VEIN : Sheep Health & Production : Chapter 7. Reproductive management and diseases in naturally mated flocks

The reproductive capacity of grazing animals serves two essential functions. First, animals are produced for sale, and this is often a fundamental production objective of the herd or flock owner; and second, replacement animals are bred to maintain flock and herd size as older animals die or are cast for age. In stud flocks and herds, reproduction also provides the capacity to select animals with desired characteristics and to change the gene frequency of heritable traits in the population.

In prime lamb flocks, the role of reproduction seems fairly clear - the higher the reproductive rate, the more lambs are sold per ewe present. Higher reproductive rates have higher biological efficiency, but this may or may not translate into increased economic efficiency - a point which will be discussed further.

In self-replacing flocks, the role of reproduction involves both functions. In some flocks, all male offspring are sold as lambs or hoggets. In many flocks, however, very few young animals are sold and the major source of income is derived from the sale of wool. Reproductive capacity chiefly serves to replace older animals which had been retained as wool growers only or wool growers and breeders, in the case of ewes. Flock owners who view themselves primarily as wool producers maintain a ewe flock chiefly to provide a source of efficient wool growers - ie, wethers. The ewe flock is seen as a means to that end rather than as a producer of sale sheep.

This chapter discusses reproduction in sheep in Australia and reviews the major veterinary activities associated with reproductive management and diseases. The reproductive performance of Australian sheep flocks is primarily limited by the relatively low genetic potential of Merino ewes and the level of nutrition made available to them under normal commercial management. Nutrition is often limiting because of the need to compromise reproductive rate, on a per-ewe basis, for the sake of increasing overall productivity on a per-hectare basis. Additionally, other husbandry strategies may adversely affect reproduction and ultimately a compromise is reached which, hopefully, maximises profit rather than any one index of sheep flock performance. It is essential that veterinarians who are requested to investigate apparently poor reproductive performance are aware of all of the major factors which influence reproductive rates, or there is a danger that much time and money could be wasted on unnecessary investigations in search of some improbable disease.

The potential financial benefits for the producer from increasing reproductive rate are also discussed to provide a context for planning rational veterinary intervention. A proper evaluation of reproductive rate and its contribution to the economic performance of a sheep flock requires a systems approach, as discussed in Chapter 3 of these notes. It is important to review all of the ramifications of changes in reproductive performance for they are unlikely to be limited to a change in numbers of sale sheep only.

Factors determining reproductive rate

Reproductive rate (RR) can be measured in a number of ways. Producers commonly report lamb marking rates because accurate counts are made of lambs present at marking and, under usual circumstances, the death rate of lambs between marking and weaning is low. The rate is reported either as lambs marked per 100 ewes present at marking, or per 100 ewes present at joining. It is important to know which number is used as the denominator - there will often be up to 5 percentage points difference between the two figures.

A short-hand way to record the method of calculation is to use abbreviations; lambs marked per ewe joined is written as LM/EJ. Lambing rates (LB/EJ) are rarely known in commercial flocks, although estimates can be made if ultrasound pregnancy diagnosis is used.

In Australian Merino flocks, marking rates of 75% to 85% are commonly achieved and considered satisfactory by most producers. In areas well suited to the health and productivity of Merino sheep, such as the medium to low rainfall areas of southern Australia, marking rates are commonly 85% to 95%, particularly in flocks of South Australian strain Merinos. In areas not so well suited, either through nutritional limitations, predation or other environmental effects, marking rates may be less than 70% and flock owners may find it difficult to maintain the size of the ewe flock without retaining ewes into old age.

From a mathematical point of view, rather than a physiological one, marking rates are determined by fertility, fecundity and the survival rate of lambs from birth to marking. By definition, fertility is the proportion of ewes present at lambing which lamb; fecundity is the average number of young born per lambing ewe. Fertility is sometimes reported as the proportion of ewes detected pregnant in mid-pregnancy by ultrasound. This measure of fertility is generally valid but ignores foetal losses beyond mid-pregnancy.

Fertility, fecundity and survival rate of lambs to marking age

The fertility of mature ewes is usually high; often over 90% of ewes conceive in a 5 week joining period, provided no adverse factors, such as oestrogenic pastures, are operating. It does vary, however, with breed, date of joining, duration of mating and other management factors. Fecundity varies markedly with season, nutrition, age, breed, strain and bloodline. Lamb survival rates also vary markedly. For Merinos, approximately 80% to 90% of single and 60% to 80% of twin-born lambs should survive, if conditions are good. Parity greater than two is unusual in commercial Merino flocks and survival rate of triplet or higher parity lambs is very low under paddock conditions.

Table 7.1 Two different combinations of fertility, fecundity and lamb survival rate

As an illustration of how they contribute to marking rate, Table 7.1 shows two possible ways by which an 85% marking rate can be achieved. Of the two examples, the second involves higher lamb losses and is a less efficient process, both in biological and economic terms.

The fertility of a flock can be estimated by pregnancy testing and by observations at lambing time. When fertility is low, however, it is instructive to further consider the factors which contribute to fertility so that appropriate corrective action can be taken. Infertility is defined as a failure to lamb. Because abortion in ewes is uncommon in Australia, it is generally true that infertility results from failure to mate, failure of fertilization in ewes which do mate, or embryo mortality, and is influenced by ovulation rate. Infertility or prenatal wastage, if measured by pregnancy diagnosis in mid-pregnancy, must, therefore, be explained in terms of deficiencies in the management of ewes and rams before and during joining. If fertility is recorded at lambing, the abortion rate must be considered as contributing to the estimate of fertility. Before we further examine problems in the management activities relevant to failures in reproduction, some reproductive physiology must be revised .

Physiological, management & disease factors affecting fertility up to mid-pregnancy

To achieve high fertility, ewes must ovulate and be mated, the rams that mate them must have good semen quality and the maternal environment must be conducive for fertilization and embryo development. If rams and ewes are in good health and free of some specific disease conditions, the ovulation rate is the most labile determinant of fertility and the key determinant of fecundity. In this section the factors which influence these components of fertility will be discussed. Some of these factors are physiological and/or nutritional and are most strongly controlled by flock husbandry decisions; some are specific disease entities which operate independently of husbandry decisions; some involve aspects of physiology, nutrition and disease.

Photoperiodicity in the ewe

On breeding properties a key management decision is when to join. The decision is usually based upon consideration of (a) the optimal time for marketing the resulting progeny, such as prime lambs, ram lambs, stud 2‑tooth rams et cetera and (b) the reliability, quantity and quality of pasture available at different times of the year to support late pregnant and lactating ewes and to permit good lamb growth and weaning weights. (The inter-relationships are discussed, with an example, in Chapter 3.) However, the decision should also take some account of the underlying physiology of reproduction in the ewe and ram.

Sheep are short‑day breeders and, in the breeding season, ewes cycle or return to oestrus every 16‑18 days. Figure 7.1 shows the incidence in Australia of spontaneous ovulation in Merino, British breed-Merino crossbred (XB) and British breed ewes throughout the year. It illustrates the pattern of photoperiodic regulation of breeding activity. Increasing daylength synchronizes the onset of cyclic activity and decreasing daylength sustains this activity. Most British breeds have a sharply defined breeding season, from late February to the end of June. In these breeds and in XB ewes ovulation rate (OR) (and consequently also conception rate) declines during the breeding season. For example, (Border Leicester x Merino) XB ewes often exhibit a mean OR of about 1.7 in late February‑March but only about 1.3 in May‑June.

Figure 7.1 The incidence of ovulation in Merino, crossbred and British Breed sheep throughout the year.

In the Merino ewe there is spasmodic andvariable spontaneous breeding activity at other times of the year. The level of activity and depth of anoestrus is markedly influenced by type/bloodline and environment. More importantly, the introduction of rams outside the breeding season will usually cause the majority of Merino ewes to cycle. The manipulation of the ’ram effect’ is discussed in Chapter 8. Table 7.2 contrasts typical results of spring and autumn joinings, in terms of several indices of reproductive performance. To interpret these data, assume that the ewes werejoined for 6 weeks with 2% rams; that spring means October/November and autumnmeans March/April. The ORs in these ewes were about 1.2 and 1.5 in spring and autumn, respectively. The table shows clearly the superiority of in‑season joinings for Merinos. Nevertheless, for other economically more important reasons, Merinos are often joined out‑of‑season. A summer joining in December/January produces a result intermediate to those shown in Table 7.2. Merino studs in NSW commonly sell flock rams as 2‑tooths at sale times late in the year. This results in pressure to join in summer rather than autumn, to produce rams which are better grown at sale. The proportion of ewes which lamb after spring and summer joinings can sometimes be increased by extending the period of joining by 2‑4 weeks and can certainly be increased by utilizing certain controlled breeding techniques (Chapter 8). Merino ewes are not joined early in the non‑breeding season since lambings in December‑February are not desired. This is fortunate, since in July‑September the ewes are in deeper anoestrus and exhibit quite unsatisfactory reproductive performance.

Table 7.2 : Effect of time of mating on reproductive performance of Merino ewes at Trangie, NSW (averages of 4-6 easons)

Effects of bodyweight and nutrition on ewe fertility and ovulation rate

In mature Merino ewes there is a good correlation between bodyweight and OR. Of course suitable bodyweights for joining mature ewes will depend on the Merino type/bloodline. For medium wool Merino types a target of 45‑50 kg is often recommended. For Merinos in general, it is probably more useful to specify target condition scores (3‑4) rather than target bodyweights. Bodyweight influences fertility as well as OR. Thus a number of studies have suggested that over a specified weight range in adult Merinos every kilogram increase in weight at joining yields about an extra lamb per 100 ewes lambing and two extra lambs per 100 ewes joined. Ovulation rates in maiden or 2‑tooth Merino ewes are generally low, so that here the relationship between bodyweight and OR is not so obvious. On the other hand, bodyweight is usually the key determinant of fertility in maiden flocks.

Flushing ewes

Flushing is the practice of increasing the feed available to ewes prior to and during joining, to raise OR and fertility. Table 7.3 shows some effects of flushing on bodyweight and twinning rate in spring and autumn joined Merinos. Note that flushing had a large impact on OR in autumn joined ewes. As already noted, OR is higher in autumn and more responsive to nutritional manipulation. Of course many clients with Merino flocks are not desirous of large increases in the twinning rate and, consequentially, higher lamb losses but rather seek to utilize some degree of flushing to increase the proportion of ewes which lamb (fertility). Giving additional feed to ewes which are 3 score or less over several weeks can be expected to raise both bodyweight and OR. However, OR is more sensitive to changes in feeding, and following the commencement of flushing, increased OR can often be seen before any change in bodyweight can be detected. Flushing Merino ewes with lupins has become popular. The ewes typically receive lupin grains at the rate of 500 g per day. Increases in OR can be seen within 7 days of commencing feeding. It is usually recommended that ewe flocks be fed grain for one week prior to and during the first 3 weeks of joining. The responses obtained vary considerably between flocks. In flocks which respond well, the OR increases by 0.3‑0.4, and the % ewes lambing by 10‑15%. Methods for feeding out lupins and the possible occurrence of lupinosis are discussed elsewhere. The mechanism by which flushing affects OR remains unclear, but appears to involve elevated plasma insulin levels.

