Fetal Disease and Abortion

Chapter 54
Fetal Disease and Abortion: Diagnosis and Causes

Wes Baumgartner

Department of Pathobiology and Population Medicine, College of Veterinary Medicine, Mississippi State University, Starkville, Mississippi, USA


Reproductive failure is a significant problem in breeding management that arises from physiological, anatomical, inherited, and infectious causes. The inability to achieve or maintain a pregnancy may be divided into four main stages: failure to ovulate after estrus, failure of fertilization, embryonic death (prior to gestation day 42), and fetal death.1 Pregnancy wastage, which probably comprises the largest portion of these losses, encompasses the combined embryonic, fetal, and neonatal deaths that achieve nothing. It has been estimated that about 75% of pregnancy wastage occurs in the embryonic stage.2,3 The majority of reproductive failure occurs in the first 2 weeks, at the time of development from a morula to blastocyst where the conceptus begins enhanced protein synthesis and placental development.3,4 Despite the importance of wastage at this time of development, the mechanisms contributing to embryonic death are poorly understood and in most cases the cause is never established.1 Factors typically thought to contribute to embryonic death include heat stress, infections of the uterus/gametes/embryo, local trauma, genetic factors, heavy lactation in dairy cattle causing energy imbalances, maternal illness, aged oocytes from persistent follicles, small follicles, fetal–maternal incompatibilities, twinning, postpartum breeding intervals, and abnormal progesterone levels due to estrus synchronization.1,3–5 Investigation into the causes of early loss are hampered by the rarity of available early conceptuses that are either expelled or resorbed and go unnoticed, only to result in a cow that returns to estrus or fails to deliver a calf.

Abortion typically refers to pregnancy loss in the fetal stage, between days 42 and 260. It is in this stage of gestation that the tissues of conception cannot be resorbed and, when expelled, are more easily noticed. During the fetal period there is a progressive decrease over time in the risk of abortion, with a slight increase in the last month.6 Although losses during this time are a minority of overall wastage, the cost of investment by the cow and the manager are substantial. A mid-term abortion represents a loss of at least US$600–1000.6 For practical purposes, unavoidable losses of 3% after pregnancy confirmation (6 weeks’ gestation), with 1–2% loss in the periparturient period, may be considered acceptable or typical, although opinion in this area varies.6–8

This discussion will concentrate on fetal death and the approach to diagnosis, but will necessarily include some aspects of embryonic death, congenital abnormalities, and common gross findings. Additionally, a brief overview of anatomy and development are included to familiarize the reader with general concepts.

The investigation of abortion is a vital part of herd management and its importance is hard to overemphasize. Accurate diagnosis is the only path to the effective control of disease. It should go without saying that a focused, efficient, and thorough investigation technique with a definite purpose by prepared veterinarians is the only relevant way to identify and understand the etiologies of abortion. The necropsy itself contributes to this in several ways: by establishing definitive causes of death, identifying unsuspected findings, providing information concerning zoonotic disease, contributing to discovering new diseases and pathogenic mechanisms, and providing a means to test new diagnostic and treatment techniques.9


The expression of disease in the conceptus is remarkably varied in a general sense, in that it gives rise to bizarre developmental defects of potentially every sort. This is due to the intricate physiology and morphology of fertilization and gestation that is shared between the dam and fetus. The sequential stages of organ system development in utero provide unique opportunities for infectious and noninfectious etiologies to manifest themselves at the gross level, if pregnancy is maintained. In addition the placenta, a unique organ of gestational necessity, is a target of many disease-causing agents and can itself develop anomalous defects that in turn directly affect the fetus.

Despite this, in many cases aborted tissues from infectious and noninfectious causes exhibit little if any recognizable changes of significance. This is partly due to autolysis in utero masking subtle changes; the relative ease and rapidity by which fetuses succumb to disease, allowing only a brief window for gross changes to manifest; and a rudimentary inflammatory response to injury.10 Not only does the conceptus vary in its susceptibility to particular insults across the gestational period, but the degree and duration of insult also determines the outcome, whether it be life, death, malformation, or inflammation.7

The physiology of pregnancy is well studied and dealt with in detail in preceding chapters. Despite our understanding of normal pregnancy, the physiology of abortion and the mechanisms involved are poorly understood. In many cases abortion may be mediated through the same pathways that occur in normal parturition, but different mechanisms and pathways are also possible.6

Categories of reproductive loss

The cause of abortion in many cases is not known, which is a consistent source of frustration for manager and clinician alike. In all species, abortion may be caused by infectious and noninfectious etiologies. Specific causes and agents are dealt with in detail later in this and subsequent chapters. Of these, infectious causes of abortion (bacteria, viruses, fungi, protozoa) are probably the best understood and characterized. It is common to see reports where the percentage of cases with a specific diagnosis is less than 50%.11 Of these, at least half are due to infectious agents, with the majority of these due to bacterial infection.6

Bacteria involved in abortions can be broadly grouped into those that are contagious and those that are opportunistic. The majority of bacterial abortions are caused by opportunists, and these may be further divided into those that are part of the natural flora, such as Trueperella pyogenes (formerly Arcanobacterium pyogenes) and Histophilus somni, and those from the environment, such as Bacillus spp. and Escherichia coli.12 The significance attached to abortion by opportunists depends on the situation in the herd. If these bacteria are only seen in isolated cases, then the significance to the herd is minimal.12 However, if these organisms are consistently associated with abortions, then further investigation is warranted.

Noninfectious causes of abortion are similar to those known to cause embryonic loss, including nutritional imbalances, malnutrition, stress, environmental toxins, teratogenic compounds, hormone imbalances, and genetic abnormalities. An expanded list of etiologic agents is shown in Table 54.1 and in the following chapters.

Table 54.1 Disease-causing agents associated with endemic fetal losses.

Source: Whittier W. Investigation of abortions and fetal loss in the beef herd. In: Anderson DE, Rings M (eds) Current Veterinary Therapy: Food Animal Practice, 5th edn. St Louis, MO: Saunders, 2009, pp. 613–618.

Histophilus somni, Listeria monocytogenes, Trueperella pyogenes, Leptospira spp., Ureaplasma diversum
Bluetongue virus, BVDV
Neospora caninum, fungi, epizootic bovine abortion
Inbreeding, sire-derived lethal traits, chromosomal abnormalities
Feed estrogens (silage, poultry litter), progesterone aberrations (high pasture protein)
Protein, vitamin A, iodine, selenium deficiency
Protein/urea, copper, iodine excess
Endotoxins due to Gram-negative bacterial sepsis in dam
Endotoxin in Gram-negative bacterial vaccines, especially given during first or last 2 months
Pine needle, broomweed, locoweed, narrow leaf sumpweed toxicosis
High plant estrogens
Aflatoxin, ergotamine, fusarium (zearalenone), nitrate fertilizer, organophosphate toxicosis

Pathophysiology of injury to the conceptus

Maintenance of the first half of gestation (the first 200 days) in cattle requires a persistent corpus luteum (CL), which is maintained by the fetus.7,13 Luteolysis may occur in pregnant cows due to excess prostaglandins (exogenous administration or secondary to heat stress) or Gram-negative bacterial septicemia.14 If the CL is destroyed at an early stage, death and rapid loss of the embryo with minimal degeneration may be seen.15 If there is fetal death prior to luteolysis, the CL may regress with eventual expulsion of autolyzed fetal tissues. However, in some cases the CL is maintained after fetal death, which can result in expulsion, resorption, or mummification.16 Early abortions are typically not recognized; most are occultly expelled, severely autolyzed, or mummified.

