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Second E coli outbreak linked to meat from Nebraska Beef

flounder

Well-known member
Second E coli outbreak linked to meat from Nebraska Beef

Nebraska Beef, Ltd., a processor based in Omaha, has recalled 1.2 million pounds of its beef after federal and state officials linked its products to a second multistate Escherichia coli O157H7 outbreak that has so far sickened 31 people in 12 states and Canada. Read article...



http://www.cidrap.umn.edu/cidrap/content/fs/food-disease/news/aug1108ecoli.html




TSS
 

mrj

Well-known member
There is more information and good explanation of reasons for further recalls from NE Beef at www.meatingplace.com in their daily news and posts in reply to the one about NE Beef.

Some posting are experienced in the packing business and seem reasonably knowledgeable about it and understand how it is happening.

I've read enough about great sounding solutions to arrest E. coli in packing plants to know it is extremely difficult to contain and eliminate that bacteria.

The current High Plans Journal has an interesting story about efforts and difficulties re getting rid of the e coli problem. Their website: www.hpj.com, but I don't know if you can access the story or not. The information re. fighting e coli is at www.bifsco.org where you will learn that the cattle/beef industry spends about $350 Million per year, with most of that money coming from all segments other than cattle production, which contributes $1.5 to $2 Million per year. That seems appropriate to me. E. coli O157:H7 does originate in nature among many animals and birds, including those pooping pastures and riparian areas and dropping dung onto the grass our cattle eat. How about you?

mrj
 
A

Anonymous

Guest
Mike said:
Seems to me E-Coli would be very easy to contain on the kill floor.

Just keep the crap off the meat!

And do some better testing/inspection- or they will end up with government mandated testing......Industry lately has done a horrific job of policing themselves- especially with imports- and that is not going to be allowed to continue....
 

Mike

Well-known member
Sandhusker said:
I'd like to know why contaminated product leaves the building.

Contaminated product can be sold to processors that cook it.

It can then be put into the human food supply.

Anyone know how the vaccines are working out?
 

Kato

Well-known member
Here's the newsroom for the company that makes the vaccine.

http://www.bioniche.com/newsroom.cfm

This would be the simplest answer. Prevention is always better than trying to find a cure. 8)
 

RobertMac

Well-known member
Mike said:
Contaminated product can be sold to processors that cook it.
Unless you are a small operator...then they don't let you do anything except destroy it!!!! Won't let you run a confirmation test...even if it is still going to be destroyed...could have been a lab mistake????? The impression I got from my processor...he was being setup to be taken out, so he quite USDA labeling beef to hopefully get back under their radar!!!!! :mad: :mad:
 

flounder

Well-known member
Research Project: DEVELOP BEEF CATTLE BETTER SUITED FOR SUSTAINABLE PRODUCTION Location: Miles City, Montana

Title: The Use of an Experimental Vaccine in Gestating Beef Cows to Reduce the Shedding of Escherichia coli O157:H7 in the Newborn Calf

Authors

Standley, T - MONTANA STATE UNIV. Paterson, John - MONTANA STATE UNIV. Skinner, K - MONTANA STATE UNIV. Rainey, B - MONTANA STATE UNIV. Roberts, Andrew Geary, Thomas Smith, G - COLORADO STATE UNIV. White, R - FT DODGE ANIM HEALTH LAB

Submitted to: Professional Animal Scientist Publication Type: Peer Reviewed Journal Publication Acceptance Date: March 15, 2008 Publication Date: June 3, 2008 Citation: Standley, T., Paterson, J., Skinner, K., Rainey, B., Roberts, A.J., Geary, T.W., Smith, G., White, R. 2008. The Use of an Experimental Vaccine in Gestating Beef Cows to Reduce the Shedding of Escherichia coli O157:H7 in the Newborn Calf. Professional Animal Scientist 24:260-263.

