Chapter 4

FEMALE GENITAL SYSTEM

 

4.1 PRE-INSTRUCTIONAL SELF-EXAMINATION

Prior to embarking on a study of the female genital system, the student should provide appropriate answers for the following questions. Please review the material in your textbook.

 

Questions

  • 1. What is the so-called estrus cycle?
  • 2. How long is the gestation period in dogs, cats, pigs, cows, horses, sheep and goats?
  • 3. What two reproductive hormones are secreted by the pituitary gland?
  • 4. What is the role of the follicle stimulating hormone?
  • 5. What is the role of the luteinizing hormone?
  • 6. What hormone is responsible for the induction of ovarian follicle formation?
  • 7. What hormone is responsible for maintaining the corpus luteum?
  • 8. What hormone is produced and liberated by the graafian follicle?
  • 9. What hormone is elaborated by the corpus luteum?
  • 10. What is the interrelationship between the graafian follicle and the corpus luteum?
  • 11. what is the interrelationship between progesterone and the luteinizing hormone?
  • 12. What is the interrelationship between estrogen produced by the graafian follicle and the follicle stimulating hormone?
  • 13. What is the so-called corpus albicans?
  • 14. What influence does estrogen have on the uterine endometrium?
  • 15. What influence would you expect progesterone to have on the uterine endometrium?
  • 16. What is endometriosis?
  • 17. What is a placenta? Give the role and/or function of this tissue.
  • 18. Distinguish between the maternal placenta and fetal placenta.
  • 19. What is the allanto-chorion?
  • 20. What is a so-called diffuse placenta? In what animal species would you expect to find such a placenta?
  • 21. What is a zonary placenta? In what animal species would you expect to find a zonary placenta?
  • 22. What is a cotyledonary placenta?
  • 23. What is epitheliochorial placenta?
  • 24. Please define and/or describe the following:
    • a. Syndesmochorial placenta
    • b. Endotheliochorial placenta
    • c. Hemochorial placenta
    • d. Deciduate placenta
    • e. Non-deciduate placenta 

4.2 GENERAL:

Diseases of the female genital system consist of a rather complex interrelationship of endocrine disturbances, infectious diseases, non-infectious diseases, immaturity and senility. These factors, individually or collectively, interfere with ovulation, fertilization and reproduction. Some of these conditions lead to sterility, others to premature expulsion of a dead or living fetus and some are reflected in diseases in the offspring.

The organization of the gonads and the basic pattern of the genital tract are established early in embryogenesis. In the early undifferentiated state, each individual is anatomically bisexual and potentially able to develop phenotypic characters of the male or female (independently of the genetic sex). The early gonad consists of cortical and medullary parts. If the medulla predominates, the gonad is a testis; however, if the cortex predominates, the gonad is an ovary. The embryogenesis of the tubular genitalia is also bisexual. If the gonads are testes, the Wolffian duct persists. If the gonads are ovaries, the Mullerian duct persists.

Each structure of the female genital tract (ovaries, uterus, cervix, etc.) tends to react to disease in a characteristic manner. Since the clinical manifestation of disorders of the female genital tract parallel anatomic divisions, this handout is divided according to anatomic structure. 

4.3 ANOMALIES OF THE GENITAL TRACT:

4.3.1 HYPOPLASIA:

Hypoplastic ovaries are normal in immature animals. However, with sexual development, they should reach the normal size and functional state of the species. when certain endocrine disturbances are present, the ovary persists in its infantile form (the condition has been studies extensively only in cattle). The primary morphologic defect in hypoplastic ovaries in cattle is a deficiency in the number of germ cells in the ovary. The degree and severity of hypoplasia may vary considerably; however, the left ovary is more frequently and severely hypoplastic than the right. In severe hypoplasia, there is an absence of follicles and luteal scars. Microscopically, the ovary is composed largely of medullary connective tissue and blood vessels. There is a deficiency of ovarian cortex.

4.3.2 FREEMARTIN:

The bovine freemartin is a genetic female born co-twin with a male. Over 90% of such females have severe hypoplasia of the genital tract and are subsequently sterile. The pathogenesis of freemartinism has not been completely elucidated. However, the condition appears to be associated with the fact that the male and female co-twin share a common placental circulation in utero.

Androgenic hormones produced by the testicles of the male fetus may enter the circulation and suppress the development of the female genitalia (the male gonads develop earlier than the female gonads and fusion of the allantoic circulation occurs prior to gonadal differentiation).

Embryonal cells are interchanged between the male and female co-twin via the circulation (the cells from one embryo establish themselves in the co-twin, producing chimerism).

The morphologic degree of modification of the female genitalia may vary. There may be varying degrees of modification from ovaries to testes, or the gonads may be represented by only a cord-like thickening in the anterior border of the ovarian ligament. The tubular genitalia may vary from cord-like structures to well-developed uterine horns. However, communication with the vagina is absent (no matter how well-developed the uterus may be). The vagina is hypoplastic or non-patent with a complete hymen. The vulva and vestibule are hypoplastic and the clitoris is enlarged. Also, the mammary gland fails to reach normal size. The male co-twin may be sterile or fertility may be reduced. 

4.4 OVARIES:

4.4.1 INFLAMMATION OF THE OVARIES:

The term oophoritis refers to inflammation of the ovaries. The condition is rare and, when it occurs, it is usually pyogenic.

4.4.2 HEMORRHAGE OF THE OVARIES:

Hemorrhage of the ovaries occurs during ovulation in all species of domestic animals, but it is usually minimal and confined largely to the collapsed follicles. Intrafollicular hemorrhage occurs in calves (for unknown reasons), in follicular cysts of the bitch and occasionally in atretic follicles of cows. The most significant and severe hemorrhage occurs following manual enucleation of the corpus luteum in cattle (blood loss may be several gallons and result in death of the animal).

