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BSE TESTING USDA VS CREEKSTONE Case 1:06-cv-00544-JR

flounder

Well-known member
GREETINGS,

i have four different pdfs and wanted to post all in pdf, so as to be much shorter, but there was no way to post pdf file without url. so here is plain text. ...TSS


Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 1 of 52

IN THE UNITED STATES DISTRICT COURT

FOR THE DISTRICT OF COLUMBIA
CREEKSTONE FARMS PREMIUM BEEF, LLC, )

Plaintiff, )

vs. ) Civil Action No. 06-544 (JR)

UNITED STATES DEPARTMENT OF AGRICULTURE, )

and MIKE JOHANNS, IN HIS CAPACITY AS THE )

SECRETARY OF AGRICULTURE, )

Defendants. )

_________________________________________________ )

REPLY IN SUPPORT OF PLAINTIFF’S MOTION FOR SUMMARY JUDGMENT AND

OPPOSITION TO DEFENDANTS’ CROSS-MOTION FOR SUMMARY JUDGMENT

Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 2 of 52

TABLE OF CONTENTS

SUMMARY OF
ARGUMENT.........................................................................................1

ARGUMENT......................................................................................................................4

I. THIS COURT HAS JURISDICTION TO HEAR CREEKSTONE’S CLAIMS.4

A. Creekstone’s Claims Are Not Moot.
..............................................................4

B. Creekstone Has Standing To Present Its Claims.
........................................6

II. USDA’S EXPANSIVE INTERPRETATION OF THE VSTA TO APPLY TO

DIAGNOSTIC TESTS AND TO THE USE OF BIOLOGICAL PRODUCTS

IS UNPERSUASIVE AND NOT ENTITLED TO DEFERENCE.....................10

A. The VSTA Is Neither Ambiguous Nor Susceptible to USDA’s

Interpretations...............................................................................................10


1. Regulation of the Use of Biological Products
...............................12

2. Regulation of Diagnostic
Tests.......................................................18

B. USDA’s Expansive Interpretation of the VSTA Is Not Entitled to

Deference.
......................................................................................................21


1. No Deference for Interpretations Expanding the Scope of the Agency’s

Authority.............................................................................................21


2. No deference for Statutory Interpretations Not Accompanied by Further

Explication..........................................................................................22


3. Little Deference for Statutory Interpretations that Were Far from

Contemporaneous or
Consistent.........................................................25

C. The Reenactment Doctrine Does Not Save USDA’s Unsupported

Interpretation of the VSTA
..........................................................................27


III. USDA LACKS STATUTORY AUTHORITY TO REGULATE BSE TEST KITS

IN PARTICULAR
..................................................................................................29


A. BSE Test Kits Are Not “Analogous Products.”
..........................................30


Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 3 of 52

B. BSE Test Kits Are Not, and Would Not Be, Used in the Treatment of

Animal Disease
..............................................................................................33


C. BSE Test Kits Are Not Worthless, Contaminated, Dangerous or Harmful.34

IV. USDA’S RESTRICTIONS ON BSE TEST KITS ON ECONOMIC GROUNDS

ARE OUTSIDE ITS AUTHORITY UNDER THE VSTA
.................................39

V. USDA IS NOT ENTITLED TO SUMMARY JUDGMENT ..............................45

CONCLUSION
................................................................................................................45

EXHIBIT 1 Supplemental Declaration of John D. Stewart

EXHIBIT 2 Declaration of Boyd R. Oase of Kowalski’s Markets

EXHIBIT 3 Declaration of James R. Kiley of Wild by Nature Markets

EXHIBIT 4 Declaration of Darin Parker of Parker International Inc.

EXHIBIT 5 Declaration of Kyu O Kim of NY-SK Trading, LLC

EXHIBIT 6 Declaration of Steve Erdley of Penn Traffic Company

EXHIBIT 7 Hearing before the Committee on Agriculture on the Estimates of

Appropriations for the Fiscal Year Ending June 30, 1914, H.R. 28283, 62d

Cong. 20-32 (1913) (testimony of Dr. A.M. Farrington, Asst. Chief, Bureau

of Animal Indus., Dept. of Agric.)

EXHIBIT 8 Declaration of Paul W. Brown, M.D.

EXHIBIT 9 Report on the Monitoring and Testing of Ruminants for the
Presence of

Transmissible Spongiform Encephalopathy (TSE) in the EU in 2005

EXHIBIT 10 Declaration of Linda A. Detwiler, D.V.M.

EXHIBIT 11 Supervie and Castagliola, “The Unrecognized French BSE
Epidemic,” 35

Vet. Res. 349-362 (2004)

iii

Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 4 of 52

TABLE OF AUTHORITIES 1

FEDERAL CASES

62 Cases of Jam v. United States, 340 U.S. 593 (1951)
....................................................43

AFL-CIO v. Brock, 835 F.2d 912 (D.C. Cir. 1987)
...........................................................28

*Adamo Wrecking Co. v. United States, 434 U.S. 275 (1978)
..............................22, 23, 26

American Fin. Servs. Ass'n v. FTC, 767 F.2d 957 ), cert. denied, 475
U.S. 1011

(1986
............................................................................................................................42

American Petroleum Institute v. EPA, 52 F.3d 1113 (D.C. Cir. 1995)
.............................11

*Animal Health Institute v. USDA, 487 F. Supp. 376 (D. Colo. 1980)
.............................13

Area Transp., Inc. v. Ettinger, 219 F.3d 671 (7th Cir. 2000)
..............................................8

Arnold v. Intervet, Inc., 305 F. Supp. 2d 548 (D. Md.
2003).............................................21

Babbitt v. Sweet Home Chapter of Communities for a Greater Oregon, 515 U.S.

687
(1995)..............................................................................................................15,
28

*Barnett v. Weinberger, 818 F.2d 953 (D.C. Cir. 1987)
...........................23, 24, 26, 27, 28

Better Government Assoc. v. U.S. Dept. of Interior, 780 F.2d 86 (D.C.
Cir. 1986) ............5

*Bowen v. Georgetown Univ. Hospital, 488 U.S. 204
(1988)...........................................25

Burlington Northern R.R. Co. v. Surface Transportation Bd., 75 F.3d 685,
688

(D.C. Cir. 1996)
............................................................................................................6


Central Bank of Denver, N.A. v. First Interstate Bank of Denver, N.A.,
511 U.S.

164
(1994)....................................................................................................................29

Lorillard v. Pons, 434 U.S. 575 (1978)
.............................................................................29

Chevron. Public Citizen, Inc. v. U.S. Dept. of Health and Human
Services, 332

F.3d 654 (D.C. Cir.
2003)....................................................................17,
18, 22, 23, 26

Christensen v. Harris Cty., 529 U.S. 576
(2000)...............................................................25

*City of Chicago v. Environmental Defense Fund, 511 U.S. 328
(1994)....................16, 17

City of New Haven v. HUD, 809 F.2d 900 (D.C. Cir. 1987)
...............................................5

Continental Airlines, Inc. v. U.S. Department of Transportation , 856
F.2d 209

(D.C. Cir. 1988)
...........................................................................................................26


Dolan v. United States Postal Service, 126 S. Ct.1252 (2/22/2006)
.................................14

Edward J. DeBartolo Corp. v. Florida Gulf Coast Building & Constr. Trades

Council, 485 U.S. 568 (1988)
......................................................................................44

Engine Mfrs. Ass'n v. EPA, 88 F.3d 1075 (D.C. Cir.
1996)...............................................22

Ethyl Corp. v. EPA, 51 F.3d 1053 (D.C. Cir. 1995)
....................................................11, 22

*ExxonMobil Gas Marketing Co. v. FERC, 297 F.3d 1071 (D.C. Cir.
2002)...................18

*FDA v. Brown & Williamson Tobacco Corp., 529 U.S. 120 (2000)
.........................13, 29

Federal National Mortgage Ass'n v. United States, 56 Fed. Cl. 228 (Ct.
of Claims

2003)
............................................................................................................................23

*Friends of the Earth, Inc. v. EPA, 446 F.3d 140 (D.C. Cir. 2006)
..................................22

*Friends of the Earth v. Laidlaw, 528 U.S. 167 (2000)
......................................................4

*Garrelts v. Smithkline Beecham Corp., 943 F. Supp. 1023 (N. D. Ia.
1996) ............28, 44

*General American Transp. Corp. v. ICC, 872 F.2d 1048 (DC Circuit 1989)
.................28

1 Asterisk denotes authorities principally relied on.

iv

Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 5 of 52

Gettman v. DEA, 290 F.3d 430 (D.C. Cir.
2002).................................................................8

*Grand Laboratories, Inc. v. Harris, 488 F. Supp. 618, 619 (D.S.D.
1980), rev’d

on other grounds, 660 F.2d 1288 (8th Cir.
1981).........................................................33

Independent Insurance Agents of America, Inc. v. Hawke, 211 F.3d 638
(2000) .............15

International Union, UAW v. Brock, 816 F.2d 761 (D.C. Cir.
1987)................................28

Investment Co. Inst. v. Camp, 401 U.S. 617 (1971)
..........................................................23

*John Hancock Mut. Life Ins. Co. v. Harris Trust & Sav. Bank, 510 U.S. 86

(1993)..........................................................................................................................22


Kelley v. U.S. EPA, 15 F.3d 1100 (D.C. Cir. 1994), cert. denied, 513
U.S. 1110

(1995)].........................................................................................................................17

Koszola v. F.D.I.C., 393 F.3d 1294 (D.C. Cir.
2005)........................................................28

Lorillard v. Pons, 434 U.S. 575 (1978)
.............................................................................29

*Lujan v. Defenders of Wildlife, 504 U.S. 555 (1992)
....................................................7, 8

Lynn Martin v. Occupational Safety and Health Review Commission, 499 U.S.

144
(1991)....................................................................................................................26


McBryde v. Committee To Review Circuit Counsel and Disability Orders, 264

F.3d 52 (D.C. Cir.
2001)............................................................................................7,
8

*Michigan Citizens for an Independent Press v. Thornburgh, 868 F.2d 1285

(D.C. Cir. 1989)
...........................................................................................................17

Michigan v. EPA, 268 F.3d 1075 (D.C. Cir.
2001)............................................................11

Miller v. AT&T Corp., 250 F.3d 820 (4th Cir. 2001)
........................................................19

*Natural Resources Defense Council v. Reilly, 983 F.2d 259 (D.C. Cir.
1993) ...............22

Pacific Power & Light Co. v. FPC, 184 F.2d 272 (D.C. Cir.
1950)..................................28

PanAmSat Corp. v. F.C.C., 198 F.3d 890 (D.C. Cir. 1999)
..............................................25

Pegram v. Herdrich, 530 U.S. 211
(2000).........................................................................19

Public Citizen, Inc. v. U.S. Dept. of Health and Human Services, 332
F.3d 654,

662 (D.C. Cir. 2003)
...................................................................................................23


*Railway Labor Executives' Ass'n v. National Mediation Bd., 29 F.3d 655,
cert.

denied, 514 U.S. 1032 (1995)
................................................................................21,
26

*Railway Labor Executives' Ass'n v. National Mediation Bd., 988 F.2d 133
(D.C.

Cir. 1993), aff'd on rehearing en banc, 29 F.3d 655 (1994), cert.
denied, 514

U.S. 1032
(1995)..............................................................................................17,
18, 42

Reno v. Flores, 507 U.S. 292 (1993)
.................................................................................11

Rodriguez v. United States, 480 U.S. 522 (1987)
........................................................12, 42

*SEC v. Sloan, 436 U.S. 103
(1978)..................................................................................23

Sea-Land Serv., Inc. v. Dep't of Transp., 137 F.3d 640 (D.C. Cir.
1998)..........................11

Sea Robin Pipeline Co. v. FERC, 127 F.3d 365 (5th Cir. 1997)
.......................................14

*Sierra Club v. Morton, 405 U.S. 727 (1972)
.....................................................................7

Solid Waste Agency of Northern Cook County v. U.S. Army Corps of Engineers,

531 U.S. 159
(2001).....................................................................................................29

Texas & Pacific Railway Co. v. Pottorff, 291 U.S. 245
(1934).........................................15

United States v. Mead, 533 U.S. 218 (2001)
.....................................................................23

*Whitman v. American Trucking Ass'ns, 531 U.S. 457
(2001)..........................................13

Whitmore v. Arkansas, 495 U.S. 149 (1990)
.......................................................................8

STATE CASES

v

Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 6 of 52

*Hall v. Nebraska, 100 Neb. 84, 158 N.W. 362 (1916)
....................................................16

STATUTES

Administrative Procedure Act, 5 U.S.C. § 706(2)
.....................................30, 38, 39, 40, 42

Act of July 1, 1902, ch. 1378, 32 Stat.
728..................................................................13, 31

Agricultural Bioterrorism Protection Act of 2002, 7 U.S.C. § 8401
...........................15, 29

Virus Serum Toxin Act, 21 U.S.C. §§
151-154......................................................... passim

21 U.S.C. §
151..........................................................................................11,
19, 29, 35, 43

21 U.S.C. §
152................................................................................................11,
19, 25, 29

21 U.S.C. §
153..................................................................................................................25

21 U.S.C. §
154....................................................................................12,
13, 18, 19, 29, 38

28 U.S.C. § 2680(b)
...........................................................................................................14

29 U.S.C. § 2611(11)
.........................................................................................................19

P.L. 99-198, 99 Stat.
1654-56............................................................................................27

Sections 211-213 of the Public Health Security and Bioterrorism
Preparedness

and Response Act of 2002, P.L. 107-188, 116 Stat. 647
.............................................29

REGULATORY MATERIALS

9 C.F.R. Chapter I Subchapter
E........................................................................................25

9 C.F.R. § 101.2(2)
..........................................................................................20,
21, 33, 34

9 C.F.R. § 102.5(d)
......................................................................................................12,
39

9 C.F.R. §
104.1...........................................................................................................25,
29

29 C.F.R. § 825.114(b)
......................................................................................................19

62 Fed. Reg. 31,326 (June 9, 1997)
.............................................................................27,
32

70 Fed. Reg. 460, 461 (Jan. 4, 2005)
.................................................................................32

LEGISLATIVE MATERIALS

Hearing before the Committee on Agriculture on the Estimates of
Appropriations

for the Fiscal Year Ending June 30, 1914, H.R. 28283, 62d Cong. 20-32

(1913) (Reply Memo Exh.
7).....................................................................................16

S. Rep. No.
99-145.............................................................................................................28

MISCELLANEOUS

OIE Terrestrial Animal Health Code – 2005, Appendix 3.8.4, Surveillance

for Bovine Spongiform Encephalopathy
.....................................................................37

Report on the Monitoring and Testing of Ruminants for the Presence of

Transmissible Spongiform Encephalopathy (TSE) in the EU in
2005........................35

Supervie and Castagliola, "The Unrecognized French BSE Epidemic," 35 Vet.

Res. 349-362
(2004).....................................................................................................37

2B Sutherland Stat. Constr. §
49.09...................................................................................28

vi

Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 7 of 52

SUMMARY OF ARGUMENT

With hardly a word of analysis (prior to this case), the Department of
Agriculture

(“USDA”) has interpreted a statute designed to keep companies from
producing and marketing

fraudulent vaccines and serums for treatment of diseases in animals as
an almost unlimited grant

of authority to restrict or preclude activities related in any way to
animal diseases. Even if it were

appropriate to uphold such an action on the basis of post hoc
rationalizations of counsel, here

those rationalizations are inconsistent with basic principles of
statutory interpretation, often lack

citation or plausible support, and in some instances simply do not make
sense even on their face.

For example, USDA’s argument that this case is moot is based entirely on
USDA’s

improper characterization of plaintiff Creekstone Farms Premium Beef’s
case as solely an

attempt by Creekstone to export beef to Japan. Neither the Complaint,
Creekstone’s Motion for

Summary Judgment, nor the Declaration filed by Creekstone’s founder and
then-CEO

characterized Creekstone’s claims that narrowly. To the contrary,
Creekstone continues to have

strong, valid reasons for wanting to use BSE test kits.

USDA’s claim that Creekstone lacks standing rests on a similarly narrow
view of what

this case is about and the relief Creekstone is seeking. Clearly
Creekstone, which believes the

benefits to its business of testing all its cattle for BSE warrants the
multi-million-dollar cost of

testing, is suffering both economic and non-economic injuries from
USDA’s unlawful refusal to

allow Creekstone access to BSE test kits, injuries that this Court
obviously could alleviate by

striking down USDA’s restrictions on BSE test kit use.

USDA’s defense of its regulations restricting the use of diagnostic
tests, as well as its

actions concerning BSE test kits in particular, is based on a convoluted
reading of the simple

Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 8 of 52

language of the VSTA and on its observation that Congress did not
specifically prohibit USDA

from regulating BSE test kits. But the Supreme Court and the U.S. Court
of Appeals for the

District of Columbia have consistently rejected such attempts to find
congressional authorization

from the absence of a prohibition. The VSTA on its face does not extend
to restrictions on the

use of biological products, nor the restriction of access to diagnostic
tests (especially diagnostic

tests, like the BSE test kits at issue here, which do not operate
through stimulation of an animal’s

immune system). USDA’s interpretation of the VSTA is not subject to
deference, because (1) it

expands the Department’s authority beyond the literal bounds of the
statute; (2) it is not a

contemporaneous interpretation of the statute but rather one that USDA
invented 60 years later;

(3) USDA’s regulations were not accompanied by any analysis of the
VSTA’s statutory language

or legislative history, or really by any explanation; and (4) at least
with respect to import permits

and to BSE test kits in particular, USDA’s regulations were not
announced in a rulemaking or

any similar formal pronouncement.

But even if USDA’s regulatory authority under the VSTA extended to
controlling who

uses biological products, and for what purpose, and to regulating
diagnostic tests that operate in a

manner analogous to viruses, serums, or toxins, USDA cannot legally ban
all private use of BSE

test kits. First, BSE test kits do not function as “analogous products;”
and second, they are not

used in the treatment of an animal disease. (In fact, USDA claims it can
bar Creekstone from

using BSE test kits precisely because they are not being used in the
treatment of animals.) Third,

using BSE test kits to screen cattle slaughtered for human consumption
for BSE hardly makes

them “worthless.” To the contrary, even USDA’s improperly limited view
of the benefits of BSE

testing admits that testing can identify carcasses infected with this
fatal disease months before the

cattle would have any outward signs of BSE that might keep them out of
the food chain. And

- 2 -


Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 9 of 52

renowned BSE experts submitting declarations in support of this Reply
Memorandum establish

the benefits of more extensive BSE testing, a practice adopted by almost
every country in the

world that has been exposed to BSE.

Finally, even assuming that USDA’s regulations were authorized by the
VSTA, and

assuming also that USDA could, consistent with the VSTA, assert
jurisdiction over the use of

BSE test kits in particular, USDA’s filings in this case now make it
clear that USDA is not

really regulating BSE test kits in order to protect animal health or
even to protect the economic

well-being of farmers and ranchers. Rather, USDA is trying to protect
large meatpackers from

competition that Creekstone and others who want to test will pose. Put
another way, USDA

wants to deprive American consumers of the opportunity to buy beef from
BSE-tested cattle.

This goal not only is far beyond what Congress authorized in the VSTA,
it is contrary to basic

tenets about the role of government to protect competition and foster
this nation’s free-market

economy.

For any one of these reasons, Creekstone is entitled to summary judgment
on its claims

that USDA’s actions preventing Creekstone from conducting BSE tests on
the cattle it

slaughters are beyond USDA’s statutory authority. Moreover, even if the
Court were to

determine that Creekstone has not demonstrated that it is entitled to
summary judgment on

those claims, that still would not mean that USDA has carried its burden
of justifying summary

judgment for USDA on those claims. Nor, of course, would it mean that
USDA is entitled to

summary judgment on Creekstone’s third claim: that USDA acted
arbitrarily and capriciously

even if it was within its statutory authority—a claim that has yet to be
briefed.

- 3 -


Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 10 of 52

ARGUMENT

I. THIS COURT HAS JURISDICTION TO HEAR CREEKSTONE’S CLAIMS.

A. Creekstone’s Claims Are Not Moot.

USDA’s argument that Creekstone’s claims are moot is easily disposed of.
Contrary to

USDA’s misreading of Creekstone’s Complaint, Creekstone’s desire to test
voluntarily for BSE

is not limited to gaining access to Japan’s market. In addition to
expanding its customer base,

voluntary testing would enable Creekstone to enhance its brand and
competitiveness. Creekstone

domestic and international customers will purchase more Creekstone beef,
and at a higher price,

if Creekstone can assure those customers that its products come from
cattle that were tested for

BSE. Moreover, because of lingering concerns over the safety of U.S.
beef, Creekstone and other

U.S beef producers have not been able to recapture market share in the
Japanese and Korean

markets—making BSE testing still relevant for those markets.

USDA mistakenly states that “plaintiff’s primary concern is with its
ability to sell beef in

the Japanese market.” USDA Consolidated Memorandum in Support of
Defendants’ Cross-

Motion for Summary Judgment and in Opposition to Plaintiff’s Motion for
Summary Judgment

(“USDA Memo”) at 15. Creekstone’s Complaint and the Supplement
Declaration of its former

CEO and current consultant John Stewart make clear that Creekstone is
challenging the USDA’s

ban against voluntary testing for BSE, not a foreign government’s trade
policy. See Stewart

Supplemental Declaration, Exhibit 1 to this Reply, ¶¶ 2-3, 5, 8. “It is
well settled that a

defendant’s voluntary cessation of a challenged practice does not
deprive a federal court of its

power to determine the legality of that practice.” Friends of the Earth
v. Laidlaw, 528 U.S. 167,

189 (2000). Here, by contrast, there has been no cessation of USDA’s ban
on voluntary BSE

- 4 -


Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 11 of 52

testing, making mootness not even an issue. By definition, this case is
not moot. See Better

Government Assoc. v. U.S. Dept. of Interior, 780 F.2d 86, 91 (D.C. Cir.
1986) (challenges “to the

legality of the standards utilized” by a government agency were not moot
where “the utilization

of the guidelines and the regulation . . . has continued,” even though
specific claim seeking relief

was moot where agency had granted relief); City of New Haven v. HUD, 809
F.2d 900, 904 (D.C.

Cir. 1987) (same).

Access to the Japanese market is but one component of Creekstone’s
desire to conduct

voluntary BSE testing. In addition to Japan, Creekstone wishes to gain
access to Korean and

other overseas markets as well as to expand its U.S. sales by offering
beef from BSE-tested cattle.

Exh. 1 (Stewart Supp. Decl.) ¶ 2. And beyond access to markets,
Creekstone will be able to sell

more beef at higher prices to both its foreign and domestic customers if
the beef is from cattle

tested for BSE. Id. ¶¶ 2, 6, 7; Creekstone customer declarations,
Exhibits 2-6. Thus, irrespective

of Japan’s lifting its ban, Creekstone could increase the demand for its
beef if it can test for BSE.

In addition, Creekstone’s business model is to sell the finest Angus
beef in the world. By

offering its customers beef from BSE-tested cattle, Creekstone intends
to reinforce its reputation

for excellence, safety, and superior beef products. See Exh. 1 (Stewart
Supp. Decl.) ¶ 8. USDA

concedes this point by admitting that one of its reasons for denying
Creekstone permission to test

for BSE is USDA’s concern that Creekstone’s competitors would feel
obligated to BSE test as

well lest they be at a disadvantage. See USDA Memo at 52 n.30. USDA’s
recognition that

allowing Creekstone to offer customers BSE-tested beef would boost
Creekstone’s brand and

provide a competitive edge alone defeats USDA’s mootness argument.

Moreover, despite Japan and Korea lifting their respective U.S. beef
bans, Creekstone

(and other U.S. beef producers) still cannot sell as much U.S. beef as
before. Exh. 1 (Stewart

- 5 -


Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 12 of 52

Supp. Decl.) ¶¶ 2-6 and attachments. This is because Japanese and Korean
customers remain

concerned about the safety of U.S. beef. Exh. 1 ¶¶ 3, 4, 6 and
attachments. In contrast to U.S.

beef, Japan requires all of its beef to be tested for BSE, and Australia
has never had a case of

BSE, putting Creekstone and other U.S. beef producers at a competitive
disadvantage. Exhibit 1

¶ 3 and Attach. A. Creekstone’s desire to test for BSE is motivated in
part to compete more

effectively for overseas customers, again defeating USDA’s mootness
argument.

In sum, there is absolutely nothing about Japan’s lifting its U.S. beef
ban that “make it

impossible to grant [Creekstone] effective relief.” USDA Memo at 15,
quoting Burlington

Northern R.R. Co. v. Surface Transportation Bd., 75 F.3d 685, 688 (D.C.
Cir. 1996) (emphasis

added). The relief Creekstone seeks from this Court is an order
permitting it to test for BSE, not

to open or keep open Japan’s beef market. Creekstone has set forth a
host of reasons for wanting

to conduct voluntary BSE testing irrespective of Japan resuming U.S.
beef imports. USDA’s

mootness argument that “plaintiff’s alleged injury has disappeared”
(USDA Memo at 16) is best

understood as an Article III standing challenge. But for the reasons set
forth in the next Part, that

challenge also fails.

B. Creekstone Has Standing To Present Its Claims.

USDA claims that Creekstone lacks standing to pursue its claims because
(a) Creekstone

has not made a sufficiently concrete demonstration that Creekstone could
be selling more beef

and/or at a higher price were it not for USDA preventing Creekstone from
testing its cattle for

BSE and (b) Creekstone has not “provided convincing evidence” that being
able to test its cattle

for BSE would remedy that injury. USDA Memo at 17.1 USDA misstates
Creekstone’s basis for

1 The weakness of USDA’s argument is exposed by its facially untenable
claim that Creekstone

“has creatively alleged” this injury in “an attempt to save its case
from mootness as a result of

- 6 -


Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 13 of 52

standing, misstates the legal standards for standing, and attempts to
substitute its own speculation

about consumer demand for Creekstone’s specific information.

Creekstone’s basic injury is that it is prohibited from testing its
cattle for BSE in order to

enhance its brand and distinguish Creekstone beef in the marketplace and
to fulfill the demands

of its customers, many of whom will buy more beef at higher prices if it
is tested for BSE. The

direct cause of that injury is USDA’s unlawful actions, restricting the
licensing and permitting of

BSE test kits, preventing the manufacturers of BSE test kits and the
Kansas State University

laboratory authorized to conduct BSE testing from cooperating with
Creekstone, and refusing to

approve Creekstone’s proposed Hazard Analysis Critical Control Points
(HACCP) program for

voluntary BSE testing. Memorandum of Points and Authorities in Support
of Plaintiff’s Motion

for Summary Judgment (“Pl. Memo”) at 11-14. This Court can redress
Creekstone’s injuries by

invalidating the USDA regulations and actions that prevent Creekstone
from BSE testing and by

ordering USDA not to interfere with Creekstone activities that are
outside USDA’s jurisdiction.

See Pl. Memo at 2.

USDA argues that Creekstone must show a definite economic injury, and a
definite

economic benefit from a ruling in its favor, in order to have standing
to challenge the USDA’s

unlawful action. USDA Memo at 17-23. But the law is very clear that
economic injury is not the

only kind of injury that establishes standing. See, e.g., Sierra Club v.
Morton, 405 U.S. 727, 73445

(1972); Lujan v. Defenders of Wildlife, 504 U.S. 555, 562-63 (1992).
Indeed, the very case

that USDA principally relies upon in its mootness argument, McBryde v.
Committee To Review

Circuit Counsel and Disability Orders…, 264 F.3d 52 (D.C. Cir. 2001),
(cited at USDA Memo at

Japan’s recent lifting of its ban against U.S. beef.” USDA Memo at 17.
In fact, Japan lifted its

ban on U.S. beef 12 days after Creekstone filed its Motion for Summary
Judgment (see USDA

Memo at 16) and four months after Creekstone described this basis for
standing in Paragraph 1718

and 26 of its Complaint.

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Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 14 of 52

16-17) held that Judge McBryde had standing to challenge a reprimand
handed down by the Fifth

Circuit—clearly not an action to remedy an economic injury. Id. at
56-57. USDA makes no

argument, nor could it, that there is anything speculative about
Creekstone’s desire to perform

BSE testing on its cattle, or about USDA’s actions that are preventing
Creekstone from doing so.2

If USDA’s position were the law, then businesses’ fundamental right to
judicial review of

unlawful agency actions would be thwarted. Indeed, in USDA’s view, its
refusal to approve a

new vaccine could not be subjected to judicial review because the
vaccine manufacturer could

not provide “convincing evidence” that it could sell the vaccine if it
were approved!

The law instead, as set down by the Supreme Court, is that a private
party aggrieved by

government action directed at it has standing to challenge that action:
“When the suit is one

challenging the legality of government action or inaction, the nature
and extent of facts that must

be averred (at the summary judgment stage) or proved (at the trial
stage) in order to establish

standing depends considerably upon whether the plaintiff is himself an
object of the action (or

forgone action) at issue. If he is, there is ordinarily little question
that the action or inaction has

caused him injury, and that a judgment preventing or requiring the
action will redress it.” Lujan,

504 U.S. at 561.

2 Creekstone’s assertions of injury and redressability thus are not
dependent on the actions of

third parties, as USDA assumes. USDA Memo at 19, 22. The cases that USDA
cites for its

standing argument all involve indirect claims involving third parties,
not attempts to redress

government action directed at the plaintiff. Whitmore v. Arkansas, 495
U.S. 149 (1990),

considered whether a third party could challenge a death sentence
imposed on a capital murder

defendant. The injury in Area Transp., Inc. v. Ettinger, 219 F.3d 671,
673 (7th Cir. 2000), rested

on whether, if the Federal Transit Agency issued the order to a
competing school bus operator

that the plaintiff sought, the competitor would choose to forego future
federal grants. The

plaintiff in Gettman v. DEA, 290 F.3d 430, 435 (D.C. Cir. 2002) hoped
that he could sell

consulting services to third parties who would use marijuana if the DEA
legalized its use. There

is no comparison at all between Creekstone’s demonstrated interest in
pursuing its business plan

involving BSE testing and Mr. Gettman’s “at best reciting injury to his
philosophical interest.”

Id. at 435.

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Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 15 of 52

But even if economic injury were necessary to demonstrate standing,
there is no question

that Creekstone has suffered and is continuing to suffer economic
injury. See Stewart Decl., Pl.

Memo Exh. 1, at ¶¶ 3, 6, 17 (Creekstone has lost about 35% of its
revenue due to BSE concerns

and is prepared to spend $6,000,000 per year to perform BSE testing
itself to help recover that

lost demand); see also Stewart Supplemental Decl., Exh. 1 to this Reply,
at ¶ 4 (Creekstone’s

average sales to Japan in the past two months have been less than
one-twentieth of what they

were prior to the discovery of BSE in the United States), ¶ 8. USDA’s
purported evidence to the

contrary is both speculative and beside the point. The agency spends
pages in its memorandum

arguing about the accuracy or significance of polls that have
consistently shown Japanese

consumers to be reluctant to purchase U.S.-origin beef, and a poll of
over 75,000 Americans

reporting that more than a third are “very concerned” about BSE. Compare
USDA Memo at 1822

with Pl. Memo Exh. 1 at ¶¶ 4-5. Yet one of USDA’s own exhibits confirms
that “polls show

many Japanese consumers still have some doubts about the safety of the
U.S. product and are

reluctant to buy” U.S. beef. USDA Memo Exh. 12. USDA even asserts,
bizarrely, that a poll

indicating that 75% of Japanese respondents were unwilling to eat
U.S.-origin beef now that BSE

has been found in the United States “does not necessarily suggest that
U.S. beef sales in Japan

will fail to return to the levels they were prior to the Japanese ban.”
USDA Memo at 20.

