To say that it was a pleasure to judge for this friendly group of fanciers early in October 2010, would be an understatement. They were very hospitable and had a good time enjoying the friendly competition. In spite of a severe depression (the worst in Europe and possibly the world at this time) caused by a careless banking industry and lack of government safeguards, the tiny Arctic country is slowly recovering. The total entry of the show was down from what was expected, but still enough to keep the sole judge (me) busy for the two day event. It made economic sense to do it this way rather than have a one-day show with multiple judges. And, since Iceland is a country smaller than Ohio, with about 300,000 people (most living in the Reykjavik-Keflavik corner), it makes good sense to bring in foreign judges. Last spring’s show was judged by a Canadian. This fall’s show had a preponderance of smaller breeds, which may reflect the economy.

Although Iceland has ethnic derivation first from the Norwegian Vikings who discovered the island, and then from the Danes and other Scandinavians, the population also shows some influence from red-haired Irish (some brought as slaves, others arriving as explorers, but all becoming assimilated), a few tall Hollanders, and some from other northern-European areas. Listening to their different language, I hear some words that are nearly the same as German.

The climate belies the name of the country, as there are great sections of pasture, and the remnant of the Gulf Stream keeps it moist and moderate most of the year. It would have made sense for Greenland and Iceland to have exchanged names centuries ago. Both had been colonies of tiny Denmark, but Iceland became independent in 1944, which is surprising, due to Denmark still being under Nazi control at the time.

Iceland’s economy is slowly starting to revive, the most obvious sign being the numerous tourist buses, vans, and oversize-wheel Jeep-type vehicles that line up at hotel doors to load folks going on excursions. But many signs of the continuing recession continue, such as the many unemployed and the many unfinished buildings guarded by idle construction cranes. One notable giant is the civic and conference center building, started in 2006, with work just now resuming. Plans are to complete it in 2011.

The country is unique in many ways. It does not burn coal or oil or nuclear fuel for heat, but relies on the abundance of volcanic and geyser activity. Its electricity comes from waterfalls, this source of energy coming from ice thawing and descending from glacial mountains. If the country were to switch its automobile use to electric vehicles, there would be nearly zero pollution (already so low that it is not noticed). There is such an abundance of geothermal and waterfall/dam energy, that they don’t feel the need for windmills, despite constant strong wind. Too bad they can’t export that! I noticed a high percentage of smokers (something I see in China, France, and a few other countries) but I also noticed quite a few joggers in this land of contrasts, this land of cold air and hot springs. The principal economies of Iceland are aluminum mining, fishing (including whaling) and tourism.

The show is run at a slightly more leisurely pace than in many countries or clubs, partly because we judges have to dictate a written, detailed (point by point) critique on each dog, and the scribe apparently does not use shorthand. Some of the items seem unnecessary, especially if there is nothing remarkable about the specific physical characteristic on the checklist.

One of the highlights for me was the entry of a number of Icelandic Sheepdogs, their “national breed” —a breed of which I had previously seen only a couple examples. It was a honor, privilege, and pleasure to do this breed in its country of origin. Somewhat related to several other Nordic and Arctic breeds, this is a herding dog that is a little shorter than most Border Collies and Australian Shepherds, but with compact sturdy bodies and good bone. Very suitable for working sheep in this climate. Since there are no predators, the dogs need not be like the Great Pyrenees or German Shepherd Dog, but strong enough to convince stubborn sheep.

The only large predators, by the way, ever to have been in this isolated island have been occasional polar bears that rode on drifting icebergs. Although these have been very rare, and quickly dispatched, Icelanders have a fascination with these fierce visitors, and many shops sport statues and pictures of the great white beasts.

There is a quarantine, as to be expected in an island country that has no endemic rabies. Dogs coming from other rabies-free countries have an easier time getting in. Otherwise, there is a waiting period and a minimum age requirement. Importation is allowed only once a month.
(For details, see: IBS.IS website and the importation guidelines )

I am attaching a number of pictures to this short report on Iceland and its dog scene. Readers are welcome to reproduce this report provided that the following mention is made of my books and availability. Fred Lanting

The author is a long-time breeder, a teacher & lecturer in canine topics, and a dog show judge. Order his book, Canine HD and Other Orthopedic Disorders, directly from him. The Total German Shepherd Dog, is also available, and he can be contacted at Mr.GSD @ netscape.com . Info on books can be found through direct e-mail to “Mr.GSD” himself.

As a retired SV Zuchtrichter (breed judge), and a trainer of many dogs to their Schutzhund titles, I am qualified to analyze, educate, and discuss in both of these areas. As a writer for dog magazines and Internet sites, I can also share these expert observations with those who were not able to come to the show. I give descriptions of most of the adult dogs’ Friday protection work (that hopefully qualifies them to enter the breed competition on Saturday and Sunday) and then their anatomical characteristics. The top dogs usually move and look very similar.

This year, in spite of very hard economic times, I had my largest group ever. Fourteen of us for the whole tour and four more (Australians) for a couple days of kennel and scenic visits. As always, it was an international group: four Uruguayans (Sergio & Eliana Fernandez and Pablo & Analía Keizler), two Argentinians (Valeriano and Estella Garcia), four from Washington DC (Jerry Lin -originally from Taiwan- with his wife & 2 daughters), two who work in Iraq (Nabil Nouman and Lori Saunders), and one from Michigan (Nabil’s wife Susie on their second honeymoon). The recession in the U.S. was the reason more Americans were not in the group. My practice is to not charge a fee, but to divide my own expenses among the rest of the group. The smaller group of five in 2009 paid me about $680 each, and the larger group of 13 in 2010 gave me $370 each (less for the Aussies who were only on part of the tour). This was for vans and my own expenses, and they paid directly for their own room and food. So, the bigger the group, the more they save.

First, let me tell you about the tour, and then I will describe the show. Everybody flies to the same airport where I have arranged rental vans. Because of jet lag, it is best to have the group arrive by mid-day on Wednesday, a day-and-a-half before the first day of the show. The first half-day is normally spent getting to the first hotel, but this year we were fortunate to have our first host fairly close to the Frankfurt airport. It was at the working-lines kennel and club of Inge and Heinz Balonier, who are some of the best of such breeders and SchH judges in Europe. Their club has about 100 members, and on the last day of the tour (the next Wednesday) we returned there to see some of them work their dogs. They impressed my group greatly.

Thursday was spent sightseeing. Leaving the autobahn (super highway) at Würzburg, we took the scenic “Romantic Road” south through several picturesque villages, cameras clicking away. The name of this off-the-highways route comes from the era hen the Roman empire flourished. When we came to Rothenburg on the Tauber River, we turned onto what is called the “Castle Road” for obvious reasons. Then east past Ansbach to Nürnberg where the show was held this year. This city is the site of the post-WW2 trials of some of the most notable Nazi fiends that were apprehended and convicted of “crimes against humanity” (many others escaped this judgment by fleeing with false papers to other European and South American countries.

Following the three-day show, the group was enlarged by the addition of the Aussies from Queensland. They were Steve & Hetty Choy, and Paul & Daphne Murray. In the days they were with us, the caravan of three vehicles and 18 people continued the odyssey. Monday we visited the Kirschental kennels, famed for herding and all-around family-&-working dogs. In the afternoon, we were treated by Herr Dieterich of Grabfeldgau to an array of various-age puppies at the home of the late Zamp Thermodos, a dog that has stamped the breed with exceptional anatomy. By the way, anyone who is seriously looking for a beautiful show or working-lines prospect can e-mail me and I can pass the request on to the various breeders.

The next day, most of us visited the Reichertshof kennels of Friedrich and Michael Reichert and saw some extremely high-quality dogs. Unfortunately, it was rainy and we couldn’t get good photos. I and one of the Aussies spoke a little German, so we could translate for the group. This father-&-son team breeds and trains for search-and-rescue as well as the show ring. That evening, we went to the grounds of the club in Laudenbach north of Heidelberg and watched the members training. We also visited the kennel and dogs of Franz Schlenzig (Vierhundert Hertz). Rain continued.

After saying bon voyage to the Uruguay and Australian contingents, the remainder of the group had a relaxing morning and then a visit to the Grossostheim club again to eat and watch dogs work. The enthusiasm and performance perfection of these dogs compared to most of the show dogs at the show was obvious. It is partly a matter of selective breeding and partly due to emphasis and time spent in training. Then, the next morning I delivered my people to their airplanes at FRA and waited for my long ride to my next destination.

With the Sieger Show tour concluded for this year, I started on my next assignment, which was a fortnight lecture tour in Belgium, the Netherlands, and Great Britain, sponsored by the combined Boerboel clubs of western Europe. This is a South African molossoid breed similar in some ways to the English Mastiff, American Bulldog, Tosa, and others. I had done a similar teaching engagement a couple of years earlier for the Belgian group. Starting in Geel, an ancient village in the northern part, I made sure I had plenty of the foods the Belgians are famous for: chocolate, seafood, and beer (much of the last is home-brewed).

On the next weekend, I was part of a panel of experts on cynology from Denmark, South Africa, and Holland. Subjects in this mini-seminar included veterinary, psychology, structure-and-gait, and breed type information. Attendees were from Scandinavia and the low countries, mostly. The following weekend in Great Britain we taught their residents.

The last time I judged and lectured in the British Isles, the “chunnel” (tunnel under the English Channel) had not been built, so getting from France to England by that route was a new experience for me. Autos and trucks are driven onto enclosed railcars for the trip. As a minor WW2 buff, I was interested in the fact that we drove through famous battlegrounds of Calais and Dunkirk to get to the tunnel.

The Big Show

OK. Now, as promised, the report of the salient features (for most serious breeders) of the big show. On the first day (Friday), there is a lot of activity in the fields where the lower-ranked dogs from 12 to 24 months are evaluated in four enormous rings. These age groups must be split into a number of separate groups, or ease of judging would not be feasible. This year, the pre-absentee numbers (entered and listed in the catalogue) were about 450 in the 18-to-24 month classes and 600 in the 12-to-18 month age group. This boiled down to, respectively, only 297 and 390, after absentees. There were also rings for the 32 HGH (herding-degree titled) dogs.

On this first day, I always analyze the bitework. This is tested in the big arena that is split by a curtain and fence so you can alternate between watching the males and the females. I saw enough of the bitches to be impressed with their work. I think that because of the distance and cost, plus the minimal return on any fame garnered here, only the best-performing females are likely to show up.

This courage test consists of two excerpts from the Schutzhund routines, now called the “TSB Uberprüfung” — one bad-guy surprise attack from a blind, and then one long-bite wherein the threatening attacker runs toward the handler from the far side of the field and the dog is sent to intercept him.

Most of the serious breeders in my group and others evaluate these performances and take notes. That’s because it is here that the official show results fail to adequately describe the true character of the dogs. If a dog barely passes its courage test thanks to marginal or questionable performance, or lenient judges, it has as much chance to get a high show placing as the dogs that are truly courageous and better for the breed. That’s why I emphasize to my groups that they should see for themselves how the dogs work, rather than rely on the pass-or-fail paper records. The judges doing the evaluations of body structure and gait is not told how well the dogs actually do in the protection phase.

On Saturday morning, the higher-ranked 12-24 month dogs are sorted in the rings outside the stadium, and by early afternoon, the crowd moves into the main stadium to get the best seats they can. First, some special presentations, such as the HGH and top-20 winners of the younger classes, and the stud dogs’ progeny classes. I have included some of my observations of these progeny presentations in the section describing the adult males.

