Clinical Signs and Diagnosis

Early in the course of the disease IPV is characterized by a mucopurulent vaginal discharge, inflammation of the vaginal and vulvar mucosa, and painful urination. Pustules develop over lymphoid follicles and progress from small (<3 mm) ulcers to coalescing erosions. The virus causes inflammation of the penis and prepuce (balanoposthitis) leading to considerable pain. Therefore animals of both sexes with IPV are reluctant to mate. The clinical signs subside in 10 to 30 days, leaving the recovered animals with transient immunity. Early in the course of IPV, lesions may be similar to those of granular vulvitis (see later section), but the lesions of IPV rapidly become more severe. Vulvovaginitis caused by Haemophilus somnus, should be a differential diagnosis.

Treatment and Prognosis

Treatment of IPV is usually not required, although lavage of the vagina with dilute antiseptic solutions and emollients has been recommended. Mating among infected animals should be suspended until the disease subsides. The prognosis for recovery is excellent.

Prevention and Control

Vaccination against IBR is not likely to be beneficial in the face of an outbreak, but cattle may be protected if they are vaccinated before exposure. The IPV virus may survive in cryopreserved semen used for AI; therefore semen donors and semen should be free of the virus. Genital carriers may be responsible for sporadic outbreaks of IPV.

Clinical Signs and Diagnosis

Clinical signs of varicose veins vary from no signs to persistent and profuse vaginal hemorrhage. Vaginoscopy or fiber endoscopy of the vagina reveals varicose veins in the vagina or the vestibulovaginal transverse fold. Vaginal hemorrhage from varicose veins should be differentiated from vaginal trauma and premature separation of the placenta in periparturient mares.

Treatment and Prognosis

Most mares with vaginal varicose veins do not require treatment. Surgical ligation, treatment with phenylephrine HCl cream,²⁰⁴ or laser surgery of the veins may be necessary in cases of severe bleeding. The short-term prognosis after surgery is good, but the condition often recurs.

Clinical Signs and Diagnosis

The disease is recurrent, is usually mild and transient, and affects the vulva and perineum of mares and the penis and prepuce of stallions. Lesions are initially small papules that rapidly progress to pustules and then ulcers. Lesions may rarely appear on the conjunctiva, lips, nares, and mucosa of the upper respiratory tract. Rare secondary bacterial infection and systemic signs occur. Intranuclear inclusion bodies are apparent in epithelial cells on histologic sections taken from the active edge of ulcers. Coital exanthema does not affect fertility in mares, but libido may be decreased in affected stallions because of pain during coitus.

Treatment and Prognosis

Lesions usually heal spontaneously within 14 days, leaving depigmented spots. Treatment is unnecessary unless secondary bacterial infection occurs. There is no available vaccine for EHV-3. Sexual rest until the lesions are healed is recommended to prevent further spread of the disease. Prognosis is excellent.

Clinical Signs and Diagnosis

Granular vulvitis is characterized by the formation of raised granules or papules in the vulvar mucosa and around the clitoris with variable amounts of mucopurulent exudate. In the mild form of granular vulvitis associated with U. diversum, only a few granules develop, and the infection has minimal effect on fertility. However, acute severe cases are characterized by hyperemia of the vulva, a profuse mucopurulent discharge, and depressed fertility. Purulent discharge during the acute phase persists for 3 to 10 days, after which the disease becomes chronic. In chronic cases the lesions are reduced in severity, and there is little or no purulent discharge. The chronic form may persist for several months, and the disease may become enzootic in some herds. The clinical signs of granular vulvitis may be similar to early signs of IPV.

Clinical Pathology

Samples for microbiologic culture should be obtained from the vulva, cervicovaginal mucus, and uterus. Use of a transport medium for submission of samples to a laboratory is mandatory. The organisms may be eliminated before the samples are obtained, yielding false-negative results. Conversely, microorganisms incriminated as causing granular vulvitis may be isolated from the genital tracts of normal animals.

Treatment and Prognosis

Most cases of nonspecific vulvitis resolve spontaneously. Infertility associated with U. diversum, infections is treated by preventing transfer of organisms to the uterus by using double-sheathed AI instruments. Natural breeding should be suspended. In addition, infusion of 1 g of tetracycline or spectinomycin in a nonirritating vehicle into the uterus 24 hours after breeding has been recommended to reduce the population of organisms that may have been transferred to the uterus. Local treatment of vulvar lesions with tetracycline or spectinomycin has also been suggested.

Prevention and Control

In chronically infected herds, fertility rates may approach normal if double-sheathed AI instruments are used and affected cows are treated with appropriate antibiotics.

Clinical Signs and Diagnosis

Mares should be evaluated with transrectal ultrasound 12 to 14 days after documented ovulation during a breeding cycle. The uterus should be carefully scanned from the tip of one horn to the other and along the uterine body to the cervix. Equine embryos at this stage are highly mobile within the uterus and may be located anywhere within the uterus. Increased uterine edema and fluid within the uterine lumen are often negative signs of pregnancy, but pregnancy should not be ruled out until the entire uterine tract has been scanned for the presence of embryos. After one embryo is found, the remainder of the uterus still must be visualized to ensure the absence of a twin. The embryo proper per se is not visible at this stage of pregnancy, but the embryonic vesicle is easily visualized. Care must be taken not to confuse endometrial cysts with embryos, which sometimes can look deceptively similar. It is very helpful to have scanned the mare’s uterus with ultrasound before breeding to document the size and location of endometrial cysts.

Treatment and Prognosis

If twins are confirmed before 16 days of pregnancy, the best way to treat the mare is to manually crush one of the vesicles. This is done by visualization of the twins using transrectal ultrasound and spatially separating them from each other within the uterus. One twin is moved away from the other to the tip of a uterine horn where it is crushed manually. The remaining embryo should be evaluated 1 to 2 days later to determine its status. Survival of the remaining embryo is greater than 90% when twin reduction is performed in this manner before day 20.²¹⁴

It is the established practice of some veterinarians to treat mares with a nonsteroidal antiinflammatory agent (e.g., flunixin) and/or altrenogest after a twin-crush procedure. The reasoning behind this practice is that manual stimulation of the uterus may cause a release of oxytocin, signaling a prostaglandin cascade that will result in luteolysis and complete pregnancy loss. There have been no studies performed to support this theory; to the contrary, other studies have shown that the release of prostaglandin after the routine twin-crush procedure does not cause a drop in progesterone and that supplementation with antiinflammatory drugs or progesterone makes no difference in the outcome.^214,215

Other techniques described for reduction of twins to a single embryo include transvaginal, ultrasound-guided fetal aspiration²¹⁶; transcutaneous, ultrasound-guided fetal intracardiac injection of procaine penicillin or potassium chloride²¹⁷; and craniocervical dislocation.²¹⁸ The success of these techniques is lower than that of manual crush, and they are performed later in gestation, after the window for manual crushing has been missed. These are all specialty techniques and are beyond the scope of this chapter.

