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Imminent on non-O157 STECs?
Posted on September 28, 2010 by Drew Falkenstein
The momentum seems to be bulding for action by the USDA-FSIS on strains
of E. coli that produce shiga-toxins, which cause HUS, other than E.
coli O157:H7, the most notorious strain of the bug. Last week, after
a meeting with Bill Marler, John Munsell (a former meat packer), and
Nancy Donley (who's son died of E. coli after eating a contaminated
hamburger), Dr. Elizabeth Hagen (USDA's newly announted Undersecretary
for Food Safety) signaled FSIS's intention to take decisive action on
non-O157 STECs, which currently are not regulated by the USDA. In a
written statement to the New York Times recently, Dr. Hagen said:
In order to best prevent illnesses and deaths from dangerous E. coli
in beef, our policies need to evolve to address a broader range of these
pathogens, beyond E. coli O157:H7.¡± She added, ¡°Our approach should
ensure that public health and food safety policy keeps pace with the
demonstrated advances in science and data about food-borne illness to
best protect consumers.
Dr. Hagen later echoed her concerns about non-O157 STECs in remarks
at the 2010 National Food Policy Conference on September 23, 2010.
The debate over the regulation of non-O157 STECs centers around several
basic issues. First, the beef industry argues that not only are non-O157
STEC strains not nearly as common as E. coli O157 in beef, they are
just not very common at all. Second, the industry argues that there
does not exist a viable rapid test for the detection of all non-O157
STEC strains. And finally, given the first and second issues, the industry
would argue that a mandatory testing program for non-O157 STECs would
be misdirected, difficult, and too costly.
Nevertheless, we are only one month removed from Cargill's recall of
8,500 pounds of ground beef contaminated by E. coli O26 which caused
at least three illnesses in New York and Maine. Also, the CDC estimates
that "non-O157 STECs (like O26, O45, 0103, O111, O121, and O145)
cause 36,700 illnesses, 1,100 hospitalizations and 30 deaths in America
each year." In speaking about the May E. coli O145 outbreak linked
to romaine lettuce, Patricia M. Griffin, chief of CDC's Enteric Diseases
Epidemiology branch, said it is likely that E. coli O145 [and others
have] caused previous food poisonings but has gone undetected because
only about 5 percent of clinical laboratories are able to detect it.
"The fact that we found it now doesn't mean it wasn't there before,"
she said. "The ability to look for the organism in ill people and
in outbreaks and food has been increasing. We're gradually finding more
of these organisms."
A series of articles by Andrew Schneider on AOLnews this morning make
great reading for any student of this debate. See the three-part series
of articles (1) USDA may be ready to take on the other e coli in your
beef, (2) Food Safety Lawyer William Marler Puts his Money where your
Mouth is, and (3) The "Holy Six" Strains of E. coli that Many
workers trudge into work regardless, study says
By Danielle Koagel
October 04, 2010
A new study suggests consumers may have more to worry about when dining
out than the bill. The restaurant workers¡¯ union, Restaurant Opportunities
Centers United, conducted a study involving more than 4,000 workers;
the majority of whom admitted to working while sick.
Sixty-three percent of restaurant employees said they cooked or served
food while ill during the last 12 months because they needed the money.
Many foodborne illnesses can be spread from person-to-food, with the
potential to sicken hundreds of people. Diseases such as Salmonella,
E. coli and Norovirus can be transmitted from sick food handlers who
don¡¯t wash their hands properly or handle ready-to-eat foods and utensils.
In April, sick food workers at an Illinois Subway restaurant sickened
at least 125 people with Shigella, hospitalizing 13 people.
ROCU argues the study highlights the need for more paid sick days to
protect workers and consumers.
"The main thing that I think I took away from the research was
that when restaurant workers are unhealthy, there's a real potential
for consumers to be unhealthy," ROC Policy Coordinator Jose Oliva
said to The News-Herald. "In the context of this great recession,
we're seeing that employers are pushing workers more and more, and that's
manifested in a lot more workers in restaurants working longer hours
and doing it for less pay. As the study demonstrates, they are without
some basic standards, as well as health insurance."
Other alarming statistics the study found:
-38 percent of workers said they had done something while working that
put their safety at risk.
-36 percent said their kitchens sometimes get so hot that conditions
-Almost half said they had been either cut or burned on the job.
-Almost 90 percent don¡¯t get health insurance through their employers.
Sludge as Fertilizer: Safe?
by Jill Richardson | Oct 04, 2010
Using sewage sludge - one of two end products from any wastewater treatment
plant (the other is effluent) - as fertilizer on food crops is a hotly
debated food safety issue, but only among a very small group of people.