The maintenance of late-stage pregnancy requires both the fetus and placenta. At this stage in development, sufficient fetal stress can induce parturition through natural endocrine mechanisms. In this way, chronically diseased fetuses can initiate their own premature delivery.

Fetal death often leads to abortion within a few days rather than immediately, allowing sufficient time for autolytic changes to occur. The mechanism for expulsion of dead fetuses is unknown, but may share many similarities with normal parturition.16 Autolytic changes include generalized edema, pallor, and hemoglobin-stained fluids in the body cavities. Visceral tissues become pulpy or semi-liquid.16 In some cases, the time between fetal death and expulsion may be characteristic for a pathogen, and may therefore be useful to the clinician. Fetal infections due to Listeria monocytogenes, Trueperella pyogenes, nonseptate fungi (Absidia spp., Mucor spp., Rhizopus spp.), and bovine herpesvirus (BHV)-1 may lead to fetal death with expulsion days later. Fetuses infected by Campylobacter fetus and Aspergillus spp. may be delivered alive.17

It is important to recognize that infection of the conceptus does not necessarily lead to fetal death. The ability of a pathogen to injure the conceptus is influenced by the dam (general health, previous exposure), the stage of fetal development, and the virulence of the infectious agent. Fetal development is a continuum of organogenesis, physiological development, and immune development. Early stages of gestation are more prone to infection and severe disease, as the capabilities of the fetus are underdeveloped. The closer the fetus is to parturition, the stronger and more capable it is of defending itself from pathogens. Thus infection at different stages of development will produce different outcomes in the fetus.

Bovine viral diarrhea virus (BVDV) infection is a good example of this. Infection in the first trimester often leads to fetal death and resorption, while infection in the second trimester may lead to developmental anomalies. The character of the developmental defects depends on which cells or tissues are susceptible to the virus at the time of infection. In the second trimester, cerebellar growth is maximal and BVDV infection at this time may lead to cerebellar necrosis and cerebellar hypoplasia. Also at this time, hair growth is highly active and BVDV infection may damage follicles, resulting in hypotrichia. By the third trimester, the immunocompetent fetus may react to BVDV infection by mounting a sufficient immune response with antibody production and virus elimination. The only evidence for such an infection would be fetal specific antibody titers.18

Other viruses, such as BHV-1, cause extensive cell necrosis and hemorrhage, leading to rapid fetal death. Neospora caninum infection in the third trimester may cause only mild inflammation, with the birth of asymptomatic calves.

Effects of maternal disease

Infectious pathogens may cause abortion either by directly infecting the conceptus, or by affecting the dam such that severe physiological disturbance leads to abortion. The dam is predisposed to infection through nonspecific immunosuppression that occurs during pregnancy.19 Fever (mastitis, pneumonia), circulatory disease (myocarditis, severe anemia), hypoxia, and endotoxemia (Gram-negative sepsis) are possible conditions that may cause abortion indirectly.18 Prostaglandins may be elevated in febrile states, which can lead to luteolysis and abortion.20 The likelihood of abortion probably increases with the number of pregnancies or previous abortions by the dam.6

Routes of infection to the conceptus

In cases where infectious organisms invade the conceptus, four routes are likely.18 Hematogenous spread from the dam to the placenta is commonly suspected in cases of infectious abortion, particularly due to Listeria monocytogenes, Leptospira interrogans, Salmonella enterica, Brucella abortus, fungus, BHV-1, or BVDV infection. Ascending infection from the vagina through the cervix can occur from primary vaginitis (characteristic of Tritrichomonas foetus) or contamination at insemination. The presence of pathogens within the uterus (endometritis due to Campylobacter fetus, Trueperella pyogenes) and descent from the abdomen via the uterine tubes (mycobacteriosis) are also possible pathways for organisms to reach the conceptus.

Route from the placenta to the fetus

Once a pathogen reaches the placenta, it may proceed to the fetus through the blood, via the umbilical veins, or by contamination of the amniotic fluid18 (Figure 54.1). For example, BVDV primarily infects the fetus hematogenously whereas BHV-1 may first infect the placenta, and then proceed to the fetus. Primary placental infection with subsequent amniotic fluid contamination is characteristic of fungal infections. In some cases a pathogen need not infect the fetus, such as with Salmonella enterica infection, where severe infection of the placenta may lead to generalized fetal hypoxia and subsequent death.


Figure 54.1 Fetus, omphalitis, ascending bacterial infection from the placenta. Purulent material is easily expressed from the cord.

Photo courtesy of J. Edwards.

Lesions in placenta

Placentitis most commonly develops by one of three ways: hematogenous spread, extension from a diseased uterus, or an ascending vaginal infection. Gross placental lesions are characteristic of chronic bacterial and fungal disease, while viral infections generally produce no lesions.21 Changes of significance may occur in both the cotyledons and/or intercotyledonary spaces. The presence of fibrin (yellow, stringy, friable material) on cotyledons is an indication of inflammation (Figure 54.2). Fibrin must be distinguished from necrotic inflammatory exudate or entrapped caruncle fragments (necrotic uninfected endometrial tissue). The presence of ecchymosis and extension of the changes to the intercotyledonary space are suggestive of an infectious inflammatory process. With chronicity, stereotypical changes of placentitis include (i) placental fibrosis and edema; (ii) cupping of cotyledons; (iii) exudate on chorionic surfaces; and (iv) necrosis of the cotyledons.10


Figure 54.2 Chorioallantois, placentitis. The cotyledons are thickened with yellow discoloration due to fibrin and necrosis. Intercotyledonary tissues are relatively unaffected.

Photo courtesy of J. Cooley.

Fungal and bacterial inflammation of the cotyledons is often associated with necrosis, which imparts a firm to friable, tan, irregular or nodular consistency to the tissues with interspersed ecchymoses. Fungal organisms prefer to grow along and within blood vessels; this often leads to thrombosis, hemorrhage, and necrosis (Figure 54.3). Fungal organisms may be particularly abundant at the periphery of lesions rather than in the centers. A useful feature for interpretation is the extension of the pathologic process into the pericotyledonary chorioallantois. Such infiltrates may bridge cotyledons and often impart a leathery thickened texture. Another differential for such a change would be adventitial placentation (discussed in the section on pathology). Leptospirosis and BHV-1 infections may also produce a placentitis and appear similar to one another.22


Figure 54.3 Chorioallantois, fungal placentitis; maternal aspect on right, fetal aspect on left. Cotyledons are thick, irregular, and tan to hemorrhagic. Intercotyledonary areas are thickened. The fetal side shows yellow discoloration and multiple discrete infarcts (arrows) due to vascular thrombosis.

Photo courtesy of J. Edwards.

Ureaplasma diversum is known to produce a rather characteristic hemorrhagic amnionitis, where the membranes are thickened, opaque, and ecchymotic with fibrin, necrosis, and fibrosis.23

Lesions in fetus

Gross lesions of the fetus, aside from malformations, are generally uncommonly noticed. They may be inapparent for four reasons: (i) the fetal immune system is not of sufficient robustness to mount a response that is easily observed at the gross level; (ii) fetuses often die before lesions appear; (iii) lesions are masked by autolysis, and (iv) fetal pathology may manifest itself in ways that are difficult to recognize.24 Table 54.2 lists some causes for commonly encountered lesions in aborted fetuses.

