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D Kinden

Publications and source records attributed to D Kinden.

3 recordsLinked to original sources
PubMed1994

Pathogenicity of a bovine attaching effacing Escherichia coli isolate lacking Shiga-like toxins.

Escherichia coli isolate 7996-90, obtained from a calf with diarrhea, had negative results of tests for K-88, K-99, 987P, F41, CS31A, F1845, F165 or E. coli adherence factor adhesins and had negative results of tests for the toxins heat-labile, heat-stable A, heat-stable B, Shiga-like toxin (SLT)-I or SLT-II. Strain 7996-90 had localized adherence to HEp-2 cells, caused actin rearrangement in host cells to which it adhered, hybridized with the eaeA probe, and produced the 94-kd outer membrane protein associated with attaching effacing lesions. This isolate caused attaching effacing lesions in Caco-2 cell polar monolayers, rabbit intestinal loops, and the intestines of gnotobiotic pigs. The isolate belongs to serotype O26: NM and is considered a class-II attaching effacing enteropathogenic E coli. Until recent addition of more sensitive assays at veterinary diagnostic laboratories, isolates such as 7996-90 were not readily recognized as pathogens because they failed to fit into the enterohemorrhagic E coli group, members of which, be definition, produce SLT. The assays described can facilitate diagnosis of attaching effacing E coli infection when histologic evaluation is hampered by autolysis.

Animals↗
PubMedDate not supplied

Atherosclerosis in rabbits fed a low cholesterol diet for five years.

Rabbits were fed a low cholesterol atherogenic diet for up to 5 years. Arterial lesions during the first 12 months consisted of smooth muscle cell and lipid accumulation in the intima, with smaller amounts of elastin and collagen. By 24 months, considerable degeneration and necrosis of smooth muscle foam cells had occurred, lipid had decreased in relative proportion, and collagen was predominant. These trends continued during the final 3 years. By 48 months most plaques were calcified and a few had hemorrhage. Atherosclerosis was extensive in rabbits with serum cholesterol concentrations greater than 300 mg/100 ml and minimal in rabbits with concentrations consistently less than 150 mg/100 ml. Thicker lesions tended to have more atheromas while thinner ones were more fibrous and less fatty. Significant regression of fatty streaks occurred in a group of rabbits fed the atherogenic diet for 2 years and a stock diet during the third year but more advanced lesions did not regress. This study illustrates the importance of time as a variable in atherogenesis, and demonstrates that modest hypercholesterolemia can lead to atherosclerosis in rabbits that is qualitatively unlike atherosclerosis induced in rabbits by cholesterol rich diets and that resembles several stages of human atherosclerosis.

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