become
atrophied, and disappear. In abscess formation, due to acute
inflammations, the entire organ becomes enlarged, markedly hyperaemic,
and infiltrated with leucocytes. Necrotic areas appear here and there in
the parenchyma. The rete often shows a marked degeneration of the lining
epithelium, and atrophy caused by increase of the interstitial
connective tissue.


EPIDIDYMIS: This organ not infrequently presents gross abnormalities,
and very often is pathological on microscopic examination. Acute,
inflammation, with induration or abscess formation, is very common in
the tail, but less so in the head and body. Possibly this is caused by
the fact that the tail is the most pendant portion of the organ. In
these cases, the tail is enlarged, soft, and quite hot and painful on
physical examination. Enlargement, due to a connective tissue
induration, occurs occasionally in all three parts, and the inflammation
may produce adhesions to the adjacent serous membranes. Inflammation of
both the parietal and visceral layers of the tunica vaginalis is very
common. In those cases, the membrane usually is quite hyperaemic, and on
the surface it presents many small reddened tufts of newly-formed
connective tissue. In adult bulls it is exceptional not to find at least
slight evidence of some previous inflammation. In all of the numerous
bulls examined, both apparently normal and sterile, I have found but one
in which some evidence of inflammation (either present or past) could
not be found. Along with the fibrous tufts, are numerous fine strands of
connective tissues passing from the covering of the tail of the
epididymis to the adjacent portion of the parietal layer of the tunica.
The strands often extend even to the upper part of the head.

Microscopically, inflammation of the part is shown by hyperaemia, loss
of cilia of the lining cells, and exudation. In the more severe forms,
the lining cells which furnish considerable secretion for the
nourishment and stimulation of the sperms, become degenerated, and are
exfoliated into the lumen, as in Fig. 21. This condition is very common
in sterile bulls, and those of lowered fertility. In the chronic types,
the interstitial connective tissue is increased in amount, leading to
degeneration and atrophy of part or all of the tubules, as in the case
of Bull 2. Infiltration with leucocytes, and necrosis, are the
predominating lesions in the pyogenic types of inflammation.


DUCTUS DEFERENS: This tube seems to be peculiarly free from severe
inflammatory processes, and when these appear they are limited to the
mucosa. The cells of the lining membrane not infrequently show a mild
type of degeneration and exfoliation, or in the more chronic forms, the
entire membrane degenerates and disappears. In man, the duct
occasionally becomes occluded, but so far I have failed to find this
condition in the bull. Undoubtedly, when the occlusion does occur, it is
near the origin of the duct at the tail of the epididymis.


SEMINAL VESICLES: The seminal vesicles and epididymis, especially the
tail, seem to be the parts most subject to extensive pathological
changes, and bacterial invasion. In most instances, diseased vesicles
present gross manifestations recognizable on clinical examination, while
on the other hand microscopic changes may be present in the absence of
gross lesions. As diagnosed on physical examination, or even on post
mortem examination of the tract, the various forms may be classified
into:

1. _Acute Catarrhal Type_: In this form, the vesicles are usually
enlarged, soft, and more or less reddened by hyperaemia. On physical
examination of the animal, distinct flinching is produced when pressure
is applied to the organ. Enlargement may even be absent in the early
stages, and the diagnosis may be made from the extreme sensitiveness
alone.

2. _Suppurative or Cystic Types_: In both of these types, the vesicles
are usually enlarged, either uniformly, or, as is usually the case, in
localized areas. The suppurative form may extend over the entire gland,
forming one large encapsulated abscess, or on the other hand, it may
take the form of variable sized abscesses with thick sclerotic, or thin
fluctuating walls. Occasionally the abscesses rupture and discharge
their contents into the rectum. Dr. Williams presented one case of this
type. One vesicle was apparently normal, whereas the other was about
five times larger than normal, and consisted of a dense outer capsule
which was adherent to all surrounding parts. On dissection, it was found
that the organ consisted of abscesses of various sizes, the larger one
of which had ruptured some time previously into the rectum, leaving the
distinct remains of an opening into that part. The cystic form may occur
either with or without suppuration. One case came to my attention in
which both vesicles were made up of abscesses of varying sizes as well
as of a smaller number of cysts. Evidently the cysts were of the
retention type, and were secondary to the pyogenic infection.

3. _Chronic or Sclerotic Type_: This form is characterized by a distinct
firmness with or without marked enlargement. The condition may be
accompanied by disease of the parenchymatous tissue or it may take the
form of a chronic productive inflammation of the interstitial tissue.
This inflammation may be simply a superficial thickening, or it may
extend in between the lobules.

4. The _Peri-vesicular or “pan-inflammatory” Type_ usually is the result
of severe inflammation of the vesicles, with probable rupture of some of
the smaller cysts or abscesses upon the surface. The vesicles are, as a
rule, considerably enlarged and buried in a dense mass of adhesions
which involve neighboring structures. The vesicles cannot be palpated on
physical examination, and it is only on careful post mortem dissection
that they may be studied. This type, however, is quite rare,—two cases
only having come to my attention. In both, the vesicles themselves were
markedly affected.

Microscopically, changes in the vesicles are quite frequently
encountered, even in the absence of gross manifestations. In the acute
catarrhal forms, the mucosa and submucosa are hyperaemic. The lining
cells show various forms of degeneration, and there are, as a rule,
inflammatory exudates in the lumen. As the inflammation progresses, the
lining cells degenerate further, and become cast off into the lumen of
the glandular cavities, as in Plate VI. The normal clear mucous
secretion becomes mixed with fibrin, leucocytes, and cellular debris.
These changes may involve merely parts of the organ, or they may be
quite extensive. With large sections, one may find the inflammation in
all stages, from the mildest catarrhal type, to complete degeneration
and exfoliation of the secretion-forming mucosal cells, and filling of
the cavities with degenerated cells, leucocytes, and debris. Frequently
the interstitial tissue is in no way affected, but at times it is
thickened by oedematous exudates, leucocytes, and fibrin. The chronic
interstitial form is characterized by a considerable increase of
connective tissue,—producing marked atrophy, or even complete
obliteration of the glandular cavities. Microscopically the suppurative
form may be diffuse over the entire gland, or as stated previously, may
be in the form of localized abscesses, with or without a thick
connective tissue wall. The parenchyma in these cases is usually
extensively degenerated and atrophied in those parts that have not
undergone suppuration and necrosis. The cysts appear to be of the
ordinary retention type, and may or may not be accompanied by extensive
changes in the lining epithelium.

Both the abscess formation and cystic conditions are undoubtedly
initiated by an obstructive inflammation of all or part of the excretory
duct. This is, however, a protective mechanism, for where the duct is
closed the bacteria and exudates are unable to reach the urethra and
contaminate the semen.


PROSTATE AND COWPER’S GLANDS: These glands were more or less neglected
in the early part of the work, but later were subjected to the same
examination as other parts. Of the thirty-six of each type of gland
examined, I failed to find one with any gross changes, but two prostates
were found that presented a mild catarrhal inflammation of the mucosa.
It is probable that Cowper’s glands, as well, occasionally undergo
inflammatory changes.


SEMEN: The semen, made up as it is of mixed products of the testes and
accessory sexual glands, is very often abnormal, as would be expected in
view of the frequency with which changes occur in the glands
contributing to its formation. The normal semen is remarkably adapted to
its function of nourishment and stimulation of the spermatozoa, and
their conveyance to the internal female genital organs. The spermatozoa
are extremely sensitive to changes in their environment, with the result
that any alteration of the physical or biochemical content of the
seminal fluid may cause death of the sperms. With this in view, we must
remember that disease of any of the contributing organs is a potential
danger, and threatens the potency of the animal. Each or all of the
glands may add bacteria, acid secretions, or inflammatory exudates. On
the other hand, they may not function at all. In each case, however, the
semen is altered.

Unfortunately it is impossible with present methods to obtain the fluid
absolutely free from vaginal mucus, but with care it may be secured
reasonably free from contamination by douching the prepuce of the bull
and vagina of the cow before service. This method was used as often as
possible in collecting the samples. The usual amount of semen obtained
was from six to ten cubic centimeters.

With a hypersecretion of one or all of the glands, the semen becomes
quite thin and watery, with a deficiency of solid matter, together with
changes in reaction. On the other hand, hypofunction results in a
secretion too viscid, which is equally unsuited to the requirements of
the spermatozoa. The thin watery semen clots imperfectly or not at all,
and clotting is essential in protecting the spermatozoa from the acid
secretions of the vagina. Likewise, a medium too viscid is a distinct
hindrance to motility. Changes in reaction are very frequently
encountered. The sperms are very sensitive to dilute acids, so that with
even a slight acidity motility may diminish or entirely cease. Purulent
inflammatory exudates are occasionally mixed with the semen, and
although the pus cells themselves have not been found to be destructive
to the sperms, certain degeneration products in the exudate are very
toxic, and inhibit or destroy the motility. So far, I have failed to
find red corpuscles present. One very interesting sample of semen was
quite thick, of a yellowish green color, and of a distinctly acid
reaction. The secretion from the vesicles was later found to be of this
same character, and was due to a _Ps. pyocyaneus_ infection. The
vesicles were highly inflamed and degenerated. The spermatozoa were in
this case markedly decreased in number, and devoid of motility.

The early precipitation of the “Boettcherchen” crystals seems to be
intimately connected with sterile semen, or spermatozoa of lowered
vitality. Likewise, a decrease in solid matter is often seen in a
deficient secretion. In normal semen, the clot disappears after standing
a time, and a thick sediment settles out. This sediment is decreased in
amount as a rule in abnormal semen.