On Sunday, the top adult females (SchH-titled and over 24 months) were brought into the main ring, in approximately the order that they will end up, and walked around the perimeter of the big ring while their judge rearranges some where he sees fit. In groups of about six, they do their fast running on-leash (leading the handler) and off-leash (heeling). As well as a final down-and-back check to see if any minor changes need to be made based on that view.

After this has been accomplished and the judged females leave the arena, we saw the special presentations such as honoring the best protection performances (both sexes), then the breeder groups competition, etcetera. These used to be done at the end, but so many people left after the judging of the males, that the SV stuck these events in between.

The same procedure as for females was then carried out for the males over 24 months and titled. These adult classes have been known by various names over the years, depending on language and country. In the SV’s homeland, they are now called the Gebrauchshundklasse Rüden (males)and Gebrauchshundklasser Hündinnen (bitches); in many English-speaking countries they may be known as “adult males/females” or (AKC-style) “open males/females” although in the WUSV such classes are “open” only to training-titled (SchH or HGH) dogs over 24 months.

The top percentage of such males as have proven worthy in both the individual evaluations this weekend and at shows since early spring next come into the big arena. The same evaluation procedure is carried out for them as for the bitches. The results of this class are what most attendees rate as of highest importance on their list of things to se and evaluate. Because a male can be bred up to 90 times a year (60 to German bitches and 30 to foreign dogs), his effects on the breed are much greater than those of even the most frequently-bred bitches.

Who Did What

And now, to the placings and my comments, as I have done for so many years. My forecasts have been very accurate, once the unexpected absentees and sales to other countries have been factored in. The Zuchtwert numbers will be in parentheses; the lower the number, the better the odds of producing superior hips. It is not foolproof, but every bit of data is helpful.

• VA-1: This year’s Sieger Ober von Bad-Boll (ZW-82) is fully worthy of the title, having shown very good work in the courage test on Friday, and offering genes from notable ancestors. He is a paternal grandson of VA2 Quantum von Arminius, and his dam’s grandsires are Sieger Ursus and Sieger Rikkor. VA5 last year, he is another top offering from Hans-Peter Rieker, who historically has put much emphasis on working-dog character. Ober’s progeny were very uniform, with strong males very much in evidence.
• VA2: Remo Fichtenslag (71), bred by Marco Ossman and owned by Josephine Kao of Taiwan, did good work in the protection phase also. His good-gaiting progeny were uniform and very promising, though young. His hip score, courage, and progeny make him a great candidate for Sieger in the next year or two.
• VA3: Yerom Haus Salihin (86) had been an early favorite for one of the two top spots, but tired too soon and lost his last chance to be Sieger. He is over 5, and that’s usually the age limit for success in the conformation (show) ring, although I have seen many top dogs at the BSP at that age and older. His slightly steep croup was accentuated by low head carriage (fatigue, out of condition). Progeny were not very uniform, and many had the same steep pelvis fault. He has reportedly been sold to… (somewhere?), and I wonder if the buyers had a queasy feeling watching him in the big ring this year.
• VA4: Kwantum Klostermoor (95), a Sieger Zamp Thermodos son who had the same ranking last year, performed OK in the courage test and looked great gaiting. This 5-year-old’s progeny class, while not numerous, was notable for its mature, strong males. I’m not wild about his relatively high ZW number, but his attitude and anatomy are impressive. The new owners in Japan will be happy enough with him.
• VA5: Shicco Freiheit Westerholt (83) is a handsome son of Maestro Osterberger Land, but his protection work this year was only fair. He was VA6 in 2009. His progeny class showed good uniformity, although several could have had better front reach. I hope he lives longer than his sire who died recently, after being sold to China.
• VA6: Arex Wilhelmswarte (83) is a Sgr Vegas son who was not very serious in the bitework. His small progeny class was pretty uniform with some who stepped too wide in front (a trademark of Vegas) and had toplines not as good as those by another Vegas son, Vanos van Noort (79). Arex is now half Taiwanese, but I don’t know where he’ll be residing. Vanos also reportedly died not long after moving to China recently.
• VA7: Ustinov v Römerland (82), last year’s V-1, again had OK protection work, and his progeny over all had nice structure. This 4-year-old Quantum Arminius son should be back next year for a chance at a higher ranking.
• VA8: Gigolo Bärenschlucht (94), is disappointing to me because of his weak bites, but also because he presented no progeny class, and has a high ZW number. I would like to see the return to the practice of giving VA (excellent-outstanding) only to dogs with a progeny class presented at the show, and preferably with successful adult offspring.
• VA9: Quattro Partnachklamm (a Zamp son with an admirable 75 ZW) is a good-looking dog but, again, I feel that VA recognition should be reserved for proven producers who present fairly mature progeny in the group.
• VA-10: Sultan Jahnhöhe (Vegas son with ZW of 75) did very good work, especially on the first bite (to the attack out of the blind). No progeny class, but a very nice dog with much promise.
• VA-11: Nino v Tronje (an uncomfortable 98) is an almost-3-year-old, handsome son of 2007 V-17 Irok Karanberg (91). No progeny class, of course. In 2009, Nino was SG-2 in the 18-24-month Junghundklasse behind Sultan.
• VA-12: Guccy Heinrichplatz (86) from Berlin, a really good-working and good-looking son of the super producer Odin Holtkämper Hof, is only a few months short of 3 years old, but I predict a bright future for him. He is owned by Jurgen Manser, whom we were going to visit, but his vacation plans did not allow it this year.
• VA-13: Paer Hasenborn (78), a very handsome Quenn son out of an American-bred Mittelwest bitch, is 4 years old and owned by Mrs. Jani of London. His man-work this year could have been stronger, but he had a large, very impressive, and uniform class of medium-size progeny. I would have given this Quenn son a much higher placing—probably VA6—because he produces so well.
• V-1: Peik Holtkämper Hof (76) This Ilbo/Roma son has very nice structure and did pretty good work, though I would liked to have seen a little more confidence and enthusiasm in the courage tests. His dam is a terrific producer, and Peik should [prove his promise in coming years.

At this point, I feel I must insert or express my ambivalent feelings about the increasing number of VA’s awarded in years when overall numbers of adult dogs competing in this main breed show have been falling. On one hand, it might encourage more entries, but on the other hand, it seems counter-intuitive to give the same number of VA’s when total competition is low, as the number awarded when it was at its highest. There were 9 VA males in 1999 at Karlsruhe for the 100th anniversary of the SV, out of a total catalog entry of 406 adult males (233 present). Compare that 3.86% of VA’s to today’s 6.5%, and you’ll see what I mean. I would have stopped at seven VA’s this year, I think.

In the 2010 Gebrauchshund classes (over-2 years & titled), actually competing in the show ring (out of 318 total entered and in the catalog) were 167 adult males plus another 33 that showed up only to do their bitework and then were pulled. This is an abysmally small participation for what used to be the largest single-breed adult-dog show in the world. The females over 2 years old started with an entry of 283 but only 151 showed in the big ring (plus 10 “excused”—presumably because the owners felt they were working-lines without a chance, or some other reason to leave after the bitework).

I did not see as many females working the courage routine as I would have liked, as I was kept busy taking notes on the males. But I chanced to see a few, and I got the impression that they did an over-all better average job than did the males. Perhaps this is because there is not much to be gained by an outstanding performance, the way that can enhance a stud-dog’s use and value. As predicted, the Siegerin was the Vegas daughter Chakira v Pendler (89), but we were deprived of double pleasure because her half-sister Boogie (95) didn’t show up… I remember her great work last year. The Vegas daughter VA2 Egga Osterberger-Land (75) had superior fast gait. So did V43 Flora dei Verdi Colli (91) of Italy, whose sire Arex Haus Neoplantum (86) is now Korea Sieger (his parents were Croatia Sieger and Siegerin), and I mention him because I was very impressed when I saw him a few years ago. I was impressed by the Quenn daughter Fendi Agilolfinger (77) and by Jurgen Oster & Christine Klefisch’s Cheyenne Karthäuser Lowentor, now owned by Reiner Gunst and managed by Uday Jani. The Bruno Vierhundert Hertz Dutch daughter Vannesca Lentfert Hoeve (76) did very good work, but a litter sister was rated insufficient. V-30 was Nickolaus Messler’s beautiful and energetic Martha v Tronje (103). Excellent work was shown by Mona Mohnwiese (78), the only SG-rated bitch, Gert Lammertink’s Lonca Lammersbeek from Holland (81), and V-12 Quickie Hohen-Haus from Austria (also 81). A Sgr Ober daughter, VA9 Nathalie Alcudia (83), was the only VA with a black mask, something I’d like to see more of. The beautiful Viana Fichtenslag (94) got VA3.

I missed only a very few male dogs on Friday because of hurried trips to the toiletten, so my notes in the catalog are fairly complete. Notable courage test performances were given by a good number of dogs, although I would have preferred a higher percentage to have been bred and/or trained for proof of better character. For me, the most impressive (after some of the working-lines dogs) were the sons of Odin Holtkämper Hof. Those that caught my eye in the defense performance were VA-12 Guccy, V8 Hatto Hühnegrab (72), the future-great V-10 Ballack Worringer Rheinaue (73), V28 Chivas Bad-Boll (74), the superbly-trained V61 dog from Holland Azuro Haus Katsboghte (73), and V62 Uso Freiheit-Westerholt (whose brothers have 86 to 89 ZW).

Several Bazi Urbecke sons and daughters represented him very well in both the bite-work and the show ring. The V51 Gaucho Estherlager (ZW-76 Belgian son of the very good worker Tiras Roten Feld) performed very well. Margit van Dorssen’s V-16 Bix (70), Canadian-owned V29 Bobo (88), and Yang (86) Arlett (pulled from breed competition) ranged from fair to excellent in the Schutzdienst exercise. The V-103 Harvey Oostweg (87-ZW son of the notable Javir Talka Marta), a Sirio Real Favorita son named William Suentelstein (87), the V95 Xwattro Stieglerhof (76-ZW son of Idol Holtkämper Hof), and V20 Pardo Baruther Land (91) all did nice jobs in protection.

An amazing performance, considering his eight years of age, was given by Puk Bad Wäldle (79). Carrying on the great work of his sire Olly v Grauen was the very nicely-structured and well-trained super sable, V47 Odin toten Niersarm (87). Really terrific work was shown by the V-104 Bricards Jazco from Sweden, trained and handled by a lady in a wheelchair. He was one of those with special recognition for outstanding work. The V99 Bastian Real Favorita (Vegas/Roma) gave very nice hits.

A beautiful dog that my group saw a few days later at a training club was the Maestro son Darko Vierhundert Hertz (85), owned and trained by Franz Schlenzing. Unfortunately, he did not “let out” on command, which disqualifies for breed-ring showing that weekend. Another of Franz’ dogs with good bites is V-19 Baru Fürstenbrunn (80), a very handsome son of Bruno Vierhundert Hertz (79), whom we also saw working at the training club. Bruno in turn is a son of the wonderful Arko Butjenter Land (94).

A super gray (sable) dog with very good protection work, named Watz Neudenauer-Holzsteige (93), was V31 and handled by John Henkel of the USA. Another impressive-working USA-connection dog was V84 Azlan Petit Geant (94), bred by Irina Deresh of Massachusetts. Another New Englander, Erin O’Shea’s Zambo Riedschlurgi (a great 73 ZW), did excellent work, which made me very proud since I have a daughter of his who is a fireball of a pup—fearless, and promising to be a good Schutzhund dog if I ever stay home long enough to train her. I have so many foreign assignments this year that I have to show her my passport before she will let me on the property!