4.4.3 CYSTIC OVARIES:

Cystic ovaries is the clinical term used to refer to one or more cysts in the ovaries. The condition may occur in all species, but it is most common in cattle and swine. Several kinds of cysts are recognized:

4.4.3.1 CYSTIC GRAAFIAN FOLLICLE

Is the most common form of cystic ovarian degeneration. It arises from failure of the mature follicle to rupture. The condition is most common in heavy-producing cows and may be associated with nymphomania (nymphomania is believed to be due to the estrogenic substances present in the cyst fluid). The pathogenesis of this condition has not been completely elucidated, but there is evidence to suggest that the pituitary gonadotrophin is not released in a normal manner during early estrus. Thus, the mature follicle is not exposed to the ovulating and luteinizing action of the luteinizing hormone. Grossly, one or more large follicles are present on one or both ovaries (apart from their greater size, these follicular cysts may be difficult to distinguish from normal follicles). There is an absence of corpus lutea in the ovaries. The uterus and vulva are edematous and flabby. The cervix is enlarged and produces a tough gray-white mucus. Also, the clitoris may be enlarged. Microscopically, the ovum is absent and there is degeneration of the granulosa cells.

4.4.3.2 LUTEINIZED CYSTS

Develop when there is delayed or insufficient release of luteinizing hormone during estrus. Ovulation fails to occur and the theca interna undergoes luteinization. Grossly, there is no ovulation papilla, the luteal mass is smooth and rounded and the cyst cavity is spherical and lined by a layer of fibrous connective tissue adjacent to the zone of luteinized theca cells. The clinical manifestations of estrus are suppressed but the length of the estrus cycle may be normal. It appears that luteinized cysts are less severe manifestations of cystic graafian follicles and the pathogenesis is probably the same (the two conditions are assumed to be expression of different degrees of the same dysfunction). In cows that develop cystic graafian follicles, there is little or no release of the luteinizing hormone. In cows that develop luteinized cysts, the hormone is slowed and not completed for some days.

4.4.3.3 CYSTIC CORPUS LUTEUM

occurs following ovulation with the formation of a cystic cavity in the center mass of the developing luteal tissue. Grossly, an ovulation papilla is present and the cystic cavity is irregularly shaped. Pathologic corpus luteum cysts usually measure from 10 to 15 mm in diameter (small cystic cavities, less that 5 mm in diameter, are normal and common in cattle shortly after ovulation).

4.4.3.4 PARAOVARIAN CYSTS

Refer to a variety of cystic structures located adjacent to the ovaries. Such cysts may arise from mesonephric or paramesonephric ducts.

4.4.4 CYSTIC OVARIES IN HORSES:

Cystic graafian follicles comparable to that of cows and sows apparently do not occur in horses. Remember, the normal mature graafian follicle of the mare is very large (4 to 6 cm) and is easily mistaken for a cystic follicle. Also, cystic granulosa cell tumors and germinal inclusion cysts can be confused with cystic follicles.

4.4.5 CYSTIC FOLLICLES IN DOGS AND CATS:

Functional graafian follicular cysts can be responsible for nymphomania, vulva tumefaction, cystic endometrial hyperplasia, cystic mammary hyperplasia and genital fibroleiomyomas in dogs and cats. Functional corpora luteal cysts can cause exaggerated progestational proliferation (cystic endometrial hyperplasia) of the endometrium. Thus, the cystic corpus luteum (as well as the retained corpus luteum of pseudopregnancy) makes the uterus more susceptible to infection because of excessive progestational activity. Pyometra is a common sequela.

4.4.6 EXTRAOVARIAN LESIONS OF CYSTIC OVARIES IN COWS:

The changes that occur in various organs and tissues of cows with cystic ovaries (cystic graafian follicles) are believed to be due to the effects of estrogen. This is especially so in those cows exhibiting signs of nymphomania. The cyst fluid contains estrogenic substances. Large amounts of estrogen are actually found in normal mature graafian follicles. However, the toxicity of estrogen depends not only on the level of circulating estrogen, but more importantly, on the continuity of its action, even though exciting levels are relatively minute. In established cases of follicular cysts in cattle, the following may be observed:

4.4.7 ATRETIC FOLLICLES:

Atresia is a normal process for those follicles that do not attain maturity (during the estrus cycle of uniparous animals, many follicles develop but only one is suppose to mature and ovulate. The remainder undergo atresia, degenerate and disappear). Follicular atresia is pathological when unnatural influences inhibit the final maturation process (as occurs in the case of anestrus of inanition and debility).

Follicular growth is independent of pituitary gonadotrophins up to the stage of antrum formation. Thereafter, growth and maturation depend on stimulation by pituitary gonadotrophins in proper proportion and sequence. Debilitated and malnourished animals are capable of synthesizing the gonadotrophins and the ovaries are capable of responding to them. However, the defect is in the pituitary gland, which does not release its stored gonadotrophins or does so in insufficient quantities. 

4.4.8 NEOPLASMS OF THE OVARIES:

Primary ovarian tumors occur most commonly in the bitch and cow.

4.4.8.1 GRANULOSA CELL TUMORS

arise from the granulosa cells of the ovarian follicle. These tumors have the potential to produce estrogen or androgen (estrogen and androgen are chemically similar and readily inter-convertible). Androgenic activity in an ovarian tumor may be the result of disturbed chemistry in a primary estrogen-producing neoplasm. Cows and mares with granulosa cell tumors may show no significant clinical signs or they may exhibit signs of nymphomania or act like males. The clinical signs are believed to be due to excessive estrogen production by the neoplasm. In the bitch, granulosa cell tumors are likely to produce endometrial hyperplasia (probably associated with the production of progesterone).

Grossly, the tumor surfaces are smooth and the incised surfaces may be cystic or solid. Microscopically, there are gland-like or rosette patterns of abortive follicles (some tumors contain secretory globules resembling an ovum which is referred to as "Call-Exner" bodies). Also, granulosa cell tumors may develop a tubular pattern similar to that of sertoli cell tumors of the testes.

4.4.8.2 DYSGERMINOMAS

Are rare ovarian tumors with gross and microscopic features similar to seminomas of the testes. However, no hormone is secreted and the origin of the dysgerminoma is unknown. 

4.5 FALLOPIAN TUBES:

Primary lesions in the fallopian tubes (oviducts) are rare. Hydrosalpinx, pyosalpinx and salpingitis may occur but these are usually secondary to diseases of the uterus or to manual manipulation of the ovaries. SALPINGITIS refers to inflammation of the oviduct. The inflamed oviducts are seldom significantly enlarged and lesions are usually not detectable with the naked eye. The exudate may be serous, catarrhal or fibrinous. Salpingitis is usually the result of extension of infection from the uterus. PYOSALPINX refers to an accumulation of purulent exudate in the oviducts. It usually follows metritis. HYDROSALPINX refers to an accumulation of fluid in the oviducts following some form of obstruction. In addition, fluid filled cysts may be present in the oviducts. 