Table 7.3 : Effect of flushing on lambing in Merinos

* 3 weeks prior to joining and first 3 weeks of joining
” increase in kg during period of flushing

Effect of ewe age on fertility and ovulation rate

Both the ovulation rate of ewes and their maternal ability increase with age. Ovulation rate peaks at 5 to 7 years of age. Mature ewes out-compete maiden ewes for the attention of rams at joining. Compared to mature (22 years or more) ewes, maiden ewes have a shorter oestrus and less overt oestrous behaviour, are less attractive to rams and are mated on fewer occasions during each oestrus. These effects all contribute to the lower fertility of maiden ewes compared to older ewes. The inexperience and age of maiden ewes contribute to their poorer maternal ability and the lower survival rate of lambs born to maiden ewes.

Ovulation without oestrus

Some ovulations in the ewe are unaccompanied by oestrus and, hence, mating. Such ovulations occur at the onset of puberty, at the start and perhaps the end of each breeding season and, in the case of Merinos, quite commonly during spring and summer. Silent heats occur when ovulation is not immediately preceded by a period of progesterone priming in the brain. Within the breeding season this priming is reliably supplied by the corpus luteum of the previous oestrous cycle. Note that this ’luteal progesterone’ has other important roles, permitting normal functioning of the new corpus luteum and uterine endometrium after the next ovulation. Whereas ovulation without oestrus is quite common, oestrus without ovulation appears to be very unusual.

Failure of fertilization due to maternal factors

Fertilization may fail due to faults in the maternal reproductive tract environment. Pasture oestrogens interfere with sperm transport through the cervix, as detailed below. Various controlled breeding techniques (eg synchronization of oestrus with progestagen sponges and superovulation of donor ewes for MOET) also alter cervical function and impair sperm transport. Many studies have indicated that in naturally cyclic ewes which ovulate more than one ovum, fertilization is nearly always ’all‑or‑none’, ie if a ewe ovulates three ova, the outcome is three zygotes or no zygotes.

Little is known about possible causes of defective oocytes in ewes where natural ovulation and mating occur, and their occurrence is probably rare.

Phyto-oestrogenic infertility

Phyto-oestrogenic infertility in ewes occurs as a result of the oestrogenic activity of isoflavone metabolites which are found mainly in the laminae of green legumes, notably some cultivars of subterranean clover (Trifolium subterraneum) and red clover (T pratense). Temporary infertility occurs when ewes are mated on green oestrogenic clover. The reduction in fertility recovers to normal levels within a few weeks of removal from the pasture. Permanent infertility (’clover disease’) occurs when the ewes graze such pastures for extended periods, leading to permanent changes in the reproductive tract. While the most severe forms of this disease are rarely seen now, sub-clinical permanent infertility is probably very common.

Pathophysiology

Chronic phyto-oestrogenism is histologically a syndrome of masculinisation. Transsexual differentiation of glandular and epithelial tissues leads to reproductive disorders in ewes and urinary tract problems in wethers. Rams do not appear to be affected.

Biochemistry

Two of the ingested isoflavones, formononetin and daidzein, are converted in the rumen to equol. Equol is absorbed and most of it is conjugated in the plasma with glucuronic acid. The small proportion of unconjugated equol is strongly oestrogenic and is the major active oestrogen responsible for clover infertility[1].

Oestrogenic cultivars

The ’sub-clover’ cultivars with the highest isoflavone levels are Yarloop, Dwalganup and Dinninup. Medium levels are found in Geraldton and Tallarook.

Permanent infertility

The abnormalities induced by the chronic ingestion of phyto-oestrogens are totally different from those of temporary infertility and are not an extension of the responses occurring during episodes of temporary infertility[2]. The principal lesions causing lower reproductive rates occur in the cervix. These lesions, which present no clinical signs, are the most important abnormalities occurring in sub-clinical permanent infertility.

Cervical changes

The superficial epithelium of the cervix of ewes exposed chronically to oestrogenic clovers contains a lower proportion of stratified squamous and mucus cells and a greater proportion of single layered columnar cells. The changes in the cervix are, in effect, a transdifferentiation of the endocervix so that it resembles endometrium[2]. As a consequence of both structural changes and a loss of ability to respond to endogenous oestrogen, the cervical mucus in affected ewes is very watery; it has a decreased spinnbarkheit (visco-elasticity). Without this normal mucus structure, sperm transport through the cervix is greatly impaired[3]. There is a large decrease in the number of sperm reaching the oviducts of clover-affected ewes.

Uterine changes

Chronically affected ewes develop endometrial cysts as a result of cystic hyperplasia of the endometrium. This may be complicated by a bacterial endometritis. The endometrial pathology, however, appears to have less effect on conception rates than the poor sperm transport.

Dystocia

Clover affected ewes often suffer from dystocia due to secondary uterine inertia consequent on a failure of the cervix to dilate. Septic metritis is a common sequel.

Lactation in maiden ewes and wethers

The mammary secretion varies from a yellow viscous fluid to apparently normal milk. The degree of teat elongation in wethers has been used as an index of pasture oestrogenicity but may be too sensitive to distinguish differing levels of oestrogenic intake.

Other effects on wethers

Uroliths containing crystals of equol metabolites can obstruct the urethra, particularly at the urethral process. The squamous metaplasia of the prostate and bulbourethral glands which also occurs in wethers grazing oestrogenic pastures may contribute to the formation of crystals and may encourage obstruction in the pelvic urethra[1].

Effects on fertility

While the lesions of ’permanent infertility’ are indeed permanent, the infertility is not complete. Affected ewes can still produce lambs. The effect of the phyto-oestrogens is to reduce the probability of each ewe conceiving under normal flock management and hence to reduce the flock’s reproductive capacity. Although the classical ’clover disease’ is now rarely seen, on properties where it does occur ewe survival rates are reduced by conditions such as hydrops uteri, dystocia and uterine prolapse. With both the severe form and the sub-clinical form, phyto-oestrogens have their predominant effect on the number of ewes lambing. As the effects accumulate, ewe conception rates progressively decline with age.

Diagnosis

Phyto-oestrogenic infertility must be differentiated from other common causes of low marking percentages, particularly under-nutrition of ewes at joining and in late pregnancy, infertility of rams, particularly that caused by ovine brucellosis, and high perinatal lamb mortalities from a variety of causes. Pregnancy diagnosis of ewes and examination of the rams will assist the diagnosis.

Classical clover disease can be diagnosed by the presence of clinical signs in ewes and wethers, the high incidence of dystocia and the history of severely depressed marking rates. Sub-clinical permanent infertility is more difficult to diagnose because clinical signs are absent and the history is often unremarkable - marking rates may be lowered by only 10% to 20%. Definitive diagnosis will be made on the cervical histopathology of a sample (minimum of 12) of older ewes from the flock[4] and the agronomic identification of a significant content of oestrogenic cultivars of T subterraneum in the pastures.

Control

The long term solution is pasture renovation - to replace the oestrogenic cultivars. This is neither easy nor cheap; the cost of the problem must be weighed up against the potential loss of often very productive pastures[5].

Short term control includes the assessment of the risk associated with each pasture on the farm. The young ewes (weaners and hoggets) are grazed on the least oestrogenic pastures during the times of the year when the pastures are green. Dry ewes (never to be mated), wethers and old ewes (with short breeding futures) are grazed on the high risk pastures.

Extension of the breeding season by leaving the ram in with the ewes for long periods may increase the lambing percentage and is practised on some properties to allow the production of sufficient ewe hoggets for breeder replacements.

Temporary infertility

Ewes grazed on green oestrogenic pastures during joining may show reduced conception rates. The effects of the phyto-oestrogens include a reduction in the incidence of oestrus, interference with ovum transport and a reduction in sperm transport[6]. Some experiments have also shown a negative effect on ovulation rate[7]. Some of the effects of grazing plant oestrogens may persist for 3 weeks after removal from the pasture but not for 5 weeks[7].

Coumestans in Medicago spp

Coumestans in lucerne (Medicago sativa) and some other medic species are also oestrogenic but their effects are always temporary. They reduce ovulation rate during the period that ewes are grazing them but the effects disappear upon removal. Lucerne often develops high coumestan levels late in its growing season[8].

Photoperiodicity in the ram

The full transformation from spermatogonia to spermatozoa through several intermediate cell types and both mitotic and meiotic cell divisions is called the spermatogenic cycle and takes about 49 days in the ram. Hence, to get the best responses, treatments applied to rams to improve their production of sperm should begin 7‑8 weeks before joining. Rams are also short‑day breeders, but seasonality is less marked in the ram than the ewe. Merino rams will generally perform satisfactorily at all times of the year. The degree of seasonality in rams of different breeds can be estimated from the difference between maximum and minimum testis volume (or weight) during the annual cycle. The ratios of minimum to maximum volumes for Merino and Romney rams are about 0.8 and 0.5, respectively. The rams of some British breeds perform quite poorly out‑of‑season.

Bodyweight, nutrition and fertility in the ram

There are important relationships between nutrition, condition score, testis size, libido, semen quality and semen volume in mature rams. A condition score of 3‑4 at the commencement of joining is recommended. At this time, Merino rams should have at least 400 ml of testes or a scrotal circumference of 30 cm. Good active rams lose condition during joining, especially during the first three weeks (or ewe cycle length). This is associated with reduced grazing. The same rams should not be used for successive joinings, unless they are given a spell of 6‑8 weeks, with adequate feeding. Excessive feeding resulting in obesity may reduce libido, whereas inadequate nutrition certainly reduces testis size, libido and semen volume. In general, plane of nutrition has little influence on semen quality. Each gram of testes in Merinos produces on average about 20 x 10[6] spermatozoa per day. However, high planes of nutrition also increase the rate of spermatozoa production per gram of testes; so that additional feeding increases sperm production more than the increase in testicular weight would suggest. Lupin supplementation is often used to increase ram testes volume and fertilizing ability. A supplement fed at the rate of 500 g lupin grain per day for 8‑10 weeks can increase testes volume in Merinos from around 400 ml to about 600 ml. This should enable the use of fewer rams at joining, and the saving related to purchasing fewer rams easily covers the cost of feeding the supplement.

Puberty and age effects in rams

Well grown Merino ram lambs reach puberty at around 6 months of age and by 12 months can produce ejaculates containing a high concentration of highly motile spermatozoa. However, the process of sexual maturation is slow, and 22 ‑year‑old rams usually produce considerably more spermatozoa than 12 ‑year‑olds. Young rams are less experienced at mating behaviour than older rams and are subject to social domination by older rams if they are used in mixed age ram syndicates. The question of how long rams should be retained has genetic, economic and disease control implications, but as a general rule producers should aim to replace 1/4 ‑1/3 of rams annually.

