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Biomedical subjects

P B Hamilton

Publications and source records attributed to P B Hamilton.

At least 73 records · Page 4Linked to original sources
PubMed1982

In vitro antifungal activity of gentian violet.

Gentian violet, a compound that gained wide acceptance in the poultry industry as a mold inhibitor in feed, was tested for its activity against eight aflatoxigenic strains of Aspergillus flavus and A. Parasiticus. In a simple nutrient medium, it completely inhibited growth of all strains at 8 micrograms/ml. When chicken feed was added to the medium, the inhibition by the same concentration ranged from 12 to 44% depending on the strain. Observations suggested that both the feed and the fungi were involved in the resistance conferred by chicken feed. Growth and aflatoxin production on moist rice was inhibited in one strain but not in a second strain. Inoculating autoclaved chicken feed of varying moisture contents with pure cultures revealed that the activity of gentian violet was better at high moisture contents than at low moisture contents approximating those found in poultry feed. It was not possible to assess the activity of gentian violet in unaltered chicken feed. Attempts failed because the formation of reproducible levels of aflatoxin could not be attained.

Animal Feed↗
PubMed1982

Experimental aflatoxicosis in young Japanese quail.

Japanese quail from the university colony fed graded levels of dietary aflatoxin (0, 1.25, 2.5, 5.0, 10.0, and 20.0 micrograms/g) from hatching to 4 weeks of age were comparatively resistant to aflatoxin as growth inhibition occurred at a dose of 5.0 micrograms/g or more as about 50% mortality occurred at a dose of 20 micrograms/g. The acute oral LD50 was 19.5 +/- 4.8 mg/kg. These values are up to ten times those reported in the literature for other quail. The most sensitive indicators of aflatoxicosis were depressed serum proteins and serum carotenoids and enlarged liver and pancreas, all of which occurred at 1.25 micrograms/g, the smallest dose administered. Unlike chickens, the serum lipids, liver lipids, hemoglobin, serum uric acid, and spleen size of quail were not affected significantly (P less than .05). The sizes of the proventriculus and gizzard were increased by doses of 5.0 micrograms/g or higher, whereas the bursa of Fabricius was regressed by the same dose.

Administration, Oral↗
PubMed1982

Increased severity and new symptoms of infectious bursal disease during aflatoxicosis in broiler chickens.

A factorial design for the presence and absence of infection with a mild strain of infectious bursal disease (IBD) virus and graded levels of dietary aflatoxin (0, .625, 1.25, 2.5, 5.0, and 10.0 microgram/g of diet) in young broiler chickens revealed several interactions which greatly changed and character of the IBD infection. An infection that was essentially free of mortality became lethal to about half the birds. A coagulopathy as indicated by prolonged prothrombin times and by the occurrence of slight hemorrhages in skeletal muscles, a hypoproteinemia, a hypocalcemia, and a markedly enlarged kidney were observed in combined aflatoxicosis and IBD, but not in IBD alone. The size of the bursa of Fabricius following an initial hypertrophy was atrophied 4 days after inoculation and the spleen was enlarged. The effects of aflatoxin and IBD on these two glands were additive. Packed blood cell volume and hemoglobin values were decreased by aflatoxin only. Thus, aflatoxin had the effects of making IBD a much more severe disease and of changing the symptoms.

Aflatoxins↗
PubMed1982

Comparison of ochratoxin, aflatoxin, and T-2 toxin for their effects on selected parameters related to digestion and evidence for specific metabolism of carotenoids in chickens.

Aflatoxicosis, ochratoxicosis, and T-2 toxicosis were produced by feeding diets containing graded concentration of the appropriate toxin to broiler chicks from hatching unit 3 weeks of age. Aflatoxin, even at levels not growth inhibitory, produced a malabsorption syndrome characterized by steatorrhea, hypocarotenoidemia, and decreased concentrations of bile salts and pancreatic lipase, trypsin, amylase, and RNase. The T-2 toxin at concentrations higher than required to inhibit growth produced a mild malabsorption syndrome characterized by steatorrhea and decreased levels of pancreatic lipase, trypsin, amylase, and RNase. The only suggestion of malabsorption during ochratoxicosis was a severe hypocarotenoidemia. The following observations indicated a lack of correlation between lipid malabsorption and hypocarotenoidemia. The T-2 toxicosis exhibited lipid malabsorption in the absence of hypocarotenoidemia, ochratoxicosis exhibited hypocarotenoidemia in the absence of lipid malabsorption, and aflatoxicosis exhibited both symptoms. These findings imply that carotenoids are physiologically active compounds with specific metabolic processes and are not inert substances swept along with lipids as is commonly assumed from the ability to grow apparently healthy birds free of carotenoids. The current findings also indicate that great specificities exist in mycotoxicoses despite superficial similarities.

