Review on the epidemiology and dynamics of BSE epidemics
Review on the epidemiology and dynamics of BSE epidemics
How to cite this article: Vet. Res. (2008) 39:15 DOI: 10.1051/vetres:2007053
Review on the epidemiology and dynamics of BSE epidemics
Christian Ducrot1, Mark Arnold2, Aline de Koeijer3, Dagmar Heim4 and Didier Calavas5
1 INRA Unité d'Épidémiologie Animale, 63122 Saint-Genès-Champanelle, France 2 VLA Sutton Bonington, The Elms, College Road, Sutton Bonington, Loughborough, LE12 5RB, England 3 Division of Infectious Diseases, Animal Sciences Group, Wageningen, University and Research Center, PO Box 65, 8200 AB Lelystad, The Netherlands 4 Office vétérinaire fédéral, Schwarzenburgstrasse 155, Case Postale 3003, Bern, Suisse 5 AFSSA Lyon, Unité Épidémiologie, 31 avenue Tony Garnier, 69364 Lyon Cedex 07, France
(Received 24 April 2007; accepted 23 October 2007 ; published online 11 January 2008)
Abstract - The paper describes how the comprehensive surveillance of bovine spongiform encephalopathy (BSE) and studies carried out on these data has enhanced our knowledge of the epidemiology of BSE. Around 7 000 BSE cases were detected through the screening of about 50 million cattle with rapid tests in Europe. It confirmed that the clinical surveillance had a poor capacity to detect cases, and also showed the discrepancy of this passive surveillance efficiency between regions and production types (dairy/beef). Other risk factors for BSE were being in a dairy herd (three times more than beef), having a young age at first calving (for dairy cattle), being autumn-born (dairy and beef), and being in a herd with a very high milk yield. These findings focus the risk on the feeding regimen of calves/heifers. Several epidemiological studies across countries suggest that the feedborne source related to meat and bone meal (MBM) is the only substantiated route of infection - even after the feed ban -, while it is not possible to exclude maternal transmission or milk replacers as a source of some infections. In most European countries, the average age of the cases is increasing over time and the prevalence decreasing, which reflects the effectiveness of control measures. Consistent results on the trend of the epidemic were obtained using back-calculation modelling, the R0 approach and Age-Period-Cohort models. Furthermore, active surveillance also resulted in the finding of atypical cases. These are distinct from previously found BSE and classified in two different forms based on biochemical characteristics; their prevalence is very low (36 cases up to 1st September 2007), affected animals were old and some of them displayed clinical signs. The origin and possibility of natural transmission is unknown.
Corresponding author: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000292/!x-usc:mailto:ducrot@clermont.inra.fr
© INRA, EDP Sciences 2008
http://www.vetres.org/index.php?option=article&access=doi&doi=10.1051/vetres:2007053
http://www.vetres.org/articles/vetres/pdf/2008/04/v07232.pdf
USA
THE june 2004 enhanced bse surveillance program was flawed from the beginning, and proven so later by OIG and GAO. also, even cdc's top prion God says he does not trust them ;
In this context, a word is in order about the US testing program. After the discovery of the first (imported) cow in 2003, the magnitude of testing was much increased, reaching a level of >400,000 tests in 2005 (Figure 4). Neither of the 2 more recently indigenously infected older animals with nonspecific clinical features would have been detected without such testing, and neither would have been identified as atypical without confirmatory Western blots. Despite these facts, surveillance has now been decimated to 40,000 annual tests (USDA news release no. 0255.06, July 20, 2006) and invites the accusation that the United States will never know the true status of its involvement with BSE.
http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm
PAUL BROWN COMMENT TO ME ON THIS ISSUE
Tuesday, September 12, 2006 11:10 AM
"Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency."
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=8125
CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006
The U.S. Department of Agriculture was quick to assure the public earlier this week that the third case of mad cow disease did not pose a risk to them, but what federal officials have not acknowledged is that this latest case indicates the deadly disease has been circulating in U.S. herds for at least a decade.
The second case, which was detected last year in a Texas cow and which USDA officials were reluctant to verify, was approximately 12 years old.
These two cases (the latest was detected in an Alabama cow) present a picture of the disease having been here for 10 years or so, since it is thought that cows usually contract the disease from contaminated feed they consume as calves. The concern is that humans can contract a fatal, incurable, brain-wasting illness from consuming beef products contaminated with the mad cow pathogen.
"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."
Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.
USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.
