Daily Freeman Journal, 6/30/09 (Iowa)

Summer in a jar.

Iowa State University Extension Nutrition and Health Specialist Paulelda Gilbert started hearing the speculation early this year that a tighter economy would see many Iowans returning to the ways of their grandmothers to cut costs and savor the taste of summer through home-canning of fresh fruits and vegetables.

But Gilbert waited to see if the proof would be in the pudding - or, in this case, in the pickling department.

Gilbert was in Webster City Tuesday afternoon to promote a new DVD filled with canning basics that is available for loan from the Hamilton County Extension office. And, of course, to offer free testing of home canner pressure gauges.

“Now that I have started to do the canner testing, the average number for the five counties that I’ve done is higher. I’ve had a couple of counties that were very low, but I’ve had a couple of counties that have almost doubled,” in the number of folks testing to make their sure their canning equipment is working properly, she said.

“That makes me wonder a little bit if people are thinking that, if their garden does well, they’ll be ready,” Gilbert added.

The Extension Service has offered annual canner testing for decades, in the interest of promoting food safety. Now, with folks dusting off old canners from a grandmother’s basement, or picking up a bargain at an auction, it’s more important than ever to make sure the canner works correctly, according to Gilbert.

It’s quite unusual, she said, to see anyone purchasing a new canner. For one thing, with many small towns no longer having a hardware store, the canners can be more difficult to find. Although some farm supply or discount stores may carry home canning equipment.

However, Gilbert cautioned that a new canner can run from $100 to $125, which could quickly defeat any cost-saving efforts of home-canning.

“That’s a pretty big investment, You’re going to have to do a lot of canning to make that pay off,” she said.

Older canners will often do just fine, as long as the proper equipment checks are made.

“It’s very reasonable to use the older canners, as far as I’m concerned. They’re well made. If they have been taken care of at all, they’re going to be fine to use,” Gilbert said.

The most important thing is to have the canner gauge tested, which assures the gauge is reading correctly and the proper pressure has been achieved when canning.

Gilbert said it’s also a good idea to have a practice run before attempting to can any produce.

“I recommend people put a couple inches of water in the bottom, and tighten down the lid. Go through all the steps, without actually having jars in there. And just make sure that the lid holds the seal,” she said.

This test will help determine if a new gasket is needed and if all the parts are working correctly.

When looking to buy an old canner at an auction or garage sale, Gilbert said the buyer should make sure that all the equipment is included and make sure the lid fits securely.

However, even if some parts are missing, replacement parts can usually be ordered. The Extension office has a list of 800 numbers in order to help locate missing parts for old models, she added.

Why safety?

But why is it so important that the gauge be accurate and the lid fit just so? Being off just a little bit can’t hurt, can it?

“Our concern is botulism is the main food bacteria that will be in home-canned foods,” Gilbert said.

Botulism can thrive where other food-borne pathogens are easily destroyed. High acidic fruits are perfectly safe for the less-cumbersome hot water bath, boiling water, method of home canning. But meat, vegetables, and even tomatoes, lack the acidity that kills bacteria.

What’s more, the person who opens the jar will not be able to tell the difference between a safe batch of home-canning and one contaminated with botulism.

That’s because botulism is odorless and tasteless, and it does not change the appearance of the food.

In addition, because botulism spores survive in a vacuum, the seal on the jar will still be in place.

The solution is to follow approved canning methods and, Gilbert emphasized, tested recipes. This is not the time, she said, to add a personal twist to, for example, a salsa recipe.

The purpose of testing recipes is to verify the acid content, which in turn ensures that the acid level is high enough to protect the produce. Even minor changes in ingredients can alter the acid level, and risk making the food unsafe for consumption.

If a person wants to test recipes of their own, Gilbert recommended freezing those items, rather than canning.

Tomatoes, she said, are often a misleading fruit, even for experienced canners.

“We think of them as an acidic fruit, but they aren’t as acidic as they used to be. Hybrids have changed that,” she said.

And, without accurate testing of “heirloom” varieties, Gilbert said it’s safer to go with tested recipes.