Interpretive Summary: Reducing the amount of E. coli O157:H7 shed through animal feces will be useful in preventing contamination of meat. Beef cows in the last trimester of pregnancy were used to determine if vaccinating against E. coli O157:H7 would increase antibody titers in the serum and also result in the transfer of these antibodies to the neonatal calf. Results from this research indicate that vaccinating the gestating cow with an experimental vaccine against E. coli O157:H7 increased antibody titers against this organism in both the cow and suckling calf. Because animals in this study exhibited little or no fecal shedding of 0157:H7, efficacy of the vaccine in reducing shedding could not be evaluated. Technical Abstract: Beef cows in the last trimester of pregnancy were used to determine if vaccinating against E. coli O157:H7 would increase antibody titers in the serum and also result in the transfer of these antibodies to the neonatal calf. Seventy-one cows were vaccinated 30 d prior to parturition with an experimental vaccine and then commingled with 66 non-vaccinated cows. Cow fecal and venous blood samples were collected at trial initiation and again ~14 d after parturition. Calf feces and serum were collected at ~14 d after parturition and 60 d later. The serum was analyzed for antibody titers to E. coli O157:H7 while the prevalence of E. coli O157:H7 in feces was determined by the Barkocy-Gallagher procedure. Initial cow antibody titers to O157:H7 were not different (P=0.50) between treatments but by parturition the antibody titers for O157:H7 in vaccinated cows were ten times higher (P<0.001) than for control cows (917 vs. 83). The serum titers for calves suckling vaccinated cows were higher (P<0.001) than control calves (1485 vs.135) at ~14 d after calving. By 60 d, titer levels were still higher (P<0.001) for calves suckling vaccinated cows. Initial fecal O157:H7 concentrations for cows were negative for both treatments and remained low. There were no differences in fecal O157:H7 at 60 d post partum among 14 calves; less than 5% of calves were shedding. Results suggest that vaccinating gestating cows for E. coli O157:H7 resulted in elevated antibody titers cows and these antibodies transferred to the calf.


http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=221584


Loneragan said, "This tells us that efficacious interventions that predictably reduce the burden of E. coli O157 on cattle entering packing plants are needed. Successful interventions will reduce the burden of E. coli O157 to a level that is within the capacity of in-plant interventions to handle. If this can be achieved, then tremendous progress toward preventing E. coli O157 from ever getting into ground beef has been made. This vaccine appears to fit this purpose and has great promise."

Thomson and his colleagues studied Siderophore receptor and porin -- SRP -- technology, which was developed by Epitopix, LLC in Willmar, Minn.

"Siderophore receptor and porin proteins are utilized by food borne pathogens like E. coli to acquire iron," Thomson said. "The SRP vaccine technology immunizes animals against these mechanisms and does not allow the bacteria to take up iron. Iron is to bacteria, as oxygen is to humans. Without iron consumption, the bacteria suffocate and can't grow or replicate."

"We conducted a challenge study, a natural infection study and two large pen field studies at commercial feedyards," Thomson said. "All studies showed positive results of this vaccine, making an impact on decreasing not only the number of the cattle shedding the bacteria but also decreasing the concentration of the bacteria being shed."

Super shedder cattle are cattle that shed E. coli in very high concentrations. "Our natural field study showed that the SRP technology vaccine reduces the number of super shedder cattle," Thomson said.

The two large pen feeding studies the team conducted utilized 20 pens and more than 1,200 head of cattle, Thomson said. The first study conducted in 2006 was funded in part by beef and veal producers and importers through their $1-per-head checkoff and was produced for the Cattlemen's Beef Board and state beef councils by the National Cattlemen's Beef Association. The second study was sponsored by Epitopix, LLC in 2007.