Clinical Signs and Diagnosis

Mares that abort because of placentitis often show clinical signs of pending abortion before the actual pregnancy termination. Premature udder development and vaginal discharge are common signs of pending abortion caused by placentitis. Transrectal ultrasonography of the allantochorion in an area close to the cervix is useful to detect early signs of placentitis and impending abortion (Fig. 43-8).²²⁴ Ultrasound evaluations may reveal hyperechoic fetal fluids, placental separation, increased or decreased fetal heart rates (normal range 75 ± 7 bpm²²⁵), and thickening of the combined thickness of the uterus and placenta (CTUP). Consistently low or high fetal heart rates are associated with fetal stress. Foals experiencing fetal distress often become bradycardic initially and then become tachycardic in the terminal phase of life.^226,227 Serial examinations should be performed to verify fetal well-being or distress. Mares considered “at risk” for pregnancy loss are often examined on a daily basis. Fetuses experiencing distress are often evaluated several times a day. Normal measurements of CTUP have been established (Fig. 43-9).^228,229 Mares with placentitis may show increased CTUP, edema of the allantochorion, and separation from the endometrium. A 5-MHz linear transducer should be used for transrectal ultrasonography. The transducer should be positioned 1 to 2 inches cranial to the cervical-placental junction and then moved laterally until a major uterine vessel (possibly the middle branch of the uterine artery) is visible at the ventral aspect of the uterine body.²²⁸ The CTUP should then be measured between the vessel and the allantoic fluid (see Fig. 43-5). It is important to obtain all CTUP measurements from the ventral aspect of the uterine body, because physiologic edema of the dorsal aspect of the allantochorion has been noted in normal pregnant mares during the last month of gestation.²²⁸ In addition, care should be exercised to be certain that the amniotic membrane is not adjacent to the allantochorion, because this may result in a falsely increased CTUP. To examine the placenta from a transabdominal approach, a 3.5-MHz sector transducer is used most frequently. A 5-MHz linear transducer can be used for transabdominal evaluation; however, depth penetration can limit evaluation of the areas such as the placenta. All four quadrants of the placenta should be examined; right cranial, right caudal, left cranial, and left caudal. Measurements of the CTUP can be made with this technique if the fetus is not in close apposition with the uterine wall. Mares with normal pregnancies should have a minimum combined thickness of the uterus and the placenta (CTUP) of 7.1 ± 1.6 mm, and a maximal CTUP of 11.5 ± 2.4 mm.²³⁰ Pregnancies with an increased CTUP have been associated with the delivery of abnormal foals.²³⁰

Fig. 43-8 Transrectal imaging of the combined thickness of the uterus and the placenta (CTUP). Measurements of the CTUP (distance between + and +) were recorded from the ventral part of the uterine body, close to the cervix. a, Placenta adjacent to the cervix; b, allantoic fluid; c, amniotic fluid; d, the amnion.

Modified from Renaudin CD, Troedsson MH, Gillis CL, et al: Ultrasonographic evaluation of the equine placenta by transrectal and transabdominal approach in the normal pregnant mare, Theriogenology, 47:559, 1997.

Fig. 43-9 Monthly recordings of transrectal ultrasonographic measurements of the combined thickness of the uterus and the placenta (CTUP) in normal mares from 4 months of gestation and throughout the pregnancy. Month 4 is 91 to 120 days; month 5 is 121 to 150 days; month 6 is 151 to 180 days; month 7 is 181 to 210 days; month 8 is 211 to 240 days; month 9 is 241 to 270 days; month 10 is 271 to 300 days; month 11 is 301 to 330 days; month 12 is 331 to 360 days.

Modified from Renaudin CD, Troedsson MH, Gillis CL, et al: Ultrasonographic evaluation of the equine placenta by transrectal and transabdominal approach in the normal pregnant mare, Theriogenology, 47:559, 1997.

The gross lesions of the fetus are not specific. An increased amount of fluid in the thoracic and abdominal cavities and an enlarged liver are frequently observed in aborted fetuses. Placental lesions are most severe on the chorionic surface at an area from opposite the cervix (“cervical star”) to the body of the placenta. The affected area is edematous, thickened, and discolored or brown with a mucoid or fibronecrotic exudate on the surface. The placenta is characteristically thickened and leathery in cases of mycotic placentitis, with lesions well demarcated from the rest of the chorionic surface. Microorganisms can be isolated from the placenta and several fetal organs, most consistently from the stomach.

Animals with nocardioform placentitis may have premature mammary development but will not have vulvar discharge, owing to the location of the infection. Placental lesions in mares infected with nocardioform actinomycetes are located ventrally in the uterine body and at the base of the uterine horns (Fig. 43-10). Affected areas are avillous, thickened, and covered by thick brown or reddish exudate. Because of the location of the lesions away from the cervical star, transabdominal ultrasonography is needed to diagnose the condition in pregnant mares. Differential diagnoses for this clinical presentation include twins and Cellulosimicrobium cellulans, placentitis.²²¹

Fig. 43-10 Placenta from a mare with nocardioform placentitis. The characteristic lesions are located ventrally in the uterine body and base of the uterine horns.

Prevalence of fungal abortions varies greatly with region. The most common route of fungal infection is ascending via the cervix, and fungal infections may be seen with a mixed bacterial infection. Abortions are observed from mid to late gestation. Usually no clinical signs in the mare precede the abortion. The chorion generally shows marked evidence of placentitis with edema, thick plaques, and a thick, mucoid exudate. In rare cases, amniotic thickening may be noted. The aborted fetus is often small and emaciated owing to chronic placental insufficiency. Culture of the chorion may be diagnostic but takes time. Culture of the fetus is rarely rewarding. Impression smears of the chorion, and sometimes the fetal stomach, may reveal hyphae.

The equine placenta is part of an endocrine fetal-placental interaction that synthesizes and metabolizes progestagens.²³¹ This endocrine function of the placenta is important for maintenance of pregnancy after the endometrial cups and the secondary corpora lutea disappear at approximately day 120 to 150 of gestation. Fetal-placental progesterone is rapidly metabolized to 5α-pregnanes. Mares with placental pathology may have increased plasma concentrations of progestagens as a result of stress to the fetal placental unit.^232,233 Unfortunately, 5α-pregnanes are not readily assayed in a commercial setting, so diagnosis of placental disease using 5α-pregnane concentrations is not possible. There is cross-reactivity between 5α-pregnanes and progesterone using some commercial radioimmunoassays for progesterone. In recent studies^233,234 using an experimental model to induce placentitis, it was found that mares that develop a chronic form of placentitis responded with increased plasma progesterone concentrations. Conversely, mares that developed acute placentitis and abortion soon after infection experienced a rapid drop in plasma progesterone concentrations. It was suggested that measurement of repeated samples of plasma progestin concentrations in mares with placentitis might be a useful method to identify mares that may abort or deliver prematurely.²³³ Furthermore, sensitivity of progesterone assays can be improved when they are combined with evidence of placental thickening as detected using transrectal ultrasonography.²³⁴

Treatment and Prognosis

Treatment efforts should be directed at combating infection, reducing inflammation, and controlling myometrial activity. Pregnant mares with clinical signs of placentitis should be treated with systemic broad-spectrum antimicrobials and antiinflammatories. Recent studies have demonstrated that commonly used antibiotics such as penicillin G (22,000 IU/kg q6h), gentamicin (6.6 mg/kg q24h), and trimethoprim-sulfadiazine (30 mg/kg bid) cross the placenta and reach therapeutic concentrations in both placental tissues and the allantoic fluid.²³⁶ Flunixin meglumine (1 mg/kg q12h) and pentoxifylline (8.5 mg/kg bid) have been used to control proinflammatory cytokines associated with placentitis. Treatment with progestins has long been advocated to promote uterine quiescence in mares with uterine pathology. Presumably the antiprostaglandin effect of progestins contributes to reduced myometrial activity by interfering with upregulation of prostaglandin and oxytocin receptors.²³⁷ Without receptor formation, gap junction formation would be inhibited and uterine contractility prevented. Altrenogest at twice the recommended dose (0.088 mg/kg PO q24h) is commonly used.

