Morphologic characteristics of oviducts from hens producing eggs of different Haugh units caused by genetics and by feeding vanadium as determined with computer software-integrated digitizing technology.

Magnum and isthmus morphologic characteristics (surface epithelium height, fold height and diameter, and periodic acid-Schiff-positive area and surface epithelium cells) of stained 6-micron tissue sections were measured by light microscopy, with data acquisition using a digitizing tablet interfaced to a microscope and to a personal computer with morphometric-dimensional software. Tissues were obtained from Leghorn layers in two separate experiments in which production of eggs with low and high Haugh unit (HU) values was induced by either genetic selection or by feeding V. Eggs produced by these hens had HU differences between the high and low groups of 11 to 14 units (both experiments, P = .0001) and had a greater volume of thick albumen fraction in high-HU groups (both experiments, P = .0001). The computer software-integrated digitizing system enabled rapid measurements of multiple characteristics. In the genetic lines, higher magnum fold height and magnum and isthmus surface epithelium height were detected at moderate significance (all at P < .05) in the tissues of the layers producing high-HU eggs than in tissues from the low-HU line. Other morphologic variables were not different between genetic lines. In response to feeding V, none of the morphological characteristics were affected, although magnum fold height approached difference at P < .07. Based on the observations in these two experiments, magnum fold height may be a further important factor related to egg albumen condition, in addition to surface epithelium height. It appears, however, that layers producing eggs of considerably different HU values, due in these experiments to genetics or V feeding, can have magnum or isthmus morphological characteristics that are indistinguishable, or only moderately different, as detected by integrated digitizing technology.

Evidence of multiple metabolic routes in vanadium's effects on layers. Ascorbic acid differential effects on prepeak egg production parameters following prolonged vanadium feeding.

The development of V toxicity was followed over a 28-d period in 25-wk-old Leghorn layers fed 20 mg ammonium metavanadate/kg diet (Days 1 to 14) followed by 30 mg/kg diet (Days 15 to 28). Then, over a second 28-d period, the responses to V and supplemental ascorbic acid (AA) fed at 500 or 1,000 mg/kg diet (Days 29 to 42) followed by 1,500 or 3,000 mg/kg diet (Days 43 to 56) were examined. Feed consumption, egg weight, Haugh units (HU), and BW measurements indicated that the response to V was multifactorial, but of differing intensities and time-frames for the variables. Haugh units were lowered rapidly (3 d, P < .05) in response to V feeding, but HU values decreased only slightly when dietary V was increased to 30 mg/kg. In contrast, egg production was decreased moderately by 20 mg V/kg and a considerable further reduction in egg production resulted from increasing the V to 30 mg/kg. Ascorbic acid supplementation differentially affected these responses: BW, egg production, and egg weight were improved significantly in the V-fed group receiving an AA supplement, as compared with those fed V only. Haugh unit values, however, were not improved by AA supplementation in groups receiving V. Foam functional properties, which also were changed by V feeding, were not corrected by AA feeding. The results suggest that the toxic effects of V are mediated through more than one physiological mechanism. One mechanism, which includes negative effects on BW, egg production, and egg weight, is responsive to the additional reducing equivalents provided by supplemental AA. Another mechanism, which is apparent from the effect of V on egg HU values, is not ameliorated by AA supplementation after toxicity developed.

Coordinate suppression of liver acetyl-CoA carboxylase and fatty acid synthetase by polyunsaturated fat.

Polyunsaturated fats (PUFA) suppressed hepatic fatty acid synthesis and the activities of lipogenic enzymes more effectively than did saturated fats. The activity of glycolytic enzymes--glucokinase, phosphofructokinase and pyruvate kinase--were not affected by PUFA. The absolute rate of liver fatty acid synthesis after meal ingestion was very similar to the maximal activities of acetyl-CoA carboxylase and fatty acid synthetase. When PUFA was supplemented to a fat-free diet, the activities of carboxylase and synthetase decreased similarly over 3 days. During the 3 days, the concentration of liver malonyl-CoA (after meal ingestion) did not significantly differ between the fat-free and PUFA dietary treatments. Apparently PUFA feeding caused a coordinate decrease in the utilization and production of malonyl-CoA which resulted in no net change in malonyl-CoA pool size. Thus the mechanism by which PUFA suppresses fatty acid synthesis appears to be by coordinately and specifically reducing the amount of carboxylase and fatty acid synthetase.

