Chapter 3 Diseases of the newborn
This chapter considers the principles of the diseases that occur during the first month of life in animals born alive at term. Diseases causing abortion and stillbirth are not included. The specific diseases referred to are presented separately under their own headings.
The inclusion of a chapter on diseases of the newborn, and at this point in the book, needs explanation. The need for the chapter arises out of the special sensitivities which the newborn have:
• Their immunological incompetence
• Their dependence on adequate colostrum containing adequate antibodies at the right time
• Their dependence on frequent intake of readily available carbohydrate to maintain energy
• Their relative inefficiency in maintaining normal body temperature, upwards or downwards.
All these points need emphasizing before proceeding to the study of each of the body systems.
There are no particular aspects of a clinical examination that pertain only to or mostly to neonates. It is the same clinical examination as is applied to adults, with additional, careful examination for congenital defects and diseases, which may involve the umbilicus, the liver, the heart valves, the joints and tendon sheaths, eyes and meninges. Although one should avoid any suggestion that an examination of an adult could be cursory, it is necessary to ensure that an examination of a newborn animal is as complete as practically possible. This is partly for an emotional reason: the neonate always evokes a sentimental reaction. It is also important for the economic reason that in most species the offspring, when already on the ground, represents a very considerable part of the year’s investment and productivity. There is also the much greater susceptibility to infectious disease, dehydration and death, and diagnosis and treatment must be reasonably accurate and rapid. Supportive therapy in the form of fluids, electrolytes and energy and nursing care are especially important in the newborn in order to maintain homeostasis.
One of the difficulties in the study of these diseases is the variation in the type of age classification that occurs between publications, which makes it difficult to compare results and assessments. The term perinatal is usually used to describe morbidity or mortality that occurs at birth and in the first 24 hours of life. The term neonatal is usually used to describe morbidity or mortality between birth and 14 days. However, there is variation in the use of these terms. To ensure that our meanings are clear, we set out below what we think is the most satisfactory classification of all the diseases of the fetus and the newborn, which is adapted from a scheme proposed for lambs. The importance of this type of classification is with the assessment of risk for a given type of disease and in the prediction of likely causes that should be investigated by further examinations. This approach is not of major importance in the assessment of disease in an individual animal, although it is of importance in helping establish the priority in diagnostic rule-outs. The classification is, however, of considerable value in the approach to perinatal morbidity and mortality in large flocks or herds where an assessment of the age occurrence of morbidity and mortality can guide subsequent examinations to the probable group of cases, with optimal expenditure of investigative capital.
These are diseases of the fetus during intrauterine life, e.g. prolonged gestation, intrauterine infections, abortion, fetal death with resorption or mummification, goiter.
These are diseases associated with dystocia, causing cerebral anoxia or fetal hypoxemia, and their consequences and predispositions to other diseases; injury to the skeleton or soft tissues and maladjustment syndrome of foals are also included here.
These are divided into early, delayed and late types:
• Early postnatal disease (within 48 hours of birth). Deaths that occur during this period are unlikely to be caused by an infectious disease unless it has been acquired congenitally. Most diseases occurring in this period are noninfectious and ‘metabolic’, e.g. hypoglycemia and hypothermia due to poor mothering, hypothermia due to exposure to cold, low vigor in neonates due to malnutrition. Congenital disease will commonly manifest during this period but may sometimes manifest later. Infectious diseases are often initiated during this period but most manifest clinically at a later age because of their incubation period; some, e.g. navel infection, septicemic disease and enterotoxigenic colibacillosis, have a short enough incubation to occur during this period
• Delayed postnatal disease (2–7 days of age). Desertion by mother, mammary incompetence resulting in starvation and diseases associated with increased susceptibility to infection due to failure of transfer of colostral immunoglobulins (the predisposing causes to these occur in the first 12–24 hours of life). Examples include colibacillosis, joint ill, lamb dysentery, septicemic disease, most of the viral enteric infections in young animals, e.g. rotavirus and coronavirus
• Late postnatal disease (1–4 weeks of age). There is still some influence of hypogammaglobulinemia, with late-onset enteric diseases and the development and severity of respiratory disease in this period, but other diseases not directly associated with failure of transfer of immunoglobulins such as cryptosporidiosis, white muscle disease and enterotoxemia start to become important.
Diseases of the newborn and neonatal mortality are a major cause of economic loss in livestock production. In cattle, sheep and pigs the national average perinatal mortalities exceed by far the perinatal mortality experienced in herds and flocks with good management. In these species the identification of the management deficiencies that are the cause of a higher than acceptable mortality in a herd or a flock is a most important long-term responsibility of the practicing veterinarian and, in most instances, is more important than the identification of the causal agent or the short-term treatment of individual animals with neonatal disease. In contrast, in horses the individual is of extreme importance and the primary thrust is in the treatment of neonatal disease.
All animals must be born close to term if they are to survive in a normal farm environment. Minimal gestational ages for viability (in days) for each of the species are:
Neonatal lamb mortality is one of the major factors in impairment of productivity in sheep-raising enterprises around the world.1-3 Mortality can obviously vary with the management system (intensive versus extensive lambing, highly supervised versus minimally supervised, variations in the provision of shelter, etc.), and according to whether there is a particular disease problem in a given flock. Nonselective mortality surveys have shown population mortality rates in lambs, from birth to weaning, that vary from 9–35% and there are flocks that may exceed this upper figure in the face of a major problem. In well-managed flocks neonatal mortality is less than 10% and in some is below 5%. The majority of neonatal mortality is due to noninfectious disease.
Surveys from various sheep-raising areas in the world consistently show that the majority of lamb mortalities can be attributed to three main causes:1-4
These syndromes have a multifactorial etiology but can account for over 65% of the mortality that occurs in the first few days of life.4,5
Infectious abortion can cause considerable fetal, parturient and postnatal mortality in infected flocks but it is a relatively minor cause of perinatal mortality overall. In contrast to other large animal species, abortion storms in sheep are often accompanied by significant mortality in liveborn animals. Many agents associated with abortion in ewes produce placentitis and cause abortion in late pregnancy. This frequently results in the birth of liveborn, growth-retarded and weak lambs that die during the first few days of life. Any investigation of perinatal mortality in sheep should also consider the presence of agents causing abortion, although abortion and the birth of dead lambs is always prominent in abortion outbreaks.
Stillbirth occurs largely as a result of prolonged birth and fetal hypoxemia. Prolonged birth and dystocia is a particular problem in large single lambs.6 Higher rates of stillbirth can also occur in flocks that are in poor condition. Prolonged birth is a major risk factor for subsequent postnatal disease.4
The hypothermia/exposure/hypoglycemia/starvation complex is the most important cause of postnatal disease. The determinants for the occurrence of this complex are the birth size of the lamb, the energy reserves of the lamb, and environmental factors at birth and during the following 48 hours which influence heat loss. These include environmental temperature, wind velocity and evaporative cooling determined by the wet coat of the lamb at birth or the occurrence of rain.
Birth size is determined by the nutrition and genetics of the ewe, and by litter size which is also determined by the parity and genetics of the ewe. Reflecting these influences, most surveys of neonatal mortality in lambs show:
• A significant association between the body condition score or nutrition of the late pregnant ewe and perinatal mortality
• A relation between birth weight and mortality (depending upon the breed, a birth weight of less than 2.5–3.0 kg has increased risk for death)
• A higher mortality in lambs from multiparous ewes
• A pronounced effect of litter size, with mortality in lambs born as triplets being higher than in those born as twins, which in turn is higher than that in lambs born as singles.
These relationships can be confounded by an increase in mortality in large-birth-weight lambs born as singles because of dystocia and by the greater mortality in lambs born to maiden ewes associated with poor mothering and desertion.
Environmental factors of temperature, wetness and wind also confound the above relationships; their influence varies according to the management system.
The identification of the above determinants of mortality is of more than academic value as almost all can be changed by the identification of at-risk groups and the institution of special management procedures, or by the identification and mitigation of adverse environmental factors.
Infectious disease can be important in some flocks and occurs after 2 days of age. The major infectious diseases of lambs that cause mortality are enteritis and pneumonia.7 Their prevalence varies with the management system – enteric disease and liver abscess are more common in shed lambing systems than with lambing at pasture.8 Risk for pneumonia is greatest in very light or heavy lambs and in lambs from maiden ewes and ewes with poor milk production.9
Other factors can be important in individual flocks or regions. Lambs found dead or missing may account for significant losses under some conditions, such as mountain or hill pastures.2 Predation, or predation injury, is an important cause of loss in some areas of the world and, depending upon the region, can occur from domestic dogs, coyotes, birds or feral pigs. Poor mothering and an inability of the ewe to gather and bond to both lambs of twins can be a problem in Merinos and can cause permanent separation of lambs from the ewe and subsequent death from starvation.
Management at lambing can also influence the patterns of mortality. Intensive stocking at the time of lambing to allow increased supervision can allow a reduction in mortality associated with dystocia and the hypothermia/exposure/hypoglycemia/starvation complex. It can ensure the early feeding of colostrum to weak lambs but it can also result in a greater occurrence of mismothering associated with the activities of ‘robber’ ewes and it also increases the infection pressure of infectious agents, resulting in an increased incidence of enteric and other disease.7
Mortality rate can differ between breeds and lambs from crossbred dams may have higher survival rates.
Simple systems for recording, determining and evaluating the major causes of lamb mortality in a flock, for determining the time of death in relation to birth and relating the deaths to the weather and management system are available.4,10 These systems of examination are effective in revealing the extent of lamb losses and the areas of management that require improvement and are much more cost-effective than extensive laboratory examinations, which may give little information on the basic cause of the mortality. More intensive examination systems that combine these simple examinations with selected biochemical indicators of determinant factors are also described.5
A 1992 review of publications on calf mortality reported mortality rates in dairy calves that varied from a low of approximately 2% to a high of 20% with mortality on individual farms varying from 0–60%.11 A survey of calf mortality in 829 dairy operations in the USA showed considerable variation with region and with management system.12 The best estimate for the average on-farm calf mortality rate is 6%.11 This mortality is in addition to that associated with stillborn or weak-born calves which is reported to occur in 11% of primiparous and 5.7% of multiparous Holstein cows in the USA.13
The exact cause of death in these stillborn or weakborn calves is not known. In addition to the influence of parity, dystocia has a major influence on rates and rates are also higher where gestation length was shorter than 280 days. Calving-associated anoxia may be an important contributing factor in these deaths.14
Mortality in twin-born calves is approximately three times that of single-born calves. Disease morbidity rates also vary with the farm and, as might be expected, with the disease under consideration and the age of the calf.12,15,16
Fetal disease and the postnatal septicemic, enteric and respiratory diseases are the most common causes of loss.
Definition of fetal loss and abortion varies between studies but the median frequencies of observed abortions is approximately 2% and of fetal loss in dairy cattle diagnosed pregnant 6.5%.17 The majority of these have no diagnosed cause.
Calving in dairy cattle is usually supervised, but prolonged calving with consequent hypoxemia (and occurring with or without dystocia) and twin birth is associated with significantly higher risk for mortality in the first 21 days of life.12,18,19
Calves are at highest risk for death in the first 2 weeks of life and especially in the first week. Septicemic and enteric disease are most common during this period, with respiratory disease being more common after 2 weeks of age.14,20,21 Failure of transfer of colostral immunoglobulins is a major determinant of this mortality.12 The economic significance of neonatal disease can be considerable and the occurrence of disease as a calf can also subsequently affect days to first calving intervals and long-time survival in the herd.14,22 Death also causes a loss of genetic potential both from the loss of the calf and the reluctance of the farmer to invest in higher-price semen in the face of a calf mortality problem.
Meteorological or seasonal influences may have an effect on dairy calf mortality rate and this can vary with the region. In cold climates during the winter months, an increase in mortality may be associated with the effects of cold, wet and windy weather, whereas in hot climates there may be an increase in mortality during the summer months in association with heat stress.
Management is a major influence and in well managed dairy herds calf mortality usually does not exceed 5% from birth to 30 days of age. Risk factors for disease morbidity and mortality in dairy calves relate to the infection pressure to the calf and factors that affect its nonspecific and specific resistance to disease. It is generally recognized that mortality is associated with the type of housing for calves, calving facilities, the person caring for the calves and attendance at calving. Thus calves that are born in separate calving pens have a lower risk of disease than those born in loose housing or stanchion areas23 and the value of good colostrum feeding practices is apparent.11,12 Studies on the role of calf housing and the value of segregated rearing of calves in reducing infection pressure generally show beneficial health results7,21,24,25 but the value of this system of rearing is probably best measured by its adoption in many dairies where climatic conditions allow this to be an option for housing young calves. The quality of management will be reflected in rates of failure of transfer of passive immunity and will also affect the infection pressure on the calf during the neonatal period. Quality of management is very hard to measure but is easily recognized by veterinary practitioners.
The epidemiological observations that calf mortality is lower when females or family members of the ownership of the farm manage the calves, rather than when males or employees perform these duties, is probably a reflection of this variation in quality of management and suggests that owner–managers and family members may be sufficiently motivated to provide the care necessary to ensure a high survival rate in calves. Even so, calf health can be excellent with some hired calf-rearers and very poor with some owner calf-rearers. Besides visual assessments of hygiene an effective measure of the quality of calf management can be provided by a measure of rates of failure of transfer of passive immunity.