"Everything they did on the Texas cow makes everything USDA did before 2005 suspect," Brown said. ...snip...end
http://www.upi.com/ConsumerHealthDaily/view.php?StoryID=20060315-055557-1284r
CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...
http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm
Geographical BSE Risk (GBR) assessments covering 2000-2006
Date : 01.08.2006
http://www.efsa.europa.eu/EFSA/Scientific_Document/GBR_assessments_table_Overview_assessed_countries_2002-2006.pdf
Audit Report
Animal and Plant Health Inspection Service
Bovine Spongiform Encephalopathy (BSE) Surveillance Program - Phase II
and
Food Safety and Inspection Service
Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat Recovery Products - Phase III
Report No. 50601-10-KC January 2006
Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain
Our prior report identified a number of inherent problems in identifying and testing high-risk cattle. We reported that the challenges in identifying the universe of high-risk cattle, as well as the need to design procedures to obtain an appropriate representation of samples, was critical to the success of the BSE surveillance program. The surveillance program was designed to target nonambulatory cattle, cattle showing signs of CNS disease (including cattle testing negative for rabies), cattle showing signs not inconsistent with BSE, and dead cattle. Although APHIS designed procedures to ensure FSIS condemned cattle were sampled and made a concerted effort for outreach to obtain targeted samples, industry practices not considered in the design of the surveillance program reduced assurance that targeted animals were tested for BSE.
USDA/OIG-A/50601-10-KC Page 27
observe these animals ante mortem when possible to assure the animals from the target population are ultimately sampled and the clinical signs evaluated.
snip...
http://www.usda.gov/oig/webdocs/50601-10-KC.pdf
GAO-05-51 October 2004 FOOD SAFETY
over 500 customers receiving potentially BSE contaminated beef .....
* GAO-05-51 October 2004 FOOD SAFETY (over 500 customers receiving potentially BSE contaminated beef) - TSS 10/20/04
October 2004 FOOD SAFETY USDA and FDA Need to Better Ensure Prompt and Complete Recalls of Potentially Unsafe Food
snip...
REPORTS
1. Food Safety: USDA and FDA Need to Better Ensure Prompt and Complete Recalls of Potentially Unsafe Food. GAO-05-51, October 7.tss
http://www.gao.gov/new.items/d0551.pdf
Highlights -
http://www.gao.gov/highlights/d0551high.pdf
3. Mad Cow Disease: FDA's Management of the Feed Ban Has Improved, but Oversight Weaknesses Continue to Limit Program Effectiveness. GAO-05-101, Feb. 25.
www.gao.gov/cgi-bin/getrpt?GAO-05-101
Highlights -
www.gao.gov/highlights/d05101high.pdf
SADLY, DEC 2005 SHOWS THAT WE STILL HAVE A SERIOUS PROBLEM WITH BSE/TSE MAD COW DISEASE FEED
GAO
GAO-06-157R FDA Feed Testing Program
October 11, 2005
SNIP...FULL TEXT 29 PAGES ;
http://www.gao.gov/new.items/d06157r.pdf
Mad Cow Disease: An Evaluation of a Small Feed Testing Program FDA Implemented in 2003 With Recommendations for Making the Program a Better Oversight Tool. GAO-06-157R, October 11
http://www.gao.gov/cgi-bin/getrpt?GAO-06-157R
USA MAD COW CASES IN ALABAMA AND TEXAS
***PLEASE NOTE***
USA BASE CASE, (ATYPICAL BSE), AND OR TSE (whatever they are calling it today), please note that both the ALABAMA COW, AND THE TEXAS COW,both were ''H-TYPE'', personal communication Detwiler et al Wednesday, August 22, 2007 11:52 PM. ...TSS
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=19779
confusious is confused again ;-)
omitting the hypothesis of a literal spontaneous happening for the BASE cases there is absolutely no proof for a spontaneous TSE anywhere in the field. some scientist are trying to claim now that the BASE cases arise spontaneously like they claim the 85%+ of all cases of CJD are sporadic/spontaneous without any cause. i prefer to believe in santa clause instead. there's more proof for that.
aside from that myth ;
i keep hearing that these atypical BSE h-base and l-base, similar to some subtypes of sporadic CJD and GSS pathologically, that these atypical BSE BASE cases are just 'aged' BSE cases. SO, would it not be that what's good for the goose is good for the gander i.e. sporadic CJDs are nothing more than 'aged' nvCJD. i mean, if that hypothesis plays out with the 'aged' BSE=ing BASEs in cows, why not humans. it's just all the same BSe. just 'aged' brains = different pathology, different symptoms and such. it goes back to the old myth with the first nvCJD 10 cases that only young kids with CJD have amyloid kuru type plaques, until the elderly started showing up with them. confusious just pondering out loud again. ...TSS
or these new phenotypes may be found, at least in part, to result from infections at an older age by a typical BSE agent, rather than neonatal infections with new "strains" of BSE. Neither alternative has yet been investigated.
http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm
SEAC unusual cases of BSE
http://www.seac.gov.uk/papers/96-2.pdf
PAUL BROWN COMMENT TO ME ON THIS ISSUE
Tuesday, September 12, 2006 11:10 AM
"Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency."
http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=8125
Wednesday, February 27, 2008
BEEF RECALL NATIONWIDE - SCHOOL LUNCH PROGRAM UPDATE
http://downercattle.blogspot.com/2008/02/beef-recall-nationwide-school-lunch.html
TSS
http://bse-atypical.blogspot.com/2008/03/review-on-epidemiology-and-dynamics-of.html
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