Determination of serum aflatoxin B1-lysine and biochemical parameters in broiler chicks fed an aflatoxin B1-contaminated diet.

In the present trial, the levels of serum aflatoxin B1 (AFB1)-lysine and their relationship with biochemical parameters in broiler chicks fed an AFB1-contaminated diet were determined. The experimental design was completely randomized with two treatments (control and 222.17 µg/kg AFB1) and 20 bird per treatment. Feeds were offered to broiler chicks for 14 days, from 28 to 42 days of age. Animals were vaccinated against Newcastle's and Marek's diseases on the 14th day of life, and were killed at 42 days of age. Broilers receiving AFB1 did not demonstrate any sign of toxicity. Compared with controls, aspartate aminotransferase and globulin levels were not affected in the AFB1-treated group. However, higher levels of gamma-glutamyl transferase and lower concentrations of total protein and albumin were observed in the group receiving AFB1 on days 35 and 42. AFB1-lysine were detected in the serum of all broilers fed the AFB1-contaminated diet, at mean levels of 56.52-77.83 ng/mg albumin on days 35 and 42 of age, respectively. These values indicated the internal dose of AFB1 in birds, which negatively correlated with total protein, albumin, and globulin levels. Data indicated that AFB1-lysine shows the potential to be a sensitive and specific biomarker for the evaluation of broiler exposure to dietary aflatoxin, as well as for diagnostic purposes. Further studies are necessary to determine physiologically-based toxicokinetics of serum AFB1-lysine in broilers.

Effects of different sources of Saccharomyces cerevisiae biomass on milk production, composition, and aflatoxin M1 excretion in milk from dairy cows fed aflatoxin B1.

The aim of the present study was to evaluate the effect of different sources of Saccharomyces cerevisiae (SC) biomass (20.0 g/d) obtained from sugarcane (cell wall, CW; dried yeast, DY; autolyzed yeast, AY) and the beer industry (partially dehydrated brewery yeast, BY) on milk production, fat and protein percentages, and aflatoxin M1 (AFM1) excretion in milk from dairy cows receiving 480 µg aflatoxin B1 (AFB1) per day. A completely randomized design was used with 2 lactating cows assigned to each of 10 dietary treatments, as follows: negative controls (no AFB1 or SC-based biomass), positive controls (AFB1 alone), DY alone, DY + AFB1, BY alone, BY + AFB1, CW alone, CW + AFB1, AY alone, and AY + AFB1. The cows in the aflatoxin treatment group received AFB1 from d 1 to 6, while the SC biomass was administered with the AFB1 bolus from d 4 to 6. Aflatoxin B1 or SC-based products did not affect milk production or milk composition during the experimental period. Aflatoxin M1 was detected in the milk from all aflatoxin treatment group cows, reaching maximum levels at d 3 and varying from 0.52 ± 0.03 to 1.00 ± 0.04 µg/L. At end of the treatment period, CW, AY, DY, and BY removed 78%, 89%, 45%, and 50% of AFM1 from the milk, respectively, based on the highest level found on d 3. Results indicate a potential application of industrial fermentation by-products, especially CW and AY, as a feed additive in the diets of dairy cows to reduce the excretion of AFM1 in milk.

Effect of peracetic acid on biofilms formed by Staphylococcus aureus and Listeria monocytogenes isolated from dairy plants.

This research investigated the removal of adherent cells of 4 strains of Staphylococcus aureus and 1 Listeria monocytogenes strain (previously isolated from dairy plants) from polystyrene microtiter plates using peracetic acid (PAA, 0.5%) for 15, 30, 60, and 120 s, and the inactivation of biofilms formed by those strains on stainless steel coupons using the same treatment times. In the microtiter plates, PAA removed all S. aureus at 15 s compared with control (no PAA treatment). However, L. monocytogenes biofilm was not affected by any PAA treatment. On the stainless steel surface, epifluorescence microscopy using LIVE/DEAD staining (BacLight, Molecular Probes/Thermo Fisher Scientific, Eugene, OR) showed that all strains were damaged within 15 s, with almost 100% of cells inactivated after 30 s. Results of this trial indicate that, although PAA was able to inactivate both S. aureus and L. monocytogenes monospecies biofilms on stainless steel, it was only able to remove adherent cells of S. aureus from polystyrene microplates. The correct use of PAA is critical for eliminating biofilms formed by S. aureus strains found in dairy plants, although further studies are necessary to determine the optimal PAA treatment for removing biofilms of L. monocytogenes.

Storage of refrigerated raw goat milk affecting the quality of whole milk powder.

The aim of this study was to evaluate the influence of the growth of lipolytic bacteria in raw goat milk stored under refrigeration for different periods on quality parameters of goat milk powder during its shelf life. Fresh goat milk (100L) was collected after milking, divided into 3 identical fractions, and stored at 4°C for 1, 3, and 5d. On d 1, 3, and 5, one sample (1L) was collected and used for microbiological and chemical analysis, and the remaining fraction (almost 30L) was spray dried and stored at 25°C. Milk powder was submitted to microbiological, chemical, and sensory analysis immediately after production, and on d 60, 120, and 180. Lipolytic psychrotrophic counts and total free fatty acid content did not increase in raw milk during storage. However, peroxide value, caprylic and capric acid concentrations, and total free fatty acid content of milk powder increased during 180d of storage, with higher levels found in milk powder manufactured with raw milk stored for 5d. Capric odor and rancid flavors increased in milk powder during storage, regardless the of storage of raw milk for 1, 3, or 5d. Heat treatments used during powder processing destroyed lipolytic psychrotrophic bacteria, but did not prevent lipolysis in milk powder. Results of this trial indicate that the storage of raw goat milk at 4°C should not exceed 3d to preserve the quality of goat milk powder during its shelf life of 180d.