Mortality in beef herds is usually recorded as birth to weaning mortality and has ranged from 3–7% in surveys, with higher rates in calves born to heifers; significantly higher mortality can occur in herds with disease problems.26-31 The majority of this mortality occurs within the first week of life and most of it occurs in the parturient or immediate postnatal period as a result of prolonged birth or its consequences.30-32
Dystocia resulting in death is common and dystocial calves, twin-born calves and calves born to heifers are at greater risk for postnatal disease.31-34 Enteric and respiratory disease occurs in outbreaks in some years and very cold weather can result in high loss from hypothermia. In a survey of 73 herds in the USA the overall mortality rate was 4.5% and causes were dystocia (17.5%), stillbirths (12.4%), hypothermia (12.2%), enteric disease (11.5%) and respiratory infections (7.6%).31
Abortion rates appear to be lower than in dairy cattle, usually less than 1%.30 The majority of these are not diagnosed as to cause but of those that are, infectious abortion is the most common diagnosis.35
Accurate prospective and retrospective studies have shown that 50–60% of the parturient deaths in beef calves are associated with slow or difficult birth and that the mortality rate is much higher in calves born to heifers than from mature cows.26,30,32 Dystocial birth can lead to injury of the fetus and to hypoxemia and may not necessarily be associated with fetal malposition. Birth size is highly heritable within all breed types of cattle36 and perinatal mortality will vary between herds depending upon their use of bulls with high ease of calving ratings in the breeding of the heifer herd. Milk fever and over-fatness at calving are other preventable causes. Selective intensive supervision of calving of the heifer herd can also result in a reduction of perinatal mortality.
Scours and pneumonia are the next most important causes of mortality in beef calves, followed by exposure to extremely cold weather or being dropped at birth into deep snow or a gully. The incidence of diarrhea is greatest in the first 2 weeks of life and there is considerable variation in incidence between herds.37 However, explosive outbreaks of diarrhea or exposure chilling can be significant causes of mortality in certain years.29 The purchase of a calf for grafting, often from a market, is a significant risk for introduction of disease to a herd.
Body condition score of the dam can influence calf mortality, with high condition scores having a higher risk for dystocial mortality and low scores for infectious disease. Mortality from diarrhea is often higher in calves born to heifers, possibly because heifers are more closely congregated for calving supervision or because of a higher risk for failure of transfer of passive immunity in this age group. Congenital abnormalities can be an occasional cause of mortality in some herds.27
Preweaning mortality ranges from 5–48%, with averages ranging from 12–19%, of all pigs born alive.38,39 More than 50% of the preweaning losses occur before the end of the second day of life. Mortality increases as the mean litter size increases and as the mean birth weight of the pig decreases. In most herd environments the minimal viable weight is approximately 1 kg. The mean number of piglets weaned is related to the size of the litter up to an original size of 14 and increases with parity of sows up to their fifth farrowing. Preweaning mortality is negatively correlated with herd size and farrowing crate utilization, and positively correlated with the number of farrowing crates per room.39
Surveys of neonatal mortality in piglets have repeatedly indicated that the most important causes of death in piglets from birth to weaning are noninfectious in origin.38-40 The major causes are starvation and crushing (75–80%) (although these may be secondary to, and the result of, hypothermia), congenital abnormalities (5%) and infectious disease (6%). The major congenital abnormalities are congenital splayleg, atresia ani and cardiac abnormalities. Infectious diseases may be important on certain individual farms but do not account for a major cause of mortality.
Fetal disease rates in most herds are low unless there is an abortion storm or poor control of endemic infections such as parvovirus. In contrast to other species, the majority of abortions are diagnosed and are infectious.
Stillbirths account for 4–8% of all deaths of pigs born and 70–90% are type II or intraparturient deaths, in which the piglet was alive at the beginning of parturition. The viability of newborn piglets can be accurately evaluated immediately after birth by scoring skin color, respiration, heart rate, muscle tone and ability to stand. Stillbirths are more commonly born in the later birth orders of large litters and it is a relatively common practice for sows to be routinely given oxytocin at the time of the birth of the first piglet in order to shorten parturition. Controlled trials have shown that, while oxytocin administration at this time will result in a significant decrease in farrowing time and expulsion intervals there is a significant increase in fetal distress, fetal anoxia and intrapartum death and an increase in piglets born alive with ruptured umbilical cords and meconium staining.41
The large percentage of mortality caused by crushing and trampling probably includes piglets that were starved and weak and thus highly susceptible to being crushed. The estimated contribution of crushing and starvation to neonatal mortality varies from 50–80%. The body condition score of the sow at the time of farrowing, the nursing behavior of the sow, her ability to expose the teats to all piglets and the sucking behavior of the piglets have a marked effect on survival.42
Cold stress is also an important cause of loss and the provision of a warm and comfortable environment for the newborn piglet in the first few days of life is critical. The lower critical temperature of the single newborn piglet is 34°C (93°F). When the ambient temperature falls below 34°C (93°F) the piglet is subjected to cold stress and must mobilize glycogen reserves from liver and muscle to maintain deep body temperature. The provision of heat lamps over the creep area and freedom from draughts are two major requirements.
Minimizing the mortality rate of newborn piglets will depend on management techniques, which include:
• Proper selection of the breeding stock for teat numbers, milk production and mothering ability
• The use of farrowing crates and creep escape areas to minimize crushing injuries
• Surveillance at farrowing time to minimize the number of piglets suffering from hypoxia and dying at birth or a few days later
• Batch farrowing, which allows for economical surveillance
• Fostering to equalize litter size
• Cross-fostering to equalize non-uniformity in birth weight within litters
• Artificial rearing with milk substitutes containing purified porcine gammaglobulin to prevent enteric infection.41
Foals are usually well supervised and cared for as individual animals. Neonatal death is less frequent than in other species but equivalent rates of morbidity and mortality occur on some farms.43 Infectious disease is important, along with structural and functional abnormalities that are undoubtedly better recognized and treated than in any of the other large animal species. In a large survey of thoroughbred mares in the UK, only 2% of newborn foals died;44 only 41% of twins survived and 98% of singles survived. In contrast, a mortality rate of 22% between birth and 10 days is recorded in an extensively managed system.45 Between 25–40% of mares that are bred fail to produce a live foal46 and an extensive study of breeding records indicated that 10% of mares that are covered either aborted or had a nonsurviving foal.47
This is a major cause of loss and in one study infections accounted for approximately 30% of abortions.46 In a retrospective study of 1252 fetuses and neonatal foals submitted for postmortem examination over a 10-year period in the UK, equine herpes virus and placentitis accounted for 6.5% and 9.8% of the diagnoses respectively.48 The placentitis occurred in late gestation and was concentrated around the cervical pole and lower half of the allantochorion associated with ascending chronic infections of bacteria or fungi resident in the lower genital tract.
Neonatal asphyxia, dystocia, placental edema and premature separation of the placenta, umbilical cord abnormality and placental villous atrophy are other important causes of mortality in this period. In the UK study48 umbilical cord disorders accounted for 38.8% of the final diagnoses. Umbilical cord torsion usually resulted in death of the fetus in utero but the long cord/cervical pole ischemia disorder resulted in intrapartum death and a fresh fetus with lesions consistent with acute hypoxia.
Postnatal disease causing mortality from birth to 2 months of age includes: lack of maturity 36%, structural defect 23%, birth injury 5%, convulsive syndrome 5%, alimentary disorder 12%, generalized infection 11% and other (miscellaneous) 9%. Of the infectious diseases, gastrointestinal and septicemic disease have greatest importance.49,50 Whereas in the past many of these conditions would have been fatal, there have been significant advances in the science of equine perinatology in the 1980s and 1990s and protocols for the treatment of neonatal disease have been developed that have been based on equivalents in human medicine. These have proved of value in the management and treatment of prematurity, immaturity, dysmaturity and neonatal maladjustment syndromes in newborn foals, as well as in enteric and septicemic disease. Different levels of intensive care have been defined that start from those that can be applied at the level of the farm and increase in sophistication, required facilities and instrumentation to those that are the province of a specialized referral hospital. Early followup studies indicate that this approach is of considerable value in foals with neonatal disease and that most surviving foals become useful athletic adults.51
The following protocol is a generic guide to the investigation of deaths of newborn animals. It will require modification according to the species involved.
1. Determine the duration of pregnancy to ensure that the animals were born at term
2. Collect epidemiological information on the problem. Where possible, the information should include the following:
3. Conduct a postmortem examination of all available dead neonates. The determination of body weight is essential and measures of crown–rump length can also give an indication of gestational age. In order of precedence the purpose of the postmortem examination is to determine:
4. If abortion is suspected, specimens of fetal tissues and placenta are sent for laboratory examination. Examinations requested are pathological and microbiological for known pathogens for the species of animal under consideration
5. A serum sample should be collected from the dam for serological evidence of teratogenic pathogens followed by another sample 2 weeks later. Samples from unaffected dams should also be submitted. A precolostral serum sample from affected animals may assist in the diagnosis of intrauterine fetal infections
6. Investigate management practices operating at the time, with special attention to clemency of weather, feed supply, maternalism of dam and surveillance by the owner – all factors that could influence the survival rate.51,52 Where possible, this should be performed using objective measurements. For example, in calf-rearing establishments the efficacy of transfer of colostral immunoglobulins should be established by the bleeding of a proportion of calves and actual measurement; food intake should be established by actual measurement, etc.
Edwards BL. Causes of death in new-born pigs. Vet Bull. 1972;42:249.
Randall GCB. Perinatal mortality. Some problems of adaptation at birth. Adv Vet Sci. 1978;22:53.
English PR, Morrison V. Causes and prevention of piglet mortality. Pig News Info. 1984;4:369-376.
Rossdale PD, Silver M, Rose RJ. Equine perinatal physiology and medicine. Equine Vet J. 1984;4:225-398.
Rook JS, Scholman G, Wing-Procter S, Shea M. Diagnosis and control of neonatal losses in sheep. Vet Clin North Am Food Anim Pract. 1990;6:531-562.
Haughey KC. Perinatal lamb mortality: its investigation, causes and control. J South Afr Vet Assoc. 1991;62:78-91.
Rossdale PD, McGladdery AJ. Recent advances in Equine neonatology. Vet Annu. 1992;32:201-208.
Kasari TR, Wikse SE. Perinatal mortality in beef herds. Vet Clin North Am Food Anim Pract. 1994;10:1-185.
Edwards SA. Perinatal mortality in the pig: environmental or physiological solutions. Livestock Prod Sci. 2002;78:3-13.
Herpin P, Damon M, Le Dividitch J. Development of thermoregulation and neonatal survival in pigs. Livestock Prod Sci. 2002;78:25-45.
Mellor DJ, Stafford KJ. Animal welfare implications of neonatal mortality and morbidity in farm animals. Vet J. 2004;168:118-133.
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2 Morrison D, Young J. Aust J Agric Res. 1991;42:227.
3 Gumbrell RC. Surveillance NZ. 1985;12:5.
4 Haughey KG. J South Afr Vet Assoc. 1991;62:78.
5 Barlow RM, et al. Vet Rec. 1987;120:357.
6 Wooliams C, et al. J Agric Sci. 1983;100:553.
7 Binns SH, et al. Prevent Vet Med. 2001;52:287.
8 Greene LE, Morgan KL. Prevent Vet Med. 1994;21:19.
9 Nash ML, et al. Small Rumin Res. 1997;26:53.
10 Eales FA, et al. Vet Rec. 1986;118:227.
11 Bruning-Fann C, Kaneene JB. Vet Bull. 1992;62:399.
12 Wells SJ, et al. Prevent Vet Med. 1996;29:9.
13 Meyer CL, et al. J Dairy Sci. 2000;83:2657.
14 Szenci O. Vet Bull. 2003;73(7):7R.
15 Curtis CR, et al. Prevent Vet Med. 1988;5:293.
16 Waltner-Toews D, et al. Prevent Vet Med. 1986;4:125. 137 & 159
17 Forar AL. Theriogenology. 1995;43:989.
18 Szenci O, et al. Vet Q. 1988;10:140.
19 Cross S, Soede N. Aust Vet J. 1988;42:8.
20 Sivula NJ, et al. Prevent Vet Med. 1996;27:155.
21 Svensson C, et al. Prevent Vet Med. 2003;58:179.
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23 Curtis CR, et al. Prevent Vet Med. 1988;6:43.
