Mad-cow proteins created in the lab

By CBC News

Scientists have firmed up the evidence that misshapen protein are responsible for brain-wasting diseases by showing how these infectious prions are created.
Scientists have firmed up the evidence that misshapen protein are responsible for brain-wasting diseases by showing how these infectious prions are created.

Researchers from the United States and China have artificially created a disease-causing prion using proteins from mice.

Prions are proteins that occur naturally in the cells of mammals. Infectious prions are abnormal, misshapen versions of this protein that cause neurodegenerative diseases such as Creutzfeldt-Jakob disease and bovine spongiform encephalopathy, also known as mad cow disease.

The scientists used a mouse prion protein, called PrP, created through genetic engineering in bacterial cells in their experiments.

They found that the protein interacts with lipids, the fatty molecules in the structures of cell membranes, and becomes contorted and improperly folded, changing it into a disease-causing prion.

Jiyan Ma of Ohio State University said the experiment, published this week in Science, is the strongest evidence yet that prions are the cause of these brain-wasting diseases.

"The major thing we showed in this study is that the infectious agent in these diseases is truly a misfolded protein," Ma said in a statement.

Ma and his colleagues at Ohio State and East China Normal University injected the artificially created prions into the brains of mice.

The mice started showing symptoms of brain-wasting disease about four months later. After the mice died, the researchers dissected their brains and found microscopic holes throughout, the classic sign of spongiform encephalopathy.

"We folded recombinant mouse prion protein into its normal shape, then converted it into a different conformation and showed that when it infected an animal, it caused full-blown prion disease, with all of the characteristics," Ma said.

Ma said there is still much more research to be done on prions and brain-wasting disease.

"For example, we still don't know what actually makes prions infectious or how their propagation causes damage in the brain," he said.

EQUINE PIROPLASMOSIS - USA (02): (TEXAS)

****************************************
A ProMED-mail post

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


Date: 28 Jan 2010
Source: Caller.com [edited]



Rare horse disease affects horses in 12 states
----------------------------------------------
King Ranch, Texas, is the epicenter of a months-long outbreak of a
deadly horse disease rarely seen in the United States that kills as
many as 20 percent that it infects. As of 20 Jan 2010, 364 cases of
equine piroplasmosis had been confirmed. Of those, 289 are on King
Ranch. The rest are scattered across Texas, Alabama, California,
Florida, Indiana, Louisiana, Minnesota, North Carolina, New Jersey,
Tennessee, Utah and Wisconsin, according to the World Animal Health
Information System.

A South Texas ranch, identified by the Texas Animal Health Commission
as the outbreak's source, has sold horses with equine piroplasmosis
in 15 states since 2004. Jack Hunt, the CEO of King Ranch, confirmed
the outbreak started on the ranch.

Horses, donkeys, mules and zebras are susceptible to the disease,
which is caused by 2 parasitic organisms. More severely affected
animals can have fever, anemia, jaundiced mucous membranes, swollen
abdomens and labored breathing.

"It will kill a horse," said Mike Vickers, a Brooks County
veterinarian and commissioner on the Texas Animal Health Commission.
"It's very, very serious."

No horses have died, officials believe. The ranch's 300-plus horses
have since been quarantined. Piroplasmosis had never been seen in
Texas and rarely had been found in the United States, according to
the Texas Animal Health Commission, the state's livestock and poultry
health regulatory agency. It is prevalent in 90 percent of the world
and commonly found in Mexico.

Once a horse is infected, the parasitic organisms remain in the
horse's system permanently, making the horse a potential carrier. It
does not affect humans or other non-equine mammals. Ticks usually
transmit the disease to horses, but it also has been spread from
animal to animal by contaminated needle. There is some concern that
it might be spread by biting horse flies, Vickers said.

Hunt, who has been in the ranching business for 35 years, said he had
never heard of the disease when it was discovered in October 2009.

A total of 8 other ranches in Jim Wells, Kleberg, and Brook counties
have been quarantined and tied to the initial outbreak, said James
Lenarduzzi, a veterinarian with the Texas Animal Health Commission.
Horses from ranches adjacent to King Ranch will be tested in coming
weeks to determine if they are infected.

The 825 000-acre King Ranch includes most of Kleberg and Kenedy
counties and portions of Brooks, Jim Wells, Nueces and Willacy
counties. It is renowned for its horses, including 1946 Triple Crown
winner Assault and 1950 Kentucky Derby and Belmont Stakes winner Middleground.

Though the ranch still has a horse breeding program, no horses have
been sold since the quarantine, Hunt said.

The Texas Animal Health Commission issued its 1st directive on the
South Texas-based infection 20 Oct 2009, noting that the disease had
been confirmed on an undisclosed ranch. Canada promptly banned
imports of Texas horses, though later relaxed the restrictions. A
total of 10 states have stringent restrictions in place that call for
testing and other controls before a horse can be imported from Texas.

State Rep. Yvonne Gonzalez Toureilles, D-Alice, who chairs the House
Committee for Agriculture and Livestock, got involved this week after
several South Texas ranchers complained that King Ranch has kept its
name away from the outbreak, which started in October 2009.

Hunt said King Ranch self-reported the infection, which was required
by law, and has worked openly with state and federal agencies since.
"We are putting a lot of resources and energy into trying to figure
out a way to take care of the problem," Hunt said. "What we don't do
is cover up stuff, which we have been accused of in this case."

The state has 1 million horses. Owners, family members and volunteers
spend USD 3 billion per year attending competitive events with more
than 250 000 horses, according to a Texas A&M University report. And
horse owners have more than USD 13 billion invested in barns, towing
vehicles, trailers, tack and related equipment and spend more than
USD 2.1 billion annually to maintain their horses.

Some South Texas ranchers are angry that the state and federal
government have been tight-lipped on the disease's origin, said
Lavoyger Durham, who manages the 13 000-acre El Tule Ranch near
Falfurrias for Brown and Root heiress Nancy Brown Negley.

Lenarduzzi met with Durham and about 25 fellow South Texas ranchers
Thursday [28 Jan 2010] to discuss the disease but would not say where
it started, which Lenarduzzi said is standard operating procedure.

Gonzalez Toureilles said she will meet with Texas Animal Health
Commission officials by Monday [1 Feb 2010] to make sure the outbreak
is being handled correctly.

King Ranch also is working with the U.S. Department of Agriculture
and some of the nation's top epidemiologists on experimental
procedures to remove the parasite from a horse's system, Hunt said.
"They have sent great people to work on this project, and we have had
lots of interaction," Hunt said. "It's just a process we are all
going to have to go through. It's not pleasant for anybody affected by it."

[Byline: Jaime Powell]

--
Communicated by:
ProMED-mail


[Equine piroplasmosis results from infection by the protozoa _Babesia
caballi_ or _B. equi_ (phylum Apicomplexa). The 2 organisms may
infect an animal concurrently.

Equine piroplasmosis is a tick-borne protozoal infection of horses.
Piroplasmosis may be difficult to diagnose, as it can cause variable
and nonspecific clinical signs. The symptoms of this disease range
from acute fever, inappetence, and malaise, to anemia and jaundice,
sudden death, or chronic weight loss and poor exercise tolerance. The
disease may be fatal in up to 20 percent of previously unexposed
animals. The tick vectors exist in the United States, and epidemics
of piroplasmosis were seen in Florida in the 1960s.

The incubation period for _B. equi_ infections is 12 to 19 days, and
infections are more severe. For _B. caballi_ infections, it is 10 to 30 days.

The clinical signs of piroplasmosis are variable and often
nonspecific. In rare peracute cases, animals may be found dead or
dying. More often, piroplasmosis presents as an acute infection, with
a fever, inappetence, malaise, labored breathing, congestion of the
mucus membranes, and small, dry feces. Anemia, jaundice,
hemoglobinuria, sweating, petechial hemorrhages on the conjunctiva, a
swollen abdomen, and posterior weakness or swaying may also be seen.
Subacute cases may have a fever (sometimes intermittent),
inappetence, malaise, weight loss, signs of mild colic, and mild
edema of the distal limbs. The mucus membranes can be pink, pale
pink, or yellow, and may have petechiae or ecchymoses. In chronic
cases, common symptoms include mild inappetence, poor exercise
tolerance, weight loss, transient fevers, and an enlarged spleen
(palpable on rectal examination). Foals infected in utero are usually
weak at birth, and rapidly develop anemia and severe jaundice.

In acute cases, the animal is usually emaciated, jaundiced, and
anemic. The liver is typically enlarged and dark orange-brown. The
spleen is enlarged, and the kidneys are pale and flabby. Petechial
hemorrhages may be seen in the kidneys, and subepicardial and
subendocardial hemorrhages in the heart. There may also be edema in
the lungs and signs of pneumonia.

The differential diagnosis for piroplasmosis includes surra, equine
infectious anemia, dourine, African horse sickness, purpura
hemorrhagica, and various plant and chemical toxicities.

Equine piroplasmosis can be diagnosed by identification of the
organisms in Giemsa stained blood or organ smears. _B. caballi_
merozoites are joined at their posterior ends, while _B. equi_
merozoites are often connected in a tetrad or "Maltese cross."
Organisms can often be found in acute infections, but may be very
difficult to find in carrier animals. In carriers, thick blood films
can sometimes be helpful.

Because _Babesia_ organisms can be difficult to detect in carriers,
serology is often the diagnostic method of choice. Serologic tests
include complement fixation, indirect fluorescent antibody (IFA), and
enzyme-linked immunosorbent assays (ELISA). The IFA test can
distinguish between _B. equi_ and _B. cabali_.

Other methods of diagnosis include DNA probes, in vitro culture, and
the inoculation of a susceptible (preferably splenectomized) animal
with blood from a suspected carrier. In addition, pathogen-free
vector ticks can be fed on a suspect animal, and _Babesia_ identified
either in the tick or after the tick has transmitted the infection to
a susceptible animal.

Disinfectants and sanitation are not generally effective against the
spread of tick-borne infections. However, preventing the transfer of
blood from one animal to another is vital.

The state of Texas in the South Central United States, can be located
on the HealthMap/ProMED-mail interactive map at:


Portions of this commentary have been extracted from
.
- Mod.TG]

[see also:
Equine piroplasmosis - USA 20100129.0309
2009
----
Equine piroplasmosis - USA 20100129.0309
Equine piroplasmosis - USA (12): (NM) 20091230.4394
Equine piroplasmosis - USA (11): multi-state 20091203.4128
Equine piroplasmosis - USA (10) 20091117.3963
Equine piroplasmosis - USA (09): (NJ ex TX) 20091111.3912
Equine piroplasmosis - USA (08): (TX) alert 20091030.3749
Equine piroplasmosis - USA (07): (TX) 20091024.3675
Equine piroplasmosis - USA (06): (TX) OIE 20091022.3631
Equine piroplasmosis - USA (05): (TX) 20091021.3617
Equine piroplasmosis - USA (04): (KS, MO) resolved 20090917.3262
Equine piroplasmosis - Ireland 20090909.3183
Equine piroplasmosis - USA (03): (KS, MO) 20090729.2662
Equine Piroplasmosis - USA (02): (MO) 20090612.2172
Equine Piroplasmosis - USA: (FL) quarantine lifted 20090225.0771
2008
----
Equine Piroplasmosis - USA (04): (FL) 20080930.3088]
....................sb/tg/ejp/dk

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Global Warming, Western Ranching, and the Bovine Curtain

By George Wuerthner, 10-06-07


Just like the old Iron Curtain that squelched any critical discussion of Communism’s failures, we in the West live behind a “Bovine Curtain.” The Bovine Curtain is—like the Iron Curtain—operated by the state, using taxpayer dollars to continuously broadcast propaganda about the virtues of ranching in the West and suppressing any negative or critical information. The mantra “cows are good” is repeated so often that it has attained cult status, even among many conservation groups—who should know better.

Eating meat (domestic livestock), particularly beef, has one of the biggest environmental impacts on the planet. In many ways making a change from a livestock based diet to plants (or wild game) is one of the easiest things that most of us can modify in our personal behavior to lessen our collective burden upon the planet. Producing one calorie of animal protein requires more than 10 times as much fossil fuel input—releasing more than 10 times as much carbon dioxide—than does a calorie of plant protein.