Husbandry procedures and ram fertility

Heat stress decreases semen quality. This occurs commonly in shedded rams (Merinos and British breeds) where ventilation and temperature control are inadequate. Under paddock conditions heat stress is uncommon in Merinos but more common in British breeds. The difference is explained in part by the more pendulous nature of the Merino’s scrotum. Testicular temperature should be 5EC lower than body temperature in Merinos. Merino rams with heavy skin wrinkle have a relatively poor ability to control testicular temperature and should not be used where joining coincides with high temperatures.

Semen quality often declines for some weeks after shearing. For example, this phenomenon is seen if shearing coincides with hot weather or is associated with dipping in certain chemicals. Merino rams are best shorn twice a year and first joined when they are carrying 3‑4 months wool. The scrotum should not be shorn. Keeping rams in good general health and free of infectious disease is an important component of reproductive management. It is also one of the easiest. The ram team is a numerically small component of the sheep flock so it is relatively inexpensive to provide them with excellent nutrition and health care. Failure of the rams to perform satisfactorily is rarely a cause of severely low reproductive rates. More often, poor ram performance is only a contributing factor to reproductive wastage.

Management of joining

Ewes

Ewes are sometimes joined in age groups or, more commonly, the maidens are joined as a separate mob. Maidens tend to be poor competitors with older, more experienced ewes exhibiting a longer and stronger oestrus. However, experience varies, and some producers obtain satisfactory or good fertility in the maidens when all ewes are joined as a single mob. Maiden medium wool Merinos should have reached a bodyweight of 40‑45 kg at joining to ensure reasonable fertility.

Merino ewes may be usefully crutched just prior to joining, but it unwise to join recently shorn ewes. For about 10 weeks after shearing, shorn ewes are less sexually attractive to rams than are woolly ewes.

Ewes and rams

It is preferable to organize the farm management calendar so that few, if any, procedures need to be carried out on the ewes or rams during the joining period. Repeated mustering, yarding and handling interferes with ram‑ewe contact and may reduce flock mating activity and fertility. It is worth keeping in mind also the possibility that chemicals employed to control parasites and other diseases just before or during joining may interfere with fertilization or embryo development.

Duration of joining

In practice, management decisions about the joining ratio and duration of joining are considered together, since they are somewhat interrelated. It is not easy to determine in advance on a particular property the minimal number of rams and minimum length of joining period which will result in good flock fertility. For in‑season joinings, where the ewes should be cycling regularly, 6 weeks is adequate. This gives each ewe 2 or 3 opportunities to become pregnant, depending on how soon after the commencement of joining that oestrus occurs. For out‑of‑season joinings, where most or all the ewes are in anoestrus at the commencement of joining, a period of 8 weeks is required, and this is sometimes increased to 10 weeks. The optimal duration of joining is probably always a compromise between seeking to maximize flock fertility and avoiding the several management penalties associated with prolonged lambings. These include such problems as the reduced efficiencies of vaccinations and drenching, the greater unevenness of the lambs at marking and weaning and the inferior condition and fertility of some ewes at the next joining.

Composition of ram syndicates

A group of rams which is joined to one mob of ewes is termed a ram syndicate. Normal practice is for syndicates to consist of some mature, experienced rams and some (maiden or 12 inexperienced rams. Under these conditions, the dominance behaviour of older rams will generally ensure the young rams are under-represented in successful matings. Some producers join young rams separately from older rams but this may lead to slightly reduced fertility in the flock. In the interests of maximising flock fertility, maiden rams should probably be omitted from syndicates joined to maiden ewes and it is unwise to mate syndicates composed only of maiden rams to mobs of maiden ewes.

Joining ratio

As a general rule, rams seem able to cover ewes adequately at a ratio of 1% rams to ewes. With autumn joinings it may be useful to reduce the number of rams after the first 18 days; surplus rams can then be used for joining to other flocks, if required. This practice is unwise with out‑of‑season joinings. The problem with using 1% rams routinely is that there are several circumstances where 1% is probably not enough. Examples to consider are where:

Joining ratios should be increased above 1% where one or more of these circumstances are present; it is unusual but sometimes the case that 2% rams are not enough. In practice, many producers simply run 2% of rams with their ewe flocks and leave it at that. If some of the circumstances listed above do not apply, this policy could be quite wasteful. As already mentioned, the joining ratio can be reduced somewhat if rams to be used for joining have been selected on the basis of a thorough soundness examination, testicular volume and perhaps serving capacity tests.

Failure of fertilization due to too few rams

When adequate rams are employed, nearly all ova should be fertilized (probably >95%). As the joining ratio diminishes, conception rates will tend to fall. Table 7.4 shows the percentages of ewes in a flock which will lamb following joinings of one, two and three cycle lengths. A conception rate of 70% (% ewes lambing to one oestrus) is quite satisfactory for Merinos. As conception rate decreases with diminishing rams so too does the % of ewes lambing, but note how the effect of conception rate on % lambing is moderated by increasing the length of the joining period. Most of the reduction in conception rate is due to oestrous ewes not being mated at all; but some of the reduction may be associated with failure of fertilization in mated ewes. The data in Table 7.4 are probably a little in error; where the conception rates to the first cycle were only 60 and 50%, due to too few rams, they probably rose to around 70% for the second and third cycles (by which time the ’functional’ joining ratio was much increased).

Failure of fertilization due to other ram factors

As already noted, where natural mating is well managed nearly all ova should be fertilized. Failure of the ram to deposit into the vagina adequate normal, motile sperm may be a problem. This could possibly result from the use of too few, overworked rams. However, it is more likely that the problem is related to abnormalities of the testes and/or male reproductive tract, due to infectious diseases or injury. Note, however, that rams with brucellosis and some other genital infections can often still produce ejaculates with good numbers of normal, motile sperm. Defective spermatozoa commonly result from excessive heating of rams. Some rams routinely produce ejaculates of low quality for no obvious reason.

Non-specific abnormalities of the epididymis which affect ram fertility

A spermatocoele is a cystic dilatation of the epididymal duct with the accumulation of sperm in the cyst. It follows acquired or congenital occlusion of the duct. If extravasation of sperm occurs the stromal tissue produces a characteristic granulomatous response. Spermatic granulomas which develop secondarily to congenital occlusion are usually in the head of the epididymis. Congenital obstruction in rams and goats is not uncommon and is usually unilateral.

Obstruction of the epididymal duct in the head, body or tail leads only slowly to testicular degeneration. The efferent ducts are able to resorb most of the products of the seminiferous epithelium except sperm. Obstruction of the efferent ducts, on the other hand, leads rapidly to testicular atrophy[9].

Spermatic granulomas which develop secondary to bacterial infection are usually found in the tail of the epididymis because the majority of bacterial infections start and are most severe at that site. The two most common bacterial infections of epididymes in Australian sheep flocks are those caused by Brucella ovis and by Actinobacillus seminis. The palpable lesion of the epididymis typical of Br ovis infection is, in fact, a spermatic granuloma in the tail of the epididymis. Spermatic granulomas following obstruction of the duct caused by trauma has been reported in Dorset rams[10].

Epididymitis caused by Brucella ovis infection (Ovine brucellosis, OB)

Epididymitis caused by Br ovis is the most common lesion of the genitalia of Merino rams culled from Australian flocks. In one survey, epididymitis was identified in 19% of rams and Br ovis was associated with 47% of those[11]. There is a lower flock prevalence of infection in Merinos than in British breeds. The prevalence of infection on some properties may exceed 50% of rams but this is uncommon. Generally, fertility is not compromised until the proportion of rams with chronic, palpable lesions exceeds 10% to 20%. Economic wastage occurs from extension of the lambing period[12][14], reduction of lambing percentage and an increased size and rate of turnover of the ram team[14].

Epidemiology

Rams can become infected as young as 4 months of age[15]. Transmission of infection occurs mainly from ram to ram, via the ewe’s vagina principally but also by homosexual activity between rams[16]. Rams can become infected by inoculation of mucosal surfaces including the prepuce, conjunctiva and nasal mucosa. Infection in ewes is usually short-lived. Experimental infection of ewes at mating[12][17][18] indicate that infection can persist in the ewe, leading to returns to service, abortion, birth of weak lambs and perinatal mortality. The incidence of infection in the field is, however, low and the role of persistently infected ewes in the maintenance of infection in the ram flock is insignificant. In chronically infected rams, active excretion of bacteria in semen probably persists indefinitely.

Pathogenesis[12]

Following a bacteraemia there is localization in the epididymis, usually unilaterally and in the tail, producing degenerative, inflammatory and proliferative changes. The resulting sperm stasis and epithelial damage may result in extravasation of sperm with subsequent spermatic granuloma formation. Histopathological and bacteriological studies suggest that the epididymal tail, ampulla ductus deferens and seminal vesicles are the most frequently involved sites of infection; the testis and the head of the epididymis are involved less frequently[19][20].

Seroconversion (as detected by the warm CFT) occurs 10 to 66 days after artificial infection, earlier with more sensitive testing procedures[21]. Semen culture is generally positive 5 to 10 weeks post-infection[21] and lesions caused by the initial infection are usually palpable from 9 weeks onwards. (Both of these events can occur sooner than this - positive semen culture and clinically palpable lesions may be detected as soon as 4 weeks post-infection[16].) Some challenged rams never develop any evidence of infection, others develop serological evidence only. These rams recover and are said to have had ’abortive’ infections[22]. Serological reactions decline in recovered animals over a period of 4 to 5 months. In animals which remain chronically infected, serological responses remain relatively constant[15].

Clinical findings

A deterioration in semen quality occurs early in the disease, and the semen contains many leucocytes. In the acute stages of the disease, there is oedema and inflammation of the epididymis and tunics, palpable as a general swelling and loss of definition of the scrotal contents. There is a systemic reaction which is rarely detected. Regression of the acute syndrome is followed by a latent period of 2 to 3 months before chronic lesions with palpable abnormalities develop in one or both sides of the scrotum.

The usual chronic lesion is an enlargement of one or both the epididymes, usually in the tail, which is hard due to fibrosis. The epididymis may be 2 to 3 times normal size or even more. There is no orchitis and initially the testes feel normal, but degeneration and atrophy lead to a decline in the size and firmness of the testes. Less commonly, the enlargement and hardening may involve more of the epididymis, or the head only or may not involve the epididymis at all, being restricted to one or more of the accessory sex glands.

