Header graphic for print

Food Safety News

Breaking news for everyone's consumption

Food Safety Spending in Canada Might Be Cut

At some date soon in February or March, Canadian Finance Minister Jim Flaherty may follow the tradition of putting on new shoes and walking into the House of Commons with a proposed new federal budget.

Ever since it received the report of an independent inquiry into the deadly 2008 Listeria outbreak that was traced back to Maple Leaf Foods in Toronto, Ottawa has approved budgets that have favored food safety with more financial support.

Now, the tide may go the other way.   

The Conservative government has to deal with a projected budget deficit totaling $31 billion.   It also wants to increase spending on trade, research and development, and cut red tape to help businesses.

Government departments, including the Canadian Food Inspection Agency (CFIA), have been asked to work on budgets cuts of 5 to 10 percent. Budget cuts at CFIA could take away 234 jobs, cutting the agency’s current annual spending of $744 million by about $21.5 million.

The union representing Canada’s federal meat inspectors held a news conference Monday to loudly complain about the possible cuts that they claim would take CFIA back to pre-Listeria outbreak levels by taking away 170 inspectors hired after the Listeria outbreak.

Agriculture Minister Gerry Ritz, in an email response to the union news conference, said, “Canadian families can be assured that the safety of our food supply will not be affected as federal departments and agencies look for ways to more efficient and more financially prudent with taxpayer’s dollars.”

Since 2008, Ottawa added $75 million to implement the recommendations of Sheila Weatherill, the independent investigator who looked into the deadly outbreak that killed 22 mostly elderly Canadians.

It then added $13 million in 2010 for added meat inspection capacity, and $100 million in 2011 for increased scientific and technology capacity, with $18 million going directly to CFIA.

As of March 2011, CFIA’s total staff, including inspection staff, “as well as additional essential positions relating to audit and evaluation, legal, human resources and corporate services” stood at 7,544, up from 6,961 in March 2008.  

Overall, that’s a bump of 583 employees.

In March 2008, inspection staff at CFIA totaled 4,571. Three years later it was up 327 to 4,898 total inspection staffers in March 2011.  

That translates to 56 percent of the new hires being in inspection.

But it is not all about new hires.   

The number of front-line inspectors and inspection manger working in the field in food processing plants was up 472, to 3,502, in March 2011, from 3,030 in March 2008.

That means 81 percent of the new hires have ended up in field positions, apparently through both new hires and new assignments.

Food Safety News has asked CFIA to update the employment totals for 2012 and the project has been assigned, but the latest figures are not yet available.

The possible cuts outlined in CFIA’s funding estimates “would leave the food safety program reeling and severely diminish an inspector’s ability to complete assignments,” asserted Bob Kingston, the union president said.  He said any cuts increase the risk of another major food-borne outbreak.

He was joined by Karen Clark, whose 89-year-old mother, Frances died from listeriosis after eating contaminated ready-to-eat meats processed by Maple Leaf Foods.  Clark says she fears Canadians have forgotten about the Listeria outbreak.

CFIA investigations most recently peaked in the April 2008 to March 2009 period at 3,439, before declining to 2,956 during April 2010 to March 2011.

Jobs and housing are much stronger in Canada, but its economy is stuck between Europe’s instability and USA’s weak recovery. Since the Conservatives took over in 2006, Canada has added about 33,000 federal jobs at a cost of $75 billion.

Meanwhile, the minority New Democratic Party (NDP) is asking Prime Minister Stephen Harper to just spare food safety of any cuts.

While vocal in the aftermath of the outbreak and during the independent investigation, neither Michael H. McCain, Maple Leaf’s president and chief executive officer, nor Randall Huffman, the Toronto company’s chief food safety officer, responded to  invitations from Food Safety News to comment about the possible cuts.

Huffman, the former head of the American Meat Institute Foundation, joined Maple Leaf after the 2008 outbreak.

