FDA Warning Letters This Week 2/22/17

warning-letters

The week goes by and new letters come out. Looks like we’ve only got one food letter this week so let’s get into it.

Don’t know what warning letters are? Check out this post for a brief overview of what they are and why FDA sends them out.

WL# 17-PHI-04

CDC Public Health Image library #2287 Credit Elizabeth White (2002)
CDC Public Health Image library #2287 Credit Elizabeth White (2002)

Subject: CGMP/Food/Prepared, Packed or Held Under Insanitary Conditions/Adulterated/L. monocytogenes

Ohhhhh it’s an L. mono letter, always interesting. Already we have to pause for some background.

At the end of 2013, CDC and FDA partnered up to stop foodborne outbreaks of Listeria monocytogenes through the utilization of whole genome sequencing (WGS). This technology used to be effectively impossible 30 years ago, and prohibitively expensive and time consuming even 10 years ago.

What this means is that when L. mono is found in foods or a sick person in the hospital, they can sequence it’s entire genome to determine how closely it might be related to other L. mono cultures found in the network. The network consists of genome databases Pulsenet, GenomeTrakr, and The Listeria Initiative, which are jointly managed by CDC, FDA, and local health departments.

Once L. mono has been found and sequenced, in tandem with a traditional epidemiological investigation (interviews, additional sampling of products and environments, illness reporting), the sequence is compared to those in the database to determine if the strain that was found is “closely related” to others and see if there is a link. This is how the listeria found in the Blue Bell products/plant was traced to 10 illnesses that occurred as early in 2010, even when the listeria in the ice cream wasn’t found until 2015. Across several states and 5 years no firm link was established until WGS sequencing revealed the relationship.

There’s some debate about how transparent CDC is about determining when related isolates are causal, or to what level this data should be considered definitive in the absence of confirmed positives in products. However, FDA is going full steam ahead with using WGS as a new enforcement and Epi tool, and CDC has some good data to support the effect on outbreaks it may have had. Whether that’s because manufacturers are more careful in light of the enforcement activities or because the enforcement activities have prevented outbreaks is unclear. But no matter the end result, it’s a win for public health.

The last bit of debate is as to the extent that L. mono can be considered an adulterant. Here in the U.S. we’ve made the determination that if there is any present in the food, it’s adulterated. This is different from several other countries, including Australia/New Zealand and the UK, which allow a non-zero legal limit if L. mono is not expected to be able to grow in the product over it’s shelf life. There’s debate over that as well.

So back to the warning letter:

FDA’s laboratory analysis of fifty environmental swabs collected on September 12, 2016, confirmed that eighteen of the fifty environmental swabs were positive for L. monocytogenes. Of most importance:

Three positive environmental swabs were collected from the following direct food contact surfaces in your cheese processing room during the production of your RTE cheeses:
  • The top of the cheese slicer
  • The cheese slicer string
  • The inside of a plastic crate used to store finished cheese before packaging
–    The remaining fifteen positive environmental swabs were collected from locations adjacent to food contact surfaces and from non-direct food contact surfaces.
–    One positive sample was collected from your RTE feta cheese

They also found a positive in unpasteurized cheese during the facility visit.

This is a pretty solid connection given they found Listeria in the product itself, especially a post-pasteurization product, and that they found it on product contact surfaces where it could continuously inoculate that pasteurized product.  There are other warning letters that claim the products are adulterated when “we found it in the threshold of your entryway to the plant” that don’t always feel solid, but this one is not one of them.

On September 12, 2016, the lift arm and bowl support brackets of the mixer contained areas which appeared to be rusted and contained rough surfaces. In addition, the beater shaft housing area of the mixer, directly above the bowl support brackets, was observed to contain areas which appeared to be rusted and contain food particulates and/or foreign matter.
Food processing tools like my hand mixer have hard to clean areas that can collect food particles like cookie dough, you’ve got to check those areas every time!

Rust happens, and plants have to do regular walkthroughs and replace what needs to be replaced as it ages. But even with the best of intentions, not everything always gets replaced by the time FDA walks through. This makes it a common violation (do you have any rusty or damaged bowls or pots in your cupboard that you plan to replace soon?). But the food particulates are a good find and an indicator of a less-than-robust sanitation standard. Small, hard-to-clean areas around bolts and inside moving parts like the underside of a kitchen-aid (see picture to left) don’t get properly inspected and cleaned unless you have a dedicated program to seek these areas out.

The floors in the processing room and walk-in cooler were observed to be in disrepair, containing areas where the concrete is cracked, rough, and peeling

This one is also common, as mentioned on this site before, cracked/pitted/porous floors are a potential point where environmental pathogens like listeria and salmonella can hide from getting properly cleaned, waiting to jump back out. It’s also a common finding because refinishing or extensive repair of floors is expensive, normally planned on a long-term basis (maybe the slow season so the plant can close or when the contractor has availability), and because in other manufacturing industries it isn’t always a problem (e.g. machine shops).

We have reviewed your written responses to the Form FDA-483, received October 24, 2016, and December 7, 2016…We will ascertain the adequacy of your corrective actions during our next inspection.

Also as discussed here in the past, this is a good sign that FDA knows this company is taking the findings seriously and making real change. Otherwise they would respond with “this is inadequate” and request additional action or proof of change before closing the letter.

Greater than twenty flies landing on the floor, food processing equipment, food processing utensils, and other food contact surfaces and non-food contact surfaces…Three fly catcher tapes containing multiple flies hanging in different areas of the processing room… Dead flies on the window sills near the batch pasteurizer and three bay sink areas.

Well, they had fly catchers, so they know that flies aren’t supposed to just keep flying around, so there’s that. The manufacturer responded that they would purchase a fly zapper and new tapes, but FDA wasn’t satisfied. With pest control, you’re supposed to keep them out of the building and away from your products. So your interventions need to prevent access (find access points, block holes and unscreened windows, create breezeways and air curtains, etc.), and keep them from getting to products with interventions like ILTs.

Your maintenance of the grounds is inadequate to protect against contamination of food, as required by 21 CFR 110.20(a)… Live chickens and pigs coming within approximately one foot of the main door to the production facility and what appeared to be remnants of dead chickens and goats in close proximity to the production facility…Multiple items within approximately twenty feet of the outside perimeter to your production facility which may constitute an attractant, breeding place, and  harborage areas for pests, including, but not limited to, a chicken coop, an abandoned truck, a small four-wheeled loader, wood paneling, vegetation over six feet tall, and other small items which appear to be refuse.

Yep, sounds like a small farm/dairy. I can just picture it, can’t you? Some animals wandering, tall grass, chicken coop, and a couple old trucks and tractors getting overtaken by weeds

Outside of the animal carcasses (obvious pest and disease attractant), this is FDA throwing a little muscle at this farm to clarify that they need to treat it as a food processing facility and not as just a farm. The letter indicates that the company took action to clean up all of these items, however FDA was unsatisfied because they apparently didn’t send them pictures of the cleaned up areas nor discuss how they would keep livestock from hovering around the entrances of the food plant. FDA again noted that they would confirm the changes made were effective at the next inspection, continuing to show that that the inspection itself and initial 483 response must have gone well and the company is doing the right things post-inspection.

Sounds like this company has some work left to do, and that in this case FDA found some tangible and realistic findings of sanitation and facility problems. It helps that the findings were also supported by the L. mono data to really drive home to the company why they should be doing these things. Always nice when cause and effect tie together with GMP’s to drive positive food safety changes home.

New FDA 483: Euthanasia drug found in canned dog food, misc. facility findings, and questions for FDA

fda-483-footerI would be remiss in the goal of this blog if I didn’t do some digging into the form 483 that was just released by FDA this week following a recall for canned dog food containing Pentobarbital. For information on the products recalled and company involved check out the FDA recalls page and search for the issue. As usual I’ll refrain from writing company and product names on this blog when there isn’t any pending civil or criminal action associated with an event. But that information is readily available for anyone by clicking through the links or performing a simple search.

The 483 is short, just two pages. What the goal of this post will be is to go over each of the observations and try to provide additional information that isn’t included in the document to hopefully provide a complete picture.

All FDA observations began with the heading clarifying which portion of the law (FDCA) the firm violated:

The following observations were found to be adulterated [sic] under the Federal Food, Drug, and Cosmetic Act: A food shall be deemed to be adulterated if it bears or contains any added poisonous or added deleterious substance that is unsafe within the meaning of section 402.