24 Quigley JD, et al. J Dairy Sci. 1995;78:893.
25 Quigley JD, et al. J Dairy Sci. 1994;77:3124.
26 Berger PJ, et al. J Anim Sci. 1992;70:1775.
27 Bellows RA, et al. Theriogenology. 1988;28:573.
28 McDermott JJ, et al. Can Vet J. 1991;32:407. 413
29 Olson DP, et al. Bovine Pract. 1989;24:4.
30 Toombs RE. Vet Clin North Am Food Anim Pract. 1994;10:137.
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Congenital defects
Etiology Genetic, infectious, toxic and physical causes are recognized for some defects but the etiology of most is not known
Epidemiology Low but significant incidence in all animals. Epidemiology depends on cause
Clinical findings Congenital defects can be structural or functional. Clinical signs depend on organ system(s) affected
Clinical pathology Specific serological and chemical tests can be used in the diagnosis and control of some congenital disease and, if available, are detailed under specific disease headings
Necropsy findings Specific to the particular problem
Diagnostic confirmation Abnormalities of structure or function that are present at birth are obviously congenital defects. They may or may not be inherited, and inherited defects may or may not be manifest at birth
Control Avoidance of exposure to teratogenic agents. Vaccination for some teratogenic infections, identification of carriers for genetic defects
Congenital disease can result from defective genetics1,2 or from an insult or agent associated with the fetal environment. A neonate with a congenital defect is an adapted survivor from a disruptive event of a genetic or environmental nature or of a genetic–environmental interaction at one or more of the stages in the sequences of embryonic and fetal development.3
Genetic abnormalities, detailed in Chapter 35, may result in a wide spectrum of disorder that can vary from severe malformations with deformation to the presence of inborn errors of metabolism in animals that may be born apparently normal and develop storage disease later in life.3
Susceptibility to injurious environmental agents depends upon the nature and the severity (dose size and duration of application) of the insult, and decreases with fetal age. Prior to attachment, the zygote is resistant to teratogens but susceptible to chromosomal aberrations and genetic mutations. Agents that disrupt blastula and gastrula stages and that interfere with normal apposition of the uterine mucosa are usually embryotoxic and induce early embryonic death.
The period during which an organ system is being established is a particularly critical period for that system and different teratogens, if applied at that time, can produce similar defects. One example would be the complex of arthrogryposis and cleft, which can occur in the calves of cattle grazing certain species of lupine,4 in calves infected in utero with Akabane virus5 and as an inherited disease in Charolais calves.6
Many noninherited congenital defects in animals occur in ‘outbreaks’, which is a reflection of the exposure of the pregnant herd to a viral, plant or other teratogen during a period of fetal susceptibility. Because this occurs in early pregnancy it is often very difficult to determine the nature of this exposure at the time the animals are born.
Some teratogens are quite specific in the defect that they produce and their action may be limited to a single species; a tentative diagnosis as to cause can be based on this association. Others produce a wide variety of abnormality that may also occur with other teratogens and cause is less obvious.
The exact etiology of most congenital defects is unknown. Influences that are known to produce congenital defects are presented here.
Most chromosomal abnormalities are associated with poor fertility and early embryonic death.7 A few are structural or numerical aberrations of chromosomes. The importance of chromosomal abnormality to congenital defects in farm animals has not been studied extensively but a study of 55 aborted and stillborn calves found six with an abnormal chromosome component.8 Chromosomal abnormality is usually associated with multiple deformations.8-11 Most chromosomal abnormalities are mutant genes and the majority are inherited as recessive traits. There are many examples among domestic animals (see Ch. 35).
Members of the Bunyavirus (Akabane virus, Cache valley virus and Rift Valley fever virus), Orbivirus (bluetongue virus, epizootic hemorrhagic disease virus and Chuzan virus), Pestivirus (bovine virus diarrhea virus, border disease virus, hog cholera virus) families, Japanese B encephalitis virus and Wesselsbron virus are recognized teratogens.12 Other viruses also can result in fetal death without malformation. Examples are as follows:
• Akabane virus – this infection of pregnant cattle, sheep and goats causes arthrogryposis, microencephaly and hydrocephalus.12 Infection of, and disease of, the fetus depends on the stage of pregnancy and the fetus’s immunological status. In cattle infected between 76–104 days of pregnancy hydranencephaly predominates; arthrogryposis predominates with infections between 104–173 days gestation and poliomyelitis after 173 days. In sheep the window of susceptibility for congenital defects is between 30 and 50 days
• Cache valley virus – congenital infection of lambs with Cache valley virus13 produces disease very similar to that produced by Akabane virus in cattle. The period of susceptibility for congenital defects is 36–45 days of pregnancy
• Rift valley fever virus infection of pregnant sheep results in placentitis and abortion but attenuated vaccine strains produce arthrogryposis and brain defects
• Bluetongue virus – vaccination of ewes with attenuated vaccine virus between days 35 and 45 of pregnancy causes a high prevalence of porencephaly in lambs. Natural infections of sheep (50–80 days of gestation) and cattle (60–120 days of gestation) can result in fetal death and resorption, or the birth of stillborn and weakborn animals and animals with hydrocephalus and hydranencephaly and occasionally arthrogryposis. Similar defects are produced by Chuzan, Aino and Kasba virus infections
• Bovine virus diarrhea – infection with cytopathogenic strains before 100 days can result in abortion and mummification, cerebellar hypoplasia and optic defects, including cataracts, retinal degeneration and hypoplasia and neuritis of the optic nerves. Other defects are brachygnathia, curly coats, abortion, stillbirth and mummification. Infection of the bovine fetus between 45 and 125 days of gestation with a noncytopathic biotype of the virus can result in the development of a persistently viremic and immunotolerant calf that is carried to term, born alive, remains persistently viremic and may later develop mucosal disease
• Border disease virus – the window of susceptibility is from 16–90 days gestation, and, depending upon the fetal age at infection and the presence of a fetal immune response, fetal infection may result in fetal death, growth retardation, the birth of persistently infected lambs or lambs born with hypomyelinogenesis, hydranencephaly and cerebellar dysplasia. Coat defects may also be seen
• Hog cholera virus – vaccination of sows with modified vaccine virus between days 15 and 25 of pregnancy produces piglets with edema, deformed noses and abnormal kidneys. Natural infection with field virus can cause reproductive inefficiency and cerebellar hypoplasia in piglets
• An unidentified virus is associated with the AII type of congenital tremor in pigs
• Congenital infection with Wesselsbron virus and with Rift Valley fever is recorded as producing central nervous system disease in cattle and sheep14
• Japanese B encephalitis virus in pigs can result in abortion or in the birth of weak, mummified or stillborn piglets and live piglets with neurological abnormalities. The window of susceptibility is from 40–60 days gestation
• Pseudorabies virus infection of the pregnant sow can result in myoclonia congenita in piglets
• Viral, bacterial and protozoal agents that produce abortion in animals can also produce intrauterine growth retardation and the birth of weakborn neonates that are highly susceptible to mortality in early life.
There are many congenital defects in animals that are known to be caused by deficiencies of specific nutrients in the diet of the dam. Examples are as follows:
• Iodine – goiter and increased neonatal mortality is caused in all species; prolonged gestation occurs in horses and sheep. Congenital musculoskeletal lesions are seen in foals (congenital hypothyroid dysmaturity syndrome). Deficiency may be due to a primary deficiency, or induced by nitrate or Brassica spp. Syndromes are also produced by iodine excess, often associated with feeding excess seaweed or seaweed products
• Copper – enzootic ataxia in lambs is due either to a primary copper deficiency or to a secondary deficiency where the availability of copper is interfered with by other minerals, e.g. molybdenum and iron
• Manganese – chondrodystrophy and limb deformities in calves15
• Vitamin D – neonatal rickets
• Vitamin A – eye defects, harelip and other defects in piglets
• Vitamin E and/or selenium – congenital cardiomyopathy and muscular dystrophy
• Congenital cobalt deficiency is reported to reduce lamb vigor at birth and to increase perinatal mortality because of impaired immune function in the lamb.16 A similar effect on immune function in neonatal lambs and calves has been proposed with copper deficiency17
• Malnutrition of the dam can result in increased neonatal mortality and is suspected in the genesis of limb deformities17 and in congenital joint laxity and dwarfism in calves18,19
• Vitamin A deficiency induced by feeding potato tops or water with high nitrate content has been associated with congenital blindness in calves.
Their teratogenic effects have been reviewed in detail.20 Some examples are given below.
• Veratrum californicum fed to ewes at about the 14th day of pregnancy can cause congenital cyclopia and other defects of the cranium and brain in lambs, as well as prolonged gestation.6 When fed at 27–32 days of pregnancy it can produce limb abnormalities. Tracheal stenosis has been produced by feeding at 31–33 days of gestation. The alkaloid cyclopamine is the teratogenic substance20
• ‘Crooked calf disease’ is associated with the ingestion of Lupinus sp. during pregnancy. This is a major problem on some range lands in western North America. There are approximately 100 species of Lupinus in Canada and the USA but the disease has been mainly associated with L. sericeus, L. leucophyllus, L. caudatus and L. laxiflorus.21 These are believed to be toxic because of their content of anagyrine, but some piperidine alkaloids may also produce the disease.22 The disease has been reproduced by feeding anagyrine-containing lupines to pregnant cattle between 40 and 90 days of gestation but can occur with later feeding in natural grazing. The syndrome is one of arthrogryposis, torticollis, scoliosis and cleft palate4
• Astragalus and Oxytropis spp. locoweeds cause limb contracture in calves and lambs, also fetal death and abortion
• Tobacco plants – ingestion of Nicotiana tabacum (burley tobacco) and N. glauca (tree tobacco) by sows between 18 and 68 days, with peak susceptibility between 43 and 55 days of gestation, can cause limb deformities in their piglets. The teratogen is the piperidine alkaloid anabasine. Cleft palate and arthrogryposis has also been produced experimentally in the fetuses of cattle and sheep fed N. glauca during pregnancy but the plant is not palatable and this is an unlikely cause of natural disease20
• Conium maculatum, poison hemlock, fed to cows during days 55–75 of pregnancy, to sheep in the period 30–60 days of pregnancy and to sows in the period 30–62 days of pregnancy will cause arthrogryposis, scoliosis, torticollis and cleft palate in the fetuses.20 Cattle are most susceptible. Piperidine alkaloids coniine and – coniceine are responsible22,23
• Leucaena leucocephala (or mimosine, its toxic ingredient) causes forelimb polypodia (supernumerary feet) in piglets when fed experimentally to sows
• Fungal toxicosis from the feeding of moldy cereal straw has been epidemiologically linked to outbreaks of congenital spinal stenosis and bone deformities associated with premature closure of growth plates in calves.24
• Some benzimidazoles (parbendazole, cambendazole, oxfendazole, netobimin) are important teratogens for sheep, producing skeletal, renal and vascular abnormality when administered between 14 and 24 days of pregnancy25
• Methallibure, a drug used to control estrus in sows, causes deformities in the limbs and cranium of pigs when fed to sows in early pregnancy
• Apholate, an insect chemosterilant, is suspected of causing congenital defects in sheep
• The administration of trichlorfon to pregnant sows can result in the birth of piglets with cerebellar hypoplasia and congenital trembles26
• Organophosphates have been extensively tested and found to be usually nonteratogenic.27 A supposed teratogenic effect is probably more a reflection of the very common usage of these substances in agriculture (see under poisoning by organophosphates)
• Griseofulvin given to a mare in the second month of pregnancy is suspected of causing microphthalmia and facial bone deformity in a foal.28
• Severe exposure to beta or gamma irradiation, e.g. after an atomic explosion, can cause a high incidence of gross malformations in developing fetuses
• Rectal palpation of pregnancy using the amniotic slip method between 35 and 41 days of pregnancy in Holstein Friesian cattle is associated with atresia coli in the calf at birth,29 but there is also a genetic influence.30 It is probable that the cause is palpation-induced damage to the developing colonic vasculature
• Hyperthermia applied to the dam experimentally causes congenital deformities, but this appears to have no naturally occurring equivalent. The most severe abnormalities occur after exposure during early pregnancy (18–25 days in ewes). Disturbances of central nervous system development are commonest. Defects of the spinal cord manifest themselves as arthrogryposis and exposure of ewes to high temperatures (42°C, 107.5°F) causes stunting of limbs; the lambs are not true miniatures as they have selective deformities with the metacarpals selectively shortened. The defect occurs whether nutrition is normal or not.31 Hyperthermia between 30 and 80 days of pregnancy in ewes produces growth retardation in the fetus. Developmental abnormalities have been reproduced experimentally in explanted porcine embryos exposed to environmental temperatures similar to those that may be associated with reproductive failure due to high ambient temperatures in swine herds.32
Currently, there is considerable interest in the possible teratogenic effects of manmade changes in the environment. The concern is understandable because the fetus is a sensitive biological indicator of the presence of some noxious influences in the environment. For example, during an accidental release of polybrominated biphenyls much of the angry commentary related to the probable occurrence of congenital defects. The noxious influences can be physical or chemical. In one examination of the epidemiology of congenital defects in pigs, it was apparent that any environmental causes were from the natural environment; manmade environmental changes, especially husbandry practices, had little effect.33 A current concern in some regions is an apparent increase in congenital defects believed to be associated with exposure to radiofrequency electromagnetic fields associated with mobile telephone networks,34,35 but there is little hard data.
Individual abnormalities differ widely in their spontaneous occurrence. The determination of the cause of congenital defects in a particular case very often defies all methods of examination. Epidemiological considerations offer some of the best clues but are obviously of little advantage when the number of cases is limited. The possibility of inheritance playing a part is fairly easily examined if good breeding records are available. The chances of coming to a finite conclusion are much less probable. Some of the statistical techniques used are discussed in Chapter 34 on inherited diseases. The determination of the currently known teratogens has mainly been arrived at following epidemiological studies suggesting possible causality followed by experimental challenge and reproduction of the defect with the suspected teratogen.
An expression of the prevalence of congenital defects is of very little value unless it is related to the size of the population at risk, and almost no records include this vital data. Furthermore, most of the records available are retrospective and based on the number of cases presented at a laboratory or hospital.
