Category Archives: Health & Genetics

Temperament vs Genetics Dr. Karen Overall

Today we’re sharing a link to Pure DogTalk’s podcast about the genetics of temperament by Dr. Karen Overall, Senior Research Scientist at the University of Pennsylvania.

Click the title to go to the podcast and enjoy the learning!

Sally Gift, Mesa AZ

Feature photo by Bob Segal

Temperament vs Genetics

Dr. Karen Overall, Senior Research scientist at the University of Pennsylvania

Temperament in purebred dogs plays a vital part in how the dogs fit into their families and society. Along with that comes the inevitable nature vs nurture argument. In other words, does separation anxiety, for example, have a genetic basis or is it caused by well-intentioned but misguided owners.

According to Dr. Karen Overall, it’s some of each.

“It was a lot more complex than what we thought’”

Research in purpose bred working dogs indicates that genetics are responsible for 30 percent of a dog’s behavior, with environment, at some level, responsible for the rest.

“When you look at a pedigree, if 50 percent of dogs in that family line have a variant of a certain condition, the chances are that there’s a genetic contribution to that,” Overall said, “especially if that condition has been identified in another species, if that model exists, chances are that pedigree is representative of an increased risk that’s genetic.”

OVERALL AND THE “SPINNING DOG”

Overall’s work is the baseline for many in the field of behavioral medicine. Her books and protocols are used in clinics around the country. But she describes her work here as sort of an “accidental tourist.” She planned to work in strictly research until a residency in behavioral medicine introduced her to a dog who couldn’t quite spinning… for two and a half hours.

“That dog said to me, whoa, this is interesting, this looks like human OCD,” Overall said. “There’s a good chance it has a genetic basis. There are a number of clear cut behavioral concerns that look to have genetic predispositions.”

Overall has dedicated her career to researching and teaching owners of pets with behavior issues. “Education may not work, may not take,” Overall said. “But that doesn’t give you the option to not do it. Without it, guaranteed, what you have is ignorance.”

BEHAVIOR MODIFICATION PROTOCOLS

This dedication to behavior medicine has paid off for Overall. She has developed and promotes protocols which help clients address and overcome with behavior modification. And she has identified seven “risk genes” that approach significance in the field.

In all the instances Overall discusses, the genetic basis is polygenic and influenced by the environment. And she notes that frequently the phenotypical disease is not actually expressed due to the dog not experiencing a triggering environment.

“I think they’ll put it on my tombstone, ‘It was a lot more complex than what we thought”.

She added that many of what we as breeders and owners identify as behavioral issues are linked with performance and the jobs the dogs were designed to do.

“In those cases, there has been selection for the job, selection against the extremes of pathology, but not that midrange,” Overall noted. “There has been no ‘cost’ to enhancing the behavior.”

RELAXATION TOOL

Amongst the tools Overall has provided to owners and breeders is this type of protocol for creating a “relaxed” dog in various situations. Please investigate the various links for more information on her amazing work. Enjoy today’s conversation, with valuable insight from one of the country’s foremost practitioners in behavioral medicine and research.

https://www.boulderhumane.org/sites/default/files/ProtocolforRelaxation.pdf

http://www.akcchf.org/educational-resources/podcasts/podcast-transcripts/Dr-Karen-Overall-Separation-Anxiety.pdf

http://www.journalvetbehavior.com/article/S1558-7878%2806%2900115-8/abstract

https://www.aaha.org/professional/resources/behavior_management_guidelines.aspx

https://www.boulderhumane.org/sites/default/files/ProtocolforRelaxation.pdf

Blastomycosis – Fungal infection August

Blastomycosis – A Potentially Lethal Fungal Infection in Our Pets

Christopher G. Byers, DVM, DACVECC, DACVIM (SAIM), CVJ

When most folks think of infection, they think of bacteria. Yet not all infections are caused by bacteria. Many infections are caused by other infectious organisms, including fungi. If you live in certain parts of the United States, fungal infections are actually quite common. One of the more common fungal infections is called blastomycosis. This week, I’ve dedicated some time to disseminating some helpful information about this infection. Happy reading!

blastomycosis

Blastomycosis – What is it?

Blastomycosis is a fungal infection caused by a fungus called Blastomyces dermatitidis. This fungus is predominantly found in North America while occurring only sporadically in Central America, Africa, India, and Europe. Within the terrestrial borders of North America, certain regions have a preponderance of the fungus, particularly the Mississippi, Ohio, Missouri, Tennessee, and St. Lawrence river valleys.

blastomycosis

Blastomyces dermatitidis is found in two distinct forms – as yeast and mycelia. Mycelia are found in the environment; as they grow, mycelia form segments called conidia (also known as spores) that are ultimately inhaled by our pets. At body temperature, conidia transform and grow as yeast in the lungs, specifically terminal airways. After establishing an infection in the lungs, the fungus disseminates to other areas through blood and lymph vessels, particularly to the following regions/organs:

  • Skin
  • Eyes
  • Bone
  • Subcutaneous tissues
  • Lymph nodes
  • Nostrils (called nares)
  • Brain
  • Testicles

Blastomycosis – What does it look like?

Both dogs and cats may become infected with blastomycosis after 5-12 weeks of incubation.. In dogs, large breeds are more commonly affected than small breeds. Sporting breeds are over-represented, likely due to the fact they are brought to high-risk areas to hunt and work more frequently. Males are more frequently affected than females. In cats, there is no age, breed, or sex predilection.

Common clinical signs in dogs include:

  • Reduced (or loss of) appetite
  • Weight loss
  • Cough
  • Labored breathing
  • Lameness
  • Skin lesions
  • Nasal discharge
  • Eye changes
  • Depression

Clinical signs are similar in cats. Breathing changes, skin lesions, vision changes, and weight loss are most commonly reported.

blastomycosis

Blastomycosis – How is it diagnosed?

After gathering a complete medical history and performing a thorough physical examination, a veterinarian will recommend testing to confirm their clinical suspicion of blastomycosis. Testing may include:

  • Complete blood count / biochemical profile / urinalysis
  • Evaluation of cells from skin lesions (cytology and/or biopsy)
  • Urine antigen testing
  • Antibody screening
  • Chest radiographs (x-rays)
  • Abdominal sonography
  • Airway sampling

Pet parents may find it helpful to partner with a board-certified veterinary internal medicine specialist to develop a cost-effective and logical treatment plan.

Blastomycosis – How is it treated?

