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From: TSS ()
Date: October 13, 2006 at 11:25 am PST



BSE Surveillance

Since 1990, the U.S. Department of Agriculture (USDA)

has taken aggressive measures to prevent the introduction

and potential spread of BSE. Following confirmation

of BSE in an imported cow in December 2003, USDA

designed and implemented an Enhanced BSE Surveillance

Program to more accurately determine the level of disease

present in the U.S. cattle population.

The Enhanced BSE Surveillance Program tested as many

cattle as possible in the targeted high-risk population

beginning June 1, 2004. Collection at an enhanced level

has continued beyond 18 months to ameliorate concerns

of trading partners. Experience in the United Kingdom

and Europe has shown that, if present, BSE is most likely

to be detected in adult cattle exhibiting clinical signs

consistent with the disease.

In general, the highest risk categories are adult cattle

showing clinical signs involving the central nervous

system (CNS) and dead and nonambulatory cattle with

clinical signs that could not be adequately evaluated. This

population was estimated to total 445,886 adult cattle per

year in the United States. This number was derived in part

from National Animal Health Monitoring System (NAHMS)

surveys of livestock producers and other estimates.

This estimate includes adult cattle in the following


Condemned at slaughter for CNS signs;

Moribund, dead, injured, or emaciated (FSIS data


CNS abnormalities reported for FAD investigations

(APHIS data 2003);

Died onfarm of unknown causes;

Lameness or injury that resulted in euthanasia; and

Cattle that died with signs of incoordination or severe


The sampling strategy was designed to target animals in

these categories.

Between June 1, 2004, and March 17, 2006, BSE samples

were collected from 5,776 unique locations across the

United States. These locations included slaughter plants,

renderers, farms, public health laboratories, veterinary

diagnostic laboratories, and salvage slaughter (3D–4D)1


To determine the extent to which the U.S. surveillance is

consistent with OIE guidelines, we have evaluated and

classified surveillance data over the past 7 years according

to OIE standards (table 5).

In May 2005, the OIE general Assembly approved a

new chapter and appendix for BSE surveillance. This

approach assigned point values to each sample, based on

animal age and the subpopulation it was from, and the

likelihood of detecting infected cattle of that age in that

subpopulation. (Prior to May 2005, OIE had recommended

a surveillance level based on the size of the adult cattle

population—for the United States that number was 433

samples with clinical signs consistent with BSE per year.)

Sample values were classified in the OIE system as

belonging to four surveillance strata (streams): clinical

suspect, casualty slaughter, fallen stock, and healthy

slaughter. Samples were also stratified by age.

Cattle were categorized in the clinical suspect stream

if they were submitted under the submission types of

highly suspicious for BSE, rabies suspects, CNS signs,

or antemortem-condemned by FSIS with condemnation

codes for CNS signs or rabies. In addition, many samples

with a clinical history of signs likely to be associated with

BSE were submitted in other categories. Many of these

represented valuable samples, but the OIE definition of

“clinical suspect” did not readily differentiate them from

animals with other clinical signs compatible with BSE.

Some of these cattle were subsequently categorized as

clinical suspects by comparing the likelihood of finding

the signs in histopathologically confirmed cases reported

in the United Kingdom2 with the likelihood of finding

the signs in uninfected animals from the enhancedsurveillance

targeted population. For example, if a sign or

combination of signs were found 30 percent of the time

in BSE cases but only once in every 1,000 uninfected

animals (0.1 percent), then it would be 0.30/0.001 = 300

times more likely to occur in the cases (likelihood ratio =

300 in this case). A likelihood ratio threshold of 807 was

established as a cutoff value for determination of clinical

suspects. This threshold was estimated using input data

from the United Kingdom in the BSurvE3 model, which

provided the average (expected) value for the ratio of

probability of an infected animal showing clinical signs

to an uninfected animal showing clinical signs. Thus, if a

sample was submitted from an animal with combinations

of clinical signs at least 807 times more likely to have

been seen in BSE cases than in the U.S. high-risk

population, it was classified as a clinical suspect.

Cattle with likelihood ratios below the threshold were

allocated into surveillance streams according to the

animal’s submission type as follows:

Submission types of “Nonambulatory” were classified

in the “casualty slaughter” stream;

Submission types of “Other clinical signs that may be

associated with BSE” were classified in the “casualty

slaughter” stream;

Submission types of “FSIS antemortem condemned”

were classified in the “casualty slaughter” stream as

long as the condemnation reason was not “dead”;

Submission types of “FSIS antemortem condemned”

with a condemnation code of “dead” were classified in

the “fallen stock” stream;

Submission types of “dead” were classified in the

“fallen stock” stream;

Submission types of “apparently healthy” were

classified in the “healthy slaughter” stream.

BSE surveillance samples from 1999 through 2003

were collected before the OIE surveillance streams

were established in 2005 and were not submitted with

the same clinical history as that used for the enhanced

surveillance in 2004–05. In order to apply the OIE point

tables, data about these samples were requested from

the National Veterinary Services Laboratories (NVSL) and

were sorted by Centers for Epidemiology and Animal

Health (CEAH) epidemiologists based on the history

included with the sample.

This information is excerpted from the report Summary

of BSE Surveillance in the United States accessed and

available on the Web as of May 2, 2006, at


06.pdf>. Details on the Enhanced BSE Surveillance

Program are posted at issues/bse/BSEOIg.pdf>.

2 Wilesmith, J. W.; Ryan, J. B.; Hueston, W. D. 1992. Bovine spongiform

encephalopathy: case-control studies of calf feeding practices and

meat and bonemeal inclusion in proprietary concentrates. Research in

Veterinary Science 52(3): 325–331.

3 Available, as of April 20, 2006, at . The

BSurvE tool is a Microsoft Excel™ spreadsheet application designed to

estimate BSE prevalence based on targeted sampling strategies.

35 Chapter 2: National Animal Health Surveillance System (NAHSS)

TABLE 5: OIE points from BSE surveillance in the U.S. accumulated for 7 years

Year of testing1










slaughter OIE points3

10/1/05 to 03/17/064 181,564 438 142,337 18,991 19,798 285,491

FY5 2005 413,647 1,527 361,557 50,557 6 899,642

FY 2004 90,085 1,066 62,054 25,096 1,869 592,369

FY 2003 20,778 577 3,106 16,613 482 267,480

FY 2002 20,380 569 2,818 16,045 948 251,740

FY 2001 5,340 665 1 4,515 159 299,177

FY 2000 2,753 664 0 2,064 25 266,891

4/1/99 to 9/30/996 666 265 15 351 35 111,014

Total surveillance

(including enhanced surveillance)

7735,213 5,771 571,888 134,232 23,322 2,973,804

Total for enhanced surveillance only

6/1/04 to 3/17/06

667,767 2,602 559,546 84,534 21,085 1,583,127

1 Testing includes the most recent 7 years of data collected from Apr. 1, 1999, through March 17, 2006.

2 Number of samples and clinical suspects represents animals eligible for surveillance according to the Terrestrial Animal Health Code Article 3.8.4.

3 Note: Animals counted as eligible for OIE points included animals older than 1 year according to the OIE point allocation table. Removal of points from the “juvenile”

category of the OIE points table would decrease the total by 2,843 points. Other documents showing U.S. data may vary due to inclusion or exclusion of young animals.

4 Includes 6 months of fiscal year 2006.

5 The U.S. Government’s fiscal year extends from October 1 through September 30 (e.g., FY 2005 began on 10/1/2004 and ended on 9/30/2005).

6 Includes 6 months of FY 1999.

7 Total includes two positive indigenous animals and one positive animal imported from Canada.

1 3D–4D facilities are slaughter facilities that salvage meat from dead,

dying, disabled, or diseased animals, the meat from which would not

likely pass inspection for human consumption (i.e., edible meat). Much

of this meat goes into either pet food or rendering.

34 2005 United States Animal Health Report

Scrapie Surveillance Evaluation

In general, evaluating a surveillance program entails a

systematic review to assess the degree to which the

program fulfills its stated objectives and meets accepted

surveillance standards. Program strengths and areas for

improvement are identified, and the program’s ability to

adapt to changing situations is evaluated. Evaluating the

surveillance component of one VS program disease was

identified as a key action item in the NAHSS strategic

plan (see nahss/NAHSS_Strategic_Plan_2005_0216.pdf>).

The surveillance component of the VS scrapie

program was chosen for evaluation. Led by the NSU,

an interdisciplinary working group was developed

consisting of an economist, statistician, several veterinary

epidemiologists, and an industry representative.

The evaluation process focused on four main areas:

surveillance structures (organization and communication),

surveillance processes (data collection, data analysis and

interpretation, and dissemination of results), qualitative

attributes (i.e., simplicity, flexibility, acceptability), and

resource distribution and utilization. Characteristics of the

system were compared with the draft VS Surveillance

Standards, as noted throughout the evaluation.

The evaluation and data gathered focused primarily on the

Regulatory Scrapie Slaughter Surveillance Program testing

and other nonslaughter surveillance testing in sheep

implemented since 2001. Although most of the evaluation

results should be applicable to scrapie surveillance in

goats, this component was not specifically evaluated.

Phone interviews were conducted with State and/or VS

field personnel involved in scrapie surveillance activities

in nine different States representing both APHIS’ Eastern

and Western Regions. Questions addressed the general

objectives, importance, and efficiency of the program; the

communication within the program; and the acceptability,

compliance, and coverage of the program. Personnel

interviewed were assured anonymity.

The evaluation report has been completed and delivered

to VS’ National Center for Animal Health Programs.



Animal Disease Eradication Programs and Control and Certification Programs

The following Veterinary Services (VS) programs are

designed to eradicate, control, or prevent diseases that

threaten the biological and commercial health of the U.S.

livestock and poultry industries.

Eradication Programs

VS eradication programs include scrapie in sheep and

goats, tuberculosis in cattle and cervids, pseudorabies and

brucellosis in swine, and brucellosis in cattle and bison.

Scrapie in Sheep and Goats

Disease and Program History—Scrapie was first

discovered in the United States in 1947 in a Michigan

flock that, for several years, had imported sheep of

British origin from Canada. Since 1952, VS has worked

to control scrapie in the United States. As a result of

increasing industry and public concern about transmissible

spongiform encephalopathies (TSEs) and the discovery of

new TSE diagnostic and control methods, VS initiated an

accelerated scrapie eradication program in 2000.

Current Program—The primary aspects of the scrapie

eradication program are animal identification, surveillance,

tracing of positive and exposed animals, testing of sheep

and goats in exposed flocks, cleanup of infected flocks,

and certification of flocks.

Animal Identification—Identification of breeding

sheep and culled breeding sheep is mandatory when

ownership changes. The only sheep that do not have to

be identified are those less than 18 months old and, in

the case of ewes, those that also have not lambed or

become pregnant and are in slaughter channels. As of

September 30, 2005, 103,580 premises with sheep and/or

goats were recorded in the scrapie national database. (In

this database, a premises that contains both sheep and

goats might be listed once for each species.) Of these

premises, 73,807 have requested and received official

eartags (tags approved for use by the Animal and Plant

Health Inspection Service [APHIS] in the official scrapie

eradication program).

Regulatory Scrapie Slaughter Surveillance (RSSS)—

The RSSS program, initiated on April 1, 2003, is the

primary surveillance method for scrapie in the United

States. RSSS identifies scrapie-infected flocks through

targeted slaughter surveillance of sheep and goat

populations that have been recognized as having higherthan-

average scrapie prevalence. These are defined as

mature black- or mottle-faced sheep and any mature

sheep or goats showing clinical signs that could be

associated with scrapie, such as poor body condition,

wool loss, or gait abnormalities. Only sheep with some

form of identification (e.g., such as United States

Department of Agriculture [USDA]-approved eartags,

electronic ID, backtags, and tattoos or lot identification)

are sampled. This arrangement allows for tracing positive

animals back to the farm of origin.

During FY 2005, as part of the RSSS program, 30,247

sheep and goat samples, collected from 78 slaughter

plants in 24 States, were tested for scrapie using

immunohistochemistry on brain or lymphoid tissue, or

both. Of the 106 animals diagnosed as positive for scrapie,

93 were black-faced, 11 were mottle-faced, 1 was whitefaced,

and 1 was unknown.

Under the scrapie program, positive test results are traced

back to the animal’s flock of origin, and the flock is placed

under movement restrictions until all high-risk animals

(genetically susceptible females) are removed. High-risk

animals that had been moved from these flocks before

being placed under movement restrictions are traced and


Testing Summary—In response to epidemiologic

suspicions of disease, field Veterinary Medical Officers

conduct testing to determine if scrapie is present. Such

cases are known as regulatory field cases. In addition to

the 30,247 samples tested under the RSSS program in

2005, about 5,200 additional tests were conducted for

scrapie—either by third-eyelid testing or necropsy—in

response to epidemiologic suspicions of disease.

