The effect of post-ruminal infusion of protein or energy on the pathophysiology of Trichostrongylus colubriformis infection and body composition in lambs

Abstract

The effect of post-ruminal infusion of protein or energy on the pathophysiology of Trichostrongylus colubriformis infection and body composition in lambs was investigated using the comparative slaughter technique. Of 52 Dorset DownxCoopworth wether lambs (mean body weight 30.5, s.e. 0.44 kg), 8 comprised an initial slaughter group (IC), 36 were infected daily, per os, with 3000 Trichostrongylus colubriformis larvae per animal, and the remainder (C) were parasite-free controls. Groups of 12 infected animals were given either a continuous infusion (via abomasal catheter) of 50.4 g/day crude protein as sodium caseinate (PI), glucose (EI) in isocaloric amounts to PI, or a solution containing P and Na at the same rate as the caseinate infusions (SI). Uninfected controls (C) were also infused with this solution. Animals were slaughtered after 6 and 12 weeks for estimation of worm count and body composition. All animals were offered, ad libitum, meadow hay (118 g crude protein/kg dry matter (DM); 930 g organic matter/kg DM; 0.65 organic matter digestibility). DM intake of infected animals decreased by approximately 22% in PI and EI and by 32% in SI animals. Mean total metabolizable energy (ME) intake during the experiment (inclusive of infusions) was C, 0.607; PI, 0.687; EI, 0.704; SI, 0.617, s.e.d. 0.0308 MJME (kg W)-0.75 day-1. Nitrogen retention in infected sheep was increased fourfold by protein infusion and twofold by energy infusion. The rate of energy retention was reduced by infection, increased by protein infusion but only partly by energy infusion. Protein infusion reduced mean faecal egg output and mean total parasite count. Increased endogenous plasma loss into the gastrointestinal tract was similar in all infected groups. It was concluded that a major limiting factor in efficient food utilization in animals with gastrointestinal nematode infections is a parasite-induced protein rather than energy deficiency, possibly the result of increased endogenous protein losses into the gastrointestinal tract. The debilitating effect of internal parasites could be markedly reduced by increasing duodenal protein supply.