CDC: Tainted ground beef may be linked to 2 deaths

[flounder]

CLASS I RECALL Congressional and Public Affairs
HEALTH RISK: HIGH Atiya Khan (202) 720-9113
FSIS-RC-059-2009
NEW YORK FIRM RECALLS FRESH GROUND BEEF
PRODUCTS DUE TO POSSIBLE E. COLI O157:H7 CONTAMINATION
WASHINGTON, October 31, 2009 – Fairbank Farms, an Ashville,
NY, establishment, is recalling approximately 545,699 pounds of fresh ground
beef products that may be contaminated with E. coli O157:H7, the U.S.
Department of Agriculture's Food Safety and Inspection Service (FSIS)
announced today.
FSIS became aware of the problem during the course of an
investigation of a cluster of E. coli O157:H7 illnesses. Working with the
Centers for Disease Control and Prevention (CDC) and state health and
agriculture departments, FSIS determined that there is an association between
the fresh ground beef products subject to recall and illnesses in Connecticut,
Maine and Massachusetts. FSIS is continuing to work with the Massachusetts
Department of Public Health, the Connecticut Department of Public Health,
other state health and agriculture departments and the CDC on the
investigation. Anyone with signs or symptoms of foodborne illness should
consult a physician.
The following products are subject to recall:
Trader Joe's
• 1-pound packages of "TRADER JOE'S BUTCHER SHOP FINE
QUALITY MEATS GROUND BEEF 85/15."
• 1-pound packages of "TRADER JOE'S BUTCHER SHOP FINE
QUALITY MEATS GROUND BEEF 80/20."
NOTE: The sell-by dates for the above two products may be October 6 or
7, 2009.
• 1-pound trays of "TRADER JOE'S BUTCHER SHOP FINE
QUALITY MEATS GROUND BEEF PATTIES 96/4 EXTRA
LEAN."
• 1-pound trays of "TRADER JOE'S BUTCHER SHOP FINE
QUALITY MEATS GROUND BEEF PATTIES 85/15."
Price Chopper
• 1- and 2.5-pound trays of "PRICE CHOPPER MEATLOAF &
MEATBALL MIX."
• 1-pound trays of "PRICE CHOPPER EXTRA LEAN GROUND BEEF 96/4."
• 1-pound trays of "PRICE CHOPPER FRESH GROUND BEEF CHUCK FOR CHILI 80% LEAN 20%
FAT."
Lancaster and Wild Harvest
• 1-pound trays of "LANCASTER BRAND 96/4 EXTRA LEAN GROUND BEEF."
• 1- and 2-pound trays of "LANCASTER BRAND 90/10 GROUND BEEF."
• 1-pound trays of "WILD HARVEST NATURAL 85/15 ANGUS GROUND BEEF."
Shaw's
• 1- and 2-pound trays of "SHAW'S FRESH GROUND BEEF 93/7."
• 1-, 2- and 3-pound trays of "SHAW'S FRESH GROUND BEEF 80/20."
• 1- and 3-pound trays of "SHAW'S FRESH GROUND BEEF 75/25."
• 1.3-pound trays of "SHAW'S FRESH GROUND SIRLOIN BEEF PATTIES 90/10."
• 1.3-pound trays of "SHAW'S FRESH GROUND ROUND BEEF PATTIES 85/15."
• 1.3-pound trays of "SHAW'S FRESH GROUND BEEF PATTIES 80/20."
• 3-pound trays of "SHAW'S FRESH GROUND BEEF PATTIES FAMILY PACK 80/20."
• 1-pound trays of "SHAW'S ANGUS GROUND BEEF 85/15."
• 1-, 2- and 3-pound trays of "SHAW'S FRESH GROUND ROUND BEEF 85/15."
• 1-pound trays of "SHAW'S 90% NATURAL GROUND BEEF."
• 1-pound trays of "SHAW'S 85% NATURAL GROUND BEEF."
• 1-, 2- and 3-pound trays of "SHAW'S FRESH GROUND SIRLOIN 90/10."
• 1-pound trays of "MEATLOAF & MEATBALL MIX."
BJ's
• 5-pound trays of "FRESH GROUND BEEF, CONTAINS 15 % FAT" patties.
• 3- and 5-pound trays of "LEAN GROUND BEEF, CONTAINS 7% FAT."
• 2.5-pound trays of "MEATLOAF & MEATBALL MIX."
Ford Brothers
• 3-pound trays of "FRESH GROUND BEEF, CONTAINS 20% FAT" patties.
Giant
• 1-pound trays of "GIANT EXTRA LEAN GROUND BEEF 96/4."
• 1-pound trays of "GIANT MEATLOAF & MEATBALL MIX."
• 1-pound trays of "GIANT NATURE'S PROMISE GROUND BEEF."
• 1-pound trays of "GIANT NATURE'S PROMISE GROUND BEEF PATTIES."
Each package bears the establishment number "EST. 492" inside the USDA mark of inspection or on the
nutrition label. These products were packaged on September 15 and 16, 2009, and may have been labeled at the
retail stores with a sell-by date from September 19 through 28, 2009, unless otherwise noted above. Consumers
should ask at their point of purchase if the products they have are subject to recall. The products were sent to
distribution centers, intended for further distribution to retail establishments in Northeast and Mid-Atlantic
regions. When available, the retail distribution list(s) will be posted on FSIS' Web site at
http://www.fsis.usda.gov/FSIS_Recalls/O ... /index.asp.
Products for further processing:
• Cases of 10-pound "FAIRBANK FARMS FRESH GROUND BEEF CHUBS."
Each case bears the establishment number "EST. 492" inside the USDA mark of inspection; has
package dates of "09.14.09," "09.15.09," or "09.16.09;" and sell-by dates of "10.3.09," "10.4.09," or "10.5.09.
These products were distributed to retail establishments in Maryland, Massachusetts, North Carolina, New
Jersey, New York, Pennsylvania, and Virginia for further processing. However, these products at retail will
likely not bear the package dates and sell-by dates listed above. Customers with concerns should contact their
point of purchase.
E. coli O157:H7 is a potentially deadly bacterium that can cause bloody diarrhea, dehydration, and in
the most severe cases, kidney failure. The very young, seniors and persons with weak immune systems are the
most susceptible to foodborne illness. Individuals concerned about an illness should contact a physician.
FSIS routinely conducts recall effectiveness checks to verify recalling firms notify their customers of the
recall and that steps are taken to make certain that the product is no longer available to consumers.
FSIS advises all consumers to safely prepare their raw meat products, including fresh and frozen, and
only consume ground beef or ground beef patties that have been cooked to a temperature of 160° F. The only
way to be sure ground beef is cooked to a high enough temperature to kill harmful bacteria is to use a food
thermometer to measure the internal temperature.
Media questions regarding the recall should be directed the company's Media Representative, Agnes
Schafer at (866) 460-8017. Consumer questions should be directed to the company's Consumer Hotline at
(877) 546-0122.
Consumers with food safety questions can "Ask Karen," the FSIS virtual representative available
24 hours a day at AskKaren.gov. The toll-free USDA Meat and Poultry Hotline 1-888-MPHotline (1-888-674-
6854) is available in English and Spanish and can be reached from l0 a.m. to 4 p.m. (Eastern Time) Monday
through Friday. Recorded food safety messages are available 24 hours a day.
#
NOTE: Access news releases and other information at FSIS' Web site at http://www.fsis.usda.gov/Fsis_Recalls/
USDA is an equal opportunity provider, employer and lender. To file a complaint of discrimination, write:
USDA, Director, Office of Civil Rights, 1400 Independence Avenue, SW, Washington, DC 20250-9410 or call
(800) 795-3272 (voice), or (202) 720-6382 (TDD).