© Food Safety News
  • THIS is not surprising. Seems Canada has taken the bad habits of the USDA et al. Canada now refuses to release any information on their mad cows. Canada and the USA are both rated as BSE GBR III.
    bottom line, the USDA, CFIA, OIE, and officials there from, have concluded, a slow incubating disease, one that is 100% fatal once clinical in humans and animals does not matter, only the trade there from does$
    Friday, December 30, 2011
    Feds back Quebec R+D for SRM removal equipment Canada
    Friday, March 4, 2011
    Alberta dairy cow found with mad cow disease
    Wednesday, August 11, 2010
    Thursday, August 19, 2010
    Thursday, February 10, 2011
    TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31
    Increased Atypical Scrapie Detections
    Press reports indicate that increased surveillance is catching what otherwise would have been unreported findings of atypical scrapie in sheep. In 2009, five new cases have been reported in Quebec, Ontario, Alberta, and Saskatchewan. With the exception of Quebec, all cases have been diagnosed as being the atypical form found in older animals. Canada encourages producers to join its voluntary surveillance program in order to gain scrapie-free status. The World Animal Health will not classify Canada as scrapie-free until no new cases are reported for seven years. The Canadian Sheep Federation is calling on the government to fund a wider surveillance program in order to establish the level of prevalence prior to setting an eradication date. Besides long-term testing, industry is calling for a compensation program for farmers who report unusual deaths in their flocks.
    Thursday, December 22, 2011
    Chronic Wasting Disease discovered on game farm Saskatchewan Wednesday Dec. 21, 2011
    PRIONET CANADA Canada’s prion research network Annual Report 2010 / 2011
    J Vet Diagn Invest 21:454-463 (2009)
    Nor98 scrapie identified in the United States
    Christie M. Loiacono,’ Bruce V. Thomsen, S. Mark Hall, Matti Kiupe!, Diane Sutton, Katherine O’Rourke, Bradd Barr, Lucy Anthenill, Deiwyn Keane
    A distinct strain of scrapic identified in sheep of Norway in 1998 has since been identified in numerous countries throughout Europe. The disease is known as Nor98 or Not-98-like scrapic. among other names. Distinctions between classic scrapie and Nor98 scrapie are made based on histopathologv and immunodiagnostic results. There are also differences in the epidemiology, typical signalment, and likelihood of clinical signs being observed. In addition, sheep that have genotypes associated with resistance to classic scrapie are not spared from Nor98 disease. The various differences between classic and Nor98 scrapie have been consistently reported in the vast majority of cases described across Europe. The current study describes in detail the patholo gic changes and diagnostic results of the first 6 cases of’ Nor98 scrapic disease diagnosed in sheep of the United States.
    Key words: Hisiopathology: Nor98: PrP imniunolabeling; scrapie: sheep.
    Case I
    The first case identified as consistent with Nor98 scrapie had nonclassic PrP distribution in brain tissue, no PrPSC in lymph tissue, and nonclassic migration of protein bands on a Western blot test. The animal was an aged, mottled-faced ewe that was traced back to a commercial flock in Wyoming. …
    Case 2
    The second case was a clinically normal 8-year-old Suffolk ewe that had been in a quarantined flock for 5 years at a USDA facility in Iowa.
    Case 3
    A 16-year-old, white-faced, cross-bred wether was born to a black-faced ewe. He lived his entire life as a pet on a farm in California.
    Case 4
    The fourth case of Nor98 scrapie was identified in an approximately 8-year-old Dorset ewe that was born into a flock of approximately 20 ewes in Indiana.
    Case 5
    The fifth case was a clinically normal, approximately 3-year-old, white-faced, cross-bred ewe from an approximately 400 head commercial flock in Minnesota.
    Case 6
    The sixth case of Nor98 scrapie was identified in a 4-year-old, white-faced ewe that was purchased and added to a commercial flock in Pennsylvania
    see full text ;
    Wednesday, February 16, 2011
    Sunday, April 18, 2010
    Monday, April 25, 2011
    Experimental Oral Transmission of Atypical Scrapie to Sheep
    Volume 17, Number 5-May 2011
    Sunday, March 28, 2010
    Nor-98 atypical Scrapie, atypical BSE, spontaneous TSE, trade policy, sound science ?
    Monday, November 30, 2009
    I strenuously urge the USDA and the OIE et al to revoke the exemption of the legal global trading of atypical Nor-98 scrapie TSE. …TSS