Work from a large scale clinical trial examined the efficacy of multipronged, long-term therapy for equine placentitis.²³⁸ Investigators examined records of 477 mares over 6 years. Fifteen mares were diagnosed with placentitis. Criteria for treatment included increased thickness of the uteroplacental unit using transrectal ultrasound, placental separation, and/or vulvar discharge and udder development. The average gestational age at diagnosis was 8.6 months. Mares were treated with a combination of systemic antibiotics (trimethoprim-sulfa, ceftiofur, or penicillin and gentimicin), pentoxifylline, altrenogest, and nonsteroidal antiinflammatory agents. Mares were treated until abortion or delivery of a foal. Twelve of 15 treated mares (80%) carried their foals to term, and 11 of 15 (73%) delivered live foals. Birthweights of surviving foals from mares treated for placentitis were similar to those of foals from nonaffected mares. The benefit of this treatment strategy is supported by recent data from a controlled study on experimentally induced placentitis.²³⁸ Data from these studies suggest that long-term antibiotic, antiinflammatory, and progestin treatment may positively affect pregnancy outcome in mares with placentitis.

Although most mares are capable of conceiving and successfully carrying a foal to term in subsequent breedings, reproductive performance may be negatively affected after ascending and hematogenous placentitis. Treatments for endometritis, such as uterine lavage and intrauterine infusions of appropriate antibiotics, should also be implemented after abortion. Most mares affected by nocardioform placentitis do not require subsequent treatment and show no signs of infertility the following breeding season.

Clinical Signs and Diagnosis

The primary lesion of EHV-1 is necrotizing vasculitis and thrombosis resulting from lytic infection of the capillary endothelium. The fetus may become infected or remain uninfected, depending on whether or not the virus crosses the uteroplacental barrier. If transplacental fetal infection occurs late in gestation, a live, infected foal may be born but will not usually survive. Stage of pregnancy during which abortions may occur varies, but the vasculitis is most pronounced from the fifth to ninth months of gestation, and 95% of abortions occur in the last trimester of pregnancy.²⁴³

Abortions occur suddenly without maternal clinical signs. The aborted fetus is fresh with minimal signs of autolysis. Increased fluid in the thoracic and abdominal cavities; congestion and edema of the lungs; an enlarged liver with small (approximately 1 mm) necrotic, yellow-white lesions; subcutaneous edema; and icterus are commonly found gross lesions in the fetus. Samples for histopathologic diagnosis should be submitted in Bouin’s solution. Histologically, the most characteristic lesion consists of areas of necrosis in lymphoid tissue, liver, adrenal cortex, and the lung, with large intranuclear eosinophilic inclusion bodies. In addition, a hyperplastic necrotizing bronchiolitis is often found. Lymphoid tissues are most commonly affected (nodes, thymus, spleen, and Peyer’s patches). Other histopathologic lesions may include mild, multifocal, necrotizing lesions in the liver and adrenal cortex and a hyperplastic, necrotizing bronchiolitis. The placenta may be grossly normal or edematous with no specific microscopic lesions.

Available diagnostic methods include serologic tests, virus isolation, and polymerase chain reaction (PCR). Serologic tests are not considered reliable in EHV-1 diagnosis, and virus isolation remains valuable as a method that allows classification and comparative evaluations. Laboratory diagnostics include fluorescent antibody (FA) staining of fetal tissue, virus isolation from aborted fetuses, virus isolation from maternal whole blood, presence of viral inclusion bodies in liver, lung, and thymus, and fetal serology. Equine fetuses have been found to be capable of producing antibodies to EHV-1 at 200 days of gestation. Maternal serology is of limited diagnostic value because mares may abort several weeks after infection. The rise in serologic titer may have disappeared by the time of the abortion.

Treatment and Prognosis

Studies offer conflicting results as to the efficacy of vaccinations in reducing viremia and abortions. Many studies do suggest a beneficial effect of vaccination, and the current recommendation is to vaccinate during the fifth, seventh, and ninth months of gestation.^239,243 Both killed and modified live vaccines are available. The vaccines are not fully protective, and abortion may occur in vaccinated mares. However, consistent vaccination of pregnant mares should be expected to decrease the incidence of abortion storms and sporadic abortions in a herd.

For the effectiveness of a vaccination program to be maximized, it needs to be combined with a management strategy that minimizes exposure of mares to the virus and prevents activation of a latent viral infection. All horses, young, adult, nonpregnant, and pregnant, should be vaccinated to restrict shedding of the virus. Unnecessary stress such as transportation and overcrowding should be avoided. Pregnant mares should be kept separate from other horses on the farm. Newly arrived horses should be isolated from the resident population for 3 weeks, during which time they should be monitored daily for signs of respiratory disease.

After abortion, the fetus and fetal membranes should be transported away from the area without contaminating the surrounding environment. The stall in which the mare aborted should be disinfected with a phenolic or iodinophoric compound, and the bedding should be prevented from contaminating other areas on the farm. All pregnant mares on an infected farm should remain on the farm until they have foaled. No horse should leave the farm until 3 to 4 weeks after the last abortion.

History and Clinical Signs

Clinical signs may be absent or highly variable and may include pyrexia, depression, anorexia, leukopenia, limb edema, stiffness of gait, rhinorrhea and epiphora, conjunctivitis, rhinitis, urticarial rash, localized or diffuse edema, and abortion. Abortion typically occurs at 5 to 10 months of gestation and follows the onset of clinical signs by several days but up to 2 months. Less frequently, severe respiratory distress, ataxia, mucosal papular eruptions, submaxillary lymphadenopathy, and intermandibular and shoulder edema may be observed.²⁴⁴ Infection is rarely fatal in adults but is more frequently fatal in neonates. The virus may be transmitted in the semen, and infected stallions may serve as long-term carriers. Clinical pathologic findings are variable, inconsistent, and nonspecific and include hypoxia, hypercapnia, respiratory or metabolic acidosis, lymphocytosis or lymphopenia, neutrophilia or neutropenia, thrombocytopenia, and hyperfibrinogenemia. Gross and histologic lesions differ in severity with the virulence of the particular viral strain. Edema, congestion, and hemorrhage of the subcutaneous and lymphoid tissues and viscera are the most common gross lesions. Histologic lesions may be found in the vasculature, lymphoid tissues, lungs, intestines, adrenal glands, kidneys, and skin.²⁴⁴ Abortion may occur without any clinical signs in the mare, and the fetus may be fresh or autolyzed. Fetal lesions are uncommon.

Laboratory Diagnosis

Diagnosis is by serologic testing in conjunction with complement-dependent virus neutralization. There are no characteristic features of EVA infection in the fetus, although autolysis and myocardial arteritis have been reported. EAV is readily isolated or detected by PCR techniques in fetal tissues and the placenta.

Epidemiology and Control

Transmission may occur venereally from infected stallions to mares. Reproductive performance of venereally infected mares is not affected, but contact transmission from venereally infected mares to late gestational mares may cause abortion. Outbreaks were reported in 1953, 1984, and 2006 in the United States. With the exception of these incidents, occasional outbreaks have occurred, with abortion occurring at low incidence.²⁴⁵ Mares may be isolated after infection but usually do not become carriers. A proportion of naturally infected stallions become persistently infected with EAV and shed the virus constantly in semen. Incidence of seropositive animals is higher in standardbreds than in thoroughbreds, and regulatory guidelines may govern the use of seropositive thoroughbred stallions. Carrier stallions may be the reservoir for the disease between outbreaks and should be isolated and bred only to immune mares. Mares bred in this way should be isolated for 3 weeks. A modified live vaccine is available for mares and stallions. Control involves vaccination of seronegative stallions under the guidance of regulatory authorities. There is some evidence that prepubertal infection of colts does not result in permanent carrier status.

