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From: TSS (
Subject: Re: Barriers to Creutzfeldt-Jakob Disease Autopsies, California
Date: August 27, 2004 at 1:41 pm PST

In Reply to: Barriers to Creutzfeldt-Jakob Disease Autopsies, California posted by TSS on August 24, 2004 at 2:48 pm:

-------- Original Message --------
Subject: re-Barriers to Creutzfeldt-Jakob Disease Autopsies, California
Date: Fri, 27 Aug 2004 15:43:05 -0500
From: "Terry S. Singeltary Sr."

IN reply to ;

Barriers to Creutzfeldt-Jakob Disease Autopsies, California

I would kindly like to comment on the above study/publication please.
MY previous comments first and my comments today;

March 27, 2003 at 7:15 am:

RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob
disease in the United States

IN the reply from Dr. Maddox to Terry S. Singeltary Sr., he states;


If BSE causes a sporadic CJD-like illness in humans, an increase in
sporadic CJD cases would be expected to first occur in the United
Kingdom, where the vast majority of vCJD cases have been reported. In
the United Kingdom during 1997 through 2002, however, the overall
average annual mortality rate for sporadic CJD was not elevated; it was
about 1 case per million population per year. In addition, during this
most recent 6-year period following the first published description of
vCJD in 1996, there was no increasing trend in the reported annual
number of UK sporadic CJD deaths.[3, 5] Furthermore, surveillance in the
UK has shown no increase in the proportion of sporadic CJD cases that
are homozygous for methionine (Will RG, National CJD Surveillance Unit,
United Kingdom, 2003; personal communication)...


THERE seems to be some difference of opinion;

Mouse model sheds new light on human prion disease


Professor John Collinge said “We are not saying that all or even most
cases of sporadic CJD are as a result of BSE exposure, but some more
recent cases may be – the incidence of sporadic CJD has shown an upward
trend in the UK over the last decade. While most of this apparent
increase may be because doctors are now more aware of CJD and better at
diagnosing it, serious consideration should be given to a proportion of
this rise being BSE-related. Switzerland, which has had a substantial
BSE epidemic, has noted a sharp recent increase in sporadic CJD.



ALSO, Dr. Maddox states;

make routine mortality surveillance a useful surrogate for ongoing CJD

THIS has proven not very useful in the U.K.;



One reason for this was the _inaccuracy_ in coding of cases correctly
certified as CJD Coding is carried out by staff who are not medically
qualified and it is not surprising that coding errors occur in the
processing of large numbers of certificates. In 1982, 12,000
certificates per week were processed at the office of population
censuses and surveys bu 15 coders and 6 checkers (Alderson et al.,
1983). The occurrence of both inter- and intra-observer coding errors
has been described (Curb et al., 1983) and the _inaccuracies_ of BOTH
certification and coding discovered in this study _support_ the
introduction of a more accurate system of death certificates and a more
detailed and specific coding system...


AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE
to other species will invariably present pathology typical of a
scrapie-like disease.


DR. Maddox states here;

In collaboration with appropriate local and state health departments and
the National Prion Disease Pathology Surveillance Center, CDC is
facilitating or conducting such surveillance and case- investigations,
including related laboratory studies to characterize CJD and CWD prions.

HOWEVER in a recent article in the UPI out of Washington;

CJD screening may miss thousands of cases

By Steve Mitchell UPI Medical Correspondent Published 7/21/2003 3:00 PM


In addition, the NPDPSC sees less than half of all the CJD cases each
year, so the CDC's investigational system not only is missing many of
the misdiagnosed CJD cases, it also is not conducting autopsies on most
of the detected cases.


ALSO in Philip Yams book 'The Pathological Protein';

''Answering critics like Terry Singeltary, who feels that the US
undercounts CJD, Schonberger _conceded_ that the current surveillance
system has errors but stated that most of the errors will be confined to
the older population''....