Creekstone’s standing to bring this lawsuit does not stand or fall on
any poll. The import

of those polls is that they support and confirm Creekstone’s own
information regarding the effect

of BSE on U.S. and foreign markets. Whatever the accuracy of these
polls, they certainly

influence the thinking of the distributors and retail chains to which
Creekstone sells its products,

and they supplement Creekstone’s personal communications with those
distributors and with

consumers (and thus are not hearsay because they are offered to show
their existence, and not the

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Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 16 of 52

truth of the reported consumer sentiments). Cf. Exhibits 2-6
(declarations of Creekstone’s

brokers and of supermarket chains). USDA’s speculation that demand for
beef will increase

(and, apparently, will be totally unaffected by BSE concerns) cannot
defeat direct information

about the market obtained by Creekstone, which of course is an expert in
factors affecting

demand for its products. See Pl. Memo Exh. 1 (Stewart Decl.) ¶¶ 4-5,
16-17; Exh. 1 (Stewart

Supplemental Decl.) ¶¶ 2-4.3 While Creekstone’s own declaration ought to
suffice, the attached

declarations from Creekstone’s customers that they would purchase more
Creekstone beef, and

would pay a higher price, if Creekstone could provide beef from
BSE-tested cattle, conclusively

defeat USDA’s speculations and arguments that Creekstone is not
suffering injury from the

agency’s test ban. See Exhibits 2 -6.

II. USDA’S EXPANSIVE INTERPRETATION OF THE VSTA TO APPLY TO

DIAGNOSTIC TESTS AND TO THE USE OF BIOLOGICAL PRODUCTS IS

UNPERSUASIVE AND NOT ENTITLED TO DEFERENCE.

A. The VSTA Is Neither Ambiguous Nor Susceptible to USDA’s Interpretations.

USDA claims that the VSTA authorizes it to control not only the
manufacture and sale of

a virus, serum, toxin, or analogous product (which USDA refers to as
“biological products”), but

also who may use such biological products and for what purpose. USDA
also claims that the

“biological products” that it can regulate the use of include
“diagnostic products” like BSE test

kits. But those authorizations cannot be found in the plain language of
the VSTA.

USDA has taken a very simple statute, which gives the Department
authority to regulate

the manufacture and sale of specific products, and transformed it into a
license to control other

products and other kinds of activities. Some of USDA’s ostensible
reasons may appear noble –

USDA’s assertion that information previously provided by Creekstone does
not reflect recent

improvements in the Japanese market is contradicted by Exh. 1 ¶¶ 3-4.
Additionally, it ignores

the fact that access to the Korean market is still highly restricted.
Exh. 1 ¶¶ 2, 5-6 and Attach. E.

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Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 17 of 52

to benefit public health and welfare – but that kind of generic goal
does not give an agency carte

blanche to regulate whatever it wishes.

The law could not be more clear: “Agency authority may not be lightly
presumed. ‘Were

courts to presume a delegation of power absent an express withholding of
such power, agencies

would enjoy virtually limitless hegemony, a result plainly out of
keeping with Chevron and quite

likely with the Constitution as well.’” Michigan v. EPA, 268 F.3d 1075,
1082 (D.C. Cir. 2001)

(quoting Ethyl Corp. v. EPA, 51 F.3d 1053, 1060 (D.C. Cir. 1995).
“‘Thus, we will not presume

a delegation of power based solely on the fact that there is not an
express withholding of such

power.’” Id. (quoting American Petroleum Institute v. EPA, 52 F.3d 1113,
1120 (D.C. Cir.

1995)).4

“Mere ambiguity in a statute is not evidence of congressional delegation
of authority.”

Sea-Land Serv., Inc. v. Dep’t of Transp., 137 F.3d 640, 645 (D.C. Cir.
1998). But in this case,

there is not even ambiguity. The statute states very clearly what
products are covered: a “virus,

serum, toxin or analogous product used in the treatment of domestic
animals.” 21 U.S.C. § 151.

It states clearly what activities are covered: the preparation, sale,
barter, exchange, or importation

of such products. Id. at §§ 151-152. And it states clearly when those
activities may be

prohibited: when such products are “worthless, contaminated, dangerous,
or harmful”; are not

“prepared, under and in compliance with regulations prescribed by the
Secretary of Agriculture,

at an establishment holding an unsuspended and unrevoked license issued
by the Secretary of

Agriculture”; or are imported without a permit. Id.

4 USDA’s reliance on Reno v. Flores, 507 US 292, 300-301 (1993), to say
that Creekstone must

“demonstrate that ‘no set of circumstances exists under which the
regulation would be valid’”

(USDA Memo at 23) is misplaced. In that case, the respondents were not
challenging the

regulation’s application in a specific instance, it had not yet been
applied in a particular instance,

and there was no record concerning the INS’s interpretation of the
regulation. Id. That clearly is

a very different situation than is presented in the instant case.

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Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 18 of 52

The statute simply does not authorize USDA to regulate activities other
than the

preparation, sale, barter, exchange, or importation of biological
products. It does not say that

USDA can prohibit or regulate the use of a biological product—in this
case, who may use it and

for what purpose.5 Nor does the statute authorize regulation of
diagnostic tests—products that

are not analogous to a virus, serum, or toxin—just because they are used
in the treatment of

animals. Ignoring those simple, albeit inconvenient for USDA, truths,
USDA resorts to

(illogical) claims that its actions promote public health and welfare
and protect the interests of

ranchers, encouraging this Court to “simplistically…assume[e] that
whatever furthers the

statute’s primary objective must be the law.” Rodriguez v. United
States, 480 U.S. 522, 526

(1987) (per curiam) (emphasis in original).

1. Regulation of the Use of Biological Products

USDA asserts that its authority in 21 U.S.C. § 154 to issue regulations
“as may be

necessary to prevent the preparation, sale, barter, exchange, or
shipment… of any worthless,

contaminated, dangerous, or harmful virus, serum, toxin, or analogous
product for use in the

treatment of domestic animals” “explicitly authorizes restrictions on
the uses for which viruses,

serum, toxins, or analogous products may be prepared, sold, bartered,
exchanged, or shipped.…”

USDA Memo at 25. This contention is absurd on its face. Saying that USDA
can regulate the

manufacture and sale of products intended for use in the treatment of
domestic animals is not the

same as saying USDA can regulate the use of such products. (And indeed,
Congress knows well

how to regulate the use of products when it wishes to do so. See Pl.
Memo at 24-25, 31-32.)

5 USDA’s assertion that “regulation 102.5(d) is not a direct use
restriction on buyers of biological

products” (USDA Memo at 25) is pure semantics (and irrelevant). Without
congressional

authorization to regulate how and by whom biological products are used,
and for what purpose,

USDA cannot indirectly do so through unlawful limitations in licenses
and permits issued to

biological product manufacturers.

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Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 19 of 52

Under USDA’s theory of how the statutory language should be read, if a
statute authorized DOT

to regulate seat belts, air bags, and other safety devices intended for
use in motor vehicles, DOT

would be authorized to regulate who may drive motor vehicles, and where,
as well!

Not surprisingly, USDA offers no case law in support of its unorthodox
reading of the

VSTA, nor even any formal interpretation previously published by USDA.
The phrase “for use

in the treatment of domestic animals” clearly limits, rather than
expands, “virus, serum, toxin, or

analogous product.” Just as clearly, the phrase must have been used in
the VSTA to distinguish it

from the Act of July 1, 1902, ch. 1378, 32 Stat. 728, which authorized
the Public Health Service

to regulate any “virus, therapeutic serum, toxin, antitoxin, or
analogous product...applicable to the

prevention, treatment, or cure of diseases or injuries of man.” See
Animal Health Institute v.

USDA, 487 F. Supp. 376, 378-79 (D. Colo. 1980) (VSTA modeled after the
1902 Act).

Contrary to USDA’s theory of statutory construction, authority to
regulate a whole new

class of activities, affecting vastly more businesses and individuals,
must be found in a clear

statement of congressional delegation of that authority, not in a
strained and ungrammatical

interpretation offered by the agency in litigation to justify its
desired scope of authority.6

“Congress…does not alter the fundamental details of a regulatory scheme
in vague terms or

ancillary provisions—it does not, one might say, hide elephants in
mouseholes.” Whitman v.

American Trucking Ass’ns, 531 U.S. 457, 468 (2001); see also FDA v.
Brown & Williamson

Tobacco Corp., 529 U.S. 120, 159–160 (2000).

Remarkably, USDA also argues that 21 U.S.C. § 154, because it authorizes
USDA to

issue regulations “as may be necessary to prevent the preparation, sale,
barter, exchange, or

6 Moreover, even if USDA were correct that the phrase “for use in the
treatment of domestic

animals” allowed it to regulate how a biological product is used, that
still would not authorize

USDA to dictate who may use the product and for what purpose.

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Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 20 of 52

shipment” of worthless or dangerous biological products, “also expands
the ability of USDA to

regulate beyond just the ‘preparation, sale, barter, exchange, or
shipment’ of products.” USDA

Memo at 26. Once again, USDA offers no case law, legislative history, or
even its past

statements or rulemaking interpreting the VSTA to support or explain
this contention. USDA

contends that “clearly” restrictions on how a biological products may be
used, by whom, and for

what purpose “may be necessary to close loopholes and remove incentives
to circumvent

regulations directed at the ‘preparation, sale, barter, exchange, or
shipment’ of products.” Id.

Apparently USDA believes that Congress made it a crime not only for a
manufacturer to produce

and sell a dangerous biological product, but for a farmer to continue to
use such a product, as

well. See id. Quite simply, it is not for USDA to decide to “close
loopholes” that Congress

chose not to regulate. Even if there were such a need for this kind of
regulation, this supposed

“[n]eed for regulation cannot alone create authority to regulate.” Sea
Robin Pipeline Co. v.

FERC, 127 F.3d 365, 371 (5th Cir. 1997).

Over and over, courts have rejected interpretations of a series of words
in a statute that go

beyond the scope of the words in the series, as does USDA’s
interpretation here. USDA’s claim

of authority to regulate the use of biological products parallels a
claim that the Supreme Court

rejected earlier this year: The plaintiff in Dolan v. United States
Postal Service, 126 S. Ct. 1252

(Feb. 22, 2006), relied on a provision concerning liability for “loss,
miscarriage, and negligent

transmission” of mail, 28 U.S.C. § 2680(b). The Court observed that,
since both “loss” and

“miscarriage” “refer to failings in the postal obligation to deliver
mail in a timely manner to the

right address, it would be odd if ‘negligent transmission’ swept far
more broadly to include

injuries like those alleged here—injuries that happen to be caused by
postal employees but

involved neither failure to transmit mail nor damage to its contents.”
126 S. Ct. at 1254.

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Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 21 of 52

Similarly, in this case it would be odd indeed if Congress intended, in
authorizing regulation of

the preparation, sale, barter, exchange, or shipment of dangerous or
worthless products used to

stimulate or enhance the immune system of animals, to regulate how such
products may be used,

by whom, and for what purpose—activities carried out by the users of the
products rather than

their manufacturers, and after the products have already been prepared,
sold, and shipped.

Texas & Pacific Railway Co. v. Pottorff, 291 U.S. 245, 257-59 (1934),
also resembles the

instant case, in that the Court both (a) refused to find that a national
bank could expand its

statutory authorization for “banking” to include pledging its assets to
secure a private deposit, and

(b) also reasoned that, if that power had been authorized, there would
have been no need to

amend the banking statute later to provide a limited power to pledge.7
So, too, in this case the

enactment of the Agricultural Bioterrorism Protection Act of 2002, 7
U.S.C. § 8401, which gave

USDA limited authority to regulate the possession and use of dangerous
biological products, is

evidence that the VSTA should not be read to give broad authorization to
regulate who may use

biological products and for what purpose (as is the legislative history
confirming that Congress

did not believe the VSTA empowered USDA to regulate the use of
biological products). Cf. Pl.

Memo at 24-25.8 USDA offers no response to that application of the canon
of statutory

construction, followed in Pottorff, to the history of the VSTA and
related legislation.

7 As the D.C. Circuit observed in Independent Insurance Agents of
America, Inc. v. Hawke, 211

F.3d 638 (2000), “[t]he pre-Chevron vintage of Pottorff is irrelevant,”
since the Supreme Court

had already made clear at that time that decisions of the Comptroller of
the Currency were

generally entitled to deference.

Cf. Babbitt v. Sweet Home Chapter of Communities for a Greater Oregon,
515 U.S. 687, 696701

(1995) (fact that Congress in 1982 authorized the issuance of permits
for “incidental take” of

endangered species is strong evidence that Congress understood the
preexisting statutory

prohibition on “take” of endangered species to include indirect as well
as direct “take”).

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Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 22 of 52

USDA does offer one reference to legislative history of the VSTA that
mentions use of

biological products. USDA Memo at 31.9 But that mention of use, put into
context, in no way

suggests that Congress meant to include regulatory authority over how a
biological product may

be used or by whom. Rather, the passage refers to “controlling the use”
of dangerous and

worthless viruses, serum, and analogous products “by preventing the
interstate shipment” of such

products that may be manufactured within the United States. The focus of
the passage from the

Senate Report, like the focus of the statutory language that Congress
ultimately adopted, is not on

how biological products are used, or by whom, but on regulating the
manufacture, sale, and

shipment of dangerous or worthless products.10 In any event, this phrase
from the Senate Report

could not endow USDA with authority not set out forth the statute. 11

USDA asks this Court to ignore the venerable principle expressio unius
est exclusio

alterius, on the grounds that the “principle does not contemplate the
expansive phrases ‘for use in

9 USDA also refers to “ubsequent legislative commentary,” by which it
means its own 1997

description of the VSTA. USDA Memo at 31. But it is hard to see how the
passage from a

USDA Federal Register notice that USDA quoted, that the “main purpose of
VSTA is to protect

those who use veterinary products from products which are worthless,
contaminated, dangerous,

or harmful” in any way justifies USDA’s conclusion here that “[c]learly
the use restrictions

contemplated by regulation 102.5(d) are consistent with the purposes of
VSTA.” See USDA

Memo at 31. What should be clear from that passage instead is that the
purpose of the VSTA is

to protect those who use biological products from harmful or worthless
products, not to regulate

and constrain those who use biological products.

10

Cf. Exhibit 7 at 23-25 (USDA official explaining request for authority
over toxins and viruses,

with no mention of restricting who could use toxins and viruses or
regulating diagnostic

products); Hall v. Nebraska, 100 Neb. 84, 88-89, 158 N.W. 362, 363-64
(1916) (“We do not

understand that the federal government undertakes to regulate those who
sell serum after it has

been disposed of by the manufacturer.”)

11

See City of Chicago v. Environmental Defense Fund, 511 U.S. 328, 337
(1994) (where Senate

Committee report included statement that “all waste management
activities of such a facility,

including the generation, transportation, treatment, storage and
disposal of waste shall be covered

by the exclusion,” Court declined to find that waste generation was
excluded, because “it is the

statute, and not the Committee Report, which is the authoritative
expression of the law, and the

statute prominently omits reference to generation.”). Moreover, the
“controlling the use” phrase

in the Senate Report relates only to domestic manufacture of products,
and not to those that are

imported into the United States, like Bio-Rad’s BSE tests. Cf. USDA Memo
at 30-31.

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Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 23 of 52

the treatment of domestic animals’ or ‘as may be necessary to prevent’
modifiers of the list of

items….” USDA Memo at 26-27. USDA offers no authority for this claimed
corollary to the

principle, nor any further explanation why it would be that phrases that
make the list more

specific or otherwise qualify it would suggest that Congress did not
intend the agency’s authority

to be limited to the enumerated list of items or activities. This Court
should reject USDA’s

unsupported attempts to expand its jurisdiction beyond the authorities
enumerated in the VSTA,

just as other courts have consistently rejected agency claims that
authority to regulate one thing

implies authority to regulate something else, because it would be
consistent with or helpful to the

stated or intended purposes of the statute. See, e.g., City of Chicago,
511 U.S. at 329, supra n.11;

Railway Labor Executives’ Ass’n v. National Mediation Bd., 988 F.2d 133,
139 (D.C. Cir. 1993),

aff’d on rehearing en banc, 29 F.3d 655 (1994), cert. denied, 514 U.S.
1032 (1995) (Board

cannot assume duties not given to it by Congress); Michigan Citizens for
an Independent Press v.

Thornburgh, 868 F.2d 1285, 1293 (D.C. Cir. 1989) (canon of expressio
unius est exclusio alterius

can determine whether statute is clear, and therefore no need to resort
to Chevron deference).12

Arrogating to itself regulatory authority over a whole different set of
activities, conducted

by a different group of people, is simply not the kind of necessary
filling of ‘gaps” in a statute’s

regulatory scheme that Chevron contemplated. Cf. USDA Memo at 36. The
“mere existence of

an agency does not give it the power to assert authority that Congress
has not delegated. It is

absurd to suggest that, under the second prong of Chevron, there is a
statutory ‘gap to fill’ or a

12 USDA disputes the relevance of Kelley v. U.S. EPA, 15 F.3d 1100 (D.C.
Cir. 1994), cert.

denied, 513 U.S. 1110 (1995). USDA Memo at 27 n. 13. The citation
Creekstone provided in its

Memo in Support was, unfortunately, incorrectly limited (citing to p.
1108 rather than pp. 11061108).

But the case indeed is relevant as an example of how courts look to the
list of things a

statute has authorized an agency to do and decline to find statutory
authority for the agency to

regulate in additional areas (in that case, specifying who will be
subject to statutory liability for

hazardous waste cleanup).

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Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 24 of 52

statutory ‘ambiguity’ to cure whenever a statute fails to specify some
authority that an agency

seeks to invoke. This cannot be the meaning of Chevron, for it would
allow federal agencies to

claim limitless authority except in those few circumstances where
Congress has expressly said

‘thou shalt not’ exercise such authority.” Railway Labor Executives’
Ass’n, 988 F.2d at 194

(Edwards, J., concurring).

2. Regulation of Diagnostic Tests

USDA admits that the VSTA says nothing about regulating diagnostic
products (USDA

Memo at 35), but “neither does it specifically exclude such tests from
its purview.” Id. at 36.

The latter is true, but it falls short of authorizing USDA’s regulation
of diagnostic tests. The

Supreme Court and the D.C. Circuit have repeatedly admonished regulatory
agencies that

statutory authority for an agency to act “may not be presumed based
solely on the fact there is not

an express withholding of jurisdiction.” ExxonMobil Gas Marketing Co. v.
FERC, 297 F.3d

1071, 1088 (D.C. Cir. 2002).

The interpretation of the VSTA that USDA advances for purposes of this
lawsuit is that

“diagnostic products are certainly used in the treatment of animals,
which is all that is required

under section 154 of VSTA.” USDA Memo at 37. Again, USDA vastly
overstates the meaning

of the qualifier “intended for use in the treatment of domestic
animals,” appearing to suggest that

anything broadly defined as “treatment” is therefore regulated under the
VSTA. Moreover, even

if Congress had given USDA authority to regulate a product just because
it is used in the

“treatment of domestic animals,” that would not include authority to
regulate products that are

used solely to detect a disease (and especially those, such as BSE test
kits, used solely to detect

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Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 25 of 52

infection in dead animals).13 The cases USDA cites (USDA Memo at 41)
provide no support for

its position: Pegram v. Herdrich, 530 U.S. 211, 228 (2000) contains a
discussion of two types of

actions by HMO administrators: “eligibility decisions,” which concern
whether a particular

condition or medical procedure for its treatment is covered by the
patient’s health insurance plan,

and “treatment decisions,” which “are choices about how to go about
diagnosing and treating a

patient’s condition: given a patient’s constellation of symptoms, what
is the appropriate medical

response?” Id. Not only to did the Pegram court not define “treatment,”
but it used the terms

“diagnosing” and “treating” as if they are two different types of
activities, joined by the

conjunction “and.” Nor does Miller v. AT&T Corp., 250 F.3d 820, 830-31
(4th Cir. 2001),

contain any independent analysis of the meaning of the word
“treatment”—it merely applies a

Family and Medical Leave Act regulation, 29 C.F.R. § 825.114(b), which
defines “treatment” to

include “examinations to determine if a serious health condition exists
and evaluations of the

condition,” and defers to an agency determination that the statutory
phrase “continuing treatment

by a health care provider,” 29 U.S.C. § 2611(11), is broad enough to
cover such examinations.

This is a far different question than whether Congress meant for “virus,
serum, toxin, or

analogous product used in the treatment of domestic animals” to include
a test procedure and

reagents used to determine whether an animal has (or had) a disease.

Additionally, to be susceptible to regulation under the VSTA, a
diagnostic product would

have to be both a “virus, serum, toxin, or analogous product” and “used
in the treatment of

domestic animals.” 21 U.S.C. §§ 151, 152, 154. Something is not
“analogous” to a virus, serum,

USDA claims its open-ended regulation of diagnostic products is
justified because the VSTA

refers to viruses, serums, toxins, or analogous products “for use in the
treatment of domestic

animals,” rather than “for treatment of domestic animals.” USDA Memo at
37. USDA does not

explain how a biological product that is not “for treatment of domestic
animals” could be “used

in the treatment of domestic animals.” Creekstone suggest that to the
extent there is a distinction,

though it seems unlikely there could be, it is a distinction without a
difference.

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Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 26 of 52

or toxin just because it is “used in the treatment of domestic animals,”
but that is what USDA

seems to assume. In USDA’s expansive view of the VSTA’s targeted
language, presumably

even a thermometer could be regulated under the VSTA, simply because it
is “used in the

treatment of domestic animals.” USDA’s attempt to turn a limiting
qualifier into a very broad

congressional delegation of regulatory authority is simply not borne out
by the language or

legislative history of the VSTA.14

USDA regulations state that “biological products,” include vaccines,
antibodies,

antitoxins, immunostimulants, “and diagnostic components, that are of
natural or synthetic origin,

or that are derived from synthesizing or altering various substances or
components of

substances….” 9 C.F.R. § 101.2. Read literally, a “diagnostic component”
(an undefined term)

need not have anything to do with the defining characteristic of
“viruses, serum, toxins, or

analogous products,” which is that they “act primarily through the
direct stimulation,

supplementation, enhancement, or modulation of the immune system or
immune response.”15

Similarly, USDA defines “analogous products” to include either
ubstances…which are

similar in function to biological products in that they act, or are
intended to act, through the

stimulation, supplementation, enhancement, or modulation of the immune
system or immune

response, or ubstances… which are intended for use in the treatment
of animals through the

detection or measurement of antigens, antibodies, nucleic acids, or
immunity;…” Id. (emphasis

added). Thus, USDA has explicitly de-coupled these diagnostic tests from
any requirement that

14 It also conflicts with a number of more-specific statutory
authorities over diagnostic tests,

including the Food, Drug and Cosmetic Act, as noted in Pl. Memo at
31-32, 38 n.14.

15 9 C.F.R. § 101.2 (definition of “biological products”). USDA offers
no response to the fact

that USDA has, in other regulations, made a clear distinction between
products that operate

through an immune response—and are subject to regulation under the
VSTA—and those that do

not, even if the same or similar components are involved. See Pl. Memo
at 36, 38.

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Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 27 of 52

th
 

flounder

Well-known member
- 20 -


Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 27 of 52

they be similar in function to the viruses, serum, toxins, and analogous
products that VSTA by its

terms covers.

Under the interpretation of “analogous product” advanced by USDA’s
counsel, if

Congress authorized the Department of Transportation to regulate the
manufacture and

distribution in commerce of automobiles, motorcycles, trucks, and
analogous products, DOT

could regulate the construction (and use) of highways or racetracks, as
well. The definitions in 9

C.F.R. § 101.2 do not represent “gap-filling” of an ambiguous statute.
Rather USDA’s “position

in this case amounts to the bare suggestion that it possesses plenary
authority to act within a

given area simply because Congress has endowed it with some authority to
act in that area.”16

See Railway Labor Executives’ Ass’n v. National Mediation Bd., 29 F.3d
655, 671 (D.C. Cir.

1994) (en banc), cert. denied, 514 U.S. 1032 (1995). The D.C. Circuit
has “categorically

reject[ed] that suggestion.” Id.

B. USDA’s Expansive Interpretation of the VSTA Is Not Entitled to
Deference.

USDA claims that its interpretations of the VSTA as authorizing it to
regulate types of

products and activities not addressed in the statute are entitled to
great deference. But USDA

cannot overcome the large body of precedent rejecting just such claims
by agencies seeking to

expand the authority granted to them by Congress.

1. No Deference for Interpretations Expanding the Scope of the Agency’s

Authority

16 USDA cites an opinion of the District Court for the District of
Maryland which described

USDA as having “plenary authority granted by Congress to regulate the
field of animal

vaccines.” USDA Memo at 27, quoting Arnold v. Intervet, Inc., 305 F.
Supp. 2d 548, 550 (D.

Md. 2003). But the question there was whether USDA’s regulatory
authority to approve and

regulate the manufacture of animal vaccines preempted state tort law
claims against vaccine

manufacturers, not whether USDA has authority to regulate everything
remotely related to animal

vaccines. Even “plenary authority” to regulate the field of animal
vaccines does not on its face

imply authority to regulate tests for detecting animal diseases.

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Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 28 of 52

USDA virtually ignores the extensive precedent declining to accord any
deference to an

agency interpretation of a statute that gives itself expanded authority.
See Pl. Memo at 27; see

also John Hancock Mut. Life Ins. Co. v. Harris Trust & Sav. Bank, 510
U.S. 86, 108-109, (1993);

Natural Resources Defense Council v. Reilly, 983 F.2d 259, 266 (D.C.
Cir. 1993). An agency

simply “may not ‘avoid the Congressional intent clearly expressed in the
text simply by asserting

that its preferred approach would be better policy.’” Friends of the
Earth, Inc. v. EPA, 446 F.3d

140, 145 (D.C. Cir. 2006), quoting Engine Mfrs. Ass’n v. EPA, 88 F.3d
1075, 1089 (D.C. Cir.

1996); see also Ethyl Corp. v. EPA, 51 F.3d 1053, 1060-61 (D.C. Cir.
1995) (rejecting

interpretation that added factors to a list of factors to be considered,
even though there were

policy justifications for the additional factors, observing “Congress
has neither explicitly or

implicitly delegated discretionary authority to the Agency to consider
other factors ‘in the public

interest’….” Id. at 1060.).

2. No Deference for Statutory Interpretations Not Accompanied by Further

Explication

Creekstone has established that USDA’s interpretations of the VSTA are
entitled to

little or no weight because they were announced with virtually no
explanation of how they were

derived. Pl. Memo at 26-27, 30-31, 41. USDA does not deny this. Rather,
its principal

response is to assert that one of the cases Creekstone cited, Adamo
Wrecking Co. v. United

States, 434 U.S. 275, 287 (1978), was decided before Chevron and is
therefore no longer good

law. USDA Memo at 34 n.16. Unfortunately for USDA’s argument, the
principal for which

Creekstone cited Adamo Wrecking, that an agency’s statutory
interpretation announced without

explanation or analysis is entitled to little weight, has been relied
upon by the Supreme Court

and the D.C. Circuit many times since Chevron.

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Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 29 of 52

For example, Public Citizen, Inc. v. U.S. Dept. of Health and Human
Services, 332 F.3d

654, 662 (D.C. Cir. 2003) discusses the inapplicability of Chevron
deference to situations where

the agency has not provided any explanation for its interpretation.
“Because the manual thus

contains no reasoning that we can evaluate for its reasonableness, the
high level of deference

contemplated in Chevron’s second step is simply inapplicable.” Id.,
citing Adamo Wrecking, as

well as SEC v. Sloan, 436 U.S. 103, 118 (1978) (reaching the same
conclusion “where this Court

can only speculate as to the Commission’s reasons for reaching the
conclusion that it did”

because the agency’s orders did not “address[ ] in any detail the
statutory authorization under

which it took [the] action”).17

Barnett v. Weinberger, 818 F.2d 953, 960-64 (D.C. Cir. 1987), another
post-Chevron

decision, declined to accord Chevron-like deference to the Department of
Defense’s

interpretation of a statute under circumstances quite similar to the
instant case:

In sum, the regulations in question were issued after what appears to

have been cursory consideration, were accompanied by neither explanation
nor

justification, and were given a breadth that does not comport with the
purposes

animating the statute purportedly interpreted. These elements buttress our

conclusion that the regulations are not entitled to significant weight in

delineating the scope of the statute’s “custodial care” provision.

Id. at 963 (footnote omitted). The Court considered it important that
the Department offered no

explanation or discussion of the regulations providing the
interpretation at the time they were

issued, “nor was any attempt made to support the regulations by an
analysis of the legislative

history underlying the statute.” Id., citing Adamo Wrecking, 434 U.S. at
237 n.5, SEC v. Sloan,

436 U.S. at 117-18, and Investment Co. Inst. v. Camp, 401 U.S. 617, 627
(1971) (declining to

See also Federal National Mortgage Ass’n v. United States, 56 Fed. Cl.
228, 236-37 (Ct. of

Claims 2003) (noting that United States v. Mead, 533 U.S. 218 at 228
(2001), held no Chevron

deference is due to an IRS interpretation for which “no reasoning is
given” (citing Adamo

Wrecking)).

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Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 30 of 52

defer to an agency “in significant part because agency failed to
buttress its interpretation with an

opinion or other supportive statement,” 818 F.2d at 963).

The interpretations of the VSTA USDA relies on to prevent Creekstone
from testing its

cattle for BSE were all announced by USDA with virtually no explanation
of why they

represent permissible and reasonable interpretations of the targeted
language of the VSTA.18

See Pl. Memo at 26-27, 30-31, 41. USDA’s argument now that it has
explained the basis for

those interpretations in subsequent Federal Register notices related to
other provisions of its

VSTA regulations would make no sense even if those explanations were
adequate. See USDA

Memo at 39 (apparently claiming that recent developments in genetic
engineering technology

and other “advances in scientific knowledge” somehow justified USDA
deciding 60 years after

the passage of VSTA that it should regulate the use of biological
products to promote public

health and welfare and that diagnostic tests are analogous to vaccines
and serums). But aside

from the fact that these would be post facto rationalizations in any
event, the passages USDA

cited do not even state, much less purport to explain, that scientific
advances justify expanding

USDA’s regulations under the VSTA to address use of biological products
and regulation of

diagnostic products. If general scientific advancement were sufficient
to justify an agency

regulating outside the terms of a statute, the words and choices of
Congress could be rendered

meaningless with each new discovery or invention.

18 In its opposition to Creekstone’s Motion for Summary Judgment, USDA
relies on opinions

interpreting comprehensive, far-reaching statutes, like the securities
and labor laws, in which

Congress delegated to administrative agencies broad authority to
regulate a whole sector of the

economy or aspect of commerce. USDA Memo at 27, 33. Such statutes
necessarily imply

broader authority for the agency and greater leeway to adopt
implementing regulations than a

statute like the VSTA, enacted to address specific concerns about
particular types of products in

particular uses.