Case and Infected Flock Summary—In FY 2005, 165

newly identified infected flocks were reported, and

598 scrapie cases were confirmed and reported by the

National Veterinary Services Laboratories (NVSL) (table

6). A scrapie case is defined as an animal for which a

diagnosis of scrapie has been made by the NVSL using a

USDA-approved test (typically immunohistochemistry on

the obex or a peripheral lymph node). During FY 2005, two

scrapie cases were reported in goats. Figure 30 presents

the geographic location of U.S. mature ewe populations

(National Agricultural Statistics Service 2002 Census)

relative to flocks found to be positive for scrapie through

RSSS sampling or another regulatory or surveillance

method (denoted by NVSL-positive flocks).

40 2005 United States Animal Health Report

TABLE 6. Scrapie cases, FY 2003 through FY 2005

Number of cases

Tests or examinations FY 2003 FY 2004 FY 2005

Necropsies 315 374 461

Regulatory third-eyelid 32 20 31

RSSS 123 86 106

Total 370 480 598

1 Includes part of FY 2003 (April 1–September 30, 2003).

FIgURE 30: Distribution of mature ewe populations, by county, compared to positive flocks

(FY 2003–early FY 2006).


Scrapie susceptibility in sheep in the United States has

been associated with two codons that encode for amino

acids in the PrP protein. These codons are at positions

136 and 171, the latter of which is thought to be the major

determinant of scrapie susceptibility in the United States.

For all the scrapie-positive sheep with known genotypes

in FY 2005, 98.4 percent were QQ at codon 171. Of these,

82.6 percent were AA at codon 136, 5.4 percent were

AV at codon 136, 0.4 percent were VV at codon 136, and

11.6 percent did not have results for codon 136. Of the

remaining 1.6 percent that were not QQ at codon 171,

0.3 percent were AAQH and 1.3 percent were AVQR at

codons 136 and 171.

Scrapie Flock Certification Program (SFCP)—The SFCP

is a cooperative effort among producers, State and Federal

animal health agencies, and industry representatives.

Through the SFCP, a flock becomes certified if, during

a 5-year monitoring period, no sheep in the flock are

diagnosed with scrapie and no clinical evidence of scrapie

is found in the flock. The program categories are described

in the following paragraphs.

Complete Monitored Category—A flock in this category

is approved to participate in the program. There are two

status levels for flocks in this category:

Enrolled flock: A flock entering the program is

assigned enrolled status and is a “complete monitored

enrolled flock.”

Certified flock: An enrolled flock that has met program

standards for 5 consecutive years advances to certified

status, meaning that it is unlikely to contain any sheep

infected with scrapie.

Selective Monitored Category—This category, though

open to any flock, was designed for producers of slaughter

lambs to allow for scrapie surveillance in large production

flocks. Only male animals over 1 year of age must have

official identification. Producers agree on the basis of

flock size to submit for scrapie diagnosis a portion of

the mature animals that are culled or die. Additionally,

an accredited veterinarian must inspect all cull ewes for

clinical signs of scrapie before slaughter. Selective status

is maintained indefinitely as long as the flock meets the

category requirements.

Trends in Plan Enrollment—Enrollment in the SFCP

has increased since 2002. As of September 30, 2005,

1,961 flocks were participating, and of these 188 were

certified flocks (table 7). One possible reason for the

increased number of certifications in 2005 was participant

awareness of standards changes, which now allow rams

from lower status flocks to be added to certified flocks

without lowering the certified flock’s status.



Challenges—For the coming year, major challenges

are to continue expanding surveillance efforts into

underrepresented areas and to increase the traceability of

sheep and goats presented for sampling. Traceability will

be enhanced by increasing compliance activities and by

improving methods for identifying and tracking sheep and

goats through review and testing of available identification

systems and integration with the National Animal

Identification System. A second tier of challenges includes

upgrading the scrapie national database, improving

field data collection by refining sample collection and

submission, and streamlining data entry and analysis.


Control and Certification Programs

Chronic Wasting Disease (CWD) in Cervids

Disease and Program History—First recognized in 1967

as a clinical “wasting” syndrome in mule deer at a wildlife

research facility in northern Colorado, CWD was identified

as a TSE in 1978. There is no known relationship between

CWD, which occurs in cervids, and any other TSE of

animals or humans.

In the mid–1980s, CWD was detected in free-ranging

deer and elk in contiguous areas of northeastern Colorado

and southeastern Wyoming. In May 1999, CWD was

found in free-ranging deer in the southwestern corner of

Nebraska (adjacent to Colorado and Wyoming) and later in

other areas in western and central Nebraska. Since 2002,

CWD has also been detected in wild deer, elk, or both

in south-central Wisconsin, southwestern South Dakota,

the western slope of the Rocky Mountains in Colorado,

southern New Mexico, northern Illinois, eastern and

central Utah, central New York, the eastern arm of West

Virginia, and northwestern Kansas. (Note: The Kansas

positive deer was harvested in late 2005, but test results

were not completed and confirmed until early 2006.)

The first infected free-ranging moose was detected in

Colorado in 2005.

49 Chapter 3: Animal Disease Eradication Programs and Control and Certification Programs

The first CWD-positive farmed elk herd in the United

States was detected in 1997 in South Dakota. Through

December 31, 2005, 31 additional CWD-positive farmed

elk herds and 8 CWD-positive farmed deer herds have

been found, for a total of 40 infected farmed cervid herds.

Current Program—APHIS–VS and State CWD surveillance

in farmed animals began in late 1997 and has increased

each year since. APHIS–VS pays laboratory costs for

all surveillance testing of farmed cervids. Responses

to onfarm CWD-positive cases include depopulation

with indemnity or quarantine. Additionally, VS conducts

traceforward and traceback epidemiologic investigations.

A proposed rule for a CWD herd-certification program for

farmed-cervid operations was published for comment in

the Federal Register on December 24, 2003. Program

goals are to control and eventually eradicate CWD from

farmed cervid herds. The program would certify herds

that demonstrate 5 years of CWD surveillance with no

evidence of disease. The proposed program requirements

include fencing, identification, inventory, and surveillance.

The rule is intended to limit interstate movement of

farmed cervids to herds enrolled in the herd-certification

program. State programs meeting or exceeding Federal

standards will be included in the Federal program. The final

rule for this program will be published and the program

implemented in 2006.

APHIS–VS has also supported CWD surveillance in wildlife

beginning in 1997. Since the national “Plan for Assisting

States, Federal Agencies, and Tribes in Managing Chronic

Wasting Disease in Wild and Captive Cervids” was

adopted in June 2002, APHIS–VS has cooperated with the

International Association of Fish and Wildlife Agencies to

promote uniform, nationwide surveillance while allowing

flexibility to meet individual State situations and needs.

Since beginning to receive line-item funding for CWD

in FY 2003, APHIS-VS has been providing assistance to

State wildlife agencies and tribes through cooperative

agreements to address the disease in free-ranging deer

and elk. This funding has covered surveillance testing

for some 90,000 hunter-killed and targeted animals in

the 2002–03 and the 2003–04 hunting seasons. Similar

numbers were projected for 2004–05 and 2005–06. All

50 States participated in the first 2 years of the program,

and 47 States requested and received funding in FY 2005.

Funding is distributed through a tiered system based on risk

of disease developed in consultation with the International

Association of Fish and Wildlife Agencies. In addition to

individual tribal assistance, an agreement with the Native

American Fish and Wildlife Society funds five regional CWD

tribal biologists to assist tribes with CWD activities.

Disease Status—In FY 2005, 15,628 farmed cervids were

tested for CWD as compared to more than 15,000 animals

in FY 2004 and more than 12,000 in FY 2003. From 1997

through 2005, CWD had been found in 32 farmed elk

herds and 8 farmed deer herds in 9 States (table 11).

Of the 40 positive herds identified as of December 31,

2005, 6 (4 in Colorado and 2 in Wisconsin) remained

under State quarantine and 33 had been depopulated.

The quarantine was lifted from one herd that underwent

rigorous surveillance for more than 5 years with no further

evidence of disease.

Challenges—The key challenges in managing CWD result

from the fact that cervids fall under multiple jurisdictions.

In 2002, at the request of Congress, an interagency group

was convened to develop a management plan to assist

States, Federal agencies, and Native American tribes in

managing CWD in captive and wild herds. Currently, this

plan is implemented by State and Federal agencies, as

budgets permit. A progress report on the implementation

of the plan was completed and presented to Congress in

May 2004.

Additional challenges are related to the difficulties

associated with testing wild cervids. High sample

throughput and more rapid test technology were needed

to meet the needs of wildlife agencies. By expanding

its contract group of State and university laboratories,

NVSL now has 26 laboratories approved to conduct CWD

testing. In addition, the Center for Veterinary Biologics has

approved four CWD antigen test kits based on enzymelinked

immunosorbent assay (ELISA), allowing faster

testing and greater throughput for surveillance testing of

wild cervids.

50 2005 United States Animal Health Report

snip...full text 120 pages ;


In cattle, BSE is one of the FAD differential diagnoses

of concern for the complaint of central nervous system

(CNS) signs, such as changes in temperament, abnormal

posture, and ataxia. In 2005, VS continued surveillance

for BSE through its Enhanced BSE Surveillance Plan

established in 2004, testing 419,268 brain submissions

and conducting

12 FAD investigations for the complaint of

CNS signs in bovines. ....


Cattle Death Loss by Cause, 2005

Since 1990, the percentage of cattle inventory lost to all

causes has remained relatively constant at approximately

2 percent. The percentage of calf crop lost decreased

from 7.25 percent in 1990 to just over 6 percent in 2005

(fig. 27).

Cause of Loss—Predator and nonpredator cause-of-loss

estimates for cattle and calves started in 1991 and were

repeated for 1995, 2000, and 2005 as a cooperative effort

between NASS and APHIS. The most recent estimates

(2005) are presented here (fig. 28). Overall, 98.0 percent

of cattle losses and 93.3 percent of calf losses were due

to nonpredator causes. Important causes of loss for cattle

were calving problems (11.1 percent), digestive problems

(11.1 percent), and respiratory problems (24.8 percent).

The most frequently reported causes of loss for calves

were respiratory problems (31.8 percent), digestive

problems (21.2 percent), and calving problems

(17.7 percent) (fig. 29).


NOW, for the rest of the story FROM ABOVE THAT ;
12 FAD investigations for the complaint of

CNS signs in bovines. ....WHAT A HOOT !!!


Non-Ambulatory Cattle and Calves

Released May 5, 2005, by the National Agricultural Statistics Service (NASS), Agricultural Statistics Board, U.S. Department

of Agriculture. For information on Non-ambulatory Cattle and Calves call Mike Miller at 720-3040, office hours 7:30 a.m. to

4:30 p.m. ET.

Non-Ambulatory Cattle and Calves

Non-ambulatory cattle and calves in the United States totaled 465,000 head during 2003 and

450,000 head during 2004. The number of non-ambulatory cattle 500 pounds or greater totaled

280,000 head in 2003 and 270,000 head in 2004. The number of calves under 500 pounds reported

as non-ambulatory totaled 185,000 head in 2003 and 180,000 head in 2004.

The number of operations that reported non-ambulatory cattle and calves was 103,000 in 2003 and

81,000 in 2004. In 2003, there were 66,800 beef cow operations reporting non-ambulatory cattle

and calves compared to 49,700 in 2004. There were 22,800 dairy operations reporting nonambulatory

cattle and calves in 2003 compared to 23,000 in 2004.

This report is released as a cooperative effort between the National Agricultural Statistics Service

and Animal and Plant Health Inspection Service - Veterinary Services. Data for this report were

collected on the January 1, 2004 and 2005 Cattle Surveys.


Audit Report

Animal and Plant Health Inspection Service

Bovine Spongiform Encephalopathy (BSE) Surveillance Program – Phase II


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.

In our prior report, we recommended that APHIS work with public health and State diagnostic laboratories to develop and test rabies-negative samples for BSE. This target group is important for determining the prevalence of BSE in the United States because rabies cases exhibit clinical signs not inconsistent with BSE; a negative rabies test means the cause of the clinical signs has not been diagnosed.

APHIS agreed with our recommendation and initiated an outreach program with the American Association of Veterinary Laboratory Diagnosticians, as well as State laboratories. APHIS also agreed to do ongoing monitoring to ensure samples were obtained from this target population.

Although APHIS increased the samples tested from this target group as compared to prior years, we found that conflicting APHIS instructions on the ages of cattle to test resulted in inconsistencies in what samples were submitted for BSE testing. Therefore, some laboratories did not refer their rabies negative samples to APHIS in order to maximize the number tested for this critical target population. In addition, APHIS did not monitor the number of submissions of rabies negative samples for BSE testing from specific laboratories.