THERE has been a _documented_ case of nv/v CJD in a 74 year old, so the
errors Schonberger speaks of (above) would be of significant importance,
if one believes in the nv/v CJD 'only' theory.

NOW we have _documented_ cases of very young CJD victims in the USA
continuing to appear in several different states.

HOW does Dr. Maddox explain this, and does he still believe that a
National CJD surveillance program with a CJD questionnaire to every
victims family is still not warranted?

WITH CWD and Scrapie running rampant in the USA, with BSE now
_documented_ in North America, with the feeding of ruminant-to-ruminant
animal protein still happening in the USA in 2003 even though there has
been a partial voluntary ban on ruminant feeding since 8/4/97, with only
48,000 BSE/TSE tests done on USA cattle in some 14 years of
surveillance, when in any given year there are 100 million cattle in the
USA, with all this, i think refusing to make CJD/TSEs reportable
Nationally in the USA is not ONLY a grave mistake, but in my opinion,
should be looked at with great suspicion...END

NOW, we have new atypical TSEs showing up in animals and
humans all across the Globe. Studies warning us of these
new atypical TSEs;

BASE in cattle in Italy of Identification of a
second bovine amyloidotic spongiform encephalopathy: Molecular
similarities with
sporadic Creutzfeldt-Jakob disease

Identification of possible animal origins of
prion disease in human beings


A further comparison6 of BASE with sCJD in
people revealed that, at least in terms of PrPSc characteristics,
BASE was similar to a particular type of sCJD
sCJD(MV2) (figure). These researchers conclude not only
that BASE is a new strain of BSE, but also that characteristics
of human and animal PrPSc could help to identify
potential risk factors for disease in individuals with sCJD of
unknown origin.


THE LANCET " Vol 363 " June 19, 2004 " 2013

Characterization of two distinct prion strains derived from bovine
spongiform encephalopathy transmissions to inbred mice
S. E. Lloyd, J. M. Linehan, M. Desbruslais, S. Joiner, J. Buckell,
S. Brandner, J. D. F. Wadsworth and J. Collinge
J Gen Virol 2004 85 (8): p. 2471-2478

J Gen Virol -- Future Table of Contents Alert
(not yet published...TSS)

THE findings from Corinne Ida Lasmézas*, [dagger] , Jean-Guy Fournier*,
Virginie Nouvel*,

Hermann Boe*, Domíníque Marcé*, François Lamoury*, Nicolas Kopp [Dagger

] , Jean-Jacques Hauw§, James Ironside¶, Moira Bruce [||] , Dominique

Dormont*, and Jean-Philippe Deslys* et al, that The agent responsible
for French iatrogenic growth hormone-linked CJD taken as a control is
very different from vCJD but is similar to that found in one case of
sporadic CJD and one sheep scrapie isolate;

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

The EMBO Journal Vol. 21 No. 23 pp. 6358±6366, 2002

BSE prions propagate as either variant CJD-like or
sporadic CJD-like prion strains in transgenic mice
expressing human prion protein

A ProMED-mail post

ProMED-mail is a program of the
International Society for Infectious Diseases

Date: Tue 6 Jan 2004
From: Terry S. Singeltary Sr.
Source: EMBO Reports, 5, 1, 110­115, 2004 (published online: 19 Dec2003)

Distinct Molecular Phenotypes in Bovine Prion Diseases
The following paragraph is the Abstract from a report with the above title
by Anne-Gaelle Biacabe, Jean-Louis Laplanche, Stephen Ryder, and Thierry
Baron, published in EMBO (European Molecular Biology Organisation) Reports.
19 Dec 2003.

