Producing milk with uniform high selenium concentrations on commercial dairy farms

Six herds on five commercial dairy farms were involved in the production of high selenium (Se) milk. The farms had a range of herd sizes, herd structures, feeding systems and milk production per cow. On all farms, pelleted concentrate supplements containing Se yeast were fed twice daily in the dairy for 16 days. The objectives were to: (1) produce milk with Se concentrations exceeding 225 mu g/kg on the five farms for pilot-scale production of a high protein milk powder; (2) validate a predictive relationship between Se intake and milk Se concentration developed in research; and (3) examine the time taken from the introduction of Se yeast to steady-state concentrations of Se in milk under a range of commercial farming conditions. We hypothesised that the relationship between Se intake and its concentration in milk found in research would apply on commercial farms. Daily Se intake, which was primarily from Se yeast in the pelleted concentrates, varied from 35 to 51 mg Se/cow. Grazed pasture and conserved forage contributed less than 1 mg Se/cow on all farms. The time taken from the introduction of pellets containing Se yeast to steady-state milk Se concentrations was 4-7 days. The steady-state Se concentrations in milk varied from 166 to 247 mu g/kg, but these concentrations were only 55-72% of predicted values. All the milk produced from the five farms on the last 2 days of feeding of Se-enriched pellets was used to produce a milk protein concentrate with a Se concentration of 5.4 mg/kg. Factors that might have affected Se incorporation into milk and the implications of these results for commercial production of high Se milk or milk products are discussed

The anti-sigma factor TcdC modulates hypervirulence in an epidemic BI/NAP1/027 clinical isolate of Clostridium difficile

Nosocomial infections are increasingly being recognised as a major patient safety issue. The modern hospital environment and associated health care practices have provided a niche for the rapid evolution of microbial pathogens that are well adapted to surviving and proliferating in this setting, after which they can infect susceptible patients. This is clearly the case for bacterial pathogens such as Methicillin Resistant Staphylococcus aureus (MRSA) and Vancomycin Resistant Enterococcus (VRE) species, both of which have acquired resistance to antimicrobial agents as well as enhanced survival and virulence properties that present serious therapeutic dilemmas for treating physicians. It has recently become apparent that the spore-forming bacterium Clostridium difficile also falls within this category. Since 2000, there has been a striking increase in C. difficile nosocomial infections worldwide, predominantly due to the emergence of epidemic or hypervirulent isolates that appear to possess extended antibiotic resistance and virulence properties. Various hypotheses have been proposed for the emergence of these strains, and for their persistence and increased virulence, but supportive experimental data are lacking. Here we describe a genetic approach using isogenic strains to identify a factor linked to the development of hypervirulence in C. difficile. This study provides evidence that a naturally occurring mutation in a negative regulator of toxin production, the anti-sigma factor TcdC, is an important factor in the development of hypervirulence in epidemic C. difficile isolates, presumably because the mutation leads to significantly increased toxin production, a contentious hypothesis until now. These results have important implications for C. difficile pathogenesis and virulence since they suggest that strains carrying a similar mutation have the inherent potential to develop a hypervirulent phenotype