Blastomycosis should be treated with an antifungal medication. Common drugs that may be prescribed include:

  • Itraconazole
  • Fluconazole
  • Amphotericin B

Treatment is prolonged, often more than two months’ duration. In general, the prognosis for patients who are promptly and effectively treated is good. Dogs with central nervous system involvement typically die but treatment is occasionally successfully. Dogs with marked lung involvement carry a more guarded prognosis with 50% of dog succumbing to infection within the first week of treatment. Approximately 25% of dogs will experience a relapse after treatment. The relapse typically occurs within six months.

The take-away message about blastomycosis in dogs & cats…

Blastomycosis is a meaningful fungal infection in many parts of North America. Clinical signs reflect the organ(s) affected by infection, and may including coughing, appetite changes, skin lesions, and eye changes. With prompt identification and treatment, prognosis is good.

To find a board-certified veterinary internal medicine specialist, please visit the American College of Veterinary Internal Medicine.

Wishing you wet-nosed kisses,

CriticalCareDVM

CriticalCareDVM

FDA List Dog Food Brands Linked to Heart Disease

Dog food brands most linked to heart-disease reports named

U.S. FDA tallies 560 dogs affected since 2014

VIN News Service

June 27, 2019 By Edie Lau; Lisa Wogan

The U.S. Food and Drug Administration today for the first time publicly identified the pet food brands most frequently associated with cases of dilated cardiomyopathy (DCM), a serious and potentially fatal heart disease. The vast majority of cases involve dogs, but a few cases involving cats have been reported, as well.

In an update on its investigation into the potential link between certain diets and canine DCM, the FDA listed 16 pet food brands that have been named in 10 or more reports of the disease.

The top three brands are Acana, named in 67 reports; Zignature, named in 64 reports; and Taste of the Wild, named in 53 reports.

Starting in 2014 and through April 30, 2019, the FDA has received reports of 560 dogs and 14 cats diagnosed by veterinarians to have DCM. Of those, 119 dogs and five cats have died.

Not included in the figures are counts from “the many general cardiac reports” the agency received that did not involve a diagnosis of DCM. “However,” the FDA said, “this case information is still valuable, as it may show heart changes that occur before a dog develops symptomatic DCM.”

DCM is a condition resulting in an enlarged, weak heart that cannot pump blood efficiently. Dogs with DCM may tire easily, cough and have trouble breathing. More dramatically, they might exhibit sudden weakness, collapse, faint or die with no warning.

The large majority of reports received by the FDA were made in 2018 and 2019. The agency has been investigating the problem since last year. It announced in July that it had learned of cases of DCM in dogs eating certain pet foods, many labeled as “grain-free” and containing as main ingredients peas, lentils, other legume seeds (known as pulses) and/or potatoes.

While particular dog breeds are known to be genetically predisposed to DCM — breeds such as Doberman pinscher, Great Dane, Newfoundland, boxer, Irish wolfhound and cocker spaniel — many of the affected dogs were not of those breeds. That is what caught veterinary cardiologists’ attention early on.

The cause of the problem is unknown, and most researchers investigating the problem suspect the answer won’t be easy to identify. The FDA cannot say with certainty that diet is the culprit, although in an investigation update posted in February, the agency reported that some dogs diagnosed with DCM improved simply by changing their diet. Other investigators have reported similar observations.

At that time and again today, the FDA said: “Based on the data collected and analyzed thus far, the agency believes that the potential association between diet and DCM in dogs is a complex scientific issue that may involve multiple factors.”

Because of the uncertainty, the agency has not asked the companies behind the implicated brands to recall them. “We have shared case report information with these firms so they can make informed decisions about the marketing and formulation of their products,” the FDA wrote in a Q&A on its canine DCM investigation.

The agency added, “We are also sharing this information with the public, but encourage pet owners to work with their veterinarians, who may consult with a board-certified veterinary nutritionist, prior to making diet changes.”

In analyzing ingredients and ingredient proportions of the identified diets eaten by affected animals, FDA researchers have found that more than 90% of implicated products were “grain-free,” meaning they did not contain corn, soy, wheat, rice, barley or other grains. Ninety-three percent contained peas and/or lentils.

Early on, some veterinarians investigating the problem posited that novel animal protein sources in diets, such as kangaroo, bison or duck, might be a factor. But in its latest update, the FDA reported: “The most common proteins in the reported diets were chicken, lamb and fish; however, some diets contain atypical protein sources such as kangaroo, duck and bison. No one animal protein source was predominant.”

The FDA said most of the identified foods in the canine cases are dry formulations, but not all. There also are raw food, semi-moist food and wet foods reported.

A representative from one company owning a frequently implicated brand expressed concern about the issue while questioning the premise that its formulations could be culpable.

Dr. Alexia Heldman, director of veterinary affairs for Diamond Pet Foods, which owns Taste of the Wild, said in a telephone interview, “Over the last year, there have been a lot of theories …. Where we are now, there are more questions unanswered than there were a year ago.”

Heldman said Taste of the Wild is the largest brand of grain-free food, noting that 29 million bags have been sold in the U.S. since September 2017.

She said that 53 reports of disease cases should be considered in the context of sales. “If the numbers were presented as a percentage of bags sold, we would be at the other end of the list,” Heldman said.

At the same time, the numbers aren’t inconsequential, she said. “I certainly want to make sure we don’t in any way minimize what those pets and pet owners have been through.”

Heldman has taken some of the calls made to the company by affected pet owners. “It is devastating. My heart really does break when I talk to pet owners. I and everyone else at the company really hate that this is happening.”

Heldman noted that Taste of the Wild formulations have been largely unchanged during the past four to five years. “[H]ow did this come out of nowhere?” she wondered.

The FDA wonders the same. “Another puzzling aspect of the recent spike in DCM cases is that they have occurred just in the last few years,” the agency wrote in today’s update.

It noted that formulation is not the only possible variation: “The FDA is working with the pet food industry to better understand whether changes in ingredients, ingredient sourcing, processing or formulation may have contributed to the development of DCM.”

Diamond Pet Foods encourages veterinarians and pet owners who have questions or concerns to contact them, Heldman said. The company number is 800-342-4808. “We take meticulous notes, because we want to share with everyone, especially the FDA, anything that we can do to help potentially figure out what is truly going on,” Heldman said. “It’s a top priority.”

Similarly, Pets Global, owner of the Zignature line, said in a prepared statement, “Ensuring the health of all our pet customers continues to be our top priority.”