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Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 31 of 52

Moreover, USDA’s interpretation of the VSTA’s provisions for permitting the

importation of biological products, 21 U.S.C. §§ 152-153, as
additionally authorizing

regulation of the use of those products once they have been imported, is
not even contained in

the USDA regulations implementing those provisions, much less supported
by any

explanation.19 See Pl. Memo at 19-20. For that reason, it is entitled to
little or no deference

under Christensen v. Harris Cty., 529 U.S. 576 (2000).

In fact, the only explanation that we have for USDA’s interpretations of
its authority

under the VSTA to regulate the use of diagnostic products like BSE test
kits is that provided by

USDA’s counsel in this litigation. Pursuant to well-established
precedent, this Court should

reject such post hoc rationalizations of counsel. See, e.g., Bowen v.
Georgetown Univ.

Hospital, 488 U.S. 204, 212-13 (1988); PanAmSat Corp. v. F.C.C., 198
F.3d 890, 897 (D.C.

Cir. 1999). This Court also should not accord any deference to USDA’s
interpretations of its

USDA asserts that Creekstone is barred from requesting that the Court
strike down 9 C.F.R. §

104.1—which on its face says nothing of restricting the manner in which
an imported biological

product can be used, or by whom, or for what purpose—if, contrary to
Creekstone’s position, the

Court finds that that particular regulation does authorize such
restrictions, because Creekstone did

not include a demand in its complaint that 9 C.F.R. § 104.1 be
overturned. See USDA Memo at

30; cf. Pl. Memo at 19-20. Creekstone’s Complaint did, however, state
that “If USDA’s

regulations implementing the VSTA, at 9 C.F.R. Chapter I Subchapter E
are broad enough to

cover the BSE test kits as described above, then those regulations are
beyond the scope of the

rulemaking authority granted to USDA in the VSTA.” Complaint Count 1 ¶
31. The USDA

regulation on import permits, 9 C.F.R. § 104.1, is contained in 9 C.F.R.
Chapter I Subchapter E.

The prayer for relief in the Complaint also asks the Court to “Enter
judgment declaring that

USDA lacks authority to restrict the use of BSE rapid test kits or to
issue licenses for the

production of such test kits that limit to whom they may be distributed
or how they may be used”

and to enjoin USDA “from implementing or enforcing any prohibition on
Creekstone acquiring

or using USDA-approved BSE rapid test kits for purposes of routinely
screening for BSE cattle

that Creekstone processes (including any restriction on the sale of such
test kits to Creekstone).”

Creekstone does not believe that 9 C.F.R. § 104.1 authorizes
restrictions on the use of imported

diagnostic tests like the Bio-Rad BSE test kits, and so it does not need
to be vacated, but if the

Court concludes that it does give that authority to USDA, then
Creekstone submits that the

provisions of the Complaint noted here provide a sufficient request for
relief to allow the Court to

hold the regulation ultra vires and vacate it in this summary judgment
proceeding.

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Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 32 of 52

authority under the VSTA, consistent with Adamo Wrecking and subsequent
cases, and should

conduct its own analysis of the breadth of the VSTA provisions, using
the traditional tools of

statutory construction described above and in Creekstone’s Memorandum in
Support.

3. Little Deference for Statutory Interpretations that Were Far from

Contemporaneous or Consistent

As Creekstone established, agency interpretations that are not
contemporaneous with a

statutes’s enactment and that do not reflect long-held positions of the
agency generally are

entitled to less deference than more contemporaneous interpretations.
See Pl. Memo at 30.

USDA’s primary response is to claim—again without any citation—that this
principle of

statutory interpretation no longer applies after the Supreme Court’s
Chevron decision. See

USDA Memo at 38-39. In fact, this principle has been applied repeatedly
and consistently

post-Chevron: “It is well established that the prestige of a statutory
construction by an agency

depends crucially upon whether it was promulgated contemporaneously with
enactment of the

statute and has been adhered to consistently over time.” Barnett v.
Weinberger, 818 F.2d at

961-62 (footnote omitted) (giving little weight to an interpretation
first announced 11 years

after enactment of statute). See also Continental Airlines, Inc. v. U.S.
Department of

Transportation , 856 F.2d 209, 216-217 (D.C. Cir. 1988) (relying on an
agency’s 1979

contemporaneous interpretation of applicable statute rather than a more
recent one); Lynn

Martin v. Occupational Safety and Health Review Commission, 499 U.S. 144
(1991) (stating

that the consistency of application of interpretations bears on the
reasonableness of the

agency’s position under Chevron); Railway Labor Executives, 29 F.3d at
669-70 (finding it

“telling” that the Board had not asserted its claim that it had latent
authority under the statute to

allow carriers or the Board itself to initiate investigations for the
first 50-plus years of the

statute’s 60-year history).

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Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 33 of 52

USDA has given virtually no explanation for why the Department failed,
for the first

two-thirds of the life of the VSTA, to recognize that it had the
authority it now claims:

authority to regulate who may use biological products and for what
purpose and to regulate

diagnostic tests as well as biological products themselves. In fact, so
far as Creekstone has

been able to determine, the instant case is the first time ever that
USDA has exercised this

purported authority to prevent a company from performing tests on its
own livestock (let alone

on the carcasses of animals it has already slaughtered). See also Exh.
(10 Detwiler Decl.) ¶ 24.

C. The Reenactment Doctrine Does Not Save USDA’s Unsupported
Interpretation of the

VSTA.

Finally, USDA claims that its interpretation of the VSTA as authorizing
USDA to

restrict who may have access to biological products and for what purpose
they may use them

has been blessed by Congress and must be deferred to under the
“reenactment” doctrine.20

USDA Memo at 28 n.14. Under that doctrine, courts “have frequently
considered whether

reenactment of a statute after promulgation of an agency interpretation
that is highly publicized

or otherwise communicated to Congress may be regarded as ratification by
acquiescence.”

Barnett v. Weinberger, 818 F.2d at 963 n.89. But the VSTA was not
reenacted when it was

amended in 1985; rather, Congress simply expanded a few of the
provisions of the VSTA,

primarily to eliminate a dichotomy that had existed between regulation
of biological products

shipped across state lines and those manufactured and used within the
same state. See P.L. 99198,

99 Stat. 1654-56; S. Rep. No. 99-145, Sept. 30, 1985, at 338-39,
reprinted in 1985

20 USDA seems to make that claim only with respect to its asserted
authority over the use of

biological products, and not its claim that diagnostic tests are
“analogous products” subject to

regulation under the VSTA. See USDA Memo at 28 n.14. Presumably that is
because the

expansion of the definition of “analogous product” in 9 C.F.R. § 101.2
to include substances

“which are intended for use in the treatment of animals through the
detection or measurement of

antigens, antibodies, nucleic acids, or immunity” did not occur until
1997. See 62 Fed. Reg.

31,326 (June 9, 1997).

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Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 34 of 52

U.S.C.C.A.N. 2004-2005; Garrelts v. Smithkline Beecham Corp., 943 F.
Supp. 1023, 1065-66

(N. D. Ia. 1996) (legislative history of 1985 amendments indicates
narrow purpose of

amendments); see also Pl. Memo at 22-23; cf. Babbitt v. Sweet Home, 515
U.S. at 729 (Scalia,

J., dissenting) (subsequently enacted provision authorizing permits for
“incidental take” of

endangered species does not implicate reenactment doctrine for agency
interpretation of the

prohibition on “take” of endangered species).

Moreover, for the reenactment doctrine to apply, Congress must have been
made aware

of the agency interpretation at issue. See, e.g., Barnett v. Weinberger,
818 F.2d at 963 n.89. In

particular, “application of the legislative reenactment doctrine
requires a showing of both

Congressional awareness and ‘express congressional approval of an
administrative

interpretation if it is to be viewed as statutorily mandated.’” General
American Transp. Corp.

v. ICC, 872 F.2d 1048, 1053 (DC Circuit 1989) (quoting AFL-CIO v. Brock,
835 F.2d 912, 915

(D.C. Cir. 1987)); accord, International Union, UAW v. Brock, 816 F.2d
761, 767 (D.C. Cir.

1987) (finding no “affirmative step taken by Congress that indicates an
intent to ratify the

agency’s interpretation” (emphasis in original)); accord, Koszola v.
F.D.I.C., 393 F.3d 1294

(D.C. Cir. 2005); see also Pacific Power & Light Co. v. FPC, 184 F.2d
272, 275 (D.C. Cir.

1950) (“before a mere reenactment can be given conclusive effect as a
congressional adoption

of an administrative interpretation, it must be shown that Congress was
conscious that it was

doing so.”); 2B Sutherland Stat. Constr. § 49.09 (reenactment doctrine
“does not apply when

nothing indicates that the legislature had its attention directed to the
administrative

interpretation upon reenactment.”).21 USDA offers no evidence to this
effect. And in fact, the

Cf. Lorillard v. Pons, 434 U.S. 575, 581–85 (1978), the case relied on
by USDA (detailing

Congress’s familiarity with the statute and judicial interpretations of
it and describing indications

of Congress’s intention to incorporate a contemporaneous construction of
the statute).

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Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 35 of 52

regulation that USDA claims authorizes restrictions on the use of an
imported biological

product, and which was promulgated prior to the amendment of the VSTA in
1985, does not

make any mention at all of such restrictions. Cf. 9 C.F.R. § 104.1; see
also Pl. Memo at 34

n.11 (no mention of regulating diagnostic tests in legislative history
of 1985 VSTA

amendments).

USDA also implies that its interpretation of the VSTA as authorizing
prohibitions on

private BSE testing must be deferred to because of a vote by the House
Appropriations

Committee not to adopt a rider to an appropriations bill that would have
required USDA to

allow Creekstone and others to conduct private BSE testing. USDA Memo at
10. But even a

negative vote by Congress on a bill is “a particularly dangerous ground
on which to rest an

interpretation of a prior statute.” Solid Waste Agency of Northern Cook
County v. U.S. Army

Corps of Engineers, 531 U.S. 159, 169-70 (2001). Accord, Central Bank of
Denver, N.A. v.

First Interstate Bank of Denver, N.A., 511 U.S. 164, 187 (1994); Brown &
Williamson, 529

U.S. at 155. A failed committee vote on an appropriations rider lacks
any legal significance.22

III. USDA LACKS STATUTORY AUTHORITY TO REGULATE BSE TEST KITS IN

PARTICULAR.

To be subject to USDA’s regulatory authority under the VSTA, something
must be

both a “virus, serum, toxin, or analogous product” and “used in the
treatment of domestic

animals.” 21 U.S.C. §§ 151, 152, 154. And for USDA to “prevent the
preparation, sale, barter,

22 In contrast, USDA offers no response to Creekstone’s demonstration,
from the text and

legislative history of the Agricultural Bioterrorism Protection Act of
2002, sections 211-213 of

the Public Health Security and Bioterrorism Preparedness and Response
Act of 2002, P.L. 107188,

116 Stat. 647, that Congress did not believe USDA’s regulatory authority
extended to who

may use biological products. See Pl. Memo at 24-25; see also Brown &
Williamson, 529 U.S. at

133 (“the meaning of one statute may be affected by other Acts,
particularly where Congress has

spoken subsequently and more specifically to the topic at hand.”)
(citations omitted).

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Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 36 of 52

exchange, or shipment” of such a product, it must be “worthless,
contaminated, dangerous, or

harmful.” Id. at § 154. As Creekstone showed in its Pl. Memo at 34-40,
test kits used for BSE

screening of apparently healthy cattle at slaughter do not meet any of
those criteria.23

A. BSE Test Kits Are Not “Analogous Products.”

The commonsense meaning of “virus, serum, toxin, or analogous product”
is that

analogous products are other products that, similar to the viruses,
serums, and toxins mentioned

specifically in the VSTA, are given to animals to supplement the
animal’s antibodies or to cause

the animal’s immune system to generate more of its own antibodies, to
prevent or mitigate the

effects of disease. USDA itself has expressed that understanding of what
“analogous product”

means. See Pl. Memo at 29, 38 n.14. Creekstone has demonstrated that
this interpretation of

“analogous products” is also consistent with the legislative history of
the VSTA, is reflected in

USDA’s own regulations contemporaneous with and extending for decades
after enactment of the

VSTA, and is similar to the way courts have interpreted virtually
identical language to “virus,

therapeutic serum, toxin, antitoxin, or analogous product” in the human
version of the VSTA, the

USDA attempts to narrow the scope of this argument by distinguishing
between “whether

USDA’s authority to regulate diagnostic tests extends as a general
matter to BSE test kits” and

“whether USDA was required to make an exception to license restrictions
prohibiting the sale of

BSE test kits for purposes other than government surveillance testing,
in order to permit plaintiff

to conduct private testing for its own marketing purposes.” USDA claims
that the latter is the

subject of Count 3 of the Complaint and therefore not covered by the
current process and motions

for summary judgment. USDA memo at 40 n.21. To the contrary, the issue
Creekstone has

raised is whether the VSTA authorizes USDA to prohibit the sale of BSE
test kits for uses other

than government surveillance testing. That is a question of whether
USDA’s license restrictions

and other actions regarding by whom BSE test kits may be used and for
what purposes are “in

excess of statutory jurisdiction, authority, or limitations, or short of
statutory right,” in violation

of 5 U.S.C. § 706(2)(C)—the subject of Counts 1 and 2 of the Complaint.

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Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 37 of 52

Act of July 1, 1902, ch. 1378, 32 Stat. 728, on which the VSTA was
modeled. Pl. Memo at 23

25, 27-30.24

Even if USDA is correct that “[d]iagnostic test kits frequently rely on
the interaction of

antibodies and antigens to stimulate, modulate, or detect the immune
system of an animal, as do

products made with viruses, serums, or toxins” (USDA Memo at 36), that
would not mean that

such test kits are “analogous products” to vaccines and similar products
used to prevent or cure

diseases. See pp. 19-21, supra. But in any event, as Creekstone has
shown, USDA itself has

recognized that certain products made from microorganisms may be
“analogous products” in

some settings and products unregulated by the VSTA in others. Pl. Memo
at 36-38. So even if

diagnostic test kits “frequently” involve the stimulation or modulation
of the immune system of

an animal, as USDA maintains, that does not suggest that all diagnostic
test kits, including BSE

test kits, must be “analogous products” subject to USDA’s regulatory
authority under the VSTA.

For example, EPA provided this description of substances that may or may
not be

“analogous products,” depending on how they are used:

It is now recognized in the scientific literature that the generation or
stimulation

of an immune response involves both antigens and certain protein regulatory

factors referred to as cytokines. Some cytokines (e.g. interleukins)
serve as an

essential components in the generation and expression of an immune
response,

without which the vaccine would be worthless…. Cytokines are also
produced in

many body tissues and act on cell types other than those of the immune
system.

Cytokines of natural or synthetic origin can be prepared as products for

administration to animals. Because of the diverse biological activity of
the

cytokines, not all products consisting of these substances would be
regulated

under the VSTA. Many of these cytokines intended to be used as drugs
would fall

under the jurisdiction of the Food and Drug Administration. In such
instances,

the VSTA would not apply.

USDA tries to dismiss the cases cited by Creekstone as irrelevant
because they were not

interpreting the VSTA. USDA Memo at 36 n.18. But, as Creekstone
indicated, the language of

the human version of the VSTA is almost identical, and courts have held
that they should be

interpreted similarly. See p. 13, supra; Pl. Memo at 30 n.10

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Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 38 of 52

Both cytokines and immunomodulators are analogous to biological products

when they are used to stimulate, supplement, enhance, or modulate the
immunity

of animals in the treatment of disease. Products consisting of these
substances

that work through the immune mechanisms in the treatment of specific
disease

appropriately fall within the definition of “biological products.”

62 Fed. Reg. 31,326, 31,327 (June 9, 1997) (emphasis added.) BSE test
kits, which are used to

determine whether an animal carcass is infected with a disease that does
not even involve the

animal’s immune system, are not a product that works through the immune
system to treat a

specific disease, and therefore should not be considered an “analogous
product” under this USDA

rulemaking precedent.

USDA’s declarant, Dr.Rippke (whose declaration provides no information
about his

training and qualifications other than that he has worked at USDA for 20
years and in the

implementation of the VSTA—which addresses hundreds of products besides
the few related to

BSE—for the last 10 years), provides only the barest of analysis to
support his conclusion that

BSE test kits are analogous to viruses, serums, and toxins. Cf. USDA
Memo Exh. 2 ¶¶ 7-8. In

contrast, in Exhibit 8 to this Reply, Paul W. Brown, M.D., a real expert
in neurology and in

transmissible spongiform encephalopathies in particular, explains that
“BSE tests do not involve

the immune system of the animal that is tested. There is a sharp
distinction between using

immunological means to prevent foreign pathogen infections (e.g., active
and passive

immunization) and the use of an immunologic reagent (e.g., an antibody)
to detect infectious

prion proteins obtained from the body of an infected host. The use of
such a test has nothing

whatsoever to do with the immune system of the infected (and now dead)
animal.” Id. ¶ 16. In

fact, USDA has already acknowledged that BSE itself does not even work
through the immune

system of the cattle it afflicts: “The BSE agent does not evoke any
demonstrated immune

response or inflammatory reaction in host animals.” 70 Fed. Reg. 460,
461 (Jan. 4, 2005). As

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Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 39 of 52

Dr. Brown says, “USDA thinking on this point is very confused.” Exh. 8 ¶
16. Dr. Rippke’s

conclusory statements notwithstanding, there is nothing about BSE test
kits, which do not involve

the immune system of cattle and in fact can only be administered to dead
cattle, that makes them

analogous to vaccines and therapeutic serums administered to animals to
prevent or cure

disease.25

B. BSE Test Kits Are Not, and Would Not Be, Used in the Treatment of Animal

Disease.

USDA sets out a circular argument: BSE test kits are “intended for use
in the treatment of

domestic animals,” even though there is no treatment for BSE and USDA
claims that routine

testing of normal-appearing cattle at slaughter has no BSE mitigation
benefit. USDA Memo at

40-44. USDA then claims authority to prevent access to BSE test kits for
routine testing because,

it alleges, they are worthless for the treatment of domestic animals in
that use. The Court should

reject this attempt to “have it both ways.”

USDA’s claim that a test which is used to determine whether meat from a
slaughtered

animal might be infected is “intended for use in the treatment of
domestic animals” is

nonsensical, especially given that there is no known treatment for the
infection and the test can

USDA also relies on its regulation (which, as Creekstone has already
shown, is inconsistent

with the VSTA in any case, Pl. Memo at 29-31), 9 C.F.R. § 101.2(2)(ii),
which defines

“analogous products” to include substances that do not even act on the
immune system but rather

are used for “the detection or measurement of antigens, antibodies,
nucleic acids, or immunity.”

USDA asserts that BSE test kits fall under that definition and are
therefore analogous products in

any event because they are tests for “antigens.” USDA Memo at 41 n.22.
But USDA’s reference

for that contention, ¶¶ 7-8 of the Rippke declaration, refers to BSE
test kits as acting “through the

immunological detection of specific antigens found in animal tissue
indicative of disease,” even

though it also states that “antigens” are materials “that, as a result
of coming in contact with

appropriate tissues of an animal body, stimulate an immune response.”
Id. ¶ 7. See also Grand

Laboratories, Inc. v. Harris, 488 F. Supp. 618, 619 (D.S.D. 1980), rev’d
on other grounds, 660

F.2d 1288 (8th Cir. 1981) (referring to “antigen” as “the biological
component intended to

produce an immune response”). Given that BSE does not involve an immune
response in cattle

(see text supra), Dr. Rippke’s description of BSE test kits as
identifying “antigens,” meaning the

prion proteins believed to cause BSE, is internally inconsistent and
should be disregarded.

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only be used on cattle that are already dead. See USDA Memo at 41-42.
USDA relies in part on

its regulations that the determination of whether a product is intended
for the use in the treatment

of domestic animals is to be based on objective criteria indicating the
intent of the manufacturer.

9 C.F.R. § 101.2(1); see USDA Memo at 43 n.24. Here, BSE test kit
manufacturers, such as Bio-

Rad, market millions of BSE test kits a year to countries that conduct
BSE tests on the carcasses

of all animals presented for slaughter (mandatory above a certain age in
EU countries). Given

USDA’s assertion that BSE test kits are ineffective for BSE disease
mitigation purposes unless

applied to targeted cattle with symptoms that might be indicative of
BSE, the marketing of BSE

test kits for other purposes provides an incontrovertible objective
indication that BSE test kits, as

the manufacturer intends them to be used and as intended to be used by
Creekstone, are not

“intended for use in the treatment of domestic animals,” despite USDA’s
assertion to the

contrary. Cf. id. Thus, USDA’s actions dictating that BSE test kit
manufacturers and importers

cannot sell the test kits for purposes other than treating BSE in cattle
are ultra vires.

C. BSE Test Kits Are Not Worthless, Contaminated, Dangerous or Harmful.

Having asserted authority to regulate the use of BSE test kits by
Creekstone and other

meat producers because BSE test kits are intended for use in the
diagnosis of BSE in cattle,

USDA turns around and claims (for the first time in writing, cf. Pl.
Memo Exh. 1 Attachments

5, 7, and 10) that BSE test kits are “ineffective…and essentially
worthless as an animal health

measure when used, as proposed by plaintiff, to diagnose the disease in
all slaughter-aged

normally-looking cattle.” USDA Memo at 42. Since Creekstone never
claimed that its planned

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BSE testing would be valuable as an animal human health measure and
never proposed to use it

to diagnose BSE for the purpose of treating animals, this is really a
“straw man” argument.26

In any case, USDA’s claim that the VSTA authorizes it to ban private use
of BSE test kits

because they are worthless when applied to brain tissue from
“slaughter-aged normally-looking

cattle” is contradicted by a wide array of facts and indeed even USDA’s
own assertions. The

countries of the European Union performed BSE tests on almost 9 million
cattle that were

healthy-appearing at slaughter in 2005 alone. Report on the Monitoring
and Testing of

Ruminants for the Presence of Transmissible Spongiform Encephalopathy
(TSE) in the EU in

2005, European Commission, 20 June 2006, p. 12 Table B1, available at

http://ec.europa.eu/food/food/biosafety/bse/annual_reps_en.htm (attached
as Exhibit 9). A

significant portion of the BSE cases found in the EU in 2005 (114 of 491
cases) were in healthy-

looking cattle tested at slaughter. Id. at p. 18 Chart B3. France,
Germany, and Italy currently test

all cattle over 24 months of age, and Germany allows voluntary testing
of cattle 24 months and

younger. Id. at p. 8 Table 2. Japan currently tests cattle of all ages
at slaughter, and Japanese

officials consider BSE testing a measure for “ensuring the safety of
meat.” Pl. Memo at 9-10 and

Exh. 5 at 2-3. While most cattle slaughtered in the U.S. are under 30
months of age, BSE has

been detected in cattle younger than that, although infrequently.
Declaration of Linda A.

Detwiler, D.V.M. (Exh. 10) ¶ 22; Ferguson Decl. (USDA Memo Exh. 1) at ¶
5; Pl. Memo Ex. 5

at 2 (BSE in 21 and 23 month old cattle in Japan). In addition, the
usual method of estimating the

age of cattle, dentition, is inherently inaccurate. Exh. 8 (Brown Decl.)
¶ 11.

USDA does not contend that BSE test kits are “contaminated, dangerous,
or harmful,” 21

U.S.C. § 151. USDA’s claim that BSE test kits as proposed to be used by
Creekstone are

“misleading” (USDA Memo at 42) does not relate directly to any criterion
for regulation under

the VSTA. In any event, USDA does not suggest that BSE test kits are
ineffective at determining

whether concentrations of BSE prions above the detection limit of the
test are found in the tested

tissue. Thus there is nothing inherent about the test itself that is
misleading.

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Under these facts, USDA cannot simply declare that BSE test kits are
worthless when

used on healthy-looking cattle under 30 (or 24) months of age (which
USDA refers to as

“slaughter-age”). USDA’s arguments do not hold up to even cursory
examination. USDA

asserts that BSE test kits applied to healthy-appearing cattle at normal
slaughter age could “miss”

BSE-infected cattle—but only because the BSE infection in the animal has
not progressed far

enough for the BSE tests to detect it. USDA Memo at 43. But if no BSE
testing is performed on

slaughter-aged, healthy-appearing cattle, then 100% of those infected
cattle will enter the food

chain. Catching even a few such cases of this fatal, incurable disease
would obviously be of great

value. Exh. 8 (Brown ) ¶ 11; Exh. 10 (Detwiler) ¶ 21. In fact, neither
of USDA’s declarants say

that BSE testing would be worthless; the closest they come is to say
that USDA’s targeted testing

“is the most efficient method” of monitoring for BSE. USDA Memo Exh. 1 ¶
6.27

USDA asserts that BSE can only be detected ‘two to three months before a
cow would

demonstrate clinical signs of the disease.” USDA Memo at 43. Even that
would be valuable, of

USDA describes its targeted testing of a fraction of the cattle most
likely to test positive for

BSE as testing “to accurately diagnose the presence or absence of the
disease” (USDA Memo at

49), and a negative inference could be made from Dr. Ferguson’s
declaration that USDA’s

targeted testing can “be interpreted to mean that the animal is
necessarily ‘BSE-free’” (Ferguson

Decl. ¶ 6). But in fact, the testing USDA is conducting, just like the
testing Creekstone proposes

for its cattle, will only diagnose the presence of BSE if the disease
has progressed quite far. See

Ferguson Decl. at ¶ 6 (“there is a long period in the life of an
infected animal when current tests

would not detect the disease”). Thus, even USDA’s “targeted” testing can
result in “false

negative” test results, if infected animals that are non-ambulatory or
suspect for other reasons are

BSE-tested at a time when infectious prions are not concentrated enough
in their brain stem to be

identified in available tests. Only if cattle fall into one of the
groups which USDA is testing

(because, e.g., they are having trouble walking, or have died of unknown
causes) and they have

BSE which has spread to the point where the animal will die of BSE
within a few months will the

testing USDA is conducting identify BSE-infected cattle. USDA’s emphasis
on “false negative”

results in tests that Creekstone proposes to perform, when USDA’s own
testing also could result

in false negative results, is additional confirmation that USDA’s claim
that BSE tests are

“worthless” is just that—an assertion unsupported by the facts.

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course, but it seriously understates the value of BSE testing.28 USDA
simply chooses to ignore

information that demonstrates the inaccuracy of its “2-3 months”
argument. For example, on

August 24, 2006 the Canadian Food Inspection Agency (CFIA) issued a
report on a 50-month-old

cow from Alberta, Canada that was confirmed to be BSE-infected on July
13, 2006. See

(Detwiler Decl.) Attach. B. The conclusion of the CFIA (which has dealt
with four times as

many BSE cases as USDA), was that “in this instance, had the cow not
succumbed to an

unrelated disease and had a brain stem sample submitted for BSE testing,
it would probably have

been four to eight months longer before the cow would have displayed
symptoms that might have

caused it to be tested because of suspicion of BSE.” Exh. 8 (Brown
Decl.) ¶ 5.

Moreover, it is undisputed that, when countries have gone from testing
only cattle with

outward signs that might indicate BSE to testing all cattle above a
certain age, they have detected

many more cases of BSE. Analysis of the experience in France as it went
from “passive” testing

only of suspect animals, to testing of all cattle over 30 months of age,
to testing all cattle over 24

months, shows that passive surveillance was picking up only a fraction
of the cases of BSE

infection that were detectable with BSE rapid tests. Supervie and
Castagliola, “The

Unrecognized French BSE Epidemic,” 35 Vet. Res. 349, 351-52, 358, 361
(2004) (attached as

Exhibit 11). This may be in part because the clinical signs of BSE are
“very subtle.” See USDA

Memo Exh. 26 at Article 3.8.4.2 ¶ 1. In fact, both of the indigenous
cases of BSE discovered in

the U.S. were in cattle with ambiguous or no clinical features. Exh. 8
Attach. C at 1817.

28 The OIE Terrestrial Animal Health Code – 2005, Appendix 3.8.4,
Surveillance for Bovine

Spongiform Encephalopathy, on which USDA relies in part (USDA Memo Exh.
26), recognizes

that cattle where BSE is detectable but clinical signs have yet to
appear is a larger group than

those showing clinical signs. Id. at Article 3.8.4.1 ¶ 2.c.

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USDA also ignores the growing data about “atypical” BSE infection, which
usually is

not accompanied by any outward signs even at an advanced state of
infection. See Exh. 8 ¶ 8

and Attach. C. “Thus, some cattle that on visual inspection appear
normal are infected, and this

fact negates any argument about a limited window of ‘pre-clinical’
positivity in BSE tests, as

there are no signs leading to a suspicion of infection. The only way
that these cattle are

identified as BSE-infected is through testing.” Exh. 8 (Brown Decl.) ¶ 8
(citation omitted). Far

from making BSE testing of asymptomatic cattle worthless, it makes such
testing essential for

an understanding of this aspect of the disease. Id. ¶ 14.

In short, “[p]reventing voluntary testing while at the same time
dramatically reducing

government testing does not make any sense for the protection of animal
and human health and

is further indication that voluntary BSE testing is not ‘worthless.’”
Exh. 8 (Brown Decl.) ¶ 15.

USDA’s statutory authority under the VSTA to prevent the sale or
shipment of biological

products extends only to those that are “worthless, contaminated,
dangerous, or harmful.” 21

U.S.C. § 154. When USDA acts to prevent distribution of BSE test kits to
all but USDA

contractors because USDA believes that it is not cost-effective to use
USDA-approved test kits

on all healthy-looking, slaughter-age cattle (or because USDA believes
the use of those test kits

will have economic consequences for beef producers or national and
international consumer

confidence in beef, as discussed in the following section), USDA is not
acting to ban a

“worthless” product, and therefore it is acting outside its statutory
authority in violation of the

Administrative Procedure Act, 5 U.S.C. § 706(2)(C).

Much of the declaration of Lisa Ferguson (USDA Memo Exh. 1) seems to be
aimed at

convincing the Court that BSE is a dwindling, not-very-serious problem.
Although overstated,

that is in any case beside the point, since nothing about the VSTA would
authorize USDA to

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prevent the sale or shipment of a vaccine or a diagnostic test for a
rare disease.29 If a vaccine

were developed to treat a rare but invariably fatal disease, which only
0.001% of the U.S. cattle

herd of 90 million head may contract, could USDA prohibit the
manufacture and sale of that

vaccine because USDA decided the disease was not important enough to
warrant ranchers’

purchasing the vaccine?

IV. USDA’S RESTRICTIONS ON BSE TEST KITS ON ECONOMIC GROUNDS ARE

OUTSIDE ITS AUTHORITY UNDER THE VSTA.

As Creekstone has explained, USDA acts outside of its statutory
authority, in violation

of section 706(2)(C) of the Administrative Procedure Act when it
prevents access to and use of

BSE test kits for reasons outside of the purposes and criteria expressed
in the VSTA. Pl.

