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Biomedical subjects

P B Hamilton

Publications and source records attributed to P B Hamilton.

At least 91 records · Page 5Linked to original sources
PubMed1980

Intestinl fragility during ochratoxicosis and aflatoxicosis in broiler chickens.

Graded concentrations of dietary ochratoxin (0, 0.5, 1.0, 2.0, 4.0, and 8.0 microgram/g) and aflatoxin (0, 0.625, 1.25, 2.5, 5.0, and 10.0 microgram/g) were fed to broiler chicks from hatching to 3 weeks of age. The breaking strength of the large intestines was decreased significantly (P < 0.05) by ochratoxin (2, 4, and 8 microgram/g), but not by aflatoxin. This fragility was accompanied by an increase in the weight of the large intestine relative to body weight of birds fed ochratoxin (4.0 and 8.0 microgram/g), whereas aflatoxin had no significant (P < 0.05) effect on this parameter. Lipid content of the large intestine was decreased significantly (P < 0.05) by aflatoxin (10.0 microgram/g) and increased by ochratoxin (8.0 microgram/g). Microscopic examination of cross sections of large intestines stained for collagen gave the impression of a great decrease in collagen content of birds fed ochratoxin, but not aflatoxin. The radial length of the collagenous longitudinal folds of the large intestine was decreased significantly (P < 0.05) by ochratoxin (2.0, 4.0, and 8.0 microgram/g). These observations, plus a field case characterized by intestinal ruptures causing carcass condemnations on the processing line and by the occurrence of aflatoxin and ochratoxin in the chicken feed, suggest a novel way in which mycotoxins cause economic loss to agriculture.

Aflatoxins↗
PubMed1980

Evaluation of penicillic acid for toxicity in broiler chickens.

Penicillic acid is a mycotoxin produced by various fungi. It may occur in high concentrations in corn and can also be produced concomitantly with other mycotoxins in poultry feed. This mycotoxin was evaluated for its toxicity in broiler chickens by feeding graded concentrations (0, 100, 200, and 400 microgram/g of diet) to 4 groups of 10 birds per treatment. No significant (P greater than .05) effects were measured on growth rate, feed conversion, relative size of pancreas, spleen, liver, heart, bursa, or kidney or on hemoglobin, packed cell volume, liver lipid, plasma protein, or glucose. The only significant effects were a slight reduction in the size of the proventriculus and gizzard at dose levels of 200 and 400 microgram/g. Neither the salt nor lactone forms of penicillic acid had any detectable effect. The acute oral LD50 for the sodium salt form was 92 +/- 9 mg/kg. These data suggest that penicillic acid by itself has little toxicity (less than 1% of that of aflatoxin) in chickens.

Animals↗
PubMed1980

Inhibition of the glycogen phosphorylase system during ochratoxicosis in chickens.

Graded doses of ochratoxin A incorporated into the diet (0, 0.5, 1.0, 2.0, 4.0, and 8.0 micrograms/g) of broiler chickens significantly (P < 0.05) inhibited activity of protein kinase, the initiator enzyme of the glycogen phosphorylase system, in the livers at all dose levels. Only the highest dose, 8.0 micrograms/g, significantly reduced the total activity of phosphorylase kinase, which is activated by protein kinase. The total activity of phosphorylase, which is activated by phosphorylase kinase, was unaltered by ochratoxin A at any level. Additon of ochratoxin A to liver extracts control birds inhibited protein kinase but not phosphorylase kinase. When added to extracts of livers from control birds, cyclic adenosine 3',5'-monophosphate stimulated protein kinase but not phosphorylase kinase. The cyclic adenosine 3',5'-monophosphate had no effect when added to extracts from birds fed ochratoxin A. These results suggest that ochratoxin A affects primarily the cyclic adenosine 3',5'-monophosphate-dependent protein kinase which initiates the enzymatic cascade leading to glycogenolysis. Furthermore, these results conform an earlier assignment on morphological criteria of the glycogenosis of ochratoxicosis as a type X glycogen storage disease.

Animals↗
PubMed1980

Protocols for surveys, sampling, post-collection handling, and analysis of grain samples involved in mycotoxin problems.

This report examines and summarizes current knowledge regarding mycotoxin surveys, sampling techniques, conditions conducive to post-collection production of mycotoxins in grain samples, and analytical methods for mycotoxin analysis. Priority attention is given to samples of corn suspected of containing aflatoxin. The report includes recommendations where deems appropriate by the Ad Hoc Work Group.

Aflatoxins↗
PubMed1979

Decreased glycogen mobilization during ochratoxicosis in broiler chickens.

Graded doses of pure ochratoxin A (0, 0.5, 1.0, 2.0, 4.0, and 8.0 microgram of toxin per g of feed) were incorporated into a commercial diet which was fed to chickens from hatching to 3 weeks of age, at which time the experiments were terminated. Liver glycogen levels were elevated significantly (P less than 0.05) by 4.0 and 8.0 microgram/g but not lower doses. Glucagon stimulation of glycogen mobilization was inhibited at the same concentrations. Histopathological examination revealed cytoplasmic but not nuclear deposits of glycogen in cells at the periphery of liver lobes. These data demonstrated that ochratoxin inhibited glycogenolysis. Impaired ability to generate glucose from glycogen could account for the increased susceptibility to cold stress previously reported to occur in ochratoxicosis. Based on present and prior observations, it seems possible that ochratoxin induces a syndrome which mimics the glycogen storage disease of type X which is caused by a deficiency in the cyclic AMP-dependent enzyme of the glycogenolytic enzymatic cascade.