This wouldn’t be FF&F if I didn’t pause here for some definitions. Adulterated is a condition of food by which it cannot be sold in commerce. It includes both reasons of safety as this case demonstrates, but it could also be forms of “economic adulteration”, where something claims to be what it isn’t or has otherwise been robbed of characteristics that the consumer would expect. Like if I were to sell you caviar but it was actually flavored gelatin balls or something.

Poisonous or added deleterious substance is a substance that when added to food “may render it injurious to health; but in case the substance is not an added substance such food shall not be considered adulterated under this clause if the quantity of such substance in such food does not ordinarily render it injurious to health.” (emphasis mine)

FDA says two things there. First, don’t add anything poisonous to food (Protip). Second, if the food happens to contain something poisonous naturally, you need to make sure it occurs at a level where it isn’t toxic. This is the often cited”dose makes poison” principal. An example would be that I can’t sell food into which I accidentally spilled some cyanide (whoops) no matter how much or little it was, but I can sell fruits that may have trace amounts of cyanide precursors in the seeds, because it’s not expected to cause an issue in both the actual dose of the seeds and the expectation that people will avoid them when eating. This clarification is actually pretty critical as we try to make sense of past FDA guidance in this case and why the food was adulterated.

So, how did these dog food products cause themselves to be adulterated?

Your low-acid canned dog food product…was found by chemical analysis to contain the barbiturate drug pentobarbital.

By Harbin (Own work) [Public domain], via Wikimedia Commons
By Harbin (Own work) [Public domain], via Wikimedia Commons
Pentobarbital is a sedative that in the form sodium pentobarbital is used as a euthanasia drug. This recall/483 event was initiated when 5 dogs became sick and one subsequently died. Several new updates have occurred since then and I encourage you to follow the story on a site like food safety news.

Here’s the thing about this finding, it’s annoying that the 483 made no mention of the dose that was recovered. This is important because FDA did a study on pentobarbital in dog food in 2002. In that study, the samples (not randomized/representative, convenience samples selected for likely positives) tested positive for the presence of pentobarbital in more or less than 50% of the samples. However, in the same study FDA made a determination of dose that caused adverse effects:

Based on the data from this study, CVM scientists were able to determine that the no-observable-effect level – which is the highest dose at which no effects of treatment were found – for pentobarbital was 50 micrograms of pentobarbital per day

Dogs would have to consume 5-10 micrograms of pentobarbitol per Kg body weight to hit that dose. The highest value FDA found in their samples was 32ppb (32 micrograms per Kg of food). This means that 7 Kg (15.4 lb) dog would need to eat between 35-70 micrograms to reach the minimum dose, which would have been a little over 1Kg of the highest testing food. Pet food isn’t very dense (canned pet food is denser but contains more water that dilutes other ingredients) and 2.2 lbs of it is a lot of food for a 7Kg dog. Therefore FDA concluded:

the results of the assessment led CVM to conclude that it is highly unlikely a dog consuming dry dog food will experience any adverse effects from exposures to the low levels of pentobarbital found in CVM’s dog food surveys

Which means that FDA concluded that the mere presence of pentobarbital does not make the product adulterated because “the quantity of such substance in such food does not ordinarily render it injurious to health” per the FDA study.

Now, because there is report of adverse events and an Oregon State College of Veterinary Medicine report out there showing that the levels in this food were high enough to cause an effect, this food is clearly adulterated. But it seems like FDA should have included a note about the concentration of the drug found in the food in this 483 to clarify why it was legally adulterated, given the past study.

Now for the findings not related to the chemistry analysis and recall:

Condensate dripped throughout your processing facility from the building…including condensate dripping directly into open cans of the in-process low-acid canned dog food product…and also into multiple open totes of raw meats including beef intended for your canned dog food product

steam-hood
Example: steam hood over my stove that I apparently need to clean…gross.

Condensate is found wherever foods are heated and cooled, and FDA has been addressing it more and more. Condensate was noted in the Blue Bell 483’s as well. The logic is that while steam or vapor may be clean, once it collects on a surface like the ceiling or whatever else, it can carry bacteria from these “non product contact” areas back onto your food. Think of it this way, would you lick the underside of the steam hood/vent above the stove if you hadn’t just cleaned it? Now imagine that the steam from your stroganoff was condensing on the underside of the hood and dripping back into it, carrying all that old grease and dust. Yum.

The floors throughout your processing facility are pitted, cracked, and otherwise damaged causing pooled water in areas where food is exposed including where open cans of…dog food are staged

pitted-concrete
Source: my patio.

Uncleanable floors = environmental pathogens. While they didn’t go on a “swab-a-thon” in this facility (yet), uncleanable floors are essentially considered harborage points for things like Listeria and Salmonella. In any other business than food, pitted floors aren’t normally an issue, which makes it a common finding in plants holding themselves to a manufacturing efficiency standard rather than a “food grade” standard.

Additional sanitary conditions observed…include peeling paint and mold on walls throughout the processing facility including in areas where food is exposed, a live fly-like insect in the …hand-packing area during processing, and an open sanitary sewer within approximately 25 feet of two food storage trailers and one food processing trailer at the rear exterior of the facility.

Really just shows a lack of preventative maintenance and facility investement when there wasn’t a clear ROI. This particular company has been in business for a long time in the same location, so it’s possible they themselves put that old coat of paint in years ago to spiff it up and make it look nice and be good for food. These kinds of things are expensive preventative maintenance tasks (mold removal, repainting) because it causes downtime as well as the expense of the repair. Typically FDA will show discretion depending on risk to product (e.g. if you only have closed containers in a room with old paint), but the inspectors here probably determined that this was facility neglect and should be noted. Same thing happens in restaurants and retail establishments where facilities have aged but there’s been no spiffing up.

You lack operating refrigerated storage facilities or other means of controlling the temperature exposure of raw meats during thawing, storage, and processing.

Ding, ding, ding! We have a winner, here’s where we demonstrate the true lack of food safety commitment/appreciation at this facility. The last findings all relate to proper temperature control:

…raw beef and other meats in various stages of thawing were stored in ambient temperature inside your processing facility and also at abmient temperature inside three trailers…the exterior ambient temperatures were below freezing…there was frozen ice containing a blood-like substance across the floors of the three trailers and also on the ground…

Open cans of beef were staged on a pallet at ambient temperature during the hand packing process [from the start of operations until 2:00 PM]

So here’s what the deal is with food safety here. This product is going to be retorted, which means that as a low-acid product, it’s going to be cooked until it’s commercially sterile.

So, in theory, it doesn’t matter if your raw meat doesn’t stay refrigerated, since you’ll kill anything that might grow on it! Heck, you can pack it in a dirty facility with dirty tools if you wanted to…

That was sarcasm.

Processors who think like this fail to understand how cooking and kill steps work, and don’t have respect for your food at all stages of production.

FDA expects the thermal process for low-acid foods to provide a minimum of a 5 or 7-log reduction for spores and pertinent pathogens. What this means is that the process should destroy a minimum 99.999% of spores/bacteria in the product, or alternatively, it would sterilize meat that contained 10,000 spores/gram (bacteria are easier to kill than spores, and would have a much higher log reduction with the same process).

This would work for most “raw” products used in this process. However, if you don’t refrigerate or otherwise control raw meat to keep it out of the danger zone of 40-140ºF, bacteria will start to grow. And with the average piece of beef trim having anywhere from 100 to 100,000 bacteria/gram, if these bacteria are allowed to multiply to the ten-millions from lack of refrigeration suddenly that 5-log reduction doesn’t work anymore!

99.999% of 10,000,000=100

While 100 un-killed spores may not seem like much, one of them could be C. botulinum, and with a shelf life of years in a can of dog food, it only has time to grow.

Take this home: every cook or “kill” step in food processing has a log-reduction value. So while you can technically cook spoiled meat until all the bacteria are dead, you have no way of knowing (without testing) that your standard procedure of cook until 165ºf will work if the number of bacteria are 100 fold higher than what the cook was intended for.

If you still think you can throw away your refrigerator and just cook everything through, I recommend purchasing an autoclave to really sock-it-to-em. Don’t think what comes out will be very tasty though. Oh, and general autoclave parameters will give you a 12-log reduction. Happy cooking.