The Norwegian dog, V63 Ausenberg’s Amir, did very good work, as did V-112 Max Zöller (78), V-83 Falkos Liebeswarte (75), V81 Inox Valtenberg (74-ZW Naxos Holtkämper See son from Romania), V-102 Warso Simonhoff from Czech Republic (90-ZW son of Yenno Hühnegrab), V70 Karlos d‘Ulmental (80-ZW son of the beautiful and great-working bitch Lea), and the only bicolor I saw, the 73-ZW Xoro Anrachtal who was a joy to watch.

Many great-performing dogs are entered in the Sieger Show purely to let the public see their courage tests, and are pulled right after that Friday event because owners know that they have no chance of high placings. This is most often because the dog has not been entered in several shows under several top judges during the year (sort of like qualifying for a starting position in racing) or were from working lines, or maybe had not been given high enough placings already by the judge who is doing the class at this show. Some dogs were absent for various reasons: age, sale overseas, a feeling that the judge would not appreciate them, etc. Notable absentees (for various reasons) were Godalis Tino and his son Iceman Amur (now in China), the Arko son Nick Holtkämper Hof, Yukon, Tyson, Paul Bierstadter Hof, Mexx Hauswalder Bach, Dux Intercanina, Furbo, and a bunch of working-lines dogs who made such an impression last year.

Some miscellaneous comments fit here as well as in any other place. Notable courage performances were given by the Quenn sons V5 Bill Fürstenau (73) and Floro degli Achei (72). A Quenn son who was absent this year, Tyson Köttersbusch (83), had his own very respectable progeny class. A couple years ago, Quenn Löher Weg’s progeny were too young for some people to appreciate his value to the breed, but my prediction then of his future value has been justified in both rings. Odin Holtkämper Hof is one of the best producers of anatomically beautiful dogs since Zamp. Also outstanding in conformation were offspring of the Hill Farbenspiel son Yukon Bastillie, and sons of Floro and Furbo, both of which latter studs were unfortunately absent from the breed-judging lineup. Rumors about these great degli Achei brothers were flying, and concerned spinal injury, cauda equine, aggression, etc., but nothing reliably confirmed. Pretty reliable, however, is the report that both have been sold to China, which country found a great prize in their fortune cookies when they got these boys! It’s getting harder to make my predictions when dogs are zipping off to money-laden China right and left!

editor’s note: Fred is a superannuated SV Zuchtrichter (breed judge) who has judged numerous countries’ Sieger Shows and Landesgruppen events,. He is author of several books, among them are The Total GSD, and the monumental work on Orthopedic Disorders. You can get autographed books directly from the author, and schedule judging or lectures/seminars by e-mailing him: fred@fredlanting.org

Articles can be found on: http://siriusdog.com/sphider/search.php?query=lanting&search=1 Also on: http://vonjagenstadt.com/ and www.fredlanting.org/ or do a Google-type search for his name.

Request permission to reprint these copyright pieces and add this or a similar notice at the end.

Thanks to that excellent research recently done by Johnston, we now have a better understanding of the disease, although no more hope than before regarding its prognosis. I have taken the liberty to edit her work, rephrasing where helpful to the organization of this article and clarifying for the lay reader. Where I have repeated her work verbatim or nearly so, I use a different inset-page width and italics, which I trust anyone reprinting this will honor. My comments within her paragraphs are in brackets. Some typically British spellings in Johnston’s dissertation have been retained. You will also see, in place of “DM”, the frequent use of the abbreviation CDRM, which stands for Chronic Degenerative Radiculomyelopathy. As her study was “dedicated solely to the investigation of CDRM in GSDs”, the most populous breed in the world, “it would provide the largest database so far collected on this disorder.”

Chronic degenerative radiculomyelopathy (CDRM) is a well-recognised neuro-degenerative disease of unknown aetiology which affected large breed dogs, primarily the German Shepherd Dog (GSD). There were other progressive neurodegenerative conditions which had been reported in a number of different dog breeds, but these conditions were too dissimilar to CDRM to warrant discussion in this thesis. CDRM affects selected areas of the spinal cord and brain stem.  The underlying aim of the Glasgow study was to improve the clinical knowledge of CDRM by regularly examining a large group of affected dogs. The most common presenting sign(s), the age at onset, and whether there was any previously unreported sex predisposition were of particular interest. Additional aims were to tabulate rates of degeneration and note the most commonly seen clinical “syndrome.” This project is the first to study a large number of affected dogs repeatedly throughout the course of disease. The previously reported clinical signs have been confirmed and the relationship between age of onset and rate of deterioration has been addressed for which no definite correlation was found.

First described as a specific, separate disease in 1973, it gets its common name from the fact that German Shepherd Dogs are affected most often (studies report a range from 56% to 82% in this breed) and relatively often (one estimate is that 20% of the breed population develop clinical signs of DM at some stage in their lives). GSDs are not the only breed affected. It is much less common in a few other large or medium-size breeds and large breed crosses such as German Shepherd Dog, Irish Setter, Collie cross, Rough Collie, Rhodesian Ridgeback, and Labrador cross.

Dr. R. M. Clemmons, neurology professor at University of Florida’s veterinary school, feels that the peculiar syndrome seen in our breed is also seen only (and even then rarely) in the Belgian Shepherd and the Old English Sheepdog, and he has believed that what is seen in other breeds may well be a different disorder. Those other degenerative myelopathies are probably not caused by the same immune-system-related deficiency as we have in the GSD, he thinks. The president of the Kerry Blue Terrier Club reported DM in her breed, and there has been another indication that Auburn University was about to publish a study of a disorder that appears to be DM in Bernese Mountain Dogs. It is important to remember, though, that while other breeds apparently get some spinal myelopathies that are also degenerative, the DM of the GSD, at least, is probably an autoimmune disease. Dr. Dennis O’Brien from the University of Missouri has been working with the PWCCA (Pembroke Welsh Corgi Club of America) Genetics Committee, according to correspondence from Dr. Sylvia Lueck of Lacey, WA.  A $45,000 grant proposal was submitted to the AKC Canine Health Foundation with support from the PWCCA to do a 2-year study, with 9 investigators, on DM in Pembrokes.  Researchers include Dr. O’Brien and principal investigator Dr. Joan Coates of Texas A & M who had been doing a DM project in German Shepherd Dogs.  The Corgi project was to be different, quite a bit more involved, Dr. Lueck says.  Three major projects (DNA fingerprinting, epidemiologic data collection and a leflunomide trial) were proposed.  At the time I corresponded with Dr. Lueck, she was unable to get any response regarding cooperation from the GSD Club of America.

CLINICAL SIGNS

“Diagnosis” (purposely put in quotation marks here) is by process of elimination, since regular neurological tests aren’t satisfactory, except perhaps for the presence of a brain fluid protein in the lumbar area of the cord. True diagnosis is only possible upon autopsy. Your best bet for a clue while the dog is living would be to consult an experienced breeder who’s been through it with his own dog or dogs, read the literature (this is a good start), and consult your vet for confirmation and medication.  He will see what you have seen, including some of the following.

Initially, the dog does not seem to realize what position his rear legs are in; soon he will begin to drag his toenails and the top part of his paws, and may tremble as if palsied. The dog sooner or later begins to atrophy in the haunches and croup. He may “dance” with the rear limbs because he does not realize how high he is stepping. Proprioception is the ability of the animal to recognize the location of his limbs, and this is increasingly lost in the afflicted dog. He will get his hocks “tangled up” (one hooked behind the other) and trip over them or drag both. Later, he will have more difficulty getting up and “steering” the rear quarters. Eventually, he will be unable to get up on all four legs, and by this time most owners will have decided upon euthanasia. There were only two cases in the U.K. study, that were maintained for two years after first signs of thoracic limb involvement, such as stumbling in front; these had both been in a “K-9 Kart” for more than 12 months, their back halves being supported by the wheeled contraption. My own cut-off date for euthanasia is when a dog can no longer get up and squat to defecate. Everyone has to decide on his own deadline, but you must have a plan and stick to it, or the event will be even harder on you.

It is not possible to diagnose CDRM definitively in life.  A presumptive diagnosis [best guess] could be made, however, based on typical history and clinical signs. Clinical signs of CDRM had been well documented. The dogs showed a slowly progressive pelvic limb ataxia and paresis with loss of proprioception. Initially they scuffed the middle two toes of one or both hind feet. Subsequently they developed problems with circling and with stairs, especially going down; they often scuffed, misjudged distances and showed hypermetria (ataxia in which intended movements overreach the intended goal). The dogs were often affected asymmetrically [more or earlier in one limb than the other] although both pelvic limbs were usually involved. Disuse muscle atrophy developed over the trunk and hindquarters several months after disease onset. With time, prolonged scuffing resulted in excoriation and ulceration of the feet. Eventually the disease resulted in marked paraparesis; the dogs could not rise without assistance and would pull themselves along with their thoracic limbs. A degree of faecal and urinary incontinence would often develop late in the disease.  Dogs maintained beyond this stage could show thoracic limb signs. It had been reported that brain stem involvement eventually occurred (Clemmons, 1992) which could result in a number of signs including asymmetrical tetraparesis, cranial nerve abnormalities and altered mental status. The clinical signs were inexorably progressive and whilst they may have stabilised for short periods of time, improvement did not occur.  Typically, the signs, which developed as the disease progressed, were as follows: wearing of the nails became increasingly noticeable and more persistent; all dogs started to have problems turning, developing a tendency for the hindquarters to fall to the outside on a turn. These difficulties were more obvious on slippery surfaces and on stairs. Most cases were still keen to exercise at this stage. Crossing of the pelvic limbs then developed, where one leg would get caught behind the other, which often resulted in the dog falling over. Collapsing to one side when walking in a straight line followed. Eventually, after a period of six to 18 months, the dogs were unable to rise to a standing position, so pulled themselves along with their thoracic limbs.

In the brain, the lateral vestibular nucleus (LVN) is the one most commonly affected in CDRM. The axons of all these cells pass to the spinal cord in the vestibulospinal tract. Cerebello-vestibular fibres from the cerebellar cortex provide a feedback mechanism between the vestibular nuclei and the cerebellum. Maintenance of equilibrium or orientation of the body in the vestibular righting reflex is largely reflex activity governed primarily by general proprioceptive impulses from muscles, tendons and joints in the trunk and limbs, and special proprioceptive nerve endings which initiate impulses conveyed via the vestibular nerve to the vestibular nuclei. The LVN, by way of that vestibulospinal tract, exerts a facilitatory effect on spinal reflexes that control muscle tone, especially to maintain appropriate posture or strength of supporting and balancing movements. This is compromised in the case of DM, and the dog is unable to sense that its rear feet are not in the right place or doing the right thing, and likewise is unable to exercise normal control over them. These tracts have an effect on the spinal cord nuclei supplying the antigravity (i.e. the postural and extensor) muscles. [Thus, the DM-affected dog will tend to gallop or bunny-hop rather than trot or walk with as much extension of the hocks as previously or normally.] A failure in the normal activity of the vestibular system due to DM or other lesions may cause disequilibrium, staggering, postural changes, falling or rolling to the same side, and other reactions. [Most owners choose euthanasia long before these symptoms appear.]

METHODS

[From Johnston’s work]: A full case history was obtained from the owner and referring veterinary surgeon and the relevant details were recorded. All cases underwent full systemic examination, full physical assessment, and neurological examination and the following functions were found to be the most useful in the assessment of CDRM.

Gait was assessed initially for lameness, coordination and weakness with the animal moving in a straight line on a flat surface. This was observed from the side, in front and behind the animal.  This was followed by assessment of gait during circling or when going up and down stairs.