The team's findings will be presented at the 2008 Beef Industry Safety Summit in Dallas March 5.



http://www.sciencedaily.com/releases/2008/02/080227125115.htm



Cattle Vaccine
Guy Loneragan, B.V.Sc., DVM, West Texas A&M University
Summary: Preharvest beef safety research examining the
potential of a siderophore receptor and porin protein (SRP)
based vaccines for control of E. coli O157:H7 was presented.
• A vaccine that would inhibit bacteria’s ability to acquire
iron was examined through a challenge study. Trends
to decrease pathogen populations were seen; however,
prevalence in study animals was so low that biological
significance was questionable. A second field study
demonstrated a vaccine efficacy of 86% with a 98%
reduction in pathogen concentration in fecal samples.
• The vaccine did not negatively affect animal performance
and demonstrated effectiveness in reducing the burden of
E. coli O157:H7.
• A vaccine using the same technology is conditionally
licensed and widely accepted in dairy production to control
Salmonella, which unlike E. coli can negatively affect
animal performance.
• The purpose of preharvest interventions such as vaccines is
to reduce pathogen levels so that the entire safety system
is enhanced.



http://www.bifsco.org/uDocs/2008safetysummitexecutivesummary.pdf



CAN VACCINATION REDUCE THE PROBABILITY THAT FEEDLOT CATTLE SHED ESCHERICHIA COLIESCHERICHIA COLIO157:H7?O157:David R. Smith, DVM, PhDDavid PhDUniversity of NebraskaUniversity Nebraska--LincolnLincoln



http://www.bifsco.org/uDocs/vaccineresearch_smith.pdf



VACCINATION AS AN INTERVENTION STRATEGY FOR REDUCTION OF ESCHERICHIA COLI0157:H7 IN CATTLE FECESVACCINATION FECESChoat, W.T., J.A. Paterson, B.M. Rainey, K.E. Belk and G.C. SmithChoat



http://www.bifsco.org/uDocs/vaccineresearch_choat.pdf



HACCP stands for Hazard Analysis and Critical Control Points. HACCP is a preventative food safety system, first developed for astronauts in space. HACCP includes seven basic principles: hazard analysis, critical control point identification, establishing critical limits, monitoring procedures, corrective actions, verification procedures, and record-keeping.

please note, the USDA, FDA, et al have failed terribly at all points. these failed points pointed out time and time again here on this site.



From: Terry S. Singeltary Sr. [[email protected]] Sent: Tuesday, July 29, 2003 1:03 PM To: [email protected] Cc: [email protected]; [email protected]; BSE-L Subject: Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION TO DOCKET 2003N-0312]

Greetings FDA,

my name is Terry S. Singeltary Sr., i lost my mother to hvCJD (Heidenhain Variant Creutzfeldt Jakob Disease).

i would kindly like to comment on the proposed HACCP method of detecting and or preventing TSEs in the human/animal feed supply.

it seems to me by implementing something that was designed for Astronauts instead of cattle, something that the GAO has already stated is terribly flawed (HACCP), i find it very disturbing to continue to insist on refusing to use rapid TSE TESTING in sufficient numbers to find TSEs, as with other Countries that they too once thought they were BSE free. for example, it took Italy 1 MILLION rapid TSE tests since 2001 to find 102 cases of BSE. THE USA has only tested 48,000 cattle in the 14 years of surveillance. there is documented proof that indeed the USA cattle have been infected with a TSE for decades, but the FDA/USDA and other USA Gov. agencies continue to conveniently ignore these findings. YOU must not ignore what Richard Marsh found. Plus, you must not ignore Asante/Collinge new findings that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest _sporadic_ CJD. The USA has been feeding ruminant by-products back to cattle, deer, elk and sheep for decades, and TSEs in these species have been recycled for feed for decades in the USA. The rendering process here in the USA will not kill this agent. to implement any HACCP over massive rapid TSE testing is only prolonging the inevitable, and will only allow the agent to spread further. it is simply a band-aid approach to something that needs a tourniquet...

3. Meat and Poultry: Better USDA Oversight and Enforcement of Safety

Rules Needed to Reduce Risk of Foodborne Illnesses. GAO-02-902, August 30.