According to the Procedure Manual for BSE Surveillance, dated October 2004, the target population includes:

Central nervous system (CNS) signs and/or rabies negative - sample animals of any age (emphasis added):

a. Diagnostic laboratories –samples submitted due to evidence of CNS clinical signs.

Rabies Negative Samples

USDA/OIG-A/50601-10-KC Page 19 USDA/OIG-A/50601-10-KC Page 20

b. Public health laboratories – rabies negative cases.

c. Slaughter facilities – CNS ante mortem condemned at slaughter, sampled by FSIS.

d. On-the-farm – CNS cattle that do not meet the criteria for a foreign animal disease investigation.

For FYs 2002, 2003, and 2004 (through February 2004), NVSL received 170, 133, and 45 rabies-negative samples, respectively. Between June 1, 2004, and May 29, 2005, the number of samples received for testing increased to 226 rabies suspect samples. The collection sites submitting these samples follow.

Number of Rabies
Suspect Submissions *

Slaughter Plant



Public Health Lab

Diagnostic Lab



Collection Site



* 26 were tested but not counted by APHIS towards meeting the target goals because the obex was not submitted.

We obtained a copy of a memorandum, dated July 13, 2004, that APHIS sent to diagnostic and public health laboratories providing them instructions on submitting samples for cattle showing signs of CNS diseases, but testing negative for rabies. The letter was sent to about 170 State veterinary diagnostic and public health laboratories and discussed the need to submit specimens to NVSL of all adult cattle (emphasis added) that showed signs of CNS diseases, but tested negative for rabies. This directive did not specify the age of the cattle. The Procedure Manual for BSE Surveillance, dated October 2004, specified samples of cattle of any age should be submitted.

We contacted laboratories in six States to determine if it was standard procedure to submit all negative rabies samples to NVSL. We found that, because of the lack of specificity in the APHIS letter and inadequate followup by APHIS, there were inconsistencies in the age of cattle samples submitted for BSE testing. For those States contacted, the following samples were submitted versus tested as negative for rabies.

USDA/OIG-A/50601-10-KC Page 21

Rabies Negative Tests Not Sent for BSE Testing Since June 1, 2004
Negative Rabies Tests

Not Sent for BSE Testing
Pennsylvania a/

Kansas b/

Wisconsin c/

South Dakota d/

Arizona e/

Mississippi e/


Sent for BSE Testing










a/ A Pennsylvania laboratory official said only rabies negative cattle over 20 months of age were submitted for BSE testing. The laboratory did not submit 18 samples for BSE testing because the animals were less than 20 months of age.

b/ Kansas laboratory officials said early in the expanded surveillance program, there was confusion as to the cattle ages that should be submitted for BSE testing. They did not know if cattle should be submitted that were above 20 months or 30 months of age. Of the 16 animals not submitted for BSE testing, 14 were under 20 months of age from early in the expanded surveillance program. The other two animals were not tested due to internal laboratory issues. The Kansas and Nebraska area office officials contacted the laboratory and told the officials to submit rabies negative cattle of any age for BSE testing. The laboratory now submits all rabies negative cattle for BSE testing.

c/ A Wisconsin laboratory official said only rabies negative cattle samples 30 months of age or older are submitted for BSE testing. Of the 11 animals not submitted for BSE testing, 8 were less than 30 months of age. Wisconsin laboratory officials were not certain why the other three samples were not submitted.

d/ Laboratory officials from South Dakota said they did not receive notification from APHIS regarding the submission of rabies negative cases for BSE testing. The section supervisor and laboratory director were not aware of any letter sent to the laboratory. The section supervisor said most bovine rabies tests at the laboratory are performed on calves. We confirmed the laboratory’s address matched the address on APHIS’ letter distribution list. However, there was no evidence that the South Dakota area office contacted the laboratory. The laboratory was not listed on the documentation from the APHIS regional office detailing the area office contacts with laboratory personnel. We contacted the South Dakota area office and were advised that while some contact had been made with the laboratory, the contact may have involved Brucellosis rather than BSE. On May 4, 2005, the area office

33 Report from the Secretary’s Advisory Committee on Foreign Animal and Poultry Diseases, February 13, 2004.

advised us they recently contacted the laboratory regarding the submission of rabies negative samples for BSE testing.

e/ Arizona and Mississippi laboratory officials said they submitted all rabies negative samples for BSE testing regardless of the age of the animal.

An NVSL official stated that APHIS is not concerned with rabies negatives samples from cattle less than 30 months of age. This position, however, is contrary to APHIS’ published target population.

Our prior audit recognized the significant challenge for APHIS to obtain samples from some high-risk populations because of the inherent problems with obtaining voluntary compliance and transporting the carcasses for testing. USDA issued rules to prohibit nonambulatory animals (downers) from entering the food supply at inspected slaughterhouses. OIG recommended, and the International Review Subcommittee33 emphasized, that USDA should take additional steps to assure that facilitated pathways exist for dead and nonambulatory cattle to allow for the collection of samples and proper disposal of carcasses. Between June 1, 2004, and May 31, 2005, the APHIS database documents 27,617 samples were collected showing a reason for submission of nonambulatory and 325,225 samples were collected with reason of submission showing "dead."

APHIS made extensive outreach efforts to notify producers and private veterinarians of the need to submit and have tested animals from these target groups. They also entered into financial arrangements with 123 renderers and other collection sites to reimburse them for costs associated with storing, transporting, and collecting samples. However, as shown in exhibit F, APHIS was not always successful in establishing agreements with non-slaughter collection sites in some States. APHIS stated that agreements do not necessarily reflect the entire universe of collection sites and that the presentation in exhibit F was incomplete because there were many collection sites without a payment involved or without a formal agreement. We note that over 90 percent of the samples collected were obtained from the 123 collection sites with agreements and; therefore, we believe agreements offer the best source to increase targeted samples in underrepresented areas.

We found that APHIS did not consider industry practices in the design of its surveillance effort to provide reasonable assurance that cattle exhibiting possible clinical signs consistent with BSE were tested. Slaughter facilities do not always accept all cattle arriving for slaughter because of their business requirements. We found that, in one State visited, slaughter facilities pre-screened and rejected cattle (sick/down/dead/others not meeting business

Downers and Cattle that Died on the Farm

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34 FSIS regulations do not specifically address the designation of an establishment’s "official" boundaries; however, FSIS Notices 29-04 (dated May 27, 2004) and 40-04 (dated July 29, 2004) make it clear that FSIS inspection staff are not responsible for sampling dead cattle that are not part of the "official" premises.

35 APHIS’ area office personnel stated that it was their understanding that some establishments in the State were not presenting cattle that died or were down on the transport vehicle to FSIS for ante mortem inspection. The dead and down cattle were left in the vehicle, if possible. In rare circumstances, dead cattle may be removed from the trailer by plant personnel to facilitate the unloading of other animals.

36 A May 20, 2004, Memorandum between the Administrators of APHIS and FSIS.

standards) before presentation for slaughter in areas immediately adjacent or contiguous to the official slaughter establishment. These animals were not inspected and/or observed by either FSIS or APHIS officials located at the slaughter facilities.

FSIS procedures state that they have no authority to inspect cattle not presented for slaughter. Further, APHIS officials stated they did not believe that they had the authority to go into these sorting and/or screening areas and require that the rejected animals be provided to APHIS for BSE sampling. Neither APHIS nor FSIS had any process to assure that animals left on transport vehicles and/or rejected for slaughter arrived at a collection site for BSE testing. FSIS allows slaughter facilities to designate the area of their establishment where federal inspection is performed; this is designated as the official slaughter establishment.34

We observed animals that were down or dead in pens outside the official premises that were to be picked up by renderers. Animals that were rejected by plant personnel were transported off the premises on the same vehicles that brought them to the plant.35

A policy statement36 regarding BSE sampling of condemned cattle at slaughter plants provided that effective June 1, 2004, FSIS would collect BSE samples for testing: 1) from all cattle regardless of age condemned by FSIS upon ante mortem inspection for CNS impairment, and 2) from all cattle, with the exception of veal calves, condemned by FSIS upon ante mortem inspection for any other reason.

FSIS Notice 28-04, dated May 20, 2004, informed FSIS personnel that, "FSIS will be collecting brain samples from cattle at federally-inspected establishments for the purpose of BSE testing." The notice further states that, "Cattle off-loaded from the transport vehicle onto the premises of the federally-inspected establishment (emphasis added), whether dead or alive, will be sampled by the FSIS Public Health Veterinarian (PHV) for BSE after the cattle have been condemned during ante mortem inspection. In addition, cattle passing ante mortem inspection but later found dead prior to slaughter will be condemned and be sampled by the FSIS PHV."

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37 FSIS Notice 40-04, dated July 29, 2004.

38 FSIS Notice 29-04, dated May 27, 2004.

APHIS has the responsibility for sampling dead cattle off-loaded onto plant-owned property that is adjoining to, but not considered part of, the "official premises.37 FSIS procedures38 provide that "Dead cattle that are off-loaded to facilitate the off-loading of live animals, but that will be re-loaded onto the transport vehicle, are not subject to sampling by FSIS.

While performing our review in one State, we reviewed the circumstances at two slaughter facilities in the State that inspected and rejected unsuitable cattle before the animals entered the official receiving areas of the plants. This pre-screening activity was conducted in areas not designated by the facility as official premises of the establishment and not under the review or supervision of FSIS inspectors. The plant rejected all nonambulatory and dead/dying/sick animals delivered to the establishment. Plant personnel refused to offload any dead or downer animals to facilitate the offloading of ambulatory animals. Plant personnel said that the driver was responsible for ensuring nonambulatory animals were humanely euthanized and disposing of the carcasses of the dead animals. Plant personnel informed us that they did not want to jeopardize contracts with business partners by allowing unsuitable animals on their slaughter premises.

In the second case, one family member owned a slaughter facility while another operated a livestock sale barn adjacent to the slaughter facility. The slaughter facility was under FSIS’ supervision while the sale barn was not. Cattle sometimes arrived at the sale barn that were sick/down/dead or would die or go down while at the sale barn. According to personnel at the sale barn, these animals were left for the renderer to collect. The healthy ambulatory animals that remained were marketed to many buyers including the adjacent slaughter facility. When the slaughter facility was ready to accept the ambulatory animals for processing, the cattle would be moved from the sale barn to the slaughter facility where they were subject to FSIS’ inspection.

We requested the slaughter facilities to estimate the number of cattle rejected on a daily basis (there were no records to confirm the estimates). We visited a renderer in the area and found that the renderer had a contract with APHIS to collect samples for BSE testing. In this case, although we could not obtain assurance that all rejected cattle were sampled, the renderer processed a significant number of animals, as compared to the slaughter plants’ estimates of those rejected. Due to the close proximity (less than 5 miles) of the renderer to the slaughter facilities, and the premium it paid for dead cattle that were in good condition, there was a financial incentive for transport drivers to dispose of their dead animals at this renderer.

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In our discussions with APHIS officials in Wisconsin and Iowa, they confirmed that there were plants in their States that also used pre-screening practices. On May 27, 2005, we requested APHIS and FSIS to provide a list of all slaughter facilities that pre-screened cattle for slaughter in locations away from the area designated as the official slaughter facility. Along with this request, we asked for information to demonstrate that either APHIS or FSIS confirmed there was a high likelihood that high-risk animals were sampled at other collection sites.

In response to our request, the APHIS BSE Program Manager stated that APHIS did not have information on slaughter plants that pre-screen or screen their animals for slaughter suitability off their official plant premises. To their knowledge, every company or producer that submits animals for slaughter pre-sorts or screens them for suitability at various locations away from the slaughter facility. For this reason, USDA focused its BSE sample collection efforts at other types of facilities such as renderers, pet food companies, landfills, and dead stock haulers. Further, in a letter to OIG on June 14, 2005, the administrators of APHIS and FSIS noted the following:

"…we believe that no specific actions are necessary or appropriate to obtain reasonable assurance that animals not presented for slaughter are being tested for BSE. There are several reasons for our position. First, we do not believe that the practice is in fact causing us to not test a significant enough number of animals in our enhanced surveillance program to invalidate the overall results. Second, OIG has concluded that because of the geographical proximity and business relationships of the various entities involved in the case investigated, there is reasonable assurance that a majority of the rejected cattle had been sampled. Third, it is also important to remember that the goal of the enhanced surveillance program is to test a sufficient number of animals to allow us to draw conclusions about the level of BSE (if any) in the American herd…We believe that the number we may be not testing because of the "pre-sorting" practice does not rise to a significant level. The number of animals tested to date has far exceeded expectations, so it is reasonable to infer that there are few of the animals in question, or that we are testing them at some other point in the process…APHIS estimated…there were approximately 446,000 high risk cattle…[and APHIS has]…tested over 375,000 animals in less than 1 year. This indicated that we are missing few animals in the high-risk population, including those that might be pre-sorted before entering a slaughter facility’s property."

