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Biomedical subjects

J E Bellamy

Publications and source records attributed to J E Bellamy.

32 records · Page 2Linked to original sources

Thymic dependence of immunity to Eimeria falciformis var. pragensis in mice.

Athymic (nude) mice, their normal littermates, and Swiss white mice were infected with 750 oocysts of Eimeria falciformis var. pragensis and reinfected twice with 20,000 oocysts, 20 and 40 days after the primary infection. The prepatent and patent periods of the primary infection were similar in each group of mice; however, the athymic mice discharged more oocysts. The normal littermates and Swiss white mice developed immunity to the parasite after the first or second infection, whereas the athymic mice never developed immunity. Infection with E. falciformis var. pragensis induced the production of antibodies in the normal littermates and Swiss white mice, whereas antibody production was impaired in athymic mice. Passive administration of immune serum did not protect athymic mice from reinfection by the parasite. Immunity to the parasite was thymus dependent, and "effector" T-lymphocytes seemed to be required for protection.

Animals↗

Enterotoxigenic colibacillosis in colostrum-fed calves: pathologic changes.

Enterotoxigenic colibacillosis was experimentally produced in 8 of 9 colostrum-fed calves orally given 10(11) Escherichia coli. The eight calves developed profuse diarrhea accompanied by dehydration and depression. At 12 hours after exposure, all calves were euthanatized for necropsy and for collection of tissues for microscopic examination. Histopathologic changes included stunted villi in the jejunum and ileum, focal degeneration and exfoliation of absorptive epithelial cells at the tips of jejunal and ileal villi, and focal emigration of neutrophils which was especially prominent above the dome area of aggregated lymphatic follicles (Peyer's patches). A layer of E coli adhered to the epithelial surface of the jejunum and ileum. In the duodenum, lesions were minimal or absent and bacteria were not adhering to the mucosa. Histopathologic changes were not observed in other tissues. In two calves examined 24 hours after they were inoculated and in two calves euthanatized 24 to 36 hours after spontaneously developing enteric colibacillosis, lesions were similar to those observed in the calves at 12 hours after exposure.

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Cold-agglutinin hemolytic anemia and Haemobartonella canis infection in a dog.

Cold-agglutinin hemolytic anemia in a dog was manifested by weakness, progressive hemolytic anemia, hematuria, and hemoglobinuria. Corticosteroid therapy failed to alleviate the anemia. The condition became complicated by Haemobartonella canis infection berminally. Prominent postmortem findings included disseminated thrombosis and infarction, glomerulonephritis, and thickened alveolar membranes.

Agglutinins↗

Zinc, cadmium, and iron interactions during intestinal absorption in iron-deficient mice.

Zinc absorption from a test dose of (65Zn) zinc chloride was increased in mice with a high capacity to absorb iron induced by a low-iron diet. When radiolabelled zinc chloride in concentrations varying from 0.025 to 0.30 mM was perfused through open-ended duodenal loops of mice fed this diet, the proportion of zinc taken up from the lumen and transferred to the body was greater from lower than from higher doses. The addition of iron to the perfusate inhibited zinc uptake and transfer, and zinc had a similar effect on iron absorption. Cadmium, a potent inhibitor of iron uptake in mice fed a low-iron diet, impaired zinc uptake under these dietary conditions. These results suggest that in dietary-induced iron deficiency there are analogous mucosal binding sites for the uptake of iron and zinc. There also appear to be mutually exclusive binding sites for the absorption of these metals: radiolabelled iron absorption from an intragastric test dose was enhanced in mice with a high capacity to absorb iron produced by bleeding, whereas the absorption of zinc was not increased.

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The life cycle of Eimeria falciformis var. pragensis (Sporozoa: Coccidia) in the mouse, Mus musculus.