While this is a significant finding, it isn’t related to the issue causing the current recall (and subsequent enforcement). The issue with the product had to do with pentobarbital in the food, which is a supplier sourcing issue (pentobarbital didn’t make it’s way in at the plant unless it was a malicious act). This plant has had a poor history with supplier approval (sourcing duck that wasn’t actually duck for example), and also has a history of being ignored by the FDA based on inspection history.

What this warning letter serves to do is show that FDA is doing it’s job (or backtracking to do so) enforcing all the regs at this plant regardless of the specifics of the current problem. But I have a lingering problem with this timeline:

12/31/17: Dogs become sick after eating the implicated food.

1/3/17: Oregon State University receives the samples for autopsy and analysis, report indicates FDA was informed.

1/10/17: FDA shows up at the plant to perform inspection that led to the facility 483 findings

1/17/17: Michigan State University confirms Pentobarbital contamination

2/1-2/2/17: FDA continues inspection according to the 483, no new findings noted from the later dates

2/3/17: Recall initiated, presumably this was a result of the meeting with FDA from the previous two days where they informed them of the results and helped identify the scope of the recall and “recommended” a “voluntary” recall.

2/8/17: FDA continues inspection according to the 483, no new findings noted from later dates.

2/17/17: FDA releases their own independent press release through CVM updates

This facility had multiple problems in 2011 and 2012 that led to FDA action, and FDA had last interacted with them (according to the inspections database, which does not include contracted inspections through the state) on 2/28/13.

Did FDA inspect a facility, find problems, and then decide not to go back for 4 years? And from this timeline above, did they only go back to this facility because they had a potential poisoning related to it on file?

Thorough and rapid response to a crisis FDA, good job! But shouldn’t you have been inspecting a known problem facility to prevent problems like this from happening?

After all, in 2011, you said this:

The FDA Food Safety Modernization Act (FSMA), signed into law by President Obama on Jan. 4, enables FDA to better protect public health by strengthening the food safety system. It enables FDA to focus more on preventing food safety problems rather than relying primarily on reacting to problems after they occur.

We can’t say whether increased visits from FDA (which should have been every 3 years at minimum) would have prevented this from happening. But it certainly couldn’t have hurt.

Anatomy of a “Serving”

NFPIs it how much you’re expected to eat? How much you should eat? Pardon me, but if I want to eat an entire bag of potato chips, that’s exactly what I’m going to do.

I say this as the guy who helps create nutrition facts panels for food products for a living. I have read, reread, proof read, and colored red hundreds of these little tables in my time, and believe it or not, people aren’t lining up at parties to hear my thrilling stories.

I know!

Right now you’re thinking, “But Austin, I remember back in 2008 the FDA called 2,584 adults from the US to ask them questions about their diet. And 24% of the respondents said they had no idea if serving sizes were determined by government rules or by manufacturers.”

Your oddly specific observation would be correct, and I should have at least ¼ of the room hovering around me in rapt attention, waiting for me to clarify this confusing point. Time has shown however that everyone is clearly too intimidated to approach and ask the simple questions, even when I’m subtly firing off labeling trivia from the empty cracker box carelessly left by the cheese platter, or establishing my mastery of the dance floor.

Fact: Every party has a dance floor, here’s the label. dance floor Well let’s clear this up right now while I’ve got you at home/work/somewhere, on your computer/phone/tablet (scary that I know where you are, isn’t it?). Who determines serving sizes, manufacturers or the government?

Answer: The government!…ish.

Well that was unsatisfying, but it’s the most accurate answer I can give. Essentially what happens is that our government, via the FDA and FSIS (Food Safety Inspection Service), determine how serving sizes are to be calculated and presented, but also leave manufacturers options in specific situations.

So how are serving sizes determined?

Step 1, what are you eating?

he first step companies need to take when determining serving size is to determine what type of product they are selling. Back in 1993 when they had to decide all of this stuff, FDA determined that they could use data collected in the NHANES dietary surveys conducted in 1978 and 1988 to set these standards. These were nationwide surveys that collected all sorts of data, including nutritional intake and food frequency data. With this information, FDA created “Reference Amounts Customarily Consumed,” or RACC, for different categories of food.

The first step is easy, find the category that a food falls into, and look up the RACC used to determine the serving size in 21 CFR 101.12 (for non-meat items). For example, if I was making mashed potatoes, my category would be “Potatoes and Sweet Potatoes/Yams: Mashed, candied, stuffed, or with sauce” and my RACC would be 140 grams.

Step 2, how can someone measure it out?

Here’s where the variation begins! You might just want to use that 140 grams we saw above; however, not everyone has a scale in their kitchen, and let’s see you try to guess how much mashed potato makes up 140 grams. Can you think of the last time you weighed your food, much less with metric weights (provided you live in the U.S.)?

So at this juncture, the government instructs manufacturers to determine what the closest “common household measurement” to one RACC of your product is. So if we take 140g of our potatoes and see that that’s about 2/3 of a cup, our serving size becomes 2/3 of a cup!

>THIS IS IMPORTANT<

Imagine we made a new, super fluffy mashed potato with more butter, and 140 grams of these potatoes actually wind up closer to ¾ of a cup. This means that even though both potato products were based on a RACC of 140g, they might have two completely different serving sizes, and the manufacturer arrived at each using the same government reference amount!

So there you have it, two serving sizes created based on a government standard, but completely different once observed on the store shelf. How could there be even more variation?

Single Serving

Ah, right. For many products, if the entire container contains less or near 200% of the RACC amount, then there are different rules to play by. In most cases, the product will be considered a single serving, but in others, manufacturers have the choice to label them as one or two servings. This is why you see different types of labeling in small containers such as ice cream, muffins, soda, and other “single serving” containers that appear significantly larger than the usual RACC amount.

As eaten, not as sold

Ah, and this is critical. When you ask someone how much cake they eat, they typically don’t respond with, “about 1/3 of a box of cake mix”. RACC values are based on products as they are consumed. However, serving sizes are based on products as they are sold. The reasoning? Because it would be bizarre to buy a bag of flour and see “two slices of bread” for a serving size. This makes more sense for some products than others, but ultimately serving sizes for products that require further preparation are the amount of packaged product it takes to make about 1 RACC of product as eaten. And remember, this must be rounded off at a common household measure!

Final thoughts

As we realize that our beloved nutrition facts panel is now old enough to drink (enforcement began in ’94), we look back and start to wonder if that data from the 70’s and 80’s used to determine RACC values still holds water. I can’t think of anyone who eats ½ cup of ice cream in a sitting, nor leaves the potato chip bag untouched after their first 10-20 chips.

But how about we think about RACC values in a different way. These values were never intended to be an expectation, but simply a way to bring nutrition information into context using consumer data. The thousands of calories in a 20 lb. bag of rice don’t have a lot of context when I eat it one bowl at a time, but that’s also not to say that I’ll never eat an obscene amount of rice in one sitting just because I’m starving.

Instead think of it this way, if these values are simply references to what we customarily consume at a time, we’ve got a great tool on our hands. I wouldn’t expect you to eat only ½ cup of ice cream, but have you noticed that many ice cream scoops happen to portion about ½ cup of ice cream at a time? And while I’ve been known to turn a bag of kettle fried chips into a meal, I still eat them one handful at a time, which just so happens to contain approximately 10-15 chips.

If only some sort of reference was available so that I could tell about how many calories I ate with each handful…

To learn more about how serving sizes are determined for all food products, check out the labeling and nutrition documents on the FDA website, this PowerPoint provided by the FSIS, or the Guide to Federal Food Labeling Requirements for Meat, Poultry, and Egg Products. Check out what consumer opinions of labels are looking like since 2008 in the FDA’s consumer research.

Choinière C. & Lando A. (2008). 2008 Health and Diet Survey, DOI:

ResearchBlogging.org

Conrad J. Choinière, & Amy Lando (2008). 2008 Health and Diet Survey FDA Consumer Behavior Research Foos Safety Surveys (FSS)

Why isn’t the USDA declaring the invisible feces in our meat?

No, that wasn’t a typo. Today I came across this petition for rulemaking to FSIS from the Physicians Committee for Responsible Medicine.

First off: PCRM has some great programs that promote research, animal welfare, and better medicine. The overall merit of their organization cannot be judged by a single program or campaign they have in place.

