pei daze fall 2008.p1-25 - dog shows by design

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1 Volume 12, Issue 4 Official Publication of Star of the North Chinese Shar-Pei Club Fall, 2008 PEI PEI PEI PEI-DAZE DAZE DAZE DAZE Our new website is up!! STAR OF THE NORTH CHINESE SHAR-PEI CLUB WEBSITE http://www.starofthenorthsharpeiclub.com/ THANKS TO WEBSITE COMMITTEE MEMBERS Arlene Dannemiller, Kay Harney, Barb Hartman & Kate Kester, And to Deb Walker who is keeping the site updated each month* FOR ALL YOUR WORK ON THIS PROJECT Deadline for monthly site update information will be the 15th of every month. Send items for website to Deb at [email protected].

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Page 1: Pei Daze Fall 2008.p1-25 - Dog Shows By Design

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Volume 12, Issue 4 Official Publication of Star of the North Chinese Shar-Pei Club Fall, 2008

PEIPEIPEIPEI----DAZEDAZEDAZEDAZE

Our new website is up!! STAR OF THE NORTH CHINESE SHAR-PEI CLUB WEBSITE

http://www.starofthenorthsharpeiclub.com/ THANKS TO WEBSITE COMMITTEE MEMBERS

Arlene Dannemiller, Kay Harney, Barb Hartman & Kate Kester, And to Deb Walker who is keeping the site updated e ach month*

FOR ALL YOUR WORK ON THIS PROJECT Deadline for monthly site update information will b e the 15th of every month.

Send items for website to Deb at [email protected] om.

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STAR OF THE NORTH CHINESE SHARSTAR OF THE NORTH CHINESE SHARSTAR OF THE NORTH CHINESE SHARSTAR OF THE NORTH CHINESE SHAR----PEI CLUBPEI CLUBPEI CLUBPEI CLUB

PEIPEIPEIPEI----DAZEDAZEDAZEDAZE

Editor: Peggy O’Hare (320) 963-7705 [email protected]

Send articles, notices and items to: Editor, Peggy O’Hare 8221 Griffith Ave NW Maple Lake, MN 55358

[email protected]

Director Linda Jokela (2007-2008) 15375 - 110th Street Foreston, MN 56330-9526 (320) 294-5897 [email protected] Director Beth Haas (Term 2008-2009) 17949 Wedgewood Dr Zumbrota, MN 55992 (507) 732-5201 Director Barbara Hartman ( 2006-2008) 5362 Logan St SE Rochester, MN 55904 (507) 281-2679 [email protected] Director Judy Hetland (Term 2008-2009) 2722 Aldrich Ave No Minneapolis, MN 55411 (612) 588-1206 [email protected]

STAR OF THE NORTH CHINESE SHAR-PEI CLUB

BOARD DIRECTORS

Director Vicki O’Neill (Term 2007-2008) 4506 50th Avenue SE Rochester, MN 55904 (507) 282-9753 [email protected] Director Deb Walker (Term 2008-2009) 7748 Unity Ave N Brooklyn Park MN 55443 763-503-3439 [email protected]

Rescue Committee

Cate Stewart (763) 682-9196

[email protected]

Beth Haas (507) 732-5201

[email protected]

STAR OF THE NORTH CHINESE SHAR-PEI CLUB

BOARD OFFICERS President Cate Stewart (2007-2008) 2374 Dempsey Ave NW Buffalo, MN 55313 (763) 682-9196 [email protected] Vice-President Cindy O’Hare (Term 2008-2009) 8221 Griffith Ave. NW Maple Lake, MN 55358 (320) 963-7705 [email protected] Treasurer Carole Sorensen (2007-2008) 2515 - 50th Ave SE Rochester, MN 55904-9002 (507) 289-5368 [email protected] Secretary Peggy O’Hare (Term 2008-2009) 8221 Griffith Ave. NW Maple Lake, MN 55358 (320) 963-7705 [email protected]

INSIDE THIS ISSUEINSIDE THIS ISSUEINSIDE THIS ISSUEINSIDE THIS ISSUE SECTION 1

Welcome New Member ----p.3 Dates To Remember --------p.3 Trophy Donors Thanks - p.4-5 September Rochester Specialty Winners -------p.6-10 Rochester Fund Raiser--- p.11 Club Products-------------- p.12 New CHIC Chick---------- p.13 HEALTH & OUR PEI -- p.14 FSF --------------------- p.14-15 Amyloidosis ----------- p.16-17 Plan of Action for Amyloidosis ----------- p.18-20 BEHAVIOR ---------- p.21

Your Dog’s Body Language--------- p.21-25 Thyroid Testing

Answers --------------p.25

INSIDE THIS ISSUEINSIDE THIS ISSUEINSIDE THIS ISSUEINSIDE THIS ISSUE Get Well Wishes------------p.42 Upcoming Dog Shows-----p.43 Birth Announcements-----p.43 Birthday Greetings ----p.44-48 Breeze-----------------------p.44 Legend, Deuce, Will ----- p45 Malcolm & Asia ----------p.46 Diva, Dani, Lacey -------- p47 Jackie Chan & Xander--p 48 In Memoria -------------p.49-53 Matt -------------------------p.49 Logan -----------------------p.50 Malcolm --------------------p.51 Lucy -------------------------p.52 Daisy ------------------------p.53 Ringing News ---------------p.54

INSIDE THIS ISSUEINSIDE THIS ISSUEINSIDE THIS ISSUEINSIDE THIS ISSUE Special Brag at Sun Tea--p.55 What A Performance -p.56-57 Membership Renewal Form-------------------------- p58 New Member Application----------------- p. 99

INSIDE THIS ISSUEINSIDE THIS ISSUEINSIDE THIS ISSUEINSIDE THIS ISSUE SECTION 2

Rescue News------------ p.27-30 Ti’s Story ----------------- p.27 Dewey NotAPei ---------- p.28 Newton Update ---------- p.28 Minnie & Mazie --------- p.28 Sally’s Story------------- -p.29 Chocolate The Sable---- p.29 Sydney Then & Now --- p.30 New Therapy Dog Deuce ---------------------- p. 31 Holiday Safety -------- p. 32-33 It’s The Law—BSL --- p.34-38 New Arrivals ----------- p.39-40 What’s Up With Our Members -------------- p. 41-42 Carole’s New Champ -- p.41 Martha’s Beau Tox ----- p.42

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Melissa Allard is a new member sponsored by Cate Stewart. Melissa and her two rescue Pei, Beauty and Jazzy, live in Blaine, Minnesota. Melissa is interested in rescue, public education, obedience and agility.

Beauty Allard Relaxing Jazzy Allard in her red snuggy

Melissa Allary with Jazzy & Beauty

Beauty and Jazzy Allard

Beauty and Jazzy with mom and dad, Melissa & Mike

A Nominating Committee has been appointed to secure nominations for the following positions on the Star of the North Board of directors: Position Person Currently Holding The Position President Cate Stewart Treasurer Carole Sorensen Director Barbara Hartman Director Linda Jokela Driector Vicki O’Neill For further information contact: Nominating Committee Chair: Beth Haas,@ [email protected]

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Event Date Location Annual Meeting & Winter Party Jan 10, 2009, 1p.m. Barb Hartman’s Home, Rochester

Watch email and website for further details

Our sincere thanks go out to everyone who contributed to our Specialty Show Trophy Fund!

