Protein metabolism in parasite infected lambs

Abstract

Aspects of the effect of gastro-intestinal parasitism on protein metabolism in lambs were investigated. Particular reference was made to the effect of parasitism on endogenous protein losses into the gastrointestinal tract, the absorptive capacity of the gastro-intestinal tract and to the deposition of protein in the body. In addition, the influence of supply of protein and energy to the small intestine on the effects of gastro-intestinal parasitism was investigated.

An initial investigation examined the effect of a concurrent infection of Trichostrongylus colubriformis and Ostertagia circumcincta on digestion and absorption of protein across the sites of infection in the GIT. This was achieved by reference to enteric plasma protein losses, to the absorption of albumin over the proximal and distal small intestine and to the changes in nitrogen flow across these regions of the GIT.

Twelve animals, paired on the basis of liveweight were cannulated at the abomasum, proximal jejunum and terminal ileum. Six lambs were infected with 3000 T. colubriformis and 3000 O. circumcillcta per day for 18 weeks. The remaining six lambs were pair-fed to the infected lambs. Dry-matter intake, liveweight, faecal egg concentration, plasma pepsinogen and plasma protein concentrations were measured throughout the experiment. During week 7 and week 17 post-infection measurement of the flow of digesta along the gastro-intestinal tract in infected and control animals was made together with measurement of enteric plasma loss and true digestion and absorption of albumin along the small intestine. Digesta pH and digesta transit time were also measured during these periods.

Parasitism caused a depression in dry-matter intake (1223±98.5 vs. 434±31.5 vs. 529±50.7 g/d during weeks 3, 7 and 17 respectively) and was associated with a reduction in N retention in both infected and control animals. During week 7 parasitism caused a significant increase in the flow of N past the the proximal jejunum and increased faecal N output, though during week 17 parasitism increased N flow throughout the GIT. Plasma protein N loss into the gastro-intestinal tract increased two- to threefold over the experiment (week 7, 0.68±0.091 vs. 1.97±0.139 and week 17, 0.85±0.158 vs. 1.96±0.346 gN/d for controls vs. infected respectively). Parasitism increased pH of digesta in the abomasum during week 7 (2.6±0.04 vs. 3.2±0.23 for control vs. infected respectively). True digestion and absorption of albumin across the site of infection in the small intestine was very low and was not affected by parasitism (mean 0.08). Across the whole small intestine absorption of albumin was high (mean 0.87) and again was not affected by parasitism. The low protein absorption in the duodenum of both infected and control animals was associated with low digesta pH in this region (4.8±0.14 vs. 5.0±0.21 for control vs. infected respectively) and also a very short transit time between the abomasum and proximal jejunum (mean 11±1.5 minutes). Transit time through the whole small intestine was increased by parasitism during week 7 (150±10.9 vs. 204±19.4 min. for control vs. infected respectively).

It was concluded that parasitism caused an increase in endogenous protein loss into the gastro-intestinal tract of which plasma protein loss was only a small proportion (10 - 36%). Despite the endogenous protein losses and increased digesta pH and transit time, digestion and absorption of protein was not affected by parasitism and occurred in the distal small intestine. Depression in feed intake was apparently a major factor responsible for the reduction in N retention in both infected and control animals.

Concurrently with this investigation, the effect of gastrointestinal parasitism on absorption and plasma concentrations of Ca, P and Mg was investigated. Depression of feed intake by parasitism was associated with reduced retention of Ca, P and Mg in both infected and control animals. Parasitism increased Ca flow past the abomasum during week 7 and week 17 by approximately 18% and P flow past the ileum during week 17 by 26%. These changes were reflected in increased faecal excretion of Ca and P apparently due to increased endogenous loss of Ca and P and' impairment of absorption of Ca and P from the gastro-intestinal tract. Plasma concentrations of Ca and P were correspondingly depressed. Magnesium metabolism was not affected by parasitism.

In a second investigation, a comparative slaughter experiment examined the effect of post-ruminal infusion of protein or energy on the animal body composition and pathology of Trichostrongylus colubriformis infection in lambs. Lambs infected with 3000 larvae per day were infused with casein (50.5 gCP/day; PI) or glucose (isocaloric with protein infusions; EI) or solvent/diluent (SI). Uninfected controls (C) were also infused with solvent/diluent. DM intake, liveweight, faecal egg concentration, endogenous plasma protein loss and total parasite burden were measured.

Mean liveweight gain over the experimental period was 8.0±0.91; 6.9±0.97; 3.7±0.92; 3.1±0.72 kg for C, PI, EI and SI respectively. Faecal egg output was not affected by the infusion treatments (PI, 1.299±0.5657; EI, 2.851±1.0775; SI; 2.017±0.3691 eggs/d x 10⁶). The increased endogenous plasma loss into the GIT due to parasitism was similarly unaffected by infusion (C, 73.3±4.34; PI, 251.6±21.18; EI, 281.5±95.31; SI, 200.1±32.98 ml/d). However, casein infusion reduced total parasite burden at slaughter (PI, 17800±5320; EI, 45700±6700; SI, 39300±6700). Neither total plasma protein nor albumin concentration was altered by parasitism or infusion treatment but globulin concentration in plasma was apparently increased by parasitism. Plasma Ca and P concentrations were also reduced by parasitism but the reduction in Ca concentration was apparently reversed by casein infusion. Plasma P concentration was not affected by the casein infusions.

After increasing for four weeks DM intake of infected animals decreased by approximately 22% for PI and EI and by 32% for SI animals. Total ME intake (inclusive of infusions) was C, 0.607; PI, 0.687; EI, 0.704; SI, 0.617 MJME/W º•⁷⁵). /d suggesting that ME intake of infected animals was not regulated by energy satiety. At slaughter the protein energy: total energy ratio in the empty body was similar for all groups (0.31), but the rate of energy retention was different (C, 0.077±0.014; PI, 0.094±0.015; EI, 0.069±0.018; SI, 0.041±0.009 MJ/Wº•⁷⁵). Nitrogen retention was increased five-fold by protein infusion and was doubled by energy infusion. The rate of Ca retention was reduced by parasitism but this effect was apparently moderated by casein infusion (C, 0.000±0.0083; PI, -0.018±0.0187; EI, -0.048±0.0191; SI, -0.052±0.0071 g/W º•⁷⁵). /d). Retention of P was reduced by parasitism but was apparently not affected by the infusion treatments (P, 0.014±0.0046; PI, -0.006±0.0077; EI, -0.001±0.0129; SI, -0.014±0.0047 g/W º•⁷⁵)./d).

It was concluded that the effect of the parasite on N retention in the host was a result of increased irreversible loss of endogenous protein from the small intestine rather than catabolism of protein to supply energy. It was possible to alleviate, in part, the deleterious effects of parasitism on N retention by supplementing the protein arriving at the small intestine by an amount calculated to be equivalent to that of the irreversible endogenous loss.