Thursday, January 5, 2012

Horse Meat, slaughter for consumption USA

Horse slaughter in Texas and everywhere else should be against the law


Posted Wednesday, Dec. 07, 2011


By Nicole Paquette


Special to the Star-Telegram


When it comes to the issue of horse slaughter, the Star-Telegram's Monday editorial got one thing right: The American people, and Texans in particular, love their horses -- but because they are trusted companions, not dinner. (See: "State horse slaughter ban needs revisiting")


American horse lovers, breeders and owners shudder at the thought of any horse of theirs ending up as a high-priced appetizer in Belgium or Japan.


The facts surrounding horse slaughter make it clear why Americans find it to be such a despicable end for horses. The process is brutal and innately inhumane. Inside the bloody, panic-stricken environment of a slaughterhouse, horses endure torture during often-repeated attempts to render them unconscious.


The USDA documented horrendous cruelty at the foreign-owned plants in Texas prior to their closure, despite the presence of federal inspectors. There's no reason to believe it won't be the same if plants reopen here.


The horse slaughter industry was never good for the economy -- it was good for the profiteers, and no one else. The foreign-owned horse slaughter plants that operated in Texas until 2007 caused nothing but controversy and problems. They employed no more than a few dozen people in low-paying, highly dangerous jobs. Profits didn't benefit local economies, but were instead pocketed overseas by foreign corporations. The communities that hosted the plants were constantly beset by pollution and the unending stench of rotten blood and offal. In their quest to improve their profit margin, these foreign-owned businesses did everything they could to avoid paying their property taxes and the fines levied against them for their environmental violations.


The negative image created by these operations caused other businesses to look elsewhere for a place to set up shop.


All of these unpleasant factors led Paula Bacon, former mayor of Kaufman (where one of the plants was located), to say, "As a community leader where we are directly impacted by the horse slaughter industry, I can assure you the economic development return to our community is negative. The foreign-owned companies profit at our expense -- it is time for them to go."


Slaughtering horses at plants in Texas never prevented the illegal acts of horse neglect and abandonment, nor has their export to plants across our borders. In the midst of today's difficult economic times, neglect and abandonment continue, though the same number of our horses are still being slaughtered. There's no single fix to the problem of homeless or neglected horses, just like there is no single fix to the pet overpopulation problem. These challenges can be solved only with a blend of wise policy solutions, rescue and sanctuary work and a large dose of personal responsibility.


For its part, the American Quarter Horse Association should stop equating the horror of the slaughter plant with "humane euthanasia." There is nothing peaceful or dignified about hauling a horse thousands of miles in terrible conditions to a harrowing death in the kill box. The horse industry should discourage the overbreeding of America's horses and relying on the cruel and predatory killer buyers to snatch up the excess. Reducing the supply of horses and focusing on improved quality are the best and most sustainable ways to give the equine industry the boost it needs.


Opinion polls are clear: The vast majority (more than 70 percent) of Americans and nearly 80 percent of Texans oppose the slaughter of horses. It is absurd to consider repealing a law that has been on the books since 1949 and has continuously been upheld in the Texas Legislature and in the courts. The majority of Texans have spoken, and it is high time we listen.


Horses are members of the family, trusted companions and partners in recreation and sport. Those few but noisy individuals clamoring for slaughter should find other ways to "help" horses, if that is their aim. Let's start by finally banning horse slaughter all across the country, by passing the American Horse Slaughter Prevention Act (S.1176/H.R. 2966).


Nicole G. Paquette of Austin is the Texas senior state director of the Humane Society of the United States.








Horse slaughter in Texas needs revisiting


Posted Sunday, Dec. 04, 2011



Americans, and Texans in particular, have long had a romance with the horse, that noble-looking animal that has served for work, sport and as a big barnyard pet.


It also once was served for food -- though the very thought of that is repulsive to some people. Until recently, that use was illegal following a 2006 maneuver by Congress to not fund federal inspections of horse meat. That congressional gimmick shut down horse slaughter houses in the United States the following year.


But things changed again recently, when Congress passed an agriculture appropriations bill that omitted the ban on USDA horse meat inspections. That means horse slaughter is legal again in the United States, except in states that have their own prohibition against it.


Texas has a 1949 law on the books that bans the possession or transport of horse meat for human consumption, a statute that was upheld by a state attorney general's ruling in 2002 and by the 5th U.S. Circuit Court of Appeals. That means there will be no equine steaks served in this state unless legislators change the law.


That's something they should do.


Before Congress cut off funding for inspections and the 5th Circuit ruled on Texas' law, three horse slaughter plants operated in the U.S.: two were in Texas, one of them in Fort Worth. They processed meat mostly for consumption overseas.


Animal-rights advocates' efforts to save horses from slaughter apparently didn't stop the killing, even after the packing plants shut down.


A report by the Government Accountability Office showed that, since the closing of domestic slaughter houses in 2007, about the same number of American horses are being killed -- about 138,000 in 2010. The only difference is they are being transported to Mexico and Canada for slaughter.


In other words, three American businesses were forced to shut down and the work (and profit) went to foreign countries.


"From 2006 through 2010, U.S. horse exports for slaughter increased by 148 percent to Canada and 660 percent to Mexico," the GAO reported.


Since the ban, the GAO also reported, there has been a dramatic increase in reports of horse neglect, a trend expected to get even worse in this down economy. The American Quarter Horse Association had argued in 2006 that processing of unwanted horses was "a necessary aspect of the equine industry, because it provides a humane euthanasia alternative for horses that might otherwise continue a life of discomfort and pain, or inadequate care or abandonment."


Texans might not want to see this industry return to the state, insisting that eating horse flesh is sacrilege in a place where the cowboy is heralded as a heroic figure and his trusted four-legged companion is idealized.


But other states are eager for the business. Nine have passed resolutions calling for the return of horse slaughter. The Star- Telegram reported Thursday that in a few states plans are underway to retrofit facilities to handle processing of horse meat, and a former representative of the three closed Texas packing plants predicts that a plant could be operational in six months to a year.


The 1949 Texas law banning consumption of horse meat is outdated and needs to be repealed.


At the very least, the Legislature should take up the issue when it convenes in 2013 and let Texans have their say on this important -- albeit emotional -- public policy issue.








Horse Meat


Horse Slaughter Information Page






Greetings,



for what it’s worth.


I am against horse slaughter for consumption or any other purpose i.e. fertilizer, plastic, fuel, etc.


I am against the use of primates in scientific studies. because arguments will always persist on proof of human relation from any given study. However, I am for Human use in place of Primates in these studies. I said it long ago. Death Row inmates. compensate the families and do the studies on these death row inmates. it could be the last good thing they ever do. just my opinion.


For horses, they should use the same policy they use in the USA for old diseased mad cows, i.e. SSS policy. shoot, shovel, and shut up. either bury them or incinerate them. again, just my opinion.


there is no humanity anymore $$$


It brings me to the old movie. how many times do old movies come true? strange...



'soyent green'.


see ;


Soylent Green is a 1973 dystopian science fiction movie depicting a future in which overpopulation lead to depleted resources, which in turn leads to widespread unemployment and poverty. Real fruit, vegetables, and meat are rare, commodities are expensive, and much of the population survives on processed food rations, including "soylent green" wafers.


The film overlays the science fiction and police procedural genres as it depicts the efforts of New York City police detective Robert Thorn (Charlton Heston) and elderly police researcher Sol Roth (Edward G. Robinson) to investigate the brutal murder of a wealthy businessman named William R. Simonson (Joseph Cotten). Thorn and Roth uncover clues which suggest that it is more than simply a bungled burglary.


snip...


After Roth dies, Thorn sneaks into the basement of the government-assisted suicide facility, where he sees corpses being loaded onto waste disposal trucks. He secretly hitches a ride on one of the trucks, which is driven to a heavily guarded waste disposal plant. Once inside the plant, Thorn sees how the corpses are processed into Soylent Green wafers. After Thorn escapes from the plant and heads for the supreme exchange with the information, he is ambushed by Fielding and several other gunmen. In the shootout, Thorn kills some of the gunmen, but is himself wounded. He retreats into a cathedral filled with homeless people. After a desperate fight, Thorn stabs and kills Fielding.


When police backup arrives, the seriously wounded and nearly hysterical Thorn confides to Hatcher the horrible secret behind Soylent Green and urges him to spread the word: "Soylent Green is people! We've got to stop them somehow!"





don’t believe me, were almost there ;





IN CONFIDENCE


SUSPECT BSE IN A HORSE


CYO BSE 1 9


IN CONFIDENCE


SUSPECT BSE IN A HORSE


The Parliamentary Secretary (Mr Maclean) will wish to be aware that, in making his differential diagnosis, a veterinary surgeon in the Reading area has included the possibility of BSE in a horse under his care. Although it is unlikely to be BSE, because of the symptoms exhibited the veterinarian believes that he cannot exclude the possibility. The case was brought to the notice of one of the veterinary staff at the CVL by the owner's veterinary surgeon and liaison is being maintained.


