Enzon sells specialty drug business for $300M

Enzon sells specialty drug business for $300M

(AP) – Nov 9, 2009

BRIDGEWATER, N.J. — Enzon Pharmaceuticals Inc. said Monday it is selling most of its business to Italian drugmaker sigma-tau Group and will focus on its experimental cancer drugs and technologies.

Enzon will get $300 million upfront, along with milestone payments of as much as $27 million. Sigma-tau could also pay Enzon royalties on Enzon’s four approved drugs through 2014. Sigma-tau is also acquiring a manufacturing facility in Indianapolis in the deal.

Enzon stock reached an annual high of $9.60 on the news. That was its highest price since December 2007.

The specialty drugs sigma-tau is buying are cancer drug Oncaspar, fungal infection treatment Abelcet, meningitis drug DepoCyt, and Adagen, which is used for severe combined immunodeficiency disease, or “Bubble Boy Disease.”

In 2008, Enzon announced plans to spin off its biotechnology business into an independent company so it could focus on developing treatments for cancer. It canceled those plans in December due to the weak state of the financial markets. With the specialty drug unit sold, the company said it will focus on potential cancer treatments including the drug candidate Peg SN38.

The transaction, which is subject to financing and approval by Enzon shareholders, is expected to close in the first quarter next year.

In morning trading, Enzon shares rose 43 cents, or 4.7 percent, to $9.41.

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Bubble Boy: Six-Week-Old Boy Recovers in Dallas

Bubble Boy Comes from Family of Bubble Boys

 

DALLAS, TX – Six-week-old Brady Stewart is one in a million. He’s also one of about 100 kids a year in the United States diagnosed with severe combined immunodeficiency syndrome, or SCID. It’s probably better know as ‘bubble boy disease.’ Brady was born without an immune system, he’s not in a bubble. His mother Jeanie says doctors and nurses who wear scrubs and masks are among the few who get to be near him.

“So he is protected in there as much as he can be. I’m just really careful; I mean, I wash my hands a thousand times a day it seems,” says Jeanie.

And for good reason. Medical City Children’s Hospital hematologist Dr. Stan Goldman says that without an immune system, any germ could be deadly.

“Left untreated, SCID is usually fatal in the first few years of life, not because of the immunodeficiency, but because of the infections you can’t fight off.” Says Dr. Goldman.

About a month ago, Brady received a bone marrow transplant from his dad. Doctors are now waiting for immune cells to grow. Bubble boy disease is transmitted from mothers to sons and only boys can have the disease. Jeanie’s brothers, Matt and Daniel, were bubble boys, Daniel almost died. Brady has two nephews, Trey and Clayton, who are also bubble boys. Jeanie says that all are now leading normal lives.

“Knowing that, it was comforting, going into it, I mean, I always knew we were going to have children, even though this was an issue and I wouldn’t trade it for the world.” Says Jeanie.

Brady was diagnosed with the disease at eighteen weeks. He was born in Oklahoma City and then taken to Medical City Children’s Hospital where his mom says he is thriving in isolation.

“He’s doing amazing, he’s gaining weight everyday and he just seems like a normal baby.” Says Jeanie. “You would never know anything were wrong with him if we didn’t know in advance.”

And until he grows an immune system, Jeanie says his hospital room will be home.

“He’s pretty protected, but if he was out in the real world, it would be very scary.”

linkback url: http://www.the33tv.com/news/kdaf-dallas-bubble-boy-story,0,1523581.story

 

SCID’s The Worst of Primary Immune Deficiency Disease or The Bubble Boy Disease

SCID’s The Worst of Primary Immune Deficiency Disease or The Bubble Boy Disease

SCID Kids Leading Healthy, Normal Lives 25 Years After ‘Bubble Boy’

Oct 12, 2009 – 1:00:27 PM

(HealthNewsDigest.com) – DURHAM, N.C. – Mention the words “bubble boy” and many will recall David Vetter, the kid with big eyes and a thick thatch of dark hair who died 25 years ago after spending almost the entire 12 years of his life in a germ-free, plastic bubble.

