Posts Tagged ‘Food’

Beer consumption increases your attractiveness – to mosquitoes

Friday, March 19th, 2010

Mosquito Malaria and alcohol consumption both represent major public health problems. Alcohol consumption is rising in developing countries and, as efforts to manage malaria are expanded, understanding the links between malaria and alcohol consumption becomes crucial. Our aim was to ascertain the effect of beer consumption on human attractiveness to malaria mosquitoes in semi field conditions in Burkina Faso. We used a Y tube-olfactometer designed to take advantage of the whole body odour (breath and skin emanations) as a stimulus to gauge human attractiveness to Anopheles gambiae (the primary African malaria vector) before and after volunteers consumed either beer (n = 25 volunteers and a total of 2500 mosquitoes tested) or water (n = 18 volunteers and a total of 1800 mosquitoes). Water consumption had no effect on human attractiveness to An. gambiae mosquitoes, but beer consumption increased volunteer attractiveness. Body odours of volunteers who consumed beer increased mosquito activation (proportion of mosquitoes engaging in take-off and up-wind flight) and orientation (proportion of mosquitoes flying towards volunteers’ odours). The level of exhaled carbon dioxide and body temperature had no effect on human attractiveness to mosquitoes. Despite individual volunteer variation, beer consumption consistently increased attractiveness to mosquitoes. These results suggest that beer consumption is a risk factor for malaria and needs to be integrated into public health policies for the design of control measures.

Beer Consumption Increases Human Attractiveness to Malaria Mosquitoes. PLoS ONE 5(3): e9546. doi:10.1371/journal.pone.0009546

Vineyardomics: SOS – Save our Shiraz!

Friday, February 26th, 2010

Shiraz Grapevines are an important global crop which are widely planted throughout temperate regions. Viruses are a significant factor in reducing the quality and quantity of the yield and are known to reduce the productive life of vineyards. Grapevines are subject to infection by more than 60 different viruses, the most known for any crop plant. Most important grapevine virus diseases are caused by complexes of viruses, with up to nine different viruses having been identified in a single vine. In South Africa, as in most grape-growing regions of the world, grapevine leafroll is regarded to be the most significant virus disease affecting grapevine, with Shiraz disease and Shiraz decline becoming more prominent as emerging diseases in the industry.

Present disease diagnostics rely on ELISA or RT-PCR and target the viruses that have historically been associated with these diseases. While these tests are highly specific, they may not result in an accurate reflection of the etiological status of the tested plant, or of the particular disease, since none of the current diagnostic techniques address the potential contribution of other known or unknown viruses that may be involved in the etiology of a particular disease. Moreover, the error prone replication of RNA viruses leads to quasispecies, which can further complicate PCR-based detection assays as not all variants of the virus may be detected.

New and powerful technologies which are able to sequence viruses from environmental samples without the need for laborious and costly purification, cloning and screening techniques can result in the generation of sequence information for the complete virome in an unbiased fashion. This paper describes the use of sequencing-by-synthesis technology on the massively parallel Illumina Genome Analyzer II, to sequence an environmental sample composed of 44 randomly selected vines, to determine the virus profile of a severely diseased vineyard.

Deep sequencing analysis of viruses infecting grapevines: Virome of a vineyard. Virology. Feb 19 2010
Double stranded RNA, isolated from 44 pooled randomly selected vines from a diseased South African vineyard, has been used in a deep sequencing analysis to build a census of the viral population. The dsRNA was sequenced in an unbiased manner using the sequencing-by-synthesis technology offered by the Illumina Genome Analyzer II and yielded 837 megabases of metagenomic sequence data. Four known viral pathogens were identified. It was found that Grapevine leafroll-associated virus 3 (GLRaV-3) is the most prevalent species, constituting 59% of the total reads, followed by Grapevine rupestris stem pitting-associated virus and Grapevine virus A. Grapevine virus E, a virus not previously reported in South African vineyards, was identified in the census. Viruses not previously identified in grapevine were also detected. The second most prevalent virus detected was a member of the Chrysoviridae family similar to Penicillium chrysogenum virus. Sequences aligning to two other mycoviruses were also detected.

