Michelle Obama's 'Let's Move' School Lunch Program Inadvertently Puts Children at Risk
By Michele Simon
The United Fresh Produce Association Foundation says it’s “proud to be a Founding Partner of the Let’s Move Salad Bars to Schools Initiative.” I thought the First Lady should know this trade group is responsible for killing a vital produce testing program that helps keep kids safe from infection.
Dear Mrs. Obama,
I am writing out of deep concern over Let’s Move’s partnerships with the United Fresh Produce Association and the Produce Marketing Association. These two groups have lobbied to kill a vital pathogen testing program. While the Let’s Move Salad Bars to Schools program is to be applauded, its association with these trade groups is not.
You may be unaware of a small produce testing program tucked away at the U.S. Department of Agriculture (USDA) called the Microbiological Data Program (MDP). At a cost of only $4.5 million a year, it’s one of the most efficient and successful uses of taxpayer dollars; and yet, it’s been zeroed out of the 2013 budget. Here is how Food Safety News recently described it:
This “tiny” program was launched in 2001 simply to collect data about fresh produce contamination, but it now regularly sparks produce recalls when participating state labs find pathogens. Perhaps more importantly, the labs upload any positive test results to the Centers for Disease Control’s PulseNet, which helps public health officials link foodborne illness cases to food products. MDP is also the only federal program that tests for non-O157 E. coli strains like the one that caused the deadly, high profile sprout outbreak in Germany last year.
While industry argues that the Food and Drug Administration (FDA) is better suited to the task than USDA, Food Safety News found that leaving the job up to FDA will mean an 80 percent reduction in produce testing. This translates to potential lives being lost. Again, from Food Safety News:
From 2009 to 2012, MDP found Salmonella 100 times, E. coli O157:H7 twice, and Listeria monocytogenes 8 times. Over the same time period, the program sparked 23 Salmonella recalls, 2 E. coli O157:H7 recalls, and 5 Listeria recalls. Of the pathogens the program identified during that time, 39 Salmonella isolates were matched to human illnesses — as were both E. coli O157:H7 and all 8 Listeria isolates.
Industry leaders from United Fresh Produce Association and other major trade associations have repeatedly pushed the government in recent years to get rid of the comprehensive testing program, saying it has cost growers millions in produce recalls and unfairly targeted farmers who aren’t responsible for contaminating the food.
Yes, those pesky recalls of contaminated food that can kill and ruin lives. Mrs, Obama, the produce industry is quite simply putting profits ahead of people.
The Chicago Tribune has also reported how the produce lobby wants to kill MDP. According to United Fresh representative David Gombas, over time the testing program “got twisted and it turned into a regulatory program where they were finding contamination and turning it over to the FDA and causing recalls.”
Finding contamination. Causing recalls. This must stop?
Moreover, in this document outlining the United Fresh Produce Association’s 2012 lobbying agenda, the trade group clearly states its desire to put the final nail in the MDP coffin: “Now that Congress has zeroed out funding for the Microbiological Data Program (MDP), it will be necessary to ensure that USDA sunsets the program and that protocols shift to FDA.”
If all that isn’t enough damning evidence, this disclosure form filed by a lobbying firm (The Russell Group) for United Fresh lists MDP funding in the 2012 Agriculture Appropriations Act as one of the issues the firm lobbied upon late last year. (It wasn’t to save the program.)
While it would be nice if FDA took up the slack, all signs are that it won’t, due to inadequate funding. As the Washington Post reported this week, neither President Obama nor Congress have put the program into the budget or any agriculture spending bills.
Mrs. Obama, I hope you are aware that with their still-developing immune systems, children are especially vulnerable to inflections from foodborne illness. I am sure your desire to get children to eat more fresh produce isn’t just about good nutrition. Don’t you also care that the produce children eat is free of life-threatening bacteria such as E. coli and salmonella? Of course you do. That’s why I am pleading with you to use your connections to the leaders of the fresh produce lobby to demand an explanation for why they are killing this program, and in the process, putting our kids at risk.
Many others are also calling on the federal government to save the program. For example, The New York Times editorial board called MDP “A Tiny Food Program that Matters," explaining:
There is too much at stake. Last fall, for instance, an outbreak of listeria in cantaloupe killed 30 people. Raw alfalfa sprouts, spinach, lettuce and tomatoes have sickened consumers in recent years. Keeping food safe requires consistent monitoring by the federal government. Ending this small program would harm those efforts.
Spinach, lettuce, tomatoes, sprouts, the good stuff school salad bars are made of, and all high-risk produce for potential contamination. Parents shouldn’t have to worry that the salad bars being put into their children’s schools by Let’s Move are tainted with deadly bacteria. Don’t you agree? Wouldn’t it be nice if the funders of Let’s Move Salad Bars to Schools did too?
Please do whatever you can to help save this vital program. Thank you.
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By Jacob L. Steenwyk and Antonis Rokas
From the mythical minotaur to the mule, creatures created from merging two or more distinct organisms – hybrids – have played defining roles in human history and culture. However, not all hybrids are as fantastic as the minotaur or as dependable as the mule; in fact, some of them cause human diseases.