David was born with severe combined immune deficiency, or SCID, a condition that robbed him of an immune system.

Since David’s death however, researchers have refined treatment options for children with SCID, and today, as scientists at Duke University Medical Center report in The Journal of Pediatrics, most of them who undergo related donor bone marrow transplants manage to grow up, go to school, and for the most part, lead pretty normal lives.

That conclusion comes from the longest and largest study to date of children with SCID treated at a single center. Led by Rebecca H. Buckley, M.D., professor of pediatrics and immunology at Duke, researchers followed for up to 26 years 110 of the 124 surviving SCID children out of the 161 who had come to Duke for bone marrow transplants. The study involved periodic questionnaires and visits to Duke for reassessment of various aspects of their lives, including immune function, growth, behavior, nutritional needs, mental, physical, and emotional well-being and any trouble with recurrent infections.

Buckley says the data clearly show that SCID infants who receive a related donor bone marrow transplant within the first 14 weeks of life are significantly more likely to survive and have fewer problems over time than those who receive transplants later in infancy or who have already developed an infection.

Buckley says the findings underscore the need for SCID testing at birth. “If we can identify children with SCID at birth, we can save more lives. When we transplant these babies prior to the onset of infections, 94 percent survive. But if they are older or if they have already developed an infection, only 71 percent will live.”

There are at least 13 subtypes of SCID, but all arise from genetic mutations that are either inherited or arise in the infant. SCID is described as a rare disorder, but Buckley points out that no one really knows how often it occurs because testing for the condition at birth is not done. “Babies frequently die from infections, but no one thinks about SCID,” Buckley says, “and autopsies are rarely done any more, so the death certificate simply lists ‘infection’ as the cause.” Buckley believes SCID may actually be as prevalent as PKU, an inherited metabolic disorder that is routinely identified and treated through newborn screening.

Buckley has been advocating for over a decade about the need for routine screening for SCID in newborns.

So far, the only states to perform it are Wisconsin and Massachusetts, which are conducting pilot studies.

In the Duke study, 77 percent of the children survived and 86 percent of those were considered healthy by their parents, says Buckley. Still, growing up with a corrected immune system is not always a sunny experience. Investigators found that 58 percent of the children needed periodic antibody therapy because of inadequate B cell function, and about one-third required antibiotics. In addition, about 10 percent had some sort of developmental delay and about 20 percent had attention deficit disorder, often due to the lack of an enzyme called adenosine deaminase, one of the causes of SCID. Other conditions appearing in a minority of the patients include diarrhea, rashes and HPV infection. Some of the conditions appeared more frequently in certain SCID subtypes than others.

At least two other centers specializing in SCID have recently published long-term outcome data on their patients, but more of Buckley’s patients survived and the survivors are healthier, in general, than their SCID Kids Leading Healthy, Normal Lives 25 Years After ‘Bubble Boy’ Buckley, director of Duke’s Immune Deficiency Foundation Center of Excellence for Primary Immunodeficiency Diseases and a member of the Institute of Medicine, says the difference may lie in Duke’s therapeutic approach.

Unlike other centers, Duke does not use chemotherapy before performing a bone marrow transplant in a SCID infant. “SCID babies do not have any T cells, so they cannot reject a graft. Chemotherapy can harm the lungs, liver and other organs and those who receive it may be sterile as adults.”

Even though a tissue-matched related donor – the ideal donor – is rarely available for these infants (only 16 had them in her series), Buckley was able to use half-matched parental donors in the other 145 by using a process to strip away the donor’s T cells from the marrow graft to prevent potentially fatal graft-versus-host disease. If T cells are not removed from half-matched marrow, the SCID infant would die of graft-versushost disease—a reaction of donor T cells against the infant. Removing the T cells from the donor bone marrow also allows omission of immunosuppressive drugs after the transplant, a practice routinely used in many centers. “Giving a SCID infant drugs to suppress the immune system is counterproductive if you are trying to build a new immune system,” she says.