FSIS Is Not Ensuring that Plants' HACCP Plans Meet Regulatory Requirements

snip...

According to FSIS's food safety systems correlation reviews, inspectors are not consistently identifying and documenting failures of plants' HACCP plans to meet regulatory requirements. Furthermore, FSIS does not expect its inspectors to determine whether HACCP plans are based on sound science--the cornerstone of an effective plan. While in-depth verification reviews examine the scientific aspects of HACCP plans, they have been conducted in very few plants, and consumer safety officers hired to review the scientific soundness of HACCP plans may take several years to assess the plans at all plants. Moreover, inspectors in 55 percent of the 5,000 plants nationwide did not document any HACCP violations during fiscal year 2001. When we brought this information to the attention of FSIS officials, they were surprised that so many plants had no HACCP violations for an entire year.

snip...

2. USDA believes that the title of the report is misleading. We disagree. We believe the title accurately reflects the concerns detailed throughout the body of the report.

snip...

http://www.gao.gov/cgi-bin/getrpt?GAO-02-902

http://www.gao.gov/new.items/rc00255.pdf

FDA acknowledges that it has not yet identified and inspected all firms subject to the ban” pg. 3 ;

http://www.gao.gov/new.items/d02183.pdf

The report concludes that “federal actions do not sufficiently ensure that all BSE-infected animals or products are kept out or that if BSE were found it would be detected promptly and not spread to other cattle through animal feed or enter the human food chain” italics added pg. 3 ;

http://www.gao.gov/new.items/d02183.pdf

and why does everybody conveniently ignore these findings;

Asante/Collinge et al, that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest _sporadic_ CJD;

http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm

To be published in the Proceedings of the Fourth International Scientific Congress in Fur Animal Production. Toronto, Canada, August 21-28, 1988

Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle

R.F. Marsh* and G.R. Hartsough

•Department of Veterinary Science, University of Wisconsin-Madison, Madison, Wisconsin 53706; and ^Emba/Creat Lakes Ranch Service, Thiensville, Wisconsin 53092

ABSTRACT Epidemiologic investigation of a new incidence of transmissible mink encephalopathy (TME) in Stetsonville, Wisconsin suggests that the disease may have resulted from feeding infected cattle to mink. This observation is supported by the transmission of a TME-like disease to experimentally inoculated cattle, and by the recent report of a new bovine spongiform encephalopathy in England.

INTRODUCTION

Transmissible mink encephalopathy (TME) was first reported in 1965 by Hartsough and Burger who demonstrated that the disease was transmissible with a long incubation period, and that affected mink had a spongiform encephalopathy similar to that found in scrapie-affecied sheep (Hartsough and Burger, 1965; Burger and Hartsough, 1965). Because of the similarity between TME and scrapie, and the subsequent finding that the two transmissible agents were indistinguishable (Marsh and Hanson, 1969), it was concluded that TME most likely resulted from feeding mink scrapie-infecied sheep. The experimental transmission of sheep scrapie to mink (Hanson et al., 1971) confirmed the close association of TME and scrapie, but at the same time provided evidence that they may be different. Epidemiologic studies on previous incidences of TME indicated that the incubation periods in field cases were between six months and one year in length (Harxsough and Burger, 1965). Experimentally, scrapie could not be transmitted to mink in less than one year. To investigate the possibility that TME may be caused by a (particular strain of scrapie which might be highly pathogenic for mink, 21 different strains of the scrapie agent, including their sheep or goat sources, were inoculated into a total of 61 mink. Only one mink developed a progressive neurologic disease after an incubation period of 22 mon..s (Marsh and Hanson, 1979). These results indicated that TME was either caused by a strain of sheep scrapie not yet tested, or was due to exposure to a scrapie-like agent from an unidentified source.