Table 54.2 Possible causes for gross and microscopic lesions in bovine fetuses.

Source: Njaa BL. Kirkbride’s Diagnosis of Abortion and Neonatal Loss in Animals, 4th edn, 2012.

Gross lesion
Mummification BVDV, Neospora
Ascites/anasarca Congenital heart defect, BVDV, Neospora
Arthrogryposis, musculoskeletal deformities Akabane/bunyaviruses, reduced in utero motility
Fibrinous peritonitis/pleuritis Bacteria (Trueperella, Campylobacter, Bacillus, Brucella) and fungi
Fibrinous pericarditis Bacillus, Campylobacter
Icterus Leptospira
Cerebellar hypoplasia BVDV
Hydrocephalus, hydranencephaly, porencephaly BTV, BVDV
Microphthalmia BVDV
Pulmonary/renal hypoplasia BVDV
Dermatitis/hyperkeratosis Fungi, EBA
Multifocal liver necrosis Listeria, BHV-1, Yersinia, Salmonella
Splenomegaly/lymphadenopathy EBA
Placentitis, infarctions Fungi
Microscopic lesion
Encephalitis Neospora, BHV-1, BVDV
Meningitis EBA, Leptospira, Brucella, other bacteria
Myocarditis Neospora, BVDV
Suppurative bronchopneumonia Bacteria
Bronchointerstitial pneumonia Ureaplasma, Brucella
Multifocal hepatic necrosis BHV-1, Listeria, Salmonella, Yersinia
Interstitial nephritis Neospora, Leptospira
Abomasitis/enterocolitis Bacteria, fungi
Conjunctivitis Bacteria, Ureaplasma, fungi
Placentitis Bacteria, fungi

BVDV, bovine viral diarrhea virus; BTV, bluetongue virus; EBA, epizootic bovine abortion; BHV-1, bovine herpesvirus 1.

The most common finding in abortion is autolysis, the degree of which depends on the cause of death, the time from death to abortion, and the time from abortion to examination.22 In experimentally induced, sterile, dead ovine fetuses, changes associated strictly with autolysis included (i) lack of odor, (ii) subcutaneous blood-tinged gelatinous edema, (iii) blood-tinged fluids in body cavities, (iv) renal cortex softening, (v) liver softening, (vi) abomasal content that was cloudy yellow to red, and (vii) uniform color (pink/red) of tissues25 (Figures 54.4 and 54.5). By 12 hours after death, the fetal corneas were cloudy, the liver and kidneys were friable, and abomasal content became cloudy with brown flecks. After 36 hours, the subcutis contained edema and the skin would slough. By 144 hours, progressive dehydration was obvious (mummification).25 Signs of fetal infection include fibrinous exudates in body cavities, white to tan foci in the liver or lungs, and evidence of abnormal development22 (Figure 54.6).


Figure 54.4 Aborted fetus, opened chest and abdomen. The lungs are uninflated (congenital atelectasis) and red with a shiny smooth pleura. Autolytic change is present (generalized reddening of tissues, friable liver).

Photo courtesy of J. Edwards.


Figure 54.5 Fetus and placenta. The fetus exhibits generalized red discoloration due to autolysis.

Photo courtesy of J. Cooley.


Figure 54.6 Aborted fetus, Trueperella pyogenes infection; opened chest and abdomen. Fibrin strands are present on the pleural surfaces. Autolytic change (generalized reddening of tissues) is evident.

Photo courtesy of J. Cooley.

Pathogens that invade the fetus via umbilical veins may produce lesions in the liver, as it is the first organ encountered (Figure 54.7). Listeria monocytogenes, BHV-1, Yersinia pseudotuberculosis, and Salmonella enterica infections are often associated with liver necrosis. For pathogens that infect the amniotic fluid, exposure of the skin, lung, and intestines may occur. Skin lesions are particularly well known in cases of fungal infection, where pale patches of thickened skin are evident (Figure 54.8). Lung and pleural disease may be manifestations of hematogenous systemic spread or inhalation of infected amniotic fluid during fetal distress.18


Figure 54.7 Fetus, liver section, hepatitis. Multiple tan foci of necrosis are surrounded by hyperemic parenchyma.

Photo courtesy of J. Cooley.


Figure 54.8 Fetus, fungal dermatitis. Coalescing, mildly bulging, gray/tan foci are present in the skin of the neck.

Photo courtesy of J. Edwards.

Epizootic bovine abortion causes distinctive lesions in the fetal liver, lymph nodes, and spleen. The liver is irregular and nodular; however this change may also be seen in cases of congenital heart disease where chronic passive congestion occurs (Figure 54.9). The spleen and lymph nodes are characteristically enlarged due to lymphoid and mononuclear cell hyperplasia.16


Figure 54.9 Fetal liver. The surface is tan and coarsely irregular. This change may be seen with chronic passive congestion (heart anomalies) or epizootic bovine abortion.

Photo courtesy of J. Edwards.

Outcome of exposure to abortifacient agents

Fetuses exposed to abortifacient agents or conditions may die (resorption/abortion/stillbirth), they may be infected (with or without disease), they may be malformed (live/dead), or they may be normal.19

Death in the embryonic stage leads to resorption. In the fetal stage the presence of skin and musculoskeletal structures, in addition to placental endocrine activity, prevents resorption. Instead fetal death leads to autolysis and expulsion, or retention with mummification/maceration. In late gestation, a sick or stressed fetus may precipitate its own premature delivery with one of three results: the fetus may be born and then die, it may be born and fail to thrive, or it may be born and thrive even if infected.18

Disease may impair fetal motion, a necessary requirement for proper musculoskeletal development. In such cases, the calves may exhibit severe changes, including arthrogryposis, ankylosis, scoliosis, torticollis, and similar defects that lead to dystocia, stillbirth, or death in the perinatal period.


Abnormal development (congenital defects) in the fetus may be caused by teratogens: toxic substances, infectious disease agents (particularly viruses), nutritional imbalances, endocrine imbalances, hypoxia, extreme temperatures, and inherited or spontaneous genetic mutations. The manifestation of these defects includes resorption/abortion, malformation, alteration of growth, and functional deficits. The late embryonic period and early fetal periods are the times of greatest susceptibility for the conceptus. During this time, each organ system is established in an orderly fashion with morphogenesis occurring in “critical periods.” During these periods organs are at their most sensitive to teratogens.

In many cases congenital defects have no defined cause. Seasonal occurrence, history of stress, or maternal disease are often noted, with or without a familial component.26 The genetic composition of the fetus as well as the nature and degree of insult figure largely in the outcome.11 Genetic considerations are discussed in greater detail in Chapter 66.

In cattle, viral infections are well-known causes of defects. BVDV, infectious bovine rhinotracheitis (BHV-1), Wesselsbron, bluetongue, Akabane (bunyaviruses), and Rift Valley fever viruses are commonly associated with embryonic loss and neuromuscular defects.27,28 In addition, toxic plants such as lupines, Conium maculatum, and locoweeds are associated with defects.26 Further discussion of such toxins is presented in Chapter 65.

