Action de la lactation sur le parasitisme des rats par Strongyloides ratti

Abstract

In lactating females of many animal species infested by Nematoda, the self-cure is, if not suppressed, at least very distinctly delayed. It does not appear that an immunological deficiency is the cause of this. We show that this phenomenon also exists in lactating female rats with Strongyloides ratti parasites. In fact, for Strongyloides ratti, the maintenance of the worms is not the only notable modification determined by lactation; much more important is the decrease in the intensity of the parasitism. This aspect is not mentioned by writers who have only studied the different parasitic states in their final phase. Parallel to these alterations in the parasitism, the evolution of the corticosteronemy differs, from two points of view, from that described in infested virgin rats: --Suppression of the hypercorticosteronemy which normally appears 48 hours after infestation; --Attenuation of the hypocorticosteronemy which usually sets in from the tenth day of infestation. This opposition of lactation to the variations in the corticosteronemy induced by the worms is explained by the effect of lactation on the secretion of gluco-cortico-steroids, described under the term of "buffer effect of lactation". The decrease in the intensity of the parasitism may be explained by the fact that lactation, by preventing the hypercorticosteronemy normally caused by larval migration, permits the intervention of aspecific defences. As for the prolongation of the parasitism, it would seem to result on one hand, from a reduced solicitation of the means of defence owing to a smaller number of worms and, on another hand, from the slowing down of the hypocorticosteronemy through the buffer effect of lactation with all the consequences flowing from this at the level of the specific and aspecific defence reactions.