When Salmonella typhimurium and Clostridium perfringens were tested in conventional chickens, larger numbers of S typhimurium and C perfringens adhered to Eimeria tenella-infected ceca than to uninfected ceca. In germ-free chickens, S typhimurium and C perfringens adhered to the E tenella-infected cecal mucosa more than to the uninfected cecal mucosa, but fewer Bacteroides vulgatus and Bifidobacterium thermophilum adhered to the E tenella-infected ceca than to the uninfected ceca. Many bacteria adhered to the lesions caused by E tenella as observed by scanning electron microscopy. On the basis of our findings, we suggest that infection with E tenella upsets the balance of competitive adherence of bacteria, allowing more colonization of S typhimurium and C perfringens.

Development of age-dependent resistance to enterotoxigenic Escherichia coli was studied, using isolated enterocytes and brush border membranes (BBM) from 7-day-old and 7-week-old pigs. Binding of 125I-labeled heat-stable (125I-STa) enterotoxin to enterocytes and BBM was specific, temperature- and time-dependent, saturable, and partially reversible. Scatchard analysis revealed a single class of receptors. Mean +/- SD avidity of binding (apparent affinity constant, Ka) of 125I-STa to enterocytes from 7-day-old and 7-week-old pigs was 2.14 +/- 0.29 X 10(8) and 2.72 +/- 0.25 X 10(8) L/mol, respectively. Numbers of STa receptors were calcuated to be 64,903 +/- 2,900/enterocyte for 7-day-old pigs and 53,029 +/- 3,117/enterocyte for 7-week-old pigs. Numbers of STa receptors expressed per milligram of BBM protein from 7-day-old pigs were 2.66 X 10(11), compared with 2.29 X 10(11) for BBM from 7-week-old pigs. By 5 minutes after addition of STa to reaction mixtures, intracellular cyclic guanosine monophosphate concentration increased 13.9-fold in enterocytes from 7-day-old pigs and 8.7-fold in enterocytes from 7-week-old pigs. The particulate guanylate cyclase activity associated with BBM from 7-week-old pigs was slightly more sensitive to low amounts of STa, compared with BBM from 7-day-old pigs; however, differences were not observed at intermediate and high amounts. These data indicate that lack of a secretory response to STa by older pigs is not attributable either to decreased numbers of STa receptors or to decreased signal response between the STa receptor and membrane-bound guanylate cyclase. Development of age-dependent resistance by porcine small intestine to STa appears to be attributable to steps in the secretory pathway that respond to increased concentration of cyclic guanosine monophosphate.

The relation between average duodenal mast cell count, duodenal mucosal mast cell numbers, duodenal connective tissue mast cell numbers, circulating basophil numbers, heterophil-to-lymphocyte ratio, and lesion score were studied to gain an understanding of the events that may lead to intestinal lesion formation associated with hemorrhagic enteritis virus (HEV) infection. Changes in vascular permeability in the duodenum in birds inoculated with HEV were examined, using colloidal carbon and ferritin as vascular markers. Turkeys inoculated with HEV had significantly (P < 0.05) higher duodenal mast cell counts than did noninfected controls. Birds inoculated with HEV had significantly (P < 0.05) more mucosal mast cells than did phosphate-buffered saline solution-inoculated birds. Connective tissue mast cell and basophil numbers were unaffected by viral inoculation. Thermal stress did not have significant effect on lesion severity, but did increase number of birds that developed the characteristic intestinal lesions. The heterophil-to-lymphocyte ratio was significantly (P < 0.05) higher in HEV-inoculated birds, compared with phosphate-buffered saline solution-inoculated controls. Increase in vascular permeability was only detected in HEV-inoculated birds with intestinal lesions. Results indicate that mast cells, and the vasoactive mediators contained within mast cells, may be important in the early manifestation of HEV infection. They also provide a possible mechanism through which biochemical and physiologic changes characteristic of HEV infection can occur.