“The wheelbarrow” [in which the dog is picked up at either end and made to walk on the other two legs] and hopping tests were used primarily to detect weakness of limbs and to highlight any asymmetry between limbs.

Neurological tests used to evaluate the sensory modality of proprioception also required adequate motor function by the animal to perform properly. Conscious proprioception and motor function were assessed by paw position, reflex step, and hip sway tests. The hip sway test was carried out by holding the dog either side of the midline in the flank region and gently moving the dog over to one side then the other. A dog with normal proprioception will immediately move the relevant foot such that the body is properly supported.  Proprioception was severely affected either unilaterally or bilaterally, depending to some extent on the duration of disease.

Muscle tone was assessed by passive flexion and extension of the limb; muscle bulk and symmetry were assessed by palpation; and the local spinal reflexes (patellar reflex and pedal reflex) were assessed in the pelvic limbs with the dog in lateral recumbency. The pedal reflex was tested to evaluate flexor muscle group strength and to assess cutaneous sensory fields in the distal limb.  In the thoracic limbs a similar examination was made. Joints were examined for the presence of musculoskeletal disease.

Mentation [mental activity] and posture were noted and the owners questioned about any change in behaviour or attitude.  The presence or absence of conscious pain perception was noted.  Additional signs of importance were a lack of any spinal pain and no evidence of faecal or urinary incontinence (except very late in the course of the disease).

The clinical signs indicated both motor (paresis) and sensory deficits (abnormal proprioception) and suggested that the major abnormalities occurred within the T3 to L3 region of the spinal cord. Based on these and other findings, an attempt was made to localise the lesion to this region.

ACTUAL DIAGNOSIS

Previous studies had identified the major clinical signs of pelvic limb ataxia and weakness to have resulted from degeneration of tracts in the white matter portions of the spinal cord.

Autopsy will not help you or your dog, but would find the obvious demyelination (loss of the insulating sheath) of the spinal cord, destruction of some large axons (nerve cells leading from the cord to smaller branch nerves), and abnormal cells (or certain cells in abnormal locations).  Similar signs may be seen in the brain’s white matter, and plasma cell infiltrates in the kidneys and intestines give further evidence of the immune system failure at the root of this disease.

PATHOLOGY
It had been reported that brain stem involvement eventually occurred (Clemmons, 1992) which could result in a number of signs including asymmetrical tetraparesis, cranial nerve abnormalities, and altered mental status. The pathology in the spinal cord had been described in detail by a number of authors. Lesions were considered to be typical of Wallerian-type degeneration and affected both the axon and myelin sheath.  Observed clinical asymmetry correlates with pathological asymmetry. This loss of axons and myelin sheaths is seen in many cervical and cranial thoracic segments, but occasional axon and myelin sheath loss is also noted in the lumbar and sacral cord segments.  In an area of the cord known as the lateral funiculus, the corticospinal tract is most severely affected in the caudal thoracic segments. In the thoracic cord, Clemmons saw vacuolation, swollen axons, and other things that represented degenerate and regenerate axons. The present study [Johnston] also identified significant brain pathology.    The intermediate horn [column of cells] is the region in the grey matter of the cord that is most often affected in CDRM, but most agreed that the white matter areas of the spinal cord were the most consistently affected, with degeneration involving both axons and myelin, often with an associated gliosis. The caudal thoracic segments were consistently the most severely affected. Only one author suggested that there was evidence of axonal regeneration in the spinal cord (Clemmons, 1989), the same author mentioned the possibility of changes occurring in unspecified white matter areas of the brain.  Detailed examination of the brains of affected dogs revealed novel (not seen in other disorders) pathological changes in specific brain nuclei. Such changes included neurones with eccentric nuclei, chromatolytic neurones and neuronal loss often with an associated gliosis. These changes affected the red nucleus, lateral vestibular nucleus and lateral (dentate) nucleus to varying extents. Such changes were found consistently in CDRM dogs but only rarely in dogs with focal spinal cord lesions. Furthermore, gliosis in the red nucleus was found only in the dogs with CDRM.

Dogs with DM often develop lick granulomas, which are ulcerations or (if you are lucky) callous-like reactions of the skin to extremely frequent licking, sometimes chewing, at the location of a supposed itch. It is probably a case of the limb feeling as if it has “fallen asleep”, to put it into terms familiar to human experience. The tingling sensation caused by incomplete and erroneous signals by the nerves serving that place is much like the irritation caused by an ant bite, or hairs out of place, or anything in between. In trying to lick it away, the dog actually softens and wears away the hair and skin. The best I could do for my dog was prick a vitamin E capsule, squeeze out a little for topical application to the granuloma, pop the rest into his mouth, and then give him some distraction such as go for a walk. These ulcers on the feet or elsewhere don’t easily respond, but the battle must be waged if the dog’s life and comfort are to be prolonged. If vitamin E does help in immune system insufficiency, it may be temporary, though it is more often just “managed” or covered up, or it may be worth the effort. It may limit itself to just one or two symptoms such as the biting/nibbling/licking.

Symptoms and histological changes of canine DM are very similar to those in human multiple sclerosis (MS) but most scientists do not admit to the probability of a genetic relationship. Still, I cannot help but suspect that most of these various canine immune-system deficiencies might be related: DM, demodex sensitivity, hormone and endocrine gland irregularities, corneal dystrophy, cauda equina, some allergies, pannus, and other problems, and perhaps even some human ailments. A big problem is that so many gene-mediated disorders of these types also have a large environmental component.

Since DM is so similar to multiple sclerosis, many thought it worth trying the nutritional approaches used by some who treat that human disorder. Wheat germ oil contains octocosanol, a fatty or waxy high molecular-weight alcohol also given to patients with encephalitis and cerebral palsy, and also contains linoleic acid (as do several vegetable oils). But one fatty acid, docosahexanoic acid, is not at all abundant in normal diets, yet seems to be the first one depleted from the nerves’ myelin sheaths in such disorders as MS. In many diets for MS patients, foods such as sardines and mackerel are emphasized, because they are among the very few foods that can supply this compound.  Of course, vitamin B complex high in inositol, B6, B12, and choline frequently is also highly recommended as an adjunct to vitamin E for nerve-muscle disorders.  Since only a percentage of patients with MS or DM respond satisfactorily to a vitamin-only approach, the concomitant use of drugs and exercise perhaps should always be prescribed. As of this writing, there were three FDA-approved drugs for MS that not only help manage symptoms but also appear to “impact disease course” in relapsing MS, according to the National Multiple Sclerosis Society. They are Copaxone (Teva Marion), Avonex (Biogen), and Zanaflex (Athena Neurosciences).  Your vet would have to decide whether or not he wanted to “go off-label”, since these have not (yet) been approved for dogs.

For several years, there was no generally accepted treatment, but as breeders became aware of the benefits of high vitamin E dosages in other immune-related disorders, the veterinary profession began to look into its efficacy and the relation to the immune system.  When I first encountered it, I imagined that I got an extra one or two years useful life out of one of my dogs by giving him 800 units (IU) a day, plus vitamin C for its synergistic effect. Years later Clemmons and others claimed that 2000 IU of vitamin E daily, 500 mg of vitamin C twice a day, and a high-strength vitamin B complex twice a day was the best dosage. Vitamin E is an important nutrient with a number of physiologic and pharmacological effects. As an antioxidant it helps reduce oxidation of fats and increases the production of HDL cholesterol. At higher doses it decreases production of prostaglandins and has anti-inflammatory action. There are no known side-effects to vitamin E at levels less than 4000-6000 IU per day (except in cats, where levels above 100 IU/day can create hepatolipidosis.  In DM, low serum and tissue concentrations of vitamin E have been observed, although recent research by Johnston indicates this may be equivocal.  I recommend that vitamin E be given to older German Shepherd Dogs for a variety of benefits.  Dr. Clemmons recommends the vitamin E be dropped temporarily to about 100 IU if the dog has to be given aspirin for any reason during the treatment, and recommends that daily DEC (diethylcarbamazine) replace the monthly heartworm medications ivermectin (Heartgard, Heartgard Plus, Ivomec brands) and Interceptor (a different antifilarial drug) because these increase immune responsiveness; also use the DEC in place of styrid caracide or Filaribits, he says.  Personally, I would simply stop all use of heartworm medication, because the dog with DM probably isn’t going to last as long as it takes for a case of heartworm to become life threatening, anyway.  Flea control should possibly be limited to Precor™ for the house, and carbamates or pyrethrin/pyrethrum on the dog.

Chemical-pharmacological treatment has largely been via the use of aminocaproic acid, something my friend Wayne Riser (founder of OFA) told me about many years ago — he recommended it for pain relief in hip dysplasia patients.  More recently, acetylcysteine three times a day has found acceptance.  To Clemmons, it appeared the best treatment is a combination of all three approaches (these two and the vitamin therapy), along with exercise.  According to some, alternate-day dosage with a steroid such as prednisone, plus acetylcysteine, added to the aminocaproic acid and vitamin formula, is enough to keep the dog owner very busy and tied to the home, but it might offer a chance at reducing progression, thus prolonging life considerably more than in the past. More recently, Clemmons has been quoted as saying that steroids are no longer recommended for DM dogs. He found that steroids lead to muscle wasting. Therefore, giving steroids to a dog with DM is like pouring gasoline onto a fire. A dog with DM that is given steroids will lose muscle mass much more rapidly than one that is not on steroids. Hydergine, a prescription drug derived from ergot fungus, is being studied, since it seems to promote nerve regeneration. For dogs with advanced DM, Dr. Clemmons suggested trying 5 mg three times a day for at least three months. There is still some disagreement among researchers as to both the nature and the preferred treatment of DM, but the work by Johnston is the most comprehensive and detailed, and she indicates that these approaches are, at best, dubious in reputed value.

Unpublished reports from the U.K. indicate that, of the dogs diagnosed with DM, 88% of those still walking at 12 months and 80% of those walking at 18 months after symptoms were recognized, were being treated with aminocaproic acid, at least.

I mentioned exercise, and this is the third of what might be considered a four-part fight against the disease.  Every other day, the dog perhaps should be given 30 minutes of aerobic activity such as vigorous walking or swimming; if you start late, build up to the strenuous level gradually.  If your dog can’t do the most, do less, but make it regular and stretch the limits where you can.  The alternating days of relaxation are important for repair and renewal. If the dog acts sore, give him the analgesic prescribed by your vet (after he has “read up” on the interactions of medications in regard to DM).

NUTRITION AND “ALTERNATIVE MEDICINE” CLAIMS

The fourth part in the semi-holistic Clemmons approach is stress reduction. The vitamin C, that anti-stress vitamin, is in his recommendations for a good reason, but take steps to avoid stressful situations, including surgery. If the dog needs surgery, make sure he gets the acetylcysteine as well.

The approach to treatment of DM that has been proposed by Dr. Clemmons is what he calls “integrative treatment”.  It combines conventional pharmaceutical treatment with “alternative medicine” or “supportive therapy”.  Paraphrasing some of his comments might be helpful here.  Conventional drug therapy (medicines) has been of little lasting help to patients with DM. However, the combination of exercise, vitamins, and certain drugs (he says) has delayed the progression of DM in many dogs. Treatment has been directed at suppression of symptoms, and since until recently the actual cause or causes of this autoimmune disease were not known, little had been done in the way of finding out how to prevent it. We now know that the genetic component is the major factor.  Saying that Degenerative Myelopathy is an autoimmune disease means that the animal’s immune system attacks its own cells; in this case, the central nervous system.  The myelin insulation sheath around the nerves and axons (fibers) is gradually destroyed.  It’s worst in the thoraco-lumbar area of the spinal cord, but can also affect the brain stem and other nerve tissue.