In the summer 2007 report, Livestock’s Long Shadow, UN researchers concluded that livestock production is one of the … most significant contributors to the most serious environmental problems, at every scale from local to global.” According to the UN, livestock contributes to “problems of land degradation, climate change and air pollution, water shortage and water pollution, and loss of biodiversity.” But few environmental groups mention this report or its findings, particularly if they are located in the cowboy West behind the Bovine Curtain. They would have to admit that the findings conclusions apply equally as well to the western U.S.

In particular the report singled out livestock production as a major contributor to global warming emissions, yet even Al Gore ignored livestock’s role in global warming during his Live Earth Concert. I don’t want to denigrate Gore’s efforts for he has brought much needed attention to global climate change. Nevertheless, while it’s well and good to ask people to screw in florescent light bulbs to reduce energy demands, the single biggest change that anyone could do to immediately reduce their contribution to greenhouse gases is to eat less meat.

Eating less meat has a surprisingly big bang for effort. Ranch and farm raised livestock produce millions of tons of carbon dioxide and methane annually. These two gases account for 90 percent of US greenhouse emissions. For instance, all the trucks, SUVs, cars, airplanes, trains and other transportation combined accounts for 13 percent of global warming emissions, while livestock production is responsible for an astounding 18 percent of all US greenhouse gases.

Not only are there the carbon dioxide emissions from livestock production, but livestock, particularly cattle, are responsible for the majority of emissions of several other greenhouse causing gases. According to the U.N., animal agriculture is responsible for an whopping 65 percent of worldwide nitrous oxide emissions. Bear in mind that nitrous oxide is about 300 times more effective as a global warming gas than carbon dioxide.

Methane is another gas produced by livestock. Methane traps 20 times more heat than carbon dioxide. The EPA reports that livestock production is the single greatest source of methane emissions in the US.

But when you live behind the Bovine Curtain most people are afraid to speak the truth or have internalized group think so completely that it does not even occur to people to ponder livestock’s central role in a host of environmental and health problems. Given their role as obsequious hand maidens to the livestock industry, it’s not surprising that federal and state governments hide the connection between meat production and global warming. But it’s totally unacceptable for environmental organizations to ignore this inconvenient truth.

For instance I recently checked the Sierra Club’s global climate change web site. They list ten things one can do to reduce global warming, from driving a more energy efficient auto to supporting renewable energy sources—but eating less meat is not one of them. It’s hard to believe that the Sierra Club is not aware of the UN report or other recent research linking livestock production with global warming, but one must assume that saying anything about livestock production is off limits when you live behind the Bovine Curtain. Worse yet, some Sierra Club chapters even promote ranching, despite the obvious impacts on global climate. A recent article the Sierra Club’s California/Nevada desert newsletter extolled the virtues of livestock grazing in the Great Basin—a region that is likely to suffer greatly from global climate change.

Similarly I reviewed National Parks and Conservation Association’s new report, “Unnatural Disaster,” which describes the multiple ways that global warming will impact our national parks. The report suggests a host of solutions that range from more efficient energy use to adoption of renewable energy, but I could not locate any mention of eating less meat in the 48 page report. And the Wilderness Society, while advising members to support carbon sequestration, mileage efficiency for vehicles, and other common remedies, did not mention of the role of livestock production and a meat diet in contributing to global warming.

Given that these national groups do not appear to see or more likely wish to avoid talking about a connection between diet and environmental issues, it’s not surprising that many regional or local environmental groups seldom mention livestock production as a global warming issue. They may express great concern about the decline of whitebark pine or large wildfires due to higher global temperatures, but they don’t go the next step to tie these issues to ranching and livestock production. Try to raise any linkage to ranching and livestock and the Bovine Curtain slams down. In the West, we don’t talk about cows except to laud the ranchers for being “good stewards of the land” or some other fawning palaver.

Global warming is only one reason to end livestock production, particularly western ranching. Production of livestock is the single greatest source of non-point pollution in the West. Livestock are among the prime reasons for the spread of invasive plants like cheatgrass. Producing hay and other irrigated forage for livestock is the reason our rivers are dewatered each summer. Livestock are the reason bison and wolves are killed outside of national parks. Livestock spread disease to wildlife. Livestock are the reason native wildlife like prairie dogs are being slaughtered. The list goes on, but few groups are willing to even list these impacts, much less tackle the source of the problem—cows.

The obvious omission of diet preferences among the proposed solutions to global warming is particularly noteworthy, especially when it involves no new technologies, no major policy changes in government, and no significant investment in new infrastructure. Eating less meat won’t cure global warming, but it’s the easiest and more cost effective mechanism available to ordinary citizens to start us on a new pathway towards global sustainability.

If you can’t afford a Prius, you can afford to eat less meat. Even if you can’t switch to solar energy, you can switch to a reduced meat diet. While most of us can’t design a wind mill, we can design a better diet. Eating less meat is not only good for the planet’s health, it‘s good for your health. It’s time for all of us to begin to view eating and our choice of diet as more than a culinary decision, but as an environmental act.







http://www.newwest.net/topic/article/global_warming_western_ranching_and_the_bovine_curtain/C38/L38/

Who Let The Cows Out ?

Click on title above to see who (jus 4 fun)

USDA Assures US: Pork From Pigs Exposed To H1N1 Safe To Eat

AMI: USDA Research - 01/21/2010 04:12PM

This is just to friggin funny to take serious. USDA says pigs sick with H1n1 safe to eat! Guess I will just run out and see if I can find a H1N1 infected pig carcass to gnaw on......if not, I guess I will have to settle for some other taint in the meat,....like e coli or salmonella, BSE, Scrappie, CWD, TB, H&M, etc.. AS IF H1N1 were the only animal/food-borne disease we had to worry about in our meat.


__________

Pork from pigs exposed to the H1N1 virus is safe to eat, according to a recent study by the USDA Agriculture Research Service (ARS).

Researchers noted that sick hogs are not allowed entry into the U.S. food supply as per USDA Food Safety and Inspection Service (FSIS) criteria, but stated that their findings support the World Health Organization (WHO) recommendation that pork harvested from H1N1-infected hogs is safe to eat.

In this study, non-respiratory tract tissues were analyzed for the virus following infection of the young pigs with the pandemic H1N12009 virus. Researchers found that while the H1N1 virus can induce respiratory disease in hogs there was no evidence for systemic infection that would contaminate meat with the infectious virus, which is consistent with other swine influenza illnesses.







http://www.cattlenetwork.com/AMI--USDA-Research----Pork-From-Pigs-Exposed-To-H1N1-Safe-To-Eat/2010-01-21/Article.aspx?oid=977702

Rhode Island Firm Recalls Italian Sausage Products Due to Possible Salmonella Contamination

Recall Release CLASS I RECALL
FSIS-RC-006-2010 HEALTH RISK: HIGH

Congressional and Public Affairs
(202) 720-9113
Atiya Khan

WASHINGTON, January 23, 2010 - Daniele International Inc., an establishment with operations in Pascoag and Mapleville, R.I., is recalling approximately 1,240,000 pounds of ready-to-eat (RTE) varieties of Italian sausage products, including salami/salame, in commerce and potentially available to customers in retail locations because they may be contaminated with Salmonella, the U.S. Department of Agriculture's Food Safety and Inspection Service (FSIS) announced today.

FSIS became aware of the problem during the course of an ongoing investigation of a multi-state outbreak of Salmonella serotype Montevideo illnesses. The Centers for Disease Control and Prevention (CDC), the Food and Drug Administration (FDA), FSIS, state health and agriculture departments, and Daniele International are cooperating in this investigation. The CDC has posted information about the multi-state outbreak on its website (http://www.cdc.gov/salmonella) but the investigation is ongoing, and has not yet definitively identified a food vehicle(s).

During the course of that investigation, a sample of product found in commerce was tested on behalf of a participating state department of health and found to contain Salmonella, which FSIS has a zero tolerance for in RTE products. The product tested was similar to products bought by customers who later became sick in the Montevideo investigation, but currently there is not a direct link. The Salmonella strain in the tested product does not appear to be the Montevideo strain of interest and further testing of the sample is ongoing at a state health partner laboratory. FSIS is continuing to work with the CDC, affected state public health partners, and the company on the investigation and will update the public on the progress of this investigation as information becomes available.

In addition, the company presented information to FSIS and took the additional action to voluntarily recall all products in commerce associated with black pepper, which the company believes is a possible source of contamination.

The products subject to recall include [View Labels, PDF One, PDF Two]:
10-ounce packages of "DANIELE NATURALE SALAME COATED WITH COARSE BLACK PEPPER."
Catch weight packages of "DANIELE PEPPER SALAME."
9-ounce packages of "BLACK BEAR OF THE BLACK FOREST BABY GENOA PEPPER SALAME."
20-ounce packages of "DANIELE DELI SELECTION, GENOA SALAME, SMOKED SALAME, PEPPERED SALAME, RUSTIC SALAME."
340- and 454-gram packages of "DANIELE SURTIDO FINO ITALIANO, SALAMI GENOA CON PIMIENTA, LOMO CAPOCOLLO, SALAMI CALABRESE."
16-ounce packages of "DANIELE ITALIAN BRAND GOURMET PACK, HOT CALABRESE, PEPPER SALAME, HOT CAPOCOLLO."
8-ounce packages of "DIETZ & WATSON ARTISAN COLLECTION PARTY PLATTER PACK, HOT CALABRESE, PEPPER SALAME, HOT CAPOCOLLO."
8-ounce packages of "DANIELE ITALIAN BRAND GOURMET PACK, HOT CALABRESE, PEPPER SALAME, HOT CAPOCOLLO."
16-ounce packages of "DANIELE GOURMET COMBO PACK, PEPPER SALAME, CAPOCOLLO, CALABRESE."
500-gram packages of "DANIELE ITALIAN BRAND GOURMET PACK EMBALLAGE ASSORTI GOURMET ITALIEN, HOT CALABRESE, PEPPER SALAME, CALABRESE PIQUANT, SALAMI AU POIVRE, HOT CAPOCOLLO, CAPOCOLLO PIQUANT."
8-ounce packages of "BOAR'S HEAD BRAND ALL NATURAL SALAME COATED WITH COARSE BLACK PEPPER."
Catch weight packages of "DIETZ & WATSON ARTISAN COLLECTION, BABY GENOA PEPPER SALAME, MADE WITH 100% PORK COATED WITH BLACK PEPPER AND PORK FAT."
20-ounce variety packages of "DANIELE DELI SELECTION, GENOA SALAME, SWEET SOPRESSATA, PEPPERED GENOA, MILANO SALAME."
21-ounce variety packages of "DANIELE GOURMET ITALIAN DELI SELECTION, SWEET SOPRESSATA SALAMI, PEPPERED GENOA SALAMI, HOT SOPRESSATA SALAMI, MILANO SALAMI, SALAMI SOPRESSATA DOUX, SALAMI GENOA POIVRÉ, SALAMI SOPRESSATA PIQUANT, SALAMI MILANO."
7-ounce packages of "DANIELE SALAME BITES PEPPER SALAME."
14-ounce packages of "DANIELE GOURMET ITALIAN DELI SELECTION ASSORTMENT DE FINES CHARCUTERIE ITALIENNE, SWEET SOPRESSATA SALAMI, MILANO SALAMI, SALAMI SOPRESSATA DOUX, SALAMI MILANO."
Catch weight packages of "DANIELE NATURALE SALAME COATED WITH COARSE BLACK PEPPER."
32-ounce variety packages of "DANIELE DELI SELECTION, GENOA SALAME, SWEET SOPRESSATA, PEPPERED GENOA, MILANO SALAME."


Recommendations for Preventing Salmonellosis:

Wash hands with warm, soapy water for at least 20 seconds before and after handling raw meat and poultry. Also wash cutting boards, dishes and utensils with hot soapy water. Clean up spills right away.

Keep raw meat, fish and poultry away from other food that will not be cooked. Use separate cutting boards for raw meat, poultry and egg products and cooked foods.

Cook raw meat and poultry to safe internal temperatures before eating. The safe internal temperature for meat such as beef and pork is 160° F, and 165° F for poultry, as determined with a food thermometer.