http://www.fairbankfarms.com/059%20%20N ... 0FINAL.pdf



CDC: Tainted ground beef may be linked to 2 deaths
By BEN DOBBIN (AP) – 19 hours ago



http://www.google.com/hostednews/ap/art ... QD9BNKQ482



Report of the committee Evolutionary Trends of Salmonella enteritidis Linked to Subpopulation Biology and Virulence Attributes a Time Specific Paper was presented by Dr. J. Guard Bouldin, ARS-USDA. The complete text of the presentation is included in these proceedings at the end of this report. Dr. Bouldin reported that Salmonella enterica serovar enteritidis (S. Enteritidis) is currently the world's leading cause of food borne salmonellosis. It is the only serotype out of over 1400 within Salmonella enterica I that contaminates the internal contents of the egg by vertical transmission from the reproductive tract of otherwise healthy hens. Epidemiological studies have shown that this exceptionally invasive pathogen with an unusual tissue tropism has a more clonal population structure than most other broad-host range Salmonella serotypes. Dr. Guard Bouldin presented research findings that showed how this egg tropism is likely to have occurred. FSIS Salmonella initiatives for meat, poultry, and processed egg products presentation was given by Daniel L. Engeljohn, Office of Policy, Program and Employee Development, FSIS. Dr. Engeljohn presented FSIS's mission, its public health performance measures, policies on pathogen control including Salmonella. As the public health regulatory agency in USDA, FSIS is responsible for ensuring that the nation's commercial supply of meat, poultry, and processed egg products are safe, wholesome, and correctly labeled and packaged www.fsis.usda.gov/about_fsis/index.asp. In FY07, FSIS had approximately 7,800 full-time inspectors that visited around 6,200 facilities. Processing establishments receive daily inspection, slaughter establishments receive daily inspection along with every animal afforded a critical inspection before slaughter.

FSIS inspected approximately 44 billion pounds of livestock, 57 billion pounds of poultry, 3.5 billion pounds of liquid egg product, 3.8 billion pounds of product reinspected at the border, and conducted about 8 million inspection procedures. A progress review was presented for the federal Healthy People 2010 program Morbidity and Mortality Weekly Report (MMWR) April 11, 2008; 57(14):366-370

www.cdc.gov/mmwr/preview/mmwrhtml/mm5714a.htm



He described preliminary surveillance data for 2007 and compared them with data for previous years. In 2007, the estimated incidence of infections caused by Campylobacter, Listeria, Shiga toxin-producing Escherichia coli O157 (STEC O157), Salmonella, Shigella, Vibrio, and Yersinia did not change significantly, and Cryptosporidium infections increased compared with 2004--2006. Progress toward the targets for Healthy People 2010 national health objectives and targets regarding the incidence of foodborne infections occurred before 2004; however, none of the targets were reached in 2007. Salmonella incidence was the furthest from its national health target, suggesting that reaching this target will require new approaches.

474

DISCUSSION


Serotyping results are presented for 18,267 Salmonella isolates. This year 44 percent of the isolates were from clinical cases and 56 percent were from monitor samples, compared to 38 percent and 62 percent last year, repectively.1