Clinical Signs and Diagnosis

Clinical signs may include pyrexia, hemoglobinuria, jaundice, and abortion. Aborted chorioallantoic lesions are similar to those of other bacterial placentitis cases (nodular cystic allantoic masses, edema, necrotic areas of chorion, and necrotic mucoid exudate coating the chorion) but may show a diffuse pattern of distribution, indicating a hematogenous source of placental infection. Funisitis has been reported in leptospira cases of abortion, and examination, both gross and histologic, of the umbilical cord should always be a part of every abortion investigation.²⁴⁹ Serologic antibody conversion lasts for years, and so serologic diagnoses are not very helpful. Gross lesions are nonspecific. Diagnosis is best done by FA tests or Warthin-Starry silver stain (WS) staining of the allantochorion and umbilical cord. Demonstration of leptospirosis could aid in rapid diagnosis and have important clinical and therapeutic indications in the case of live-born, weak foals.²⁴⁹

Treatment and Control

Horses may shed spirochetes in urine for up to 90 days; therefore affected animals should be isolated and treated with antibiotics. Aborting mares should be isolated, and the stalls should be disinfected. Infected mares may be treated with streptomycin (10 mg/kg twice daily), penicillin (10 to 15,000 IU/kg twice daily), or oxytetracycline (5 to 10 mg/kg) for a period of 1 week. Because Leptospira, Pomona is the most common isolate in the United States, mares should be separated from other leptospiral hosts such as ruminants and pigs. Vaccines for cattle are not effective in horses.

Clinical Signs and Diagnosis

Abortions have been observed 2 to 3 months after clinical signs of ehrlichiosis.²⁵² Abortions were associated with placentitis and RFMs. Fetal histologic lesions include enterocolitis, periportal hepatitis, myocarditis, and lymphoid hyperplasia with necrosis of the mesenteric lymph nodes and spleen. Recovery of the protozoan may be from fetal bone marrow, spleen, lymph node, colon, or liver.^250,251 The diagnosis can be confirmed by identifying a small number of rickettsiae by PCR assay.

Treatment and Prevention

Treatment with oxytetracycline (6.6 mg/kg IV once daily) for 5 days in pregnant mares with clinical signs of ehrlichial colitis may prevent or reduce the incidence of abortion. Commercial vaccines against equine ehrlichiosis are available, but the protective effect of vaccines against abortion is unknown.

Neospora caninum, is a known protozoal abortifacient in cattle. This protozoan has not been definitively shown to cause abortion in the mare, but its presence has been documented in aborted foals, suggesting the need for further investigation.²⁵³

Clinical Signs and Diagnosis

Clinical signs preceding abortion and failure to maintain pregnancy are typically not observed. Both early (40 to 150 days’ gestation) and late (near term) pregnancies are affected. Hyperechoic amniotic and allantoic fluids can be noted on ultrasonographic examination, along with a dead or dying fetus (slow heart rate, <75 beats/min), which would then be expelled within several days.^257,258 Characteristic histologic lesions are noted in the placenta and umbilical cord. In many cases, endometrial cultures are positive for non—beta-hemolytic streptococci and actinobacilli. Actinobacillus, species identified in cases of MRLS are identical to commensal organisms found in the oral cavities and alimentary tracts of healthy horses.²⁵⁹ Larval hairs (cetae) are hypothesized to migrate through gastrointestinal system and translocate commensal organisms from the oral cavity and intestines to other sites.²⁵⁶

Treatment and Prevention

Because clinical signs are absent in the mare before fetal death, treatment is not possible. Prevention is aimed at limiting exposure to M. americanum, larvae. Applying insecticides, physically removing caterpillar nests from trees, removing black cherry trees, muzzling mares in pasture, and supplementing hay feeding in pastures to minimize grazing have all been used.

Clinical Signs and Diagnosis

Abortions follow a recent episode of stress induced by endotoxemic shock or gram-negative endotoxemia. Pregnancy loss at early stages of gestation may go undetected unless fetal membranes or parts are found in the stall. Abortions during later stages of the pregnancy may be observed as vaginal discharge or the detection of an expelled fetus.

Treatment and Prevention

Daily administration of a progestagen (Altrenogest 0.044 mg/kg PO) has been shown to effectively prevent experimental endotoxin-induced abortion.²⁶⁰ If the animal is treated while the pregnancy is still CL dependent (approximately <day 80), analysis of serum progesterone concentrations after the acute episode of the disease helps in deciding if the supplementation needs to continue. Serum progesterone concentrations of less than 1 ng/mL indicate the loss of an active CL, and supplemental progestagen treatment should continue until the fetoplacental unit is known to be capable of maintaining the pregnancy. For practical reasons supplementation until day 100 is commonly recommended. Serum progesterone concentrations greater than 1 ng/mL are compatible with a functional CL, and the progestagen treatment can gradually be discontinued. Treatments with flunixin meglumine or other prostaglandin inhibitors have not been proven to effectively prevent endotoxin-induced fetal losses unless the agents are administered before clinical signs appear.

History and Clinical Signs

Although fetal death is most common during the first trimester, abortion can occur at any stage of gestation.^263,264 Pathogenicity of the disease depends on gestational time of infection, the viral strain, viral biotype (cytopathic or noncytopathic), and fetal immunocompetence.²⁶⁵ Often there is a history of repeat breeding and a recent episode of febrile disease in the herd before the onset of abortions.²⁶⁶

Laboratory Diagnosis

Fetal loss generally occurs 10 to 27 days postexposure, with expulsion of the fetus up to 50 days later.²⁶⁵ As a result the fetus is most often autolyzed, although in some cases it may be mummified or fresh. The aborted fetus may have a variety of dysplastic lesions, including cerebellar hypoplasia, cerebral malformations (hydrencephaly, porencephaly, microencephaly) and cataracts, brachygnathia, arthrogryposis, alopecia, thymic hypoplasia, and intrauterine growth restriction.^{5,263,266,267} Microscopic lesions include a mild nonsuppurative placentitis. Nonsuppurative vasculitis may be observed in the placenta, liver, or lymph nodes.²⁶⁶

Virus isolation from fetal tissue is seldom successful, likely because of the protracted time before fetal expulsion generally occurs after infection. Viral antigen may be detected by FA test on kidney, lung, or lymph node.²⁶⁶ Virus neutralization and enzyme-linked immunosorbent assay are used to detect antibodies in fetal thoracic fluid, which indicate prenatal exposure to the virus but do not necessarily incriminate BVDV as the cause of abortion. Maternal titers are seldom of diagnostic value because a rise in titer generally occurs before abortion.⁵

Pathophysiology

BVDV may be shed in most body secretions. The effects of exposure to BVDV vary greatly depending on the gestational time during which exposure occurred (Fig. 43-11). In seronegative cows, exposure to BVDV at the time of breeding prevents conception.²⁶⁸ Placental attachment at approximately 35 days’ gestation seemingly must precede fetal infection. During the first 4 months of gestation, infection usually causes fetal death and abortion.¹⁶⁶ Fetuses that survive infection with noncytopathic strains between 18 and 125 days’ gestation will be persistently infected (PI), are typically seronegative at birth, and subsequently shed BVDV continuously.²⁶⁵ They may develop mucosal disease later in life from superinfection with cytopathic BVD virus.^269,270 Fetuses infected at between 100 and 150 days’ gestation, considered congenitally infected (CI), are at risk for the development of dysplastic lesions including teratologic defects in the brain, skin, or bronchioles. Fetuses infected after 150 days usually recover without dysplastic lesions.²⁶³ Recent evidence, however, suggests that those fetuses born with neutralizing titers to BVDV are more likely to develop a serious illness within the first 10 months of life and less likely to conceive as heifers than those calves born without neutralizing titers to BVDV.^271,272

Fig. 43-11 Potential clinical reproductive outcomes after infection with bovine virus diarrhea virus. EED, Early embryonic death.²⁶⁵

Epidemiology

Most cattle have serum antibodies to the virus. The abortion rate may approach 25% with new infection of a susceptible herd.⁵

Control

BVDV is not fully controlled with vaccination. Herd health plans must focus on elimination of PI animals and prevention of new PI animals being introduced into the herd.