SPERMATOZOA: Spermatozoa, the essential germinal elements, are very
frequently abnormal, changes in which may be manifested in many ways. We
may divide the deviations into changes in structure, and changes in the
motility which is so indicative of the intrinsic vitality of the sperm.
Reynolds (34) describes two forms of abnormal motion. The first is
“rotary swimming,” in which the sperms move forward progressively, and
sometimes with fair rapidity, but in a spiral screwlike manner. He
states that this type of swimming is very awkward, easy to recognize,
and is usually of quite long duration. The other form termed “pendulum
swimming,” he states, is less common than the rotary swimming and is
usually confined to relatively fewer sperms in a given field. “In this
the middle piece and upper tail seem to lose their flexibility and
balance to a considerable degree, and the lower tail motion swings the
forward part of the spermatozoon to and fro with a pendulum movement.
This type of swimming yields very poor progress.”

One factor we must bear in mind in the study of the semen obtained from
the vagina, is that the spermatozoa may be highly motile before
ejaculation, but the admixture of hostile vaginal mucus may inhibit or
destroy the motility. On the other hand, the conditions may be reversed.
Cary (35), in one instance, found that the spermatozoa in a sample of
semen collected from a condom, appeared to be of very low vitality,
while when they were mixed with the vaginal secretions, an exaggerated
activity was manifested. May we not have to contend with this factor in
some herds in which there is a very distinct acid and toxic vaginal
secretion from the products of cervicitis and vaginitis?

In a study of motility, we must consider not only the abnormal types
which may be encountered but the percentage of motile cells, and the
duration of the movement. In _necrospermia_ all the ejaculated cells are
motionless or dead. In other specimens, varying percentages of the cells
are without motion, and the others may be possessed of full and lasting
motility. On the other hand, the motility in some cases is very active
at first, but quickly subsides even under the best of conditions. The
appearance in freshly ejaculated semen of numerous sperms that have a
tendency to take on the “undulatory tactile” type of motion when they
should be in a highly active state, is very indicative of lowered
vitality. Many specimens present this very picture, whereas the very
active progressive movement should, under proper conditions, survive for
a considerable time before it gives way to the second, and slower type.
The cells frequently early bunt into epithelial cells or clumps of
immotile sperms, then back out and move around sluggishly, only to
repeat the same performance till they stop moving entirely. I have seen
one specimen in which the sperms all tended to clump. Whether this was
the result of some agglutinative substance in the vaginal secretion is
problematical. I have seen several specimens of semen in which
practically all the sperms were motile when first examined, but the
motion did not survive for any great length of time. Even a small
percentage of motionless sperms or of those showing lowered vitality is
a considerable factor in potency. Although millions of the germinal
elements are ejaculated into the vagina, large numbers of them are
destroyed or become motionless there, and a small number is left behind
in the cervix and uterus; so that even though but a single sperm is
required for fertilization, the chances of impregnation are diminished
in proportion to the number of dead or defective sperms.

_Aspermia_: Absence of spermatozoa in the semen is rarely encountered,
and is probably due either to total cessation of spermatogenesis, or to
an obstruction at some point in the system of excretory ducts. I have
seen but one case of this character. The semen of this bull was greatly
increased in amount, and of a thin watery consistency. Due to lack of
cooperation on the part of the owners, the tract could not be obtained
for study. _Oligospermia_, or a diminution of the number of spermatozoa,
is quite common, and is undoubtedly associated with defective
spermatogenesis, either as a result of poor mitosis of the seminal
epithelium, or degeneration of the elements before maturity. This
condition may vary from the finding of only occasional dead sperms in
the field, to but a slight decrease in the usual number of normal sperms
observed.

Abnormalities in morphology may be classified into immature types, and
deformities or imperfect development of the head and tail. Defective
spermatogenesis occurs so frequently that it is not surprising to find
spermatozoa in various stages of development cast into the excretory
ducts. The various stages passed through in the development, from
spermatogonia to adult sperm, are numerous, and it therefore is to be
expected that we should see in abnormal semen many different immature
forms. No classification of the various types can be made, but a clearer
understanding of them can best be obtained by a review of the process of
spermatogenesis.

Spermatocytes and spermatids are seen in the more severe types of
defective spermatogenesis, and are relatively uncommon, while the more
mature forms that result from the transformations of spermatid to adult
cell are very often seen. Some of these intermediate types are large
oval cells without distinct nuclei and as a rule with poorly developed
tails. Cells with no tails or distinct nuclei, those with protoplasmic
appendages to the head or tail, and various other types, are
occasionally encountered. Most of these are motionless and incapable of
producing impregnation. Others are active, but survive a comparatively
short time. According to Cary, the production of the immature cells is
an effort on the part of the testes to supply an abnormal demand, and
their presence indicates that the fertility of the semen is impaired.

The deformities, which may be divided into cephalic and caudal groups,
are also the product of defective spermatogenesis, or they represent a
degenerative process induced possibly by abnormalities of the fluid
environment. It is rather difficult, however, to distinguish between
deformities and immature types. The two most common cephalic deformities
are what might be called macro and microcephalic forms. In the former,
the head is enlarged to a greater or less extent, it is usually
defective in staining qualities, and its outline is indistinct, due to
degeneration of the covering membrane. This type is seen in Fig. 32.
Also the shape of the head is usually abnormal, being either quite
rounded, long and narrow, or short and very broad. Cells with
protoplasmic appendages, though they are more properly an immature type,
occasionally give the head a greater volume. Microcephalic sperms vary
from those slightly smaller than normal to those in which the head is
represented by a slight knob. In some cells, the head is small and
round, in others, short and stubby, while another type is normal in
outline but diminutive in size. These forms likewise are, as a rule,
deficient in staining qualities, and are undoubtedly degeneration forms,
occurring either as the result of faulty development, or degeneration
subsequent to their formation. Cary believes they are degeneration types
because in the majority of cells the tail is apparently fully formed,
and in the normal process of evolution the tail is the last part of the
cell to be exhibited. Double headed forms are quite rare, but they
nevertheless appear at times. Their significance is difficult to
explain. Another very frequent deformity of the head is a marked
constriction at the posterior part so that it is the shape of a pear or
top as in Fig. 27. In some, the head is otherwise normal in size, while
in others it is much elongated, as in Fig. 28, or considerably
atrophied. A constriction at the middle of the head, as in Fig. 29, is
not uncommon. Both defects are undoubtedly the result of nuclear
deficiency, as the nuclear part of the head in these cases is much
diminished in size, and stains very deeply or not at all. I have seen
spermatozoa, the heads of which were like an inverted cone, with a
bulging rounded base. Other heads are even somewhat contorted and bent
on themselves, as shown to some extent in Fig. 26.

Under caudal deformities, the most frequent form encountered is a
thickening of the connecting piece. This may occur as a uniform
thickening, or as a bulging appendage. Rudimentary development of the
tail, the presence of two poorly formed tails, and defective development
of the connecting piece occur rather infrequently.

All these immature and defective types are, as a rule, motionless, and
of course incapable of producing fertilization. Their presence indicates
lowered fertility of the semen. Besides these deformities, there are
sperms showing a curvature of the tail at an acute angle just posterior
to the neck,—the so-called “wry neck.” Their significance is difficult
to explain, but they occur frequently in semen fixed and stained by the
same routine methods used on samples in which they are absent. They
probably are not the result of the methods used in fixing and staining.
Some think they are slightly immature types, or that the condition is
produced by abnormal contractions of the tail. The majority of sperms,
however, especially those from highly fertile bulls, do not show this
type at all.

The most common changes in the spermatozoa, are those in which there is
a separation of the head from the tail, and degeneration of the head as
evidenced by reaction to stains. The separation of the head from the
tail always occurs at the neck, and often is associated with
degeneration or abnormalities of the head. The separation, in the
majority of cases, indicates some lowering of vitality in the elements,
although in many instances traumatism produced in making smears or
collecting the samples is responsible. Various forms of abnormal
staining of the head are very common. The cell membrane, which is
normally distinct and sharp, becomes blurred in outline. Normally, the
head takes a good differential stain, the anterior part staining
lightly, and the posterior part somewhat deeper. The nucleus is distinct
in outline and well defined. The lighter “inner body” stands out in well
stained specimens. As the result of degeneration, the whole head may
take the stain uniformly, either slightly or much deeper than normal,
according to the degree of degeneration. The whole problem of staining,
however, depends very much upon the methods used, and the care with
which they are applied. When a good method is obtained, it should be
adhered to, and used uniformly on all specimens. As a rule, however, a
certain amount of practice will enable one to differentiate between the
sharply outlined, clearly staining normal forms, and those that show
abnormal reactions to the stains.


                              BACTERIOLOGY

A complete bacteriological study was made of the genital tracts of
fourteen normal young veal calves (six to twelve weeks old), four mature
fertile bulls, and sixteen mature bulls, either sterile or impotent to
some degree. Together with these, the tracts of eleven aborted fetuses,
seven calves dying from calf infections (scours or pneumonia), and
sixteen bulls slaughtered at an abattoir were studied bacteriologically.
Occasionally, studies were made of individual seminal vesicles or
testes, when these parts alone were brought or sent in. The history of
the abattoir animals was, of course, quite indefinite or entirely
negative. On the killing floor, many tracts could be studied for
pathological changes, but in the bacteriological work it was difficult
to care for more than two tracts on each visit.