Of the clinical isolates, 35 percent were of bovine origin and 32 percent were isolated from swine. Thirty-nine percent of the monitor samples were isolated from chickens and 12 percent were recovered from turkeys. A total of 253 serotypes were identified from isolates recovered from animals, their environment, or feed in 40 states and the District of Columbia. The 10 most common serotypes (Table 1) accounted for 58 percent of the total isolates reported. Table 2 lists the 10 most common serotypes by clinical role: those from clinical cases and those from monitor samples. Salmonella Typhimurium, S. Heidelberg, S. Cerro, S. Senftenberg and S. Montevideo are found in both lists. Salmonella Typhimurium was again the most frequently identified serotype from all sources and clinical roles. (Table 1) It was the most common serotype from clinical cases and the third most common serotype from monitor samples (Table 2). Salmonella Typhimurium was among the five most frequently identified serotypes isolated from chickens, swine, horse and dog/cat (Tables 3, 6, 7 and . Fourteen percent of all isolates, 22 percent of isolates from clinical cases, and 8 percent of isolates from monitor samples were identified as S. Typhimurium, compared to 13 percent, 21 percent, and 9 percent, respectively, last year.1 Fifty-one percent of the S. Typhimurium isolates were identified as S. Typhimurium var. Copenhagen this year, compared to 53 percent last year.1 The majority of S. Typhimurium isolates recovered from swine were S. Typhimurium var. Copenhagen (73 percent); whereas 37 percent of isolates of chicken origin were S. Typhimurium var. Copenhagen, and 19 percent of equine origin were S. Typhimurium var. Copenhagen. An untypable serotype 4,5,12:i:- decreased to 164 this year from 262 last year1 and 43 7 in 20062. Sixty-seven of these were isolated from chickens, 20 from cattle, and 25 from horses. This serotype is believed to be S. Typhimurium that has lost the ability to express the phase 2 flagellar antigen. Salmonella Newport was the seventh most frequently identified serotype from all sources (Table 1) and third in clinical cases. (Table 2). It was the fourth most common serotype from clinical cases in cattle (Table 5) and accounted for 6 percent of the isolates of bovine origin. Salmonella salmonella 494 Report of the comite Newport was the second most common serotype from clinical cases in horses (Table 7) and accounted for 5 percent of the isolates of equine origin. Four percent of the total isolates from all sources and all clinical roles were S. Newport, compared with 4 percent last year1, 5 percent in 20062, and 9 percent in 2005.3 The number of Salmonella Enteritidis isolated decreased this year to 551 isolates compared to 774 isolates last year. Fifty-four percent of the isolates were of chicken origin and it was the most frequently identified serotype from chicken clinical cases and the third most common serotype from chicken monitor samples (Table 5). Eleven different phage types were identified among the 329 S. Enteritidis isolates that were phage typed. The most frequently identified phage types were type 8 (54 percent), type 13 (13 percent), and type 23 (11 percent). Two percent were untypable, and 2 percent reacted, but did not conform (RDNC.) Fifteen different phage types were identified among 150 S. Typhimurium isolates that were phage typed. The most common phage types were DT104 and variants (67 percent) and U302 (9 percent). Five percent were untypable and 5 percent reacted, but did not conform.

REFERENCES Morningstar, B.R, et al. 2007. Salmonella Serotypes From Animals and Related Sources Reported During July 2006-June 2007. Proc U.S. Animal Health Assoc.111:633 -635 Morningstar-Flugrad, B.R., et.al. 2006. Salmonella Serotypes From Animals and Related Sources Reported During July 2005-June 2006. Proc U.S. Animal Health Assoc. 110:564-570 Ferris, K.E., et.al. 2005. Salmonella Serotypes From Animals and Related Sources Reported During July 2004- June 2005. Proc U.S. Animal Health Assoc. 109:559-562 Ferris, K.E., et.al. 2004. Salmonella Serotypes From Animals and Related Sources Reported During July 2003- June 2004. Proc U.S. Animal Health Assoc. 108:501-502. Ferris, K.E., et.al. 2003. Salmonella Serotypes From Animals and Related Sources Reported During July 2002- June 2003. Proc U.S. Animal Health Assoc. 107:463-469.

http://www.usaha.org/meetings/2008/2008 ... edings.pdf





TSS

 

[flounder]

Foodborne Pathogens and Disease

The Effects of Transport and Lairage on Counts of Escherichia coli O157 in the Feces and on the Hides of Individual Cattle

--------------------------------------------------------------------------------

To cite this article: Narelle Fegan, Glen Higgs, Lesley L. Duffy, Robert S. Barlow. Foodborne Pathogens and Disease. November 2009, 6(9): 1113-1120. doi:10.1089/fpd.2009.0338.

-------------------------------------------------------------------------------- Published in Volume: 6 Issue 9: November 4, 2009 Online Ahead of Print: July 24, 2009

--------------------------------------------------------------------------------

Full Text: • PDF for printing (4,681.3 KB) • PDF w/ links (155.8 KB)

Narelle Fegan,1 Glen Higgs,2 Lesley L. Duffy,2 and Robert S. Barlow2 1Food Science Australia, CSIRO, Werribee, Victoria, Australia. 2Food Science Australia, CSIRO, Brisbane, Queensland, Australia. Address correspondence to:

Narelle Fegan, Ph.D.

Food Science Australia, CSIRO

671 Sneydes Road

Werribee, Victoria 3030

Australia E-mail: Abstract

Objectives: The main objective of this study was to determine the impact of transport and lairage on the isolation rate and the number of Escherichia coli O157 on cattle.

Materials: Ninety animals, divided into three groups (A, B, and C) of 30 animals each, were used in this study. Individual animals were tagged, and samples were collected from the hides and feces of each at a feedlot and again after slaughter. The carcass of each animal was also sampled. Samples were also collected from the feedlot pens, the sides and floors of the transport trucks, and abattoir holding pens. The isolation rate and the number of E. coli O157 were estimated using a combination of immunomagnetic separation and the Most Probable Number technique.

Results: Cattle hides were more likely to be contaminated with E. coli O157 at the feedlot (31%) than at the abattoir (4%). E. coli O157 was detected in 18% and 12% of cattle feces collected at the feedlot and after slaughter, respectively. E. coli O157 was isolated from truck floors (26%), truck sides (11%), abattoir pen rails (47%), and pen floors (42%). The mean count of E. coli O157 in positive feces was log10 1.17 and 2.37MPN/g at the feedlot and slaughter, respectively. A 3 log10 increase in the number of E. coli O157 was observed between the feedlot (2.66MPN/g) and slaughter (5.66MPN/g) in the feces of one animal in group B. E. coli O157 was isolated from the hide and carcass of this animal.

Conclusions: Transport and lairage did not lead to an increase in the number or isolation rate of E. coli O157 from cattle.

Applications: Intervention strategies for reducing E. coli O157 contamination of cattle carcasses should target mechanisms that limit the impact of animals shedding a high number throughout production and processing.


http://www.liebertonline.com/doi/abs/10 ... istoryKey=



TSS

 

[Oldtimer]

Some more from Munsell

Q&A With 'Meatpacking Maverick' Munsell



by Helena Bottemiller | Nov 16, 2009

Food Safety News - Marler Clark LLP, PS.



John Munsell, dubbed the "meatpacking maverick" by Mother Jones, has spent much of his life on the front lines of food safety.



In 2002, Munsell told the U.S. Department of Agriculture (USDA) that his small meat grinding operation had been receiving E. coli-positive beef from ConAgra's massive plant in Greeley, Colorado and that something needed to be done about it. Instead of launching an investigation into the Greeley plant, the USDA shut down Munsell's business for four months after an agency inspector collected a positive E. coli sample from ground beef produced in his plant.



