Bovine Abortion and Embryo Loss Study Guide

Overview and Clinical Importance

Bovine abortion and embryo loss represent significant causes of reproductive failure and economic loss in both dairy and beef cattle operations. The diagnostic success rate for determining the cause of bovine abortion ranges from only 25-45%, making this a challenging area of veterinary medicine.

Pregnancy loss in cattle can be categorized by timing: early embryonic death (conception to day 42), late embryonic/early fetal death (days 42-60), and fetal abortion (day 60 to term). Normal abortion rates should be less than 3-5% annually; rates exceeding this threshold warrant investigation.

Early Embryonic Death

Early embryonic death (EED) accounts for the majority of reproductive loss in cattle, occurring primarily before day 16 post-breeding (before maternal recognition of pregnancy). Fertilization rates in cattle typically exceed 90%, but only 50-60% of inseminations result in confirmed pregnancies at day 30.

Timing and Magnitude of Loss

Causes of Early Embryonic Death

Non-Infectious Causes

Progesterone insufficiency: Inadequate CL function results in failure of maternal recognition of pregnancy. Both too-high and too-low progesterone concentrations negatively affect embryo survival.

Heat stress: Maximum embryonic losses occur during early cleavage divisions (days 1-7). Heat stress interferes with protein synthesis and causes oxidative cell damage. Bos indicus embryos show greater thermotolerance than Bos taurus.

Negative energy balance: Energy balance and dry matter intake during the first 4 weeks postpartum critically affect conception rates at 70-100 days post-calving.

Genetic abnormalities: Chromosomal aberrations (e.g., 1/29 Robertsonian translocation) cause embryonic death within the first 1-2 weeks.

Nutritional factors: Excess crude protein/rumen degradable protein with inadequate fermentable carbohydrate leads to elevated ammonia and reduced conception rates.

Infectious Causes

BVD virus: Fetal infection before 125 days can cause embryonic death, resorption, mummification, or persistent infection. BVDV disrupts follicular growth and estradiol secretion.

Campylobacter fetus subsp. venerealis: Venereal transmission causes endometritis and early embryonic death. Most cows recover in 3-5 months.

Tritrichomonas foetus: Venereal protozoan causing infertility, early embryonic death, and occasionally abortion in first half of gestation.

Leptospirosis and Bovine Abortion

Etiology and Epidemiology

Leptospirosis is a bacterial zoonotic disease caused by pathogenic spirochetes of the genus Leptospira. The disease occurs worldwide and represents one of the most commonly identified infectious causes of bovine abortion.

Important Serovars in Cattle

Pathogenesis

Leptospires are transmitted through direct contact with infected urine or indirect exposure to contaminated water sources. The organisms penetrate intact mucous membranes or abraded skin and enter the bloodstream (leptospiremia). During the bacteremic phase, organisms spread to multiple organs including kidneys, liver, and reproductive tract.

Reproductive tract pathogenesis: Leptospires cause diffuse placentitis with avascular, light tan cotyledons and edematous, yellowish intercotyledonary areas. The fetus typically dies 1-2 days before expulsion. Serovar Hardjo can establish lifelong infection in kidneys and reproductive tracts, causing chronic shedding in urine.

Clinical Signs

Abortion: Generally occurs in the second half of gestation (last 3 months), 2-5 weeks after infection. Fetuses are typically autolyzed.

Milk drop syndrome (Hardjo): Sudden drop in milk yield 2-7 days after infection. Udder becomes soft and flabby with colostrum-like or blood-tinged secretions.

Acute disease (Pomona): Fever, icterus (yellow mucous membranes), hemoglobinuria (red urine), anorexia, lethargy.

Weak/premature calves: Infected fetuses that survive may be born weak or premature.

Reduced fertility: Hardjo can cause embryonic death and reduced conception rates in carrier cows and cows bred to carrier bulls.

Diagnosis

Fetal/Placental Examination

Gross findings: Autolyzed fetus, icterus (especially with Pomona late in gestation), serosanguinous fluid in body cavities

Histopathology: Renal tubular necrosis, interstitial nephritis, bile retention (cholestasis) in liver, non-suppurative meningitis

Fluorescent antibody test (FAT): Detection of Leptospira antigen in fetal kidney and lung - best available test for abortion confirmation

PCR: Detection of Leptospira DNA in liver, kidney, or placenta. Highly sensitive and specific

Maternal Testing

MAT (Microscopic Agglutination Test): Titers greater than 1:100 considered significant. For Hardjo, titers may fall rapidly after infection and be negative at abortion. For incidental serovars (Pomona), expect high titers (greater than 1:400).

