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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.

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.

Thirty-three samples of wheat of the 1982 crop year from Kansas and Nebraska were analyzed for deoxynivalenol, T-2 toxin, zearalenone, and aflatoxin. Deoxynivalenol was identified in 31 of 33 samples, zearalenone was identified in 3 of 33 samples, and aflatoxin B1 was identified in 23 of 31 samples. One 1982 wheat sample from Illinois and one from Texas were also contaminated with deoxynivalenol at 1,200 and 600 ng/g, respectively. None of the samples contained detectable T-2 toxin. The mean concentration of deoxynivalenol was 1,782 +/- 262 ng/g, and the concentrations of aflatoxin B1 ranged from 0.8 to 17.0 ng/g, with a mean of 3.37 +/- 0.7. Zearalenone concentrations of the three positive samples were 35, 90, and 115 ng/g. However, density segregation of two other samples which tested negative yielded light fractions, comprising less than 2% of the samples, contaminated at 230 and 254 ng of zearalenone per g; calculated zearalenone concentrations for these two samples were below the limit of detection of the method. The high frequency of aflatoxin B1 and deoxynivalenol in wheat from the 1982 crop is unprecedented, as is the simultaneous contamination of some samples with deoxynivalenol, zearalenone, and aflatoxin B1.

Crude extracts of filtrates of cultures of Fusarium sambucinum NRRL 13495 were acetylated or hydrolyzed. After chromatography on cartridge columns of silica gel and recrystallization three times from mixtures of ethyl acetate and hexane, 3,4,15-triacetoxyscirpenol (435 +/- 10 mg/liter of filtrate; mean +/- standard error [n = 3]) and the parent alcohol scirpentriol were isolated (261 +/- 29 mg/liter of filtrate; mean +/- standard error [n = 3]) in 68 and 53% yield for a 130- and 14-fold improvement, respectively, over prior reports.

Filtrates of Fusarium sambucinum NRRL 13495 grown in a stagnant culture for 9 days contained up to 458 +/- 60 (mean +/- standard error; n = 3) mg of 4,15-diacetoxyscirpenol per liter depending on culture conditions. Extraction with ethyl acetate, chromatography on a column of silica gel, and crystallization from mixtures of ethyl acetate and hexane provided pure material in 96% yield.

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.

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.

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.