The horse in question is a five-year old eventing gelding which was purchased by the present owner about four months ago. Approximately two months after purchase the animal became a little apprehensive, developed mild nervous symptoms and became over-sensitive to noise. The nervous symptoms have increased and the horse is now practically impossible to ride. Investigations by the owner's private veterinary surgeon are continuing but it is likely that the animal will have to be destroyed.


If the horse should die or be destroyed, a full post-mortem examination will be required for insurance purposes and will probably be carried out at a non-Ministry laboratory. However, Mr Bradley of the Pathology Department, CVL, has informed the private veterinary surgeon that he is willing to provide a second opinion on the brain histology if requested.


I will keep the Parliamentary Secretary informed of any further developments in the case.


I CRAWFORD


14 May 1990


Mr M P H Hill, PS/Parliamentary secretary (Mr Maclean) - by FAX


cc:


Private Offices


Mr K C Meldrum


Mrs E A J Attridge D J Evans Mr K C Taylor Mr R Lawson Mr R Bradley. CVL


(hand written notes i cannot read all (cut short) as follows...tss)


The Parliamentary Secretary (Mr Maclean was grateful for this. He said that we must keep very close to ...on it, and when the horse dies, or is put down we must be told immediately. He also feels it is very important that our veterinary staff be involved in the brain examination. .........(cannot read the rest .............TSS)


90/05.14/10.1





Mr A Huws Principal WOAD2A CP2


SUSPECT BSE IN A HORSE


You will wish to be aware that on Thursday afternoon 25 June the T/DVO Powys received a phone call from a veterinary Surgeon reporting his suspicion that a horse had ___contracted BSE after having been fed cattle cake___.


The clinical symptoms described were similar to those shown by cattle there ___being a similar case some months ago on the same premises___.


The owner' s name and address is:


Irene Thomas J Thomas & Company Riding Stables Penybryn Llangorse Brecon


The horse is a 12 year old gelding used for pony trekking.


By yesterday evening the horse was in a comatose state and on humane grounds was destroyed by the veterinary Surgeon. At his request a full post mortem and laboratory investigation will be carried out at the Carmarthen Veterinary Investigation Centre this morning to ascertain the exact cause; I have been told this will take at least two weeks. Charges to the veterinary Surgeon have been waived in this instance.


I will inform you immediately I receive a diagnosis.


26 June 1990


D SUMMERS DRVO


cc


Mr D R Williams, RVO


Mr A R Hunter, SVIO


90/06.26/10.1





Mr A Huws Principal WOAD2A CP2


SUSPECT BSE IN A HORSE


You will wish to be aware that on Thursday afternoon 25 June the T/DVO Powys received a phone call from a veterinary Surgeon reporting his suspicion that a horse had contracted BSE after having been fed cattle cake. The clinical symptoms described were similar to those shown by cattle there being a similar case some months ago on the same premises.


The owner' s name and address is:


Irene Thomas J Thomas & Company Riding Stables Penybryn Llangorse Brecon


The horse is a 12 year old gelding used for pony trekking.


By yesterday evening the horse was in a comatose state and on humane grounds was destroyed by the veterinary Surgeon. At his request a full post mortem and laboratory investigation will be carried out at the Carmarthen Veterinary Investigation Centre this morning to ascertain the exact cause; I have been told this will take at least two weeks. Charges to the veterinary Surgeon have been waived in this instance.


I will inform you immediately I receive a diagnosis.


26 June 1990


D SUMMERS DRVO


cc


Mr D R Williams, RVO


Mr A R Hunter, SVIO


90/06.26/10.1





full text ;






we know that horses, especially quarter horses and show horses are fed feed with high animal protein content, and it’s perfectly legal.



see ;




Nonprohibited Materials:



These feed materials CAN be fed to ruminants.


A. The following protein products derived from mammals, including ruminants, are exempt from the Ruminant Feed Ban rule and CAN be fed to ruminants:


Blood and blood products


Milk products (milk and milk protein)


Pure porcine (pork) protein


Pure equine (horse) protein


Gelatin Inspected meat products, such as plate waste, which have been cooked and offered for human food and further heat processed for animal feed.


snip... see full text ;







From: TSS


Subject: MAD COW/HORSE FEED BAN VIOLATIONS WARNING LETTER July 20, 2001 USA


Date: August 14, 2001 at 11:36 am PST


DEPARTMENT OF HEALTH AND HUMAN SERVICE


July 20, 2001


CERTIFIED MAIL RETURN RECEIPT REQUESTED


WARNING LETTER Ref. KAN 2001-028


Mr. Eric N. Blomkuist, CEO Farnam Companies, Inc. 301 W. Osborn P.O. Box 34820 Phoenix, AZ 85013


Dear Mr. Blomkuist:


An inspection of your Council Bluffs, Iowa facility that serves as a manufacturing/repackaging site for animal feed and as a distribution operation for animal drugs and feeds conducted on June 13-20, 2001 by an Investigator representing this office found significant deviations from the requirements set forth in Title 21, Code of Federal Regulations, Part 589.2000 - Animal Proteins Prohibited in Ruminant Feed. This regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalophathy (BSE) within the borders of the United States. Such deviations cause products being manufactured and/or distributed by your facility to be adulterated within the meaning of Section 402(a)(4) and misbranded within the meaning of Section 403(F) of the Federal Food, Drug, and Cosmetic Act (the Act).


The inspection revealed the following:


There are no written procedures demonstrating the clean-out process used to prevent the cross- contamination of product. Your firm uses common equipment for product manufactured with prohibited material and for feed and/or drugs that are not.


Your firm distributes products that may contain prohibited material, specifically Flex Free, Equinyl, Generation and Max Flex, that are not labeled with the required cautionary statement "Do Not Feed to Cattle or Other Ruminants"


The above is not intended to be an all-inclusive list of violations. As a manufacturer of products intended for animal feed use you are responsible for assuring that your overall operation and the products you manufacture and distribute are in compliance with the law. At the conclusion of the inspection Form FDA483, List of Inspectional Observations was issued to Ronald G. Adler, Plant Manager identifying these and other deviations. A copy is enclosed for your information.


Our Investigator reported a telephone discussion with Mr. Barry G. Harrison who identified himself as the Corporate Counsel of the Farnam Companies, Inc. During this discussion Mr. Harrison, reportedly, claimed the products in question are exempt from the cautionary statement requirement. This claimed exemption is based on the fact the products are intended only for the equine market and your firm defines horses as pets. We cannot accept this claimed exemption because while some horses may be held as pets, horses are also working animals and in some parts of North America, food animals.


Based on our knowledge of working ranches, horse feed is often stored in the same general area as ruminant feed making a conspicuous cautionary statenmit vital on feeds and supplements, containing prohibited materials.


You should take prompt action to correct the above violations and to establish procedures whereby such violations do not recur. Failure to make immediate and lasting corrections may result in regulatory actions without further notice including but not limiting to product seizure and/or injunction.


You should respond, in writing, Within 15 working days of the steps you have taken to bring your firm into compliance with the law. Please include all the steps you plan to take, the timeframe for completing these actions and any documentation demonstrating the action's completion.


Your response should be directed to Ralph J. Gray, Compliance Officer at the above address.


Sincerely, Charles W. Sedgwick District Director Kansas City District Office


Cc: Mr. John C. Williams CEO, Manufacturing and Distribution Farnam Companies, Inc, 1302 Law Ross Road Council Bluffs, IA 51501






Subject: Re: MAD COW/HORSE FEED BAN VIOLATIONS WARNING LETTER July 20, 2001


Date: Tue, 14 Aug 2001 23:43:26 –0400


From: "Robert A. LaBudde"


Reply-To: Bovine Spongiform Encephalopathy


To: BSE-L@uni-karlsruhe.de


######## Bovine Spongiform Encephalopathy #########


At 01:41 PM 8/14/01 -0700, Terry wrote: >DEPARTMENT OF HEALTH AND HUMAN SERVICE > >July 20, 2001 > >Our Investigator reported a telephone discussion with Mr. Barry G. >Harrison who identified himself as the Corporate Counsel of the Farnam >Companies, Inc. During this discussion Mr. Harrison, reportedly, claimed >the products in question are exempt from the cautionary statement >requirement. This claimed exemption is based on the fact the products >are intended only for the equine market and your firm defines horses as >pets. We cannot accept this claimed exemption because while some horses >may be held as pets, horses are also working animals and in some parts >of North America, food animals. > >Based on our knowledge of working ranches, horse feed is often stored in >the same general area as ruminant feed making a conspicuous cautionary >statenmit vital on feeds and supplements, >containing prohibited materials.