ELISA: Remains positive longer than MAT. Bulk milk ELISA useful for herd surveillance.

Urine PCR/Dark-field microscopy: Direct detection of leptospires in urine samples.

Treatment and Prevention

Neosporosis and Bovine Abortion

Etiology and Epidemiology

Neospora caninum is an apicomplexan protozoan parasite first recognized in dogs in 1984 and described as a new species in 1988. It is now recognized as the most common infectious cause of bovine abortion worldwide, responsible for 12-45% of aborted dairy fetuses in various studies.

Key epidemiologic points: Seroprevalence in US dairy herds ranges from 16-36%. Seropositive cows are 3-7 times (up to 20 times) more likely to abort than seronegative cows. The parasite is efficiently transmitted, with infection rates reaching 90% within some herds.

Life Cycle and Transmission

Definitive hosts: Dogs and other canids (coyotes, wolves, foxes). These animals shed oocysts in feces after consuming infected tissues.

Intermediate hosts: Cattle (primary), also sheep, goats, horses, deer, and other species.

Transmission Routes

1. Vertical (transplacental) transmission: PRIMARY route - accounts for greater than 90% of transmission. Infected dams pass infection to fetus during pregnancy. Congenitally infected calves remain infected for life and transmit to their offspring. This is the main way infection spreads within herds.

2. Horizontal (postnatal) transmission: Cattle ingest oocysts shed in dog feces that contaminate feed or water. This route is less efficient but can cause "point-source" abortion outbreaks.

Pathogenesis

After ingestion of oocysts, sporozoites excyst and transform into rapidly dividing tachyzoites that disseminate hematogenously. In immunocompetent animals, the immune response drives conversion to slowly dividing bradyzoites that form tissue cysts and remain dormant in neural and muscle tissue.

Pregnancy and abortion: During pregnancy, immunosuppression allows reactivation of tissue cysts. Tachyzoites reach the placenta and fetus via the bloodstream. Abortion occurs through direct fetal/placental damage and/or prostaglandin release causing luteolysis.

Fetal outcome depends on gestational age at infection:

Before day 95: Fetus unlikely to survive (no immune response)

Middle third (90-180 days): Fetus may mount immune response - survival variable

Third trimester: Fetus usually survives but is born congenitally infected for life

Clinical Signs

Abortion timing: Characteristically 4-6 months gestation (range 3-9 months). This mid-gestation timing is relatively unique among infectious causes.

Pattern: May be sporadic or epidemic (abortion storms when infection first introduced). Repeat abortions in individual cows are reported.

Dam clinical signs: NONE - adult cattle show no clinical illness. Placental retention is uncommon.

Fetal findings: Moderate autolysis, rarely mummified. Usually no gross lesions. Some calves born weak with neurologic deficits (proprioceptive deficits, ataxia, paralysis).

Congenital infection: 95% of calves born to seropositive dams are born infected but clinically normal.

Diagnosis

Fetal Examination

Histopathology: Characteristic lesions include multifocal nonsuppurative necrotizing encephalitis (brain), nonsuppurative myocarditis, and focal hepatic necrosis. Fetal brain is the BEST tissue for diagnosis.

Immunohistochemistry (IHC): Identifies N. caninum organisms in tissue sections. Relatively low sensitivity due to low parasite numbers.

PCR: Superior sensitivity and specificity for detecting N. caninum DNA in fetal brain, heart, liver, and placenta.

Fetal serology: Precolostral antibodies in late-gestation fetuses indicate in-utero infection.

Maternal Testing

ELISA: Detects Neospora-specific antibodies. PP values greater than 25 = positive. Titers fluctuate during pregnancy (highest 10-4 weeks before calving). A positive test indicates exposure but does NOT confirm Neospora as abortion cause.

IFAT: Immunofluorescent antibody test on fetal fluids.

Treatment and Control

CRITICAL: There is NO effective drug treatment to clear Neospora infection in cattle. Infected animals remain infected for life. Control focuses on prevention and herd management.

Differential Diagnosis of Bovine Abortion

Comparison of Major Infectious Causes

Diagnostic Sample Collection

Optimal submission: Intact fetus with placenta plus maternal serum. The placenta is often MORE valuable diagnostically than the fetus.

Required Samples

Fresh tissues (refrigerated, NOT frozen): Brain (whole), lung, liver, spleen, kidney, heart, adrenal, abomasal contents, placenta (3+ cotyledons)

Fixed tissues (10% neutral buffered formalin): Same tissues in 1/4 inch thick sections

Fluids: Fetal heart blood or thoracic fluid (3-5 ml), maternal serum (red top tube)