Diagnosis

The presence in a flock of a prevalence of chronic epididymal lesions greater than 5% is suggestive of brucellosis. Lesions of chronic epididymitis must be differentiated from those caused by trauma and other bacteria, particularly Actinobacillus seminis. Lesions caused by A seminis generally show a more acute reaction and are located in the head of the epididymis more frequently than lesions caused by Br ovis. Either semen examination and demonstration of the weakly acid fast bacilli in smears or semen culture for Br ovis is necessary for a definitivediagnosis. Neither test is particularly sensitive, primarily because of intermittent shedding of the organism by infected rams, and culture may be the more sensitive technique when laboratory procedures are commenced soon after sample collection[23][24].

The CF test has long been used in Australia and New Zealand to eradicate the disease from flocks. In 1983, an ELISA test was developed with a specificity comparable to the warm CF test (0.5% false positives) but significantly more sensitive[25]. (The increased sensitivity, however, means that some CF negative, ELISA positive rams are detected which will never excrete Br ovis and will eventually become ELISA negative.)

If an investigation is carried out soon after Br ovis is introduced a high proportion of rams which will never become excretors may be detected serologically. This fact should be considered when planning eradication programs. Testing immediately after joining or soon after sexual activity has started in flocks of young rams, could lead to the identification and culling of recently infected animals, many of which will ultimately recover and become serologically negative.

Rams with low CFT titres (1:8 or 1:16) are frequently found to be uninfected and are, probably, recovering from abortive infections. Currently, it is recommended that low titre positive animals with no palpable lesions be isolated from other rams and re-tested after 4 weeks. Persistent low titres may warrant the slaughter and detailed necropsy examination of the rams so that the status of the flock can be determined[26].

Eradication

Isolation of old rams from young rams - in commercial flocks, brucellosis can be readily eradicated by isolating the existing, infected ram flock, purchasing replacement rams from accredited OB free studs and keeping them at all times separate from the old rams. Eradication from the older rams can be attempted, by test and slaughter, or they can be used for mating and cast for age progressively over 3 to 4 years. There is a significant danger that the infected rams will gain access to the young rams and cause a breakdown, so the shorter the duration of the ’two flock’ system the safer.

Test and slaughter - in ram breeding flocks, a program of test (ELISA serology) and slaughter will successfully eradicate brucellosis provided new cases are detected before they commence excretion of Br ovis organisms, which can occur as soon as 4 weeks post-infection[16]. Serial testing should be performed, therefore, every 3 weeks and all positive reactors slaughtered[27]. Any older rams with lesions of epididymitis should be culled regardless of the serological result because some false negative results can occur with chronically infected animals[21]. Infection of ewes is potentially a source of breakdown during eradication but this is rarely a problem of any practical significance.

Vaccination, but NIA - vaccination against OB has been used in Australia as a control measure. The usual practice was the simultaneous administration of a formalin-killed Br ovis saline-in-oil emulsion and Br abortus strain 19 vaccine although the equal efficacy of some Br ovis vaccines when administered twice, 2 weeks apart, was demonstrated[28]. Vaccination is no longer used for control in Australia but is used as an eradication method in New Zealand.

Accredited OB free flock scheme

A voluntary accreditation scheme for ram breeders was introduced into NSW in 1981. In flocks desiring accreditation, all rams, cryptorchids and teasers over 4 months of age are examined by palpation of the scrotal contents and those over 10 months of age are serologically tested. Initial accreditation requires 2 consecutive negative tests at an interval of 60 to 180 days, and inspection of the boundary fencing to ensure it is adequate. Subsequent testing, performed annually for 3 years then biennially, involves the palpation of all rams, cryptorchids and teasers over 10 months and blood testing of all over 22 months of age. In large ram flocks, provisions exist for testing a sample of the sale rams, rather than the entire flock, provided the retained stud sires have been tested and found clean.

The testing procedure is performed by private practitioners and the register of accredited flocks is maintained by NSW Agriculture. The flock owner pays all costs incurred by the practitioner and the laboratory. Similar programs operate in all other Australian states[29].

Other causes of epididymitis

Actinobacillus seminis

A seminis causes chronic epididymitis in rams and polyarthritis in lambs. Unlike brucellosis, orchitis may also be present. The organism may be a common inhabitant of the genital tract of normal rams and ewes. Some rams, however, develop an epididymitis which is clinically indistinguishable from brucellosis. Most of these remain fertile but at reduced levels. Serology can be used but many normal animals have antibodies.

A seminis is very closely related to Histophilus ovis and one may be a variant of the other[30]. H ovis has also been reported as causing epididymitis, suppurative arthritis in lambs and mastitis.

Miscellaneous infections

Actinobacillus pyogenes, A ligneriesi, A actinomycetes-comitans, Corynebacterium pseudotuberculosis, Yersinia pseudotuberculosis, Escherichia coli (causing abscessation with fistula formation in the scrotum and orchitis[31] and Br abortus (strain 19) have been reported in sporadic cases of epididymitis.

Testicular abnormalities

Cryptorchidism

In sheep this appears to be a sex-limited trait inherited as a recessive gene with a low degree of penetrance or as a threshold polygenic trait.

Hypoplasia

Testicular hypoplasia occurs in rams and can be either unilateral or bilateral. Both unilateral or bilateral forms may have an inherited basis. Hypoplasia of the testes has been associated with zinc deficiency.

Degeneration

The testicular germinal epithelium is very sensitive to many adverse influences. Degeneration may be unilateral or bilateral, often reflecting whether the cause is systemic or local. The degenerated testis may remain a normal size but be soft and flabby or become small and firm. Softness and flabbiness often indicate rapidly progressing degeneration. Fibrosis takes a long time to develop. There follows a reduction in sperm production and the semen becomes thin and milky or watery. Regeneration can occur but takes longer than the degeneration.

Other lesions of the male genitalia

Balanoposthitis

Balanoposthitis is principally a problem of wethers but also occurs in rams. A special disease of Border Leicester rams - balanitis - has been reported.

Varicocoele

A varicocoele is a dilatation of the spermatic vein and is usually of little or no significance. Bilateral varicocoeles of long duration may adversely affect semen quality (possibly due to anoxia) or, if large enough, incapacitate rams for walking due to pain. They do, however, increase in size very slowly and rarely reach large proportions.

Scrotal mange

Mange of the scrotum, caused by Chorioptes bovis, is associated with seminal degeneration and testicular atrophy[32]. (See also the section on skin diseases.)

Embryo mortality

Except in occasional flocks a large majority of prenatal mortality occurs in embryos and not in foetuses (ie, during the interval from fertilization to attachment). More specifically, about 20‑30% of all fertilized ova are lost in the first month and very few losses occur after about day 35. In the majority of cases the embryos are lost before they would normally exert their anti‑luteolytic activity on the uterine endometrium and ovary (i.e. the ewes return to oestrus after 16‑18 days). This implies that the embryos must be dead or at least retarded by about day 12, since the normal anti‑luteolytic signal acts on days 12‑13. Hence, in the field, embryonic death cannot be distinguished from failure of fertilization, even where harnesses and crayons are used. Less commonly, embryo loss in specific flocks or geographical regions may be associated with delayed returns to oestrus (or apparent failure to return to oestrus, depending on the length of the joining period). This is seen most clearly in the case of selenium deficiency.

Aetiology

The reasons for most embryo losses in commercial flocks are unknown. Some losses are attributable to intrinsic faults within the embryo and hence are desirable (rather than the subsequent abortion or birth of abnormal foetuses). There is evidence that some embryo loss may result from the fertilization of ova by heat damaged spermatozoa. However, in vitro culture and in vivo embryo transfer studies suggest that most losses are due to failures in the uterine environment. Faulty nutrition, abnormal temperatures, endocrine imbalances and asynchronous development of embryo and endometrium have all been suggested as causes. It takes a severe nutritional insult, more than can normally be experienced in the field, to kill sheep embryos. However, deficiencies of zinc, iodine and selenium have occasionally been implicated. Again, the environment of the ewe has to be very hot before embryo losses occur. A progesterone influence on the uterus is essential, but within a fairly wide range of plasma concentrations it seems to have no controlling influence. Experiments involving the transfer of embryos between asynchronous donors and recipients have clearly indicated that embryos will not survive and develop in inappropriate endocrine and endometrial environments. However, the extent to which ’asynchronous development’ may occur after natural mating in commercial flocks remains unclear. Studies in countries where ewe lambs are mated in their first year of life clearly implicate age as a factor, with low embryo survival rates in ewes less than 12 months of age. However, studies of 12‑year‑old maidens in Australia have not revealed any differences from adult sheep.

Partial or full embryo loss

It is useful to distinguish between full and partial embryo loss after multiple ovulation. In the latter case (sometimes designated PFMO), the pregnancy proceeds with no outward signs of loss. PFMO becomes more important as mean flock OR increases. Eggs ovulated as singles seem to have a higher chance of surviving than eggs ovulated as twins, etc. For example, if the mean OR in a Merino flock is 1.3, you might expect about 10‑15% of lambing ewes to give birth to twins. Nevertheless, it follows that flock fertility should generally increase with increasing OR. Typical conception rates to one oestrus in Merino and XB ewes with mean ovulation rates of 1.2 and 1.7 are about 70% and 80% respectively. The causes of PFMO are not understood. Supplementary progestagens given before day 12 have reduced PFMO in some but not all studies. Such treatments cannot presently be recommended. Some researchers consider PFMO to be a physiological adaptation rather than a problem, i.e. the ewe (or the uterus) has mechanisms to reduce the number of embryos to match uterine capacity. However, since the uterus in the Booroola Merino ewe seems quite capable of supporting the development of up to five foetuses, this explanation is not very convincing.

The relative importance of embryo mortality

In individual flocks experiencing an infertility problem, the relative importance of failure to mate, failure of fertilization and embryo mortality will obviously vary. Sometimes failure to mate is the main problem, especially with out‑of‑season joinings. Provided mating occurs and there is adequate ram power, embryo loss is usually considerably more important than failure of fertilization. Thus with normal return rates of 20‑30% (depending mainly on OR?) only one third or less of returns seem to be due to failure of fertilization. However, this statement will be incorrect where pasture oestrogens are involved or some controlled breeding procedures are employed.

Abortion in ewes and prenatal diseases of lambs

Depending on the stage of gestation at which it occurs, abortion can contribute to infertility or to perinatal mortality. Generally, abortion is an uncommon cause of reproductive wastage in sheep in Australia. It appears to be more important in countries where more intensive systems of lambing management are used and, when abortion storms do occur in Australia, they are often associated with unusually high stocking densities. As well as causing sporadic outbreaks of abortion and neonatal lamb deaths, many of the causative agents probably also cause a low level of undetected losses on many farms. One would particularly expect this to be the case with toxoplasmosis.