Memo at 41-43. In particular, since USDA is banning access to BSE test
kits for purposes

unrelated to the purposes of the VSTA, such as promoting domestic and
international

confidence in beef, controlling costs of meatpackers, and the like, USDA
is acting outside its

statutory authority. Pl. Memo at 42, 44.30

USDA asserts that this issue goes to whether USDA acted in an arbitrary
and capricious

manner (Count 3 of the Complaint), and not Counts 1 and 2, which are the
subject of

Creekstone’s current Motion for Summary Judgment. But to the extent that
USDA has

promulgated regulations that it now asserts authorize it to restrict the
use of biological products

29 The declarations of Drs. Brown and Detwiler (Exhibits 8 and 10 to
this Reply Memo) make it

very clear that (1) much of what Dr. Ferguson states as unqualified fact
is actually more of an

educated guess and (2) BSE is far from eliminated and indeed recent
developments (ignored by

Dr. Ferguson’s declaration) make voluntary BSE testing even more
important. See also, e.g.,

Exh. 11 at 357 (referring to “animals slaughtered in the late stage of
incubation when it is

hypothesized that infected tissues are infectious” (emphasis added);
Exh. 8 Attach. C at 1820; Pl.

Memo Exh. 3 at 91 (Dr. Prusiner explaining why the feed ban will reduce
but not eliminate BSE.)

30 Creekstone also noted that, if the reference in USDA regulations at 9
C.F.R. § 102.5(d) to “the

protection of domestic animals or the public health, interest, or
safety, or both” could be read to

authorize restrictions on biological products for purposes unrelated to
the efficacy or safety of

such products, then that regulation should be struck down as ultra
vires, as well. Pl. Memo at 43.

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for reasons other than for animal health and has issued product
licenses, advisories, and other

communications concerning BSE tests for purposes that have nothing to do
with its regulatory

authority in the VSTA, USDA has acted “in excess of statutory
jurisdiction, authority, or

limitations, or short of statutory right,” in violation of 5 U.S.C. §
706(2)(C)—the subject of

Counts 1 and 2 of the Complaint.31 (Of course, if the Court believes
that this issue more

appropriately falls under Count 3 of the Complaint, then the Court could
simply defer ruling on

this particular argument until it is briefed in connection with a
summary judgment motion on

Count 3 (should Creekstone be denied summary judgment on both Counts 1
and 2).)

USDA’s substantive response is to assert (1) that its actions preventing
private parties

from BSE testing further the purposes of the VSTA by protecting animal
health and (2) that

regulating BSE test kits to achieve various economic or market ends is
also authorized by the

“purpose” of the VSTA. Neither of these arguments makes sense.

USDA has said or implied numerous times that its policy of preventing
BSE testing of

healthy-appearing cattle at slaughter (i.e., those least likely to have
BSE) promotes animal

health. See, e.g., USDA Memo at 48. But USDA has never explained how
that could be. Just

because BSE testing of healthy-appearing younger cattle is unlikely to
identify a case of BSE

does not mean that such testing would be harmful to animal health. A
“false negative” result

(which USDA in any case would expect to be extremely rare, since it
estimates that there are

seven or fewer BSE-infected cattle in the U.S., Defendants’ Statement of
Undisputed Material

Facts ¶ 5) could not be more “harmful” to animal health than not testing
the animal at all.

31 In contrast, Creekstone would be presenting an argument covered by
Count 3 of the Complaint

if it were arguing here that, even if USDA were authorized by the VSTA
to regulate the use of

biological products for reasons other than to protect domestic animals
(and, indirectly, their

owners) from ineffective or harmful biological products, it was
arbitrary and capricious for

USDA to exercise that authority in order to protect Creekstone’s
competitors from having to test

themselves or for other unreasonable reasons.

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USDA’s illogical pretext for banning private BSE testing is further
exposed by the fact

that virtually every developed country with BSE tests 100% of cattle
over 24 or 30 months of

age, and Japan tests all cattle presented for slaughter. See Section
III.C., supra. The value of

large-scale testing is reinforced by the statements of internationally
recognized experts on BSE

and the management of BSE and similar diseases, Dr. Paul Brown and Dr.
Linda Detweiler

(Exhs. 8 and 10), that it is important to perform a greater amount of
BSE testing in the United

States and that any data on the presence or absence of BSE in cattle
slaughtered in the United

States is of value. Since Creekstone’s proposed voluntary testing would
not prevent any

government testing for BSE, but would only provide supplemental data,
there is simply no

reason to conclude that Creekstone’s proposed use of BSE test kits would
adversely affect

animal health.32 USDA does not even attempt to explain its bald
assertion that Creekstone’s

voluntary testing would interfere with USDA’s efforts “to accurately
diagnose the presence or

absence of the disease” and, “through its surveillance testing, to
manage the disease.” USDA

Memo at 49. Cf. Rippke Decl. (USDA Memo Exh. 2) (stating that current
USDA BSE testing

“will contribute to the knowledge of the disease and may increase the
chances of developing

therapies or potential cures for the disease in the future,” but
omitting any mention of the effect

of voluntary BSE testing as proposed by Creekstone); Ferguson Decl.
(USDA Memo Exh. 1)

(stating that USDA’s testing of targeted animals is “the most efficient
method for detecting the

presence of BSE” (¶ 6), but never even claiming that Creekstone’s
proposed testing would

interfere with USDA’s “surveillance testing” for BSE).

32 Perhaps an argument could be made to that effect if Creekstone’s
testing would use up limited

laboratory capacity or test kit manufacturing capacity that otherwise
could be used for higher-

priority BSE testing. But USDA has not made such an argument, and in
fact Creekstone has

constructed its own laboratory for BSE testing and there is no shortage
of BSE test kit

manufacturing capacity (especially now that USDA has reduced its BSE
testing by 90%).

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If there was any doubt before, it is clear after reading the USDA Memo
that USDA’s

prohibition of the manufacture and sale of BSE test kits, except for use
in USDA’s own BSE

testing program, is an action to further USDA’s views of what is good
for domestic and foreign

markets for beef and for the financial health of U.S. meatpackers,
rather than to prevent the

manufacture and sale of a worthless or harmful biological product as the
VSTA directs. It

therefore is an action “in excess of statutory jurisdiction, authority,
or limitations, or short of

statutory right.” 5 U.S.C. § 706(2)(C). USDA openly acknowledges that it
was acting for

purposes of “maintaining domestic and international confidence in U.S.
cattle and beef

products,” “protecting consumers from paying more for privately BSE
tested beef,” and

“correcting market deficiencies and information asymmetries pertaining
to the effectiveness of

BSE test kits.” USDA Memo at 51-52. Tellingly, for the first time USDA
admits its

motivation that prohibiting private BSE testing “also prevents beef
producers from having to

incur increased costs of conducting the BSE testing, which, although
useless for animal health

and food safety purposes, might otherwise be necessary to remain
competitive if private BSE

testing were permitted.” Id. at 52 n.30.

USDA’s defense of its actions is to claim that, although not directly
authorized by any of

the provisions of the VSTA, they are “consistent with VSTA’s purpose.”
USDA Memo at 52.

Creekstone does not dispute that Congress enacted the VSTA in part to
protect the economic

interests of livestock owners from biological products that would harm
their livestock or would

be worthless. But a regulatory action is not authorized by a statute
just because it is consistent

with the statute’s purposes. A specific grant of authority from Congress
is necessary. Rodriguez

v. United States, 480 U.S. 522, 526 (1987); American Fin. Servs. Ass’n
v. FTC, 767 F.2d 957,

965), cert. denied, 475 U.S. 1011 (1986)); Railway Labor Executives’
Ass’n, 988 F.2d at 141 n.10

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(“However sensible the Board’s view that stability in labor relations
would be promoted by [the

challenged regulation] …, Congress has not so provided.”) If USDA’s
position were the law,

then USDA could also, for example, dictate to biological products
manufacturers the maximum

amount they could charge for each product, because keeping prices low
would benefit the

economic interests of livestock owners and beef producers. See also 62
Cases of Jam v. United

States, 340 U.S. 593, 600 (1951) (“In our anxiety to effectuate the
congressional purpose of

protecting the public, we must take care not to extend the scope of the
statute beyond the point

where Congress indicated it would stop.”)

A biological product is not “worthless, contaminated, dangerous, or
harmful” for “use

in the treatment of domestic animals,” 21 U.S.C. § 151, because USDA
thinks that its use

would put others at a competitive disadvantage or would interfere with
“maintaining domestic

and international confidence in U.S. cattle and beef products.”33 This
Court should be

particularly cautious about inferring in the VSTA authority to restrict
access to biological

products for purposes of preventing competition among meat
producers—even competition on

grounds that USDA believes would be inappropriate—or consumer access to
information.

Other government agencies are charged with regulating competition and
fraudulent

representations to consumers. Imposing such limitations on speech
carries with it important

Constitutional constraints. And action by USDA—or indeed any government
agency—

specifically designed to favor one set of competitors (large meatpackers
with low margins) over

33 USDA Memo at 51-52. In any event, USDA provides no explanation for
this contention,

which is counterintuitive, especially given that 100% testing (of all
cattle, in Japan, and of cattle

over 24 months in France and Germany, and over 30 months in the
remainder of the EU, see p.

35, supra) is already the norm in many of those international markets,
and consumers in Asia

have been seeking testing for imported beef. This Court should not
simply accept USDA’s

unsupported assertion that more testing for BSE would make consumers
less confident in the

safety of U.S. beef. See also Exhibits 1-6.

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Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 50 of 52

others (Creekstone and other high-end meatpackers with an interest in
BSE testing) is not only

inappropriate as a matter of policy, it likely is unconstitutional. The
Court should refrain from

interpreting the “VSTA’s purpose” as authorizing such potentially
unconstitutional actions.

See Edward J. DeBartolo Corp. v. Florida Gulf Coast Building & Constr.
Trades Council, 485

U. S. 568, 575 (1988) (courts should construe a statute to avoid
constitutional problems “unless

such construction is plainly contrary to the intent of Congress”).

In any event, USDA’s argument is that its restriction of access to BSE
test kits is

consistent with the VSTA’s purpose to protect farmers and ranchers from
economic losses

associated with harmful or ineffective biological products. USDA Memo at
50-51. But even

this broad, vague claimed authority does not support USDA’s claim that
actions to protect

consumers from paying more for BSE-tested beef (USDA Memo at 52) are
consistent with the

VSTA’s purpose “to protect the economic interests of livestock owners
and beef producers”

(id.), since actions to protect consumers of meat do not relate to the
financial well-being of

farmers and ranchers per se at all. (Instead, USDA now makes the
remarkable claim that the

VSTA authorizes it to “regulate the economic condition of [the beef]
market.” Id.) Even if

authorization to ban private use of BSE test kits could be derived
solely from the purposes of

the VSTA, none of those purposes supports USDA actions ostensibly
directed at providing

accurate information to beef consumers or protecting beef producers from
competition.34

Contrary to USDA’s assertion (USDA Memo at 51 n.27), Garrelts v.
Smithkline Beecham

Corp., 943 F. Supp. 1023 (N. D. Ia. 1996), is very relevant to this
case. After an extensive

analysis of the 1913 enactment of the VSTA and its amendment in 1985,
the Garrelts court

concluded that in both instances “Congress’s concern was regulation of
the worthlessness,

contamination, dangerousness, or harmfulness of animal vaccines to
livestock, not the general

duties of product manufacturers…to safeguard human users of their
products….” Id. at 1068

(emphasis in original); see also id. at 1066-67. Obviously, the economic
interests of beef

processors and consumers are even further removed from that
congressional purpose.

- 44 -


Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 51 of 52

V. USDA IS NOT ENTITLED TO SUMMARY JUDGMENT.

USDA has offered almost no argument directed specifically to its
cross-motion for

summary judgment, apparently believing that, if its arguments against
Creekstone’s summary

judgment motion are successful, then USDA will be entitled to summary
judgment itself. That

is, of course, not the way the law works.

First, as USDA has noted, by agreement Creekstone has only moved for
summary

judgment on Counts 1 and 2 of its Complaint, leaving Count 3 for a
fuller development of the

record if the Court should conclude that Creekstone is not entitled to
summary judgment on

either Count 1 or Count 2.35 See Pl. Memo at 1 n.1; USDA Memo at 13 n.7.
Secondly, the

Court could decide that Creekstone has not qualified for summary
judgment on Counts 1 and 2,

without finding that USDA has met its burden of demonstrating that there
is no genuine issue

as to any material fact and that USDA is entitled to judgment as a
matter of law on those counts

(which USDA certainly has not). See Fed. R. Civ. P. 56(c).

CONCLUSION

For the reasons explained above and in Creekstone’s Memorandum in
Support of its

Motion for Summary Judgment, Creekstone is entitled to summary judgment
on Counts 1 and

2 of its Complaint, and for the relief sought therein.

Dated: November 3, 2006 Respectfully submitted,

__/s/ Russell S. Frye _

Russell S. Frye (D.C. Bar No. 331124)

35 The only argument that USDA has even asserted that could apply to
Count 3 of Creekstone’s

complaint is that the Court lacks jurisdiction to hear Creekstone’s
claims because they are moot

or do not present a redressable injury. As Creekstone has demonstrated
in Section I of this

memorandum, those arguments are misguided and unavailing.

- 45 -


Case 1:06-cv-00544-JR Document 14-1 Filed 11/03/2006 Page 52 of 52

FryeLaw PLLC

P.O. Box 33195

Washington, DC 20033-0195

(202) 572-8267

[email protected]

__/s/ William L. Miller ________

William L. Miller (D.C. Bar No. 443191)

The William Miller Group, PLLC

1666 Connecticut Avenue, N.W.

Washington, DC 20009

(202) 256-2306

[email protected]

__/s/ Peter C. Choharis ________

Peter C. Choharis (D.C. Bar No. 444787)

2771 Woodley Place, NW

(202) 422-8312

Washington, D.C. 20008

[email protected]

Attorneys for Plaintiff

CREEKSTONE FARMS PREMIUM BEEF, LLC

- 46 -
TSS
 

flounder

Well-known member
Case 1:06-cv-00544-JR Document 14-9 Filed 11/03/2006 Page 1 of 47

Creekstone Farms Premium Beef v. USDA

Civ. Action No. 06-544 (JR)

Plaintiff’s Summary Judgment Reply and Opposition

EXHIBIT 8

Case 1:06-cv-00544-JR Document 14-9 Filed 11/03/2006 Page 2 of 47

IN THE UNITED STATES DISTRICT COURT

FOR THE DISTRICT OF COLUMBIA


)

CREEKSTONE FARMS PREMIUM BEEF, LLC, )

)

Plaintiff, )

)

vs. ) Civil Action No. 06-544 (JR)

)

UNITED STATES DEPARTMENT OF AGRICULTURE, )

and MIKE JOHANNS, IN HIS CAPACITY AS THE )

SECRETARY OF AGRICULTURE, )

)

Defendants. )

__________________________________________________)

DECLARATION OF PAUL W. BROWN, M.D.

Paul W. Brown, MD, certifies and states as follows:

1. My entire 43-year career has been devoted to the study of the
Transmissible

Spongiform Encephalopathies (TSEs, or ‘prion diseases’) in the National
Institutes of Health (NIH)

laboratory of Nobel Laureate D. Carleton Gajdusek; and for the last 15
years of my career I held the

position of Senior Investigator at the National Institute of
Neurological Disorders and Stroke

(NINDS) at the NIH. In this capacity I oversaw and conducted research
involving these invariably

fatal, neurodegenerative diseases, which include both bovine spongiform
encephalopathy (BSE),

commonly referred to as “mad cow” disease, and variant Creutzfeldt-Jakob
Disease (vCJD), a

human TSE infection acquired by the consumption of BSE-contaminated meat
products.

2. Since leaving the NIH two years ago, I have continued to engage in
research, writing,

and scientific advisory activities in various aspects of TSE. Ongoing
research projects include an

ultra-high pressure methodology to inactivate the agent of BSE; a
pre-clinical diagnostic blood

screening test for TSEs in general, and variant CJD in particular; and a
study to determine whether


Case 1:06-cv-00544-JR Document 14-9 Filed 11/03/2006 Page 3 of 47

blood infectivity in humans with CJD can be diluted to extinction
(important in the context of the

size of plasma pools used for the extraction of therapeutic proteins
such as anti-hemophilic factor). I

have continued to participate in scientific advisory boards, including
chairing the safety committee

of LFB (the plasma fractionator in France), co-chairing the scientific
research committee of a

pharmaceutical consortium to award research contracts, and advising the
EuroCJD committee on

global BSE and CJD surveillance, and the Argentine Agriculture
Department on BSE issues. I have

also continued to accept invitations to chair and/or lecture at numerous
scientific meetings on TSEs

in the Americas and Europe.

I am a member of the American College of Physicians, the American
Epidemiological

Society, the Infectious Diseases Society of America, the American
Society for Virology, the Société

Française de Neurologie, and the American Neurological Association. I
have authored or coauthored nearly 400 papers, mainly dealing with TSE,
and especially the topics of epidemiology,

infectivity, and inactivation. (A list of scientific papers (published
from 1991 to the present or that

are in press) of which I am an author, primarily regarding TSEs, is
attached as Attachment A.) Since

1990, I have been an Associate Editor of the European Journal of
Epidemiology, and from 1991 until

1997, was an Associate editor of the Journal of the Neurological Sciences.

3. Before entering the NIH in the US Public Health Service, I attended
Harvard College

(A.B., Magna cum Laude), and the Johns Hopkins School of Medicine (M.D.,
Alpha Omega Alpha

Honor Society), and undertook Medical Internship and Residency training
at both the Johns Hopkins

Hospital in Baltimore, Maryland, and the University of California School
of Medicine in San

Francisco, California. I am a Diplomate of the American Board of
Internal Medicine.

(My curriculum vitae is attached to this declaration as Attachment B.)

-2


Case 1:06-cv-00544-JR Document 14-9 Filed 11/03/2006 Page 4 of 47

4. At the request of William L. Miller of the William Miller Group, PLLC
(outside

counsel for Creekstone Farms Premium Beef, LLC), on October 11, 2004, I
agreed to prepare this

declaration regarding the current scientific understanding of bovine
spongiform encephalopathy

(BSE) in support of the litigation by Creekstone Farms Premium Beef, LLC
to be allowed to

voluntarily test for BSE in cattle processed at its plant in Arkansas
City, Kansas. Prior to October

11, I have had no relationship with Creekstone Farms. The opinions
expressed in this declaration are

based solely on my knowledge of BSE and other TSEs that I have gained
from my experience as a

physician and neuroscientist over the past 45 years.

5. Based on current science, we do not know with certainty how far in
advance of

displaying clinical signs of BSE a bovine animal could test positive
using a BSE rapid test such

as the rapid test technology developed by Bio-Rad Laboratories, Inc.,
and currently used by the

United States Department of Agriculture to test for BSE. For example,
the Canadian Food

Inspection Agency (CFIA) recently issued a report on a 50-month-old cow
from Alberta, Canada

that on July 13, 2006 was confirmed as BSE-infected. The CFIA reports
states as follows:

This animal was detected and diagnosed with BSE during a pre-clinical
phase of the

disease. The normal disease course to expression of clinical signs in
this animal would be

expected to have included an additional three to six months of
incubation followed by an

additional one to two months of clinical expression prior to being
recognized as

symptomatic of BSE and targeted for testing. Had an unrelated disease
not hastened her

entry into the surveillance stream, this animal would most likely have
demonstrated

clinical signs sometime between 54 and 56 months, not significantly
different from the

age range of previous cases.

-3


Case 1:06-cv-00544-JR Document 14-9 Filed 11/03/2006 Page 5 of 47

Canadian Food Inspection Agency, Report On The Investigation Of The
Seventh Case Of

Bovine Spongiform Encephalopathy (BSE) In Canada, available at

http://www.inspection.gc.ca/english/anima/heasan/disemala/bseesb/ab2006/7investe.shtml.


Thus, in this instance, had the cow not succumbed to an unrelated
disease and had a brain stem

sample submitted for BSE testing, it would probably have been four to
eight months longer

before the cow would have displayed symptoms that might have caused it
to be tested because of

suspicion of BSE.

6. Experimental studies to determine range of intervals between positive
tests and the

onset of clinical signs have not been done (a critical experiment has in
fact been done in the UK,

but only infectivity was measured, and tests for the presence of prion
protein have not been

done). Wells, G. A. H., S.A. Hawkins, R.B. Green, A.R. Austin, I.
Dexter, Y.I. Spencer, M.J.,

Chaplin, M.J. Stack, and M Dawson, 1998, Preliminary observations on the
pathogenesis of

experimental bovine spongiform encephalopathy (BSE): an update, Vet.
Rec. 142:103-106;

Wells, G.A.H., J. Spiropoulos, S.A.C. Hawkins, and S. J.Ryder, 2005,
Pathogenesis of

experimental bovine spongiform encephalopathy: preclinical infectivity
in tonsil and

observations on the distribution of lingual tonsil in slaughtered
cattle, Vet. Rec. 156:401-407.

Equally important, field experience in countries that have gone to
universal testing (including

universal testing above a certain age) has shown that such testing
(active surveillance) identifies

considerably more cases than only testing cattle whose behavior happens
to attract the attention

of authorities happens to attract the attention of authorities (passive
surveillance).

Report on the Monitoring and Testing of Ruminants for the Presence of
Transmissible

Spongiform Encephalopathy (TSE) in the EU in 2005, Final Annual Report,
2005, European

Commission, 20 June 2006. (Section 4.2, Chart B2), available at

-4


Case 1:06-cv-00544-JR Document 14-9 Filed 11/03/2006 Page 6 of 47

http://ec.europa.eu/food/food/biosafety/bse/annual_reps_en.htm.

7. Assumptions about the likely course of BSE infection in cattle and
its significance for

potential vCJD infection in humans who consume cattle tissues are
largely just that—

assumptions or extrapolations from limited data, not tested conclusions.
We have little or no

direct evidence of such things as when in life a bovine is most
susceptible to BSE; how much

less susceptible, if at all, humans are than cattle; whether shorter
incubation times in cattle are

the result of exposure to a high dose at a young age or some other
factor(s) (such as genetic

susceptibility or the strain of prions); how many humans may ultimately
be shown to have vCJD;

or how effective SRM removal is at reducing the risk of transmission of
BSE from an infected

animal.

8. The question of the interval between when cattle may test positive
for BSE and

when those cattle exhibit clinical signs of the disease has in any case
been made irrelevant by the

recent discovery of atypical cases of BSE that usually occur in older
asymptomatic animals that

for one reason or another are culled, and are then discovered to test
positive. Thus, some cattle

that on visual inspection appear normal are infected, and this fact
negates any argument about a

limited window of 'pre-clinical' positivity in BSE tests, as there are
no signs leading to a

suspicion of infection. The only way that these cattle are identified as
BSE-infected is through

testing. The frequency of such infections is not yet known, but so far
has ranged from less than

1% all the way up to 15% of the total number of test positives.
International Conference on

Prion Diseases of NeuroPrion, Network of Excellence, Prion2006, Turin,
Italy, 4-6 October

2006, Book of Abstracts (hereinafter “Prion2006 Abstracts”), See

http://www.neuroprion.com/en/ev_prion2006.html; Brown P, McShane LM,
Zanusso G,

Detwiler L, On the question of sporadic or atypical bovine spongiform
encephalopathy and

-5


Case 1:06-cv-00544-JR Document 14-9 Filed 11/03/2006 Page 7 of 47

Creutzfeldt-Jakob disease, Emerg. Inf. Dis., 2006, 12: 1816-21, in
press, December 2006. (A

copy of the article is attached to this declaration as Attachment C.)

9. Although these cases of asymptomatic, atypical BSE have been found in
older

cattle, we do not currently know the concentration and distribution of
infection and infectivity

that might have been found in these cattle at an earlier age. Another
issue concerns evidence that

atypical BSE may be more virulent for humans than typical BSE. This
evidence comes from

experimental transmission studies in at least 4 different laboratories.
All have shown more rapid

onset of disease (shorter incubation periods) following inoculation with
atypical BSE than with

typical BSE, and in one study, BSE did not transmit at all. These
studies involved the use of

wild-type mice, bovinized and humanized transgenic mice, and (most
worrisome) non-human

primates as recipient animals. Prion2006 Abstracts, See

http://www.neuroprion.com/en/ev_prion2006.html.

10. We do not have any direct evidence of how few BSE prions need to be
consumed

in order for a human to be at risk of vCJD. Just because the disease has
not progressed far

enough in a bovine to produce clinical symptoms does not mean that there
are insufficient

concentrations of BSE prions in that bovine's tissue to present a risk
of vCJD if consumed. (In

fact, logic suggests the contrary, because it would imply that all of
the people with vCJD were

infected by the consumption of meat products from cattle that were
displaying signs of BSE at

the time of slaughter, which seems highly unlikely.) The available tests
for BSE are generally

believed to have lower limits of detecting concentrations of prions
that, if ingested, could cause

BSE in other cattle, or potentially vCJD in humans. In cattle, the
minimum amount of tissue

needed to infect a cow by the oral route is only 0.001 gram (Dr. Gerald
Wells, personal

-6


Case 1:06-cv-00544-JR Document 14-9 Filed 11/03/2006 Page 8 of 47

communication), and this figure has been used for risk analyses in
humans (a hypothesized

bovine to human 'species barrier' effect has never been documented).

11. Just because cattle are under 30 months of age does not mean that
they present no

risk of BSE, both because of the facts discussed above about the
uncertain relationship between

testing positive for BSE and having sufficiently concentrated prions to
cause infection in

humans, and because BSE has been detected in younger cattle in Europe
and Japan.

Additionally, the way that the age of cattle to be slaughtered is often
determined (dentition) is

not very precise. As a matter of protecting animal and human health from
the fatal consequences

as BSE, detecting even a handful of cases that otherwise would be missed
is very valuable.

USDA requires testing of agricultural products for numerous diseases
which are (thankfully)

extremely rare, such as E. coli.

12. The USDA has performed BSE tests on thousands of cattle younger than 30

months, including thousands that had no clinical signs of BSE.

13. Measures that the United States (and Canada) has put in place to
reduce the

transmission of BSE have substantially reduced the risk in the United
States, but have not

eliminated it. Experience has shown that the feed bans are incomplete,
both because the bans are

limited and because of imperfect implementation.

14. Collecting additional BSE test data from cattle less likely to have
detectable levels

of BSE (because they are younger and do not display other risk factors),
while not as cost-

effective, is not worthless and produces data that could help better
understand BSE and its

distribution in U.S. cattle. (For example, if authorities only tested
cattle suspected of having

BSE, the Canadians would not have found BSE in the 50 month old Alberta
cow that did not

have outward signs that might have suggested BSE and was born long after
exposure to BSE in

-7


Case 1:06-cv-00544-JR Document 14-9 Filed 11/03/2006 Page 9 of 47

cattle feed was believed to have ceased; nor is it likely that either of
the two indigenously

infected US cows with atypical BSE that tested positive would have been
identified.) Evolving

knowledge about atypical BSE, where there are only rarely outward signs
that might cause the

animal to be singled out and tested based on suspicion of BSE, makes the
value of testing

asymptomatic cattle even clearer. Voluntary testing does not interfere
with or dilute government

efforts to test for BSE and to understand the disease. Additionally,
while most cattle slaughtered

in the U.S. are under 30 months of age, many thousands every year are
over 30. I am not aware

of any other programs under which USDA has prohibited testing for a
disease because it is

unlikely that the disease will be found.

15. The USDA recently announced a dramatic (ten-fold) reduction in the
number of

cattle it will test for BSE. USDA plans to reduce the current annual
rate of over 400,000 cows to

only 40,000 (less than 1 % of the cattle that are slaughtered or die
each year). USDA News

Release No. 0255.06, July 20, 2006, available at

http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB?contentidonly=true&contentid=2006/


07/0255.xml. Preventing voluntary testing while at the same time
dramatically reducing

government testing does not make any sense for the protection of animal
and human health and

is further indication that voluntary BSE testing is not "worthless."
Although the USDA and the

OIE have stated that targeted testing of cattle most likely to have BSE
is the most effective way

of detecting and monitoring BSE infection in a country's cattle herd,
most developed countries

known to have BSE nonetheless have chosen to go far beyond such targeted
testing in their

domestic BSE monitoring programs, especially in view of the growing
proportion of infected

cattle that have atypical (and asymptomatic) forms of BSE when slaughtered.

-8


Case 1:06-cv-00544-JR Document 14-9 Filed 11/03/2006 Page 10 of 47

16. BSE tests do not involve the immune system of the animal that is
tested. There is

a sharp distinction between using immunological means to prevent foreign
pathogen infections

(e.g., active and passive immunization) and the use of an immunologic
reagent (e.g., an

antibody) to detect infectious prion proteins obtained from the body of
an infected host. The use

of such a test has nothing whatsoever to do with the immune system of
the infected (and now

dead) animal. USDA thinking on this point is very confused.

17. The USDA allows suppliers of meat and other products to certify that
those

products meet criteria unrelated to food safety (or least, where USDA
does not have data to

conclude that there is a food safety benefit). I believe this is true,
for example, of "organic,

"natural," "hormone-free, "grass-fed," and other descriptors that USDA
allows. Given the

legitimate role of the USDA to protect consumers from industry
incompetence, it nevertheless

seems unreasonable for USDA to prohibit the private use of its own
validated test method. The

desire on the part of some consumers to have a higher standard of safety
with respect to what

they eat should not be circumvented by this kind of attitude, even if
most people are satisfied

with government assurances of safety based on its own evaluation.

I declare under penalty of perjury that the foregoing is true and correct.

Executed on October 27, 2006. Paul Brown, M.D.

-9


Case 1:06-cv-00544-JR Document 14-9 Filed 11/03/2006 Page 11 of 47

ATTACHMENT A

Paul W. Brown, M.D.

List of Publications 1991 to Present


Case 1:06-cv-00544-JR Document 14-9 Filed 11/03/2006 Page 12 of 47

Paul W. Brown, M.D.

LIST OF PUBLICATIONS 1991 TO PRESENT

153. Goldfarb, L.G., Brown, P. and Gajdusek, D.C. Multiple mutations in

kuru, Creutzfeldt-Jakob disease, and Gerstmann-Sträussler syndrome.

Brain Research, 16: 1 (January), 98-99, 1991.

154. Brown P. and Gajdusek, D.C. New studies on the resistance of scrapie

agent to enzymatic digestion, heat and chemical denaturation, and

natural weathering. Brain Research, 16: 1 (January), 100-103, 1991.

155. Brown, P. and Gajdusek, D.C. Survival of scrapie virus after 3 years’

interment. Lancet, 337: 8736 (February 2), 269-270, 1991.

156. Goldfarb L.G., Haltia, M., Brown, P., Nieto, A., Kovanan, J.,

McCombie, W.R., Trapp, S. and Gajdusek, D.C. New mutation in scrapie

amyloid precursor gene (codon 178) in Finnish Creutzfeldt-Jakob

kindred. Lancet, 337: 8738 (February 16), 425, 1991.

157. Nieto, A., Goldfarb, L.G., Brown, P., McCombie W.R., Trapp, S.,

Asher, D.M. and Gajdusek, D.C. Codon 178 mutation in ethnically

diverse Creutzfeldt-Jakob disease families. Lancet, 337: 8741

(March 9), 622-623, 1991.