Calves with congenital defects often die during parturition or soon thereafter. In many cases the anomalies are grossly obvious, often affecting the neural and musculoskeletal systems. A wide range of malformations have been described, some of which have been intensively studied and a genetic component has been found. For the purposes of this chapter, relevant anomalies are generally discussed for those which are caused by infectious agents (BVDV, Akabane virus) or those that are not known to be inherited but are particularly puzzling when encountered (acardiac twins, moles). Reviews are available.11,29


Congenital tumors and neoplasms are rare in calves and are most often diagnosed as lymphomas, mesotheliomas, embryonic tumors, and hamartomas. They have been reviewed.30


The placenta is a transient metabolic organ derived from the fetal chorion and maternal endometrium to provide nutrition and metabolic exchange between mother and calf. Gestation can be divided into the embryonic stage with organogenesis, and the fetal stage with fetal growth. The embryonic stage extends to around day 45; the fetal stage continues until delivery. Together, the chorioallantois and amnion form the extraembryonic fetal membranes.

After fertilization, the zygote undergoes cleavage to form a ball of cells (morula). With further division the morula develops into the blastocyst, which is an inner cell mass (the embryo proper) and a blastocele (fluid-filled cavity) lined by the trophoblast cell layer. The blastocyst, now about 1.5 mm wide, hatches from the zona pellucida at 9–11 days after ovulation in order to attach to the endometrium of the uterus.31 By 19 days, the bovine blastocyst trophoblast enlarges as a threadlike emanation/sac along the entire length of the uterine horn.28,32 At this time, defective embryos will die and be resorbed or expelled. Also, the CL is developing and producing progesterone.11

The primitive endoderm from the inner cell mass migrates along the inner aspect of the trophoblast, lining the cavity that will become the yolk sac. The yolk sac provides nourishment to the conceptus early in development, but will quickly regress to an inapparent rudiment.32,33 At this time, prior to uterine attachment, the conceptus derives nourishment from the secretions of the uterine mucosal glands, known as histotrophe. This material is a yellow/white, opaque, thick secretion sometimes mistaken for purulent exudate.11. Once the fetomaternal placental circulation develops, fetal nutrition is supplied by diffusion of nutrients from the blood across the placentome (hemotrophe).28

The primitive mesoderm migrates between the endoderm and trophoblast (now a trophectoderm) to form the chorion. The chorion then rapidly expands as a transparent sac to fill the uterine lumen.34 Around this time, dorsomedially migrating folds composed of mesoderm/trophectoderm surround the embryo between days 13 and 16, providing complete envelopment of the embryo in an amniotic cavity. The site where these folds meet, the raphe or mesamnion, persists as a broad attachment of the dorsum of the amnion to the chorioallantois in Bovidae. The amnion is therefore composed of an inner trophectoderm and subjacent mesoderm with extensive attachment to the allantois.

Between days 14 and 21, a diverticulum of the hindgut extends from the embryo into the mesoderm to form the allantois and, along with it, the vasculature supplying the chorion and amnion.21 The allantois continues to expand to fill both uterine horns, with widespread apposition and eventual fusion to the chorion (chorioallantois). It is thus T-shaped, with the stem of the T as the allantoic stalk of the umbilicus and the other ends of the T as extensions of the chorioallantois into both uterine horns.28 The chorioallantois attaches at 4 weeks’ gestation to the uterus, forming irregular villous projections over the uterine caruncles, with eventual development into placentomes.

By days 30–35, three to four fragile attachments (early placentomes) are present in the pregnant horn; by day 40 attachments are present in both horns. At day 70, 40–50 placentomes are present, which will number 75–140 by mid gestation. Placentome size may vary widely, from 5 to 15 cm in diameter. The fetal cotyledon has a velvety red surface (Figure 54.10). Both the weight and size of placentomes increase during gestation, particularly in the pregnant horn.35 Between placentomes, there is minimal chorioallantoic villous proliferation, which may be seen as fine red villous proliferation occurring diffusely or in multiple, 5–10 mm wide, regularly spaced foci. Such proliferation may cover nongravid horns that contain no cotyledons.


Figure 54.10 Normal placenta. A cotyledon has a red velvety surface. The intercotyledonary spaces are smooth, shiny, opaque, and white.

Placentomes are usually arranged in two dorsal and two ventral rows along both horns, although an extra row or reduced rows may be seen (see Figure 54.14). They become progressively larger the closer they are to the fetus and the majority of cotyledons are present in the gravid horn. The largest placentomes are closest to the main arteries and become progressively smaller toward the periphery. In some cases all cotyledons are present in the gravid horn with few to no cotyledons on the nongravid side. The cotyledonary rows may be interrupted by a circular bare area associated with the junction of the horns, near the cervix.36

As development progresses, there is fusion of membranes to one another in the areas where they come into contact. These attachments may be transient. In early gestation, the amnion is relatively large and compresses the allantois laterally. As the amnion grows and contacts the chorion, the amniochorion is formed; on the opposite side of the calf where the amnion contacts the allantois, the allantoamnion is formed. With maturity, the allantois increases in volume to almost entirely surround the amnion.

Thus the fetus is immediately surrounded by the amniotic fluid, which is produced by transamniotic fluid fluxation, fluid from the fetal lungs, oral glands, and urination. Initially the amniotic fluid is watery, slightly yellow and clear; later in development it becomes viscous, translucent, opaque, and white or yellow. Urine throughout early development is excreted through the urachus and umbilicus to the allantois, but it may also be excreted through the urethra. The contribution of urine to the amniotic fluid after 240 days’ gestation in cattle has not been conclusively decided; both increasing and decreasing late-term transurethral urination has been reported.21,28 Amniotic fluid in full-term cattle varies from 2 to 8 L, with reported averages at 2.2 or 5–6 L. Allantoic fluid at term ranges from 4 to 15 L, with an average of 9.5–10 L.11,37

The umbilicus is relatively short, being about one-quarter the length of the fetus, or about 30–40 cm.11 As such, rupture of the cord occurs during parturition when the fetal pelvis passes through the dam’s pelvis.38 The umbilicus is exclusively within the amnion, and is composed of two arteries, two veins (which merge into one prior to entering the fetus), the allantoic stalk, and rarely yolk sac remnants. The umbilical arteries and veins are sheathed in smooth muscle, which contracts during parturition due to stretching, stopping blood flow after birth.28 The umbilical arteries arise from the caudal aortae, running cranioventrally along the urachus, exiting with the allantoic stalk to supply the chorioallantois. In necropsied neonates, it is common to see swollen, purple, thrombosed umbilical arteries at the level of the urachus; this is a normal inflammatory reaction to the severing of fetomaternal circulation (Figure 54.11).


Figure 54.11 Calf, umbilical artery thrombosis. Bilaterally the arteries alongside the urinary bladder (asterisk) are focally swollen and red due to the tearing and thrombosis associated with parturition.

By day 45, fetal organogenesis is complete and the fetal growth stage then begins. Average weights, crown–rump lengths, and external characteristics achieved during growth are summarized in Table 54.3.

Table 54.3 Gestational age estimates of bovine fetuses.

Source: Njaa BL. Kirkbride’s Diagnosis of Abortion and Neonatal Loss in Animals, 4th edn, 2012. This material is reproduced with permission of John Wiley & Sons, Inc. Original content from Roberts S. Veterinary Obstetrics and Genital Diseases (Theriogenology), 3rd edn, 1986, p. 19.