A few months later, the Greeley plant recalled 19 million pounds of beef after an E. coli outbreak that sickened 45 people in 23 states was tied to its product. Over 80 percent of the recalled meat had already been consumed by the public by the time USDA announced the recall in the Summer of 2002.



Munsell operated his small-scale USDA-inspected meat plant in Montana for 34 years. The business had been in his family for almost six decades when he sold it in 2005 after becoming fed up with USDA politics and 'burdensome' federal regulations.



Food Safety News had a chance to chat with Munsell about the ConAgra outbreak, the current state of meat regulation, and what he thinks should be done to improve food safety.



Q: How did you become a meat regulation activist?



A: It boils down to this... in 2002 we were involved in a recall of about 270 pounds of ground beef that was contaminated with E. coli. That was a result of at test that was collected by the USDA inspector assigned to my plant.



The inspector and I both knew and we stated that the meat that was sampled was from an outside plant--it wasn't my meat. Our plant not only slaughtered animals, but we brought in a lot of meat from the outside. In this particular sample, the inspector and I both stated it was meat purchased from the outside.



At that time, whenever a plant did have a recall, the USDA had to follow it up with 15 subsequent consecutive days of additional sampling. In the midst of that there were three consecutive days in which the samples collected by the inspector turned up positive for E. coli. Both the inspector and we observed that [the meat that tested positive] all came from ConAgra.



Now the battle was on.



The USDA intentionally hung me out to dry. They ignored the fact the bad meat I had had come from an outside plant. So, I had to make some changes to my HACCP plan. I made about 14 changes and they kept turning them down. It was probably unprecedented in the history of American inspection--14 changes all denied.



Finally, what happened is that the ConAgra plant that sold me this meat announced a 19 million pound recall. Well then, all of the sudden, overnight, the USDA accepted my changes and allowed me to grind again--but for four months I was not allowed to grind.



I came to realize real quickly how disingenuous they were. And I realized that if they could pull this off at my plant, obviously they could do it at all small plants across America. Secondly, I came to realize--I had two young grandkids at that time--that the USDA could really care less about the health of my grandkids.



So, when I came to those conclusions, I decided to fight them every inch of the way and to expose problems within the USDA's meat inspection program. I continue working on that to this day.



Q: You called the recent E. coli beef outbreaks out of New England "embarrassing..."



A: I say it's embarassing, because it should be embarassing to the USDA that, in spite of their "science-based" meat inspection program we have all these ongoing outbreaks and recalls. It should also be embarrassing to our industry.



It's been 11 year since the biggest packers implemented the HACCP program. You'd think that by this point the program would be maturing and paying dividends, but in fact it's going the opposite direction.



We've got to finally realize that the consuming pubic are going to see through this--this façade. At times I wonder if the word "embarrassing" is not the right word. The overarching, more important concern is food safety and sick consumers and people who are dying.



People are dying. A lot of people are getting sick, this should be an embarrassment to this industry, and to the USDA.



Q: Have you been keeping up on the media attention on meat safety--in the New York Times, Larry King Live, Time, etc?



A: Yes, I keep up on all that. A great many people read [the New York Times article] and the big players in our industry shot it down.



Unfortunately, Michael Moss hit the nail on the head. We do have ongoing problems. The USDA is not the least bit concerned about going to the root of the problem, and getting the source to clean up their act.



USDA is much more willing to go down to your local Safeway store--which unwillingly inherits previously contaminated meat--the USDA is much more likely to throw its enforcement hammer against the destination of previously contaminated meat instead of going to the source, which is these big multinational packers.



Q: What is the root of the problem--do you think there is a tension at USDA between promoting the industry and protecting the consumer?



A: Have you heard of the term "agency capture"? That's the terminology used to describe the situation in which a government regulatory agency is captured by the very industry that it supposedly regulates. That is precisely what has happened here.



I contend that the agency has been captured by, is controlled by, big packer interests. The revolving door certainly is also detrimental to the cause of public health.



There is a direct conflict between promoting agricultural products and regulating the industry that creates those products.



If indeed a big packer produces some bad meat, the USDA is less likely to take aggressive steps against that big packer. And you know, let's just face it--the big packers get bigger all the time. Probably five years ago it was stated that 80 percent of the feedlot cattle in this country--feedlot fattened steers and heifers--80 percent were slaughtered by the top four companies. Now its 88 percent.



The big get bigger, the small get smaller, and go out of business.



Q: You've been very vocal about your belief that HACCP [Hazard Analysis and Critical Control Points] systems employed by the meat industry are 'a hoax.' If you were writing the meat safety rules, what would they look like?



A: Number one, HACCP was advertised as being science-based, and it is not. HACCP was designed by Pillsbury 20-30 years ago. They were making fully-cooked, ready-to-eat food for the astronaut program and it had to be guaranteed safe. Well, those were highly-processed, fully-cooked ready-to-eat-foods--the pathogens would be cooked out--they all had a real "kill step."



Well, the USDA saw the HACCP program and thought, 'Gee, that sounds really good. Lets apply that meat inspection.' The problem is the vast majority of what we process in meat plants is not fully-cooked, ready-to-eat, it is raw.



The USDA shouldn't use the term HACCP unless the products they are working with are fully cooked.



Number two, when the agency required the industry to implement HACCP, the agency said that under the program the USDA's role would be hands-off. That is an absolute disaster.



The USDA cannot be hands-off.



Under the transition to HACCP, the USDA knowingly acquiesced its authority back to the industry. It's an absolute disaster waiting to happen.



The natural long-term consequences of the agency adopting a hands-off, non-involvement role is ongoing outbreaks and recurring recalls all the time now.



HACCP cannot work in the raw meat industry.



I really think that meat inspection should be moved from the USDA, and that a separate agency should be created to perform inspection of not only meat and poultry but also produce, which is currently assigned to the FDA.



Q: Lets talk about the point of contamination. Where in the supply chain should we be focused? If the downstream processors are punished for contaminated meat, how would you solve that problem?



A: We know that Salmonella and E. coli are enteric, which means it is being introduced into the food stream at the slaughterhouse.