4.6 UTERUS:

4.6.1 INFLAMMATION OF THE UTERUS:

Inflammation of the uterus limited to the endometrium is termed endometritis. Involvement of the entire uterine wall is referred to as metritis. Inflammation of the uterine serosa is called perimetritis.

The normal non-pregnant uterus is highly resistant to infections (even specific genital organisms such as Brucella, Vibrio and Trichomonas are incapable of persisting for long periods in the non-pregnant uterus). The exact mechanism of this resistance has not been completely elucidated. However, experimental evidence indicates that the uterus under the influence of estrogen (as in the case of the normal non-pregnant uterus) is highly resistant to infection. On the other hand, the uterus under the influence of progesterone (as in the case of the pregnant uterus) is highly susceptible to many specific and non-specific bacterial infections.

4.6.1.1 ENDOMETRITIS:

Endometritis refers to inflammatory processes in which the endometrium is primarily involved (actually, the reaction is limited to the endometrium only in very mild forms of infections). Almost all uterine infections begin as an endometritis, but they may progress very rapidly to involve the entire wall. There is a tendency for Vibrio fetus and Trichomonas fetus to cause mild infections limited to the endometrium. In mild forms of endometritis, gross lesions are absent or insignificant. Microscopically, there is a mild infiltration of inflammatory cells (the best indication of mild metritis is the presence of infiltrated plasma cells and lymphocytes in the stroma because a few neutrophils may be present in a normal uterus). A more severe form of endometritis occurs following parturition. Grossly, the uterus is enlarged, flabby and collapsed (rather that firm and contracted). The uterine lumen contains chocolate-colored lochia, with or without a foul odor. The endometrium is reddened, swollen and edematous. 

4.6.1.2 METRITIS:

Metritis is characterized by inflammation of the entire uterine wall (including the endometrium). The term septic metritis is oftentimes used when referring to severe and often fatal inflammation of the uterus. Metritis is usually due to infections introduced at or shortly after parturition. Organisms most likely to be responsible are streptococci, staphylococci and other pus-formers. Grossly, the uterine wall is flaccid, thickened, reddened, edematous and friable (rupture may occur and result in a secondary peritonitis). There may be a scanty or abundant secretion of fetid uterine exudate via the vagina. Microscopically, inflammatory cells may be found throughout the uterine wall (in acute cases, neutrophils dominate, whereas in chronic cases, lymphocytes are prominent). Severe metritis may lead to a septicemia. However, cases may recover with proper treatment.

4.6.2 ABSCESSATION OF THE UTERUS:

Uterine abscesses occur most frequently in cows. They often result from localization of infection to one part of the uterine wall following severe metritis or localized traumatic injury.

4.6.3 PYOMETRIA:

Pyometria is an acute or chronic suppurative infection of the uterus with an accumulation of pus in the lumen in the presence of a "closed" cervix (the cervix may not be completely closed but there is never a heavy discharge from the uterus). The condition occurs with frequency only in the cow, bitch and cat. There are two primary mechanisms:

4.6.4 ABNORMAL ENDOMETRIAL GROWTH:

4.6.4.1 ATROPHY OF THE ENDOMETRIUM:

Endometrial atrophy may be associated with ovariectomy, hypopituitarism, a pituitary lesion or chronic inanition/wasting disease. Grossly, the endometrium is flat, thin and grayish. Microscopically, only remnants of endometrial glands remain.

4.6.5 HYPERPLASIA OF THE ENDOMETRIUM:

Endometrial hyperplasia may be cystic or non-cystic. Cystic hyperplasia (sometimes referred to as "Swiss cheese" endometrium) is an extreme degree of hyperplasia. Endometrial hyperplasia is probably an exaggeration of the normal proliferative changes of the endometrium in response to ovarian hormones. In the bitch, prolonged progesterone stimulation is the major factor in the induction of endometrial hyperplasia. However, in cattle, endometrial hyperplasia is associated with prolonged estrogenic stimulation (hyperestrogenism as seen with ovarian follicular cysts and with granulosa cell tumors). In sheep, endometrial hyperplasia has been reported in animals grazing on pasture legumes with high estrogenic activity (especially Trifolium subterraneum and T. pratense). These plants may have similar effects in cattle.

Non-cystic hyperplasia of the endometrium is usually not recognizable grossly. In cystic endometrial hyperplasia, the uterine wall is soft, thick and spongy. There are numerous submucosal cysts that bulge into the lumen of the uterus. Infection superimposed on endometrial hyperplasia is common only in the dog and cat. Endometrial hyperplasia is a significant precancerous lesion in the human. This is not true in domestic animals. 

4.6.6 ADENOMYOSIS (endometrosis):

Adenomyosis is a condition characterized by the presence of endometrial glands and stroma between muscle fibers of the myometrium. The condition may result from congenital malformations or it may arise subsequent to hyperplasia and overgrowth of the endometrium.

4.6.7 TORSION OF THE UTERUS:

Torsion of the uterus may occur in any species, but the condition is most frequently observed in pregnant cattle. Torsion of 180 degrees or more will cause dystocia and circulatory embarrassment. Minor twists of 90 degrees or less are fairly common and will apparently resolve themselves. In uniparous species (cow), the twist occurs at the level of the mesovarium, vagina or cervix with involvement of the entire uterus (these animals have a well-developed intercornual ligament which prevents very much independent movement of the uterine horns). In multiparous animals (bitch, cat), there is no intercornual ligament and the torsion may involve part of one horn or it may involve the entire uterus.

4.6.8 PROLAPSE OF THE UTERUS: 

Uterine prolapse occurs with some frequency in ruminants. The condition occurs most commonly after parturition in the previously gravid uterine horn. The pathologic sequelae are comparable to those of intestinal intussusception with the added factor of trauma.

4.6.9 THE PREGNANT UTERUS:

The pregnant uterus is under the influence of estrogen and is highly susceptible to a variety of diseases and conditions. 