Reported prevalence rates of 0.5–3.0% for calves and 2% for lambs are comparable with the human rate of 1–3%.36 A much higher rate for animals of 5–6% is also quoted.21 A study of over 3500 cases of abortion, stillbirth and perinatal death in horses found congenital malformations in almost 10%.37 A very extensive literature on congenital defects in animals exists and a bibliography is available.38-40
Some breeds and families have extraordinarily high prevalence rates because of intensive inbreeding. The extensive use, by artificial insemination, of certain genetics can result in a significant increase in the occurrence and nature of congenital defects when the bulls are carriers of genetic disease. The use of bulls that were carriers for the syndrome ‘complex vertebral malformation’ resulted in an approximately threefold increase in the presence of arthrogryposis, ventricular septal defect and vertebral malformations in Holstein–Friesian calves submitted to diagnostic laboratories in the Netherlands between 1994 and 2000.41
In the USA an extensive registry has been established at the veterinary school at Kansas State University.
Checklists of recorded defects are included in the review literature.
The pathogenesis of many of the congenital defects of large animals is poorly understood but it is apparent that disease produced by each teratogen is likely to have its own unique pathogenesis. Congenital defects in large animals have examples of defects induced from structural malformations, from deformations, from the destruction of tissue by extraneous agents and from enzyme deficiencies – or from a combination of these.
Structural malformations result from a localized error in morphogenesis. The insult leading to the morphogenic error takes place during organogenesis and thus is an influence imposed in early gestation. Deformations occur where there is an alteration in the shape of a structure of the body that has previously undergone normal differentiation. Deforming influences apply later in the early gestational period, after organogenesis.
Deformation is the cause of arthrogryposis and cleft palate produced by the piperidine alkaloids from Conium maculatum and Nicotiana spp. and by anagyrine from Lupinus spp., which produce a chemically induced reduction in fetal movements. Ultrasound examination of the normal fetus shows that it has several periods of stretching and vigorous galloping during a 30 minute examination period. In contrast, the fetus that is under the influence of anagyrine has restricted movement and lies quietly, often in a twisted position. Restricted fetal limb movement results in arthrogrypotic fixation of the limbs, and pressure of the tongue on the hard palate when the neck is in a constant flexed position inhibits closure of the palate. In experimental studies there is a strong relation between the degree and duration of reduced fetal movement, as observed by ultrasound, and the subsequent severity of lesions at birth.21
Restriction in the movement of the fetus, and deformation, can also result from teratogens that produce damage and malfunction in organ systems, such as the primary neuropathy that occurs in the autosomal recessive syndrome in Charolais cattle and the acquired neuropathy in Akabane infection, both of which result in arthrogryposis through absence of neurogenic influence on muscle activity.
It has been suggested, with some good evidence, that the etiology and pathogenesis of congenital torticollis and head scoliosis in the equine fetus are related to an increased incidence of transverse presentation of the fetus.42,43 Flexural deformities of the limbs are also believed to be due to errors in fetal positioning and limited uterine accommodation, which may be further complicated by maternal obesity. Abnormal placental shape may also be important in the genesis of skeletal deformations.44
Viral teratogenesis is related to the susceptibility of undifferentiated and differentiated cells to attachment, penetration and virus replication, the pathogenicity of the virus (cytopathogenic versus noncytopathogenic strains of bovine virus diarrhea), the effects that the virus has on the cell and the stage of maturation of immunological function of the fetus at the time of infection. Viral infections can result in prenatal death, the birth of nonviable neonates with severe destructive lesions, or the birth of viable neonates with growth retardation or abnormal function (tremors, blindness). The gestational age at infection is a major influence. In sheep infected with border disease virus between 16 and 90 days of gestation, the occurrence of the syndromes of early embryonic death, abortion and stillbirth or the birth of defective and small weak lambs is related to the fetal age at infection. Certain viruses cause selective destruction of tissue and of organ function late in the gestational period and the abiotrophies are examples of selective enzyme deficiencies. The pathogenesis of the viral diseases is given under their specific headings in later chapters.
A number of inherited congenital defects, some of which are not clinically manifest until later in life, are associated with specific enzyme deficiencies. Examples are maple syrup urine disease (MSUD), citrullinemia, factor XI deficiency in cattle and the lysosomal storage diseases. Inherited lysosomal storage diseases occur when there is excessive accumulation of undigested substrate in cells. In mannosidosis, it is due to an accumulation of saccharides due to a deficiency of either lysosomal α-mannosidase or β-mannosidase. In GM1 gangliosidosis, disease is due to a deficiency of β-galactosidase and in GM2 gangliosidosis a deficiency of hexosaminidase.45
The age at development of clinical signs and their severity is dependent on the importance of the enzyme that is deficient, the biochemical function and cell type impacted and, in storage disease, the rate of substrate accumulation. Factor XI deficiency is manifest with bleeding tendencies but is not necessarily lethal. In contrast, calves with citrullinemia and MSUD develop neurologic signs and die shortly after birth, whereas the onset of clinical disease can be delayed for several months with α-mannosidosis.
It is not intended to give details of the clinical signs of all the congenital defects here but some general comments are necessary. Approximately 50% of animals with congenital defects are stillborn. The defects are usually readily obvious clinically. Diseases of the nervous system and musculoskeletal system rate high in most published records and this may be related to the ease with which abnormalities of these systems can be observed. For example, in one survey of congenital defects in pigs, the percentage occurrence rates in the different body systems were as follows:
• Combined alimentary and respiratory tracts (mostly cleft palate and atresia ani) 27%
• Miscellaneous (mostly monsters) 9%
In a survey of congenital defects in calves the percentage occurrence rates were:
• Respiratory and alimentary tracts 13%
• (Anomalous-joined twins and hydrops amnii accounted for 20%).
In a survey of foals the approximate percentage occurrence rates were:
Contracted foal syndrome and craniofacial abnormalities were the most common congenital defects in a study of stillbirth and perinatal death in horses.37,46
Many animals with congenital defects have more than one anomaly: in pigs, the average is two and considerable care must be taken to avoid missing a second and third defect in the excitement of finding the first. In some instances, the combinations of defects are repeated often enough to become specific entities. Examples are microphthalmia and cleft palate, which often occur together in piglets, and microphthalmia and patent interventricular septum in calves.
There are a number of defects that cannot be readily distinguished at birth and others that disappear subsequently. It is probably wise not to be too dogmatic in predicting the outcome in a patient with only a suspicion of a congenital defect or one in which the defect appears to be causing no apparent harm. A specific instance is the newborn foal with a cardiac murmur.
Sporadic cases of congenital defects are usually impossible to define etiologically but when the number of affected animals increases it becomes necessary and possible to attempt to determine the cause.
The use of clinical pathology as an aid to diagnosis depends upon the disease that is suspected and its differential diagnosis. The approach varies markedly with different causes of congenital defects: specific tests and procedures are available for some of the viral teratogens, for congenital defects associated with nutritional deficiencies and for some enzyme deficiencies and storage diseases, and the specific approach for known teratogens is covered in the individual diseases section.
When an unknown viral teratogen is suspected, precolostral blood samples should be collected from the affected neonates and also from normal contemporaries that are subsequently born in the group. Precolostral serum can be used for investigating the possible fetal exposure of the group to an agent and the buffy coat or blood can be used for attempted virus isolation. IgG and IgM concentrations in precolostral serum may give an indication of fetal response to an infecting agent even if the agent is not known and there is no serological titer to known teratogenic agents.
Enzyme-based tests have been used to virtually eradicate carriers of α mannosidosis in cattle breeds in Australia and New Zealand47 and DNA-based tests are used to detect and eliminate the carriers of diseases such as generalized glycogenosis in cattle.48
• The diagnostic challenge with congenital defects is to recognize and identify the defect and to determine the cause
• Syndromes of epidemic disease resulting from environmental teratogens are usually sufficiently distinct that they can be diagnosed on the basis of their epidemiology combined with their specific clinical, pathological and laboratory findings and on the availability of exposure
• Congenital defects occurring sporadically in individual animals pose a greater problem. There is usually little difficulty in defining the condition clinically, but it may be impossible to determine what was the cause. With conditions where there is not an obvious clinical diagnosis, an accurate clinical definition may allow placement of the syndrome within a grouping of previously described defects and suggest possible further laboratory testing for further differentiation.
The examination for cause of an unknown congenital defect is usually not undertaken unless more than a few newborn animals in a herd or area are affected in a short period of time with similar abnormalities. A detailed epidemiological investigation will be necessary which will include the following:
• Pedigree analysis. Does the frequency of occurrence of the defect suggest an inherited disease or is it characteristically nonhereditary?
• Nutritional history of dams of affected neonates and alterations in usual sources of feed
• Disease history of dams of affected neonates
• History of drugs used on dams
• Movement of dams during pregnancy to localities where contact with teratogens may have occurred
The major difficulty in determining the cause of nonhereditary congenital defects is the long interval of time between when the causative agent was operative and when the animals are presented, often 6–8 months. Detailed clinical and pathological examination of affected animals offers the best opportunity in the initial approach to determine the etiology based on the presence of lesions that are known to be caused by certain teratogens.
Dennis SM, Leipold HW. Ovine congenital defects. Vet Bull. 1979;49:233.
Parsonson IM, Della-Porta AJ, Snowdon WA. Development disorders of the fetus in some arthropod-bovine virus infection. Am J Trop Med Hyg. 1981;30:600-673.
Leipold HW, Huston K, Dennis SM. Bovine congenital defects. Adv Vet Sci Comp Med. 1983;27:197-271.
Leipold HW. Cause, nature, effect and diagnosis of bovine congenital defects. In: Proceedings of the 14th World Congress on Diseases of Cattle. 1986;1:63-72.
Rousseaux CG. Developmental anomalies in farm animals. I. Theoretical considerations. Can Vet J. 1988;29:23-29.
Rousseaux CG, Ribble CS. Developmental anomalies in farm animals. II. Defining etiology. Can Vet J. 1988;29:30-40.
De Lahunta A. Abiotrophy in domestic animals: a review. Can J Vet Res. 1990;54:65-76.
Angus K. Congenital malformations in sheep. In Pract. 1992;14:33-38.
Panter KE, Keeler RC, James LF, Bunch TD. Impact of plant toxins on fetal and neonatal development. A review. J Range Manag. 1992;45:52-57.
Dennis SM. Congenital abnormalities. Vet Clin North Am Food Anim Pract. 1993;9:1-222.
Rousseaux CG. Congenital defects as a cause of perinatal mortality of beef calves. Vet Clin North Am Food Anim Pract. 1994;10:35-45.
Mee JF. The role of micronutrients in bovine periparturient problems. Cattle Pract. 2004;12:95-108.
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2 Huston K. Vet Clin North Am Food Anim Pract. 1993;9:1.
3 Leipold HW, et al. Adv Vet Sci. 1983;27:197.
4 Finnell RH, Gay CC. Handbook Nat Toxins. 1991;6:27.
5 Konno S, et al. Vet Pathol. 1982;19:246.
6 Russell RG, et al. Vet Pathol. 1985;22:32.
7 McFeeley RA. Vet Clin North Am Food Anim Pract. 1993;9:11.
8 Schmultz SM, et al. J Vet Diagn Invest. 1996;8:91.
9 Agerholm JS, Christensen K. J Vet Med Assoc. 1993;40:576.
10 Saito M, et al. J Jpn Vet Med Assoc. 1995;48:848.
11 Oberst RD. Vet Clin North Am Food Anim Pract. 1993;9:23.
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This is a special form of congenital defect. It is a failure to grow properly, as apposed to a failure to gain body weight, and occurs when the developmental age is less than the chronological (gestational) age. Runt is a common colloquial agricultural term. Normal fetal growth rate is determined by genetic and epigenetic factors and cross-breeding experiments suggest that fetal size is regulated by the embryonic/fetal genotype and also an effect of maternal genotype.1 Litter size has an effect on birth weight in all species. A genetic association with intrauterine growth retardation has been shown in Japanese Black calves.2
There is a strong positive association between placental mass and fetal size at birth in all species and the majority of cases of growth retardation result from inadequate placentation, disturbance in utero-placental blood flow or placental pathology.
There are a number of different etiologies.
Heat stress to ewes in the final third of pregnancy will result in intrauterine growth retardation but it is not as severe as when ewes are exposed in the second third of pregnancy – the period of placental growth.3,4 Hyperthermia results in a redistribution of blood away from the placental vascular bed and a decrease in cotyledon mass with consequent reduction in birth weight. The degree of growth restriction is directly related to the degree of hyperthermia to which the ewe is exposed and her heat tolerance. The growth retardation affects fetal weight more than fetal length and, while there is some reduction in the growth of the brain, it is relatively less than that of the internal organs, resulting in an increased brain:liver weight ratio at birth.5
Viral infections, such as border disease and bovine virus diarrhea in ruminants and parvovirus in pigs, produce growth-retarded neonates,6,7 as do bacterial and other infections that result in placentitis.
