An outbreak of goitre occurred in the spring 2010 and autumn 2011 lambs from a stud Poll Dorset flock in the Central West of NSW.
On this property the pasture type is predominantly improved pastures with significant weed infestation, notably purple top (Verbena bonariensis). In addition to the grass-based pastures there has been a paddock sown with fodder canola (Brassica napus) which is used for grazing while the ewes are pregnant. The main water sources are troughs. There have not been any significant health or reproductive problems on this property until the current problem arose. There have not been any management practices changed in the past two years.
There are 185-190 ewes with both a spring and autumn lambing. The rams are changed at three weeks in the six-week joining. The lambs are marked 2-3 days after the last lamb is born and weaned at 14-16 weeks depending on the season. At marking, the lambs receive the first booster of clostridial vaccine (ULTRAVAC™ 5-in-1). Gudair™ vaccine is also administered at marking with the second booster of the clostridial 5-in-1 vaccine at weaning. The lambs are also given a vitamin injection (A, D, E and B12) at weaning and they are drenched with abamectin. The ewes receive a pre-lambing drench and clostridial vaccine. There has not been any supplement feeding performed until the current problem was identified.
Last spring lambing (2010), the producer noted a reduced lambing rate compared with normal years, in addition to an increased number of late term abortions and stillbirths. These dead neonates often had bilateral large swellings on the ventral aspect of the neck and were often of significantly lower birth weights than the normal lambs. At the same time in the mob, there was some evidence of wool breakage, particularly in the autumn 2010 lambs. A number of the live lambs were also observed to have the large bilateral rounded swellings on the ventral aspect of the neck. This autumn (2011) the problem has developed to the point that approximately one quarter of the flock are exhibiting wool break and the lambing rate was reduced to 50% of the ewes joined. Over this time, there has also been an increase in prevalence of foot abscess in the ewes, to approximately four times the normal level at the time of presentation. All of these animals had been grazing the fodder canola or were born to ewes grazing the fodder canola during gestation.
We aimed to investigate the reproductive and production problems that have been identified in this flock. One of these problems was the bilateral swellings on the ventral aspect of the neck in the neonatal lambs, identified as a congenital goitre. To determine the prevalence of congenital goitre in the lambs born in the last two lambing seasons (spring 2010 and autumn 2011) the lambs were yarded and palpated individually to identify enlarged thyroid glands. The spring 2010 lambs were examined and it was determined that of the 25 lambs, there were 19 with palpably enlarged thyroid glands.
The autumn 2011 lambs, of which there were only 10 at the time of presentation; there were nine lambs with palpably enlarged thyroid glands. Other courses of investigation would have been to determine the thyroid-weight: birthweight ratio (g/kg). If this ratio was in excess of 0.4g/kg, this is indicative of an iodine deficiency. Another option for investigation would be to perform histopathology on the thyroid glands to identify histological changes associated with hypertrophy, notably the presence of columnar epithelium lining the thyroid follicles (Knowles and Grace 2007).
Neither of these options were possible in this case as there were no neonatal lambs in the flock at presentation and the sacrificial post-mortem or biopsy of a thyroid gland were not economically viable in this flock with the reduced lambing rate this autumn. Blood samples of the animals were also not possible, as the animals had been supplemented with iodine prior to presentation. If blood collection was a possibility, total T4 assays may have been performed in the ewes post-parturition, however it must be noted that the T4 serum level is affected by other biological factors, notably the presence of internal parasites (Clark et al. 1998).
Congenital goitre is the term given to a lamb that has an enlarged thyroid gland present at birth. Knowles and Grace (2007) state that the most common causes of congenital goitre in lambs include both absolute and relative iodine deficiencies in the ewes. An absolute iodine deficiency arises when the ewes are grazing pastures grown on iodine deficient soils (Knowles and Grace 2007). A induced iodine deficiency in the ewes is caused by some factor preventing the uptake of the available iodine; goitrogenic compounds will interfere with the uptake of iodine by the thyroid gland and thus ewes may become iodine deficient despite having normal iodine levels in the blood (Robertson, Friend and King 2008; Knowles and Grace 2007). Congenital goitre is a clinical sign of hypothyroidism (Robertson, Friend and King 2008). Hypothyroidism will cause a reduced metabolic rate and the lambs will be more susceptible to hypothermia. They will be less active and have reduced suckling behaviour (Robertson, Friend and King 2008; Knowles and Grace 2007). Their wool follicles may also be affected. In some cases, the lamb may be born without wool or the wool may be sparse and soft. In adult sheep the wool will be brittle and break easily (Robertson, Friend and King 2008; Knowles and Grace 2007).
Therefore, the most common clinical signs related to iodine deficiency in a sheep flock include reduced birth rates, increased neonatal mortality with smaller birth weights and increased prevalence of wool break within the flock (Robertson, Friend and King 2008; Knowles and Grace 2007). This flock exhibited all of these clinical signs in the spring 2010 and autumn 2011 lambings.
