The Femal Genital System

Developmental anomalies of the female genital system

True hermaphrodites

True hermaphrodites (Fig. 1) have both ovarian and testicular tissue either in form of a combined gonad (ovotestis) or as separate organs. Hermaphrodites have a genital tract that can not easily classed as male or female.

Pseudohermaphrodites

Pseudohermaphrodites have the gonads of only one sex, either tests or ovaries, but the external genitalia have features of the opposite sex (Fig.2) . They are classified as male or female depending upon the type of gonad present.

Fig. 1: Cattle showing true hermaphrodites.

Fig. 2: Horse showing male pseudohermaphrodites.

Freemartins is a form of ovarian dysgenesis that has been described only in ungulates. It occurs most often in cattle.

A freemartin is a sterile female co-twin of a set heterosexual twins. The condition results from fusion of placental vessels and the sharing of blood between twins during early embryonic development, Such twins are bone marrow chimeras.

Ovary

Ovary is a site of many Pathological changes and affections as:

1. Ovarian cysts

Ovarian cysts occurs in all animals, especially cows, sows, laying hens and mares. The ovarian cysts may be:

a. Follicular cysts

The follicular cysts may be regarded as follicles, which approached, but didn’t attain, normal maturity.

Macroscopically:

The follicular cysts are single or multiple, involving one or both ovaries. They are minute or up to a fist in size. Their wall is thin and usually tense. The cyst contain a clear, serous fluid of low albumin.

Microscopically:

The ovum is absent, the membrana granulosa is shrunk and represent by a layer of flat cells, which lines the inner wall of the cysts (due to pressure atrophy). By the time the cysts are entirely disappears (Fig. 3).

Fig.3: Ovary showing absence of ovum. The membrana granulosa is shrunk and represent by a layer of flat cells, which lines the inner wall of the cysts (due to pressure atrophy). By the time the cysts are entirely disappears. H&E.

b) Lutein cysts (corpus luteum cysts)

These represent an abnormal accumulation of fluid at the centre of the corpus luteum. The difference between corpus luteum cyst and follicular cysts by the presence of spherical or polyhedral, lipoid containing cells, remenants of the atrophic and degenerated corpus luteum. The cause is unknown but may be due to insufficient blood supply (Figs 4& 5).

Fig. 4: Corpus luteum cysts  represent an abnormal accumulation of fluid at the centre of the corpus luteum. The difference between corpus luteum cyst and follicular cysts by the presence of spherical or polyhedral, lipoid containing cells. H&E.

Fig. 5: Corpus luteum cysts  represent an abnormal accumulation of fluid at the centre of the corpus luteum. The difference between corpus luteum cyst and follicular cysts by the presence of spherical or polyhedral, lipoid containing cells. H&E.

c. Theca leutein cysts:

These cysts are similar to the ordinary leutein cysts but the polyhedral, lipid containing cells are derived from the theca interna. These cysts are connected with the chorionic villi and similar to the neoplasm arising from the chorionic villi. No report of this type of cysts in domestic animals.

d.  Endometerial cysts:

These cysts are develop from ectopic endometrium like tissue in human.

e.  Dermoid cysts:

These cysts are discussed in teratoma. They are readily recognizable by the hair which they almost contain.

f. Retained corpus luteum:

Retained corpus luteum occurs in bovine, which fails to undergonorml involution with the advance of the cycle into its di-estrual phase. It appeared enlarge reaching to 4 cm. The cause is usually due to excess of L.H. Retained corpus leuteum lead to anestrum without pregnancy. The removal of corpous 1euteum      by the digital expulsion per rectum retain the cycle to normal.

2. Parovarian cysts:

One or several cysts are frequently present in bovine, they are found attached to the mesovarium or mesosalpinx (Fig. 6) . They are clear spherical cyst of several centimetres in size. They 1ined with simple columnar, cuboidal or flattened epithelium. They arise from the distal vestigal segments of the embryonic Wolffian body. Sometime cysts are referred to cystic Hydatids of morgagni. Taenia hydatigena may present in the ovary and confused with the parovarian cysts but the scolex of the tapeworm is the difference.

Fig. 6: Paraovarian cyst showing contain fluid attached to mesovarium.

Tumors of the ovary

Cystadenoma (Fig. 7) cystadenocarcinoma granulosa cell tumor (Fig. 8) and teratoma are the main tumours of the ovary (Figs 9 &10).

Fig. 7: Ovary showing microscopic picture of cystadenoma.  H&E.

Fig. 8: Gross picture of ovarian cystadenocarcinoma.

Fig. 9: Ovary showing teratoma. The ovary containing hairs.

Fig. 10: Ovary showing microscopic picture of ovarian adenoma showing cartilaginous tissue. H&E.

