Reprinted with Permission
This article first appeared in the July 2003 issue of the AKC Gazette and is reprinted with permission.
To ensure the best results in your breeding program, it is vital to recognize symptoms and treat affected dogs.
Your prize titled champion has been diagnosed with hypothyroidism. You worry if the dog can fully recover. Happily, a small pill given twice daily produces improvement, even a disappearance of symptoms. The dog regains vitality, energy, and luster. You sigh with relief. Life can return to normal. Or can it?
Do you put this dog back in the show ring or the field? Have you identified and eliminated possible environmental stressors that triggered the initial signs of disease? Do you switch from commercial kibble to raw foods or home cooking? Do you measure annual titers instead of revaccinating? Is your dog genetically predisposed to thyroid disease? Have you researched the pedigree for inheritance factors? Have you already bred this dog? Can you breed away from this problem? Will you breed the dog now that lifelong medication is required? What are the consequences of breeding dogs with thyroid disease? How you answer these medical and ethical questions will depend on your understanding of the thyroid gland and the diseases that hormonal dysfunction causes and perpetuates. Although thyroid research has developed diagnostic tools and painless treatment, breeders must still make though decisions, adjusting their breeding programs to ensure the health of their dogs and safeguard the reproductive viability of their breed.
The thyroid gland secretes hormones through the blood, affecting the entire body from the smallest cell to the most complex system. Thyroid function regulates metabolism. When a healthy thyroid transmits the correct amount of hormone, body processes and activities are energized, stimulating tissue protein production and cellular oxygenation. When thyroid malfunction occurs, hormonal levels typically fall and metabolic rates decline, altering growth, maturation, and potentially all parts of the body. Outward changes in weight, musculature, excretion, skun, coat, mood, and sensory sensitivity are apparent. Other, more serious internal changes are less observable.
According to W-Jean Dodds, DVM, [Director of the Kerry Blue Terrier Foundation and] a pioneer in thyroid research and a specialist in hematology and immunology, hypothyroidism-the most common thyroid disease-can affect all major organs and systems of the body. Isolated symptoms do not always indicate thyroid disease, but a trend toward ill health or a combination of abnormal factors should alert the conscientious breeder to consider this important gland. A complete blood thyroid panel will confinn or deny a provisional diagnosis.
Veterinarians traditionally measured total T4 (free plus protein-bound thyroxine) in the blood as the sole indicator of thyroid disease. Most experts now realize that T4 results alone can misrepresent the presence or absence of disease because thyroxine, when protein-bound, is influenced by other diseases or drugs active in the body. Advances in hematology and endocrinology have yielded several diagnostic tools that detect thyroid disease in its initial stages of inflammation (thyroiditis) as well as in its later stages (hypothyroidism), when the gland has significandy reduced or ceased hormonal secretion. Specific thyroid function/blood profiles, measuring total T4, total T3, free T4, free T3, and their autoantibodies (T4AA and T3AA), are available through major commercial veterinary laboratories. University veterinary diagnostic labs also provide such vital assays as TSH and TRH stimulation and TgAA measurement (canine thyroglobulin autoantibody), a key component when pinpointing the genetic form of thyroid disease.
Not all thyroid diseases are inheritable or autoinummebased. The gland may become irritated and normal hormonal production interrupted by other diseases, such as Cushing-'s (hyperadrenocorficism); by potentiated sulfonamide antibiotics or combined worm-and-flea preventives; by diets with chemical preservatives or ones too rich in iodine; or by overuse of combination vaccines including rabies. But genetics plays a key role when a dog is diagnosed with autoinimune lymphocytic thyroiditis or idiopathic primary hypothyroidism. In fact, a dog may have autoimmune thyroiditis for years before showing clinical signs of hypothyroidism.
Raymond F. Nachreiner, DVM, a dedicated veterinary researcher at Michigan State University's Animal Health Diagnostic Laboratory, stresses the necessity of TgAA testing when clari~dng the cause-and-effect relationship between autoimmune thyroiditis and hypothyroidism. "Dogs with autoimmune thyroiditis have a positive TgAA," says Nachreiner. "This disease is the most common cause of hypothyroidism (50 percent in most reports), but new data indicate that many of the 45 percent of hypothyroids classified as idiopathic are actually in the end stage of autoimmune thyroiditis. Hence, as many as 95 percent of hypothyroids may be a result of autoirnmune thyroid disease and can be detected early in life with the TgAA procedure."