You make it possible for Star of the North to show our appreciation to exhibitors who show the Pei who will become the sires and dams of our future generations of beloved Pei. The purpose of the conformation dog show is to present dogs who represent the very best characteristics of their breed. It is these wonderful dogs who will pass on their health, beauty and temperament to the next generation of Shar-Pei.

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Sept. 12, 2008 Star of the North Chinese Shar-Pei C lub Specialty Show

Best of Breed, Etched Glass Trophy ..................................................offered by Cindy O’Hare, Riverwind Shar-Pei. Best of Opposite Sex, Etched Glass Trophy .......................................offered by John and Cate Stewart,

Nordic Star Shar-Pei To our past, present and future champions. High In Trial, Etched Glass Trophy...................................................... offered Cheri Katzung

in memory of: Mintcreek Have Gun Will Travel CD, RA, CGC - "Paladin" - forever in my heart

Best of Winners, Etched Glass Trophy ............................................... offered by Barbara Hartman, XingFu SharPei, in honor of all our Pei who have gone to the Bridge.

Winners Dog, Etched Glass Trophy .................................................... offered by Linda Jokela, Jokela Shar-Pei Reserve Winners Dog, Etched Glass Trophy .....................................offered by Jean Woodring. Winners Bitch, Etched Glass Trophy...................................................offered by Kate Kester, Roka Shar-Pei

in honor of Roka Veterans Reserve Winners Bitch, Etched Glass Trophy ....................................offered by Kate Kester, Roka Shar-Pei

in honor of Roka Veterans Best Junior Handler, $15 Target Gift Certificate .................................offered by Wayne Harmon, Award of Merit, Etched Glass Trophy..................................................offered by Carole Sorensen Best Veteran, Etched Glass Trophy ....................................................offered by Arlene Dannemiller -

Sun Tea Shar-Pei in memory of Tsi Mai Main Man of Bang *Maynard*

First Place 7-9 yr Veteran Dog, Glass Trophy.....................................offered by Kay Harney in memory of Grayland's No Mystakin

First Place 7-9 yr Veteran Bitch, Glass Trophy ...................................offered by Kay Harney,

In Memory of Grayland’s No Mystakin First Place 9-10 yr Veteran Dog, Glass Trophy................................... offered by Lee and Nancy Annett,

in Honor of Annie and Java First Place 9-10 yr Veteran Bitch, Glass Trophy ................................offered by Kay Harney,

In Memory of Grayland’s No Mystakin First Place 10+ yr Veteran Dog ................................... , Glass Trophyoffered by Lee and Nancy Annett,

in Honor of Annie and Java First Place 10 + yr Veteran Bitch ................................... Glass Trophyoffered by Vicki O’Neill, Jihlo Shar-Pei Best Puppy in Match, Etched Glass Trophy.......................................offered by Arlene Dannemiller -

Sun Tea Shar-Pei To the future of our breed. Best Opposite Sex Puppy in Match, Etched Glass Trophy .................offered by Kate Kester – Roka Shar-Pei

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CH O-Na-Pei Trip Around The Sun, owned and handled by Dorothy Schuer-man, Springfield, IL took Best In Sep-cialty Show, September 12, 2008 No Picture Available.

Furrows Jolly Jac-O-Lantern, bred, owned and handled by Susan Beck took Best Veteran. Sorry no picture available.

CH China Fleet’s Nordic Breeze, owned and handled by Cate Stewart, taking Best of Opposite Sex

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Topline Thor, bred, owned and handled by Tim & Nancy Bergeron, took Winners Dog September 12, 2008 Sorry no picture available.

Oak Lane’s Secret Treasure (Cairo), bred by Liz Forss & Beth Haas, co-owned & handled by Kris Henning took Winners Bitch and Best of Winners September 12, 2008.

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Arlene Dannemiller and CH Sun Tea If I Could Only Win Your Love (Emmy Lou) taking an Award Of Merit at the Star of the North Specialty in Rochester, Minnesota September 12, 2008.

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Cherie Katzung and Mintcreek’s Indy’s Full Circle t aking High In Trial at the Star of the North CSPC Specialty Show in Rochester. Septemb er 12, 2008.

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Topline Queen of the Universe (Rhea), owned by Tim and Nancy Bergeron, took Best Opposite in Match September 12, 2008.

Destiny’s Fire It Up (Torch) at home telling everyone about his Best In Match win at the Star of the North Specialty Show in Rochester, MN on September 12, 2008

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Huge thanks to everyone who worked so hard to make the Specialty, the fund-raiser and the party a huge success!.

Pictured above is a portion of the Star of the North fund raiser table at the Rochester Show

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Our club logo as seen in this ad embroidered on t-shirts, fleece pull-over shirts with neck zipper, and hooded sweat-shirts with zippered front. Gray T-shirts sm-xlg, $15.00 Black Fleece shirts med, large $15.00 Gray Hooded sweat-shirts $30.00 Save on Shipping charges by picking up products at club events! Order now!

Product Size Quan-tity

Unit price Shipping Total

Gray T-Shirt $15.00 $5.00

Black Fleece Shirt $15.00 $5.00

Gray Hooded Sweat-Shirt $30.00 $5.00

Send orders to: Carole Sorensen 2515 - 50th Ave SE Rochester, MN 55904-9002 [email protected]

Gray Only- Gray Only-

Black Only-

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Cate Stewart is proud to announce that Breeze (CH C hina Fleet’s Nordic Breeze) is the latest CHIC Chick at Star of the North!!! Breeze passed all of her OFA, Thyroid and CERF requ irements to be-come CHIC certified. Hugh Congratulations Cate!

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The following information is intended to raise awar eness levels, not to prescribe medical treatment or offer self diagnosis. The following articles hig hlight some of the more notable health problems. Responsible owners and breeders should be aware of these health concerns and try to eliminate them using pedigree analysis and careful selection of breeding partners. Never embark on treatment of any type without consu lting your Veterinarian!

It has been some time since we have published anything about the two major health issues in our breed. Many new Pei people in the club are not familiar with the symptoms of FSF and Amyloid. Thus as 2008 draws to a close, it seems appropriate to re-publish the articles by Dr Jeffrey Vidt on Familial Shar-Pei Fever and Amyloidosis.