Inadequate placentation is the cause of runt piglets. Runts are smaller, thinner and have disproportionately larger, domed heads than normal pigs. A deficiency in specific trace elements is suspect in some field cases of growth retardation in ruminants but there is no evidence for deficient trace element nutrition in runt pigs.8
Inadequate nutrition can result in in-utero growth retardation. Growth retardation can be produced in fetal pigs, lambs and calves by maternal caloric undernutrition. Nutritional restriction in ewes reduces the number of placental lactogen receptors that mediate amino acid transport in fetal liver and glycogen synthesis in fetal tissue, leading to depletion of fetal liver glycogen stores. This has been postulated as a possible cause of the fetal growth retardation that accompanies maternal caloric undernutrition;9 runt pigs have a reduced metabolic rate and lower skeletal muscle respiratory enzyme activity.10 This deficiency persists after birth – runt pigs have a lower core temperature and a lessened ability to increase their metabolic rate and heat production in response to cold.11
Paradoxically, overnourishing the adolescent ewe will also result in placental growth restriction and in in-utero growth retardation.4,12 This effect is most evident in the second third of pregnancy. This syndrome is accompanied by the birth of lambs with a shorter gestational age, commonly reduced by 3 days. It is thought that the fetal hypoxia and hypoglycemia that accompanies placental insufficiency might stimulate the maturation of the fetal hypothalamic–pituitary–adrenal axis, initiating early parturition. The growth of those lambs that survive initially lags behind that of normal lambs but there is compensatory growth and no difference in weight at 6 months-of age.13
Measurements that can be used to determine the presence of growth retardation in a dead fetus include crown– rump (anal) length, brain weight, body weight, brain to body weight ratios, long bone weight and appendicular ossification centers. Formulas are available to determine the degree of growth retardation.14
In the live animal the presence of radiodense lines in long bones and the examination of closure of ossification centers can provide evidence for prior stressors in pregnancy that induce fetal growth retardation, such as malnutrition or infection of the dam, that may not be found by other examinations.7,15,16
Intrauterine growth retardation is accompanied by an impaired cellular development of tissues such as the small intestine and skeletal muscle and disproportionately large reductions in the growth of some organs such as the thymus, spleen, liver, kidney, ovary and thyroid. There is an associated impairment of thermogenesis, immune and organ function at birth.17-19 In lambs there is impaired development of secondary wool follicles.
The survival of fetuses with growth retardation requires special nutritional care and the provision of adequate heat, and is discussed in the section on Critical care for the newborn. In large piggeries that practice batch farrowing, the survival of runts can be significantly improved by the simple practice of fostering them together in one litter on one sow so that they do not have to compete with larger-birth-size and more vigorous pigs, by ensuring adequate colostrum intake and adequate environmental warmth and by feeding using a stomach tube in the first few hours of life if indicated.
Fowden AL, Rossdale PD. Foetal maturation; comparative aspects of normal and disturbed development. Equine Vet J Suppl. 1993;14:1-49.
Redmer DA, Wallace JM, Reynolds LP. Effect of nutrient intake during pregnancy on fetal growth and vascular development. Domestic Anim Endocrinol. 2004;27(3):199-217.
1 Ousy JC, et al. Equine Vet J. 2004;36:616.
2 Ogata Y, et al. J Jpn Vet Med Assoc. 1997;50:271.
3 McCrabb GJ, et al. J Agric Sci. 1993;120:265.
4 Wallace JM, et al. J Physiol. 2005;565:19.
5 Wallace JM, et al. Placenta. 2000;21:100.
6 Done JT, et al. Vet Rec. 1980;106:473.
7 Caffrey JF, et al. Res Vet Sci. 1997;62:245.
8 Gurtler H, et al. In: Proceedings of the 6th International Trace Element Symposium. 1989;2:534.
9 Freemark M, et al. Endocrinology. 1989;125:1504.
10 Dauncey MJ, Geers R. Biol Neonate. 1990;58:291.
11 Hayashi M, et al. Biol Neonate. 1987;51:205.
12 Wallace JM, et al. Biol Reprod. 2004;71:1055.
13 Da Silva P, et al. Reproduction (Cambridge). 2001;122:375.
14 Richardson C, et al. Vet Rec. 1990;126:279.
15 O’Connor BT, Doige CE. Can J Vet Res. 1993;57:25.
16 Smyth JA, Ellis WA. Vet Rec. 1996;139:599.
17 Greenwood PL, Bell AW. Proceedings of the 6th International Symposium on Reproduction in Domestic Animals. 2003;6:195.
18 Holdstock NB, et al. Pferdheilkunde. 2001;17:659.
19 Da Silva P, et al. Reproduction (Cambridge). 2003;126:249.
Congenital neoplasia is rare, occurring at a substantially lower rate than in adults, and accounts for a minor percentage of findings in surveys of neonatal mortality.1,2 It is probable that genetic rather than environmental factors influence its development.
Clinical signs depend upon the type of neoplasm and its site and they can result in dystocia or abortion. A variety of tumors have been recorded in all large animal species and are predominantly of mesenchymal origin.2,3
In calves, malignant lymphoma is most commonly reported. It is usually multicentric and also affects the skin. Sporadic bovine leukosis of young calves may also be present at birth Other tumors reported predominant in calves include diffuse peritoneal mesothelioma, mixed mesodermal tumor, mast cell tumor, hemangiomas and cutaneous melanoma.2,4
Melanomas (both benign and malignant) also occur in foals and piglets. Duroc Jersey, Vietnamese pot-bellied pigs and Sinclair miniature pigs have a high incidence of congenital malignant melanoma, which is fatal in approximately 15% of affected pigs but regresses spontaneously, and without recurrence, in the remainder.5,6
A breed predisposition to cardiac rhabdomyoma is recorded in Red Wattle pigs.7
Papillomatosis is rare but lingual papillomatosis is reported as a cause of enzootic disease of piglets in China.5
Physical and environmental causes of perinatal disease
Disease in the neonate can result directly from noxious influences in the postnatal period but it can also be predisposed or produced by noxious influences in the period before and during birth.
The clinical care of the newborn animal in large animal veterinary medicine has traditionally started at the time of birth but there is a growing recognition of the importance of antenatal and parturient events to the subsequent viability of the neonate. This has been particularly recognized by equine clinicians and has led to the clinical concept of perinatology.1 One purpose of perinatology is to expand the care of the neonate into the antenatal and parturient period by measurements that reflect fetal health or that can predict risk to fetal viability. Measures that can be used are still being developed and evaluated but the following include those that have apparent value.2,3
In the horse, fetal heart rate recorded by electrocardiography (ECG) or by ultrasound can be used as a measure of fetal viability, for the detection of twins and as a monitor for fetal distress during parturition. Fetal heart rate decreases logarithmically from approximately 110 beats/min at 150 days before term to 60–80 beats/min near to term.4 It has been suggested that a base heart rate of 80–92 beats/min with baseline variations of 7–15 beats/min and occasional accelerations above this is normal for the fetal heart rate of equines, and that bradycardia is evidence of abnormality.2 Continued monitoring traces may be needed to assess fetal distress. Cardiac arrhythmia is common at the time of birth and for the first few minutes following and is believed to result from the transient physiological hypoxemia that occurs during the birth process.5
The foal can be examined by ultrasound to establish the presentation, the presence of twins, the heart rate, the presence and quality of fetal movement, the presence of placentitis, placental thickness, the presence of echogenic particles in the amniotic fluid and an estimate of body size from the measurement of the aortic and orbit diameters. Measurements of fetal heart rate, fetal aortic diameter, uteroplacental contact, maximal fetal fluid depths, uteroplacental thickness and fetal activity have allowed the development of an objective measurement profile to assess fetal wellbeing.2,6
The examination of the amniotic fluid for the determination of pulmonary maturity and other measures of foal health may be limited as there is a cosiderable risk for abortion and placentitis, even with ultrasound-guided amniocentesis, and the technique is not recommended for routine clinical use.7,8
Foals born at less than 320 days of gestational age are considered premature and those less than 310 days are at significant risk for increased mortality. Traditionally, external signs have been used to predict a premature foaling and the common signs used are the enlargement of the udder, milk flow and the occurrence of vaginal discharge. Causes of early foaling include bacterial or fungal placentitis and twin pregnancy.9 Several assays are used as alternate methods of determining if foaling is imminent and if problems are present.
Plasma progestogen concentrations decline in pregnancy to reach a low around 150 days of gestation. In Thoroughbreds, they remain below 10 ng/mL until approximately 20 days prior to foaling when they start to increase but in ponies there is a greater variation.10,11 Concentrations decline 24 hours before parturition. Plasma progestogen cannot be used to accurately predict the time of foaling and a single sample is not diagnostic.8 There is a strong correlation between the presence of plasma progestogen concentrations above 10 ng/mL before a gestational age of 310 days and the presence of placental pathology2 and a rapid drop in concentration to below 2 ng/mL that persists for more than 3 days indicates impending abortion. Current research is examining the profiles of individual progestogens during pregnancy to determine if the profile of any one can be used as a predictor of fetal distress.12
During the last week of gestation the concentration of calcium and potassium in milk increases and that of sodium decreases. The rise in calcium concentrations are the most reliable predictor of fetal maturity3 and milk calcium concentrations above 10 mmol/L, in combination with a concentration of potassium that is greater than sodium, are indicative of fetal maturity. Milk calcium concentrations above 10 mmol/L in the earlier stages of pregnancy are suggestive of fetal compromise.2 Commercial milk test strips are available for estimating mammary secretion electrolyte concentrations; however, it is recommended that testing be done in an accredited laboratory.13
Rossdale PD, Silver M, Rose RJ. Equine. Equine Vet J Suppl. 1988;5:1-61.
Ellis DR. Care of neonatal foals, normal and abnormal. In Pract. 1990;12:193-197.
Rossdale PD, McGladdery AJ. Recent advances in Equine neonatology. Vet Annu. 1992;32:201-208.
Rossdale PD. Advances in Equine perinatology 1956–1996: a tribute. Equine Vet Educ. 1997;9:273-277.
Davies Morel MCG, Newcombe JR, Holland SJ. Factors affecting gestation length in the Thoroughbred mare. Anim Reprod Sci. 2002;74:175-185.
1 Rossdale PD. Equine Vet Educ. 1997;9:273.
2 Rossdale PD, McGladdery AJ. Equine Vet Educ. 1991;3:208.
3 Vaala WE, Sertich PL. Vet Clin North Am Equine Pract. 1994;10:237.
4 Matsui K, et al. Jpn J Vet Sci. 1985;47:597.
5 Yamamoto K, et al. Equine Vet J. 1992;23:169.
6 Reef VB, et al. Equine Vet J. 1996;28:200.
7 Schmidt AR, et al. Equine Vet J. 1991;23:261.
8 LeBlanc MM. Equine Vet J. 1997;24:100.
9 Ellis DR. In Pract. 1990;12:192.
10 Rossdale PD, et al. J Reprod Fertil Suppl. 1991;44:579.
11 Ousey JC, et al. Pferdheilkunde. 2001;17:574.
Foals that are born before 300 days are unlikely to survive and foals born between 300 and 320 days of gestation are considered premature but may survive with adequate care.1,2 Premature foals are characterized clinically by low birth weight, generalized muscle weakness, poor ability to stand, lax flexor tendons, weak or no suck reflex, lack of righting ability, respiratory distress, short silky haircoat, pliant ears, soft lips, increased passive range of limb motion, and sloping pastern axis. Radiographs may show incomplete ossification of the carpal and tarsal bones and immaturity of the lung and there may be clinical evidence of respiratory distress. Full term foals born after 320 days of gestation but exhibiting signs of prematurity are described as dysmature.
Premature foals have hypoadrenal corticalism. They are neutropenic and lymphopenic at birth and have a narrow neutrophil to lymphocyte ratio.3,4 In premature foals older than 35 hours the neutrophil count can be used to predict survival and foals that remain neutropenic after this time have a poor prognosis.4,5 Premature foals also have low plasma glucose, low plasma cortisol and a blood pH of less than 7.25. An extensive collaborative investigation of equine prematurity has been conducted and information on foal metabolism6-9 and guidelines for laboratory and clinical assessment of maturity are available.5,10
The placenta is critical to the fetus in the antenatal period and pregnancies involving placental pathology commonly result in foals that suffer premature-like signs at whatever stage they are delivered.11 Placental edema, placental villous atrophy and premature separation of the placenta are significant causes.12,13
Precocious lactation of the mare can be associated with placentitis. The examination of the placenta for evidence of placentitis and for the presence of larger than normal avillous areas should be part of normal foaling management. A study of the equine placenta showed a high correlation between both allantochorionic weight and area and foal weight in normal placentas. Normal placentas had a low association with subsequent perinatal disease in the foals. In contrast, abnormal placental histology was associated with poor foal outcome (three normal foals from 32 abnormal placentas). Cords longer than 70 cm were often associated with fetal death or malformation. Edema, sacculation and strangulation are other abnormalities and can be associated with microscopic deposits of mineral within the lumen of placental blood vessels.12
1 Mee JF. Vet Rec. 1991;128:521.
2 Koterba AM. Equine Vet Educ. 1993;5:271.
3 Rossdale PD, McGladdery AJ. Equine Vet Educ. 1991;3:208.
4 Chavatte P, et al. J Reprod Fertil Suppl. 1991;44:603.
5 Vaala WE. Compend Contin Educ Pract Vet. 1986;8:S211.
6 Wilsmore T. In Pract. 1989;11:239.
7 Silver M, et al. Equine Vet J. 1984;16:278.
8 Fowden AL, et al. Equine Vet J. 1984;16:286.
9 Pipkin FB, et al. Equine Vet J. 1984;16:292.
10 Rossdale PD. Equine Vet J. 1984;16:275. 300
11 Rossdale PD, et al. J Reprod Fertil Suppl. 1991;44:579.
During parturition extreme mechanical forces are brought to bear upon the fetus and these can result in direct traumatic damage or can impair fetal circulation of blood by entrapment of the umbilical cord between the fetus and the maternal pelvis, which may lead to hypoxemia or anoxia and death of the fetus during the birth process. Neonates that suffer birth trauma and anoxia but survive are at risk for development of the neonatal maladjustment syndrome,1 have reduced vigor, are slower to suck and are at increased risk for postnatal mortality.