Now let’s tear this petition apart, because I actually had to check their website to make sure it was real, and not an over-the-top satire from The Onion.

The concern the committee wishes to correct via this petition is thus:

“Inconsistent with its statutory mandate, USDA regularly passes at inspection meat and poultry that is  contaminated with feces. Although USDA implements a “zero tolerance” policy for fecal contamination, this policy applies to visible fecal contamination only. The result is that fecally contaminated meat and poultry products pass inspection as long as the feces on them are not “visible” to the naked eye.

This inspection policy conveys a misleading promise of “wholesomeness.” Feces may contain round worms, hair worms, tape worms, and leftover bits of whatever the animal excreting the feces may have eaten, not to mention the usual fecal components of digestive juices and various chemicals that the animal was in the process of excreting. Americans deserve fair notice that food products deemed “wholesome” by USDA would be deemed disgusting by the average consumer and adulterated under any reasonable reading of federal law.”

Not to quote without context, the petition goes on to list the ways in which non-obvious feces may be introduced to meat product, the most valid being shared scald/chill tanks in processing operations.

Ultimately, the corrections the committee is seeking are removal of the “wholesome” description from USDA inspected meats, begin treating feces as an adulterant, and:

“USDA should amend sections 317.2(l)(2) and 381.125(b)(2)(i) of the Code of Federal Regulations to exclude from the current mandatory label the sentence that reads, “This product was prepared from inspected and passed meat
and/or poultry.” USDA should amend sections 317.2(l)(2), 381.125(b)(2)(i), and 381.125(b)(2)(ii) of Title 9 to include in the mandatory label the following as the second-to-last sentence: “This product may be permeated with feces, which cooking does not remove.”

That’s some pretty heavy language, perfectly stated to play on the fears and squeamishness of your average consumer. However, I see nothing written there about food safety, so the intention of the change is obvious: prevent people from eating meat.

While the about page for PCRM mentions nothing about being proponents of animal rights, the amount of articles devoted to encouraging a purely vegan diet clearly shows that they have an anti-meat agenda. While they correctly advertize the health benefits of vegan foods, a quick search of their website saturates any visitor with the message “meat is bad, and animal agriculture is always cruel”.

The petition shines a light on a group that is ready to intentionally scare and mislead consumers into changing their lifestyle. As part of their justification that feces is everywhere, they cite one of their own studies, “Fecal Contamination in Retail Chicken Products“. In this study, the committee proved that invisible fecal contamination is everywhere by “testing for the presence of feces.”

No such test exists.

What they actually did was test for generic E. coli, which can act as an indicator organism for fecal contamination.  HACCP programs in slaughter facilities use on-line enumeration of E. coli and other coliforms to validate critical control points for just that purpose. But in this case, rather than setting limits and using a statistical rationale to make a conclusion about the level of contamination, it appears that any evidence of the presence of E. coli  led to the determination that the sample was contaminated with feces. Because there are no methods declared, this evidence could be as mundane as RNA fragments from a non-pathogenic strain recovered in an enriched sample.

The study is absolutely meaningless. There is no available data to review in terms of the levels of contamination, no methods listed for how the E. coli was enumerated, and finally no legitimate publication, suggesting that the construction of the study and its conclusions would not have passed peer review.

As part of the rule change, PCRM would like feces to be declared as an adulterant. Generally, USDA inspectors cannot allow adulterated products to enter commerce, adding to the ludicrosity of this proposal. By the PCRM’s definition, all meat products are covered in invisible feces, and the presence of invisible feces should prevent any product from entering commerce. In one swift move, PCRM will ensure that only clean, wholesome meats will be sold, i.e. none.

But have things changed over the years to make eating meat less safe? The PCRM thinks so. I have no data to argue whether or not Americans are cooking less (PCRM also neglected to provide data), and eating more RTE products, but I did think it was funny that when I read this:

“Americans today consume far more meat and poultry than ever before, thereby increasing their potential exposure to fecal contamination in these products”

When the first link I read on their website contained this graph…
http://www.pcrm.org/media/blog/nov2013/youre-in-good-company-with-a-vegan-thanksgiving
http://www.pcrm.org/media/blog/nov2013/youre-in-good-company-with-a-vegan-thanksgiving
Which is it PCRM? Whichever is more convenient for the ad campaign at the time?
(side note: if people indeed are eating out more in restaurants, that would mean they are eating at inspected restaurants where county health inspectors ensure adequate cooking temperatures, rather than at home where people rarely if ever have proper process control)

Finally, the idea that the USDA needs to declare the presence of invisible feces on every product that passes inspection makes no logical sense,  and does nothing but mislead the consumer, not only by implying that the product isn’t safe in general, but that fully cooking the product makes no difference. If it wasn’t obvious by now that this proposed rule change isn’t solely to earn points with vegans, look closely the wording. In order to turn consumers off meat, PCRM would risk undoing years of public education and trust in proper cooking temperatures.

Clearly I took this proposal too literally, but because FSIS will actually have to review the proposal, and PCRM wants to brag about how these changes might occur, I offer one last piece of evidence to support my view that this proposal belongs on a tabloid.
Proposed legends

…one of their proposed inspection marks literally contains a DO NOT EAT symbol.

ResearchBlogging.org

Physicians Committee for Responsible Medicine (2013). Re: Fecal Contamination of Poultry and Meat USDA Petition for Rulemaking

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The poultry microbiome, once again proving that culture-based ecology misleads us all

Shigella penetrating the intestinal wall. Source: cellimagelibrary.org

If the world was enriched and homogenized, we would actually have a very good idea of what the microbiological community within looks like. Fortunately, the world is much more complex than the miniature environments we culture in the lab, and high throughput sequencing (HTS) is allowing us to fully appreciate micro-biodiversity. As new information becomes available, many of our models for microbial communities continue to be challenged by the actual composition of species in natural environments.

In the world of food safety, we rely on these models to set policy on a regulatory level, and to set critical limits down at the production level. Which tests we run on what products depend directly on what organisms (that cause food borne illness or spoilage) are supposed to be found on that type of food. The authors of this study that came out in PLOS ONE this February examined the microbiome associated with poultry products from farm to fork (meaning from clucking chicken to packaged poultry product) using HTS rather than culture/enrichment methods. The results indicate that there is an unappreciated amount of diversity between different stages of the poultry production process, and that we may not acknowledge the presence of some organisms as much as we should.

In the study, samples were taken from multiple steps in the poultry production process: wet and dry litter, fecal samples, fluid from carcasses collected during the cooling process following slaughter, and fluid from raw retail poultry products (legs, wings, and breasts). Other than the retail portion, all of the samples collected were from the same batch of birds from start to finish. The available RNA from viable cells in each sample was amplified and identified as belonging to specific species using a combination of Illumina sequencing and database referencing (blastn and usearch).

From this pile of data, lists of organisms were compiled to compare the ecosystem profile for each point in production.

The numbers refer the the number of unique taxa found in each group

The authors were very surprised by the amount of diversity between the two litter samples (wet and dry) and the fecal sample. They expected to see very similar profiles, as all of the predicted microbes in those groups would be inoculated from contact with fecal material (young chicks have no inherited microflora, and are coprophagous); however, all of the groups’ microbial communities had very little in common. As shown above, of the hundreds of unique species identified, only 52 were actually found at every stage from farm to fork.

In evaluating food safety, several results are of concern. The first was that the authors found significant amounts of Shigella spp., which have traditionally not been associated with poultry products and may not be a part of many sanitation programs. The second is that in one of their dry litter samples, the authors found a large amount of C. jejuni. It’s presence was interesting as previous studies have found it difficult to cultivate C. jejuni onto dry litter, suggesting that it will not grow in that environment. This discovery further shows that our attempts to cultivate bacteria are not indicative of their behavior in “the wild”. There may be nutrient gradients or a symbiont in play that allows C. jejuni to grow; therefore the possible contamination of dry litter has to be acknowledged in that facility’s Campylobacter monitoring program.

The last point of interest I’ll discuss here is the large amount of unique species that were found in samples following slaughter. This suggests that these species did not come from the farm, but rather were introduced during slaughter and processing. Interestingly, among Campylobacter spp., there was little to no abundance of C. jejuni in the samples, but differing amounts of other Campylobacter spp. This is revealing, as we have been predisposed to expect C. jejuni to be present due to our use of selective media.

