Investigations into the poor recovery of sulphadimidine from medicated animal feeds have
shown that irreversible drug-feed binding, and not drug degradation, is responsible for the
poor recoveries. The experimental work involved the novel use of C-sulphadimidine in
analytical studies and in autoradiography of C-sulphadimidine-bound feed. The latter
showed that the drug was not bound preferentially to specific feed constituents but was widely
distributed on nearly all the feed particles.
Further work on sulphadimidine recovery from feeds demonstrated an inverse relationship
between drug recovery and feed moisture content. The role of moisture in the binding
mechanism was then considered, and experiments conducted on the adsorption of moisture
by feeds showed that the rate controlling mechanism was diffusion.
A hypothesis is presented in which sulphadimidine is partially dissolved by the moisture in
the feed and the resulting solution then diffuses into the internal regions of the feed particles
via pores and cracks in the constituent particles. The deep penetration of the drug into the feed
prevents the drug from being recovered by the extraction solution. Experimental evidence was
found to support this hypothesis.
Experimental work also investigated the causes of poor recoveries of sulphadiazine,
trimethoprim and dinitolmide.
A Doctoral Thesis. Submitted in partial fulfilment of the requirements for the award of Doctor of Philosophy of Loughborough University.