The statement also says in part: “While the vast majority of our customers thrive with our high quality, grain-free pet formula, we are taking the FDA’s recent announcement very seriously. As such, we have created a dedicated customer care line (888-897-7207) so we can understand more to further ensure the safety of all pets. As the FDA said in its release, it still does not have enough information to fully understand these cardiac issues. Any pet owners or veterinarians who have information on this matter are strongly encouraged to contact our dedicated customer care line backed by our team of veterinary experts and nutritionists.”

Mike Fuccillo, a spokesperson for Champion PetFoods, which owns Acana, the most frequently named brand on the list, and Orijen, another brand on the list, said the company had no comment.

Jennifer Fiala contributed to this report.

URL: //news.vin.com/doc/?id=9164603

Feature photo courtesy of Bob Seagal

Osteosarcoma: Beyond Amputation and Euthanasia

Veterinary Practice News

Osteosarcoma: Beyond amputation and euthanasia

When amputation is not an option, please don’t go straight to euthanasia

March 12, 2019 1:00 pm

[1]
Osteosarcoma of the radius in an eight-year-old Labrador.

When a patient is diagnosed with osteosarcoma, we tend to focus on three options:
• the “gold standard,” i.e. amputation with or without chemotherapy;
• what many call palliative care, meaning pain medication and rest; or
• euthanasia.

But what if amputation is not an option? What if chemotherapy or radiation is out of the owner’s financial capabilities? Or a couple of medications are not enough to numb the pain? What if visible metastasis to the lungs is already present?

Bob Stein, DVM, pain management guru and founder of the Veterinary Anesthesia & Analgesia Support Group (www.vasg.org), recently shared another valid option.*

“With my suggested approach, we can often provide quality of life to even large-breed dogs for six to 12 months and sometimes more than 20.”

Let’s detail Dr. Stein’s protocol.

Pamidronate

Pamidronate, a bisphosphonate, is an injectable drug that is inexpensive and easy to administer (ref: TM Fan et al. JVIM 2007). It helps to reduce pain (in 30 to 50 percent of patients), inhibit bone osteolysis, and has potential cancer-suppression effects by impeding proliferation and inducing apoptosis. The drug has a wide safety margin and can even be used on patients with renal or liver insufficiency. While side effects such as esophagitis, allergic reactions, and gastritis have been described, Dr. Stein has not yet observed those adverse effects at his practice. Note: If pamidronate is backordered when you read this, use zoledronic acid instead.

NSAIDs

NSAIDs are a mainstay in pain management, but they are not particularly well suited to the management of bone cancer pain. Dr. Stein hopes NSAIDs can contribute, but consistently utilizes them for their antiangiogenic, cancer-suppressant properties. They also help with pain related to degenerative joint disease (DJD) in other limbs and discomfort related to weight shifting.

Tramadol

Tramadol has been shown multiple times to be unpredictable and, generally speaking, ineffective when managing canine pain, so we won’t dwell on it. When reaching for a reuptake inhibitor, Dr. Stein chooses amitriptyline or duloxetine as noted later in this column.

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Gabapentin

Several studies have been conducted to prove the effectiveness and safety of gabapentin. Like amitriptyline and duloxetine, gabapentin is better suited to bone cancer pain than NSAIDs. Initially used to treat seizures, gabapentin treats pain by blocking calcium channels. Patients with osteosarcoma receive a starting dose of 10 mg/kg three times daily, but Dr. Stein increases the dose as rapidly as tolerated to as high as 60 to 70 mg/kg three times daily. Due to gabapentin’s nonlinear pharmacokinetic profile, it is very difficult to overdose gabapentin, but you can see lethargy and sedation if you increase the dose too quickly.

Trazodone

Our patients are unaware they have a life-threatening disease. If their activity needs to be slowed down, prescribe trazodone. It doesn’t play well with tramadol (yet another reason not to use tramadol), but works well with gabapentin to provide safe and effective sedation. Use with caution, if at all, when utilizing a reuptake inhibitor like tramadol, amitriptyline, or duloxetine.

Cymbalta

Cymbalta (duloxetine), a serotonin reuptake inhibitor (SNRI), has been shown to provide pain control by increasing serotonin in synapses. Care must be taken to ensure there are no drug interactions with other medications, such as aspirin or over-the-counter supplements the patient may be on.

Amitriptyline

Amitriptyline, a tricyclic antidepressant, can be used to treat neuropathic pain via a broad variety of mechanisms. Unlike tramadol, amitriptyline can be effective when dosed twice daily. Doses as high as 3 to 4 mg/kg twice daily may be required for peak analgesic benefit.

Amantadine

Initially used as an antiviral medication, amantadine is a N-Methyl-D-aspartate (NMDA) receptor inhibitor. It can disrupt the nervous system response to prolonged pain signaling. Also showing evidence of chronic osteoarthritis pain alleviation, this drug can be used for relieving osteosarcoma-related pain.

Food

What we feed a cancer patient is more important than most pet owners realize. Food can either “feed” the cancer or help “starve” it, while boosting the immune system. Prescription diets for cancer patients offer:
• Low levels of carbohydrates (sugar is blamed with “feeding” cancer cells)
• High levels of protein, fat, and omega-3 fatty acids

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Weight control

Weight control is critical in cancer patients. Many veterinary professionals believe weight loss and cachexia are a classic consequence of cancer. Until the disease takes over, being overweight is a far greater risk. Quite often, the owner feels bad for their dog’s fate and tends to use food to offer comfort. Sadly, extra weight puts extra pressure on joints. In addition, adipose tissue releases cytokines that can exacerbate a multitude of inflammatory processes, including DJD, which can contribute to discomfort.
Weight maintenance or weight loss should be a critical part of the discussion regarding a cancer patient. Remember to include serial weight checks and follow-ups to tailor the food amount to your patient’s needs.

Supplements

Glucosamine, chondroitin, injectable supplements, and methylsulfonylmethane (MSM) have been recommended to help with arthritis present in joints unaffected by cancer.

Omegas

Not all omega-3 fatty acids are created equal. There is a lot of over-the-counter junk. Proper manufacturing and conservation are critical to prevent the supplement from becoming rancid. According to Dr. Stein, docosahexaenoic acid (DHA) supplementation can provide anti-angiogenesis properties. Calculate the dose of various supplements with a free calculator located at http://www.vasg.org.**

Harness

Using a harness, such as Help ’Em Up, can help owners lift or support dogs with osteosarcoma in a back leg. It can also alleviate extra strain on the back end when a front limb is affected. An effective harness also reduces the likelihood the client will be injured while assisting their dog.