“Integrative” or supportive treatment of DM, as promoted by Clemmons at the University of Florida vet school, suggests the use of dietary alternatives and supplements to combat the immune system, and is derived from an approach to treating Multiple Sclerosis.  You probably know at least one person with MS, and can recognize the similarity in symptoms.  It has been postulated that besides the vitamins E and C, the drugs, and the exercise mentioned above, avoidance of toxins such as is found in pesticides and lawn chemicals, and perhaps in some processed foods, is possibly helpful. Clemmons recommends “stress formula” B-complex containing 100 mg of most of the B vitamin components. Or use yeast as a good source of these B-complex vitamins, trace minerals, and some protein.  It is relatively inexpensive; try half a tablespoon mixed in each meal. If your dog gets flatulence from this, as most do, use a discount or mail-order vitamin B complex pill instead.

Antioxidant vitamins E and C are synergistic; i.e., they work together better than they do separately.  While dogs produce vitamin C, those with DM may need more than they can manufacture.  In excess, it also can cause flatulence.  Tolerance in the intestines may be for as much as 3000 mg per day, but up to 1000 mg twice a day should be enough unless it causes diarrhea.  Selenium also is synergistic, helping vitamin E to be more effective.  It can be toxic to medium-size dogs if given at more than 200 µg (micrograms) of selenium per day.  I take 200 µg whenever I feel I’m not getting much western grain (good source of selenium) in my daily diet (which is rarely, such as when I’m out of the country for an extended time), and I weigh twice as much as my largest German Shepherd Dog. I keep it in the house to give it (100 micrograms daily) along with vitamin E to my old stud dog in an attempt to control prostate enlargement.

Clemmons says that “Omega-3 fatty acids such as EPA (eicosapentanoic acid) and DHA (docosahexanoic acid) are constituents of fish oils that act as anti-inflammatory agents and may be worth trying if your dog has an autoimmune disorder or arthritis.” If so, fortunate is the owner who can give an afflicted dog a couple of cooked sardines or a small piece of salmon as a daily, natural source of such fatty acids.  A 1000-mg fish oil capsule, tablespoon of ground flax seeds, or flaxseed or wheat germ oil supplement can do about the same thing.  If you are really “into” the health-food store shopping, 500 mg twice a day of GLA (gammalinolenic acid), a fatty acid found in evening primrose and black currant oils, is an alternative anti-inflammatory without the side effects of most anti-inflammatory drugs.  All of the above should be considered as optional adjuncts to conventional treatment with the drugs, vitamins, and exercise, not replacements for them. Johnston found none of these therapies to be effective, however:

Clemmons (1992) suggested, among other ideas, the presence of an 85kDa antigen in dogs with CDRM.  However, no other authors have mentioned such a possibility. He has also made numerous other observations and conclusions that have not been duplicated by other researchers, so one must look with care at his “data” until verified in the scientific community. His treatment regimen has also been controversial, as the claims made therein have not been substantiated elsewhere. High doses of vitamin E (2000 IU/day), high-potency B vitamin complex, and epsilon aminocaproic acid (EACA) had all been used as treatments (Clemmons, 1989 & 1992) although their efficacy appeared questionable. Since EACA has anti-protease activity, Clemmons considered that it would therefore be helpful in CDRM, as it would presumably block the final step in the inflammatory pathway, thus helping to prevent tissue destruction. There was no further evidence suggesting that any of the therapies suggested by Clemmons were beneficial in the treatment of CDRM, which was still considered untreatable. All authors agreed that maintenance of regular exercise and optimal body weight seemed beneficial to affected dogs.  Clemmons has been the only author in the scientific literature who suggested a treatment regime would be effective which included vitamin E, vitamin B, and EACA; this was not confirmed by other workers in the field.  Clemmons in 1989 and 1992 suggested that a combination of vitamins, evening primrose oil, and essential fatty acids might slow the rate of neuro-degeneration in cases of CDRM. These claims remained to be substantiated, although a number of owners have decided to give their dogs these therapies.  The rate of deterioration in the studies reported by Johnston was not obviously altered in the cases given the vitamins and evening primrose oil therapies.

Clinical and pathological similarities between CDRM and neurodegenerative disorders due to vitamin E deficiency in horses and humans had implicated vitamin E as a potential factor in the aetiology of CDRM. This stimulated a study of serum vitamin E concentrations. Data presented in this thesis suggests that affected GSDs do not have significantly lower serum vitamin E concentrations than other breeds of dog. In contrast, GSDs with CDRM appear to have elevated levels of serum vitamin E in comparison with the general canine population. [That may be because owners are supplementing.]

[Johnston found that]: The significance of the possible involvement of vitamin B 12 must be questioned, as the study this idea was based on did not include a control population of unaffected dogs. CDRM may occur due to the abnormal absorption of some other nutrient(s) such as vitamin E, or the reported biochemical abnormalities might be occurring secondary to (a result of) the neurologic dysfunction.  It has been postulated that since “ataxia with vitamin E deficiency” (AVED) in man responds to the administration of high doses of vitamin E, and that loss of axons and myelin sheaths had been associated with chronic vitamin E deficiency in rats and rhesus monkeys as well as humans, the deficiency of this free radical scavenger that protects neuronal cell membranes from peroxidation could lead to increased membrane fragility and ultimately neuronal cell death. Barclay and Haines (1994) suggested that an immune-mediated spinal cord destruction might be occurring, because they found immunohistochemical evidence in the spinal cords of affected dogs which was not present in the normal dog. Further, the pathogenesis for this or a similar condition in horses is not understood.

As the owners in the U.K. study represented a highly motivated population, the inevitable result was that the vast majority of cases seen were on the dietary supplements (26/34). A further problem with analysing this information was the fact that dogs with CDRM do deteriorate such that they have periods of deterioration interspersed with periods of no apparent deterioration. Thus in the short term, the supplements could have appeared to slow down the degeneration depending on the precise timing of the initiation of therapy.  However, as the dogs were being objectively reassessed at Glasgow on a regular basis throughout the clinical course of disease, any such discrepancies should have been minimized.

Analysis of vitamin E concentrations for dogs in the preliminary investigation using the two-sample t-test, suggested that there was no significant difference between vitamin E concentrations in GSDs with CDRM and non-GSDs unaffected by CDRM. Williams et al (1985) investigated a small number of GSDs with CDRM (n=7) and found that they had a slightly lower serum vitamin E concentration than control dogs. These latter authors consider that the GSDs with CDRM also had an enteropathy which could cause improper absorption of essential nutrients. Williams (1984) investigated the possible involvement of vitamin B 12 deficiency but ruled this out as a possible cause of CDRM.  Serum vitamin E concentrations, when measured, were lowered in neurological disorders in other species which had been attributed to vitamin E deficiency.  Work done in other species had suggested that serum vitamin E concentration was decreased quite considerably before any associated disease occurred.  The data presented in this work, in the light of findings associated with vitamin E deficiency and disease in the dog and other species, suggested that deficiency of vitamin E is unlikely to be a primary factor in the aetiology of CDRM.

GENETIC EVIDENCE

The finding of CDRM in several littermate pairs, combined with the acknowledged high incidence of the disease in the German shepherd breed in general suggested that a genetic factor may well be involved in the aetiology of the disease, as previously suggested  (Clemmons, 1989). Due to this unusually high incidence of CDRM in one breed of dog and the discovery of at least two pairs of affected littermates, the investigation of a possible genetic factor was indicated. Following a literature search for diseases in other species with clinical and pathological similarities to CDRM, a working hypothesis was established: CDRM is caused by a CAG trinucleotide repeat expansion in an unknown gene. A number of molecular biological techniques were employed to test this theory, including the Repeat Expansion Detection (RED) technique. This work is still in progress but there is some evidence, still inconclusive, that CDRM may be the result of a trinucleotide repeat expansion. Undoubtedly, CDRM has a complex aetiology which probably involves several different factors but most authors agree there is almost certainly a genetic factor due to the very high incidence of the disease in one breed. [The results from the Glasgow experiments provided some evidence that CDRM is principally genetic, and specifically of an “expansion” as noted, in the CAG nucleotide sequence on a gene that yet has to be found or marked.]

CONCLUSIONS BY JOHNSTON

This project aimed to examine clinically and pathologically a large number of GSDs affected by CDRM. Clinically, we wished to confirm the previously reported clinical signs, and look for any that may not have been reported. We proposed to follow the dogs through the clinical course of the disease, re-examining on a regular basis to establish whether the rate of degeneration was constant or variable. If variable, were there a number of recognisable patterns, which might suggest we were dealing with a syndrome rather than a single disease? In addition, we wished to confirm whether or not GSDs with CDRM had lower serum vitamin E concentrations than other dogs, since this vitamin had been associated with a number of neurodegenerative diseases in other species.  The initial aim of the pathology investigation was to carefully examine the spinal cord using immunocytochemistry and electron microscopy, as well as classical techniques, to confirm the pathology previously reported and to look for new clues to the pathogenesis and aetiology using the more modern techniques. The next step was to carefully search through the brain, in particular those structures which, on the basis of the clinical signs, were most likely to be involved in CDRM. This search resulted in the discovery that specific brain nuclei and areas of white matter were altered in dogs with CDRM. These findings suggested marked clinical and pathological similarities between CDRM and a group of late-onset progressive human neurodegenerative conditions which were the result of CAG trinucleotide expansions. This led into an investigation of the hypothesis that “CDRM is the result of a [genetic] CAG trinucleotide repeat expansion”. However, further work would be required to definitively prove whether or not this was the case.

According to an e-mail someone sent me in 2002, “…in an article by W. Marvin Davis (U. of MS School of Pharmacy), he wrote, ‘Promising research on a monoclonal human antibody has shown it to favor re-myelination in laboratory animals after demyelinating disease or spinal cord injury. Such an action could conceivably reverse CNS damage in Multiple Sclerosis’….”.  Johnson had said, (re “antibody method of searching for the responsible DNA?”): “However, there was no clear distinction of western profiles between CDRM cases and control dogs. The technique requires improvement and application to a tighter control population — i.e., aged GSDs with no clinical signs of CDRM.”

DISORDERS WITH SIMILAR SYMPTOMS

Cauda equina syndrome, giant axonal neuropathy, tumors, and other disorders may also mimic or be mistaken for signs of DM.  Many cases of spinal and related nerve damage are due to sudden trauma, but some can result from encroachment of bone or tumors into the space occupied by the cord. Since nervous tissue generally does not regenerate, such conditions result in partial or complete paralysis. Symptoms similar to myelopathy may be brought on by a nerve cell degeneration normally associated with age. However, with the latter disorder, the rapidly progressive nature of GSD myelopathy is not seen. Neoplasms also cause the dog to display symptoms similar to those of GSD myelopathy. These tumors on the spinal cord, neuroepitheliomas, have a special predilection for German Shepherd Dogs from six months to maturity at three years of age. There were other progressive neurodegenerative conditions that had been reported in a number of different dog breeds, but these conditions were too dissimilar to DM to warrant discussion in Johnston’s thesis.

CONCLUSION

Much effort has gone into the attempt to find the cause, avoidance, and best treatment for this neurological disease that brings premature death to our beloved canine companions. The best, most scientific and thorough work is that of Dr. Johnston of Glasgow. People often are desperate to try anything, disregarding science and logic, when their faithful pet begins to show signs of this debilitation, resulting in much anxious grasping at shadows. We can’t blame distraught people for going on wild-goose chases, but we can offer them understanding and sympathy as well as the hard facts.