In the future, other therapies may be possible. “Gene therapy is likely to be the best option — if the problems encountered to date can be worked out,” says Buckley. Gene therapy trials were halted in 2003 after some patients developed cancer following the therapy, but new trials that may be safer may start soon.

The research was funded by the National Institutes of Allergy, Immunology and Infectious Diseases.

Duke coauthors of the study include Mary D. Railey, M.D. and Yuliya Lokhnygina, Ph.D.

linkback url: http://www.pbn.com/detail/46159.html

Edgar toddler first ‘bubble boy’ survivor

Edgar toddler first ‘bubble boy’ survivor

State-mandated test at birth identified fatal disease

By Megan Loiselle
Wausau Daily Herald

EDGAR — A 1-year-old Edgar boy has become the first child in the world to be saved from a fatal immunodeficiency disease, just months after Wisconsin became the only state to test for it at birth.

Dawson Bornheimer’s family on Sept. 25 celebrated the first anniversary of a lifesaving bone marrow transplant that treated his Severe Combined Immunodeficiency, or SCID — also known as “bubble boy disease.” The disease is fatal if not treated in the first few months of life.

The state’s pilot program for the screening was funded in part by the Jeffrey Modell Foundation, established by Vicki and Fred Modell in memory of their son who died at age 15. Dawson was honored as the “man of the year” by the foundation at a gala this spring in New York. The screening now is routine for the estimated 70,000 births in the state annually.

“They caught it, and because of that, we get to play with you every day,” his mother, Melissa Bornheimer, said during an interview at her home, as she patted Dawson’s leg.

Twelve days after Dawson was born on June 12, 2008, the Bornheimers received a call saying he had failed the test for SCID — a test they didn’t even know he had been given.

Melissa said at first she thought the test had to be wrong because Dawson seemed fine.

Hours after the call, the Bornheimers took Dawson to the hospital with a fever. He was released with what doctors said was a viral infection. Days later, his belly button became infected so badly that it had to be removed at a hospital in Madison.

In a span of a few weeks in August, Dawson was checked into the Children’s Hospital of Wisconsin in Milwaukee for a blood transfusion as well as surgeries to remove abscesses growing on his neck and to fix a hole in his trachea. Test results showed his bone marrow wasn’t producing white blood cells strong enough to attack infections in his body. The only cure would be a bone marrow transplant.

On Sept. 25, 2008, he received the transplant, with marrow donated from a baby in Germany. Some of Dawson’s vital organs shut down as his body struggled to adjust to the donor’s marrow, but Melissa said his body eventually accepted the bone marrow.

One year after the transplant, Dawson still has 100 percent of his donor’s bone marrow, which means chemotherapy he received last year was successful in eradicating all of his own bone marrow.

Melissa, 35, said the couple had great health insurance through Mike’s work as a material handler at Wausau Supply Co. It allowed the family to focus on Dawson rather than worrying about his $1 million in treatment costs.

Today, Dawson often crawls around the floor and plays at home with his 9-year-old brother, Dylan. Dawson will start walking soon.

His grandmother Ione Bornheimer of Athens said every time she and her husband, Harvey, visit, they see more improvements.

“He’s making big strides,” she said. “It has been very hard on the family but he’s our little miracle baby.”
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‘Olivia’s Fund’ gets barbecue boost

‘Olivia’s Fund’ gets barbecue boost

The Silliker family and supporters are grateful to the community for its support. As a result of that support, Olivia Silliker’s (small photo) future is considerably brighter following a bone marrow transplant courtesy of her four-year-old sister Mackenzie.

Community support

Family and friends of Olivia Silliker are overwhelmed by the community spirit and generosity displayed at a fund-raising barbecue outside Chrissy’s Variety Store.