Most likely, the majority of Americans who are even aware of the issue
actually work in the sewage industry.
Despite sludge's relative obscurity, the newly formed Food Rights Network,
founded by John Stauber, former Executive Director of the Center for
Media and Democracy and author of the book "Toxic Sludge is Good
For You," is taking on sewage sludge as its flagship issue. Simply
put, the group says that it is not safe to grow food in sewage sludge.
Why isn't it safe?
Sewage sludge regularly tests positive for a host of heavy metals, flame
retardants, polycyclic aromatic hydrocarbons, pharmaceuticals, phthalates,
dioxins, and a host of other chemicals and organisms. Of the thousands
of contaminants that have been found in sludge, the U.S. government
regulates exactly 10 of them (nine heavy metals and fecal coliform)
if you want to spread the sludge on farm fields growing food crops.
When industry, hospitals, and households send their waste to wastewater
treatment plants, the plants remove as many contaminants as possible
from the water and then discharge the water as effluent. The leftover
solids are sludge.
Sewage sludge is typically treated to remove some--but not all--of the
contaminants. In recent decades, the sludge lobby (yes, there is one)
has rebranded the treated sludge as "biosolids."
Sludge that is applied to farmland--or even golf courses, home gardens,
and, in the past, the White House lawn--comes in two flavors: Class
A Biosolids and Class B Biosolids. The only regulatory difference between
the two is the level of fecal coliform, which is lower in Class A.
Class B Biosolids may be applied only to land where crops fed to animals
are grown. No restrictions apply to Class A Biosolids. You as a home
gardener can even buy these at your local gardening store and grow your
own food in them. Various cities get very creative at "branding"
their sludge, so that gardeners can choose between "Milorganite"
from Milwaukee, "Hou-Actinite" from Houston, or "GroCo"
Often, but not always, the various contaminants are found in sewage
sludge at low levels. What happens to them once the sludge is applied
to the soil is anyone's guess. Some chemicals bind to the soil; others
do not. Some chemicals leach into groundwater; others are insoluble
Some chemicals are taken up by plants--perhaps into the roots only,
or into leaves, or all the way into fruits. Some chemicals break down
into harmless components, others break down into dangerous components,
and others don't break down at all.
Understanding the path that low levels of thousands of chemicals take
in the environment is a daunting task.
Once a contaminant makes its way from sewage sludge to soil, and into
the human food supply, what happens?
Again, it depends.
Some chemicals are stored in the human body, and others pass through
it. Some break down in our digestive system and others don't. And each
person is different, with a different body size, stage of development,
and metabolism. The same chemical may wreak devastating effects if a
pregnant woman eats it but go unnoticed if eaten by a man.
Consider also the interaction between the many contaminants individuals
may be exposed to if they regularly eat food grown in sludge. While
the effects of individual chemicals are often studied, less is known
about the interactions between low levels of large numbers of chemicals.
To provide a more concrete example, take the chemical triclosan. It
has been used for several decades in antibacterial products like soaps,
deodorants and cosmetics. It is also nearly universally found in sewage
sludge. A recently published study found that soybeans planted in soil
containing triclosan took the triclosan up into their beans.
Triclosan is a suspected endocrine disruptor and recent CDC reports
show more than a 40 percent increase in triclosan levels in the urine
of Americans over a recent two-year period. The amount in our bodies
isn't entirely due to sewage sludge; humans can absorb triclosan through
their skin and those who use triclosan-containing toothpastes put the
chemical directly into their mouths.
Scientists are also finding that triclosan breaks down into dioxins
in the environment.
A more extreme example of sewage sludge posing health risks
Andy McElmurray was a Georgia dairy farmer who accepted sewage sludge
to fertilize his fields where he grew food for his cows over many years.
As the years went by, he noticed that his land was becoming more and
more acidic. McElmurray applied lime to raise the pH of his soil. Soon
after he did so, his cows became sick.
After many tests, he traced the cows' illnesses back to the sludge.
The sludge he had applied contained high levels of molybdenum, cadmium,
and thallium. Molybdenum and cadmium are regulated in sewage sludge,
whereas thallium is not.
When McElmurray applied the lime, the contaminants became more bioavailable
to the plants, and the cows ate the plants. His cows suffered from telltale
signs of molybdenum poisoning, and their milk was contaminated with
thallium (a rat poison toxic to humans in small doses).