Terry:


Perhaps you should pester FDA about this "loophole". Apparently, "pet food" does not have to bear the warning labels specified for food animals.


I can't see any serious objection to expanding the label requirement to ALL animal food, not just food animals.


Also, horses are "ruminants", so it's disturbing that they might escape the feed ban by being classified as "pets". Another good reason to extend the warning labels and regulation to all animal foods.


Perhaps you could submit a request for ruling to the FDA on this issue to propose amending the regulation to include all animal foods, including pet foods.




================================================================



Robert A. LaBudde, PhD, PAS, Dpl. ACAFS e-mail: ral@lcfltd.com Least Cost Formulations, Ltd. URL: http://lcfltd.com/ 824 Timberlake Drive Tel: 757-467-0954 Virginia Beach, VA 23464-3239 Fax: 757-467-2947


"Vere scire est per causas scire"




================================================================





Subject: Re: Horses & ruminants


Date: Wed, 15 Aug 2001 12:41:29 +0200


From: Roland Heynkes


Reply-To: Bovine Spongiform Encephalopathy


To: BSE-L@uni-karlsruhe.de


######## Bovine Spongiform Encephalopathy #########


Dear Robert and Oz,


>> Also, horses are "ruminants", so it's disturbing that they >> might escape the feed ban by being classified as "pets". >> Another good reason to >extend the warning labels and >> regulation to all animal foods. > > Just a note that horses are NOT ruminants, as I am sure > robert knows from the quotes. > They are however herbivores. > It's also worth noting problems with x-infection found > in the EU. > although horses are not ruminants, it is of course a very poor idea to exclude them from a feed ban. Unfortunately exactly this is the case even in Germany, where horses are still excluded from the ban, if they are not intended to become human food. As Oz mentioned, this opens an absolutely unnecessary possibility for cross contaminations. Of course I repeatedly informed the involved German politicians and authorities about this problem, but they are not interested.


This perfectly fits to the fact, that most German authorities are still not prepared to inform the public about the German BSE cases. If you are interested in some information about this cases, you have to visit private Internet sites. Instead most German authorities provide the public with down playing statements and links to meat industry and marketing agencies. Links to sites with scientific information about TSE safety problems are not allowed on this official sites. Official sites with useful information comparable with those that we all know from the UK, are not wanted in Germany.


This also perfectly fits to the fact, that it is at least in Germany well known since 5 days for those who are interested in such information, that Dr. Margit Herbst won the Whistleblower-Prize. You may be not surprised to learn, that this prize is from a scientific association, not from politics. She gets it, because she lost her job, just because she informed the public about the fact that her superiors were not prepared to run the necessary pathological examinations with more than 20 cattle, that she had found to show BSE symptoms between 1990 and 1994 in just one German abattoir. At that time this was the political signal for all German vets not to find any German BSE cases. And as you know, the Bavarian vets were not prepared to let my speak about German BSE risks even in May 2001.


I was interested to see, if any of the German members of this list would forward this good news about Dr. Margrit Herbst. In my opinion it is absolutely typical that this was not the case and that again I had to do this.


By the way, studying the British BSE statistics I found that the risk to become infected, was sharply declining from birth to the age of about 6 months and that for a given period of time the risk of infection was about 5-times as high for a calf in comparison to adult animals. It is therefore clear, that many cattle became infected only as adults. The detailed analysis will be on my site until the end of this week.


kind regards


Roland






Subject: Re: MAD COW/HORSE FEED BAN VIOLATIONS WARNING LETTER


July 20, 200 1 Date: Thu, 16 Aug 2001 13:52:58 –0400


From: "Cook, Nancy" Reply-To: Bovine Spongiform Encephalopathy


To: BSE-L@uni-karlsruhe.de


######## Bovine Spongiform Encephalopathy #########


Robert, just wanted to comment on your request that the "Do not feed to Cattle or other Ruminants" statement be placed on all animal feeds. In 1997, we undertook a broad, five city survey to determine what effect that statement might have in the marketplace if it occurred on pet food labels.


Overwhelmingly, and in all locations, an immediate and severe effect was projected, not only into pet food, but into the Meat Counter as well, as people struggled with the idea that "if it's not good for ruminants (whatever they are?), why should I feed it to my pets, and oh, by the way, why should I eat beef at all if it's a problem?"


The Office of Management and Budget agreed with our findings and advised FDA that the labeling was not needed on pet food for retail sale or for laboratory animal feed. However, salvage products are required to bear the statement, since those products are often used for swine feed.


In most states, pets are classified as dogs and cats. Specialty pets are other caged and "aquariumed" critters. Horses and rabbits are classified as livestock.


Hope this is helpful.


Nancy K. Cook Pet Food Institute 2025 M Street, Suite 800 Washington, DC 20036 202-367-1120 202-367-2120 (fax)




Subject: Re: MAD COW/HORSE FEED BAN VIOLATIONS WARNING LETTER July 20, 2001


Date: Fri, 17 Aug 2001 14:37:50 –0700


From: "Terry S. Singeltary Sr."


Reply-To: Bovine Spongiform Encephalopathy


To: BSE-L@uni-karlsruhe.de References: 1


######## Bovine Spongiform Encephalopathy #########



Greetings again List Members,


here is a bit of what was thought of pet foods and TSEs in the early days of the BSE Inquiry;


. What is meat and other material from scrapie-infected sheep used for - does it include pet food and material for biological products?


Pet Food


As initial preclinical multiplication of the agent takes place in the spleen and other parts of the lympho-reticular system (LRS) there is obviously the possibility that scrapie infected material is used for pet food in addition to material from clinically affected sheep. Sheep spleens are used exclusively for pet foods and processed sheep heads are undoubtedly included.


Commercial canned pet food is subject to heat treatment. The following treatments are employed by . . .


[A table has been deleted here for commercial-in-confidence reasons.]


snip...





18. As it will probably be some months before the answer to No. 17 is known, what steps if any would it be prudent to take in the meantime in clinically affected animals covering a) meat, offal and meat products for human consumption, b) milk, c) material used in the preparation of biologicals and d) pet food?


snip...


Given the difficulties in abattoirs of identifying parts of a given carcass it may be prudent to condemn, for any use, the whole carcass of affected animals. This would seem to be politic given the possible fears from the public of the risk of consuming products from affected animals and therefore unfairly bring all animal products into disrepute.





6. Might there be a human risk from other animals, eg domestic pets?


If scrapie-infected sheep offal is the source of infection for cows, and similar material has gone into pet food, what is the chance of dogs/cats also being infected? Even if they do not show symptoms of disease (say because the incubation period is longer than the natural life span) might they still be infectious? Would there be any chance of transmission to humans through scratches or bites?




10.10 The recommendation that carcasses of affected animals should be destroyed was also designed to protect pets by preventing the incorporation of potentially infective material in their food.


10.11 Question 18 of the Key Questions (see paragraph 1.25 and the Annex) had asked what steps it would be prudent to take in respect of clinically affected animals covering, among other things, the use of meat offal and meat products for human consumption and for pet food. Mr Wilesmith had answered:


Given the difficulties in abattoirs of identifying parts of the given carcass it may be prudent to condemn, for any use, the whole carcass of affected animals.


10.12 Dr Pickles, for DH, had responded to the question simply and tersely: 'Not acceptable.'




CONFIDENTIAL BSE FEB. 9, 1989




10.113 The Working Party considered the possibility of transmission of BSE to cats and dogs and recommended that the surveillance of the health of domestic pets should be brought to the attention of the Consultative Committee on Research (the Tyrrell Committee) and the veterinary profession. 3




f. some pet foods may need to be looked at, although it appeared that the time/temperature combinations employed in the preparation of canned products was sufficient to reduce the titre of the Scrapie agent to a very low level. Mention was made of a USA standard of 132*C for one hour. Althought mink encephalopathy had been recorded there was no record of pets having succumbed...




6. Are there routes to other animals (farm or domestic) from products of infected cattle? What are the risks of a species jump?


If BSE is a result of cattle becoming infected with the scrapie agent, it will be some time, if ever, [before it is known] whether only a particular strain, and possibly a new one, is involved. Similarly the effects of passage of the agent in cattle, in terms of altered risks for other species, will be difficult to ascertain.