The recent barbecue raised $1,500, for which the family and supporters wished to express thanks from the bottom of their hearts.

Olivia was born June 9th to parents Mark and Anna and hospitalized August 5th with a diagnosis of ADA SCIDS (Severe Combined Immunodeficiency). In layman’s terms, the rare (one in every two million births) condition means her immune system does not function properly, and a common cold can be deadly

Treatment for ADA SCIDS is a bone marrow transplant.

The immediate family was tested and a perfect match found in Olivia’s four-year-old sister Mackenzie. One week after admission to Sick Kids hospital in Toronto, the transplant took place with the support of a very brave older sister. Mackenzie has since recovered from the procedure and attended her first day of school September 22nd.

Olivia remains in Sick Kids, in an isolation room, which filters air 500 times per hour. To interact with Olivia, her family needs to protect her from germs by using sterile gowns, gloves, hairnet, boots and masks.

It is unknown how long she must be in the hospital, but her family has been told to prepare for a lengthy stay. Olivia’s blood is taken regularly to ensure her white blood cells are increasing and tests are done to determine whether the bone marrow transplant was a success. She will not be released until it is positive that she has developed an immune system and will be able to fight infection on her own.

In the interim, Anna’s desire to remain with her daughter is being challenged by financial realities. Her maternity leave from a subsequently-closed plant (DDM) will come to an end, highlighting the additional financial pressures of living costs and travel expenses exacerbating the family’s natural stress caused by their daughter’s medical challenges.

Fund-raising efforts have been organized, including the barbecue, in order to provide financial assistance for Anna to stay by Olivia’s side through accommodation at Ronald McDonald House in Toronto, as well as with monthly bills and everyday living expenses.

“I would rather sell my house than leave her there all alone,” said Anna.

Additional fundraisers will occur over the next few months, however friends and family are encouraging the public to donate whenever possible to assist the Silliker family.

Donations can be made at St. Mary’s Roman Catholic Church in Tillsonburg. Cheques are to be made payable to St. Mary’s RC Church specifying that the donation is for “Olivia’s Fund” and a tax receipt will be issued.

linkback url: http://www.tillsonburgnews.com/ArticleDisplay.aspx?e=2047035

Scientists Identify Genetic Cause of Previously Undefined Primary Immune Deficiency Disease

Scientists Identify Genetic Cause of Previously Undefined Primary Immune Deficiency Disease

Researchers at the National Institutes of Health have identified a genetic mutation that accounts for a perplexing condition found in people with an inherited immunodeficiency. The disorder, called combined immunodeficiency, is characterized by a constellation of severe health problems, including persistent bacterial and viral skin infections, severe eczema, acute allergies and asthma, and cancer.

The team that made the discovery was led by Helen Su, M.D., Ph.D., at the National Institute of Allergy and Infectious Diseases (NIAID), and included collaborators from NIAID and the National Cancer Institute (NCI). The research is reported in this week’s New England Journal of Medicine.

“NIH clinicians have cared for people with unusual and difficult-to-treat immune disorders for decades,” says NIAID Director Anthony S. Fauci, M.D. “This study exemplifies their commitment to improving the lives of people with these diseases by trying to uncover the causes of these disorders and thereby better understanding how to treat them.”

Combined immunodeficiency is a type of primary immune deficiency disease (PIDD) in which several parts of the immune system are affected. This inherited disorder is characterized by increased susceptibility to bacterial, viral and fungal infections of various organs of the body. In some cases, susceptibility to cancers also may be seen.

There are 150 known PIDDs. Approximately 500,000 people in the United States have been diagnosed with a PIDD, while many more remain undiagnosed.

The NIAID and NCI investigators recognized that certain patients with an undefined form of combined immunodeficiency shared enough clinical features to make it likely that the cause might be a common genetic mutation. Originally, these individuals were thought to have a variant form of hyper-immunoglobulinema E syndrome (HIES), a disorder characterized by increased levels of a class of antibodies known as immunoglobulin E, superficial and systemic bacterial and fungal infections, and atopic dermatitis, also known as eczema.