I think it makes obvious sense for the USDA to increase their inspection of and sampling at the slaughter plants. And when they find problems there, they need to force the source plants to clean up their act. Unfortunately the agency's primary focus now is at the downstream plants.



They are so intentionally deceptive. The USDA says downstream plants should put pressure on source or slaughter providers to ship them consistently safer meat. Well, these downstream plants have no power. They cannot control the wholesomeness of the meat they receive from the big packers, nor can they put pressure on them.



It would be my suggestion that the USDA implement a horrendous increase in the amount of samples that the agency collects at the originating slaughter plants, and that the results of all those tests should be made available to the public. My contention is that, within two weeks, the whole world would know which slaughter plants are noncompliant and have a high percentage of positive tests.



Q: Since you are so familiar with meat processing, I really want to dig into this issue about how to prevent contamination--you sent me an email about CAFOs (Concentrated Animal Feeding Operations), and their right to exist. In a concentrated feedlot you're going to have animals covered in feces, that is just the reality, but isn't that part of the problem, that the animals are so filthy?



A: In our facility, we were very small, we would kill maybe 15 to 20 beef in one day is all. We were not automated. The big plants, the maximum speed they are allowed is 390 head per hour.



Q: Have you been to one of these big plants?



A: Mhmm. It's amazing how automated and how fast they are. I'm not criticizing them--I'm just saying, it's part of the American dream, you know to be highly automated. Because of the fact that the carcasses are going down the line so quickly, it appears to me that neither the USDA, nor the employees of the packing plant have an adequate amount of time to inspect those carcasses, and in fact that is part of the whole ideal of HACCP is that--you know, everyone admits that those big packers are leaving hair and fecal matter on carcasses--but at the big plants they have implemented certain interventions. For example, they will spray lactic acid on the carcasses, or steam vacuum them. The industry claims these are 100 percent safe and successful, well obviously it's not safe enough.



E. coli exists in cattle naturally--and maybe 20 percent have the bad kind of E. coli in their gut. So in the CAFOS, all those animals in there shed their manure and then roll around and sleep in each other's manure--in fact in the spring when the ice melts they really are living in a pathogen soup--they are sharing each other's pathogens.



For right now, we need to put a lot of emphasis on finding vaccines.



But lets just say a vaccine removes 90 percent of the bad E. coli, well what about the remaining 10 percent? Whose responsibility is it that the bad E. coli doesn't end up in raw meat? Well, that still then falls on the slaughterhouse. The slaughterhouses are not doing an adequate job of preventing cross-contamination.



It might mean that they have to slow down their chain speeds, and they have to put more people on the line, whatever is necessary.



Obviously the interventions they have now do not remove all the pathogens, so I say until they can come up with interventions that do, they need to slow down chain speeds.



The bottom line is they need to test more often and find out where those problems are and how to fix them.



foodsafetynews.com

 

[vclavin]

http://www.cattlenetwork.com/Minnesota- ... 7487feac75

Does cooking the meat properly kill the E coli?

If yes, wouldn't it then be the fault of whoever cooked the meat?

Blessings
Valerie Clavin

 

[flounder]

>>>Does cooking the meat properly kill the E coli?

>>>If yes, wouldn't it then be the fault of whoever cooked the meat?

>>>Blessings

>>>Valerie Clavin





yes it does, it kills _most_ dangerous pathogens, please see ;


How the Consumer Can Fight Foodborne Illness

The Centers for Disease Control and Prevention (CDC) recommendations for prevention of an infection caused by Escherichia coli O157:H7 include:

Cook all ground beef or hamburger thoroughly. Make sure that the cooked meat is gray or brown throughout (not pink), any juices run clear, and the inside is hot.
The temperature of the meat should reach a minimum of 160 degrees F, as measured with a digital instant-read meat thermometer.
If you are served an undercooked hamburger in a restaurant, send it back.



http://www.fda.gov/AnimalVeterinary/New ... 083980.htm



However, cooking does NOT kill the PrP i.e. the TSE or Transmissible Spongiform Encephalopathy aka mad cow type diseases, and there are many, with atypical TSE cases spreading. There are many here in the USA and all of North America. THE c-BSE, atypical h-BSE and l-BSE have all been documented in North America. The USDA have absolutely no idea how bad the mad cow type disease is here in the USA, and we been trading products from Canada live and dead that could very well be tainted with TSE, like two lovers swapping spit. but in my opinion, the argument of defense to the consumer by comparison, when you buy a car, you get some sort of warranty, unless it is a clunker program i.e. 'buy as is'. is that how you want your industry to be construed as i.e. clunker program? at least with a car, you can trace the owners, you can trace parts, but not with a product we are to consume each day and hope it does not kill us, and if it does, oh well, you cannot trace it ??? which brings me to the infamous USDA dead stock downer cow school lunch program, the top 'clunker program' of all ;


New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication

Paul Brown*,dagger , Edward H. RauDagger , Bruce K. Johnson*, Alfred E. Bacote*, Clarence J. Gibbs Jr.*, and D. Carleton Gajdusek§

* Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, and Dagger Environmental Protection Branch, Division of Safety, Office of Research Services, National Institutes of Health, Bethesda, MD 20892; and § Institut Alfred Fessard, Centre National de la Recherche Scientifique, 91198 Gif sur Yvette, France

Contributed by D. Carleton Gajdusek, December 22, 1999

Abstract

One-gram samples from a pool of crude brain tissue from hamsters infected with the 263K strain of hamster-adapted scrapie agent were placed in covered quartz-glass crucibles and exposed for either 5 or 15 min to dry heat at temperatures ranging from 150°C to 1,000°C. Residual infectivity in the treated samples was assayed by the intracerebral inoculation of dilution series into healthy weanling hamsters, which were observed for 10 months; disease transmissions were verified by Western blot testing for proteinase-resistant protein in brains from clinically positive hamsters. Unheated control tissue contained 9.9 log10LD50/g tissue; after exposure to 150°C, titers equaled or exceeded 6 log10LD50/g, and after exposure to 300°C, titers equaled or exceeded 4 log10LD50/g. Exposure to 600°C completely ashed the brain samples, which, when reconstituted with saline to their original weights, transmitted disease to 5 of 35 inoculated hamsters. No transmissions occurred after exposure to 1,000°C. These results suggest that an inorganic molecular template with a decomposition point near 600°C is capable of nucleating the biological replication of the scrapie agent.