History and Clinical Signs

In cattle, Leptospira, Hardjo is associated with infertility, early embryonic death, abortions from 4 months’ gestation to term, and birth of weak calves. Abortion rate is usually less than 10% but may approach 50% in some areas.²⁷³Leptospira, Pomona abortion usually occurs in the last 3 months of gestation, with an abortion rate as high as 50%.⁵ Clinical signs of leptospirosis in the cow may include icterus, hemoglobinuria, anemia, fever, and mastitis that is characterized by a flaccid udder and thick ropy secretions from all four quarters, but usually cows abort without clinical illness.²⁶⁶ Dead or weak calves may be delivered at term.²⁷³ Abortions caused by serovar Hardjo tend to occur sporadically rather than in storms (as may be seen with serovars Pomona or Grippotyphosa).

Laboratory Diagnosis

The aborted fetus is usually autolyzed, icteric, and edematous. Histologically, renal tubular necrosis is accompanied by lymphocytic interstitial nephritis, pneumonia, and placentitis.^5,266

Leptospires are rapidly destroyed by autolysis or freezing. Isolation from fetal liver, kidney, or brain is possible but slow and impractical. Leptospires may be isolated or demonstrated by darkfield microscopy, FA staining, or histologic techniques in fetal or placental tissues or in the urine of the aborting dam within approximately 2 weeks after abortion.^5,266

Diagnosis is usually based on serology. A few infected fetuses develop microagglutination titers of 1:10 or more. It is difficult to distinguish among vaccinated, acutely infected, and recovered animals, but titers to Leptospira, Pomona greater than 1:12,800 in the dam suggest leptospiral abortion. Maternal titer usually has peaked by the time of abortion. Single titers of 1:800 or more in unvaccinated animals, seroconversion, or fourfold changes in titers in paired sera indicate leptospirosis in the herd. Titers to Leptospira, Hardjo are often less than 1:100 in affected cows and seldom exceed 1:1600.²⁶⁶

Pathophysiology

Hematogenously spread leptospires colonize the gravid uterus up to 142 days after infection. Abortion occurs 1 to 6 weeks after acute disease with Leptospira, Pomona infection and 1 to 3 months with Leptospira, Hardjo.⁵Leptospira, Hardjo remains in the oviducts of infected cows up to 22 days after calving.²⁷³

Epidemiology

Leptospira, organisms are ubiquitous and an important cause of abortion in all cattle-producing regions. Leptospira, organisms persist in the genital tract and kidneys. The organisms localized in the kidneys of infected animals are shed in the urine and serve as a source of infection for other animals. The organisms localized in the female reproductive tract are responsible for abortions. Aborted tissues are infectious to other animals and humans and should be handled with caution.²⁷⁴ Vaccination may be useful in endemic areas.

Treatment and Control

In abortion outbreaks, pregnant cows can be vaccinated with killed bacterin and treated with oxytetracycline (antibiotic treatment can be limited to sick cows in dairy herds).²⁷⁵ Aborting cows should be isolated and treated with streptomycin if they are not destined for slaughter. Aborted fetuses and placentas should be removed from the premises.²⁷⁶ Preventing exposure to swine, rodents, and contaminated water lessens the opportunities for infection.^5,202Leptospira, Pomona usually has no permanent effect on fertility, but infection with Leptospira, Hardjo has been associated with persistent herd infection and recurring abortions.⁵

Herd vaccination is recommended at 6-month intervals or more frequently in areas with heavy exposure to leptospires. Vaccination programs are aimed at reducing urinary shedding of leptospires and decreasing fetal loss. However, a commercial pentavalent leptospiral vaccine (serovar Leptospira, Hardjo type hardjo-prajitno is used for the Leptospira, Hardjo component of U.S. Department of Agriculture [USDA]—licensed leptospiral vaccines) did not prevent renal colonization, urinary shedding, or fetal infection after conjunctival instillation of cows with serovar Leptospira, Hardjo type hardjo-bovis (the only type of Leptospira, Hardjo isolated from cattle in the United States).²⁷⁷

History and Clinical Signs

Late abortion or delivery of weak calves occurs in affected herds. Many fetuses in the sixth to seventh month of gestation may be aborted, especially from heifers without premunition immunity from natural exposure to the causative agent. Older native cows show no clinical signs of infection.

Laboratory Diagnosis

A 3-month period is required for full development of pathologic changes in the fetus. Superficial cervical lymph nodes are enlarged up to 16 g, the spleen is enlarged up to 250 g, the thymus is slightly smaller than normal, and the liver may be enlarged and nodular.^266,278,280 Histologically there is loss of thymic cortical lymphocytes; remaining lymphocytes are enlarged and poorly differentiated. Follicular hyperplasia, histiocytosis, vasculitis, necrosis, and pyogranulomas occur in lymph nodes and spleen. Lymphohistiocytic proliferation may also occur around vessels in the liver, lung, and meninges.²⁶⁶

EBA has been diagnosed mainly by pathologic examination of the fetus. Recent studies have demonstrated high levels of IgG (3 mg/mL or more) in fetal blood.^266,278 A spirochete-like agent can be demonstrated in the plasma of aborted fetuses but also may occur in plasma of normal fetuses.²⁷⁹ Currently no serologic test for EBA exists because the cause is uncertain.

Pathophysiology

Infection is transmitted by the soft-shell tick Ornithodoros coriaceus.,^280,281 The disease also can be transmitted with fresh or frozen fetal tissue.²⁷⁸ Transformation and proliferation of fetal lymphocytes and macrophages occur by 50 days but are not severe enough for diagnosis until 100 days after maternal exposure to the tick vector. IgG and IgM are deposited in vascular lesions, but increase in fetal serum immunoglobulin is not detectable until at least 80 days after tick exposure.^278,281 Repeated superinfection may be necessary to result in fetal death.²⁸⁰ Because at least 90 days are required for development of fetal lesions, infection after 6 months’ gestation is not likely to result in abortion.^5,266

Epidemiology

EBA is limited to the range of the tick vector in the foothills bordering the central valley of California.²⁷⁸ Of the annual calf loss in California, 5% to 10% is attributed to EBA.²⁸¹ The prevalence of infection by the spirochete is far greater than the prevalence of abortion.²⁸⁰ Abortion occurs 3 to 4 months after exposure to ticks but almost always late in gestation, regardless of the time of tick exposure.²⁸² Older native cows from enzootic areas usually do not abort, and introduced cows and heifers generally abort only once.²⁷⁸ The abortion rate may be 30% to 80% in susceptible animals.^266,282

Treatment and Control

Chlortetracycline therapy (2 to 5 g/day in the feed) reduces the rate of abortion.²⁸¹ Currently no vaccine exists for EBA, but abortions can be controlled by exposing heifers to the tick vector before breeding or by changing from spring to fall calving,⁵ which takes advantage of limiting exposure to the last trimester of gestation in some management systems. Therefore exposure of susceptible pregnant cattle to the tick only after the sixth month of pregnancy is a practical solution for ranchers using summer foothill pastures and fall calving. The tick lives in ground duff (e.g., leaves) and is not found on cattle that graze in irrigated pastures and most other areas outside of brushy foothills.