Refrigerate raw meat and poultry within two hours after purchase (one hour if temperatures exceed 90° F). Refrigerate cooked meat and poultry within two hours after cooking.


Each package bears a label with establishment number "EST. 9992" or "EST. 54" inside the USDA mark of inspection. The establishment is recalling all the products listed above which are currently in commerce. These products were distributed to retail establishments nationwide, as well as internationally. When available, the retail distribution list(s) will be posted on FSIS' Web site at http://www.fsis.usda.gov/FSIS_Recalls/Open_Federal_Cases/index.asp.






http://www.fsis.usda.gov/News_

California Firm Recalls Beef Products Due to Possible E. coli

Recall Release CLASS I RECALL
FSIS-RC-004-2010 HEALTH RISK: HIGH

Congressional and Public Affairs
(202) 720-9113
Adrian Gianforti

WASHINGTON, January 18, 2010 - Huntington Meat Packing Inc., a Montebello, Calif. establishment, is recalling approximately 864,000 pounds of beef products that may be contaminated with E. coli O157:H7, the U.S. Department of Agriculture's Food Safety and Inspection Service (FSIS) announced today.

The problem was discovered during a Food Safety Assessment (FSA) by FSIS personnel. The FSA led to the determination that a further investigation of establishment records was warranted. The investigation is ongoing and the following products are subject to recall.

The following products, consisting of all ground beef products produced by the plant from January 5, 2010 to January 15, 2010, are subject to recall:


40 lb. boxes of "Huntington Meats Ground Beef"
40 lb. boxes of "HUNTINGTON MEAT PKG. INC. BEEF GROUND FOR FURTHER PROCESSING"
40 lb. boxes of "BEEF BURRITO FILLING MIX"
10 lb. boxes of "IMPERIAL MEAT CO. GROUND BEEF PATTY"
20 lb. boxes of "IMPERIAL MEAT CO. GROUND BEEF PATTY"
10 lb. boxes of "El Rancho MEAT & PROVISION ALL BEEF PATTIES"

SAFE PREPARATION OF FRESH AND FROZEN GROUND BEEF

USDA Meat and Poultry Hotline
1-888-MPHOTLINE or visit
www.fsis.usda.gov


Wash hands with warm, soapy water for at least 20 seconds before and after handling raw meat and poultry. Wash cutting boards, dishes and utensils with hot, soapy water. Immediately clean spills.

Keep raw meat, fish and poultry away from other food that will not be cooked.

Consumers should only eat ground beef or ground beef patties that have been cooked to a safe internal temperature of 160° F, whether prepared from fresh or frozen raw meat products.

Color is NOT a reliable indicator that ground beef or ground beef patties have been cooked to a temperature high enough to kill harmful bacteria such as E. coli O157:H7.

The only way to be sure ground beef is cooked to a high enough temperature to kill harmful bacteria is to use a thermometer to measure the internal temperature.

Refrigerate raw meat and poultry within two hours after purchase or one hour if temperatures exceed 90° F. Refrigerate cooked meat and poultry within two hours after cooking



Each box bears the establishment number "EST. 17967" inside the USDA mark of inspection on a label. The products were produced between January 5, 2010, and January 15, 2010, and were shipped to distribution centers, restaurants, and hotels within the State of California. FSIS has received no reports of illnesses associated with consumption of these products. Individuals concerned about an illness should contact a physician.

During a subsequent review of the establishment's records, FSIS also determined additional products produced and shipped in 2008 to be adulterated because they may have been contaminated with E. coli O157:H7. As a result, the following products produced from February 19, 2008 to May 15, 2008, are subject to recall:

40 lb. boxes of "Huntington Meats Ground Beef"
40 lb. boxes of " HUNTINGTON MEAT PKG. INC. BEEF GROUND FOR FURTHER PROCESSING"
40 lb. boxes of "BEEF BURRITO FILLING MIX"
10 lb. boxes of "IMPERIAL MEAT CO. GROUND BEEF PATTY"
20 lb. boxes of "IMPERIAL MEAT CO. GROUND BEEF PATTY"
10 lb. boxes of "El Rancho MEAT & PROVISION ALL BEEF PATTIES"

Each box bears the establishment number "EST. 17967" inside the USDA mark of inspection on a label. The products were produced between February 19, 2008, and May 15, 2008, and were shipped to distribution centers, restaurants, and hotels within the State of California.

While these products are normally used fresh, the establishment is taking this action out of concern that some product may still be frozen and in commerce.

FSIS has received no reports of illnesses associated with consumption of these recalled products. Individuals concerned about an illness should contact a physician.

E. coli O157:H7 is a potentially deadly bacterium that can cause bloody diarrhea, dehydration, and in the most severe cases, kidney failure. The very young, seniors and persons with weak immune systems are the most susceptible to foodborne illness.

FSIS routinely conducts recall effectiveness checks to verify recalling firms notify their customers (including restaurants) of the recall and that steps are taken to make certain that the product is no longer available to consumers.

FSIS advises all consumers to safely prepare their raw meat products, including fresh and frozen, and only consume ground beef or ground beef patties that have been cooked to a temperature of 160° F. The only way to be sure ground beef is cooked to a high enough temperature to kill harmful bacteria is to use a food thermometer to measure the internal temperature.

Media and consumer questions regarding the recall should be directed to the company owner, Robert Glenn, at (888) 894-8242.

Consumers with food safety questions can "Ask Karen," the FSIS virtual representative available 24 hours a day at AskKaren.gov. The toll-free USDA Meat and Poultry Hotline 1-888-MPHotline (1-888-674-6854) is available in English and Spanish and can be reached from l0 a.m. to 4 p.m. (Eastern Time) Monday through Friday. Recorded food safety messages are available 24 hours a day.
#





http://www.fsis.usda.gov/News_

Mad Deer Update / Kansas

Four More CWD Positive Tests In Kansas
Saturday, January 23rd, 2010 at 1:58 pm
Tags: Chronic Wasting DiseaseCWDKansas

Four More Chronic Wasting Disease Presumptive Positive Tests In Kansas
Just more than half the samples collected have been tested.


Kansas Department of Wildlife and Parks

PRATT, KS —-(AmmoLand.com)- It’s likely that four more deer taken in northwest Kansas will be confirmed to have had chronic wasting disease (CWD).

So far, a total of 10 samples taken from deer killed by hunters this fall have shown presumptive positive results for CWD at the K-State Diagnostic Veterinary Lab in Manhattan.

Those presumptive positives have been sent to the National Veterinary Services Lab (NVSL) in Ames, Iowa for confirmation. Six samples that showed presumptive positive results in December were recently confirmed positive by the NVSL.

The four recent presumptive positive samples came from deer taken in Rawlins, Decatur, and Logan counties. If confirmed, this would be the first case of CWD in Logan County.

More than 1,000 samples still wait to be tested in an ongoing effort by KDWP to monitor the prevalence and spread of CWD. The fatal disease was first detected in a deer taken in Cheyenne County in 2005. Three infected deer were taken in Decatur County in 2007 and 10 tested positive in 2008, from Cheyenne, Decatur, Rawlins and Sheridan counties. This year, about 2,300 samples will be collected, with emphasis in northwest Kansas.

CWD is a member of the group of diseases called transmissible spongiform encephalopathies (TSEs). Other diseases in this group include scrapie in sheep and goats, bovine spongiform encephalopathy (BSE or Mad Cow Disease) in cattle, and Cruetzfeldt-Jacob disease in people. CWD is a progressive, fatal disease that results in small holes developing in the brain, giving it a sponge-like appearance under the microscope. An animal may carry the disease without outward indication but in the later stages, signs may include behavioral changes such as decreased interactions with other animals, listlessness, lowering of the head, weight loss, repetitive walking in set patterns, and a lack of response to humans.

There is no vaccine or other biological method that prevents the spread of CWD. There is no evidence that CWD poses a risk to humans or livestock, but precautions are advised. Hunters are advised not to eat meat from animals known to be infected and common sense precautions are advised when field dressing and processing meat from animals taken in areas where CWD is found.

More information on CWD can be found on KDWP’s website, www.kdwp.state.ks.us or at the Chronic Wasting Disease Alliance website, www.cwd-info.org

Distributed to you by - AmmoLand.com – The Shooting Sports News source.


http://www.ammoland.com/2010/01/23/cwd-positive-tests-in-kansas/

U.S. urged to show respect over beef dispute

U.S. urged to show respect over beef dispute

TAIPEI, Taiwan -- Premier Wu Den-yi and several lawmakers yesterday called for U.S. understanding and respect for Taiwan people after four House representatives called on the Office of the U.S. Trade Representative to halt new trade talks with Taiwan.



The House representatives said the U.S. should suspend the negotiations on trade and investment with Taipei untilthe dispute over Taiwan's ban on imports of some American beef products is settled.

Premier Wu said Taiwan has allowed the entry of 90 percent of U.S. beef products with only a tiny portion of 2 percent related to ground beef and internal organs remaining on the prohibition list due to public health concern.

He said the government will continue communicating with the U.S. to solve the trade friction.

Officials at the Ministry of Foreign Affairs said the nation's representative to Washington has been engaged in active dialogue with U.S. lawmakers to seek understanding.

But they said the beef issue should not hinder the progress on other talks on trade and investment between Taiwan and the U.S. for the sake of greater mutual benefits.

Lawmakers of both the ruling Kuomintang (KMT) and the opposition Democratic Progressive Party (DPP), who passed the new revision to the Act Governing Food Sanitation to tighten beef imports, said it is unrealistic for the U.S. to postpone the resumption of regular talks concerning the Taiwan-U.S. trade and investment framework agreement (TIFA).

They said the rules are meant to better safeguard the people's health from possible infection of beef products affected by mad cow disease.

The move is not singly targeted at the U.S. products but covers all import sources around the world, they said.

Legislator Tsai Huang-liang of the DPP said the U.S. should respect the decision made by the elected representatives of the people in Taiwan and Washington should not take actions that will affect Taiwan people's affection toward the U.S.

Furthermore, the overall benefits of the trade and investment relations between the two nations are far too high to be affected by the beef issue, he said.



http://www.chinapost.com.tw/taiwan/foreign-affairs/2010/01/23/241972/US-urged.htm

ENZOOTIC BOVINE LEUKOSIS - UNITED KINGDOM ex CANADA VIA COLOSTRUM

*****************************************************************
A ProMED-mail post

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


Date: Fri 22 Jan 2010
Source: Farmers Weekly Interactive [edited]



Cattle test positive for enzootic bovine leukosis
-------------------------------------------------
Cattle fed on imported colostrum substitute have tested positive for
enzootic bovine leukosis. The Department for Environment Food and Rural
Affairs (DEFRA) tests on 3 UK farms found calves had picked up the disease
from Calf's Choice Total, a Canadian-produced colostrum which is
distributed by Alta UK.

DEFRA said there was no direct animal health risk from using the product,
but said the herds affected had been placed under movement restriction.

--
communicated by:
Sabine Zentis
Gut Laach 52385 Nideggen, Germany


[The following information has been abridged from DEFRA's Summary profile
for enzootic bovine leukosis (EBL), available at
.