We obtained 123 APHIS sampling agreements and contracts with firms and plotted their locations within the United States (see exhibit F). We also analyzed the samples tested to the BSE sampling goals allocated to each State under the prior surveillance program. This analysis showed that there are

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39APHIS noted that sites with agreements do not necessarily reflect the entire universe of collection sites and at some sites APHIS collects samples with no payment involved and no agreement in place. OIG agrees that not all collection sites are reflected in our presentation of the 123 sites with reimbursable agreements. OIG believes obtaining sampling agreements is one of the primary methods available to increase sample numbers in areas with sampling gaps.

sampling gaps in two large areas of the United States where APHIS did not have contracts with collection sites. These two areas are shown in the following chart (Montana, South Dakota, North Dakota and Wyoming – Group 1 and Louisiana, Oklahoma, Arkansas, and Tennessee – Group 2):

Original Sampling Goal Based on (268,500 sampling goal)

Samples collected as of May 31, 2005

No. of BSE Sampling Agreements/




















APHIS notes that for the current surveillance program, it had established regional goals and APHIS was not trying to meet particular sampling levels in particular States. However, we believe that it would be advantageous for APHIS to monitor collection data and increase outreach when large geographical areas such as the above States do not provide samples in proportion to the numbers and types of cattle in the population.

We also disagree with APHIS/FSIS’ contention that because they have tested over 375,000 of their 446,000 estimate of high risk cattle, few in the high-risk population are being missed, including those that might be pre-screened before entering a slaughter facility’s property. In our prior audit, we reported that APHIS underestimated the high-risk population; we found that this estimate should have been closer to 1 million animals (see Finding 1). We recognize that BSE samples are provided on a voluntary basis; however, APHIS should consider industry practice in any further maintenance surveillance effort. Animals unsuitable for slaughter exhibiting symptoms not inconsistent with BSE should be sampled and their clinical signs recorded. However, this cited industry practice results in rejected animals not being made available to either APHIS or FSIS veterinarians for their observation and identification of clinical signs exhibited ante mortem. Although these animals may be sampled later at other collection sites, the animals are provided post mortem without information as to relevant clinical signs exhibited ante mortem. For these reasons, we believe APHIS needs to

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observe these animals ante mortem when possible to assure the animals from the target population are ultimately sampled and the clinical signs evaluated.


USDA Testing Protocols and Quality Assurance Procedures

In November 2004, USDA announced that its rapid screening test produced an inconclusive BSE test result. A contract laboratory ran its rapid screening test on a brain sample collected for testing and produced three high positive reactive results. As required, the contract laboratory forwarded the inconclusive sample to APHIS’ National Veterinary Services Laboratories (NVSL) for confirmation. NVSL repeated the rapid screening test, which again produced three high positive reactive results. Following established protocol, NVSL ran its confirmatory test, an immunohistochemistry (IHC) test, which was interpreted as negative for BSE.

Faced with conflicting results between the rapid screening and IHC tests, NVSL scientists recommended additional testing to resolve the discrepancy but APHIS headquarters officials concluded that no further testing was necessary since testing protocols were followed and the confirmatory test was negative. In our discussions with APHIS officials, they justified their decision to not do additional testing because the IHC test is internationally recognized as the "gold standard" of testing. Also, they believed that

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conducting additional tests would undermine confidence in USDA’s testing protocols.

OIG obtained evidence that indicated additional testing was prudent. We came to this conclusion because the rapid screening tests produced six high positive reactive results, the IHC tests conflicted, and various standard operating procedures were not followed. Also, our review of the relevant scientific literature, other countries’ protocols, and discussions with experts led us to conclude that additional confirmatory testing should be considered in the event of conflicting test results.

To maintain objectivity and independence, we requested that USDA’s Agricultural Research Service (ARS) perform the Office International des Epizooties (OIE) Scrapie-Associated Fibrils (SAF) immunoblot test. The additional testing produced positive results. To confirm, the Secretary of Agriculture requested that an internationally recognized BSE laboratory in Weybridge, England (Weybridge) perform additional testing. Weybridge conducted various tests, including their own IHC tests and three Western blot tests. The tests confirmed that the cow was infected with BSE. The Secretary immediately directed USDA scientists to work with international experts to develop new protocols that include performing dual confirmatory tests in the event of an inconclusive BSE screening test.

We attribute the failure to identify the BSE positive sample to rigid protocols, as well as the lack of adequate quality assurance controls over its testing program. Details of our concerns are discussed in Findings 3 and 4.


Section 2. Testing Protocols and Quality Assurance Controls In November 2004, USDA announced that its rapid screening test, Bio-Rad Enzyme Linked Immunosorbent Assay (ELISA), produced an inconclusive BSE test result as part of its enhanced BSE surveillance program. The ELISA rapid screening test performed at a BSE contract laboratory produced three high positive reactive results.40 As required,41 the contract laboratory forwarded the inconclusive sample to the APHIS National Veterinary Services Laboratories (NVSL) for confirmatory testing. NVSL repeated the ELISA testing and again produced three high positive reactive results.42 In accordance with its established protocol, NVSL ran its confirmatory test, an immunohistochemistry (IHC) test, which was interpreted as negative for BSE. In addition, NVSL performed a histological43 examination of the tissue and did not detect lesions44 consistent with BSE. Faced with conflicting results, NVSL scientists recommended additional testing to resolve the discrepancy but APHIS headquarters officials concluded no further testing was necessary because testing protocols were followed. In our discussions with APHIS officials, they justified their decision not to do additional testing because the IHC is internationally recognized as the “gold standard.” Also, they believed that conducting additional tests would undermine confidence in USDA’s established testing protocols. However, OIG obtained evidence that indicated additional testing was prudent to ensure that USDA’s testing protocols were effective in detecting BSE and that confidence in USDA’s testing procedures was maintained. OIG came to this conclusion because the rapid tests produced six high positive reactive results, confirmatory testing conflicted with the rapid test results, and various standard operating procedures were not followed. Also, our review of scientific literature, other country protocols, as well as discussions with internationally recognized experts led us to conclude that confirmatory testing should not be limited when conflicting test results are obtained. To maintain objectivity and independence in our assessment, we requested the USDA Agricultural Research Service (ARS) perform the Office International des Epizooties (OIE) Scrapie-Associated Fibrils (SAF) 40 ELISA test procedures require two additional (duplicate) tests if the initial test is reactive, before final interpretation. If either of the duplicate tests is reactive, the test is deemed inconclusive. 41 Protocol for BSE Contract Laboratories to Receive and Test Bovine Brain Samples and Report Results for BSE Surveillance Standard Operating Procedure (SOP), dated October 26, 2004. 42 The NVSL conducted an ELISA test on the original material tested at the contract laboratory and on two new cuts from the sample tissue. 43 A visual examination of brain tissue by a microscope. 44 A localized pathological change in a bodily organ or tissue.

immunoblot.45 ARS performed the test at the National Animal Disease Center because NVSL did not have the necessary equipment46 (ultracentrifuge) to do the test. APHIS scientists observed and participated, as appropriate, in this effort. The additional tests conducted by ARS produced positive results. To confirm this finding, the Secretary requested the internationally recognized BSE reference laboratory in Weybridge, England, (Weybridge) to perform additional confirmatory testing. Weybridge conducted various tests, including their own IHC methods, as well as three Western blot methods. The tests confirmed that the suspect cow was infected with BSE. Also, Weybridge confirmed this case as an unequivocal positive case of BSE on the basis of IHC. As a result of this finding, the Secretary immediately directed USDA scientists to work with international experts to develop a new protocol that includes performing dual confirmatory tests in the event of another inconclusive BSE screening test. Finding 3 Rigid Protocols Reduced the Likelihood BSE Could be Detected APHIS relied on a single test method, as well as a histological examination of tissue for lesions consistent with BSE, to confirm the presence of BSE even though discrepant test results indicated further testing may be prudent. When IHC test results were interpreted as negative, APHIS concluded the sample tested negative for BSE. Subsequent independent tests initiated by OIG using a different testing method, as well as confirmatory testing by Weybridge, determined that the suspect sample was a positive case of BSE. APHIS Declares BSE Sample Negative Despite Conflicting Results When the tissue sample originally arrived at NVSL in November 2004 from the contract lab, NVSL scientists repeated the ELISA screening test and again produced three high positive reactive results. NVSL scientists cut out two sections of the brain sample for IHC testing. One section was used for an experimental procedure that was not part of the confirmatory testing protocol, and the other cut was for normal IHC testing using scrapie for a positive control.47 According to NVSL scientists, the experimental test results were inconclusive but the IHC test was interpreted as negative. The NVSL scientists were concerned with the inconsistencies and conducted 45 The OIE SAF immunoblot is an internationally recognized confirmatory test, often referred to as a Western blot test. There are different types of Western blots; the OIE SAF immunoblot includes enrichment steps taken with the sample prior to the standard Western blot steps. 46 APHIS has now ordered the necessary equipment for NVSL. USDA/OIG-A/50601-10-KC Page 32

47 A positive control is a sample that is known to contain a given disease or react in the test. The sample then can be used to make sure that the test for that disease works properly. In the case of BSE, tissue infected with either scrapie or BSE can serve as a positive control for an IHC test for BSE since both are different forms of the same disease (transmissible spongiform encephalopathy or TSE).

another IHC test using BSE as a positive control.48 The test result was also interpreted as negative. Also, according to the NVSL scientists, the histological examination of the tissue did not detect lesions consistent with BSE. After the second negative IHC test, NVSL scientists supported doing additional testing. They prepared a plan for additional tests; if those tests had been conducted, BSE may have been detected in the sample. The additional tests recommended by NVSL scientists, but not approved by APHIS Headquarters officials, were the IHC using other antibodies (IHC testing using different antibodies ultimately produced positive results); IHC testing of additional regions of the brain (the cerebellum tested positive); regular and enriched (OIE-like) Western blots (the obex and cerebellum tested positive); and variable rapid tests (the obex and cerebellum tested positive with two different rapid tests). NVSL officials also recommended that the sample be sent to Weybridge for confirmatory testing (to conduct IHC and OIE Western blot tests). In June 2005, Weybridge conducted IHC testing with three different antibodies, including the antibody used in the United States (tested positive), the OIE Western blot (tested positive), a modified commercial kit Western blot (negative) and the NaPTA49 Western blot (tested positive). We obtained information as to the differing protocols used by other countries. We found that while APHIS determined that additional testing was unnecessary after the IHC test, other countries have used multiple tests to confirm positives. In Japan, for example, all reactive screening test samples are examined by both IHC and a Western blot (different from the OIE SAF immunoblot). In the United Kingdom (U.K.), IHC and Western blot (different from the OIE SAF immunoblot) tests are used for all animals that test positive with a screening test. When IHC and the Western blot fail to confirm a positive rapid test, the U.K. resorts to a third test, the OIE SAF immunoblot. With these procedures in place, both Japan and the U.K. have found BSE cases that were rapid test reactive, IHC negative, and finally confirmed positive with a Western blot. Evidence Indicated Additional Testing Would Be Prudent We also spoke with an internationally recognized BSE expert regarding the advisability of limiting confirmatory testing when conflicting results are obtained. This official expressed concern about limiting confirmatory tests to the IHC despite its status as one of the “gold standard” tests. He advised that the IHC is not one test; it is a test method that can vary significantly in sensitivity from laboratory to laboratory. New antibodies can improve or

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48 The NVSL uses scrapie as the positive control as part of its normal IHC testing procedures. Due to the conflicting results between the ELISA and IHC tests, the NVSL conducted another IHC test with BSE as the positive control. Subsequently, the NVSL modified the Confirming Inconclusive Results from BSE Testing Laboratories at the NVSL SOP to show that all IHC tested BSE inconclusive samples from contract laboratories will use BSE as the positive control. 49 Sodium phosphotungstic acid.