For the past several years, the recommendation has been to add 1 tablespoon of 100 percent bottled lemon juice for each pint of low-acid canned products. The lemon juice, she said, will not change the flavor, but will increase the acid level sufficiently to protect the food.

Vinegar, of course, is a common ingredient in many recipes and also serves to raise the acid level. Again, Gilbert said it’s important to use only a tested recipe to make sure enough vinegar is used.

Reliable sources

So, where can you find these “tested recipes?”

The Ball Blue Book is a good source, according to Gilbert. But make sure it’s a current copy. Grandma was canning an entirely different variety of fruits and vegetables and the recipes of yesteryear may not work for today’s produce.

The USDA also offers tested recipes.

Why bother?

Now, with all these concerns, is it really worth the trouble?

Gilbert said a real positive of canning your own food is that you know what goes into it - and what doesn’t.

“Knowing where your food comes from is important to a lot of people,” she added.

Picture a cold winter day, with the snow blowing outside and a pot of chili on the stove. Now try smelling that pot of chili knowing that the tomatoes, onions, and peppers all came fresh from the garden, via a root cellar filled with jars of canned tomatoes, peppers and bin of onions.

And, Gilbert agreed, the pride of knowing you did it all yourself.

Summer in a jar - all year long.

For more information, contact Gilbert at the Webster County Extension Office, 515-576-2119, or E-mail pgilbert@iastate.edu,

Contact Lori Berglund at editor@freemanjournal.net



Link:  http://www.theglobeandmail.com/news/national/how-a-european-cargo-ship-kills-a-great-lakes-loon/article1199297/

Erin Anderssen

From Saturday’s Globe and Mail

“Two years ago, a tiny shrimp-like creature with a creepy name – the bloody red mysid – was discovered in Lake Ontario, the latest in a long line of foreign invaders believed to have arrived by cargo ship through the St. Lawrence Seaway.

1 ZEBRA MUSSELS

Ravenous, it travels in packs and upsets the food chain wherever it takes up residence. It’s still too early to predict how much damage the bloody red mysid will do to its new home, but scientists aren’t about to rule out the worst.

They know this from experience. Here is how researchers believe that one early interloper, travelling in the belly of a boat from another continent, has led to thousands of loons washing up dead on the shores of the Great Lakes.

1. A freighter leaves a European port, bound for ports such as Duluth, Minn., on the southwest shore of Lake Superior, or Thunder Bay, to the north. Sloshing around in the bowel of the ship is a muddy mix of sand and water – the ballast used to maintain the vessel’s stability as it traverses the oceans. The amount of ballast depends on how much cargo the ship is carrying, but even fully loaded ships that technically need “no ballast on board” – called NoBObs – still have some leftover slop in their holds. Foreign freshwater species from ports near rivers are pumped in with the water, and because of faster travel times, they survive the ocean crossing. On one occasion at least – but probably many more times – the stowaway is a striped, freshwater mollusk, the quagga mussel, or its cousin, the zebra mussel.

2. The freighter makes it way up the St. Lawrence, through the locks and canals, usually offloading its cargo at ports such as Hamilton as it moves west through the system into Lake Superior, dumping its ballast as needed. Sometimes the foreign marine life dies: The season is off, or its numbers are too small, or the location proves inhospitable. “An invasion is a roulette wheel spin,” says Anthony Ricciardi, a biologist at McGill University in Montreal. “You may not get in on the first try, but keep trying and you get in.”

This time, the species gets in, and flourishes. Soon, zebra mussels, first discovered in Lake St. Clair, have hopped into the other lakes, carried by other ballast loads or hitching a ride on the hulls of various boats.

3. Zebra mussels spread like a contagion across the lake bottom, sucking life out of the water, filtering everything around them. They probably breed undiscovered for a decade or more. To boaters above, the lakes seem clearer, when, in fact, a deathly brew is stewing. With more light and the waters warming, weedy algae called Cladophora begin to grow. (The algae do their own damage: In 2007, weeds clogged intake pipes and forced a nuclear-power plant in New York State to close three times.)