Aflatoxins↗
PubMed1982

Natural occurrences of ochratoxicosis in poultry.

Five independent episodes of ochratoxicosis in about 970,000 turkeys, two episodes in about 70,000 laying hens, and two episodes in about 12,000,000 broiler chickens were investigated. Ochratoxin A concentrations in suspect feed and ingredients ranged from less than .2 to 16 ppm. Feed samples tested for T-2 toxin, F-2 toxin, heavy metals, and polychlorinated biphenyls were negative. Minor amounts of aflatoxin (less than 60 ppb) were found in suspect feed from two episodes. The main symptoms in turkeys were mortality (up to 59%), nephrotoxicity (pale, swollen kidneys that became tan colored in the sequel to acute toxicity), decreased feed consumption (as little as 20% of the normal feed intake) prior to death, and secondary air sacculitis. Histopathology revealed edema and necrosis of the proximal tubules of the kidneys and no changes in the liver or other organs. Suspect feed containing 2 ppm ochratoxin A increased uric acid levels in serum when fed to poults in the laboratory. The episodes in laying hens were characterized by reduced egg production, poor egg shell quality, and nephropathy. The episodes in broiler chickens were characterized by poor growth rate, poor feed conversion efficiency, poor pigmentation, nephropathy, and increased incidence of air sacculitis. Obtaining feed and ingredients free of ochratoxin, cleaning the feed and ingredient handling equipment, and adding antifungal agents to the feed proved beneficial. Eight of the 9 episodes were traced to the corn supply and the ninth episode was traced to corn gluten meal that became contaminated during storage after manufacture. Evidence was obtained that the ochratoxin was unstable and declined in concentration during storage. Aqueous acetone was a better solvent for extracting ochratoxin than was the recommended phosphoric acid: chloroform. The ochratoxin extracted from high potency samples consisted of ochratoxins A, B, and C in ratios of about 90:8:2.

Animals↗
PubMed1981

Experimental ochratoxicosis in turkey poults.

Graded concentrations of ochratoxin A (0, 1, 2, 4, and 8 micrograms/g of feed) incorporated into the diet of turkey poults from hatching until 3 weeks of age resulted in a decreased growth rate, enlarged proventriculus and gizzard, and a regressed thymus (all at 4 and 8 micrograms/g) and the sizes of liver, spleen, pancreas, kidneys, bursa of Fabricius were unaffected. Feed conversion ratio increased from 1.63 (control value) to 2.07 (8 micrograms/g). Mortality was increased significantly (P less than .05) at 8 micrograms/g. Water consumption and plasma uric acid were increased at 4 and 8 micrograms/g. Plasma glucose and the dry weight of the kidneys decreased significantly at 8 micrograms/g while total plasma proteins, prothrombin time, plasma carotenoids, and phenol red clearance rate were unaltered. A leucocytopenia, which was primarily a lymphocytopenia, was observed at 4 and 8 micrograms/g. Heterophils decreased while basophils increased at 8 micrograms/g. The oral LD50 for day-old and 3-week-old poults was 4.63 +/- .31 and 7.84 +/- .94 mg/kg, respectively. Intraperitoneally, the value for day-old birds was .16 +/- .03 +/- mg/kg and for 3-week-old birds was .34 +/- .09 mg/kg. These data suggest that ochratoxin is a potent nephrotoxin in turkeys, but that ochratoxicosis in turkeys differs markedly from the disease in other species.

Animal Feed↗
PubMed1981

Glycogen storage disease type X caused by ochratoxin A in broiler chickens.