Summary profile for enzootic bovine leukosis (EBL)
--------------------------------------------------
1. Description: A viral disease of cattle causing malignant tumours in
affected animals. Clinical signs only appear in a very small proportion of
infected cattle usually when they are at least 4-5 years old. Tumours
develop in many parts of the body; there is loss of appetite, loss of
weight and a fall in milk production. Once these clinical signs appear the
disease rapidly leads to death of the animal. The virus is present in the
white blood cells of infected animals and the disease is transmitted
through close physical contact and the transfer of tissues containing
blood. Transmission by contaminated needles, surgical instruments or biting
insects is possible.
2. Rationale for government intervention:
2.1 Protection of human health: the disease does not affect humans.
2.2 Society: as only a small proportion of infected animals develop
clinical signs, the economic consequences of the disease are relatively low
at an industry level although the impact on individual farms may be
considerable.
2.3 Trade: assurances on EBL status are required for trade in live animals
and products.
2.4 Welfare: not the primary reason for intervention but welfare is
compromised as a result of infection and subsequent illness.
3. Legislative overview: EU and domestic legislation aims to eradicate the
disease and to prevent its spread through trade in live animals and products.
4. Geographic distribution:
GB ­ The disease was eradicated from Great Britain (GB) in 1996 following a
national programme of blood and milk testing. GB is classified as
officially EBL-free by the EU.
EU ­ A number of countries and regions of the European Union (EU) have
achieved officially EBL-free status. The disease however remains common in
many European countries.
International ­ The disease is common in Canada, the USA, and in South
America. There is a low level of infection in Australia and New Zealand.
5. Risk of introduction/spread: low ­ Although the disease is widespread
throughout the world, imported cattle are subject to certification and
testing requirements which minimise the risk of introduction. Potential
routes of entry of the disease to GB: importation of infected carrier
animals. Importation of semen containing infected blood cells.
6. Human health implications: the disease does not affect humans and there
is no risk to human health.
7. GB Disease control strategy: the disease control strategy in GB is to
maintain EBL free status by regular serological screening of the national
herd through blood and milk sampling and to stamp out any disease which is
introduced into the country.
8. Current Surveillance: EBL is a notifiable disease and there is a
national testing programme. Tumours in live animals or in carcases must be
notified to the divisional veterinary manager, who ensures that tests are
carried out for EBL. Structured surveys of the national cattle herd take
place by regular tests on bulk milk samples or blood samples. These show
that the country remains free from the disease. - Mod.AS]

[see also:
2009
---
Enzootic bovine leukosis - New Zealand (03): Europe 20091004.3449
Enzootic bovine leukosis - New Zealand (02): eradicated, not 20091001.3417
Enzootic bovine leukosis - New Zealand: eradicated 20090928.3388
2008
---
Enzootic bovine leukosis - Finland: OIE 20080404.1241
2005
---
Enzootic bovine leukosis - Switzerland: susp 20050625.1783]

....................arn/ejp/sh



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Mad Deer / WV

CHRONIC WASTING DISEASE, CERVID - USA: (WEST VIRGINIA) 2009
***********************************************************
A ProMED-mail post

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


Date: Sat 16 Jan 2009
Source: West Virginia Metro News [edited]



16 new CWD cases found in Hampshire County
------------------------------------------
The slow growth and spread of chronic wasting disease [CWD] continues in
West Virginia. DNR [Division of Natural Resources] Biologists report 16
deer killed by hunters in the 2009 deer season tested positive for the
presence of CWD. The DNR pulled those positives from 1091 deer killed by
hunters in Hampshire at local checking stations during the season.

"It's not the greatest news and certainly wasn't the Christmas present I
was hoping to open, but you know when you're dealing with CWD and lots of
unknowns associated with it, having a result with 16 positives was not
necessarily unexpected at all," said Paul Johansen, chief of the DNR's Game
Management on West Virginia Outdoors.

The 16 infected whitetails included one 4.5 year old doe, a 2.5 year old
doe, one 1.5 year old buck, ten 2.5 year old bucks, and three 3.5 year old
bucks.

The DNR discovered chronic wasting disease in 2005 in a road killed deer
near the community of Slanesville. Since that time a containment zone was
established north of Route 50 in Hampshire County with special restrictions
on hunting and constant monitoring. This year's [2009] count included
13-infected deer within that zone and 2 from outside the border, but still
within Hampshire County.

"This is not the 1st time we've detected a positive outside that
containment zone," said Johansen. "We're going to have to take a look at
that containment zone and see if it should be expanded."

CWD is an incredibly slow disease. Although deer may be infected, they show
no signs of the illness until in the very last stages when they become
emaciated and disoriented. Otherwise, infected deer show no signs they are
carrying the virus without testing of the brain or spinal tissue.
Researchers conclude feeding or baiting deer is one of the fastest ways to
spread the virus with nose-to-nose contact. Restrictions have been placed
on feeding and baiting deer in the containment area.

"Despite our agency's best efforts, we continue to struggle with CWD in
Hampshire County," said DNR director Frank Jezioro. "I am particularly
concerned that some individuals are not complying with regulations
prohibiting the feeding and baiting of deer within the Hampshire County CWD
Containment Area."

"In certain areas of the containment zone we have information to indicate
there is some baiting and feeding activity that's going on," said Johansen.
"That concerns us as we try to grapple with this disease." The agency plans
to renew efforts to engage the public's help in controlling the spread and
compliance with restrictions enacted to slow the spread. Those efforts will
include additional law enforcement activities if needed.

"As we strive to meet this wildlife disease challenge and implement
appropriate management strategies, the continued support and involvement of
landowners and hunters will be essential," Jezioro said. "The WVDNR remains
committed to keeping the public informed and involved in these wildlife
disease management actions as we go forward."

The CWD Management Strategy to this point includes the following
restrictions in Hampshire County:
- implemented CWD testing efforts designed to determine the prevalence and
distribution of the disease;
- established antlerless deer hunting regulations designed to increase
hunter opportunity to harvest female deer, adjust deer populations to
desired levels, and reduce the risk of spreading the disease from deer to
deer;
- established deer carcass transport restrictions designed to lower the
risk of moving the disease to other locations;
- established regulations designed to prohibit the feeding and baiting of
deer within the affected area and reduce the risk of spreading the disease
from deer to deer.

Hunters concerned about consumption of venison from infected animals are
advised to use their own judgment. Researchers and DNR biologist say
there's no known instance of CWD affecting humans.

[byline: Chris Lawrence]

--
communicated by:
HealthMap Alerts via ProMED-mail


[As hunting seasons across the United States draw to a close, we are likely
to see several reports indicating a slow spread in some states as the
surveillance of hunter-killed animals become tested, tabulated, and
reported. It is important to remember that CWD has not been shown to have
transmissibility to humans. - Mod.TG

West Virginia can be located on the HealthMap/ProMED-mail interactive map
at . Hampshire County can be seen on the map
at . -
Sr.Tech.Ed.MJ]

[see also:
2009
---
Chronic wasting disease, cervids - USA (04): (WV) 20090601.2041
Chronic wasting disease, cervids - USA: (WV) 20090101.0004
2008
---
Chronic wasting disease, cervids - USA (09): (WV) 20081223.4039
Chronic wasting disease, cervids - USA (04): (WV) 20080509.1580]

.................tg/mj/sh



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are posted, but the accuracy and completeness of the
information, and of any statements or opinions based
thereon, are not guaranteed. The reader assumes all risks in
using information posted or archived by ProMED-mail. ISID
and its associated service providers shall not be held
responsible for errors or omissions or held liable for any
damages incurred as a result of use or reliance upon posted
or archived material.
************************************************************
Become a ProMED-mail Premium Subscriber at

************************************************************
Visit ProMED-mail's web site at .
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Austrailia's Cattle Dying in Droves from Mystery Disease

UNDIAGNOSED DEATHS, BOVINE - AUSTRALIA: (NEW SOUTH WALES) REQUEST FOR
INFORMATION
***************************************************************************
A ProMED-mail post

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


Date: Fri 8 Jan 2010
Source: The Daily Advertiser [edited]



Cattle farmers in western [New South Wales] are counting a mounting
death toll as herds of corpses litter paddocks after succumbing to an
unknown disease.

The disease is causing growing concern as it continues to spread
among livestock properties, with farmers from Mildura, Hillston,
Ivanhoe, and Mossgiel reporting mystery deaths in their herds.

Head veterinarian with the Western Division of DPI [Department of
Primary Industries] Dr Greg Curran yesterday [7 Jan 2009] admitted
the disease behind the deaths was yet to be identified, expressing
his unease at the severity of the illness.

Early speculation had salmonella poisoning blamed as the cause of the
deaths but as more necropsies are carried out a rare salmonella
outbreak is becoming less and less likely to be the sole culprit.

"There are various possibilities," he said. "We are finding
salmonella damage in some of the cattle but then we are opening other
up and finding damage from something else. We are still working on an
overall diagnosis. It has been quite severe in some mobs."

A Mossgiel farmer is feeling the full brunt of the unknown sickness,
with 66 percent of one of his herds struck with the virus. [At this
point, they do not know if it is a virus, but it is causing death. - Mod.TG]

He is said the biggest worry of the illness is the speed in which
calves and cows are affected before death. "We only have 22 left in
the mob," he said. "They look healthy 3 to 4 days before they are
sick, then they get diarrhea before they start to slime something
from the mouth. Then they are dead."

In order to quarantine his farm, [the farmer] has moved the 2 healthy
herds to the far corners of the property to limit their contact with
the sick livestock. "We are keeping them to one side of the property," he said.

"I know of at least 7 other farmers that have this happening on their
property but we are the only property so far that has had it go
through the whole lot.

"It was just attacking the calves early in December [2009] and the
older ones were standing up to it better, but now it is killing the
cows as well."

[The farmer] and Dr Curran share a growing anxiety over the inability
to find an antibiotic or treatment showing a response in the sick
animals. "We have attempted various treatments but at this point
antibiotics and treatments have not been as successful as hoped," he said.

"We saw something similar to this in 2006; we saw what appears to be
the same sort of problem."

Local farmers will be relieved to hear at this stage it looks
unlikely the disease will spread into the Riverina, with Dr Curran
confident the disease will be contained in the affected region.

[Byline: Stephanie Muir]

--
Communicated by:
ProMED-mail


[The article is relatively vague, only giving us a few signs, of
diarrhea, and slime at the mouth, and then presumably, acute death.
We are not even told what antibiotics they tried. However, either
this is not bacterial, or they treated with an antibiotic the agent
is not sensitive to.

If there is a pattern here, then we should learn from this. How
similar is this outbreak to the one in 2006? What stopped the spread
of the illness? Is it spread via air? Fomites? Or nose-to-nose contact?

What kinds of investigations have been done? Do these animals have a
fever? Are they off feed before showing signs of illness? Do all
affected areas have anything in common? Water? Hay? Feed?

I could speculate on several diseases, but there are presently too
many unknown pieces. If there is someone with more information, not
speculation, ProMED-mail would welcome the input. - Mod.TG]

[New South Wales can be located on the HealthMap/ProMED-mail
interactive map of Australia at
. - Sr.Tech.Ed.MJ]

[see also:
2009
----
Theileria, bovine - Australia: (NSW), RFI 20090313.1045
Ephemeral fever, bovine - Australia: (NSW) 20090313.1043
Fascioliasis, bovine - Australia: (NS) 20090306.0934
Bovine viral diarrhea - Australia (02) 20090120.0244
Bovine viral diarrhea - Australia: susp., RFI 20090106.0051
2008
----
Bluetongue, bovine - Australia: (NT) 20080417.1374
Tick fever, bovine - New Caledonia ex Australia (04) 20080401.1205
Tick fever, bovine - Australia: (NSW), babesiosis 20080401.1201
Tick fever, bovine - New Caledonia ex Australia (03) 20080330.1184
Tick fever, bovine - New Caledonia ex Australia (02) 20080320.1073
Tick fever, bovine - New Caledonia ex Australia 20080313.1006
2007
----
Undiagnosed deaths, bovine - Australia (NSW) (02) 20070329.1088
Undiagnosed deaths, bovine - Australia (NSW): RFI 20070324.1028
2006
----
Johne's disease, bovine - Australia (WA) 20060711.1904
Botulism, bovine - Australia (02) 20060629.1797
Botulism, bovine - Australia 20060524.1464
Lupinosis, ovine, bovine - Australia (SA) 20060406.1029]
...................................sb/tg/mj/dk

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ProMED-mail makes every effort to verify the reports that
are posted, but the accuracy and completeness of the
information, and of any statements or opinions based
thereon, are not guaranteed. The reader assumes all risks in
using information posted or archived by ProMED-mail. ISID
and its associated service providers shall not be held
responsible for errors or omissions or held liable for any
damages incurred as a result of use or reliance upon posted
or archived material.
************************************************************
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************************************************************
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WORLDWIDE HOOF & MOUTH OUTBREAK / CATTLE

A ProMED-mail post

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


Date: Fri 18 Dec 2009
Source: Report of the 5th Annual Meeting of the Network of OIE/FAO
Reference Laboratories for Foot-and-Mouth Disease, 23-27 Nov 2009,
Delhi [extracts, pages 9-12, edited]



Regional discussions
--------------------
The participants split into groups to discuss current threats and
vaccine priorities according to regional virus pools and under the
following headings: (1) significant epidemiological events; (2)
antigenic changes noted; (3) serological vaccine matching tests done;
(4) priority vaccines; (5) gaps in submission; (6) gaps in vaccine
selection; (7) threats for 2010.