This newly described group, however, had far more severe eczema than is typical in people with variant HIES.  They also had extensive and difficult-to-manage viral infections of the skin, such as warts, molluscum contagiosum—a type of poxvirus that only infects the skin—and herpes simplex. Some in this group also developed skin cancers, as well as lymphoma of the skin.

“Even though these individuals were diagnosed with a more uncommon form of HIES, they were still considered to have a mystery disease, because they had severe allergies and had developed cancers,” says Dr. Su.

Using a technique called comparative genomic hybridization, a process by which large amounts of DNA is fixed to a computer chip and analyzed for changes in the genes, scientists examined the genes in the tissue samples from five different groups:  the 11 individuals with the unknown immunodeficiencies, people with the variant form of HIES, people with classic HIES, those with other immunological diseases, and healthy individuals.

The researchers discovered that people with the unique form of HIES had mutations in a gene called DOCK8 that led to deletions in parts of the gene. The normal function of DOCK8 is currently unknown.

When compared with healthy individuals, the people with DOCK 8 mutations had fewer CD8 positive T cells, immune cells needed to fight viral infections; fewer antibody-producing B cells; and increased numbers of eosinophils—immune cells associated with allergy.

According to Dr. Su, these findings indicate that DOCK8 is essential for defense against viral infections and for preventing the development of cancer and allergies.

Although further study is required to determine if DOCK8 mutations occur in other people with similar disease symptoms, DOCK8 immunodeficiency syndrome may be a new PIDD. These findings mean that individuals with this rare disease will be able to receive a more accurate diagnosis. Identifying a genetic cause for the disease provided comfort to some of those diagnosed who had battled an unknown immune disease for years, according to Dr. Su.

“The study of inherited disorders and the genetic alterations that are responsible for their complex array of disease symptoms has often resulted in the discovery of causative genes that play a role in cancer initiation,” said NCI Director John E. Niederhuber, M.D. “The disease mutations found in this study in the DOCK8 gene exemplify that kind of important finding.  As with any discovery of a genetic defect, the challenge going forward is to develop a complete knowledge of the cascading pathways of biological function for which DOCK8 is responsible.”

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NIAID conducts and supports research—at NIH, throughout the United States, and worldwide—to study the causes of infectious and immune-mediated diseases, and to develop better means of preventing, diagnosing and treating these illnesses. News releases, fact sheets and other NIAID-related materials are available on the NIAID Web site at http://www.niaid.nih.gov.

NCI leads the National Cancer Program and the NIH effort to dramatically reduce the burden of cancer and improve the lives of cancer patients and their families, through research into prevention and cancer biology, the development of new interventions, and the training and mentoring of new researchers. For more information about cancer, please visit the NCI Web site at http://www.cancer.gov or call NCI’s Cancer Information Service at 1-800-4-CANCER (1-800-422-6237).

The National Institutes of Health (NIH)—The Nation’s Medical Research Agency—includes 27 Institutes and Centers and is a component of the U. S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.

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Reference:

Zhang et al. DOCK8 mutations underlie a new form of combined immunodeficiency with allergy, hyper-immunoglobulinemia E, lymphocyte dysfunction, viral infections, and cancer. New England Journal of Medicine DOI: 10.1056/NEJMoa0905506 (2009).

linkback url: http://www3.niaid.nih.gov/news/newsreleases/2009/DOCK8.htm

The Second Coming of Gene Therapy

The Second Coming of Gene Therapy
09.02.2009
For years, gene therapy produced tons of hype but no results. Recently, though, new approaches have yielded its first successes: breakthrough treatments for blindness, cancer, and the deadly bubble boy disease.
by Jill Neimark

“For the first two years of her life, my daughter, Katlyn, was knocking on heaven’s door every day,” says Daisy Demerchant, a 26-year-old mom living in Centreville, New Brunswick, just north of Maine. “Two months after she was born she started getting sick, and she never got better.” At six months Katlyn was diagnosed with “bubble boy” disease, formally known as severe combined immunodeficiency (SCID), which robs the immune system of the ability to fight infection. There are many causes of this disorder; in Katlyn’s case it was lack of the enzyme adeno­sine deaminase, or ADA, which rids the body of a natural toxin called deoxyadenosine. When the toxin builds up, it destroys T and B lymphocytes, the body’s infection-fighting immune cells. As a result, Katlyn’s immune cells were dying.