If you have lost a dog to this neurological disorder, I offer my condolences in the form of a poem:

Rondeau on the Death of a Dog

They whimper in their darkness and their pain,

But oh, so softly that one has to strain

To hear.  The life that Folly whispered low

Would stay (and how we wished that it were so!)

Ebbs out, although we grasp for it in vain.

Steady the flow, invisible the stain

Their life-blood leaves on those who here remain.

Unwilling to desert us as they go,

They whimper in their darkness.

We pity pets who painfully are slain,

Or even gently enter Death’s domain,

But human-folk will feel Fate’s cruelest blow,

For, long after they lay their friends below,

And sorrow weighs them down like iron chain,

They whimper in their darkness.

Fred Lanting  ©, 1980

************************************************************************

Here is another sentiment for those of you who are still struggling with the problem:

The Season for Old Friends

In my green youth spring beauties bloomed,

Violets jeweled my life with friendly faces.

Each promised purpled constancy

And each I clasped and cherished.

Years, clustered, ripened in my summer’s sun,

Bade me dream of wine to share.

Friendships warmed in lengthening days

While butterflies, spiraling, ascending, danced.

Now fallen acorns wait for leaf burial;

Now wither white rays and golden heart

Of pearly everlasting, false to its name.

Trees rust in cold, damp nights

To mirror my own autumn oxidation.

The harvest falls to foxes

And purple verities are dun and done with.

Strange, in the grimness of winter’s glare,

Hope ripens orange on persimmon trees

Whose bitter fruit begins to shrink,

To soften, yes, to die.

But mystery unfolds as just before release

It is transformed to total sweetness.

Hold on, my heart, relinquish naught

Which through the seasons love has bought.

Old dogs are dearer than the rest;

Old wine is good, old friends are best.

©  1980, Fred Lanting.  Use poems and articles only with permission

*************************************************************************

© copyright (entire article above, or any part of it) by Fred Lanting; reprint only with permission of author, who would appreciate your adding the information in the paragraphs below.

Fred Lanting is an international all-breed judge with AKC and SV experience, and presents seminars on orthopedic disorders as well as on gait-&-structure, which latter is useful for judging, picking puppies, or choosing breeding partners. He is reached at < Mr.GSD@netscape.com> and you will find some of his dogs and/or articles on several websites, as for example, www.FredLanting.org, (or)  http://vonjagenstadt.com/articles.html (or)
siriusdog.com/sphider/search.php?query=lanting&search=1 , and others.

Inquire about copies of “The Total GSD” by Fred Lanting. 360 pages, 8.5 x 11”, $50 plus $4 p&h (in the US; ask about overseas). “It should be part of any personal library on the canine.” –Erich Renner. “This book has a unique ability to appeal both to the novice and veteran dog owner, something that is very rare in any dog book.” –Cheryl Carlson.  This is the expanded and enlarged second edition, a book with 17 of its 20 chapters applicable and valuable to fanciers of all breeds and a must for every GSD lover’s library. Postage paid if ordered from the author along with the big Canine Orthopedics book, which is $68 including postage. Ask about overseas delivery rates.

********************************************************************************

ADDITIONAL INFORMATION & UPDATES, 2010:

Test for Degenerative Myelopathy gene now available

Dr. Gary Johnson at the Animal Molecular Genetics Laboratory and Dr. Joan Coates at the Comparative Neurology Program of the University of Missouri and Drs. Claire Wade and Kerstin Lindblad-Toh at the Broad Institute of MIT/Harvard and their colleagues have identified a DNA mutation that is a major risk factor for development of degenerative myelopathy in dogs. See the article in the Proceedings of the National Academy of Sciences for details.

A DNA test is now available for use by veterinarians, breeders and pet owners. This test is available through the OFA (Orthopedic Foundation for Animals). The test clearly identifies dogs that are clear (have 2 normal copies of the gene), those who are carriers (have one normal copy of the gene and one mutated copy of the gene), and those who are at much higher risk for developing DM (have 2 mutated copies of the gene).

However, having two mutated copies of the gene does not necessarily result in disease.

Dogs that have clinical signs and a confirmed diagnosis of DM have tested as genetically affected. A relatively high percentage of dogs in several breeds (including Boxers, Pembroke Welsh Corgis, Chesapeake Bay Retrievers and Rhodesian Ridgebacks) have the predisposing mutation. It is important to note that there are a large number of dogs that have tested as genetically affected, but are reported as clinically normal by their owners. It may be that many of these dogs will develop clinical signs as they get older or it is possible that symptoms will never manifest in these dogs. Research is still needed to determine the frequency of the mutation in breeds known to have DM (German Shepherd Dogs, Rhodesian Ridgebacks, Pembroke and Cardigan Welsh Corgis, Boxers, Chesapeake Bay Retrievers, Standard Poodles). In the future, we may identify other risk factors in those dogs that have tested as genetically affected. Wise use of this test can reduce the incidence of dogs at risk for DM in the long-term, particularly if other low frequency risk factors are identified that can more easily be reduced. It is likely to take many generations to reduce the frequency of this disease in breeds with higher frequency of the mutation.

As part of an ongoing collaborative effort by research scientists at the University of Missouri and the Broad Institute, a free DNA test is offered for dogs that have been diagnosed with DM, and for older dogs in selected breeds. Details are outlined in the research section of this website: http://www.caninegeneticdiseases.net/DM/ancmntDM.htm

This research was funded by the AKC Canine Health Foundation, American Boxer Charitable Foundation, Pembroke Welsh Corgi Club of America, Rhodesian Ridgeback Club of the United States, French Bulldog Club of America, and French Bulldog Rescue League. To them and the many breeders, pet owners, and veterinarians who assisted, thank you!

———————————————————————————————————-

The following articles are not covered by my copyright:

Degenerative Myelopathy Research  —  Ongoing and Additional

http://www.caninegeneticdiseases.net/DM/ancmntDM.htm

As explained in the DM test announcement and the “Using the DNA test” sections of this website: <http://www.caninegeneticdiseases.net/DM/resrchDM.htm>, we have recently discovered a mutation that can greatly increase a dog’s risk of developing degenerative myelopathy. We have found that dogs with 2 copies of the mutation (testing “affected”) are at risk for developing DM although many dogs that test “affected” remain free from symptoms. On the other hand, dogs that test “carrier” (one mutant copy and one normal copy) or “clear” (two normal copies) are highly unlikely to develop DM.

We are trying to determine if there are genetic or environmental factors that explain why some dogs that test “affected” develop symptoms, while others are spared. If genetic or environmental modifiers do exist, we want to identify them. We are also trying to develop therapies that will slow or halt the progression of symptoms once they start. We expect this ongoing research will yield benefits not only for dogs at risk of developing DM and their owners, but also for people at risk of developing the human equivalent of DM. The entire research team would like to thank all who have participated in the research so far, and encourage participation from owners and breeders and their veterinarians to assist the ongoing research.

One target of ongoing research is determining why some at risk dogs develop symptoms and others do not. Researchers at the Broad Institute are searching for possible modifier genes that may influence onset of symptoms. For this work, we need information and samples from additional dogs. We are offering a free DNA test for dogs that fit our research criteria.

DOGS ELIGIBLE FOR A FREE DNA TEST:

Dogs must meet one of the following criteria to be eligible for a free DNA test:

1) Any dog (any breed) with a presumptive diagnosis of DM made by your veterinarian or a veterinary neurologist. To locate a neurologist use the “Find a Specialist” link on the ACVIM website – www.ACVIM.org

2) Any dog, healthy or not, that is 10 years of age or older from the breeds listed below only:

• Boxer
• Chesapeake Bay Retriever
• French Bulldog
• Pembroke Welsh Corgi
• Rhodesian Ridgeback

Samples for free testing must be sent as blood samples to provide the quality and quantity of DNA needed for the additional research. Please go to the website to download the instructions and the form for sending these samples or for a link to the online store at OFA where you can order the test. Dogs that do not qualify for the free test still may be tested using the screening test offered by OFA.

TISSUE SAMPLES ALSO NEEDED

We also are continuing to study the pathology of this disease. To do this, we are examining tissues from the nervous system of dogs with DM symptoms, as well as older dogs that do not show any symptoms of DM. When it comes time to have your dog humanely euthanized we would be very grateful for your assistance in obtaining an autopsy. We have a protocol that will assist with collection of tissues from specific areas of the nervous system – see the website for this protocol.

BREEDS AT RISK for Degenerative Myelopathy

As part of this research, we have been surveying many breeds for the presence of the newly discovered mutation. As of May 19, 2009 we have found the mutation present in over 75 breeds as well as mixed breed dogs. Some of these breeds have been previously reported with individuals diagnosed with DM and others have not. We are very interested in blood samples and spinal cord samples from presumptively diagnosed dogs of any breed, so that we can confirm the presence of the disease using all useful diagnostic methods.

Although any dog can be tested for DM, it is possible that the genetic background that predominates in some breeds prevents the development of symptoms even in dogs testing as affected. We are reluctant to recommend testing for members of breeds where we have not yet proven susceptibility to DM through microscopic examination of spinal cords from deceased dogs that exhibited symptoms of the disease. At this time we have the required evidence that there is an association between DM symptoms and the mutation in the following breeds;

• Bernese Mountain Dog
• Boxer
• Cardigan Welsh Corgi
• Chesapeake Bay Retriever
• German Shepherd Dog
• Kerry Blue Terrier
• Pembroke Welsh Corgi
• Rhodesian Ridgeback
• Standard Poodle

We do want additional samples from these breeds for ongoing research, as stated above.

Many other breeds have been reported with DM symptoms. We will add breeds to the above list of confirmed breeds as we are able to confirm susceptibility by DNA testing and microscopic examination of spinal cords.

OFA

I have been going back and forth on a topic close to my heart and part of what my decisions will be in regards to breeding… and that is toplines. I CANNOT stand the “arched” (or roached) toplines I see in the German showlines. I tried to get used to it, tried to train my eye to it, and I just can’t do it. It seems all of the showline males available have arched toplines from very slight in the “older style” dogs like Little Man (Leri Unesco) who I used for my first breeding to almost hinge-backed dogs. I see in just about every German showline litter that most of the puppies are hump-backed. I just can’t justify breeding that. And how do I justify that to buyers? Even the pet people know a deformity when they see it! Regardless of whether or not they are what wins in the German ring, and how the German judges try to explain it, it is NOT correct to the standard, and just based on anatomy and basic physics, it is NOT more efficient. In fact, in the case of hinged-backs, it is a perfect site for osteoarthritis to set in, complete with bone spurs, and that is not a good thing to happen around a spinal cord.

So now I am left with trying to find showline dogs without roached spines who have working ability. A tall order. I would be better off looking for a V-rated working line dog, I think. The reason I say this is that given the arched dogs are winning in the ring, I would imagine there are not a whole lot of straight-backed dogs even entered in seiger shows, let alone having them place well. Fewer showline dogs still would have those traits and be good at SchH. I think I would really have better luck finding a working-line dog (who already has the temperament qualities I am looking for) with a V-rating.

I know I have been counseled by some of the best breeders in this country NOT to interbreed the lines, but my goal as a breeder is not to breed what wins in the ring, but what a good German Shepherd should be. Apparently there are many Euro breeders who do take the risk of mixing the lines and with great success. I am not looking to be a “great success” with world-wide accolades – I want to produce the best dog I can, period.

I just would be embarrassed to produce hinge-backed puppies – I wouldn’t want one and how could I awn that off on someone? Even if the pedigree is outstanding, it just is plain WRONG.