Physical injuries

Rupture of the ovary in chicken may occurs due to mechanical injury or due to pullorum disease or leukosis. The yolk disarranged into the abdominal cavity cause diffuse peritonitis.

Disturbances in circulation

• Acute active hyperemia with estrus and  called physiological acute active hyperemia. Pathological active hyperaemia with ovaritis.

• Passive hyperemia occurs at the time of ovulation. It may be pathological with the general passive hyperemia.

• Hemorrhage may also occur physiologically with injury or with pullorurn disease.

•Thrombosis of ovarian vessels is occasionally observed when bacterial infection occurs.

• Emboli and infarction are uncommon, but septic ovaritis is common with septic metritis.

• Edema is occurs with general edema but physiological edema is present during estrus.

Disturbances in growth

• Aplasia of ovaries is observed in sheep and swine and also in hermaphrodites.

• Hypoplasia are normal in immature animals, but with endocrine disturbances hypoplasia is present in mature animals and in hemphrodites (Fig. 11).

Fig. 11: Hypoplasia of ovary in hermaphrodite cattle.

Fallopian tubes

Primary lesions in the fallopian tubes are uncommon. Hydrosalpinx, pyoxalpinx and salpingitis are the only lesions which are usually detected. There are usually secondary to the diseases of the uterus or to manual manipulation of the ovary.

Hydrosalpinx

Hydrosalpinx is so called because the fallopian tubes is distended, uniformly or irregularly, up to 1.5 cm or so, with a clear watery fluid (Fig. 12) which fluctuate. The tube is also in reached in length and tortuosity and is thin walled.

Fig. 12: Fallopian tube are distended with clear fluid.

Histologically:

1. There is extensive multilocular cyst formation in the mucosa with obliteration of the lumen (Fig. 13).

2. In some chronically inflamed conditions, mononuclear cell infiltration of the substantia propria are seen. Distension of the fallopian tube by      fluid follows loss of potency   of the lumen and it doesn’t matter whether the obstruction is to the abdominal ostium or the uterine ostium. The obstruction may have a congenital or inflammatory basis.

Fig. 13: Fallopian tube showing microscopic picture of multilocular cysts in the mucosa in hydrosalpinx.

Pyosalpinx

This is less common than hydrosalpinx and typically follows metritis. Pyosalpinx is characterized accumulation of pus in the tube following obstruction of the lumen.

The obstruction may be of inspissated exudate, an inflammatory thickening and fusion of the mucosal folds or chronic granulation tissue.

The length of the tube is usually not uniformly involved by the inflammatory process, rather, there are segments in which the reaction is more acute or more advanced so that the obstruction tends to involve irregular segments with the in between portions distended with exudate.

Microscopic appearance

The entire thickness of the wall of the duct is infiltrated with neutrophils, lymphocytes and plasma cells and the same cells collect in the lumen and in the mucosal cysts formed by adhesion.

Salpingitis

It means the inflammation of the oviduct. Inflammation of the oviduct without significant enlargement is the common and most important tubular lesion.

It is usually bilateral and is usually not detectable macroscopically.

It may show any of the usual forms of inflammation, either serous, catarrhal or fibrinous.

In the mildest form of salpingitis, the mucosa alone is affected and changes of functional significance may be slight enough to be overlooked histologically.

Congestion of the mucosal vessels, mononuclear cell infiltration, loss of epithelial celia and some desquamation of the epithelium may be the only changes detectable.

In more severe infections, catarrhal exudate collects in the lumen, the mucosal folds are thickened by cellular infiltration and congestion and the epithelium is in large part destroyed. Loss of epithelium occurs first on the free edges of the mucosal folds and these denuded areas tend to fuse and adhere to produce intramucosal cysts (Fig.14).

In chronic catarrhal salpingitis, the mucosa is virtually destroyed and replaced by proliferated connective tissue and cellular infiltrations with more or less occlusion of the lumen (Fig 15).

Fig. 14: Salpingitis showing cystic dilatation of mucosal glands and infiltration of the mucosa with inflammatory cells besides congested blood vessels. H&E.

Fig. 15: Chronic catarrhal salpingitis, the mucosa is  destroyed and replaced by proliferated connective tissue and cellular infiltrations with more or less occlusion of the lumen with necrotic debri. H&E.

The uterus

Torsion of the uterus

It is exceptional in species other than cattle. In almost all cases, such twisted uteri are pregnant, but torsion may occur also with pyometra and hydrometrs. The torsion occurs about the transverse axis of the organ with the mesovarium as one fixed point.

In uniporous (cow in which a well-developed intercornual ligament doesn’t permit much independent movement of the horns, the entire organ is involved in the torsion which is about the mesovarium and vagina or cervix as fixed points.

It may result in dystocia, more severe twist may result in local circulatory disturbances, where the thinner walled veins are obstructed before the arteries and the uterus becomes congested and edematous, with the edema of the placenta and death of the foetus.