Toxoplasmosis

Toxoplasma gondii is an obligate intracellular protozoan parasite. Its asexual cycle can occur in most warm-blooded animals but the sexual cycle occurs only in cats. Wild rodents, with encysted bradyzoites in brain and muscle, act as a reservoir of infection which is spread and enormously amplified by cats. Cat faeces can contain 10⁶ oocysts/g. Theoretically, 50g of cat faeces can provide 250,000 sheep-infective doses[33]. Susceptible sheep become infected and remain so always after ingesting oocysts. Infection of the placenta and conceptus occurs when a susceptible sheep ingests oocysts when pregnant. The outcome of infection depends on the stage of pregnancy :

Diagnostic aids - Histopathology of selected foetal and placental tissues reveals characteristic lesions. Serology of ewes is of little use because Toxoplasma titres are frequently high in ewes which have not aborted but may be low in ewes aborting due to toxoplasmosis at the time of abortion. Serology of non-autolyzed foetal lambs is, however, useful as a diagnosis of congenital toxoplasmosis, particularly on a flock basis rather than an individual basis[34]. Definitive diagnosis requires the demonstration of T gondii in fixed tissue sections or bioassay in mice.

Control - Infection is from contaminated feedstuffs and pasture, there is no significant sheep to sheep transmission. Prevention of infection, therefore, involves the reduction in contamination by cats. Young cats pose the greatest threat - oocysts are usually produced during initial infection which occurs as the young cat starts to catch and eat small animals. If the environment is contaminated, sheep can be exposed to infection 2 to 3 months before joining to reduce the incidence of mid-pregnancy infections. The vaccine ’Toxovax’ has been used in NZ[35].

Campylobacteriosis

Campylobacter fetus ss fetus is transmitted by ingestion. The bacteria survive in the gall bladder and gut of infected sheep and crows and magpies can become infected for several months and thus become vectors[36]. Outbreaks of abortion are usually preceded by a period of high stocking, particularly in winter and spring, but also after periods of hand-feeding in summer and autumn[37]. If the flock has been previously exposed, the older ewes do not abort but the younger ones do. Abortion occurs in the 3rd, 4th or 5th month of gestation. Sometimes an abortion storm follows 2 to 3 weeks after the first, sporadic abortion. Ewes may retain their membranes and develop metritis. Aborting ewes develop good immunity and are unlikely to abort from this cause again. The disease has occurred repeatedly on some farms[38].

Diagnostic aids - Some aborted lambs have ’rosette-like’ necrotic foci in the liver and this can be a useful differential feature from toxoplasmosis. Definitive diagnosis is based on isolation of organisms from aborted membranes and the foetal stomach.

Control - Aborted ewes should be removed from the lambing flock. Hand-feeding should be stopped or changed to a new area each feed. The ewes should be ’spread-out’ into clean paddocks. Ewe hoggets can be grazed on lambing paddocks after an abortion storm in order to infect them while non-pregnant. The vaccine ’Campylovexin’ has been used in NZ[39].

Salmonellosis

The Salmonella Reference Laboratory in Adelaide reports that, in Australia, the salmonella serovars most commonly isolated from sheep are S typhimurium and S bovis-morbificans. There are a number of other serovars involved in outbreaks from time to time. S dublin, a common cattle isolate, occurs much less commonly in sheep. Outbreaks of salmonellosis in pregnant ewes will usually cause abortion in a large proportion of ewes in addition to signs of enteric infection. In one report, four outbreaks of S typhimurium infection in WA affecting autumn lambing ewes were characterised by significant mortality of ewes (8% to 18% of the mob), diarrhoea, foetid dark red vaginal discharge, foetal death, abortion, retained foetal membranes, septicaemia and high fever[40]. It is likely that in Australia abortion will usually be accompanied by clinical illness in the ewe. In the UK, S abortus-ovis and S montevideo have caused numerous outbreaks of ovine abortion in which other clinical signs in the ewe are largely inapparent[41]. S abortus-ovis has declined in importance in the UK since 1975[42] and the serovar is not present in Australia. S montevideo is isolated from sheep only rarely in Australia. Outbreaks of Salmonella abortion are usually associated with stressful conditions, including overcrowding, hand-feeding, undernutrition and pregnancy, as is the case in enteric salmonellosis in non-pregnant sheep (discussed further in Chapter 16).

Diagnosis - The usual presence of clinical signs related to gastro-enteritis and septicaemia, including high fever, usually differentiate abortion caused by Salmonella spp from that caused by Toxoplasma and Campylobacter. Confirmation follows isolation of the organisms from the foetal stomach and placenta.

Treatment and control - Separation of affected ewes from unaffected ewes and a reduction in stocking rate of the latter may reduce the incidence of new cases but is unlikely to stop them altogether. Affected sheep can be treated with antibiotics as a life-saving measure. Antibiotic resistance is frequent in Salmonella isolates, but least likely for ampicillin, trimethoprin/sulphadiazine, tetracyclines and neomycin. Oral medication with furazolidone, continued for up to 7 days, may be attempted to prevent salmonellosis in in-contact sheep but caution must be exercised to avoid overdosage.

Listeriosis

Listeria ivanovii (formerly L monocytogenes serotype V) is the causative agent. It is often present in the gut of normal sheep and can survive and multiply in faecal material and soil. The feeding of silage, particularly silage with a pH above 5.5, is often associated with outbreaks of listeriosis. The disease occurs commonly under wet, muddy conditions and its occurrence is sporadic and unpredictable[43]. It is probably a cause of widespread losses from abortion and perinatal death but with a generally low flock prevalence[44]. Listeriosis is a zoonosis.

Diagnosis - Listerial abortion is characterised by foetal loss at 32 - 5 months of gestation. The organism can be isolated from the foetus (liver and lungs) and placenta.

Control - Antibiotics are not generally effective. Effective control involves changing the predisposing conditions but abortions will continue for some time.

Enzootic abortion

Chlamydia psittaci is a specialised, antigenically complex, intracellular bacterium. Infections of sheep causing polyarthritis, pneumonia, and kerato-conjunctivitis are widespread in Australia, but enzootic abortion is rare[45][46]. The disease is common overseas.

Aborting ewes remain chronically infected but do not abort again. Vast numbers of infectious chlamydial elementary bodies are shed at the time of abortion which remain a potent source of infection for animals and man[33].

Brucellosis

Br ovis can cause an increase in ’returns to service’, foetal mortality and the birth of low bodyweight lambs with a reduced chance of survival when OB infected rams are mated to uninfected ewes. The infection is more likely to be a cause of perinatal mortality than of abortion, although sporadic abortion does occur[47]. The main result of infection is a placentitis which interferes with foetal nutrition. Lambs born from infected ewes are usually of normal gestational age but of significantly lower birthweight.

Infection does not appear to persist in the ewe flock. Although the placentas from infected ewes are a source of Br ovis organisms and the vaginal discharge of infected ewes contain brucellae for up to 10 days after parturition, the ewes do not appear to be a significant source of infection to other ewes or to rams[48]. It appears that it is necessary for the ram flock to remain infected for the disease to appear from year to year in the ewe flock[49].

Ovine Pestivirus

This virus causes Border Disease (Hairy Shaker Disease, hypomyelinogenesis congenita), embryonic death and abortion. The virus is serologically similar to the pestivirus of BVD-MD. The disease has been reproduced in sheep with cattle-derived virus. There is a range of strains of which most, if not all, will infect both cattle and sheep. Nevertheless, there are some differences in host-affinity, pathogenicity and cross-immunity between strains[50].

Infection of ewes less than 50 days pregnant commonly results in abortion due to placental degeneration. Infection at 50 to 80 days can result in foetal death and abortion or the birth of live or dead lambs with hairy coats and varying degrees of hypomyelinogenesis, cerebellar and cerebral dysgenesis, arthrogryposis, kyphosis and brachygnathia.

Generally only a few ewes in the flock abort. Affected lambs born alive fail to thrive and die from complicating illness.

Akabane Disease

The virus enters the blood through an insect bite; viraemia is followed by invasion of the placenta and foetus. The principal vector is the biting midge Culicoides brevitarsis. Immunity lasts for years, although cross protection with the other related arbovirus Aino may not exist[51]. There is some evidence that the sheep foetus is only susceptible to infection between 30 and 36 days. Lambs are aborted or born with congenital defects, including microencephaly, hydrocephalus, arthrogryposis, kyphosis and cerebellar agenesis[52].

Table 7.5 Summary of infectious abortion of ewes

Cause	Transmission	Time and incidence	Clinical characteristics	Diagnostic tests	Serology	Prophylaxis
Toxoplasma gondii	Ingestion of oocysts from cat faeces	Last 8 weeks, typically last 10 days, stillborn or weak lambs Up to 40% abort	Small white necrotic foci in cotyledons, intercotyledonary areas unaffected, mummified foetuses	Histopathology of foetus or placenta	Sabin Feldman dye test, Indirect Fluor antibody test and a number of others	Expose non-pregnant ewes Deal with farm cats Monensin Vaccination
Campylobacter fetus	Ingestion	Last 12 weeks, typically 2 to 6 weeks pre-term 5% to 30% abort	Severe endometritis in ewes; 40% of foetuses with ’rosette’ lesions in liver, thickenned intercotyledonary area	Isolation of organisms from foetal stomach	Agglutination test	Expose non-pregnant ewes(good flock immunity) Vaccination
Salmonella spp	Ingestion	Last 6 weeks Up to 40% abort	Metritis, septicaemia, mortality in ewes usually	Isolation of organisms from foetal stomach	Agglutination test	Avoid predisposing conditions
Listeria ivanovii	Ingestion ? inhalation ? coitus	Last 6 weeks and post-partum lamb deaths 2% to 20% abort	Metritis, septicaemia in some ewes	Isolation of organisms from foetal tissues	None	Avoid feeding (poor) silage
Brucella ovis	Coitus, ingestion	Late abortion but usually low birthweight lambs Very low incidence	Epididymitis in rams	Isolation of organisms from foetal stomach, placenta	CF test of ewes and rams	Eliminate infection in rams Br ovis vaccine, twice or with Br abortus strain 19
Pestivirus	Ingestion at 12 to 80 days gestation	Low incidence, variable timing	’Hairy shaker’ lambs	Virus isolation, histopthology of foetal nervous system	Not useful	Remove surviving lambs from flock, as they shed virus Vaccination
Akabane virus	Insect, particularly C brevitarsis	Variable timing and premature weak lambs	’Dummy’ and arthrogrypotic lambs also born	Histopathology, virus isolation not possible	Agglutination test
Chlamydia psittaci	Ingestion	Last 3 weeks	No premonitory sign, necrotic placentitis, thick, leathery intercotyledonary area, foetus looks normal, none mummified	Chlamydial EBs in cotyledon smears	Serology of little use because antibodies widespread	Usually immune after abortion Vaccination
Br melitensis	Ingestion etc	Last 10 weeks	Dull grey cotyledons	Foetal stomach isolation	CF test	Vaccination
Rift Valley fever	Mosquito		Heavy mortality in lambs	Viral antigen in blood	Several tests	Vaccination
Wesselsbron dis	Mosquito

Abortion caused by Histophilus ovis

This organism has been isolated from sporadic ovine abortions in Victoria. It is more usually associated with polysynovitis and septicaemia of lambs and epididymitis/orchitis of rams.