Need your advice and guidance on this one – my “workingline mentor” is Shelly Leibowitz and even he thinks I am crazy for wanting to mix the two… but more and more I see myself leaning towards a working line dog – I am just seeing so many issues in the extreme anatomy of showline dogs, not to mention a general lack of working ability. I am not looking to produce alligators, but I do think mixing the two lines can potentially produce the best of both worlds. And if it produces the worst…. Well, I can cull. Not something I would LIKE to do, but something necessary if I am committed to being a “breeder.” I keep my thoughts on hybrid vigor…

-Sara

You are quite right, Sara. The illustrations in the GSD book I wrote (which you have) are apropos.

If you want to improve toplines and get back to the original, you will find precious few “hochtzuchtlinie” (high-line) dogs with “normal” toplines. It started changing in the show lines in the mid-1970s because of the influence of Walter & Hermann Martin, who ran the SV for decades. Nowadays, you’ll find correct, original toplines almost exclusively in the “working-lines” dogs. See attached pictures. Even then, it’s difficult, because the “working-dawg” people have concentrated so much on bitework that they have historically neglected the correct croup length/slope and the correct length/slope of the upper arm.

So while you may find better toplines in the working lines, you will have to go to the showline dogs for correct fronts in most cases.

-Fred

Thanks! Ziggy

Ziggy,
With limited info on the specific nature of “back problems”, we can only guess; but fortunately, my experience in the breed makes them rather educated guesses. A GSD this old is likely to have one OR MORE of a few relatively common disorders: Could have hip dysplasia that is just now getting to the point that the wear-and-tear is hurting or restricting range of motion. Could have Cauda Equina or similar stenosis, although this
usually manifests much earlier in life. Could have spondylosis (see my Internet article on TVS, CAUDA EQUINA SYNDROME, AND SPONDYLOSIS, found onSiriusDog.

If it isn’t primarily spondylosis, it might be what is called chronic degenerative radiculomyelopathy (CDRM) in the UK or degenerative myelopathy in the USA. See if you can find my articles on this subject on that SiriusDog site… look for “The New Knowledge of DM (GSD Myelopathy)” or similar title. I’ll attach these for you, though VetMed cannot get attachments. Or, even better, get my book on orthopedic disorders, which treats of this even though it’s not a bone/joint problem.

Fred

I have a very serious problem occurring with one of my Labs. I came across your article “Thyroid Problems and Suggestions on Dealing with Them” this evening. It had some refreshingly different points of view and pieces of information. So, I am turning to you in the hope of receiving some useful help and advice.

Watson will turn 8 in February. He is an AKC Master Hunter and qualified for the 2008 Master National in June of that year. Shortly thereafter, his work basically fell apart for no apparent reason. He finally was diagnosed with negligible T4 in April and has been on Soloxine for the past eight months. I quickly discovered Dr. Dodds and Hemopet has done most of the bloodwork, including a full thyroid panel along with a full blood analysis.

Watson’s work has improved somewhat but is way below par. He has not passed a Master test since I became aware he had a health problem in July 2008. His T4 level has increased, but was only XX, per his latest blood test, drawn 11/30/09.

Watson is out of my breeding. I also kept one female littermate. Ladybug had her first bloodtest shortly after I persuaded my local vet (I’ve since switched) to perform Watson’s first ever bloodtest. She was found to be deficient in T4, but it was not serious, and she has responded just fine to Soloxine. However, I have not achieved nearly the success competitively with the female that I have with Watson, quite possibly due to my belief that she had hormonal/thyroid issues from a very young age that were not resolved until this past year, thanks to the medication.

The present need is to resurrect Watson’s career before age and other factors continue to cause decline. He is my first and only Master Hunter thus far. The annual Master National rotates among four quadrants of the country. We drove  from California to Minnesota in October 2008, then bombed out on the first day of the eight-day event. This year, the event is in Corning, California, at MY hunt club, only about an hour from my home. I would be much more likely to retire Watson from competition if this were not the situation or if I had an up-and-coming puppy, which I do not. Further, it was and remains my desire to breed Watson. There has been a lot of interest in him and it would be one way to recoup some of my considerable hunt test and veterinary expenses. Dr. Dodds sees no ethical issues in putting Watson out to stud provided the bitches are thyroid-clear. First though, I would have to resolve his own thyroid issue.

Dr. Dodds has no further recommendations on that. Following Watson’s last blood test, she recommended that he receive good mineral supplementation; however, I am concerned about over-supplementing him. I feed him Purina Pro Plan Performance, which already has a lot of elements in it. She was not specific as to how much of what she thinks he should have. She mentioned only selenium, and my reading on it so far has me baffled as to what amount might be optimal. If blood levels seem to rise when there is a selenium deficiency; then, it seems to me that the converse would be true. If correct, that would mean Watson’s is getting too much selenium.

With my local vet’s permission, I have tried upping Watson’s dosage of Soloxine. That seemed to worsen the situation, and I dropped him back down to 0.8 mg, 2x/day.

About a month ago, I also began administering Anipryl to Watson. Watson’s sire passed away this past July, at age 15. Both sire and dam were my dogs. The momma died in May, at age 12, after a brief fight with lymphoma. I had the sire on Anipryl for his last year and a half, and was very pleased with its results. It suddenly occurred to me one day that the symptoms of Watson’s supposed hypothyroidism are exactly consistent with Doggie Dementia; so, I figured, why not treat it as if it is Doggie Dementia? He is the only dog I’ve ever heard of who has not responded well to Soloxine, and I felt I had to compensate for that somehow.

It seems to me that Watson is responding well to the Anipryl, and it also is possible, according to my research, that Watson’s mental decline could be due to Doggie Dementia anyway. Most articles state that it tends to begin around age 6 in large breeds. He is a Lab and a rather large one, at 96 pounds. Additionally, it is more likely to be noticed in earlier stages in performance dogs with vigilant owners.

Nobody seems to know what to do about a dog not responding sufficiently to thyroxine. It doesn’t do me any good to hear about how successful it is virtually in every other case but my own. You state in your article, “One of the lessons I have learned is that, in the best treatment of hypothyroidism, there is a range of results from barely perceptible to nearly miraculous.” I was very pleased to see that remark. Apparently, everyone else has had stellar results, hasn’t learned or has some other problem.

I know I could try different brands, ground natural glands, T3, different dogfood, nutritional supplements, and perhaps, as you might say, pixie dust. The problem is, as you wisely pointed out, various claims and counterclaims come into favor and fall into disfavor on an ongoing basis. I don’t really have a handle on why my dog is messed up; so, it seems to me that it would be relatively easy to make matters worse, since it sure has been impossible so far to make them significantly better.

Hence, I need help. I am willing to incur a reasonable degree of risk while experimenting with the variables; however, I need some logical recommendations to follow.

Can you, will you, please help me?

Sincerely,

Joule

You are right in studying everything that Jean Dodds has to say on this matter. She has long been a cogent and sensible voice for dogs and dog owners’ concerns. If she has some studies showing optimum and risky levels of selenium, let me know where I might be able to read them. While I did not save hard copies, I remember reading long ago about the dangers of over-supplementation with selenium (I suppose one could wade through the tons of stuff on Internet, but I’m old-fashioned and have not the time to do that). I do know from my ancient work in chem. & biochem. etc. that mineral supplementation can very easily be carried too far by dog owners. Years ago, a host of orthopedic disorders were exacerbated by food companies trying to outdo each other in calcium levels. Just as these days, they are hurting dogs by competing for the High-Protein King position.  Dog food companies are all about profit and market share, not necessarily about what’s best for Fido.  Personally, for myself and my older males, I use selenium tablets (100 micrograms for me, 50 mcg for my GSD) to supplement natural food sources. This is because the little extra dietary Se seems to ward off or control prostate enlargement. I don’t know why it would have any effect on gundog or retriever work.

I typed in “Thyroid problems Fred Lanting” in the Google search engine, and found that several websites carry my articles. I have not checked to see which have the most recent versions (had to change my e-mail address a few years ago)…

I think the Google listing gives the most-looked-at sites first. Which one led you to e-mailing me?  The one that is in 2 parts and is called  www.thedogplace.org/Articles/DogCare/09042-Thyroid-2_Lanting.asp – is a good one, since it is the most recently updated, besides the SiriusDog site piece.

Keep experimenting with levels, don’t go to extremes, and let us know if you have any success.

Fred

All endocrine glands are “connected”; i.e., they can influence each other’s action and efficiency. If any part of the endocrine system is out if kilter, so will be the rest. If the endocrine system is not running properly for any length of time, damage could become permanent (adrenal failure, pancreas failure, etc). Two of the most important glands in this discussion will be the pituitary and the thyroid. For a detailed discussion of the pituitary dwarfism in the GSD and related breeds, see www.siriusdog.com/articles/ or use a search engine [such as Google] to find my articles elsewhere on the Internet. Also, you probably should order my book on the GSD. I recommend you get the Orthopedics book at the same time.

Additionally, function in a couple of the endocrine glands can be mitigated or influenced directly by environment. So, it’s a tricky thing to adjust all these factors and treat your affected dog. Since we are discussing the thyroid in this particular article, let’s start with what it is and what it’s supposed to do, before getting into what to try to fix your problem.

In an excellent treatise on the subject some years ago, John Cargill reported:

“In the dog, the thyroid gland consists of two lobes flanking the trachea (windpipe). It has been established that it secretes at least two related hormones, thyroxine (T4) and tri-iodothyronine (T3). The only difference between the two is that T4 has four iodine atoms attached to it and T3 only has three. Even though the thyroid gland secretes mostly T4 (about 90%), it is T3 that is considered the active form of the hormone. [and…] In a series of complex steps that involve mainly the liver and kidneys, T4 is stripped of an iodine atom and is converted to T3 when needed.”

Other signs, though less common and certainly attributable to different disorders, might include neurological symptoms such as behavioral changes (including, at worst, unprovoked aggression), head tilting, circling such as in tail chasing or appearing to search for a good spot to lie down in but never getting there), what appears to be seizures, ataxia, and lack of control of facial muscles. Remember, these are the extremes, and in most dogs you will find only the hair loss, ear crud, and one or two other indications. Abnormal behavior in dogs can have a variety of medical causes, and one might be sub-optimal thyroid function. However, behavior is very complex because it not only reflects the functioning of the whole physical and psychological organism, but it changes as a result of environmental influences.

She found an increase, over the decade previous to her reports, in dogs showing various types of abnormal behavior such as aggression, extreme shyness or seizure-like activity, and that in the majority of the cases studied, significant abnormalities were found, attributable to abnormal thyroid function. The diagnosis in most of these was autoimmune thyroiditis. Her conclusion: physiological change at the cellular level leads to the aberrant behavior. She found that treatment for thyroiditis in these dogs, namely, twice daily thyroid hormone, along with a one-month tapering course of low-dose corticosteroids, successfully reversed the behavioral problems within 10 days to eight weeks.

Thyroxine treatment is apparently a good approach even without the corticosteroid, as her team found out when they had to treat a dog with facial demodectic mange; such steroids are contraindicated in demodectic mange cases. This dog got only the T4/T3 treatment: T4 at 0.1 milligram per 10 pounds plus a one-third dose of T3 at 1 microgram per pound, both given twice daily. The dog’s behavioral aggression subsided.