Day-old broiler chickens fed graded concentrations of ochratoxin A (0, .5, 1.0, 2.0, 4.0, and 8.0 micrograms/g of diet) for 3 weeks were examined histopathologically for glycogen accumulation in muscle tissue using both formalin and ethanol fixatives with periodic acid-Schiff stain in a duplicate diastatic slide technique. However, glycogen could not be visualized in chicken muscle by these techniques which work with human muscle. Quantitative analysis for the glycogen itself permitted demonstration of a significant (P less than .05) fourfold increase in birds fed 8 micrograms/g. Using startled birds demonstrated that this accumulated glycogen was about 99% physiologically available. These findings coupled with prior reports permit the assignment on morphologic criteria of the hyperglycogenation of ochratoxicosis as a type X glycogen storage disease.

Animals↗
PubMed1981

New evidence for intrinsic blood coagulation in chickens.

Coagulation of blood in chickens is considered the result of an extrinsic clotting system initiated, as in mammals, by tissue thromboplastin released from injured tissues. Blood coagulation in mammals depends principally on an intrinsic mechanism in which thromboplastin is generated from blood itself. Only a negligible role, if any, has been ascribed to an intrinsic system in chickens. A reevaluation of intrinsic coagulation in chickens was undertaken in this study. Whole blood of chickens was found to clot over 30% faster when contacted by suitable surface activators such as kaolin or glass than when such contact was omitted. Plasma recalcification times were significantly (P less than .02) shortened by contact activators. Clotting functions were measurable both by partial thromboplastin time and activated partial thromboplastin time, tests that bypass extrinsic factors. Intrinsic thromboplastin could be generated from dilute whole chicken blood although at a slower rate than that reported for human blood. Modification of whole blood thromboplastin generation techniques permitted measurement of activities that seem analogous to human intrinsic factors VIII and IX but not XI or XII. These data provide evidence of a functioning intrinsic clotting mechanism in chickens. A complete description and role for this mechanism remains to be defined.

Animals↗
PubMed1981

Steatorrhea during aflatoxicosis in chickens.

Graded levels of dietary aflatoxin (0, .625, 1.25, 2.5, 5 and 10 microgram/g) were tested for their effect on lipid excretion in feces of young broiler chickens. There was a highly significant (P less than .01) increase at 1.25 microgram/g and above including a threefold increase at 10 microgram/g, while growth rate was decreased only at levels of 2.5 microgram/g and above. Pancreatic lipase, the primary fat digestive enzyme, was decreased significantly (P less than .05) at all levels of aflatoxin and at 10 microgram/g was only 40% of the control value, Bile, which is required for lipid digestion and absorption, was decreased highly significantly (P less than .01) in concentration by all growth inhibition levels of aflatoxin. A slight but significant ( P less than .05) increase in bladder size at growth inhibitory levels of aflatoxin appeared adequate to compensate for decreased bile concentration. A pair feeding technique showed the effect of aflatoxin on fecal lipids and pancreatic lipase occurred in diets low (2%) or high (17%) in fat. The steatorrhea caused by aflatoxin apparently reflects a lipid malabsorption syndrome caused by an impaired ability to digest lipids.

Aflatoxins↗
PubMed1981

Aflatoxicosis and Intrinsic Coagulation function in broiler chickens.

Aflatoxin was fed (0, .625, 1.25, 2.5, 5.0, and 10.0 microgram/g) to broiler chickens from day-old to 3 weeks of age when the birds were bled and intrinsic coagulation parameters measured. Clotting times of whole blood were increased by aflatoxin (2.5, 5.0, and 10.0 microgram/g) and decreased in blood samples activated by contact with the surface of crushed glass. There was no interaction of aflatoxin with the contact phenomenon. Partial thromboplastin times were significantly (p less than .05) prolonged by 5.0 and 10.0 microgram/g aflatoxin. Intrinsic activity as judged by whole blood thromboplastin generation was reduced nearly 40% by those two levels of aflatoxin. Activity analogous to human factor VIII was depressed by the two highest doses, but factor IX was significantly (P less than .05) reduced by only the highest dose fed, 10 microgram/g. These data suggest that chickens possess an intrinsic coagulation mechanism that is sensitive to aflatoxin but that the factor or factors responsible for the contact response are refractory to this important mycotoxin.