By the time the cows' illnesses were traced to the sludge, it was too
late to save McElmurray's farm. Worse, both McElmurray and his father
became sick themselves from breathing sewage sludge dusts blowing from
In this case, the Augusta, GA wastewater treatment plant that provided
the sludge fudged its numbers and broke the law, providing McElmurray
with sludge that contained higher levels of heavy metals than allowed.
In the end, however, scientists also found that if the wastewater treatment
plant had followed the law and limited molybdenum to the legal levels,
McElmurray's cows still would have gotten sick.
Given the complexity of the many chemicals found in sewage sludge--and
consider that each wastewater treatment plant's sludge is different
over time and different from another plant's sludge--how could sewage
sludge be regulated in such a way that it is safe to use?
Regulators must consider that humans will be exposed to any contaminant
in sludge in several ways. McElmurray and his father became ill after
inhaling sewage sludge dusts. Gardeners who use sewage sludge as fertilizer
touch the soil directly, and small children may even eat soil. If it
could be done, regulating sewage sludge to guarantee safety and then
following through with those regulations would be infinitely difficult
Currently, sewage sludge is disposed of via landfills and incineration
as well as land application. According to the EPA, about half of all
sewage sludge is applied to land, but it is only applied to about one
percent of the nation's farmland. The likely result is that, if dangers
do lurk in the sludge applied to land, we rarely find out about them.
Most people's chances of eating enough tainted food from farms that
apply sewage sludge as fertilizer to cause an acute reaction are pretty
slim. The chance that anyone who got sick would be able to correctly
trace his or her illness back to the farm and to sewage sludge is even
smaller. However, a lack of easily traceable acute illnesses does not
prove that sewage sludge is safe. Health harm due to exposure to low
levels of toxins over a long period of time is no more acceptable than
acute problems, even if they are less obvious.
As a consumer, the only sure way to avoid food grown in sewage sludge
is to buy organic food (or grow your own). If you are a gardener and
you wish to avoid sewage sludge fertilizers or composts, avoid any product
that says it contains "biosolids." Last, if you wish to keep
sewage sludge from being spread on farm fields near where you live,
you can take action locally to make it illegal in your city or county.
Editor's Note: Jill Richardson has written about sewage sludge for the
Center for Media & Democracy.
variety, maturity influences salmonella response
Aging increases the risk of salmonella contamination in tomatoes. Green
tomatoes resist salmonella more than ripe red ones.
A Univ. of Fla. study found that tomato variety and maturity influence
the way salmonella bacteria respond to the fruit. It may be possible
to reduce fruit susceptibility to contamination during and after harvest
by monitoring ripeness.
The research findings suggest that tomato cultivars may be able to be
bred to have more resistance to contamination. The findings also support
the thinking that contamination isn¡¯t caused solely by hygiene problems
during pinking and handling.
Tomato varieties are being screened to determine which varieties are
most resistant to salmonella contamination. The researchers also plan
to examine filed irrigation and fertilization to determine if they impact
resistance to 14 antimicrobial agents tested
By Lisa M. Keefe on 10/5/2010
Cefotaxime, ciprofloxacin, norfloxacin or levofloxacin are likely to
be effective against salmonella, but ampicillin, cephazolin and amoxicillin-clavulanic
acid may not be, based on the results of new research published in the
Journal of Food Protection.
A researcher from Baysal University in Turkey studied resistance patterns
in salmonella found on 225 meat products (poultry, ground beef and beef
cuts) bought at retail. Of all the specimens collected, 22.2 percent
tested positive for salmonella.
None of the strains exhibited resistance to cefotaxime, ciprofloxacin,
norfloxacin or levofloxacin. The highest resistance rates, on the other
hand, were 64 percent each for ampicillin and cephazolin and 56 percent
for amoxicillin-clavulanic acid. A total of 62 percent of the 50 Salmonella
strains were multiresistant to three or more antimicrobial agents. Furthermore,
32 percent exhibited multiple resistance to four or more antimicrobial
This, despite the fact that none of the isolates exhibited beta-lactamase
Blame hospitals? Or food?
By Maryn McKenna
October 6, 2010 |
People who are interested in infections that are transmitted in hospitals
(umm, ghouls like me) have a special sick relish for Clostridium difficile,
or in its short form, C. diff. C. diff lives in the intestines, part
of a complex population of many bacteria ? you did know there are more
bacteria in your body than there are cells that belong to you, right?