Rupture of the uterus and peritonitis may take place.

Prolapse of the uterus

It occurs fairly commonly in ruminants, exceptionally in other species.

In cows it is most common associated with prolonged dystocia, relieved by forced traction, retained placenta and post parturient hypocalcaemia.

Uterine prolapse after parturition is a common complication of the hyperaestrogenism, which results from ingestion of 1egumes with a high content of estrogens.

The pathogenic sequelae of prolapse are comparable to those of intestinal intussusception with the added factor of trauma. Congestion and edema are followed by hemorrhage, necrosis and gangrene may occur.

Rupture of the uterus

It may occur spontaneously, but it is usually a result of obstetrical manipulations.

Most ruptures occur in the fundus adjacent to the pelvic edge as irregular tears which may involve the full width of the wall or only the mucosa.

Mucosal ruptures are of no consequence. Complete rupture are often fatal either by virtue of haemorrhage, or spread of uterine inflammation to the peritoneum, or displacement of retained membranes into the abdominal cavity.

The majority of ruptures occur in uteri, which are devitalized as a result of torsion or prolonged dystocia.

Circulatory disturbances

Endometrial hyperemia and edema occur normally at estrus and reach the greatest relative development in the bitch in preoestrus.

Hemorrhage is common in older cows and occurs immediately after estrus.

The source of hemorrhage is the endometrial capillary bed immediately anterior to the cervix.

Hemorrhage of pathologic important follows torsion and inversion, by obvious mechanisms.                                              

Disturbance in growth

Atrophy

Atrophy of the endometrium results from loss of atrophic ovarian function.

Atrophy is common after ovarectomy, but may reflect hypopituitorism of chronic inanition (Exhaustion from lack of food or defect in assimilation), or most disease or a primary hypophyseal lesion.

The endometrium is flat, thin and greyish in appearance. The more superficial portions of the endometrium are the more atrophic and in advanced atrophy the lining mucosa covers a thin layer of condensed stroma, in the depth of which are the inactive glandular remnants which are sometimes cystic.

Hyperplasia

Endomaterial hyperplasia is usually called cystic hyperplasia of the endometrium or cystic hyperplastic endometrium or cystic hyperplastic endometritis (Figs 16 & 17).

Fig. 16: Endometrium showing cystic endometrial hyperplasia.

Fig. 17: Microscopic picture of endometrium showing cystic endometrial hyperplasia.

Non-cystic hyperplastic endometritis is really only an inflammatory complication of cystic hyperplasia.

Endometrial hyperplasia is also of pathological importance. The origin of endometrial hyperplasia can be attributed to excessive and prolonged estrogenic activity.

Cystic endometrial hyperplasia in the cow is invariably associated with ovarian follicular cysts or granulosa cell tumours, both of which are potential sources of hyperestrogenism.

Non-cystic endometrium hyperplasia isn’t recognizable macroscopically, except as an suspicious thickening of the endometrium. The thickening is due to an increase in the size and number of glands which are irregular in their distribution and coarse. The stroma isn’t hyperplastic but is edematous. The glands may show both proliferative and secretory activity.

Cystic endometrial hyperplasia is recognizable grossly. In the mare in which it is a rather rare condition,      the uterine wall is soft thick and spongy. If the opened uterus is placed on a table and jarred, the endometrium shivers like a gelatinous mass. The lining has a glistening appearance is moist, the numerous submucosal cysts bulge like blisters of clear fluid into the lumen. In the cow, cystic hyperplasia is typically non-uniform and in long standing cases is often associated with the presence of excess mucous (mucometra) or fluid (hydrometra) or pus (hyperplasia pyometra complex) in the uterine lumen (Fig. 18).

Fig. 18: Microscopic picture of cystic hyperplasia pyometra complex. H&E.

Adenomyosis

This terms applies to the presence of endometrial glands and stroma between the muscle bundles of the myometrium. In some cases it is a malformation and in others it arises by hyperplastic overgrowth of the endometrium.

It isn’t a common lesion in any domestic species, but is seen in the bitch with cystic endometrial hyperplasia.

Adenomyosis is observed occasionally in cows as a part of the local disorder of segmental aplasia. It may also be present as a malformation of the tips of the uterine horns in cows (Fig 19).

Fig. 19: Adenomyosis showing endometrial gland between the muscle bundles of the myometrium. . H&E.

(Endometriosis)

It is the presence of endometrium outside the uterine cavity (Ectopic sites). It occurs in menstruate species, which include women. This ectopic endometrium respond to the normal cyclic ovarian hormonal changes and under goes monthly desquamation and bleeding (menstruation) in the pelvic cavity results in strong inflammatory reaction which leads to fibrosis and adhesions between pelvic organs.  