Age (months) Relative size Crown–rump length (cm) Weight External characteristics
2 Mouse  6–8 8–30 g Claw buds and scrotum present
3 Rat 13–17 200–400 g Hair on lips, chin, and eyelids
4 Small cat 22–32 1–2 kg Fine hair on eyebrows, claws developed
5 Large cat 30–45 3–4 kg Hair on eyebrows and lips, testes in scrotum, teats developing
6 Small dog, beagle 40–60 5–10 kg Hair on inside of ear and around horn pits, tip of tail and muzzle
7 Dog 55–75 8–18 kg Hair of metatarsal, metacarpal, and phalangeal region of extremities and beginning on back, long hair on tail tip
8 Large dog 60–85 15–25 kg Fine short hair all over body, incisor teeth not erupted

Approach to the problem

Fetal loss in a herd may be divided into four epidemiologic presentations, which may simplify and better direct investigations. These four include (i) baseline losses, (ii) endemic losses that exceed baseline and occur consistently and chronically, (iii) epidemic losses characterized by high losses in a specific time frame, and (iv) fetal losses that are confused with conception failure or neonatal losses.24

Baseline losses, as mentioned in the introduction, are considered largely unavoidable and may be due to illness in the dam, lethal genetic make-up of the fetus, trauma, or physiological abnormalities. It is important to monitor such losses from a management standpoint as it will aid the discovery of endemic problems. While it is prudent to thoroughly investigate all abortions, it is also costly. However, with continued monitoring and testing, the manager and veterinarian have a clearer picture of herd health and are better prepared to identify endemic problems. Furthermore, upcoming epidemics may be identified at a stage where losses can be minimized.24

Endemic abortions significantly affect herd productivity due to chronic excessive losses. Not only may it be difficult to realize that there is a problem, but it may be equally difficult to identify the source of the losses. Accurate record keeping and routine pregnancy diagnosis is therefore vitally important in order to recognize these issues.24 Table 54.1 lists many disease-causing agents that are associated with endemic losses in cattle. BVDV, Neospora caninum, and Leptospira spp. are of particular importance.

Epidemic abortion storms may be due to many of the same agents that cause endemic losses. BHV-1, Brucella abortus, and Leptospira spp. are well-known causes.19 Herd health status, vaccination history, pathogen virulence, access to toxic agents, and clustering of pregnancies all have relevance in determining the likelihood of epidemic loss. Herds with tight pregnancy patterns are more susceptible to this type of outbreak. Investigations should make note of the particular time/season and area where the losses are occurring as this will aid in determining differentials.24

Finally, managers should be encouraged to document and report all abortions, stillbirths, premature births, dysmature calves, and abnormal calves.

History/background investigation

The importance of a thorough history cannot be overstated; essential information is found in a systematic query of farm details. Abortion is both an individual and potential herd problem, and lack of investigation in both will severely hamper efforts to alleviate unacceptably high losses. It is important to keep in mind that more than one agent may be involved in abortion. Similarly, although more than one infectious agent may be present in an aborted fetus, only one may be the cause of death. Organisms regarded as low virulence may be the cause of abortion, but are also commonly present as contaminants.17

Sporadic abortions may be a manifestation of an ongoing herd problem or they may be the beginning of an outbreak; in either case investigation is warranted. Standard forms are used to reliably collect important cow and herd information (see Appendix); systematic evaluation of management practices will help direct investigations. Pertinent questions are listed below.39 These questions and other information are incorporated into the investigation form provided. An expanded questionnaire has been published.40

Aborted calf

  • When was it due?
  • Was it born alive?

Aborting cow

  • Breed, age, lactation/parity number, source, dam/sire, bred naturally or AI, conception date/last service, date of last normal parturition, previous abortions and any work-up done.
  • Vaccination history, vaccine brand/lot number, vaccine handling and storage.
  • Deworming history.
  • Any clinical signs?


  • Number of animals, number that are immature, number purchased in last year, health problems/body condition.
  • Herd abortion history (sporadic/recurrent/recent, how many in last week/month/year, which trimester affected, affects older/younger/all cows, any particular time of year), problems with term calves (congenital defects).
  • Are postpartum examinations performed routinely?


  • Feeding regime, types of forage, concentrates, minerals, selenium.
  • Any changes in management, housing, pasture?
  • What is the quality of the forage?
  • Water source/quality?


  • Access of herd to other cattle, animals, predators.
  • Nature and quality of pasture.
  • Any toxic plants on pasture?
  • Nutrient deficiencies in area pasture.

Examination of the cow

In some cases, the health condition of the cow has direct implications as to the cause of abortion (plane of nutrition, respiratory/intestinal disease, Anaplasma sp. infection). Any vaginal discharge or cervical mucus should be collected and sent to the diagnostic laboratory for microbiological analysis. Blood samples for serology should be taken from the dam as well as unaffected cows and those that have recently aborted. Serum should be acquired 2–3 weeks later in order to provide paired samples. Collecting serum from 10 other herdmates (or 10% of the herd) will make serological assessment more meaningful.6 Whole blood in EDTA is useful for blood smear and serum chemistry analysis of the dam. Gloves are to be worn during all examinations, as zoonotic agents may be present.

Examination of tissues

A necropsy is an examination with a definite purpose in order to yield the maximum amount of information. As such, it is vitally important to be systematic so that a full complement of tissues is taken during each examination. Optimally one should send the entire fetus and membranes to a diagnostic laboratory for evaluation. It is of primary importance to send fetal membranes as these may be diagnostic. If this is not convenient, then a standard approach should be adopted, as described here.

Examinations should be directed toward suspected etiologies, but keep in mind that more than one pathogen may be present. Typical findings in aborted calves that died in utero include edematous red tissues that lack normal tinctorial distinction, clear red fluids in body cavities, pale soft livers, and friable autolytic kidneys. Digital photographs are an excellent way to document lesions and may be useful in communications with diagnostic laboratories.

Examination of the fetus

It is important to verify the approximate time of death, which can be done based on gross findings. In antepartum fetal death, tissues are autolyzed or mummified and include the findings described above. Partum death is characterized by signs of life (localized head or limb edema, partial lung aeration, limb/rib fractures, subcutaneous shoulder hemorrhage, liver fractures with hemorrhage) in addition to proper degrees of fetal maturation/formation. Neonatal deaths are characterized by aeration of the lungs, umbilical artery thrombosis (swollen purple/red nodules along the arteries that run lateral to the urinary bladder), loss of the eponychium (soft fetal hoof keratin), and milk in the stomachs.41

The method of necropsy for aborted fetuses is basically the same as for any animal. The degree of autolysis and weight of the fetus and placenta are noted. Even if severely autolyzed, fetal tissues may be of use for polymerase chain reaction (PCR) screening for pathogens. Estimation of gestational age can be accomplished by the following formula: x = 2.5(y + 21), where y is crown–rump length in centimeters and x is gestation age in days.7 The crown is a point midway between the orbits on a line traversing the frontal eminence; the rump is the base of the tail or first coccygeal vertebra.42 In embryos, the greatest total length may be used instead of crown to rump. For stillbirths, fetal weight is useful in the diagnosis of dystocia due to fetal–maternal disproportion. Also, comparison of calf weight to thyroid weight in cases of suspect hyperthyroidism (goiter) may be useful. Reports of normal thyroid weight in calves vary from 6.5 to over 18 g.43 Further discussion on this subject can be found in the section on noninfectious causes of abortion.

Most aborted calves have no gross lesions. Small white/tan foci in the lungs, liver, and kidneys may be present and indicate necrosis or inflammation. The presence of fibrin on organ surfaces is helpful for confirming inflammation. Meconium on the perineum or in airways/stomach indicates fetal stress and anoxia, typically associated with placentitis or dystocia (Figure 54.12). Hemorrhage and fractures of shoulder and hip joints are most often seen as a result of dystocia.