? but it roars out of control if those other bacteria are wiped out
by a course of antibiotics, especially clindamycin. Removing the other
bacteria clears out space for C. diff to reproduce in much greater numbers;
the toxins it produces irritate the lining of the intestine, producing
colitis, and triggering fever, cramps and diarrhea, and in the worst
cases, sepsis. miscarriage and death.
C. diff colitis is one of the most common and serious hospital-acquired
infections because ? if you¡¯re reading this over breakfast, you might
want to stop eating now ? severe diarrhea in a hospital patient who
is confined to a bed and using a bedpan tends to get everywhere. Really,
everywhere: bed linens and bedrails, floors and walls, stethoscopes,
telephones, computer keyboards, and the hands of the healthcare personnel
who operate those devices and then touch another patient.
C. diff persists so spectacularly because in the outside air, it forms
a hard-shelled spore that protects its genetic material from assault
? including from the alcohol in the hand gel that most healthcare workers
use to clean their hands in between patients, and from the stomach acid
of patients who swallow it. (See, I told you to stop eating.) Because
of that, and because it¡¯s such a devastating infection, hospitals toil
incredibly hard at sanitizing to get rid of it.
C. diff colitis is a stubborn and ugly infection. Earlier this summer,
an Illinois man named Ed Corboy Jr. described his mother Joan¡¯s experience
with it to the Infectious Diseases Society of America:
I watched helplessly as [she] grew weaker, more dehydrated, and nearly
died. She was started on intravenous fluids and standard antibiotics
while in the hospital two different times that December. Her blood pressure
dipped dangerously low on many occasions. She had lost almost 55 pounds
in the previous five months, and she was so profoundly exhausted, tired,
and wasting away that it became apparent in early January she might
die from this. She could hardly get to a bedside commode without two
people helping her. Prior to this she was able to walk to her bathroom
with her walker on her own for years.
Starting about 10 years ago, C. diff got dramatically more problematic:
more virulent, more resistant to treatment, and more commonly occurring
in people who would not have been expected to have it ? often, healthy
young people who had not been in hospitals, who seemed to be developing
the illness in the outside world. Two CDC researchers said in 2008:
In the United States, the number of hospital discharges where (C. diff
associated diarrhea, CDAD) was listed as any diagnosis doubled between
2000 and 2003, with a disproportionate increase for persons aged >
64 years. By 2003, regional reports of CDAD outbreaks from hospitals
throughout the US and in Quebec, Canada emerged, describing severe disease
associated with greater numbers of complications, including colectomies,
treatment failures, and deaths. In 2004, the attributable mortality
rate of nosocomial CDAD in Quebec hospitals was 6.9%, compared to 1.5%
among Canadian hospitals in 1997. In the US, death certificate data
suggest mortality rates due to CDAD increased from 5.7 per million population
in 1999 to 23.7 per million in 2004. (Gould, Critical Care, 2008)
The reason for the surge has been understood to be the emergence of
a new, hypervirulent strain of C. diff that produces up to 20 times
more toxin than earlier ones. (C. diff nomenclature will make your brain
hurt, but the strain is generally known as NAP1/027/BI, toxinotype III.)
But increased virulence doesn¡¯t explain the increased incidence, and
the transmission patterns of the new strain have been murky.
An emerging line of inquiry suggests that the transmission patterns
become much more clear if you look in a different place for the bacterium¡¯s
origin: not in hospitals, but in food.
C. diff has been identified in live pigs, cows and chickens. The bacterium
has been found in retail meat in the United States and in Canada (in
three separate studies), and in salad greens in Scotland. And in a paper
published this month, the main authors from those Canada studies establish
that minimum recommended cooking temperatures for ground beef don¡¯t
kill C. diff spores.
(You¡¯re really not eating now, right?)
So, OK: But are the C. diff strains found in animals the same ones that
are causing human disease? The answer turns out to be Yes. Several researchers
have found overlaps, in 2007, 2009 and earlier this year, in a study
with the perfect title: ¡°Innocent bystander or serious threat?¡±.
And in what looks certain to be a provocative presentation, a team of
researchers from Houston is going to present a paper at the annual meeting
of the Infectious Diseases Society of America in a few weeks, titled:
¡°Potential Foodborne Transmission of Clostridium Difficile Infection
In a Hospital Setting.¡± (Uh-oh.)
The case for C. diff as a foodborne illness still isn¡¯t made. In an
excellent paper published last month, L. Hannah Gould and Brandi Limbago
of the CDC go over the findings so far, and detail what evidence and
further research are still needed.
It is reasonable to assume that the general public is and has been often
exposed to low numbers of potentially infectious C. difficile spores.
