This study was carried out to establish whether cattle can develop resistance to re-infection by Calicophoron microbothrium by assessing the response of intestinal mucosal globule leukocytes, eosinophils, mast cells and basophils, and the establishment of the parasite in the host. A total of 24 1-year-old Tuli steers were randomly divided into four groups of six animals each and infected with C. microbothrium metacercariae. On the first day of the study, animals in Groups I and II were immunized with 5 000 metacercariae and then challenged with 15 000 metacercariae on Day 150 post-immunization. Animals in Group III were immunized with 15 000 metacercariae at the same time that Groups I and II animals were challenged to act as a positive control group. Animals in Group IV were left uninfected and acted as a negative control group. Three animals from each group were slaughtered on Day 28 post-challenge and the remainder were slaughtered on Day 42 post-challenge. The established amphistomes were recovered and histopathological and cytological examinations were done on the jejunum, duodenum, abomasum and the rumen. The establishment rates of the challenge infection in the immunized and challenged groups were lower and ranged from 0 to 0.2 % as compared to 6 %> from naive animals infected as positive controls. Animals immunized and then challenged with C. microbothrium had significantly higher eosinophil, mast cell and globule leukocytes counts in the intestinal mucosa (P < 0.05) as compared to those of the control group. The study indicates that cattle can develop resistance to C. microbothrium re-infection and that eosinophils and mast cells may be important cells in the rejection of the parasite.

Major clinical signs were depression, vomiting, abdominal pain, weakness, recumbency, paddling convulsions terminating in death from 6 to 96 hours after ingestion. Gross pathological findings included ascites with fibrin strands, enlarged, congested and friable livers with accentuation of lobulation on the capsule. Microscopically, acute hepatic congestion and hemorrhage, centrilobular hepatocyte necrosis, with occasional binucleation together with discoid lysis of skeletal and cardiac muscle fibers were remarkable changes. Binucleation of hepatocytes and degenerative changes in active muscles have not been reported before in relation to cocklebur plant toxicosis. These findings suggest that X. strumarium is a potential cause of sudden death in pigs extensively reared in Zimbabwe.