Familial Shar-Pei Fever Familial Shar-Pei Fever (FSF) is a hereditary inflammatory disorder seen in Shar-Pei. It is inherited as an autosomal recessive condition. Clinical signs: Episodic fever is the most important and consistent clinical sign of this disorder. The temperature commonly is in the 105-107°F range. The fever is generally self-limiting lasting 12-36 hours. Another common clinical sign often accompanying the fever is swelling of a joint, usually the hock (tibiotarsal) joint and is known as Swollen Hock Syndrome (SHS). This painful, hot swelling can also in-volve the carpus (wrist) and the lips. Dogs with FSF are sick -- they are reluctant to move and when they do walk they have a charac-teristic "walking on eggs" gait. They often are painful in the abdomen and have a characteristic "roached" back. Pathogenesis: What we do know about this disease is as follows:

Shar-Pei with FSF have increased levels of the cytokine Interleukin-6 (IL-6). IL-6 is involved with the fever response and and is an integral part of triggering the production of Acute Phase Reactant Proteins by the liver. IL-6 is also involved in the Sys-temic Inflammatory Response Syndrome (SIRS). Dysregulation of IL-6 is the cause of much of the disease in Shar-Pei with FSF. IL-6 also plays a major role in the body's stress response and serves to "prime" the immune system.

Shar-Pei with FSF are at risk from early death from systemic amyloidosis. About 25% of the FSF dogs will develop renal failure including renal amyloidosis -- a smaller percentage will develop hepatic amyloidosis. This is usually seen in Shar-Pei between the ages of 2-5 years of age. They also seem more susceptible to immune-mediated kidney disease such as membranous glomerulonephritis, protein-losing glomerulopathies, DIC, thromboembolic phenomena such as mesenteric, splenic and pul-monary embolism and Streptococcal Toxic Shock Syndrome (STSS).

FSF in Shar-Pei was hypothesized to be an animal model of Familial Mediterranean Fever (FMF) in humans. Recent work indicates this is not true, although FSF is very similar to FMF in man.

FSF is a heredofamilial disease with a genetic basis. It appears to be inherited as an autosomal recessive condition. Laboratory Findings: Unfortunately there are no blood test, etc. which are specific for FSF. During a fever episode there will often be an increased white blood cell count, an increase in liver enzyme levels and other non-specific findings. Work done by Dr. Gary Johnson at the University of Missouri College of Veterinary Medicine to develop a DNA blood test to screen for the disease was unsuccessful and the research effort will still continue. Treatment: It is very important to monitor the temperature in this condition. Initially, fever can be treated using aspirin. Usually a regular strength adult aspirin is given every 6 hours for the first 24 hours and then twice a day for 3-5 day thereafter. In rare cases where aspirin doesn't work of for extremely high fevers, dipyrone is given. Some patients will require supportive care with intravenous fluid therapy and in extreme cases emergency treatment similar to heat stroke treatment. Antibiotics are not normally indicated in this condition. Colchicine: Colchicine is a drug that has been in use in people with FMF to prevent amyloidosis. It is currently being recommended in Shar-Pei with FSF for the same purpose. No studies have been completed to determine if it is useful for this purpose in the Shar-Pei or not. The clinical impression is that it does help. Those dogs on colchicine seem to have fewer FSF episodes and less severe signs while on the drug. Side-effects appear to be minimal at this time and are primarily gastrointestinal such as vomiting, diarrhea, anorexia (decreased appetite), etc.

(FSF, Continued on page 15)

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Prevention: Shar-Pei with FSF only show symptoms sporadically. It would appear that there are "triggers" involved in initiation of the FSF episodes. One of the major triggers appears to be stress. This may be a dog training class, a dog show, another illness, a dog in heat, excessive exercise, etc. If the owner can recognize these triggers and take steps to avoid them the number of FSF episodes can often be reduced. Diet does not appear to be helpful in prevention of FSF or kidney disease. Surely diet has a role in the management of the kidney dis-ease once clinical signs are apparent. Low dose aspirin therapy may be useful in decreasing the incidence of FSF and its severity as well. Aspirin may also be useful as an adjunct therapy in the prevention of thromboembolism. Monitoring: Monitoring for the complications which often accompany FSF is one of the major goals of the owner of an FSF dog. The primary and most consistent sequela to FSF is kidney failure either due to immune-mediated kidney disease or renal amyloidosis. I currently recom-mend monitoring a urinalysis every 3 months. The sample should be collected first thing in the morning after the water has been taken up overnight. I primarily look at the urine specific gravity which is a measure of the concentration of the urine and the protein levers in the urine. When the kidneys begin to fail the initial indication is a loss in the ability to produce a concentrated urine. This occurs before there are blood changed related to kidney failure. Increased water consumption, increased urination are the clinical signs associated with the loss of concentrating ability, but these signs are often not recognized. I also thing it is wise to do a blood panel every 6-12 months and certainly do one in the urinalysis is abnormal. Weighing your dog periodically is very important. We often don't recognize a significant weight loss because it is very subtle over a longer period of time. Water consumption and appetite are other important indi-cators to watch. Complications of FSF: We have already discussed the kidney complications in this condition. Other Complications which have been documented include throm-boembolism (mesenteric, splenic, pulmonary), DIC (disseminated intravascular coagulation), SIRS (systemic inflammatory response syndrome), MODS (multiple organ dysfunction syndrome), STSS (streptococcal toxic shock syndrome), hypertension associated with renal failure. Many of the deaths following an acute FSF episode are due to these complications. No FSF episode should be treated lightly! Diagnosis: There is no specific diagnostic test for FSF at this time. Diagnosis is based on the clinical sign of episodic fever in a Shar-Pei. I think every Shar-Pei that dies should be autopsied to determine the cause of death, but this is even more critical in cases involving FSF. Re-nal amyloidosis can only be diagnosed based on kidney biopsy and staining with Congo Red stain. This stain is specific for the presence of amyloid. Amyloid has been found in other tissues in Shar-Pei as well so special staining should be requested on all tissues submitted for histopathology. Many dogs with FSF will not have amyloid in the tissues at the time the tissues were harvested -- this means the absence of amyloid in a biopsy specimen does not mean that dog will not or would not have gone on to develop amyloidosis at a later time. To further confuse the issue, not all Shar-Pei with amyloidosis have shown signs of FSF. Future: Research is currently underway at the University of Missouri College of Veterinary Medicine by Dr. Gary Johnson to develop a DNA blood test. The gene for human FMF was sequenced in the Fall of 1997 and with that information Dr. Johnson had hoped to sequence the FSF gene. That information was applied by Dr. Gary Johnson to FSF in a research project founded by the CSPCA Charitable Trust. That pro-ject did determine that the mutations causing FMF in man do not exist in FSF in the Shar-Pei, hence they are two distinct, although similar diseases. There are other hereditary inflammatory fever disorders in man and Dr. Kastner ant the National Institutes of Health are looking at the disorder with information supplied by Dr. Tintle. Familial Hibernian Fever in man has also been ruled out as the cause of FSF by Dr. Johnson with information supplied by NIH. Work will continue to find the genetic mutation(s) responsible for FSF in Shar-Pei. As of this writing the mutation responsible for FSF has not been found. If a test can be developed, a screening program can be estab-lished to screen breeding stock and determine normal individuals, carriers and affected dogs. With this information Shar-Pei breeders can gradually eliminate this genetic disease from the breed. One of the major obstacles to research revolves around the unpredictable phenotype of FSF. There is no consistent age range when clinical signs develop, the clinical signs can be variable, some dogs develop amyloidosis, some don't, etc. This makes it very difficult to use genetic selection methods which are based on phenotype. Recommendations: All Shar-Pei with FSF should be on colchicine and be regularly monitored via urine samples and blood work for development of complica-tions. Dogs with FSF should not be used in breeding programs and should be neutered. Dogs with a family history of FSF should be on colchicine and monitored. Dogs with FSF should be maintained as stress-free as possible.