There is currently limited epidemiologic evidence to support or refute
the hypothesis that C. difficile is transmitted by the foodborne route;
the presence of C. difficile on retail foods suggests but does not prove
that some proportion of infections is acquired this way. The food supply
may thus serve as a source of new strains causing human infections;
alternatively, food could be another constant and normally innocuous
exposure. (Gould, Emerging Infectious Diseases, 2010)
What¡¯s really interesting, though, is that microbiologists aren¡¯t the
only ones noticing this accumulation of evidence. C. diff as a possible
foodborne pathogen caught the attention of foodborne-illness attorney
Bill Marler early last year. If Marler ? the most aggressive and, I
suspect, successful foodborne-injury lawyer on the planet, dating back
to the 1993 Jack-in-the-Box outbreak ? is starting to notice the evidence
tying C. diff outbreaks to food, there might be a lot more attention
paid to this connection fairly soon.
Talk About Feeding Antibiotics to Animals
by Ralph F. Loglisci | Oct 06, 2010
It is time for some straight talk about the risks of using massive amounts
of antibiotics in livestock and poultry. I don't know one infectious
disease expert who would disagree that there are direct links between
antibiotic use in food animals and antibiotic resistance in people.
If you don't believe me just ask Rear Admiral Ali Kahn, Assistant Surgeon
General and Acting Deputy Director for the Center for Disease Control
and Prevention's National Center for Emerging and Zoonotic Infectious
Just this summer, during a hearing before the House Energy and Commerce
Committee, Dr. Kahn testified that, "there is unequivocal evidence
and relationship between [the] use of antibiotics in animals and [the]
transmission of antibiotic-resistant bacteria causing adverse effects
Knowing this, I continue to be frustrated with the fact that Agriculture
Secretary Tom Vilsack does not publically recognize that the industrial
food animal production system is a leading contributor to the increase
of antibiotic resistance in pathogens that infect people and animals.
Earlier this month at a National Cattlemen's Beef Association meeting,
Vilsack reportedly responded to a question about the Preservation of
Antibiotics for Medical Treatment Act (PAMTA) by saying the, "USDA's
public position is, and always has been, that antibiotics need to be
used judiciously, and we believe they already are."
That quote had me scratching my head when I read it in a New York Times
Op-Ed a couple of weeks ago. The Times' editors interpreted the statement
as saying Vilsack believes there is no need to change antibiotic use
policy among food animal producers. That contradicts the positions of
both the FDA and CDC. The Times pointed out that while neither regulatory
agency is doing enough to address the problem both, at least, recognize
that current antibiotic use should change.
U.S. Rep. Louise Slaughter (D-NY) and Sen. Dianne Feinstein (D-CA),
the primary sponsors of PAMTA, which calls for limits on the non-therapeutic
use of certain antibiotics in livestock production, were perplexed with
Secretary Vilsack's comment, too.
They recently requested that Vilsack clarify his stance on the issue.
In a letter, Slaughter and Feinstein wrote, "Media reports suggest
that you may have mischaracterized our legislation and made statements
that run contrary to previous positions taken by Department officials.
We hope that you can provide us with reassurance that your off-the-cuff
remarks were taken out of context, and that you remain committed to
protecting human and animal health."
I called the Secretary's office for a clarification myself. A USDA spokesperson
sent me the following statement:
"USDA believes that antibiotic use should be used judiciously to
slow the development of resistance in animals. USDA believes livestock
producers are good stewards, use antibiotics judiciously, but there
are some bad actors, and continued use can develop resistance. USDA
wants to be a partner with Congress, producers and other federal partners
to address this important issue."
This statement does little to address the issue at hand.
The problem does not lie with a few rogue producers. Rather, there is
an industry standard of feeding livestock and poultry low concentrations
of antibiotics and other antimicrobials, like arsenicals, in their feed
to promote growth. (All of which is approved by the FDA, by the way.)
Considering industry produces more than 10 billion food animals a year
(the majority chicken and hogs) the amount of antibiotics used in food
animals is astronomical.
Case in point, researchers at Johns Hopkins Bloomberg School of Public
Health estimate that the amount of antibiotics North Carolina hog producers
use in their swine feed every year exceeds the total amount of antibiotics
used to treat infections in people nationwide. It is estimated that
as much as 70 percent of the antimicrobial drugs used in the US are
administered to animals not to treat disease, but to purportedly promote
growth or prevent the spread of pathogens among livestock and poultry
living in intensive confinement.