Induced paragonimiasis in cats: clinical signs and diagnosis.

Twenty-eight specific-pathogen-free cats were inoculated with 14 to 50 metacercariae of Paragonimus kellicotti obtained from the hearts of naturally infected crayfish. Young flukes excysted in the intestine of cats and appeared in the peritoneal cavity from 1 to 14 days after inoculation (DAI) and in the pleural cavity from 5 to 23 DAI. Flukes penetrated the pulmonary parenchyma and formed hemorrhagic subpleural lesions within 5 weeks after inoculation. Marked eosinophilia developed between 2 and 12 weeks after inoculation. Fluke-containing pulmonary lesions were detected by radiography 3 to 4 weeks after inoculation. Lesions developed most frequently in the right caudal lung lobe. Clinical signs were mild and did not appear until 4 weeks after inoculation. Thereafter, cats appeared dull and coughed intermittently. One cat became dyspneic due to pneumothorax. Paragonimus eggs were first detected at the 34th DAI, using a fecal sedimentation technique.

Albendazole therapy for experimentally induced Paragonimus kellicotti infection in cats.

The effect of albendazole therapy was studied in 6 cats with pulmonary paragonimiasis induced by experimental inoculation of metacercariae (25/cat) of Paragonimus kellicotti. At 76 to 101 days after they were inoculated, 5 cats were administered an oral aqueous suspension of albendazole in 2 divided doses totaling 20 mg (2 cats), 50 mg (1 cat), or 100 mg (2 cats)/kg of body weight each day for 14 to 21 days. The 6th cat (control) was not administered albendazole. Nine days after cats were given the 50- and 100-mg/kg dosages, Paragonimus ova were not seen in the feces of 3 cats. There was marked reduction in ova production in the feces of the 2 cats administered 20 mg/kg of albendazole. Live flukes were not recovered from the lungs of 3 cats necropsied 4 or 5 weeks after dosing with 50 or 100 mg/kg, but the lungs of the 2 cats administered 20 mg of albendazole/kg yielded 9 and 7 apparently viable flukes. Seventeen live flukes were recovered from the control cat not treated with albendazole. In 4 noninoculated normal cats administered 20 mg (1 cat), 100 mg (1 cat), and 200 mg (2 cats) of albendazole/kg of body weight each day for 14 days, there were no gross or microscopic lesions attributable to the drug.

Sarcocystis fayeri sp. n. from the horse.

Hearts, diaphragms, esophagi, and spinal cords from 266 horses were obtained at slaughter in Creston, Ohio. Tissues were examined microscopically for Sarcocystis in sections, digested in trypsin to obtain bradyzoites, and fed to 10 dogs and 10 cats. Intramuscular cysts were found in selections of two hearts from 57 horses and four esophagi from 107 horses. The cysts were up to 900 micron long and up to 70 micron wide. The cyst wall was 1 to 2 micron thick and cross-striated. The enclosed bradyzoites were banana-shaped, 15 to 20 by 20 to 3 micron, and contained several PAS-positive granules. Bradyzoites were found in trypsin digests of seven of 57 (13%) equine tissues (heart, diaphragm, esophagus but not spinal cord) in one experiment and 10 of 47 (21%) esophagi, eight of 47 (17%) diaphragms but none of 47 hearts and spinal cords in another experiment. All of 10 dogs shed sporulated sporocysts or oocysts in feces 12 to 15 days (12 in one, 13 in eight, and 15 days in one) after digesting tissues from 169 horses. The sporocysts were 11 to 13 (12.0 +/- 0.5) by 7 to 8.5 (7.9 +/- 0.5) micron. In histologic sections of canine small intestine the sporocysts were located in the lamina propria near the tips of the villi. The 10 cats fed tissues from 266 horses did not shed Sarcocystis. A new name, S. fayeri, is proposed for this organism. Sarcocystis fayeri sporocysts (12 by 8 micron) are shorter than those of S. betrami (15 by 10 micron), the other species of Sarcocystis from the horse. The prepatent period is 12 to 15 days for S. fayeri and 8 days for S. bertrami (synonym S. equicanis Rommel and Geisel 1975).