Hydrometra and Mucometra

The two conditions are considered together and differ only in physical, properties and depends on the degree of dehydration of the mucin, which in turn may be related to the relative activity of estrogenic hormone (Fig 20).

Fig. 20: Uterus showing hydrometra.

The accumulation of thin or viscid fluid in the uterus occur in the same time with the development of endometrial hyperplasia or is proximal to an obstruction of the lumen of the uterus, cervix or vagina.

In the first instance, the amount of fluid may be several litres and the greater the volume of fluid, the less viscous. Small amounts of mucin give the mucosal surface a gummy stickness.

In the second instance, that of obstruction to the lumen the volume of fluid depends on the site of the obstruction to the lumen.

The fluid is slightly cloudy and watery but, in some cases of segmental aplasia, where the volume of retained secretion isn’t great, it may be very viscid and sometimes inspissated to rubbery masses of mucin and cellular detritus.

Inflammatory diseases of the uterus

Inflammation limited in extent   to the endometrium is termed endometritis, involvement of the entire thickness of the wall is metritis, of the serosa, perimetritis and of the suspensory ligaments, parametritis.

Endometritis

Mostly all uterine infections begin as an endometritis, but may progress so rapidly to any of numerous.

Variations and manifestations that definitions have little worth.

The mildest forms are seen post-coitus, they are caused by Trichomonas fetus and vibrio-fetus or pyogenic cocci and coli forms of low pathogenicity (Fig. 21).

There are no gross lesions in this simple form of endormetris. A slight opacity of the normally crystal clear oestrual mucous, may be all that is seen.

Microscopically:

1- The change aren’t striking and consist for the most part of a diffuse but light infiltration of inflammatory cells with slight desquamation of the superficial epithelium.

2- There is no significant vascular changes.

3- The best indications of mild endometritis are infiltrated plasma cells and foci of lymphocytes in the stroma.

Resolution of this type of endometritis occurs with no more residue, than a few cystic glands with priglandular fibrosis, although during its course it may be responsible for a series of aborted embryos.

More severe grades of endometritis such as acute and chronic catarrhal  are common to the purerperm (the period from the termination of labour to complete involution of the Nothing of significance may be visible on the serosal surface, but the organ is enlarged.

The lumen contains chocolate colored lockia which is slightly viscous and often without foul odor. With the admixture of inflammatory exudate and placental detritus, the uterine content becomes progressively dirty grayish-yellow in color.

The endometrium is congested and the intercotylodenary areas are rigged, with shreds of mucosa free in the lumen.

Small haemorrhages are common in the congested mucosa and there is prominent leukocytic infiltration involving all muscosal elements, including the glands and massing at the surface, where suppuration and superficial necrosis produce the tattered mucosa, the surface is comparable to a pyogenic membrane (Figs 22 & 23).

Fig. 21: Uterus showing mild endometritis characterized by infiltration of the endometrium with inflammatory cells. H&E

Fig. 22: Acute catarrhal endometritis showing desquamation of epithelial lining and infiltration of lamina propria with inflammatory cells with cystic dilatation of endometrial glands. H&E.

Fig. 23: Catarrhal endometrium showing inflammatory cells and accumulation of mucus in gland. H&E.

Metritis

The difference between endometritis and metritis is that the later all layers of the uterine wall show evidence of acute inflammation characterized by the following changes:

1. The uterus is paretic and there may be little or no vaginal discharge.

2. The wall of the uterus is thickened with suffused blood and edema fluid and is very friable.

3. The serosa is dull and finally granular, with point brush hemorrhages and a thin deposition of fibrin or the subserosal vessels may be darkly congested.

4. The secretion may be scant or abundant, feted, and is dirty yellow to red in color.

The microscopic picture is that of a purulent inflammation, where the following changes can be detected:

1. The subserosal connective tissue are edematous and infiltrated with leukocytes and the same process surrounds the blood vessels of the myometriurn and spread between the bundles of individual muscle fibres, which then undergo granular degeneration.

2. In metritis as in acute endometritis, the leukocytes mass on the mucosal surface are associated with extensive hemorrhage, necrosis and sloughing.

3. Thombosis of blood vessels, which may extend to the vessels of mesometrium with the usual sequllae.

Sequelae of metritis and endometritis

1. Many of the milder cases of endometritis recover.

2. Many of the acute cases of metritis are fatal in spite of therapy.

3. Complicating conditions, as chronic endometris, uterine abscess, parametritis, salpingitis, pyemia and pyometra occur.

4. Pyelonephritis is an occasional complication.

Chronic endometritis

It may be a sequelae of acute phase. With greater or lesser degrees of endometrial destruction and replacement by granulation scar tissue. The uterus takes on the nature of a fistulous tract.