Treatment options ranged from risky to grim. One was a bone marrow transplant, in which imported donor cells could manufacture healthy T cells to fight invading germs. But bone marrow transplants can have lethal complications and often require drugs that further inhibit the patient’s immune system, leaving a window of vulnerability until the transplant kicks in. Another potential treatment involved injections of the ADA enzyme itself. But there was a risk Katlyn would develop antibodies to the drug, rendering it useless. Without any treatment at all, she would simply die.

While weighing their options, doctors put the little girl on protective antimicrobials and sent her to a hospital eight hours from her home. She became another fragile bubble baby sequestered from the world. “My husband quit his job building fire trucks, and we lived with Katlyn in the hospital for 15 months,” Demerchant says. The parents had to wear sterile gowns, booties, masks, and gloves, and the urge to touch their child—let alone hug and kiss her—had to be put on hold.

Just when it seemed as if Katlyn’s life might never improve, science and fate intervened. Her specific condition, called ADA-SCID, had long tantalized researchers seeking to repair genetic defects with a technique called gene therapy. Rare, deadly, and caused by a single gene mutation, it was a perfect proof-of-principle condition for anyone seeking to replace damaged DNA with genes that did the job. With all her troubles, little Katlyn Demerchant had been almost made to order for Fabio Candotti, a senior investigator at the National Human Genome Research Institute at the National Institutes of Health in Bethesda, Maryland.

Before Katlyn showed up at NIH, the doctors there were already well prepared: They had inserted healthy human ADA genes into a modified mouse retrovirus—a type of virus that can enter human cells and transfer new genetic material right into the DNA strands in their nuclei.

Once Katlyn arrived in May 2007, Candotti and his team removed stem cells from her bone marrow and exposed them to the engineered retrovirus, creating a human-virus hybrid. Then they injected the hybrid cells back into Katlyn. Like heat-seeking missiles, the retooled stem cells automatically found their way back home to the marrow. There, they began to specialize, creating all of the secondary or “daughter” cells that such stem cells normally produce—including healthy T cells with functioning ADA genes.

Everybody waited while Katlyn, still stuck inside the bubble, learned to walk on the floor of her sterile isolation room and to play through the protective window with a visiting dog named Toffee. On September 3, blood tests showed Katlyn’s immune system was being populated with robust, functioning T cells. She was so restored, in fact, that her parents were able to take her outside for the first time since she was an infant. “The first day we took her out she was really quiet and a little terrified,” Daisy Demerchant says. “The second time she started running around and asking us a million questions. She’d point to the sun, clouds, leaves, cars, everything imaginable, and ask us what it was. Ever since that day, she has never wanted to stay inside.”

Six months after her gene therapy transplant, Katlyn was so healthy that doctors let her return home to Canada. It can take a year or longer for the immune system to reconstitute itself in full, so Katlyn still takes antimicrobials as a precaution, but today she plays outside, even in the dirt, and is resistant enough to fly on a commercial plane.

The new DNA treatments for Katlyn Demerchant and other bubble babies are nothing short of remarkable, the culmination of a major push to perfect gene therapy for the disease, Candotti says. Across the ocean, in Italy, bubble babies with ADA-SCID are also being cured: A trial led by Alessandro Aiuti, a molecular biologist at San Raffaele Telethon Institute for Gene Therapy in Milan, restored the immune system in eight of ten children, while a ninth had significant improvement.