Physical therapy

As osteosarcoma progresses, weight shifting can cause strain to the other limbs. Physical therapy and massage can lessen the impact of the increased load.

Acupuncture,  myofascial trigger point needle therapy

Needle therapy can be part of a multimodal program for pain control. Acupuncture has been shown to boost beta-endorphins, which are the body’s natural opioids. Acupuncture also can help reduce chemotherapy-related gastrointestinal side effects, such as vomiting, diarrhea, and nausea. Myofascial trigger point needle therapy can relieve the painful contracture knots that often form when muscles are overtaxed or injured.

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Others

Countless other modalities, including Reiki, have been recommended to help fight cancer, along with all kinds of nutritional supplements. Claims include cancer growth inhibition and overall support. We will leave it up to you to pick and choose what you believe in. Working with a veterinarian who is familiar with these modalities is recommended. Laser, however, is not recommended anytime cancer is suspected or proven.

When amputation is not an option, please don’t go straight to euthanasia. As Dr. Stein suggests, using some of the modalities mentioned here can significantly improve a patient’s quality of life, as well as their longevity.

Phil Zeltzman, DVM, DACVS, CVJ, Fear Free Certified is a board-certified veterinary surgeon and author. His traveling surgery practice takes him all over Eastern Pennsylvania and Western New Jersey. You can visit his websites at http://www.DrPhilZeltzman.com and http://www.VeterinariansInParadise.com. AJ Debiasse, a technician in Stroudsburg, Pa., contributed to this article.

References
* VIP conference, April 2018, Cabo, Mexico (www.VeterinariansInParadise.com).
** http://vasg.org/drug_delivery_calculators.htm and bit.ly/2R7fDsL

Source URL: https://www.veterinarypracticenews.com/osteosarcoma-beyond-amputation-euthanasia/

Spay-neuter considerations to maximize health

Feature photo by Bob Segal, Illinois

VACCINATION AGAINST CANINE CANCER STUDY

Thank you Barbara Manson, Stoughton WI for bringing this to our attention!

Attention all Gordon Setter owners – our breed is included among those being recruited for this study. If interested, follow the link below to submit your information online.

Sally Gift, Mesa AZ

VACCINATION AGAINST CANINE CANCER STUDY

UW Veterinary Care’s Oncology Service is recruiting dogs for the Vaccination Against Canine Cancer Study (VACCS trial), the largest clinical trial conducted to date for canine cancer.

The goal of the VACCS trial is to evaluate a new vaccine strategy for the prevention, rather than treatment of dogs with cancer. Healthy dogs of certain breeds, 6 to 10 years old, will be randomized to receive either a series of vaccines similar to other routine vaccines that are given to dogs currently, or placebo vaccines. Dogs will live at home and be checked 2-3 times yearly for 5 years after enrollment. A financial incentive will be offered to defray the cost associated with diagnostics and treatment of any cancers that dogs develop, regardless of whether they are receiving vaccine or placebo.

In addition to potentially providing a new strategy for cancer prevention in dogs, if successful, this study could provide important justification for eventually looking at a similar approach in humans.

TO QUALIFY, DOGS MUST MEET THE FOLLOWING CRITERIA:

  • Owners must live within 150 miles of one of the participating trial sites
    • University of Wisconsin–Madison · Madison, Wisconsin
    • Colorado State University · Fort Collins, Colorado
    • University of California–Davis · Davis, California
  • Age: 6 to 10 years old
  • Weight: 12 pounds (5 kg) or more
  • No history of previous cancer
  • No significant other illness that could result in a life span of less than 5 years
  • No history of previous autoimmune disease
  • No current treatment with oral or injectable immunosuppressive medications such as prednisone, cyclosporine, mycophenolate, or tacrolimus

THIS TRIAL IS NOW BEGINNING THE PATIENT ENROLLMENT PROCESS.

If you believe your pet meets the study criteria and would like to receive more information, please click the button below to enter your contact details and preliminary information about your dog.

A member of the Oncology team will contact you within a week of your entry to collect further information and schedule an appointment.

Questions? To learn more about this study, please email us: vaccs@vetmed.wisc.edu.

DOGS MUST BE ONE OF THE FOLLOWING BREEDS:

  • Mixed Breed
  • Afghan Hound
  • Airedale Terrier
  • Alaskan Malamute
  • Basset Hound
  • Beagle
  • Bernese Mountain Dog
  • Borzoi
  • Boston Terrier
  • Boxer
  • Briard
  • Bullmastiff
  • Cocker Spaniel
  • Corgi
  • Deerhound
  • English Setter
  • Field Spanie
  • Flat-coated Retriever
  • French Bulldog
  • German Shepherd
  • German Shorthaired Pointer
  • Giant Schnauzer
  • Golden Retriever
  • Gordon Setter
  • Great Pyrenees
  • Irish Setter
  • Irish Water Spaniel
  • Irish Wolfhound
  • Italian Spinone
  • Keeshond
  • Labrador Retriever
  • Leonberger
  • Newfoundland
  • Norwegian Elkhound
  • Nova Scotia Duck Tolling Retriever
  • Old English Sheepdog
  • Petit Basset Griffon Vendeen
  • Rhodesian Ridgeback
  • Rottweiler
  • Saluki
  • Scottish Terrier
  • Shetland Sheepdog
  • Siberian Husky
  • Springer Spaniel
  • Staffordshire Bull Terrier
  • Standard Poodle
  • Tibetan Terrier
  • Viszla
  • Welsh Terrier
  • West Highland White Terrier

FDA Investigating Potential Connection Between Diet and Cases of Canine Heart Disease

My heart goes out to a member of our Gordon Setter community who lost her beautiful Gordon companion to canine dilated cardiomyopathy (DCM). Her heart is broken. Learning, while doctoring to save her Gordon, that the food she had so carefully chosen to ensure her Gordon’s health and longevity, cost him his life instead, added unbearable pain to an already devastating loss.

We want you to be aware that DCM caused by diet has been confirmed in our beloved breed.

Sally Gift, Mesa AZ

Link between Diet and Canine Heart Disease

July 12, 2018

The U.S. Food and Drug Administration is alerting pet owners and veterinary professionals about reports of canine dilated cardiomyopathy (DCM) in dogs eating certain pet foods containing peas, lentils, other legume seeds, or potatoes as main ingredients. These reports are unusual because DCM is occurring in breeds not typically genetically prone to the disease. The FDA’s Center for Veterinary Medicine and the Veterinary Laboratory Investigation and Response Network, a collaboration of government and veterinary diagnostic laboratories, are investigating this potential association.