These possibilities aside, and assuming that a straightforward analogy with scrapie can be made, the risk of transmission to pet animals would appear to be unchanged. There is however, the potential problem of an increase in exposure to all species receiving rendered products or 'raw' products of infected animals, because we now have scrapie infected sheep and BSE infected cattle entering the food chain. Hounds, at least, have been fed uncooked carcass of dead and diseased animals for some time without becoming a maintenance host of a scrapie-like agent. It could also be argued from an evolutionary and dietary standpoint that cats and dogs are unlikely to become infected.




37.Putative TSE in hounds - work started 1990 –(see para 41)


Robert Higgins, a Veterinary Investigation Officer at Thirsk, had been working on a hound survey in 1990. Gerald Wells and I myself received histological sections from this survey along with the accompanying letter (YB90/11.28/1.1) datedNovember 1990. This letter details spongiform changes found in brains from hunt hounds failing to keep up with the rest of the pack, along with the results of SAF extractions from fresh brain material from these same animals. SAFs were not found in brains unless spongiform changes were also present. The spongiform changes were not pathognomonic (ie. conclusive proof) for prion disease, as they were atypical, being largely present in white matter rather than grey matter in the brain and spinal cord. However, Tony Scott, then head of electron microscopy work on TSEs, had no doubt that these SAFs were genuine and that these hounds therefore must have had a scrapie-like disease. I reviewed all the sections myself (original notes appended) and although the pathology was not typical, I could not exclude the possibility that this was a scrapie-like disorder, as white matter vacuolation is seen in TSEs and Wallerian degeneration was also present in the white matter of the hounds, another feature of scrapie.


38.I reviewed the literature on hound neuropathology, and discovered that micrographs and descriptive neuropathology from papers on ‘hound ataxia’ mirrored those in material from Robert Higgins’ hound survey. Dr Tony Palmer (Cambridge) had done much of this work, and I obtained original sections from hound ataxia cases from him. This enabled me provisionally to conclude that Robert Higgins had in all probability detected hound ataxia, but also that hound ataxia itself was possibly a TSE. Gerald Wells confirmed in ‘blind’ examination of single restricted microscopic fields that there was no distinction between the white matter vacuolation present in BSE and scrapie cases, and that occurring in hound ataxia and the hound survey cases.


39.Hound ataxia had reportedly been occurring since the 1930’s, and a known risk factor for its development was the feeding to hounds of downer cows, and particularly bovine offal. Circumstantial evidence suggests that bovine offal may also be causal in FSE, and TME in mink. Despite the inconclusive nature of the neuropathology, it was clearly evident that this putative canine spongiform encephalopathy merited further investigation.


40.The inconclusive results in hounds were never confirmed, nor was the link with hound ataxia pursued. I telephoned Robert Higgins six years after he first sent the slides to CVL. I was informed that despite his submitting a yearly report to the CVO including the suggestion that the hound work be continued, no further work had been done since 1991. This was surprising, to say the very least.


41.The hound work could have provided valuable evidence that a scrapie-like agent may have been present in cattle offal long before the BSE epidemic was recognised. The MAFF hound survey remains unpublished.


Histopathological support to various other published MAFF experiments


42.These included neuropathological examination of material from experiments studying the attempted transmission of BSE to chickens and pigs (CVL 1991) and to mice (RVC 1994).





Feline Spongiform Encephalopathy


Total to date: 88 (Plus 1 in N Ireland, 1 in Norway, 1 in Lichtenstein)





Simultaneous occurrence of spongiform encephalopathy in a man and his cat in Italy


Gianluigi Zanusso, Ettore Nardelli, Anna Rosati, GianMaria Fabrizi, Sergio Ferrari, Antonella Carteri, Franco De Simone, Nicola Rizzuto, Salvatore Monaco


Transmissible spongiform encephalopathies (TSE) encompass inherited, acquired, and sporadic mammalian neurological disorders, and are characterised by the conversion of the cellular prion protein (PrP) in an insoluble and protease-resistant isoform (PrPres). In human TSE, four types of PrPres have been identified according to size and glycoform ratios, which may represent different prion strains. Type-1 and type-2 PrPres are associated with sporadic Creutzfeldt-Jakob disease (CJD), type 3 with iatrogenic CJD, and type 4 with variant CJD.1,2 There is evidence that variant CJD is caused by the bovine spongiform encephalopathy (BSE)-prion strain.2­4 The BSE strain has been identified in three cats with feline spongiform encephalopathy (FSE), a prion disease which appeared in 1990 in the UK.5 We report the simultaneous occurrence of sporadic CJD in a man and a new variety of FSE in his cat.




Volume 4: The Southwood Working Party, 1988-89 10. Discussion The baby food recommendation Susceptibility of babies





kind regards, Terry S. Singeltary Sr., Bacliff, Texas USA




====================================



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


Subject: Re: MAD COW FEED BAN WARNING LETTER USA (a real hum dinger) !


Date: Tue, 24 Jun 2003 16:59:41 –0500


From: "Terry S. Singeltary Sr."


To: Bovine Spongiform Encephalopathy References: 3EE5D269.9040504@wt.net



i hate to keep kicking a mad cow here, but i thought since the FDA et al still refuses to tell us about _all_ the ruminant-to-ruminant feed ban violations, i thought i would go over a few of the old ones i might have missed. BOY, did i miss one. has all this feed been confirmed to have been recalled? how much is still out there?


RECALLS AND FIELD CORRECTIONS: VETMED -- CLASS II ________


PRODUCT & CODES: Animal feed products, packaged in 5, 25, 50, and 55 pound bags, and in bulk, intended for both ruminant and non-ruminant animals. The products are as follows: Recall # V-195-1 through V-350-1.


RUMINANT FEED PRODUCTS: RECALL NO. PRODUCT NO. PRODUCT NAME


V-195-1 40150 B. 30% Calf Pellet V-196-1 40250 B. 16% Calf Pellet V-197-1 40350 B. 16% Calf Ration V-198-1 40450 B. 18% Calf Starter V-199-1 40600 B. 38% Dairy Pellet V-200-1 40650 B. 38% Dairy Pellet V-201-1 40750 B. 16% Dairy Feed V-202-1 40950 B. 40% Beef Pellet V-203-1 41150 B. 18% Lamb Starter Pellet V-204-1 41250 B. 39% Lamb Conc. Pellet V-205-1 41350 B. 14% Lamb & Beef Pellet V-206-1 41450 B. 16% Goat Feed V-207-1 42150 B. 32% Expectation Pellet V-208-1 42250 B. Llama & Alpaca Pellet V-209-1 42350 B. 32% Calf Grower Pellet V-210-1 42650 B. Llama & Alpaca Crums V-211-1 42750 B. 38% Hay Booster 2 V-212-1 42850 B. 25% Pasture Booster V-213-1 43100 B. 16% Grower/Dev Pellet V-214-1 43150 B. 16% Grower/Dev Pellet V-215-1 43700 WH 32% Calf Gro Pellet V-216-1 43750 WH 32% Calf Gro Pellet V-217-1 43850 B. 38% Dairy Mix V-218-1 44250 B. 17% Doe Pellet V-219-1 44350 B. 21% Buck Pellet V-220-1 44450 Legends Ranch Pellet V-221-1 44500 Legends 17% Breeder Pellet V-222-1 1652 B. Vitamin E-20 V-223-1 1614 B. Vitamin A-30 V-224-1 44550 Legends 17% Breeder Pellet V-225-1 44650 Legends 13.5% Rut Pellet V-226-1 44750 Deer Starter (J) V-227-1 44940 Llama Premix (J) FSC V-228-1 45150 Empire 25% Calf Pellet V-229-1 45450 Berry Llama Pellet V-230-1 45950 50% Beef Conc. (Meal) V-231-1 46250 B. 12% Sweet Livestock V-232-1 46350 B. 1440 Bovatec Pellet V-233-1 46400 Liberty 38% Dairy Pellet V-234-1 46450 Liberty 38% Dairy Pellet V-235-1 47150 B. 14% Gold-n-Grower V-236-1 47250 B. 12% Gold-n-Conditioner V-237-1 47450 B. 18% Gold-n-Lamb V-238-1 47800 Homeworth Dairy Pellet V-239-1 47850 Homeworth Dairy Pellet V-240-1 47900 B. 36% Hi Fat Dairy Pellet V-241-1 47950 B. 36% Hi Fat Dairy Pellet V-242-1 48550 B. 16% Calf Pellet CA V-243-1 49200 Mastead Dairy Base V-244-1 49300 KLEJKA Dairy Base V-245-1 49650 Deer Premix (J) HFB V-246-1 49750 39% Lamb Premix (J) HFB V-247-1 49850 Lamb Starter Premix (J) HFB V-248-1 120850 Brood Cow Deluxe Mineral V-249-1 152850 B. A-D-E Mix