Figure 54.12 Fetus and amnion (opened). The amniotic fluid and skin are stained yellow/brown due to meconium.

Photo courtesy of J. Cooley.

Slightly raised, white skin plaques that are firmly adherent, particularly around the eyes and face indicate fungal infection. Sometimes calves will have scattered white mineral on the hair, which is easily removed; this finding is not significant but must be distinguished from adherent fungal plaques (Figure 54.13). In calves born dead, the lungs are uninflated; they are uniformly dull red/plum, heavy, and sink in formalin (see Figure 54.4). In cases of dystocia where fetuses may have taken a partial breath, there may be incompletely inflated lungs; assess lung aeration in sections of cranial and caudal lobes by degree of the flotation in fixative/fluid. Make note of any milk in the stomachs, as this indicates colostrum consumption, which will interfere with bacteriological and serological findings.7


Figure 54.13 Fetus with white mineral grit present over the shoulder. Not to be confused with fungal dermatitis.

Photo courtesy of J. Edwards.

Necropsy method

It is best to have an abortion kit prepared beforehand; Table 54.4 enumerates materials to have in a kit. Zoonotic pathogens may be present, so always wear gloves, protective clothing, eye/face protection, and use careful technique when examining dams and fetal tissues. In addition, materials used in standard field necropsies are needed: clean water, bucket, brush, and disinfectant. Make sure to disinfect contaminated sites and equipment. If there are questions as to which samples are best to take, contact the diagnostic laboratory to which samples will be submitted for advice. Taking photographs of lesions is a relatively simple and excellent practice which will aid diagnosis.

Table 54.4 Contents for abortion kit.

Knife (15-cm boning) and steel
Nitrile/rubber gloves
String and ruler for measurements
Shears (small tree limb variety works well)
Culturette swabs
Overalls, washable apron, rubber boots
Alcohol swabs, syringes, needles to draw blood/fluids
Scalpel blades and handle
Red-top glass vacutainer tubes, purple-top EDTA tubes
Hatchet/cleaver and hacksaw
Sterile rat-tooth forceps and scissors
Styrofoam box/cooler for temporary specimen storage
Sterile containers/whirltop bags/ziplock bags, permanent pen
Fixative (10% neutral buffered formalin), at least 500 mL in plastic sealable container/jar

  1. Measure crown–rump length along the vertebral ridge (see above) and weigh fetus and placenta separately. Examine skin for exudate and abnormalities, around the eyes and face in particular for signs of fungal infection.
  2. Examine the body for congenital abnormalities, umbilical hernias, cleft palates, facial anomalies.
  3. Wash the surface of fetus with water to remove gross contaminants.
  4. With the left side down, reflect right legs with a knife and continue the incision from cranial to caudal, reflecting the skin to the dorsal and ventral midlines. Collect any pooled blood between incised tissue planes with a syringe if available (for serology).
  5. Open abdomen at the highest point along the caudal aspect of the ribs, being careful not to contaminate any peritoneal fluid or tissues. Aspirate any abdominal fluids with a sterile syringe, place in sterile tube, label, refrigerate. Continue the cut along the caudal aspect of the ribs, along the lumbar area, and cranial to the pelvis to expose the abdominal viscera. Note any lesions, and volume, character and color of fluids.
  6. Incise the diaphragm (noting if negative pressure is present) and cut the ribs at the costal angles and along the sternum; remove the chest wall. Aspirate any thoracic fluids with a sterile syringe, place in sterile tube, label, refrigerate. Note any lesions, and volume, character and color of fluids. The pleural surface of the removed chest wall may be used as a makeshift cutting board/sterile field for dissection.
  7. Aspirate fluids from the unopened abomasum with sterile syringe, place in sterile tube, label, refrigerate. Note the character of the abomasal fluid. Take samples of any other suspicious fluids at this time.
  8. Examine the body cavities and organs in situ, making note of fibrin, hemorrhages, or abnormally situated organs.
  9. Remove thoracic viscera from tongue to lung (pluck). Examine the mouth; one may split the mandibular symphysis with a knife. Incise the esophagus along the entire length; incise the dorsal tracheal membrane from the larynx to the bronchi. Examine the chest for any fractures. Slice multiple lung lobes, examining the cut sections for changes in the lobules and airways. Examine the thyroid gland. Collect tissues, especially lesions (see numbers 16 and 17).
  10. Examine the heart, making sure to inspect all four main valves and four chambers. Look for ventricular septal defects or other anomalies.
  11. Collect visceral organs, examining gastrointestinal tract last. Identify the kidneys, ureters, and urinary bladder. Remove the gastrointestinal tract by incising the root of the mesentery and continuing the cut to the diaphragm along the dorsum, avoiding the urinary tract. The tract may then be lifted out of the abdomen, leaving the colon attached and uncut. Collect tissues, especially lesions (see numbers 16 and 17).
  12. Remove the adrenal glands.
  13. Remove the urinary tract, making multiple slices through the kidneys. Identify genital organs.
  14. Serially section the liver and spleen.
  15. Open the forestomachs and abomasum, examine for content. Continue into the intestine, making several incisions along each major section (duodenum, jejunum, ileum, cecum, colon). Examine content and the mucosa.
  16. Collect organs (kidney, liver, lung, spleen, thymus, adrenal) in sterile bags (placenta kept in separate bag), refrigerate.
  17. Collect in formalin for histopathology: lung, liver, kidney, spleen, heart, adrenal glands, skeletal muscle (three to four sections including tongue, diaphragm), thyroid, ileum, skin (including eyelid), thymus, and mesenteric lymph node in 5-mm sections.
  18. Remove the head from the body at the atlanto-occipital joint. Harvest entire brain, even if severely autolyzed, and place whole in formalin. If the fetus is severely autolyzed, take a swab culture of the brain tissue prior to fixation. The skull is relatively soft and can be easily opened with a saw, making two cuts along the inner aspects of the occipital condyles, cranially (and somewhat laterally along the curve of the calvaria) toward the inner aspects of the orbital rims. Make a third incision across the orbital ridge, connecting the first two cuts. Pry the cranium from the skull in one piece. Place the brain in the palm of your hand and with a scalpel gently cut the nervous attachments of the base of the brain, allowing the brain to fall into your hand.
  19. Collect ocular fluid with a needle/syringe for nitrate/nitrite levels if needed, freeze.
  20. Open several joints, looking for purulent exudate, fibrin, and hemorrhage.
  21. Examine fetal membranes for exudates, lesions, abnormalities (see next section for detailed instruction). Remove dirt/debris from the membranes prior to sampling.
  22. Place two to three sections with cotyledons in a sterile bag, refrigerate; make impression smears of any lesions.
  23. Harvest the placenta for histopathology (at least three to four sections including cotyledons and intercotyledonary areas).
  24. Collect amniotic fluid if available, refrigerate.
  25. Collect dam blood in red top tube (herdmate blood samples may be collected as well; 10 cows or 10% of the herd has been suggested).

Examination of the membranes

Collect as much of the membranes as possible and carefully examine the chorioallantois and amnion, as lesions may be subtle, focal, and easily overlooked. In many cases, little if any placenta can be examined. It is important to try to verify if all membranes have been expelled. Because of the attachments of the amnion to the chorion, as well as the short umbilicus, calves will rupture and escape both the amnion and chorioallantois at delivery. Typically membranes are found with cotyledons on the outside.