Animals↗
PubMed1979

Ochratoxin A-induced iron deficiency anemia.

Ochratoxin A at 8 micrograms per g of diet, but not at lower doses, fed to chickens from 1 day to 3 weeks of age resulted in significantly (P less than 0.05) decreased packed blood cell volume and hemoglobin concentration without altering the number of circulating erythrocytes. Serum iron and percentage of transferrin saturation were lowered at 4 and 8 micrograms/g. Therefore, anemia was characteristic of severe ochratoxicosis of young chickens, and the anemia was categorized as a hypochromic-microcytic anemia of the iron deficiency type. These data indicate that ochratoxin A by itself does not cause hemorrhagic anemia syndrome of chickens and that an anemia caused by a nutritional deficiency can be elicited by a mycotoxin.

Anemia, Hypochromic↗
PubMed1979

A leucocytopenia induced in chickens by dietary ochratoxin A.

Ochratoxin A was fed (0, .5, 1.0, 2.0, 4.0, and 8.0 microgram/g) to broiler chickens from day-old to three weeks of age when the birds were bled and total leucocyte and differential counts were performed. Ochratoxin A significantly (P less than .05) reduced leucocyte counts at every dose level of ochratoxin A administered. The leucocytopenia was characterized by an increase in the relative concentration of heterophils and decrease in the relative concentration of lymphocytes. From total leucocyte and differential leucocyte counts the number of circulating cells was calculated for each type of leucocyte. The total number of circulating lymphocytes of blood decreased significantly (P less than .05) at every dose level of ochratoxin A administered, and the number of monocytes decreased at 2.0 microgram/g and above. However, the number of circulating heterophils was not altered. These data demonstrated that ochratoxin A induced a severe leucocytopenia (lympocytopenia primarily and monocytopenia to a lesser extent) and implied that the functioning of the immune system might be altered.

Animals↗
PubMed1979

Refractory phagocytosis by chicken thrombocytes during aflatoxicosis.

The percentage phagocytosis of chicken thrombocytes was insensitive to dietary aflatoxin (10 microgram/g diet) while the mean phagocytosis was slightly but significantly (P less than .05) reduced by 5 or 10 microgram/g but not lower levels. Thrombocytic phagocytosis was dependent on a heat sensitive serum factor which is not affected during aflatoxicosis. These findings contrast with reports that other phagocytic types such as heterophils, macrophages, and monocytes are sensitive to low levels (e.g., .625 microgram/g) of dietary aflatoxin.

Animals↗
PubMed1979

Impairment of phagocytosis in chicken monocytes during aflatoxicosis.

Graded doses of dietary aflatoxin (0, .625, 1.25, 2.5, 5.0, and 10.0 microgram/g) were tested for their effect on the phagocytic and locomotive capacities of monocytes from chicken blood. The percentage and mean phagocytic activites were decreased significantly (P less than .05) at 2.5 microgram/g and above and at 1.25 microgram/g and above, respectively. Both the directed and undirected locomotion of monocytes were impaired significantly (P less than .05) at 2.5 microgram/g and above. A serum factor with the heat sensitivity of complement and which was required for optimal phagocytosis by monocytes also was reduced in activity during aflatoxicosis. Thus, the circulating element of the mononuclear phagocyte series has reduced capacity to perform its role in host defense during aflatoxicosis.

Animals↗
PubMed1977

Interrelationships of mycotoxins with nutrition.

Mycotoxins interact with lipid, protein, carbohydrate, and vitamin nutrition. Diets high in lipid have a mortality-sparing effect against aflatoxicosis and, if high in unsaturated fatty acids, a growth-sparing effect. Aflatoxicosis causes a lipid malabsorption syndrome coupled with decreased digestive enzymes and bile salt excretion, a decreased synthesis of fatty acids, and impaired transport. Deficiencies of vitamins A, D, or riboflavin make animals more sensitive to aflatoxin while a thiamin deficiency has the opposite effect. Interaction with vitamins E and K has not been clearly demonstrated as yet. Mycotoxins increase the protein requirements of animals and apparently alter the enzymes that regulate glycogen catabolism and neogenesis.

Animals↗
PubMed1976

Survey of aflatoxicosis in farm animals.

Over a 22-month period, 278 submissions of farm animals were made to the North Carolina Diagnostic Laboratory for suspected aflatoxicosis, and 94 cases were confirmed on the basis of finding aflatoxin in the feed and the occurrence of bile ductule proliferation. There was an annual variation in the incidence of aflatoxicosis, as well as a seasonal variation: the peak incidence occurred in the winter, and the minimum incidence occurred during the summer. The annual increase coincided with the corn harvest. All confirmed cases occurred on farms that raised and stored their own corn, and 88% were in swine. The cases were geographically localized in the eastern section of North Carolina (94% of the total cases) where 82% of the swine and 79% of the corn are produced. Mean concentration of aflatoxin in feed samples from the confirmed cases was 3,890 mug/kg, and the mean value for corn used in making the feed was 5,180 mug/kg. Only aflatoxin B1 was found in the samples. These data were interpreted to mean that the incidence and severity of aflatoxicosis is greater than previously suspected, that poor on-farm storage of corn is a primary contributing factor, that aflatoxin formation continues during and after the milling process, and that mycotoxicoses other than aflatoxicosis may cause equal or greater problems.

Aflatoxins↗