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reduce sensitivity, as can variations in many of the reagents50 used. He explained that his laboratory had experienced cases where an initial confirmatory IHC test was challenged by either a more extensive IHC test or “…applying a more sensitive immunoblot.” He emphasized the importance of having additional confirmatory testing to resolve discrepant results since there are many variables, and most of the variability appears to be due to test performance of the laboratory. OIG became concerned that APHIS relied on its confirmatory test methods when rapid screening tests produced high positive reactive results six times.51 Also, we found that APHIS did not pursue and/or investigate why the ELISA produced high reactive positives. An official from the manufacturer of the ELISA test kit told us that they requested, but did not receive, information on the inconclusive reported by USDA in November 2004. These officials requested this information in order to understand the reasons for the discrepant results. The Bio-Rad ELISA rapid screening test is internationally recognized as a highly reliable test and is the rapid screening test used for USDA’s surveillance effort. According to APHIS officials, they felt it would be inappropriate to collaborate on the one sample because Bio-Rad is a USDA-APHIS regulated biologics company and only one of several competing manufacturers. To maintain confidence in USDA’s test protocols, it would have been a prudent course of action for USDA to determine why such significant differing results were obtained. The fact that they did not pursue this matter caused concerns relating to testing quality assurance procedures. In this regard, we found lack of compliance with SOPs relating to laboratory proficiency and quality assurance (see Finding 4), and, in this case, the storage of sampled material and reporting of test results. We found that the NVSL did not prepare a report to document its confirmatory testing of the November 2004 sample. The SOP52 states that the BSE network laboratory initiating the inconclusive will receive a report of the case. NVSL officials could not explain why a final report had not been prepared. We also found that the inconclusive sample was frozen prior to IHC confirmatory testing. APHIS protocols state that samples are not to be frozen prior to laboratory submission. The OIE Manual of Diagnostic Tests and Vaccines for Terrestrial Animals states that the tissues for histological or IHC examination are not to be frozen as this will provide artefactual53 lesions that may compromise the identification of vacuolation,54 and/or target site location. Although the sample was frozen, APHIS did not conduct a Western 50 A substance used in a chemical reaction to detect, measure, examine, or produce other substances. 51 The six high positive reactive results were from three tests of the submitted sample (multiple runs of the same test). 52 Confirming Inconclusive Results from Bovine Spongiform Encephalopathy Testing Laboratories at the NVSL SOP, dated August 13, 2004. 53 A structure or feature not normally present but visible as a result of an external agent or action, such as one seen in a microscopic specimen after fixation. 54 A small space or cavity in a tissue.

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blot test on the sample. An NVSL official said freezing the sample does not make it unsuitable for IHC. APHIS determined that the sample was suitable for IHC and therefore, in accordance with its SOP, did not conduct a Western blot test. APHIS also handled the December 2003 BSE positive differently than the November 2004 sample. For the December 2003 BSE positive sample, APHIS conducted several confirmatory tests in addition to the IHC testing and histological examination (unlike the November 2004 sample tests, both of these were interpreted as positive). ARS performed two Western blots (Prionics Check Western blot and an ARS developed Western blot). When we questioned why the samples were handled differently, APHIS officials stated that the Western blots were done because the IHC in December 2003 was positive. The additional testing was done to further characterize the case, because it was the first U.S. case; the additional testing was not done to decide whether the case was positive or negative. We discussed our concerns with limiting confirmatory testing, particularly given conflicting results, with the APHIS Administrator and staff in May 2005. He explained that international standards recognized more than one “gold standard” test. In setting up its testing protocols, USDA had chosen one as the confirming test, the IHC test, and stayed with it. APHIS protocols only allow a Western blot in cases where the sample has become unsuitable for IHC tests (e.g., in cases where the brainstem architecture is not evident). International standards, he continued, accept a tissue sample as negative for BSE if its IHC test is negative. Once the test is run in accordance with protocols, additional tests undermine the USDA testing protocol and the surveillance program. He concluded that since APHIS’ protocols accepted the IHC test as confirming the presence or absence of BSE, no further testing was necessary. According to protocol, the tissue sample was determined to have tested negative for BSE. On June 24, 2005, USDA announced that the additional testing by the BSE reference laboratory in England confirmed the presence of BSE in the tissue sample. To obviate the possibility that a future sample would be declared negative and then found positive, the Secretary of Agriculture announced a change to APHIS’ testing protocols that same day. He called for “dual confirmatory tests in the event of another ‘inconclusive’ [reactive] BSE screening test.” He also indicated that he would reinforce proper procedures so that samples will not be frozen, and to spot-check the laboratories to see that they complete reports as required. APHIS issued a SOP on the new confirmatory testing protocols on November 30, 2005.

Office Note


A The Present Position with respect to Scrapie
A] The Problem

Scrapie is a natural disease of sheep and goats. It is a slow
and inexorably progressive degenerative disorder of the nervous system
and it ia fatal. It is enzootic in the United Kingdom but not in all

The field problem has been reviewed by a MAFF working group
(ARC 35/77). It is difficult to assess the incidence in Britain for
a variety of reasons but the disease causes serious financial loss;
it is estimated that it cost Swaledale breeders alone $l.7 M during
the five years 1971-1975. A further inestimable loss arises from the
closure of certain export markets, in particular those of the United
States, to British sheep.

It is clear that scrapie in sheep is important commercially and
for that reason alone effective measures to control it should be
devised as quickly as possible.

Recently the question has again been brought up as to whether
scrapie is transmissible to man. This has followed reports that the
disease has been transmitted to primates. One particularly lurid
speculation (Gajdusek 1977) conjectures that the agents of scrapie,
kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of
mink are varieties of a single "virus". The U.S. Department of
Agriculture concluded that it could "no longer justify or permit
scrapie-blood line and scrapie-exposed sheep and goats to be processed
for human or animal food at slaughter or rendering plants" (ARC 84/77)"
The problem is emphasised by the finding that some strains of scrapie
produce lesions identical to the once which characterise the human

Whether true or not. the hypothesis that these agents might be
transmissible to man raises two considerations. First, the safety
of laboratory personnel requires prompt attention. Second, action
such as the "scorched meat" policy of USDA makes the solution of the
acrapie problem urgent if the sheep industry is not to suffer



Prion protein in cardiac

elaphus nelsoni)

Odocoileus virginianus)

wasting disease


infectivity in skeletal muscle of CWD-infected mule deer (Angers et al.,

2006) has raised the level of concern on the issue of potential

human health risks that might be encountered by consuming

prion-containing meat.

Prions in Skeletal Muscles of Deer with Chronic Wasting Disease

Rachel C. Angers,1* Shawn R. Browning,1*† Tanya S. Seward,2 Christina J. Sigurdson,4‡ Michael W. Miller,5 Edward A. Hoover,4 Glenn C. Telling1,2,3§

1Department of Microbiology, Immunology and Molecular Genetics, 2Sanders Brown Center on Aging, 3Department of Neurology, University of Kentucky, Lexington, KY 40536, USA. 4Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, CO 80523, USA. 5Colorado Division of Wildlife, Wildlife Research Center, Fort Collins, CO 80526, USA.

*These authors contributed equally to this work.

†Present address: Department of Infectology, Scripps Research Institute, 5353 Parkside Drive, RF-2, Jupiter, Florida, 33458, USA.

‡Present address: Institute of Neuropathology, University of Zurich, Schmelzbergstrasse 12, 8091 Zurich, Switzerland.

§To whom correspondence should be addressed: E-mail:

Prions are transmissible proteinaceous agents of mammals that cause fatal neurodegenerative diseases of the central nervous system (CNS). The presence of infectivity in skeletal muscle of experimentally infected mice raised the possibility that dietary exposure to prions might occur through meat consumption (1). Chronic wasting disease (CWD), an enigmatic and contagious prion disease of North American cervids, is of particular concern. The emergence of CWD in an increasingly wide geographic area and the interspecies transmission of bovine spongiform encephalopathy (BSE) to humans as variant Creutzfeldt Jakob disease (vCJD) have raised concerns about zoonotic transmission of CWD.

To test whether skeletal muscle of diseased cervids contained prion infectivity, Tg(CerPrP)1536 mice (2) expressing cervid prion protein (CerPrP), were inoculated intracerebrally with extracts prepared from the semitendinosus/semimembranosus muscle group of CWD-affected mule deer or from CWD-negative deer. The availability of CNS materials also afforded direct comparisons of prion infectivity in skeletal muscle and brain. All skeletal muscle extracts from CWD-affected deer induced progressive neurological dysfunction in Tg(CerPrP)1536 mice with mean incubation times ranging between 360 and ~490 d, whereas the incubation times of prions from the CNS ranged from ~230 to 280 d (Table 1). For each inoculation group, the diagnosis of prion disease was confirmed by the presence of PrPSc in the brains of multiple infected Tg(CerPrP)1536 mice (see supporting online material for examples). In contrast, skeletal muscle and brain material from CWD-negative deer failed to induce disease in Tg(CerPrP)1536 mice (Table 1) and PrPSc was not detected in the brains of sacrificed asymptomatic mice as late as 523 d after inoculation (supporting online material).

Our results show that skeletal muscle as well as CNS tissue of deer with CWD contains infectious prions. Similar analyses of skeletal muscle BSE-affected cattle did not reveal high levels of prion infectivity (3). It will be important to assess the cellular location of PrPSc in muscle. Notably, while PrPSc has been detected in muscles of scrapie-affected sheep (4), previous studies failed to detect PrPSc by immunohistochemical analysis of skeletal muscle from deer with natural or experimental CWD (5, 6). Since the time of disease onset is inversely proportional to prion dose (7), the longer incubation times of prions from skeletal muscle extracts compared to matched brain samples indicated that prion titers were lower in muscle than in CNS where infectivity titers are known to reach high levels. Although possible effects of CWD strains or strain mixtures on these incubation times cannot be excluded, the variable 360 to ~490 d incubation times suggested a range of prion titers in skeletal muscles of CWD-affected deer. Muscle prion titers at the high end of the range produced the fastest incubation times that were ~30% longer than the incubation times of prions from the CNS of the same animal. Since all mice in each inoculation group developed disease, prion titers in muscle samples producing the longest incubation times were higher than the end point of the bioassay, defined as the infectious dose at which half the inoculated mice develop disease. Studies are in progress to accurately assess prion titers.

While the risk of exposure to CWD infectivity following consumption of prions in muscle is mitigated by relatively inefficient prion transmission via the oral route (8), these

/ / 26 January 2006 / Page 1 / 10.1126/science.1122864

results show that semitendinosus/semimembranosus muscle, which is likely to be consumed by humans, is a significant source of prion infectivity. Humans consuming or handling meat from CWD-infected deer are therefore at risk to prion exposure.


Human health implications

14. Epidemiological data on possible CWD infection of humans are

very limited. The possibility that clinical symptoms of CWD in

humans differ from those of Creutzfeldt-Jakob Disease (CJD)

cannot be excluded. There is no significant difference between the

prevalence of CJD in CWD endemic areas and other areas of the

world. However, because CJD surveillance in the USA is relatively

recent, not all CJD cases may have been identified. Additionally,

detection of a small increase in prevalence of such a rare disease

is very difficult. Investigation of six cases of prion disease in young

people ((> 54 years of age) diagnosed

with sporadic CJD, no link with consumption of venison from CWD

endemic areas was found. No causal link was found in an

investigation of three men with neurological illnesses who were

known to partake in “wild game feasts”. Only one of these subjects

was found to have a prion disease and this was also

indistinguishable from sporadic CJD.



217. To date there are no known cases of human prion disease attributable to CWD

transmitted to humans (Belay et al., 2004). While limited epidemiological investigations to

date have not shown any links between CWD and humans with spongiform encephalopathies

CWD Review / Dr Debra Bourne / October 2004 / For SEAC / Page 45 of 66

this data must be considered along with a caveat: “because CWD is a relatively new TSE, it is

unlikely that enough people have consumed enough CWD-affected cervids to result in a

clinically or pathologically recognizable disease attributable to CWD, especially considering

the very long incubation periods characteristic of TSE diseases.” (Race et al., 2002)

Epidemiological investigations

218. Epidemiological investigations have failed to show any links between cases of prion

disease in unusually young people or in hunters in the USA and CWD (CDC, 2003). Two

major epidemiological investigations have been carried out, one on cases of CJD in unusually

young individuals in the USA, the second on a group of men from Wisconsin who developed

neurological diseases.

219. The first study (Belay et al., 2001) focused on three individuals, two 28 years of age

and the third 30 years old, diagnosed with CJD in the USA between 1st January 1997 and 31st

May 2000, and without any established risk factors for CJD (family history, receipt of human

growth hormone, receipt of grafts of dura mater or cornea, or previous neurological surgery)

and concluded that there was no strong evidence for a causal link with CWD. None of the

individuals had travelled to Europe (therefore a link with BSE was unlikely). Two of the

individuals were hunters who regularly consumed game meat while the third (case 1) had, as a

young child, regularly consumed venison from animals hunted by family members and on two

occasions from a family friend. Two of the individuals (cases 1 and 2) had undergone tonsillar

surgery as children; the third had never received any surgical treatment. One individual (case

1) had eaten venison mainly hunted in Maine, occasionally hunted in New Jersey, and, on two

occasions at about six years old, elk meat which had probably been harvested in Wyoming.