All uses of antibiotics contribute to drug resistance. While human medicine
plays a large role in the antibiotic drug resistance problem, new research
is clearly showing that resistant bugs from food animals are starting
to show up in people more and more.
Johns Hopkins Bloomberg School of Public Health and Hershey Medical
Center researchers recently published a study that confirms other research
indicating that hospitals are no longer the main source of exposure
for methicillin resistant Staphylococcus aureus or MRSA. And researchers
in Europe have published evidence that livestock production is increasingly
becoming a major source for the Super Staph bug.
The reason why PAMTA is focusing on the non-therapeutic use of antibiotics
in animals is that it is contrary to everything we have known for 70
years about preserving these drugs. The amounts of antibiotics used
in animal feeds are low and are not intended to kill bacteria. That
creates a problem first recognized by the inventor of penicillin, Alexander
Fleming, who warned in 1945 that, "the greatest possibility of
evil in self-medication is the use of too small doses so that instead
of clearing up infection, the microbes are educated to resist penicillin."
Many infectious disease experts believe that we may very well be close
to a post-antibiotic era, which could mean a return to a time when a
simple bacterial infection could cause your child, your parents or you
serious health problems or even death.
In their letter to Vilsack, Feinstein and Slaughter tried to clear up
what they call common misperceptions about their legislation:
"The Preservation of Antibiotics for Medical Treatment Act does
not ban the use of antibiotics. And in fact we share your belief banning
all uses of antibiotics would be counterproductive. Instead, the Preservation
of Antibiotics for Medical Treatment Act addresses usage of seven antibiotics
that are critical in human medicine, phasing them out for non-therapeutic
uses in livestock production."
I respectfully suggest that the common misconception about PAMTA Feinstein
and Slaughter should focus on is the misguided belief by many people
that their bill would ban the use of antibiotics to treat sick food
animals. The legislation allows veterinarians to authorize proper use
of antibiotics to treat or prevent disease.
While I support the proposed legislation to limit antibiotic use in
food animals, I have continually made it clear that the current language
in PAMTA should be stronger. I believe the concession to focus only
on the so-called "seven antibiotics that are critical in human
medicine" weakens the bill. If we are going to be up front with
the public, we must make it clear that bacteria don't differentiate
between types of antibiotics, whether they are approved for human medicine
Dr. Ellen Silbergeld, professor of environmental health sciences at
the Johns Hopkins Bloomberg School of Public Health, recently testified
before Pennsylvania's state Legislature regarding its own proposed legislation
to limit antibiotic use in food animals. She warned that, "bacteria
respond to chemical structures, not brand names, and resistance to one
member of a pharmaceutical class results in cross resistance to all
other members of the same class."
For example, she noted that resistance in Campylobacter (a nasty bug
that the USDA says is the second most frequently reported cause for
foodborne illness) to the antibiotic enrofloxacin (an antibiotic approved
for pets and other domestic animals, commonly called Baytril) results
in resistance to the very important human therapeutic antibiotic ciprofloxacin.
Both antibiotics are two of more than 30 variations of the fluroquinolone
class of antibiotics. As Silbergeld explains, when bacteria develop
resistance to one member of that class of antibiotics, they can be resistant
Authors made certain that language in PAMTA would ensure that any "derivative
of a drug that is used in humans or intended for use in humans to treat
or prevent disease or infection caused by microorganisms" would
be banned from being used as a growth promoter in food animals. But--and
this is a big "but"--the bill does not address the fact that
the use of any antibiotic can lead to a pool of resistance that can
affect every antibiotic class--important to both human and animal medicine.
Silbergeld has long warned that antibiotic resistant bacteria can share
the genes (bits of DNA) that code for resistance with other bacteria
in the environment and therefore readily transfer antibiotic resistance.
Sharing genes between bacteria is almost as easy for these organisms
as forwarding an email to a friend; only bacteria are exchanging genetic
code information. Resistance genes for multiple classes of antibiotics
can be shared in the same "email," or what scientists call
For instance, some isolates of Salmonella and Campylobacter have been
found to have taken up a "cassette" of resistance genes that
protect them from as many as 17 different antibiotic drugs.
What this means is that not only can bacteria share resistance genes
within the same class of antibiotics such as the fluoroquinolines class
antibiotics containing enrofloxacin (restricted for veterinary use)
and ciprofloxacin (critical to human medicine), but also bacteria have
the capability of exchanging resistance genes between different classes
of antibiotics like we've seen in Salmonella and Campylobacter.
Allowing the non-therapeutic use of any antibiotic in food animals,
regardless of whether it is defined as important to human medicine or
not, could still lead to the development of bacteria that are resistant
to an antibiotic that you and I may one day depend on.