OBSERVATIONS AND RESULTS

A New Incidence of TME. In April of 1985, a mink rancher in Stetsonville, Wisconsin reported that many of his mink were "acting funny", and some had died. At this time, we visited the farm and found that approximately 10% of all adult mink were showing typical signs of TME: insidious onset characterized by subtle behavioral changes, loss of normal habits of cleanliness, deposition of droppings throughout the pen rather than in a single area, hyperexcitability, difficulty in chewing and swallowing, and tails arched over their _backs like squirrels. These signs were followed by progressive deterioration of neurologic function beginning with locomoior incoordination, long periods of somnolence in which the affected mink would stand motionless with its head in the corner of the cage, complete debilitation, and death. Over the next 8-10 weeks, approximately 40% of alt the adult mink on the farm died from TME. Since previous incidences of TME were associated with common or shared feeding practices, we obtained a careful history of feed ingredients used over the past 12-18 months. The rancher was a "dead stock" feeder using mostly (>95%) downer or dead dairy cattle and a few horses. Sheep had never been fed.

Experimental Transmission. The clinical diagnosis of TME was confirmed by histopaihologic examination and by experimental transmission to mink after incubation periods of four months. To investigate the possible involvement of cattle in this disease cycle, two six-week old castrated Holstein bull calves were inoculated intracerebrally with a brain suspension from affected mink. Each developed a fatal spongiform encephalopathy after incubation periods of 18 and 19 months.

DISCUSSION These findings suggest that TME may result from feeding mink infected cattle and we have alerted bovine practitioners that there may exist an as yet unrecognized scrapie-like disease of cattle in the United States (Marsh and Hartsough, 1986). A new bovine spongiform encephalopathy has recently been reported in England (Wells et al., 1987), and investigators are presently studying its transmissibility and possible relationship to scrapie. Because this new bovine disease in England is characterized by behavioral changes, hyperexcitability, and agressiveness, it is very likely it would be confused with rabies in the United Stales and not be diagnosed. Presently, brains from cattle in the United States which are suspected of rabies infection are only tested with anti-rabies virus antibody and are not examined histopathologically for lesions of spongiform encephalopathy. We are presently pursuing additional studies to further examine the possible involvement of cattle in the epidemiology of TME. One of these is the backpassage of our experimental bovine encephalopathy to mink. Because (here are as yet no agent- specific proteins or nucleic acids identified for these transmissible neuropathogens, one means of distinguishing them is by animal passage and selection of the biotype which grows best in a particular host. This procedure has been used to separate hamster- adapted and mink-udapted TME agents (Marsh and Hanson, 1979). The intracerebral backpassage of the experimental bovine agent resulted in incubations of only four months indicating no de-adaptation of the Stetsonville agent for mink after bovine passage. Mink fed infected bovine brain remain normal after six months. It wili be essential to demonstrate oral transmission fiom bovine to mink it this proposed epidemiologic association is to be confirmed.

ACKNOWLEDGEMENTS These studies were supported by the College of Agricultural and Life Sciences, University of Wisconsin-Madison and by a grant (85-CRCR-1-1812) from the United States Department of Agriculture. The authors also wish to acknowledge the help and encouragement of Robert Hanson who died during the course of these investigations.

REFERENCES Burger, D. and Hartsough, G.R. 1965. Encephalopathy of mink. II. Experimental and natural transmission. J. Infec. Dis. 115:393-399. Hanson, R.P., Eckroade, R.3., Marsh, R.F., ZuRhein, C.M., Kanitz, C.L. and Gustatson, D.P. 1971. Susceptibility of mink to sheep scrapie. Science 172:859-861. Hansough, G.R. and Burger, D. 1965. Encephalopathy of mink. I. Epizoociologic and clinical observations. 3. Infec. Dis. 115:387-392. Marsh, R.F. and Hanson, R.P. 1969. Physical and chemical properties of the transmissible mink encephalopathy agent. 3. ViroL 3:176-180. Marsh, R.F. and Hanson, R.P. 1979. On the origin of transmissible mink encephalopathy. In Hadlow, W.J. and Prusiner, S.P. (eds.) Slow transmissible diseases of the nervous system. Vol. 1, Academic Press, New York, pp 451-460. Marsh, R.F. and Hartsough, G.R. 1986. Is there a scrapie-like disease in cattle? Proceedings of the Seventh Annual Western Conference for Food Animal Veterinary Medicine. University of Arizona, pp 20. Wells, G.A.H., Scott, A.C., Johnson, C.T., Cunning, R.F., Hancock, R.D., Jeffrey, M., Dawson, M. and Bradley, R. 1987. A novel progressive spongiform encephalopathy in cattle. Vet. Rec. 121:419-420.