Romulosis

Onion grass (Romulea rosea var australis previously R bulbocodium) occurs in unimproved and low fertility pastures in some areas of south-eastern Australia. Ingestion of the plant, or a fungus (Helminthosporium) infesting the plant, has been associated with infertility and abortion in sheep in Victoria[53]. Infertility is characterised by extremely low (even near zero) lambing rates in one year, with normal rates in the previous and subsequent years. Abortion, if it occurs, does so in mid-pregnancy. Surviving full-term lambs may have long bone deformities[54]. Nervous signs, including posterior paresis, may occur in flocks experiencing onion grass poisoning.

Health and management at lambing

Nutrition

Implantation in the ewe is a diffuse, gradual process that involves only the superficial tissues of the endometrium. Initially the trophoblast adheres to the epithelium lining the caruncles. Firm attachment is not apparent until around day 30. The growth of the cotyledonary placenta proceeds rapidly after day 40 and exceeds foetal growth until about days 90‑100. After this time the mass of cotyledons tends to decline slowly, until term. At day 90 a typical single Merino foetus weighs about 500 g. Thereafter its growth rate accelerates, to maximum rates of about 70‑80 g per day during days 120‑140 and at term it weighs 3‑5 kg. The maintenance of pregnancy requires an adequate supply of progesterone. Initially progesterone comes from the corpus luteum, but after about day 50 the cotyledons are the principal source of this steroid.

There are probably no nutritional requirements specific to pregnancy until about day 90. Plane of nutrition prior to day 90 may influence placental weight, but variation in feeding at this stage has relatively little influence on lamb birthweight. Commencing at about this stage ewes require additional nutrients to support adequate foetal growth and at the same time maintain a satisfactory ewe condition score. During the last 3‑4 weeks of gestation nutrients are also required to support mammogenesis.

Table 7.6 : Effect of level of nutrition of grazing ewes during the last 5 weeks of pregnancy on birth weights

Table 7.6 gives some data for the birthweights of single and twin lambs as well as changes in ewe liveweight associated with three different levels of nutrition during only the last five weeks of pregnancy. Note that at this late stage of gestation, adjustments to feeding had a greater influence on the birthweights of twin rather than single lambs. It would be interesting to know also how these three levels of feeding influenced udder development and maternal behaviour in the ewes at lambing. As noted above, the optimization of lamb birthweights may require that adjustments to feeding commence at least eight weeks before lambing.

Undernutrition of ewes in late pregnancy leads to a spectrum of disease ranging from minor losses of production, to increased lamb mortality, reduced lactation and, at the most obvious, to mortalities of ewes. Many of the syndromes which are sub-clinical at lambing time have serious consequences in later weeks and months - including death of lambs at a few weeks of age from malnutrition/parasitism, poor growth rate of lambs to weaning, difficulties in weaner management in summer and autumn as a consequence of low weaning weights, and poor wool production and subsequent reproductive performance from the ewes. Pregnancy toxaemia is the clinical ’tip’ of a sub-clinical ’iceberg’.

Pregnancy Toxaemia

This is a disease of ewes in late pregnancy characterised by dullness, inappetence and recumbency which, unless treated early, progresses to death. The condition arises when dietary and body reserve sources of glycogenic precursors are unable to meet the glucose requirements of the ewe and the foetus or foetuses.

Predisposing factors

Restriction of feed intake or low feed quality in late pregnancy, especially in ewes with multiple foetuses, are the usual predisposing factors. In general terms, the disease occurs when the energy balance of the ewe and the foetuses is disturbed and so factors which increase foetal requirements or decrease the ewe’s intake are relevant risk factors. These include :

Pathogenesis

Ruminal digestion of all carbohydrates, from simple sugars and starches to cellulose, pentosans and pectins, produces for absorption volatile fatty acids (VFAs). Three of these, acetic, propionic and butyric, provide most of the energy supply for the animal. Acetic acid predominates, with approximately 4 moles produced for every mole of propionic acid. Butyric acid is largely converted to the ketone bodies acetoacetate and ß—hydroxybutyrate in the ruminal epithelium[55].

Acetate and propionate metabolism - Acetate is rapidly metabolised via the TCA cycle in skeletal muscle, heart and kidney to produce energy in those tissues. Acetate is also used for fat synthesis in adipose tissues. When alternative energy producing substrates are insufficient, lipolysis releases free fatty acids (FFAs) for energy production.

Propionate is, in contrast, gluconeogenic. It is rapidly converted to glucose in the liver and kidney cortex. Propionate is the major source of glucose in the ruminant; amino acids, lactic acid and glycerol released from fat stores are minor sources[56]. 60% to 70% of the oxidative energy production of sheep uses acetate, ketones, glucose and FFAs as substrates. The energy requirements of the brain, eye, erythrocytes and mammary gland (for the production of lactose) must be met by glucose.

Blood glucose, free fatty acid and hyperketonaemia - There is an inverse relationship between blood glucose concentration and that of FFAs. When blood glucose levels are low, plasma FFA concentration rises. These FFAs are oxidised in peripheral tissues and in the liver, producing acetyl-CoA. The raised plasma concentration of FFAs also leads to increased hepatic lipogenesis, raising liver fat levels. Acetyl-CoA can enter the TCA cycle but some is diverted to the synthesis of the ketone bodies acetoacetate and ß—hydroxybutyrate. With increased fat mobilization, the supply of FFA to the liver increases; an increasing proportion of this FFA is converted to ketone bodies, producing hyperketonaemia, and reconverted to fat, producing fatty infiltration of the liver.

Foetal requirement for glucose - Foetal blood concentrations of acetate and ketone bodies are low relative to maternal concentrations. The foetus, however, has a high requirement for glucose and will take up 8 to 9g per kg of foetal weight per day. 5kg of foetus require approximately 45g of glucose daily. For comparison, a dietary intake of 750g of roughage - sufficient to maintain a non-pregnant ewe - will provide about 110g of glucose. Maternal hypoglycaemia is readily induced in ewes in late pregnancy because of the high foetal demand for glucose and the limited amounts produced by gluconeogenesis from propionate and amino acids. The foetus is also highly efficient at capturing maternal glucose - foetal blood levels may remain near normal even when the ewe is severely hypoglycaemic and has virtually no liver glycogen reserves.

Figure 7.2 Relationship between diet and hyperketonaemia in twin-bearing ewes fed chopped hay. 0.75 kg/day is maintenance for the non-pregnant ewe.

Insufficiency of glucose precursors - When glucose deficiency occurs, oxaloacetate is diverted from energy production in the TCA cycle to gluconeogenesis. Under these conditions, energy production in the liver is shifted to oxidation of FFAs with the production of acetyl-CoA. Without the TCA cycle to utilize acetyl-CoA, the ketone bodies acetoacetate and ß-hydroxybutyrate are formed. Hypoglycaemia and hyperketon-aemia, therefore, occur simultaneously, preceded slightly by an increase in plasma FFA concentration.

Development of clinical signs - Severe hypoglycaemia, hyperketonaemia and weight loss can occur in ewes without the development of clinical pregnancy toxaemia. All the reasons for the development of clinical signs in some cases of hyper-ketonaemia and not in others are not clear.

The relationship between diet, stage of pregnancy and ketonaemia is illustrated in Figure 7.2. Hypoglycaemia is expected to develop similarly. The degree to which these changes occur depends on the degree of undernutrition and the foetal load. In most field situations, some degree of hypoglycaemia is inevitable in multiple-bearing ewes because their voluntary feed intakes are unlikely to allow the ingestion of sufficient roughage to meet the total demand for energy substrates without using body reserves.

Elevated plasma cortisol - Although hypoglycaemia and hyperketonaemia do not consistently lead to the development of clinical disease, one consistent association is the presence of elevated blood cortisol levels in ewes with clinical signs - a feature not present in hyperketonaemic, but clinically normal ewes. The high level of serum cortisol is a feature of the ovine disease not present in bovine ketosis and which, among other things, may lead to the wool break in affected but surviving ewes.

Progression to irreversibility - The development of clinical signs amounts to a metabolic collapse following a period of precarious nutritional balance. Excessive production of ketone bodies produces an acidosis. Prolonged urinary excretion results in loss of sodium and potassium and a lowering of plasma alkali reserve[56]. With sudden cessation of dietary intake the hyperketonaemia worsens, exacerbating the CNS depression. Ewes become comatose, dehydrated, anuric and uraemic.

Clinical signs

In an affected flock, pregnancy toxaemia usually appears as a continuing outbreak over a period of 2 to 3 weeks, with a few ewes developing clinical signs each day. The course of the disease is usually 4 to 7 days although ewes are not always observed in the early stages. Affected ewes separate from the mob and, initially, stand with head low and appearing depressed. They do not graze and are easily approached. They appear blind but may make some movement to face an approaching dog or human or to walk away. The gait is staggery and weak and they collapse readily, particularly as the disease progresses.

The pupillary light reflex is diminished and the eye preservation reflex is absent. Ruminal movements are normal or reduced. They are usually constipated, disinterested in food and become more sleepy as the disease progresses. Recumbency follows 2 or 3 days after the ewes are first observed to separate from the flock. Death follows in a further few days.

Signs of nervous derangement may be observed at all stages of the disease. These include muscle tremors of the face, jaw champing and lateral or dorsal head flexion. There may even be tonic-clonic convulsions. Foetal death is a sequel when the disease is prolonged.

Clinical pathology

The presence of ketone bodies in the plasma and urine may be detected using sodium nitroprusside reagents (Acetest^R tablets, Ketostix^R test strips). Ten fold dilution of urine before testing is recommended to reduce the possibility of false positive reactions. In advanced cases, plasma bicarbonate concentrations are measurably reduced and BUN concentrations elevated. Terminally, ewes may become hyperglycaemic.

Necropsy

The presence of two or more near-term foetuses is common. The liver is fatty and pale yellow, friable and greasy on cut section. The adrenal glands are enlarged.

Diagnosis

The disease must be differentiated from hypocalcaemia, which is more characterised by paralysis and muscle weakness and, if uncomplicated, responds to treatment with calcium borogluconate. Pregnancy toxaemia is, however, often superimposed on hypocalcaemia unless it is treated promptly.

Treatment

The response to treatment depends on the manner in which the disease developed and the duration of time which passes before treatment is instituted. A small proportion of cases will recover spontaneously without treatment, either because dietary intake recommences or because the foetuses are born or die in utero. In this latter case, of course, death from septicaemia is also a likely outcome.