4.6.9.1 EMBRYONAL DEATH:

A degenerate ovum, zygote or early embryo may be absorbed or expelled from the uterus. The incidence of zygotic and early embryonal death is estimated to be high (15-30%) in all species studied extensively. Early embryonal death is usually manifested by signs of infertility and irregular estrus cycles in the female (there may be no evidence of an aborted fetus or lesions in the genital tract of the female). The causes of such mortality are presumably diverse; however, chromosomal abnormalities may play an important role.

4.6.9.2 FETAL DEATH:

A developing dead fetus may be mummified, macerated or aborted. (Abortion may be defined as the expulsion of a fetus prior to the time of expected viability. Whereas, a fetus delivered within the time of expected viability is referred to as a stillborn).

In uniparous domestic species, the dead fetus may be expelled or retained. In early pregnancy, when the main source of progesterone is the maternal ovary, death of the conceptus results in resorption, maceration or mummification. However, later in gestation, when the progesterone which maintains pregnancy is produced primarily by the fetal-placental unit, death is usually followed by expulsion of the fetus.

In multiparous species, it is most common for one or several dead fetuses to be retained with the viable ones and delivered at parturition. However, if most of the fetuses die at the same time, all are likely to be aborted (live and dead fetuses). 

4.6.9.3 MUMMIFICATION OF THE FETUS:

A mummified fetus is one that dies and undergoes subsequent autolysis (there is an absence of infection and putrefaction does not occur). This condition occurs most commonly in multiparous species. In mummification, the fetal fluids are resorbed and the soft tissues gradually liquify. These fluids are concurrently resorbed via the maternal blood and lymphatics. Eventually, the entire fetus becomes brown or black and leather-like (there is no exudate or odor). A completely mummified fetus consists of dried wrinkled skin and bones. The time required for complete mummification will depend on the size of the fetus. It takes about 6 to 8 months in the case of a 6-month-old bovine fetus. In uniparous species, the mummified fetus may be retained indefinitely.

4.6.9.4 MACERATION AND EMPHYSEMA OF THE FETUS:

Maceration refers to a dead, retained fetus that undergoes autolysis in the presence of a uterine infection. The usual causes of fetal death and maceration are not potent gas producers. If the cervix is open and putrefactive organisms are able to invade the uterus and dead fetus, the result is fetal emphysema.

4.6.10 ADVENTITIAL PLACENTATION:

The development of intercotyledonary placentation occurs primarily in ruminants. This is a mechanism of compensation for inadequate development of the placentomes (which is primarily endometrial). There are normally between 75 and 125 caruncles in the cow. However, this number may be reduced due to infection or congenital disorders. Subsequently, compensation occurs through a great increase in size of the remaining caruncles during pregnancy and by the development of a more primitive villous placentation between the placentomes. The process may involve virtually all of the intercotyledonary placenta. Abortion and hydrallantois are common complications.

4.6.11 AMNIOTIC PLAQUES:

Amniotic plaques are foci of squamous epithelium on the internal surface of the amnion. These plaques are flat and measure between 2 and 5 mm in diameter. They resemble the lesions of the poxes. Amniotic plaques are more numerous on the umbilical stump. The plaques are apparently normal and they constantly occur on the bovine placenta during the middle trimester of gestation.

4.6.12 PLACENTAL CALCIFICATION :

Placental calcification refers to the presence of visible calcium deposits around small blood vessels of the placenta. These deposits appear as white streaks or spots in the amnion and allantois. They occur in many species from about the end of the first trimester to the end of the second trimester. The reason(s) for this deposition of calcium is unknown and there is apparently no ill effect on the fetus.

4.6.13 HYDRAMNIOS AND HYDRALLANTOIS:

Hydramnios and hydrallantois refer to an accumulation of fetal fluid in the amniotic and allantoic cavities, respectively. Normally, there is 6 to 15 liters of allantoic fluid and 3 to 6 liters of amniotic fluid in the cow with the maximum amounts being reached around mid-gestation. The fluid is then progressively decreased until termIn hydramnios and hydrallantois, the excessive fluid may reach a total volume of up to 50 gallons. The pathogenic mechanism is seldom determined; however, the excess fluid should have an obstructive origin. The fluid may accumulate slowly or rapidly and there is usually an accompanying fetal anasarca. Important sequelae are dystocia, uterine paresis, retention of the placenta and acute metritis. Also, abortion may occur. 

4.7 SOME SPECIFIC CAUSES OF ABORTION IN ANIMALS: 

4.7.1 BRUCELLOSIS 

Bacteria of the genus Brucella are small, Gram-negative bacilli or coccobacilli which prefer an intracellular habitat. Important species include:

All of the Brucella organisms are capable of producing systemic infections with relapsing bacteremic phases. Localization and persistence of infection may occur in many organs and tissues (especially in the genital tract and in the placenta). 

Brucella abortus causes abortion around the 7th and 8th months of gestation. The non-pregnant uterus is not highly susceptible to infection and, following abortion, the organisms disappear from the uterus. However, the organisms have a special affinity for the pregnant placenta and endometrium. Grossly, the pregnant uterus is not remarkable. The placenta may be normal or characteristic lesions may be present. There is mild to severe necrosis of the cotyledons (they are soft and yellow). A dirty yellow sero-purulent exudate develops between the endometrium and chorion in the intercotyledonary areas. Affected areas of the intercotyledonary placenta are thickened, opaque, tough and leather-like in appearance. There is usually edema of the placenta and umbilical cord. Microscopically, the placenta is edematous and there is an infiltration of neutrophils and mononuclear cells. In the fetus, the most important lesion is a bronchopneumonia which may be mild or severe. The abomasal contents are turbid, yellow and flaky (normal abomasal contents should be clear,translucent, thick and viscous). 

Brucella melitensis is considered to be a major cause of abortion in sheep and goats. In most respects, the disease resembles that caused by Brucella abortis in cattle. However, mastitis is an early sign and the milk is watery and clotted. Organisms are excreted in the milk. 

Brucella ovis causes placentitis and abortion in the ewe (the organism is not very pathogenic compared to the other Brucella spp.) Periarteritis and arteritis are distinctive features of the disease. Placental lesions are similar to those described for Brucella abortus in cattle. The fetus is edematous and fluid in the body cavities may contain strands of fibrin. Also, a mild bronchopneumonia and a lymphadenitis may be observed in the fetus. In general, the greatest susceptibility to intrauterine exposure is from 21 to 90 days of gestation.

