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One hundred fifty 1-d-old quail chicks (Coturnix coturnix japonica) were divided into 2 groups. The 2 groups were designated as controls (CX) and fumonisin-fed birds (FX) with each containing 50 and 100 chicks, respectively. The birds in group CX were maintained on quail mash alone, whereas the birds in group FX were maintained on diets supplemented with 300 ppm of fumonisin B1 from Fusarium verticillioides (formerly Fusarium moniliforme) culture material from 1 d. Quail chicks in both groups were examined daily for clinical signs and mortality. Five randomly selected quail from each group were individually weighed on 0, 7, 14, 21, and 28 d post-feeding (DPF). After weighing, blood was collected from these birds at 7, 14, 21, and 28 DPF for hematological studies and at 14, 21, and 28 DPF for biochemical studies. Fumonisin B1-fed birds (FX) had ruffled feathers, reduced feed and water intake, poor body growth, and greenish mucus diarrhea with 59% mortality. Nearly 30% of the fumonisin B1-fed birds showed nervous signs during the 4-wk experimental period. From 7 DPF onward, BW in group FX were significantly lower than those in group CX. Fumonisin feeding significantly increased hemoglobin, packed cell volume, total erythrocyte count, and total leukocyte count. There was also a significant increase in aspartate transaminase and alanine transaminase in the fumonisin-fed group. Fumonisins significantly increased concentrations of total serum protein and albumin on 14 and 21 DPF, serum calcium and cholesterol levels from 14 DPF onward, and creatinine from 21 DPF onward. This study revealed that the addition of F. verticillioides culture material supplying a level of 300 ppm of FB1/kg of diet is highly toxic to quail chicks, resulting in heavy mortality, decreased growth rate, and significant alterations in hemato-biochemical parameters.

Experiments with topically applied T-2 trichothecene mycotoxin were undertaken to determine whether lesions caused by this toxin could be differentiated from autolysis. Two pathologists, who had previously seen lesions caused by T-2 toxin, graded lesions without knowledge of treatment group and stated whether the animal had received the toxin or not. Both pathologists differentiated T-2 toxin-treated mice up to 6 h post-mortem. Failure to distinguish between treated and control mice resulted in false-negative diagnoses only. It was concluded that the diagnosis of trichothecene mycotoxicosis would probably be missed more than 6 h post-mortem.