a1 Agriculture and Life Sciences Division, PO Box 84, Lincoln University, Canterbury, New Zealand
The nutritional cost of both the acquisition and maintenance of immunity to gastro-intestinal nematodes was investigated using immunologically naïve 5-month-old lambs and immunologically competent 17-month-old ewes. Within each age cohort, animals were either infected with the equivalent of 80 L3 Trichostrongylus colubriformis larvae per kg live weight (LW) per day (IF), similarly infected and concurrently immuno-suppressed with weekly injections of 1·3 mg/kg LW of the glucocorticoid methylprednisolone acetate (ISIF), immuno-suppressed only (IS) or remained as controls (C). Body composition of all animals was estimated using X-ray computer tomography on days -14 and 76 relative to the start of infection. Body weight and faecal nematode egg counts (FEC; eggs per gram of fresh faeces (e.p.g.)) were taken weekly and blood samples for serum proteins and antibodies were obtained every 2 weeks. FEC in IF lambs peaked at 1250 e.p.g. before a typical decline as immunity developed to less than 100 e.p.g. by day 75. FEC of less than 100 e.p.g. in IF ewes indicated immunity was maintained. Successful immuno-suppression in ISIF lambs and ewes was indicated by FEC of 4000 e.p.g. on day 75 and was confirmed by comparative worm burdens and serum antibody titres. The typical reduction in voluntary food intake (VFI) as a consequence of infection was observed in IF lambs (proportionately 0·30, P < 0·001) but not in IF ewes, ISIF lambs or ISIF ewes. Gross efficiency of use of metabolizable energy for net energy deposition was reduced by proportionately 0·20 in lambs during acquisition of immunity and by 0·16 in ewes maintaining an established immunity. Infection in immuno-suppressed animals reduced efficiency by 0·05 and 0·15 for lambs and ewes, respectively. These findings allowed the hypothesis that the reduction in VFI and loss in performance in young parasitised sheep is caused by physiological signalling associated with the acquisition phase of the host immune response to infection, rather than simply the damage caused by the parasite per se.
(Received June 24 2004)
(Accepted September 08 2004)