    Friday, February 11, 2011
    Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues
    Monday, January 16, 2012
    Tuesday, December 20, 2011
    CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011
    Tuesday, January 17, 2012
    Annual report of the Scientific Network on BSE-TSE EFSA-Q-2011-01110 Issued: 20 December 2011
    last two _DOCUMENTED_ mad cows in the USA (EXCLUDING THE OTHER DOCUMENTED, UNDOCUMENTED stumbling and staggering mad cow in Texas that was rendered without being tested), and excluding the c-BSE case old Dave bolted in Washington.
    LET’S take a closer look at this new prionpathy or prionopathy, and then let’s look at the g-h-BSEalabama mad cow. This new prionopathy in humans? the genetic makeup is IDENTICAL to the g-h-BSEalabama mad cow, the only _documented_ mad cow in the world to date like this, ……wait, it get’s better. this new prionpathy is killing young and old humans, with LONG DURATION from onset of symptoms to death, and the symptoms are very similar to nvCJD victims, OH, and the plaques are very similar in some cases too, bbbut, it’s not related to the g-h-BSEalabama cow, WAIT NOW, it gets even better, the new human prionpathy that they claim is a genetic TSE, has no relation to any gene mutation in that family. daaa, ya think it could be related to that mad cow with the same genetic make-up ??? there were literally tons and tons of banned mad cow protein in Alabama in commerce, and none of it transmitted to cows, and the cows to humans there from ??? r i g h t $$$ ALABAMA MAD COW g-h-BSEalabama In this study, we identified a novel mutation in the bovine prion protein gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United States of America. This mutation is identical to the E200K pathogenic mutation found in humans with a genetic form of CJD. This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene. We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in “the approximately 10-year-old cow” carrying the E221K mutation.
    her healthy calf also carried the mutation (J. A. Richt and S. M. Hall PLoS Pathog. 4, e1000156; 2008).
    This raises the possibility that the disease could occasionally be genetic in origin. Indeed, the report of the UK BSE Inquiry in 2000 suggested that the UK epidemic had most likely originated from such a mutation and argued against the scrapierelated assumption. Such rare potential pathogenic PRNP mutations could occur in countries at present considered to be free of BSE, such as Australia and New Zealand. So it is important to maintain strict surveillance for BSE in cattle, with rigorous enforcement of the ruminant feed ban (many countries still feed ruminant proteins to pigs). Removal of specified risk material, such as brain and spinal cord, from cattle at slaughter prevents infected material from entering the human food chain. Routine genetic screening of cattle for PRNP mutations, which is now available, could provide additional data on the risk to the public. Because the point mutation identified in the Alabama animals is identical to that responsible for the commonest type of familial (genetic) CJD in humans, it is possible that the resulting infective prion protein might cross the bovine-human species barrier more easily. Patients with vCJD continue to be identified. The fact that this is happening less often should not lead to relaxation of the controls necessary to prevent future outbreaks. Malcolm A. Ferguson-Smith Cambridge University Department of Veterinary Medicine, Madingley Road, Cambridge CB3 0ES, UK e-mail: maf12@cam.ac.uk Jürgen A. Richt College of Veterinary Medicine, Kansas State University, K224B Mosier Hall, Manhattan, Kansas 66506-5601, USA NATURE|Vol 457|26 February 2009
    Saturday, August 14, 2010
    BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY (see mad cow feed in COMMERCE IN ALABAMA…TSS)
    Saturday, June 25, 2011
    Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque
    “BSE-L in North America may have existed for decades”
    When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
    This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.
    Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
    The rancher was a ”dead stock” feeder using mostly (>95%) downer or dead dairy cattle…
    Transmission of atypical BSE in humanized mouse models
    Liuting Qing1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5, Qingzhong Kong1 1Case Western Reserve University, USA; 2Instituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University (Previously at USDA National Animal Disease Center), USA