(FSF, Continued from page 14)

Note: An aspirin given at the first sign of symptoms along with 500 mg of amoxicillin will almost always alleviate symptoms within 24 hours and usually less.

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Amyloidosis is the deposition of an abnormal substance called amyloid in the tissues of the body. Amyloidosis is not a disease as much as it is a specific biochemical arrangement in which a precursor protein or protein fragment accumulates and forms filaments. These filaments align and stack themselves in a beta-sheet conformation forming fibrils that twist around each other and are depos-ited in the tissues as amyloid deposits. Amyloid deposits differ due to the nature of the protein precursors that form there. Due to this structure amyloid is insoluble and can be thought of as “wax". There are currently at least 11 different protein precursors in amyloidosis. Many of these have specific tissues they accumulate in and have specific clinical signs or syndromes associated with them. As an example in humans Alzheimer’s patients have amyloid deposition in the brain due to an unknown precursor protein. In animals the only form of amyloidosis shown to occur at this time is reactive amyloidosis. Here the precursor protein is serum amy-loid A protein and amyloid A composes the fibrils in the amyloid deposits. All amyloid deposits stain with Congo Red and have a char-acteristic green color with birefringence under polarized light. Of the many types of amyloidosis which stain with Congo Red only reactive amyloid and beta-2 microglobulin amyloid are decolorized by potassium permanganate oxidation. Beta-2 microglobulin amyloid has only been described in humans on long-term hemodialysis for chronic renal failure and has not been found in animals. The amyloid in Shar-Pei is definitively reactive amyloidosis. It is also important to realize that amyloidosis is not a single disease, but can be the end point of many diseases. This form of systemic amyloidosis, reactive amyloidosis, usually occurs with chronic inflammatory diseases and is characterized by the presence of amyloid protein AA. Amyloid protein AA is derived from an acute phase protein called serum amyloid A protein (SAA) produced by the liver. There are many other acute phase proteins produced by the liver which have important roles in the inflamma-tory process and in tissue repair after injury. It is important to understand that amyloid protein AA is a normal protein and that it’s production is a normal response to tissue injury and inflammation. It is also important to realize that many diseases, traumatic inju-ries, cancer disorders, stresses, etc. can stimulate the production of the acute phase proteins. There appears to be a balance be-tween the production of SAA and the degradation and excretion of SAA from the body. It is not known whether the development of amyloidosis in the Shar-Pei is due to prolonged excessive SAA production by the liver which overwhelms the degradation mecha-nisms or a defect in the degradation process itself, or a combination of both. We do know that Familial Shar-Pei Fever is an inflam-matory process which does stimulate the synthesis and release of acute phase proteins from the liver. That this occurs can be sur-mised from the changes seen on the hemogram and biochemical profiles of Shar-Pei during, or shortly after, an FSF episode. It cer-tainly appears that the cause of amyloidosis in Shar-Pei has a genetic basis. Reactive amyloidosis results in extracellular deposition of amyloid protein in tissues. This means the “waxy” amyloid is surrounding the cells and slowly crushes them as well as interfering with nutrition of the cells. These cells die and the structures they make up are replaced by fibrous, nonfunctional scar tissue. There are species differences as to which tissues amyloid will accumulate in. In dogs, the kidney is the primary organ involved with the spleen and liver affected less often. The kidney is especially vulnerable due to its decreased ability to replace damaged cells and ultimately, when a certain number of cells have been irreparably damaged, kidney failure with its accompanying clinical signs develops. Once amyloid is deposited in the tissues it appears that nothing can remove it although recently a new class of drugs have been discovered which may do just that. It is important to realize that amyloidosis occurs in all dog breeds and in a number of inflammatory and immune-mediated condi-tions. The majority of amyloidosis in dogs is idiopathic or of unknown cause. Amyloidosis can occur secondary to heartworm disease, tick-borne diseases, various cancers, systemic lupus, immune-mediated arthritis, IBD, etc. I suspect that the tendency to develop amyloidosis in response to inflammatory or immune-mediated disease or triggers is a separate genetic disease in dogs which leads to failure to degrade amyloid, failure to excrete amyloid degradation products or increased production of amyloid precursors. Why does amyloidosis have so many different clinical presentations? Why does it occur in some Shar-Pei at 2 years of age and in others at 10 years of age? Why do some Shar-Pei develop amyloidosis and others don’t? Why is it a genetic disease in Shar-Pei? There are many questions which have no answers at this time. I think several theories are plausible to explain the variations we see: The underlying trigger of amyloidosis in Shar-Pei is Familial Shar-Pei Fever (FSF). It is quite possible that FSF has variable age of onset and variable degrees of severity in terms of the inflammatory disease it causes. This may result in a variable rate of progres-sion in the development of amyloidosis in different individuals. For example, the response of the liver to FSF and the synthesis and release of the acute phase proteins, especially SAA, may be more acute in some dogs resulting in a more rapid deposition of amy-loid. In other individuals, the response to FSF may be more chromic and result in slower deposition of amyloid. In effect, there may be milder forms and more severe forms of the same disease. The exact mechanism of amyloid deposition may be different in differ-ent individuals. There may be other effects of FSF on the body which are additive with the amyloidosis. As an example, we know Shar-Pei are more susceptible to disseminated intravascular coagulation (internal blood clotting) during an episode of FSF and blood clots in the kidneys may cause more kidney damage than just amyloid deposition itself. Some dogs may have other disease proc-esses going on which can be additive with the effects of amyloidosis. These are just some ideas on why we see different presentations of the same disease. One fact remains – any amyloid deposits found in a Shar-Pei have to be regarded as related to FSF and genetic until proven otherwise. It really doesn’t matter whether a little or a large amount of amyloid is found. Another point to keep in mind is that the mechanisms initiating amyloid deposition are normal protective responses seen in any breed of dog. It appears in our breed that the mechanisms, which regulate the inflammatory re-sponse, don’t work properly allowing this normal response to go out of control and cause disease. Relationship of FSF and Amyloidosis There is a definite relationship between FSF and amyloidosis. FSF is undoubtedly a genetic condition which is inherited much as the periodic fever episodes seen in humans. FSF is a built-in trigger resulting in intense inflammation and the release of acute phase proteins from the liver one of which is serum amyloid A. I think there are several explanations for the wide variety of clinical presen-tations we see with FSF/amyloidosis. I suspect that there are several different mutations which can result in FSF. We know in hu-mans with Familial Mediterranean Fever that there are at least 8 mutations in the FMF gene leading to differences in severity of clini-