158. Fradkin, J.E., Schonberger, L., Mills, J.L., Gunn, W.J., Piper, J.M.,

Wysowski, D.K., Thomson, R., Durako, S. and Brown, P. Creutzfeldt-

Jakob disease in pituitary growth hormone recipients in the United

States. Journal of the American Medical Association, 265: 7

(February 20), 880-884, 1991. Also as abstract:

Fradkin, J.E., Schonberger, L., Mills, J.L., Gunn, W.J., Piper, J.M.,

Wysowski, D.K., Thomson, R., Durako, S. and Brown, P. Creutzfeldt-

Jakob disease in pituitary growth hormone recipients in the United

States. In: “Program and Abstracts, The Endocrine Society 72nd

Annual Meeting, Atlanta, GA, June 20-23, 1990, p. 350.

159. Brown, P., Goldfarb, L.G., Brown, W.T., Goldgaber, D., Rubenstein, R.,

Kascsak, R. J., Piccardo, P., Boellaard, J.W. and Gajdusek, D.C.

Clinical and molecular genetic study of a large German kindred with

Gerstmann-Sträussler-Scheinker syndrome. Neurology, 41: 3 (March),

375-379, 1991.

160. Brown, P., Goldfarb, L.G. and Gajdusek, D.C. The new biology of

spongiform encephalopathy: infectious amyloidoses with a genetic

twist. Lancet, 337: 8748 (April 27), 1019-1022, 1991.

161. Pocchiari, M., Peano, S., Conz, A., Eshkol, A., Maillard, F., Brown,

P., Gibbs, C.J., Jr., Geng Xi, Y., Tenham-Fisher, E. and Macchi, G.

Combination ultrafiltration and 6 M urea treatment of human growth

hormone effectively minimizes risk from potential Creutzfeldt-Jakob

disease virus contamination. Hormone Research, 35: 3-4

(March-April), 161-166, 1991.


Case 1:06-cv-00544-JR Document 14-9 Filed 11/03/2006 Page 13 of 47

1991 (Con’t.)

162. Brown, P., Goldfarb, L.G., Gibbs, C.J., Jr. and Gajdusek, D.C.

The phenotypic expression of different mutations in transmissible

familial Creutzfeldt-Jakob disease. European Journal of

Epidemiology, 7:5 (September), 469-476, 1991.

163. Goldfarb, L.G., Brown, P., Mitrová, E., Haltia, M., Cervenáková, L.,

Goldin, L., Korczyn, A., Chapman, J., Galvez, S., Cartier, L.,

Rubenstein, R. and Gajdusek, D.C. Familial Creutzfeldt-Jakob disease

associated with the PRNP codon 200Lys mutation: an analysis of 45

families. European Journal of Epidemiology, 7:5 (September), 477486, 1991.

164. Mitrová, E., Brown, P., Hroncová, D., Tatara, M. and Zilák, J. Focal

accumulation of CJD in Slovakia: retrospective investigation of a new

rural familial cluster. European Journal of Epidemiology, 7:5

(September), 487-489, 1991.

165. Haltia, M., Kovanen, J., Goldfarb, L.G., Brown, P. and Gajdusek, D.C.

Familial Creutzfeldt-Jakob disease in Finland: epidemiological,

clinical, pathological and molecular genetic studies. European

Journal of Epidemiology, 1991, 7:5 (September), 494-500, 1991.

Also as abstracts:

Haltia, M., Kovanen, J., Goldfarb, L.G. and Gajdusek, D.C. Novel

mutation in the PRNP amyloid precursor gene co-segregates with

Creutzfeldt-Jakob disease in a Finnish family. Abstracts of the 36th

Annual Meeting of the Deutsche Gesellschaft für Neuropathologie und

Neuroanatomie Düsseldorf, September 16-18, 1991. Clinical

Neuropathology, 10: 5 (September/October), 257, 1991

Haltia, M., Kovanen, J., Goldfarb, L.G., Brown, P. and Gajdusek, D.C.

A new mutation (at codon 178) in the PRNP amyloid precursor gene
cosegregates with Creutzfeldt-Jakob disease in a large Finnish kindred.

Abstracts of the First Hungarian Conference of Neuropathology and the

5th Hungarian-Polish Neuropathological Symposium, Budapest, September

26-28, 1991. Ideggyógyászati Szemle (Neurological Review), 44

(Suppl. 1), 35, 1991.

166. Liberski, P.P., Kwiecinski, H., Barcikowska, M., Mirecka, B.,

Kulczycki, J., Kida, E., Brown, P. and Gajdusek, D.C. PrP amyloid

plaques in Creutzfeldt-Jakob disease of short duration:

immunohistochemical studies of 5 cases from Poland. European Journal

of Epidemiology, 7:5 (September), 505-510, 1991.

167. Brown, P. The clinical epidemiology of Creutzfeldt-Jakob disease in

the context of bovine spongiform encephalopathy. In: “Sub-acute

Spongiform Encephalopathies”, R. Bradley, M. Savey and B.A.

Marchant, editors. Kluwer Academic Publishers, Dordrecht

(The Netherlands), 1991, pp.195-202.

168. Brown, P. and Gajdusek, D.C. The human spongiform encephalopathies:

kuru, Creutzfeldt-Jakob disease, and the Gerstmann-Sträussler-

Scheinker syndrome. In: “Transmissible Spongiform Encephalopathies:

Scrapie, BSE and Related Disorders”, B.W. Chesebro, editor. Current

Topics in Microbiology and Imunology, volume 172, Springer Verlag,

Berlin, 1991, pp.1-20.

2


Case 1:06-cv-00544-JR Document 14-9 Filed 11/03/2006 Page 14 of 47

1991 (Con’t.)

169. Brown, P. Molecular genetics of spongiform encephalopathy.

Neuroscience Facts, 2:19 (October 3), 2, 1991.

170. Brown, P., Goldfarb, L.G., Cathala, F., Vrbovská, A., Sulima, M.,

Nieto, A., Gibbs, C.J., Jr. and Gajdusek, D.C. The molecular

genetics of familial Creutzfeldt-Jakob disease in France. Journal

of the Neurological Sciences, 105:2 (October), 240-246, 1991.

171. Scrimgeour, E.M. and Brown, P. BSE and potential risks to

slaughtermen. Veterinary Record, 129: 17 (October 26), 390-391,

1991.

172. Liberski, P.P., Brown, P., Shu-Yan, X. and Gajdusek, D.C. The

ultrastructural diversity of scrapie-associated fibrils isolated

from experimental scrapie and Creutzfeldt-Jakob disease. Journal

of Comparative Pathology, 105:4 (November), 377-386, 1991.

173. Trabattoni, G., Lechi, A., Bettoni, L., Macchi, G., Masullo, C.,

Brown, P. and Pocchiari, M. Creutzfeldt-Jakob disease in Italy

(letter to the editor). European Journal of Epidemiology, 7: 6

(November), 713-714, 1991.

174. Goldfarb, L.G., Brown, P., McCombie, W.R., Goldgaber, D.,

Swergold, G.D., Wills, P.R., Cervenáková, L., Baron, H.,

Gibbs, C.J., Jr. and Gajdusek, D.C. Transmissible familial

Creutzfeldt-Jakob disease associated with five, seven, and eight

extra octapeptide coding repeats in the PRNP gene. Proceedings of

the National Academy of Sciences (USA), 88:23 (December 1), 1092610930,
1991.

175. Laplanche, J.-L., Chatelain, J., Thomas, S., Brown, P. and Cathala, F.

Analyse du gene PrP dans une famille d’origine Tunisienne atteinte de

maladie de Creutzfeldt-Jakob. Revue Neurologique (Paris), 147: 12

(December), 825-827, 1991.

176. Korczyn, A.D., Chapman, J., Goldfarb, L.G., Brown, P. and Gajdusek,

D.C. A mutation in the prion protein gene in Creutzfeldt-Jakob

disease in Jewish patients of Libyan, Greek, and Tunisian origin.

Annals of the New York Academy of Sciences, 640:(December 3), 171176, 1991.

177. Brown, P., Goldfarb, L.G., McCombie, W.R., Nieto, A., Squillacote, D.,

Sheremata, W., Little, B.W., Godec, M.S., Gibbs, C.J., Jr. and

Gajdusek, D.C. Atypical Creutzfeldt-Jakob disease in an American

family with an insert mutation in the PRNP amyloid precursor gene.

Neurology, 42:2 (February), 422-427, 1992.

178. Goldfarb, L.G., Brown, P., Haltia, M., Cathala, F., McCombie, W.R.,

Kovanen, J., Goldin, L., Nieto, A., Godec, M.S., Asher, D.M.and

Gajdusek, D.C. Creutzfeldt-Jakob disease co-segregates with the

codon 178Asn PRNP mutation in families of European origin.

Annals of Neurology, 31:3 (March), 274-281, 1992.

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1992 (Con’t.)

179. Brown, P., Goldfarb, L.G., Kovanen, J., Haltia, M., Cathala, F.,

Sulima, M., Gibbs, C.J., Jr. and Gajdusek, D.C. Phenotypic

characteristics of familial Creutzfeldt-Jakob disease associated with

the codon 178Asn mutation. Annals of Neurology, 31:3 (March), 282-285,

1992.

180. Brown, P. The phenotypic expression of different mutations in

transmissible human spongiform encephalopathy. Revue Neurologique

(Paris), 148:5 (May), 317-327, 1992.

181. Chapman, J., Brown, P., Rabey, M.J., Goldfarb, L.G., Inzelberg, R.,

Gibbs, C.J., Jr., Gajdusek, D.C. and Korczyn, A.D. Transmission of

spongiform encephalopathy from a familial Creutzfeldt-Jakob disease

patient of Jewish Libyan origin carrying the PRNP codon 200 mutation.

Neurology, 42:6 (June), 1249-1250. 1992. Also as abstract:

Brown, P., Goldfarb, L.G., Gibbs, C.J., Jr., Gajdusek, D.C.,

Chapman, J., Rabey, M.J., Inzelberg, R. and Korczyn, A.D.

Transmission of spongiform encephalopathy from a Creutzfeldt-Jakob

disease (CJD) patient of Jewish Libyan origin carrying the PRNP

codon 200 mutation. Abstract no. 781S in: “ American Academy of

Neurology 44th Annual Meeting”, San Diego, May 3-9, 1992.

Neurology, 42:4 (April), Supplement 3, 370, 1992.

182. Brown, P., Preece, M.A. and Will, R.G. “Friendly fire” in medicine:

hormones, homografts, and Creutzfeldt-Jakob disease. Lancet,

340:8810 (July 4), 24-27, 1992.

183. Goldfarb, L.G., Brown, P., Vrbovská, A., Baron, H., McCombie, W.R.,

Cathala, F., Gibbs, C.J., Jr. and Gajdusek, D.C. An insert mutation

in the chromosome 20 amyloid precursor gene in a Gerstmann-

Sträussler-Scheinker family. Journal of the Neurological Sciences,

111:2 (September), 189-194, 1992.

184. Brown, P., Gálvez, S., Goldfarb, L.G., Nieto, A., Cartier, L.,

Gibbs, C.J., Jr. and Gajdusek, D.C. Familial Creutzfeldt-Jakob

disease in Chile is associated with the codon 200 mutation of the

PRNP amyloid precursor gene on chromosome 20. Journal of the

Neurological Sciences, 112:1,2 (October), 65-67, 1992.

185. Goldfarb, L.G., Petersen, R.B., Tabaton, M., Brown, P, LeBlanc, A.C.,

Montagna, P., Cortelli, P., Julien, J., Vital, C., Pendelbury, W.W.,

Haltia, M., Wills, P.R, Hauw, J.J., McKeever, P.E., Monari, L.,

Schrank, B., Swergold, G.D., Autilio-Gambetti, L., Gajdusek, D.C.,

Lugaresi, E. and Gambetti, P. Fatal familial insomnia and familial

Creutzfeldt-Jakob disease: disease phenotype determined by a DNA

polymorphism. Science, 258:5083 (October 30), 806-808, 1992.

Also as abstract:

Petersen, R.B., Goldfarb, L., Tabaton, M., Brown, P, LeBlanc, A.,

Montagna, P., Cortelli, P., Monari, L., Autilio-Gambetti, L.,

Gajdusek, D.C., Lugaresi, E. and Gambetti, P. Fatal familial

insomnia and one subtype of familial Creutzfeldt-Jakob disease:

effect of a polymorphism on a pathogenic mutation in the prion

protein. The FASEB Journal, 7: 4 (February 23), A627, 1993.

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1992 (Con’t.)

186. Bertoni, J.M., Brown, P., Goldfarb, L.G., Rubenstein, R. and

Gajdusek, D.C. Familial Creutzfeldt-Jakob disease (codon 200

mutation) with supranuclear palsy. Journal of the American Medical

Association, 268:17 (November 4), 2413-2415, 1992.

187. Goldfarb, L.G., Brown, P. and Gajdusek, D.C. The molecular genetics of

human transmissible spongiform encephalopathy. In: “Prion Diseases

of Humans and Animals”, S.B. Prusiner, J. Collinge, J. Powell and

B. Anderton, editors, Ellis Horwood, Chichester (England), 1992,

pp.139-153.

1993

188. Brown, P. The molecular biology and genetics of spongiform

encephalopathy. In: “Light and Electron Microscopic Neuropathology

of Slow Virus Disorders”, P.P. Liberski, editor. CRC Press, Boca

Raton, Florida, 1993, pp.63-100.

189. Liberski, P.P., Guiroy, D.C., Williams, E.S., Yanagihara, R.,
Brown, P.

and Gajdusek, D.C. The amyloid plaque. In: “Light and Electron

Microscopic Neuropathology of Slow Virus Disorders”, P.P. Liberski,

editor. CRC Press, Boca Raton, Florida, 1993, pp.295-347.

190. Liberski, P.P. and Brown, P. Scrapie-associated fibrils. In: “Light

and Electron Microscopic Neuropathology of Slow Virus Disorders”,

P.P. Liberski, editor. CRC Press, Boca Raton, Florida, 1993, pp.393414.

191. Brown, P., Kaur, P., Sulima, M.P., Goldfarb, L.G., Gibbs, C.J., Jr.
and

Gajdusek, D.C. Real and imagined clinicopathological limits of

“prion dementia”. Lancet, 341:8838 (January 16), 127-129, 1993.

192. Brown, P. “Prion dementia”: Author’s reply to Letters to the Editor

concerning Real and imagined clinicopathological limits of “prion

dementia”. Lancet, 341:8845 (March 6), 627-628, 1993.

193. Gibbs, C.J., Jr., Asher, D.M., Brown, P.W., Fradkin, J.E. and
Gajdusek,

D.C. Creutzfeldt-Jakob disease infectivity of growth hormone derived

from human pituitary glands. New England Journal of Medicine, 328:5

(February 4), 358-359, 1993.

194. Goldfarb, L.G., Brown, P., Haltia, M., Ghiso, J., Frangione, B. and

Gajdusek, D.C. Synthetic peptides corresponding to different mutated

regions of the amyloid gene in familial Creutzfeldt-Jakob disease

show enhanced in vitro formation of morphologically different amyloid

fibrils. Proceedings of the National Academy of Sciences (USA),

90:10 (May 15), 4451-4454, 1993.

195. Brown, P. EEG findings in Creutzfeldt-Jakob disease (Questions and

Answers section). Journal of the American Medical Association, 269:

24 (June 23), 3168, 1993.

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1993 (Con’t.)

196. Brown, P. Infectious cerebral amyloidosis: clinical spectrum, risks

and remedies. In: “Developments in Biological Standardization”,

F. Brown, editor. Karger, Basal, 1993, volume 80, pp.91-101.

Also as abstract:

Brown, P. The clinico-pathologic features of transmissible human

spongiform encephalopathy, with a discussion of recognized risk

factors and preventive strategies. In: Abstracts of an International

Meeting on Transmissible Spongiform Encephalopathies: Impact on

Animal and Human Health, Heidelberg, June 23-24, 1992, p.4.

197. Goldfarb, L.G., Brown, P., Little, B.W., Cervenáková, L., Kenney, K.,

Gibbs, C.J., Jr. and Gajdusek, D.C. A new (two repeat) octapeptide

coding insert mutation in Creutzfeldt-Jakob disease. Neurology, 43:

11 (November), 2392-2394, 1993.

198. Barcikowska, M., Liberski, P.P, Boellaard, J.W., Brown, P.,

Gajdusek, D.C. and Budka, H. Microglia is a component of the

prion protein amyloid plaque in the Gerstmann-Sträussler-Scheinker

syndrome. Acta Neuropathologica, 85: 6 (May), 623-627, 1993.

199. Chapman, J., Brown, P., Goldfarb, L.G., Arlazoroff, A., Gajdusek, D.C.

and Korczyn, A.D. Clinical heterogeneity and unusual presentations

of Creutzfeldt-Jakob disease in Jewish patients with the PRNP codon

200 mutation. Journal of Neurology, Neurosurgery and Psychiatry, 56:

10 (October), 1109-1112, 1993.

1994

200. Brown, P. Transmissible human spongiform encephalopathy

(infectious cerebral amyloidosis): Creutzfeldt-Jakob disease,

Gerstmann-Sträussler-Scheinker syndrome, and kuru. Chapter 48

in: “Neuro-degenerative Diseases”, D.B. Calne, editor.

W.B. Saunders Co., Philadelphia, 1994, pp.839-876.

201. Brown, P. Infectious cerebral amyloidoses: Creutzfeldt-Jakob disease

and the Gerstmann-Sträussler-Scheinker syndrome. Chapter 14 in:

“Handbook of Dementing Illnesses”, J C. Morris, editor. Marcel

Dekker, Inc., New York, 1994, pp.353-375.

Also as abstract:

Brown, P. Clinical and laboratory diagnosis of spongiform

encephalopathy. XIVth European Congress of Pathology, September

5-10, 1993, Innsbruck, Austria. Pathology Research and Practice,

189: 6-7 (August), 661, 1993.

202. Brown, P., Cervenáková, L., Goldfarb, L.G., Gajdusek, D.C.,

Haverkamp, A., Haverkamp, C., Horwitz, J., Creacy, S.D., Bever, R.A.,

Wexler, P., Sujansky, E. and Bjork, R.J. Molecular genetic testing of a

fetus at risk of Gerstmann-Sträussler Scheinker syndrome. Lancet, 343:

8890 (January 15), 181-182, 1994.

203. Goldfarb, L.G., Brown, P., Cervenáková, L. and Gajdusek, D.C.

Genetic analysis of Creutzfeldt-Jakob disease and related disorders.

Philosophical Transactions of the Royal Society of London (Series B),

343: 1306 (March 29), 379-384, 1994.

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1994 (Con’t.)

204. Brown, P., Goldfarb, L.G., Cervenáková, L., McCombie, W.R.,

Rubenstein, R., Will, R.G., Pocchiari, M., Martinez-Lage, J.F., Scalici,

C., Masullo, C, Graupera, G., Ligan, J. and Gajdusek, D.C. Iatrogenic

Creutzfeldt-Jakob disease: an example of the interplay between ancient

genes and modern medicine. Neurology, 44: 2 (February), 291-293, 1994.

205. Monari, L., Chen, S.G., Brown, P., Parchi, P., Petersen, R.B.,

Mikol, J., Gray, F., Cortelli, P., Montagna, P., Ghetti, B., Goldfarb,

L.G., Gajdusek, D.C., Lugaresi, E., Gambetti, P. and Autilio-Gambetti,

L. Fatal familial insomnia and familial Creutzfeldt-Jakob disease:

different prion proteins determined

by a DNA polymorphism. Proceedings of the National Academy of Sciences

(USA), 91: 7 (March 29), 2839-2842, 1994.

206. Lane, K.L., Brown, P., Howell, D.N., Crain, B.J., Hulette, C.M.,

Burger, P.C. and DeArmond, S.J. Creutzfeldt-Jakob disease in a pregnant

woman with an implanted dura mater graft. Neurosurgery,

34: 4 (April), 737-740, 1994.

207. Alperovitch, A., Brown, P., Weber, T., Pocchiari, M., Hofman, A.
and Will,

R. Incidence of Creutzfeldt-Jakob disease in Europe in 1993. Lancet,

343: 8902 (April 9), 918, 1994.

208. Garruto, R.M. and Brown, P. Tau protein, aluminium, and Alzheimer’s

disease (Commentary). Lancet, 343: 8904 (April 23), 989, 1994.

209. Brown, P., Gibbs, C.J., Jr., Rodgers-Johnson, P., Asher, D.M.,

Sulima, M.P., Bacote, A., Goldfarb, L.G. and Gajdusek, D.C.

Human spongiform encephalopathy: the National Institutes of

Health Series of 300 cases of experimentally transmitted disease.

Annals of Neurology, 35: 5 (May), 513-529, 1994.

210. Brown, P. The “brave new world” of transmissible spongiform

encephalopathy (infectious cerebral amyloidosis). Molecular

Neurobiology, 8: 2-3 (April-June), 79-87, 1994.

211. Goldfarb, L.G., Brown, P., Cervenáková, L. and Gajdusek, D.C.

Molecular genetic studies of Creutzfeldt-Jakob disease.

Molecular Neurobiology, 8: 2-3 (April-June), 89-97, 1994.

212. Petersen, R.B., Goldfarb, L.G., Tabaton, M., Brown, P., Monari, L.,

Cortelli, P., Montagna, P., Autilio-Gambetti, L., Gajdusek, D. C.,

Lugaresi, E. and Gambetti, P. A novel mechanism of phenotypic

heterogeneity demonstrated by the effect of a polymorphism on a

pathogenic mutation in the PRNP (prion protein gene). Molecular

Neurobiology, 8: 2-3 (April-June), 99-103, 1994.

213. Brown, P., Cervenáková, L., Boellaard, J.W., Stavrou, D., Goldfarb,
L.G.

and Gajdusek, D.C. Identification of a PRNP mutation in Jakob’s

original Creutzfeldt-Jakob disease family. Lancet, 344: 8915

(July 9), 130-131, 1994.

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1994 (Con’t.)

214. Haltia, M., Viitanen, M., Sulkava, R., Ala-Hurula, V., Poyhonen, M.,

Goldfarb, L., Brown, P., Levy, E., Houlden, H., Crook, R., Goate, A.,

Clark, R., Korenblat, K., Pandit, S., Keller, H.D., Lilius, L.,

Liu, L., Axelman, K., Forsell, L., Winblad, B., Lannfelt, L. and Hardy,

J. Chromosome 14-encoded Alzheimer’s disease: genetic and

clinicopathological description. Annals of Neurology, 36: 3

(September), 362-367, 1994.

215. Brown, P. [Debate] Vertical transmission of prion disease [response

to an article entitled “The transmission of prion disease: vertical

transfer of prion disease” by R.W. Lacey and S.F. Dealler]. Human

Reproduction, 9: 10 (October), 1796-1797, 1994.

216. Martinez-Lage, J.F., Poza, M., Sola, J., Tortosa, J.G., Brown, P.,

Cervenáková, L., Esteban, J.A. and Mendoza, A. Accidental transmission

of Creutzfeldt-Jakob disease by dural cadaveric grafts. Journal of

Neurology, Neurosurgery and Psychiatry, 57: 10 (October), 1091-1094,

1994.

217. Cervenáková, L., Brown, P., Goldfarb, L.G., Nagle, J., Pettrone, K.,

Rubenstein, R., Gibbs, C.J., Jr and Gajdusek, D.C. Infectious amyloid

precursor gene sequences in primates used for experimental transmission

of human spongiform encephalopathy. Proceedings of the National Academy

of Sciences (USA), 91, 25, (December 6), 12159-12162, 1994.

1995

218. Goldfarb, L.G. and Brown, P. The transmissible spongiform

encephalopathies. Annual Review of Medicine, 46: 57-65, 1995.

219. Lang, C.J.G., Schüler, P., Engelhardt, A., Spring, A. and Brown, P.

Probable Creutzfeldt-Jakob disease after a cadaveric dural graft.

European Journal of Epidemiology, 11: 1 (February), 79-81, 1995.

220. Billette de Villemeur, T., Fournier, J-G., Robain, O., Escaig-Haye,
F. and

Brown, P. Electronmicroscopic detection of prion-protein-positive

fibres in brain from iatrogenic Creutzfeldt-Jakob disease. Lancet, 345:

8953 (April 1), 861-862, 1995.

221. Barcikowska, M., Kwiecinski, H., Liberski, P.P., Kowalski, J.,

Brown, P. and Gajdusek, D.C. Creutzfeldt-Jakob disease with Alzheimer-

type Ab-reactive amyloid plaques. Histopathology,

26:5 (May), 445-450, 1995.

222. Reder, A.T., Mednick, A.S., Brown, P., Spire, J.P., Van Cauter, E.,

Wollmann, R.L., Cervenáková, L., Goldfarb, L.G., Garay, A.,

Ovsiew, F., Gajdusek, D.C. and Roos, R.P. Clinical and genetic studies

of fatal familial insomnia. Neurology, 45: 6 (June),

1068-1075, 1995. Also as abstract:

Mednick, A.S., Reder, T., Spire, J.P., Van Cauter, E., Brown, P.,

Wollmann, R.L., Goldfarb, L.G., Garay, A., Ovsiew, F., Gajdusek, D.C.

and Roos, R.P. Fatal familial insomnia (FFI). Proceedings of the 46th

Annual Meeting of the American Academy of Neurology, May 1-7, 1994 in

Washington, D.C. (Abstract 629P). Neurology, 44: (Suppl 2)

4 (April), A285-286, 1994.

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1995 (Con’t.)

223. Hainfellner, J.A., Brantner-Inthaler, S., Cervenáková, L., Brown, P.,

Kitamoto, T., Tateishi, J., Diringer, H., Liberski, P.P., Regele, H.,

Feucht, M., Mayr, N., Wessely, P., Summer, K., Seitelberger, F. and

Budka, H. The original Gerstmann-Stäussler-Scheinker family of Austria:

divergent clinicopathological phenotypes but constant PrP genotype.

Brain Pathology, 5: 3 (July), 201-211, 1995.

224. Budka, H., Aguzzi, A., Brown, P., Brucher, J-M., Bugiani, O.,

Collinge, J., Diringer, H., Gullotta, F., Haltia, M., Hauw, J-J.,

Ironside, J.W., Kretzschmar, H.A., Lantos, P.L., Masullo, C., Pocchiari,

M., Schlote, W., Tateishi, J. and Will, R.G. Consensus Report: Tissue

handling in suspected Creutzfeldt-Jakob disease (CJD) and other human

spongiform encephalopathies (prion diseases). Brain Pathology, 5: 3

(July), 319-322, 1995.

225. Budka, H., Aguzzi, A., Brown, P., Brucher, J-M., Bugiani, O.,

Gullotta, F., Haltia, M., Hauw, J.-J., Ironside, J.W., Jelinger, K.,

Kretzschmar, H.A., Lantos, P.L., Masullo, C., Schlote, W.,

Tateishi, J. and Weller, R.O. Consensus Report: Neuropathological

diagnostic criteria for Creutzfeldt-Jakob disease (CJD) and other human

spongiform encephalopathies (prion diseases). Brain Pathology, 5: 3

(July), 459-466.

226. Tateishi, J., Brown, P., Kitamoto, T., Hoque, Z.M., Roos, R.,

Wollman, R. and Gajdusek, D.C. First experimental transmission

of fatal familial insomnia. Nature, 376: 6539 (August 3), 434-435,

1995.

227. Brown, P., Kenney, K., Little, B., Ironside, J., Will, R.,

Cervenáková, L., San Martin, R.A., Safar, J., Roos, R., Harris, S.,

Haltia, M., Gibbs, C.J., Jr. and Gajdusek, D.C. Intracerebral

distribution of infectious amyloid protein in spongiform encephalopathy.
Annals of Neurology, 38: 2 (August), 245-253, 1995.

Also as abstract:

Brown, P., Kenney, K., Little, B., Ironside, J., Safar, J., Rohwer, R.,

Roos, R., Wollmann, R., Gibbs, C.J., Jr and Gajdusek, D.C. Comparison

of clinical features, neuropathology, and intracerebral distribution of

PrP amyloid protein in the brains of patients with spongiform

encephalopathy. Neurobiology of Aging, 15 (Supplement 1), p.S150

(Abstract No. 619), 1994.

228. Beekes, M., Baldauf, E., Cassens, S., Diringer, H., Keyes, P.,

Scott, A.C., Wells, G.A.H., Brown, P., Gibbs, C.J., Jr. and

Gajdusek, D.C. Western blot mapping of disease-specific amyloid

in various animal species and humans with transmissible spongiform

encephalopathies using a high-yield purification method.

Journal of General Virology, 76: 10 (October), 2567-2576, 1995.

229. Brown, P. Can Creutzfeldt-Jakob disease be transmitted by transfusion?

Current Opinion in Hematology, 2: 6 (November), 472-477, 1995.

230. Brown, P. [Education and Debate] Creutzfeldt-Jakob disease and bovine

spongiform encephalopathy: any connection? The jury is still out.

British Medical Journal, 311: 7017 (November 25), 1416, 1995.

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231. Masullo, C., Brown, P.W. and Macchi, G. Creutzfeldt-Jakob disease

in an Iranian: the first clinico-pathologically described case.

Clinical Neuropathology, 15: 1 (January), 26-29, 1996.

232. Budka, H., Aguzzi, A., Brown, P., Brucher, J.-M., Bugiani, O.,

Collinge, J., Diringer, H., Gullotta, F., Haltia, M., Hauw, J.-J.,

Ironside, J.W., Kretzschmar, H.A., Lantos, P.L., Masullo, C.,

Pocchiari, M., Schlote, W., Tateishi, J. and Will, R.G.

Konsensusbericht: gewebsbehandlung bei verdacht auf Creutzfeldt-Jakob-

Krankheit und andere spongiforme enzephalopathien (prionen-krankeiten)

des menschen. Pathologe, 17: 2 (February), 171-176, 1996.

233. Chapman, J., Arlazoroff, A., Goldfarb, L.G., Cervenáková, L., Neufeld,

M.Y., Werber, E., Herbert, M., Brown, P., Gajdusek, D.C. and Korczyn,

A.D. Fatal insomnia in a case of familial Creutzfeldt-Jakob disease

with the codon 200Lys mutation. Neurology, 46: 3 (March), 758-761,

1996.

234. Liberski, P., Yanagihara, R., Brown, P., Kordek, R., Kloszewska, I.,

Bratosiewicz., J. and Gajdusek, D.C. Microwave treatment enhances the

immunostaining of amyloid deposits in both the transmissible

and non-transmissible brain amyloidoses. Neurodegeneration, 5: 1

(March), 95-99, 1996.

235. Brown, P. Bovine spongiform encephalopathy and Creutzfeldt-Jakob
disease:

the link is unproved but no better explanation is presently

forthcoming. British Medical Journal, 312: 7034 (March 30), 790-791,

1996.

236. Salvatore, M., Galvez, S., Brown, P., Macchi, G., Fieschi, C.,

Cardone, F., Petraroli, R., Colosimo, C., D'Allessandro, M. and

Pocchiari, M. Codon 200 mutation in a new Creutzfeldt-Jakob disease

family of Chilean origin. Journal of Neurology, Neurosurgery, and

Psychiatry, 61: 1 (July), 111-112, 1996.