"Bovine spongiform encephalopathy (BSE) in cattle, the most likely cause of
variant Creutzfeldt­Jakob disease [abbreviated as CJD (new var.) or vCJD in
ProMed-mail] in humans, is thought to be caused by a unique infectious
agent, with stable features, even when transmitted to other species. Here,
we show the existence of an atypical molecular phenotype among cattle
diagnosed with BSE in France. Following western blot analyses, 3 cases
showed unusual features of the electrophoretic profiles of the
protease-resistant prion protein (PrPres) accumulating in the brain. The
PrPres patterns were similar in these 3 atypical cases, showing a higher
molecular mass of unglycosylated PrPres and strong labelling by P4
monoclonal antibody compared to 55 typical BSE cases. This finding suggests
either some phenotypic modifications of PrPres following infection by the
BSE agent or the existence of alternative origins of such diseases in

Terry S. Singeltary Sr

[The following paragraphs comprise extracts from the authors' discussion of
their findings. The original article should be consulted for the
appropriate references.

"Our results demonstrate the finding of a distinct molecular phenotype of
prion diseases in cattle among routinely diagnosed BSE cases following
active surveillance of the disease using rapid tests for the detection of
PrPres in cattle at a slaughterhouse or in rendering plants. The 3 cases
described here had not been reported as having clinical signs suggestive of
BSE during their life and were found in old cattle.

This atypical molecular phenotype is mainly characterized by a higher
molecular mass of the unglycosylated PrPres and PrPres labelling by P4
monoclonal antibody. This is an unexpected finding since it is believed
that this cattle disease is caused by a single strain of infectious agent,
which has shown very stable and uniform features, including following its
transmission to other species.

Several hypotheses can be considered to explain this finding. This may be a
manifestation of the BSE agent with different molecular features in cattle,
as recently described following transmission in transgenic mice expressing
the human prion protein. Mechanisms involved in such observations remain to
be established, but it should be emphasized that such PrPres changes were
only found following transmission of cattle BSE, not of human vCJD, to
these human transgenic mice.

Genetic differences in the prion genes between these atypical cattle and
the general cattle population might be expected to give rise to variants in
electrophoretic profiles of PrPres, as the sequence of the human PRNP gene
is known to influence the molecular features of PrPres in some cases of
human [sporadic] CJD. Sequencing of the entire open reading frame of the
prion genes of 2 of the atypical cases that showed the known sequence for
cattle excluded this hypothesis. Importantly, with regard to the single
polymorphism described in the bovine prnp gene, which can contain 5 or 6
repeats of the octapeptide region, no differences were observed between the
atypical and typical BSE cases, which could otherwise be distinguished by
labelling with P4 monoclonal antibody that recognizes an epitope very close
to this region of the protein.

In human [sporadic] CJD, it has also been shown that 2 distinct PrPres
types could be inter-converted in vitro by altering their metal ion
occupancy. Treatment with metal ion chelator EDTA, in the range of
concentrations that was shown to modify the PrPres profiles in human CJD,
did not modify the electrophoretic patterns of cattle-BSE cases. The
differences between atypical cases and typical cattle BSE were maintained,
with regard to both molecular mass of unglycosylated PrPres and P4
labelling of PrPres.

Cattle may also have been infected by another source of infectious agent,
such as scrapie from sheep and goats. Interestingly, experimental infection
of cattle with a British natural sheep scrapie source indeed led to similar
differences in the PrPres electrophoretic profiles compared to typical
cattle BSE.

Finally, it has been suggested that a spontaneous rare sporadic form of
these diseases could exist in cattle as in humans, and might have been the
origin of the BSE epidemic. As different PrPres profiles were found between
sporadic and variant CJD in humans, this hypothesis might also explain our

Further studies are now required to determine the frequency of such novel
molecular phenotypes in cattle and the biological features of the involved
infecting strain. These may be carried out by means of mouse transmission
studies in a panel of wild-type mice with different prn-p genotypes, as
well as in bovine transgenic mice. However, in a 1st hypothesis, our
results would reinforce the possibility that BSE might have different
manifestations, and in this case might be hardly recognized when
transmitted to other species as previously suggested.