4. When the algae die and decompose, they suck oxygen out of the water, and in that environment, the botulism bacteria thrives. It, in turn, is sucked up by the voracious quagga and zebra mussels.

5. The only fish that eats the mussels is itself a non-native – the round goby, an aggressive bottom-dweller that scientists believe also was probably introduced by transoceanic ships in the early 1990s.

6. The goby eats the botulism-carrying mussels and then along comes the loon, fishing for its dinner. The goby, especially if it is sick and slowed by the bacteria in its system, makes for an easy catch. The botulism spreads to the loon.

7. The loon dies , to be found belly-up on shore.

Scientists call this “invasional meltdown.” Since the St. Lawrence Seaway opened, 57 non-native species are believed to have invaded the Great Lakes through the ballast of ocean-crossing ships. New regulations require all ships to flush out their tanks before entering, but biologists point out that, unlike chemical spills, it takes only one ballast dump to introduce an environmentally disastrous life form.

Scientists such as Dr. Ricciardi are now watching for the arrival of another species dubbed the “killer shrimp” – which is tiny and insatiable, and snacks on much larger creatures. “It’s an amazing little beast,” he says. “That one might cause trouble if it gets over here.”

How much trouble, scientists can’t be certain. After all, when zebra mussels were discovered in 1988, no one was thinking of loons belly-up in 2007.

“Who could have predicted that?” Dr. Ricciardi asks. “We can figure it out now, we think. But risks assessment of the zebra mussel would never have considered that. You put some invaders together, you change some conditions around, you mix it all together and you get this witches’ brew that leads to ecological surprises like this.”



Link:  http://www.570news.com/news/local/more.jsp?content=20090627_062102_4472

TheHorse.com, 6/25/09  

Botulism in Horses: A Deadly Disease

Botulism is a deadly disease caused by the toxins produced by the bacterium Clostridium botulinum. The botulinum toxin is a potent neurotoxin that impairs nerve function, including those of the diaphragm, leading to paralysis. When the nerves to the diaphragm are paralyzed, the affected animal stops breathing and will die as a result.

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C. botulinum is an anaerobic (lives without oxygen), gram-positive, sporeforming bacterium. The toxin produced by C. botulinum is one of the most potent toxins known to science. The Clostridium family is known for causing rapid, severe, and deadly diseases, including botulism, tetanus, blackleg, malignant edema, etc. Sometimes the onset of clostridial disease is so rapid that no clinical signs are noted, and the owner simply finds the animal dead.

The botulism toxin blocks the release of acetylcholine in the neuromuscular junction. Acetylcholine is a neurotransmitter, which transmits information from the nerve cell to the muscle cell. It is released in the neuromuscular junctions (the space where nerves communicate and stimulate muscles), and it enables muscle contraction; therefore, without acetylcholine, the muscles will not contract. A very important muscle in any mammal’s survival is the diaphragm, which, when contracted, enables breathing. Ultimately, without acetylcholine, a horse infected with botulism will die of respiratory failure and asphyxia, due to the paralysis of the diaphragm.

There are seven types of botulism recognized (A, B, Ca, Cb, D, E, F, and G), based on the antigenic specificity of the toxin produced by each strain. Types A, B, E, and F cause human botulism. Types A, B, C, and D cause most cases of botulism in animals. In horses, type B botulism is responsible for more than 80% of the cases.

The bacterium and its spores are widely distributed in nature. They are found in soil, sediments of streams and lakes, and in the intestinal tracts of fish and mammals. The bacteria will produce toxins under conditions of decaying plants and animals.

A horse can get botulism in three ways:

  • By consuming forage or feed containing the bacteria, which will then produce the toxins in the intestinal tract (more commonly found in foals, known as shaker foal syndrome, or toxicoinfectious botulism).
  • By consuming feed or forage containing the pre-formed toxins of C. botulinum (known as forage poisoning). 
  • Through wounds contaminated with the bacteria, generally puncture wounds. Wound borders will close, providing an anaerobic environment, which is a favorable condition for the bacteria to produce the toxins.