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Dance till you can’t dance no more

Friday, January 22nd, 2010

dance In 1518, one of the strangest epidemics in recorded history struck the city of Strasbourg. Hundreds of people were seized by an irresistible urge to dance, hop and leap into the air. In houses, halls and public spaces, as fear paralyzed the city and the members of the elite despaired, the dancing continued with mindless intensity. Seldom pausing to eat, drink or rest, many of them danced for days or even weeks. And before long, the chronicles agree, dozens were dying from exhaustion. What was it that could have impelled as many as 400 people to dance, in some cases to death?

Medieval dancing epidemics were not unrelated events: they were linked both in time and space. Every one of the ten or so outbreaks between the late 1300s and 1518 happened along the Rhine and Mosel rivers. In 1374, for instance, the crazed dance gradually spread out from an epicentre around Aachen, Liege and Maastricht to neighbouring towns such as Ghent, Utrecht, Metz, Trier and, eventually, Strasbourg. Moreover, outbreaks of compulsive dancing virtually always struck in or close to places affected by earlier outbreaks. Maastricht, Trier, Zurich and Strasbourg each experienced two or more episodes. There are also several reports of compulsive dancing after 1518. All of these, crucially, took place close to the Rhine, and all but one within a short ride of Strasbourg itself.

How can we explain this striking epidemiological picture? One suggestion is that wild dancing formed part of the ecstatic ritual of a heretical sect, an energetic counterpart of the flagellant’s cult. There are two main difficulties with this theory. First, in lucid moments the dancers implored bystanders and priests to come to their aid. There is absolutely no evidence that the dancers wanted to dance. On the contrary, they expressed fear and desperation. Second, the authorities consistently saw the afflicted not as heretics but as the victims of diabolical possession or divine curse, and treated them accordingly. The dancers were subject to exorcisms or sent on pilgrimages. Never were they hauled before the inquisition.

Other authors have sought a chemical or biological origin for the dancing mania, and the chief contender has been ergot, a mould that grows on the stalks of damp rye. While seductively simple, this hypothesis is untenable. The chemicals contained in ergot do not allow for sustained dancing. They can certainly trigger violent convulsions and delusions, but not coordinated movements that last for days. Yet while the dancers were free from ergot, they almost certainly were delirious. Only in an altered state of consciousness could they have tolerated such extreme fatigue and the searing pain of sore, swollen and bleeding feet. Moreover, witnesses consistently spoke of the victims as being entranced, seeing terrifying visions and behaving with wild, crazy abandon. So what could have plunged hundreds of people into trances so deep that remorseless dancing became possible? Psychologists, neurologists and anthropologists have identified severe psychological distress as a factor increasing the likelihood of an individual entering an altered state. It is unlikely to be a coincidence, therefore, that in the year 1518 many people in Strasbourg were experiencing truly exceptional levels of hunger and mental anguish.

In a spin: the mysterious dancing epidemic of 1518. Endeavour. 2008 32(3): 117-121. doi: 10.1016/j.endeavour.2008.05.001

Is that chicken bugged?

Wednesday, October 7th, 2009

BBC News

Two-thirds of chicken on sale in the UK is contaminated with a bacterium which can cause severe food poisoning. Campylobacter, which can cause diarrhoea, cramping and abdominal pain, causes 55,000 cases of food poisoning a year in the UK. Cooking the meat properly kills the bug. The Food Standards Agency said the poultry industry should take action. Levels of Campylobacter in chicken were the same as when a similar survey was last carried out in 2001.