transmissible spongiform encephalopathy | scrapie | prion | medical waste | incineration

Introduction

The infectious agents responsible for transmissible spongiform encephalopathy (TSE) are notoriously resistant to most physical and chemical methods used for inactivating pathogens, including heat. It has long been recognized, for example, that boiling is ineffective and that higher temperatures are most efficient when combined with steam under pressure (i.e., autoclaving). As a means of decontamination, dry heat is used only at the extremely high temperatures achieved during incineration, usually in excess of 600°C. It has been assumed, without proof, that incineration totally inactivates the agents of TSE, whether of human or animal origin. It also has been assumed that the replication of these agents is a strictly biological process (1), although the notion of a "virus" nucleant of an inorganic molecular cast of the infectious beta -pleated peptide also has been advanced (2). In this paper, we address these issues by means of dry heat inactivation studies.

see full text:

http://www.pnas.org/cgi/content/full/97/7/3418


PLoS ONE. 2008; 3(8): e2969. Published online 2008 August 13. doi: 10.1371/journal.pone.0002969. PMCID: PMC2493038

Copyright This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production

Cathrin E. Bruederle,1* Robert M. Hnasko,1 Thomas Kraemer,2 Rafael A. Garcia,3 Michael J. Haas,3 William N. Marmer,3 and John Mark Carter1 1USDA-ARS WRRC, Foodborne Contaminants Research Unit, Albany, California, United States of America 2Forensic Toxicology, Institute of Legal Medicine, Saarland University, Homburg/Saar, Germany

3USDA-ARS ERRC, Fats, Oils and Animal Coproducts Research Unit, Wyndmoor, Pennsylvania, United States of America Neil Mabbott, Editor

University of Edinburgh, United Kingdom * E-mail: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000089/!x-usc:mailto:cat

Conceived and designed the experiments: CEB RMH WNM JMC. Performed the experiments: CEB RMH TK. Analyzed the data: CEB TK JMC. Contributed reagents/materials/analysis tools: CEB RMH TK RAG MJH JMC. Wrote the paper: CEB. Received April 21, 2008; Accepted July 24, 2008.

http://www.pubmedcentral.nih.gov/articl ... id=2493038

P04.08 Environmental Persistence of TSEs - Extraction of PrPSc from Soil Smith, A; Fernie, Karen; Somerville, R Neuropathogenesis Unit, UK Background: There are concerns about the potential spread of transmissible spongiform encephalopathies (TSEs) by environmental routes following, for example, burial of infected carcasses or the disposal of waste water. The extent to which TSE infectivity survives or is disseminated within soil and soil water is unclear as is the likelihood of ensuing infection. Aim: As part of this environmental project, soil samples are being collected from lysimeters containing either infected bovine heads or boluses of infectivity. The aim of this experiment is to devise a method for the extraction of PrPSc from soil and examines the interaction between soil and its components and TSE infectivity. Methods: Samples from two soil types (clay and sandy loam) were spiked with known amounts of TSE infected brain homogenate and subjected to various extraction methods including combinations of freeze/thaw, boiling, sonication and mixing with various solvents and detergents. Any recovery was determined on western blot using PrPSc as a surrogate marker for the presence of TSE infectivity. Results: These experiments have shown that PrPSc binds strongly to both sandy and clay soil, and to pure sand (quartz). Elution from quartz and the soils was only achieved in the presence of the detergent sarkosyl, and in the case of clay soil, satisfactory elution was only achieved if PrPSc was digested with proteinase K. This finding suggests that components in clay soil may bind differently to PrP than those of sandy soil, and that the N-terminal domain of PrP is involved in this binding. Conclusion: These results form the basis of a method for the extraction of PrPSc from soil and will be used to assay samples from a large scale lysimeter experiment. Samples testing positive for the presence of PrPSc will be selected for bioassay in mice. Results to date suggest that TSE infectivity may bind strongly to soil components and could therefore persist in the environment for long periods of time.

P04.61

Survival of PrPSc during Simulated Wastewater Treatment Processes

Pedersen, J1; Hinckley, G1; McMahon, K2; McKenzie, D3; Aiken, JM3 1University of Wisconsin, Soil Science/Civil and Environmental Engineering, USA; 2University of Wisconsin, Civil and Environmental Engineering, USA; 3University of Wisconsin, Comparative Biosciences, USA

Concern has been expressed that prions could enter wastewater treatment systems through sewer and/or septic systems (e.g., necropsy laboratories, rural meat processors, private game dressing) or through leachate from landfills that have received TSE-contaminated material. Prions are highly resistant to degradation and many disinfection procedures raising concern that they could survive conventional wastewater treatment. Here, we report the results of experiments examining the partitioning and survival of PrPSc during simulated wastewater treatment processes including activated and mesophilic anaerobic sludge digestion. We establish that PrPSc can be efficiently extracted from activated and anaerobic digester sludges with 1% sodium dodecyl sulfate, 10% sodium undecyl sulfate, and 1% sodium N-lauryl sarcosinate. Activated sludge digestion does not result in significant degradation of PrPSc. The protein partitions strongly to the activated sludge solids and is expected to enter biosolids treatment processes. A large fraction of PrPSc survived simulated mesophilic anaerobic sludge digestion. Our results suggest that if prions were to enter municipal waste water treatment systems, most of the agent would partition to activated sludge solids, survive mesophilic anaerobic digestion, and be present in treated biosolids. Land application of biosolids containing prions could represent a route for their unintentional introduction into the environment. Our results argue for excluding inputs of prions to municipal wastewater treatment facilities that would result in unacceptable risk of prion disease transmission via contaminated biosolids.