http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf

02N-0273 - Substances Prohibited From ... [PART 1 TSS SUBMISSION] ... compare search on 8/8/01...tss =====ANIMAL PROTEIN ... had to request to the FOIA >>for the USA madcow feed ban warning letters. ... www.fda.gov/ohrms/dockets/dailys/ 03/Jan03/012403/8004be07.html - 68k -

http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be07.html

Docket Management Docket: 02N-0273 - Substances Prohibited From ... [PART 2 TSS SUBMISSION]

http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be09.html

SNIP...

The problem is diminishing in most of the 15 EU nations, but in Britain there were 260 positive tests between January and May, compared with 156 for the same period last year.

The higher number could be explained partly by the greater number of tests carried out this year in Britain: 198,143 compared with 122,801.

The European Commission carried out about 4.1 million tests across member states - about 10% of cattle in the bloc.

It found 591 positive cases of bovine spongiform encephalopathy in the first five months of the year, down from 603 over the same period last year.

snip...

http://icberkshire.icnetwork.co.uk/


USA TEST ONLY 48,000 CATTLE IN 14 YEARS, from 100 MILLION CATTLE IN ANY GIVEN YEAR, to 2003, TOTAL TSE TEST EVER IN USA BOVINE;

As of April 30, 2003, over 48,000 brains have been examined for BSE or another form of a TSE in cattle (figure 3 <http://www.aphis.usda.gov/lpa/issues/bse/surveillance/figure3.html>). No evidence of either condition has been detected by histopathology or immunohistochemistry.

http://www.aphis.usda.gov/lpa/issues/bse/surveillance/figure3.html

For the USA to continue to _flounder_ with these TSEs, as they have done for the past 30 years or so, will only allow the agent to spread. to continue to ignore what every other Country around the globe has dealt with and is still dealing with, and to think that the USA is any different, should be taken with great suspicion $

PLUS, if the USA continues to flagrantly ignore the _documented_ science to date about the known TSEs in the USA (let alone the undocumented TSEs in cattle), it is my opinion, every other Country that is dealing with BSE/TSE should boycott the USA and demand that the SSC reclassify the USA BSE GBR II risk assessment to BSE/TSE GBR III 'IMMEDIATELY'. for the SSC to _flounder_ any longer on this issue, should also be regarded with great suspicion as well. NOT to leave out the OIE and it's terribly flawed system of disease surveillance. the OIE should make a move on CWD in the USA, and make a risk assessment on this as a threat to human health. the OIE should also change the mathematical formula for testing of disease. this (in my opinion and others) is terribly flawed as well. to think that a sample survey of 400 or so cattle in a population of 100 million, to think this will find anything, especially after seeing how many TSE tests it took Italy and other Countries to find 1 case of BSE (1 million rapid TSE test in less than 2 years, to find 102 BSE cases), should be proof enough to make drastic changes of this system. the OIE criteria for BSE Country classification and it's interpretation is very problematic. a text that is suppose to give guidelines, but is not understandable, cannot be considered satisfactory. the OIE told me 2 years ago that they were concerned with CWD, but said any changes might take years. well, two years have come and gone, and no change in relations with CWD as a human health risk. if we wait for politics and science to finally make this connection, we very well may die before any decisions or changes are made. this is not acceptable. we must take the politics and the industry out of any final decisions of the Scientific community. this has been the problem from day one with this environmental man made death sentence. some of you may think i am exaggerating, but you only have to see it once, you only have to watch a loved one die from this one time, and you will never forget, OR forgive...yes, i am still very angry...but the transmission studies DO NOT lie, only the politicians and the industry do...and they are still lying to this day...

