To determine their capacity to host Brucella abortus, face flies were examined 1 to 120 hours after feeding on broth containing bacteria and bovine erythrocytes. Brucella abortus was cultured in large numbers from whole flies for 12 hours after feeding, but not after 72 hours. Histologic analysis showed that brucellae were rapidly taken into the midgut, sequestered from erythrocytes, transiently stored, and shed in the feces; there was no evidence of bacterial replication within epithelial cells. Immunoperoxidase and immunogold techniques revealed that most brucellae in the gut were confined to the lumen by the peritrophic membrane, that brucellae were degraded in secondary lysosomes of midgut epithelial cells, and that intact brucellae passed into connective tissues surrounding the midgut. Bacterial excretion without midgut replication is consistent with transient, but not long-term, insect transmission in nature.

The role of bile salt in biliary lipid excretion was studied in 3 healthy ponies with chronic external biliary fistulas. After endogenous bile salt pool depletion, micelle-forming taurocholate or taurochenodeoxycholate was infused to replace excreted bile salt. Enterohepatic circulations were held open (total biliary diversion) throughout each study. Results indicated that biliary lipid excretion in ponies (113 +/- 21 nmol/in/kg of body weight) is approximately 10 times less than that reported in rodents. Although the lipid composition (4.4% cholesterol, 5.6% phospholipid, and 90% bile salt) was within the predicted range for a single phase of micellar (or vesicular) liquid in solution, it was supersaturated with cholesterol because of low absolute concentrations of bile salt and phospholipid. Ponies, like guinea pigs, were determined to have a high bile salt-independent secretion of biliary lipid with little (or no) coupling to endogenous bile salt output. However, bile salt excretion induced by higher taurocholate infusion rates (ie, those greater than the physiologic range of 61 to 125 nmol/min/kg) was positively correlated with an increase in biliary phospholipid excretion, but not cholesterol excretion, thus indicating that a threshold intracellular bile salt concentration may be associated with enchanced biliary phospholipid excretion in ponies. The apparent cholerectic effects of endogenous bile salts, taurocholate, and taurochenodenoxycholate (that is, the increment in bile flow per increment in bile salt recovered) were greater in ponies than reported for any other mammal.

The 51Cr-labeled EDTA was validated as a suitable permeability probe in dogs for measurement of passive, unmediated diffusion across intestinal mucosa via intercellular pathways. The 51Cr-labeled EDTA was stable in aqueous solution and did not bind to biologic tissue and fluids. After incubation of 51Cr-labeled EDTA in isolated jejunal loops, analytic subcellular fractionation of jejunal mucosa on reorientating sucrose-density gradients was performed, and no association of 51Cr-labeled EDTA with particulate intracellular organelles was detected. Intravenously administered 51Cr-labeled EDTA was rapidly and completely excreted in urine. Intestinal permeability to 51Cr-labeled EDTA after oral administration was assessed in healthy dogs. The percentage of the administered dose of 51Cr-labeled EDTA excreted in the urine in 24 hours ranged from 2.3 to 17.6% (median, 13%).

Twelve male cats were fed 2 diets that differed in the source of P. In diet 1 (1.4% P), 62.7% of P originated from poultry, meat, and fish meal, and the remainder from other organic ingredients of food. In diet 2 (1.6% P), 63.5% of P was derived from neutral monobasic/dibasic salts, and the remainder from other organic ingredients of the food. The P intake was nearly the same with both diets, but there was a significant (P less than 0.05) difference between diets in the percentage of ingested P that was excreted in the urine (14.7 +/- 5.3% for diet 1; 34.9 +/- 8.4% for diet 2), and in 6-day urinary P excretion (774 +/- 290 mg for diet 1; 2,004 +/- 556 mg for diet 2). The P concentrations in urine samples obtained by cystocentesis after cats ate were significantly (P less than 0.05) higher when cats were fed diet 2 than when those same cats were fed diet 1. Plasma P concentrations increased after ingestion of diet 2, but were unchanged after ingestion of diet 1. Seemingly, urinary excretion of P was markedly influenced by dietary composition. Diets with the same P content have potential for different biologic effects because of differences in availability of P.

The virulence of 2 porcine group-A rotavirus isolates was compared. Forty hysterotomy-derived 3-day-old gnotobiotic pigs were inoculated orally with 2 ml of intestinal homogenate containing either the Ohio State University (OSU) or the South Dakota State University (SDSU) strain of porcine rotavirus or were inoculated with medium only. Clinical signs of disease, body weight, distribution of viral antigen, fecal excretion of virus, and histologic lesions (observed by light and scanning electron microscopy) were determined. Morphometric measurements of villi and crypts were made. In pigs inoculated with OSU or SDSU strains, diarrhea began at postinoculation hours (PIH) 19 to 48 and PIH 24 to 54, respectively. None of the virus-infected pigs died as a consequence of infection and all had similar clinical signs of disease, body weight changes and virus-shedding patterns, regardless of the strain of rotavirus with which they were infected. Microscopic findings in the small intestine of virus-infected pigs were similar, except that the SDSU strain caused more severe villus atrophy and villus fusion in the duodenum at PIH 72 and 168 than was associated with the OSU strain. Viral antigen in the small intestine of pigs infected with either virus was observed by use of immunofluorescence at PIH 24 and 72, but was seldom seen at PIH 168.