The results of the bacteriological examinations are given in the
appended tables, in which the tracts are divided into six groups. The
results in Group I. consisting of normal veal calves, indicate that the
genital organs of young male calves are, under normal conditions, free
from bacteria. Carpenter (9) obtained like results in examining the
genital tracts of heifer calves. The cultures made from the seminal
vesicles and testes of all these veal calves were, with two exceptions,
negative. Both seminal vesicles of one tract and one of another yielded
cultures of _Staphylococcus albus_.

Adult bulls of known fertility were naturally difficult to obtain, only
the four animals in Group II being available for examination. Two of
these (Nos. 1 and 2) were from the experimental herd kept by the
department, and at all times had a good breeding history. The other two
were good breeders, but were slaughtered because of poor pedigrees. Bull
1, raised in the department herd, had a severe attack of scours when a
few weeks old, while the calfhood history of the other is not known, he
having been purchased after reaching sexual maturity. The cultures from
the genital organs of the former (Bull 1) were entirely negative, except
those from the left epididymis and scrotal sac, which yielded growths of
_Streptococcus viridans_. All the organs of the tract from this animal
were normal, except for the fact that numerous strands of connective
tissue extended from the serous covering of the tail of both epididymes
to the adjacent part of the parietal layer of the tunica. The tract of
the other failed to show any organisms. The only evidence of any
abnormality was the presence of the same connective tissue strands on
the tail of the epididymis, as in the first tract. The other two bulls
gave negative cultures from all parts.

Of the sixteen bulls in Group III, slaughtered at abattoirs, and in
which no history was available, eight failed to show the presence of any
organisms in their genitalia. Of the others, the vesicles yielded
cultures of _Staphylococcus albus_ nine times, and _streptococci_ four
times. _Staphylococcus albus_ was recovered once from the prostate, and
once from Cowper’s glands. The testes gave cultures of staphylococci in
two cases, and _Bact. abortum_ in one. No observable anatomical changes
accompanied the presence of the Bang bacillus in this case. The
epididymes showed growths of staphylococci five times, and streptococci
on three occasions. _Streptococci_ were isolated from the scrotal sacs
of eight testes.

The results in Group IV (aborted fetuses) show that bacteria are often
present in the seminal vesicles or testes of these animals. As a rule,
however, the organisms are identical with those isolated from the blood
or other parts of the animal. This is to be expected, however, for
because of the feeble resistance of the fetus to any infection, the
organisms circulating in the blood may be isolated, as a rule, from many
different organs and tissues. All samples of blood set with _Bact.
abortum_ antigen were negative, irrespective of whether or not the
organism was recovered from the blood or other tissues. This is in
accordance with the findings of Carpenter in the female fetus,—the
resistance is so feeble that few or no antibodies are formed to combat
any existing infection. _Bact. abortum_ was recovered in two cases from
the vesicles, and in four cases from the testes, but in each instance
the same organism was present in the blood or other tissues of the body.

The results from the tracts of the calves dying of calf infections are
given in Group V, and show that five were negative. The other two showed
_B. coli_, staphylococci, and streptococci, in the organs indicated by
the chart.

In Group VI, the mature infertile or sterile bulls, there was a
comparatively wide variation in the type of organisms encountered, but
streptococci and micrococci were the most common invaders. In the order
of the frequency of infection, the organs would be enumerated as
follows: Vesicles, epididymis (usually the tail), scrotal sac, testes,
prostate, and Cowper’s glands. The first three parts mentioned usually
contained bacteria. A streptococcus was the usual invader of the scrotal
sac, and very probably was the cause of the connective tissue tufts and
strands so frequently seen. The vesicles and epididymes gave, in the
order of the frequency of their occurrence, staphylococci, streptococci,
_B. coli_, and _Ps. pyocyaneus_. The streptococci were usually of the
viridans group, though a few were hemolytic, and two strains were
indifferent to blood. The testes gave growths in only eleven
instances,—staphylococci eight times, streptococci two times, and an
unidentified rod once. The prostate yielded staphylococci twice and
Cowper’s gland once.

As emphasized previously, the vesicles and tail of the epididymis are
most subject to infection and degenerative changes. At the same time,
they are intimately connected with the secretion of the semen. Once the
epididymis becomes infected, there is nothing to prevent the organisms,
together with inflammatory products, from being mixed with the semen and
ejaculated during coitus. Also in the vesicles, unless the inflammation
is so severe as to occlude the excretory duct, the organisms are mixed
with the vesicular secretion, which is emptied into the urethra during
ejaculation. Carried along with the bacteria, are, of course, toxic
products, degenerated cells, and the otherwise altered secretion of the
glands. One interesting case noted was that of a bull that had passed
from a state of fertility to that of complete sterility during a period
of two months. The semen was semi-fluid, greenish yellow in color, and
contained a very few non-motile spermatozoa. Post mortem examination
showed that the vesicles had undergone abscess formation and that they
contained yellowish green material similar to that which had been
discharged during copulation. _Streptococcus hemolyticus_ and _Ps.
pyocyaneus_ were isolated from both vesicles, and from the semen.
_Micrococcus albus_ was isolated in nearly all cases of vesiculitis and
was often associated with _Streptococcus viridans_ or _hemolyticus_.

Bacteriological studies of the semen are, on the whole, more or less
unsatisfactory, due to the present difficulty in obtaining samples free
from any chance of contamination. In most of the abnormal bulls,
bacteria of various types were isolated from the semen, most of which
agreed culturally with those later isolated from the internal genital
organs of the same tracts. The method of culturing consisted of douching
the prepuce of the bull and vagina of the female with sterile saline
solution before breeding. Samples of vaginal mucus were taken before
service, and the flora compared to that after douching. This method of
douching produced vaginal samples relatively free from bacteria, at
least so much so that the post coital fluid demonstrated that many
organisms must have been introduced from without. Whether or not they
came in with the semen is problematical, but in all probability this was
the method of introduction.

I have so far failed to obtain _Bact. abortum_ from the tract of an
adult animal, either by direct culture or guinea pig inoculation, except
from the testicle of one abattoir bull. The agglutination tests with
_Bact. abortum_ antigen were all negative, except for two abattoir
bulls. The results so far obtained would seem to indicate that, in
accordance with the findings of other workers, the Bang organism seldom
invades the male genital tract, or does not thrive there after its
introduction. Schroeder (12) and others, have, however, on various
occasions, recovered the organism from the bull, and the former author
even states that it invades the vesicles and is eliminated with the
semen.


                               DISCUSSION

A complete discussion of those factors which have a bearing on
reproduction and fertility in an animal, includes not only a thorough
study of the genital tract, but an appreciative consideration of various
extrinsic factors. The effect of environment has long been known to have
a marked influence upon breeding, particularly with reference to animals
in domestication. Diet, though long relegated to a minor phase of the
question, has, within recent years, come to be a matter of prime
importance with regard to its bearing upon the entire body metabolism.
The endocrine organs preside over and regulate the growth and
functioning of the genital organs from the earliest embryonic stage to
the cessation of sexual life. Any derangement in one results in
functional or organic changes in the other. In a given mating, we must
take into consideration such factors as impediments to coitus, as well
as those numerous agencies in the female which may interfere with the
union of sperm and ovum, or with the successful implantation of the
fertilized egg in the uterus, and its growth and development there till
normal parturition takes place. Successful reproduction depends upon the
mating of sexually sound females to equally sound males. Considering the
various factors which govern reproduction, sexual soundness must
necessarily depend, to a large extent, upon a good general condition of
the entire body.


ENVIRONMENT: The effect of environment on fertility in the bull is no
doubt a minor factor. Cases in which changes in environment affect
fertility probably occur, however, particularly when fear and other
psychic disturbances play a part. Marshall (29) states: “It would seem
probable that failure to breed among animals in a strange environment is
due not, as has been suggested, to any toxic influence on the organs of
generation, but to the same causes as those which restrict breeding in a
state of nature to certain particular seasons, and that the sexual
instinct can only be called into play in response to certain
stimuli,—the existence of which depends to a large extent upon
appropriate seasonal and climatic changes.”


DIET: Under this heading we may include not only the effect of deficient
food, but also constitutional disorders, as a result of which the organs
of generation and those glands guarding their function receive
insufficient nourishment. It is a well known fact, and long has been,
that animals fail to breed when they are in a run down condition or when
they are fed a deficient diet. Cary (35), quoting Hagner, states that
the virility of the spermatozoa is often in direct proportion to the
general physical condition of the patient.

Reynolds (34) emphasizes the fact that it is an established principle
among animal breeders that a high protein diet in both sexes is
essential to full fertility. “Oligospermia with deficient vitality of
the spermatozoa is not infrequently found from constitutional disorders.
It can easily be demonstrated in animals that both low diet and
conditions of life that produce a nervous excitable state are attended
by oligospermia.” Animals that are closely confined, those that are
over-fat (show animals), as well as those fed a deficient ration very
frequently fail to breed, but exercise and change of diet soon overcome
the impotency.

Dutscher, Hart, Steenbock, and other biological chemists have done
extensive work to show the essential importance of vitamines and
minerals in the diet. Their results indicate that animals cannot thrive
and breed normally when fed a diet composed solely of the products of
one plant. There must be variety, and there must be not only a correct
nutritive ratio, but the mineral and vitamine content must be present as
well. Cows fed on the products of one plant often failed to breed, and
if conception occurred, it invariably resulted in a premature birth, or
the birth of weak and poorly nourished calves. The work of these authors
is fundamental, and brings out many important points. Is it not probable
that the deficient diet results in weakened tissues which are easier
prey to the invasion of bacteria?

