Moniliformin (1-hydroxy-cyclobut-1-ene-3,4-dione), either purified (0, 8, and 16 mg/kg of diet) or from culture of Fusarium moniliforme strain NRRL 6322 on corn grits (8, 16, and 64 mg/kg of diet) was fed to growing broiler chicks from 1 to 21 days of age. Up to 16 mg moniliformin/kg of diet from either source was without effect on chick weight gain, feed consumption, and mortality. Chicks fed 64 mg moniliformin/kg of diet from culture had reduced weight gain and feed consumption. Total daily moniliformin consumption by these chicks was nearly twice the reported single oral 50% lethal dose. Three of 10 chicks fed 64 mg/kg of moniliformin in the diet died. No lesions were found upon necropsy. The LD50 of purified moniliformin upon intravenous injection of 7-week-old female broiler chickens was 1.38 +/- .035 mg/kg body weight. Average time to death was 65 minutes. Progressive symptoms noted included lack of muscular coordination, tachypnea from moderate to severe followed by slow labored respiration, coma, terminal agonal struggle, and death.

A total of 168 broiler chickens (6 to 9 weeks of age) and 192 turkey poults (3-1/2 to 6-1/2 weeks of age) were fed purified zearalenone at levels of 0 (control), 10, 25 (turkeys only), 50, 100, 200, 400, and 800 mg/kg diet for a 3 week period to evaluate its toxicity. Dietary zearalenone had no effect on body weight gain, feed consumption, weights of liver, heart, spleen, and bursa of Fabricius, serum calcium, phosphorus, alkaline phosphatase, total protein and cholesterol, hematocrit, hemoglobin, red blood cell count, white blood cell count, and differential leukocyte count in both chickens and turkeys. Male broiler comb and testes weights were reduced by high levels of zearalenone. Female comb weight, broiler oviduct weight, and turkey testes and ovaries were unaffected by zearalenone. Histopathological examination of tissues revealed no change due to zearalenone. Male turkeys fed 400 and 800 mg/kg zearalenone had increased development of dewlaps and caruncles and exhibited considerable strutting behavior. Muscle and fat tissue from broilers fed 800 mg/kg zearalenone had no detectable estrogenic activity as measured by mouse uterine bioassay. These studies indicate that the effects of dietary zearalenone on finishing broilers and young growing turkey poults are minimal.

Variable quantities of zearalenone (0, 10, 25, 50, 100, 200, 400, or 800 mg/kg diet) were incorporated into a practical laying hen diet and fed to 30-week-old White Leghorn females in egg production. During the 3 week pretest and 8 week experimental periods hens were inseminated weekly with .05 ml of pooled semen from males fed normal diets. Zearalenone was without effect on egg production, egg size, feed consumption, change in body weight, fertility, hatchability of fertile eggs, growth of progeny to 3 weeks of age, comb, weight, oviduct weight, heart weight, liver weight, spleen weight, egg shell thickness, Haugh units, blood hematology, serum calcium, serum inorganic phosphorus, and serum alkaline phosphatase. Zearalenone above 50 mg/kg of diet caused reduced serum cholesterol. In a reciprocal study, adult male New Hampshire chickens were fed diets containing 0, 100, or 800 mg/kg zearalenone for an 8 week period. Semen was collected and inseminated into White Leghorn females fed normal diets. Zearalenone was without effect on fertility or hatch of fertile eggs resulting from matings of these males. Zearalenone resulted in reduced serum inorganic phosphorus, serum cholesterol, and serum alkaline phosphatase in males. Histological examination of a number of tissues in both males and females revealed no changes due to zearalenone feeding. It is concluded that zearalenone up to 800 mg/kg of diet is without effect on reproductive performance of mature chickens.

Abstract. Broiler chickens were started and maintained on rations containing 2%, 5%, and 10% grain contaminated with Fusarium roseum. There was mortality of 75% and loo%, respectively, in chicks fed 5% and 10% levels, and osteochondrosis was present in chicks which died at 12 to 17 days of age. Chicks on 2% or 3% F. roseum-contaminated grain survived the experimental period and osteochondrosis was well-developed in the proximal tibias of 85 or 90% of these chicks. The number of chondroclasts was reduced markedly in the affected bones. Defective chondroclasis may play a role in the pathogenesis of osteochondrosis associated with F. roseum.Tibial dyschondroplasia is a common abnormality in growing broiler chickens and turkeys throughout the world. The lesion is characterized by the presence of a cone of cartilage which extends distally from the proximal tibiotarsal physis [l-4, 6, 8, 13-15, 18, 191. Abnormalities of this type are not limited to the tibiotarsus; they also occur in the tarsometatarsus, humerus, and femur [9, 101. Similar lesions occur in swine, horses, bulls, and dogs, and the term osteochondrosis has been recommended for the lesion in all species [7].A number of factors have been cited as causes of osteochondrosis in poultry. Rapid weight gain, nutritional deficiencies, and genetic factors frequently are implicated. Poorly defined management factors, such as litter contamination [ 191 and stress, also are incriminated. Scientific investigations have substantiated the influence of genetics and dietary factors on the development of osteochondrosis. Strains of chickens having high and low incidences of osteochondrosis were established by genetic selection [4, 5 , 111. High dietary levels of chloride increased the incidence and severity of osteochondrosis in the genetically susceptible strain, but not in the low incidence strain [5, 111. The incidence and severity of osteochondrosis was greater in randomly bred broiler chickens fed a high energy diet than in those fed a low energy diet [9, 101. The chicks on high energy feed gained weight more rapidly, and it was concluded that the added weight exacerbated osteochondrosis.Previously, Fusarium roseum-contaminated corn was found to induce a high 544

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