The changes depend on the duration and severity of the inflammation, but consist essentially of productive fibrosis and leucocytes in which the plasma cells predominate.

The endometrium is thickened, the glands are empty or atrophic or flattened and attenuated or cystic due to the periglandular fibrosis (Figs 24, 25 & 26).

Fig. 24: Chronic endometritis showing periglandular infiltration with round cells.

Fig. 25: Chronic catarrhal endometritis showing periglandular fibrosis. H&E.

Fig. 26: Uterus showing chronic catarrhal endometritis.

Fig. 27: Uterus showing pyometra.

1. Pyometra in association with mechanical obstruction to discharge:

This   type of uterine infection is sometimes seen in the uterus is a sequelae to prolonged endometritis.

The causative microorganism is usually streptococci. These genital infections     in the more typically productive meteritis, cervicitis and endometritis.

In the course of chronicity of the chronically inflamed cervix become indurated and may become stenotic, there by preventing the expulsion of uterine exudate.

Anoma1es development of the uterus, for example the segmental aplasias, results also in the obstruction of the cervix.

2. Pyometra in association with functional obstruction to discharge

This occur as a result of endometrial pyogenic infection together with retained corpus lutein.

The role of retained luteal tissue in the pathogenesis of pyometra appears clear. The secreted progesterone endows the uterus with a high degree of susceptibility to infection, maintains functional closure of the cervix and inhibits myometrial contractility.

The amount of pus retained in the uterus of a cow with pyometra varies from a few ounces to more than a gallon and is thick, creamy or greyish green in color.

The wall of the uterus is thick, doughy, but in long standing cases the walls are then fibrosed.

Pyometra in bitch and cat is a more acute lesion than in cow and typically, there is demarkable distension of the uterine horns, which may come to occupy most of the peritoneal cavity.

The cervix is completely closed. The serosal surface of the uterus is dark in color and the vessels are congested and prominent. The wall is friable and either rupture or perforation with secondary peritonitis isn’t uncommon.

The nature of the uterine content is variable.

In the more severe cases, usually those infected with Escherichia coli and proteus spp., the exudate is thick, viscid, tenacious, opaque, red brown in color and with a characteristic fetid odor. In there infected with Streptococci and Staphylococci the exudate is more typically purulent.

Macroscopically

When the exudate is removed, the mucosa is seen to be irregular in thickness, necrotic and ulcerated in portions with irregular superficial hemorrhage and in other portions, obviously hyperplastic, dull-white and dry in appearance with small cysts visible in these hyperplastic areas.

Microscopically

The most significant feature is the remarkable endometrial hyperplasia and progestational proliferate in almost all cells

The cells of such progestational epithelium are enlarged, columnar, vacuolated has a small pyknotic nucleus. In some cases, the normal side layer of cells piles up to produce pseudostratification or localized papillary proliferation.

Whatever remains of the endometrial lining may show this development or it may be patchy and alternating With normal or even with metastatic squamous epithelium which develops response to irritation as a protective phenomena.

Extragenital lesions associated with pyometra in the bitch are common and due to severe intoxication and probably also to intermittent bacteremia.

1. Depression of bone marrow leads to anemia and prominent extra-medullary elaboration of leucocytes, especially in the liver, kidney, spleen, lymph nodes, lung and adrenal glands and there is typically a severe leukocytosis.

2. A variety of degenerative and inflammatory lesions, including glomerulosclerosis occur in the kidneys.

3. There may be hemorrhage and necrosis of the adrenal cortex and congestion of viscera.

The cervix

Cysts of the cervix

It occurs in cows and probably all are retention cysts formed by fusion of the rugae.

Loss of the original epithelium of the rugae is first necessary and may be incident to the lacerations of parturation, artificial insemination, or inflammation. The cysts are usually small not significant. Larger ones may cause partial occlusion of the cervical canal, but this is seldom of importance.

Stenosis of the cervix

It is extraordinary. It is acquired rather than congenital and consists of fusion across epithelial surface and scarification. It may follow severe laceration or long standing inflammation.

Cervicitis

It is regarded as an extension of an endormetritis or vaginitis. The usual form of bovine simple cervicitis is seen as a swelling of the first (caudal) annular rugae, which are edematous and hyperemic.

They soon protrude through the external os into the vagina and a thin mucopurulent exudate accumulates between the folds collects in the vagina.

In more acute suppuration (Fig. 28 ) may be seen, although in older calves, the prolepse and tunefaction of the rings may be quite seen.

Chronic cervicitis may lead to in time to enlargement and induration of the cervix with some stenosis.

Cervical abscesses or suppurative fistulous tracts occasionally result from accidental injury, acquired during uterine irrigation or artificial insemination.

Fig. 28 : Cervix showing acute cervicitis represented by severe infiltration of lamina propria with inflammatory cells besides accumulation of mucus secretion. H&E.