Canine DCM is a disease of a dog’s heart muscle and results in an enlarged heart. As the heart and its chambers become dilated, it becomes harder for the heart to pump, and heart valves may leak, leading to a buildup of fluids in the chest and abdomen. DCM often results in congestive heart failure. Heart function may improve in cases that are not linked to genetics with appropriate veterinary treatment and dietary modification, if caught early.

The underlying cause of DCM is not truly known, but is thought to have a genetic component. Breeds that are typically more frequently affected by DCM include large and giant breed dogs, such as Great Danes, Boxers, Newfoundlands, Irish Wolfhounds, Saint Bernards and Doberman Pinschers. It is less common in small and medium breed dogs, except American and English Cocker Spaniels. However, the cases that have been reported to the FDA have included Golden and Labrador Retrievers, Whippets, a Shih Tzu, a Bulldog and Miniature Schnauzers, as well as mixed breeds.

Diets in cases reported to the FDA frequently list potatoes or multiple legumes such as peas, lentils, other “pulses” (seeds of legumes), and their protein, starch and fiber derivatives early in the ingredient list, indicating that they are main ingredients. Early reports from the veterinary cardiology community indicate that the dogs consistently ate these foods as their primary source of nutrition for time periods ranging from months to years. High levels of legumes or potatoes appear to be more common in diets labeled as “grain-free,” but it is not yet known how these ingredients are linked to cases of DCM. Changes in diet, especially for dogs with DCM, should be made in consultation with a licensed veterinarian.

In the reports the FDA has received, some of the dogs showed signs of heart disease, including decreased energy, cough, difficulty breathing and episodes of collapse. Medical records for four atypical DCM cases, three Golden Retrievers and one Labrador Retriever, show that these dogs had low whole blood levels of the amino acid taurine. Taurine deficiency is well-documented as potentially leading to DCM. The Labrador Retriever with low whole blood taurine levels is recovering with veterinary treatment, including taurine supplementation, and a diet change. Four other cases of DCM in atypical dog breeds, a Miniature Schnauzer, Shih Tzu and two Labrador Retrievers, had normal blood taurine levels. The FDA continues to work with board certified veterinary cardiologists and veterinary nutritionists to better understand the clinical presentation of these dogs. The agency has also been in contact with pet food manufacturers to discuss these reports and to help further the investigation.

The FDA encourages pet owners and veterinary professionals to report cases of DCM in dogs suspected of having a link to diet by using the electronic Safety Reporting Portal or calling their state’s FDA Consumer Complaint Coordinators. Please see the link below about “How to Report a Pet Food Complaint” for additional instructions.

Additional Information

Let’s Talk Linebreeding

“One of the most bandied about terms among breeders today seems to be linebreeding. Despite it’s widespread use, however, linebreeding is frequently misunderstood and miscommunicated; in fact, it is not altogether uncommon for an outcrossed pedigree to be mistakenly viewed as linebreeding by the novice. The present discussion defines linebreeding and how we can more accurately define our linebred litters.”

From – “Let’s Talk Linebreeding” written by Claudia Waller Orlandi, Ph.D. published in ‘Tally Ho’ the Basset Club of America Newsletter (July-August ’97). The online article may be found by clicking here.

(While this article was written with the Basset Hound breeder in mind, one can change the name to  Gordon Setter, or any breed for that matter, as the material is “one size fits all” when it comes to the topic of breeding.)

Linebreeding and Inbreeding: A Family Affair

Inbreeding and Linebreeding involve the mating of animals within the same family. Breeding relatives is used to cement traits, the goal being to make the offspring homozygous (pure) for desirable characteristics. Homozygous dogs tend to be prepotent and produce offspring that look like themselves (Walkowicz & Wilcox 1994)

Willis (1989) defines Inbreeding as the mating of animals “more closely related to one another than the average relationship within the breed.” Inbred pairings would include brother/sister (the closest form) father/daughter, mother/son, and half-brother/half-sister.  Linebreeding involves breeding relatives other than the individual parents or brother and sisters. Typical linebred matings are grandfather/granddaughter, grandmother/grandson, grandson/granddaughter, great-grandmother/great-grandson, uncle/niece, aunt/nephew and cousin crosses. Linebreeding is a less intense form of inbreeding. Because of their focus on a dog’s potential genetic contribution, inbreeding and line breeding are termed genetic breeding systems.

figure-1-genetic-breeding-systems Definition:  For a dog to be linebred there must be an ancestor in the pedigree that is common to both the sire and the dam.  Figure 2 illustrates this concept. Kelly is linebred because the dog, Brahms, appears twice in the sire’s side and once in the dam’s side of the pedigree.figure-2-linebreedingCommon Misconception:  A pedigree may show either the sire and/or the dam to be linebred but no ancestor common to both the sire and dam. This is outcrossing, not linebreeding (see figure 3).  Similarly, because the same kennel prefixes (Windy, Hill, Castle) are common to both the sire’s and dam’s ancestors, the newcomer may mistakenly view the pedigree as linebreeding.figure-3-outcrossingWhere to draw the “Line”?

Breeders do not always agree on what constitutes linebreeding, with some feeling that common ancestors within the first five or six generations is linebreeding. Willis (1989) indicates that the farther back linebreeding is in a pedigree the less intensive it will be, pointing out that a dog appearing 12 times (out of a possible 32) in the 6th generation of a pedigree would have a Coefficient of Inbreeding (CI) of only 1.8% (by comparison, a sire to a granddaughter cross has a CI of 12.5%). The CI tell us the proportion of genes for which the inbred ancestor is likely to be homozygous, that is carrying the same genes from each parent. (Remember that homozygous animals have a higher potential for reproducing themselves.) In Willis’s (1992) view, a common ancestor farther back than the 2nd or 3rd generation will have little influence on the litter. Linebreeding beyond the fourth generation has even less genetic impact.

How much bang will we get for our buck (or Basset!)

Several modern writers (Walkowitz & Wilcox 1994; Willis 1992, 1989; Onstott 1962) view linebreeding and inbreeding as essentially the same  and differing only in degree of intensity. Whether one considers inbreeding and linebreeding to be the same or feels they are two distinct breeding systems, quantifying the degree to which an animal is linebred (or inbred) provides important information regarding its potential genetic contribution. As Willis (1989) states: “When describing inbreeding [or linebreeding] breeders often say their dog is inbred or linebred without further qualification. This is a very inadequate description. We need to know which dog the animal is inbred [linebred] to and the degree of inbreeding [linebreeding].” Put another way, how much “bang” will we get from our linebreeding?