(Amyloidosis, Continued on page 17)

By Dr Jeff Vidt

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cal signs, duration, illness and death in different populations. I think we see the same thing in Shar-Pei, some having mild episodes and some having very severe episodes. This may also explain why some dogs succumb to STSS, DIC, heat stress, and other com-plications but others don’t. That being said I also suspect that there are variations in the genetic defect predisposing to amyloidosis in dogs in general. One can imagine in a dog with a severe form of FSF resulting in dramatic increases in serum amyloid A and having a genetic defect leading to a decrease in degradation of amyloid that the rate of amyloid deposition would be very high. On the other hand if the type of FSF resulted in mild increases in serum amyloid A in a dog with no amyloid defect then amyloidosis would not develop. The same seems to hold true with the dog population in general since not all dogs with inflammatory/immune-mediated diseases develop amyloidosis and some dogs with amyloidosis have no discernable underlying disease to blame for it. I think it is safe to say that FSF is not the only precursor to the development of amyloidosis in the Shar-Pei but certainly is the major factor since FSF is only seen in our breed. Is it possible that FSF is revealing those animals with an amyloidosis defect of some kind? The high fever seen in FSF certainly results in increased levels of serum amyloid A thus facilitating the development of amyloidosis. Thus it appears FSF and amyloidosis most often occur together in Shar-Pei but can occur separately as well. Since idiopathic amyloidosis occurs in dogs in general (the most common cause of amyloidosis in other breeds) we can expect it would occur in the Shar-Pei also so not all cases of amyloidosis in our breed are related to FSF.

H & E Stain: The pink-staining material in the collecting ducts, tubules and glomeruli is amyloid. Unfortunately protein in the tu-bules will also appear the same. Only Congo Red staining can differentiate amyloid deposits.

Congo Red Stain: The areas of birefringence are due to amyloid

(Amyloidosis, Continued from page 16)

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By Dr Jeff Vidt

This article by Dr. Vidt presents a plan to monitor Shar-Pei with the goal of uncovering renal amyloidosis as early as possible and then instituting appropriate dietary and medical intervention. It does contain some technical terms which your veterinarian may be able to simplify for you. The author urges you to discuss this article with veterinarian and then both of you can work together in dealing with this troubling disease. Renal amyloidosis has hit the Shar-Pei fancy in recent years and left many of us feeling helpless as we watch young Shar-Pei sicken and die before our very eyes. We don't have to sit and take it, but can gather the facts and formulate a plan of action. What I propose in this paper is based on the information available today about renal amyloidosis. Currently, there is no test available to help pinpoint Shar-Pei at risk for developing the condition and due to ethical considerations, information concerning pedigree analy-sis is not available to help determine those dogs who have the condition in their background. What we are left with is to try to un-cover the condition in our dogs as early as possible and to institute steps to minimize the effects on our dogs and increase longevity. The following plan has no guarantees and certainly will change as new information becomes available, but it represents a starting point and a step to build on further. Keeping a Watchful Eye for the Health of your Shar-Pei As a Shar-Pei owner you can do the following simple steps:

Monitor weight - This involves weighing your dog at regular intervals using a scale. Do not rely on eyeball judgements. Too of-ten I see dogs in an advanced state of weight loss which the owner has just noticed, but which has been going on for sev-eral weeks. Remember, we are trying to uncover this condition at its earliest point - minor weight loss can indicate early renal amyloidosis.

Monitor appetite - Daily fluctuations in appetite do occur, but a change in what is normal for your dog may indicate early kidney problems.

Monitor water consumption - A normal dog consumes approximately 1 oz. of water per pound of body weight per day. This var-ies with activity level, season of the year, type of food being fed (canned vs. dry), etc. I advise measuring water intake periodically by measuring how much water is put down in the morning and measuring it again at night. Obviously this will involve a little more ingenuity on the owner's part when multiple dogs are involved. Increased water consumption may indicate early kidney failure

In addition to the above home monitoring program, I also advise having your veterinarian check a urine sample every three months on any Shar-Pei over two years of age. The main parameters I watch in the urine are the urine specific gravity and the urine protein reading. Urine specific gravity is a measure of the concentration of the urine. If the kidneys were not functioning at all this reading would be 1.008 - 1.012 (a dilute urine). Normal concentration should be above 1.025 and usually is greater that 1.045 (a concentrated urine). Ideally the urine sample should be a morning sample collected after the dog's water bowl has been removed overnight (remember to close the toilet lid!). By depriving the dog of water overnight we force the kidneys to concentrate the urine, if they are able to do so. Inability to concentrate urine indicates that approximately 75% of the kidneys are non-functional - this is still compatible with life, but treatment needs to be started quickly to preserve the remaining kidney function. The other urine test I heavily rely on is the urine protein level. The stick test routinely run by veterinarians primarily measures urine albumin levels. An elevated urine albumin level means that protein is being lost in the urine and correlates with glomerular damage (the glomerulus is the filtration unit of the kidney and serves to filter out the waste products of the body). High levels of protein in the urine indicates significant kidney disease and additional testing need to be done to obtain a diagnosis. It appears that there are three separate syndromes associated with renal amyloidosis in the Shar-Pei:

Glomerular - If the amyloid deposits occur primarily in the glomerulus, we see increased protein levels in the urine. Tubular - If the amyloid deposits occur in the tubular part of the kidney we see loss of concentrating ability which manifests as a

dilute urine. Combination - This occurs when amyloid is deposited in both the glomeruli and the kidney tubules and we see increased protein

levels in the urine and dilute urine. The clinical signs and the routine urine check constitute the first level of diagnostics. If the urine sample is abnormal and one or more clinical signs are present, then we immediately proceed to the second level of diagnostics. This level incorporates the following tests:

A complete blood count - This includes a packed cell volume, a white blood cell count, red blood cell count, platelet count, and a (Plan, Continued on page 19)

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white blood cell differential count. A health panel - This includes at least a BUN, creatinine, sodium, potassium, calcium, phosphorous, cholesterol, total protein, albu-

min, globulin and, glucose. It often includes liver tests and thyroid hormone levels. An immune panel - This should consist of a direct Coomb's test, an anti-nuclear antibody test (ANA), a Rheumatoid arthritis factor

test (RA), and an LE prep for systemic lupus. A urine protein/creatinine ratio - A value above 1.0 is considered abnormal and indicates excessive urine protein loss. Abdominal radiographs - Used to evaluate kidney size and shape.