The second person (case 2) had hunted cervids mainly in Utah, but had harvested an elk in

southwestern Wyoming on one occasion (less than three years before onset of clinical signs)

and had hunted in British Columbia on one occasion nine years before onset of illness. The

third person (case 3) had hunted close to home and never in Colorado or Wyoming although

the plant where he took his carcasses for processing did also process some elk from Colorado

each year. The clinical signs, duration of illness and histopathological findings for the three

individuals showed no obvious similarities to one another. One individual was

methionine/methionine homozygous at codon 129 of the PRNP (case 1), one was

homozygous for valine at this gene (case 2) and the third (case 3) was heterozygous

methionine/valine. Immunohistochemistry revealed strong staining with a “synaptic” pattern

in the first individual and weak staining with a “synaptic” pattern in the second case; in case

3, based on a brain biopsy sample obtained at an early point in the illness, staining was

questionable and possibly showed a synaptic pattern. Cases 2 and 3 showed a “Type 1”

immunoblot pattern, this test had not been carried out for case 1. It was noted that none of

these three individuals had a definite history of consumption of venison from the geographical

areas in which CWD was known to be endemic in Colorado and Wyoming, and no CWD had

been identified in 299 deer and sampled from the area in which most of the venison consumed

by patient 1 had originated, nor in 404 deer and 196 elk sampled from the area in which most

of the venison consumed by patient 2 had originated, nor in 138 deer samples from the area in

which most of the venison consumed by patient 1 had originated. Additionally, there was no

homogeneity in phenotypic expression of the disease and all three possible options for coding

at codon 129 of the PRNP gene were represented. Since a survey had indicated that

approximately 40% of blood donors in the USA consumed venison from wild cervids, it was

considered most likely that coincidence explained why three of the four young (30 years old

or younger) individuals with sporadic CJD reported in the USA after March 1996 had

consumed such meat (Belay et al., 2001).

CWD Review / Dr Debra Bourne / October 2004 / For SEAC / Page 46 of 66

220. The second major epidemiological investigation centred around three men from

Wisconsin and Minnesota who had died from degenerative neurological illnesses and who

had participated in “wild game feasts” in northern Wisconsin. Full investigation including

examination of fixed brain tissue confirmed CJD in only one of the three individuals. Wild

game eaten during the feasts was harvested mainly in Wisconsin but also in areas of

Colorado, Wyoming and Montana; CWD was not known to be endemic in the areas where the

game was hunted at the time that the game was harvested. Further investigations of other

possible attendees of the feasts revealed 34 participants, all male, of whom a total of seven

were deceased, including the three individuals in the initial investigation. Causes of death in

the other four deceased individuals were not attributed to nor associated with any

degenerative neurological disorder and no signs or symptoms associated with a degenerative

neurological disorder were noted for any of the remaining living participants of the feasts. It

was noted that only one case of CJD had occurred among known participants at the feasts,

that this case was consistent with the commonest form of sporadic CJD, that this individual

had only participated in one feast and that it was unlikely that he had consumed CWDinfected

venison at the feasts “because venison and other game from outside Wisconsin that

was served at these feasts did not originate from known CWD-endemic areas.” Limitations of

the investigations were noted to include reliance on recall of events from up to 25 years

previously and the fact that not all participants in the feasts could be contacted and

interviewed. However, those who were interviewed agreed in their recall of events (CDC,


221. It is important to recognise that the limited epidemiological investigations that have

been carried out are not able to rule out the possibility that CWD might play a role in causing

illness in humans (CDC, 2003).

222. Three further cases of prion disease in young humans in the USA have been

investigated for possible links to CWD (Belay et al., 2004). The first case was a 25-year-old

man who died in 2001 after about 22 months of illness. Gerstmann-Sträussler-Scheinker

syndrome (GSS) was diagnosed by analysis of the prion gene, with a P102L mutation

together with valine at codon 129 in the mutant allele. It was noted that the disease had

occurred at an unusually young age, even for GSS, and the possibility that exposure to CWDinfected

venison contributed to early onset of the disease could not be ruled out; the patient’s

grandfather had regularly hunted in southeastern Wyoming, around the known CWD-endemic

area, and had given venison to the patient’s family. Two other cases of prion disease occurred

in individuals of 26 and 28 years of age, from adjacent counties, and with onset of illness only

months apart, therefore an environmental source of infection was investigated. However,

these two individuals were finally diagnosed with different prion diseases: sporadic CJD in

one case and GSS in the other, indicating that a common cause was unlikely. In the first case

CJD was confirmed from autopsy samples (by histopathology, immunohistochemistry and

immunoblotting); the individual had no history of hunting nor of regular consumption of

venison, and although he may have eaten venison originating from the Upper Peninsula of

Michigan while at college CWD has never been detected in deer from Michigan.

Phenotypically this individual fit the “MM2 sporadic CJD” phenotype described by Parchi et

al. (1999). In the other case post mortem immunohistochemistry revealed prion deposition

which was consistent with GSS and a GSS P102L mutation was detected in a blood sample

from one parent (appropriate samples were not available from the affected patient); this

individual may possibly have eaten venison from Michigan on one occasion at about two

years of age (Belay et al., 2004).

223. A further three cases of CJD in individuals of 54 to 66 years old who were deer and

elk hunters (two individuals) or ate wild-harvested venison (one individual) have been

CWD Review / Dr Debra Bourne / October 2004 / For SEAC / Page 47 of 66

investigated. There was no evidence that any of these individuals had hunted in known CWDendemic

areas; information available indicated hunting or eating venison from Washington

State and Pennsylvania. Two individuals were V/V at codon 129 the third was M/M; they

were considered to fit known subtypes of sporadic CJD (MM1, VV1 and VV2 subtypes as

described by Parchi et al. (1999)). Further investigations were also made on the only two

nonfamilial cases of CJD in individuals with a history of eating venison from the known

CWD-endemic areas. One was reported to have eaten venison from two deer harvested in an

area with endemic CWD, but both deer had been tested and not found to be CWD-positive;

the patient’s illness was consistent with the CJD subtype MM1. The other individual grew up

in a CWD-endemic area and ate locally-harvested venison; her disease fit the MM1 CJD

phenotype and no atypical neurological features were noted (Belay et al., 2004).

224. Additional epidemiological notes are that the incidence and age distribution of CJD in

Colorado and Wyoming, where CWD is thought to have been endemic for decades, are

similar to those found in other areas of the USA. In Wyoming, seven cases of CJD have been

reported between 1979 and 2000 with an average annual age-adjusted CJD death rate of 0.8

per million and no cases reported in humans less than 55 years old. In Colorado in the same

period 67 cases of CJD have been reported, with an average annual age-adjusted CJD death

rate of 1.2 per million (Belay et al., 2004).

225. In summary, there is no evidence of an increase in incidence of CJD in Colorado and

Wyoming, nor have epidemiological investigations carried out so far found any evidence of a

link between CWD and cases of CJD in persons in the USA (Belay et al., 2001; CDC, 2003;

Belay et al., 2004).

Laboratory studies

226. There is evidence from an in vitro cell-free system that there may be a considerable

“species barrier” reducing the probability that CWD will affect humans. It was shown that

PrPres associated with chronic wasting disease (PrPCWD) from elk, mule deer or white-tailed

deer was able to readily induce substantial conversion of recombinant cervid PrPsen

molecules form any of these three species to the protease-resistant state. In the same system,

CWD-associated PrPres was shown to convert human PrPsen but at a much lower efficiency:

more than 14-fold lower efficiency than inter-cervid conversion reactions and more than fivefold

lower than conversion of human PrPsen by PrPres from the brains of humans with CJD

(Raymond et al., 2000). While encouraging, interpretation of this study is complicated by the

fact that conversion of human PrPC by PrPBSE and PrPSc from sheep were of similar efficacy,

both being more than 10-fold less efficient compared with corresponding homologous

conversions) and one of these appears to be orally transmissible to humans (BSE) while the

other (scrapie) appears not to be (Raymond et al., 2000). In previous experiments PrPBSE had

showed 10-fold greater conversion efficacy for bovine PrPsen than for human codon 129-M

(methionine) PrPsen and 30-fold greater conversion efficacy than for human codon 129-V

(valine) PrPsen, while ovine PrPSc showed five-fold greater conversion efficacy for ovine

PrPsen than for human 129-M PrPsen and eight-fold greater conversion than for human 129-

V PrPsen (Raymond et al., 1997).

227. Results of recent work in transgenic mice expressing human PrP (see paragraph 71), in

which transmission of CWD from elk by intracerebral inoculation failed, was considered to

“strongly suggest” a species barrier to transmission of elk CWD to humans (Kong et al.,


CWD Review / Dr Debra Bourne / October 2004 / For SEAC / Page 48 of 66

Potential risk from consuming cervid products

Velvet antler

228. Limited studies to date indicate risk from this product may be very low. No CWDspecific

PrP accumulation was detected in a sample of velvet from an elk stag which

developed clinical CWD about three months later; there were severe brain lesions and

extensive CWD-specific PrP staining in both the brain and peripheral lymphoid tissue of the

stag (Kahn et al., 2004).

Consumption of venison and other parts of the animal

229. PrPCWD has not been detected in muscle tissue from infected cervids (Spraker et al.,

2002c). However, it has been recommended by the World Health Organisation that no parts or

products of any animal know to be CWD-positive should be consumed (WHO, 2000). Public

health authorities in the USA and Canada have indicated agreement with this (Canadian Food

Inspection Agency, 2003; Chronic Wasting Disease Alliance, 2004). It has been suggested

that if a harvested cervid is being tested for CWD, the test results should be awaited before

the meat is eaten (Wisconsin Department of Agriculture, Trade and Consumer Protection,

2002). Authorities in North America have widely advised that (a) tissues likely to contain the

greatest amount of CWD agent in infected cervids, including the brain, spinal cord, lymph

nodes, spleen, tonsils and eyes, should not be consumed from any harvested deer; (b) meat

should be boned out and fat and connective tissue removed (which would also remove lymph

nodes); and (c) hunters should avoid eating meat from deer or elk which look sick or which

test positive for CWD (Buege, 2002; Chronic Wasting Disease Alliance, 2004; Williams et

al., 2002; Wisconsin Department of Agriculture, Trade and Consumer Protection, 2002;

Belay et al., 2004).

Potential risk from handling and processing cervids

230. In order to minimise any potential risk from exposure to the agent of CWD, hunters,

meat processors and taxidermists handling cervid carcasses are advised to wear latex or

rubber gloves when handling or dressing cervids from CWD-endemic areas, to minimise

handling of brain and spinal cord, and to thoroughly wash knives and other implements after

use on deer or elk carcasses (Belay, 2004; Williams et al., 2002). It has been suggested that

the risk of “build-up” of infectious CWD agent in a venison processing plant would be

unlikely (Buege, 2002).

Potential risk from disposal of carcasses and subsequent contamination of


231. In 2002, a risk analysis was produced on disposal of deer from Wisconsin in

municipal solid landfills. It was noted that it is not known how much infected material a

human (or animal) must consume or be exposed to in order to be infected with CWD. The

report took into account the probable species barrier for transmission to humans (Raymond et

al., 2000). It was noted that the CWD agent is hydrophobic and likely to adhere to organic

materials within a landfill, taking several months to move through the landfill, and that any

infectivity exiting the landfill would be captured in the landfill effluent. If effluent was

transferred to a wastewater plant (rather than recirculated in the landfill) the agent would be

expected to partition with the sludge fraction, which would be diluted greatly with other

solids and mixed with nine inches (22.5 cm) of topsoil, providing “an extremely large dilution

factor.” It was concluded that there was no significant risk to human health from disposing of

deer infected with CWD in properly constructed landfill sites (Olander, 2002).

snip...full text 66 pages ;

1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype
of 'UNKNOWN' strain growing. ...


Animal Prion Diseases Relevant to Humans (unknown types?)
Thu Oct 27, 2005 12:05

About Human Prion Diseases /
Animal Prion Diseases Relevant to Humans

Bovine Spongiform Encephalopathy (BSE) is a prion
disease of cattle. Since 1986, when BSE was recognized,
over 180,000 cattle in the UK have developed the
disease, and approximately one to three million are
likely to have been infected with the BSE agent, most
of which were slaughtered for human consumption before
developing signs of the disease. The origin of the
first case of BSE is unknown, but the epidemic was
caused by the recycling of processed waste parts of
cattle, some of which were infected with the BSE agent
and given to other cattle in feed. Control measures
have resulted in the consistent decline of the epidemic
in the UK since 1992. Infected cattle and feed exported
from the UK have resulted in smaller epidemics in other
European countries, where control measures were applied

Compelling evidence indicates that BSE can be
transmitted to humans through the consumption of prion
contaminated meat. BSE-infected individuals eventually
develop vCJD with an incubation time believed to be on
average 10 years. As of November 2004, three cases of
BSE have been reported in North America. One had been
imported to Canada from the UK, one was grown in
Canada, and one discovered in the USA but of Canadian
origin. There has been only one case of vCJD reported
in the USA, but the patient most likely acquired the
disease in the United Kingdom. If current control
measures intended to protect public and animal health
are well enforced, the cattle epidemic should be
largely under control and any remaining risk to humans
through beef consumption should be very small. (For
more details see Smith et al. British Medical Bulletin,
66: 185. 2003.)

