Pathophysiology of nematodiasis in cattle.
Recent detailed studies of the physiologic changes occurring in cattle infected with some of the common gastrointestinal nematodes have shown that the weight loss and reduced carcass values resulting from these infections are a consequence of major alterations in host metabolism. Dramatic changes in protein metabolism were consistently found to involve decreased muscle synthesis and increased urinary nitrogen excretion. Because of the well-recognized loss of plasma proteins into the gut lumen and cellular damage at the mucosa occurring during nematode infections of the abomasum and duodenum, it has been assumed that protein was being lost in feces or not absorbed; however, this loss has proved not to be as significant as postabsorptive protein catabolism in these infections. Only when the colon and cecum are involved in protein-losing infections is the loss of protein into the feces significant. The mechanisms by which gastrointestinal nematode infections result in such altered host metabolic states are not known, but suggestions have been made that parasites directly or indirectly alter gut hormone levels. Gut hormone changes may also be responsible for diarrhea and anorexia. Another mechanism of altering metabolism has been proposed for chronic parasitisms that stimulate macrophages. Macrophages produce a peptide called cachectin, and cachectin is thought to mediate protein and lipid catabolism. This mechanism obviously could be contributing to weight loss and anorexia whenever nematodes cause sufficient macrophage activation, including during lungworm infections, which do not have enteric involvement.