237. Brown, P. Environmental causes of human spongiform encephalopathy.

In: “Methods in Molecular Medicine: Prion diseases", H. Baker and

R. Ridley, editors, Humana Press, Totowa, New Jersey, pp.139-154, 1996.

238. Brown, P. Transmissible cerebral amyloidosis. Journal of Neural

Transmission, Supplement 47, 219-229, 1996.

239. Scrimgeour, E.M., Brown, P and Monaghan, P. Disposal of rendered

specified offal. Veterinary Record, 139: 9 (August 31), 219-220, 1996.

240. Cochran, E.J., Bennett, D.A., Cervenáková, L., Kenney, K., Bernard,
B.,

Foster, N.L., Benson, D.F., Goldfarb, L.G. and Brown, P. Familial

Creutzfeldt-Jakob disease with a five-repeat octapeptide insert

mutation. Neurology, 47: 9 (September), 727-733, 1996.

241. Scrimgeour, E.M., Chand, P.R., Kenney, K. and Brown, P.
Creutzfeldt-Jakob

disease in Oman: report of two cases. Journal of the Neurological

Sciences, 142: 1-2 (October), 148-150, 1996.

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1996 (Con’t.)

242. Will, R.G., Zeidler, M., Brown, P., Harrington, M., Lee, K.H. and

Kenney, K.L. Cerebrospinal-fluid test for new-variant Creutzfeldt-Jakob

disease. Lancet, 348: 9032 (October 5), 955, 1996.

243. Silburn, P., Cervenáková, L., Varghese, P., Tannenberg, A., Brown,
P. and

Boyle, R. Fatal familial insomnia -a seventh family. Neurology, 47: 5

(November), 1326-1328, 1996.

244. El Hachimi, K.H., Cervenáková, L., Brown, P., Goldfarb, L.G.,
Rubenstein,

R., Gajdusek, D.C. and Foncin, J.-F. Mixed features of Alzheimer

disease and Creutzfeldt-Jakob disease in a family with a presenilin-1

mutation in chromosome 14. Amyloid, 3: 4 (December), 223-233, 1996.

245. Goldfarb, L.G., Cervenáková, L., Brown, P. and Gajdusek, D.C.

Genotype-phenotype correlations in familial spongiform

encephalopathies associated with insert mutations. In:

"Transmissible Subacute Spongiform Encephalopathies: Prion Diseases".

(Proceedings of the IIIrd International Symposium on Transmissible

Subacute Spongiform Encephalopathies: Prion Diseases, 18-20 March

1996, Val de Grâce, Paris, France). L. Court and

B. Dodet, editors, Elsevier, Amsterdam, 1996 pp.425-431.

246. Cervenáková, L., Brown, P., Piccardo, P., Cummings, J.L., Nagle, J.,

Vinters, H.V., Kaur, P., Ghetti, B., Gajdusek, D.C. and Goldfarb,

L.G. 24-nucleotide deletion in the PRNP gene: analysis of associated

phenotypes. In: "Transmissible Subacute Spongiform Encephalopathies:

Prion Diseases". (Proceedings of the IIIrd International Symposium

on Transmissible Subacute Spongiform Encephalopathies: Prion

Diseases, 18-20 March 1996, Val de Grâce, Paris, France). L. Court

and B. Dodet, editors, Elsevier, Amsterdam, 1996, pp.433-444.

247. Brown, P. The risk of blood-borne Creutzfeldt-Jakob disease.

In: "Transmissible Subacute Spongiform Encephalopathies: Prion

Diseases". (Proceedings of the IIIrd International Symposium on

Transmissible Subacute Spongiform Encephalopathies: Prion Diseases,

18-20 March 1996, Val de Grâce, Paris, France). L. Court and

B. Dodet, editors, Elsevier, Amsterdam, 1996, pp.447-431.

Also, with slight modification:

Brown, P. The risk of blood-borne Creutzfeldt-Jakob disease.

In: Proceedings of the 4th NATO Military and Civil Blood Conference, The

Hague, The Netherlands, 5-8 May, 1996. Netherlands Military Medical

Review, vol.49 (June-December), pp.37-38.

248. Hainfellner, J.A., Liberski, P.P., Guiroy, D.C., Cervenáková, L.,

Brown, P., Gajdusek D.C. and Budka, H. Pathology and
immunohistochemistry of a kuru brain. Brain Pathology, 7: 1 (January),

547-554, 1997.

249. Epstein, L.G. and Brown, P. Bovine spongiform encephalopathy and a

new variant of Creutzfeldt-Jakob disease. Neurology, 48: 3 (March),

569-571, 1997.

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1997 (Con’t.)

250. Parchi, P. Capellari, S., Chen, S.G., Petersen, R.B., Gambetti, P.,

Kopp, N., Brown, P., Kitamoto T., Tateishi, J., Giese, A. and

Kretzschmar, H. Typing prion isoforms. Nature, 386: 6622

(March 20), 232-234, 1997.

251. Liberski, P.P., Brown, P., Cervenáková, L. and Gajdusek, D.C.

Interactions between astrocytes and oligodendroglia in human and

experimental Creutzfeldt-Jakob disease and scrapie. Experimental

Neurology, 144: 1 (March), 227-234, 1997.

252. El Hachimi, K.H., Chaunu, M.-P., Cervenáková, L., Brown, P. and

Foncin, J.-F. Putative neurosurgical transmission of Creutzfeldt-

Jakob disease with analysis of donor and recipient agent strains.

Comptes Rendus de l’Académie des Sciences (Paris), 320: 4 (April),

319-328, 1997.

253. Cervenáková, L., Rohwer, R., Williams, E.S., Brown, P. and

Gajdusek, D.C. High sequence homology of the PrP gene in mule deer

and Rocky Mountain elk. Lancet, 350: 9072 (July 19), 219-220, 1997.

254. McLean, C.A., Storey, E., Gardner, R.J.M., Tannenberg, A.E.G,

Cervenáková, L. and Brown, P. The D178N (cis-129M) "fatal familial

insomnia" mutation associated with diverse clinicopathological

phenotypes in an Australian kindred. Neurology, 49: 2 (August),

552-558, 1997.

255. Chen, S.G., Parchi, P., Brown, P., Capellari, S., Zou, W.,

Cochran, E.J., Vnencak-Jones, C.L., Julien, J., Vital, C., Mikol, J.,

Lugaresi, E., Autilio-Gambetti, L. and Gambetti, P. Allelic origin

of the abnormal prion protein isoform in familial prion diseases.

Nature Medicine, 3: 9 (September), 1009-1015, 1997.

256. Heckmann, J.G., Lang, C.J.G., Petruch, F., Druschky, A., Erb, C.,

Brown, P. and Neundörfer, B. Transmission of Creutzfeldt-Jakob

disease via a corneal transplant. Journal of Neurology,

Neurosurgery, and Psychiatry, 63: 3 (September), 388-390, 1997.

257. Brown, P. The risk of bovine spongiform encephalopathy ("mad cow

disease") to human health. Journal of the American Medical

Association, 278: 12 (September 24), 1008-1011, 1997.

258. Liberski, P.P., Brown, P. and Gajdusek, D.C. The evolution of views

on the nosological position of transmissible spongiform
encephalopathies. Folia Neuropathologica, 35: 4 (October-December),
214-225,

1997.

259. Walis, A., Liberski, P.P., Brown, P. and Gajdusek, D.C. Electron

microscopic studies of the optic nerve in experimental scrapie and

the panencephalopathic type of Creutzfeldt-Jakobd disease. Folia

Neuropathologica, 35: 4 (October-December), 255-258, 1997.

260. Martínez-Lage, J.F, Poza, M., Brown, P., Cervenáková, L., Bremón, A.R.

and de Pedro, J. Enfermedad de Creutzfeldt-Jakob en Neurocirugía:

una revisión de riesgos y medidas de prevención. Neurocirugía,

8: 4 (December), 284-293, 1997.

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1997 (Con’t.)

261. Brown, P. Spongiform encephalopathies: B-lymphocytes and

neuroinvasion. (News and Views). Nature, 390: 6661 (December

18/25), 662-663, 1997.

262. Brown, P., Cervenáková, L., McShane, L., Goldfarb, L.G., Bishop, K.,

Bastian, F., Kirkpatrick, J., Piccardo, P., Ghetti, B. and

Gajdusek, D.C. Creutzfeldt-Jakob disease in a husband and wife.

Neurology, 50: 3 (March), 684-688, 1998.

263. Brown, P. Donor pool size and the risk of blood-borne Creutzfeldt-

Jakob disease. Transfusion, 38: 3 (March), 312-315, 1998.

264. Zeidler, M. and Brown, P. More patients should be excluded from

being tissue donors. British Medical Journal, 316: 7138 (April 11),

1170-1171, 1998.

265. Brown, P. Commentary. BSE: the final resting place. Lancet, 351:

9110 (April 18), 1146-1147, 1998.

266. Fournier, J-G., Escaig-Haye, F., Billette de Villemeur, T., Robain,
O.,

Lasmézas, C.L., Deslys, J-P., Dormont, D. and Brown, P. Distribution

and submicroscopic immunogold localization of cellular prion protein

(PrPc) in extracerebral tissues. Cell and Tissue Research, 292: 1

(April), 77-84, 1998.

267. Heldt, N., Boellaard, J.W., Brown, P., Cervenáková, L.,

Doerr-Schott, J., Thomas, C., Scherer, C. and Rohmer, F.

Gerstmann-Sträussler-Scheinker disease with A117V mutation in

a second French-Alsatian family. Clinical Neuropathology, 17: 4

(July-August), 229-234, 1998.

268. Parchi, P., Chen, S.G., Brown, P., Zou, W., Capellari, S., Budka, H.,

Hainfellner, J., Reyes, P.F., Golden, G., Hauw, J.J., Gajdusek, D.C.

and Gambetti, P. Different patterns of truncated prion protein

fragments correlate with distinct phenotypes in P102L Gerstmann-

Sträussler-Scheinker disease. Proceedings of the National Academy

of Sciences (USA), 95: 14 (July 7), 8322-8327, 1998.

269. Brown, P. Commentary. On the origins of BSE. Lancet, 352: 9124

(July 25), 252-253, 1998.

270. Zanusso, G., Liu, D., Ferrari, S., Hegyi, I., Yin, X., Aguzzi, A.,

Hornemann, S., Liemann, S., Glockshuber, R., Manson, J.C., Brown, P.,

Petersen, R.B., Gambetti, P. and Sy, M-S. Prion protein expression

in different species: analysis with a panel of new mABs. Proceedings

of the National Academy of Sciences (USA), 95: 15 (July 21), 88128816,
1998.

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1998 (Con’t.)

271. McLean, C.A., Ironside, J.W., Alpers, M., Cervenáková, L.,

Anderson, R.McD., Brown, P.W. and Masters, C.L. Comparative

neuropathology of kuru with the new variant of Creutzfeldt-Jakob

disease: evidence for strain of agent predominating over genotype

of host. Brain Pathology, 8: 3 (July), 429-437, 1998.

272. Brown, P., Cervenáková, L. and Powers, J.M. FFI cases from the United

States, Australia, and Japan. Brain Pathology, 8: 3 (July), 567-570,

1998.

273. Chapman, J., Cervenáková, L., Petersen, R.B., Estupinan, J.,

Richardson, S., Vnencak-Jones, C.L., Gambetti, P., Gajdusek, D.C.,

Korczyn, A.D., Brown, P. and Goldfarb, L.G. APOE in non-Alzheimer

amyloidoses: transmissible spongiform encephalopathies. Neurology,

51, 2 (August), 548-553, 1998.

274. Brown P., Rohwer, R.G., Dunstan, B.C., MacAuley, C., Gajdusek, D.C.
and

Drohan, W.N. The distribution of infectivity in blood components and

plasma derivatives in experimental models of transmissible spongiform

encephalopathy. Transfusion, 38: 9 (September), 810-816, 1998.

275. Brown, P. Author’s Reply to a Letter to the Editor: Origins of BSE.

Lancet, 352: 9133 (September 26), 1068-1069, 1998.

276. Brown, P. Transmission of spongiform encephalopathy through biological

products. In: “Developments in Biological Standardization”.

Brown, F., Griffiths, E., Horaud, F. and Petricciani, J.C., editors.

Developments in Biological Standardization, volume 93, Karger, Basel,

1998, pp.73-78.

277. Brown, P., Cervenáková, L., McShane, L., Kleihues, P., Foncin, J.-F.,

Collins, G., Bastian, F., Goldfarb, L.G. and Gajdusek, D.C.

Polymorphic genotype matching in acquired Creutzfeldt-Jakob disease:

an analysis of donor/recipient case pairs. In “Prions and Brain

Diseases in Animals and Humans”. D.R.O. Morrison, editor. Nato ASI

Series A: Life Sciences volume 295, Plenum, New York, 1998, pp.19-24.

278. Piccardo, P., Dlouhy, S.R., Lievens, P.M.J., Young, K., Bird, T.D.,

Nochlin, D., Dickson, D.W., Vinters, H.V., Zimmerman, T.R.,

Mackenzie, I.R.A., Kish, S.J., Ang, L-C., De Carli, C.,

Pocchiari, M., Brown, P., Gibbs, C.J., Jr., Gajdusek, D.C.,

Bugiani, O., Ironside, J., Tagliavini, F. and Ghetti, B.

Phenotypic variability of Gerstmann-Sträussler-Scheinker disease

is associated with prion protein heterogeneity. Journal of
Neuropathology and Experimental Neurology, 57: 10 (October) 979-988, 1998.

279. Liberski, P.P., Barcikowska, M., Cervenáková, L., Bratosiewicz, J.,

Marczewska, M., Brown, P. and Gajdusek, D.C. A case of sporadic

Creutzfeldt-Jakob disease with a Gerstmann-Sträussler-Scheinker

phenotype but no alterations in the PRNP gene.

(Berlin), 96: 4 (October), 425-430, 1998.

Acta Neuropathologica

280. Liberski, P.P., Kordek, R., Brown, P. and Gajdusek, D.C. Astrocytes in

transmissible spongiform encephalopathies (prion diseases). Chapter 7

in: “Astrocytes in Brain Aging and Neurodegeneration”, Schipper,H.M.,

editor, R.G. Landes Co., Austin, Texas, 1998, pp.127-163.

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1998 (Con’t.)

281. Cervenáková, L., Goldfarb, L.G., Garruto, R., Lee, H.-E., Gajdusek,

D.C. and Brown, P. Phenotype-genotype studies in kuru: implications

for new variant Creutzfeldt-Jakob disease. Proceedings of the

National Academy of Sciences (USA), 95: 22 (October 27), 1323913241, 1998.

282. El Hachimi, K.H., Chaunu, M.-P., Brown, P. and Foncin, J.-F.

Modification of oligodendroglial cells in spongiform

encephalopathies. Experimental Neurology, 154: 1 (November),

23-30, 1998.

283. Brown, P. Transmissible spongiform encephalopathy. Chapter 43 in:

"Textbook of Clinical Neurology", Goetz, C.G. and Pappert, E.J.,

editors, W.B. Saunders Co., Philadelphia, 1998, pp.869-875.

284. Brown, P. Iatrogenic Creutzfeldt-Jakob disease. In: “Sterilization of

Medical Products”, Morrissey, R.F. and Kowalski, J.B., editors.

Proceedings of the VIIth International Kilmer Memorial Conference on

the Sterization of Medical Products, Scottsdale, Arizona, March 2-4,

1998. Polyscience Publications, Inc., Champlain NY, 1998, pp.212-218.

285. Brown, P. and Bradley, R. 1755 and all that: a historical primer of

transmissible spongiform encephalopathy. British Medical Journal,

317: 7174 (December 19-26), 1688-1692, 1998.

286. Hogan, R.N., Brown, P., Heck, E. and Cavanagh, H.D. Risk of prion

disease transmission from ocular donor tissue transplantation.

Cornea, 18: 1 (January/February), 2-11, 1999.

287. Bons, N., Mestre-Frances, N., Belli, P., Cathala, F., Gajdusek, D.C.

and Brown, P. Natural and experimental oral infection of nonhuman

primates by bovine spongiform encephalopathy agents. Proceedings of

the National Academy of Sciences (USA), 96: 7 (March 30); 4046-4051,

1999.

288. Lee, H.S., Sambuughin, N., Cervenáková, L., Chapman, J., Pocchiari,
M.,

Litvak, S., Qi, H.Y., Budka, H., del Ser, T., Furukawa, H.,

Brown, P., Gajdusek, D.C., Long, J.C., Korczyn, A. and Goldfarb, L.G.

Ancestral origins and worldwide distribution of the PRNP 200K

mutation causing familial Creutzfeldt-Jakob disease. American

Journal of Human Genetics, 64: 4 (April), 1063-1070, 1999.

289. Grigoriev, V., Escaig-Haye, F., Streichenberger, N., Kopp, N.,

Langeveld, J., Brown, P. and Fournier, J-G. Submicroscopic
immunodetection of PrP in the brain of a patient with a new-variant of

Creutzfeldt-Jakob disease. Neuroscience Letters, 264: 1-3 (April 2),

57-60, 1999.

290. Brown, P., Bradley, R. and Cathala, F. Bref historique des
encéphalopathies spongiformes transmissibles. Revue du Praticien: 49: 9

(May 1), 928-933, 1999.

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1999 (Con’t.)

291. Parchi, P., Giese, A., Capellari, S., Brown, P., Schulz-Schaeffer, W.,

Windl, O., Zerr, I., Budka, H., Kopp, N., Piccardo, P., Poser, S.,

Rojiani, A., Streichemberger, N., Julien, J., Vital, C., Ghetti, B.,

Gambetti, P. and Kretzschmar, H. Classification of sporadic

Creutzfeldt-Jakob disease based on molecular and phenotypic analysis

of 300 subjects. Annals of Neurology, 46, 2 (August), 224-233, 1999.

292. Brandel, J-P., Cathala, F. and Brown, P. Maladies à prions:

encéphalopathies spongiformes subaiguës transmissibles humaines et

animales. Chapitre 4 in: Neurogénétique. Affections hérédodégénératives,
A. Brice and D.F. Schorderet, editors. Doin, Paris,

1998, pp.35-61.

293. Brown, P. A brief history of scrapie before the prion. In:”The Science

and Culture Series”, K. Goebel, editor. International Seminar on

Nuclear War and Planetary Emergencies (23rd Session), Erice, Italy,

19-24 August 1998. World Scientific, Singapore, 1999, pp.35-36.

294. Brown, P. Transmissible spongiform encephalopathies. Chapter 59 in:

“Neurology in Clinical Practice”, W.G. Bradley, R.B. Daroff, G.M.

Fenichel and C.D. Marsden, editors. Butterworth-Heinemann, Newton

MA, 1999, volume II, pp.1423-1430.

295. Parchi, P., Brown, P., Capellari, S., Gibbs, C.J., Jr. and
Gambetti, P.

Agent strain variation in human prion diseases: insight from

transmission to primates. In: “Alzheimer’s Disease and Related

Disorders”, K. Iqbal, D.R. Swaab, B. Winblad and H.M. Wisniewski,

editors. John Wiley & Sons, London, 1999, pp.561-567.

Also as abstract:

Parchi, P., Brown, P., Capellari, S., Gibbs, C.J., Jr. and Gambetti, P.

Biochemical analysis of strain variation in human prion diseases:

insight from transmission to primates. Abstract No.722 in Book of

Abstracts, 6th International Conference on Alzheimer’s Disease and

Related Disorders, Amsterdam, July 18-23, 1998

296. Brown, P. The risk of blood-borne Creutzfeldt-Jakob disease. In:

“Developments in Biologicals”, Brown, F. and Vyas, G., editors.

Karger, Basel, 1999, volume 102, pp.53-59.

297. Boellaard, J.W., Brown, P. and Tateishi J. Gerstmann-Sträussler-

Scheinker disease -the dilemma of molecular and clinical

correlations. Clinical Neuropathology, 18, 6 (November-December),

271-285, 1999.

298. Brown, P., Cervenáková, L., McShane, L.M., Barber, P., Rubenstein, R.

and Drohan, W.N. Further studies of blood infectivity in an

experimental model of transmissible spongiform encephalopathy, with

an explanation of why blood products do not transmit Creutzfeldt-

Jakob disease. Transfusion, 39: 11/12 (November-December),

1169-1178, 1999.

299. Cervenáková, L., Buetefisch, C., Lee, H-S., Taller, I., Stone, G.,

Gibbs, C.J., Jr., Brown, P., Hallett, M. and Goldfarb, L.G. Novel

PRNP sequence variant associated with familial encephalopathy.

American Journal of Medical Genetics (Neuropsychiatric Genetics),

88: 6 (December), 653-656, 1999.

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1999 (Con’t.)

300. Dickson, D.W. and Brown, P. Multiple prion types in the same brain.

Is a molecular diagnosis of CJD possible? Neurology, 53: 9

(December), 1903-1904, 1999.

2000

301. Blanquet-Grossard, F., Sazdovitch, V., Jean, A., Deslys, J-P.,

Dormont, D., Hauw, J-J., Marion, D., Brown, P. and Cesbron, J.-Y.

Prion protein is not detectable in dental pulp from patients with

Creutzfeldt-Jakob disease. Journal of Dental Research, 79: 2

(February), 700, 2000.

302. Brown, P., Rau, E.H
 

flounder

Well-known member
302. Brown, P., Rau, E.H., Johnson, B.K., Bacote, A.E., Gibbs, C.J., Jr.
and

Gajdusek D.C. New studies on the heat resistance of hamster-adapted

scrapie agent: threshold survival after ashing at 600°C suggests an

inorganic template of replication. Proceedings of the National

Academy of Science (USA), 97: 7 (March 28), 3418-3421, 2000.

303. Brown, P. and Lamb, G. Creutzfeldt-Jakob disease and the mortuary

profession. The Director, 72: 3 (March), 58-62, 2000.

304. Majtényi, C., Brown, P., Cervenáková, L., Goldfarb, L.G. and
Tateishi, J.

A three-sister sibship of Gerstmann-Sträussler-Scheinker disease with

a CJD phenotype. Neurology, 54: 6 (June), 2133-2137, 2000.

305. Brown, P. and Cervenáková, L. Authors’ Reply to a Letter to the

Editor: Infectivity of buffy coat in variant CJD. Transfusion, 40: 6

(June), 754-755.

306. Fournier, J.C., Kopp, N., Streichenberger, N., Escaig-Haye, F.,

Langeveld, J. and Brown, P. Electron microscopy of brain amyloid

plaques from a patient with new variant Creutzfeldt-Jakob disease.

Acta Neuropathologica, 99: 6 (June), 637-642, 2000.

307. Parchi, P., Zou, W., Wang, W., Brown, P., Capellari, S., Ghetti, B.,

Kopp, N., Schulz-Schaeffer, W.J., Kretzschmar, H.A., Head, M.W.,

Ironside, J.W., Gambetti, P. and Chen, S.G. Genetic influence on the

structural variations of the abnormal prion protein. Proceedings of

the National Academy of Science (USA), 97: 18 (August 29), 1016810172,
2000.

308. Liberski, P.P., Bratosiewicz, J., Barcikowska, M., Cervenakova, L.,

Marczewska, M., Brown, P. and Gajdusek, D.C. A case of sporadic

Creutzfeldt-Jakob disease with a Gerstmann-Sträussler-Scheinker

phenotype but no alterations in the PRNP gene.

100: 2 (August), 233-234, 2000.

Acta Neuropathologica

309. Cervenáková, L., Protas, I.I., Hirano, A., Votiakov, V.I.,

Nedzved, M.K., Kolomiets, N.D., Taller, I., Park, K.-Y.,

Sambuughin, D., Gajdusek, D.C., Brown, P. and Goldfarb, L.G.

Progressive muscular atrophy variant of familial amyotrophic

lateral sclerosis (PMA/ALS). Journal of the Neurological Sciences,

177: 2 (August), 124-130, 2000.

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2000 (Con’t.)

310. Brown, P. BSE and transmission through blood [Commentary].

356: 9233 (September 16), 955-956, 2000.

Lancet,

311. Brown, P., Preece, M., Brandel, J.-P., Sato, T., McShane, L.,

Zerr, I., Fletcher, A., Will, R.G., Pocchiari, M., Cashman, N.R.,

d’Aignaux, J.H., Cervenáková, L., Fradkin, J., Schonberger, L.B. and

Collins, S.J. Iatrogenic Creutzfeldt-Jakob disease at the Millennium.

Neurology, 55: 8 (October 24), 1075-1081, 2000.

312. Goldfarb, L.G., Bütefisch, C. and Brown, P. Ataxia in the
transmissible

spongiform encephalopathies. In: Handbook of Ataxia Disorders,

T. Klockgether, editor. Marcel Dekker, New York, 2000, pp.523-543.

313. Brown, P. Risk of Creutzfeldt-Jakob disease associated with blood or

blood products. Proceedings of an INFARMED Workshop held in Evora,

Portugal, December 11-12, 1999. In: Jornada Sobre Medicamentos:

Hemoderivados e vCJD, J.A. da Silva, editor. INFARMED, Lisboa, 2000,

pp.79-84.

314. WHO Infection Control Guidelines for Transmissible Spongiform

Encephalopathies. Report of a WHO Consultation, Geneva, Switzerland,

23-26 March 1999. WHO/CDS/CSR/APH/2000.3

2001

315. Brown, P., Cervenáková, L. and Diringer, H. Blood infectivity and

the prospects for a diagnostic screening test in Creutzfeldt-Jakob

disease. Journal of Laboratory and Clinical Medicine, 137: 1

(January), 5-13, 2001. [Erratum 137: 4 (April), 230, 2001]

316. Lee, H.-S., Brown, P., Cervenáková, L., Garruto, R.M., Alpers, M.P.,

Gajdusek, D.C. and Goldfarb, L.G. Increased susceptibility to kuru

of PRNP 129 MM genotype carriers. Journal of Infectious Diseases,

183: 1 (January); 192-196, 2001.

317. Brown, P., Will, R.G., Bradley, R., Asher, D.M. and Detwiler, L.

Bovine spongiform encephalopathy and variant Creutzfeldt-Jakob

disease: background, evolution, and current concerns. Emerging

Infectious Diseases, 7: 1(January/February), 6-16, 2001.

318. Brown, P. The pathogenesis of transmissible spongiform encephalopathy:

routes to the brain and the possibility of therapeutic barricades.

Cellular and Molecular Life Sciences, 58: 1 (February): 259-265,

2001.

319. Brown, P. Authors’ Reply to a Letter to the Editor: Iatrogenic

Creutzfeldt-Jakob disease at the millennium. Neurology, 56: 7

(April 10) 987, 2001.

320. Liberski, P.P., Bratosiewicz, J., Walis, A., Kordek, R., Jeffrey, M.

and Brown, P. A special report. I.Prion protein (PrP) – amyloid

plaques in the transmissible spongiform encephalopathies, or prion

diseases revisited. Folia Neuropathology, 39: 4 (April), 217-235,

2001.

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2001 (Con’t.)

321. Kennedy, R.H., Hogan, R.N., Brown, P., Holland, E., Johnson, R.T.,

Stark, W. and Sugar, J. Eye banking and screening for Creutzfeldt-

Jakob disease. Archives of Ophthalmology, 119: 5 (May); 721-726,

2001.

322. Brown, P. Afterthoughts about bovine spongiform encephalopathy and

variant Creutzfeldt-Jakob disease. Emerging Infectious Diseases,

7: 3 (June Supplement), 598-600, 2001.

323. Brown, P.

tests.

2001.

Creutzfeldt-Jakob disease: blood infectivity and screening

Seminars in Hematology, 38: 4 (October, Supplement 9), 2-6,

324. Brown, P. Transmissible Spongiform Encephalopathies. Chapter 29 in

“Baker’s Clinical Neurology”. R.J. Joynt and R.C. Griggs, editors.

CD-ROM, Lippincott Williams & Wilkins, Baltimore, 2001.

325. Panegyres, P.K., Toufexis, K., Kakulas, B.A., Cervenáková, L.,

Brown, P., Ghetti, B., Piccardo, P. and Dlouhy, S.R. A new PRNP

mutation (G131V) associated with Gerstmann-Sträussler-Scheinker

disease. Archives of Neurology, 58: 11 (November), 1899-1902, 2001.

326. Brown, P. Transmissible spongiform encephalopathies. In: “Early Onset

Dementia”, Hodges, J.R., editor. Oxford University Press, Oxford,

2001, pp.367-384.

327. Brown P. The scientist’s dilemma. In: “Proceedings of Joint

WHO/FAO/OIE Technical consultation on BSE: public health, animal

health and trade”, Paris, 11-14 June, 2001, pp.74-75.

328. Bons, N., Lehmann, S., Nishida, N., Mestre-Frances, N., Dormont, D.,

Belli, P., Delacourte, A., Grassi, J. and Brown, P. BSE infection of

the small short-lived primate Microcebus murinus. Comptes Rendus de

l’Academie de Science (Paris) 325: 12 (December), 1-8, 2001.

329. Cervenáková, L., Brown, P., Hammond, D.J., Lee, C.A. and Saenko, E.L.

Factor VIII and transmissible spongiform encephalopathy: the case for

safety. Hemophilia, 8: 2 (March) 63-75, 2002.

330. Brown P. What are the current human risks from mad cow disease? MD

Consult Infectious Disease, May 9, 2002. http://www.mdconsult.com

331. Liberski, P.P., Bratosiewicz-Wasik, J., Gajdusek, D.C. and Brown, P.

Ultrastructural studies of experimental scrapie and Creutzfeldt-Jakob

disease in hamsters. I. Alterations of myelinated axons. Acta

Neurobiologiae Experimentalis, 63: 3 (June), 121-129, 2002.

332. Liberski, P.P., Bratosiewicz-Wasik, J., Gajdusek, D.C. and Brown, P.

Ultrastructural studies of experimental scrapie and Creutzfeldt-Jakob

disease in hamsters. II. Astrocytic and macrophage reaction towards

axonal destruction. Acta Neurogiologiae Experimentalis, 63: 3

(June), 131-139, 2002.

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2002 (Con’t.)

333. Liberski, P.P., Gajdusek, D.C. and Brown, P. How do neurons degenerate

in prion diseases or transmissible spongiform encephalopathies

(TSE’s): neuronal autophagy revisited. Acta Neurogiologiae

Experimentalis, 63: 3 (June), 141-147, 2002.

334. Brown, P. Current issues related to the origin and etiology of BSE.

Relationship with variant Creutzfeldt-Jakob disease. In: “Report

of the PAHO/WHO Consultation on Bovine Spongiform Encephalopathy:

Scientific Bases for Policy Decisions in the Americas”, Montevideo,

Uruguay, 9-11 April 2001. Veterinary Public Health Program, Pan

American Health Organization, Washington, D.C., 2002.

335. Bons, N., Lehmann, S., Mestre-Francès, N., Dormont, D. and Brown, P.

Brain and buffy coat transmission of bovine spongiform encephalopathy

(BSE) to the primate Microcebus murinus. Transfusion, 42: 5 (May),

513-517, 2002.

336. Brown, P. Drug therapy in human and experimental transmissible

spongiform encephalopathy. Neurology, 58: 12 (June 25), 1720-1725,

2002.

337. Brown, P. Transmission of Creutzfeldt-Jakob disease by transfusion.

In: “Rossi’s Principles of Transfusion Medicine”, 3rd Edition.

