Lactating rats experience a breakdown of immunity to parasites, i.e. they carry larger worm burdens after re-infection compared to their non-lactating counterparts. Feeding high-protein foods to lactating rats results in reduced worm burdens. This could be attributed to changes in gastrointestinal environment or to overcoming effects of nutrient scarcity on host immunity. The latter hypothesis was addressed through a manipulation of nutrient demand by manipulating litter size. Twenty-three rats were immunized prior to mating and re-infected on day 2 of lactation with 1600 infective Nippostrongylus brasiliensis larvae. From parturition onwards, rats received ad libitum a low-protein food (100 g crude protein/kg). Litter sizes were standardised to nine (LS9), six (LS6) or three (LS3) pups, by day 2 of lactation. After a further 10 d, LS9 and LS6 rats carried more worms than LS3 rats. However, feeding treatments did not affect concentrations of mucosal inflammatory cells. Achieved feed intake did not differ consistently between the treatment groups. However, LS9 and LS6 rats lost weight, whilst LS3 rats gained weight during lactation. The results support the view that resistance to N. brasiliensis is sensitive to changes in nutrient demand, and the improved resistance to N. brasiliensis is likely due to effects of overcoming nutrient scarcity on host immunity.

Lactating mammals usually exhibit a breakdown of immunity to parasites, i.e. they have larger worm burdens than their non-lactating counterparts. Here, we tested the hypothesis that a secondary infection with Nippostrongylus brasiliensis in lactating rats is sensitive to dietary protein content. We also tested whether this infection affects host food intake. Rats either remained uninfected throughout the study or were given a single infection before mating (primary infection) and re-infected on day 2 of lactation (secondary infection) with 1600 infective larvae. Infected rats were fed foods during lactation formulated to supply 100 (low protein; LP), 200 (medium protein; MP) or 300 (high protein; HP) g crude protein per kg DM; non-infected rats were fed either the LP or HP food. Litter size was standardized to ten pups between parturition (day 0) and secondary infection (day 2). Ten days after secondary infection, MP and HP rats had excreted fewer nematode eggs, and had fewer adult nematodes in their small intestine and nematode eggs in their colon than the LP rats. Primary infection increased food intake in late pregnancy, and increased maternal body weight and litter size at parturition. Secondary infection did not affect mean food intake, maternal and litter weight, although food intake was reduced for 1 d following infection. These results support the view that a secondary infection with N. brasiliensis is sensitive to dietary protein content, and that the latter infection does not impair lactational performance. Future studies may focus on elucidating the nutritional sensitivity of immune responses underlying the reduced secondary N. brasiliensis infection.

The nutritional basis of breakdown of immunity to parasites may be addressed in a rodent model. We hypothesized that lactating rats would show a breakdown of immunity to Nippostrongylus brasiliensis, and that this breakdown of immunity would be sensitive to protein supply. Rats were immunized with 1600 infective N. brasiliensis larvae and subsequently mated. During lactation, these rats were offered foods with 90 (low protein; LP) or 210 (high protein, HP) g crude protein (N X 6.25)/kg and re-infected with 400, 800 or 1600 larvae on day 2 post-parturition. Immunized non-reproducing rats were offered a food containing 60 g crude protein/kg and re-infected with 1600 larvae. Seven days after secondary infection, lactating rats had more adult nematodes in their small intestine and nematode eggs in their colon contents than the non-reproducing rats. Protein supply did not affect worm or egg counts, although LP rats carried relatively more female nematodes than the HP rats. All lactating rats had lower intakes than expected from previous studies using similar nutritional protocols. This may have resulted in insufficient protein supply, even for the HP rats, and this could explain the absence of effects of protein supply on egg and worm counts. We conclude that a breakdown of immunity to N. brasiliensis can occur in lactating rats; this strongly suggests that the lactating rat is a suitable model for elucidating a possible nutritional basis of breakdown of immunity to parasites. However, sufficient protein intake must be achieved to address the hypothesis that breakdown of immunity to N. brasiliensis is sensitive to protein supply.