 Brucella suis is the organism of importance in swine (however, swine are susceptible to B. abortus as well as to B. melitensis). Transmission is primarily via coitus. The uterine lesions consist of multiple yellow-white nodules or granulomas that vary in size from 1 to 3 mm in diameter. The placenta may be normal or it may be congested and edematous with many small hemorrhages. The fetuses are edematous and their stomach contents may be yellowish and slimy. In general, abortion occurs between the 2nd and 3rd months of gestation. There is also a high incidence of stillborns and weak piglets delivered at term. The placenta may or may not be retained. 

Brucella canis has been incriminated as the cause of abortion and epidymitis in the dog. Aborted fetuses may be dead or alive at the time of expulsion. Live pups usually die within a few hours after birth. Lesions in the fetuses consist of pneumonia, endocarditis and hepatitis. Affected bitches may exhibit a sero-sanguinous vaginal discharge for 1 to 6 weeks after abortion. 

4.7.2 VIBRIOSIS

BOVINE GENITAL VIBRIOSIS is a venereal disease caused by vibrio fetus veneralis and characterized by infertility and early embryonal death (abortion may occur in a small percentage of infected cows). Coitus is the usual means of transmission. Temporary infertility and irregularity of the estrus cycle may be the only clinical signs noted in infected cows (irregularity of the estrus cycle is believed to be due to interruption of very early pregnancy by infection). There may be a very mild endometritis, cervicitis and vaginitis. In the small percentage of cows that abort, the abortion occurs around the 5th to 7th months of gestation. Grossly, placental lesions are similar to those described for Brucella abortus in cattle, but they are less severe. Many of the cotyledons are yellow and necrotic and sero-purulent or sero-fibrinous exudate is present between the endometrium and chorion. The intercotyledonary areas are thickened, edematous and leather-like. Following infection, there is no permanent maternal injury.

4.7.3 EPIZOOTIC BOVINE ABORTION: 

EPIZOOTIC BOVINE ABORTION (sometimes referred to as Chlamydial abortion or "foothill" abortion) is an infectious disease caused by a strain of Chlamydia psittaci and characterized by abortion between the 5th and 7th months of gestation. The disease has been reported primarily from the western U.S.A. 

Fetal lesions consist of petechial hemorrhages which may be found throughout the subcutaneous tissue, oral cavity and in the conjunctiva. The fetal liver is enlarged and friable with a granular or roughened surface. Microscopically, there is a diffuse or focal proliferation of reticuloendothelial cells in many organs and tissues (liver, spleen, brain, lymph nodes, myocardium, etc.). Also, foci of necrosis may be found in the liver and spleen. 

4.7.4 LISTERIOSIS: (Please refer to your Central System Notes)

Abortion due to listeria monocytogenes occurs during the last trimester of gestation in both sheep and cattle. If uterine infection develops during the early part of the last trimester, the placenta is quickly invaded by the organisms and the fetus dies as a result of septicemia. The dead fetus is expelled in approximately 5 days. By this time, autolytic changes will mask any pathologic lesions that may have been present. However, if the fetus is near term when the infection develops, dystocia occurs and there is severe metritis with septicemia of the fetus. The placental lesions consist of necrosis that involves the tips of villi. Multiple foci of necrosis may be found throughout the fetal liver. 

4.7.5 EQUINE VIRAL RHINOPNEUMONITIS: (Please refer to your Respiratory System Notes)

The equine herpesvirus I causes abortion in mares between the 8th and 11th months of gestation. The most consistent lesion in the fetus is severe lung edema. The fetal liver is characterized by multiple tiny foci of necrosis. Microscopically, intranuclear inclusion bodies are found in the liver, spleen and bronchial epithelial cells.

4.7.6 GENITAL TRICHOMONIASIS: 

Trichomoniasis is a contagious protozoan disease of cattle characterized by sterility, pyometria and abortion. Infection in the bull remains in the preputial cavity indefinitely. Characteristically, trichomoniasis in the female results in signs of infertility and irregular estrus cycles. A few days after infection, an acute vaginitis develops with a mucoid discharge. Subsequently, the vaginitis resolves and the infection localizes in the uterus and cervix, resulting in endometritis and cervicitis. There may be a rather copious (up to a gallon) accumulation of purulent exudate in the uterus (pyometria). There are no specific characteristic placental or fetal lesions. 

4.7.7 MYCOTIC ABORTION 

Mycotic abortion occurs sporadically in cattle and it is usually caused either by Aspergillus or Mucor (Absidia and Rhizopus have also been incriminated). These agents apparently reach the uterus via the blood stream causing abortion in late gestation. There is usually necrosis of the cotyledons and thickening of the intercotyledonary areas. Fetal skin lesions may be present and they appear as irregular elevated plaques (resembling the lesions of ringworm). 

4.8 CERVIX: 

4.8.1 INFLAMMATION

Inflamation of the cervix (cervicitis) is usually an extension of uterine or vaginal infections. Actually, cervicitis is seldom a separate disease entity. Most inflammations are superficial. In general, the mucous-secreting epithelium of the cervix provides a good defense against bacterial invasion. 

4.9 VAGINA AND VULVA:

4.9.1 INFLAMMATION

Inflamation of the vagina and vulva is a frequent sequela of parturition in which the mucous membranes are bruised or lacerated. Other causes of vaginitis and vulvitis include malicious injury, foreign bodies, etc. The inflamed vagina is painful, reddened and edematous. necrosis and a fetid discharge are common. 

4.9.2 INFECTIOUS PUSTULAR VULVOVAGINITIS OF CATTLE

Is caused by the same virus as that which causes infectious bovine rhinotracheitis. In general, the respiratory and vaginal infections behave as separate and distinct disease entities (however, the syndromes may occur together in individual animals). 