BBC News

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Mushroom Expert

Saturday, September 19th, 2009

Mushroomexpert.com Mushroomexpert.com is a great website by Michael Kuo for anyone interested in identifying fungi, whether edible or poisonous! As well as Mushroom of the Month, the site also includes great sections on:

Although they are beautiful, there is no simple way of knowing which fungi are safe to eat and which poisonous. Do not experiment with edible fungi, and get expert advice if you are in any doubt. Do not trust visual identification alone, whether from books or websites, as fungi vary tremendously in size, shape, colour and sometimes even in growing habitat.

Why not grow your own?

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Novel genetic tools for studying food-borne Salmonella

Wednesday, July 1st, 2009

Salmonella typhimurium Nontyphoidal Salmonellae are responsible for an estimated 1.4 million cases of gastrointestinal disease with 500 associated deaths in the United States, at a cost of $2 billion. The number of cases worldwide probably exceeds 100 million each year. Infection generally occurs after the ingestion of contaminated food or water, and usually leads to a self-limiting enterocolitis. The disease is characterized by diarrhea, abdominal cramps, nausea, fever, vomiting, and headache lasting 7–10 days, followed by a longer period of subclinical fecal shedding. Infants, the elderly, and immunocompromised individuals are at risk for serious systemic complications and death as a result of infection.

Contaminated foods, including beef, pork, poultry, and egg products are frequent vectors responsible for the transmission of these organisms to humans. Livestock can harbor Salmonellae subclinically resulting in carcass contamination at slaughter and in the laying of contaminated eggs. In recent years, as the traditional routes of infection are better controlled, large outbreaks of nontyphoidal Salmonella infection in the United States have been attributed to fruits, vegetables, and processed foods including jalapeño peppers, cantaloupe, cereal, and peanut butter (CDC).

Serology based on surface antigens is the standard method of classification of Salmonella. The host-range and disease can differ considerably between serovars, making such classification important. Throughout the world, the most prevalent nontyphoidal serovars isolated from human sources are serovars Typhimurium and Enteritidis and these two serovars comprise nearly 40% of isolations from human sources in the United States. These serovars can be harbored subclinically in livestock for prolonged periods of time and are thus very difficult to eradicate in the absence of a detailed knowledge of the biology of the organism in this niche.

The bacterial factors necessary for Salmonellae to persist subclinically in the gastrointestinal tract of livestock and to survive and grow in other reservoirs such as crops and processed foods are only beginning to be elucidated. This knowledge will allow the development of new strategies and the identification of points in the production chain where producers can intervene to improve the safety of foods. We review the current status as well as the uses of complete genome sequence information for Salmonellae, and enhancements of genetic techniques that may rapidly increase our knowledge of the biology of this organism in these important food safety niches.

Complete genome sequencing of Salmonellae is allowing us to better understand their genetic diversity, to develop novel tools, and to improve existing genetic techniques to understand the complex biology of these important food-borne pathogens. Approximately half of the genes in Salmonella still have no known phenotype in the environment. Frontiers for further study of Salmonella for improved food safety using modern genetic tools are likely to include determination of the genes necessary for environments where Salmonella must survive outside the host, such as in feces, soil, water, and plants. Understanding how Salmonella completes its entire host-to-host life cycle in agriculture may reveal previously unknown vulnerabilities that will be susceptible to novel intervention and allow us to break the chain of transmission.

Novel genetic tools for studying food-borne Salmonella. Curr Opin Biotechnol. 2009 Apr;20(2):149-57.
Nontyphoidal Salmonellae are highly prevalent food-borne pathogens. High-throughput sequencing of Salmonella genomes is expanding our knowledge of the evolution of serovars and epidemic isolates. Genome sequences have also allowed the creation of complete microarrays. Microarrays have improved the throughput of in vivo expression technology (IVET) used to uncover promoters active during infection. In another method, signature tagged mutagenesis (STM), pools of mutants are subjected to selection. Changes in the population are monitored on a microarray, revealing genes under selection. Complete genome sequences permit the construction of pools of targeted in-frame deletions that have improved STM by minimizing the number of clones and the polarity of each mutant. Together, genome sequences and the continuing development of new tools for functional genomics will drive a revolution in the understanding of Salmonellae in many different niches that are critical for food safety.