Pool 1. Eastern Asia
--------------------
A small number of cases of serotype A and Asia 1 have been detected
in China this year [2009]. The Asia 1 viruses appear to be matched by
the current vaccine used in China, whilst the suitability of vaccines
to cover the serotype A viruses is still under study. In South East
Asian (SEA) countries, serotypes O and A have predominated with no
reports of Asia 1. Whereas all serotype A viruses in SEA appear to be
derived from the same lineage that has evolved within the region for
many years, the situation for serotype O is more complex with a
mixture of indigenous and introduced viruses. Samples have been
analysed at Pakchong from Myanmar, Laos, Vietnam, Cambodia, and
Thailand. The vaccines used in the different countries are as follows:
1. China, O China 99, A China F/72, Asia 1 China JSWX052;
2. Viet Nam, O Manisa and O 3039, A May 97 and A22 Iraq, Asia 1 Shamir;
3. Malaysia, O Manisa and O 3039, A May 97, Asia 1 Shamir;
4. Thailand, O 189/87 (Manisa-like), A 118/87, Asia 1/85 (Asia 1 Shamir-like).
There were considered to be no major gaps in submission, although the
number of samples analysed is quite small and there have been no
submissions this year [2009] to Pakchong from Malaysia. In 2010, the
main concern in China is over possible continuation of outbreaks
caused by serotype A, whilst outbreaks of both serotype O and A are
expected to recur in South East Asia.

Pool 2. Southern Asia
---------------------
In India, outbreaks of serotype O have predominated. About 10 percent
of the approximately 334 isolates made thus far have undergone
testing for vaccine matching to O IND R2/75 and 95 percent have shown
a good match. Until this year [2009], the PanAsia 2 strain was the
main one, but in 2009, the "India 2001" strain has predominated.
PanAsia 2 has been associated with significant disease in wildlife
during 2005-08. Most of the 26 serotype A isolates have shown a match
to A IND 40/00 and all of the 16 Asia 1 field isolates matched to
Asia 1 63/72. These A and Asia 1 virus lineages seem to be unique to
India. The predominant strain of serotype A is genotype VII, which
has an amino acid deletion in an antigenic site of VP3. This virus is
distinct from the A Iran 05 strain found throughout the Middle East.
The priority vaccine strains are those stipulated in India, namely O
IND R2/75, A IND 40/00 and Asia 1 IND 63/72. The meeting agreed on
the importance of making a full antigenic and genetic comparison
between representative Indian strains and those held in the WRLFMD database.

Pool 3. Eurasia
---------------
The main epidemiological events have been the continued spread and
circulation of serotype O and A viruses belonging to O PanAsia 2 and
A Iran 05 strains. It seems probable that antigenic changes may have
conferred an advantage for the spread of the A Iran 05 strain, but
this is less clear for O PanAsia 2 which mostly still matches O
Manisa vaccine. An isolated case of Asia 1 virus was reported in
Bahrain caused by an isolate with closest match to earlier Indian
sequences held in the WRLFMD database. An outbreak in 2009, fatally
affecting gazelle in the United Arab Emirates, was caused by viruses
of the O India 2001" strain. Recent isolates sent to WRLFMD from
Pakistan show continued evolutionary change, with some A and a single
Asia 1 viruses showing a poor match to A Turkey 06 (A Iran 05 strain)
and Asia 1 Shamir, respectively. Elsewhere in the region, Egypt
continues to submit samples containing unique viruses of serotype O
(related to the O Sharquia 72 vaccine strain) and type A (of the A
Africa topotype closely related to that introduced into the country
in 2006). In all, about 35 isolates have been matched to a variety of
vaccine strains as well as 10 O PanAsia 2 viruses isolated in 2008.
The priority vaccines are O Manisa (or similar strains), A Iran 05
strain and Asia 1 Shamir (or similar strains). The major gaps in
submission are considered to be from some central Asian Republics,
the Caucasus, and some Middle East countries concerned about the
impact of transparency on trade. The main problems for vaccine
selection are an inability to compare vaccine matching results
between centres due to the use of different vaccine strains,
unstandardised methods, and field isolates that are not shared. Based
on previous experience, it may be expected that serotype O but not A
will be sustained within the region. An Asia 1 epidemic may be due,
since cases are occurring in Pakistan, whilst countries like Iran and
Turkey will by now have a low population immunity to this serotype
(last seen in 2004). Plans to increase imports of live cattle and
small ruminants into the Middle East from Africa and through new
trade routes may increase the risk of African strains being
introduced. It was felt that the discrepancy between the vaccine
strain recommendations from the WRLFMD and those made on a regional
basis by the Network caused confusion and it needed to be clearer
that the former were intended primarily as a guide for vaccine bank
managers in free countries and only included vaccine strains
available to WRLFMD and that met the standards of the European Pharmacopoeia.

Pool 4. Western Africa
--------------------
There is very little available information. In 2008, viruses
submitted from Nigeria to WRLFMD were of serotypes O and SAT 2 and
revealed a link to other African regions such as Sudan. In 2009, 31
samples were submitted to PIADC-FADDL [Plum Island Animal Disease
Center - Foreign Animal Disease Diagnostic Laboratory]. Epithelial
samples had been collected from an outbreak affecting mainly cattle
that had lasted from October 2008 to February 2009. 21 of 31 samples
were positive and typed as serotype A. Phylogenetic analysis of the
P1 and VP1 regions revealed close identity to A Kenya 1984 virus.
Collectively, these isolates are more linked to the European and
South American old isolates rather than to those of Asiatic lineage
of Thailand, Iraq, Iran, Pakistan, and India.

Pool 5. Eastern Africa
----------------------
Samples from Kenya have been typed as SAT 1, SAT 2, O, and A, with
SAT 1 predominating. The samples were also referred to WRLFMD who
have also received samples from some neighbouring countries. Within
the region, there are gaps in laboratory capacity and both in
technical capability and ability to interpret results. There is a
need to develop a strategic plan and network for the region. It would
be helpful to identify a specialist from each country who could act
as a local animator to encourage action on FMD control initiatives.

Pool 6. Southern Africa
-----------------------
In Southern Africa, SAT 1 isolates from 2001-2006 belonged to
topotypes I, II and III with outbreaks characterised in Mozambique
during 2001-2002, Zimbabwe in 2003, Zambia during 2005 and 2006 and
Botswana in 2006. The SAT 2 isolates were from Botswana 2002 and
2006; Zimbabwe during 2000/2001-2003, and recently from Namibia and
Malawi during 2008 and 2009. Recently, SAT 1 had infected domestic
cattle in the buffer zone (Makoko diptank and Phameni diptank). They
had heard of outbreaks in Zimbabwe but no confirmation had been
received so far. In Botswana, after 20 years with no outbreaks, a
series of 9 outbreaks have occurred since 2002. These have been
mostly of SAT 2 and attributed either to incursions from neighbouring
countries or due to contact between domestic cattle and wildlife. The
2008 outbreaks appeared to have been exacerbated by antigenic
mismatch between the field virus and the vaccine strains. To try to
address the problems associated with lower vaccine matches, efforts
are being made to increase antigen payload, introduce new vaccine
strains and improve the surveillance of buffalo. The priority
vaccines are SAT 2 and SAT 1, but there is insufficient information
to be more precise about the strains that should be included. For SAT
1, past vaccine matching results have indicated that vaccine strains
are relevant. For SAT 2, recent outbreaks have shown some
differences. However, viruses with good correlation to vaccine caused
outbreaks recently as well.

Pool 7. South America
---------------------
There are multiple zones (regarding OIE FMD status) in different
countries of the region and maps need to be carefully drawn in order
to illustrate the situation accurately. Most of the countries are now
FMD-free with or without vaccination. 9 samples were received at
PANAFTOSA from Ecuador (n=6) and Colombia (n=3), whilst 19 samples
from Ecuador were sent to the Argentinean OIE Reference Laboratory.
All of the samples were of serotype O and are of strains indigenous
to the region. Venezuela has reported during 2008-2009 a total of 60
FMD outbreaks, (25 serotype O virus and 35 serotype A virus) but has
not submitted samples to an OIE reference Laboratory. Nationally,
both serotypes O and A have been confirmed. The vaccines used in the
region are all single oil emulsions. O Campos and A24 Cruzeiro are
used throughout the region, whilst C3 Indaial is included in Bolivia,
Brazil, and Paraguay. The justification has been the Amazonas
outbreak in 2004. In Argentina, a tetravalent vaccine is used
incorporating A ARG 2001 in addition to O Campos and A24 Cruzeiro and
C3 Indaial. The role of the OIE reference Laboratories in advising on
methodology and standards for vaccine control is considered extremely
important. Cattle up to 2 years old are vaccinated every 6 months and
thereafter annually, aiming for 100 percent coverage. For vaccine
matching, r1 values of 0.25 or greater are considered acceptable and
the 2009 type O viruses gave values over this threshold when tested
at 2 OIE Reference Laboratories. In some cases r1 values from Ecuador
strains were slightly over threshold. Considering the importance of
vaccine potency, expectancy of protection is also used to gauge
antigenic match rather than relying on r1 values alone.

[Byline: David Paton]

--
Communicated by:
ProMED-mail


[The information above, addressing the very recent worldwide FMD
situation, provided by those on the frontline of FMD surveillance and
diagnosis, is timely and useful. Additional information on discussed
topics such as collaborative vaccine matching trials, proficiency
test schemes, recent research subjects, and others, can be found in
the full report (21 pages) at the source URL above.

The early publication of this report by the WRLFMD, Pirbright is
exemplary. - Mod.AS]

[see also:
Foot & mouth disease, bovine - South Korea: (KG), OIE 20100108.0089
2009
----
Foot & mouth disease, bovine - Viet Nam (06): vaccination, RFI 20091203.4120
Foot & mouth disease, bovine - Viet Nam (05): (PY), (YB) 20091202.4112
Foot & mouth disease - Turkey, Syria: susp. RFI 20091129.4081
Foot & mouth disease, bovine - China (06): (XJ), OIE 20091128.4080
Foot & mouth disease, bovine - India: (KL), susp., RFI 20091120.4002
Foot & mouth disease, bovine - Congo (DR): (IT) susp. RFI 20090920.3293
Foot & mouth disease - South Africa: suspected, RFI 20090915.3241
Foot & mouth disease, porcine - Taiwan (08): (TY) 20090905.3123
Foot & mouth disease, bovine - Viet Nam (02): (QG) RFI 20090826.3005
Foot & mouth disease, bovine - Bangladesh: susp., RFI 20090823.2974
Foot & mouth disease - Middle East (06): WRLFMD update, vac. 20090808.2806
Foot & mouth disease, bovine - Rwanda: (ES) susp, RFI 20090807.2795
Foot & mouth disease, bovine - Ecuador (02): conf 20090804.2755
Foot & mouth disease, domestic ruminants - India: (SK), RFI 20090804.2751
Foot & mouth disease - Israel: serotype A, resolved, OIE 20090803.2732
Foot & mouth disease - Middle East (05): FAO/OIE surveill., control
20090731.2686
Foot & mouth disease - Israel, Palestinian Authority: serotype A 20090714.2510
Foot & mouth disease - Nepal 20090625.2318
Foot & mouth disease, porcine - Taiwan (04): (TY) sentinels 20090624.2301
Foot & mouth disease, bovine - China (05): (SD) serotype A 20090609.2129
Foot & mouth disease, bovine - Angola: (CC) OIE 20090605.2082
Foot & mouth disease, bovine - Ecuador: susp. 20090601.2036
Foot & mouth disease - Middle East (04): FAO 20090509.1735
Foot & mouth disease - Lebanon: serotype A 20090422.1519
Foot & mouth disease - Middle East (03): serotypes, update 20090410.1377
Foot & mouth disease - Bahrain: serotype A 20090409.1366
Foot & mouth disease - Taiwan, Lebanon 20090404.1295
Foot & mouth disease, bovine - China (04): (SC) serotype Asia 1 20090403.1283
Foot & mouth disease - Middle East (02): serotypes A, O, update 20090331.1242
Foot & mouth disease, porcine - Taiwan (03): conf.OIE 20090331.1239
Foot & mouth disease - Middle East: serotypes A, O, update 20090317.1082
Foot & mouth disease - Malaysia (02): (Peninsular) clarificn. 20090305.0903
Foot & mouth disease, bovine - Laos: (BL) RFI 20090304.0877
Foot & mouth disease, cattle, buffaloes - Egypt: serotype A 20090303.0865
Foot & mouth disease - Malaysia (Peninsular) 20090303.0864
Foot & mouth disease - Palestinian Auton Terr: (JN), RFI 20090227.0816
Foot & mouth disease, bovine - China (03): (HB, SH) serotype A 20090223.0757
Foot & mouth disease - Lebanon: OIE, untyped 20090222.0734
Foot & mouth disease, porcine - Taiwan: serotype O 20090219.0689
Foot & mouth disease - Israel (02): OIE, serotype O, spread 20090218.0680
Foot & mouth disease - Iraq: (BA) 20090208.0577
Foot & mouth disease - Saudi Arabia (02): vaccination 20090201.0447
Foot & mouth disease - Saudi Arabia: east, RFI 20090128.0387
Foot & mouth disease, bovine - Uganda (03): (N., E, & Central) 20090127.0364
Foot & mouth disease, bovine - China: (HB, A), (XJ, Asia1) 20090124.0318
Foot & mouth disease, bovine - Viet Nam: (LA, KT) serotype A 20090122.0273]
...................................arn/mj/dk