In all species, but in ruminants in particular, the condition of the dam can have a marked influence on the prevalence of birth injury and its consequences. The effect is well illustrated in sheep, where the two extremes of condition can cause problems. Ewes on a high plane of nutrition produce a large fetus and also deposit fat in the pelvic girdle, which constricts the birth canal, predisposing to dystocia. Conversely, thin ewes may be too weak to give birth rapidly.2 Pelvic size can influence the risk of birth injury and ewe lambs and heifers mated before they reach 65% of mature weight are at risk. Pelvimetry is used to select heifers with adequate pelvic size for breeding but the accuracy and validity is seriously questioned.3,4 Breed is also a determinant of length and ease of labor and the subsequent quickness to time to first suckle.5
Traumatic injuries can occur in apparently normal births, with prolonged birth and as a result of dystocia, which may or may not be assisted by the owner. Incompatibility in the sizes of the fetus and the dam’s pelvis is the single most important cause of dystocia, and birth weight is the most important contributing factor. In cattle, expected progeny difference (EPD) estimates for calf birth weight are good predictors of calving ease.3 In foals, calves and lambs the chest is most vulnerable to traumatic injury but there is the chance of vertebral fracture and physical trauma to limbs with excessive external traction.
Fractured ribs are common in foals and can lead to laceration of the lungs and heart and internal hemorrhage.6 Rupture of the liver is common in some breeds of sheep7,8 and can also occur in calves and foals. A retrospective study of rib and vertebral fractures in calves suggests that most result from excessive traction and that as a result smaller dystocial calves are more at risk.9 Vertebral fractures occur as the result of traction in calves with posterior presentations and in calves with hip lock. Trauma is a major cause of neonatal mortality in piglets but it occurs in the postparturient phase and is associated with being overlain or stepped on by the sow. It is possible that the underlying cause of crushing mortality in piglets is hypothermia.10
Intracranial hemorrhage can result in damage to the brain. A high proportion (70%) of nonsurviving neonatal lambs at, or within 7 days of birth have been shown to have single or multiple intracranial hemorrhages, the highest incidence being in lambs of high birth weight. Similar lesions have been identified in foals and calves. Experimentally controlled parturition in ewes showed that duration and vigor of the birth process affected the severity of intracranial hemorrhages and further studies indicated that these birth-injured lambs had depressed feeding activity and that they were particularly susceptible to death from hypothermia and starvation.11,12
Birth anoxia associated with severe dystocia in cattle can result in calves with lower rectal temperatures in the perinatal period than normal calves and a decreased ability to withstand cold stress.13
Intracranial hemorrhage, especially subarachnoid hemorrhage, occurs in normal full-term deliveries as the result of physical or asphyxial trauma during or immediately following delivery.14 The forceful uterine contractions associated with parturition can result in surges of cerebral vascular pressure resulting in subarachnoid hemorrhage. It is also of common occurrence in foals born before full term.15 In one study, the highest incidence occurred in pony foals in which parturition was induced prior to 301 days of gestation. Similar hemorrhage occurred in pony foals born by cesarean section at 270 and 280 days of gestation and appeared associated with anoxic damage.
In a prolonged birth, edema of parts of the body, such as the head and particularly the tongue, may also occur. This occurs particularly in the calf and the lamb, possibly because of less close supervision at parturition and also because the young of these species can sustain a prolonged birthing process for longer periods than the foal without their own death or death of the dam. The edema can interfere with subsequent sucking but the principal problem relative to neonatal disease is the effect of the often prolonged hypoxia to which the fetus is subjected. There is interference with the placental circulation and failure of the fetus to reach the external environment. The hypoxia may be sufficient to produce a stillborn neonate, or the neonate may be alive at birth but not survive because of irreparable brain damage. Intrapartum deaths due to prolonged parturition occur in piglets.
Kasari TR, Wikse SE. Perinatal mortality in beef herds. Vet Clin North Am Food Anim Pract. 1994;10(1):1-185.
Sanderson MW, Chenoweth PJ. Compend Contin Educ Pract Vet. 2001;23(9 Suppl):S95.
Szenci O. Role of acid-base disturbances in perinatal mortality of calves: a review. Vet Bull. 2003;73(7):7R-14R.
Redmer DA, Wallace JM, Reynolds LP. Endocrine regulation of tissue differentiation and development with focus on the importance of nutrition and IGFs. Domestic Anim Endocrinol. 2004;27:199-217.
1 Hess-Dudan F, Rossdale PD. Equine Vet Educ. 1996;8:24. 79.
2 Wilsmore T. In Pract. 1989;11:239.
3 Rice LE. Vet Clin North Am Food Anim Pract. 1994;10:53.
4 Vestweber JG. Vet Clin North Am Food Anim Pract. 1997;13:411.
5 Dwyer CM, et al. Reprod Fertil Develop. 1996;8:1123.
6 Giles RC, et al. J Am Vet Med Assoc. 1993;203:1170.
7 Johnston WS, Maclachlan GK. Vet Rec. 1986;118:610.
8 Greene LE, Morgan KL. Prevent Vet Med. 1993;17:251.
9 Schuijt G. J Am Vet Med Assoc. 1990;197:1196.
10 Edwards SA. Livestock Prod Sci. 2002;78:3.
11 Haughey KG. Aust Vet J. 1980;56:49.
12 Haughey KC. Wool Technol Sheep Breed. 1984;31:139.
13 Bellows RA, Lammoglia MA. Theriogenology. 2000;53:803.
14 Hess-Dudan F, Rossdale PD. Equine Vet Educ. 1996;8:24. 79.
Hypoxemia and hypoxia can occur as a result of influences during the birth process or because of pulmonary immaturity in premature births.1,2
Transient tachypnea occurs following birth and is believed to be due to transient hypoxemia associated with the birth process and the absorption of pulmonary fluid.
Prolonged tachypnea, with flaring of the nostrils, open-mouth breathing, exaggerated rib retraction and paradoxical breathing patterns, is highly suggestive of primary pulmonary abnormality. Failure of respiration can occur at this stage and creates an urgent need for resuscitation measures. In the foal, body position can have a major effect on arterial oxygen tension.3 A foal that is unable to stand or to right itself from lateral recumbency is at risk from atelectasis4 and should be moved frequently. Hypoxia and hypercapnia resulting from mismatching of ventilation and perfusion are accentuated by prolonged recumbency.
Placental dysfunction or occlusion of the umbilicus in the second stage of labor can result in a much more serious situation so that the neonate is born in a state of terminal, as distinct from primary, apnea. It will be stillborn unless urgent and vigorous resuscitation is initiated immediately. Resuscitation includes:
• Establishing a patent airway by extending the head and clearing the nostrils of mucus and, if necessary, by postural drainage to clear excess fluids from the airways
• Artificial ventilation. This is easier if the foal is intubated but can also be achieved by sealing one nostril by hand and breathing forcibly into the other (or inflating with a rubber tube from an oxygen cylinder, delivering at a rate of 5 L/min). The chest wall should be moved only slightly with each positive breath. Continue at 25 ventilations/min until respiration is spontaneous
• Administering 200 mL 5% sodium bicarbonate solution intravenously to counter acidosis. However, respiratory acidosis with hypoxemia and hypercapnia should be primarily treated by assisted ventilation.
In general, the response of the neonate to hypoxemia is an increase in blood pressure and a redistribution of cardiac output with increased blood flow to the brain, heart and adrenal gland and a reduction in flow to the lungs, kidney, gastrointestinal tract and carcass.5,6 These regulatory changes fail with developing hypoxia and metabolic acidosis and failure leads eventually to cerebral anoxia. The avoidance of acidemia and the maintenance of an adequate oxygen supply are essential in the care of hypoxemic and premature foals.
A special cause of hypoxia, due usually to hypovolemia in addition to inadequate oxygenation of blood, occurs in the foal as a result of an inadequate placental blood transfusion, when the umbilical cord is severed too early after birth. This is one cause of the neonatal maladjustment syndrome, which is detailed in another section of this text.
Intrapartum hypoxemia due to prolonged parturition is common,7 particularly in calves born to first-calf beef heifers, and is considered to be one cause of the ‘weak calf syndrome’ described in Chapter 36.
A similar syndrome has been produced experimentally by clamping the umbilical cord of the bovine fetus in utero for 6–8 minutes, followed by a cesarean section 30–40 minutes later. Calves born following this procedure may die in 10–15 minutes after birth or survive for only up to 2 days.8 During the experimental clamping of the umbilical cord, there is a decline in the blood pH, Po2 and standard bicarbonate levels and an increase in Pco2 and lactate levels.8 There is also increased fetal movement during clamping and a release of meconium, which stains the calf and the amniotic fluid. Those that survive for a few hours or days are dull, depressed, cannot stand, have poor sucking and swallowing reflexes and their temperature is usually subnormal. They respond poorly to supportive therapy. A slight body tremor may be present and occasionally tetany and opisthotonus occur before death. Calves that are barely able to stand cannot find the teats of the dam because of uncontrolled head movements. At necropsy of these experimental cases, there are petechial and ecchymotic hemorrhages on the myocardium and endocardium, an excess of pericardial fluid, and the lungs are inflated. When the experimental clamping lasts only 4 minutes, the calves usually survive.
Meconium staining (brown discoloration) of the coat of the newborn at birth is an important indicator that it has suffered hypoxia during or preceding the birth process; such neonates require close supervision in the early postnatal period. In lambs, severe hypoxia during birth results in death shortly following birth and there is an increased risk in those that survive for metabolic acidosis and depressed heat production capacity, which causes hypothermia.9
Fetal anoxia associated with premature expulsion of the placenta occurs in all species but may be of greatest importance in cattle.10 It occurs in all parities of cow and with little relation to calving difficulty, although malpresentation is a predisposing factor. Prepartum diagnosis in cattle is hindered by the low prevalence of prepartum vaginal hemorrhage, and the majority of fetuses die during the birth process. The placenta is expelled with the fetus. Premature separation of the placenta (‘red bag’) occurs in foals when foals experience difficulty in breaking through the cervical star region of an edematous thickened placenta. This is an emergency and requires immediate attention.
In all species the prevention of intrapartum hypoxia depends on the provision of surveillance. Universal surveillance is usually not practical for species other than the horse, and in cattle, for example, it tends to concentrate on the group at most risk so that surveillance, and assistance if necessary, is provided for first-calf heifers at the time of calving. Heifers that do not continue to show progress during the second stage of parturition should be examined for evidence of dystocia, and obstetrical assistance should be provided if necessary.
The treatment and care of foals with this syndrome is described under Critical care of the newborn later in the chapter. The monitoring, treatment and care of agricultural animals with this syndrome should follow the same principles but is usually limited by the value of the animal and the immediate access to a laboratory. Measures such as the time from birth to sternal recumbency, time from birth to standing and time from birth to first suckle have been used to grade calves and identify those that might require intervention and treatment, but the best method of evaluation is an assessment of muscle tone.11 There is no effective practical treatment for calves affected with intrapartum hypoxia other than the provision of ventilation as for the foal and the correction of the acidosis. The airway should be cleared and, if physical stimulation of ventilation gives no response, then mechanical ventilation should be attempted. The practice of direct mouth-to-mouth ventilation assistance should be strongly discouraged, especially in lambs, because of the risk from zoonotic disease agents. Doxapram hydrochloride has been used in calves to stimulate respiration.11
The provision of warmth, force-feeding of colostrum and fluid therapy are logical support approaches.
1 Hess-Dudan F, Rossdale PD. Equine Vet Educ. 1996;8:24. 79
2 Rose R. Equine Vet J Suppl. 1987;5:11.
3 Chavatte P, et al. J Reprod Fertil Suppl. 1991;44:603.
4 Rossdale PD, McGladdery AJ. Vet Annu. 1992;32:201.
5 Ruark DW, et al. Am J Physiol. 1990;258:R1108. R1116
6 Rossdale PD. Vet Clin North Am Large Anim Pract. 1979;1:205.
7 Vestweber JG. Vet Clin North Am Food Anim Pract. 1997;13:411.
8 Dufty J, Sloss V. Aust Vet J. 1977;53:262.
9 Eales FA, Small J. Res Vet Sci. 1985;39:219.
The environment of the neonate can have a profound effect on its survival. This is especially true for lambs and piglets, in which hypothermia and hypoglycemia are common causes of death. Hypothermia can also predispose to infectious disease and can adversely affect the response of neonates in coping with an exogenous endotoxin challenge. Endotoxin exposure of hypothermic pigs results in an even greater reduction in body temperature.1
Lambs are very susceptible to cold and hypothermia is an important cause of mortality in the early postnatal period. Cold stress to neonatal lambs exists in three forms, ambient temperature, wind and evaporative cooling. The healthy newborn lamb has a good ability to increase its metabolic rate in response to a cold stress by shivering and nonshivering thermogenesis (brown adipose tissue). The energy sources in the neonatal lamb are liver and muscle glycogen, brown adipose tissue and, if it sucks, the energy obtained from colostrum and milk. The ingestion of colostrum can be essential for early thermogenesis in lambs, especially twin lambs.2
The critical temperature (the ambient temperature below which a lamb must increase metabolic heat production to maintain body temperature) for light birth-weight lambs is 31–37°C in the first days of life.
