Aflatoxin (af)-contaminated and fumonisin B1 (fb1)-contaminated (culture material from Fusarium moniliforme) diets were fed singly and in combination to growing cross-bred barrows. Six barrows (3 replicates of 2 each; mean body weight, 17.5 kg) per group were fed: 0 mg of af and 0 mg of fb1/kg of feed (control); 2.5 mg of af/kg of feed; 100 mg of fb1/kg of feed; or 2.5 mg of af plus 100 mg of fb1/kg of feed for 35 days. The effects on production performance, serum biochemical, hematologic, immunologic, and pathologic measurements were evaluated. Body weight, gain, and feed consumption were significantly (P < 0.05) decreased by af and af plus fb1 diets. The fb1 diet decreased feed consumption, and although body weight was numerically decreased, it was not statistically significant. Aflatoxin increased serum γ-glutamyltransferase (GGT) activity and total iron concentration and decreased urea nitrogen concentration and unsaturated iron-binding capacity. The fb1-alone diet increased serum GGT activity, whereas the af plus fb1 diet increased serum aspartate transaminase, Cholinesterase, alkaline phosphatase, and GGT activities, increased rbc count, triglycerides, and total iron concentrations, and decreased unsaturated iron-binding capacity and urea nitrogen concentration. For the most part, the effects of the af plus fb1 diet on body weight and hematologic measurements could be considered additive. However, the effect of the af plus fb1 diet on cholinesterase and alkaline phosphatase activities was greater than additive and was a synergistic response. One pig in the fb1-diet group and 2 pigs in the combination-diet group died. Postmortem lesions in pigs of the fb1-diet group consisted of ascites and increased liver weight. Observations at necropsy for pigs of the af plus fb1-diet group consisted of hydrothorax, ascites, pulmonary edema, gastric erosions and ulceration, and increased liver and spleen weights. The af diet increased relative liver weight and resulted in liver that was pale, rubbery, and resistant to cutting. Histologic lesions consisted of hepatic necrosis or degeneration, or both, with variable degrees of bile duct proliferation in barrows of the af-diet groups. Renal tubular nephrosis was observed in barrows of the fb1-diet group, but this was not consistent in the af plus fb1-diet group. Cell-mediated immunity, as measured by mitogen-induced lymphoblastogenic stimulation index, was decreased in barrows of the af and fb1-diet groups, and values in barrows given the combination diet were significantly decreased from those in barrows given the single toxin diets. It was concluded that af and fb1 (from culture material), singly or in combination, can adversely affect clinical performance, serum biochemical, hematologic, and immunologic values and induce lesions in growing barrows. For most of the variables we evaluated under our study conditions and dosages of toxins, measurements were affected more by the combination diet than by either single toxin diet, and the toxic responses could be described as additive or more than additive, particularly for induction of liver disease. Aflatoxin (af)-contaminated and fumonisin B1 (fb1)-contaminated (culture material from Fusarium moniliforme) diets were fed singly and in combination to growing cross-bred barrows. Six barrows (3 replicates of 2 each; mean body weight, 17.5 kg) per group were fed: 0 mg of af and 0 mg of fb1/kg of feed (control); 2.5 mg of af/kg of feed; 100 mg of fb1/kg of feed; or 2.5 mg of af plus 100 mg of fb1/kg of feed for 35 days. The effects on production performance, serum biochemical, hematologic, immunologic, and pathologic measurements were evaluated. Body weight, gain, and feed consumption were significantly (P < 0.05) decreased by af and af plus fb1 diets. The fb1 diet decreased feed consumption, and although body weight was numerically decreased, it was not statistically significant. Aflatoxin increased serum γ-glutamyltransferase (GGT) activity and total iron concentration and decreased urea nitrogen concentration and unsaturated iron-binding capacity. The fb1-alone diet increased serum GGT activity, whereas the af plus fb1 diet increased serum aspartate transaminase, Cholinesterase, alkaline phosphatase, and GGT activities, increased rbc count, triglycerides, and total iron concentrations, and decreased unsaturated iron-binding capacity and urea nitrogen concentration. For the most part, the effects of the af plus fb1 diet on body weight and hematologic measurements could be considered additive. However, the effect of the af plus fb1 diet on cholinesterase and alkaline phosphatase activities was greater than additive and was a synergistic response. One pig in the fb1-diet group and 2 pigs in the combination-diet group died. Postmortem lesions in pigs of the fb1-diet group consisted of ascites and increased liver weight. Observations at necropsy for pigs of the af plus fb1-diet group consisted of hydrothorax, ascites, pulmonary edema, gastric erosions and ulceration, and increased liver and spleen weights. The af diet increased relative liver weight and resulted in liver that was pale, rubbery, and resistant to cutting. Histologic lesions consisted of hepatic necrosis or degeneration, or both, with variable degrees of bile duct proliferation in barrows of the af-diet groups. Renal tubular nephrosis was observed in barrows of the fb1-diet group, but this was not consistent in the af plus fb1-diet group. Cell-mediated immunity, as measured by mitogen-induced lymphoblastogenic stimulation index, was decreased in barrows of the af and fb1-diet groups, and values in barrows given the combination diet were significantly decreased from those in barrows given the single toxin diets. It was concluded that af and fb1 (from culture material), singly or in combination, can adversely affect clinical performance, serum biochemical, hematologic, and immunologic values and induce lesions in growing barrows. For most of the variables we evaluated under our study conditions and dosages of toxins, measurements were affected more by the combination diet than by either single toxin diet, and the toxic responses could be described as additive or more than additive, particularly for induction of liver disease.