Application of a Swab Sampling Method for the Detection of Norovirus and Rotavirus on Artificially Contaminated Food and Environmental Surfaces

Noroviruses and rotaviruses are the leading causes of non-bacterial gastroenteritis in humans worldwide. Virus-contaminated food and surfaces represent an important risk to public health. However, established detection methods for the viruses in food products are laborious and time-consuming. Here, we describe a detailed swabbing protocol combined with real-time RT-PCR for norovirus and rotavirus detection on artificially contaminated food and environmental surfaces. Recovery rates between 2 and 78% for norovirus and between 8 and 42% for rotavirus were determined for contaminated food surfaces of apple, pepper, cooked ham and salami. From contaminated environmental surfaces (stainless steel, ceramic plate, polyethylene, wood), recovery rates between 26 and 52% (norovirus) and between 10 and 58% (rotavirus) were determined. The results demonstrate the suitability of the swab sample method for virus detection on food and environmental surfaces. Compared to other methods, it is easy to perform and significantly time-saving, predestining it for routine testing.     

A review of predator diet effects on prey defensive responses

Numerous studies have examined how predator diets influence prey responses to predation risk, but the role predator diet plays in modulating prey responses remains equivocal. We reviewed 405 predator–prey studies in 109 published articles that investigated changes in prey responses when predators consumed different prey items. In 54 % of reviewed studies, prey responses were influenced by predator diet. The value of responding based on a predator’s recent diet increased when predators specialized more strongly on particular prey species, which may create patterns in diet cue use among prey depending upon whether they are preyed upon by generalist or specialist predators. Further, prey can alleviate costs or accrue greater benefits using diet cues as secondary sources of information to fine tune responses to predators and to learn novel risk cues from exotic predators or alarm cues from sympatric prey species. However, the ability to draw broad conclusions regarding use of predator diet cues by prey was limited by a lack of research identifying molecular structures of the chemicals that mediate these interactions. Conclusions are also limited by a narrow research focus. Seventy percent of reviewed studies were performed in freshwater systems, with a limited range of model predator–prey systems, and 98 % of reviewed studies were performed in laboratory settings. Besides identifying the molecules prey use to detect predators, future studies should strive to manipulate different aspects of prey responses to predator diet across a broader range of predator–prey species, particularly in marine and terrestrial systems, and to expand studies into the field.     

Comparison of intake of nicotine from environmental tobacco smoke between nose and mouth breathers

Two experiments were carried out in order to investigate nicotine intake through passive smoking. In the first study, carboxyhemoglobin (COHb) and serum cotinine were found to increase to a similar extent in seven subjects breathing through the nose only and in another seven subjects breathing through the mouth only during exposure to environmental tobacco smoke. Similarly, no significant difference was found in urinary excretion of nicotine and cotinine over a period of 72 hours, although nicotine and cotinine excretion tended to be slightly higher after inhalation through the nose only. In the second study, nicotine was measured in four subjects who held mainstream or sidestream smoke in the mouth without inhaling. Cotinine levels in serum and amounts of nicotine and cotinine excreted in the urine were low compared with those measured in the breathing study. Nicotine from sidestream smoke, however, is more effectively absorbed by the oral mucosa than nicotine from mainstream smoke. The data suggest that nicotine intake from passive smoking largely takes place in the bronchial tree and that nicotine absorption via the nasal or the oral mucosa is only of minor significance.