Macomber and Reynolds (39) experimented upon white rats to determine the
effect of defective diet as a cause of sterility. They call attention to
the confusion caused by the application of the term sterility to most,
or all, infertile matings. They believe that failure of reproduction is,
in fact, the result of decreased fertility rather than of actual
sterility on the part of the two individuals concerned. “There are
certainly a large number of infertile matings which are purely
functional and due to physiologic alterations or local conditions. Such
physiological alterations moreover coexist in the sterilities of
pathologic origin and when unrecognized and consequently unremedied,
undoubtedly explain a large proportion of the continued infertilities
after operation.” Is it possible for a bull to be infertile to the cows
in his herd that have been fed a deficient diet, and at the same time to
breed well when mated to animals outside this herd? This is rather
improbable in practice, but there is always the possibility of its
occurrence. In the experimental work, white rats were used: one strain
from the Wistar Institute with a fertility of about 65 per cent, and the
other from a Dr. Castle’s strain with a fertility of about 90 per cent.
The Wistar rats were fed in groups, each group receiving a diet
deficient in a certain substance: calcium, protein, or fat soluble
vitamine. To this group was added a diet deficient in both calcium and
protein (war diet). These diets reduced the fertility of the groups from
the original 65 per cent, to 55, 31, and 14 per cent respectively. It
delayed the appearance of fertility in young rats raised on these diets,
and lowered its degree in the mature animals. Most of these rats,
however, though infertile to each other, bred promptly when mated to the
Castle rats of known fertility. This demonstrates clearly that relative
infertility of given matings does occur. One interesting feature of the
work is the fact that in the matings on the single deficiency diets,
four deliveries of macerated fetuses occurred and there were two more in
eight deliveries from those reared on the war diet. No cases of this
kind had previously occurred in this strain, which had been under
observation for several years. Does this throw any light upon the cause
of macerated fetuses in cattle? Microscopically the testes and ovaries
of these infertile rats showed no observable changes, a fact which is of
great importance to bear in mind.

Williams, in his book on disease of the genital organs, brings out quite
clearly the relation of defective diet, overfeeding, and lack of
exercise, to reproductive efficiency.

Novarro (40) observed that pigeons fed on a diet without vitamine B
showed degeneration of the seminal epithelium, with hypertrophy and
hyperplasia of the interstitial cells of the testis. Another author
(Allen) showed that reduction in the quantity of water-soluble vitamine
in the diet of rats resulted in total degeneration of all the germ
cells, but it did not interfere with growth and development in other
respects.

The observations of Williams (41), in a pure bred beef herd in Hawaii,
clearly demonstrate the intimate correlation between poor fodder as the
result of extreme drought, and the accentuation of, or increased
susceptibility to, genital infections, as demonstrated by clinical
findings. The genital disorders started soon after the onset of the
drought, and immediately took a downward trend with the advent of the
rainy season.

Judging by the work quoted, we will observe that deficient diet, though
it does not always affect the general health, has a profound effect upon
the genital organs of both sexes, associated with disturbances of
spermatogenesis in the male. In most debilitated and weakened conditions
of the male, spermatogenesis ceases or is markedly defective. We must,
undoubtedly, explain this fact upon the ground of deficient nourishment
to the reproductive organs or possibly the endocrines. The vitamines
have been termed nuclear nourishers, and their absence probably results
in nuclear deficiency.


ENDOCRINES: Bell (42) emphasizes the fact that not only the structure
but also the function of every part of the body is in close correlation
with the rest. “This is essentially true of the ductless glands: the
shadow of their influence is over all.” Further he states that when we
remember that the individual exists to perpetuate the species, it is not
difficult to realize that the metabolic factors concerned in
reproduction are the same as those related to the individual metabolism.
It follows, therefore, that the ductless glands which regulate the
individual metabolism concern equally the reproductive. Brown (43),
discussing the same subject brings out the generalization that the
sympathetic, since it is the most primitive part of the nervous system,
is closely associated with the endocrine system, a still more elemental
means of communication in the body. Also since specialized reproductive
cells appear before the nervous system, the organs of reproduction
remain closely associated with the older chemical reactions now
specialized in the endocrine glands. “The endocrine glands, the
reproductive organs, and the sympathetic nervous system, therefore,
remain as a basic tripod, and it is not likely that a disturbance will
occur for long in one limb without affecting the other two.” The former
author believes that the gonad keeps the other ductless glands informed
of the needs of the genital tract, they in turn influencing the general
metabolism. Jump (44) states: “We are therefore justified in believing
that there is a correlation of function between these (endocrine) glands
and that some cases of sterility are probably due to a derangement of
this correlation.” Biedl (45) concludes: “There appears to be an
intimate anatomical and physiological interrelationship between the
different blood glands which is manifested clinically by the fact that
the pathological disturbance of one gland is accompanied by symptoms
pointing to the functional derangement of one or more of the others.
Knowing, as we do, the many sided interactivity which subsists between
the different internal secretory organs, it is readily conceivable that
isolated diseases of single organs of this group are very much rarer
than, at the first glance, they would appear to be. In the present state
of our knowledge, the only course of investigation which is open to us
is to start with the known results of the functional derangement of any
organ, and, by following these up, to seek the primary link in the
pathological chain.”

Most workers seem to agree that a special connection exists between the
normal function of the adrenal cortex and the sexual organs. Tumors of
the former are usually associated with sex abnormalities, and feeding
young animals the gland substance seems to stimulate growth of the
testes.

Many arguments have been brought forward to show that the prostate
produces an internal secretion. It is a well known fact that this organ
atrophies after castration, and enlarges as the sex life dwindles. As
has been previously stated, Serrlach and Pares reached the conclusion
that the gland produces an internal secretion which controls the
testicular functions and regulates the process of ejaculation. Also they
state that if the prostate is removed, spermatozoa are no longer
produced in the testes, and that the secretory activity of the accessory
genital gland ceases. The secretion is, at any rate, a stimulus to the
internal secretion of the testis.

The thyroid bears a distinct biological relationship to the sexual
glands. Removal of the gland results in imperfect development of the
gonads, infantilism, and general torpor. Bell (42) believes that the
association between the thyroid gland and the genitalia is as intimate
as the relation of the pituitary to the genital functions.

Of all the endocrines, perhaps the anterior lobe of the hypophysis is in
most intimate correlation with reproduction. Castration results in
hypertrophy of this organ, while removal of the anterior lobe usually
leads to death. In those cases in which death does not ensue, it results
in genital atrophy, stunting, and reduction of sexual activity. In young
animals, spermatogenesis ceases entirely even after partial extirpation
of the anterior lobe. Biedl (45) states that “in disease of the
hypophysis, derangement of sexual activity occurs very early in the
course of the disease, shown in women by the cessation of menstruation,
and in men by impotence.”

The thymus, as is well known, is quite intimately associated with the
development of the genital organs. Its normal disappearance is always
associated with the development of sexual maturity in the individual.
Hewer (46) conducted experiments to ascertain the effect of thymus
feeding on the activity of the reproductive organs in the rat. She
concludes in part: “Male rats appear more susceptible to the influence
of thymus feeding than female rats. With moderate doses of thymus,
sexual maturity in the animals treated is delayed, a phenomenon which is
attributed to delayed development of the testis. With large doses of
thymus, in the male, the testis is structurally affected: in the young
animal in the direction of retardation of development, in the mature
animal in the direction of degeneration. This degeneration is confined
to the testes. In the degenerating testis, cells of Sertoli appear to be
absent: the spermatogonia are present, also dividing, and may lie free
in the lumen of the tubule; spermatids, many with abnormal nuclei, are
shed into the lumen in large numbers; spermatozoa are practically
absent. In the later stages, only a few dividing spermatogonia appear
among the debris of the other unrecognizable cells of the tubule. In the
epididymis which itself is normal, when the testis is showing
degeneration, very few spermatozoa appear, in the later stages none.
Many spermatids are present in various stages, and some spermatocytes.
Animals in the hyper-thymic condition appear to be sterile.”

The foregoing references will, I hope, serve to bring out the facts that
environment and diet, together with the general body metabolism and the
endocrines, have a more or less profound effect upon the development,
growth, and functioning of the genital system. In the experiments it has
been shown that sterility is not necessarily accompanied by any apparent
microscopical changes in the gonads, or even at times in the general
body health. Nor can we exclude impotency of the male entirely even when
the spermatozoa are normal in shape, and motility. Carnett, and others
(38), years ago stated: “Indeed, there is abundant clinical proof to the
effect that systemic conditions which have no appreciable effect upon
the motility or conformation of the spermatozoa materially interfere
with reproductive power.” The entire complex genital system is
inseparably linked up with the body as a whole, a fact which we must
bear in mind at all times.

_Impediments to coitus_ may be due to great difference in the size of
the two mated individuals, psychic disturbances, or inability to
protrude the penis. Williams (17) mentions several physical impediments,
as deformity of the limbs or feet, sore feet, overloading of the rumen,
obesity, fear of falling, and paralysis. Coitus may be somewhat delayed,
or even not performed as the result of a severe inflammation with
sensitiveness of the penis or prepuce. Occasionally tumors of the penis
are encountered which may interfere with protrusion of the penis, or its
entrance into the vagina. Not infrequently the penis is rendered
incapable of protrusion as the result of inflammatory adhesions,
tuberculosis of the preputial lymph glands, etc.