NON-RUMINANT FEED PRODUCTS:


V-250-1 10150 B. Miracle Starter V-251-1 10350 B. 21% Broiler Starter V-252-1 10450 B. Pullet Grower & Developer V-253-1 10550 B. 18% Layer Breeder Pellets V-254-1 10750 B. 20% Gold Std. Laying Crum V-255-1 10950 B. 17% Complete Laying Crums V-256-1 11050 B. 16% Prosperity Layer Crums V-257-1 11100 B. 40% Poultry Concentrate V-258-1 11150 B. 40% Poultry Concentrate V-259-1 11250 B. 28% Turkey Starter Crums V-260-1 11350 20% Gig "4" Pellets V-261-1 11450 B. 16% Prosperity Layer Pellets V-262-1 11550 18% Game Bird Breeder Pellets V-263-1 11650 B. 19% Ratite Grower Diet V-264-1 11750 B. 23% Ratite Breeder Diet V-265-1 12100 B. 40% Poultry Concentrate Crums V-266-1 12550 B. 32% Base Poultry Mix V-267-1 13250 B. 28% Turkey Starter V-268-1 13450 B. 20% Poultry Grower V-269-1 14325 B. Game Bird Mix - Coarse V-270-1 20150 B. 18% Pig Starter Pellets V-271-1 20250 B. 16% Pig Grower Pellets V-272-1 20450 B. 14% Porkmaker 100 Pellets V-273-1 20550 B. 40% Gro 'Em Lean V-274-1 21850 B. 27% Hi-Fat Swine Base V-275-1 23000 Mt. Hope Hevy Hog V-276-1 30050 12% Pleasure Horse - Sweet V-277-1 30150 Alfa + Performer 10 Sweet V-278-1 30250 14% Grass + Perf Sweet V-279-1 30450 12% Wrangler - Complete V-280-1 30550 B. 12% Pleasure Horse Pellets V-281-1 30650 B. 32% Gro' N Win Pellets V-282-1 30750 12% Wrangler Cubes V-283-1 30950 18% Foal Starter V-284-1 31050 B. 14% Alfa + Dev Pellets V-285-1 31150 B. Alfa + Performer 10 Pel V-286-1 31200 Grass +Performer 14 Pel V-287-1 31250 Grass +Performer 14 Pel V-288-1 31350 12% Mustang V-289-1 31450 Endurance - 101 Extruded V-290-1 31550 B. Equine Energy - UK V-291-1 31650 B. 16% Grass + Dev Pellets V-292-1 31750 16% Grass + Dev Cubes V-293-1 31850 16% Grass + Dev Sweet V-294-1 31950 B. 11% Alfa Gro 'N Win Pel V-295-1 32050 B. Sho' Win Pellets V-296-1 32250 B. Senior Formula V-297-1 32350 Oscar Horse Mix V-298-1 32450 B. Ultimate Finish V-299-1 32550 Crossfire Horse Feed V-300-1 32650 B. Equine 16% Growth V-301-1 32750 B. Reduced Energy Formula V-302-1 32850 B. Training Formula V-303-1 32950 B. Cadence Formula V-304-1 33150 B. Track 12 Horse Feed V-305-1 33350 Spears 16% GR + Dev Cubes V-306-1 33400 B. 14% Supreme Horse Pellets V-307-1 33450 B. 14% Supreme Horse Pellets V-308-1 33650 B. Race'N Win V-309-1 33750 B. 14% Prominent Horse Feed V-310-1 33850 B. Unbeetable Horse Feed V-311-1 34750 Cargill Senior Horse V-312-1 34850 Cargill Vitality Gold V-313-1 35150 Chagrin 12% Sweet Fd V-314-1 35250 Smith Pure Pleasure V-315-1 35750 Roundup 10% Horse Pellets V-316-1 35850 12% Summerglo Horse V-317-1 36255 B. Grass +Min&VitBase - Mexico V-318-1 36850 Miller's 12% Horse Feed V-319-1 37155 B. Gro'Win Base Mix - Mexico V-320-1 38000 B. 32% Premium Mixer Pellets V-321-1 38050 B. 32% Premium Mixer Pellets V-322-1 38100 36% Maintenance Mixer Pellets V-323-1 38150 36% Maintenance Mixer Pellets V-324-1 50150 Terramycin Crumbles V-325-1 60105 16% Rabbit Pellets V-326-1 60125 16% Rabbit Pellets V-327-1 60150 B. 16% Rabbit Pellets V-328-1 60205 18% Rabbit Developer V-329-1 60250 B. 18% Rabbit Developer V-330-1 60450 B. 16% Rabbit Maintenance V-331-1 90150 B. Buckeye Scratch V-332-1 90225 Gold Standard Scratch V-333-1 90250 Gold Standard Scratch V-334-1 90350 Intermediate Scratch V-335-1 90450 B. Chick Grains V-336-1 90525 B. Shelled Corn V-337-1 90550 B. Shelled Corn V-338-1 90650 B. Cracked Corn V-339-1 90825 B. Fine Cracked Corn V-340-1 90850 B. Fine Cracked Corn V-341-1 91000 Steam Flaked Corn V-342-1 91050 Steam Flaked Corn V-343-1 91750 Oats - HP Crimped V-344-1 91850 B. HP Sweet Crimped Oats V-345-1 95550 Land O' Lakes Shelled Corn V-346-1 95650 Land O' Cracked Corn V-347-1 95850 Land O' Lakes Chick Crack V-348-1 100850 B. Alfalfa Pellets V-349-1 101850 Cooked Full Fat Soybean V-350-1 122200 Magnatone M-4-B Pels Bulk MANUFACTURER: Buckeye Feed Mills, Dalton, Ohio.


RECALLED BY: Manufacturer visited local customers on April 17, 2001. On April 18 and 19, 2001, manufacturer mailed and faxed recall notices. Firm initiated recall is ongoing.


DISTRIBUTION: Al, CT, DE, FL, GA, IL, IN, IA, KY, ME, MD, MA, MO, MN, MS, NH, NJ, NY, NC, OH, OR, PA, RI, TN, VA, WV, and WI.


QUANTITY: 2,790 tons of ruminant feed products and 14,000 tons of non-ruminant feed products.


REASON: The animal feed products may contain protein derived from mammalian tissues.


snip...


END OF ENFORCEMENT REPORT FOR June 6, 2001.






SEE MORE MAD COW FEED FOR HORSES AND EVERYTHING ELSE UNDER THE SUN ;










TSE & HOUNDS

GAH WELLS (very important statement here...TSS)

HOUND STUDY

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.

snip...

http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf





I thought that in Britain dogs had contracted BSE, but perhaps not.

not so fast here;

The spongiform changes were not pathognomonic (ie. conclusive proof) for prion disease, as they were atypical, being largely present in white matter rather than grey matter in the brain and spinal cord. However, Tony Scott, then head of electron microscopy work on TSEs, had no doubt that these SAFs were genuine and that these hounds therefore must have had a scrapie-like disease. I reviewed all the sections myself (original notes appended) and although the pathology was not typical, I could not exclude the possibility that this was a scrapie-like disorder, as white matter vacuolation is seen in TSEs and Wallerian degeneration was also present in the white matter of the hounds, another feature of scrapie.

38.I reviewed the literature on hound neuropathology, and discovered that micrographs and descriptive neuropathology from papers on 'hound ataxia' mirrored those in material from Robert Higgins' hound survey. Dr Tony Palmer (Cambridge) had done much of this work, and I obtained original sections from hound ataxia cases from him. This enabled me provisionally to conclude that Robert Higgins had in all probability detected hound ataxia, but also that hound ataxia itself was possibly a TSE. Gerald Wells confirmed in 'blind' examination of single restricted microscopic fields that there was no distinction between the white matter vacuolation present in BSE and scrapie cases, and that occurring in hound ataxia and the hound survey cases.

39.Hound ataxia had reportedly been occurring since the 1930's, and a known risk factor for its development was the feeding to hounds of downer cows, and particularly bovine offal. Circumstantial evidence suggests that bovine offal may also be causal in FSE, and TME in mink. Despite the inconclusive nature of the neuropathology, it was clearly evident that this putative canine spongiform encephalopathy merited further investigation.

40.The inconclusive results in hounds were never confirmed, nor was the link with hound ataxia pursued. I telephoned Robert Higgins six years after he first sent the slides to CVL. I was informed that despite his submitting a yearly report to the CVO including the suggestion that the hound work be continued, no further work had been done since 1991. This was surprising, to say the very least.