Although the incidence of the disease is low, it is of considerable concern because of its high mortality rate if not addressed and treated immediately and properly. The mid-Atlantic region of the eastern United States and especially Kentucky is where botulism is most commonly found, although the disease is reported worldwide. The spores of C. botulinum Type B can be found in the soil of most regions of the United States, although they are more frequently found in the northeastern and Appalachian regions. The western region is more abundant with C. botulinum type A, and type C occurs mainly in Florida. The frequency of occurrence of foodborne botulism in humans and in horses correlates with the distribution of the types of spores in the soil.

The Different Faces of Botulism
Forage poisoning can occur when  horses eat spoiled forage or any type of feed contaminated by a decaying animal. Spoilage is common in hay that was baled with a high moisture content. In cases associated with hay, horses eating roundbaled hay are at higher risk of developing the disease. Also, horses consuming hay that is spilled on the ground and then allowed to be mixed with soil and feces are at increased risk for botulism. Moreover, botulism can occur when dead animals accidentally get baled in hay during harvest. The decomposing carcass is an excellent anaerobic incubator for botulism spores present in the intestinal tract of the dead animal or bird. Once toxin is formed in the carcass, it leaches out and contaminates the hay or other feed material. Improperly ensiled silage and haylage with a high moisture content and alkaline pH (pH >4.5) provide optimal conditions for the production of botulinum toxin. Improperly fermented silage (pH >4.5) should not be fed to horses because it predictably causes botulism. In contrast, cattle are more resistant to botulism and may not develop the disease as readily as horses when fed spoiled silage, although there have been several reports of cases of botulism in cattle.

Botulism in foals, also known as shaker foal syndrome, happens when the foal starts to nibble at hay and grass, between 2 and 12 weeks of age, and ingests the bacteria directly from the soil. The bacteria will form spores in the intestinal tract of the foal and produce toxins. One interesting fact is that the normal flora of adult horses inhibit the intraintestinal growth of botulinum spores, limiting the occurrence of toxicoinfectious botulism to neonates. The toxins are absorbed into the bloodstream and cause the blockage in the neuromuscular junction, which keeps the muscles from contracting. The foal will start to show signs of difficulty in standing, shaking (thus, the name of the syndrome), and then falling down over and over again. The foal will not be able to suckle and will, if not diagnosed and treated in time, eventually die of respiratory failure.

Wound botulism occurs when C. botulinum contaminates a wound, such as a deep puncture wound, where the wound borders close, creating an anaerobic environment. The bacteria then produce the deadly toxins anaerobically. It has been seen after castration and been associated with injection abscesses, puncture wounds, trauma, and surgery in adult horses and in foals with umbilical hernias treated with clamps. This mechanism is similar to tetanus infection.

Regardless of the port of entry, the sequence of events that follow is the same for every horse. Once the toxin enters the body, it reaches the bloodstream and is distributed to nerves throughout the body. The toxin then prevents the transmission of impulses from the nerve to the muscle, impeding muscle contraction and leading to paralysis. The course of the disease is very rapid, taking only one to two days to cause death, depending on the dose of toxin or bacteria ingested.

Clinical Signs and Diagnosis
Clinical signs of botulism in horses are weakness; decreased muscle tone of the tail, eyelid, and tongue; trembling; dilated pupils; lying down; difficulty in swallowing; drooling; and green or milky nasal discharge. Foals will nurse for about one minute, start to shake, and collapse on the floor. They will not be able to swallow the milk, and the owner will notice the milk all around the muzzle of the foal or the foal drooling the milk. In the same way, adult horses may drop the grain, push the grain around the feed bucket, cover it in saliva, and not be able to actually eat it. Eventually, the horse will be lying down more often, be unable to stand, or stand with an “elephant-on-a-ball” posture, with all four feet placed close together under the body. As the horse gets weaker and cannot stand anymore, it may collapse instead of deliberately folding its legs under itself as a normal horse would do. Finally, as the chest muscles and diaphragm get involved, respiratory failure occurs, and the horse dies of asphyxia.