Alternatively, this may argue that different forms of the disease may
affect cattle, possibly meaning that some cases of such diseases could be
detected beyond any possibility of contamination by infected meat-and-bone
meal. While contamination and recycling of a scrapie agent in cattle has
been a major hypothesis of the origin of BSE, [direct] infection of cattle
by scrapie agents may have occurred. This may have happened through
contamination of feed as possibly occurred at the origin of the BSE
epizootic, but direct infection could also be considered since scrapie can
be transmitted between sheep and goats by contact and/or through
environmental contamination."

Japanese workers have reported recently that an atypical form of the BSE
agent was associated with cases of disease in Japan. It remains to be
established whether the atypical form detected in these French cattle in
any way resembles the atypical form described by the Japanese scientists. -

[see also:
CJD (new var.) - UK: update 2004 (01) 20040106.0064
Scrapie - Norway: new phenotype 20031117.2857
BSE - Japan (08): 9th case, lab findings 20031115.2838
BSE, atypical case - Italy: OIE 20031022.2649
BSE - Japan (06): atypical 20031009.2547
BSE - Japan (05): atypical 20031008.2526
BSE - Japan (04): atypical 20031007.2511
CJD, iatrogenic: strain differences 20030718.1765]

Greetings CDC et al,

WITH all this data, the risk of iCJD from all these different
TSEs, I find it extremely disturbing that CDC/NIH et al
are still insisting that CJD not be made reportable in
every state. FURTHERMORE, in the 25 or so that CJD
is reportable, in some, I find it even more disturbing
that there is a clause for an age bracket in some of those
states. THERE have been documented cases of nv/v CJD
in the elderly. WE have young victims of CJD mounting
in the USA, but it's all sporadic? Something is terribly
wrong here and by refusing to make all human TSE reportable
Nationally, will only spread this agent further. To think that
85%+ of all CJD (sporadic) happens spontaneously without
route and source of any agent, to believe in this nonsense,
is like believing in Santa Claus. THE USA BSE GBR was
just raised to III with the findings stating that ;

> USA, Summary of the GBR Assessment, July 2004 GBR Level : III**
> 1980-1990: Moderate
> 1991-1995: Very High
> 1996-2003: Extremely high
> 1980-2003: Extremely unstable
> Live Cattle imports MBM imports Feeding Rendering SRM-removal BSE
> surveillance
> Any external challenge would have met the
> extremely unstable system and infectivity
> would have been recycled.
> An internal challenge was possibly present
> from 1980 to 1990 and was likely to be present
> and growing from 1991 to 2003
> From UK:
> 323 (CD*)
> or
> 327 (other sources of
> data)
> From other BSE risk
> countries:
> 16.656.490 (CD)
> or
> 15.496.449 (other
> sources of data).
> *CD: country dossier
> From UK:
> 5 tons (CD)
> or
> 101 tons (other
> sources of data)
> From other BSE risk
> countries:
> 406.547 tons (CD)
> or
> 229.701 tons (other
> sources of data)
> 1980-2003:
> Not OK.
> Feeding of
> ruminant MBM to
> cattle legally
> possible until
> August 1997.
> 1980-2003:
> Not OK.
> No proof of an
> effective process in
> reducing BSEinfectivity
> is given.
> 1980-2003:
> Not OK.
> SRM are still
> rendered for feed.
> Passive but
> improving with
> some testing of risk
> groups.
> As long as there are no significant changes in
> rendering or feeding, the stability remains
> extremely/very unstable. Thus, the probability
> of cattle to be (pre-clinically or clinically)
> infected with the BSE-agent persistently
> increases.
> ** GBR level III: ‘it is likely but not confirmed’ that domestic cattle
> are (clinically or pre-clinically) infected with the BSE-agent.

WITH all the different animal TSEs being rendered and fed back
to animals for human and animal consumption here in the USA for
decades, there is no telling what kind and how many different strains
of CJD/TSEs are here in the USA.