The life cycle of Eimeria falciformis var. pragensis, established from a single oocyst, is described in experimentally infected mice (Mus musculus). The coccidium had a prepatent period of 7 days and a patent period of 10--16 days. Oocysts were spherical to ellipsoidal in shape and measured 21.2 x 18.3 micron. Sporulation time was 3 to 3.5 days. Sporocysts measured 12.2 x 7.2 micron and contained a circular to avoid granular sporocyst residuum measuring 5.5 X 5.0 micron. One, 2 or 3 circular to rectangular polar granules were observed within each sporulated oocyst. The endogenous stages developed primarily in the cecum and colon and only occasionally in the lower ileum. Four generations of schizonts were found. Mature 1st-generation schizonts, first observed 48 hr postinfection (PI), measured 17.8 x 12.3 micron and had 12 merozoites that measured 13.3 x 2.0 micron. Mature 2nd-generation schizonts appeared 78 hr PI. They measured 10.2 x 9.3 micron and had 8 merozoites measuring 5.0 x 1.6 micron. Mature 3rd-generation schizonts appeared first at 114 hr PI and measured 17.5 x 10.2 micron and had 10 merozoites that measured 12.4 x 1.8 micron. Mature 4th-generation schizonts appeared first at 144 hr PI. They measured 18.2 x 15.3 micron and had 18 merozoites. The merozoites of the 4th-generation schizont were 4.5 x 1.2 micron. Mature macrogamonts and microgamonts developed simultaneously appearing at 156 hr PI. Macrogamonts measured 16 x 14.5 micron and microgamonts were 18.2 x 15.3 micron. In experimentally infected rats (Rattus norvegicus), development of E. falciformis var. pragensis progressed only as far as mature 1st-generation schizonts.

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The pathological changes caused by Eimeria falciformis var pragensis in mice.

Groups of Swiss white mice weighing 25-28 grams were infected orally with 500, 2,000, 5,000 or 20,000 oocysts of Eimeria falciformis var pragensis. Depression, anorexia, weight loss, diarrhea or dysentery, and dehydration were most pronounced at eight to ten days postinfection. The highest mortality, 31%, occurred in mice infected with 20,000 oocysts. None of the mice infected with 500 oocysts died. The pathological findings were equally severe in mice infected with 5,000 and 20,000 oocysts. The enteric lesions, most pronounced at eight to ten days postinfection, were restricted mainly to the large intestine and consisted initially of both cryptal and absorptive epithelial cell destruction and submucosal edema. These changes were followed in 12 to 24 hours by a transient influx of neutrophils into the lamina propria followed by mononuclear cell infiltration which lasted for five to ten days. As the infective dose decreased, the inflammatory response occurred later and was less extensive. When seen, hemorrhage occurred seven to 11 days postinfection. In 50% of the mice infected with 5,000 and 20,000 oocysts, varying degrees of a nonselective mucosal necrosis were seen at eight to 12 days postinfection. In mice infected with 500 oocysts, mucosal destruction was restricted to the epithelium. Neutrophils predominated when necrosis was extensive, otherwise, mononuclear cells were the main inflammatory cells. Two to three days following necrosis, crypt hyperplasia was marked and mucosal integrity was restored. Ulcers, some of which extended into the submucosa, healed by days 14 to 20. Localized granulomatous colitis, induced by trapped oocysts within the lamina propria, was seen until the experiment was terminated at 25 days postinfection. Infection was followed by lymphoid hyperplasia in the lymph nodes and the spleen.

Animals↗

Effects of immune-mediated enteroluminal neltrophil emigration on intestinal function in pigs.

Intestinal function was assessed in cannulated loops of porcine proximal jejunum during immune-mediated emigration of neutrophils into the intestine. Net water, net sodium, net chloride, undirectional sodium and unidirectional chloride fluxes were measured before and after intestinal exposure to an antigen in both sensitized and nonsensitized pigs. Neutrophil emigration was assessed histologically. The results indicate that fluid and electrolyte movements in the intestine are not significantly altered during immune-mediated enteroluminal neutrophil emigration suggesting that the neutrophil response does not interfere with intestinal function.

Animals↗

Myopathy and myoglobinuria in a wild white-tailed deer.

Fatal myopathy similar to "capture myopathy" described for African game was diagnosed in a wild white-tailed deer. Clinical signs included depression, inability to rise or stand, and myoglobinuria. Values for serum creatine phosphokinase, glutamic oxaloacetic transaminase, and blood urea nitrogen were high. The deer died 42 hours after capture. At necropsy the muscles of the limbs had a waxy, "cooked" appearance and the kidneys were brown. Microscopic findings included severe degeneration and fragmentation of skeletal muscle fibers, nephrosis, centrilobular hepatic necrosis, myocardial degeneration, and anoxic neuronal degeneration.

Animals↗

Suppression of growth of Vibrio cholerae in the intestine of immunized mice.