T.L. Simon, W.H. Dzik, E.L. Snyder, C.P. Stowell and R.G. Strauss,

editors. Lippincott Williams & Wilkins, Philadelphia, 2001,

pp.784-788.

338. Dagvadorj, A., Petersen, R.B, Lee, H.S., Cervenakova,L, Budka, H.,

Boyle, R., Brown, P., Gambetti, P. and Goldfarb, L.G. Spontaneous

mutations in the prion protein gene causing transmissible spongiform

encephalopathy. Annals of Neurology, 52: 9 (September), 355-359,

2002.

339. Stenland C.J., Lee, D.C., Brown, P., Ironside, J., Petteway, S.R., Jr.

and Rubenstein, R. Partitioning of human and sheep forms of the

pathogenic prion protein during the purification of therapeutic

proteins from human plasma. Transfusion, 42: 11 (November),

1497-1500, 2002.

340. Brown, P. Special precautions for autopsies of patients with

Creutzfeldt-Jakob disease. Chapter 13 in: “Autopsy Performance and

Reporting”, K.A. Collins and G.M. Hutchins, editors, College of

Amercian Pathologists, Northfield, Illinois, 2003, pp.105-110.

341. Cervenáková, L., Brown, P., Soukharev, S., Yakovleva, O., Diringer,
H.,

Saenko, E.L. and Drohan, W.N. Failure of immunocompetitive

capillary electrophoresis assay to detect disease-specific prion

protein in buffy coat from humans and chimpanzees with Creutzfeldt-

Jakob disease. Electrophoresis, 24: 6 (March), 853-859, 2003.

20


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2003 (Con’t.)

342. Ricketts, M. and Brown, P. Transmissible spongiform encephalopathy:

update and implications for blood safety. Clinics in Laboratory

Medicine, 23: 1 (March), 129-137, 2003.

343. Liberski, P.P., Sikorska, B., Bratosiewicz-Wasik, J., Walis, A,

Brown, P. and Brown, D. Exuberant cellular reaction of the optic

nerves in experimental Creutzfeldt-Jakob disease. Acta

Neurobiologiae Experimentalis, 63: 3 (March), 309-318, 2003.

344. Brown, P., Transmissible Spongiform Encephalopathy as a Zoonotic

Disease. ILSI Europe Report Series, International Life Sciences

Institute, ILSI Press, Brussels, March 2003, 47 pp.

345. Brown, P. Variant CJD transmission through blood: risks to predictors

and “predictees”. Transfusion, 43: 4 (April), 425-427, 2003.

346. Brown, P., Meyer, R., Cardone, F. and Pocchiari, M.
Ultra-highpressure inactivation of prion infectivity in processed meat: a

practical method to prevent human infection. Proceedings of the

National Academy of Science (USA), 100: 10 (May 13), 6093-6097,

2003.

347. WHO Guidelines on Transmissible Spongiform Encephalopathies in
relation

to Biological and Pharmaceutical Products. Report of a WHO

Consultation, Geneva, Switzerland, 3-5 February 2003.

http://www.who.int/bloodproducts/tse/en

348. Brown, P. Creutzfeldt-Jakob disease (CJD). In: “Encyclopedia of the
Neurological Sciences”,

M.J. Aminoff and R.B. Daroff, editors, Academic Press, San Diego, 2003,
volume 1, pp.795802.

349. Brown, P. Transmissible Spongiform Encephalopathy. Chapter 43 in:

“Textbook of Clinical Neurology”, 2nd Edition, C.G. Goetz, editor,

Saunders, Philadelphia, 2003, pp.945-954.

350. Brandel, J.-P., Preece, M., Brown, P., Croes, E., Laplanche J.-L.,

Will, R. and Alpérovitch, A. Distribution of codon 129 genotypes

in human growth hormone-treated CJD patients in France and the

United Kingdom. Lancet, 362: 9378 (July 12), 128-130, 2003.

351. Walis, A., Bratosiewicz, J., Sikorska, B., Brown, P., Gajdusek, D.C

and Liberski, P.P. Ultrastructural changes in the optic nerves of

rodents with experimental Creutzfeldt-Jakob disease (CJD),

Gerstmann-Sträussler-Scheinker disease (GSS) or scrapie. Journal of

Comparative Pathology, 129: 2-3: (August-October), 213-225, 2003.

352. Cervenakova, L., Yakovleva, O., McKenzie, C., Kolchinsky, S.,

McShane, L., Drohan, W.N. and Brown, P. Similar levels of

infectivity in the blood of mice infected with human-derived vCJD

and GSS strains of transmissible spongiform encephalopathy.

Transfusion, 43: 12 (December), 1687-1694, 2003.

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353. Brown, P. Fall-out from a possible transfusion-related transmission of

vCJD. The Lancet Neurology, 3: 4 (April), 203, 2004.

354. Mills, J.L., Schonberger, L.B., Wysowski, D.K., Brown, P., Durako,

S.J., Cox, C., Kong, F. and Fradkin, J.E. Long Term Mortality in

the United States cohort of pituitary-derived growth hormone

recipients. J Pediatrics, 2004 144: 4 (April), 430-436, 2004.

355. Sikorska, B., Walis A., Bratosiewicz-Wasik, J., Brown, P. and

Liberski, P.P. Fate of myelinated fibres in the optic nerves in

experimental Creutzfeldt-Jakoc disease in rodents: an

ultrastructural study. Folia Neuropathologica 42: 2 (April-June),

101-105, 2004.

356. Liberski, P.P. and Brown, P. Kuru: a half-opened window onto the

landscape of neurodegenerative diseases. Folia Neuropathologica 42:

Supplement A (June), 3-14, 2004.

357. Liberski, P.P. and Brown, P. Prion diseases: from transmission

experiments to structural biology – still searching for the cause.

Folia Neuropathologica, 42: Supplement A (June), 15-32, 2004.

358. Brown, P. Mad cow disease in cattle and human beings. American

Scientist, 92: 4 (July-August), 334-341, 2004.

359. Fichet, G., Comoy, E., Duval, C., Antloga, K., Dehen, C.,
Charbonnier, A.,

McDonnell, G., Brown, P., Lasmézas, C.I. and Deslys, J-P. Novel

methods for disinfection of prion-contaminated medical devices.

Lancet, 364: 9433 (August 7), 521-526, 2004.

360. Brown, P. and Cervenáková, L., The modern landscape of
transfusion-related

iatrogenic Creutzfeldt-Jakob disease and blood screening tests. Current

Opinion in Hematology, 11: 5 (September), 351-356, 2004.

361. Brown, P., Rau, E.H., Meyer, R., Lemieux, P., Cardone, F. and

Pocchiari, M. ‘Extreme’ inactivation methods for transmissible

spongiform encephalopathy agents. In: “Proceedings of the Eighth

International Kilmer Conference”, J.B. Kowalski and R.F. Morrissey,

editors, Osaka, Japan, October 6-9, 2003. Polyscience Publications

Inc., Laval, Canada, 2004, pp.104-111.

362. Brown, P., Rau, E.H., Lemieux, P., Johnson, B.K., Bacote, A. and

Gajdusek, D.C. Infectivity studies of both ash and air emissions

from simulated incineration of scrapie-contaminated tissues.

Environmental Science and Technology, 38: 22 (November 15),

6155-6160, 2004.

363. Yakovleva, O., Janiak, A., McKenzie, C., McShane, L., Brown, P. and

Cervenakova, L. Effect of protease treatment on plasma infectivity

in variant Creutzfeldt-Jakob disease mice. Transfusion, 44: 12

(December), 1700-1705, 2004.

364. Cervenáková, L. and Brown, P. Advances in test development for

transmissible spongiform encephalopahies. Expert Review of

Anti-infective Therapy, 2: 6 (December), 873-880, 2004.

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2005

365. Brown, P. and Abee, C.R. Working with transmissible spongiform

encephalopathy agents. Institute for Laboratory Animal Research

(ILAR) Journal, 46: 1 (January), 44-52, 2005.

366. Brown, P. and Cervenáková L. A prion lexicon (out of control).

Lancet, 365: 9454 (January 8), 122, 2005.

367. Lasmézas, C., Comoy, E., Hawkins, S., Herzog, C., Mouthon, F.,

Konold, T., Auvré, F., Correia, E., Lecoutra-Etchegaray, N.,

Salès, N., Wells, G., Brown, P. and Deslys, J.P. Risk of oral

infection with bovine spongiform encephalopathy agent in primates.

Lancet, 365: 9461 (February 26), 781-783, 2005.

368. Brown, P. Pathogenesis and transfusion risk of transmissible

spongiform encephalopathies. In: “Advances in Transfusion Safety”,

G. Vyas and A. Williams, editors, Developments in Biologicals,

volume 120, Karger, Basel, 2005, pp.27-33.

369. Brown, P. Blood infectivity, processing and screening tests in

transmissible spongiform encephalopathies. Vox Sanguinis,

89: 2 (August), 63-70, 2005.

370. Sowemimo-Coker, S., Kascsak, R., Kim, A., Andrade, F., Pesci, S.,

Kascsak, R., Meeker, C., Carp, R. and Brown, P. Removal of

exogenous (spiked) and endogenous prion infectivity from red cells

with a new prototype of leukocyte reduction filter. Transfusion,

45: 12 (December), 1839-1844, 2005.

371. Kennedy, R.H., Mills, C.R. and Brown, P. Risk of infectious disease

transmission through the use of Allografts. In: “Essentials in

Ophthalmology: Oculoplastics and Orbit”, R. Guthoff and

J. Katowitz, editors, Springer-Verlag, Berlin, 2005, pp.3-18.

2006

372. Thomzig, A., Cardone, F., Krüger, D., Pocchiari, M., Brown, P. and

Beekes, M. Pathological prion protein in muscles of hamsters and

mice infected with rodent-adapted BSE or vCJD. Journal of General

Virology, 87: 1 (January), 252-254, 2006.

373. Cardone, F., Brown, P., Meyer, R., and Pocchiari, M. Inactivation of

transmissible spongiform encephalopathy agents in food products by

ultra-high pressure-temperature treatment. Biochimica et Biophysica

Acta (Proteins and Proteomics), 1764: 3 (March), 558-562, 2006.

374. Walis, A, Liberski P.P. and Brown, P. Ultrastructural alterations

in the optic nerve in transmissible spongiform encephalopathies – a

review. Folia Neuropathologica 42: Supplement B (March), 153-160, 2006.

375. Liberski, P.P., Jaskolski, M. and Brown, P. Gerstmann-Sträussler-

Scheinker disease. II. An effect of GSS mutation on PRP structure.

Folia Neuropathologica 42: Supplement B (March), 153-160, 2006.

23


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2006 (Con’t)

376. Liberski, P.P. and Brown, P. Astrocytes in transmissible spongiform

encephalopathies (prion diseases). Folia Neuropathologica 42:

Supplement B (March), 153-160, 2006.

377. Brown, P. The quest for a pre-clinical blood screening test for TSE.

Neuroprion News, No. 5 (April), 2006, p.1.

378. Brown, P. Letter to God. British Medical Journal. 332: 7553 (3 June),

1341.

379. Brown, P. Blood infectivity in the transmissible spongiform

encephalopathies. Chapter 4 in: “Creutzfeldt-Jakob Disease:

Managing the Risk of Transmission by Blood, Plasma, and Tissues”,

Turner M.L., editor. ABBA Press, Bethesda, MD, 2006, pp. 95-118.

380. Minor, P. and Brown P. Diagnostic tests for CJD for ante-mortem

screening. Chapter 5 in: “Creutzfeldt-Jakob Disease: Managing the

Risk of Transmission by Blood, Plasma, and Tissues”, Turner M.L.,

editor. ABBA Press, Bethesda, MD, 2006, pp. 119-148.

381. Baribeau, A-M., Bradley, R.B., Brown, P., Goodwin, J., Kihm, U.,

Lotero, E., O’Conner D., Schuppers, M., and Taylor D. Biodiesel

from Specified Risk Material Tallow: an Appraaisal of TSE Risks and

Their Reduction. ATF Advanced Technologies & Fuels Canada, Inc.,

Ottowa, July 2006.

382. Brown, P., Brandel, J.-P., Preece, M. and Sato, T. Iatrogenic

Creutzfeldt-Jakob disease: the waning of an era. Neurology,

67:3 (August 8), 389-393.

^^^. Brown, P. Atypical BSE. Neuroprion News, No. 6 (November), 2006, p.1.

^^^. Brown, P., McShane, L. Zanusso G and Detwiler, L. On the question of

sporadic or atypical bovine spongiform encephalopathy and

Creutzfeldt-Jakob disease. Emerging Infectious Diseases, 2006

[IN PRESS]

^^^. Brown, P. and Detwiler, L. Bovine spongiform encephalopathy. In: Food

Microbiology: Fundamentals and Froniers”, 3rd edition, Doyle, M.F,

^^^^^^^^^^^^^^^^^^^^^^, editors. ASM Press, Washington D.C.,

pp.^^^-^^^. [IN PRESS]

^^^. Sikorska, B., Liberski, P. and Brown, P. Neuronal autophagy and

aggresomes constitute a significant part of neurodegenerations in

experimental scrapie. [IN PRESS]

2007

^^^. Georgsson, G., Sigurdarson, S. and Brown, P. The infectious agent of

sheep scrapie may survive in the environment for at least sixteen

years. Journal of General Virology, [IN PRESS]

24


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2007 (Con’t)

^^^. Williams, L., Brown, P., Ironside, J., Gibson, S., Will, Rl, Ritchie,

D., Kreil, T.R.and Abee, C. Clinical, neuropathological, and

immunohistochemical features of sporadic and variant forms of

Creutzfeldt-Jakob disease in the squirrel monkey (Saimiri sciureus}.

Journal of General Virology, 2007. [IN PRESS]

^^^. Larramendy-Gozalol, C., Berret, A, Daudigeos E, Mathieu, E.,

Antonangeli, L., Riffet, C., Petit, E., Papy-Garcia, D.,

Barritault, D., Brown, P. and Deslys, J.-P. Characterization of

CR36, a new heparan mimetic, and Pentosan Polysulfate in the

treatment of prion diseases.

[SUBMITTED]

Journal of General Virology, 2007

^^^. Brown, P. Transmissible spongiform encephalopathy. Chapter 43 in:

“Textbook of Clinical Neurology”, 3rd edition, Goetz, C., editor.

W.B. Saunders, Philadelphia, 2007, pp. ^^^-^^^. [IN PRESS]

^^^. Martinez-Lage, J.F., Brown, P. and Martin, P.M. Enfermedades por

priones adquiridas: enfermedad de Creutzfeld-Jakob yatrógena.

Chapter 11 in: “^^^^^^^^^^^^^^^^^^^^^^ [IN PRESS]

^^^. Liberski, P.P., Brown, D.R., Caughey, B. and Brown, P. Neuronal cell

death caused by a misfolded protein in transmissible spongiform

encephalopathies (prion diseases).

^^^-^^^, 2006 [IN PRESS].

Autophagy 2: 3 (Oct/Nov/Dec),

^^^. Pan, T., Sethi, J., Nelsen, C., Cervenakova, L., Lohman, K.,

Wegrzyn, R., Rucolph, A., Brown, P. and Orser, C.S. Evidence for

PRPTSE in blood by the misfolded protein diagnostic Assay.

Transfusion, [IN PREPARATION]

25


Case 1:06-cv-00544-JR Document 14-9 Filed 11/03/2006 Page 37 of 47

ATTACHMENT B

Paul W. Brown, M.D.

Curriculum Vitae


Case 1:06-cv-00544-JR Document 14-9 Filed 11/03/2006 Page 38 of 47

CURRICULUM VITAE

Present address

Birthdate/Place

Education and

experience

Society

affiliations

Paul W. Brown, M.D.

7815 Exeter Road

Bethesda, Maryland 20814

Telephone (301) 652-5940

Fax (301) 652-4312

e-mail [email protected]

12 March 1936, Hackensack, New Jersey, USA

A.B. (Magna cum Laude), Harvard College, 1957

M.D., The Johns Hopkins School of Medicine, 1961

Internship and 1st year medical residency:

Osler Medical Service, The Johns Hopkins Hospital,

1961-1963

Research Associate, NINDS, NIH, 1963-1965.

Staff Associate, National Institute of Child Health and

Human Development, (NICHHD), NIH, 1965-70

2nd year medical residency, University of California San

Francisco Medical Center, 1965-66

3rd year medical residency, Osler Medical Service,

The Johns Hopkins Hospital, 1966-67

Chargé de Recherche, L'Institut National de la Santé et de

la Recherche Médicale (INSERM), and Medical

Consultant, American Embassy, Paris, 1971-72

Staff Associate, NINDS, NIH, 1971-89

Visiting Scientist, INSERM, Laboratoire de

Neurovirologie, Clinique des Maladies du Système

Nerveux, Hôpital de la Salpêtrière, Paris, 1977-78

Medical Director, US Public Health Service, 1979-1999

Senior Investigator, NINDS, 1990-2004

American College of Physicians

American Epidemiological Society

Infectious Diseases Society of America

American Society for Virology

Société Française de Neurologie

American Neurological Association


Case 1:06-cv-00544-JR Document 14-9 Filed 11/03/2006 Page 39 of 47

Languages English and French

Publications Over 380 papers during a span of 40 years, mainly dealing with

transmissible spongiform encephalopathy (TSE), and especially the topics

of epidemiology, infectivity, and inactivation

Editorial European Journal of Epidemiology, Associate editor,
1990positions Journal of the Neurological Sciences, Associate editor,
1991-97

Honors and -Henry Strong Denison Scholar, The Johns Hopkins School

recognitions School of Medicine, 1961

-Alpha Omega Alpha (AOA), Johns Hopkins Chapter, 1961

-Diplomate, American Board of Internal Medicine, 1968

-Prix Léopold Trasbot, Académie Vétérinaire de France,

1980

-Fellow, National Multiple Sclerosis Society, 1971-72

-Fellow, Committee to Combat Huntington’s Chorea, 1973

-Chairman, DHHS Interagency Epidemiology

Subcommittee on Human Growth Hormone and

Creutzfeldt-Jakob disease, 1985 to present

-Lawson Wilkins Pediatric Endocrine Society Lecture,

Los Angeles, California, 1987

-Thomas Campione Lecture,

Northwestern University School of Medicine, 1987

-USPHS Commendation Medal, 1990

-Arnold Barnett Lecture,

Wichita Society of Neuroscience, 1991

-Member, WHO Expert Advisory Panel on Neurosciences,

1991-1993

-Consultant to PAHO (Pan American Health Organization)

for the evaluation of bovine spongiform encephalopathy

in Latin America, 1992

-USPHS Outstanding Service Medal, 1992

-Consultant to EEC Biomed 1/2 Project: Surveillance of

Creutzfeldt-Jakob disease in the European Community,

1992 to present

-Andrew Mark Lippard Memorial Lecture, College of Physicans

and Surgeons of Columbia University, 1995

-Chairman, WHO consultation on TSE and Medical Products

(1997)

-Transmissible Spongiform Encephalopathies Advisory

Committee, Center for Biologics Evaluation and Research,

FDA: Chairman 1997-2001; Ad hoc member 2001-present

-Chairman, Neurodegererative Diseases Working Group,

World Federation of Scientists, 1998-2000

2


Case 1:06-cv-00544-JR Document 14-9 Filed 11/03/2006 Page 40 of 47

Honors and -Chairman, WHO consultation on TSE and Infection Control

recognitions Guidelines (1999)

(continued) -Distinguished Scientist Seminar Lecturer,

University of South Alabama School of Medicine, 2000

-Marie C. and Joseph C. Wilson Memorial Lecture,

University of Rochester Medical Center, 2000

-Bill Stone Distinguished Speaker, 2001

South Texas Blood & Tissue Center

-Convocation Lecture and Seminar, Berea College, 2001

-Fredrich Deinhardt Lectureship, 18th Annual Clinical Virology

Symposium, Clearwater Beach, Florida, 2002

-Board of Governors and Board of Scientific Directors,

The Memorial Institute for Neurodegenerative Diseases

of Saskatchewan, Canada, 2003

-Eagleson Lecture, American Biological Safety Association

Conference, 2004

-Plenary Lecture, European Network of Excellence Neuroprion

Conference, Paris, 2004

-Co-Chairman, Dominique Dormont Memorial Conference,

Paris, 2005

-Co-President, Fondation Alliance de Biotechnologie,

Paris, 2006 onwards

3


Case 1:06-cv-00544-JR Document 14-9 Filed 11/03/2006 Page 41 of 47

ATTACHMENT C

Brown, P, McShane, LM, Zanusso, G, Detwiler, L, On the question of
sporadic or atypical

bovine spongiform encephalopathy (BSE) and Creutzfeldt-Jakob disease


Case 1:06-cv-00544-JR Document 14-9 Filed 11/03/2006 Page 42 of 47

PERSPECTIVE

On the Question of Sporadic

or Atypical Bovine SpongiformEncephalopathy and

Creutzfeldt-Jakob Disease

Paul Brown,* Lisa M. McShane,† Gianluigi Zanusso,‡ and Linda Detwiler§

Strategies to investigate the possible existence of sporadic

bovine spongiform encephalopathy (BSE) require

systematic testing programs to identify cases in countries

considered to have little or no risk for orally acquired disease,

or to detect a stable occurrence of atypical cases in

countries in which orally acquired disease is disappearing.

To achieve 95% statistical confidence that the prevalence

of sporadic BSE is no greater than 1 per million (i.e., the

annual incidence of sporadic Creutzfeldt-Jakob disease

[CJD] in humans) would require negative tests in 3 million

randomly selected older cattle. A link between BSE and

sporadic CJD has been suggested on the basis of laboratory

studies but is unsupported by epidemiologic observation.

Such a link might yet be established by the discovery

of a specific molecular marker or of particular combinations

of trends over time of typical and atypical BSE and various

subtypes of sporadic CJD, as their numbers are influenced

by a continuation of current public health measures that

exclude high-risk bovine tissues from the animal and

human food chains.

Bovine spongiform encephalopathy (BSE) was first recognized

in 1986 in the United Kingdom and quickly

reached epidemic proportions, affecting >30,000 cattle per

year by 1992. Because of continuing exportation of both

live cattle and meat and bone meal rendered from the carcasses

of slaughtered cattle, the disease spread throughout

most of Europe and a few non-European countries.By

2006, 20 years after its first appearance in the United

Kingdom, the disease had been reported in an additional

24 countries (1).

*Bethesda, Maryland, USA; †National Institutes of Health,

Bethesda, Maryland, USA; ‡University of Verona, Verona, Italy;

and §Virginia-Maryland Regional College of Veterinary Medicine,

College Park, Maryland, USA

Beginning toward the end of the 1980s in the United

Kingdom, and in the 1990s in other countries, numerous

regulations were enacted to minimize the entry of contaminated

tissues into both the animal and human food chains

and to eliminate the international spread of disease. These

measures have been extraordinarily successful, to the

extent that no new countries have been added to the list

during the past year and the number of new cases has dramatically

diminished in most countries in which BSE has

appeared (the situation in some countries with insufficient

surveillance remains unclear).

Although the origin of the epidemic is thought to have

been caused by a species-crossing contamination by sheep

scrapie during the course of rendering and recycling carcass

meat and bone meal as cattle feed, an alternative

hypothesis suggested an origin in a similarly recycled case

of spontaneously occurring disease in cattle. The pros and

cons of these competing ideas have been argued elsewhere

(2,3), and neither will ever be convincingly proved or disproved.

Thus, the phenomenon of spontaneous disease

remained in limbo until the recent discovery of “atypical”

strains of BSE reopened the question. In this article we

consider the importance of atypical BSE within the overall

concept of sporadic (spontaneous) disease and whether

such cases, if they exist, could account for at least some

cases of apparently sporadic Creutzfeldt-Jakob (CJD) in

humans.

Sporadic BSE

Obviously, the ideal country in which to examine the

question of sporadic BSE would have a large national herd

that was guaranteed never to have been exposed to environmental

sources of infection. Such an ideal will never be

realized. Until recently, the United States appeared to have

at least approached the ideal by having a large national

Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 12, No. 12,
December 2006


Case 1:06-cv-00544-JR Document 14-9 Filed 11/03/2006 Page 43 of 47

herd, an adequate testing program, and an apparently small

risk for contamination by imported cattle or cattle feed.

That position was made vulnerable in late 2003 by the discovery

of a case of BSE imported from Canada and was

eliminated altogether by the subsequent discovery of 2

indigenously infected animals in widely separate regions

of the country. Although the 2 indigenous cases might represent

sporadic disease, the continuing identification of

cases in western Canada, coupled with a history of substantial

numbers of cattle imported from Canada into the

United States (both indigenous US animals had the same

molecular “signature” as the most recent Canadian case),

makes it difficult to ignore the possibility of undetected

instances of feed contamination from imported and recycled

infectious carcasses.

At present, the 2 best countries in which to undertake

testing programs would be Argentina and Australia; both

have large national herds (˜50 million and 30 million animals,

respectively), and both are considered to be free of

orally acquired BSE infections, on the basis of importation

history, nutritional practices, and adequacy of surveillance

(4). Even in these countries, however, the discovery of a

case of BSE could not be guaranteed to be spontaneous

because of the widespread global distribution of potentially

infected cattle and cattle feed and the vagaries of international

trade: imperfect record keeping, lack of

compliance, and just plain deception.

By way of illustration, an incident occurred many years

ago that involved a particularly bulky shipment labeled as

a pesticide. The large quantity seemed unusual to the customs

inspector, who opened it and discovered that the shipment

contained meat and bone meal destined to be spread

on fields to inhibit grazing by deer, a serious agricultural

pest. Thus, a study of sporadic BSE would only be truly

convincing if no cases were identified.

Moreover, the criteria for answering the question of

sporadic BSE are different than for orally acquired BSE.

Most importantly, we do not know at what age sporadic

cases of BSE might occur, but they are unlikely to be in the

3- to 5-year-old age group in which orally acquired BSE is

most prevalent. If the age distribution of sporadic disease

in cattle were to mimic that of sporadic CJD in humans, it

would not peak until 14–20 years of age (the last third of

the ˜20-year natural life span of a cow). Substantial numbers

of such older cattle do not exist, and thus it may never

be possible to state with assurance that spontaneous BSE

does not occur.

Even if we accept this practical constraint, we can still

take advantage of the fact that in many countries a proportion

of the total slaughter population consists of breeding

stock and dairy cows that are culled at >7 years of age, and

animals that go directly to rendering plants or die “on

farm” further increase this number. Argentina, for exam

Bovine Spongiform Encephalopathy and CJD

ple, with a national herd of ˜50 million cattle, in 2005

recorded nearly 1.4 million deaths from slaughter and natural

causes in animals >7 years (L. Mascitelli, pers.

comm.).

Approximately 10% of cases of sporadic CJD occur in

patients 25–50 years of age; this age in humans corresponds

to the middle third of a cow’s normal life span, or

7–13 years of age (Figure 1). If the age distribution of sporadic

BSE followed the same pattern, negative test results

in a total of ˜3 million animals randomly selected from

this group would allow us to be 95% confident that sporadic

BSE is not present at a prevalence >1 per million,

and ˜4.5 million negative animals would raise the level of

confidence to 99%. Larger numbers of BSE-negative animals

would be required to achieve these levels of confidence

for a maximum prevalence <1 per 10 million cattle

(Table 1, Figure 2).

Even the least rigorous negative result—a prevalence

not greater than that of sporadic CJD in humans, or 1 per

million—would require several years to achieve, and it is

perhaps unrealistic to suppose that the motivation to prolong

the testing program will endure much beyond the

global disappearance of orally acquired BSE and variant

CJD. Nevertheless, to the degree that testing older as well

as younger adult animals approached these numbers, both

statistical and consumer confidence would increase, and at

the very least provide reassurance that the occurrence of

sporadic disease must be exceedingly rare, with little likelihood

of posing a risk to either human or animal nutrition.

Atypical BSE

Because of its contemporary nature, the study of atypical

BSE is very much a work in progress, with comparatively

little published data and many unknowns. The first 2

cases to be identified were a serendipitous discovery made

in the course of an unrelated experimental study that

required a detailed neuropathologic and immunochemical

Figure 2. Maximum prevalence according to number of negative

cattle at 95% (solid line) and 99% (dashed line) confidence levels.

See Table 1 for exact numbers and statistical method.

Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 12, No. 12,
December 2006


Case 1:06-cv-00544-JR Document 14-9 Filed 11/03/2006 Page 44 of 47

PERSPECTIVE

examination of the entire brain (5). The absence of clinical

signs in these older animals, the unusual distribution of

PrPTSE, together with amyloid plaques, and a Western blot

pattern that differed from the stereotypic pattern seen in

typical BSE left little doubt about the probability that a

new “atypical strain” had been identified (bovine amyloidotic

spongiform encephalopathy[BASE]).

Although no further cases were found in nearly 200 cattle

examined in Italy, the initiation of Western blot studies

of animals in other countries with screening test programs

began to yield additional atypical patterns (Table 2, Figure

3) (6–14; P. Lind, pers. comm.). Two major patterns have

been described, named L (resembling the original Italian

case pattern with a lower molecular weight than typical

BSE) and H (for a distinct pattern first seen in France with

a higher molecular weight than typical BSE). It is not yet

clear whether other mixed patterns result from technical

procedures in different laboratories or whether a more

complicated scheme of classification will evolve as more

atypical patterns are discovered.

In addition, Western blots of PrPTSE are a fragile basis

on which to define a BSE phenotype. Little or no information

is available about either the clinical status or neuropathologic

features of these animals. We know that cases

have occurred in different breeds and PrP genotypes, and

we also know that very few of the animals have had the

typical clinical picture of BSE (behavioral disturbances,

sensory signs, ataxia, and tremors), but a cloud of ambiguity

surrounds the clinical picture even in those animals for

which an extensive post-hoc investigation was undertaken.

The fact that few detailed neuropathologic results are

available is explained by the need to preserve at least a full

half brain for examination, which is presently not done in

any of the various countries that have screening test programs.

In the future, the brain as well as the carcass must

be retained in cold storage until the test results are known.

The frequency of atypical cases is another unknown.

Published (7,12) and unpublished (11,13) observations

indicate that in some countries it might be as high as

5%–10% of the total number of older animals diagnosed

by rapid screening tests (e.g., 2/27 in Germany, and 1/9 in

Canada), which would seem to be a surprisingly high proportion

of spontaneously occurring cases. However, data

are not yet sufficient to estimate the overall prevalence of

atypical BSE, i.e., cases per million tested animals of all

ages.

In this context, a word is in order about the US testing

program. After the discovery of the first (imported) cow in

2003, the magnitude of testing was much increased, reaching

a level of >400,000 tests in 2005 (Figure 4). Neither of

the 2 more recently indigenously infected older animals,

with ambiguous or no clinical features, would have been

detected without such testing, and neither would have been

identified as atypical without confirmatory Western blots.

Despite these facts, surveillance has now been decimated

to 40,000 annual tests (USDA news release no. 0255.06,

July 20, 2006) and invites the accusation that the United

Figure 1. Distribution of ages at onset of illness in 500 cases of

neuropathologically verified or experimentally transmitted sporadic

Creutzfeldt-Jakob disease. Approximately 10% of cases occur in

patients during the middle third (25–49 years) of a human lifespan,

which corresponds to age in cattle of ~7–13 years.