Infectious vulvovaginitis is an acute contagious disease characterized by inflammation, necrosis and pustule formation on the mucosa of the vulva and vagina (occasionally, similar lesions may occur on the skin of the penis and prepuce). The syndrome is frequently transmitted by coitus, but it can also be transmitted by other mechanical means. Initially, there is hyperemia of the vaginal and vulval mucosa and focal hemorrhages in lymphoid follicles of the submucosa. Subsequently, pock-like lesions (2 to 3 mm in diameter) which are slightly elevated, pale, soft and friable, replace the hemorrhage over the lymphoid follicles. The affected epithelium becomes necrotic, ulcerates or erodes. Microscopically, intranuclear inclusion bodies may be observed in epithelial cells early in the disease. The disease usually subsides in 10-12 days 

4.10 MAMMARY GLAND 

4.10.1 INFLAMMATION OF THE MAMMARY GLAND:

The term mastitis refers to inflammation of the mammary glands. The condition is of greatest economic importance in dairy cattle; however, all species may be affected. 

4.10.1.1 BOVINE MASTITIS:

The causes of mastitis in cattle are diverse with more than 50 species of bacteria and more than 20 species of fungi being incriminated. Factors that predispose to mastitis are poor milking hygiene, faulty milking machines, trauma, etc. The bacterial pathogens most commonly recovered from mastitis (in approximately decreasing order of frequency) are Staphylococcus aureus, Streptococcus agalactiae, other streptococci, coliform organisms, Corynebacterium pyogenes and Pseudomonas aeruginosa.

The morphological patterns of mastitis are usually divided into several types based largely on severity and duration of the disease. 

4.10.1.1.1. ACUTE CATARRHAL MASTITIS

Is characterized by a mild systemic response of short duration. Individual quarters are affected. Secretions may be bloodstained and contain flakes of inspissated pus. Grossly, affected lobules are pale, firm and project above the cut surface. Flakes of purulent exudate are present in the cisterns and lactiferous ducts. Edema may be mild or pronounced. Microscopically, the alveoli within lobules are filled with neutrophils. 

4.10.1.1.2 ACUTE HEMORRHAGIC MASTITIS

Is characterized by marked swelling of the affected quarter and by a severe systemic response which is often fatal. The small amount of secretion that can be obtained consists of sero-sanguinous or fibrinous exudate. Grossly, the tissue is intensely hyperemic and hemorrhagic with areas of necrosis. Gangrene may occur. 

4.10.1.1.3 CHRONIC MASTITIS

Is usually a sequela of acute mastitis. However, even in the chronic stages, foci of active (acute) inflammation may be present. There is no systemic involvement. Grossly, the affected tissue is tough and smaller than normal (due to proliferation of fibrous connective tissue and glandular atrophy). 

4.10.1.1.4 SUPPURATIVE MASTITIS

Is usually associated with Corynebacterium pyogenes or Pseudomonas aeruginosa infection. Multiple abscesses are present. 

4.10.1.1.5 GRANULOMATOUS MASTITIS

Is the response to chronic inflammation by a variety of organisms (Mycobacterium, Nocardia, Cryptococcus, etc.). 

4.10.1.2 STREPTOCOCCAL MASTITIS:

STREPTOCOCCUS AGALACTIAE mastitis is one of the more important forms of bovine mastitis (presently, the condition can be readily controlled via therapy). The organisms depend on mammary tissue for survival and the mammary gland of the cow and goat is the natural and sole habitat. The organisms enter the mammary gland via the teat canal and reside in the milk or on the surface of the milk channels (they may persist without causing an inflammatory process). Under certain conditions (altered virulence, etc.), the epithelial cells lining the teat channels are briefly invaded and acute inflammation may follow. However, inflammation of mammary tissue is due primarily to the diffusion of toxic products. Once an inflammatory process is initiated, the infiltrating neutrophils will rapidly destroy the invading organisms (this destruction of organisms may at times sterilize the udder or decrease the numbers so that a bacterial count taken during a crisis may be negative). 

Grossly, more than one quarter is usually involved but not uniformly. Most of the changes take place in the distal portion of the gland around the cisterns and larger ducts. In the acute stages, the glandular tissue is swollen and turgid and lobulations are distinct on the cut surfaces. The affected mammary tissue is grayish (whereas normal lactating tissue is more or less white in color). In the chronic stages, fibrosis becomes prominent. Microscopically, the acute stage is characterized by an exudative process in which there is severe edema and an extensive infiltration of neutrophils into interlobular tissue and acini. The acinar epithelial cells become vacuolated and they desquamate. This acute exudative phase gives rise to pathologic fibrosis and/or involution. Penicillin is highly effective against Streptococcus agalactiae. 

Other streptococci that may cause mastitis include Strept. dysglactiae, Strept. uberis, Strept. zooepidemicus, Strept. pyogenes, Strept. fecalis and Lancefield groups of G and L streptococci.

4.10.1.2.1 STAPHYLOCOCCAL MASTITIS: 

Staphylococcus aureus is considered to be the most important cause of mastitis in most dairy areas. The organism is ubiquitous and can colonize the skin as well as the udder. Antibiotic treatment is not always successful for certain isolates. Staphylococcus aureus is capable of causing peracute, acute, subacute, chronic, gangrenous and subclinical types of mastitis. The acute form of the disease usually occurs shortly after parturition and tends to produce gangrene of the affected quarters with high mortality. Grossly, the affected tissues are swollen, tense, hot, firm and painful. Milk secretion is reduced. Gangrenous tissues become blue and eventually black in color. 

The acute non-gangrenous forms of the disease are characterized by lesions similar to those described for streptococcal mastitis. However, the staphylococcal organisms have the ability to invade more deeply into the interacinar tissue and establish themselves as persistent foci of infection (a granulomatous type reaction may be provoked).

4.10.1.3 COLIFORM MASTITIS: 

Coliform mastitis is usually caused by Escherichia coli and Aerobacter aerogenes. Under certain condition, coliform organisms are capable of multiplying very rapidly, producing a large pool of potential endotoxin. The resulting toxemia is responsible for the local and systemic signs of mastitis. The body temperature ranges from 103 to 108 degrees F. Milk secretion ceases and there is anorexia, depression, dehydration and rapid weight loss. The infection is usually limited to one quarter and the course is rather short (a unique feature of coliform mastitis is that the udder tissue usually returns to normal following an acute infection). If for some reason the course is prolonged, extensive necrosis occurs. Eventually, fibrosis is a prominent feature. Remember, gangrene is not produced by coliform bacilli alone. 

