Backgrounds: Unhygienic poultry feedstuffs can lead to nutrient losses and detrimental effect on poultry production and public health. Objectives: This study was to investigate the fungal contamination of poultry feed and its ingredients in broiler farms in Torbat Heydarieh, Khorasan Razavi province, Iran. Methods: A total of 240 poultry feed samples comprising three different feeds were collected and examined using dilution plating technique. Preparations of all samples from successive dilutions were prepared; and then 0.1 ml of each dilution was cultured on the surface of Potato Dextrose Agar supplemented with Chloramphenicol and was incubated at 27 °C for 7 days. Fungal colony counting was performed based on CFU/gr. The fungi were identified by gross and microscopic features. Statistical analysis of the data were done using SPSS software version 21. Results: In examined samples, fungal contamination was detected in 205 samples (85/14 %) out of 240 samples. The corn (32/5%) was most contaminated feed, followed by soybean (29/16%) and finished feed (23/75%). The predominant fungi isolated were Fusarium spp. (41/3 %), Penicillium spp. (37/9%), Cladosporium spp. (21.3 %), Paecilomyces spp. (17.1%), Aspergillus fumigatus (13/3 %), Aspergillus niger (12.9%) and Yeast spp. (12.9 %). Frequency of toxin -forming fungi was significantly higher than the non- toxin -forming fungi (P<0/001). The mean total count of fungi was estimated 2/9 × 105 CFU/gr.Conclusions: The findings of this research showed the high prevalence of fungal contamination as well as high frequency of toxin -forming fungi. Therefore, the feed raw materials are important vehicles for introduction of fungal organisms into poultry feed and fungal growth reduces the nutritional value of feeds. It should be considered to plan a program in order to control, limit and delete of the fungi from feeds.

Kikuyu poisoning occurs sporadically in South Africa. It is of major economic importance, as valuable dairy cows are often poisoned by it, and once affected, the mortality rate is high. Pennisetum clandestinum samples were collected during eight outbreaks of kikuyu poisoning in cattle in the Eastern Cape Province of South Africa from 2008 to 2010. The kikuyu grass samples were submitted specifically for the isolation and molecular identification of Fusarium species, as it was recently suggested that mycotoxins synthesised by Fusarium torulosum could be the cause of this intoxication. Ninety-four Fusarium isolates were retrieved from the grass samples, of which 72 were members of the Fusarium incarnatum/Fusarium equiseti species complex based on morphology and phylogenetic analyses of the translation elongation factor 1α sequence data. The South African isolates from kikuyu identified as members of the F. incarnatum/F. equiseti species complex grouped together in six separate clades. The other isolates were Fusarium culmorum (n = 3), Fusarium redolens (n = 4) and Fusarium oxysporum (n = 15). Although F. torulosum could not be isolated from P. clandestinum collected during kikuyu poisoning outbreaks in South Africa, the mycotoxicosis theory is still highly plausible.

The present study was carried out to investigate the effect of barley and barley bran contaminated with Fusarium spp on growth performance and feed efficiency of fattening and growing pigs. In experiment 1, total 48 fattening Landrace pigs were used in a fattening trial for 71 days. Pigs weighing around 75 kg were allocated into different substitution groups containing 0, 10, 20 and 30% of barley contaminated Fusarium spp. In experiment 2, total 16 growing Landrace pigs were used in a growing trial for 45 days. Pigs weighing around 29.4 kg were allocated into different substitution groups containing 0, 5, 10 and 20% of barley bran contaminated Fusarium spp. Mycotoxin concentrations of barley and barley bran contaminated with 30% Fusarium spp were 0.452 and 1.049 ppm for deoxynivalenol, 8.125 and 17.646 ppm for nivalenol and 0.023 and 0.029 ppm for zearalenone, respectively. In experiment 1, no differences were found in weight gain and feed intake between control group (0%) and 10 or 20% substitution groups, but in 30% substitution group, weight gain and feed intake were significantly lower (p less than 0.05) than those in control group. After slaughtering, the extended haemorrhage of the fundus region in stomach was observed in 20 or 30% substitution groups. In experiment 2, weight gain and feed intake were not significantly different among treatment groups. After slaughtering of experimental pigs, the extended haemorrhage of the fundus region in stomach was observed in pigs fed diet with 20% substitution group. These results suggest that the feeding of diet with contaminated highly levels of Fusarium spp was negative effect on growth and feed efficiency in growing and fattening pig.

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 gamma-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.

A corn culture of Fusarium roseum was added to a standard corn-soybean swine gestation ration. Low, middle, and high dosage mixed feeds contained 7, 38, and 64 mg of zearalenone/kg of feed (7, 38, and 64 ppm) and 0.5, 2.5, and 4.5 mg of deoxynivalenol/kg, respectively. Control feed was the standard ration without added F roseum corn culture. Mature gilts were bred by natural service and fed control or F roseum molded feed from 3 to 34 days after breeding. The main effect of the molded feed was an inhibition of fetal development, with decreased numbers of fetuses present in treated animals at slaughter (38 to 43 days after breeding). Normal litters were present in 7 of 8 control animals, in 2 of 4 gilts given the low-dosage feed, in 1 of 4 gilts given the medium dosage, and in 0 of 4 given the high-dosage feed. Corpora lutea were maintained in all treated animals, as evidenced by serum progesterone concentrations. Serum estradiol concentrations were decreased in gilts in the middle- and high-dosage groups. The genital system of the gilts fed low- and middle-dosage feeds had a gross and microscopic appearance similar to that of the pregnant controls and reflected prolonged progesterone stimulation. Morphologic changes in the genital system of the high-dosage group were intermediate between changes induced by progesterone and those induced by estrogen. Clinical signs of hyperestrogenism and partial feed refusal were noticed in only some of the high-dosage group animals.

Swab specimens for fungal isolation were collected from the healthy conjunctival sacs of 3 species of captive camelids (Lama glama, L guanicoe, L pacos) and llama-guanaco hybrids. Fungi were collected from over half the animals in winter (53%) and summer (56%). Fungal species of 10 genera were isolated. In both seasons, Aspergillus was the most commonly isolated genus; at least 9 species of Aspergillus were found. The fungal organisms isolated were similar to those found in healthy eyes of other domestic animals and may represent a random seeding from the environment where they are ubiquitous.

The effect of Fusarium-produced T-2 toxin on tumor growth was evaluated in ICR, CFW, and C57B6/6 mice inoculated with murine sarcoma, Ehrlich ascites carcinoma, or B16F1 melanoma tumor cell lines. Mice were given T-2 toxin intragastrically either at the rate of 2 mg of toxin/kg of body weight daily for 5 days or a single dosage of 4 mg of toxin/kg and were inoculated SC with tumor cells 1 or 2 days after administration of toxin. Tumor growth was assessed 15 to 41 days after tumor challenge by determining the frequency of tumor development and tumor weights. Significant increases in the frequency of development of murine sarcoma (P < 0.005). Ehrlich ascites carcinoma (P < 0.01), and B16F1 melanoma tumors (P < 0.05) were detected in toxin-treated mice, compared with control mice. Murine sarcoma and B16F1 melanoma tumor weights also were significantly (P < 0.01) higher in toxin-treated mice. The effect of T-2 toxin on tumor growth was more marked after 5 daily treatments than after a single dose.