The disease can hit suddenly and result in the death of horses that were perfectly healthy the day before. Botulism causes a flaccid paralysis, unlike tetanus that causes a rigid paralysis.

One of the worst aspects of botulism is that only the motor nerves are affected, the ones that are responsible for muscle movement. As such, the sensory function is left unimpaired. This means that victims of botulism will continue to experience hunger, thirst, fear, distended bladder, pain, and all other sensations, but they simply cannot move in response. 

Clinical signs, history, and environmental observation are used to make a tentative diagnosis. If one horse in a group shows signs of botulism, others may quickly follow, if they have been fed from the same source of contaminated hay or feed.

Botulism is clinically diagnosed and more challenging to diagnose with laboratory tests. It is difficult to detect botulinum toxin in animals or to isolate the toxin from feedstuffs and feces of an affected horse. Routine blood tests are found normal (suspect botulism if the blood work is normal, yet the horse is showing signs of weakness!). Therefore, there may be more actual cases of botulism than the ones that are diagnosed. If clinical signs are compatible with botulism and the hay being fed is spoiled and contains areas of moist, decomposing material or a dead animal, or if a foal is involved, one should suspect botulism.

Treatment
Treating a horse with botulism can be very costly, difficult, and often too late. It is better to prevent the disease than to treat it. Recommended treatment for botulism includes early administration of hyperimmune plasma containing antitoxin. The antitoxin binds to the toxin molecules that are free floating in the bloodstream and neutralizes them before they bind to nerve cells, but they cannot reverse the effects of bound toxin. The bond that forms between the toxin and the nerve cell is irreversible.

The horse’s body can make new neuromuscular junctions to replace the ones that are affected by the toxins; however, this process requires 7 to 10 days. It is a challenge to keep a horse alive that is recumbent and cannot eat or drink. In adult horses, being recumbent for a few days poses a problem in itself. They can develop pressure sores, colic, muscle damage, etc. Moreover, the horse will need to be mechanically ventilated and administered supportive therapy. However, it is very difficult to keep an adult horse on a ventilator for days, as the available machines are not designed to support this workload. If the paralysis has extended to the breathing muscles of an adult horse, it is humane to euthanize it.

Prevention
Horse owners should be cautious about feeding hay that has been rained on during the harvesting phases. Roundbaled hay is particularly a risk factor when baled at excessive moisture content. Any hay with rotten or decaying material should not be fed to horses. Since the spoiled material is most likely to be internal in round hay bales, it may be impossible to visually determine this condition unless the bales are opened. If the exterior of the bale is rotten with dark discoloration and moldy or if the bales feel warm, they should not be fed to horses. An unspoiled round bale, put out for a group of horses, is generally not a problem.

There is also a risk for botulism if horses are being fed silage or haylage, especially if the fermentation process was inadequate to lower the pH to inhibit the growth of the bacteria and toxin production. Haylage, silage, and high-moisture hay are more prone to spoilage. For people who own horses and cattle, and thus feed silage to all their animals, it is important to mention that cattle are not as sensitive to botulism as horses, but they do die from this disease.

Vaccination
There is a USDA-approved vaccine available to prevent botulism. The vaccine can be purchased from your veterinarian. Talk with your veterinarian about the best vaccination schedule for your herd. The following vaccination schedule is the proposed schedule of the American Association of Equine Practitioners (AAEP).–Fernanda C. Carmargo, Bob Coleman, Laurie Lawrence, Department of Animal Sciences

Vaccination Chart: Foals and Weanlings (< 12 months of age)
Mares vaccinated in the prepartum period Unvaccinated mares

Vaccination Chart: Adult Horses
Broodmares Other Adult Horses (> 1 year of age)

Acknowledgments
Special thanks to Jim Smith, DVM, Hagyard Equine Medical Institute, Lexington, Kentucky, who has been practicing equine veterinary medicine for almost 50 years; and to Jackie Smith, MS, Livestock Disease Diagnostic Center, University of Kentucky, Lexington, a very accomplished epidemiologist. They contributed essential information for this article.