4.10.1.4 CORYNEBACTERIUM PYOGENES MASTITIS: 

Corynebacterium pyogenes is commonly associated with suppurative mastitis in cattle and swine. The condition may involve lactating and dry cows. There is evidence that C. pyogenes is actually a secondary invader in most cases of mastitis. The disease is characterized by the presence of multiple abscesses.

4.10.2 NEOPLASMS OF THE MAMMARY GLAND: 

Mammary neoplasms occur frequently and are often fatal in the dog (less frequent in the cat). The hard worked bovine udder is quite susceptible to inflammation, but neoplasms are rare. Also, mammary tumors are seldom observed in other domestic species. 

IN THE DOG, mammary tumors may consist of epithelial and/or connective tissue components. Mammary tumors represent approximately 25% of all neoplasms in female dogs, about 50% of these tumors are benign mixed mammary tumors and about 25% are adenocarcinomas. The remainder are adenomas, duct papillomas, myoepitheliomas and malignant mixed mammary tumors. 

4.10.2.1 MIXED MAMMARY TUMORS

Contain neoplastic cells of both glandular (epithelial) and stromal (connective tissue) origin. Also, there may be a myxomatous portion represented by a proliferation of myoepithelial cells (myoepithelial cells play a role in the production of basement membrane material and cartilage). Frequently, the connective tissue elements will undergo metaplasia with the formation of cartilage and bone (thus, some mixed tumors may consist primarily of cartilage and bone). In addition, the glandular and stromal elements may assume the neoplastic characteristics of anaplasia, hyperchromatism, hypercellularity, etc. 

The canine mixed mammary tumors are related to the endocrine status of the individual. Ovariohysterectomy has a negative effect on tumor formation. Bitches neutered before their first estrus have only 0.5% of the mammary cancer risk of the intact female. 

4.10.2.2 ADENOCARCINOMAS OF THE MAMMARY GLAND

Are similar to those that occur in other organs and tissues. These tumors are characterized by a proliferation of neoplastic epithelial cells with the formation of acini or duct-like structures. 

4.10.2.3 FIBROADENOMAS

Occur with some frequency in the mammary tissue of aged rats (this is the most frequent benign tumor of the human female breast). These tumors are composed of both connective tissue and glandular elements. Grossly, these tumors are firm, grayish-white, with grayish-yellow specks. Microscopically, there is a loose connective tissue network with pleomorphic glandular and cystic spaces. 

4.11 POST-INSTRUCTIONAL SELF-EXAMINATION 

FEMALE GENITAL SYSTEM

 