The fetal membranes may be laid out lengthwise to identify the umbilicus and with it the internal aspect of the amnion. Examination of amniotic membranes and fluids is best done at this time. The umbilicus is composed of four muscular turgid vessels (arteries and veins) loosely enmeshed in slippery membranes. The gravid horn is easily identified as the larger half of the tissue, and should have larger placentomes. Avascular chorionic tips should be identified and inspected carefully, as true placental lesions may be present in the gravid horn near the tip.16 The umbilicus is continuous with the umbilical arteries and veins, which form a useful longitudinal axis by which to orient the placenta. From there the internal aspect of the allantoic cavity may be examined, with attention to the nature of any fluids present, thickness and color of membranes, and peculiar odors. Allantoic calculi are typically found at this time.

By placing the umbilical vessels at one side of the tissue, a lengthwise incision along the opposite side of the placenta will allow the placenta to be opened and laid flat, with the umbilical vessels forming the central axis (Figure 54.14). The horns are unequal in size, the gravid horn being much larger. In this way, vessels and cotyledon rows (normally four) may be examined thoroughly. Fresh cotyledons have a red velvety texture with a mildly irregular surface. The size variation, shape, color, consistency, and degree of cotyledon mottling should be noted, as well as degree of autolysis. Occasional small tags of attached caruncular tissue may be seen. Cotyledon margins are typically sharply defined, and the intercotyledonary chorion is white, translucent, and smooth. Adventitial placentation is a frequent finding that appears as small cotyledons or villous tuft formations adjacent to the placentomes that may cover the entire placenta.


Figure 54.14 Placental membrane examination method. (Left) The long axis of the chorioallantois is arranged perpendicular to the umbilical stalk. (Right) An incision is made along the dotted white line, allowing the chorioallantoic sac to be opened (direction of white arrow) and laid flat. In this way, the vascular axis, cotyledons, and membranes can be thoroughly examined.

Courtesy of Rachael Fishman.

Sample collection

A complete set of tissues should be collected in every case.44 Biological specimens must be properly collected, prepared, stored, and transported otherwise diagnostic accuracy will suffer. It is important to maintain aseptic technique despite apparent tissue contamination; this is necessary to maximize chances for diagnosis as well as for prevention of zoonotic infection. Microbiology samples are to be kept chilled and sent to the diagnostic laboratory as soon as possible in a Styrofoam cooler with ice packs for overnight courier shipping. If fresh tissue samples cannot be sent within 2–3 days, then freezing at –70 °C and delivering on dry ice is ideal.44 If necessary, specimens can be placed at –20 °C until dry ice can be obtained. Conventionally frozen tissues (–20 °C) are often acceptable for PCR testing of many pathogens. Abomasal and thoracic/pericardial fluid samples should be sent in sterile tubes without additives. Frozen fetal liver, lung, and kidney (2.5–5 cm chunks, –20 °C) should be kept for testing in case nutritional or toxicologic disease is suspected after initial examinations.39

Chilled or frozen tissues should be placed in sealed bags (whirlpack-type bags often leak), preferably with a secondary bag around them. Fluids shipped in glass tubes require ample padding in tight-fitting containers. Absorbent materials should also be included in the package to prevent soaking of the exterior, which complicates and may delay the shipping process. Disposable diapers are an effective option.39 Contact your diagnostic laboratory for proper packaging and shipping requirements for abortion samples as they may contain infectious and/or zoonotic agents.

Viruses may have very specific tissue tropisms and therefore require certain tissues for isolation. Specimens need to be collected as soon as possible as autolysis can be very damaging to virions. Virology samples for abortions are typically pooled, although placing tissues in separate bags is ideal. Placental tissues should be bagged separately. Do not pool samples from multiple abortions. Tissues should be kept cool but not frozen until arrival at the diagnostic laboratory. If tissues will not be immediately used, freezing at –70 °C is better than at –20 °C.39 If live viruses are sent packed in dry ice, be sure to place samples in airtight containers as the gaseous phase of dry ice is carbon dioxide, which can lower sample pH and inactivate some viruses. Certain laboratories may have preferences for virological samples, particularly if a certain pathogen is highly suspected.

Bacteriology tissue samples should be 2.5–5 cm per side in order that surfaces may be heat seared for proper culture. External and gut samples should not be bagged with internal organs. If samples are contaminated, sending a swab culture (Culturette) in addition to tissues may be helpful. For severely decomposed specimens, aseptically collected brain tissue may be useful for isolating pertinent organisms.22

Fungal sampling should at least include affected cotyledons; however it is best to send the entire placenta. Fetal infection is inconsistent, but lung, skin, and abomasal content are useful.

For histopathology, sections approximately 5 mm wide in 10% neutral buffered formalin are best. The brain, however, should be immersed whole in formalin, without dissection. If the brain is liquefied, fix separately. For small lesions, several foci should be submitted. For large lesions, a few sections including the margin with normal and abnormal tissues should be collected. Identify clearly any lesions seen in order to alert the diagnostician.

At least 10 volumes of formalin per volume of tissue is needed for proper fixation. Tissues should be allowed to fix for at least 24 hours, preferably 3 days. The brain in particular requires ample fixative over 3–4 days. Addition of 1 part ethanol to 9 parts formalin (10% ethanol, 90% formalin) may be used to prevent freezing in cold climates.45 If formalin is not available, 70% ethanol may be used. Tissues may be sent in formalin, otherwise fix tissues for 24 hours, drain, and send in bags with formalin-moistened gauze. Be sure to double-bag samples as containers may rupture in transit. Contact your diagnostic laboratory for instructions.

For blood samples, blood from the dam as well as the fetus is ideal. Fresh blood smears are particularly useful if anaplasmosis is suspected. Blood in EDTA is preferred for PCR testing. For serum samples, draw 8–10 mL of serum into tubes without additives, allow to sit for 1–2 hours until the clot begins to retract, then place in the refrigerator overnight. Centrifuge at 1000 × g for 10 min and decant serum; send in a separate sterile tube. One may freeze the serum (do not freeze whole blood) until needed.

Table 54.5 lists typical sample storage conditions.

Table 54.5 Fresh specimens collected for fetal and neonatal diagnostics.

Test Storage Specimens Notes
Bacteriology/mycology (culture, PCR) Keep refrigerated not frozen unless PCR only Stomach contents, pericardial fluid, liver, lung, brain, placenta Collect stomach contents or pericardial fluid in a syringe with a large-gauge needle
Package each specimen in separate containers
Virology (virus isolation, fluorescent antibody test, PCR) May be frozen (at –70 °C if necessary) Lung, liver, kidney, heart, blood, placenta Package each specimen in separate containers
Nutrition, toxicology May be frozen Liver, kidney, ocular fluid
Fetal/maternal fluids Keep refrigerated Dam serum/fetal fluids Paired (acute and convalescent) if possible


Arrival at an accurate diagnosis is the result of the cooperative efforts of the attending veterinarian and the diagnosticians at the laboratory. Even with the submission of proper samples, the establishment of a definitive diagnosis is problematic. Expulsion of a dead fetus often occurs hours to days after death; the resulting autolysis makes the difficult task of fetal lesion identification even more so. Fetal membranes, which may have the only significant lesions to be found, are often not present for examination. Also, in many cases examined tissues are severely contaminated, whether due to incomplete expulsion or from the environment. Finally, diagnostic laboratories run routine tests to identify well-known causes of abortion in a timely manner. As such, investigation of unusual or poorly understood etiologies is beyond their purview.17

Keep in mind that the majority of pregnancy wastage occurs at earlier stages of development, when expelled tissues are least likely to be noticed. Early gestation abortions are often detected only weeks after the fact, making investigation and diagnosis all but impossible. The majority of tissues examined by clinicians and diagnostic laboratories are of large fetuses, which may bias the interpretation of a herd problem where losses occur at various gestation stages. Late-stage abortions may be the result of injury many weeks prior to expulsion; they may not exhibit important or telling changes that could be present in earlier aborted fetuses, preventing accurate diagnosis. Worse yet, in an effort to find a cause, other coincident agents may be erroneously blamed, depending on what is found in the submitted fetus.6

It is important to realize that more than one disease or management problem may be at work in a herd, complicating the resolution of endemic problems. Multiple pathogens may be present; some may not be obvious while those that are readily evident may not be directly contributing to abortion. In these cases, determining the actual cause of abortion is challenging.

