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Biomedical subjects

B C Zook

Publications and source records attributed to B C Zook.

At least 37 records · Page 2Linked to original sources

Experimental lead paint poisoning in nonhuman primates. II. Clinical pathologic findings and behavioral effects.

Oral administration of lead-containing paint to rhesus monkeys induced anemia, more profound in older primates. Erythrocytes were microcytic and hypochromic, but tended to become macrocytic terminally. Stippled erythrocytes were increased in all poisoned monkeys, especially in those with high blood lead levels and anemia. Proteinuria, glycosuria, casts and sloughed tubular cells containing acid-fast inclusion bodies were found on urinalysis. Terminal elevations of blood urea nitrogen were associated with profound anemia and renal tubular damage. Repeated blood lead values over 200 microgram/dl were associated with a moribund termination while monkeys which had levels under 100 microgram/dl remained apparently healthy. Behavioral studies in a small number of subclinically poisoned juveniles and neonates failed to reveal deficiencies of visual acuity or cognitive ability, nor was there evidence of alterations in levels of activity.

Anemia↗

Experimental lead paint poisoning in nonhuman primates. III. Pathologic findings.

Necropsies were performed on 25 rhesus monkeys, three cebus monkeys and three baboons which had been fed leaded paint or lead acetate at various doses up to 666 days. The 31 test primates and six controls ranged in age from five days to about eight years. In addition, the brains of 13 subadult squirrel monkeys fed lead oxide and two controls were studied grossly and microscopically. Lead content of liver, kidney and brain correlated with clinical outcome and typical histologic changes. Neuropathologic lesions, most severe in the young, occurred in 28 of 43 test primates despite a paucity of neurological signs. Brain lesions were similar to those occurring in human lead encephalopathy and included degenerative and proliferative changes of small vessels, ring hemorrhages, edema, perivascular hyalin droplets, rosette-like deposits of proteinaceous exudates, focal loss of myelin, astrogliosis and necrosis of hippocampal neurons.

Animals↗

Canine anatomy as assessed by computerized tomography.

Computerized tomographic studies of normal canine anatomy were obtained, using a whole body scanner. The regions of interest were head and neck, thorax, and abdomen and pelvis. Scans were compared with gross transverse sections from one euthanatized dog. Identification and labeling of anatomic structures were aided by reference to recognized texts of canine anatomy.

Animals↗

Pathological studies in experimental Candida endocarditis.

Mycotic endocarditis was produced in rabbits by indwelling intracardiac catheters filled with a suspension of Candida albicans. Grossly, cardiac lesions consisted of massive fungoid valvular vegetations and/or "sleeve thrombi" surrounding the catheter. Microscopically, platelet-fibrin aggregates were observed to be loosely attached to the valvular cusps. With time, the vegetations became organized and more firmly attached against the endocardium. Also observed was a heavy neutrophylic collar often containing Candida cells which infiltrate the subendothelial tissues of the valvular cusps. Sterile endocardial lesions were produced by retained catheters. The lesions consisted of discrete, glistening, hemispherical nodules in the right heart; and similar elevated plaques on the mural endocardium of the left ventricle. Microscopically, these lesions consisted of fibrous connective tissues devoid of inflammatory cells. The lesions in the left ventricle were more extensive, extending into the myocardium.

Animals↗

Tyzzer's disease in Syrian hamsters.

Tyzzer's disease was diagnosed in 18 Syrian hamsters. The clinical signs included sudden onset of diarrhea, dehydration, and lethargy; all affected hamsters died within 48 hours. Gross lesions consisted of multiple white nodules in the heart; dilated cecum and colon containing semiliquid feces, sometimes bearing necrotic plaques on the mucosa; and occasionally, a few small scattered white spots in the liver. Microscopic study of those lesions revealed areas of necrosis and mixed cellular inflammation. The causative agent, Bacillus piliformis, was demonstrated within myocardial fibers, hepatocytes, and colonic epithelial cells. Inoculation of chicken embryos and a clinically normal hamster with a homogenate of cecal wall prepared from affected hamsters resulted in reproduction of the agent and transmission of the disease.

Animals↗

Experimental lead paint poisoning in nonhuman primates. I. Clinical signs and course.

Lead-containing paints were administered orally to 27 rhesus monkeys for periods of 18-667 days. Lead acetate was fed to nine monkeys of three different species for 9-156 days. Excretion of one week's dose of lead in six primates ranged from 35 to 94%. The animals incurred moderate to extreme elevations of lead in blood, most lost weight, or had depressed weight gains, and developed Burtonian lines, some died suddenly and unexpectedly, and many terminated in a moribund state with profound anemia. Only one neonate had obvious signs of lead encephalopathy. The monkeys' ages, dose and source of lead, and possibly other factors, affected their response to lead.

Age Factors↗