History and Clinical Signs

Abortion is the chief clinical sign of bovine brucellosis and usually occurs after the fifth month of gestation. Lameness, mastitis, epididymitis, and/or orchitis may be present in infected herds.²⁸³

Laboratory Diagnosis

Autolysis frequently obscures gross lesions in the fetus, but fibrinous serositis may be apparent, and abomasal content may be discolored and flocculent. Placentitis is a consistent finding. Cotyledons are necrotic; the intercotyledonary placenta is thickened and opaque with accumulation of odorless, flocculent, yellow-brown exudate between maternal and fetal membranes. Histologically there is suppurative placentitis (and endometritis in the dam). Suppurative bronchopneumonia and lymphoreticular hyperplasia are frequent histologic findings in the fetus.

Diagnosis depends on culture of B. abortus, from fetal lung, abomasum, or placenta or from maternal uterine or mammary secretions. Organisms and Brucella, antigen can be detected in fetal tissues by avidin-biotin-peroxidase complex immunostaining.²⁸⁴

No serologic test is 100% accurate, but a positive card test or titer of 1:100 or more on plate or tube agglutination suggests brucellosis. False-negative serologic reactions occur in approximately 15% of infected cows, particularly just before or after parturition. False-positive reactions are a problem in cows vaccinated with strain 19. Supplemental tests such as the Rivanol test, complement fixation, and mercaptoethanol sensitivity of agglutination are used in suspect cases. Dairy herds are surveyed by the Brucella, ring test on milk.⁵ In goats, tube agglutination titers of 1:25 or more indicate infection.²⁸³

Pathophysiology

Initial replication of B. abortus, occurs in regional lymph nodes. Bacteremia is followed by colonization of supramammary lymph nodes, the mammary gland, and the gravid uterus. Uterine infection occurs during the second trimester.^5,285 In the placenta the bacteria appear first in phagosomes of erythrophagocytic trophoblasts. Replication occurs in the rough endoplasmic reticulum of chorioallantoic trophoblasts.²⁸⁵ Preferential replication in chorioallantoic trophoblasts has been attributed to their erythritol content; however, the placentas of several laboratory rodents that lack detectable erythritol still support B. abortus, replication.²⁸⁶ The organism also occurs in fetal placental endothelial cells and capillary lumina, where it is associated with vasculitis and destruction of chorionic villi. Placental inflammation spreads along the allantochorion to involve additional cotyledons with resultant chorioallantoic ulceration, necrosis of trophoblasts, and ulcerative endometritis. Fetal death results from placental disruption and endotoxemia.^5,285 The fetus is frequently retained 1 to 3 days in utero. Numerous bacteria are expelled from the genital tract at parturition, but shedding usually stops by 3 weeks after abortion.⁵

Epidemiology

Infection with B. abortus, occurs naturally by ingestion. Contaminated materials are infectious for humans and should be handled with caution. Infection is not easily transmitted between cattle separated by fences or roads.²⁸⁷ Most calves infected at birth clear the infection, but persistent congenital infection has been documented.^288,289

Bovine brucellosis has been nearly eradicated in the United States by test and slaughter of seropositive cattle and vaccination. However, a reservoir remains in bison and elk, especially in the greater Yellowstone area.

Treatment and Control

Treatment of brucellosis is usually not effective. Combination therapy with long-acting oxytetracycline and streptomycin has been shown to reduce shedding in most cows and potentially eliminate infection in some,²⁹⁰ but because of the eradication program used in many countries, infected cows are rarely treated. In the United States, infected individuals are destroyed, and exposed herdmates are quarantined to the herd until slaughter or the herd is recertified as brucellosis-free (United States Department of Agriculture, 2003).

In the past, strain 19 vaccine was used as part of the eradication program. However, vaccinated and field strain—infected cattle could not be differentiated. A newer vaccine for B. abortus, vaccine strain RB51, was developed to overcome the serologic problems associated with the strain 19 vaccine.²⁹¹ Animals vaccinated with RB51 lack antibodies to the O-polysaccharide chain and can thus be distinguished from field-infected cattle. Strain RB51 is also less abortifacient for cattle than strain 19, although vaccination of pregnant heifers may result in abortion and subsequent zoonotic exposure if obstetric assistance is necessary (Centers for Disease Control, Morbidity and Mortality Weekly Report, March 13, 1998), and so the vaccine is to be administered only to young heifers before pregnancy.^261,290a,291

History and Clinical Signs

Infection with C. fetus, subsp. venerealis, mainly causes temporary infertility or early embryonic death, but sporadic abortions from the fourth to eighth months of gestation are possible.²⁶⁶ The usual history includes a high percentage of cows exposed for the first time returning to estrus or found nonpregnant after the breeding season, and cows calving late because they returned to estrus one or more times.

Laboratory Diagnosis

Autolysis is usually minimal, and the lungs of the term fetus may be partially inflated. Dehydration, fibrinous serositis, and necrotizing placentitis may be apparent grossly. Histologically, bronchopneumonia and hepatitis may also be evident. Diagnosis is based on demonstration or isolation of the organism. By darkfield microscopy the bacterium appears as a curved rod with darting corkscrew motility.²⁶⁶ Cows that abort may have serum antibody titers; however, they may not be diagnostic because they are not specific for C. fetus, subsp. venerealis., Culture from placenta or fetal abomasal contents requires at least 72 hours. The vaginal mucus agglutination test is used to survey herds for infection.⁵ Alternatively the penis and preputial mucosa of infected bulls may be swabbed and cultured, although culture is difficult because the organism is slow-growing and often overwhelmed by saprophytes.

Pathophysiology

Within a week of vaginal infection the organism is established in the uterus, causing mucopurulent endometritis, which persists 3 to 4 months. Intrauterine infection either prevents conception or causes embryonic death, and infected heifers typically return to estrus by 40 days. Less commonly, abortions occur at up to 8 months’ gestation.^5,266

Epidemiology

C. fetus, subsp. venerealis, is ubiquitous. Venereal transmission from infected bulls to virgin heifers approaches 100%. Cows with previous exposure to infected bulls develop immunity and therefore are less likely to experience infertility than heifers. The abortion rate seldom exceeds 10%.²⁶⁶

Treatment and Control

Infected cows usually recover spontaneously within 5 months and resist reinfection. Recovery is hastened by intrauterine infusions of streptomycin and penicillin. Infertility may be permanent if endometritis or salpingitis is severe.⁵ Heifers should be vaccinated with a killed bacterin before breeding. Most vaccines are administered 1 month before breeding and require a booster vaccination 2 weeks later.*^† Higher than normal doses of vaccine may be needed to clear the infection from bulls. Cows and bulls must be vaccinated annually. Exclusive use of C. fetus, subsp. venerealis,—negative semen via AI controls the disease by preventing transmission.

Laboratory Diagnosis

Aborted fetuses have been free of gross lesions. Necrotizing placentitis is associated with fibrinoid necrosis of placental arteries.²⁰⁷ Diagnosis is based on recovery of large numbers of the organisms in relatively pure culture from placenta or fetus, histologic evidence of placentitis, and lack of other apparent causes.

Interpretation of maternal titers to H. somnus, is difficult, and it is best to take paired serum samples. Titers between 1:256 and 1:512 in nonvaccinated herds may be the result of early active or chronic infection. Titers between 1:1040 and 1:4096 indicate recent active infection. A fourfold change in titer in paired sera is the best indicator of active infection.

