Susan McClure, DV Central West LHPA

Posted Flock & Herd July 2012


Lambs frequently fail to develop protective immunity to gastro-intestinal nematodes (GIN). This results in direct losses from mortality and decreased production, and indirect costs associated with treating parasitised lambs post-weaning. In the past this susceptibility has been attributed to age, with the argument that such lambs are not old enough to develop effective immunity (Colditz et al. 1990). However, this does not make immunological sense, as fetal lambs are immune-competent from 55 days of gestation, and neonatal lambs develop immunity to GIN (McClure et al. 1988; Emery et al. 1999). In at least some cases, this susceptibility is due rather to the interaction between liveweight and nutrition, and as such is more amenable to prevention.


In pen trials (McClure and Emery, 2007), Merino lambs weighing less than 23 kg at the time of first exposure to T. colubriformis had impaired ability to develop protective mucosal immunity and thus had reduced ability to control worm burdens and worm fecundity during second and subsequent infections. Those lambs below 15 kg had no ability to control worm infections (Figure 1). These observations were made on lambs fed 40 g/kg/day of a pelleted oat grain/lucerne ration supplemented with 1% Siromin (CSIRO, a multi-mineral mix) and containing approximately 15% crude protein, 10 MJ/kg DM, 5% soluble carbohydrate and 1 mg/kg Mo, a diet sufficient to allow moderate liveweight gain. The critical weights observed in these lambs may not apply to sheep of different genetic backgrounds. This lack of an effective immune response in lambs below 23 kg suggests that bodyweight gain had priority in terms of metabolism and nutrient partitioning over the immune response. This may explain, at least in part, the widely observed phenomenon of age-related hypo-responsiveness of lambs to gastro-intestinal nematodes. The principle may also apply to immunity against other gut pathogens and in the young of other ruminant and non-ruminant species.

Figure 1. Effect of initial liveweight on faecal worm egg count and final worm count during subsequent infection with T. colubriformis (reproduced courtesy of Aust Vet J)

There are two exceptions to this critical liveweight observed in shedded lambs and yet to be confirmed under field conditions. A very high-quality diet (added maize and fishmeal) overcame this reduced resistance in light-weight lambs (McClure, 2010), indicating that disease control strategies should consider interactions between liveweight, quality of diet and developing immunity. Secondly, lambs infected as neonates (one week of age) developed better immunity to Trichostrongylus and Haemonchus than did older lambs (one month of age) (Emery et al., 1999). This difference may be due to the brown fat reserves present in neonates. Alternatively, neonates may not be subject to the same metabolic regulation with respect to priority for growth, or the quality and quantity of the early milk supply relative to the lamb's requirements may be better. (If this observation were to hold up in the field, it would raise a question about the desirability of routinely administering long-acting anthelmintics to pre-lambing ewes.)


Thus, under field conditions, light lambs (those below 23 kg at weaning) may not have developed a functional immunity during primary exposure whilst grazing on heavily contaminated paddocks with lambing ewes. In addition, like the penned weaners above (Figure 2) they may not exhibit a functional secondary-type immune response when exposed to larval challenge after weaning, at 12 to 14 weeks of age, resulting in higher worm burdens and prolonged egg contamination of pastures. This has significant implications for sheep husbandry.

Figure 2. Faecal worm egg counts and final worm count following primary or secondary infection with T. colubriformis of lambs under or over the recommended weaning weight at time of first exposure to T. colubriformis (reproduced courtesy of Aust Vet J)

Practical advice given to farmers in south-eastern Australia is that lambs should reach a minimum of 45% of adult bodyweight by weaning or drying-off of pastures, then grow at 1 kg/month until the onset of autumn rains. This equates to 22.5 kg for a strain of Merino which averages 50 kg as a mature ewe in condition score 3 (Holmes and Sackett, 1990). As lambs below this weight have no fat reserves, a possible metabolic cause of reduced immunity in light lambs may therefore involve energy. The expected bodyweight of 3 to 4-month-old spring-born Merino lambs in the paddock in the Northern Tablelands of New South Wales is 20 to 22 kg.

Lamb weight is a function of birthweight (which in turn is a function of prenatal nutrition), sex, parental genetics, parity, stress during pregnancy and lamb growth rate. For the first 8 weeks, lamb growth rate is largely dependent on ewe nutrition, weight, condition score and parity and thus milk yield, and on lamb appetite and sex, while after 8 weeks, pasture quality and availability to the lamb become increasingly important.

Under extensive grazing conditions, lambs frequently fail to reach the desirable target weaning weight even in good seasons, and if feed quantity and quality are not maintained after weaning, lambs can quickly drop below this weight. Weaning itself has the potential to delay the development of immunity. If the goal is to ensure that lambs develop immunity before weaning, then every endeavour should be made to achieve the combination of critical bodyweight and exposure to moderate levels of nematode infection as soon as possible. In extensive systems under existing nutritional and management practices it is difficult to prevent primary exposure to internal parasites until lambs are over 23 kg. However, attention to such factors as ewe condition and nutrition, quality of the lamb diet (including the possibility of early supplementation) and the management of larval availability on pasture may permit the development of immunity before weaning.


  1. Colditz IG, Watson DL, Gray GD, Eady SJ. Some relationships between age, immune responsiveness and resistance to parasites of ruminants. Int J Parasitol 1990;26:869-877
  2. Emery DL, McClure SJ, Davey RJ, Bendixsen T. Induction of protective immunity to Trichostrongylus colubriformis in neonatal Merino lambs. Int J Parasitol 1999;2:1037-1046
  3. Holmes P, Sackett D. Weaner series - target weights and feeding. Holmes & Sackett On Farm 1990;3:23-25
  4. McClure SJ. Dietary impacts on the resistance of Merino lambs to Trichostrongylus colubriformis. N Z Vet J 2009;57:102-108
  5. McClure SJ, Emery DL. Trichostrongylus colubriformis and Haemonchus contortus infections in light bodyweight Merino lambs Aust Vet J 2007;85:1-9
  6. McClure S, McCullagh P, Parsonson IM, McPhee DA, Della-Porta AJ, Orsini A. Maturation of immunological reactivity in the fetal lamb infected with akabane virus. J Comp Path 1988;99:133-143


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