P04.71 Oral Transmission of Prion Disease Is Enhanced by Binding to Soil Particles Johnson, C; Pedersen, J; Chappell, R; McKenzie, D; Aiken, J University of Wisconsin - Madison, USA A long-unanswered question in prion biology is how certain transmissible spongiform encephalopathies (TSEs), such as sheep scrapie and cervid chronic wasting disease, spread from animal to animal. Anecdotal evidence and controlled field experiments have suggested the presence of an environmental TSE reservoir. We, and others, have speculated that soil may harbor TSE agent in the environment and allow its transfer to naïve hosts. TSE infectivity can persist in soil for years, and we previously demonstrated that the disease-associated form of the prion protein binds to soil particles and that prions adsorbed to the common soil mineral montmorillonite (Mte) retain infectivity following intracerebral inoculation. We assessed the oral infectivity of Mte- and soil-bound prions and found that prions bound to Mte are orally bioavailable and that, unexpectedly, binding to Mte significantly enhances disease penetrance and reduces incubation period relative to unbound agent. Cox proportional hazards modelling revealed that across the doses of TSE agent tested, Mte increased the effective infectious titer by a factor of 680 relative to unbound agent. Oral exposure to Mte-associated prions led to TSE development in experimental animals even at doses too low to produce clinical symptoms in the absence of the mineral. We tested the oral infectivity of prions bound to three whole soils differing in texture, mineralogy and organic carbon content, and found soil-bound prions to be orally infectious. Two of the three soils increased oral transmission of disease, and the infectivity of agent bound to the third soil was equivalent to that of unbound agent. Enhanced infectivity of soilbound prions may explain the environmental transmission of some TSEs despite the presumably low levels shed into the environment.

P04.104 Survival of Prion Proteins in Environmental Matrices Maluquer de Motes, C1; Torres, JM2; Pumarola, M3; Girones, R1 1University of Barcelona, Spain; 2Centro de Investigacion en Sanidad Animal, Spain; 3Autonomous University of Barcelona, Spain Several publications have suggested the environment as a possible route of transmission, especially for sheep scrapie and cervid Chronic Wasting Disease (CWD). The role of the environment as a reservoir for these disorders is difficult to prove and faces a considerable lack of information. In this work, different methodologies have been developed to evaluate the survival and inactivation of TSE agents in environmental matrices. Different slaughterhouse and urban sewage samples were spiked with diverse strains of either scrapie or BSE agents and kept under controlled conditions for extended periods of time. Aliquots of every experiment were sequentially collected and concentrated according to a methodology specifically selected for each type of matrix. Sensitivity of the methods developed was estimated among 2-10 ƒÊg of infected tissue. PrPres was finally detected by western blot. Films were then transformed into digital pictures, signal intensities were quantified and regression models were computed. According to the results obtained, scrapie agent showed higher stability than BSE in all the environments studied. However, no significant differences were observed among mouse-passaged scrapie strains and sheep scrapie. The regression models provided t90 and t99 values (times of incubation necessaries for 90% and 99% reduction of PrPres levels). In urban sewage, i.e., t99 was estimated as about 50 and 22 days for scrapie and BSE respectively. In general, the effect of the matrix was clearly observed in all the experiments, showing up to a 6-8 fold higher reduction of PrPres levels in comparison to PBS controls. As some of the inocula were titrated in terms of infectious doses, we approximated the decay of PrPres levels to the reduction of infectivity for both agents. In slaughterhouse wastewater, i.e., two-log reduction was observed for both agents after 30-35 days of incubation. Data on infectivity will be confirmed by a series of bioassay experiments.

P04.125 Environmental Persistence of TSE Infectivity: Field Studies Fernie, K; Smith, A; Somerville, R Neuropathogenesis Unit, Roslin Institute, UK Background: There is concern about the consequences of contamination of the environment with TSE infectivity. Infectivity may enter the environment by various routes, persist in the ground and spread from the original source to contaminate an extended area and groundwater. Aims: We are studying this problem by addressing the following questions: 1. Does infectivity with some containment (e.g. in a carcass) survive in the carcass over time; 2. Does infectivity without containment survive, and is it disseminated into the surrounding soil and water? 3. Do the environmental conditions, e.g. soil type and pH, affect the survival and/or transport of infectivity through soil? Methods: To address these questions, we are performing two field experiments (with appropriate containment) each using two soil types. Air temperature, rainfall, soil temperature and moisture content are being monitored. In one experiment a series of 10 bovine heads have been spiked with the BSE derived TSE strain 301V and buried in the two soils, contained within individual lysimeters, for exhumation and analysis at yearly intervals. Rainwater flowing through and collected as groundwater is also being analysed. In the second experiment a bolus of infected brain is buried at the centre of two 3 meter diameter lysimeters and soil samples taken from them at regular intervals. Water flow-through is also analysed. Results: To date, the first two bovine heads have been exhumed and the surrounding soil sampled. Both of the exhumed heads were apparently largely decomposed but on examination of the brain cavity were found to contain significant amounts of brain tissue. These have been sampled and are presently being analysed. The soil samples taken from around the heads and five sets of core samples taken from the soil surrounding the buried brain in the two large lysimeters are presently being analysed for PrPSc, the abnormal protein associated with the TSEs and for infectivity. Water samples have also been collected for analyses. Discussion: We will use the acquired data to build a predictive model of TSE behaviour in the environment which will inform future risk assessments.

snip...end....NEUROPRION 2007...TSS

Public release date: 11-Aug-2008

Contact: Dr. Björn Seidel mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000089/!x-usc:mailto:bjo 49-297-230-2330 Fraunhofer-Gesellschaft

Resistant prions

A flock of sheep at pasture – a seemingly idyllic scene. But appearances can be deceptive: If the animals are suffering from scrapie, entire flocks may perish. Scrapie is an infectious disease in which prions destroy the animal's brain, rather like BSE. The brain becomes porous, the sheep lose their orientation, they suffer from strong itching sensations and scrape off their fleece. Eventually, the infected animals die.

It is difficult to contain the disease – all too often, scrapie will break out again on the same farm several months or years after it has apparently been eradicated. Are the prions transmitted not only by direct contact, but also by the environment – perhaps by the pastures? How long do prions that get into the pasture via the saliva and excrements of the sick animals, persist in the ground?