Describing your Basset’s linebred pedigree: reading, writing and a little arithmetic!

Willis (1992) suggests that a concise yet meaningful way to express the extent of linebreeding (inbreeding) is to number the generations of the animal in question. The common ancestor(s) is assigned the generation number as he/she appears in the pedigree. The parents are the first generation (1), the grandparents are the second (2), great grandparents are the third (3), great-great-grandparents are the fourth (4) and so on.

As previously stated, Kelly’s pedigree (Figure 2) is an example of  linebreeding, with Brahms appearing on both the sire’s and dam’s side. On the sire’s side Brahms appears twice in the third generation (3). We can write this as 3.3. On the dam’s side, Brahms appears once in the second generation (2) and this is written simply as 2. Willis has suggested the following written and verbal formats for expressing the extent of line breeding in a pedigree:

Written Format

We would write: “Kelly is linebred on Brahms 3.3/2”

Verbal Format

We would say: “Kelly is linebred on  Brahms three, three TO two.”

In the Written Format notice we separate the sire’s and dam’s side of the pedigree by using a slash mark (think of a pencil making a slash mark); in the Verbal Format the word “TO” is used to separate the sire’s and dam’s side (think of talking “to” someone). This verbal and written format tells us the dog on which Kelly is linebred and the extent of the linebreeding. Smaller numbers indicate that a dog is more closely linebred; larger numbers of 4 and above (Willis 1989) indicate a lesser extent.

Linebreeding and pedigrees: a final caveat

Linebreeding and inbreeding are essentially the same, differing only in the degree of intensity. (In Willis’s view, the common ancestors beyond the 2nd and 3rd generations will not greatly influence the resulting litter.) We have described the ease with which an animal’s extent of linebreeding may be expressed by means of written and verbal models. Perhaps this format will be “adopted” by those Basset Hound breeders whose interest lies in linebreeding. In addition to facilitating the description of a linebred pedigree over the phone, it certainly provides important information regarding the potential outcome of a breeding. In this regard, two things bear repeating: (1) linebreeding (and inbreeding) are only as viable as a breeder’s knowledge of basic genetics (a topic which will be addressed in future columns) and (2) a linebred pedigree is only as valuable as a person’s ability to determine the virtues and faults of the dogs it contains. When we add the final ingredient of rigorous selection hopefully we are on the way to producing better Basset Hounds!

References

Onstott, K. 1980. The New Art of Breeding Better Dogs. Howell, New York.

Walkowicz, C. and Wilcox, B. 1994 Successful Dog Breeding. Howell, New York.

Will, M.B. 1968 A simple method for calculating Wright’s coefficient of inbreeding. Rev. Cubana Cienc.Agric. (Eng.Ed.) 2: 171-4

Willis, M.B. 1989 Genetics of the Dog. Howell, New York

Willis, M.B. 1992. Practical Genetics for Dog Breeders. Howell, New York

For more articles about breeding by Claudia follow the link below.

These articles were written by Claudia Waller Orlandi, Ph.D. All have been published in ‘Tally Ho’, the official newsletter of the Basset Hound Club of America

Thank you to Barbara Manson, WI for sharing this link with us.

Sally Gift, Mesa AZ

Photography by Susan Roy Nelson

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Musings on Color

The following includes many excerpts from the article “Musings on Color” published on the blogspot Musings of a Biologist and Dog Lover written by Stephanie.

I’ve added my own thoughts and comments to embellish and round out the information for the Gordon Setter lover and breeder.

Setters 1805 - sydenham-edwards-the-setter-1805
This 1805 depiction of “setters” appears in the Cynographia Britannica. Note the black and tan setter and the red setter with the white face. The white dogs was also considered a Setter and it is speculated that these may all be litter mates.

Musings of a Biologist and Dog Lover

Sunday, July 1, 2012

The Gordon setter is one of a small number of setter breeds, which also includes the English setter, Irish setter, and Irish red and white setter. Though the Gordon Setter now only comes in one acceptable color, the breed’s history included a number of other colors that are now considered to be mismarks. Part of why these colors are in the breed is due to its relationship with the other setters. So, what are these mismarks?

Dogs with more or less than than required in the standard  

*Based on the current breed standard the Gordon Setters depicted in this artwork from the 1940’s carry too much tan.

Inherited on the Brown locus, a dog must be bb to be liver

Liver Gordon
Liver colored Gordon Setter

 

Inherited on the Extension locus, a dog must be ee to be recessive red

Barn hunt image 2
Red Gordon Setter

 

Inherited on the Spotting locus, a dog with a variety of genotypes can have too much white

Looking at these mismarks, they are all recessively inherited except in dogs that are genetically solid but have too much residual white. All of theses colors were well known when the breed was young. Much like the Irish setter, the predominant color in the early years of the breed is actually not what you think it would be when looking at modern dogs. Gordons were once mostly tricolor with some dogs being solid black and tan, liver, or red, but the white markings and other colors fell out of favor and led to the production of the breed you see today.

The current breed standard for the Gordon only allows for black and tan dogs with specific tan markings. Dogs that are anything other than black and tan are disqualified and anything more than a small bit of white on the chest is not allowed. A dog with more or less than the required tan would be penalized, despite the fact that tan markings can vary greatly on dogs that are all genetically tan pointed. So far, it is known that there are modifiers that control this amount of tan, but it isn’t known where they are or how they are inherited.

This is a case where color standard is based on, basically, fashion. What once was popular was no longer liked by those who wrote the breed standard, and thus those other colors faded into obscurity. However, since the colors are basically all recessively inherited, they continue to pop up on occasion in litters that are born today. These past decisions are really problematic when looking at the breed’s history and what this holds for the future.   Stephanie


Sally says…It is at this point that as a breeder of Gordon setters I would step in to say that I disagree with Stephanie’s call that the Gordon’s color standard (black and tan) is based on fashion and that this preference is problematic for the breed.