41.The hound work could have provided valuable evidence that a scrapie-like agent may have been present in cattle offal long before the BSE epidemic was recognised. The MAFF hound survey remains unpublished.

Histopathological support to various other published MAFF experiments

42.These included neuropathological examination of material from experiments studying the attempted transmission of BSE to chickens and pigs (CVL 1991) and to mice (RVC 1994).

http://www.bseinquiry.gov.uk/witness/htm/stat067.htm

It was thought likely that at least some, and probably all, of the cases in zoo animals were caused by the BSE agent. Strong support for this hypothesis came from the findings of Bruce and others (1994) ( Bruce, M.E., Chree, A., McConnell, I., Foster, J., Pearson, G. & Fraser, H. (1994) Transmission of bovine spongiform encephalopathy and scrapie to mice: strain variation and species barrier. Philosophical Transactions of the Royal Society B 343, 405-411: J/PTRSL/343/405 ), who demonstrated that the pattern of variation in incubation period and lesion profile in six strains of mice inoculated with brain homogenates from an affected kudu and the nyala, was similar to that seen when this panel of mouse strains was inoculated with brain from cattle with BSE. The affected zoo bovids were all from herds that were exposed to feeds that were likely to have contained contaminated ruminant-derived protein and the zoo felids had been exposed, if only occasionally in some cases, to tissues from cattle unfit for human consumption.

snip...

http://www.bseinquiry.gov.uk/files/ws/s324.pdf


NEW URL ;

http://collections.europarchive.org/tna/20080102174910/http://www.bseinquiry.gov.uk/files/ws/s324.pdf



2005

DEFRA Department for Environment, Food & Rural Affairs

Area 307, London, SW1P 4PQ Telephone: 0207 904 6000 Direct line: 0207 904 6287 E-mail: h.mcdonagh.defra.gsi.gov.uk

GTN: FAX:

Mr T S Singeltary P.O. Box 42 Bacliff Texas USA 77518

21 November 2001

Dear Mr Singeltary

TSE IN HOUNDS

Thank you for e-mail regarding the hounds survey. I am sorry for the long delay in responding.

As you note, the hound survey remains unpublished. However the Spongiform Encephalopathy Advisory Committee (SEAC), the UK Government's independent Advisory Committee on all aspects related to BSE-like disease, gave the hound study detailed consideration at their meeting in January 1994. As a summary of this meeting published in the BSE inquiry noted, the Committee were clearly concerned about the work that had been carried out, concluding that there had clearly been problems with it, particularly the control on the histology, and that it was more or less inconclusive. However was agreed that there should be a re-evaluation of the pathological material in the study.

Later, at their meeting in June 95, The Committee re-evaluated the hound study to see if any useful results could be gained from it. The Chairman concluded that there were varying opinions within the Committee on further work. It did not suggest any further transmission studies and thought that the lack of clinical data was a major weakness.

Overall, it is clear that SEAC had major concerns about the survey as conducted. As a result it is likely that the authors felt that it would not stand up to r~eer review and hence it was never published. As noted above, and in the detailed minutes of the SEAC meeting in June 95, SEAC considered whether additional work should be performed to examine dogs for evidence of TSE infection. Although the Committee had mixed views about the merits of conducting further work, the Chairman noted that when the Southwood Committee made their recommendation to complete an assessment of possible spongiform disease in dogs, no TSEs had been identified in other species and hence dogs were perceived as a high risk population and worthy of study. However subsequent to the original recommendation, made in 1990, a number of other species had been identified with TSE ( e.g. cats) so a study in hounds was less

critical. For more details see- http://www.bseinquiry, gov.uk/files/yb/1995/06/21005001 .pdf


As this study remains unpublished, my understanding is that the ownership of the data essentially remains with the original researchers. Thus unfortunately, I am unable to help with your request to supply information on the hound survey directly. My only suggestion is that you contact one of the researchers originally involved in the project, such as Gerald Wells. He can be contacted at the following address.

Dr Gerald Wells, Veterinary Laboratories Agency, New Haw, Addlestone, Surrey, KT 15 3NB, UK

You may also wish to be aware that since November 1994 all suspected cases of spongiform encephalopathy in animals and poultry were made notifiable. Hence since that date there has been a requirement for vets to report any suspect SE in dogs for further investigation. To date there has never been positive identification of a TSE in a dog.

I hope this is helpful

Yours sincerely 4

HUGH MCDONAGH BSE CORRESPONDENCE SECTION



=====================



The signs of canine cognitive dysfunction syndrome or "old dog syndrome" commonly seen in dogs are: lose of house training increased barking or whining increased anxiety or fear signs disorientation-appearing lost or confused,getting stuck behind furniture or in corners, walking in circles, becoming forgetful,walking aimlessly,staring into space, repetitious or compulsive behavior change in sleep patterns-up at night, sleep all day

lack of responsiveness other changes,may not recognize you, their name,may become more docile, more aggressive.. You can liken it to human senility. An article at the petcenter says "CDS is not "normal aging". A number of pathophysiological changes are suspected to play a role in its development. These include: * deposition of amyloid plaques in the cerebral cortex and hippocampal part of the brain * alterations in neurotransmitters, including dopamine * increased levels of monoamine oxidase B (MAOB) in the brain * increased levels of free radicals L-DEPRENYL HYDROCHLORIDE SELEGILINE HYDROCHLORIDE,BRAND NAME: ANIPRYL OR ELDEPRYL is used to help treat canine cognitive dysfunction by increasing brain concentrations of the neurotransmitter dopamine. Hopefully you can see a difference in a month or so. If you don't see a difference in the first month, your vet might tell you to try two pills a day for the next month. ANIPRYL doesn't work for all dogs. A great writeup on L-DEPRENYL can be found at

http://www.petsinfo.org/elderlydogs1.html.


"One third of canine CD patients respond extremely well to treatment with deprenyl by regaining their youthful vigor; another one third respond reasonably well; and one third do not respond at all (perhaps there is a variant of CD with different neuropathology). The bottom line is that for any dog that is slowing down to the point that problems become apparent, treatment with deprenyl is the logical route once other organic causes for reduced mental function have been ruled out. Here is a write up on selegline " Selegiline has immune-system-boosting and anti-neurodegenerative effects. ....


Taken consistently in low doses, selegiline tends to extend the life-expectancy of rats by some 20%; enhances drive, libido and endurance; and independently improves cognitive performance in Alzheimer's patients and in some healthy normals. It is used successfully to treat canine cognitive dysfunction syndrome (CDS) in dogs...Selegiline protects the brain's dopamine cells from oxidative stress. " Some also use alpha lipoic acid and r-lipoic acid. powerful antioxidants to help slow down canine cognitive dysfunction. There is a dog food that is rich in antioxidants for CDS but I am assuming if you supplement with your own antioxidants you don't have to worry if your dog likes the food or not. I know my dog Hammy has become very picky and at least if I pill him, I know he is getting his antioxidants.


http://www.thensome.com/cds.htm



Doggie Dementia

Does 14-year-old Fido get lost in his own back yard?

Does he not respond when you call his name?

Does he generally seem confused?

According to Pulse, the official magazine of the Southern California Veterinary Medical Association, just as humans in the 21st Century are living longer, so is man’s best friends—more than 7.3 million dogs in the United States are age 10 or older. And with age dogs become prone to the same age-related diseases as their human companions, including dementia.

A disease of old age affects dogs and humans alike

Kazzy, a 17-year-old Lhasa Apso, is one of the 60 percent of dogs aged 11 to 15 who suffer from one or more symptoms of canine cognitive dysfunction syndrome (CDS), also known to veterinarians as doggie dementia. "He used to be the most incredible watchdog," says his owner, Olivia Feldman-Rich. "But he’s not like that anymore. He’s quite bewildered."

Experts like Dr. Maritza Perez, a veterinarian at West Orange (NJ) Animal Hospital, say that confusion is one of the four major signs of CDS (see sidebar). Dr. Perez says dogs may "pace around in circles, get stuck behind furniture, or they don’t know where the back door is anymore."

Often the most distressing sign of CDS is that, like human patients with Alzheimer’s disease, your pet seems to forget you and your family. "A lot of people notice that when you walk in the door, and this dog that was happy to see you doesn’t get up off the couch or off the floor to greet you," says Dr. Perez. "And he doesn’t come anymore when you call him."

These symptoms, coupled with others debilitating diseases affecting older dogs, such as arthritis, all add up to a serious loss in quality of life for your canine friend. The American Veterinary Medical Association reports that some 500,000 dogs are put to sleep each year because of CDS.