When Looking Through a Microscope Isn’t Close Enough.<p>For the last few years, <a href="http://www.rokaslab.org/" target="_blank">our team at Vanderbilt University</a>, <a href="https://www.researchgate.net/lab/Gustavo-Goldman-Lab" target="_blank">Gustavo Goldman's team at São Paulo University in Brazil</a> and many other collaborators around the world have been collecting samples of fungi from patients infected with different species of <em>Aspergillus</em> molds. One of the species we are particularly interested in is <a href="https://doi.org/10.1006/rwgn.2001.0082" target="_blank"><em>Aspergillus nidulans</em>, a relatively common and generally harmless fungus</a>. Clinical laboratories typically identify the species of <em>Aspergillus</em> causing the infection by examining cultures of the fungi under the microscope. The problem with this approach is that very closely related species of <em>Aspergillus</em> tend to look very similar in their broad morphology or physical appearance when viewing them through a microscope.</p><p>Interested in examining the varying abilities of different <em>A. nidulans</em> strains to cause disease, we decided to analyze their total genetic content, or genomes. What we saw came as a total surprise. We had not collected <em>A. nidulans</em> but <em>Aspergillus latus</em>, a close relative of <em>A. nidulans</em> and, as we were to soon find out, <a href="https://doi.org/10.1016/j.cub.2020.04.071" target="_blank">a hybrid species that evolved through the fusion of the genomes</a> of two other <em>Aspergillus</em> species: <em>Aspergillus spinulosporus</em> and an unknown close relative of <em>Aspergillus quadrilineatus</em>. Thus, we realized not only that these patients harbored infections from an entirely different species than we thought they were, but also that this species was the first ever <em>Aspergillus</em> hybrid known to cause human infections.</p>
Several Different Fungal Hybrids Cause Human Disease.<p>Hybrid fungi that can cause infections in humans are well known to occur in several different lineages of single-celled fungi known as yeasts. Notable examples include multiple different species of <a href="https://doi.org/10.1002/yea.3242" target="_blank">yeast hybrids</a> that cause the human diseases <a href="https://rarediseases.info.nih.gov/diseases/6218/cryptococcosis" target="_blank">cryptococcosis</a> and <a href="https://www.cdc.gov/fungal/diseases/candidiasis/index.html" target="_blank">candidiasis</a>. Although pathogenic yeast hybrids are well known, our discovery that the <em>A. latus</em> pathogen is a hybrid is a first for molds that cause disease in humans.</p>
(Left) Candida yeasts live on parts of the human body. Imbalance of microbes on the body can allow these yeasts, some of which are hybrids, to grow and cause infection. (Right) Cryptococcus yeasts, including ones that are hybrids, can cause life-threatening infections in primarily immunocompromised people. Centers for Disease Control and Prevention<p><a href="https://doi.org/10.1371/journal.ppat.1008315" target="_blank">Why certain <em>Aspergillus</em> species are so deadly</a> while others are harmless remains unknown. This may in part be because <a href="https://doi.org/10.1016/j.fbr.2007.02.007" target="_blank">combinations of traits, rather than individual traits</a>, underlie organisms' ability to cause disease. So why then are hybrids frequently associated with human disease? Hybrids inherit genetic material from both parents, which may result in new combinations of traits. This may make them more similar to one parent in some of their characteristics, reflect both parents in others or may differ from both in the rest. It is precisely this mix and match of traits that hybrids have inherited from their parental species that <a href="https://www.nytimes.com/2010/09/14/science/14creatures.html" target="_blank">facilitates their evolutionary success</a>, including their ability to cause disease.</p>
The Evolutionary Origin of an Aspergillus Hybrid.<p>Multiple evolutionary paths can lead to the emergence of hybrids. One path is through mating, just as the horse and donkey mate to create a mule. Another path is through the merging or fusion of genetic material from cells of different species.</p><p>It is this second path that appears to have been taken by our fungus. <em>A. latus</em> appears to have two of almost everything compared to its parental species: twice the genome size, twice the total number of genes and so on. But unlike other hybrids, which are often sterile like the mule, we found that <em>A. latus</em> is capable of reproducing both asexually and sexually.</p><p>But how distinct were the parents of <em>A. latus</em>? By comparing the parts contributed by each parent in the <em>A. latus</em> genome, we estimate that its parents are approximately 93% genetically similar, which is about as related as we humans are with lemurs. In other words, <em>A. latus</em>, an agent of infectious disease, is the fungal equivalent of a human-lemur hybrid.</p>
How A. Latus Differs From its Parents.<p>Elucidating the identity of closely related fungal pathogens and how they differ from each other in infection-relevant characteristics is a key step toward reducing the burden of fungal disease. For example, we found that <em>A. latus</em> was three times more resistant than <em>A. nidulans</em>, the species it was originally identified as using microscopy-based methods, to one of the most common antifungal drugs, <a href="https://www.drugbank.ca/drugs/DB00520" target="_blank">caspofungin</a>. This result provides a clear example of the potential importance of accurate identification of the <em>Aspergillus</em> pathogen causing an infection.</p><p>We also examined how <em>A. latus</em> and <em>A. nidulans</em> interact with cells from our immune system. We found that immune cells were less efficient at combating <em>A. latus</em> compared to <em>A. nidulans</em>, suggesting the hybrid fungus may be trickier for our immune systems to identify and destroy.</p><p>In the midst of the COVID-19 pandemic, our quest to understand <em>Aspergillus</em> pathogens is becoming more urgent. Growing evidence suggests that <a href="https://doi.org/10.1111/myc.13096" target="_blank">a fraction of COVID-19 patients are also infected with <em>Aspergillus</em>.</a> More worrying is that these <a href="https://doi.org/10.3201/eid2607.201603" target="_blank">secondary <em>Aspergillus</em> infections</a> can worsen the clinical outcomes for those infected with the novel coronavirus. That being said, we stress that little is known about <em>Aspergillus</em> infections in COVID-19 patients due to a lack of systematic testing, and none of the infections identified so far appear to have been caused by hybrids.</p><p>So, when it comes to hybrids, some are fantastic (the minotaur), some are helpful (the mule) and some are dangerous (<em>Aspergillus latus</em>). Understanding more about the biology of <em>Aspergillus latus</em> may help in our understanding of how microbial pathogens arise and how to best prevent and combat their infections.</p>
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