Vagina and vulva

Cysts

1- The canals of Gartner (remnants of Wolfian ducts) (Fig 28 ) may persist in cows and present a double or single row of cysts on the floor of the vagina from the external as to the extermal uretheral orifice. They    contain clear fluid or grey gelatinous masses and lined with simple epithelium.

Fig. 29: Cyst of canals of Gartner (remnants of Wolfian ducts).

2. Bartholin (glandulae vestibularez majores), located in the lateral walls of the vulva, may become cystic as a result of an inflammatory process which produces strictures of the ducts, leading to an accumulation of secretion.

Disturbance in continuity

Lacerations

They are of frequent occurrence during normal parturition or as a result of unskilful obstetrical manipulation. Occasionally they occur during copulation.

The results depend upon whether or not infection occurs.

Vaginitis and Vulvitis

The etiology of vagnitis may be mechanical traumatic, thermical or infectious agents (Fig. 30).

Fig. 30: Microscopic picture of vaginitis showing inflammatory cells and  hyperplasia of lymphoid follicles. H&E.

Infectious agents of most importance in this connection are Fusiform necrophorum, an undidentified microgram protozoan parasites Trypanosoma equiperiurn, in dourine of mares and Trichomonas foetus in cows.

Necrotic vulvitis

It occasionally affects several heifers in the same feed lot.

The cause has not always been determined, in some instances, these cases have been due to Fusiform necrophorum.

Vulvovaginitis

The etiology is unknown, but a correlation apparently exists between the occurrence of the disease and the feeding.

There has been speculation as to whether estrogenic substances present in forage plants may initiate the condition.

Macroscopic appearance

1. The vulva is swollen, smooth and firm.

2. The lips separate and display a hyperemic vaginal mucosa.

3. The condition may progress to prolapse of the vagina, resulting in passive hyperemia.

4. The prolapsed vagina is easily injured and becomes hemorrhagic and eroded and if infected, it becomes purulent.

Microscopic appearance:

There are edema, hyperemia and cellular infiltration (Fig. 31).

Infectious pustular vulvovaginitis

Infectious pustular vulvovaginitis of cows is an uncommon viral disease, in which small foci of epithelial degeneration develop in the vulva and vagina.

The degenerating epithelial cells may contain intranuclear inclusion bodies and necrosed. The necrotic foci become infiltrated with neutrophils. The adjacent necrotic foci may coalease and form ulcers (Fig. 32).

The condition may be severe enough to cause endometritis. Vulva nodules following the infection may consist of solitary lymph nodules whose surface epithelial covering didn’t regenerate.

Fig. 31: Infectious pustular vulvovaginitis showing ulceration and infiltration of the lamina propria with inflammatory cells.H&E.

Fig. 32: Infectious pustular vulvovaginitis showing ulceration and infiltration of the lamina propria with inflammatory cells.H&E.

Tumors

Various kinds of tumours occasionally occur in the vagina and vulva. Among them, are papilloma (Fig. 31) , fibromas, trausmissible fibropapilloma, fibroleiomyomas and squamous cell carcinoma (Figs 32 & 33)

Fig. 33: Buffalo, vagina , squamous cell papilloma.

Fig. 34: Goat vulva showing squamous cell carcinoma.

Fig. 35: Vulva showing squamous cell carcinoma (cell nest). H&E.

The mammary gland

Mastitis

Bovine mastitis

Mastitis is an inflammation of the mammary gland of various causes, course and consequence, affecting all species, although each has types peculiar to itself.

Bovine mastitis due to Streptococcus agalactiae:

This type of mastitis was by the most common and by for the most of the    forms of bovine mastitis.

The only significant portal of entry of Strep. agalactiae into the mammary gland is through the teat canal.

Mastitis is always a possible complication of traumatic teat injury.

Macroscopical appearance:

1. The streptococcal mastitis vary according to the stage of the disease.

2. Usually more than quarter is involved, but not uniformly.

3. Most of the changes takes of the glands about the cisterns and large ducts.

4. The affected quarter is swollen, firm, liver like in consistency and are easily cut in contrast to the normal elasticity of the mammary tissue which makes it difficult to cut.

5. The cistern and ducts are filled with secretion, in the early stage of the disease, the secretion being serous, and floccular or distinctly purulent.

6. The mucous membrane of the cistern may not be apparently altered or it may be hyperaemic granular.

7. The glandular tissue is swollen and turgid.

8. On the cut surface, the lobulation is distinct because the swollen lobules protrude.

9. The affected lobular tissue is grayish in color and can be distinguished from the milky whiteness of normal lactating tissue, but not readily from the involuted parenchyma.

10. Later on, the gland become atrophic, dry, because of fibrosis it become poorly elastic.

11.Some lobules escape for a time, often a long time only to be involved ultimately in a flare-up or by extension of the disease process.