Researchers say that deposits of beta-amyloid plaques in brain tissues are likely to play a role in CDS. These plaques build up and eventually inhibit transmission of the brain’s neural signals. Still, the recognized symptoms of CDS are behavioral, so a diagnosis is exclusionary, meaning it is arrived at only after all other physical and neurological causes are ruled out.

No cure yet, but relief for some dogs

Dr. Perez with a 14 year-old beagle who is on Anipryl.

While scientists search for a permanent cure for CDS, there is one treatment currently FDA-approved for CDS. Selegiline hydrochloride, whose brand name is Anipryl, may give some dogs relief from its symptoms. Researchers speculate that Anipryl works by increasing levels of dopamine, a neurotransmitter. Other treatments are currently being investigated, including diets high in anti-oxidants as well as a new drug, Adrafinil, in one Canadian study.

Dr. Perez says that Anipryl does cause an improvement in many dogs with CDS, meaning relief from at least one of the common symptoms. "We have lots of animals on it and it does work," she says. But it’s not a sure thing—Dr. Perez tried it on her own dog with no effect.

Feldman-Rich is debating putting Kazzy on Anipryl. "I’m hoping that it will give a little more balance to his life and make him a little more aware that he’s still here and we’re still here for him," she says. "I always told him that he couldn’t leave me too soon, and he’s definitely kept up his end of it, but I’d definitely like for him to feel a little more like he’s part of the family."

by Debra Utacia Krol

http://www.sciencentral.com/articles/view.php3?article_id=218391360&cat=1_6



[Image] Research letters Volume 352, Number 9134 [Image] 3 October 1998 [Previous] [Next]

[Image][Image]


Simultaneous occurrence of spongiform encephalopathy in a man and his cat in Italy


[Image]

Gianluigi Zanusso, Ettore Nardelli, Anna Rosati, GianMaria Fabrizi, Sergio Ferrari, Antonella Carteri, Franco De Simone, Nicola Rizzuto, Salvatore Monaco

Transmissible spongiform encephalopathies (TSE) encompass inherited, acquired, and sporadic mammalian neurological disorders, and are characterised by the conversion of the cellular prion protein (PrP) in an insoluble and protease-resistant isoform (PrPres). In human TSE, four types of PrPres have been identified according to size and glycoform ratios, which may represent different prion strains. Type-1 and type-2 PrPres are associated with sporadic Creutzfeldt-Jakob disease (CJD), type 3 with iatrogenic CJD, and type 4 with variant CJD.1,2 There is evidence that variant CJD is caused by the bovine spongiform encephalopathy (BSE)-prion strain.2-4 The BSE strain has been identified in three cats with feline spongiform encephalopathy (FSE), a prion disease which appeared in 1990 in the UK.5 We report the simultaneous occurrence of sporadic CJD in a man and a new variety of FSE in his cat.

A 60-year-old man, with no unusual dietary habits, was admitted in November, 1993, because of dysarthria, cerebellar ataxic gait, visual agnosia, and myoclonus. An electroencephalogram (EEG) showed diffuse theta-delta activity. A brain magnetic resonance imaging scan was unremarkable. 10 days later, he was speechless and able to follow only simple commands. Repeat EEGs showed periodic triphasic complexes. 2 weeks after admission, he was mute, akinetic, and unable to swallow. He died in early January, 1994.

His 7-year-old, neutered, female shorthaired cat presented in November, 1993, with episodes of frenzy, twitching of its body, and hyperaesthesia. The cat was usually fed on canned food and slept on its owner's bed. No bites from the cat were recalled. In the next few days, the cat became ataxic, with hindquarter locomotor dysfunction; the ataxia got worse and there was diffuse myoclonus. The cat was killed in mid-January, 1994.

No pathogenic mutations in the patient's PrP gene were found. The patient and the cat were methionine homozygous at codon 129. Histology of the patient's brain showed neocortical and cerebellar neuronal loss, astrocytosis, and spongiosis (figure A). PrP immunoreactivity showed a punctate pattern and paralleled spongiform changes (figure B). The cat's brain showed mild and focal spongiosis in deeper cortical layers of all four lobes (figure C), vacuolated cortical neurons (figure D), and mild astrogliosis. The cerebellar cortex and the dentate nucleus were gliosed. Immunoreactive PrP showed a punctate pattern in neocortex, allocortex, and caudate nucleus (figure E). Western blot analysis of control and affected human and cat brain homogenates showed 3 PrP bands of 27-35 kDa. After digestion with proteinase K and deglycosylation, only samples from the affected patient and cat showed type-1 PrPres, with PrP glycoform ratios comparable to those observed in sporadic CJD1 (details available from author).

[Image]

Microscopic sections of patient and cat brains

A: Occipital cortex of the patient showing moderate spongiform degeneration and neuronal loss (haematoxylin and eosin) and B: punctate perineuronal pattern of PrP immunoreactivity; peroxidase immunohistochemistry with monoclonal antibody 3F4. C: cat parietal cortex showing mild spongiform degeneration (haematoxylin and eosin).D: vacuolated neurons (arrow, haematoxylin and eosin), E: peroxidase immunohistochemistry with antibody 3F4 shows punctate perineuronal deposition of PrP in temporal cortex.

This study shows a spatio-temporal association between human and feline prion diseases. The clinical features of the cat were different from previously reported cases of FSE which were characterised by gradual onset of behavioural changes preceding locomotor dysfunction and ataxia.5 Neuropathological changes were also at variance with the diffuse spongiosis and vacuolation of brainstem neurons, seen in FSE.5 The synaptic pattern of PrP deposition, similar in the cat and in the patient, was atypical for a BSE-related condition. Evidence of a new type of FSE was further provided by the detection of a type-1 PrPres, other than the BSE-associated type 4.2 Taken together, our data suggest that the same agent strain of sporadic CJD was involved in the patient and in his cat.

It is unknown whether these TSE occurred as the result of horizontal transmission in either direction, infection from an unknown common source, or the chance occurrence of two sporadic forms.

1 Parchi P, Castellani R, Capellari S, et al. Molecular basis of phenotypic variablity in sporadic Creutzfeldt-Jakob disease. Ann Neurol 1996; 39: 767-78 [PubMed].

2 Collinge J, Sidle KCL, Meads J, Ironside J, Hill AF. Molecular analysis of prion strain variation and the aetiology of 'new variant' CJD. Nature 1996; 383: 685-90 [PubMed].

3 Bruce ME, Will RG, Ironside JW, et al. Transmissions to mice indicate that 'new variant' CJD is caused by the BSE agent. Nature 1997; 389: 498-501 [PubMed].

4 Hill AF, Desbruslais M, Joiner S, et al. The same prion strain causes vCJD and BSE. Nature 1997; 389: 448-50 [PubMed].

5 Pearson GR, Wyatt JM, Henderson JP, Gruffydd-Jones TJ. Feline spongiform encephalopathy: a review. Vet Annual 1993; 33: 1-10.

------------------------------------------------------------------------ Sezione di Neurologie Clinica, Dipartimento di Scienze Neurologiche e della Visione, Università di Verona, Policlinico Borgo Roma, 37134 Verona, Italy (S Monaco; e mail rizzuto@Gorgorna.univr.it); and Istituto Zooprofilattico Sperimentale della Lombardia e dell' Emilia, Brescia


=======================================



Terry S. Singeltary Sr. wrote:

######## Bovine Spongiform Encephalopathy #########


Greetings list members,

ODD that some FELINE in Italy seem to have this same or maybe very similar phenotype of TSE;

In October 1998 the simultaneous occurrence of spongiform encephalopathy in a man and his pet cat was reported. The report from Italy noted that the cat did not display the same clinical features as FSE cases previously seen. Indeed, the presence of a new type of FSE was suggested. The man was diagnosed as having sporadic CJD, and neither case (man nor cat) appeared to be affected by a BSE-related condition.



Subject: FDA BSE Update - Pet Food from Canadian Manufacturer & MAD DOG DATA


Date: Tue, 27 May 2003 08:07:58 –0500


From: "Terry S. Singeltary Sr." To: Bovine Spongiform Encephalopathy



snip...see full text ;











2007 10 YEARS POST PARTIAL AND VOLUNTARY FEED BAN USA




10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007


Date: March 21, 2007 at 2:27 pm PST


RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II


___________________________________


PRODUCT


Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007


CODE


Cattle feed delivered between 01/12/2007 and 01/26/2007


RECALLING FIRM/MANUFACTURER


Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.


Firm initiated recall is ongoing.


REASON


Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.