Let’s fully appreciate the amount of diversity found within the processing facility, the authors collected two post-processing samples labeled carcass rinse and carcass weep. The rinse was composed of fluid shaken off of the carcass following its removal from the chlorinated chill tanks, and the weep was the drippings from the same carcass 48 hours later. 2/3 of the unique species found the weep samples were not found in the rinse. The authors interpret this as being due to the fact that the sterilization of carcasses is not the goal of poultry processing, and provide the example that viable Salmonella can be recovered from carcasses even after they are sent through the standard antimicrobial processes. The goal is to reduce enumeration, not sterilization.

Finally, in examining the retail samples, we get what we expect. Similar organisms as the weep, with some new faces, presumably because they persisted through processing at undetectable levels, and slowly grew as the product was stored in refrigeration.

The authors conclude by examining some potential symbionts that would allow C. jejuni to persist, but ultimately say that due to the high number of environments C. jejuni can occupy, attempting to exclude it in a universal way will not be very effective.

So all in all, a thorough example of the misdirection we receive from culture bias, and a startling look at how, given enough incubation time, properly processed meat can still support a huge amount of microbial diversity, including many food borne pathogens.

Appreciate this diversity, and make sure you cook your chicken to temperature.

 

ResearchBlogging.org

Oakley BB, Morales CA, Line J, Berrang ME, Meinersmann RJ, Tillman GE, Wise MG, Siragusa GR, Hiett KL, & Seal BS (2013). The Poultry-Associated Microbiome: Network Analysis and Farm-to-Fork Characterizations. PloS one, 8 (2) PMID: 23468931

“Organizational silos,” and how they prevent effective zoonotic disease tracking

It appears that the agencies that we rely on to track disease outbreaks need to start tracking disease, not just their own jurisdiction.

An article in Sociology of Health and Illness piqued my interest this last week that reveals the amount of segregation different government agencies have when dealing with zoonotic disease. The understanding of the goals and connections between livestock, wildlife, and human health among these agencies are often apathetic at best, and antagonistic at worst.

The author of the article took it upon himself to interview several government agencies with different species and regional jurisdictions, and was able to reveal what he calls “organizational silos” that develop when the values and cultures of these different agencies prevent them from working with outside groups. When attempting to monitor emerging infectious disease (EID), identification of cross-species movement is critical to predicting and preventing pandemics. Unfortunately, while they may be able to acknowledge the geographical movement of EID’s, many organizations are blinded by their specific oversight of humans or animals.

Copied from the article: Diagram showing the crossover between domestic animals, wildlife, and human EID. Important emergence factors for each circle are listed on the outside.

There are many telling comments contained in his interviews, and I encourage you to read the article to get the whole scope of the problem, but I’ve chosen to list a few of my favorites here:

From the Director of Animal Health Division at a state Department of Agriculture:

“‘We got a positive [flu result] on one of our routine surveillance tests’ of a poultry farm, Spencer complained, and ‘we were required to contact the USDA right away because of the pandemic Asian strain’. Spencer added, ‘It seems a little silly because there was no clinical illness on the property, and the strain came back something pretty common…’ In Spencer’s eyes, it was ‘hard to justify’ reporting the flu strain to the USDA… These days, Spencer said he passes on information about disease events to the state DOH and leaves it to them to tell local health boards. ‘If somebody screws up’, he shrugged, ‘at least we can blame the [Department of Health]’.”

Not an uncommon perspective for many organizations, or even coworkers! Let’s hear from another director at the USDA Animal and Plant Health Inspection Service (APHIS):

 “Clinton argued that the ‘single biggest threat for disease’ comes from ‘wildlife intermingling with domestic livestock’. He told me, ‘You can’t control the birds’ and he rightly pointed out that ducks are flu incubators. If the bird flu – which Clinton called the top priority of his agency – becomes pandemic in humans, he told me, it will come from waterfowl.”

Interesting, I might argue that we have much more interaction with domestic fowl (can’t remember the last time I handled a wild duck), but let’s see what others had to say about this viewpoint.

“Nina Marano, a zoonotic disease expert at the CDC, told me that ‘most of the outbreaks have occurred through interaction with domestic poultry’. Another example: though poultry farmers singled out wild birds called cattle egrets as the source of a 2004 flu outbreak in California, the egrets tested negative – it turned out that contaminated egg containers circulating between farms were the culprit (McNeil 2004).”

Finally, one last example of how a zoonotic disease often isn’t treated as such by human health agencies. From a Director of the Infectious Disease Bureau of a city Public Health Commission:

“When I asked Sanders to describe a zoonose that she responded to, she mentioned a recent outbreak of salmonella…and she believed that the pathogen came from two live poultry markets in Chinatown. What I found telling was that, in Sanders’ lengthy discussion of this outbreak, she did not mention any communication with veterinary medicine agencies.While the Disease Bureau’s response to salmonella followed protocol, it did not turn to the Department of Agriculture, the USDA, or any other agencies involved in animal health for help or information. Nor did it share information with them.”

Clearly here the city health board considered this a food safety issue, but payed no attention to the implications of getting meat from an approved source (a domain which definitely belongs to the USDA), or the fact that other agriculture agencies may be interested in a salmonella outbreak. There are many other telling quotes within these interviews, and I again encourage you to check out the article.

The author of the study concludes that the only examples we get of harmonious collaboration are for those diseases which are in the public eye such as rabies and influenza (H5N1 and H1N1), though we still have lines drawn even when the public is asking for action (“‘we have enough H1N1 to worry about without worrying about turkeys’. He
concluded that turkey infection is ‘a Department of Agriculture issue’”). The most shining example of the failure to communicate by these institutions in the article is the discovery of Bird Flu in the US.

The first human cases of H5N1 in the US were wrongly diagnosed with St. Louis encephalitis, resulting in the deaths of 3 patients. A veterinary pathologist at the Bronx zoo observed neurological symptoms in some of the zoo’s birds and suspected a link, however encephalitis would not have killed her birds. Both the CDC and local DOH would not accept new information from her, instead keeping the encephalitis diagnosis. She then sent specimens to a friend at an Army Medical Research Institute of Infectious Diseases, who revealed the etiology of the disease and I’m sure had a hilarious conversation with the CDC and DOH (could you please explain to us why this veterinarian is doing your job casually on the side, and doing it better?). By the time the CDC received/accepted this information, H5N1 was endemic in the area.

Nothing against the CDC, it’s a fantastic organization, but this highlights the closed lines of communication that exist between human and animal agencies the author discusses. In order to prevent the next EID crisis, rigorous epidemiology is critical. Refusing to acknowledge the importance of cross-species movement to the virulence and emergence of a disease that falls under your agency does not only prevent you from identifying the next source of infection, but leaves you with nothing but reactive measures catered to a epidemic that you refuse to fully appreciate.

ResearchBlogging.org

Jerolmack, C. (2012). Who’s worried about turkeys? How ‘organisational silos’ impede zoonotic disease surveillance Sociology of Health & Illness DOI: 10.1111/j.1467-9566.2012.01501.x

Staphylococcus aureus diversity and subclinical mastitis

This is the first study I’ve found that was interested in cataloging bacterial diversity among subclinical (or asymptomatic) infections. While they may be less threatening to the animal’s overall health, these infections have great significance in the world of animal agriculture, where they restrict growth (or in this case, milk production), and encourage the use of medicated feeds which in turn motivate people to purchase organic products. Identifying the risk factors and causes of these infections could therefore impact both the management of food animals, and any legislation defining how and when medications can be used. With that in mind, let’s jump back into mastitis, and everyone’s favorite gram-positive, S. aureus.

It’s because of my plasmids, people can’t help but stare.
Image from http://cellimagelibrary.org/

S. aureus is one of many bacteria that cause mastitis, however it is of additional importance as it often causes chronic or recurring cases of mastitis that result in unusable milk and discomfort of the animal. In this study, the authors investigated 11 dairy farms where they expected to find S. aureus, based on previous culture findings at each farm. They defined cows that they took milk samples from as having new or chronic infections based on somatic cell counts (SCC) in the milk. If values were >200,000 cells/mL for the month of collection the infections were considered new, whereas if cell counts were  >200,000 cells/mL for more than 2 months, those infections were considered chronic. They took a single milk sample from each teat of the infected cows, for a total of 1,354 mammary glands from 350 cows.