The risk for mortality from hypothermia is highest in lambs of small birth size. Heat production is a function of body mass while heat loss is a function of body surface area. Large-birth-size lambs have a greater body mass in relation to their surface areas and are thus more resistant to environmental cold stress. In contrast, small-birth-size lambs, with a smaller body mass relative to surface area, are more susceptible. The dramatic nature of this relationship was shown in early studies on cold stress and survival in lambs many years ago. Birth weight is lower in twins and triplets and in the progeny of maiden ewes. Susceptibility is also influenced by maternal nutrition in pregnancy (see next section), as this can both influence placental mass, birth weight and the energy reserves of the neonate, and also affect the activity of the ewe at parturition, and the resultant poor mothering behavior and mismothering can result in starvation in the lamb.
Lambs are particularly susceptible to cold stress during the first 5 days of life. During this period hypothermia can result from heat loss in excess of summit metabolism or from depressed heat production caused by intrapartum hypoxia, immaturity and starvation.3
Low-birth-weight lambs born into a cool environment where there is wind are especially susceptible because of the evaporative cooling of fetal fluids on the fleece.4 To a small newborn lamb the evaporative cooling effect of a breeze of 19 km/h (12 mph) at an ambient temperature of 13°C (55°F), common in lambing seasons in many countries, can be the equivalent of a cold stress equivalent to 25°C. The heat loss in these circumstances can exceed their ability to produce heat (summit metabolism) and progressive hypothermia and death results. Hypothermia due to heat loss in excess of summit metabolism can also occur when there is rain or just with cold and wind. This mortality occurs primarily in the first 12 hours of life.
Hypothermia occurring in lambs after 12 hours of age is usually due to depletion of energy reserves in periods of cold stress. There are three major causes. Milk is the sustaining energy source.
One of the early manifestations of developing hypothermia is the loss of sucking drive; severe cold stress and developing hypothermia can result in low milk intake and depletion of energy reserves.
The second important cause is mismothering; the third is related to birth injury. Dystocia-related hypoxia results in acidemia, a reduction in summit metabolism and disturbance in thermoregulation and can result in hypothermia.5 Birth-injured lambs, usually large single-born lambs, have depressed sucking and feeding activity.6,7 Systems are available for the categorization of deaths based on postmortem examination.7-9
In lambs that have hypothermia associated with heat loss in excess of summit metabolism, heat is required for therapy, but in lambs with starvation hypothermia the administration of glucose is also necessary. Glucose is administered intraperitoneally at a dose of 2 g/kg body weight using a 20% solution. Following the administration of the glucose, the lambs should be dried with a towel if wet and rewarmed in air at 40°C (104°F). This can be done in a warming box using a radiant heater as the heat supply. Care should be taken to avoid the occurrence of hyperthermia. Careful attention must be given to the nutrition of the lambs after rewarming otherwise relapse will occur. A feeding of 100–200 mL of colostrum will also be beneficial but lambs should not be fed before they are normothermic, as aspiration pneumonia is a risk. Experimental hypothermia in lambs has shown little direct long-term pathological effect.10
In most countries the selection of time of lambing is dictated by nutritional considerations and the seasonality of the ewes’ sexual behavior and lambing occurs at a time of year when cold stress is likely. The control of loss from hypothermia in newborn lambs requires supervision at lambing and protection from cold. Shed lambing will reduce cold stress loss. The provision of shelter in lambing paddocks may be effective but site is important as birth sites in lambing paddocks are not randomly distributed and there is variation in the preferred sites between breeds.5 Some ewes will seek shelter at lambing but many ewes in wool will not. In some flocks, sheep are shorn before lambing in an attempt to force this shelter-seeking trait.
Experimentally, there is a strong relationship between breed and the degree of hypothermia produced.10 There is also convincing evidence that rearing ability is heritable in sheep, that some of this relates to traits within the newborn lamb, and that a significant reduction in neonatal mortality associated with susceptibility to hyperthermia could be achieved with a genetic approach.6,7,10-12
Lambs are also susceptible to hyperthermia and thermoregulation is not efficient at high environmental temperatures. Heat prostration and some deaths can occur in range lambs when the environmental temperature is high, especially if lambs have to perform prolonged physical exercise and if there is an absence of shade.
Hypothermia as a result of environmental influence is less common in full-term healthy calves than in lambs but mortality rates have been shown to increase with decreasing ambient temperature and increasing precipitation on the day of birth.13 The critical temperature for neonatal calves is much lower than for lambs, approximately 13°C, and Bos taurus calves are more resistant to cold stress than Bos indicus.14
Experimentally produced hypothermia in calves has also been shown to cause little overt injury except for peripheral damage to exterior tissues.15,16 During cooling, there can be significant peripheral hypothermia prior to any marked reduction in core body temperature. Calves have a remarkable ability to resist and overcome the effects of severe cold temperatures.14,16 However, there is a relationship between the occurrence of cold weather and calf deaths, including those due to the ‘weak calf syndrome’, and deficiencies in thermoregulation occur in animals born prematurely and in dystocial calves. As in lambs, dystocia will reduce teat-seeking activity and sucking drive and dystocial calves have lower intakes of colostrum17 and lower body temperatures and decreased ability to withstand cold stress.18
Rewarming of hypothermic calves can be by radiant heat but immersion in warm water produces a more rapid response and with minimal metabolic effort. The prevention of hypothermia requires the provision of shelter from wet and wind for the first few days of life. Cows can be calved in a shed, or alternately sheds for calves can be provided in the fields. Beef calves will use shelters in inclement weather; these may not improve their health status, although they are in common use.19
Hypothermia from heat loss and hypothermia/hypoglycemia from starvation are major causes of loss in neonatal pigs.20 Newborn piglets have a reasonably good ability to increase their metabolic rate in response to cold stress but they have limited energy reserves, especially limited brown adipose tissue, and they consequently rely on a continual intake of milk for their major energy source, sucking approximately every hour. Young pigs have a good ability for peripheral vasoconstriction at birth but surface insulation is deficient because at this age there is no subcutaneous layer of fat. The critical temperature for young pigs is 34°C.
Thermoregulation is inefficient during the first 9 days of life and is not fully functional until the 20th day. Newborn piglets must be provided with an external heat source in the first few weeks of life. The body temperature of the sow cannot be relied upon for this and the preferred air temperature for neonatal pigs is 32°C (89.5°F) during the first day and 30°C (86°F) for the first week. In contrast, the preferred temperature for the sow is about 18°C. A separate environment (creep area) must be provided for the piglets. Providing there is an adequate ambient temperature to meet the requirements of the piglets, and good floor insulation, hypothermia will not occur in healthy piglets of viable size unless there is a failure of milk intake.
Birth anoxia, with resultant reduced vigor, reduced teat-seeking activity and risk for hypothermia, occurs particularly in later-birth-order pigs in large litters from older sows. Failure of milk intake can also occur with small-birth-size piglets and is influenced by litter size, low number of functional teats relative to litter size and teat sucking order.
There have been few studies on thermoregulation in foals but the large body mass in relation to surface area renders healthy newborn foals, like healthy calves, relatively resistant to cold. Also, foals are less likely to be born in a hostile environment than other farm animals. Significant foal mortality from hypothermia as a result of starvation and exposure can occur in extensively managed herds and dystocia, low birth weight and poor mothering are contributing factors.21
Sick and premature foals may have difficulty in maintaining body temperature in normal environments and the metabolic rates of sick foals and premature foals are approximately 25% lower than healthy foals.22,23
The relatively larger surface area to mass ratio, lower energy reserves and lower insulation of the coat of premature foals, coupled with the lower metabolic rate, places them at particular risk for hypothermia. Dystocial foals also have lower metabolic rates but dysmature foals appear to thermoregulate normally.22,24 Methods of investigation that allow postmortem differentiation of placental insufficiency, acute intrapartum hypoxemia, inadequate thermogenesis and starvation as causes of mortality in foals are described.8
Hypothermia should be suspected in premature foals when the rectal temperature falls below 37.2°C (99°F) and should be corrected with external warmth, rugging or moving to a heated environment. If fluids are being administered they should be heated to normal body temperature.
Alexander G, Barker JD, Slee J. Factors affecting the survival of newborn lambs. In A seminar in the CEC programme of coordination of agricultural research held in Brussels, January 22–23, 1985. Brussels: Commission of the European Communities; 1986.
Rook JS, Scholman G, Wing-Proctor S, Shea M. Diagnosis and control of neonatal loss in sheep. Vet Clin North Am Food Anim Pract. 1990;6(3):531-562.
Haughey KC. Perinatal lamb mortality: its investigation, causes and control. J South Afr Vet Assoc. 1991;62:78-91.
Carstens GE. Cold thermoregulation in the newborn calf. Vet Clin North Am Food Anim Pract. 1994;10(1):69-106.
Mellor DJ, Stafford KJ. Animal welfare implications of neonatal mortality and morbidity in farm animals. Vet J. 2004;168:118-133.
1 Carroll JA, et al. Am J Vet Res. 2001;62:561.
2 Hamadeh SK, et al. Sheep Goat Res J. 2000;16(2):46.
3 Eales FA, et al. Vet Rec. 1984;114:469.
4 McCutcheon SN, et al. NZ J Agric Res. 1983;26:169. 175
5 Eales FA, Small J. Res Vet Sci. 1985;39:219.
6 Haughey KC. Wool Technol Sheep Breed. 1984;31:139.
7 Haughey KC. J South Afr Vet Assoc. 1991;62:78.
8 Rook JS, et al. Vet Clin North Am Food Anim Pract. 1990;6:531.
9 Eales FA, et al. Vet Rec. 1986;118:227.
10 Slee J, et al. Aust J Exp Agric. 1991;31:175.
11 Alexander G, et al. Aust J Exp Agric. 1990;30:759.
12 Nash ML, et al. Vet Rec. 1996;139:64.
13 Azzam SM, et al. J Anim Sci. 1993;71:282.
14 Carstens GE. Vet Clin North Am Food Anim Pract. 1994;10:69.
15 Olson DP, et al. Am J Vet Res. 1981;42:758. 876
16 Olson DP, et al. Am J Vet Res. 1983;44:564. 572, 577, 969
17 Vermorel M, et al. Can J Anim Sci. 1989;69:103. 113
18 Bellows RA, Lammoglia MA. Theriogenology. 2000;53:803.
19 Olson DP, et al. Bovine Pract. 1989;24:4.
20 English PR. Vet Annu. 1993;33:107.
21 Haas AD. Can Vet J. 1996;37:91.
22 Ousey JC, et al. Vet J. 1997;153:185.
Effects on both the dam and the fetus can occur from overfeeding or underfeeding of the dam, and there can be effects from the influences of trace element deficiencies or toxic substances. Severe undernutrition of the dam can affect fetal size, and its thermogenic rate, with consequences mentioned earlier. Prepartum protein restriction has most effect.1 Severe undernutrition of the dam can also lead to weak labor, increased rates of dystocia and can limit the development of the udder. Colostrogenesis may be impaired, with a greater risk of infectious disease in the neonate, and milk production may be significantly reduced or delayed, with a risk of starvation.
Most information is available for the effects of nutrition of the pregnant ewe on fetal growth rate, udder development, the availability of energy in the body reserves of fetuses at term, and the amount and energy content of colostrum.2-4 In sheep, maternal nutrition can have a significant influence on fetal growth rate and on placental size. The underfeeding of hill sheep in late pregnancy markedly reduces the term weight of the udder and the prenatal accumulation and subsequent rates of secretion of colostrum.4 A low plane of nutrition in late pregnancy results in a marked decrease in fetal body lipid and brown fat reserves, and marked reductions in the total production of colostrum and in the concentration in colostrum during the first 18 hours after parturition.4 However, exposure of late pregnant ewes to cold by shearing increases lamb birth weight and lamb brown fat reserves.5,6
Inadequate nutrition can also result in in-utero growth retardation. Growth retardation can be produced in fetal pigs, lambs and calves by maternal caloric undernutrition. Nutritional restriction in ewes reduces the number of placental lactogen receptors that mediate amino acid transport in fetal liver and glycogen synthesis in fetal tissue, leading to depletion of fetal liver glycogen stores. This has been postulated as a possible cause of the fetal growth retardation that accompanies maternal caloric undernutrition. Runt pigs have a reduced metabolic rate and lower skeletal muscle respiratory enzyme activity. This deficiency persists after birth – runt pigs have a lower core temperature and a lessened ability to increase their metabolic rate and heat production in response to cold. Paradoxically, overnourishing the adolescent ewe will also result placental growth restriction and in in-utero growth retardation.7,8 This effect is most evident in the second third of pregnancy. This syndrome is accompanied by the birth of lambs with a shorter gestational age, commonly reduced by 3 days. It is thought that the fetal hypoxia and hypoglycemia that accompanies placental insufficiency might stimulate the maturation of the fetal hypothalamic– pituitary–adrenal axis initiating early parturition.