In cases which have occurred following sustained undernutrition treatment is of little value, possibly because acidosis and renal failure are present from the outset. If heroic treatment is commenced, intravenous electrolytes, possibly with potassium iodide, bicarbonate solutions, glucose and insulin as indicated, are rational therapies. Oral administration of glucose precursors (propylene glycol, glycerine) are successful at raising blood glucose concentrations but rarely lead to clinical recovery. In fact, many cases are so advanced when presented that hyperglycaemia may be present before treatment can start.

In those cases where the clinical signs have developed as a result of more sudden deprivation, treatment is more likely to be successful. Treatment, to have any chance of success, must commence early and be vigorous and frequent. Once cases advance to permanent recumbency, treatment is unlikely to succeed.

Concentrated oral rehydration solutions, containing glucose, glycine, NaCl, KH₂PO₄, potassium citrate and citric acid have been shown to be more effective at raising plasma glucose concentrations than the same amount of glucose administered alone. A field trial using the concentrated oral rehydration solution (160ml every 4 to 8 hours) reported that 90% of ewes classified as having mild signs and 55% of those with severe signs recovered completely, producing live lambs[57]. Mild signs were separation from the flock, disinclination to move, anorexia. Severe signs were one or more of blindness, drowsiness or excess salivation. No other treatment was compared in the field trial.

Prevention

Supplementary feeding with high energy foodstuffs will reduce the incidence of pregnancy toxaemia. Preferably, the need for supplementation is foreseen before any cases occur; the need being recognised from an assessment of the quantity and quality of the available pasture. Often, however, supplementation is introduced or increased after some ewes have succumbed.

Feeding rates of cereal grains may vary between 400 and 700 g daily depending on the degree of nutritional deficiency. Hay is unlikely to provide sufficient energy density (megajoules of ME per kg of dry matter or MD) to prevent the development of pregnancy toxaemia in high risk flocks. Methods of feeding grain and, particularly, the need for care in introduction were discussed in the section on hand feeding.

The existence of pregnancy toxaemia in a flock is suggestive of (probably more) important sub-clinical losses of production from high lamb mortalities, poor lamb growth and poor ewe health and production. This subject is discussed by Foot (1983).

In light of that, producers who chronically suffer from the disease in their flocks or who frequently need to take action to prevent it, should possibly consider changing management strategies. If the disease is related to poor pasture quality, lambing at a time when feed quality is higher will probably be advantageous. If the disease is related to low pasture availability, decreasing the stocking rate of the ewes is advisable. If pregnancy toxaemia is related to husbandry procedures (crutching, shearing etc), changes should be made to ensure the ewes have shorter periods off-feed and less disturbance close to lambing.

Identification of ewes with multiple pregnancies by ultrasound scanning can be used to form mobs of multiple-bearers which receive differential treatment. While this strategy is highly successful, it is probably too expensive unless the twinning rate is very high and the ewes particularly valuable.

Monitoring of bodyweight and condition score can give useful guides to the need for preventive action. Single bearing ewes which maintain uterine-free bodyweight will gain at least 8 or 9 kg of liveweight over pregnancy (mostly in the last 8 weeks) due to the mass of the foetus, foetal fluids and udder development. As discussed previously, such objectives are both difficult to meet in the field and unnecessary in commercial sheep production, from an economic viewpoint. Satisfactory production and health is probably associated with liveweight gains of 2 to 5 kg in this period, equivalent to the loss of 0.5 to 0.7 of one condition score. The ability to lose that amount safely depends on bodily condition in early pregnancy - lean ewes should not be allowed to lose that much, fat ewes should be limited to losing no more than that amount of condition. For ewes with twin foetuses, liveweight gains of 5 to 8 kg are desirable.

Hypocalcaemia

Hypocalcaemia in ewes generally occurs in the last month of pregnancy rather than during lactation. The clinical syndrome is usually precipitated by sudden changes in feed intake or by stress. Moving ewes to another paddock, driving for husbandry procedures, particularly if the weather is cold and wet, can readily precipitate outbreaks. Generally, only a small proportion of the flock is affected. Occasionally the disease occurs in association with exposure following shearing and large numbers of ewes may be affected. An increase in the incidence of hypocalcaemia of ewes 2 to 6 weeks before lambing was observed in the 6 months following the end of the 1982/3 drought in southern Australia. Most cases occurred spontaneously and some were precipitated by pre-lambing crutching[59]. Older ewes are usually more frequently and more severely affected. Hypocalcaemia also occurs in weaners.

Clinical signs

Initially affected ewes are ataxic and hyperaesthetic but soon become recumbent and the paralysis becomes flaccid. They are frequently seen in sternal recumbency with legs stretched behind and head turned to the flank. The pupils are dilated. Unless treated, affected ewes usually die within 1 or 2 days of collapse.

Treatment

50 ml of 40% calcium borogluconate injected subcutaneously is effective, particularly when given early. Failures to respond may be due to intercurrent pregnancy toxaemia. In ewes which do respond, treatment with oral glucose precursors is advisable in an attempt to avoid pregnancy toxaemia.

Vaginal prolapse

Vaginal prolapse occurs in the pregnant ewe up to 4 weeks before lambing. The incidence in Merino ewes is generally low but may exceed 5% annually in some flocks of British breed sheep. There appears not to be any one aetiological factor but a number of factors which may contribute variably to the development of the syndrome. A major factor is probably the increase in intra-abdominal mass in late pregnancy, particularly in ewes on bulky feed. When the ewe lies down, the intra-abdominal pressure is transmitted to the flaccid pelvic structures, tending to balloon the relaxed and loosely attached vaginal walls through the lips of the vulva. The exposed mucosa becomes dry and irritated, stimulating tenesmus which exacerbates the prolapse[60].

Treatment

Treating the prolapse by reduction is useless if it has been present for long enough for the mucosa to be devitalised or the sub-mucosal tissues bruised or torn. Early cases can be treated by reduction after disinfection with mild antiseptics (suitable for sensitive mucous surfaces) and retention by a variety of means. Epidural anaesthesia, by reducing tenesmus for an hour or so, will facilitate reduction and allow a period following reduction for some oedema to resolve before the ewe is aware of any discomfort and stimulated to strain again. Retention is generally attempted with sutures of umbilical tape, either across the vulva or, preferably, in a ’purse-string’ suture lateral to the vulval labiae. These must be removed before the ewe lambs so it is necessary to confine the ewe for observation after treatment. With nervous Merino ewes, it is necessary to confine them in a paddock or yard in the company of 5 or 6 other sheep at least or the stress of isolation and panic when approached will not favour a successful outcome. Antibiotic therapy, locally and parenterally, is advisable.

Ewes should be culled after they have raised their lamb because of the risk of recurrence at the next lambing. If a number of ewes are affected, steps should be taken to reduce overfatness, reduce the bulkiness of the diet and to increase exercise of the ewes, where these actions are appropriate, in future pregnancies.

Husbandry at lambing

The length of pregnancy in the ewe varies between about 145 and 150 days, depending primarily on breed but also on litter size and possibly other factors. As a rule of thumb, pregnancies last for about 145, 147 and 150 days in British breeds, crossbreds and Merinos, respectively. It is the foetus rather than the dam that determines the length of gestation (worth remembering if MOET involves recipients of a different breed!). In order to survive, the lamb must promptly make certain adjustments at birth and both the ewe and lamb must exhibit behaviour patterns that ensure prompt initiation of sucking by the lamb and formation of a strong ewe‑lamb bond. Teat‑seeking activity by the healthy lamb is vigorous during the first few hours after birth. Lambs usually stand on all four feet within 2 hour and suck successfully within 1‑2 hours of birth. In the absence of effective bonding, both lamb teat‑seeking activity and ewe maternal behaviour begin to fade after about 3 hours. For high lamb survival ewes should lamb at a condition score of about 3 and in sheltered, comfortable surroundings, but this is not always possible or the most economical strategy. Points to consider in choosing the lambing paddock include:

In larger commercial Merino flocks there is commonly no surveillance of lambing. Indeed, some producers take their annual leave during the lambing period. However, where management is more intensive (eg on smaller, prime lamb and stud properties) some degree of surveillance is both desirable and feasible. Twice daily inspections (in the early morning and late afternoon) are ideal. Difficult births can be assisted with a reasonable chance of delivering live lambs. It is usually best to leave the ewe on her side with the lamb over her snout (if she has not already stood!). In the early morning, recently lambed and lambing ewes will mostly be separated from the main mob. Once daily or less frequent inspections may be all that is possible. With once daily inspection more dead lambs are delivered, but there is still a good chance of saving the ewe. If the ewe has been down for some time she may need active assistance to get up and walk again. Once she has been helped to walk about 20 metres, she should be able to look after herself. If surveillance is planned, the producer should walk through the flock for 2‑3 weeks prior to the start of lambing to accustom the ewes to inspections.

Intensive management at lambing

It is sometimes necessary to identify lambs and ewes lambing. This requires a careful effort. Where the parentage of the lambs or full identification is required, it is necessary to inspect the flock at least once daily and preferably early in the morning. Lambing ewes are flank branded and their lamb(s) eartagged. The ear tags in the lambs may need to be replaced later as the holes in the ears become larger. If parentage is not required, information on the numbers of ewes lambed and lambs born can be obtained as follows: flank brand the ewes and paint the tails of recently born lambs. Record the lambed ewes and count the painted tails. Do it at least daily, preferably early in the morning. It is not easy to get accurate data. Some newborn lambs often disappear promptly after birth! In principle, provided sufficient time and resources are invested, it is possible to reduce lamb losses almost to zero. In practice, the producer must consider how much cost and effort is warranted to reduce lamb losses. The manipulation of lamb birthweights by using ultrasound and/or adjusting feeding, the provision of shelter and frequent surveillance have been mentioned. Less commonly, other procedures include: drift lambing, where with suitable subdivisional fencing the lambing flock is gently moved each day to the next paddock, with a 3‑4 day rotation. This enables small groups of separated lambing or just lambed ewes to be left behind and alone, until the main mob catches up with them a few days later. Pen lambing of individual or small groups of ewes is more intensive and expensive. Ewes giving birth to multiples may be confined individually in pens to facilitate bonding to all lambs; two days of confinement may be required.

Shearing and lambing

Ewes in long wool may usefully be crutched before lambing commences. This may facilitate bonding of the ewe and lamb. The effect of shearing on lambing performance depends mainly on when it is carried out in relation to lambing. In severely cold districts, shearing just prior (2‑3 weeks) to the onset of lambing may reduce lamb losses. Newly shorn ewes seek out shelter and hence indirectly protect their lambs from exposure. However, more generally shearing at this time is not practical on other grounds and should not be recommended, as possible side‑effects include abortions and pregnancy toxaemia. Shearing 4‑8 weeks prior to the onset of lambing is safer and may be beneficial. Compared to ewes shorn post‑lambing, shearing at this time often results in a significant increase in lamb birthweights and decrease in lamb deaths. The increased losses in ewes shorn post‑lambing are probably explained mainly by the lower birthweights, but other factors may include poorer lactation and ability of lambs to find the teats and suckle. Shearing before lambing seems often to increase ewe mobility and feed intake. Late pregnant ewes in long wool are prone to become cast, especially when they are wet.