References
Smith, Louis DS. The occurrence of Clostridium botulinum and Clostridium tetani in the soil of the United States. Health Laboratory Science 15(2):74-80, 1978.
Clostridium botulinum: United States Food and Drug Administration, Foodborne Pathogenic Microorganisms and Natural Toxins Handbook. (www.cfsan.fda.gov/~mow/chap2.html)
Wilkins, P. Botulism. In: Equine Infectious Diseases. Editors: Sellon and Long, Saunders-Elsevier, Missouri, USA, pp. 372-376, 2007.
Whitlock, RH; McAdams, S. Equine botulism. Clinical Techniques in Equine Practice 5:37-42, 2006.
Whitlock, RH; Buckley, C. Botulism. Veterinary Clinics of North America: Equine Practice 13:107-128, 1997.
Divers, TJ; Bartholomew, RC; Messick, JB; Whitlock, RH; Sweeney, RW. Clostridium botulinum type B toxicosis in a herd of cattle and a group of mules. Journal of the American Veterinary Medical Association 188:382-386, 1986.



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The catalytic domain of Clostridium botulinum neurotoxin type F (represented as a molecular surface, gray) bound to an inhibitor molecule (colored ribbon) designed to mimic the nerve-cell protein the toxin cleaves. The mimic protein interacts with the toxin at several exosites (purple-, brown-, and green-shaded areas) in addition to the active site (red) that performs the cleaving action, suggesting that blocking these interactions could thwart the toxins deadly action.

Link:  http://www.bnl.gov/bnlweb/pubaf/pr/PR_display.asp?prID=958&template=Today



http://www.sciencexpress.net/how-botulism-paralyzes-nerve-cells-new-details-revealed/

Inhibitor molecules mimic interaction; could become drugs to block deadly poison.

UPTON, NY — New structures of a botulism toxin interacting with a mimic of the nerve-cell protein it destroys suggest new ways to block this often-fatal interaction. Indeed, the mimic molecules have such high affinity for the toxin and bind to it so tightly that they themselves could possibly serve as anti-toxin drugs with further modification, the researchers said.

The catalytic domain of Clostridium botulinum neurotoxin type F (represented as a molecular surface, gray) bound to an inhibitor molecule (colored ribbon) designed to mimic the nerve-cell protein the toxin cleaves. The mimic protein interacts with the toxin at several exosites (purple-, brown-, and green-shaded areas) in addition to the active site (red) that performs the cleaving action, suggesting that blocking these interactions could thwart the toxins deadly action. (Brookhaven National Laboratory)

The catalytic domain of Clostridium botulinum neurotoxin type F (represented as a molecular surface, gray) bound to an inhibitor molecule (colored ribbon) designed to mimic the nerve-cell protein the toxin cleaves. The mimic protein interacts with the toxin at several exosites (purple-, brown-, and green-shaded areas) in addition to the active site (red) that performs the cleaving action, suggesting that blocking these interactions could thwart the toxins deadly action. (Brookhaven National Laboratory)

The atomic-resolution structures were made at the U.S. Department of Energy’s (DOE) Brookhaven National Laboratory in collaboration with scientists from the U.S. Army Medical Research Institute for Infectious Diseases, and will be published online on June 21, 2009, in Nature Structural & Molecular Biology.

Botulism toxins are among the deadliest known poisons. Minute quantities in improperly canned goods can cause a fatal form of food poisoning. Recently, some forms have been used in medical settings to smooth facial wrinkles and to quell bladder spasms to stem urinary leakage. But fear of their use as a bioterror weapon has made the toxins notorious — and the push for developing antitoxin drugs or vaccines a high priority.

The toxins come in seven distinct varieties, but all work the same way: One portion of the toxin binds to a nerve-cell membrane; another portion moves a smaller “catalytic domain” into the cell; then this catalytic domain binds to and cleaves a nerve-cell protein, making it impossible for the nerve cell to “fire,” or send signals. The result is paralysis — and often, death.