Pulse field electrophoresis was used to identify the different subspecies/serotypes/pulsotypes (pick your word), and to identify the genes coding for enterotoxin production that had been amplified by PCR. An ELISA test was used last to detect the presence of several enterotoxins.

As the majority of exposure to enterotoxins produced my S. aureus is through milk and dairy products, subclinical infections of S. aureus are very important as a food safety control point. Unlike cows with clinical cases that are removed from production, cows with subclinical infections continue to contribute milk that makes it to the consumer, provided that the SSC is <750,000 cells/mL. The authors were unable to detect a large amount of enterotoxin in their samples, but many of the pulsotypes contained the genes coding for their production. Other studies cited by the author report the common presence of these genes in S. aureus  samples, but expression rates are inconclusive or unexplored. This means that theoretically, subclinical cows could be introducing these bacterial toxins into consumer milk in small amounts.

It’s difficult to tell how significant these amounts might be. Toxic doses of one of the enterotoxins, “Toxic Shock Syndrome Toxin 1”, has been found to be as low as 100 micrograms/Kg in miniature pigs. The concentrations that may be introduced through contaminated milk, and the bioavailability when ingested, should be explored. Takeuchi et al. (1998) were able to detect the presence of TSST- 1 in bulk milk tanks, but no one has yet to quantify the amounts of TSST- 1 potentially present in pasteurized milk.

All that being said, what good is this new information? It can be argued that because these infections are chronic and/or subclinical that these strains of S. aureus aren’t very pathogenic, but they’re still causing inflammation. By identifying common serotypes and factors leading to the subclinical infection of a herd, perhaps there are simple management changes that can prevent infection. Milking is an almost sterile procedure, with sanitation of the teats both prior and following milking, wearing gloves, and forestripping; but there could be other tricks that would target risk factors related to the spread of subclinical pathogens, especially those that are specific to a location.

 

ResearchBlogging.org

Bulanda M, Zaleska M, Mandel L, Talafantova M, Travnicek J, Kunstmann G, Mauff G, Pulverer G, & Heczko PB (1989). Toxicity of staphylococcal toxic shock syndrome toxin 1 for germ-free and conventional piglets. Reviews of infectious diseases, 11 Suppl 1 PMID: 2928643

Oliveira L, Rodrigues AC, Hulland C, & Ruegg PL (2011). Enterotoxin production, enterotoxin gene distribution, and genetic diversity of Staphylococcus aureus recovered from milk of cows with subclinical mastitis. American journal of veterinary research, 72 (10), 1361-8 PMID: 21962279

Takeuchi, S., Ishiguro, K., Ikegami, M., Kaidoh, T., & Hayakawa, Y. (1998). Production of toxic shock syndrome toxin by Staphylococcus aureus isolated from mastitic cow’s milk and farm bulk milk Veterinary Microbiology, 59 (4), 251-258 DOI: 10.1016/S0378-1135(96)01253-9

Banned antibiotics in feather meal – A discussion with an author of the study

Following my recent post where I examined an article from Johns Hopkins that found multiple contaminants in commercial feather meal (including fluoroquinolones, a class of antibiotics that have been banned from use in poultry since 2005), I was honored to be contacted by one of the Authors, Dr. David Love. Dr. Love offered to continue the discussion with me, and was happy to answer my questions regarding the study, the media frenzy it has inspired, and some of the goals of the research conducted at the Center for a Livable Future. I immediately jumped at the chance, and was able to speak with him on the phone earlier this week.

As those who read the post last week have seen, my primary concern with the study was not to do with it’s results or conclusion, but in how the press release was worded. He didn’t feel that it was as misrepresentative as I initially interpreted it, and we quickly moved on discussing just why this article was picked up so quickly.

“I’m not sure how much more clear it could be, we specifically said feather meal, and the title of the study says ‘feather meal, a previously unrecognized route for reentry into the food supply’…I think on the whole we were careful, I don’t think we can come out of this paper with twelve samples and make sweeping generalizations, it’s important to point out that our big recommendation of the study in the last line was that more research should be done…It’s really at the intersection of the media and what they’re interested in, the consumer and what their interests are, and then our story as the authors. Consumers are so interested in what’s going on with their food. We say we did a study on chicken, there’s energy there, and if that’s what they want to talk about, it tells me that we need more transparency in packaging, labeling, and more consumer education. “

I agree, everyone is interested in what they eat, and he makes a great point that we shouldn’t ignore that interest as scientists or producers as it reflects consumer demand. Another point I wanted clarification on was the statement that self-regulation and our current FDA guidelines aren’t sufficient to keep contaminants out of food.

“From the looks of the latest FDA Guidance there’s a lot of strong language, but no teeth in the language. I think for the draft guidance for 213 we’re hopeful, as there will be a larger role for veterinarians in prescribing antibiotics. As for self regulation, I would be more willing to support it if there was more transparency. Many other countries go out of their way to report use, and we in the U.S. have trouble dividing up which antibiotics are used for growth promotion, prophylaxis, and therapy. It would be hard to go about but if we could get that, and reduce or cut growth promotion uses, we would be able to actually measure progress on how we’re reducing antibiotic use in animals.”

He made a very strong point, and following publishing my post last week I came upon  a commentary published by the authors discussing the issue created by unintentional overuse of antibiotics in feed. The article actually provided many of the citations supporting their arguments that I mockingly asked for last week, and I encourage anyone interested to check out the data behind the conclusions. In wrapping up our discussion, I asked where the authors planned to go next with follow-up research.

“A lot of people want to know. Well we found this stuff in feathers, now lets look at meat, at the consumer level with what you buy at the grocery store.”

A logical next step, and one that I’m sure will have even more interest than the findings from feather meal.

Out of our discussion, I discovered a different perspective of the research that I believe was reflected in the discussion, but was completely missed by the media and myself. While the source of the contaminants is obviously a big question, that wasn’t the purpose of the study. The authors were examining feather meal as a route to antibiotic introduction that could have implications in terms of creation of AB-resistant bacteria. Regardless of how it got there (like through contaminated groundwater, as I suggested), a small percentage of chicken producers use it as a feed supplement, thus introducing fluoroquinolones into our food supply through a previously unknown method, and thus not subject to withdrawal times that prevent meat contamination. Further exploration of this research goal will probably concern testing the meat of chickens being fed feather meal for the presence of fluoroquinolones, and seeing if they do allow a sufficient amount to reenter the food supply that may warrant a withdrawal period.

In reflecting on my first post on the subject, I believe that my own response to the press release provided an excellent example of the point I was making. As this case and my interpretation of it reveal, it’s extremely easy to think that your statements were clear and representative of the science at the time, but under outside scrutiny can still be misinterpreted whether in a press release or a blog post. I’m sure I’ll remember this article when I get to publish my first paper, and take a good, hard look at the press release before approving it.

 

 

I want to sincerely thank Dr. David Love for taking the time to speak with me about his research, food safety, and agriculture research in general. I greatly enjoyed our discussion and hope that I get to work with him again. Quotes used in this post are transcribed from my notes I took during our discussion, and are used with his prior review and permission.

If you are still interested in this topic I encourage you to read all you can about it, there’s no end to the depth of the science and social issues involved. I’ve linked to the original article several times, but you can also read the supplementary material here that includes some of the anecdotal evidence in support of the presence of some of the contaminants. You can also read the National Chicken Council’s response to the NY times opinion piece that first made this research so popular. Finally, here’s some research from Chile correlating concentrations of enrofloxacin (a fluoroquinolone)  in feathers with withdrawal times in chickens treated with the drug.

Additional government resources on AB-resistant bacteria statistics and USDA residue testing: FDA NARMS report and USDA Redbook.