DUE to International travel, hospitalization and such, i still say all
human TSEs must be made reportable Nationally and Internationally ASAP,
especially sporadic CJD, because you simply do not know how many
strains are included in the sporadic CJD category and you dont know
how they would transmit and how infectious the tissues would be.

thank you,

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


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

disease in the United States

Email Terry S. Singeltary:

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

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

forms of CJD. Asante, Collinge et al [1] have reported that BSE

transmission to the 129-methionine genotype can lead to an alternate

phenotype that is indistinguishable from type 2 PrPSc, the commonest

sporadic CJD. However, CJD and all human TSEs are not reportable

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

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

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

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

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

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

intracerebral inoculation. With the known incubation periods in other

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

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

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

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

should be drastic measures to safeguard the medical and surgical arena

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

CJDs in the USA are type 2 PrPSc?


Volume 3, Number 8 01 August 2003


Tracking spongiform encephalopathies in North America

Xavier Bosch

My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost

my mom to hvCJD (Heidenhain variant CJD) and have been searching for

answers ever since. What I have found is that we have not been told the

truth. CWD in deer and elk is a small portion of a much bigger problem.

49-year-old Singeltary is one of a number of people who have remained

largely unsatisfied after being told that a close relative died from a

rapidly progressive dementia compatible with spontaneous

Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of

documents on transmissible spongiform encephalopathies (TSE) and

realised that if Britons could get variant CJD from bovine spongiform

encephalopathy (BSE), Americans might get a similar disorder from

chronic wasting disease (CWD)the relative of mad cow disease seen among

deer and elk in the USA. Although his feverish search did not lead him

to the smoking gun linking CWD to a similar disease in North American

people, it did uncover a largely disappointing situation.

Singeltary was greatly demoralised at the few attempts to monitor the

occurrence of CJD and CWD in the USA. Only a few states have made CJD

reportable. Human and animal TSEs should be reportable nationwide and

internationally, he complained in a letter to the Journal of the

American Medical Association (JAMA 2003; 285: 733). I hope that the CDC

does not continue to expect us to still believe that the 85% plus of all

CJD cases which are sporadic are all spontaneous, without route or source.

Until recently, CWD was thought to be confined to the wild in a small

region in Colorado. But since early 2002, it has been reported in other

areas, including Wisconsin, South Dakota, and the Canadian province of

Saskatchewan. Indeed, the occurrence of CWD in states that were not

endemic previously increased concern about a widespread outbreak and

possible transmission to people and cattle.

To date, experimental studies have proven that the CWD agent can be

transmitted to cattle by intracerebral inoculation and that it can cross

the mucous membranes of the digestive tract to initiate infection in

lymphoid tissue before invasion of the central nervous system. Yet the

plausibility of CWD spreading to people has remained elusive.

Part of the problem seems to stem from the US surveillance system. CJD

is only reported in those areas known to be endemic foci of CWD.

Moreover, US authorities have been criticised for not having performed

enough prionic tests in farm deer and elk.

Although in November last year the US Food and Drug Administration

issued a directive to state public-health and agriculture officials

prohibiting material from CWD-positive animals from being used as an

ingredient in feed for any animal species, epidemiological control and

research in the USA has been quite different from the situation in the

UK and Europe regarding BSE.

Getting data on TSEs in the USA from the government is like pulling

teeth, Singeltary argues. You get it when they want you to have it,

and only what they want you to have.

Norman Foster, director of the Cognitive Disorders Clinic at the

University of Michigan (Ann Arbor, MI, USA), says that current

surveillance of prion disease in people in the USA is inadequate to

detect whether CWD is occurring in human beings; adding that, the

cases that we know about are reassuring, because they do not suggest the

appearance of a new variant of CJD in the USA or atypical features in

patients that might be exposed to CWD. However, until we establish a

system that identifies and analyses a high proportion of suspected prion

disease cases we will not know for sure. The USA should develop a

system modelled on that established in the UK, he points out.