_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│       │       │        │        │
 ══════╧═══════╧═══════╧════════╧════════╧════════

 ══════╤═══════╤═══════╤═══════╤═══════╤═══════
 NUMBER│ Right │ Left  │ Left  │ Right │ Left
       │epidid.│testis │epidid.│scrotal│scrotal
       │       │       │       │  sac  │  sac
 ──────┼───────┼───────┼───────┼───────┼───────
      1│       │       │       │       │
 ──────┼───────┼───────┼───────┼───────┼───────
      2│Staph. │       │       │       │Strep.
       │  alb. │       │       │       │  vir.
       │Strep. │       │       │       │
       │  vir. │       │       │       │
 ──────┼───────┼───────┼───────┼───────┼───────
      3│       │       │       │Strep. │
       │       │       │       │  vir. │
 ──────┼───────┼───────┼───────┼───────┼───────
      4│Staph. │       │       │Strep. │Strep.
       │  alb. │       │       │  vir. │  vir.
       │Strep. │       │       │       │
       │  hem. │       │       │       │
 ──────┼───────┼───────┼───────┼───────┼───────
      5│       │       │       │       │
 ──────┼───────┼───────┼───────┼───────┼───────
      6│       │       │       │       │
 ──────┼───────┼───────┼───────┼───────┼───────
      7│       │       │       │       │
       │       │       │       │       │
 ──────┼───────┼───────┼───────┼───────┼───────
      8│       │       │Staph. │Strep. │
       │       │       │  alb. │  hem. │
       │       │       │Strep. │       │
       │       │       │  hem. │       │
 ──────┼───────┼───────┼───────┼───────┼───────
      9│       │       │       │       │
 ──────┼───────┼───────┼───────┼───────┼───────
     10│       │       │       │       │
       │       │       │       │       │
 ──────┼───────┼───────┼───────┼───────┼───────
     11│       │       │       │       │
 ──────┼───────┼───────┼───────┼───────┼───────
     12│       │       │Staph. │       │Strep.
       │       │       │  alb. │       │  hem.
 ──────┼───────┼───────┼───────┼───────┼───────
     13│       │       │       │       │
       │       │       │       │       │
 ──────┼───────┼───────┼───────┼───────┼───────
     14│       │       │       │       │
       │       │       │       │       │
 ──────┼───────┼───────┼───────┼───────┼───────
     15│Staph. │Staph. │       │Strep. │Strep.
       │  alb. │  alb. │       │  vir. │  vir.
 ──────┼───────┼───────┼───────┼───────┼───────
     16│       │       │       │       │
 ══════╧═══════╧═══════╧═══════╧═══════╧═══════

          BACTERIOLOGY OF THE GENITAL TRACTS OF ABORTED FETUSES
                               _Group IV_
 ══════╤════════════╤════════════╤════════════╤════════════╤════════════
 NUMBER│   Right    │Left seminal│Right testis│Left testis │    Remarks
       │  seminal   │  vesicle   │            │            │
       │  vesicle   │            │            │            │
 ──────┼────────────┼────────────┼────────────┼────────────┼────────────
      1│Strep. vir. │            │            │Strep. vir. │Strep. vir.
       │            │            │            │            │  from
       │            │            │            │            │  heart’s
       │            │            │            │            │  blood.
 ──────┼────────────┼────────────┼────────────┼────────────┼────────────
      2│            │            │            │            │
 ──────┼────────────┼────────────┼────────────┼────────────┼────────────
      3│B. coli     │B. coli     │B. coli     │B. coli     │B. coli from
       │            │            │            │            │  all
       │            │            │            │            │  organs.
 ──────┼────────────┼────────────┼────────────┼────────────┼────────────
      4│            │            │Bact. abort.│Bact. abort.│Bact.
       │            │            │            │            │  abortum
       │            │            │            │            │  from
       │            │            │            │            │  spleen.
 ──────┼────────────┼────────────┼────────────┼────────────┼────────────
      5│            │            │            │            │
 ──────┼────────────┼────────────┼────────────┼────────────┼────────────
      6│            │            │            │            │
 ──────┼────────────┼────────────┼────────────┼────────────┼────────────
      7│Bact. abort.│            │            │Bact. abort.│Bact.
       │            │            │            │            │  abortum
       │            │            │            │            │  from liver
       │            │            │            │            │  and
       │            │            │            │            │  heart’s
       │            │            │            │            │  blood.
 ──────┼────────────┼────────────┼────────────┼────────────┼────────────
      8│Staph. alb. │Staph. alb. │            │Staph. alb. │Staph. alb.
       │            │            │            │            │  from
       │            │            │            │            │  heart’s
       │            │            │            │            │  blood.
 ──────┼────────────┼────────────┼────────────┼────────────┼────────────
      9│            │            │            │            │
 ──────┼────────────┼────────────┼────────────┼────────────┼────────────
     10│Bact. abort.│            │Bact. abort.│            │Bact.
       │            │            │            │            │  abortum
       │            │            │            │            │  from
       │            │            │            │            │  heart’s
       │            │            │            │            │  blood.
 ──────┼────────────┼────────────┼────────────┼────────────┼────────────
     11│            │            │            │            │
 ══════╧════════════╧════════════╧════════════╧════════════╧════════════

  BACTERIOLOGY OF THE GENITAL TRACTS OF CALVES DYING OF CALF INFECTIONS
                                _Group V_
 ══════╤════════════╤════════════╤════════════╤════════════╤════════════
 NUMBER│   Right    │Left seminal│Right testis│Left testis │    Remarks
       │  seminal   │  vesicle   │            │            │
       │  vesicle   │            │            │            │
 ──────┼────────────┼────────────┼────────────┼────────────┼────────────
      1│            │            │            │            │
 ──────┼────────────┼────────────┼────────────┼────────────┼────────────
     2.│B. coli     │B. coli     │            │            │B. coli
       │Staph. alb. │Staph. alb. │            │Staph. alb. │
 ──────┼────────────┼────────────┼────────────┼────────────┼────────────
      3│            │            │            │            │
 ──────┼────────────┼────────────┼────────────┼────────────┼────────────
      4│Strep.      │Strep.      │Strep.      │            │Strep.
       │  viridans  │  viridans  │  viridans  │            │  viridans
       │            │            │            │            │  from
       │            │            │            │            │  heart’s
       │            │            │            │            │  blood.
 ──────┼────────────┼────────────┼────────────┼────────────┼────────────
      5│            │            │            │            │
 ──────┼────────────┼────────────┼────────────┼────────────┼────────────
      6│            │            │            │            │
 ──────┼────────────┼────────────┼────────────┼────────────┼────────────
      7│            │            │            │            │
 ══════╧════════════╧════════════╧════════════╧════════════╧════════════

 BACTERIOLOGY OF THE GENITAL TRACTS OF MATURE INFERTILE OR STERILE BULLS
                                _Group VI_

 ══════╤═════════╤═════════╤════════╤════════╤══════
 NUMBER│ R.S.V.  │ L.S.V.  │Prostate│Cowper’s│  R.
       │         │         │        │        │Testis
       │         │         │        │        │
 ──────┼─────────┼─────────┼────────┼────────┼──────
      1│Strep.   │Staph.   │        │        │Strep.
       │  vir.   │  alb.   │        │        │  hem.
       │Staph.   │         │        │        │Staph.
       │  alb.   │         │        │        │  alb.
 ──────┼─────────┼─────────┼────────┼────────┼──────
      2│Strep.   │Strep.   │        │        │Staph.
       │         │  vir.   │        │        │  alb.
       │(neutral)│Staph.   │        │        │
       │         │  alb.   │        │        │
 ──────┼─────────┼─────────┼────────┼────────┼──────
      3│Strep.   │Strep.   │        │        │
       │  vir.   │  vir.   │        │        │
       │         │Staph.   │        │        │
       │         │  alb.   │        │        │
 ──────┼─────────┼─────────┼────────┼────────┼──────
      4│         │         │        │        │Staph.
       │         │         │        │        │  alb.
 ──────┼─────────┼─────────┼────────┼────────┼──────
      5│B. coli. │B. coli. │        │        │
       │Staph.   │Staph.   │        │        │
       │  alb.   │  alb.   │        │        │
 ──────┼─────────┼─────────┼────────┼────────┼──────
      6│         │Strep.   │        │        │
       │         │  vir.   │        │        │
       │         │Staph.   │        │        │
       │         │  alb.   │        │        │
 ──────┼─────────┼─────────┼────────┼────────┼──────
      7│         │         │        │        │
 ──────┼─────────┼─────────┼────────┼────────┼──────
      8│Ps.      │Ps.      │        │        │
       │  pyocan.│  pyocan.│        │        │
       │Strep.   │Strep.   │        │        │
       │  hem.   │  hem.   │        │        │
 ──────┼─────────┼─────────┼────────┼────────┼──────
      9│Staph.   │Staph.   │Staph.  │        │
       │  alb.   │  alb.   │  alb.  │        │
       │         │         │        │        │
 ──────┼─────────┼─────────┼────────┼────────┼──────
     10│         │         │        │        │Staph.
       │         │         │        │        │  alb.
 ──────┼─────────┼─────────┼────────┼────────┼──────
     11│         │Staph.   │        │        │Staph.
       │         │  alb.   │        │        │  alb.
       │         │         │        │        │
       │         │         │        │        │
 ──────┼─────────┼─────────┼────────┼────────┼──────
     12│Staph.   │Strep.   │        │Staph.  │
       │  alb.   │  vir.   │        │  alb.  │
 ──────┼─────────┼─────────┼────────┼────────┼──────
     13│Staph.   │Staph.   │Staph.  │        │
       │  alb.   │  alb.   │  alb.  │        │
       │B. coli. │B. coli. │        │        │
 ──────┼─────────┼─────────┼────────┼────────┼──────
     14│Staph.   │Staph.   │        │        │
       │  alb.   │  alb.   │        │        │
 ──────┼─────────┼─────────┼────────┼────────┼──────
     15│         │Strep.   │        │        │
       │         │  hem.   │        │        │
 ──────┼─────────┼─────────┼────────┼────────┼──────
     16│Staph.   │Strep.   │        │        │
       │  alb.   │  vir.   │        │        │
 ══════╧═════════╧═════════╧════════╧════════╧══════