Based on the results of the first and second level diagnostics the following steps are taken to manage the patient: Diet - A low protein diet is initiated using Hill's Prescription Diet K/D® or its home-made counterpart. I'm also using the Iams Eu-

kanuba Veterinary Kidney Diets - Early Stages® and Advanced Stages®. Vitamin-mineral supplementation. Ascriptin® - 1/4 tablet once a day. 1 cooked egg per day - used in cases where albumin is being lost in the urine. Additional medical therapy may be instituted using either colchicine tablets or DMSO via injection or orally. The effectiveness of

both these drugs in the prevention and treatment of renal amyloidosis in the dog has yet to be substantiated, but their use is justified given the grave prognosis of this condition in the Shar-Pei. Colchicine is a human anti-gout medication whose mode of action is largely unknown. It appears to prevent the formation of amyloid in the laboratory, but whether this occurs in the living animal is not known. Dimethyl sulfoxide (DMSO) is another drug whose mode of action is unknown, but has demon-strated the property of dissolving amyloid in the laboratory. Again, whether this action occurs in the living animal is unknown. The dosages are as follows:

Colchicine - this dose can be obtained from Dr. Linda Tintle or myself (see the July/August 1992 issue of The Barker). DMSO - numerous dosages are in the veterinary literature. Your veterinarian should refer to an excellent article on renal

amyloidosis by DiBartola in Current Veterinary Therapy XI. [IMPORTANT! - DMSO imparts an odor to the breath and skin of the patient.] Again, the effectiveness of these drugs in the treatment of amyloidosis has not been proven in clinical studies and hence, they should be regarded as experimental drugs for this use. They should be used only under the supervision of your veterinarian.

Equally important is the avoidance of further kidney damage. - Avoid dehydration- provide plenty of fresh water daily. Avoid kidney-damaging drugs such as aminoglycoside antibiotics, methoxyflurane anesthesia, various chemotherapeutic

agents, sulfonamide antibiotics, etc. Avoid stress- boarding, traveling, showing, etc.

Third level diagnostics may be done depending on your veterinarian or the availability of specialists in your area. Test at the level may include:

Coagulation panel - Increased levels of fibrinogen may indicate impending thromboembolism (throwing of blood clots) associated with DIC (Disseminated Intravascular Coagulation) especially if associated with increased cholesterol and decreased albumin levels (nephrotic syndrome). This panel should include a platelet count and a measurement of FDP's (Fibrin Degradation Prod-ucts).

Fractional clearances of various eletrolytes. 24-hour urine protein excretion. Creatinine clearance testing to evaluate kidney function. Kidney ultrasound. Kidney biopsy.

The kidney biopsy is the definitive diagnosis of renal amyloidosis and the decision to biopsy should be made early in the course of the disease for a number of reasons:

Early on, the animal is a much better surgical candidate and many complications of renal amyloidosis such as bleeding tendencies and uremia are not present.

There is a real danger in the Shar-Pei to blame every kidney problem on renal amyloidosis and fail to pursue other causes of kidney disease such as kidney infection, heartworm disease, and immune-mediated diseases like systemic lupus and immune-mediated glomerulonephritis.

The information from an early kidney biopsy can guide the medical and dietary management of the case and provide valuable prog-nostic information.

Almost as important as the early diagnosis of renal amyloidosis is the continued monitoring of the patient while on therapy. This allows us not only to monitor and watch for the progression of the disease, but also to evaluate the various therapeutic modalities and deter-mine which are effective and which are not. Monitoring at one to two week intervals initially and then at monthly intervals thereafter is recommended. I usually repeat a kidney panel and cholesterol level, a CBC, and a urinalysis including a urine protein/creatinine ratio. Continued monitoring is also important in order to pick up the early signs of sequelae to renal amyloidosis such as:

Nephrotic syndrome - characterized by decreased serum albumin, increased serum cholesterol and increased protein loss in the urine. A serious complication of this syndrome is thromboembolism ("throwing blood clots"). Your veterinarian may do a blood fibrinogen level and coagulation panel to evaluate the blood clotting system. If the fibrinogen level is >300 mg/dl, aspirin ther-apy is strongly indicated. Another serious complication of this condition is the development of edema or fluid accumulation in the abdomen or chest and in the limbs. In this case, the use of diuretics such as Lasix may be necessary.

(Plan, Continued from page 18)

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Uremia - or the accumulation of body waste products which are normally filtered by the kidneys into the urine. The build-up of these wastes causes clinical signs such as appetite loss, weight loss, vomiting, diarrhea, depression and lethargy. More serious effects include anemia (decreased red blood cell production) and gastrointestinal ulceration. Treatment here may include intravenous fluid therapy, dietary therapy such as Hill's Science Diet U/Dâ, Iams Eukanuba Veterinary Kidney Diet - Advanced Stagesâ, phosphate binders such as Amphojelâ, ulcer medication such as Carafateâ and other therapy as deemed necessary by your veterinarian. Eventually, uremia will progress and lead to the death of the animal. As an aside, current nutritional research indicates that there is no advantage to instituting dietary protein restriction prior to the onset of kidney failure. This means that feeding protein-restricted diets prior to developing laboratory or clinical signs of kidney failure will not prevent kidney failure.

Hypertension - The kidneys are very important in the regulation of blood pressure. It is speculated that up to 80% of the dogs in kidney failure have significant hypertension as a consequence. The use of indirect blood pressure monitoring in animals has recently become available to the veterinarian and hopefully will lead to more advances in this area. Your veterinarian may wish to institute therapy using vasodilators and/ or diuretic medication.

Disseminated Intravascular Coagulation (DIC)- The body's coagulation system is in a fine state of balance between forming blood clots and dissolving them. When this balance is disrupted coagulation factors are used up before they can be re-placed and out of control bleeding is the result. This condition is associated with high mortality and is a poor prognostic factor. Treatment is not very effective.

Streptococcal Toxic Shock Syndrome (STSS) -This is an unusual complication which results in areas of skin death leading to skin sloughing almost like a burn. The condition seems to be caused by toxins produced by Streptococcus canis and is rapidly fatal sometimes in spite of treatment. It should be mentioned here that DIC and STSS are also complications following episodes of Familial Shar-Pei Fever (FSF). FSF appears to be a potential trigger for the Systemic Inflammatory Response Syndrome (SIRS) which can stimu-late the development of DIC and STSS. Ultimately, these end up in the development of Multiple Organ Dysfunction Syn-drome (MODS) if early and aggressive treatment is not initiated. The bottom line is that no episode of FSF should be treated lightly. I recommend that my clients call me with each FSF attack and certainly bring the dog in if the episode is not responding to aspirin, is lasting longer than usual, they notice any usual symptoms or the fever is very elevated. To what extent early diagnosis and monitoring contributes to the longevity and quality of life of renal amyloidosis pa-tients is hard to quantify at this time. My feeling is that it is possible to slow the progression of the condition and improve the short-term prognosis for these patients. We can probably add several months to their life span. It's expensive and requires diligence and hard work on the part of both the owner and their veterinarian, but the reward is some extra time with a close friend. Lastly, when the end does come, consider allowing your veterinarian to do an autopsy on your dog. Especially impor-tant is the evaluation of the kidneys through histopathology. We must verify cases of renal amyloidosis or other causes of kidney failure if we are to make headway in correcting this condition through breeding. Results can be sent to Dr. Linda Tintle, Wurstboro Veterinary Clinic, PC, 251 Sullivan Street, P.O. Box 906, Wurtsboro, New York, 12790. This site represents my own opinions based on reading the veterinary literature and in no way reflects the opinions of the CSPCA, Inc. or anyone else. The Officers and Board of Directors of the Chinese Shar-Pei Club of America supports research for Familial Shar-Pei Fever and amyloidosis.