Breeders no longer have to play Russian roulette with their breeding programs, viewing each litter as a test breeding. Instead of waiting for clinical signs of disease to develop, routine testing of breed stock and offspring alleviates genetic uncertainty when the inheritance mode is unclear or susceptibility for immune disease becomes increasingly regular. "With the tightly linebred pedigrees we have in most breeds today," says Dodds, "it would be very difficult to distinguish autosomal recessive inheritance of thyroiditis from incomplete dominance." Until a gene test is available, the best approach is breeding only to TgAA-negative dogs to reduce the prevalence of thyroid disease. "When breeding positive dogs," says Nachreiner, "the offspring will be carriers, assuming an autosomal recessive trait." By knowing which dogs in a pedigree are TgAA-positive, carriers can be predicted. Dodds agrees: "The best way to curtail the spread of this genetic disease is to eliminate known TgAA-positive dogs from breeding stock."
Some breeds are so thoroughly affected that breeders feel they must breed healthy-looking, TgAA-positive stock. Nachreiner notes that this practice persists among rare breeds with small gene pools. Dodds argues against this practice when the gene pool is large and TgAA-negative stock is available. Even with rare breeds, worldwide shipping of semen from healthy TgAA-negative stock is possible. Maintaining the genetic vitality of a breed must take priority over phenotypic breeding. Acquiring championships does not justify the proliferation of immune-compromised animals, especially now that testing is so accessible and assessing breed stock is a matter of simple mathematics.
Breeding decisions can be made with greater knowledge and certainty by testing puppies at puberty. Dodds recommends testing females during the first anestrus; after maiden heat. Both dogs and bitches should be tested annually, from 1 year of age through their breeding years, to monitor the lifespan of a breed specimen as well as validate the health of a bloodline and its evolving pedigree over several generations.
Because thyroid disease can emerge at any age, continuing to test is important Dodds cites a large English Setter family in which several great-granddams tested negative annually until age 10, when they began testing positive. "Each of these dams has produced offspring and great-offspring with significant thyroiditis," says Dodds, who promotes the whole thyroid profile plus TgAA for all breeding stock. "Without measuring T3AA and T4AA, you will definitely miss those few dogs that are consistently positive on T3AA and/or T4AA but are consistently TgAA-negafive."
Ignorance Is Not Always Bliss
Canine thyroid disease is not new. Familial occurrence of thyroiditis in Beagles was studied in 1968. Decades of ignorance and unfortunate breeding decisions have propagated widespread thyroid problems, particularly in the larger breeds. According to a 1997 AKC health survey of national breed clubs, hypothyroidism ranked among the top three diseases and was often the number-one complaint in every breed of the Sporting, Hound, Working, Terrier, Non-Sporting, and Herding groups. When hypothyroid dogs are bred generation after generation, other diseases can be exacerbated. "Almost all cells of the body are target tissues for thyroid hormones," Nacbreiner explains, "so bleeding disorders may be worse if the dog is also hypothyroid, or dermatologic condidons may be more severe because of a slowed immune system in the presence of hypothyroidism." Dodds has documented many cases in which thyroid dysfunction generated or worsened aggression, aberrant behavior, and seizure conditions, indicating a link between thyroid hormones and the central nervous system.
Dodds's breed databases can demonstrate the consequences of breeding without thyroid screening: More offspring of subsequent generations become affected, and disease is manifested at increasingly earlier ages in successive generations. In her Old English Sheepdog study, polyglandular autoimmunity (multiple genetic endocrine disease) occurred with concurrent diagnoses of thyroiditis and Addison's disease, rheumatoid arthritis, autoimmune hemolytic anemia, or immune (idiopathic) thrombocytopenic purpura. Dodds found "typically two pups in litters affected with one or more of these diseases; then three generations later, it bad increased to five to seven pups. In one specific breeding, all seven pups in a litter were sick by age 2 years.
Most alarming is the effect of hypothyroidism on the reproductive system. Nachreiner's experiments have not proven any abnormalities, but Dodds's clinical data closely links infertility and hypothyroidisrn. She attributes her findings to "an abnormal (inflamed and damaged) thyroid gland that somehow causes a misdirected message to the reproductive organs through the pituitary/hypothalamic axis, which regulates the neuroendocrinehormonal cycles in the body." When normal cycles of reproduction are disrupted, the eventual result is extinction -- first of families and bloodlines, then breeds, finally species.
Accentuate the Positive
With almost 35 years' experience in Giant Schnauzers, Christine Lietzau, a breeder-owner-handler of conformation, obedience, and schutzhund champions, acknowledges that in the early 1970s "most of the time a thyroid problem went unrecoggnized until textbook symptoms such as hair loss, weight gain, cold intolerance, and infertility began to appear." She lists typical excuses given by uneducated breeders: A dog becoming heavy or stocky has matured; a bitch hasn't become pregnant because of bad timing; hair loss around the eyes is from a dog rubbing its face against a crate.