Chronic Wasting Disease (CWD) is a prion disease of elk
and deer, both free range and in captivity. CWD is
endemic in areas of Colorado, Wyoming, and Nebraska,
but new foci of this disease have been detected in
Nebraska, South Dakota, New Mexico, Wisconsin,
Mississippi Kansas, Oklahoma, Minnesota, Montana, and
Canada. Since there are an estimated 22 million elk and
deer in the USA and a large number of hunters who
consume elk and deer meat, there is the possibility
that CWD can be transmitted from elk and deer to
humans. As of November 2004, the NPDPSC has examined 26
hunters with a suspected prion disease. However, all of
them appeared to have either typical sporadic or
familial forms of the disease. The NPDPSC coordinates
with the Centers for Disease Control and state health
departments to monitor cases from CWD-endemic areas.
Furthermore, it is doing experimental research on CWD
transmissibility using animal models. (For details see
Sigurdson et al. British Medical Bulletin. 66: 199.
2003 and Belay et al. Emerging Infectious Diseases.
10(6): 977. 2004.)

Interspecies Transmission of Chronic Wasting Disease
Prions to

Squirrel Monkeys (Saimiri sciureus)

Richard F. Marsh,1? Anthony E. Kincaid,2 Richard A.
Bessen,3 and Jason C. Bartz4*

Department of Animal Health and Biomedical Sciences,
University of Wisconsin, Madison 537061; Department of

Physical Therapy2 and Department of Medical
Microbiology and Immunology,4 Creighton University, Omaha,

Nebraska 68178; and Department of Veterinary Molecular
Biology, Montana

State University, Bozeman, Montana 597183

Received 3 May 2005/Accepted 10 August 2005

Chronic wasting disease (CWD) is an emerging prion
disease of deer and elk. The risk of CWD transmission

to humans following exposure to CWD-infected tissues is
unknown. To assess the susceptibility of nonhuman

primates to CWD, two squirrel monkeys were inoculated
with brain tissue from a CWD-infected mule deer. The

CWD-inoculated squirrel monkeys developed a progressive
neurodegenerative disease and were euthanized at

31 and 34 months postinfection. Brain tissue from the
CWD-infected squirrel monkeys contained the abnormal

isoform of the prion protein, PrP-res, and displayed
spongiform degeneration. This is the first reported

transmission of CWD to primates.


JOURNAL OF VIROLOGY, Nov. 2005, p. 13794-13796 Vol.
79, No. 21


Copyright © 2005, American Society for Microbiology.
All Rights Reserved.


The EMBO Journal, Vol. 19, No. 17 pp. 4425-4430, 2000
© European Molecular Biology Organization

Evidence of a molecular barrier limiting
susceptibility of humans, cattle and sheep to
chronic wasting disease

G.J. Raymond1, A. Bossers2, L.D. Raymond1, K.I. O?Rourke3,
L.E. McHolland4, P.K. Bryant III4, M.W. Miller5, E.S.
Williams6, M.
and B. Caughey1,7

1NIAID/NIH Rocky Mountain Laboratories, Hamilton, MT
3USDA/ARS/ADRU, Pullman, WA 99164-7030, 4USDA/ARS/ABADRL,
Laramie, WY 82071, 5Colorado Division of Wildlife,
Wildlife Research
Center, Fort Collins, CO 80526-2097, 6Department of
Veterinary Sciences,
University of Wyoming, Laramie, WY 82070, USA and
Institute for Animal Science and Health, Lelystad, The
7Corresponding author e-mail: Received
June 7, 2000;
revised July 3, 2000; accepted July 5, 2000.


Chronic wasting disease (CWD) is a transmissible
spongiform encephalopathy (TSE) of deer and elk,
and little is known about its transmissibility to other
species. An important factor controlling
interspecies TSE susceptibility is prion protein (PrP)
homology between the source and recipient
species/genotypes. Furthermore, the efficiency with which
the protease-resistant PrP (PrP-res) of one
species induces the in vitro conversion of the normal PrP
(PrP-sen) of another species to the
protease-resistant state correlates with the cross-species
transmissibility of TSE agents. Here we
show that the CWD-associated PrP-res (PrPCWD) of cervids
readily induces the conversion of recombinant cervid
molecules to the protease-resistant state in accordance
with the known transmissibility of CWD between cervids.
In contrast,
PrPCWD-induced conversions of human and bovine PrP-sen
much less efficient, and conversion of ovine PrP-sen was
intermediate. These results demonstrate a barrier at the
molecular level that should limit the susceptibility of
these non-cervid
species to CWD.


Clearly, it is premature to draw firm conclusions about
passing naturally into humans, cattle and sheep, but
the present
results suggest that CWD transmissions to humans would
be as
limited by PrP incompatibility as transmissions of BSE
or sheep
scrapie to humans. Although there is no evidence that
scrapie has affected humans, it is likely that BSE has
caused variant
CJD in 74 people (definite and probable variant CJD
cases to
date according to the UK CJD Surveillance Unit). Given the
presumably large number of people exposed to BSE
the susceptibility of humans may still be very low
compared with
cattle, which would be consistent with the relatively
conversion of human PrP-sen by PrPBSE. Nonetheless, since
humans have apparently been infected by BSE, it would
seem prudent
to take reasonable measures to limit exposure of humans
(as well as sheep and cattle) to CWD infectivity as has
recommended for other animal TSEs.


2006 mad cow protein to deer

e) "Big Jim's" BBB Deer Ration, Big Buck Blend,
Recall # V-104-6;

every wonder why they are so big......mad cow protein ;

Guidance for Industry: Use of Material From Deer and Elk In Animal Feed

Terry S. Singeltary Sr.
Vol #: 1

-------- Original Message --------

Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material
From Deer and Elk in Animal Feed; Availability
Date: Fri, 16 May 2003 11:47:37 -0500
From: "Terry S. Singeltary Sr."

Greetings FDA,

i would kindly like to comment on;

Docket 03D-0186

FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal
Feed; Availability

Several factors on this apparent voluntary proposal disturbs me greatly,
please allow me to point them out;

1. MY first point is the failure of the partial ruminant-to-ruminant feed
ban of 8/4/97. this partial and voluntary feed ban of some ruminant
materials being fed back to cattle is terribly flawed. without the
_total_ and _mandatory_ ban of all ruminant materials being fed
back to ruminants including cattle, sheep, goat, deer, elk and mink,
chickens, fish (all farmed animals for human/animal consumption),
this half ass measure will fail terribly, as in the past decades...

2. WHAT about sub-clinical TSE in deer and elk? with the recent
findings of deer fawns being infected with CWD, how many could
possibly be sub-clinically infected. until we have a rapid TSE test to
assure us that all deer/elk are free of disease (clinical and sub-clinical),
we must ban not only documented CWD infected deer/elk, but healthy
ones as well. it this is not done, they system will fail...

3. WE must ban not only CNS (SRMs specified risk materials),
but ALL tissues. recent new and old findings support infectivity
in the rump or ass muscle. wether it be low or high, accumulation
will play a crucial role in TSEs.

4. THERE are and have been for some time many TSEs in the
USA. TME in mink, Scrapie in Sheep and Goats, and unidentified
TSE in USA cattle. all this has been proven, but the TSE in USA
cattle has been totally ignored for decades. i will document this
data below in my references.

5. UNTIL we ban all ruminant by-products from being fed back
to ALL ruminants, until we rapid TSE test (not only deer/elk) but
cattle in sufficient numbers to find (1 million rapid TSE test in
USA cattle annually for 5 years), any partial measures such as the
ones proposed while ignoring sub-clinical TSEs and not rapid TSE
testing cattle, not closing down feed mills that continue to violate the
FDA's BSE feed regulation (21 CFR 589.2000) and not making
freely available those violations, will only continue to spread these
TSE mad cow agents in the USA. I am curious what we will
call a phenotype in a species that is mixed with who knows
how many strains of scrapie, who knows what strain or how many
strains of TSE in USA cattle, and the CWD in deer and elk (no
telling how many strains there), but all of this has been rendered
for animal feeds in the USA for decades. it will get interesting once
someone starts looking in all species, including humans here in the
USA, but this has yet to happen...

6. IT is paramount that CJD be made reportable in every state
(especially ''sporadic'' cjd), and that a CJD Questionnaire must
be issued to every family of a victim of TSE. only checking death
certificates will not be sufficient. this has been proven as well

7. WE must learn from our past mistakes, not continue to make
the same mistakes...


Oral transmission and early lymphoid tropism of chronic wasting disease
PrPres in mule deer fawns (Odocoileus hemionus )
Christina J. Sigurdson1, Elizabeth S. Williams2, Michael W. Miller3,
Terry R. Spraker1,4, Katherine I. O'Rourke5 and Edward A. Hoover1

Department of Pathology, College of Veterinary Medicine and Biomedical
Sciences, Colorado State University, Fort Collins, CO 80523- 1671, USA1
Department of Veterinary Sciences, University of Wyoming, 1174 Snowy
Range Road, University of Wyoming, Laramie, WY 82070, USA 2
Colorado Division of Wildlife, Wildlife Research Center, 317 West
Prospect Road, Fort Collins, CO 80526-2097, USA3
Colorado State University Veterinary Diagnostic Laboratory, 300 West
Drake Road, Fort Collins, CO 80523-1671, USA4
Animal Disease Research Unit, Agricultural Research Service, US
Department of Agriculture, 337 Bustad Hall, Washington State University,
Pullman, WA 99164-7030, USA5

Author for correspondence: Edward Hoover.Fax +1 970 491 0523. e-mail

Mule deer fawns (Odocoileus hemionus) were inoculated orally with a
brain homogenate prepared from mule deer with naturally occurring
chronic wasting disease (CWD), a prion-induced transmissible spongiform
encephalopathy. Fawns were necropsied and examined for PrP res, the
abnormal prion protein isoform, at 10, 42, 53, 77, 78 and 80 days
post-inoculation (p.i.) using an immunohistochemistry assay modified to
enhance sensitivity. PrPres was detected in alimentary-tract-associated
lymphoid tissues (one or more of the following: retropharyngeal lymph
node, tonsil, Peyer's patch and ileocaecal lymph node) as early as 42
days p.i. and in all fawns examined thereafter (53 to 80 days p.i.). No
PrPres staining was detected in lymphoid tissue of three control fawns
receiving a control brain inoculum, nor was PrPres detectable in neural
tissue of any fawn. PrPres-specific staining was markedly enhanced by
sequential tissue treatment with formic acid, proteinase K and hydrated
autoclaving prior to immunohistochemical staining with monoclonal
antibody F89/160.1.5. These results indicate that CWD PrP res can be
detected in lymphoid tissues draining the alimentary tract within a few
weeks after oral exposure to infectious prions and may reflect the
initial pathway of CWD infection in deer. The rapid infection of deer
fawns following exposure by the most plausible natural route is
consistent with the efficient horizontal transmission of CWD in nature
and enables accelerated studies of transmission and pathogenesis in the
native species.


These results indicate that mule deer fawns develop detectable PrP res
after oral exposure to an inoculum containing CWD prions. In the
earliest post-exposure period, CWD PrPres was traced to the lymphoid
tissues draining the oral and intestinal mucosa (i.e. the
retropharyngeal lymph nodes, tonsil, ileal Peyer's patches and
ileocaecal lymph nodes), which probably received the highest initial
exposure to the inoculum. Hadlow et al. (1982) demonstrated scrapie
agent in the tonsil, retropharyngeal and mesenteric lymph nodes, ileum
and spleen in a 10-month-old naturally infected lamb by mouse bioassay.
Eight of nine sheep had infectivity in the retropharyngeal lymph node.
He concluded that the tissue distribution suggested primary infection
via the gastrointestinal tract. The tissue distribution of PrPres in the
early stages of infection in the fawns is strikingly similar to that
seen in naturally infected sheep with scrapie. These findings support
oral exposure as a natural route of CWD infection in deer and support
oral inoculation as a reasonable exposure route for experimental studies
of CWD.


Date: October 5, 2006 at 1:45 pm PST

Infectious Prions in the Saliva

and Blood of Deer with Chronic

Wasting Disease

Candace K. Mathiason,1 Jenny G. Powers,3 Sallie J. Dahmes,4 David A. Osborn,5 Karl V. Miller,5

Robert J. Warren,5 Gary L. Mason,1 Sheila A. Hays,1 Jeanette Hayes-Klug,1 Davis M. Seelig,1

Margaret A. Wild,3 Lisa L. Wolfe,6 Terry R. Spraker,1,2 Michael W. Miller,6 Christina J. Sigurdson,1

Glenn C. Telling,7 Edward A. Hoover1*

A critical concern in the transmission of prion diseases, including chronic wasting disease (CWD)

of cervids, is the potential presence of prions in body fluids. To address this issue directly, we

exposed cohorts of CWD-nai¨ve deer to saliva, blood, or urine and feces from CWD-positive deer.