The color preference written into the standard was developed well over a century ago by avid bird dog breeders. They didn’t have an eye to fashion when it came to writing their standard, but they did know exactly what kind of dog they wanted to hunt over, as well as why those traits, written into the standard, were important to them. It has been my understanding that the vivid black and tan coloring of the Gordon Setter may have been written into the standard as the preferred color because of it’s contrast to the gold, tan and red foliage of the fall hunting season, the black dog contrasting, standing out against the fall foliage, making it far easier for the hunter to follow the dog while he worked the field. A red or buff dog, even a white and tan dog would more easily blend into the foliage, his coat acting to camouflage him as he worked the field. And, with the deaf link to the white gene it is certainly understandable why white was weeded out as an allowed color.

If there are other history buffs out there who can offer more insight as to the color preference we’d love to hear your thoughts and hope you’ll share those and any references for us in the comment section of this article.

Anita Aronsson, Sweden shared this stunning link to photos of Gordon Setters in many colors and patterns, be sure to check it out by clicking here!

We’d also welcome your photos, if you have some to share, of red, liver, or other mismarked Gordons to be shared here to help others learn.  Please email those to us at gordonsetterexpert@gmail.com, we will respect your privacy and photos can be published anonymously.

Charlie Royster was kind enough to share this example of Gordon Setter color photo with usColor example

Sally Gift, Mesa AZ

 

 

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Death by a Thousand Health Tests

Food for thought is always a good thing, at least in my world, it keeps my mind open to new ideas. As I’ve aged I’ve found it’s ever more important not to get stuck in my ways and thinking about what other people have to say on a topic keeps me out of ruts.  So when I read the article I’m sharing with you today about health testing, I found myself thinking. Now, a word of warning, some of my close friends would tell you, “Sally’s thinking takes some rather weird detours now and again, so when she says “I was thinking” you might wanna run for cover!”

We all talk about being a responsible breeder, and of course, we consider a part of that responsibility to be health testing of the parents. Now mind you, I’m getting to that place where I’m almost old as dirt, so I’m one of those breeders who started in the game long before the majority of the health tests of today were available. While I’m all for health testing to gain knowledge of what is in the genes I’m about to mix together, I’m also one of those breeders who will tell you to use a good ole dose of common sense when breeding. While I’d never throw health testing to the side, I am also realizing that as the population of Gordon Setters declines, so follows our number of breeding options. This is a big conundrum we face folks, and it will take dedication, smart decisions and some good old common sense to preserve the best of our breed.

Sally Gift, AZ              Photograph by Susan Roy Nelson, WY

With that said, I don’t know as I agree with everything in this article, but I do know it will give you some food for thought so I’m sharing, for your reading and thinking pleasure.  If you’d like to share your thoughts after reading this feel free to use the comment section!

Breeder On The Edge

Death From a Thousand Health Tests by Amanda Kelly

AUTHOR:  A dedicated hobby breeder in a terminally rare breed, Amanda Kelly perpetually finds herself on the edge of everything from ecstasy to bankruptcy, quitting and insanity.

I had a really interesting conversation with a geneticist the other day that got me thinking: science is offering us more and more great ways to evaluate the health of our dogs…but when does enough turn into too much? When do we cross the threshold from helpful information to complete paralysis? Or outright bankruptcy? How do we avoid both?

Prioritization
The test we were discussing is quite a new one in my breed (Toy Manchester Terriers). It is for a condition called Xanthinuria that causes dogs to form a very rare form of kidney stone. There have only been three clinically affected dogs that I am aware of (full disclosure: we bred one). After encountering the issue, a fellow breeder did a little digging and discovered that a marker associated with the condition in humans worked for our breed as well. Kudos to her for being proactive and finding out more! The American and Canadian breed clubs helped proof the test and voila, it is now available commercially at quite a reasonable cost.

When I looked at dogs in my own breeding program that came up as carriers however, I was surprised as I would have expected more of our puppies to have or be forming stones than was the case.  So, what does that say about the disease? Do all affected puppies form stones? If not, what is the rate?  I found the answers to those Qs simultaneously helpful and troubling.

Apparently, current thinking is that approximately 50% of males with two copies of the mutation form stones or have associated kidney issues, while very few females with the same status have a problem (likely because they do a better job of emptying their bladders). Now, these are just rough estimates because the disease as a whole is rare and hasn’t been extensively studied, but it does raise an important question: what are we as breeders to do with this information and associated results of the genetic test?

The Jigsaw
The simple fact is that the more tests we have, the more pieces of info we have to try and reconcile when planning a breeding. At present, Toy Manchester breeders as a group are variously clearing things like hips, patellas, eyes, thyroid, and hearts plus DNA testing for von Willebrand’s Disease, and, now, potentially xanthinuria. That’s 7 tests, some with questionable value based on anecdotal and surveillance evidence, if we’re being honest. We’re also actively working to identify a test for juvenile cardiomyopathy.

The end result of all of that testing is a ton of information, which is great from the perspective of evaluating the health of individual dogs but also creates a number of very real problems for breeders in areas like liability, reputation and cost.

In the past, these factors were certainly in play but their effects were somewhat muted. Breeders worked for years to learn about their breed and their lines so they could make informed decisions and minimize the risk of producing issues. Health tests initially concentrated on measuring phenotype as an indicator and we worked with what we had. The important thing was that we could confidently tell puppy buyers we had done everything possible to produce healthy, happy puppies and if a problem appeared we were solid in the knowledge we had used all available tools to their best advantage.

Enter the genetic test. In my breed, the first one was for von Willebrand’s Disease (a blood clotting disorder). For years this disease was monitored by assay testing that measured the actual amount of the specific type of clotting factor in the blood and projected genetic status based on corresponding ranges. It was a pain to do but everyone muddled through as it was one of the few standard health tests most breeders did in the 1980s and 90s. When the genetic marker was identified, some breeders lost their ever loving minds. Dozens of valuable dogs were promptly spayed and neutered while breeders across North America began making pronunciations about “never” breeding a carrier even to a clear.

There’s no question, needless damage was done to the gene pool — especially when you consider there had never been a documented case of a Manchester actually bleeding out because it was vWD affected (at least not one I am aware of). Eventually breeders learned how to work with the DNA results and things calmed down. Our new test allowed us to easily avoid producing “affected” puppies (i.e., a dog with two copies of the gene, not necessarily clinically affected) and, regardless of the actual effects of the condition itself, doing so quickly became “right” and “just”.  It was an approach we ourselves endorsed and followed because, after all, “responsible breeders” test.

And thus, the line in the sand was drawn. It’s a line we in the dog community drew ourselves and it’s one most of us dare not cross.