(Plan, Continued from page 19)

It is very important to have a necropsy, including Congo Red Stains, performed on all Shar-Pei. The informa-tion gained from these tests are of great value to breeders in whose hands are trusted the future of our breed. The time to plan for a necropsy and Congo Red Stains is while your Pei is young and healthy. During the stress and sadness of losing our beloved Pei, this is one less thing to remember. You can place a notation in your dog’s veterinary file authorizing a necropsy with Congo Red Stains at any time.

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In observing dogs in daycare there are some key pos tures, expressions and mannerisms that can tell you about the animal’s state of mind. As a general rule, anythin g that deviates from “normal” in the dog’s posture and expression can be a clue into an animal’s intention or feeling s about a particular situation. Canine body languag e has been well researched and documented by ethologists and behavi orists in the field of animal science. Understandin g, then ap-plying this information is one key to being success ful in providing quality of care based upon knowled ge, not experi-mentation. The following is a list of observable bo dy postures and facial expressions that will help i n evaluating and making judgements about dogs that come to our facil ity for daycare. It is vitally important to safety and providing quality care that we understand all that we can abo ut an animal. Information provided by owners is on ly part of the picture. Common behavior in a home environment wher e a dog is comfortable and familiar may not be an i ndicator of how a dog responds in the daycare environment with all the different sights and smells. This is where being able to “read” a dog’s body language is helpful. It allows us to act with insight and anticipation with our p et clients rather then responding to crisis and “mayhem”! Study this list, then start watching the dogs. The more you watch, the better you will get at seeing the postures and expressions. This will help you understand the dyn amics you are seeing in the dog’s interactions with you and with other dogs. This understanding paired with good han dling skills are necessary components to offering a safe and quality daycare experience for all our 4-legged fri ends and the owners that love them. MOUTH Open For body cooling efforts Relaxed or “happy” mindset Sometimes seeen when the dog is in highly aroused s tate Closed Key indicator that dog is no longer in relaxed mins et when you see them go from open mouth to colsed On “Alert” status Serious about something Key point for Daycare: When you are introducing ne w dogs, this is one indicator to monitor that can g ive you some information about how the dog feels about an intera ction. If you see a dog go from an open mouth and relaxed body to a colosedmouth with a stiff posture it’s time to pay close attention. This indicator, paired with other signs, can alert you to a need for sesparation or intervention. Be ready to act quickly. BODY TONE Stiffness/Freezing Paired with a closed mouth is a sign of high “alert ” status and thus a greater bite risk. Freezing paired with head turn is a commonly seen w arning that a dog is uncomfortable about something going on

with or near their hindquarters. This is a situati on one might encounter when a doing is being groome d, examind uring a vet visit or simply touched on the hindquar ters.

(Body Language, Continued on page 22)

By Nancy Nicholson

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Not uncommon to see some freezing of motion in play mode, e.g. stalking posture to invite pounce or re st between play fighting.

Relaxed/Loose Good sign in greeting and playghroups. Dog’s body will appear loose, movements are fluid and ge3neral posture

appears “normal”. Can also feel this when you are petting a dog…their general muscle tone will feel natural and moderate ly firm, not

taunt or quivering. Key point for Daycare: Be alert when you see stiff ening in a dog’s posture. If it occurs when you ar e petting them or reaching for them, stop. Warn others if you see them reaching for a dog that suddenly goes stiff. If the dog is stiffen-ing and giving a head turn when on a leash, see if there is something in your handling or the situati on that can be adjusted to remove the threat that a dog may be fee ling. For example; you can loosen the tension on t he leash and recheck for body stiffening. WAGGING TAIL Loose, relaxed tail wagging in a large arc is gener ally a positive indicator. (Can be accompanied by hindquarters as

well.) High raised tail wagging in small acrs at midsectio n only-

Need to be alert. Note whether if this is accompani ed by Other signs such as suddenly closed mouth and body stiffness. Key point for daycare: A wagging tail isn’t always a sign of happiness or an invitation to pet. In hum an communi-cation, a Word can have many meanings depending upon the tone and situation in which it is used. Similarly, a wa gging tail can indicate a variety of messages in dog “lan guage.”

Postures ( i.e. direction of dog’s energy) 1. Forward weight bearing a. Dog presents in a confindent state b. Could be friendly or offensive/aggressive *” If dog comes toward me (written from author’s personal account) willingly, wagging his tail from the shoulders back in a “full-body wag,” head lowered, mouth open and eyes squinty, I’m going to squat down and have a love frst with him. If a dog’s body is shifted forward and he’s stiff and immobile, with his mouth closed shut and his tail wagging only from the tip, I’m going to stay where I am, and ease the tension by turning away or pulling out a treat or a ball. However, if the dog is close and begins to Advance on me, mouth still shut, body still Stiff, I’ll turn my head quickly toward him and Speak in a low, sharp voice. This is a dog who Is on the offensive, and who needs to be stopped Without adding to the tension; as soon as I can I’ll face him off, but then break the tension by Saying ‘wanna go on a walk?’ of “Dinner!’” 2. Backward weight shift

Defensive stance-might indicate fear or indecision. Don’t pressure a dog in this stance, e.g. corner th em, advance toward them or reach for them. This posture might also be seen when a dog is attem ption to avoid obeying a command or evade contact

with you. Disobedience should be fairly evident wh en considered in relation to the situation in which it occurs. This would be handled differently than fear. (see training tips).

Side approach with a curved body Polite canine greeting manner.

Key points for daycare: Consider your posture and d irection of weight bearing when approaching a dog. If you sense

(Body Language, Continued from page 21)

(Body Language, Continued on page 23)

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fear-an easy way to decrease pressure is to change your orientation to a more sideways stance or sidew ays direction of approach. You could also slightly shift your weigh t backwards to your heals…they do respond to even t his small weightshift. If you need to demonstrate leadership with a pushy or dominant dog, a confident standce with slight for-ward weight shift will demonstrate your status whou t having to be threatening or physicial. Do not, h owever, use this posture in a situation where a dog appears ready to react aggressively…it is best to avoid an aggressi ve confrontation and approach the situation differently. Position of Corner of the Mouth on the Dog (commisure)

Retracted Could be a sign of submission (docile or yielding m anner); will even see this in play, not just greeti ng. Can show ambivalence (uncertainty)- see this in the dog that barks with full set of teeth showing… the y would

rather not act on their display of threat, it’s mor e of a bluff in hopes that it will make the threate ning object/person/situation go away.