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16 STATE E. COLI OUTBREAK: BAD BEEF

E. COLI O157 - USA: 2009, TENDERIZED, NON-INTACT STEAK
******************************************************
A ProMED-mail post

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


Date: Wed 6 Jan 2010
Source: CDC [edited]



The Centers for Disease Control and Prevention (CDC) is collaborating
with public health officials in several states and the United States
Department of Agriculture's Food Safety and Inspection Service (FSIS)
to investigate a multistate outbreak of human infections due to _E.
coli_ 0157:H7.

As of 5:00 PM EDT, Mon 4 Jan 2010, 21 persons infected with the
outbreak strain of _E. coli_ O157:H7 had been reported from 16
states. The number of ill persons who were identified resides in each
state as follows: CA (1), CO (1), FL (1), HI (1), IA (1), IN (1), KS
(1), MI (1), MN (3), NV (1), OH (2), OK (1), SD (2), TN (1), UT (2),
and WA (1).

Known illness onset dates range from 3 Oct 2009 through 14 Dec 2009.
Most patients became ill between mid-October and late November.
Patients range in age from 14 to 87 years and the median age of
patients is 34 years (which means half are younger than 34 years). 43
percent of patients are females. There have been 9 reported
hospitalizations, 1 case of hemolytic uremic syndrome (HUS), and no deaths.

The outbreak can be visually described with a chart showing the
number of persons who became ill each day. This chart is called an
epidemic curve or epi curve. Illnesses that occurred after 22 Dec
2009 might not yet be reported due to the time it takes between when
a person becomes ill and when the illness is reported. This takes an
average of 2 to 3 weeks.

In early December 2009, CDC's PulseNet staff identified a multistate
cluster of 14 _E. coli_ O157:H7 isolates with a particular DNA
fingerprint or pulsed-field gel electrophoresis (PFGE) pattern
reported from 13 states. The CDC's OutbreakNet team began working
with state and local partners to gather epidemiologic information
about persons in the cluster to determine if any of the ill
individuals had been exposed to the same food source(s). Health
officials in several states who were investigating reports of _E.
coli_ O157:H7 illnesses in this cluster found that most ill persons
had consumed beef, many in restaurants. CDC is continuing to
collaborate with state and local health departments in an attempt to
gather additional epidemiologic information and share this
information with FSIS. At this time, at least some of the illnesses
appear to be associated with products subject to a recent FSIS recall.

On 24 Dec 2009, FSIS issued a notice about a recall of 248 000 pounds
of beef products from National Steak and Poultry that may be
contaminated with _E. coli_ O157:H7. The recall was issued after FSIS
determined there was an association between non-intact steaks (blade
tenderized prior to further processing) and illnesses in Colorado,
Iowa, Kansas, Michigan, South Dakota and Washington.

--
Communicated by:
ProMED Rapporteur Brent Barrett


[A discussion regarding the issue of non-intact steaks and roasts,
pieces of meat that have be tenderized by needle or blade which can
introduce pathogens (especially _E. coli_ O157:H7) to the internal
aspect of the meat where it may survive better than its "surface"
cousins can be found at the previous ProMED posting on this small but
epidemiologically significant cluster at
.
- Mod.LL]

[see also:
2009
----
E. coli O157 - USA (09): tenderized, non-intact steak 20091230.4389
E. coli O157 - USA (08): ground beef 20091103.3794
E. coli O157 - USA (07): refrigerated cookie dough 20090710.2473
E. coli O157 - USA (06): beef, recall, RFI 20090702.2389
E. coli O157 - USA (05): refrigerated cookie dough, CDC 20090701.2381
E. coli O157 - USA (04): refrigerated cookie dough 20090630.2371
E. coli O157 - USA (03): beef, recall 20090629.2354
E. coli O157 - USA (02): refrigerated cookie dough 20090623.2291
E. coli O157 - USA: refrigerated cookie dough 20090619.2259
2008
----
E. coli O157 - USA (09): (WA), susp. 20081021.3336
E. coli O157 - USA (08): (CA), cooked beef 20081007.3181
E. coli O157, university students - USA (06): California lettuce 20081015.3266
E. coli O157, university students - USA: (MI) 20080922.2987
E. coli O157 - USA (07): (MA) alert 20080811.2475
E. coli O157 - USA: (OH, MI), unknown source 20080624.1947
E. coli O157, lettuce - USA: (WA) 20080606.1807
E. coli O157, restaurant - USA: (HI) 20080228.0811
2007
----
E. coli O157, ground beef - USA (multistate) (09) 20071126.3823
E. coli O157, ground beef - USA (multistate) (08): Canada 20071029.3511
E. coli O157, ground beef - USA (multistate) (04): 2nd
manufacturer 20071007.3304
E. coli O157, ground beef - USA (multistate) (03): CDC report 20071003.3272
E. coli O157, ground beef - USA (multistate): alert, recall 20070927.3201
E. coli O157, ground beef - USA (NY): alert, recall 20070926.3190
E. coli O157, ground beef - USA (WA, OR): alert 20070830.2855
E. coli O157, ground beef - USA (NY) 20070725.2387
E. coli VTEC, prisoners - USA (CO) (02) 20070714.2263
E. coli VTEC, prisoners - USA (CO): RFI 20070712.2236
E. coli O157, ground beef - USA (west) (03): expanded recall 20070611.1902
E. coli O157, ground beef - USA (west): recall 20070606.1831
E. coli O157, ground beef - USA (multistate): recall 20070514.1532
E. coli O157, steak - USA (PA): recall 20070426.1362
E. coli O157, restaurant - USA (CA) (03) 20070410.1204
E. coli O157, restaurant - USA (CA) 20070403.1131
E. coli O157, spinach - USA (multistate): 2006, FDA report 20070326.1051
E. coli O157, bagged salad greens - USA (multistate) 20070121.0288
E. coli O157, lettuce - USA (multistate): 2006 20070112.0158]
2003
----
E. coli O157, frozen steaks - USA (Midwest): recall 20030701.1617]
.................................ll/ejp/dk

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New York Times Questions Safety of Processed Beef

An in depth investigation by the New York Times has revealed some startling information about the safety of processed beef approved for human consumption. Since pet food is the very last thing of concern with government agencies, if these risks were discovered in people food, imagine what could be found in pet foods (if anyone bothered to look). It is frightening to consider.


Click on title above to go to Sues website to real original article;

http://www.truthaboutpetfood.com/articles/safety-of-processed-beef-for-humans-questioned-imagine-the-lack-of-safety-with-pet-food-meat.html

NH Gal Gets Anthrax from Playing BONGO Drums

Guess this means you can maybe catch it from wearing (or even touching) leather products? Hummmm.

ANTHRAX, HUMAN - USA: (NEW HAMPSHIRE)
****************************************
A ProMED-mail post

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


Date: 7 Jan 2010
Source: Concord Monitor/AP [edited]



A woman who was in critical condition with an extremely rare form of
anthrax is improving and is no longer in intensive care, a state
health official said yesterday [6 Jan 2010].

The young woman from Strafford County became ill with
gastrointestinal anthrax in early December 2009 and is being treated
in a Boston hospital. Authorities still are investigating how she
became infected but believe the most likely scenario is that she
swallowed anthrax spores propelled into the air by drums at a
gathering in Durham last month [December 2009].

Two of the 64 animal skin drums used during the United Campus
Ministry center's 4 Dec 2009 drum circle have tested positive for
anthrax, as has an electrical outlet in the building. 52 other drums
tested negative, and the other 10 will be tested today [7 Jan 2010],
said Dr. Elizabeth Talbot, adviser to the state Department of Health
and Human Services.

Two recent U.S. anthrax cases also were traced to drums covered with
animal hides, but those involved spores that were either inhaled into
the lungs or entered through the skin of patients who were exposed
while making drums. The gastrointestinal form usually occurs after
eating raw or under cooked contaminated meat.

Testing by the Centers for Disease Control and Prevention confirmed
that the strain of anthrax found on the drums and outlet matched the
patient's strain. Talbot said the strain in question is a very common
one worldwide, and authorities can't pinpoint where it came from. She
said there is no obvious link between the 2 infected drums, which
aren't the same type or age. The origins of the animal hides aren't
clear, Talbot said.

Investigators with the state Department of Environmental Services and
federal Environmental Protection Agency planned to conduct more
testing today [7 Jan 2010] at the campus ministry center, which has
been closed during the investigation. Talbot said officials have
contacted 52 of the approximately 60 people who attended the drum
circle, and several have taken the state up on its offer of
antibiotics and vaccinations.

--
Communicated by:
ProMED-mail

[It is good to read that this young woman is out of intensive care.
It has been a worrying time.

This woman was apparently exposed on 4 Dec 2009 at a drumming
session. Considering the inherent dangers in oral antibiotics and the
moderate persisting risk, the attendees would be wiser to go for
vaccination. This would have the additional advantage of protecting
them during drumming meetings over the next 12-18 months, something
that antibiotics would certainly not do.

Clarification is being sought on the genomic nature of the isolates
and the problems of locating them. - Mod.MHJ]

[see also:
2009
----
Anthrax, human - USA (03): (NH) 20091230.4390
Anthrax, human - USA (02): (NH) 20091229.4374
Anthrax, human - USA: (NH) 20091227.4360]
..............................................mhj/msp/dk

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ProMED-mail makes every effort to verify the reports that
are posted, but the accuracy and completeness of the
information, and of any statements or opinions based
thereon, are not guaranteed. The reader assumes all risks in
using information posted or archived by ProMED-mail. ISID
and its associated service providers shall not be held
responsible for errors or omissions or held liable for any
damages incurred as a result of use or reliance upon posted
or archived material.
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PRION DISEASE UPDATE 2010

PRION DISEASE UPDATE 2010
**************************
A ProMED-mail post

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


[With the continuing decline in the number of cases in the human
population of variant Creutzfeldt-Jakob disease -- abbreviated
previously as vCJD or CJD (new var.) in ProMED-mail -- it has been
decided to broaden the scope of the occasional ProMED-mail updates to
include some other prion-related diseases. In addition to vCJD, data
on other forms of CJD: sporadic, iatrogenic, familial, and GSS
(Gerstmann-Straussler-Scheinker disease), are included also since
they may have some relevance to the incidence and etiology of vCJD. - Mod.CP]

In this update:
[1] UK: National CJD Surveillance Unit - monthly statistics as of 5 Jan 2010
[2] France: Institut de Veille Sanitaire - monthly statistics as of 4 Jan 2010
[3] US National Prion Disease Center - not updated since 7 Nov 2009
[4] Portuguese vCJD case - pathology
[5] vCJD codon 129 heterozygote
[6] vCJD codon 129 heterozygote - Lancet paper
[7] Prion evolution & a new reagent

******
[1] UK: National CJD Surveillance Unit - monthly statistics as of 5 Jan 2010
Date: Tue 5 Jan 2010
Source: UK National CJD Surveillance Unit, monthly statistics [edited]



The number of deaths due to definite or probable vCJD cases remains
166. A total of 4 definite/probable patients are still alive, so that
the total number of definite or probable vCJD cases remains 170 for
the year 2009.