Ali Samii, a neurologist at Seattle VA Medical Center who recently

reported the cases of three hunterstwo of whom were friendswho died

from pathologically confirmed CJD, says that at present there are

insufficient data to claim transmission of CWD into humans; adding that

[only] by asking [the questions of venison consumption and deer/elk

hunting] in every case can we collect suspect cases and look into the

plausibility of transmission further. Samii argues that by making both

doctors and hunters more aware of the possibility of prions spreading

through eating venison, doctors treating hunters with dementia can

consider a possible prion disease, and doctors treating CJD patients

will know to ask whether they ate venison.

CDC spokesman Ermias Belay says that the CDC will not be investigating

the [Samii] cases because there is no evidence that the men ate

CWD-infected meat. He notes that although the likelihood of CWD

jumping the species barrier to infect humans cannot be ruled out 100%

and that [we] cannot be 100% sure that CWD does not exist in humans&

the data seeking evidence of CWD transmission to humans have been very


he complained in a letter to the Journal of the American Medical

Association (JAMA 2003; 285: 733). I hope that the CDC does not

continue to expect us to still believe that the 85% plus of all CJD

cases which are sporadic are all spontaneous, without route or source.<<<

actually, that quote was from a more recent article in the Journal of

Neurology (see below), not the JAMA article...

Full Text

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

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






BY Philip Yam

Yam Philip Yam News Editor Scientific American

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

IMPORTS FROM CANADA [takes a few minutes to load]

Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION]

Docket Management Docket: 02N-0273 - Substances Prohibited From Use in

Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed

Comment Number: EC -10

Accepted - Volume 2



File Format: PDF/Adobe Acrobat -

Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary

Sr. [] Monday, January 08,200l 3:03 PM freas ...

Asante/Collinge et al, that BSE transmission to the 129-methionine

genotype can lead to an alternate phenotype that is indistinguishable

from type 2 PrPSc, the commonest _sporadic_ CJD;

Docket Management Docket: 96N-0417 - Current Good Manufacturing Practice
in Manufacturing, Packing, or Holding Dietary Ingredients a
Comment Number: EC -2
Accepted - Volume 7

[PDF] Appendices to PL107-9 Inter-agency Working Group Final Report 1-1
File Format: PDF/Adobe Acrobat - View as HTML
Agent, Weapons of Mass Destruction Operations Unit Federal Bureau of
those who provided comments in response to Docket No. ...
Meager 8/18/01 Terry S. Singeltary Sr ...

Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION
TO DOCKET 2003N-0312]

# Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of
TSS 1/27/03 (0)

Docket Management

Docket: 02N-0276 - Bioterrorism Preparedness; Registration of Food
Facilities, Section 305
Comment Number: EC-254 [TSS SUBMISSION]

Dockets Entered On October 2, 2003 Table of Contents, Docket #,
Title, 1978N-0301,

OTC External Analgesic Drug Products, ... EMC 7, Terry S. Singeltary Sr.
Vol #: 1, ...

Daily Dockets Entered on 02/05/03

DOCKETS ENTERED on 2/5/03. ... EMC 4 Terry S. Singeltary Sr. Vol#: 2.
... Vol#: 1.

03N-0009 Federal Preemption of State & Local Medical Device Requireme. ...

Docket Management

Docket: 02N-0370 - Neurological Devices; Classification of Human Dura Mater

Comment Number: EC -1

Accepted - Volume 1

Daily Dockets - 04/10/03

... 00D-1662 Use of Xenotransplantation Products in Humans.
EMC 98 Terry S. Singeltary Sr. Vol#: 3. 01F ... - 05-20-2003
- Cached

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

Terry S. Singeltary Sr.
Vol #:

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

Terry S. Singeltary Sr.
Vol #:

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

Terry S. Singeltary Sr.
Vol #:

01N-0423 Substances Prohibited from use in animal food/Feed Ruminant

APE 5 National Renderers Association, Inc. Vol#: 2

APE 6 Animal Protein Producers Industry Vol#: 2

APE 7 Darling International Inc. Vol#: 2

EMC 1 Terry S. Singeltary Sr. Vol#: 3

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

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