Maximum lamb survival is achieved at intermediate lamb birth weights and the nutritional management of the pregnant ewe in fecund flocks is very important.9 Ewes with multiple lambs can be selected using ultrasound and fed separately from those with singles. Pregnant maiden ewes should also be fed to their separate requirements. The recommendation is for a body condition score of 3.0–3.5 at mating, with a fall of 0.5 in score during the second and third months of pregnancy and a subsequent rise in score to 3.55 to the point of lambing, and with a distinct weight gain in late pregnancy. Equivalent condition scores are also appropriate for other species.
Toxic substances and trace element deficiencies can result in increased risk for fetal and neonatal mortality and are discussed under those headings. One of particular significance is agalactia, prolonged gestation and fetal distress at birth seen in mares fed grain contaminated with ergot (Claviceps purpurea) and in mares grazing tall fescue (Festuca arundinacea) containing the endophyte fungus Acremonium coenophialum.
1 Carstens GE. Vet Clin North Am Food Anim Pract. 1994;10:69.
2 Mellar DJ. Br Vet J. 1983;139:307.
3 Mellor DJ, Murray L. Res Vet Sci. 1982;32:177. 377
4 Mellor DJ, Murray L. Res Vet Sci. 1985;39:230. 235
5 Symonds ME, Lomax MA. Proc Nutr Soc. 1992;51:165.
6 Symonds ME, et al. J Physiol. 1992;455:487.
7 Wallace JM, et al. J Physiol. 2005;565:19.
Any examination of neonatal mortality suspected of being caused by hypothermia, starvation or infection due to failure of transfer of passive immunity, and even trauma by crushing in piglets, must take into account the possibility that poor mothering and a poor mother– young bond may be the primary cause. Inadequate maternal care leads to rapid death of the newborn under extensive conditions where there is no human intervention to correct the problem. The defect is most likely to be on the side of the dam but may originate with the offspring. A poor relationship may be genetic or nutritional and, on the part of the offspring, may be the result of birth trauma.
For both the dam and the young there is a much greater chance of establishing a good bond if the animal has been reared in a group rather than as an individual. Because sight, smell, taste and hearing are all important in the establishment of a seeking and posturing to suckle activity by the dam and a seeking, nuzzling and sucking activity by the offspring, any husbandry factor that interferes with the use of these senses predisposes to mortality. Weakness of the offspring due to poor nutrition of the dam, harassment at parturition by overzealous attendants and high growth of pasture are obvious examples. This can be a problem in cattle, pigs and sheep, and occasionally in horses, especially with extensive foaling practices.1 In pigs it may be developed to an intense degree in the form of farrowing hysteria, and is dealt with under that heading. In sheep it can be a significant contributor to neonatal death from starvation, especially in highly strung breeds like the Merino.2
Bonding occurs rapidly after birth, although there is some minor variation between species with bonding starting within a few minutes of birth in sheep but taking up to 2–3 hours in some horses.3 The strength of bonding also appears to vary between species.4 The bonding of the dam to the neonate is usually quite specific, although this can be modulated by management systems, and the neonate may be less selective and will often attempt to suck other dams. With sheep lambed under intensive lambing practices, this can lead to high rates of mismothering and subsequent abandonment, when preparturient ‘robber’ ewes adopt lambs from multiple births. A high degree of shepherding is required to minimize loss in these management systems, whereas in extensive systems a strong bonding is established providing the ewe and lamb are allowed to remain relatively undisturbed on the lambing site for 6 hours.2
Vaginal cervical stimulation and the central release of oxytocin are believed to be important in initiating maternal behavior5,6 though caudal epidural anesthesia for delivery does not effect mothering or bonding.7 Sucking is also a major determinant. Recognition is olfactory and auditory and mediated by the release of neurotransmitters.8
Bonding is often slower with primiparous dams and is also delayed where there is postpartum pain. A failure of bonding leads to rejection and abandonment of the neonate.
Maternal care is also important to neonatal survival and there is significant difference in litter mortality from crushing and injury between sows related to sow behavior and their response to piglet distress calls.9 A description of normal and abnormal behavioral patterns of the mare and foal is available10 and techniques for fostering are described.3,11
1 Haas SD, et al. Can Vet J. 1996;37:91.
2 Nowak R. Appl Anim Behav Sci. 1996;49:61.
3 Chavatte P. Equine Vet Educ. 1991;3:215.
4 Hopster H, et al. Appl Anim Behav Sci. 1994;44:1.
5 Kendrick KM, et al. Brain Res Bull. 1991;26:803.
6 Romeyer A, et al. Physiol Behav. 1994;55:395.
7 Scott PR, Gessert ME. Vet Rec. 1996;138:19.
8 Ohkura S, Kendrick KM. J Reprod Dev. 1995;41:143.
9 Wechsler B, Hegglin D. Appl Anim Behav Sci. 1997;51:39.
The medical induction of parturition by the parenteral injection of corticosteroid into pregnant cows during the last 6 weeks of pregnancy has raised the question of animal welfare and of the possible effects of prematurity on the disease resistance of the newborn calf. The induction of premature parturition in cattle has found application in five main areas:
• With pastoral-based dairy production, synchronization of the calving period has allowed maximal utilization of seasonally available pastures by the synchronization of peak demand for dry matter intake with spring flush in pasture growth. In pastoral-based herds with breeding for seasonal calving, late-calving cows will be induced and these average approximately 8% of the herd1
• Ensuring that calving coincides with the availability of labor to facilitate observations and management of calving and to overcome the inconvenience caused by late-calving cows
• Minimizing dystocia in small heifers
• The therapeutic termination of pregnancy for various clinical reasons, including potential problems such are associated with pregnancy in feedlot heifers
• As an aid in the control of milk fever using vitamin D analogs.2
A variety of short-acting and long-acting corticosteroids have been used. A single injection of a short-acting formulation is used when it is desirable to induce calving in the last 2–3 weeks of gestation. Earlier in pregnancy the long-acting formulations are more reliable. Sometimes this is followed in 5–8 days by treatment with a short-acting glucocorticoid. Parturition occurs 30–60 hours (mean 48 h) after injection.
Some reports have indicated that the mortality rate of induced calves was higher than expected, and that the level of serum immunoglobulins was lower because of interference with absorption by the corticosteroid. Mortality in calves born as a result of induced parturition is primarily as a result of prematurity and calf mortality is generally low when calving is induced within 12 days of parturition, although there are welfare concerns.3 The calves are usually lighter in weight. The health of calves that survive is generally good, provided they receive adequate quantities of colostrum. When short-acting corticosteroids are used to induce calving close to term, the ability of the calves to absorb immunoglobulins from colostrum is not impaired. However, calves born earlier in pregnancy after using long-acting corticosteroid are lethargic, slow to stand and to suck properly and their ability to absorb immunoglobulins is impaired.2 Up to 60% of calves born following induction with long-acting corticosteroids are at risk for failure of transfer of immunoglobulins. The colostrum available to such calves also has a reduced content of immunoglobulins, and there may also be a reduction in the total volume of colostrum available from the induced-calving cows.
Artificial induction of parturition is an important risk factor for retention of the placenta and the incidence is reported to vary from 20% to 100%1,4,5 Subsequent reproductive performance of induced cows can be impaired.1 A risk for acute Gram-negative bacterial infections is reported in a low (0.3%) proportion of cows following induction with dexamethasone.6
When parturition is induced in large herds of beef cattle, particularly with a high percentage of heifers, increased surveillance will be necessary after the calves are born to avoid mismothering. Every attempt must be made to establish the cow–calf pair (neonatal bond) and move them out of the main calving area. Heifers that disown their calves must be confined in a small pen and be encouraged to accept the calf and let it suck – sometimes a very unrewarding chore for the cowman. Calf mortality can be very high where calving is induced earlier than 35 weeks of pregnancy.3
The induction of parturition in mares for reasons of economy, management convenience, concern at prolonged gestation or clinical conditions such as prepubic tendon rupture, or research and teaching is now being practiced.7,8
Foaling is induced with oxytocin and occurs within 15–90 minutes of its administration.9 High doses of oxytocin are potentially dangerous to the foal and low doses (10–20 IU) are preferred. Glucocorticoids, antiprogestagens and prostaglandins that are effective in inducing pregnancy in other species are either ineffective in the mare or capricious in their efficacy, and can also be associated with adverse effects on the foal.8
Induction of parturition in the mare it is not without risk and has been associated with the birth of foals that are weak, injured or susceptible to perinatal infections. The period of fetal maturation is relatively short in the horse and is considered to be the last 2–3 days of gestation. Because spontaneous parturition in healthy mares can occur between 320 and 360 days there is the risk of delivering a foal that is premature and nonviable. Fetal maturity is the major prerequisite for successful induced parturition and the three essential criteria are:8
• A gestational length of more than 330 days
• Substantial mammary development and the presence of colostrum in the mammary gland with a calcium concentration greater than 10 mmol/L
The rise in calcium concentration is the most reliable predictor of fetal maturity and milk calcium concentrations above 10 mmol/L, in combination with a concentration of potassium that is greater than sodium, are indicative of fetal maturity. Commercial milk test strips are available for estimating mammary secretion electrolyte concentrations, however, it is recommended that testing be done in an accredited laboratory.8,10-12
In mature foals, head lifting, sternal recumbency and evidence of suck reflex occurs within 5 minutes of spontaneous full-term deliveries. The foal can stand within 1 hour and suck the mare within 2 hours. The behavior and viability of the premature foal after induced parturition have been described.13 The overall survival rate of foals delivered from induced parturition before 320 days of gestation was 5%.13 Four patterns of neonatal adaptation were observed on the basis of righting, sucking and standing ability. If the suck reflex was weak or absent and the foals were unable to establish righting reflexes, the prognosis of survival was poor. Foals born before 300 days of gestation did not survive for more than 90 minutes; foals born closer to 320 days of gestation had a better chance of survival and exhibited behavioral patterns of adaptation.
In addition to the potential delivery of a premature or weak foal, other adverse effects of induction can be dystocia, premature placental separation and retained placenta.
The induction of parturition of gilts and sows on days 112, 113 or 114 of gestation is highly reliable and can be achieved by a single intramuscular injection of 175 mg of cloprostenol or 5–10 mg of prostaglandin F2α.14 The sows farrow approximately 20–24 hours later. The interval to onset can be decreased by the use of oxytocin.15
Induction of parturition has been used on large-scale farms to allow a concentration of labor and improve supervision and care at the time of farrowing, and to reduce the incidence of the mastitis/metritis/agalactia syndrome16 and reduce the percentage of stillborn piglets. The end-day of a batch farrowing system can be fixed and weekend farrowing avoided. The subsequent fertility of the sows is not impaired. Induction on day 110 may be associated with a slight increase in perinatal mortality.
The induction of parturition in sheep is not commonly practiced but it can be used to synchronize lambing in flocks where there are accurate dates of mating for individual ewes. Unless accurate dates are available there is risk of prematurity. Also, ewes that are more than 10 days from their normal parturition date are unlikely to respond.17
Induction of parturition is also used as a therapeutic ploy to terminate pregnancies in sheep with pregnancy toxemia.
Induction is usually with dexamethasone, betamethasone or flumethazone.18,19 Lambing occurs 36–48 hours later and there may be breed differences in response. Variability in lambing time can be reduced by the use of clenbuterol and oxytocin.20
MacDiarmid SC. Induction of parturition in cattle using corticosteroid: a review. Part 1. Reasons for induction, mechanisms of induction and preparations used. Anim Breed Abstr. 1983;51:403-419.
MacDiarmid SC. Induction of parturition in cattle using corticosteroid: a review. Part 2. Effects of induced calving on the calf and cow. Anim Breed Abstr. 1983;51:499-508.
Pressing AL. Pharmacologic control of swine reproduction. Vet Clin North Am Food Anim Pract. 1992;8:707-723.
Hemsworth PH, Barnett JL, Beveridge L, Mathews LR. The welfare of extensively managed dairy cattle: a review. Appl Anim Behav Sci. 1995;42:161-182.
Ingoldby L, Jackson P. Induction of parturition in sheep. In Pract. 2001;23:228-231.
Macmillan KL. Advances in bovine theriogenology in New Zealand. 1. Pregnancy, parturition and the postpartum period. NZ Vet J. 2002;50(3 Suppl):67-73.
1 Macmillan KL. NZ Vet J. 2002;50(3 Suppl):67.
2 MacDiarmid SC. Anim Breed Abstr. 1983;51:403-499.
3 Morton JM, Butler KL. Vet Rec. 1995;72:5.
4 Verkerk GA, et al. Proc NZ Soc Anim Prod. 1997;57:231.
5 Guerin P, et al. Vet Rec. 2004;154:326.
6 Browning JW, et al. Aust Vet J. 1990;67:28.
7 Camillo F, et al. Equine Vet J. 2000;32:307.
8 Ousey J. Equine Vet Educ. 2003;15:164.
9 Macpherson ML, et al. J Am Vet Med Assoc. 1997;210:199.
10 Ousey JC, et al. Equine Vet J. 1984;16:259.
11 Leadon DP, et al. Equine Vet J. 1984;16:256.
12 LeBlanc MM. Equine Vet J. 1997;24:100.
13 Leadon DP, et al. Am J Vet Res. 1986;47:1870.
14 Podany J, et al. Pig News Info. 1987;8:24.
15 Pressing AL. Vet Clin North Am Food Anim Pract. 1992;8:707.
16 Scott E. Pig J. 1994;32:38.
17 Ingoldby L, Jackson P. In Pract. 2001;23:228.
18 Niemann H. Reprod Domest Anim. 1991;26:22.