The concept behind PAMTA is an important one. We must stop wasting one
of medicine's most important lifesaving discoveries simply as a way
to increase the growth of food animals and subsequently profit for the
food industry. If PAMTA is not passed this year I hope that the next
version would follow more closely the recommendations from the Pew Commission
on Industrial Farm Animal Production's final report, which calls for
"the phasing out and then banning the non-therapeutic use of [ALL]
antimicrobials in food animal production."
Fish: Making Sure They¡¯re Always Safe To Eat
Popular fish like salmon, catfish, and tilapia are coming under the
close scrutiny of Agricultural Research Service food-safety scientists
Andy Hwang and Kathleen Rajkowski. They¡¯re discovering more about how
to prevent foodborne pathogens from contaminating these and other delicious,
good-for-you seafood. Both scientists are based at the ARS Eastern Regional
Research Center in Wyndmoor, Pennsylvania.
Hwang, a food technologist, has completed a series of studies in which
he¡¯s simulated?in his laboratory?commercial processes used today for
preparing smoked salmon. A gourmet treat, smoked salmon is typically
sold in vacuum packages that have a refrigerator shelf life of about
3 to 8 weeks, according to Hwang. Trouble is, pathogenic microbes like
Listeria monocytogenes can live at refrigerated temperatures, so it¡¯s
important to get rid of these harmful microbes before the product leaves
the processing plant.
Smoked salmon, pricey and, when properly prepared, delicate in texture,
is often served in thin slices with bagels and cream cheese or as an
appetizer, stacked on toast-type crackers with red onion and a splash
of lemon juice. Too, some sushi bars feature smoked salmon surrounded
by sticky rice and snugly wrapped in seaweed.
Hwang is looking for ways that processors can protect the pleasing flavor
and texture of smoked salmon while reducing or eliminating contamination
by L. monocytogenes or other foodborne pathogens.
At the Smokehouse
Smoked salmon is typically prepared by using what¡¯s known as ¡°wet brining¡±
or ¡°dry brining¡± to cure the raw fillets before smoking. Fish cured
with a wet brine are soaked in a solution of water, salt, and sugar,
which preserves the fish, helps it retain moisture, and enhances its
flavor. The brine may also include spices or liquid smoke, like the
kind home chefs use for a backyard barbeque.
With dry brining, the salt and other compounds are rubbed on the fillets
and later rinsed off before the fish is smoked.
The smoking process takes place in special smoking ovens in which wood
chips are burned to smoke the cured fillets. Most processors opt for
cold smoking, which uses temperatures of 68¢ªF to 86¢ªF to smoke?but not
cook?the fillets. Cold-smoking takes about 3 to 4 days.
Hot-smoking, a lesser-used option for salmon, uses temperatures of about
140¢ªF and takes about 6 to 10 hours. Hot-smoking cooks the fish, giving
it a different taste and texture than cold-smoked fish.
Many Combinations Tested
In a series of experiments, Hwang and colleagues Shiowshuh Sheen and
Vijay Juneja at Wyndmoor exposed cooked salmon samples, prepared with
various concentrations of salt and smoke compound (from burning wood
chips or liquid smoke), to midrange temperatures?between 104¢ªF and 131¢ªF.
¡°The temperatures were higher than those used for cold-smoking but not
quite as warm as hot-smoking,¡± explains Hwang. ¡°We wanted to provide
a range of alternative smoking temperatures for processors to consider
and to show them the level of Listeria inactivation they might be able
to achieve at various temperatures and various combinations of salt
and smoke compound.¡±
The scientists cooked the fillets for the tests to kill any existing
microbes before inoculating the fish with Listeria. Not surprisingly,
smoking temperature was the single most important factor for inactivating
the microbe. ¡°Every 9¢ªF increase in temperature resulted in a 10-fold
increase in rates of inactivation of the Listeria,¡± Hwang reports.
The researchers used data from the study to create a new, first-of-its-kind
formula, or mathematical model, for food processors and their food-safety
consultants to use in choosing the optimal combination of temperature
and concentrations of salt and smoke compound.
¡°Users can plug into the model the salt concentration, smoke-compound
concentration, and smoking temperature of their choice to predict what
effect this combination may have on Listeria levels,¡± says Hwang. ¡°Salt
and smoke-compound concentrations and smoking temperature affect taste,
texture, and other key qualities of the smoked fish, so processors often
have their own unique combination of these three factors. We constructed
the model to accommodate a wide range of choices.¡±
The team¡¯s 2009 article in the Journal of Food Science has details.