Microscopical appearance

1. The first response to the penetration of streptococci is remarkable interstitial edema and an extensive migration of neutrophils into the interlobular tissue and secretory acini.

2. The stromal lymphatics are widely dilated contain numerous leucocytes.

3. The aciner epithelium becomes vacuolated, desquamated or in places heaped up and ragged over accumulations of macrophages and    fibroblasts, which makes their appearance very early in the coarse of the reaction.

4. Streptococci are, very numerous at this stage both within the ducts and acini and in and under the epithelium.

5. The acute exudative reaction given place to two processes which proceed together pathologic fibrosis and in involution.

6. A few organisms still persist in the larger ducts and the neutrophils reaction is reduced, but macrophages and fibroblasts continue to increase number and eventually obliterate many of the acini.

7. Lymphatic foci begin to develop in the interstitial tissue.

8. Other acini become dilated and rounded contain a stringy coagulum with intact cells and cellular debris which continues the first indications of the involution which follows interruption of secretion and acinar stagnation.

9. Adjacent to the spot where the streptococci invade the epithelium of the    smaller ducts, granulation tissue develops rapidly, and protrude into the ducts lumen which is  dilated and contains stagnant milk, exudate and numerous organisms.

10. These polypoid proliferation may completely obstruct the duct, produce loculation resembling abscess cavities which are clearly visible macroscopically.

11. There is proliferation of periductal fibrous tissue spreading centrifugally to involve and obliterate large amounts of lobular tissue, such granulation tissue in time cicatrizes and the duct epithelium is restored.

12. Similar changes occur in, the larger ducts and teat cisterns and the epithelium is shortly transformed to a squamous, some times keratenizing type which is later desquamated and reconstructed as the acute phase subsides to the chronic one of involution and as fibrosis.

13. Later on, the processes of fibrosis and involution continue until the end stages, when some lobules show normally involuted tissue, some are obliterated by fibrosis and others show a varying balance between both processes.

Bovine mastitis caused by Staphylococcus aureus

Staphylococcal mastitis is predominantly an infection of the younger age group and there is no increase in susceptibility with age.

Staphylococcal mastitis may be peracute and fuliminating or milder more chronic, the later is the more common.

The acute forms of the disease, typically occur shortly after porturition and tend to produce gangrene of affected quarters.

Lesions of acute gangrenous form:

1. The affected quarters are swollen and tense, hot and firm and very painful.

2. There is almost complete stagnation of secretion and only a few millelitres of brownish blood  stained or straw colored watery fluid can be expressed from the teat.

3. Unaffected quarters of the same udder are also swollen and tense and the secretion is reduced.

4. Gangrene usually affects first the teat adjacent portion of the udder and may not be more extensive or it may extend even to involve the whole quarter.

5. The tissues become blue and eventually black and are softer, insensitive and colds.

6. There is pitting edema of the inguinal area, flank and ventral and in a day or so the necrotic skin begin as to exude serum and to slough and crepitating gas bubbles develop beneath it.

7. The amount of tissue involved in the gangrenous process is quite variable and groups of necrotic tubules adjoin others which are near normal.

8. Natural separation o f the gangrenous areas begin about a week after the onset, but proceeds slowly with development of a suppurative surface and fistulae.

9. The gangrenous changes are attributed to the direct action of toxin on the acinar tissue and to venous thrombosis.

The acute non gangrenous and mild forms of the    disease progress more closely along the lines already described for streptococcal mastitis, but with some important differences. The differences in the manner of progression of acute streptococcal and the milds staphylococcal mastitis depend on different toxigenicity of the genera and the ability of the staphylococci to invade more deeply into the interacinar tissue and to establish themselves there as persistent foci of infection to bring about the granulomatous reaction known as botryomycosis. The initial reaction is necrotizing and there necrotic foci are soon surrounded by an intense leucocytic: response and fibroplasias develops readily to surround the irritant foci thus obliterating large portions of the normal mammary structure.

Each granulomatous focus may be not more than 1-2 cm in diameter, but they may be numerous and involve a large portion of the gland between then, a residue of involved lobules which are surrounded by septa greatly thickened by confluence of fibrosis.

The thickened septa and the granulaomas are readily visible to the naked eye and small amount of pus can be expressed from them.

Microscopical appearance:

1.The granulornas closely resemble those of actinomycosis but the coccal organisms are easily visible in the microabscesses.

2. The granulomas are surrounded by connective tissue.

Bovine mastitis caused by Corynebacterium pyogenes:

Corynbacterium pyogenes is found in normal udders without evidence of inflammation, but it causes sporadic cases of acute mastitis as a complication of injury and as an enzootic disease, is known in England as “Summer mastitis” and in Europe a “Holstein udder plague”.