Serology results must be cautiously interpreted. A positive sample from a cow indicates exposure, which may or may not be relevant in light of vaccination status. Twofold to fourfold increases in titer over 2 weeks may be significant, particularly with herdmate samples for comparison.6 However, it is likely that dam serum antibody levels have reached their peak by the time abortion occurs, so it is not unexpected to see a lack of rise in titer 2–3 weeks later.24 Serology may be particularly useful in diagnosing BVDV, leptospirosis, anaplasmosis, and abortions where the agent is difficult to demonstrate by other methods.17 The presence of a specific antibody in fetal serum does not mean that particular agent is the cause of abortion; BVDV and Neospora caninum are two examples. Serology results must be carefully weighed with microbiology, histopathology, and herd history data. Table 54.6 lists common diagnostic tests for specific pathogens.

Table 54.6 Summary of diagnostic tests for bovine abortifacient pathogens.

Source: Njaa BL. Kirkbride’s Diagnosis of Abortion and Neonatal Loss in Animals, 4th edn, 2012.

Agent Preferred fetal tissues Preferred fetal diagnostic test Additional diagnostics
Bovine herpesvirus 1 Kidney, adrenal, liver, lung FA (frozen tissue), IHC, VI IHC of placenta if placentitis is present
Bovine viral diarrhea virus Lung, heart, kidney, placenta, skin FA, IHC, VI, PCR Antigen-capture ELISA, RT-PCR
Bluetongue virus Brain, spleen PCR, VI Fetal serology
Bunyaviruses None None Fetal/precolostral serology; congential abnormalities
Brucella Placenta, lung, abomasal content, uterine fluid Bacterial culture Culture of milk from dam; dam and fetal serology
Listeria Placenta, lung, brain, abomasal contents Bacterial culture, IHC Gram’s stain of freshly aborted tissues, PCR
Salmonella Placenta, liver, lung, abomasal contents Bacterial culture
Yersinia pseudotuberculosis Placenta, liver, lung, abomasal contents, intestines Bacterial culture
Leptospira Kidney, placenta FA (fetal kidney smear), IHC, PCR PCR of fetal urine; fetal and maternal serology
Ureaplasma Lung, abomasal content, placenta Ureaplasma culture, PCR
Campylobacter Lung, abomasal contents, placenta Campylobacter culture, IHC, darkfield microscopy Silver staining of histology tissues, PCR
Epizootic bovine abortion Thymus, spleen, lymph nodes Modified Steiner’s silver stain of histology slides, IHC Elevated fetal serum immunoglobulins
Chlamydophila Placenta PCR, IHC, FA Macchiavello’s, Gimenez, or modified acid-fast stains of histology slides
Coxiella burnetii Placenta PCR, IHC Macchiavello’s, Gimenez, or modified acid-fast stains of histology slides
Fungi Placenta, abomasal contents, lung, skin lesions Fungal culture, H&E Direct identification by KOH wet mounts of skin or placenta or GMS and PAS stained histology slides
Tritrichomonas Placenta, abomasal contents, lung Tritrichomonas culture, Bodian’s silver stain of histology slides, IHC, H&E Darkfield microscopy of abomasal contents, PCR
Neospora Brain, lung, kidney, skeletal muscle, liver, placenta IHC, PCR Fetal serology (IFA, microagglutination titer, ELISA)
Sarcocystis Brain, lung, liver, kidney, skeletal muscle, placenta IHC Genomic probe; ribosomal RNA assays

ELISA, enzyme-linked immunosorbent assay; FA, fluorescent antibody test; GMS, Gomori–methenamine silver stain; H&E, standard histopathology stains; IFA, indirect fluorescence test; IHC, immunohistochemistry (usually formalin-fixed tissues); KOH, potassium hydroxide test; PAS, periodic acid–Schiff stain; PCR, polymerase chain reaction; RT-PCR, reverse transcription PCR; VI, virus isolation.

Specific manifestations of the conceptus relating to pathology


Mummification is an uncommon event in which there is often no certain cause. It is the process of progressive dehydration and compaction of a sufficiently mature dead fetus in utero. In order for this to occur, bacterial infection (tissue lytic organisms) of the dead fetus must be absent, no air can be present in the uterus (closed cervix), and a functional CL must be present. The time course, which may take months, depends on the size of the fetus. This process generally occurs in the second and third trimesters, when fetal bones are sufficiently developed to resist resorption. As fetal fluids are absorbed, tissues become compressed, shrunken, red/brown, and sticky to dry, without odor. As the membranes atrophy and the uterus involutes, hemorrhage occurs between the uterus and fetal tissues, imparting the red “hematic” sticky material onto the tissues (Figures 54.15 and 54.16). This hematic type of mummification apparently is distinctly bovine.11,27


Figure 54.15 Opened uterus with mummified fetuses. Friable, nonodorous, hematic material obscures the fetuses.

Photo courtesy of J. Edwards.


Figure 54.16 Fetal mummy. The carcass is shrunken and contracted with diffuse red/brown discoloration, dry tissues, and sunken eyes. Tissues lack odor and emphysema.

Photo courtesy of J. Edwards.

The uterus tightly wraps around the fetal materials, compacting the mummy. The longer this proceeds, the drier and firmer the fetus becomes, remaining in utero for as much as 2 years. In the cow, mummification is most common at the end of the first and beginning of the second trimesters.46 Various infectious and noninfectious etiologies have been implicated in their occurrence (BVDV, tritrichomoniasis), but the cause is usually unknown.10,16 Mummification may be associated with certain breeds (Guernsey, Jersey) or certain breeding/genetic combinations.11 In cases of uncomplicated mummification, prognosis is good for return to fertility.27


Maceration describes the effect of dead fetal tissue softening due to fluid soaking and saprophytic digestion in utero (Figure 54.17). In cattle this is due to exposure of the retained fetal tissues to bacteria. This occurs when there is failure of fetal expulsion after death with retention of the carcass partially or entirely within the uterus. The bacteria may be those that caused fetal death or those that arrive through an open cervix.10 Maceration is distinct from autolysis, which is digestion of tissues by endogenous enzymes and requires no bacteria. When bacteria gain access to a dead fetus in the reproductive tract, they are able to multiply rapidly at body temperature and are relatively insulated from the dam’s immune system. Bacterial digestion of tissues and gas formation (emphysema) ensues. The uterus surrounds the fetus and there is an intense metritis.


Figure 54.17 Opened uterine horn with a macerated fetus. Bone fragments in purulent fluid remain. The ovary has a retained corpus luteum.

Photo courtesy of J. Cooley.

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Aug 24, 2017 | Posted by in GENERAL | Comments Off on Fetal Disease and Abortion

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