Now, Hwang intends to test these laboratory findings at a smokehouse
and monitor the safety of the smoked salmon as it makes its way through
the distribution chain, from wholesaler to retailer to restaurant or
And as a followup to a preliminary study that he and Sheen described
in another 2009 Journal of Food Science article, Hwang wants to discover
more about the extent to which other microbes?benign or harmful?can
colonize the fillets and help or hinder Listeria¡¯s survival.Powerful
Tactics That Don¡¯t Require Heat
Meanwhile, colleague Rajkowski, a food microbiologist, is determining
how to prevent certain foodborne pathogens from contaminating fish fillets.
She¡¯s using tilapia and catfish fillets for this research. ¡°Even though
foodborne illnesses are not commonly associated with either of these
fish,¡± says Rajkowski, ¡°we chose them for our research because they
are the two most commonly consumed kinds of fish fillets in the United
Microbes that she¡¯s studying include not only Listeria but also Salmonella,
Shigella, Staphylococcus, Pseudomonas, and Escherichia coli O157:H7.
In one study, Rajkowski is determining the correct cooking times and
temperatures for packaged tilapia fillets. Instructions for cooking
fillets are sometimes based on visual determination?what the fish looks
¡°Instructions might require you to know what the fillet looks like when
it ¡®flakes easily with a fork,¡¯¡± she says. ¡°Not everyone knows what¡¯s
meant by that. We want to provide science-based cooking instructions
that are precise and easier for everyone, even beginning cooks, to follow.¡±
Rajkowski is continuing research on heat-free ways to reduce levels
of harmful microbes. Overheating can easily ruin the taste and texture
In an early experiment with both frozen and thawed tilapia and catfish
fillets, Rajkowski artificially inoculated the fillets with L. monocytogenes
and then determined the amount of ionizing radiation needed to reduce
the pathogen¡¯s population by 90 percent. The dosages required to achieve
that level of safety were nearly the same for both kinds of fish, Rajkowski
found. Published in the Journal of Food Protection in 2008, the study
was the first to identify the dosages needed to effectively reduce Listeria
in these popular fish products. Her results were similar to those that
reduce Listeria in ground beef.
Rajkowski is also testing the effects of ultraviolet (UV) light in combating
another pathogen, Shigella sonnei. Like Listeria, Shigella can cause
gastrointestinal illness. For one investigation, Rajkowski applied a
solution of S. sonnei to the surface of frozen tilapia and then exposed
the samples to UV light. The treatment resulted in a 99-percent reduction
of the pathogen. In contrast, tests with small samples of fresh tilapia
showed that the UV treatment did not kill the pathogen. But exposing
the fillets to pulsating beams of high-intensity UV light reduced the
pathogen by 99 percent. Rajkowski documented the study in 2007 in Ice
Fish that Hwang and Rajkowski are investigating are a good, low-fat
source of high-quality protein. That¡¯s reason enough to make sure these
fish, and others from farm and sea, remain pathogen-free and safe for
us to eat.?By Marcia Wood, Agricultural Research Service Information
This research supports the USDA priority of ensuring food safety and
is part of Food Safety, an ARS national program (#108) described at
Cheng-An (Andy) Hwang and Kathleen Rajkowski are with the USDA-ARS Eastern
Regional Research Center, 600 E. Mermaid Ln., Wyndmoor, PA 19038; (215)
233-6416 (Hwang), (215) 233-6440 (Rajkowski).
"In-Demand Fish: Making Sure They¡¯re Always Safe To Eat" was
published in the October 2010 issue of Agricultural Research magazine.
of E. coli on leafy greens
Posted on October 6, 2010 by Drew Falkenstein
The Journal of Food Protection, Vol. 73, No. 10, 2010 recently published
a study that sought to investigate the fate of E. coli O157:H7 applied
to the surface of lettuce leaves that had either been exposed to insects
that commonly infest leafy greens or that had been injured by physical
The study's tests were complex, involving a variety of methods of applying
the E. coli O157:H7 bacteria (innoculum) to both the abaxial (underside)
and top side of spinach and lettuce leaves, including by mist and droplets,
as well innoculating with differing concentrations of bacteria. The
study also includes interesting discussion on the effect that natural
host (here, lettuce and spinach leaves) defenses against contamination
and bacterial growth, as well as on the mechanisms (aside from mechanical
abrasion or insect damage) by which E. coli O157:H7 can be internalized
into the structure of a lettuce or spinach
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