    Background: Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Atypical BSE cases have been discovered in three continents since 2004; they include the L-type (also named BASE), the H-type, and the first reported case of naturally occurring BSE with mutated bovine PRNP (termed BSE-M). The public health risks posed by atypical BSE were largely undefined.
    Objectives: To investigate these atypical BSE types in terms of their transmissibility and phenotypes in humanized mice. Methods: Transgenic mice expressing human PrP were inoculated with several classical (C-type) and atypical (L-, H-, or Mtype) BSE isolates, and the transmission rate, incubation time, characteristics and distribution of PrPSc, symptoms, and histopathology were or will be examined and compared.
    Results: Sixty percent of BASE-inoculated humanized mice became infected with minimal spongiosis and an average incubation time of 20-22 months, whereas only one of the C-type BSE-inoculated mice developed prion disease after more than 2 years. Protease-resistant PrPSc in BASE-infected humanized Tg mouse brains was biochemically different from bovine BASE or sCJD. PrPSc was also detected in the spleen of 22% of BASE-infected humanized mice, but not in those infected with sCJD. Secondary transmission of BASE in the humanized mice led to a small reduction in incubation time.*** The atypical BSE-H strain is also transmissible with distinct phenotypes in the humanized mice, but no BSE-M transmission has been observed so far.
    Discussion: Our results demonstrate that BASE is more virulent than classical BSE, has a lymphotropic phenotype, and displays a modest transmission barrier in our humanized mice. BSE-H is also transmissible in our humanized Tg mice. The possibility of more than two atypical BSE strains will be discussed.
    Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.
    Liuting Qing1, Fusong Chen1, Michael Payne1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5*, and Qingzhong Kong1 1Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA; 2CEA, Istituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University, Diagnostic Medicine/Pathobiology Department, Manhattan, KS 66506, USA. *Previous address: USDA National Animal Disease Center, Ames, IA 50010, USA
    Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Two atypical BSE strains, BSE-L (also named BASE) and BSE-H, have been discovered in three continents since 2004. The first case of naturally occurring BSE with mutated bovine PrP gene (termed BSE-M) was also found in 2006 in the USA. The transmissibility and phenotypes of these atypical BSE strains/isolates in humans were unknown. We have inoculated humanized transgenic mice with classical and atypical BSE strains (BSE-C, BSE-L, BSE-H) and the BSE-M isolate. We have found that the atypical BSE-L strain is much more virulent than the classical BSE-C.*** The atypical BSE-H strain is also transmissible in the humanized transgenic mice with distinct phenotype, but no transmission has been observed for the BSE-M isolate so far.
    I ask Professor Kong ;
    Thursday, December 04, 2008 3:37 PM Subject: RE: re–Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment
    ”IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious…..”
    Professor Kong reply ;
    ”As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete. Thanks for your interest.”
    Best regards, Qingzhong Kong, PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA
    Thursday, December 04, 2008 2:37 PM
    “we have found that H-BSE can infect humans.”
    personal communication with Professor Kong. …TSS
    BSE-H is also transmissible in our humanized Tg mice.
    The possibility of more than two atypical BSE strains will be discussed.
    Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.
    Saturday, December 01, 2007 Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model Volume 13, Number 12–December 2007 Research
    Saturday, November 19, 2011
    Novel Prion Protein in BSE-affected Cattle, Switzerland
    Friday, January 6, 2012
    OIE 2012 Training Manual on Wildlife Diseases and Surveillance and TSE Prion disease
    Tuesday, January 17, 2012
    Annual report of the Scientific Network on BSE-TSE EFSA-Q-2011-01110 Issued: 20 December 2011
    2011 Monday, September 26, 2011
    L-BSE BASE prion and atypical sporadic CJD
    Tuesday, January 17, 2012
    Canadian Inspectors criticize plan to cut inspections at meat plants
    Meat inspectors’ union warns of cuts to government’s food-safety program