 ══════╤═══════════╤════════╤════════╤═════════╤═══════
 NUMBER│R. Epidid. │   L.   │   L.   │   R.    │  L.
       │           │ Testis │Epidid. │ Scrotal │Scrotal
       │           │        │        │  Sac.   │ Sac.
 ──────┼───────────┼────────┼────────┼─────────┼───────
      1│Strep. vir.│Staph.  │Strep.  │         │
       │           │  alb.  │  could │         │
       │Staph. alb.│        │not     │         │
       │           │        │  grow. │         │
 ──────┼───────────┼────────┼────────┼─────────┼───────
      2│Strep. vir.│Staph.  │Strep.  │         │
       │           │  alb.  │  vir.  │         │
       │Staph. alb.│        │Staph.  │         │
       │           │        │  alb.  │         │
 ──────┼───────────┼────────┼────────┼─────────┼───────
      3│Strep. vir.│Strep.  │        │         │Strep.
       │           │  vir.  │        │         │  vir.
       │Staph. alb.│        │        │         │
       │           │        │        │         │
 ──────┼───────────┼────────┼────────┼─────────┼───────
      4│Strep. vir.│        │        │         │Strep.
       │           │        │        │         │  hem.
 ──────┼───────────┼────────┼────────┼─────────┼───────
      5│Staph. alb.│        │B. coli.│         │
       │           │        │Staph.  │         │
       │           │        │  alb.  │         │
 ──────┼───────────┼────────┼────────┼─────────┼───────
      6│           │        │Strep.  │         │
       │           │        │  vir.  │         │
       │           │        │        │         │
       │           │        │        │         │
 ──────┼───────────┼────────┼────────┼─────────┼───────
      7│           │        │        │         │
 ──────┼───────────┼────────┼────────┼─────────┼───────
      8│           │        │        │         │
       │           │        │        │         │
       │           │        │        │         │
       │           │        │        │         │
 ──────┼───────────┼────────┼────────┼─────────┼───────
      9│Strep. vir.│Unident.│Unident.│         │Strep.
       │           │        │        │         │  hem.
       │           │rod.    │rod.    │         │
 ──────┼───────────┼────────┼────────┼─────────┼───────
     10│           │        │Staph.  │         │
       │           │        │  alb.  │         │
 ──────┼───────────┼────────┼────────┼─────────┼───────
     11│Strep. hem.│        │Strep.  │Strep.   │
       │           │        │  vir.  │         │
       │           │        │Staph.  │(neutral)│
       │           │        │  alb.  │         │
 ──────┼───────────┼────────┼────────┼─────────┼───────
     12│Strep. vir.│        │        │         │
       │           │        │        │         │
 ──────┼───────────┼────────┼────────┼─────────┼───────
     13│Strep. vir.│        │        │         │
       │           │        │        │         │
       │           │        │        │         │
 ──────┼───────────┼────────┼────────┼─────────┼───────
     14│Strep.     │        │Strep.  │Strep.   │
       │  (neutral)│        │  vir.  │  vir.   │
 ──────┼───────────┼────────┼────────┼─────────┼───────
     15│           │        │Strep.  │         │
       │           │        │  hem.  │         │
 ──────┼───────────┼────────┼────────┼─────────┼───────
     16│           │Staph.  │Strep.  │         │Strep.
       │           │  alb.  │  vir.  │         │  hem.
 ══════╧═══════════╧════════╧════════╧═════════╧═══════

 A—PATHOLOGY OF THE GENITAL TRACTS OF MATURE STERILE OR INFERTILE BULLS

 ═╤═══════════════╤════════╤══════════════╤══════════════
  │R. Sem. Vesicle│L. Sem. │    Ductus    │  R. Testis
  │               │Vesicle │   Deferens   │
 ─┼───────────────┼────────┼──────────────┼──────────────
 1│Desquamation   │Same as │Both          │Apparently
  │  and          │  right.│  apparently  │  normal.
  │  degeneration │        │  normal.     │
  │  of lining    │        │              │
  │  membrane.    │        │              │
  │               │        │              │
  │Debris and     │        │              │
  │  exudates in  │        │              │
  │  lumen.       │        │              │
  │               │        │              │
  │               │        │              │
 ─┼───────────────┼────────┼──────────────┼──────────────
 2│Most vesicles  │Same as │Right         │Most tubules
  │  degenerating.│  right.│  apparently  │  apparently
  │               │        │  normal.     │  normal.
  │               │        │              │
  │               │        │              │
  │               │        │              │
  │               │        │              │
  │Interstitial   │        │Left shows    │Some show
  │  cellular     │        │  degeneration│  degeneration
  │  infiltration.│        │  of the      │  of the
  │               │        │  lining      │  seminal
  │               │        │  membrane.   │  epithelium.
  │Necrosis in one│        │              │
  │  large area.  │        │              │
 ─┼───────────────┼────────┼──────────────┼──────────────
 3│Entire gland   │Same as │Slight        │Some tubules
  │  degenerated. │  right.│  desquamation│  normal.
  │               │        │  and         │  Others show
  │               │        │  degeneration│  degeneration
  │               │        │  of mucosa of│  of the
  │               │        │  right       │  seminal
  │               │        │  ductus.     │  epithelium.
  │Coagulation    │        │              │
  │  necrosis of  │        │              │
  │  interstitial │        │              │
  │  tissue.      │        │              │
  │  Debris and   │        │              │
  │  exudates in  │        │              │
  │  the vesicles.│        │              │
 ─┼───────────────┼────────┼──────────────┼──────────────
 4│Same as No. 3. │Same as │Epithelium    │Much
  │               │  No. 3.│  entirely    │  degeneration
  │               │        │  denuded in  │  and
  │               │        │  both ducts. │  desquamation
  │               │        │              │  of the
  │               │        │              │  seminal
  │               │        │              │  epithelium.
 ═╧═══════════════╧════════╧══════════════╧══════════════

 ═╤══════════════╤═══════════════╤═══════════════
  │R. Epididymis │   L. Testis   │ L. Epididymis
  │              │               │
 ─┼──────────────┼───────────────┼───────────────
 1│Acute         │Apparently     │Degeneration
  │  desquamation│  normal.      │  and
  │  and         │               │  desquamation
  │  degeneration│               │  in some
  │  in some     │               │  tubules.
  │  tubules.    │               │
  │              │               │Others
  │              │               │  atrophied due
  │              │               │  to a chronic
  │              │               │  interstitial
  │              │               │  inflammation.
 ─┼──────────────┼───────────────┼───────────────
 2│Degeneration  │Most tubules   │Same as right,
  │  and         │  becoming     │  but some
  │  desquamation│  atrophied due│  tubules are
  │  of          │  to a chronic │  becoming
  │  epithelium  │  inflammation.│  atrophied due
  │  of the      │               │  to a chronic
  │  tubules.    │               │  inflammation.
  │              │               │
  │              │               │
  │              │               │
  │              │               │
  │              │               │
  │              │               │
  │              │               │
 ─┼──────────────┼───────────────┼───────────────
 3│Much of the   │Same as right. │Same as right.
  │  epithelium  │               │
  │  denuded.    │               │
  │              │               │
  │              │               │
  │              │               │
  │              │               │
  │Debris and    │               │
  │  exudates in │               │
  │  the lumen.  │               │
  │              │               │
  │              │               │
  │              │               │
  │              │               │
 ─┼──────────────┼───────────────┼───────────────
 4│Desquamation  │Same as right. │Same as right.
  │  of most of  │               │
  │  lining-     │               │
  │  membrane.   │               │
  │              │               │
  │              │               │
  │              │               │
 ═╧══════════════╧═══════════════╧═══════════════

 B—PATHOLOGY OF THE GENITAL TRACTS OF MATURE INFERTILE OR STERILE BULLS

 ═╤══════════════╤════════╤══════════════╤════════════
  │   R. Sem.    │L. Sem. │    Ductus    │ R. Testis
  │   Vesicle    │Vesicle │   Deferens   │
 ─┼──────────────┼────────┼──────────────┼────────────
 5│Epithelium    │Same as │Both          │Degeneration
  │  becoming    │  right.│  apparently  │  of many
  │  degenerated.│        │  normal.     │  tubules.
  │Vesicles      │        │              │
  │  filled with │        │              │
  │  debris and  │        │              │
  │  exudates.   │        │              │
 ─┼──────────────┼────────┼──────────────┼────────────
 6│Acutely       │Same as │Slight        │Degeneration
  │  inflamed.   │  right.│  degeneration│  of mucosa
  │              │        │  of lining   │  in some
  │              │        │  membrane of │  tubules.
  │              │        │  both.       │
  │              │        │              │
  │              │        │              │
 ─┼──────────────┼────────┼──────────────┼────────────
 7│Some          │Same as │Both          │Apparently
  │  degeneration│  right.│  apparently  │  normal.
  │  of lining   │        │  normal.     │
  │  membrane.   │        │              │
 ─┼──────────────┼────────┼──────────────┼────────────
 8│Necrosis in   │Same as │Both          │Apparently
  │  areas.      │  right.│  apparently  │  normal.
  │              │        │  normal.     │
  │Infiltration  │        │              │
  │  of          │        │              │
  │  interstitial│        │              │
  │  tissue.     │        │              │
  │Degeneration  │        │              │
  │  of lining   │        │              │
  │  membrane.   │        │              │
 ═╧══════════════╧════════╧══════════════╧════════════