And bubble babies are far from alone. In Europe and the United States, gene therapists have restored vision in individuals suffering from a rare genetic disorder that inevitably leads to blindness. In Texas, a team has manipulated genes in order to put deadly cancers into complete remission. Building on these successes, gene therapy may soon be used to correct hereditary genetic diseases like cystic fibrosis, hemophilia, and Tay-Sachs and to activate the immune response against a wide variety of infectious diseases and cancers. Gene therapy and its adjuncts may help us trick the body into growing new tissue to rejuvenate arthritic joints, fix injured hearts, and speed the healing of wounds….Continued

link url: http://discovermagazine.com/2009/sep/02-second-coming-of-gene-therapy

Campers aid area toddler

The Jeffery family is giving thanks to their newfound friends, many of whom they’ve never met.

Indeed, most of the Jefferys’ supporters are members of the Bluewater Campers’ Association, which recently presented the St. Joseph’s family with a $7,200 donation, the second of such gifts since the club first heard of the family’s plight three years ago.

“I can’t tell you what this means for our family,” says Dennis Jeffery. “This will help a lot.”

And help is what the Jefferys need as their youngest son, three-year-old André, continues with his valiant battle with Severe Combined Immunodefiency Disease (SCID), an autoimmune disease that leaves him vulnerable to a host of life-threatening illnesses and renders most of his life to the confines of what is commonly known as a plastic bubble.

André was first diagnosed with the disease at the age of four months when the Jefferys brought him to see a Stratford doctor as the baby was covered in a rash that looked like he’d been splashed with scalding water.

André has been in and out of hospitals ever since.

Most recently, the sweet-cheeked young lad with soulful brown eyes, suffered cardiac arrest, his second one due to the havoc the 34 medications medications he takes daily are wreaking on his organs.

André is now at Sick Kids’ Hospital in Toronto where his mom, Sheila, keeps vigil as the rest of the family including seven-year-old sister, Monica, and nine-year-old brother, Donavon, hold down the fort in St. Joseph’s.

Naturally, notes Dennis, the emotional, financial and physical toll of André’s plight is difficult on everyone, especially André’s siblings who must spend a lot of time away from their beloved parents who, for a time, were at André’s bedside 24 hours a day.

“It’s hard to keep everybody together,” notes Dennis. “It’s been a difficult experience. I wouldn’t wish it on my worst enemy.

And when André and his mom are able to return home, the family will once again face the additional expenses of bringing Registered Nurses in to assist with his care. Plus, only 27 of the medications André requires are covered by OHIP.

At a recent meeting at the Bluewater Campers’ meeting room, club members presented the family with the $7,200 donation, as well as $50 gift certificates for Monica and

Donavon and a stuffed animal for André. It was clearly a proud night for members as one organizer put it: “For such a small number of people, this is an amazing amount of money.”

While learning André is currently grappling with kidney problems as he recovers from cardiac arrest, the Bluewater Campers vow to continue to help where they can – even though most of them were meeting Dennis, Monica and Donavon for the first time at the cheque presentation.

“It’s going to help me large,” says Dennis, who notes there are many changes on the horizon for the Jefferys including the possibility that they will have to sell their St. Joseph’s home, a community where both Dennis and Sheila hail from, and move to Toronto to ensure Andre continues to receive the treatment he needs.

Club member Deb Jeffrey, in thanking the campers, note the relatively small park – at 140 trailers – has raised nearly $20,000 in the past three years for the Jefferys and other community-based causes including $3,000 for Habitat for Humanity and $2,500 for the CT Scanner campaign at Alexandra Marine General Hospital in Goderich last year, and about $3,000 for the Jefferys two years ago.

The fundraising events, note organizers, were made possible through a slew of events, including silent auctions and golf tournaments with prizes donated by a vast number of area businesses and community groups. A special cake made each year proves to be a hot ticket item as well as it raised $350 during the first year, $550 the second and $1,400 this year.

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