Aflatoxins↗
PubMed1981

Decreased pancreatic digestive enzymes during aflatoxicosis.

Dietary aflatoxin at concentrations of 1.25 microgram/g or above caused in broiler chickens a significant (P less than .05) decrease in the specific activities of pancreatic amylase, trypsin, lipase, RNase, and DNase. These enzymes are the primary enzymes of digestion for starches, protein, lipid, and nucleic acids. At concentrations of 2.5 microgram/g or above there was a compensatory pancreatomegaly that resulted in essentially normal total activity for trypsin, RNase, and DNase. Thus, aflatoxicosis was associated with reduced activity levels of enzymes that digest starch and lipid. This digestive deficiency could account for a malabsorption syndrome observed in field outbreaks of aflatoxicosis.

Aflatoxins↗
PubMed1981

Interactions during inhibition of growth of Aspergillus parasiticus by gentian violet.

The interrelationships of gentian violet and the growth of Aspergillus parasiticus NRRL 2999 were investigated with static cultures in a yeast extract-sucrose liquid medium. The dye was fungistatic but not fungicidal at concentrations up to 32 microgram/ml. Growth inhibition was dependent on the concentration of the added dye and on the age of the culture. At 8 microgram/ml with a spore inoculum, growth was inhibited for 6 days while 32 microgram/ml added to a 4-day-old culture inhibited for only 24 hr. Initiation of a normal rate of growth coincided with disappearance of the dye from the medium. The disappearance followed first order kinetics. The dye appeared to bind to the mycelium prior to its apparent disappearance from the medium. Gentian violet appeared to inhibit spore germination by inhibiting a critical point in the spore swelling phenomenon. In addition, growth subsequent to germination was retarded.

Animals↗
PubMed1980

Impairment of phagocytosis by heterophils from chickens during ochratoxicosis.

The effect of graded concentrations of dietary ochratoxin A (0, O.5, 1.0, 2.0, 4.0, and 8.0 microgram/g of diet) on the in vitro phagocytic, locomotory, and bactericidal capacities of heterophils from broiler chickens was investigated. Both the percentage and the mean phagocytic activities were decreased significantly (P less than 0.05) at 4.0 and 8.0 microgram/g. Both directed and undirected locomotion of heterophila was impaired significantly at the same concentrations. A crossover experiment revealed that the reduced percentage of phagocytosis was associated with the heterophil itself and not with a serum factor such as complement. Heterophila from birds that consumed 4.0 microgram/g were not impaired in ability to kill engulfed bacteria.

Animals↗
PubMed1980

Evaluation of bone strength during aflatoxicosis and ochratoxicosis.

Young chickens were fed graded levels of aflatoxin (0, 0.625, 1.25, 2.5, 5.0, and 10.0 mug/g of diet) or ochratoxin (0, 0.5, 1.0, 2.0, 4.0, and 8.0 mug/g of diet), and the breaking strength, displacement before failure, and diameter of their tibias were determined. Breaking strength was decreased at growth inhibitory levels of aflatoxin (2.5 mug/g) and ochratoxin (2 mug/g), whereas a reduction in diameter required higher levels (5.0 and 4.0 mug/g, respectively). Bones from birds with ochratoxicosis selected to have diameters equal to control bones had lower breaking strength. In an attempt to negate mathematically the effect of decreased diameter and bias in any selection process, stress at time of failure of the bones was calculated and found to be decreased by feeding aflatoxin but not ochratoxin. Total displacement of bones before breaking was increased significantly (P < 0.05) by both toxins at the highest levels administered, but this increase was primarily the result of an increase in displacement from the start of failure to complete failure. Increased displacement associated with both toxicoses was equal in bones selected to be of equal diameter or in bones from the same treatment but of different diameters. However, calculation of modulus of elasticity which is corrected for diameter revealed aflatoxin had no effect whereas ochratoxin tripled the effect. These data indicate that the material properties of bones can be altered during mycotoxicoses and suggest yet another way in which mycotoxins are detrimental to animal health.

Aflatoxins↗