Together with fellow-scientists from the Robert Koch Institute in Berlin and the Friedrich Loeffler Institute (Federal Research Institute for Animal Health) on the island of Riems, research scientists from the Fraunhofer Institute for Molecular Biology and Applied Ecology IME in Schmallenberg investigated these questions on behalf of the German Ministry for Environment, Nature Conservation and Nuclear Safety BMU. "We mixed soil samples with scrapie pathogens to find out how long the pathogens would survive," says Dr. Björn Seidel, who headed the investigations at IME. "Even after 29 months, in other words more than two years, we were still able to detect prions in the soil." But are these prions still infectious? "The soil actually seems to increase the infectiousness of the pathogens. The incubation period – the time it takes for the disease to break out – is exceedingly short even after the prions have persisted in the soil for 29 months. All of the animals that were given contaminated soil became sick within a very short time.

These results indicate that fresh incidences of scrapie among sheep are due to contaminated pastures," says Seidel in summary. The results of the study reveal that sheep may even become infected from the surface water, though the risk of infection is much lower in this case. There is no danger to humans, however: scrapie pathogens seem unable to affect them.

Another cause for concern is chronic wasting disease (CWD). Like BSE and scrapie, this is caused by prions, but it mainly affects deer. The numbers of infected animals in North America are rising steeply. How long do BSE and CWD prions survive in the ground? "To find this out, we urgently need to carry out further tests. The appropriate research applications have already been submitted," says Seidel.

http://www.eurekalert.org/pub_releases/ ... 081108.php #

snip... full text ;

http://bse-atypical.blogspot.com/2008/1 ... iform.html




Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.

snip...

The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...

http://web.archive.org/web/200305160516 ... /tab05.pdf

Food Authorities Affected by Hallmark/Westland Meat Packing Co. Beef Recall February 2006 - February 2008

http://www.fns.usda.gov/fns/safety/Hall ... yState.pdf

Members of The HSUS are also concerned about the meat products provided to their children through the National School Lunch Program. More than 31 million school children receive lunches through the program each school day. To assist states in providing healthful, low-cost or free meals, USDA provides states with various commodities including ground beef. As evidenced by the HallmarkNVestland investigation and recall, the potential for downed animals to make their way into the National School Lunch Program is neither speculative nor hypothetical.

http://biotech.law.lsu.edu/cases/FDA/hs ... plaint.pdf

>>>In the papers, the government alleges the meatpacking plant slaughtered and processed downer cows for nearly four years — from January 2004 to September 2007 — at the average rate of one every six weeks...<<<

http://downercattle.blogspot.com/2009/0 ... for-4.html

"The alleged misrepresentations by Hallmark and Westland could have impacted the health of many of our nation's most vulnerable citizens--our schoolchildren," said Tony West, Assistant Attorney General of the Justice Department's Civil Division. "Our intervention in this case demonstrates how seriously we will pursue allegations such as these."

http://downercattle.blogspot.com/2009/0 ... lmark.html


Tuesday, November 17, 2009

SEAC EFFECT OF AGE ON THE PATHOGENESIS OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES SEAC 103/2


http://downercattle.blogspot.com/2009/1 ... is-of.html



Friday, September 4, 2009

FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009

http://madcowfeed.blogspot.com/2009/09/ ... oduct.html

Saturday, August 29, 2009

FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009

http://madcowfeed.blogspot.com/2009/08/ ... oduct.html

----- Original Message ----- From: "Terry S. Singeltary Sr." <[email protected]> To: <[email protected]> Sent: Thursday, November 05, 2009 9:25 PM Subject: [BSE-L] re-FOIA REQUEST ON FEED RECALL PRODUCT contaminated with prohibited material Recall # V-258-2009 and Recall # V-256-2009

http://madcowfeed.blogspot.com/2009/11/ ... oduct.html



Tuesday, December 1, 2009


IMPORTATION OF CANADIAN CATTLE, BISON, SHEEP, AND GOATS INTO THE UNITED STATES 12/1/09


http://usdameatexport.blogspot.com/2009 ... bison.html


Monday, November 23, 2009

BSE GBR RISK ASSESSMENTS UPDATE NOVEMBER 23, 2009 COMMISSION OF THE EUROPEAN COMMUNITIES AND O.I.E.


http://docket-aphis-2006-0041.blogspot. ... pdate.html


Wednesday, November 18, 2009

R-CALF: 40 Groups Disagree With USDA's Latest BSE Court Submission


http://bse-atypical.blogspot.com/2009/1 ... usdas.html



2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006



http://bse-atypical.blogspot.com/2006/0 ... pdate.html




Monday, October 19, 2009

Atypical BSE, BSE, and other human and animal TSE in North America Update October 2009



http://bse-atypical.blogspot.com/2009/1 ... n-and.html




THE USA Bovine is not exempt from the TSE prion agent. you cannot hide from them, and you can only hide them for so long. you cannot kill them, and they know no boundaries or borders or age group (in terms of CJD reportable only in the 55 and or younger age groups only, this defies common sense and science). THE UKBSEnvCJD only theory is wrong, one of which that consists of only the UK bovine, that of only one strain, the human TSE there from i.e. nvCJD, and that there from of only one strain, in only one Geographical location of the globe, when the same feeding and rendering practices mirrored that of the UK, only the UK started some 5 years before we did, and scrapie, and all of the strains there from typical and atypical, all of which are right here in the USA, and have been, where humans of old age group, and young age group are dyeing from CJD, long and short incubation, some with kuru type amyloid plaques, some with the same symptoms as the nvCJD. the systematic failure of all agencies in the august 4, 1997 partial and voluntary mad cow feed ban, and the systematic failure in the enhanced BSE surveillance of 2004, all PROVEN to be such. ONE cannot say that many have not been exposed. one can only thank God, that only a few have been documented that went clinical, to date. but who will watch the children for the next 5+ decades? i'm serious, who will watch these kids that were exposed all across our Nation for 4 years or more to the dead stock downer cow school lunch program, where the most high risk cattle for BSE/TSE i.e. dead stock downers were fed to our kids??? this is what i don't understand, these parents will get their panty hose all twisted up because a few animals were abused, and do absolutely nothing about the fact there kids were abused, and in fact, in my opinion, poisoned. this is a disease that can incubate without symptoms for over 5 decades, or not, for some it's shorter, but once clinical, it is 100% fatal. with atypical TSE spreading, one can only guess of what the infectious dose is ??? I guess, hope it's minimal and forget about it, or hope everybody else does. ..i refuse too. ...





TSS

 

[jackquality]

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