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December 2006


Case 1:06-cv-00544-JR Document 14-9 Filed 11/03/2006 Page 45 of 47

Bovine Spongiform Encephalopathy and CJD

States will never know the true status of its involvement

with BSE.

In short, a great deal of further work will need to be

done before the phenotypic features and prevalence of

atypical BSE are understood. More than a single strain

may have been present from the beginning of the epidemic,

but this possibility has been overlooked by virtue of the

absence of widespread Western blot confirmatory testing

of positive screening test results. These new phenotypes

may be found, at least in part, to result from infections at

an older age by a typical BSE agent, rather than neonatal

infections with new “strains” of BSE. Neither alternative

has yet been investigated.

Sporadic CJD

The possibility that at least some cases of apparently

sporadic CJD might be due to infection by sporadic cases

of BSE cannot be dismissed outright. Screening programs

needed to identify sporadic BSE have yet to be implemented,

and we know from already extant testing programs that

at least a proportion of infected animals have no symptoms

and thus would never be identified in the absence of systematic

testing. Thus, sporadic BSE (or for that matter,

sporadic disease in any mammalian species) might be

occurring on a regular basis at perhaps the same annual

frequency as sporadic CJD in humans, that is, in the range

of 1 case per million animals.

Whether humans might be more susceptible to atypical

forms of BSE cannot be answered at this time.

Experimentally transmitted BASE shows shorter incuba

tion periods than BSE in at least 1 breed of cattle,

bovinized transgenic mice, and Cynomolgus monkeys

(12,13). In humanized transgenic mice, BASE transmitted,

whereas typical BSE did not transmit (13). Paradoxically,

the other major phenotype (H) showed an unusually long

incubation period in bovinized transgenic mice (12).

The limited experimental evidence bearing on a possible

relationship between BSE and sporadic CJD is difficult

to interpret. The original atypical BASE strain of BSE had

a molecular protein signature very similar to that of 1 subtype

(type 2 M/V) of sporadic CJD in humans (5).

In another study, a strain of typical BSE injected into

humanized mice encoding valine at codon 129 showed a

Figure 3. Representation of Western blots of PrPTSE patterns of

typical bovine spongiform encephalopathy (BSE) and the 2 major

types of atypical BSE. M.W., molecular weight in kilodaltons; L

type, atypical “light” pattern; H type, atypical “heavy” pattern.

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December 2006


Case 1:06-cv-00544-JR Document 14-9 Filed 11/03/2006 Page 46 of 47

PERSPECTIVE

Figure 4. Numbers of tested cattle in the United States,

2000–2007. Number tested in 2006 as of October; number tested

in 2007 proposed by the US Department of Agriculture.

glycopattern indistinguishable from the same subtype of

sporadic CJD (15). In a third study, the glycopatterns of

both the H and L strains of atypical BSE evidently did not

resemble any of the known sporadic CJD subtypes (12).

To these molecular biology observations can be added

the epidemiologic data accumulated during the past 30

years. The hypothesis that at least some cases of apparently

sporadic CJD are due to unrecognized BSE infections

cannot be formally refuted, but if correct, we might expect

by now to have some epidemiologic evidence linking BSE

to at least 1 cluster of apparently sporadic cases of CJD.

Although only a few clusters have been found (and still

fewer published), every proposed cluster that has been

investigated has failed to show any common exposure to

bovines. For that matter, no common exposure has been

shown to any environmental vehicles of infection, including

the consumption of foodstuffs from bovine, ovine, and

porcine sources, the 3 livestock species known to be susceptible

to transmissible spongiform encephalopathies.

Additional negative evidence comes from several large

case-control studies in which no statistically significant

dietary differences were observed between patients with

sporadic CJD and controls (16,17).

On the other hand, the difficulty of establishing a link

between BSE and CJD may be compounded by our ignorance

of the infectious parameters of a sporadic form of

BSE (e.g., host range, tissue distribution of infectivity,

route of transmission, minimum infectious dose for

humans, whether single or multiple). Presumably, these

parameters would resemble those of variant CJD' that is,

high infectivity central nervous system and lymphoreticular

tissues of an infected cow find their way into products

consumed by humans. Transmissions that might have

occurred in the past would be difficult to detect because

meat products are generally not distributed in a way that

results in detectable geographic clusters.

Barring the discovery of a specific molecular signature

(as in variant CJD), the most convincing clue to an association

will come from the observation of trends over time of

the incidence of typical and atypical BSE and of sporadic

and variant CJD. With 4 diseases, each of which could

have increasing, unchanging, or decreasing trends, there

could be 81 (34) possible different combinations. However,

it is highly likely that the trends for typical BSE and variant

CJD will both decrease in parallel as feed bans continue

to interrupt recycled contamination. The remaining

combinations are thus reduced to 9 (32), and some of them

could be highly informative.

For example, if the incidence of atypical BSE declines

in parallel with that of typical BSE, its candidacy as a sporadic

form of disease would be eliminated (because sporadic

disease would not be influenced by current measures

to prevent oral infection). If, on the other hand, atypical

BSE continues to occur as typical BSE disappears, this

would be a strong indication that it is indeed sporadic, and

if in addition at least 1 form of what is presently considered

as sporadic CJD (such as the type 2 M/V subtype

shown to have a Western blot signature like BASE) were

to increase, this would suggest (although not prove) a

causal relationship (Figure 5).

Recognition of the different forms of BSE and CJD

depends upon continuing systematic testing for both

bovines and humans, but bovine testing will be vulnerable

Figure 5. Diagram of 2 possible informative trends in the incidence

of bovine spongiform encephalopathy (BSE) and Creutzfeld-Jakob

disease (CJD). The left panel shows the likely trends of typical

BSE and variant CJD (vCJD). The right upper panel shows 1 possible

pair of trends of atypical BSE and sporadic CJD (sCJD)

that might occur in conjunction with the typical BSE/vCJD trends,

and would be consistent with the interpretation that atypical BSE

is not sporadic and not related to sCJD. The right lower panel

shows a second possible associated pair of trends consistent with

the interpretation that atypical BSE is sporadic and might also be

related to the type 2 M/V subset of apparently sCJD.

Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 12, No. 12,
December 2006


Case 1:06-cv-00544-JR Document 14-9 Filed 11/03/2006 Page 47 of 47

to heavy pressure from industry to dismantle the program

as the commercial impact of declining BSE cases ceases to

be an issue. Industry should be aware, however, of the

implications of sporadic BSE. Its occurrence would necessitate

the indefinite retention of all of the public health

measures that exclude high-risk bovine tissues from the

animal and human food chains, whereas its nonoccurrence

would permit tissues that are now destroyed to be used as

before, once orally acquired BSE has disappeared.

Acknowledgments

We thank Victoria E. Bridges and Chris Kopral for providing

data about annual cattle slaughter numbers from the Food

Safety and Inspection Service of the US Department of

Agriculture (USDA) and for estimates of cattle dying on farms

from data supplied by the National Animal Health Monitoring

System, Animal and Plant Inspection Services, Veterinary

Service, USDA.

This study was funded in part by grant # 4AN/F10 “Studio

dei meccanismi patogenetici delle malattie neurodegenerative per

la diagnosi e lo sviluppo di approcci terapeutici” from the Istituto

Superiore di Sanità, Rome, Italy

Dr Brown has recently retired after a 41-year career in the

Laboratory of CNS Studies at the National Institutes of Health,

where he focused on studying transmissible spongiform

encephalopathies.

References

1. World Organization for Animal Health. Bovine spongiform

encephalopathy. Geographical distribution of countries that reported

BSE confirmed cases since 1989 [cited 2006 Oct 24]. Available

from http://www.oie.int/eng/info/en_esb.htm

2. Brown P, Bradley R, Detwiler L, Dormont D, Hunter N, Wells GAH,

et al. Transmissible spongiform encephalopathy as a zoonotic disease.

International Life Sciences Institute (ILSI) Europe Report

Series. Brussels: ILSI Press; 2003.

3. Horn GM, Bobrow ME, Bruce M, Goedert M, McLean A, Webster J.

Review of the origin of BSE 2001, London: Stationery Office; 2001.

4. World Organization for Animal Health. Bovine spongiform

encephalopathy. Recognition of the bovine spongiform encephalopathy

status of member countries [cited 2006 Oct 24]. Available

from http://www.oie.int/eng/info/en_statesb.htm

Bovine Spongiform Encephalopathy and CJD

5. Casalone C, Zanusso G, Acutis P, Ferrari S, Capucci L, Tagliavini F,

et al. Identification of a second bovine amyloidotic spongiform

encephalopathy: molecular similarities with sporadic Creutzfeldt-

Jakob disease. Proc Natl Acad Sci U S A. 2004;101:3065–70.

6. Danish Institute for Food and Veterinary Research [cited 2006 Oct.

24]. Available from http://www.dfvf.dk/Default.asp?ID=8147&M=

News&PID=89507&NewsID=792

7. Polak M, Rozek W, Rola J, Zmudzinski JF. Prion protein glycoforms

from BSE cases in Poland. Bulletin of the Veterinary Institute of

Pulawy. 2004;48:201–5.

8. De Bosschere H, Roels S, Vanopdenbosch E. Atypical case of bovine

spongiform encephalopathy in an East-Flemish cow in Belgium. Int

J Appl Res Vet Med. 2004;2:52–4. Available from http://www.jarvm.

com/articles/Vol2Iss1/DEBOSSCHERE.htm

9. Yamakawa Y, Hagiwara K, Nohtomi K, Nakamurua Y, Nishijima M,

Higuchi Y, et al. Atypical proteinase K-resistant prion protein

(PrPrres) observed in an apparently healthy 23-month-old Holstein

steer. Jpn J Infect Dis. 2003;56:221–2.

10. Biacabe AG, Laplanche JL, Ryder S, Baron T. Distinct molecular
phenotypes

in bovine prion diseases. EMBO Rep. 2004;5:110–4.

11. Canadian Food Inspection Agency. Report on the investigation of the

sixth case of bovine spongiformencephalopathy (BSE) in Canada

[cited 2006 Oct]. Available from http://www.inspection.gc.ca/english/

anima/heasan/disemala/bseesb/mb2006/6investe.shtml

12. Buschmann A, Gretzshel A, Biacabe AG, Schiebel K, Corona C,

Hoffmann C, et al. Atypical BSE in Germany—proof of transmissibility

and biochemical characterization. Vet Microbiol. 2006;

117:103–16.

13. Book of abstracts. Prion 2006, International Conference on Prion

Diseases of NeuroPrion, Network of Excellence, Turin, Italy, 2006

Oct 3–6 [cited 2006 Oct 24]. Available from http://www.

neuroprion.com/en/ev_prion2006.html

14. Seuberlich T, Botteron C, Wenker C, Café-Marçal V, Oevermann A,

Haase B, et al. Spongiform encephalopathy in a miniature zebu.

Emerg Infect Dis. 2006;12:xxx–xxx. [THIS ISSUE]

15. Wadsworth JDF, Asante EA, Desbruslais M, Linehan JM, Joiner S,

Gowland I, et al. Human prion protein with valine 129 prevents

expression of variant CJD phenotype. Science. 2004;306:1793–6.

16. Wientjens DP, Davanipour Z, Hofman A, Kondo K, Matthews WB,

Will RG, et al. Risk factors for Creutzfeldt-Jakob disease: a reanalysis

of case control studies. Neurology. 1996;46:1267–91.

17. Van Duijn CM, Delasnerie-Lauprêtre N, Masullo C, Zerr I, de Silva

R, Wientjens DPWM, et al. Case-control study of risk factors of

Creutzfeldt-Jakob disease in Europe during 1993–1995. Lancet.

1998;351:1081–5.

Address for correspondence: Paul Brown, 7815 Exeter Rd, Bethesda, MD

20814, USA; email: [email protected]

Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 12, No. 12,
December 2006
TSS
 

flounder

Well-known member
UNITED STATES DISTRICT COURT

FOR THE DISTRICT OF COLUMBIA

CREEKSTONE FARMS PREMIUM

BEEF, LLC,

Plaintiff,

v.

UNITED STATES DEPARTMENT OF

AGRICULTURE, et al.,

Defendants.

WILD OATS MARKETS, INC.

3375 Mitchell Lane

Boulder, Colorado 80301

Proposed Amicus Curiae.

Civil Action No. 06-544 (JR)

MOTION FOR LEAVE TO APPEAR AS AMICUS CURIAE

IN OPPOSITION TO DEFENDANTS' MOTION FOR SUMMARY JUDGMENT

Wild Oats Markets, Inc. ("Wild Oats"), a party interested in the outcome
of this litigation

and desiring to assist the Court in resolving it, hereby files this
motion for leave to appear as

amicus curiae and to present argument in opposition to the cross-motion
for summary judgment

filed in this matter [dkt. 10] by the United States Department of
Agriculture and Secretary of

Agriculture Mike Johanns (together, "the USDA").

Reason to Appear

Wild Oats submits this motion to address one point asserted in the USDA
cross-motion:

that testing for bovine spongiform encephalopathy ("BSE") is "worthless"
when performed for

food safety or marketing purposes. See USDA Consolidated Memorandum in
Support of

_

7235557 1

Cross-Motion ("USDA Mem."), at 1, 5, 42. As discussed below, testing of
cattle for BSE

would eliminate from the food supply meat from animals with elevated
levels of this disease.

Consumers would therefore benefit from testing and from being informed
about it through

truthful, nonmisleading marketing programs.

Position of the Parties on this Motion

Prior to filing this motion counsel for Wild Oats sought consent from
both counsel to

Creekstone and counsel to USDA. Counsel for Creekstone advised that
Creekstone had no

objection to Wild Oats' participation in this matter as amicus curiae.
Counsel for USDA advised

that the government objected to Wild Oats' participation in the case as
amicus curiae.

Interest of Wild Oats

Wild Oats is a leading national retailer of natural and organic food.
The company

operates 74 full service supermarkets in 23 states, each offering
consumers a wide variety of the

highest quality food, health and wellness products. The company was
founded in 1987 and its

mission is to enhance the lives of its customers, employees, and
shareholders by operating a

successful business based on products and education that support health
and well-being.

Wild Oats uses great care in selecting the products it offers for sale
to consumers. The

company's commitment to quality is unsurpassed in the industry, and it
uses rigorous criteria

based on scientific research to ensure that all of the products it sells
are made naturally, without

artificial colorings, preservatives, flavorings or other synthetic
additives. Wild Oats strives to

feature products that contribute to its customers' health and
well-being, and does so by partnering

with product manufacturers and vendors that meet rigorous environmental
and social standards.

Wild Oats is also responsive to its customers' concerns. At the
forefront of those

concerns is the desire to know that foods Wild Oats carries are
wholesome, nutritious and safe.

7235557_1 -2

Wild Oats therefore makes every effort to ensure that they are. The
company carefully selects its

suppliers with this consideration in mind, and bases its decisions
regarding product selection on

the most current and reliable scientific research available. Wild Oats
also monitors industry

trends and scientific developments so it is knowledgeable about the
issues affecting consumers.

Facts Regarding BSE and Testing

Among the issues of greatest concern to Wild Oats customers in recent
years has been

BSE. This disease occurs when healthy cattle consume feed containing
protein derived from

other cattle infected with BSE. The disease, which is fatal in cattle,
attacks their brains, leads to

degeneration of their mental and physical abilities, and ultimately
causes their death.

BSE is of concern to consumers because the consumption of meat tainted
with BSE is

believed to cause a fatal human disease, variant Creutzfeldt-Jakob
Disease ("vCJD"). Over the

past twenty years, nearly 200 cases of vCJD have been identified, and
most of these are believed

to have resulted when consumers ate beef products contaminated with BSE.

Because of this risk to public health, the federal government has taken
several steps to

reduce the chances that consumers will exposed to beef infected with
BSE. For example, the

government has banned certain "specified risk materials" ("SRM") derived
from older cattle

from use as human food. SRM include animal parts in which BSE
concentrations are known to

be greatest in diseased cattle, such as the brain, spinal cord and
intestines. In addition, the

government has prohibited the use of meat and other bovine tissues from
being added to cattle

feed. The government has also conducted testing of older and visibly
impaired cattle to help

assess the level of incidence of BSE within the domestic cattle herd.

These measures, however, have not eliminated the risk that American
consumers could

contract vCJD from consuming beef infected with BSE. In fact, the
government's restrictions on

7235557_1 -3

the use of beef tissues in cattle feed have been criticized as being
insufficient to prevent cross-

contamination by feed intended for non-ruminants, such as hogs and
chickens, in which beef

tissues can be used.1 Questions have also been raised whether the
government's feed ban has

been adequately enforced.2 In addition, the government recently cut back
the amount of testing

it is doing by a substantial margin.3 Over the past several years at
least three cattle infected with

BSE have been identified in the domestic herd, and the government has
continued to allow cattle

imports from countries in which the incidence of BSE is believed to be
greater than in the United

States, including Canada.4

Protocols exist today to test cattle for BSE. In fact, the government
follows these

protocols in its own limited testing program. Such testing is performed
at the time of slaughter

and meat from tested cattle is either held or tracked pending receipt of
test results. See

Creekstone Mem., at 11. As the government admits, these tests are
sensitive enough to identify

cattle infected with BSE several months before they show visible signs
of the disease. See

USDA Mem., at 5-6.

Because of concerns relating to BSE, many other developed countries
where BSE has

been found now test all or a large portion of the cattle processed for
human consumption for

BSE. In Europe, several countries test all cattle in excess of 24 months
of age when they are

slaughtered, and others test all cattle in excess of 30 months of age.
These countries perform

1

In October 2005 the U.S. Food and Drug Administration proposed to ban
SRM from being used in

feed given to any animals. See 70 Fed. Reg. 58570 (Oct. 6, 2005). That
proposal has not been finalized.

2

See "Beef Delays in Mad Cow Protection," Consumer Reports (January
2005), at 29 (Ex. 1).

3

See "USDA to Cut Back BSE Testing Program," University of Minnesota
Center for Infectious

Disease Research and Policy ("CIDRAP") (July 20, 2006) (Ex. 2).

4

See "Canada Finds Eighth Case of BSE," CIDRAP (Aug. 23, 2006) (Ex. 3).

7235557_1 -4

these tests for one reason: because testing provides additional
assurance that cattle infected with

BSE are removed from the food supply.

Argument

By prohibiting beef processors in the United States from testing cattle
for BSE, USDA is

preventing them from acquiring information regarding the safety and
quality of the products they

sell, and preventing Wild Oats and other retailers from providing that
information to consumers.

Consumers want that information and would use it in making their
purchasing decisions, and

there is no valid reason for the government to prevent them from having it.

1. Speech concerning products offered for sale to consumers is protected
by the First

Amendment. Central Hudson Gas & Electric Corp. v. Public Service Comm'n,
447 U.S. 557,

566 (1980); Virginia State Bd. of Pharmacy v. Virginia Citizens Consumer
Council, 425 U.S.

748, 763 (1976). The free flow of information about consumer products is
"indispensable to the

proper allocation of resources in a free enterprise system because it
informs the numerous private

decisions that drive the system." Rubin v. Coors Brewing Co., 514 U.S.
476, 481-82 (1995)

(citation and quotation omitted). In fact, a consumer's interest in
receiving this information "may

be as keen, if not keener by far, than his interest in the day's most
urgent political debate." Id.

2. The government's ban on BSE testing implicates the First Amendment
rights of

food retailers and consumers because the purpose and inevitable effect
of that ban is to prevent

retailers from communicating information on products it sells, and to
prevent consumers from

receiving it. See United States v. O'Brien, 391 U.S. 367, 377, 384-85
(1967); see also City of

Cincinnati v. Discovery Network, Inc., 507 U.S. 410, 417-19 (1993);
Minneapolis Star &

Tribune Co. v. Minnesota Comm'r of Revenue, 460 U.S. 575, 582-83 (1983);
Linmark

Associates, Inc. v. Township of Willingboro, 431 U.S. 85, 94-95 (1977).
In this case, USDA's

7235557_1 -5

response to Creekstone's request to conduct BSE testing, and the brief
the government has

filed in this case, leave no doubt that USDA's policy is achieving its
intended result: to

prevent producers from gathering and disseminating BSE test data. See
USDA Mem., at 1,

42-44 & n.24.

3. USDA claims that representations about test results would be
"misleading"

because "a negative test on a young cow cannot be interpreted to mean
that the cow is

necessarily 'BSE-Free.'" Id. at 5-6. Assuming this is true, Creekstone
has not said it wants to

tell its customers that its products are "BSE-Free." Nor from this one
example is it reasonable

to assume that every other statement that might be made about BSE
testing is necessarily

misleading so as to warrant a blanket ban. While complete prohibitions
prevent misleading

speech, they also prevent truthful, nonmisleading speech, and the
government may not adopt one

"simply to spare itself the trouble" of distinguishing the former from
the latter. See Edenfield v.

Fane, 507 U.S. 761, 775-77 (1993); Zauderer v. Office of Disciplinary
Counsel, 471 U.S. 626,

646 (1985).

4. USDA's ban on BSE testing advances no substantial governmental interest.

According to the agency, a ban is needed (a) "to maintain domestic and
international confidence

in U.S. cattle and beef products," (b) because if individual producers
were allowed to test their

products for BSE, other producers would have no choice but to test their
products as well, and

(c) to prevent consumers from thinking that "they should pay more for
beef from BSE-tested

cattle."5

a. The claim that "confidence in American beef would decline" is
conclusory and

provides no basis for restricting the right of beef processors and
retailers to communicate truthful

5

See Declaration of John D. Stewart 12-14 (Exhibit 1 to Creekstone's
Motion for Summary

Judgment); id. Attachment 7 (Letter from B. Hawks to J. Stewart, June 1,
2004); USDA Mem., at 7-10, 51.

7235557_1 -6

information about their products to consumers. See Edenfield, 507 U.S.
at 770 (government

"must demonstrate that the harms it recites are real and that its
restriction will in fact alleviate

them to a material degree . . . [and] mere speculation or conjecture" is
not enough); Zauderer,

471 U.S. 648-49 ("unsupported assertions" about possible harms cannot
justify speech

restrictions). In fact, it is reasonable to assume that the only way
consumer confidence in the

domestic beef supply would be shaken is if testing revealed a
significant incidence of BSE in the

domestic cattle herd. If that is true, then there is a far greater
reason to allow such testing than

there could ever be to prevent it.

b. Fear about industry impact from purchasing decisions does not permit
USDA to

ban information that might drive those decisions. Whether, or the extent
to which, other beef

processors felt compelled to test their products for BSE is a matter
that should be left to market

forces. If, by their purchasing decisions, consumers signal that they
want beef that has been

tested, then other processors will follow suit. If some consumers, but
not all, demonstrate such a

preference, then some processors, but not all, will test. Moreover,
those processors who do not

test can always market their products based on other factors. See
Virginia Board, 425 U.S. at

770 (if one store is allowed to advertise drug prices, second store's
business could be hurt, but

"nothing prevents [second store] from marketing [its] own assertedly
superior product, and

contrasting it with [first store's]"); see also Peel v. Attorney
Registration and Disciplinary

Comm'n, 496 U.S. 91, 101 & n.10 (1990) (attorney can advertise he is
"certified" by trial

advocacy organization, despite potential negative inference with respect
to other, uncertified,

attorneys). This process, based on the free flow of commercial
information, ensures that

products available for sale are ones that consumers want to buy. Banning
processors from

obtaining and communicating information about their products interferes
with this process and

7235557_1 -7

undermines the efficient functioning of the market. See Ibanez v.
Florida Department of

Business and Professional Regulation, 512 U.S. 136, 144-48 (1994);
Zauderer, 471 U.S. at 640

n.9; Bates v. State Bar of Arizona, 433 U.S. 350, 364 (1977).

c. Speculation about how consumers might value information about BSE
testing is

not a valid basis to ban producers from communicating it. "The First
Amendment directs us to

be especially skeptical of regulations that seek to keep people in the
dark for what the

government perceives to be their own good." 44 Liquormart, 517 U.S. at
502. The "commercial

marketplace, like other spheres of our social and cultural life,
provides a forum where ideas and

information flourish. Some of the ideas and information are vital, some
of slight worth. But the

general rule is that the speaker and the audience, not the government,
assess the value of the

information presented." Id. See also Edenfield, 507 U.S. at 767.

Indeed that is precisely the government's approach with respect to
scores of other

products available on the market today: consumers, not government
regulators, decide whether

particular features or representations are worth any increase in cost.
For example, stores today

contain a vast array of products with characteristics that some
consumers consider valuable, but

which other consumers consider unimportant. The Court might take
judicial notice of such

products, based on nothing more than a walk through virtually any
supermarket in America,

where it will find a wide array of foods that contain "no artificial
flavors, colorings, or

preservatives," others made "without use of synthetic pesticides,
fertilizers, or hormones," and

still more that are "caffeine free," "chlorine free," arsenic free,"
"certified," "kosher," "dolphin-

safe," "organic," "natural," "hand-picked," "vine-ripened," "sun-dried,"
"stone ground," "cold

processed," "aged for three years," and "filtered through layers of
ancient rock."6

6

See generally 7 U.S.C. 205.105 (USDA rules allow product manufacturers
to label and advertise

foods as "organic" if they are produced without use of "synthetic
substances and ingredients"); 21 C.F.R. 101.29

7235557_1 -8

In sum, USDA has not articulated in its Motion for Summary Judgment any
substantial

governmental interest that is served by its policy of banning beef
processors from obtaining and

communicating BSE test data to consumers. For all the reasons set forth
in Creekstone's

Opposition to that motion, and for the reasons set forth herein, the
Court should declare that

policy null and void.

Conclusion

For all the foregoing reasons, Wild Oats seeks leave to appear as amicus
curiae in this

matter, and to present the arguments in this brief, upon which it urges
the Court to deny USDA's

Motion for Summary Judgment.

Respectfully submitted,

signature

Thomas B. Smith

D.C. Bar No. 412192

ROPES & GRAY LLP

One Metro Center

700 12th Street, NW

Washington, DC 20005

(202) 508-4600

Counsel for Wild Oats Markets, Inc.

Date: November 3, 2006

(FDA rules allow food to be labeled as "kosher," as long as they "meet
certain [unspecified] religious dietary

requirements.");
http://www.fsis.usda.gov/Fact_Sheets/Meat_&_Poultry_Labeling_Terms/index.asp
(USDA fact

sheet on labeling terms allowed, including "certified" as an official
mark of "quality").

7235557_1 -9

UNITED STATES DISTRICT COURT

FOR THE DISTRICT OF COLUMBIA

CREEKSTONE FARMS PREMIUM

BEEF, LLC,

Plaintiff,

v.

UNITED STATES DEPARTMENT OF

AGRICULTURE, et al.,

Defendants.

Civil Action No. 06-544 (JR)

ORDER

Upon consideration of the Motion for Leave to Appear as Amicus Curiae in

Opposition to Defendants' Motion for Summary Judgment filed by Wild Oats
Markets,

Inc., it is hereby

ORDERED, that said motion be and hereby is GRANTED.

Hon. James Robertson

United States District Judge

Date: _________________

Serve All Counsel

_

7235557 1

CERTIFICATE OF SERVICE

I certify that, on this 3d day of November 2006, I caused the foregoing
to be

served on the following counsel of record in this case by first class
mail, postage prepaid:

Counsel for Plaintiff Creekstone Farms Premium Beef, LLC:

Russell S. Frye

FRYELAW PLLC

P.O. Box 33195

Washington, DC 20033-0195

William L. Miller

THE WILLIAM MILLER GROUP, PLLC

2248 Hall Place, NW

Washington, DC 20007

Counsel for Defendants United States Department of Agriculture

and Mike Johanns:

James J. Gilligan

Edward H. White

U.S. DEPARTMENT OF JUSTICE

Civil Division, Federal Programs Branch

20 Massachusetts Avenue, NW, Room 6110

Washington, DC 20530

signature

Thomas B. Smith

-2

---
TSS
 

flounder

Well-known member
GREETINGS,


from this abstract of the meeting to happen in 2007, i find this most disturbing ;



3:00 Afternoon Refreshment Break, Poster and Exhibit Viewing in the Exhibit Hall

3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized Mouse Models
Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western Reserve University
Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain discovered recently in Italy, and similar or different atypical BSE cases were also reported in other countries. The infectivity and phenotypes of these atypical BSE strains in humans are unknown. In collaboration with Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have inoculated transgenic mice expressing human prion protein with brain homogenates from BASE or BSE infected cattle. Our data shows that about half of the BASE-inoculated mice became infected with an average incubation time of about 19 months; in contrast, none of the BSE-inoculated mice appear to be infected after more than 2 years. These results indicate that BASE is transmissible to humans and suggest that BASE is more virulent than classical BSE in humans.


http://www.healthtech.com/2007/tse/day1.asp


I found this most interesting, what about Familial BSE? old tom was pondering this many moons ago nov 2000;



CpG mutations in bovines yielding known CJD alleles

http://www.mad-cow.org/prion_point_mutations.html#mam

04 Nov 00 webmaster (a similar analysis could be done in sheep

Recalling that the CpG effect occurs across vertebrates, these might be
expected to cause hotspots for mutations in cows. There has always been
a concern about a steady background of one per million incidence of TSE
in any mammal (Gibbs Principle). While the the bovine prion gene has
its share of CpG occurences, the effect of hotspot changes at these is
in general unpredictable.

However, a certain subset of these gives rise to legitimate concern:
those CpG changes in bovine DNA giving rise to an amino acid
substitution that, had they occured in human DNA in the homologous
position, would cause CJD. It turns out that bovine and human sequences
are similar enough that two known human CJD hotspot mutations are
applicable to bovines: E200K and R208H.

Because prion genes are very slowly evolving, only miniscule
differences are found in comparing human and bovine sequence threaded
to known mouse and hamster nmr structures: this supports but does not
prove that the consequences of the same mutations are similar. The most
immediate concern for 'familial' BSE arises from octapeptide
insertional repeats and E200K.

The table below shows normal bovine in the first row with blue
highlighting for residues where homologous changes in humans is
associated with CJD. The second row shows in red the effect of C to T
changes from the CpG effect, the third row the effect of G to A. Where
blue and red align, I predict the change is causative for BSE. (Other
sites are not ruled out by any means, simply not supported.) E200K is a
very high frequency allele in familial CJD.

Note that in regards to human P102L, the pity here was the CpG site was
newly created in hominoids (CpG are in depleted equilibrium in
placental mammals), being the CCC codon in all species prior to
divergence with orangutan. For a similar reason, mule deer are at
special risk, unlike humans, for A117V, just as pronghorn are at T188R.

At D178N and D202N, cattle again are spared -- the problem is the
silent CAC codon at H177, mainly affecting primates and rodents,
similar to V180I, and the ACT T201.

By using the curated prion sequence database, it is a simple matter to
list all species at risk for hotspot amino acid changes that cause CJD
in humans at the comparable site. In species such as pigs, sheep, and
cows where 100's of millions of animals are kept, it is inevitable that
such mutations arise on a yearly basis.

http://www.mad-cow.org/CpG_bovine.gif



PLUS, FOR ANYONE INTERESTED IN THE CREEKSTONE PDFs FOR YOUR FILES, you can download here ;


http://vegsource.com/talk/madcow/pdf/



TSS
 
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