Non lactating and   immature glands are affected as well as lactating glands.

It isn’t clear if the corynebacterium pyogenes alone can initiate the inflammation phase or in accompany with other microorganism.

Microscopical appearance:

1. Affected quarter is swollen and hard.

2. The secretion contains large amount of pus and has a foul odor.

3. Abscesses form and they tend to rupture to the exterior near the base of the teat.

4. The abscesses may heal or produce chronically discharging fistulae.

5. In some cases there is extensive necrosis with sloughing of the necrotic tissue.

6. The cistern is narrowed by the fibrosis and teat canal may be stenotic or atretic.

Microscopical appearance:

1. Small abscesses occur in the intralobular ducts.

2. There are desquamative changes and exudation of a few leucocytes into the acini.

3. There is rapid fibroplasia and infiltration of leucocytes including many plasma cells in the septa.

4. The large abscesses are centered on the larger ducts, the wall of which are remodelled by abundant granulation tissue, although still lined in part by hyperplastic and squamous epithelium.

5. Bacteria are numerous in the abscesses and in the secretions in other parts of the duct systems.

6. The walls of the teats canal and cistern are thickened by granulation tissue and the mucosa is ragged.

Bovine tuberculous mastitis

There are three major anatomical forms of mammary tuberculosis:

1. Disseminated miliary tuberculosis.

2. Chronic organ tuberculosis.

3. Caseaus tuberculous mastitis.

In the great majority of cases, the infection is blood borne, with subsequent spread along the ducts.

1) Disseminated miliarry tuberculosis

Disseminated miliary tuberculosis develops as a part of an early generalization and isn’t common even in highly infected community.

Lesions:

1. The lesions are rather like those of miliary tuberculosis elsewhere, occurring in nodules up to 1.0 cm or so in diameter, which project above the cut surface.

2. The tubercles aren’t distributed, but rather tend to occur in groups in the deeper tissue.

3. Some are caseous, others are caseous and calcified and are of typical tubercle structure, often with very heavy capsule.

4. The foci begin to develop in the interacinar connective tissue and remain localized to lobules which are completely destroyed.

5. The interlobular ducts are also extensively involved and the dilated lumen is filled with cellular exudate.

6. The wall itself is greatly increased in thickness by tuberculous granulation tissue and epithelial hyperplasia.

7. The supra-mammary lymph nodes in such cases usually contain many typical tubercles.

2. Chronic organ tuberculosis:

It is the most common form. It is rather different from the ordinary tuberculous lesion and the regional 1ymph nodes aren’t usually involved, although some may show numerous microscopic foci of infection with few organisms.

Lesions:

1. The mammary tissue is very firm and cuts readily.

2. The lobulated structure is exaggerated when cut, projects above the surface of the organ giving a smoothy bumpy appearance surrounded by indentation of the interlobular tissue.

3. The lobules which are affected most of them tend to be vary from grayish red to white in color and the surface is dry.

4. The lesions begin as one or more foci of granulation tissue within the lobules and they expand and coalease to involve the entire lobule.

5. Few foci break down and as caseate.

Microscopic appearance:

1. The lobular outlines are retained and the interlobular septa aren’t involved.

2. The process begins in the intralobular septa and the diffuse tuberculous granulation tissue overcomes    and obliterate the acinar tissue.

3. Typical tubercles don’t form, although the cellular types involved in the reaction are as usual.

4. The intra and intetlobular are always involved and  the walls are greatly thickened by granulation tissue.

5. The surface tends to caseate although some epithelium altered to squamous type persist.

6. Caseous exudate collects the sinuses.

3. Caseous tuberculous mastitis

This form of the disease appears to develop from chronic organ tuberculosis, or possibly as port of an early generalization of the disease, in animals whose resistance is lowered.

Lesions:

1. Great enlargement of the affected glands and they are not nodular.

2. The caseous areas are large and irregular with the dry yellowish caseous appearance and hyperaemic margin suggestive of ischaemic infarction.

3. Other portions of the gland may show areas of chronic organ tuberculosis, often with commencing caseation and transformation to the diffuse type.

4. Confluence is the rule and there is no limitation of spread by interlobular boundaries.

Microscopic appearance

1. The histological change is characterized by inflammatory exudation of fibrin and numerous leucocytes.

2. The caseated areas are surrounded by a zone of hyperemic granulation tissue and hemorrhage in it occur frequently.

There is in addition, a form of mammary tuberculosis in which the process centers, on the interlobular ducts with subsequent spread to the larger ducts.

In all cases of tuberculous Mastitis, there is duct involvement, but in the types already described, duct involvement is by spread from initial foci in the intralobular tissue. This form is known as tuberculous galactopharitis.

In this form there may be no discoverable acinar lesion or if lesions are present, they and more recent than and obviously derived from the duct form.