Please feel free to leave comments on how you feel about the research, the media presentation, and my own interpretation! I know for a fact all you people from ResearchBlogging.org have opinions, I read them all the time!
ResearchBlogging.org

Love, D., Davis, M., Bassett, A., Gunther, A., & Nachman, K. (2010). Dose Imprecision and Resistance: Free-Choice Medicated Feeds in Industrial Food Animal Production in the United States Environmental Health Perspectives, 119 (3), 279-283 DOI: 10.1289/ehp.1002625

Love, D., Halden, R., Davis, M., & Nachman, K. (2012). Feather Meal: A Previously Unrecognized Route for Reentry into the Food Supply of Multiple Pharmaceuticals and Personal Care Products (PPCPs) Environmental Science & Technology, 46 (7), 3795-3802 DOI: 10.1021/es203970e

San Martín B, Cornejo J, Iragüen D, Hidalgo H, & Anadón A (2007). Depletion study of enrofloxacin and its metabolite ciprofloxacin in edible tissues and feathers of white leghorn hens by liquid chromatography coupled with tandem mass spectrometry. Journal of food protection, 70 (8), 1952-7 PMID: 17803156

Newsworthy: Banned antibiotics found in feather meal at Johns Hopkins – How did they get there, and why does your press release contain different conclusions?

An article recently published in Environmental Science and Technology details a study conducted at Johns Hopkins where when examining samples of commercially available feather meal (used as a protein supplement feed or fertilizer) they found trace amounts of fluoroquinolones, a class of antibiotics that have been banned for use in animal feed for 6 years. This is an interesting find, and definitely warrants further research before any broad sweeping conclusions can be made. You know…unless you publish a press release condemning the entire industry for breaking the law and trying to kill us all (question, if all the chicken consumers are dead, how does that lead to higher profits?).

The article itself is very well done. The authors collected samples of feather meal from several states and Canada and tested them for various pharmaceuticals. They also autoclaved the samples to see how the heating processes involved in creation of the product affected degradation/digestion of any of the compounds, and exposed E. Coli cultures to the meal to see if the presence of one or more of the compounds was enough to select for antibiotic resistant populations (they were).

The researchers examined each of the compounds of interest and proposed mechanisms for their presence. Some of them are used at various levels legally within the industry, and the presence of many others (such as caffeine) can be explained by their introduction through various feedstuffs (such as coffee pulp and green tea powder) (Love et al., 2012).

Obviously of most interest to the researchers were the levels of fluoroquinolones, and they hesitantly proposed possible mechanisms for their introduction into feather meal.

“Fluoroquinolones (enrofloxacin, norofloxacin, or ofloxacin) were detected in 6 of 10 U.S. samples, which was not expected because fluoroquinolone use in U.S. poultry production has been banned since 2005. These findings may suggest that the ban is not being adequately enforced or that other pathways, for example, through use of commodity feed products from livestock industries not covered by the ban, may inadvertently contaminate poultry feed with fluoroquinolones…To better interpret our findings, corroborating evidence in the form of antimicrobial usage practices and dosing amounts would be needed.” (Love et al., 2012)

Clearly we’re not ruling out the possibility of these antibiotics being fed, but there is no cause and effect relationship here. They also make note that feather’s contain antibiotics in higher concentrations than meat or other tissues, even after legally defined withdrawal times to remove them from edible tissue. The conclusions here are justly cautious, and place no blame or accusations upon the industry.

The other interesting find was that the feather meal tested would select for antibiotic resistant strains of E. Coli when exposed to cultures. However, this was only testable with autoclaved samples of the meal. And did we mention that the only samples tested here were sourced from China (who according to the article use many more antibiotics than we do in poultry production)?

“These initial results suggest, but cannot prove, that the inhibiting substance may be an antibiotic/bacteriostatic. Autoclaving may have attenuated the quantity and bioavailability of antimicrobial drugs originally present.” (Love et al., 2012)

Again, a cautious observation and hardly conclusive. Comparisons were made from standard cultures exposed to low levels of relevant antibiotics to see if the same strains were removed, but this data cannot be correctly compared as the feather meal was not controlled enough to isolate those compounds. The authors finish their discussion with an appreciation for the novel information they found and an invitation for others to verify, replicate, and build upon their results.

“We have previously described risks related to administration of medicated feed to food animals, which may promote selection for antimicrobial resistance. The presence of antimicrobials in feather meal, as determined in this study, is a previously unrecognized source of these drugs in animal feed. Because this is the first study of PPCPs in feather meal, we invite independent verification of our results by others. More work is needed to determine whether the detected levels of PPCPs in feather meal have an impact on the quality of food animal products and the safety of consumers.” (Love et al., 2012)

And there we have it, an exciting new study that presents a lot of questions to be used for follow-up research. So we’ll publish it and make sure to put out a press release so that not only those keeping up with the journals can read and understand what we’re currently researching.

Well…it seems like the authors like to be scientific when submitting journal articles, but prefer big headlines and sensationalizing when trying to popularize their research. In their official press release, these researchers quickly turn from cautious scientists to industry whistleblowers.

“The discovery of certain antibiotics in feather meal strongly suggests the continued use of these drugs, despite the ban put in place in 2005 by the FDA…The public health community has long been frustrated with the unwillingness of FDA to effectively address what antibiotics are fed to food animals.” – David Love, PhD

Comments from Keeve Nachman, PhD, show a level of conviction that I had no idea he possessed in the original article.

“In recent years, we’ve seen the rate of fluoroquinolone resistance slow, but not drop…With such a ban, you would expect a decline in resistance to these drugs. The continued use of fluoroquinolones and unintended antibiotic contamination of poultry feed may help explain why high rates of fluoroquinolone-resistant Campylobacter continue to be found on commercial poultry meat products over half a decade after the ban.” (I guess we know for sure they’re still being used in the US, I must have missed that citation in your introduction)

“A high enough concentration was found in one of the samples to select for bacteria that are resistant to drugs important to treat infections in humans” (Note: the concentration comment is true, however, your study stated that there was not controlled enough testing to prove that any specific compound present caused the bacterial selection)

“We strongly believe that the FDA should monitor what drugs are going into animal feed…Based on what we’ve learned, I’m concerned that the new FDA guidance documents, which call for voluntary action from industry, will be ineffectual. By looking into feather meal, and uncovering a drug banned nearly 6 years ago, we have very little confidence that the food animal production industry can be left to regulate itself.”

Wow, this press release from the actual authors of the article must be legit, after all, they wrote it, and they wouldn’t write/act completely differently so as to both dangle a carrot to the media and still get their research published in a peer-reviewed journal right?

I knew the Colonel was lying to me. Source: kfc.com

Well, the press release did its job, and Nachman can be found interviewing left and right about how he was “floored” by the result, and how that the more he learns, “the more [he is] drawn to Organic”. There’s a severe lack of integrity here, and the misrepresentation of your data and analysis to cater to anti-big-Ag sentiments is irresponsible and unethical.

So, future scientific corespondents for the Daily Mail aside, what are some other proposed mechanisms for the presence of these banned antibiotics? After all, I’m suggesting that they aren’t being fed routinely as the authors apparently really believe. Let me rephrase that, I’m not ignoring multiple unproven mechanisms for the purpose of shock science.

I spoke with James Hermes PhD, a professor and Poultry Science Extension Specialist here at Oregon State University, about the article. He had obviously heard of it and shared with me some discussions he had had with his colleagues. Their proposed mechanism for the introduction of the pharmaceuticals was through groundwater.

“Feather meal is boiled at the rendering plant, it’s processed with a lot of water, so anything in the groundwater can end up in the meal…Just recently near [Corvallis] they did some testing and found nearly everything we use at home. For years they told us to flush our excess medications…It’s always been there, we’ve just only recently been able to look at such small concentrations 1 parts per billion, trillion, or even possibly quadrillion.” – James Hermes, PhD

So in addition to whatever chickens could be exposed to via drinking the water and concentrating pollutants in their feathers, additional water and pollutants are introduced during the rendering of the product. He encouraged me to find some research showing that ground water contains any and all of the things discovered in the feather meal, and I found it.

So is this a possible mechanism for the introduction of these contaminants? I suggest the authors of the study follow their own advice in the article and explore this mechanism. Perhaps see if the levels of the pharmaceuticals change in the feathers both prior to and after rendering/boiling, explore if they are present in organically produced feather meal, and find out if there are still large concentrations of fluoroquinolones in the groundwater of the areas processing feather meal. And hey, if they want to keep on trucking with scare tactics, I think finding this stuff in the water supply will be much more frightening to the public given that we can’t buy organic water (don’t start).