Determining the iodine levels in the pastures is complex and often inaccurate (Robertson, Friend and King 2008). This is because the levels of iodine in the soil will vary depending on the season, rainfall and the pasture growth (Robertson, Friend and King 2008). It is more accurate to investigate signs of iodine deficiency in the animals, with the most simple and inexpensive method being to examine the young animals for goitre (Robertson, Friend and King 2008). The complexity of investigations of deficient soils using the clinical signs in the animals is compounded by the fact that there are various fodder species that have high concentrations of goitrogenic compounds that will induce an iodine deficiency in the animals grazing these pastures (Robertson, Friend and King 2008).
Brassica napus (canola) is a forage crop with a high concentration of goitrogens in addition to a low concentration of iodine (Mawson et al. 1994). Goitrogenic compounds suppress thyroid function, which may lead to goitre and hypothyroidism. There are two different goitrogenic compounds in canola; glucosinolates and S-methyl cysteine sulfoxide (Mawson et al. 1994). These chemicals are distinct pharmacologically working in different ways to induce iodine deficiency in the animal (Mawson et al. 1994).
The glucosinolates in the canola are released as isothiocyanates during digestion and work by interfering with the thyroidal uptake of inorganic iodine from the blood through the thyroid blood vessels (Knowles and Grace 2007). The combination of the low levels of available iodine and the goitrogenic compounds acting on the thyroid will mean that in an animal grazing fodder canola, the thyroid gland will demonstrate hypertrophy (Knowles and Grace 2007). This hypertrophy of the thyroid gland is a physiological response to the induced deficiency of the iodine. The thyroid is increasing its level of activity to utilise all of the iodine available (Knowles and Grace 2007).
The main goitrogens are found in the Brassica family (canola, broccoli, cauliflower, Brussels sprouts or cabbage) however they may also be found in soy, pine nuts, millet and peanuts (Robertson, Friend and King 2008; Knowles and Grace 2007). In southern NSW, it has been identified that white clover (Trifolium repens) is also a source of goitrogenic compounds (Robertson, Friend and King 2008).
Animals grazing pastures containing goitrogenic compounds have an increased requirement for dietary iodine; 2-4 times more dietary iodine than normal requirements (Haskell 2008; Knowles and Grace 2007). In sheep, the normal requirements of iodine vary from 0.1-0.4mg/kg dry matter feed intake (Haskell 2008).
Supplementation of sheep that have been grazing pastures containing goitrogenic compounds will rectify the iodine deficiency and prevent further production losses caused by the deficiency. However, it will not reverse the developmental changes that have occurred in the lambs (Haskell 2008; Knowles and Grace 2007). The hypertrophy of the thyroid gland will not be reversed, however if supplemented, the lamb's thyroid gland will cease increasing in size and become less obvious as the lamb grows in body size.
Haskell (2008) states that if more than 25% of the normal diet is composed of a plant source that contains goitrogenic compounds, it is necessary to supplement iodine. In this flock, both the ewes and lambs were drenched with potassium iodine. In the future, if the fodder canola is resown and grazed through gestation, it is recommended to dose the ewes with injectible potassium iodine, which is useful against the thiocyanate goitrogens in canola, in order to provide protection against the reproductive and production losses caused by the induced iodine deficiency (Haskell 2008; Knowles and Grace 2007). This supplementation may either be performed once orally in late gestation (208-300mg), once 7-9weeks prior to lambing using 1ml of iodised poppy seed oil injected intramuscularly (which may provide protection for up to two years) or weekly using tincture of iodine (1-2ml) to the inside of the flank during gestation (Haskell 2008).
It is important to monitor the flock for the clinical signs of iodine toxicity when supplementing with iodine. Haskell (2008) lists these clinical signs of iodine toxicity as 'coughing, excessive lacrimation [tears on the face], generalised scaling of the skin, partial alopecia, variable appetite and joint pain'. If any of these clinical signs are observed in iodine supplemented sheep it is recommended that the supplement be removed as iodine is rapidly metabolised and excreted thus rectifying the toxicity (Haskell 2008).
Further investigation on this property would include identifying the thyroid-weight: birthweight ratios of the neonatal lambs. This size of this ratio will give an indication of the iodine status of the flock (Knowles and Grace 2007). If this ratio is consistently <0.4g/kg the iodine status of the flock is within normal limits (Knowles and Grace 2007). Ratios of >0.8g/kg are indicative of an iodine deficiency and further supplementation is warranted (Knowles and Grace 2007). In the case that the thryoid-weight:birthweight ratio is between 0.4and 0.8g/kg then further investigation is warranted in order to determine the iodine status of the flock before implementing additional supplementation regimes (Knowles and Grace 2007).
It is also necessary to investigate the selenium status of the flock, as selenium deficiency may not only be related to reproductive problems in sheep, it can also predispose sheep to hypothyroidism. This occurs as there is a selenium enzyme (S'-deiodinase) which is required in the conversion of thyroxine to tri-iodothyronine (T3) (Clark et al. 1998).
T4 levels are generally considered unreliable for assessment of iodine status as concentrations are depressed by onset of lactation, high milk production, gastrointestinal parasitism and reduced energy intakes, and are elevated by a conconcurrent Se deficiency (selenium is involved in the selenoprotein iodothyronine deiodinase which converts T4 to the active T3). Dietary I intake is correlated with serum and milk iodine and both are reported as suitable alternatives to T4, however it would appear that serum iodine assays are not readily available in NSW.