Terry S. Singeltary Neurology Online, 27 Jan 2003 [Full text] ...snip...end...TSS



Whole Foods tightens rules for its beef suppliers

By ANNYS SHIN
Washington Post
Aug. 11, 2008, 11:00PM


WASHINGTON — It can be legal to sell steaks and roasts that carry a potentially deadly strain of E. coli. But it is not legal to sell that meat if it is going to be used to make ground beef. As meat makes its way from packer to distributor to retailer, those distinctions can get lost, as Austin-based Whole Foods found out in last week's recall.

The natural food retailer pulled fresh ground beef from some of its stores after seven customers in Massachusetts fell ill with a strain of E. coli that has sickened people in 11 other states, the District of Columbia and Canada. No one in Texas was reported affected.

The ground beef that Whole Foods recalled was made using primal or intact cuts — meat typically used for steaks and roasts — produced by Nebraska Beef under the Coleman Natural Meats brand, Whole Foods said.

Regulators do not monitor meat sold for steaks and roasts as closely as meat sold for ground beef because those primal cuts are less likely to make people sick. For example, if a steak is contaminated, the bacteria is most likely on the outside and killed during cooking. By contrast, with ground beef, the pathogen gets mixed in and can survive if the interior isn't heated to 160 degrees.

Whole Foods grinds its own beef in an attempt to assure quality and safety, spokeswoman Kate Lowery said. In this case, the company said, the cuts used had already been contaminated.


snip...full text ;

http://www.chron.com/disp/story.mpl/headline/biz/5937764.html


http://www.fsis.usda.gov/News_&_Events/Recall_031_2008_update/index.asp

http://www.fsis.usda.gov/News_&_Events/Recall_029_2008_Release/index.asp

http://www.fsis.usda.gov/News_&_Events/Recall_027_2008_Release/index.asp



TSS
 

Kathy

Well-known member
Vaccinations are not the end all to disease. In fact, many of our vaccines are very likely responsibile for the resistance of bacteria to treatment.

And don't forget that these resistant strains of bacteria can also be created by "irradiating" the meat. This process is destroying the "radiosensitive" bacteria which can still be destroyed by the antibiotics; but, the "irradiation" process is mutating and aiding the growth of "radioresistant" bacteria like e coli 0157:H7.

Another likely contributor, is the genetically modified grains which we are feeding our livestock. These foreign genes are inserted into the new cells upon "metal nano-particles" via a "particle gun accelerator". Some scientists might use gold particles, but uranium works better because it is a DNA seeker.

The GM researchers also add genes to make the new plant cells "antibiotic resistant", that way they can tell which cells have successfully been "infected" with the new genetic material. They treat the cells in these petri dishes with an antibiotic and the cells that survive are good to go (GM cells) (the cells that die, were not modified). Don't you think this has an effect on the genetic material of the plants?

There is some indication that the "inserted genetic material" has successfully jumped from the GM plants to their consuming counter-parts (animals and humans). The bacteria in the gut would be affected by this also, making them change their expression of proteins etc.

But man is God, right! That's what so many of these researchers and doctors believe. And the average, everyday people are just going along with their delusional creations and plans of grandeur. Keep buying those GM grains and spreading the seeds of destruction.

OR

Your can eat whole foods, non GM foods, and for God's sake quite using chemicals on everything. Our immune systems are under attack from so many toxins and chemicals that MAN uses for his convenience, the last thing we need to be bombarded with is vaccines full of toxic metals, chemicals and foreign proteins/material.