Although 2 new cases vCJE were recorded in 2009, the overall picture
is still consistent with the view that the vCJD outbreak in the UK is
in decline, albeit now with a pronounced tail. The 1st cases were
observed in 1995, and the peak number of deaths was 28 in the year
2000, followed by 20 in 2001, 17 in 2002, 18 in 2003, 9 in 2004, 5 in
2005, 5 in 2006, 5 in 2007, one in 2008, and 2 in 2009.

Totals for all types of CJD cases in the UK in the year 2009
--------------------------------------------
During the 12 months of 2009, there have been 143 referrals, 59 cases
of sporadic CJD, one case of familial CJD, one case of iatrogenic
CJD, 3 cases of GSS, and 2 cases of vCJD.

--
Communicated by:
ProMED-mail

******
[2] France: Institut de Veille Sanitaire - monthly statistics as of 4 Jan 2010
Date: Mon 4 Jan 2010
Source: IVS - Maladie de Creutzfeldt-Jakob et maladies apparentees
[in French, trans. & summ. Mod.CP]



During the 12 months of 2009, there were 1486 referrals, 85 cases of
sporadic CJD, 10 cases of familial CJD, 3 cases of iatrogenic CJD,
and 2 confirmed cases of vCJD.

A total of 25 cases of confirmed or probable vCJD has now been
recorded in France since 1997. The 25 confirmed cases comprise 13
females and 12 males. All 25 are now deceased. Their median age is 37
(between 19 and 58). Seven were resident in the Ile-de-France and 18
in the provinces. All the identified cases have been Met-Met
homozygotes. No risk factor has been identified. One of the 25 had
made frequent visits to the United Kingdom.

--
Communicated by:
ProMED-mail

******
[3] US National Prion Disease Center - not updated since 7 Nov 2009
Date: Sat 7 Nov 2009
Source: US National Prion Disease Pathology Surveillance Center [edited]



(Report not updated since 7 Dec 2009): During the period 1 Jan 2009
to 7 Nov 2009, there were 341 referrals, of which 198 were classified
as Prion disease, comprising 133 cases of sporadic CJD, 33 of
familial CJD, and no cases of iatrogenic CJD or vCJD.

--
Communicated by:
ProMED-mail

******
[4] Portuguese vCJD case - pathology
Date: Fri 1 Jan 2010
Source: J Neurol Neurosurg Psychiatry 2010 Jan;81(1):112-4. [edited]



Title: Variant Creutzfeldt-Jakob disease: the first confirmed case
from Portugal shows early onset, long duration and unusual pathology.

Authors: Barbot C, Castro L, Oliveira C, Carpenter S.
At: Department of Neuropaediatrics, Hospital Maria Pia, Porto, Portugal.

Summary:
We present clinical and autopsy findings in the 1st case of variant
Creutzfeldt-Jakob disease diagnosed and confirmed in Portugal. Onset
was at 11 years, the earliest onset reported, and the course (32
months) relatively long. Western blot showed protease resistant prion
protein, mainly of type 4 (2B) isoform. The cerebral cortex revealed
severe spongiform change with numerous amyloid plaques, which did not
fit the definition of florid plaques. In the striatum, spongiform
change was limited, but the extracellular space was dilated. Other
reports have found marked spongiform change in the striatum and
little in the cortex. Massive neuronal loss, in excess of what has
been described, was found in the thalamus and pontine grey. The
cerebellum showed, as expected, severe loss of granule cells,
moderate loss of Purkinje cells and marked immunopositivity for the
prion protein. Differences between our findings and previous ones
probably result from the patient's long survival.

--
Communicated by:
Terry S. Singeltary Sr.

******
[5] vCJD codon 129 heterozygote
Date: Fri 19 Dec 2009
Source: BBC News, Health [edited]



A 30-year-old man thought to have died in January [2009] from vCJD
belonged to a genetic group that had not shown any signs of the
disease, scientists say. In the UK, 166 people have died of vCJD,
linked to eating BSE [bovine spongiform encephalopathy] infected
beef, and all were thought to have shared a certain gene.

Writing in the Lancet, scientists say that the victim, a resident of,
Lanarkshire [Scotland], had a different version of the gene. They
estimate that up to 350 people in this group could get vCJD.
Scientists have always thought that a 2nd wave of vCJD cases would
emerge some time after the 1st. This is the 1st indication that this
theory is being born out, with the identification of the 1st probable
vCJD patient outside of the initial genetic group, BBC science
correspondent Pallab Ghosh reports.

The father believes his son was incubating the disease for much of
his life. It is probable because the diagnosis is based on
observations of the progression of the disease rather than
post-mortem tests which would have provided absolute confirmation of
the disease, he adds.

The case report written by Professor John Collinge of the National
Prion Clinic and colleagues is a reminder that the disease has not
gone away. Many thousands of people may be carrying the infection,
and although they will never show any symptoms, they have the
potential to infect others.

vCJD is caused by infectious agents called prions. Prion diseases
affect the structure of the brain or other neural tissue and are
currently untreatable. Disease-causing prions are thought to consist
of abnormally folded proteins, which spread by encouraging the normal
healthy prion protein found on the surface of most cells in the body
to change shape. Tests showed that the patient had a heterozygous
version of the gene which codes for the human prion amino acids
valine (V) or methionine (M). People can be V V (homozygous), M M
(homozygous) or M V (heterozygous). Since 1994, around 200 cases of
vCJD have been identified worldwide, and all those tested have been M
M homozygous. [However, genetic analysis of 2 out of 3 prion-positive
appendix samples in the tissue-based prevalence study in 2001-2004
showed that both were valine homozygous (VV) at codon 129 in the
prion protein gene (Ironside et al, Brit Med J 2006). - Mod.CP].
However, this most recent victim was M/V heterozygous. It is thought
that 47 percent of the population have this version of the gene.
Professor Collinge said: "The majority of the UK population have
potentially been exposed to BSE prions, but the extent of clinically
silent infection remains unclear. About 1/3rd of the UK population
are M/M homozygous. If individuals with other genotypes [M/V and V/V]
are similarly susceptible to developing prion disease after BSE prion
exposure, but with longer incubation periods, further cases would be expected."

The scientists have previously looked at another prion disease in New
Guinea called "kuru" [which was induced by eating infected human
brain tissue. - Mod.CP]. The original cases were all M/M, but more
recently, M/V cases have appeared. They say this indicates that M/V
people can get prion diseases like kuru but have a much longer
incubation period.

--
Communicated by:
ProMED-mail

[The abstract of the Lancet paper upon which the above report is
based is reproduced below. - Mod.CP]

******
[6] vCJD codon 129 heterozygote - Lancet paper
Date: Thu 18 Dec 2009
Source: Lancet 2009; 374: 2128 [edited]



[A Case Report published in the 18 Dec 2009 issue of the Lancet by
Professor John Collinge, MRC Prion Unit and National Prion Clinic,
UCL Institute of Neurology and National Hospital for Neurology and
Neurosurgery, London]

A 30-year-old man was admitted to hospital in June 2008 with a
13-month history of personality change, progressive unsteadiness, and
intellectual decline. He complained of severe leg pain and poor
memory. Two months later, he developed visual hallucinations and
falsely believed he had an abdominal tumour. Symptoms worsened over
the next 3 months. In October 2008, his score on the mini mental
state examination was 26/30. Pursuit eye movements were saccadic [a
rapid movement of the eye between fixation points]. He had a pout
reflex. There was mild ataxia in the arms. His legs were severely
ataxic with brisk tendon reflexes and a left extensor plantar
response. He needed 2 crutches to walk. Medical history included
tonsillectomy and removal of a cervical lymph node 15 years
previously, but he had never had a blood transfusion or received
implantation of other human tissues.

EEG showed slow wave activity. CSF protein, glucose, and cell count
were normal, but the 14-3-3 protein was positive. MRI [magnetic
resonance imaging] of the brain was consistent with the pulvinar sign
(illustrated in the original text). Although not all
neuroradiologists consulted considered the pulvinar sign positive,
quantitative assessment showed symmetrical higher signal in the
pulvinar nuclei than the caudate nuclei (illustrated in the original
text). Extensive screens for genetic, metabolic, and autoimmune
diseases, including those induced by neoplasia, were negative. PRNP
analysis did not show any known disease-associated mutations; codon
129 was heterozygous. A clinical diagnosis of variant
Creutzfeldt-Jakob disease (vCJD) was made on the basis of a
characteristic clinical onset and progression, exclusion of other
diagnoses, and MRI findings. Sporadic CJD was judged unlikely given
the combination of young age, clinical features, MRI findings, and
absence of pseudoperiodic complexes on EEG. His care givers did not
want further investigation. His condition deteriorated, and he died
in January 2009. Autopsy was not done.

Human prion diseases have acquired, sporadic, and inherited
aetiologies, show wide phenotypic heterogeneity, and are associated
with propagation of infectious prions of many distinct strain types
(1). Since 1994, about 200 cases of vCJD, causally related to
exposure to bovine spongiform encephalopathy (BSE) prions, have been
identified world-wide. vCJD is generally seen in young adults, has
characteristic neuropathological features and tissue distribution of
infectivity, and a distinctive type 4 (London classification)
molecular strain type (1). A polymorphism at codon 129 (encoding
methionine or valine) of the human prion protein gene (PRNP)
constitutes a powerful susceptibility factor in all types of prion
disease. In vCJD, every case genotyped to date has been methionine
homozygous. In the other acquired prion diseases, cases have occurred
in all genotypes but with different mean incubation periods (1),
which can span decades (2); PRNP codon 129 heterozygotes generally have!
the longest incubation periods. There is a report of a recipient of
a blood transfusion from a donor incubating vCJD who died of
unrelated causes but showed signs of prion infection at autopsy and
was PRNP codon 129 heterozygous (3). Animal studies have suggested
that different clinicopathological phenotypes could occur in people
with various PRNP codon 129 genotypes (4,5). The majority of the UK
population have potentially been exposed to BSE prions but the extent
of clinically silent infection remains unclear. About 1/3rd of the UK
population are PRNP codon 129 methionine homozygous. If individuals
with other genotypes [V/V or V/M] are similarly susceptible to
developing prion disease after BSE prion exposure, but with longer
incubation periods, further cases, which may or may not meet
diagnostic criteria for vCJD, would be expected in these PRNP codon
129 genotypes. However, prion disease susceptibility and incubation
periods are also affected by other genetic loci, and the possibility
remains that cases of vCJD to date may have unusual combinations of
genotypes at these loci, yet to be fully characterised.

References:

(1) Collinge J. Prion diseases of humans and animals: their causes
and molecular basis. Annu Rev Neurosci 2001; 24: 519-50.

(2) Collinge J, Whitfield J, McKintosh E, et al. Kuru in the 21st
century - an acquired human prion disease with very long incubation
periods. Lancet 2006; 367: 2068-74.

(3) Peden AH, Head MW, Ritchie DL, Bell JE, Ironside JW. Preclinical
vCJD after blood transfusion in a PRNP codon 129 heterozygous
patient. Lancet 2004; 364: 527-29.

(4) Asante E, Linehan J, Gowland I, et al. Dissociation of
pathological and molecular phenotype of variant Creutzfeldt-Jakob
disease in transgenic human prion protein 129 heterozygous mice. Proc
Natl Acad Sci USA 2006; 103: 10759-64.

(5) Wadsworth JD, Asante E, Desbruslais M, et al. Human prion protein
with valine 129 prevents expression of variant CJD phenotype. Science
2004; 306: 1793-96.

