Oxidative reactivity across kingdoms in the gut: Host immunity, stressed microbiota and oxidized foods.

Reactive oxygen species play a major role in the induction of programmed cell death and numerous diseases. Production of reactive oxygen species is ubiquitous in biological systems such as humans, bacteria, fungi/yeasts, and plants. Although reactive oxygen species are known to cause diseases, little is known about the importance of the combined oxidative stress burden in the gut. Understanding the dynamics and the level of oxidative stress 'reactivity' across kingdoms could help ascertain the combined consequences of free radical accumulation in the gut lumen. Here, we present fundamental similarities of oxidative stress derived from the host immune cells, bacteria, yeasts, plants, and the therein-derived diets, which often accentuate the burden of free radicals by accumulation during storage and cooking conditions. Given the described similarities, oxidative stress could be better understood and minimized by monitoring the levels of oxidative stress in the feces to identify pro-inflammatory factors. However, we illustrate that dietary studies rarely monitor oxidative stress markers in the feces, and therefore our knowledge on fecal oxidative stress monitoring is limited. A more holistic approach to understanding oxidative stress 'reactivity' in the gut could help improve strategies to use diet and microbiota to prevent intestinal diseases.

A cluster of three cases of leptospirosis in dairy farm workers in New Zealand.

AIMS: We report a cluster of three cases of leptospirosis on a New Zealand dairy farm, with regard to clinical, laboratory, and environmental findings. The cluster is discussed against the annual incidence of leptospirosis in humans and cattle, and the vaccination of cattle as one means of preventing human cases on farms. METHDOS: The three cases were investigated by case interview and review of clinical and laboratory information. A site visit was made to the farm to assess environmental risk. Relevant veterinary information relating to the cattle herds was reviewed. RESULTS: Most of the symptoms exhibited by the three patients were consistent with primary phase leptospirosis. Different methods of laboratory diagnosis were used with each case. However, two cases were confirmed as leptospirosis and in both the causative agent was Leptospira borgpetersenii serovar (sv) Hardjo. The third case had a milder illness, received doxycycline early, and was regarded as a 'probable' case as there were no confirmatory diagnostic results. All three cases had worked on the same dairy farm during their incubation period, where the highest risk environment was the milking shed and potential exposure to urine splashes from infected cattle. Also there were inadequacies in the herd vaccination programme. CONCLUSIONS: There are options for minimising risk to dairy farm workers in New Zealand. No human vaccine exists in this country. Leptospira borgpetersenii serovar (sv) Hardjo (serovar Hardjo) is endemic in New Zealand dairy cattle without causing apparent disease. L. Pomona is a sporadic infection but can cause abortions. A cattle vaccine against these serovars was introduced in New Zealand in 1979, after which there was a general fall in notifications of human cases of leptospirosis. This was attributed to the overall decrease in these two serovars among the livestock population. Vaccination of farm livestock for leptospirosis is an integral factor in preventing human cases. We note the New Zealand initiative to combine vaccination with a risk management programme operated by veterinarians, called Leptosure, to reduce the risk of human leptospirosis on dairy farms. The efficacy of using doxycycline as a prophylaxis for preventing human infection in trials is reviewed. Other preventative strategies include the use of personal protective equipment to cover the mouth and nose, eyes and all skin breaks, farm workers and rural clinicians being aware of the signs and symptoms of leptospirosis, and prompt treatment of cases with antibiotics.

Clostridium difficile in foods and animals: history and measures to reduce exposure.

Many articles have summarized the changing epidemiology of Clostridium difficile infections (CDI) in humans, but the emerging presence of C. difficile in foods and animals and possible measures to reduce human exposure to this important pathogen have been infrequently addressed. CDIs have traditionally been assumed to be restricted to health-care settings. However, recent molecular studies indicate that this is no longer the case; animals and foods might be involved in the changing epidemiology of CDIs in humans; and genome sequencing is disproving person-to-person transmission in hospitals. Although zoonotic and foodborne transmission have not been confirmed, it is evident that susceptible people can be inadvertently exposed to C. difficile from foods, animals, or their environment. Strains of epidemic clones present in humans are common in companion and food animals, raw meats, poultry products, vegetables, and ready-to-eat foods, including salads. In order to develop science-based prevention strategies, it is critical to understand how C. difficile reaches foods and humans. This review contextualizes the current understanding of CDIs in humans, animals, and foods. Based on available information, we propose a list of educational measures that could reduce the exposure of susceptible people to C. difficile. Enhanced educational efforts and behavior change targeting medical and non-medical personnel are needed.

Low prevalence of Escherichia coli O157:H7 in horses in Ohio, USA.

Manure from draft animals deposited in fields during vegetable and fruit production may serve as a potential source of preharvest pathogen contamination of foods. To better quantify this risk, we determined the prevalence of Escherichia coli O157:H7 in horses. Between June and September 2009, freshly voided fecal samples were collected from horses stabled on 242 separate premises in Ohio, USA. Overall, the prevalence of E. coli O157:H7 was 1 of 242 (0.4% prevalence, 95% confidence interval [CI] = 0.01 to 2.28). E. coli O157:H7 was recovered from none of the 107 equine fecal samples (0% prevalence, 95% CI = 0.00 to 3.39) that originated from locations without ruminant presence, and only 1 of the 135 horse fecal samples (0.7% prevalence, 95% CI = 0.02 to 4.06) from sites where ruminants were also present. The lone positive sample was collected from a horse that was costabled with a goat. Subsequent sampling at that location identified indistinguishable subtypes of E. coli O157:H7 present in the cohoused goat, in the environment, insects, sheep, and other goats housed in an adjacent field. E. coli O157:H7 was not isolated from the five subsequent samples from this horse. These data indicate that E. coli O157:H7 carriage by horses is an uncommon event.