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Prions are secreted in milk from clinically-normal scrapie-exposed sheep

Tuesday, June 9th, 2009

PrP All scientific papers are important, but some are more important than others. Aside from its scientific importance, this paper is particularly important to me in purely personal terms. It comes from my own department. Ben Maddison was a PhD student in my laboratory many years ago and now heads up his own research group within the department. It’s also one of the final papers to come from Gary Whitelam, my former head of department, who died tragically last year. And as if all that wasn’t enough, as the UK starts to forget about how close we came to disaster with BSE, we’re still not completely sure that it’s all over.

Using the cutting-edge research technique of serial protein misfolding cyclic amplification (sPMCA), my colleagues show that prions are secreted in the milk from scrapie-exposed sheep. The sPMCA method involves incubating a small amount of abnormal prion with an excess of normal prion protein, so that some conversion takes place. The growing chain of misfolded protein is then blasted with ultrasound, breaking it down into smaller chains and so rapidly increasing the amount of abnormal protein available to cause conversions. By repeating the cycle, the mass of normal protein is rapidly changed into misfolded prion.

Since scrapie is not transmissible to humans, these findings do not indicate the likely introduction of zoonotic prions from sheep into the human food chain. Nevertheless, the data do indicate caution in the risk assessment associated with such foods. Although it is unknown if analogous shedding of prions into milk occurs with bovine BSE, evidence from previous epidemiological and bioassay studies suggests that such a scenario seems unlikely to cause clinical disease. However, the present report strongly suggests that given the importance of cow’s milk in the human diet the potential presence of low levels of prions within milk warrants further investigation. Analyzing milk samples by sPMCA offers a methodology with clear potential for the identification of clinically sick animals and those with preclinical/subclinical prion disease. Such a non-invasive, live animal assay has the potential to contribute to the epidemiological study, management and control of prion diseases within farmed animals.

Prions are secreted in milk from clinically normal scrapie-exposed sheep. J Virol. Jun 3 2009. doi:10.1128/JVI.00051-09
The potential spread of prion infectivity in secreta is a crucial concern for prion disease transmission. Here, serial protein misfolding cyclic amplification (sPMCA) allowed the detection of prions in milk from clinically-affected animals as well as scrapie-exposed sheep at least 20 months before clinical onset, irrespective of the immunohistochemical detection of protease-resistant PrP(Sc) within lymphoreticular and CNS tissues. These data indicate the secretion of prions within milk during the early stages of disease progression and a role for milk in prion transmission. Furthermore, the application of sPMCA to milk samples offers a non-invasive methodology to detect scrapie during preclinical/subclinical disease.

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The Good, the Bad, and the Deadly

Saturday, May 30th, 2009

Ah, the tasty fruiting bodies of Basidiomycetes! (mushrooms to you ;-) The snag is that some are poisonous. Which ones? Well, that’s the risky bit. Taylor Lockwood is a biologist and photographer whose new DVD, The Good, the Bad, and the Deadly tries to teach you the basics about toxic mushrooms and their edible look-alikes.

Although they are beautiful, there is no simple way of knowing which fungi are safe to eat and which poisonous. Do not experiment with edible fungi, and get expert advice if you are in any doubt. Do not trust visual identification alone, whether from books or websites, as fungi vary tremendously in size, shape, colour and sometimes even in growing habitat.

Why not grow your own?

Related:

You are what you eat – but what are you eating?