[Acknowledgment: MRC Prion Unit and National Prion Clinic, UCL
Institute of Neurology and National Hospital for Neurology and
Neurosurgery, London, UK (D Kaski MRCP, S Mead PhD, H Hyare FRCR,
Prof J Collinge FRS, P Rudge FRCP); Institute of Neurological
Sciences, Glasgow University, Glasgow, UK (S Cooper MRCP, R Jampana
FRCR, J Overell FRCP); and National CJD Surveillance Unit, Western
General Hospital, Edinburgh, UK (Prof R Knight FRCP)]

--
Communicated by:
ProMED-mail

[To put this work in perspective, parts of a British Medical Journal
editorial by Maurizio Pocchiari are reproduced below. - Mod.CP.

Date: 21 May 2009
Source: BMJ 2009;338:b435 [edited]


"Prevalence of variant CJD in the UK
----------------------------
The number of cases of variant Creutzfeldt-Jakob disease (vCJD) in
the United Kingdom has decreased since 2000, but controversy remains
about how many people carry the infectious agent and will eventually
develop disease. Clewley and colleagues in a limited study add to the
debate by assessing 63 007 pairs of tonsils for the only available
marker of prion disease, the pathological, partially protease
resistant, prion protein. Although more than half of the samples came
from people born between 1961 and 1995, when the risk of exposure to
bovine spongiform encephalopathy (BSE) infection was high, no
convincingly positive tonsil specimens were detected. This study
estimated that the prevalence of vCJD in the British population is
zero, but with a large confidence interval of 0 to 113 per million.

This result agrees with one UK survey of 2000 tonsil specimens, but
it differs from another survey of 1427 tonsils and 11 247 appendices,
which found that more than 10 000 people might be incubating the
disease. However, despite the discrepancy, the 95 percent confidence
intervals of the 2 studies overlap, indicating that the results do
not differ significantly and that many people in the UK may be carriers.

The chance that no one in the UK is incubating the disease, as
suggested by the lower confidence limit of Clewley and colleagues'
study, is unlikely because backup calculations predict up to 100 new
cases of vCJD in the next 50 years. This prediction seems reasonable
unless most cases of vCJD were missed by surveillance in the past years.

Until December 2008, all 210 people reported to have vCJD (164 in the
UK, 46 in other countries) were homozygous for methionine at the
polymorphic codon 129 of the prion protein gene (PRNP), suggesting
that genetic factors strongly influence the development of disease.
Whether people who are heterozygous for methionine and valine or
homozygous for valine at this codon (about 60 percent of the
population) will develop vCJD in the future is still unknown.
However, data from gene targeted transgenic mice indicate that these
people are also susceptible to BSE and vCJD, although incubation
periods are longer than in those who are homozygous for methionine."

Interested readers should consult the original article for further
information and references. - Mod.CP]

******
[7] Prion evolution & a new reagent
Date: 1 Jan 2010
Source: BBC Health News [edited]



Abnormal prion proteins cause at least 20 fatal diseases. Scientists
have shown for the 1st time that "lifeless" prion proteins, devoid of
all genetic material, can evolve just like higher forms of life. The
Scripps Research Institute in the US says the prions can change to
suit their environment and go on to develop drug resistance.

Prions are associated with 20 different brain diseases in humans and
animals. The scientists say their work suggests new approaches might
be necessary to develop therapies for these diseases. In the study,
published in the journal Science [see below], the scientists
transferred prion populations from brain cells to other cells in
culture and observed the prions that adapted to the new cellular
environment out-competed their brain-adapted counterparts. When
returned to the brain cells, the brain-adapted prions again took over
the population.

Charles Weissmann, head of Scripps Florida's department of
infectology who led the study, said: "On the face of it, you have
exactly the same process of mutation and adaptive change in prions as
you see in viruses. This is a timely reminder that prion concerns are
not going away and that controls to stop abnormal prions being
transmitted to humans through the food system or through blood
transfusions must be vigorously maintained."

Professor John Collinge, Medical Research Council Prion Unit stated
that: "This means that this pattern of Darwinian evolution appears to
be universally active. In viruses, mutation is linked to changes in
nucleic acid sequence that leads to resistance. Now, this
adaptability has moved one level down -- to prions and protein
folding -- and it's clear that you do not need nucleic acid (DNA or
RNA) for the process of evolution."

Mammalian cells normally produce cellular prion protein or PrPC.
During infections, such as the human form of mad cow disease, known
as vCJD, abnormal or mis-folded proteins convert the normal host
prion protein into its toxic form by changing its conformation or
shape. "It was generally thought that once cellular prion protein was
converted into the abnormal form, there was no further change," Prof.
Weissmann said. "But there have been hints that something was
happening. When you transmit prions from sheep to mice, they become
more virulent over time. Now we know that the abnormal prions
replicate and create variants, perhaps at a low level initially. But
once they are transferred to a new host, natural selection will
eventually choose the more virulent and aggressive variants."

Professor John Collinge, of the Medical Research Council's (MRC)
Prion Unit, described the research as exciting confirmation of a
hypothesis that he had proposed 2 years ago, that there could be a
"cloud" or whole array of prion proteins in the body. He called it
the cloud hypothesis: "The prion protein is not a clone, it is a
quasi-species that can create different protein strains even in the
same animal. The abnormal prion proteins multiply by converting
normal prion proteins. The implication of Charles Weissmann's work is
that it would be better to cut off that supply of normal prion
proteins rather than risk the abnormal prion adapting to a drug and
evolving into a new more virulent form. You would do this by trying
to block the sites on the normal prion protein that the abnormal form
locks on to to do its conversion. We know there is an antibody that
can do this in mice, and the Medical Research Council's Prion Unit
have managed to engineer a human antibody to do this. It is currently
undergoing safety tests, and we hope to move to clinical trials by
the end of 2011."

Professor Collinge said the MRC was also trying to find more
conventional chemical compounds to do this and has been collaborating
with the chemical company GlaxoSmithKline (GSK). He said: "They have
given us access to their chemical libraries, which contain millions
of compounds, and we have already identified some that may work well.
This is a timely reminder that prion concerns are not going away and
that controls to stop abnormal prions being transmitted to humans
through the food system or through blood transfusions must be
vigorously maintained."

--
Communicated by:
ProMED-mail

[The abstract and the reference for the Science paper descried above
are the following: Science DOI: 10.1126/science.1183218, Published
Online 31 Dec 2009.
.
Darwinian Evolution of Prions in Cell Culture. By Jiali Li, Shawn
Browning, Sukhvir P. Mahal, Anja M. Oelschlegel, Charles Weissmann
At: Department of Infectology, Scripps Florida, 130 Scripps Way,
Jupiter, FL 33458, USA.

Abstract: "Prions are infectious proteins consisting mainly of PrPSc,
a sheet-rich conformer of the normal host protein PrPC, and occur in
different strains. Strain identity is thought to be encoded by PrPSc
conformation. We found that biologically cloned prion populations
gradually became heterogeneous by accumulating "mutants," and
selective pressures resulted in the emergence of different mutants as
major constituents of the evolving population. Thus, when transferred
from brain to cultured cells, "cell-adapted" prions out competed
their "brain-adapted" counterparts, and the opposite occurred when
prions were returned from cells to brain. Similarly, the inhibitor
swainsonine selected for a resistant substrain, whereas in its
absence, the susceptible substrain outgrew its resistant counterpart.
Prions, albeit devoid of a nucleic acid genome, are thus subject to
mutation and selective amplification."

From a theoretical standpoint, this work has great significance.
Nonetheless, the immediate interest of the BBC News report is the
information that Professor John Collinge's MRC group has succeeded in
engineering a humanised monoclonal antibody that interacts with the
sites on the normal prion protein that the abnormal form locks onto
to achieve its conversion and that it is hoped eventually to move to
clinical trials of this reagent. - Mod.CP]

[see also:
2009
----
Prion disease update 2009 (10) 20091103.3784
vCJD - Italy: susp. 20091024.3671
Prion disease update 2009 (09) 20091005.3461
Prion disease update 2009 (08) 20090908.3170
Prion disease update 2009 (07) 20090806.2783
Prion disease update 2009 (06) 20090706.2433
Prion disease update 2009 (05) 20090602.2054
Prion disease update 2009 (04) 20090406.1337
vCJD, 5th death - Spain (Cantabria) 20090307.0953
Prion disease update 2009 (03) 20090305.0918
Prion disease update 2009 (02) 20090202.0463
Prion disease update 2009 (01) 20090108.0076
2008
----
Prion disease update 2008 (14): new vCJD wave imminent? 20081218.3980
Prion disease update 2008 (13) 20081201.3780
Prion disease update 2008 (12) 20081103.345
Prion disease update 2008 (11) 20081006.3159
vCJD, mother & son - Spain: (Leon) 20080926.3051
Prion disease update 2008 (10) 20080902.2742
vCJD - Spain: susp. 20080410.1311
Prion disease update 2008 (05) 20080408.1285
Prion disease update 2008 (01): correction 20080104.0046
Prion disease update 2008 (01) 20080102.0014
2007
----
Prion disease update 2007 (08) 20071205.3923
Prion disease update 2007 (07) 20071105.3602
Prion disease update 2007 (06) 20071003.3269
Prion disease update 2007 (05) 20070901.2879
Prion disease update 2007 (04) 20070806.2560
Prion disease update 2007 (03) 20070702.2112
Prion disease update 2007 (02) 20070604.1812
Prion disease update 2007 20070514.1542
CJD (new var.) update 2007 (05) 20070403.1130
CJD (new var.) update 2007 (04) 20070305.0780
CJD (new var.) update 2007 (03) 20070205.0455
CJD (new var.) update 2007 (02): South Korea, susp 20070115.0199
2006
----
CJD (new var.), blood transfusion risk 20061208.3468
CJD, transmission risk - Canada (ON) 20061207.3457
CJD (new var.) update 2006 (12) 20061205.3431
CJD (new var.) update 2006 (11) 20061106.3190
CJD (new var.) update 2006 (10) 20061002.2820
CJD (new var.) - Netherlands: 2nd case 20060623.1741
CJD (new var.) - UK: 3rd transfusion-related case 20060209.0432
CJD (new var.) update 2006 (02) 20060206.0386
CJD (new var.) update 2006 20060111.0101
2005
----
CJD (new var.) update 2005 (12) 20051209.3547
CJD (new var.) update 2005 (11) 20051108.3270
CJD (new var.) update 2005 (10) 20051006.2916
CJD (new var.) update 2005 (02) 20050211.0467
CJD (new var.) - UK: update 2005 (01) 20050111.0095
2004
----
CJD, genetic susceptibility 20041112.3064
CJD (new var.) - UK: update 2004 (14) 20041206.3242
CJD (new var.) - UK: update 2004 (10) 20040909.2518
CJD (new var.) - UK: update 2004 (02) 20040202.0400
CJD (new var.) - UK: update 2004 (01) 20040106.0064
CJD (new var.) - France: 8th case 20041022.2864
CJD (new var.) - France: 9th case 20041123.3138
CJD (new var.), blood supply - UK 20040318.0758
CJD (new var.), carrier frequency study - UK 20040521.1365
2003
----
CJD (new var.) - UK: update 2003 (13) 20031216.3072
CJD (new var.) - UK: update 2003 (01) 20030108.0057
2002
----
CJD (new var.) - UK: update Dec 2002 20021207.5997
CJD (new var.) - UK: update Jan 2002 20020111.3223
2001
----
CJD (new var.), incidence & trends - UK (02) 20011124.2875
CJD (new var.), incidence & trends - UK 20011115.2816
CJD (new var.) - UK: reassessment 20011029.2671
CJD (new var.) - UK: update Oct 2001 20011005.2419
CJD (new var.) - UK: regional variation (02) 20010907.2145
CJD (new var.) - UK: update Sep 2001 20010906.2134
CJD (new var.) - UK: update Aug 2001 20010808.1872
CJD (new var.) - UK: 9th Annual Report 20010628.1231
CJD (new var.) - UK: update June 2001 20010622.1188
CJD (new var.) - UK: update 3 Jan 2001 20010104.0025]
....................................................cp/msp/dk

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