[/b]
 

Mike

Well-known member
Vaccinations are not the end all to disease. In fact, many of our vaccines are very likely responsibile for the resistance of bacteria to treatment.

Polio and smallpox come to mind. Were vaccinations responsible for their demise? yes or no?

Vaccinations are way to build a natural immunity to a particular bacteria/virus.

I fully agree with the concept.
 

Ben Roberts

Well-known member
Mike said:
Vaccinations are not the end all to disease. In fact, many of our vaccines are very likely responsibile for the resistance of bacteria to treatment.

Polio and smallpox come to mind. Were vaccinations responsible for their demise? yes or no?

Vaccinations are way to build a natural immunity to a particular bacteria/virus.

I fully agree with the concept.


I'm not sure about smallpox, but the Polio vaccine was not the demise of Polio!
 

Mike

Well-known member
Ben Roberts said:
Mike said:
Vaccinations are not the end all to disease. In fact, many of our vaccines are very likely responsibile for the resistance of bacteria to treatment.

Polio and smallpox come to mind. Were vaccinations responsible for their demise? yes or no?

Vaccinations are way to build a natural immunity to a particular bacteria/virus.

I fully agree with the concept.


I'm not sure about smallpox, but the Polio vaccine was not the demise of Polio!

Maybe demise was not the proper word, but we sure don't have Polio like we used too!! Because of vaccinations? Yes or no?

In the last 15 years, the number of cases of polio worldwide has dropped spectacularly, going from 350,000 cases in 1988 when the Global Polio Eradication Initiative began to 1,940 in 2005 (data as of March 14, 2006). This eradication initiative, whose aim is to eliminate all cases due to the wild virus throughout the world, now has tools in place to rapidly stop polio transmission everywhere except Nigeria, where, as of June 2006, another 12 months will be required.

Polio is a unique disease in the history of medicine. In more than one instance, the fight against polio has given rise to an extraordinary public reaction and mobilization. The first polio vaccine, the injectable vaccine developed by Jonas Salk, was hailed as a breakthrough in medical research. Health care for polio victims has led to advances that have become standard practice in today's hospitals. In addition, the methods used to produce the polio vaccine revolutionized manufacturing techniques, which were then applied to other vaccines.

Smallpox, eradicated in 1977 through vaccination, was the first infectious disease to ever be eliminated from the planet. Today polio is on the verge of becoming the second such disease, eradicated thanks to the efforts of countless people.
 

Ben Roberts

Well-known member
Mike said:
Ben Roberts said:
Mike said:
Polio and smallpox come to mind. Were vaccinations responsible for their demise? yes or no?

Vaccinations are way to build a natural immunity to a particular bacteria/virus.

I fully agree with the concept.


I'm not sure about smallpox, but the Polio vaccine was not the demise of Polio!

Maybe demise was not the proper word, but we sure don't have Polio like we used too!! Because of vaccinations? Yes or no?

In the last 15 years, the number of cases of polio worldwide has dropped spectacularly, going from 350,000 cases in 1988 when the Global Polio Eradication Initiative began to 1,940 in 2005 (data as of March 14, 2006). This eradication initiative, whose aim is to eliminate all cases due to the wild virus throughout the world, now has tools in place to rapidly stop polio transmission everywhere except Nigeria, where, as of June 2006, another 12 months will be required.

Polio is a unique disease in the history of medicine. In more than one instance, the fight against polio has given rise to an extraordinary public reaction and mobilization. The first polio vaccine, the injectable vaccine developed by Jonas Salk, was hailed as a breakthrough in medical research. Health care for polio victims has led to advances that have become standard practice in today's hospitals. In addition, the methods used to produce the polio vaccine revolutionized manufacturing techniques, which were then applied to other vaccines.

Smallpox, eradicated in 1977 through vaccination, was the first infectious disease to ever be eliminated from the planet. Today polio is on the verge of becoming the second such disease, eradicated thanks to the efforts of countless people.


NO
 
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