 ═╤════════════╤════════════╤══════════
  │     R.     │ L. Testis  │    L.
  │ Epididymis │            │Epididymis
 ─┼────────────┼────────────┼──────────
 5│All         │Same as     │Nearly
  │  epithelium│  right.    │  normal.
  │  denuded.  │            │
  │Debris in   │            │
  │  lumen.    │            │
  │            │            │
  │            │            │
 ─┼────────────┼────────────┼──────────
 6│Apparently  │Degeneration│Apparently
  │  normal.   │  in some   │  normal.
  │            │  tubules.  │
  │            │            │
  │            │            │
  │            │No mitosis  │
  │            │  in some.  │
 ─┼────────────┼────────────┼──────────
 7│Apparently  │Apparently  │Apparently
  │  normal.   │  normal.   │  normal.
  │            │            │
  │            │            │
 ─┼────────────┼────────────┼──────────
 8│Apparently  │Apparently  │Apparently
  │  normal.   │  normal.   │  normal.
  │            │            │
  │            │            │
  │            │            │
  │            │            │
  │            │            │
  │            │            │
  │            │            │
  │            │            │
 ═╧════════════╧════════════╧══════════

 C—PATHOLOGY OF THE GENITAL TRACTS OF MATURE INFERTILE OR STERILE BULLS

 ══╤══════════════╤══════════╤════════════╤═══════════════
   │   R. Sem.    │ L. Sem.  │   Ductus   │   R. Testis
   │   Vesicle    │ Vesicle  │  Deferens  │
 ──┼──────────────┼──────────┼────────────┼───────────────
  9│Apparently    │Apparently│Both        │Apparently
   │  normal.     │  normal. │  apparently│  normal.
   │              │          │  normal.   │
 ──┼──────────────┼──────────┼────────────┼───────────────
 10│Slight        │Same as   │Both        │Apparently
   │  desquamation│  right.  │  apparently│  normal.
   │  and         │          │  normal.   │
   │  degeneration│          │            │
   │  of the      │          │            │
   │  lining      │          │            │
   │  membrane.   │          │            │
 ──┼──────────────┼──────────┼────────────┼───────────────
 11│Apparently    │Apparently│Both        │Some tubules
   │  normal.     │  normal. │  apparently│  show no
   │              │          │  normal.   │  mitosis,
   │              │          │            │  others are
   │              │          │            │  degenerating.
 ──┼──────────────┼──────────┼────────────┼───────────────
 12│Degeneration  │Same as   │Both        │Apparently
   │  and         │  right.  │  apparently│  normal.
   │  desquamation│          │  normal.   │
   │  of          │          │            │
   │  epithelium  │          │            │
   │  of some     │          │            │
   │  vesicles.   │          │            │
   │              │          │            │
   │              │          │            │
   │              │          │            │
   │              │          │            │
   │              │          │            │
   │              │          │            │
   │              │          │            │
 ══╧══════════════╧══════════╧════════════╧═══════════════

 ══╤══════════════╤══════════╤══════════════
   │R. Epididymis │L. Testis │L. Epididymis
   │              │          │
 ──┼──────────────┼──────────┼──────────────
  9│Apparently    │Apparently│Apparently
   │  normal.     │  normal. │  normal.
   │              │          │
 ──┼──────────────┼──────────┼──────────────
 10│Degeneration  │Apparently│Same as right.
   │  of lining   │  normal. │
   │  membrane.   │          │
   │              │          │
   │              │          │
   │              │          │
   │              │          │
 ──┼──────────────┼──────────┼──────────────
 11│Degeneration  │Same as   │Degeneration
   │  and         │  right.  │  and
   │  desquamation│          │  desquamation
   │  of lining   │          │  of lining
   │  membrane.   │          │  membrane.
 ──┼──────────────┼──────────┼──────────────
 12│Degeneration  │Apparently│Apparently
   │  of          │  normal. │  normal.
   │  epithelium  │          │
   │  of all      │          │
   │  tubules.    │          │
   │              │          │
   │              │          │
   │Debris and    │          │
   │  exudates in │          │
   │  lumen.      │          │
   │Some increase │          │
   │  in          │          │
   │  connective  │          │
   │  tissue.     │          │
 ══╧══════════════╧══════════╧══════════════

 D—PATHOLOGY OF THE GENITAL TRACTS OF MATURE INFERTILE OR STERILE BULLS

 ══╤═══════════════╤═══════════════╤══════════════╤══════════════
   │R. Sem. Vesicle│L. Sem. Vesicle│    Ductus    │  R. Testis
   │               │               │   Deferens   │
 ──┼───────────────┼───────────────┼──────────────┼──────────────
 13│Degeneration of│Same as right. │Slight        │Apparently
   │  most of      │               │  catarrhal   │  normal.
   │  gland.       │               │  inflammation│
   │               │               │  of mucosa of│
   │               │               │  both.       │
   │               │               │              │
   │               │               │              │
   │Cellular       │               │              │
   │  infiltration │               │              │
   │  of           │               │              │
   │  interstitial │               │              │
   │  connective   │               │              │
   │  tissue.      │               │              │
   │Debris and     │               │              │
   │  exudates in  │               │              │
   │  lumen.       │               │              │
 ──┼───────────────┼───────────────┼──────────────┼──────────────
 14│Apparently     │Apparently     │Apparently    │Some
   │  normal.      │  normal.      │  normal.     │  degeneration
   │               │               │              │  of seminal
   │               │               │              │  epithelium
   │               │               │              │  of some
   │               │               │              │  tubules.
   │               │               │              │
   │               │               │              │
   │               │               │              │
   │               │               │              │
 ──┼───────────────┼───────────────┼──────────────┼──────────────
 15│Slight         │Acute catarrhal│Both          │Degeneration
   │  desquamation │  inflammation.│  apparently  │  of seminal
   │  and          │               │  normal.     │  epithelium
   │  degeneration │               │              │  in some
   │  of lining    │               │              │  tubules.
   │  membrane.    │               │              │
   │               │Debris and     │              │
   │               │  exudates in  │              │
   │               │  lumen.       │              │
 ──┼───────────────┼───────────────┼──────────────┼──────────────
 16│Chronic        │More acute than│Both          │Degeneration
   │  interstitial │  right.       │  apparently  │  in some
   │  inflammation.│               │  normal.     │  tubules.
   │               │               │              │
   │               │               │              │
   │               │               │              │
   │               │               │              │
   │               │               │              │
   │Atrophy of many│               │              │Some show poor
   │  tubules.     │               │              │  mitosis.
 ══╧═══════════════╧═══════════════╧══════════════╧══════════════

 ══╤══════════════╤══════════╤═══════════════
   │R. Epididymis │L. Testis │ L. Epididymis
   │              │          │
 ──┼──────────────┼──────────┼───────────────
 13│Degeneration  │Apparently│Same as right.
   │  and         │  normal. │
   │  desquamation│          │
   │  of lining   │          │
   │  membrane of │          │
   │  most        │          │
   │  tubules.    │          │
   │              │          │
   │              │          │
   │              │          │
   │              │          │
   │              │          │
   │              │          │
   │              │          │
   │              │          │
   │              │          │
 ──┼──────────────┼──────────┼───────────────
 14│Apparently    │Apparently│Acute
   │  normal.     │  normal. │  inflammation.
   │              │          │
   │              │          │
   │              │          │
   │              │          │
   │              │          │Some
   │              │          │  desquamation
   │              │          │  of lining
   │              │          │  membrane.
 ──┼──────────────┼──────────┼───────────────
 15│Desquamation  │Apparently│Apparently
   │  of lining   │  normal. │  normal.
   │  membrane.   │          │
   │              │          │
   │              │          │
   │              │          │
   │Debris in     │          │
   │  lumen.      │          │
   │              │          │
 ──┼──────────────┼──────────┼───────────────
 16│Apparently    │Same as   │Acute
   │  normal.     │  right.  │  inflammation.
   │              │          │  Some
   │              │          │  desquamation
   │              │          │  and
   │              │          │  degeneration
   │              │          │  of lining
   │              │          │  membrane.
   │              │          │
   │              │          │
 ══╧══════════════╧══════════╧═══════════════




                              BIBLIOGRAPHY


  1. BANG B. Die Aetiologie des seuchenhaften (infectiösen) Verwerfens.
       Zeit Med. Band I, S. 241, 1897. Das seuchenhaften Verwerfen der
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  2. LAW, JAMES. Contagious Abortion of Cows. Circular No. 5, Agr.
       Experiment Sta. University of California, June, 1903.

  3. Report of English Commission of Epizootic Abortion. Appendix to
       Part I, p. 17, 1909.

  4. HADLEY, F. B., and LOTHE, H. The Bull as a Disseminator of
       Contagious Abortion. Jour. Amer. Vet. Med. Assoc., L, 1916–17, p.
       143.