“This study looked specifically at how the catalytic domain of one type of neurotoxin, neurotoxin F, recognizes and binds to its target nerve-cell protein to perform this final, paralyzing step,” said Brookhaven Lab biologist Subramanyam Swaminathan, who led the research team.

The team first synthesized two different mimics of the target nerve-cell protein. They then allowed each to bind to the catalytic domain of the toxin, and analyzed the structures using high-intensity x-rays at Brookhaven’s National Synchrotron Light Source (NSLS). Analyzing how the x-rays bounce off the structure allows scientists to reconstruct extremely high-resolution, 3-D images showing the positions and relative orientations of the atoms making up the proteins.

“Our structures reveal that portions of the toxin that are distant from the ‘active site’ that cleaves the nerve-cell protein are crucial to the toxin’s ability to bind to and destroy this protein,” Swaminathan said. Biochemical analysis confirmed the existence and importance of these “exosites,” further validating the crystal structures.

“Because these exosites play such an essential role in the toxin’s ability to bind to and cleave the nerve-cell protein, they could serve as additional targets for the development of drugs designed to interfere with the toxin’s deadly action,” Swaminathan said.

The scientists are also exploring the possibility that the inhibitor molecules they used in this study as mimics for the nerve-cell protein could themselves serve as anti-toxin drugs.

“These inhibitors are attractive candidates for anti-botulinum drug development,” Swaminathan said. “To do so, we’d need to find a way for the inhibitor to reach the toxin inside nerve cells.” One possibility would be to add a transmembrane sequence or some other means of intracellular transport to the inhibitor molecule.

Work on all seven variations of the toxin is essential to understanding common mechanisms that may aid in the design of drugs that work across several different types, or ideally, broadly against all seven. Swaminathan’s group has studied six of the seven varieties. (See related links, below.)

Brookhaven biologists Subramanyam Swaminathan (left) and Rakhi Agarwal. (Brookhaven National Laboratory)

Brookhaven biologists Subramanyam Swaminathan (left) and Rakhi Agarwal. (Brookhaven National Laboratory)

“The mere existence of a vaccine or anti-toxin drugs would help mitigate the extreme fear of a bioterror attack,” Swaminathan said.

Understanding the detailed structures of the toxins and how they interact with their target proteins could also lead to advances in the ways they can be used safely in a medical setting.

This research was funded by grants from the Defense Threat Reduction Agency/Joint Science and Technology Office for Chemical and Biological Defense, U.S. Department of Defense. Data for this study were measured at beamline X29 and X12C of the NSLS, which is supported by the offices of Biological and Environmental Research and of Basic Energy Sciences within DOE’s Office of Science.



Link:  http://www.wdsu.com/news/19806760/detail.html

WDSU.com:

“There’s a new weapon in the fight against wrinkles, and doctors said it works just as well as Botox.

Tired of looking in the mirror and seeing frown lines, Kathy Loeffler turned to Botox three years ago.

“Age was starting to show up on my face,” she said.

Now there’s something new for Loeffler and the millions of others who get Botox every year. The latest injection is called Dysport.

“The difference between Botox and Dysport is very small,” said Dr. Tom Rohrer, of SkinCare Physicians.

Rohrer studied Dysport in a clinical trial. He said both drugs will contain the same main ingredient: the botulism toxin.

“What it’s doing is really blocking the signal between the nerve and the muscle, so when you tell yourself to frown, the muscle really never gets that message,” he said.

Injected in small amounts, Rohrer said Dysport and Botox offered the same results with the same side effects, too, mostly bruising at the site.

“The Dysport, like Botox, worked extremely well,” Rohrer said. “People who had it, the lines went away; they didn’t frown anymore.”

Loeffler said she thought Dysport worked better than Botox.

“The Botox didn’t seem to last as long as this did,” she said. “As I continued to use it, the times between visits were longer.”

She said she was excited to learn that, in Europe, Dysport costs less than Botox — but its manufacturer hasn’t released a price sheet just yet.