Pathophysiology

Although H. somnus, can be isolated from the genital tract of clinically normal cows,¹⁹⁴ the rate of isolation is higher in cows with endometritis or cervicitis.^207,292 Experimentally, H. somnus, can adhere to zona pellucida—intact embryos and cause degeneration.²⁹³ Vaginitis can be induced by inoculation with H. somnus,²⁹⁴ and abortion has been induced by intraamniotic, intravenous, or intrabronchial challenge with the organism.²⁹⁵ Cervical infusion with the organism has resulted in colonization of the chorioallantois and placentitis, but calves were born alive without culturable H. somnus.,^296,297

Treatment and Control

Antibiotic treatment and vaccination anecdotally increase fertility in herds affected with H. somnus,—induced vulvovaginitis.²⁰⁷

History and Clinical Signs

Bovine abortions usually occur in the last 2 months of gestation.²⁶⁶ Infected ewes and does typically abort in the last month.^5,298 Fever, depression, RFMs, or endometritis may occur,^5,266,299 but often the dam shows no clinical signs of infection.

Laboratory Diagnosis

In less severely autolyzed fetuses, fibrinous polyserositis may be apparent. Most aborted fetuses have gray-white hepatic foci up to 2 mm in diameter. Similar foci may be visible in cotyledons; exudation occurs between cotyledons. Abomasal erosions have been reported in aborted lambs.²⁶⁶ Histologically, suppurative placentitis and endometritis are consistent findings.

Listeria, is readily cultured from abortuses without cold enrichment. Serovars 1 and 4b are commonly isolated from bovine fetuses; serovars 4b and 5 are the usual ovine isolates.²⁶⁶Listeria, appears in impression smears as gram-positive pleomorphic coccobacilli.²⁶⁶

Pathophysiology

Listerial abortion can be induced experimentally in cattle 6 to 8 days after infection and in sheep 3 to 11 days after infection. Fetuses die from placentitis and septicemia and are often retained in utero several days before expulsion.²⁶⁶

Epidemiology

Listerial abortion is usually sporadic, and incidence seldom exceeds 15%.²⁶⁶ Infection is most common in the winter and has been associated with feeding of silage. The elevated pH of spoiled silage enhances multiplication of the organism. Aborted tissues are infectious for humans and should be handled with care.

Treatment and Control

The effect on fertility is usually transient, and aborting animals tend to resist reinfection. Tetracycline may be used in remaining pregnant animals in the herd.⁵ Aborting animals should be segregated, and fetuses and placentas should be removed from the premises. The feeding of spoiled silage should be avoided.

History and Clinical Signs

M. bovigenitalium, is associated with granular vulvovaginitis and less commonly with endometritis, especially in heifers. Infertility is more common than abortion. M. bovis, causes mastitis and abortion.²⁹⁹ In goats, mycoplasmal infection is associated with septicemia, arthritis, pneumonia, mastitis, and abortion.⁵

Laboratory Diagnosis

Placentitis and fetal pneumonia have been associated with bovine mycoplasmal abortion.²⁹⁹ Isolation of Mycoplasma, from the genital tract, milk, placenta, or fetus indicates infection. However, mycoplasmosis should not be considered the cause of abortion unless placentitis or fetal inflammation is present and other more likely causes of abortion have been eliminated.

Pathophysiology

M. bovigenitalium, can be isolated from the vagina of as many as 12% of clinically normal cows, but M. bovis, is isolated from fewer than 1%. Vulvitis can be induced by inoculation with mucosal scarification with M. bovigenitalium;, therefore venereal transmission may be the natural route of infection.^5,299 Experimental inoculation with M. bovis, induces abortion with placentitis and fetal pneumonia.^299,300M. bovigenitalium, is rarely isolated from abortuses or normal fetuses.⁵

Epidemiology

Mycoplasma, species are ubiquitous, but mycoplasmal abortions are not commonly documented.

Treatment and Control

Tetracycline or tylosin is the recommended antibiotic for mycoplasmal granular vulvovaginitis in heifers.²⁹⁹

History and Clinical Signs

The animal may show systemic signs before abortion. Abortion may occur at any stage of gestation and is characterized by placental necrosis, edema, and hemorrhage. RFMs and fetal autolysis may occur. Abortion may be accompanied by diarrhea, fever, or vaginal discharge, particularly in the ewe, but often infection is not clinically apparent in the dam.^266,301,302 Fetuses also may be lost as a result of stillbirth or perinatal septicemia.

Laboratory Diagnosis

The fetus is frequently autolyzed. Placentitis is usually present. Diagnosis is based on isolation of the organism and evidence of placentitis or inflammation of fetal tissues. FA techniques can identify the bacteria in impression smears or sections of placenta or fetal tissue.²⁶⁶ The dam can be tested serologically for evidence of recent active infection,³⁰¹ but at present many diagnostic laboratories do not perform Salmonella, serology.

Pathophysiology

Infected adult animals are often short-term carriers and shed salmonellae in the feces or milk. True long-term asymptomatic carriers occur mainly with the host-adapted serotypes: Salmonella, Dublin in cattle, Salmonella, Abortus ovis in sheep, and S. abortivoequina, (or Salmonella, Abortus equi) in horses. Salmonellosis caused by Salmonella, Abortus equi has been eradicated in the United States. Occasionally, long-term carriers of other serotypes are seen; these are usually intestinal carriers and fecal shedders. Infection usually occurs by ingestion. There is no evidence of venereal transmission.³⁰¹ Maternal septicemia is followed by localization of the organism in a variety of tissues, including the pregnant uterus. The bacteria multiply in and cause necrosis of connective tissues of the cotyledon.³⁰¹ The incubation period between infection and abortion varies from approximately 1 week to 1 month.^5,302 Fetal death results from placentitis and fetal septicemia.^266,303 In most cases, maternal shedding of the organism in cattle ceases by 5 weeks after calving.³⁰¹

In a second mechanism of Salmonella,-induced abortion, Salmonella, septicemia causes endotoxemia and release of endogenous PGF, which causes luteolysis and abortion. In this case the fetus and placenta are culture negative for salmonellae.

Epidemiology

Bovine abortion resulting from salmonellosis is caused mainly by Salmonella, Dublin and Salmonella, Typhimurium. Abortion is sporadic and most common in the summer and fall.³⁰¹

Ovine abortion is associated with Salmonella, Typhimurium, S., Dublin, Salmonella, Arizona, and Salmonella, Abortus ovis. Salmonella, Abortus ovis (which infects only sheep) is enzootic in parts of England and Europe but is not reported from the United States.^5,266 Young ewes in late gestation are most susceptible, and the abortion rate may approach 50%,^5,302 but usually only one or two ewes in a flock abort.²⁶⁶

Treatment and Control

Metritis is a rare complication of salmonellosis that can be fatal.²⁶⁶ Usually there is no lasting effect on fertility, but animals infected with host-adapted serotypes may become carriers and should be cultured and tested serologically and culled if positive. Salmonellosis can be controlled by hygiene and by avoiding the introduction of carrier animals. Aborting animals should be isolated; the fetus, placenta, and contaminated material should be removed from the premises. Salmonella, species are infectious for humans; therefore aborted tissues should be handled with caution.

History and Clinical Signs

Granular vulvitis appears as reddish nodules in the vulvar mucosa, with mucopurulent discharge in the early stages. The discharge is usually more copious and protracted than with IPV induced by herpesvirus.^5,299 Affected cows are not systemically ill.²⁶⁶ The organism has been recovered from embryo flushing media and can adhere to the zona pellucida, resisting removal by washing. It is believed to be responsible for an 18% reduction in pregnancy rate in embryo recipients when the transfer medium contains the organism.