Finally, in evaluating consumer exposure to the present antibiotics in feather meal, we should keep in mind the steps necessary in the shortest route to the consumer. First, there have to be high concentrations of antibiotics in feather meal; second, that feather meal must be fed to an animal used for food, third; those antibiotics must be retained and remain active until slaughter of that animal at a high enough concentration; fourth, they have to survive gastric juices and be absorbed into the small intestine of the person eating the meat/milk. Nevermind that along the way, the authors of the relevant study note that at any point the vector for the antibiotics is heated most of them will degrade.

Obviously, if the feather meal is used as fertilizer instead of a by product feed, then there are a few more steps that need to take place to get those pollutants onto the plate.

Now if you’ll excuse me, I need to finish this compelling article on how those fat cats selling nautral almond extract are trying to murder me .

 

ResearchBlogging.org
D.C. Love, R.U. Halden, M.F. Davis, & K.E. Nachman (2012). Feather Meal: A Previously Unrecognized Route for Reentry into the Food Supply of Multiple Pharmaceuticals and Personal Care Products (PPCPs) Environmental Science and Technology, 46, 3795-3802

Kolpin, D., Furlong, E., Meyer, M., Thurman, E., Zaugg, S., Barber, L., & Buxton, H. (2002). Pharmaceuticals, Hormones, and Other Organic Wastewater Contaminants in U.S. Streams, 1999−2000: A National Reconnaissance Environmental Science & Technology, 36 (6), 1202-1211 DOI: 10.1021/es011055j

 

 

Update: following this post I had a chance to talk with one of the Authors of the article, read about our discussion here.

Badger culling in the U.K. – step one: cull badgers, step two: …?, step three: profit!

Image from BBC News

A friend of mine thought this would interest me when I last visited him, and I had him send me the links discussing badger culling in the UK to control the spread of bovine tuberculosis (Mycobacterium bovis).  In addition to having an economic impact,  bovine TB also carries a zoonotic concern. I thought I would learn more about the issue, and see what the literature says about the success of the program.

Badger culling has been a part of TB control in the United Kingdom since 1973. Despite this and other programs in place, incidence of TB has only increased during that time. In the thousands of biological and environmental risk factors that have been associated with TB infection risk, Badgers have been identified as an important reservoir and potential vectors for the disease.

The politics surrounding the issue are interesting, and provides a great case example of how public perception can be skewed for certain species. The regular players are all there: the economically invested (in this case, cattle farmers and associated industries), the scientific community, outspoken animal interest groups, a generalized public perception, and the federal government trying to cater to the majority of voters (or campaign contributors, depending on the official and your own opinion). Lets break down these players.

The Economically Invested

On this issue, everyone seems to be on board that bovine TB is a problem in the UK. The ones who really care though are cattle producers, meat and dairy processing companies, and the retail ends associated with those products. When oppositional parties want to discredit this group, we see them described as “big corporations” only concerned about the bottom line. These claims are many times true, as even the small farmer has to maintain a decent profit margin to provide for him or herself. This group tends to be less publicly oppositional, preferring to exercise their strength through advertizing, lobbying, and funding research that can help support their position. Within this issue, I wasn’t able to find any ads produced by organizations in the UK, however, I did find some farmer concerns over the issue. One was the difficulty in getting approved for a badger cull in your area, and the other was the fear of response from activist groups if they did choose to participate in the program. The position of the farm interest groups is that the spread of bovine TB is an animal welfare and economic concern, and that badger culling will be critical in suppression of the disease. Local wildlife can often aid transmission of disease; however, we have also seen blame placed incorrectly on wildlife in other situations.

Animal Interest Groups

There are many groups in the UK that advocate for Animal interests, and they’re pretty much unanimous in the opinion that culling badgers is not an effective or ethical way to combat bovine TB prevalence. However, they do have different techniques in approaching opposition. While many of them strictly condemn the practice and advertize to sway public opinion, one group (with the support of many others), Gloucestershire Wildlife Trust, has been independently vaccinating wild badgers for bovine TB. At this time they haven’t investigated the effectiveness of the vaccine itself, but rather the economical viability of the process. Their results so far have shown that it would cost more than twice as much to vaccinate an entire hectare instead of culling. Typically these same groups in other controversial situations are very politically active.

The General Public

Generally the least informed and (arguably) the most powerful, the majority of public opinion represents the majority of voters and consumers. Regarding badger culling however, most of the general public has been shown in polls to oppose the practice. Agricultural controversies are often represented by government and industry actions that don’t necessarily mirror consumer or public preference, but instead are economically viable. Whether it’s often advocated for or not, above all else the majority of the public wants inexpensive food, and that benefit often outweighs other consumer preferences (though not always). An interesting examination of the public perception of badgers is discussed within this controversy, and this argument can also apply to other similar situations we have seen over the years. BBC explored the role of badgers in popular children’s stories, and related them to other species that receive special protection even if they are not endangered. An example from the states would be our attachment to wild horses as an icon of America, and some of the debates we’ve seen surrounding not only control of wild horses, but within discussions on using horses for food. Kevin Pierce from the article sums this feeling up well:

“It’s an image issue. A lot of farmers like badgers but we also want to control the disease. If your vector spreading TB was a rat, I’m sure that there’d be no problem for farmers in securing a license to take action.”

The Government

Tasked with the burden of trying to please everyone, the federal government often responds to the loudest collective voice along with their own advisers, analysts, and ethics. In this case, we do know that the government has moved forward with culling as they have in the past. Evaluating the motivation behind these decisions is an endless discussion, whether it’s a working system or corrupt is beyond the scope of this post. Feel free to express your opinions on the process in the comments below. The best I hope for is that while looking out for my interests, my officials attempt to remain objective, and speaking of objectivity…

The Scientific Community

I’ve left us for last. The example of objectivity and a lens of evidence to weigh a cost-benefit analysis of the issue not directed by personal interests, concepts of morality, or hidden goals. Or so we would hope. As a realistic scientist who has read a lot of peer-reviewed research, I know that we are never truly objective. All funding comes from somewhere, we interpret our own results, and while we try as hard as we can to be objective, there is no perfect experimental design immune to bias. However, as creator of this site, I obviously hold research in high esteem, so lets look at some of the literature regarding the effectiveness of badger culling in curbing the spread of bovine TB.

According to the sources I found, it appears that badger culling does have a positive effect on the rates of bovine tuberculosis, but strictly within the areas the culling occurs. There’s a beneficial cumulative effect after several years of a culling program (in the reduction of detrimental effects in surrounding areas), but it isn’t necessarily lasting, cost-effective, or repeatable in different situations. The consensus amongst several studies is that localized culling actually increases TB rates in the surrounding areas, due to the displacement of normally local badger populations, and additional factors that we don’t fully understand. Given these effects, there seems to be a general consensus in the literature I viewed that at best badger culling is not a cost effective way to reduce TB transmission, and at worst contributes to the spread of disease.

Culling programs always have fierce opposition from many sources, whether it be culling sea lions to protect Columbia river salmon, culling grey wolves to protect livestock, or culling tame geese that are causing damage to city parks. There are serious concerns from conservationists and animal activists about the effectiveness of such programs that can be well founded, and the controversy surrounding badger culling in the United Kingdom is a clear example  of why these decisions would be more effective if they are backed by empirical research and economic analysis before being presented as a moral dilemma.

ResearchBlogging.org
Donnelly CA, Woodroffe R, Cox DR, Bourne J, Gettinby G, Le Fevre AM, McInerney JP, & Morrison WI (2003). Impact of localized badger culling on tuberculosis incidence in British cattle. Nature, 426 (6968), 834-7 PMID: 14634671
Donnelly CA, Wei G, Johnston WT, Cox DR, Woodroffe R, Bourne FJ, Cheeseman CL, Clifton-Hadley RS, Gettinby G, Gilks P, Jenkins HE, Le Fevre AM, McInerney JP, & Morrison WI (2007). Impacts of widespread badger culling on cattle tuberculosis: concluding analyses from a large-scale field trial. International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases, 11 (4), 300-8 PMID: 17566777
Donnelly CA, Woodroffe R, Cox DR, Bourne FJ, Cheeseman CL, Clifton-Hadley RS, Wei G, Gettinby G, Gilks P, Jenkins H, Johnston WT, Le Fevre AM, McInerney JP, & Morrison WI (2006). Positive and negative effects of widespread badger culling on tuberculosis in cattle. Nature, 439 (7078), 843-6 PMID: 16357869