Unlimited Liability
The scientific advancements that brought us more genetic tests took place against an active backdrop that included the rise of animal rights, increasing anthropomorphization of pets, emergence of puppy lemon laws, and the advent of social media. Now, it may seem odd to bring those factors into a discussion of genetic testing, but they each play a very important role in describing the environment within which we are working. An environment that values reputation above all else and that pits breeding decisions against financial liability in a way many breeders don’t consider.

Any breeder with two licks of sense knows that when it comes to breeding dogs, the most important possession you have — more important than any ribbon you may ever win — is your reputation. Your reputation affects everything you do, from access to stud dogs and puppies to demand for same. In a subjective sport like ours, it can even affect your ability to succeed in the show ring.

Protecting, fostering and growing a reputation can become all-consuming. Let’s cut to the chase here: We’re operating in an environment that can make a competition out of anything — which is why sometimes reputation management, and by extension health testing, becomes as much about one upmanship and moral superiority as it is the well-being of the dogs in question. That probably explains why many of the tests done in my breed are done by rote…because they are available, not because we have objectively identified a need for them. Not because we have established that rates of thyroid problems or eye issues, for example, are any higher in our breed than in the general dog population. No, we do them because we can and because we feel (tell one another?) that we should. And why is that? It’s because we have established as fact within our community that good breeders test and bad breeders don’t. So, we all work extra hard to make sure our conduct is above reproach.

That core belief is just as strong outside of the dog community, where we have worked hard to battle animal rights messaging by establishing health testing as a key feature differentiating responsible breeders from backyard breeders. And it’s a great message — easy to understand and easy for the public to actively measure when they are talking to breeders. The trouble is, that message comes pre-loaded with expectations we can never live up to. Expectations that if you buy from a good breeder your dog will never ever have health issues. That health tested parents won’t produce problems. That responsible breeders can be God.

And therein lies the problem. The more health testing we do, the bigger the gap grows between public expectations and the reality of what we can deliver…and with it, our financial liability. Because hey, don’t forget, in addition to health testing, responsible breeders also guarantee their puppies. Whether through provision of a replacement puppy or return of purchase funds, those guarantees do carry financial risk and can’t be dismissed at the best of times and even less so as puppy lemon laws increasingly make puppy health a legal matter. So, tell me…how do you think small claims court would view a breeder that knowingly produces a problem? Or one that unknowingly produces one because they failed to use the tests available? It’s a perfect catch 22 in the making.

Risk Reduction
It’s a simple axiom that the more health testing available, the less we talk about what we’re trying to avoid producing and the more we talk about what we are willing to risk producing. There isn’t a perfect dog out there and every biological organism possesses deleterious genes for something, regardless of whether we can test for it or not.  The more tests available, the more complicated planning breedings becomes because we all naturally want to avoid the chances of producing any problem at all.  But is that a realistic goal?

What did I say we were up to in my breed – seven tests? Eight? Heck, even I lose track sometimes. And all of these tests in an era when the number of puppies being produced continues to drop at an alarming rate. Under 200 Toy and Standard Manchester Terriers “combined” were produced in North America last year, so I’m sure you can image how difficult it might be to match test results for potential breedings (particularly if we’re testing for everything under the sun). Or what the costs of doing those breedings might be as we look further and further afield, let alone the relative cost of doing the health screening to begin with in a breed with relatively small litter sizes and low purchase prices. The financials would rock your world and have you questioning my sanity, so we won’t go there other than to say red is a better quality in a new coat than a ledger (but I digress…).

I asked a few researchers and vets what they felt breeders should do with test results when there are many to consider.  The consistent response was that we need to prioritize — and that’s a completely reasonable thing for a scientist to say…and a very difficult thing for a devoted dog breeder to actually do.

Never mind the costs, appearance or liability — I genuinely don’t want to be responsible through conscious decision for producing a sick puppy. It is one thing to employ testing, tools and techniques to theoretically reduce disease and quite another to look at a plethora of results and say “This one I can live with.”

And what happens once the die is cast?  If we use Xanthinuria as an example, I could choose to breed two carriers together and test all of the puppies…but then what? Sure, knowing a puppy has two copies of the gene and is at higher risk of forming stones will be helpful to an owner who could keep the dog on a low purine diet and perhaps avoid issues altogether…but could I sell a puppy like that? For how much? Would anyone take it if I was giving it away? What level of financial responsibility do I hold if it does develop an issue two, five or 10 years down the road? What if there are multiple puppies with two copies of the gene in the litter?

And that, ladies and gentlemen, is the ethical dilemma of the future.  Perhaps we in smaller, rarer breeds are dealing with it sooner, but it is a dilemma I truly believe every breed and breeder will face at some point.  It has the potential to be absolutely paralyzing as we seek to do the right thing in a world where that is increasingly less black and white than it seemed a few short years ago.

I don’t know exactly how we can or should approach it — perhaps I’m hoping you’ll be able to tell me. I suspect that monitoring of actual breed health through health surveys and breeders sharing information on what they are seeing will be increasingly important if we wish to prioritize according to real information. And I do know that one of the things we absolutely must do is change how we discuss health testing. The way we talk about each other (oh Lordy, put a star next to that one!) and to each other as well as how we portray ourselves to the public. Just as important, we have to think about health tests and results holistically in the context of our breed and gene pool. In our rush to erase problems through testing, we are shown again and again that the devil we don’t know is often worse than the devil we can test for.

What To Do?
This article isn’t intended to form the cornerstone of a campaign against health testing. Far from it. I truly believe we need to use the tools available to us, particularly if they are able to help us avoid devastating issues facing our dogs and puppies. In fact, I and others in my breed have worked hard for more than a decade to see a genetic test developed for juvenile cardiomyopathy because it is a brutal, deadly disease and I want all of us to have a tool that will allow us to make informed choices and stop guessing at how to avoid it.

But I’m also a realist. Health management is a tough nut to crack even for trained geneticists let alone the average breeder doing their best to navigate an increasingly complex and technical landscape. Giving us the test results is the easy part, it seems — figuring out what to do with them is our next great challenge.

Blastomycosis—What Every Dog Owner Needs to Know – Life with Llewellin Setters

Blastomycosis, or Blasto as it is often called, is a very serious and potentially deadly, systemic fungal disease that can affect dogs, humans, and other mammals. Blasto is caused by inhaling the spores of the fungus Blastomyces dermatitidis. B. dermatitis grows as a mold in acidic, organically rich …

Source: Blastomycosis—What Every Dog Owner Needs to Know – Life with Llewellin Setters