Perinatal mortality

A number of specific metabolic and other diseases are associated with late pregnancy, parturition and the onset of lactation. These diseases of periparturient ewes can result, in individual flocks, in serious ewe losses. As a largely separate issue, the death of lambs in the perinatal period is a major source of reproductive wastage. These are deaths occurring shortly before, during or within 7 days of birth. Losses at this time account for 80‑90% of preweaning losses. The incidence of perinatal mortality is extremely variable. Overall, in Australia about 20% of all lambs die and about 20‑25% of pregnant ewes do not have a lamb at lamb marking. In Merinos, losses of less than 15% lambs must generally be considered acceptable. If mortalities exceed 15‑20%, then a single major cause may usually be diagnosed, but where mortalities are less than 15% there is commonly not any one predominant cause.

Certain factors concerning the breeding flock and its environment have major influences on the rate of perinatal mortality. These are:

Ultimately, nearly all losses relate to failure to rapidly establish and maintain an adequate ewe‑lamb bond. Key determinants of the onset of maternal behaviour are oestrogens, cervico‑vaginal stimulation, olfaction and maternal experience. The two distinguishable components of this behaviour of the ewe are (a) responsiveness towards (any) newborn lambs and (b) the bonding of the ewe to one or two specific lambs. Much less is known about the regulation of desirable behaviour in the neonate and young lamb towards its dam. Bonding and lamb survival are improved by management practices which increase the time spent on the birthsite by the ewe after parturition. Disturbance of lambing ewes for feeding can lead to mismothering.

There are several possible causes of perinatal lamb loss. At least 80% of deaths usually fall into two categories at autopsy. These are (1) deaths due to uncomplicated birth stress and may include small lambs dying of peracute hypothermia in very cold weather; (2) neonatal deaths due to a complex of starvation, mismothering and exposure (SME), characterised at autopsy by evidence of starvation and cold exposure.

Birth stress

Birth stress results from the effects of asphyxia and/or trauma on the foetal CNS during birth. Gross evidence of birth stress includes (1) birth injury ‑ subdural and subarachnoid haemorrhages of the brain and spinal cord; (2) subcutaneous oedema of the presented part of the foetus; (3) abdominal haemorrhage from liver trauma; (4) petechial and ecchymotic haemorrhage in subpleura, subendocardium, subepicardium and thymus. The birth coat is often meconium stained. Birth stress does not only lead to mortality of lambs at the time of parturition but also contributes to deaths from the SME complex, where evidence of birth stress is accompanied by varying degrees of catabolism of brown fat.

SME complex

Deaths from the SME complex present evidence of hypothermia ‑ brown fat catabolism, subcutaneous oedema of the extremities, inadequate quantities or absence of milk ingesta in the gut. The texture and colour of the brown fat in the perirenal, pericardial, epicardial and prescapular sites are sensitive indicators of the lambs’ exposure to cold independent of starvation. During severe, cold, wet, windy weather high rates of mortality may occur from primary hypothermia. Most SME complex deaths occur from secondary hypothermia ‑ the result of exhaustion of substrates necessary for thermogenesis because of starvation. Common causes of failure to feed include birth injury to the CNS, aberrant maternal or neonatal behaviour, udder or teat abnormalities, agalactia and management‑induced mismothering.

The relationship between climate and lamb mortality is an important consideration when choosing a joining date. Seasonal variation in environmental conditions is one of the issues, discussed in Chapter 3, which determines the best time to lamb.

Minor causes of perinatal mortalities

Perinatal mortalities from causes other than birth stress and the SME complex usually amount to only a small proportion of deaths. Nevertheless, on isolated occasions, perinatal mortalities from congenital malformations, infectious causes or trace element deficiencies can be serious.

Lethal congenital malformations

Vaccination against bluetongue, Rift Valley fever and Wesselsbron disease and teratogenic plants can cause congenital malformations.

Congenital infections

Infections acquired after birth

Trace element deficiencies

Copper, iodine and selenium deficiencies can cause heavy mortalities of lambs under particular circumstances.

Predation

The significance of primary predation as a cause of perinatal lamb losses has been difficult to assess. Many live lambs taken are probably not viable (secondary predation) and many lambs disappear or are mutilated after death from other causes (scavenging). Generally primary predation is thought to cause only minor losses, with exceptions in some seasons and in some districts where losses can be extremely high. Pigs, dogs (including dingoes) and foxes can be responsible for primary predation. With the advent of ultrasound and the realisation that more lambs often ’disappear’ in Merino flocks than was previously thought, the role of predators and especially of foxes needs re‑evaluation. Fox numbers seem to have increased substantially in recent times with the demise of the fur trade, and foxes may now be an important cause of lamb losses in many flocks.

Management and diseases of lactating ewes

Uterine prolapse

Uterine prolapse occurs occassionally in ewes after a difficult lambing, particularly where straining has been prolonged or the vagina has been damaged during the birth process. Uterine prolapse also occurs as a consequence of phyto-oestrogenism in ewes.

The prolapse can be replaced and the success rate is high, at least in terms of ewe survival if not in terms of future breeding, provided the damage done to the organ is minimal before and during treatment, provided gross contamination is removed and provided the organ is completely reverted. The foetal membranes, if still present, should be left in situ. Antibiotic therapy, with intra-uterine pessaries, seem appropriate but pessaries are often lost soon after placement. Oxytocin should be administered intra-muscularly to encourage uterine involution. A purse-string suture of umbilical tape may be placed around the vulva but probably does not add to the success rate in ewes which are ambulatory and in which involution commences within a few minutes of treatment.

Hypomagnesaemia

This appears to be a relatively uncommon condition of sheep. When it does occur, it involves ewes in the first month of lactation and, like the disease in cattle, affects those ewes with the heaviest lactations. Deaths can occur at pasture without the disturbance of handling or driving so on some occasions affected ewes are simply found dead. If seen alive, affected ewes have a stiff, uncoordinated gait and readily collapse and show repeated tetanic spasms. They are hyperaesthetic and show tremor, particularly of the facial muscles. The course of the disease is probably only a few hours.

Treatment

If ewes are found alive, treatment with both calcium borogluconate and magnesium salts is advised and often successful. Relapse, however, is common.

Prevention

The pathogenesis of the disease is probably similar to that of cattle so preventive strategies are similar. Oral supplementation with magnesium oxide or magnesium carbonate should be effective.

Figure 7.3 The lactation of the ewe varies with nutritional intake (stocking rate) Davies HL 1962.

Nutrition through lactation

Depending on body condition at lambing and the level of nutrition in late pregnancy and lactation, the milk production of Merino sheep peaks 2 to 3 weeks after lambing and then declines. By 10 weeks it is usually about 3 of the peak level (Figure 7.3)[61].

In approximate terms, lambs ingesting 1kg of milk per day through the first 4 to 6 weeks of lactation will grow at 200g per day and, therefore, weigh up to 12kg at marking at 6 weeks of age. At marking time, later born lambs may be as young as 1 week but the oldest, single reared lambs will usually weigh 10-12kg if the ewe has had satisfactory nutrition. Lambs which have grown at similar rates to marking age are very active, fast and strong, have limited rumen development and, therefore, small abdomens. They are called ’sappy’ because of their ’bloom’ and appearance of good health and vigour. Sappy lambs of 6 weeks old generally have very low parasite burdens because their grazing has been limited by their continuing good milk intake.

The consequences of undernutrition of ewes, if it does not result in the death of the ewe through pregnancy toxaemia or the perinatal death of the lamb, are inadequate and early cessation of lactation and increased grazing activity of the lambs at an early age. Lambs normally commence grazing at 3 weeks of age and, by the time they are aged 8 weeks and weigh 10 to 14kg, they have sufficient rumen development to survive on good quality pasture without milk. Before that age, inadequate rumen development and high dietary protein requirements reduce the chance of survival of lambs without adequate milk intake. These lambs may die at any age from 7 days onwards (before that the death is classed ’perinatal’). If they survive to marking they will be very light (for example, 6 kg at 6 weeks of age), will appear ’poddy’ or pot-bellied due to marked rumen development in a small body. They are weak and inactive. They

Sheep Health & Production

Chapter 7. Reproductive management and diseases in naturally mated flocks

Introduction

Factors determining reproductive rate

Fertility, fecundity and survival rate of lambs to marking age

Table 7.1 Two different combinations of fertility, fecundity and lamb survival rate

Physiological, management & disease factors affecting fertility up to mid-pregnancy

Photoperiodicity in the ewe

Figure 7.1 The incidence of ovulation in Merino, crossbred and British Breed sheep throughout the year.

Table 7.2 : Effect of time of mating on reproductive performance of Merino ewes at Trangie, NSW (averages of 4-6 easons)

Effects of bodyweight and nutrition on ewe fertility and ovulation rate

Flushing ewes

Table 7.3 : Effect of flushing on lambing in Merinos

Effect of ewe age on fertility and ovulation rate

Ovulation without oestrus

Failure of fertilization due to maternal factors

Phyto-oestrogenic infertility

Pathophysiology

Biochemistry

Oestrogenic cultivars

Permanent infertility

Cervical changes

Uterine changes

Dystocia

Lactation in maiden ewes and wethers

Other effects on wethers

Effects on fertility

Diagnosis

Control

Temporary infertility

Coumestans in Medicago spp

Photoperiodicity in the ram

Bodyweight, nutrition and fertility in the ram

Puberty and age effects in rams

Husbandry procedures and ram fertility

Management of joining

Ewes

Ewes and rams

Duration of joining

Composition of ram syndicates

Joining ratio

Failure of fertilization due to too few rams

Failure of fertilization due to other ram factors

Non-specific abnormalities of the epididymis which affect ram fertility

Epididymitis caused by Brucella ovis infection (Ovine brucellosis, OB)

Epidemiology

Pathogenesis[12]

Clinical findings

Diagnosis

Eradication

Accredited OB free flock scheme

Other causes of epididymitis

Actinobacillus seminis

Miscellaneous infections

Testicular abnormalities

Cryptorchidism

Hypoplasia

Degeneration

Other lesions of the male genitalia

Balanoposthitis

Varicocoele

Scrotal mange

Embryo mortality

Aetiology

Partial or full embryo loss

The relative importance of embryo mortality

Abortion in ewes and prenatal diseases of lambs

Toxoplasmosis

Campylobacteriosis

Salmonellosis

Listeriosis

Enzootic abortion

Brucellosis

Ovine Pestivirus

Akabane Disease

Table 7.5 Summary of infectious abortion of ewes

Abortion caused by Histophilus ovis

Romulosis

Health and management at lambing

Nutrition