Questions

  • 1. Please complete the following statements:
    • a. _______________ refers to inflammation of the uterus.b. _______________ refers to inflammation of the ovaries.
    • c. _______________ refers to inflammation of the mammary gland.
    • d. _______________ refers to a genetic female with severe hypoplasia of the genital tract that was born co-twin with a male.
    • e. _______________ is a primary ovarian neoplasm with the potential of producing estrogen or androgen.
    • f. _______________ refers to a primary ovarian neoplasm with gross and microscopic features similar to seminomas.
    • g. _______________ refers to inflammation of the fallopian tubes.
    • h. _______________ refers to inflammation of the endometrium.
    • i. _______________ refers to an acute or chronic inflammation of the uterus with an accumulation of pus in the lumen, in the presence of a closed cervix.
    • j. _______________ is the hormone which plays an important role in the pathogenesis of pyometria.
    • k. _______________ is the major hormone responsible for the induction of endometrial hyperplasia in dogs.
    • l. _______________ is the major hormone responsible for endometrial hyperplasia in cattle.
    • m. _______________ is characterized by the presence of endometrial glands and stroma between muscle fibers of the myometrium.
    • n. _______________ is the hormone that exerts the primary influence on the pregnant uterus.
    • o. _______________ refers to the expulsion of a fetus from the uterus prior to the time of expected viability.
    • p. _______________ refers to the expulsion of a fetus from the uterus within the time of expected viability.
    • q. _______________ refers to a fetus which dies and undergoes autolysis within the uterus in the absence of infection and putrefactio
    • r. _______________ refers to a dead, retained fetus that undergoes autolysis in the presence of uterine infection.
    • s. _______________ refers to the presence of visible calcium deposits around small blood vessels of the placenta.
    • t. _______________ refers to foci of squamous epithelium on the internal surface of the amnion.
    • u. _______________ refers to an excessive accumulation of fetal fluid in the amniotic cavity.
    • v. _______________ is a mammary neoplasm that contains neoplastic cells of both epithelial and connective tissue origin.
  • 2. What is a freemartin?
  • 3. What lesions would you expect to observe in a freemartin? Why would you expect such an animal to be sterile?
  • 4. Under what circumstances would you expect a freemartin to develop?
  • 5. Discuss the possible mechanisms by which a freemartin develops.
  • 6. What is chimerism?
  • 7. What alteration (clinical, morphologic, etc.) would you expect to observe in the male co-twin of a freemartin?
  • 8. What is the condition oftentimes referred to as "white heifer disease?" What lesions would you expect to observe in the ovaries and oviducts? What lesions would you expect to observe in the cervix, uterus and vagina? Under what circumstances would you expect "white heifer disease" to develop?
  • 9. How would you differentiate "white heifer disease" from "bovine freemartin?"
  • 10. Under what circumstances would you expect hypoplastic ovaries to be a normal condition in animals?
  • 11. What are cystic ovaries? In what animal species would you expect this condition to occur most commonly?
  • 12. What considerations must be taken before making a diagnosis of cystic ovaries in horses?
  • 13. Name the types of ovarian cysts that may occur in animals.
  • 14. Under what circumstances would you expect a cow with cystic ovaries to exhibit signs of nymphomania? How would you define nymphomania?
  • 15. What is the most common type of cystic ovarian degeneration you would expect to observe in animals? What hormone is most likely to be responsible for nymphomania in cattle?
  • 16. What is the role of pituitary gonadotrophin and luteinizing hormone in the development of cystic ovaries in cattle?
  • 17. Briefly discuss the gross and microscopic alterations associated with cystic graafian follicles.
  • 18. What are luteinized cysts?
  • 19. What pathologic alterations are associated with cystic graafian follicles in dogs and cats?
  • 20. Briefly discuss the extraovarian lesions associated with cystic ovaries in cattle.
  • 21. Under what circumstances are atretic follicles considered to be a normal process?
  • 22. Under what circumstances are atretic follicles a pathologic condition?
  • 23. Discuss the factors which are responsible for atretic ovarian follicles.
  • 24. What is a corpus luteum?
  • 25. What hormone is necessary for the growth and development of a corpus luteum?
  • 26. What hormone is produced by the corpus luteum?
  • 27. Name the primary neoplasms of the testis. Which one of these neoplasms is capable of producing a hormone?
  • 28. Name a primary ovarian neoplasm that has the potential to produce estrogen and/or androgen.
  • 29. Name at least two conditions that may result in nymphomania.
  • 30. Name a primary ovarian neoplasm that may be associated with endometrial hyperplasia in the bitch.
  • 31. What are "Call-exner bodies?"
  • 32. How would you define the following terms: metritis, endometritis, pyometria, perimetritis?
  • 33. Would you expect the normal non-pregnant uterus or the normal pregnant uterus to be more susceptible to infections? Explain.
  • 34. What hormone exerts the major influence on the non-pregnant uterus?
  • 35. What hormone exerts the major influence on the pregnant uterus?
  • 36. Name two specific organisms which are oftentimes the cause of abortion in cattle but tend to infect only the endometrium.
  • 37. Briefly, discuss the pathologic alterations associated with endometritis in cattle. What is lochia?
  • 38. Differentiate a metritis from an endometritis. What is a septic metritis?
  • 39. What factors may be responsible for metritis in animals?
  • 40. Under what circumstances would you expect a severe generalized peritonitis to be associated with a metritis? What is a septicemia?
  • 41. How would you distinguish uterine abscessation from a septic metritis?
  • 42. How would you characterize pyometria in animals?
  • 43. How would you distinguish a pyometria from uterine abscesses?
  • 44. What are the two primary causative mechanisms of pyometria?
  • 45. What is the most common etiologic mechanism associated with pyometria in mares?
  • 46. What is the primary etiologic mechanism associated with pyometria in cattle and dogs?
  • 47. What is the essential component associated with pyometria that develops subsequent to functional obstruction to uterine discharge?
  • 48. What hormone is associated with pyometria in animals? What effects would you expect this hormone to have on the reproductive system?
  • 49. Why would you expect endometrial hyperplasia to be associated with pyometria in the bitch and cat?
  • 50. Why would you expect pyometria in the bitch to be associated with cases of pseudopregnancy?
  • 51. What organisms are usually associated with pyometria that develops subsequent to a retained corpus luteum?
  • 52. Why would you expect bone marrow depression and anemia to be associated with cases of pyometria?
  • 53. Discuss the pathologic alterations associated with pyometria that develops subsequent to a retained corpus luteum in cattle and in bitches.
  • 54. Following ovulation, a corpus luteum develops from the ruptured follicle. Please answer the following questions.
  • a. In the absence of fertilization and pregnancy, what is the normal fate of the corpus luteum?
  • b. If pregnancy occurs, what is the fate of the corpus luteum?
  • c. What is a retained corpus luteum?
  • d. Discuss those alterations that may occur in animals subsequent to a retained corpus luteum.
  • 55. How would you characterize endometrial atrophy? What are some likely causes of this condition?
  • 56. What is a Swiss cheese uterus?
  • 57. List as many disease/conditions as possible which are named after a food ("bread and butter heart," etc.).
  • 58. What hormone is associated with endometrial hyperplasia in the bitch?
  • 59. What hormone is associated with endometrial hyperplasia in cattle?
  • 60. What factors are oftentimes associated with endometrial hyperplasia in sheep?
  • 61. Discuss the pathologic alterations associated with endometrial hyperplasia in animals.
  • 62. How would you characterize adenomyosis in animals?
  • 63. How would you characterize torsion of the uterus?
  • 64. What effects would you expect a uterine torsion of 180 degrees or more to have on a pregnant cow?
  • 65. Please define and/or describe the following terms: embryonal death, infertility, sterility, irregular estrus cycle, fetal mummification, fetal maceration, fetal abortion, stillborn fetus.
  • 66. What hormone exerts the major influence on the pregnant uterus? Give the source of this hormone during early pregnancy and during late gestation.
  • 67. Distinguish between an aborted and a stillborn fetus.
  • 68. Distinguish between fetal maceration and fetal mummification.
  • 69. Give the pathologic alterations you would expect to observe in both a mummified and a macerated fetus. What is fetal emphysema?
  • 70. How would you characterize adventitial placentation?
  • 71. Under what circumstances would you expect intercotyledonary placentation to occur?
  • 72. What are amniotic plaques? Where would you expect to observe such plaques?
  • 73. What is the clinical significance of amniotic plaques and placental calcification?
  • 74. In what animal species would you expect to observe a high incidence of amniotic plaques? During what stage of gestation would you expect to observe such plaques?
  • 75. How would you describe (grossly) amniotic plaques and placental calcification?
  • 76. During what stage of gestation would you expect placental calcification to occur?
  • 77. Distinguish between hydramnios and hydrallantois.
  • 78. Give a likely pathogenesis for hydramnios and hydrallantois.
  • 79. The following group of questions refers to brucellosis in animals:
  • a. Where in the body would you expect Brucella organisms to reside (intracellular, blood stream, etc.)?
  • b. Name the important species of Brucella organisms found in animals.
  • c. Give the important features of Brucella organisms.
  • 80. Differentiate Brucella abortus abortion from vibrio abortion in cattle based on the time period during gestation in which you expect abortion to occur.
  • 81. Briefly discuss the gross and microscopic alterations in the uterus and fetus of a cow that aborted subsequent to Brucella abortus infection.
  • 82. Briefly characterize abortions due to Brucella melitensis, Brucella ovis, Brucella suis and Brucella canis.
  • 83. Briefly characterize vibrio abortion. name the etiologic agent. What is a venereal disease?
  • 84. How is Vibrio fetus venerealis transmitted?
  • 85. What placental lesions would you expect to observe in abortions due to Vibrio fetis in cattle?
  • 86. What is the etiologic agent associated with vibrio abortion in sheep? How is this condition transmitted? At