  5. HADLEY, F. B. Contagious Abortion Questions Answered. Bulletin No.
       296, Oct. 1921, Agr. Experiment Sta., University of Wisconsin.

  6. BUCK, J. M., CREECH, G. T., and LADSON, H. H. Bacterium Abortus
       Infection of Bulls (Preliminary Report). Jour. Agr. Research,
       August, 1919.

  7. SCHROEDER, E. C., and COTTON, W. E. The Bull as a Factor in
       Abortion Disease.

  8. COTTON, W. E. Proceedings of A. V. M. A., p. 851, 1913.

  9. CARPENTER, C. M. Report of the New York State Veterinary College,
       Cornell University, 1920–21.

 10. RETTGER, L. F., and WHITE, G. C. Infectious Abortion in Cattle.
       Storrs Agr. Exp. Sta. Bulletin No. 93. January, 1916.

 11. MCFADYEAN, SHEATHER and MINETT. Researches Regarding Epizootic
       Abortion. Jour. of Comp. Path. and Therap., XXVI, 142, 1913.

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       Infections Abortion. Jour. Amer. Vet. Med. Assoc., LX, p. 542.
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       Vesicles. Bost. Med. and Surg. Jour., CLXXI, 1914, 59.

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       April, 1920.

 15. WILLIAMS, W. L. Report of the New York State Veterinary College,
       Cornell University, 1920–21.

 16. WILLIAMS. W. W. Technique of Collecting Semen for Laboratory
       Examination with Review of Several Diseased Bulls. Cornell Vet.
       X, 87, April, 1920.

 17. WILLIAMS, W. W. Diseases of the Bull Interfering With Reproduction.
       Jour. of Amer. Vet. Med. Assoc., LVIII, 29, October, 1920.

 18. HOPPER, E. B. Herd Efficiency from the Standpoint of the
       Veterinarian. North Amer. Vet., III, 71, February, 1922.

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       Herd. Cornell Veterinarian, XII, 19, January, 1922.

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       Lancet, CCI, 228. July 30, 1921.

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       Endocrinology, II, 42.

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       of the Hibernating Bat and Its Significance. C. R. Soc. de Biol.
       (Paris), 1920, LXXXIII, 67–69.

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       September, 1918.

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       Geschlechtsorgane. Oppel’s Lehrbuch der vergleichenden mikr.
       Anat. der Wirbeltiere, IV, Jena, 1904.

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       Pocularis: Its Histology, Anatomy, and Physiology. Jour. Urology,
       I, 1917, 231.

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       Veterinarian, October, 1921.

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       University, Ithaca, New York.

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       Anat. u. Physiol. 1899.

 32. BOETTCHER, W. On the Significance of the Secretions of the Male
       Accessory Genital Organs. Münch. med. Wchnschr. 1920, 67, 1, p.
       44.

 33. EDITORIAL. Jour. of Amer. Med. Assoc., LXXVII, No. 1, 42, July 2,
       1921.

 34. REYNOLDS, E. Fertility and Sterility. Jour. of Amer. Med. Assoc.,
       LXVII, 1193–1199, October 21, 1916.

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       Gynecological Aspects. Amer. Jour. of Obstetrics and Diseases of
       Women and Children. LXXIV, No. 4, 1916.

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       Jour. of Physiol. IV, 246, August 3, 1921.

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       Monograph of the Rockefeller Institute for Med. Res., 1919, IX.

 38. GARNETT, J. B., and others. The Surgical Treatment of Sterility due
       to Obstruction at the Epididymis Together with a Study of the
       Morphology of Human Spermatozoa. Univ. of Penn. Med. Bulletin,
       March, 1902.

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       Sterility. Jour. of Amer. Med. Assoc., LXXVII, 169, July 16,
       1921.

 40. NOVARRO, P. A. Tissues of the Testicle and Antaminosis. Gazetta
       degli Ospedali (Milano), 1920, XLI, 424.

 41. WILLIAMS, W. L. Observations on Reproduction in a Pure Bred Beef
       Herd. Cornell Veterinarian. January, 1922.

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       Organs of Internal Secretion and the Reproductive System. Brit.
       Med. Jour., 1920, 1, 787.

 43. BROWN, W. L. The Principles of Internal Secretion. Brit. Med. Jour,
       1920, II, 687–691.

 44. JUMP. Discussion in Penn. Med. Jour., XXV, 81.

 45. BIEDL, A. The Internal Secretory Organs.

 46. HEWER, E. E. The Effect of Thymus Feeding on the Activity of the
       Reproductive Organs of the Rat. Jour. of Physiology, XLVII,
       1913–1914, 479.

 47. LLOYD-JONES, O. and HAYS, F. A. The Influence of Excessive Sexual
       Activity of Male Rabbits. 1. On the Properties of the Seminal
       Discharge. Jour. of Exper. Zoology, 1918, XXV, 463.

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       Cattle. North Amer. Veterinarian, III, May, 1922.




                         DESCRIPTION OF PLATES


     PLATE I.

      Fig. 1. Diagrammatic sketches showing the development of a
                spermatozoon from a spermatogonium.

      Fig. 2. Diagrammatic sketch showing the minute structure of a
                spermatozoon. The middle piece is made comparatively
                thick in order to bring out the finer structures.
                Adapted from Ellenberger.

    PLATE II.

      Fig. 3. Testicle of bull, showing extensive degeneration and
                necrosis.

   PLATE III.

      Fig. 4. Inner part of wall of ductus deferens. Normal. × 230.

      Fig. 5. Same, but showing extensive degeneration and exfoliation
                of the lining membrane. × 230.

    PLATE IV.

      Fig. 6. Ductus deferens, showing entire exfoliation of the lining
                membrane. The lumen is filled with a cellular debris. ×
                50.

      Fig. 7. Same, showing the degeneration of the lining membrane, and
                debris in lumen. × 230.

     PLATE V.

      Fig. 8. Seminal vesicle of bull. High power section showing the
                normal structure of the vesicular cavities.

      Fig. 9. Seminal vesicle of bull. Low power. The membrane lining
                the cavities is degenerated and exfoliated. The cavities
                are filled with cellular debris, and exudates. There is
                some increase in the interstitial tissue, and atrophy of
                some of vesicular cavities.

    PLATE VI.

     Fig. 10. Low power section of seminal vesicle of bull. The
                condition is about the same as in Fig. 9 except that it
                is not quite as severe.

     Fig. 11. Same as Fig. 10. High power.

   PLATE VII.

     Fig. 12. Testicular tubule showing normal spermatogenesis. × 230.

     Fig. 13. Testicular tubule showing no evidence of mitosis. × 230.

     Fig. 14. Testicular tubule. The spermatogenic epithelium is
                beginning to degenerate and become cast off into the
                lumen. × 230.

     Fig. 15. Testicular tubule, showing almost total exfoliation of the
                spermatogenic epithelium. × 230.

  PLATE VIII.

     Fig. 16. Testicular tubule. The seminal epithelium is entirely
                degenerated. The membrana propria is markedly thickened.
                × 230.

     Fig. 17. Testicular tubule. The tubule is undergoing atrophy and
                degeneration. The interstitial connective tissue is much
                increased in amount. × 230.

     Fig. 18. Same as Fig. 17, except that it is in the more advanced
                stages.

     Fig. 19. Testicular tubule. The spermatogenic epithelium has
                undergone a sort of hydropic degeneration. The
                interstitial connective tissue has become much increased
                in amount and has undergone cellular infiltration.

    PLATE IX.

     Fig. 20. Normal structure of epididymis tubule. × 140.

     Fig. 21. Epididymis tubule showing exfoliation of the lining
                membrane, and cellular debris in the lumen. × 140.

     Fig. 22. Atrophy and degeneration of epididymis tubule. The
                interstitial connective tissue is much increased in
                amount. × 140.

     Fig. 23. Same, but in more advanced stage. × 140.

     PLATE X.

     Fig. 24. About the same as Fig. 22. × 140.

     Fig. 25. Marked degeneration of epididymis tubule. There is a
                cellular infiltration of the interstitial tissue. × 60.

    PLATE XI.

     Fig. 26. Spermatozoon, showing constriction at middle of head. The
                head is also somewhat contorted. × 670.

     Fig. 27. Spermatozoon. Pear shaped head. × 670.

     Fig. 28. Spermatozoon. The head is quite long, and pointed at its
                posterior end. × 670.

     Fig. 29. Spermatozoon, showing a constriction at middle of the
                head. × 670.

   PLATE XII.

     Fig. 30. Microcephalic spermatozoon. × 670.

     Fig. 31. Spermatozoon. The head is small, and pear shaped. × 670.

     Fig. 32. Macrocephalic sperm. The middle piece is much thickened. ×
                670.

     Fig. 33. Tailless spermatozoa. × 670.

[Illustration: PLATE I]

[Illustration: PLATE II]

[Illustration: PLATE III]

[Illustration: PLATE IV]

[Illustration: PLATE V]

[Illustration: PLATE VI]

[Illustration: PLATE VII]

[Illustration: PLATE VIII]

[Illustration: PLATE IX]

[Illustration: PLATE X]

[Illustration: PLATE XI]

[Illustration: PLATE XII]

------------------------------------------------------------------------




                          TRANSCRIBER’S NOTES


 Page Changed from                     Changed to

   54 [blank]                          Bacteriology of the Genital
                                       Tracts of Mature Infertile or
                                       Sterile Bulls Group VI

 ● Typos fixed; non-standard spelling and dialect retained.
 ● Enclosed italics font in _underscores_.





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