In Lietzau's breeding experience, the inheritance factor seems unpredictable. She has bred thyroid normals and produced affected offspring; she has bred affected but antibody-negative animals to normals and ended up with normals. Lietzau draws the line at breeding "dogs or bitches that show high antibodies in T4, T3, or thyroglobulin." She tests her own stud dogs annually and only breeds to bitches with normal test results within the past year. Mostly linebreeding with some outcrossing, Lietzau has produced only two hypothyroid puppies out of 25.
Susan Ralston, a veterinarian and breeder of Rhodesian Ridgebacks, is on the health committee of the Rhodesian Ridgeback Club of the United States (RRCUS). At the breed's national specialty, the committee presents expert speakers and organizes blood draws for thyroid screening. The RRCUS has worked closely with canine geneticist George Padgett, who estimates that 36 percent of Ridgebacks are carriers. "The exact mode of inheritance is unknown at this time, but it appears to be recessive and probably polygenic," says Ralston. She echoes Dodds's concern about vaccination. Hounds often exhibit greater sensitivities than other breeds. Ralston cites the Michigan State study that found dogs with abnormally high TgAA for a period of time following, routine vaccination when given combination shots. She supports the recommendation that thyroid screening panels be run within two to eight weeks after vaccination.
Veterinary medicine has taken much of the guesswork out of breeding. Utilizing research results, testing all breed-stock and progeny, removing from a breeding program and neutering those animals who don't fit basic health standards, and working with the genetic odds all aid breeders in reducing the incidence of disease. If the goal of breeding is to constantly improve one's stock and strive to attain the ideal, it is a breeder's obligation to place internal health on a par with extemal beauty.
Leslie Crone Rugg is the author of five novels and has edited several breed-oriented magazines and newsletters.
Clinical Signs of Canine Hypothyroidism
Cornpiled by W. Jean Dodds. DVM
Alterations in Cellular Metabolism
- mental dullness
- exercise intolerance
- neurologic signs
- weight gain
- cold intolerance
- mood swings
- stunted growth
- chronic infections
- laryngeal paralysis
- facial paralysis
- "tragic" expression
- knuckling or dragging feet
- muscle wasting
- head tilt
- drooping eyelids
- dry, scaly skin and dandruff
- oarse, dull, or "puppy' coat
- bilaterally symmetrical hair loss
- "rat tail"
- seborrhea or greasy skin
- pyoderma or skin infections
- chronic offensive skin odor
- lack of libido
- testicular atrophy
- prolonged interestrus interval
- absence of heat cycles
- silent heats
- weak, dying, or stillborn pups
- slow heart rate (bradycardia)
- cardiac arrhythmias
- bone marrow failure
- low red blood cells (anemia), low white blood cells, low platelets
- corneal lipid deposits
- corneal ulceration
- dry eye (keratoconjunctiyitis sicca)
- infections of eyelid glands (Meibomian gland)
- Vogt-Koyanagi-Harada syndrome
Other Associated Disorders
- IgA deficiency
- loss of smell (dysosmia)
- loss of taste
- chronic active hepatitis
- other endocrinopathies: adrenal, pancreatic, parathyroid
Natural Glandular Therapy of the Hypothyroid Dog
by Shawn Messonnier, DVM
Conventional therapy for hypothyroidism, the most common canine Gendocrine disorder, uses synthetic thyroid hormone (usually L-thyroxine) to treat the disease. Although synthetic hormones are among our safest medications, many pet owners prefer a more natural therapy. Glandular therapy uses whole animal tissues or extracts tissues for treating diseased glands and is "tissue specific" therapy (liver extracts benefit the liver, thyroid extracts benefit the thyroid gland). The glandular macromolecules are absorbed from the digestive tract into the blood and exert their biologic effects on target tissues.
Several studies show that radioactively tagged cells, when injected into the body, accumulate in the target tissues. Accumulation is more rapid in traumatized body organs or glands than in healthy tissue, which may indicate an increased requirement for those ingredients contained in glandular supplements. For example, animals with thyroid cell damage showed rapid uptake of thyroid glandular cells with active regeneration of the damaged thyroids.
Glandular supplements are a source of active lipids and steroids. They may also provide specific nutrients including hormones and other chemical constituents; function as a source of enzymes that encourage hormone production of hormones; and help maintain health or fight disease.
Most hypothyroid dogs can benefit from treatment with glandular therapy. The supplement may help support the thyroid gland in a more natural way than chemically synthesized conventional medications and can usually be administered safely on a long-term basis for the majority of pets.