“I’ve heard rumors of maybe a 10 percent drop in the price,” Rohrer said.

Dysport was just recently approved by the Food and Drug Administration, so it should be brought into doctor’s offices within the next few weeks.”



TheCalifornian.com (http://thecalifornian.com/article/20090618/NEWS01/90618016/1002/Carmel+s+Sea+Harvest+recalls+sauce+due+to+possible+health+risk)

Sea Harvest Fish Market and Restaurant in Carmel announced today it is voluntarily recalling cioppino sauce sold in jars over the counter at its Carmel store as a precaution due to potential contamination with Clostridium botulinum, which can cause botulism, a serious and sometimes life-threatening condition.

The voluntary recall covers all jars of cioppino sauce, regardless of size or date purchased.

Consumers should not consume these products, even if they appear to be normal, because of the possible serious health risk.

Consumers who have the affected products should destroy them or return them to the store for a refund.

No illnesses have been linked to jars of cioppino sauce sold at the store, and there have been no positive test results for the pathogen in product sampled.

Sea Harvest took this voluntary action in the interest of public health because the jars of cioppino sauce were not manufactured in accordance with processing controls that may be applicable.

There is no safety concern about cioppino sauce consumed at the restaurant; the only issue is the canning process.

Symptoms of botulism poisoning in humans include general weakness, dizziness, double-vision and trouble with speaking or swallowing. Difficulty in breathing, weakness of other muscles, abdominal distension and constipation may also be common symptoms. People experiencing these problems should seek immediate medical attention.

Consumers may call Sea Harvest at 831-626-3626 for further information.

The recall is being undertaken with the knowledge of the California Department of Public Health, 1-800-495-3232.



Mercury News, 6/19/09 (http://www.mercurynews.com/breakingnews/ci_12628298)

CARMEL, Calif.—Canned cioppino sauce produced and sold by Sea Harvest Restaurant of Carmel has been voluntarily recalled because of possible botulism contamination.

No illnesses have been reported.

Authorities say the restaurant is cooperating with the California Department of Public Health and the Monterey County Health Department in the voluntary recall.

The sauce was manufactured by Sea Harvest and sold at retail in the restaurant. The state says Sea Harvest does not have the required cannery license to produce the cioppino sauce.



Intro:  This is a legal blog site coming from the law firm of Eric Weinberg.  It’s meant to inform and extend assistance towards victims of food poisoning.  Botulismtoolkit.com does not endorse any law firm.  This site is also meant to inform the public about the Boiled Horse Mackeral and provide new websites for more information.  BTW, why anyone would want to eat mackerel called “Boiled Horse” I have no clue.

Botulism Legal Help Blog:  http://botulismlegalhelp.com/?p=77

According to a company press release dated June 10, 2009, the Bao Ding Seafood Company of New York, NY, has recalled its Boiled Horse Mackerel.  It was recently discovered that the recalled Mackerel product was not eviscerated prior to processing and therefore has the potential to be contaminated with Clostridium botulinum.

Clostridium botulinum is a bacterium capable of causing the life-threatening illness known as botulism. 

Someone who has eaten product contaminated with the botulinum toxin may experience some of the following symptoms:  general weakness, dizziness, double vision, and trouble speaking or swallowing.  Further symptoms that are also common include trouble breathing, weakness in other muscles, abdominal distension, and constipation.  Please see Botulism Symptoms for more information. 

The Boiled Horse Mackerel that has been recalled is packaged in vacuum packed plastic bags with a net weight of 450g, and was sold in New York State.

The Mackerel may not appear spoiled or give off any odors, and consumers are warned not to eat it even if it seems normal.  The press release cautions that individuals should seek immediate medical attention if they are experiencing any of the above symptoms.

The Law Firm of Eric H. Weinberg represents hundreds of food poisoning victims of food poisoning outbreaks nationwide.  We are ready to help you.  If you have questions regarding your legal rights, please click Free Case Evaluation, or call us toll free at 1-877-934-6274.

To learn about current food and drug recalls, please see Food Poisoning Attorney and Drug Recall Lawyer.