VOLUME OF PRODUCT IN COMMERCE


42,090 lbs.


DISTRIBUTION


WI


___________________________________


PRODUCT


Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007


CODE


The firm does not utilize a code - only shipping documentation with commodity and weights identified.


RECALLING FIRM/MANUFACTURER


Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.


REASON


Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.


VOLUME OF PRODUCT IN COMMERCE


9,997,976 lbs.


DISTRIBUTION


ID and NV


END OF ENFORCEMENT REPORT FOR MARCH 21, 2007





Saturday, August 14, 2010


BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY


*** (see mad cow feed in COMMERCE IN ALABAMA...TSS)


BANNED MAD COW FEED IN COMMERCE IN ALABAMA


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


a) EVSRC Custom dairy feed, Recall # V-130-6;


b) Performance Chick Starter, Recall # V-131-6;


c) Performance Quail Grower, Recall # V-132-6;


d) Performance Pheasant Finisher, Recall # V-133-6.


CODE None RECALLING FIRM/MANUFACTURER Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is complete.


REASON


Dairy and poultry feeds were possibly contaminated with ruminant based protein.


VOLUME OF PRODUCT IN COMMERCE 477.72 tons


DISTRIBUTION AL


______________________________





PRODUCT Bulk custom dairy pre-mixes,


Recall # V-120-6 CODE None RECALLING FIRM/MANUFACTURER Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete. REASON Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.


VOLUME OF PRODUCT IN COMMERCE 350 tons


DISTRIBUTION AL and MS


______________________________


PRODUCT


a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags, Recall # V-121-6;


b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall # V-122-6;


c) Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6;


d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6;


e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6;


f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6;


g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6


CODE All products manufactured from 02/01/2005 until 06/20/2006 RECALLING FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006. Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.


REASON Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".


VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bags


DISTRIBUTION AL, GA, MS, and TN


END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006


###





Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006


Date: August 6, 2006 at 6:16 pm PST PRODUCT


a) CO-OP 32% Sinking Catfish, Recall # V-100-6;


b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;


c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;


d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;


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


f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;


g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;


h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;


i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;


j) CO-OP LAYING CRUMBLES, Recall # V-109-6;


k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;


l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;


m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE


Product manufactured from 02/01/2005 until 06/06/2006


RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.


REASON Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".


VOLUME OF PRODUCT IN COMMERCE 125 tons


DISTRIBUTION AL and FL


END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006


###





MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22 71.248.128.67


RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II


______________________________


PRODUCT


a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6;


b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6;


c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6;


d) Feather Meal, Recall # V-082-6 CODE


a) Bulk


b) None


c) Bulk


d) Bulk


RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. Firm initiated recall is ongoing.


REASON


Possible contamination of animal feeds with ruminent derived meat and bone meal.


VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons


DISTRIBUTION Nationwide


END OF ENFORCEMENT REPORT FOR July 12, 2006


###





please see full text ;






Tuesday, March 2, 2010


Animal Proteins Prohibited in Ruminant Feed/Adulterated/Misbranded Rangen Inc 2/11/10 USA








2011




Saturday, July 23, 2011


CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE






Saturday, November 6, 2010


TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU


Berne, 2010 TAFS INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation






Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR>


Prion disease update 2010 (11) PRION DISEASE UPDATE 2010 (11)















IN CONFIDENCE SCRAPIE TRANSMISSION TO CHIMPANZEES


IN CONFIDENCE


reference...


RB3.20


TRANSMISSION TO CHIMPANZEES


1. Kuru and CJD have been successfully transmitted to chimpanzees but scrapie and TME have not.


2. We cannot say that scrapie will not transmit to chimpanzees. There are several scrapie strains and I am not aware that all have been tried (that would have to be from mouse passaged material). Nor has a wide enough range of field isolates subsequently strain typed in mice been inoculated by the appropriate routes (i/c, ilp and i/v) :


3. I believe the proposed experiment to determine transmissibility, if conducted, would only show the susceptibility or resistance of the chimpanzee to infection/disease by the routes used and the result could not be interpreted for the predictability of the susceptibility for man. Proposals for prolonged oral exposure of chimpanzees to milk from cattle were suggested a long while ago and rejected.


4. In view of Dr Gibbs' probable use of chimpazees Mr Wells' comments (enclosed) are pertinent. I have yet to receive a direct communication from Dr Schellekers but before any collaboration or provision of material we should identify the Gibbs' proposals and objectives.


5. A positive result from a chimpanzee challenged severely would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.


6. A negative result would take a lifetime to determine but that would be a shorter period than might be available for human exposure and it would still not answer the question regarding mans' susceptibility. In the meantime no doubt the negativity would be used defensively. It would however be counterproductive if the experiment finally became positive. We may learn more about public reactions following next Monday' s meeting.


R. Bradley


23 September 1990


CVO (+Mr Wells' comments)


Dr T W A Little


Dr B J Shreeve


90/9.23/1.1.






IN CONFIDENCE CHIMPANZEES


CODE 18-77 Reference RB3.46


Some further information that may assist in decision making has been gained by discussion with Dr Rosalind Ridley.


She says that careful study of Gajdusek's work shows no increased susceptibility of chimpanzees over New World Monkeys such as Squirrel Monkeys. She does not think it would tell you anything about the susceptibility to man. Also Gajdusek did not, she believes, challenge chimpanzees with scrapie as severely as we did pigs and we know little of that source of scrapie. Comparisons would be difficult. She also would not expect the Home Office to sanction such experiments here unless there was a very clear and important objective that would be important for human health protection. She doubted such a case could be made. If this is the case she thought it would be unethical to do an experiment abroad because we could not do it in our own country.


Retrospectively she feels they should have put up more marmosets than they did. They all remain healthy. They would normally regard the transmission as negative if no disease resulted in five years.


We are not being asked for a decision but I think that before we made one we should gain as much knowledge as we can. If we decided to proceed we would have to bear any criticisms for many years if there was an adverse view by scientists or­media. This should not be undertaken lightly. There is already some adverse comment here, I gather, on the pig experiment though that will subside.


The Gibbs' (as' distinct from Schellekers') study is somewhat different. We are merely supplying material for comparative studies in a laboratory with the greatest experience of human SEs in the world and it has been sanctioned by USDA (though we do not know for certain yet if chimpanzees specifically will be used). This would keep it at a lower profile than if we conducted such an experiment in the UK or Europe.


I consider we must have very powerful and defendable objectives to go beyond Gibbs' proposed experiments and should not initiate others just because an offer has been made.


Scientists have a responsibility to seek other methods of investigative research other than animal experimentation. At present no objective has convinced me we need to do research using Chimpanzees - a species in need of protection. Resisting such proposals would enable us to communicate that information to the scientist and the public should the need arise. A line would have been drawn.


CVO cc Dr T Dr B W A Little Dr B J Shreeve


R Bradley


26 September 1990


90/9.26/3.2













I AM NOT AN ADVOCATE FOR EXPERIMENTAL USE OF CHIMPANZEES AS TEST VICTIMS. However, I would be an advocate for (and i have said this before over the years), of death row inmates being used. Their families could be compensated with a monetary award, and the death row inmates could do one final thing for the good of humanity. There going to die anyway. just my opinion. ...TSS-2011




SEE FULL TEXT ;






THIS is what happens when industry runs government policy ;


STRICTLY PRIVATE AND CONFIDENTIAL 25, AUGUST 1995


snip...


To minimise the risk of farmers' claims for compensation from feed compounders.


To minimise the potential damage to compound feed markets through adverse publicity.


To maximise freedom of action for feed compounders, notably by maintaining the availability of meat and bone meal as a raw material in animal feeds, and ensuring time is available to make any changes which may be required.


snip...


THE FUTURE


4..........


MAFF remains under pressure in Brussels and is not skilled at handling potentially explosive issues.


5. Tests _may_ show that ruminant feeds have been sold which contain illegal traces of ruminant protein. More likely, a few positive test results will turn up but proof that a particular feed mill knowingly supplied it to a particular farm will be difficult if not impossible.


6. The threat remains real and it will be some years before feed compounders are free of it. The longer we can avoid any direct linkage between feed milling _practices_ and actual BSE cases, the more likely it is that serious damage can be avoided. ...



SEE full text ;












Monday, January 2, 2012


EFSA Minutes of the 6th Meeting of the EFSA Scientific Network on BSE-TSE Brussels, 29-30 November 2011











It has become appallingly obvious that our technology has exceeded our humanity.


Albert Einstein


Stupid is, as stupid does, and some times you just can’t fix stupid $$$


never say never with TSE Prions. ...


TSS

No comments:

Post a Comment