Laboratory Diagnosis

Gross lesions include thickening of placental membranes with foci of hemorrhage and fibrinous exudate. Gross lesions are seldom apparent in the fetus. Microscopically the placenta is fibrotic, with heavy mononuclear cell infiltration, multifocal necrosis, fibrin deposition, and mineralization. Cuffs of lymphocytes surround fetal intrapulmonary airways.²⁶⁶ Diagnosis is based on isolation of the organism from genital mucosa, placenta, or fetal stomach or lung and the presence of genital or fetal inflammation.

Pathophysiology

Ureaplasma, can be isolated from the genital tract of normal cows and from normal fetuses.³⁰⁴ Vulvitis has been induced by inoculation of virgin heifers with U. diversum.,³⁰⁴ Uterine involvement is considered rare but may cause conception failure, early embryonic death, or abortion. Abortion presumably results from placentitis.⁵ Intraamniotic inoculation of U. diversum, caused placentitis, abortion, and fetal alveolitis in two of four experimental cows.³⁰⁴ One cow delivered a weak calf at term. Experimental infection in ewes did not decrease fertility.³⁰⁵

Epidemiology

Bovine infection is common, but documented abortions caused by Ureaplasma, are rare.²⁹⁹ Infertility is more common in heifers than in cows.

Treatment and Control

Nonirritating tetracyclines by intrauterine infusion are recommended for treatment. Products may not be approved for intrauterine use.⁵ Uterine contamination can be avoided by use of the double-rod technique of AI.⁵

History and Clinical Signs

Infertility characterized by a high percentage of cows returning to estrus or found nonpregnant after the breeding season and cows calving late plus occasional pyometras and abortions are the most common clinical signs of trichomoniasis. Pyometra in postcoital heifers or cows suggests that trichomoniasis may be the cause. Abortions generally occur in the first half of gestation at a rate of 5% to 30%.³¹⁴ The placenta may be expelled or retained.^5,266

Laboratory Diagnosis

Diagnosis in the female is made by identifying or culturing trichomonads from cervicovaginal mucus (approximately 76% sensitivity), uterine exudate, placental fluids, or fetal abomasal contents.^{5,189,266,314,315} Preputial smegma collected from bulls by using a plastic pipette run against the mucosa can also be cultured for trichomonads (sensitivity 80% to 90%). Diamond’s medium (or modified Pastridge medium) is recommended for cultures from cows, bulls, or aborted fetuses.³¹⁵ Samples should be transported at ambient temperature, kept out of sunlight, not refrigerated, and delivered promptly to the diagnostic laboratory. The organisms are identified microscopically by their size (10 μm×15 μm), the presence of three anterior flagellae and an undulating membrane, and a characteristic jerky, rolling motion.²⁶⁶

There are no specific gross lesions in aborted fetuses. However, placentitis is a consistent microscopic lesion, and trichomonads can frequently be recognized in the placental stroma in histologic sections. Organisms may also be observed in the fetal lung in association with pyogranulomatous bronchopneumonia.³¹⁶

Pathophysiology

Trichomoniasis is transmitted venereally from infected bulls to cows or vice versa. The organisms colonize the vagina, cervix, uterus, and oviducts; yet they do not generally interfere with conception. Embryonic death frequently occurs within the first 2 months of infection,⁵ followed by a 2- to 6-month period of immunity to reinfection.¹⁸⁹ Clearance of infection in cows commonly occurs within 95 days; infection rarely persists as long as 6 months.³¹⁴ However, infection in bulls over 4 years of age is permanent and the main source of carryover from one breeding season to the next in beef cattle.¹⁸⁹

Treatment and Control

Systemic treatment of infected animals with imidazole compounds (ipronidazole, dimetridazole) is effective, but these compounds are prohibited in food animals in the United States.^242,317,318 Infected cows should be either culled or given at least 3 months’ sexual rest. The use of AI with semen from T. foetus,—negative bulls controls the disease once infected natural service bulls have been removed from the herd. In natural breeding situations, vaccination, use of young virgin bulls, and testing and elimination of positive bulls older than 3 years of age will allow herd owners to gain control over the incidence of trichomoniasis.

History and Clinical Signs

Most cattle are infected with Sarcocystis, but do not show clinical signs of infection; however, massive or repeated infections may elicit depression, anorexia, weight loss, lameness, hair loss, emaciation, or death. Abortions occur in late gestation, usually in severely affected animals.^266,326,327

Laboratory Diagnosis

There are no specific gross lesions in the aborted fetus. Histologically protozoa may be observed in villi and small arteries of the cotyledon or (more likely) the caruncle but are seldom seen in the bovine, ovine, or caprine fetus. Parasites are more likely to be observed in the fetal brain than in other tissues.³²⁶ Nonsuppurative inflammation may occur in the placenta or, less commonly, in fetal tissues, particularly the brain, heart, lung, liver, or kidney.^266,326,327

FA demonstration of numerous developing protozoa in the cotyledon or caruncle is considered diagnostic. Caruncles are reported to be atrophied.³²⁶ The protozoa can also be isolated by feeding aborted tissues to canids and recovering coccidian sporocysts from their feces.²⁶⁶

Pathophysiology

The pathogenesis of abortion in sarcocystosis is unclear. Generally, numerous spores are required to induce abortion experimentally. Fetal invasion by Sarcocystis, is rare, and abortion may result from maternal fever, anemia, or placental insufficiency.³²⁶ Pregnant does apparently have diminished immunity to Sarcocystis, because low doses of S. capracanis, result in fetal death without maternal illness if given in early pregnancy.³²⁸

Epidemiology

Ruminants are infected by consumption of canid feces that contain oocysts. Sarcocystis, occurs in the skeletal and cardiac muscle of most cows without associated lesions or clinical evidence of illness.

Control

Effective therapeutic regimens for clinically ill animals have not been developed. For the lifecycle of Sarcocystis, to be broken, feeds should be kept free of dog or cat feces. These carnivores should not be allowed to eat aborted fetuses, placentas, or other ruminant carcasses.

History and Clinical Signs

Mycotic abortions usually occur in the latter half of gestation (often near term) and seldom are associated with prodromal or postabortion clinical signs in the dam.

Laboratory Diagnosis

The most consistent lesion is placentitis with necrosis and thickening of fetal membranes. In ruminants, both cotyledons and the intercotyledonary placenta are affected. Histologically, necrotizing inflammation of the chorionic villi is associated with vasculitis and thrombosis.²⁶⁶ Gross lesions may not be apparent in the fetus, but granulomatous bronchopneumonia is frequently observed histologically.^266,330-332 In bovine aspergillosis the fetus is often near term with minimum autolysis and partially inflated lungs. Emaciation and dehydration with multifocal dry, scaly skin lesions occur in approximately 25% of affected fetuses.²⁶⁶ With other fungi the aborted fetus is often autolyzed, placentitis may be more severe, and skin lesions, if present, tend to be moister than those of aspergillosis.²⁶⁶ The placenta is characteristically thickened and leathery. The fetus may be emaciated, and granulomatous bronchopneumonia has been observed.³³¹ The fungus can be isolated from the fetus and placenta or demonstrated on histologic sections with immunostaining.

Pathophysiology

The route of fungal infection in the bovine uterus is thought to be hematogenous.¹¹

Epidemiology

Mycotic abortion generally affects only one or two animals in a herd and is more common in the winter.²⁶⁶ Fungi cause 3% to 10% of bovine abortions.^333,334Aspergillus, accounts for up to 80% of bovine mycotic abortions; Mucorales account for an additional 10% to 15%.⁵Mortierella, is a common abortifacient in Australia and New Zealand and has been associated with feeding of grass silage,^330,334 but Mortierella, abortion is rare in the United States.

Control

The only means of control of mycotic abortion is reduction of exposure to fungal agents.

INFECTIOUS CAUSES