In ligated intestinal loops of actively immunized adult mice, growth of V. cholerae 569B was suppressed approximately seven fold when compared to bacterial growth in non-immune animals. Similarly, growth of V. cholerae 569B was reduced in mice immunized with a hybrid vibrio strain, NCV569B-165, which shares only flagella antigens with V. cholerae 569B. Immunofluorescence studies of intestinal loop contents and intestinal sections indicated that, in non-immune mice, vibrios coated the intestinal mucosa. In contrast, the intestinal mucosa of immune animals was almost free of bacteria. The vibrios were found agglutinated in the intestinal lumen contents of immune animals. It was concluded that immunization suppressed the growth of V. cholerae in the intestinal lumen and the possibility that bacterial agglutination mediates this growth suppression is discussed.

Animals↗

Antibody cross-linking as a factor in immunity to cholera in infant mice.

Several antibody preparations were tested for their ability to reduce adsorption of Vibrio cholerae to isolated intestinal epithelial cells, and this ability was related to agglutination and protective activity in infant mice. The results demonstrate that (1) the reduction in adsorption of V. cholerae to epithelial cells correlates with the degree of agglutination for given antibody preparation; (2) intact tantibodies protect infant mice from cholera only at concentrations that agglutinate the bacteria; and (3) purified antibodies to flagellar antigens protect infant mice from cholera. These results indicate that cross-linking of bacteria by antibody causes a reduction in the number of organisms adsorbed to the intestinal wall. Thus antibody cross-linking plays an important role in immunity to cholera in infant mice.

Adsorption↗

Immune-mediated emigration of neutrophils into the lumen of the small intestine.

By using pigs sensitized to bovine serum albumin (BSA), it was found that exposure of the intestinal mucosa to BSA induced, in 4 h, the emigration of large numbers of neutrophils into the intestinal lumen. This response was specific for the immunizing antigen and could be transferred to nonimmune animals with immune serum. The emigration of neutrophils through the intestinal mucosa was not accompanied by the edema, hemorrhage, and thrombosis which were apparent after intracutaneous inoculation of BSA into the same animals. Twenty-four hours after a 4-h mucosal exposure to BSA, the intestinal mucosa showed no evidence of neutrophil emigration nor any other abnormal features. These observations suggested that emigration of neutrophils into the intestinal lumen can be a specific, antibody-mediated immune response which occurs in the absence of intestinal injury. Possible relationships between immune-mediated enteroluminal emigration of neutrophils, neutrophil production, and a protective role for the neutrophil in the intestinal lumen were considered.

Animals↗

A comparison between the active cutaneous Arthus reaction and immune-mediated enteroluminal neutrophil emigration in pigs.

The induction of neutrophil emigration into the intestinal lumen in bovine serum albumin immune and nonimmune pigs by mucosal exposure to bovine serum albumin was studied using a ligated intestinal loop technique. In order to compare the response in the skin to that in the intestine, test materials were inoculated intracutaneously as well as enterally. Several histochemical procedures were applied to the intestinal mucosa and skin for evaluation of responses. In immune animals, mucosal exposure to bovine serum albumin evoked the emigration of neutrophils into the intestinal mucosa and lumen. The neutrophil emigration tended to occur focally. Denudation of a few epithelial cells occurred at emigration sites. Hemorrhage, thrombosis, and edema, quite obvious after intracutaneous inoculation were not apparent after enteroluminal inoculation of bovine serum albumin into immune animals. Enteroluminal inoculation of bovine serum albumin or bovine serum albumin plus anti-bovine serum albumin into nonimmune animals did not elicit neutrophil emigration or any other pathological lesion in the intestine, whereas intracutaneous inoculation of bovine serum albumin plus anti-bovine serum albumin into the same animals elicited an Arthus reaction.

Animals↗

The vascular architecture of the porcine small intestine.

The vascular anatomy of the porcine small intestine was studied by injection of intestinal vessels with India Ink. Examination of transverse and longitudinal serial sections of the injected intestine facilitated a three-dimensional interpretation of the vascular pattern. An artery from the mesentery penetrated the tunica muscularis, supplied muscular branches and passed on to the submucosa where it formed an arterial rete. From the submucosal arteries, arterioles arose and followed a direct axial course to the tips of villi where they ramified into a subepithelial capillary plexus. Some of the capillaries, at the midpoint of the villus, fused into paraxial venules, which emptied into a "transverse venule" at the base of the villus. Other villus capillaries were continuous with those of the crypts. The pericryptal capillary plexus received a few arterial branches from the submucosal arteries. The transverse venule and the pericryptal capillary plexus emptied into large, segmentally dilated veins in the submucosa. The submucosal veins formed an extensive anastomosing network drained by large venous trunks which passed through the muscle layers to the mesentery. The observations suggest possible relationships between the vascular pattern and intestinal fluid movement.

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