Can also demonstrate fear- like a fear grimace 2. Forward(called an offensive pucker) (a) Indicates a readiness to act/go on the offensiv e. *”If your dog lunges at another dog with his commis sure forward, he’s in a very different state then i f he retracts it in a fear grimace. He could be barking and lungi ng in both cases, but the position of his mouth wil l help you understand how he’s feeling inside when he does. If your dog puckers her mouth forward when your child tries take a toy out of her mouth, she’s telling you that she’s standing up for what she believes is her pro perty, and that she’s willing to use her mouth to defend it if necessary. If she growls at a visitor with her com missures re-tracted she may be afraid of strangers, and so need s help overcoming her fear when the doorbell rings. ” Key points for daycare: observe this in play, greet ings and when a dog is barking. If there is fear in volved, one might be inclined to take measures to ease tension, reduce stress, or remove the thing that the dog pe rcieves as threatening. For instance, remove an object from th e dog’s line of vision or locate them in a differen t setting. Maybe a different partner or group for play would b e indicated. If there is a sign of an offensive or confronta-tional intent, like the situation where a dog is gr owling over a toy, bone, or food only when separate from oth-ers… the impulse to protect, acquire or hoard is in stinctual. Tongue Flicks

1. Can indicate low level anxiety- dog is sig naling or signaling or expressing they don’t feel en tirely comfortable with a situation or another do g. 2. Also an appeasement gesture from subordina te dog to a higher ranking dog (like a white truce f lag) *” Submissive or slightly nervous dogs will tongue flick in response (to handling), but status-seeking ones will go stiff and clench their jaws… A dog who wags his whole bod y and comes toward you with head down, tongue flick ing in and out, is submissively soliciting attention. If howev er, a dog stands still, tongue-flicks out of a clo sed jaw, and then stiffly turns his head away from you, mind your manners. Yo u are being told loud and clear that Fido is uncomf ortable, and isn’t interested in a date right now. Ignore this m essage at your peril. Yawning Not always an indicator of sleepiness or relaxati on; can indicate a dog is somewhat uncomfortable/sl ightly anxious. Key point for daycare: This is one technique you ca n employ to put an anxious or tense dog at ease. Ke ep your body loose, approach sideways, avert your gaze and yawn a few times. Simple, but it works! Amount of Eye Opening and Size of Pupils 1. Wrinkly or squinting eyes- seen in docile dogs during greetings. 2. Large, rounded eye a. Can show alert, fear or surprise b. High arousal 3. Dilated (large) pupils- correlate with fear or a rousal (it is normal for pupils to be constricted n ot dilated in a bright envi-roment, watch out if the pupils on a dog suddenly e nlarge!) ** Be aware that different breeds of dogs have natu rally larger or smaller eyes. Look for changes from what is normal for that breed and particular dog.

(Body Language, Continued from page 22)

(Body Language, Continued on page 24)

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Hard Eye Look of intense, focused gaze seen in dogs when the risk of aggresion is high. This is similar to a gl are in humans. This signal may be something you understand intuiti vely on an unconscious level… a red flag. Listen to your gut and take measures to protect yourself, e.g. freeze, look away, get behinde protective fencing, etc. Whale Eye Labeled by Sue Sternberg, canine aggresion expert, this appears when the dog’s head and eyes are not p ointing in the same direction. It causes the whites of the eye s to be more apparent. Key points for daycare: Take measures to reduce the threat this dog is feeling. For instance, don’t fo rce contact, let the dog approach you. If this is happening to a dog in the play setting when other dogs are being to p ushy or ignor-ing boundaries, walk between the dogs and redirect the play. If necessary, reconsider the playgroup ma keup. You may need to shuffle some dogs to get a better combi nation for all parties. Look Away 1. Another method used by dogs to diffuse tension in an encounter. This is “often the sign of well s ocialized, friendly dog.” They are showing manners by not forc ing a direct gaze or nose to nose contact. 2. Sometimes seen in a confident, high status dog i n response to a greeting by a submissive, lower sta tus dog (like royalty avoiding contact with a commoner!) 3. Also a gesture used by a nervous dog to communic ate their desire to not be approached. Key points for daycare: Respect this signal and giv e the dog space. One can also use this technique to lower the feeling of threat or tension when approaching a fea rful/aggressive dog. It gives the message, “I mean no harm.” Tail Position 1. High- confident, dominant 2. Low- submissive, maybe ambivalent (somewhat insecure or unsure) 3. Tucked- fearful, anxious, unhappy Ear Position 1. Up and forward- alert 2. Splayed (airplane ears)- ambivalent 3. Down or back- check other body language, Could correspond to offensive intent, Fear/cowering, submission; sign to be on Alert or paying attention to situation you See with the dog. ** Both ear and tail position can also be influence d by breed and may not be indicative of something b eing amiss. Head and Neck Position 1. Lowered (torpedo positioning) when associated wi th an aggressive display such as bared teeth, hard eye, growl-ing/barking is a red flag for bite risk. Might also see in conjunction with play posture like stalking or in herding breed when intent on pressuring another animal. May also see in combination with other body displays t o demon-strate submission to a higher ranking animal. 2. Raised- confident, secure in status. Other Cues of Dog’s State of Mind Aggressive 1. Hackles up 2. Teeth bared 3. Growling 4. Slow movements 5. Stalking posture

(Body Language, Continued from page 23)

(Body Language, Continued on page 25)

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Submissive 1. Rolling onto back 2. Urination 3. Running away Dominence 1. Putting paw or head over back of other dog 2. Mounting 3. Mouthing esp. around other animal’s muzzle 4. Direct gaze or approach Definitions Dominant = aggressive = assertive, confident Submissive = no bite risk = yielding, not necessarily fear Aggressive = hostile, intent to fight or harm, can be self defense. Sources: 1) McConnell, Patricia. 2005. For the Love of a Dog , Understanding Emotion in You and Your Best Friend . New York: Ballantine Books. 2) New Hire Orientation @ Kennelwood Pet Academy, w ritten by Sue Schultz, head trainer.

(Body Language, Continued from page 24)

Thoughts on thyroid questions:

1. I also think 1 year of age is early to test for thyroid function. When I proposed the CHIC testing program my thought was to have all the testing done around 2 years of age due to the OFA Hip Dys-

plasia testing. That would allow breeders to get the testing done all at once and get the CHIC certi-fication quickly.

2. The MSU thyroid testing panel I recommended was chosen for several reasons: a) It does include

autoantibody testing to screen for autoimmune thyroiditis, 2) It does allow for a diagnosis of hypo-thyroidism in most cases and 3) It can be requested to have an endocrinologist interpret the results

which I recommend. 3. We can change the requirements of the CHIC program as it now stands however it was suggested

we leave the requirements in place for a while to see if other problems arise. While I agree 1 year is probably too early for thyroid testing it does allow for normals to be established for that dog. I

would then recommend follow up testing doneevery two years unless clinical signs show up in the

dog. I would prefer to have thyroid testing begin a 2 years of age when the other CHIC tests are done.

I am certainly willing to discuss further with you about the program. We also may adjust things

based on input from Dr. Tintle. Nothing is carved in granite.

Jeff Vidt