We found infectious prions capable of transmitting CWD in saliva (by the oral route) and in blood

(by transfusion). The results help to explain the facile transmission of CWD among cervids and

prompt caution concerning contact with body fluids in prion infections.

SNIP... end


Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine
Spongiform Encephalopathy (BSE)

[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk
Materials for Human Food and Requirement for the Disposition of
Non-Ambulatory Disabled Cattle

Terry S. Singeltary


Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Singeltary, Sr et al. JAMA.2001; 285: 733-734.

RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob

disease in the United States

Email Terry S. Singeltary:

I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to

comment on the CDC's attempts to monitor the occurrence of emerging

forms of CJD. Asante, Collinge et al [1] have reported 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. However, CJD and all human TSEs are not reportable

nationally. CJD and all human TSEs must be made reportable in every

state and internationally. I hope that the CDC does not continue to

expect us to still believe that the 85%+ of all CJD cases which are

sporadic are all spontaneous, without route/source. We have many TSEs in

the USA in both animal and man. CWD in deer/elk is spreading rapidly and

CWD does transmit to mink, ferret, cattle, and squirrel monkey by

intracerebral inoculation. With the known incubation periods in other

TSEs, oral transmission studies of CWD may take much longer. Every

victim/family of CJD/TSEs should be asked about route and source of this

agent. To prolong this will only spread the agent and needlessly expose

others. In light of the findings of Asante and Collinge et al, there

should be drastic measures to safeguard the medical and surgical arena

from sporadic CJDs and all human TSEs. I only ponder how many sporadic

CJDs in the USA are type 2 PrPSc?







Date: September 6, 2006 at 7:58 am PST

a) EVSRC Custom dairy feed, Recall # V-130-6;
b) Performance Chick Starter, Recall # V-131-6;
c) Performance Quail Grower, Recall # V-132-6;
d) Performance Pheasant Finisher, Recall # V-133-6.
Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone
on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is
Dairy and poultry feeds were possibly contaminated with ruminant based
477.72 tons

a) Dairy feed, custom, Recall # V-134-6;
b) Custom Dairy Feed with Monensin, Recall # V-135-6.
None. Bulk product
Recalling Firm: Burkmann Feed, Greeneville, TN, by Telephone beginning on
June 28, 2006.
Manufacturer: H. J. Baker & Bro., Inc., Albertville, AL. Firm initiated
recall is complete.
Possible contamination of dairy feeds with ruminant derived meat and bone
1,484 tons
TN and WV

MS, AL, GA, AND TN 11,000+ TONS
Date: August 16, 2006 at 9:19 am PST


Bulk custom made dairy feed, Recall # V-115-6
Hiseville Feed & Seed Co., Hiseville, KY, by telephone and letter on or
about July 14, 2006. FDA initiated recall is ongoing.
Custom made feeds contain ingredient called Pro-Lak which may contain
ruminant derived meat and bone meal.
Approximately 2,223 tons


Bulk custom made dairy feed, Recall # V-116-6
Rips Farm Center, Tollesboro, KY, by telephone and letter on July 14, 2006.
FDA initiated recall is ongoing.
Custom made feeds contain ingredient called Pro-Lak which may contain
ruminant derived meat and bone meal.
1,220 tons

Bulk custom made dairy feed, Recall # V-117-6
Kentwood Co-op, Kentwood, LA, by telephone on June 27, 2006. FDA initiated
recall is completed.
Possible contamination of animal feed ingredients, including ingredients
that are used in feed for dairy animals, with ruminant derived meat and bone
40 tons
LA and MS


Bulk Dairy Feed, Recall V-118-6
Cal Maine Foods, Inc., Edwards, MS, by telephone on June 26, 2006. FDA
initiated recall is complete.
Possible contamination of animal feed ingredients, including ingredients
that are used in feed for dairy animals, with ruminant derived meat and bone
7,150 tons


Bulk custom dairy pre-mixes, Recall # V-119-6
Walthall County Co-op, Tylertown, MS, by telephone on June 26, 2006. Firm
initiated recall is complete.
Possible contamination of dairy animal feeds with ruminant derived meat and
bone meal.
87 tons


Bulk custom dairy pre-mixes, Recall # V-120-6
Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm
initiated recall is complete.
Possible contamination of dairy animal feeds with ruminant derived meat and
bone meal.
350 tons
AL and MS


a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet,
50 lb. bags, Recall # V-121-6;
b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet,
50 lb. bags, Recall # V-122-6;
c) Tucker Milling, LLC #31232 Game Bird Grower,
50 lb. bags, Recall # V-123-6;
d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD
Medicated, 50 lb bags, Recall # V-124-6;
e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags,
Recall # V-125-6;
f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags,
Recall # V-126-6;
g) Tucker Milling, LLC #30116, TM Broiler Finisher,
50 lb bags, Recall # V-127-6
All products manufactured from 02/01/2005 until 06/20/2006
Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit
on June 20, 2006, and by letter on June 23, 2006.
Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated
recall is ongoing.
Poultry and fish feeds which were possibly contaminated with ruminant based
protein were not labeled as "Do not feed to ruminants".
7,541-50 lb bags
AL, GA, MS, and TN



COMMERCE 27,694,240 lbs
Date: August 6, 2006 at 6:14 pm PST
Bulk custom dairy feds manufactured from concentrates, Recall # V-113-6
All dairy feeds produced between 2/1/05 and 6/16/06 and containing H. J.
Baker recalled feed products.
Vita Plus Corp., Gagetown, MI, by visit beginning on June 21, 2006. Firm
initiated recall is complete.
The feed was manufactured from materials that may have been contaminated
with mammalian protein.
27,694,240 lbs



TONS Products manufactured from 02/01/2005 until 06/06/2006
Date: August 6, 2006 at 6:16 pm PST
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) Performance Sheep Pell W/Decox/A/N, medicated,
net wt. 50 lbs, Recall # V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
d) CO-OP 32% Sinking Catfish Food Medicated,
Recall # V-103-6;
e) "Big Jim's" BBB Deer Ration, Big Buck Blend,
Recall # V-104-6;
f) CO-OP 40% Hog Supplement Medicated Pelleted,
Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020,
Carbadox -- 0.0055%, Recall # V-106-6;
Feed for Chickens from Hatch to 20 Weeks, Medicated,
Bacitracin Methylene Disalicylate, 25 and 50 Lbs,
Recall # V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying
Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
net wt 50 Lbs, Recall # V-110-6;
Recall # V-111-6;
Recall # V-112-6
Product manufactured from 02/01/2005 until 06/06/2006
Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and
visit on June 9, 2006. FDA initiated recall is complete.
Animal and fish feeds which were possibly contaminated with ruminant based
protein not labeled as "Do not feed to ruminants".
125 tons
AL and FL



Date: August 6, 2006 at 6:19 pm PST
Bulk custom made dairy feed, Recall # V-114-6
Burkmann Feeds LLC, Glasgow, KY, by letter on July 14, 2006. Firm initiated
recall is ongoing.
Custom made feeds contain ingredient called Pro-Lak, which may contain
ruminant derived meat and bone meal.


Sun Jul 16, 2006 09:22


a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals,
Recall # V-079-6;
b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg),
Recall # V-080-6;
FEED, Recall # V-081-6;
d) Feather Meal, Recall # V-082-6
a) Bulk
b) None
c) Bulk
d) Bulk
H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and
by press release on June 16, 2006. Firm initiated recall is ongoing.
Possible contamination of animal feeds with ruminent derived meat and bone
10,878.06 tons



Date: June 27, 2006 at 7:42 am PST
Public Health Service
Food and Drug Administration

New Orleans District
297 Plus Park Blvd.
Nashville, TN 37217

Telephone: 615-781-5380
Fax: 615-781-5391

May 17, 2006



Mr. William Shirley, Jr., Owner
Louisiana.DBA Riegel By-Products
2621 State Street
Dallas, Texas 75204

Dear Mr. Shirley:

On February 12, 17, 21, and 22, 2006, a U.S. Food & Drug Administration
(FDA) investigator inspected your rendering plant, located at 509 Fortson
Street, Shreveport, Louisiana. The inspection revealed significant
deviations from the requirements set forth in Title 21, Code of Federal
Regulations, Part 589.2000 [21 CFR 589.2000], Animal Proteins Prohibited in
Ruminant Feed. This regulation is intended to prevent the establishment and
amplification of Bovine Spongiform Encephalopathy (BSE). You failed to
follow the requirements of this regulation; products being manufactured and
distributed by your facility are misbranded within the meaning of Section
403(a)(1) [21 USC 343(a)(1)] of the Federal Food, Drug, and Cosmetic Act
(the Act).

Our investigation found you failed to provide measures, including sufficient
written procedures, to prevent commingling or cross-contamination and to
maintain sufficient written procedures [21 CFR 589.2000(e)] because:

You failed to use clean-out procedures or other means adequate to prevent
carryover of protein derived from mammalian tissues into animal protein or
feeds which may be used for ruminants. For example, your facility uses the
same equipment to process mammalian and poultry tissues. However, you use
only hot water to clean the cookers between processing tissues from each
species. You do not clean the auger, hammer mill, grinder, and spouts after
processing mammalian tissues.

You failed to maintain written procedures specifying the clean-out
procedures or other means to prevent carryover of protein derived from
mammalian tissues into feeds which may be used for ruminants.

As a result . the poultry meal you manufacture may contain protein derived
from mammalian tissues prohibited in ruminant feed. Pursuant to 21 CFR
589.2000(e)(1)(i), any products containing or may contain protein derived
from mammalian tissues must be labeled, "Do not feed to cattle or other
ruminants." Since you failed to label a product which may contain protein
derived from mammalian tissues with the required cautionary statement. the
poultry meal is misbranded under Section 403(a)(1) [21 USC 343(a)(1)] of the

This letter is not intended as an all-inclusive list of violations at your
facility. As a manufacturer of materials intended for animal feed use, you
are responsible for ensuring your overall operation and the products you
manufacture and distribute are in compliance with the law. You should take
prompt action to correct these violations, and you should establish a system
whereby violations do not recur. Failure to promptly correct these
violations may result in regulatory action, such as seizure and/or
injunction, without further notice.

You should notify this office in writing within 15 working days of receiving
this letter, outlining the specific steps you have taken to bring your firm
into compliance with the law. Your response should include an explanation of
each step taken to correct the violations and prevent their recurrence. If
corrective action cannot be completed within 15 working days, state the
reason for the delay and the date by which the corrections will be
completed. Include copies of any available documentation demonstrating
corrections have been made.

Your reply should be directed to Mark W. Rivero, Compliance Officer, U.S.
Food and Drug Administration, 2424 Edenborn Avenue, Suite 410, Metairie,
Louisiana 70001. If you have questions regarding any issue in this letter,
please contact Mr. Rivero at (504) 219-8818, extension 103.



Carol S. Sanchez
Acting District Director
New Orleans District

look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused
7% (1 of 14) of the cows to come down with BSE;

Risk of oral infection with bovine spongiform encephalopathy agent in

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog,
Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie
Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe
Summary The uncertain extent of human exposure to bovine spongiform
encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease
(vCJD)--is compounded by incomplete knowledge about the efficiency of oral
infection and the magnitude of any bovine-to-human biological barrier to
transmission. We therefore investigated oral transmission of BSE to
non-human primates. We gave two macaques a 5 g oral dose of brain homogenate
from a BSE-infected cow. One macaque developed vCJD-like neurological
disease 60 months after exposure, whereas the other remained free of disease
at 76 months. On the basis of these findings and data from other studies, we
made a preliminary estimate of the food exposure risk for man, which
provides additional assurance that existing public health measures can
prevent transmission of BSE to man.


BSE bovine brain inoculum

100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg

Primate (oral route)* 1/2 (50%)

Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%)
1/15 (7%)

RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)

PrPres biochemical detection

The comparison is made on the basis of calibration of the bovine inoculum
used in our study with primates against a bovine brain inoculum with a
similar PrPres concentration that was

inoculated into mice and cattle.8 *Data are number of animals
positive/number of animals surviving at the time of clinical onset of
disease in the first positive animal (%). The accuracy of

bioassays is generally judged to be about plus or minus 1 log. ic
ip=intracerebral and intraperitoneal.

Table 1: Comparison of transmission rates in primates and cattle infected
orally with similar BSE brain inocula

Published online January 27, 2005

It is clear that the designing scientists must

also have shared Mr Bradley's surprise at the results because all the dose

levels right down to 1 gram triggered infection.

2) Infectious dose:

To cattle: 1 gram of infected brain material (by oral ingestion)

Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518

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