Monday, May 25th, 2009

Salad Despite improvements in agricultural practices, leafy greens, tomatoes, salad crops and nuts were among the foods linked to recent outbreaks of gastrointestinal illnesses caused by Escherichia coli O157:H7 and non-typhoidal Salmonella (Human enteric pathogens in produce: un-answered ecological questions with direct implications for food safety. Curr Opin Biotechnol. April 4 2009). Because plants are not traditionally considered as hosts for human enteric pathogens, recent produce-associated outbreaks highlight important deficiencies in our understanding of the ecology of enteric pathogens outside of their human and animal hosts. The ongoing food safety debate focuses on answering the question whether plants are true alternate hosts for Salmonella or E. coli, or whether they are simply matrices where these organisms persist.

In a survey of several farms, up to 43% of produce sampled in the field was positive for Salmonella enterica, and the pathogen was found in the soil, irrigation water and on the hands of agricultural laborers. Following the 2006 E. coli O157:H7 spinach outbreak in the United States, the pathogen was isolated from cattle and feral swine faeces, river sediment, pasture soil, and surface water near the implicated fields. Human enteric pathogens are often recovered from surface water and untreated waste water used for irrigation. These reports establish that enteric pathogens in various environmental reservoirs may lead to food-associated outbreaks. Once deposited in soils, enteric bacteria persist for periods of time that range from a few weeks to several years. In field studies, both E. coli and Salmonella from raw manure were capable of colonizing the root zone and above ground parts of plants, supporting the hypothesis that pre-harvest contamination in the field could be a plausible route of produce contamination.

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For an enteric bacterium, it may make evolutionary sense to colonize vegetative and reproductive parts of plants that are then eaten by animals. If so, then enteric bacteria should have sophisticated, co-evolved mechanisms for getting into plants, spreading and multiplying in edible plant tissues to levels capable of populating guts of their herbivorous hosts. Salmonella enterica and enterovirulent E. coli are able to colonize tissues of plants quite effectively. This suggests that under favorable conditions enterics can exist as epi- or endophytes. If endophytic growth is truly a part of the life cycle of enterics, then this explains why current surface salad crop decontamination procedures may not be very effective. Conversely, if endo- or epiphytic growth is an important part of the life cycle of enterics, then we should be able to uncover evidence of specificity in the bacterial attachment, colonization and avoidance of plant defenses.

Recent laboratory studies identified a few of the genes and mechanisms that enterics use to colonize external surfaces of host plants. It appears that bacterial polymers and aggregative fimbriae were involved in the attachment of E. coli and/or Salmonella to plant seedlings. In their reliance on cellulose for attachment to plant surfaces, enteric pathogens are similar to plant symbiotic and pathogenic bacteria that also use cellulose fibrils to anchor themselves to plant surfaces.

Most plant pathogens and endophytes also produce hemicellulases and pectinases, enzymes that degrade polymers in plant cell walls. Unlike closely related members of the Enterobacteriaceae, Salmonella and E. coli do not seem to produce such enzymes and their genomes do not encode homologs of these enzymes. It is not yet clear whether Salmonella has unknown classes of cell wall degrading enzymes, whether it manages to gain entry and spread in plant tissues without such enzymes by moving intercellularly, or whether it relies on enzymes from the host or from other endophytes or plant pathogens to degrade plant cell walls. Regardless of their route of entry, enteric bacteria that were present inside plant seedlings were found in the intercellular spaces between host cell walls.

Although recent research has established that Salmonella and enterovirulent E. coli are capable of spending at least a part of their life cycle as plant-associated endo- or epiphytes, several important questions about the genetics and physiology of these interactions still need to be answered before plants are designated as true alternate hosts for these bacteria. Because there is evidence of specificity in the interactions of plant genotypes with enterics, defining the genetic basis and molecular markers associated with resistance to enterics may help identify crop cultivars that are less conducive to supporting growth of human pathogens. Further characterization of the attachment to plant surfaces and interactions with the resident microbiota will likely help improve pre- and post-harvest treatments to ensure safety of produce for human consumption.

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