Dodds found also that for those animals that show occasional and not very severe seizure disorders, the thyroid medication alone usually will suffice.
She also discovered that because many of the animals with behavior problems had autoimmune thyroid disease, it was wise to avoid or minimize environmental factors that challenge the immune system. She recommended a hypoallergenic diet preserved with vitamins E and C, but without added chemical preservatives; avoiding sulfonamide antibiotics and monthly heartworm preventatives that may adversely affect the immune system; and withholding vaccination boosters until the thyroid function is balanced properly and the behavioral abnormalities are resolved. Antibody titers are far preferable to automatic revaccination schedules.

The gland secretes much more T4, but T3 is considerably more active. In other organs of the dog’s body, especially the liver and kidney, T4 is converted to T3 by stripping off one iodide ion from each molecule. T3 is quite potent, and since the healthy body makes its own in those organs, it is unwise for most people to ask that T3 supplementation be attempted. T4 is quite safe in almost any reasonable amount. Along with transthyrein and albumin, a globulin type of glycoprotein synthesized in the liver transports both through the body via the circulatory system, to where the molecules are needed by “target cells”.

One breeder-researcher-writer I corresponded with came up with an interesting analogy. He said, “T3 is the work-horse hormone. If there is a need, the pituitary gland signals the thyroid gland to send out TSH (Thyroid Stimulating Hormone); the thyroid then produces T4, which in turn is converted into T3 and other thyroid hormones. T4 is the gas at the gas station, and the T3 is putting that gas to work. This is why simply measuring the T4 levels in a dog to diagnose hypothyroidism is not correct.”

In Vet School, a student may not get as much useful data as circulates among experienced breeders. This is the case in many areas, such as breeding and reproduction, nutrition, and breed-specific health issues. For example, most vets are taught (and repeat) that young dogs don’t have thyroid hormone deficiencies, so they don’t test for this unless the owner insists. So often, the suspicions of the owner are confirmed, and the surprised vet’s eyebrows are raised twice: once at the test results and again at the remarkable recovery that often occurs in these young dogs.

I will probably keep singing the same refrain about interactions and reciprocal influence between endocrine glands, the same way I do about the interdependence of heredity and environment. Adrenal gland problems are often concomitant with thyroid problems, and “fixing the thyroid usually fixes the adrenals.” An example of hypoadrenia (sub-par adrenal gland activity) is Addison’s Disease.

A recipe for health that has held up well for me for many decades of breeding has been: a well-tested & well-balanced nutrition/diet, moderation in medicine, plenty of exercise and fresh air, indoor humidifiers in winter, and watchful parasite control. Others can feed all the raw chicken, yucca, and pixie dust they want, but so far, they have not come up with any good, logical, scientific refutation for my success as a dog owner since 1937 and breeder since 1945. They can’t effectively argue with results. Nor will either camp likely convert the other. In all the hundreds of pups we’ve produced and the numerous dogs that lived their lifespans with us, I only had one that suffered from hypothyroidism and had need for regular flea control for a while and ear cleaning for a longer period. She had been sent off to travel and compete in the “care” of another professional handler (my mistake… I was too busy handling clients’ dogs to campaign her myself!) When she returned, she was in terrible condition, with the flea and thyroid condition plus a mummified puppy that was retained (she had been bred and delivered while in his hands). I bring up this incident to illustrate the complicated interaction of genetic and environmental factors in the appearance and severity of thyroid-related disorders.

In my successive roles as breeder, handler, judge, and writer, I have been witness to, and recipient of, much that deals with this subject, so I do not have to rely on my own luck or bloodlines for my data and learning. One of the lessons I have learned is that, in the best treatment for hypothyroidism, there is a range of results from barely perceptible to nearly miraculous. The treatment I refer to is the use of synthetic thyroxine. Soloxine® is one brand name; another is Synthroid®. You may also come across the Thyro-Tabs® brand, or Armour® Thyroid Tablets sold for human consumption. The website www.armourthyroid.com has lots of very good information, including effects on reproduction. Other informative websites are www.thyroid.about.com/ and www.soloxine.com/, if these are still current. Whichever you choose, you’ll have to get a prescription from the vet, if you live in the USA.

I have seen amazing results with Soloxine in a number of health needs, especially in fleabite allergy cases and in fertility of bitches that have previously failed to conceive. Many times this temporary sterility seems to be prevented by a couple weeks of administering Soloxine. Forget the T3 tests if you just want to boost conception or try it out for frank hypothyroidism or more other minor problems such as unexplained hair loss on chest, belly, and a few other places (after you’ve positively ruled out fleas). Just convince your vet to sell you a good-size bottle and let you experiment, with his/her occasional supervision. You might ask him/her to let you start with a dosage level of about 0.1 mg (milligrams) per ten pounds of body weight. In my experience and that of many vets I have discussed it with, Soloxine (or the other brands) is extremely safe; none of them were concerned about “overdosing”.

Typically, the daily dosage is divided, the tablet halves being given orally approximately 12 hours apart, though the exact timing is not important. Some of my correspondents report satisfactory results with once-a-day doses of 0.1mg per 10 pounds, while more claim or think they need to give that much two times a day. You can either experiment with this very safe product and determine for yourself what is enough, on the basis of visually observing results, or you can help pay for your vet’s Lexus by letting him run periodic blood tests for T3/T4 levels. Perhaps every month or two until you get an idea of ideal maintenance dosage. One reason for twice-daily medication is that about half of the hormone is used and excreted from the body within 12 hours. Another is that it helps control thyroiditis by shutting off TSH production in the pituitary, and “calming down” the dog’s thyroid follicular cells and thereby inhibiting production of the antithyroid antibodies that give rise to symptoms.

A correspondent in the UK told me she is treating her second hypothyroid Chow-Chow, eleven years old and 35 lbs at the time of this writing, and it has been on the medicine for four years as of this writing. In her country she is using “Forthyron-400” (had used Soloxine on the previous Chow). Her story is typical of many whose vets do not recognize the symptoms as indicative of thyroid dysfunction. Here is part of what she wrote to me:

“Heaven [the first bitch] when started on the treatment was at death’s door — she was severely hypothermic (we couldn’t get a reading on the thermometer), totally uncoordinated, her eyes were ulcerated, and still the vet was diagnosing HD and entropion. I insisted she do a full set of thyroid tests – previously, when I asked her to test, she only did a simple blood test. But by the time we tested for thyroid this next time, it was almost impossible to get blood from her. Her weight had dropped to next to nothing but her head was quite puffy. The change, once medicated was amazing. We only managed to get one test, as it was so hard to take blood. Even using a needle as big as those used to insert chips, it still clogged up as soon as the blood was being drawn up the shaft.”

Speaking of this vet and her current dog, the lady said, “I think she should always test [for hypothyroidism] when there is a change in behaviour (lethargy, grumpiness) and the brittle coat with bald areas. [This] is a pretty good indication, and we have discussed this on more than one occasion.” The dog in question is related to “Heaven” — this second one’s maternal grandsire was the first bitch’s sire. Both developed severe signs well after mid-life, which follows a general pattern in my experience. I have noticed that by the time symptoms are obvious, the affected dog is usually between four and ten years of age, more often middle-aged than geriatric.

In the UK and in vet circles elsewhere, the synthetic product chemically identical to the naturally occurring T4 is referred to as levothyroxine sodium, the active soluble isomer of thyroxine. The likely reason for the vet’s confusion (other than inexperience or perhaps absence from the classroom when the lectures on hypothyroidism were delivered) was a plethora of symptoms due to the fact that basal cellular metabolism and oxygen consumption changes affecting the function of virtually all organ systems can be confusing. Especially by the time the condition has worsened without proper treatment. The dog owner must take it upon himself to “bone up” on health matters and ask specific and leading questions. See the following website if you want more about Forthyron.

On that site, the recommended starting dosage and frequency is 10 micrograms per kilogram of body weight orally every 12 hours. A kg is 2.2 pounds, so this equates to 0.1 mg (milligrams) per 2.2 lbs. of dog, or approximately 3 mg for a 66-lb. dog instead of the 0.6 to 0.7mg tablets of Soloxine that most U.S. vets would start with. Four to five times the typical American dosage. Because of variability in absorption and metabolism, the dosage may require alterations before a complete clinical response is observed, and these represent merely a starting point. Clinical results will determine how you and your vet tweak the amounts, probably even better than plasma T4 levels retested two weeks after dosage changes could, and it could take four to eight weeks to see it in the dog’s coat, behavior, etc. Once you get satisfactory results, clinical and biochemical monitoring can be performed less often, such as every 6 months or annually. Every dog is a little different, so take your lead from the patient.

The following paragraph or two perhaps could be in the above section on treatments and testimonials, but I also feel the subject should be segregated. Some “alternative”, “naturopath”, or “holistic” writers, with variable levels of scientific training, understanding, credibility and qualifications, have suggested dietary preventive measures such as adding a bit of iodine-rich kelp to canine food rations, or avoiding soy (claiming it has thyroid depressant action) and not using “chemicals” to fight parasites… such latter statements really irk me, since as a chemist I decry the abysmally poor education the nation’s children have had for so many generations, under teachers who don’t seem to know that everything is composed of chemicals. These current “manglers of meaning and desecrators of definitions” usually are not careful enough to explain that what they should be complaining about is the overload of synthetic or harmful substances, an “unnatural” excess. Extremism, as Barry Goldwater said, is no vice in the defense of liberty, but it might be in the field of health.

On the other hand, there may be some “alternative” treatments that are beneficial. If you are willing to take the risk with your dog, you can investigate these. Elemental iodine compounded with potassium iodide (5 mg I with 7.5 mg KI per tablet) in a product called Iodoral or Lugol’s solution, made by Optimox, is one example, though I hesitate to mention it simply because I have no personal experience or close knowledge of its efficacy. I know Soloxine works, and though I’d prefer to get any medicines without prescriptions, I feel a little more confident going with what I know. The Iodoral has been promoted for treatment of corals in salt water aquariums, and a number of other things that make sense because of the antimicrobial (killing) effect of active iodine on a variety of fungi, bacteria, etc. But whether the Optimox iodine is actually taken up by the thyroid and used there to “repair/rejuvenate” the gland has not yet been proven to my satisfaction. I want to see double-blind control study results before giving much credibility to such reports.

Potassium iodide (KI) by itself, without the more toxic elemental iodine, is generally preferred by the medical profession for the purpose of adding dietary or medicinal iodine to the body via the gut and/or circulatory system. Elemental iodine is toxic in normally significant amounts (which is why it has been used as a disinfectant). The main reason the potassium iodide is in the formulation is probably because elemental iodine by itself is not water-soluble, but in this Lugol’s ratio, it is made so. The solution was at one time used in the treatment of gout and as a first-line treatment for iodine-deficiency hypothyroidism in adult humans. It has been used in a variety of “alternative medical” treatments for several health problems, and until 2007 was an unregulated over-the-counter product in the USA, sold as a general reagent, antiseptic, preservative, emergency disinfection of drinking water, or medicine for human or veterinary application. As of mid-2007, however, the DEA (Federal Drug Enforcement Agency) now regulates all solutions containing more than 2.2% iodine because they potentially may be used to make methamphetamine. However, as of this writing, you can still get up to one fluid ounce (30 ml) of Lugol’s exempt from this regulation in the USA. It is currently available over-the-counter in Canada and Mexico without such restrictions.

One must be very careful with dosages. Sometimes a tremendous excess can have the exact opposite effect from what the amateur administrator intended. Examples might include vitaminosis with A and D, overloading with calcium supplements that have the effect of shutting down the assimilation of that mineral, etc. If you “overdose” a dog with iodine, you could even cause the Wolff-Chaikoff effect, which is a hypothyroidism caused by ingestion of a large amount and consequent elevated levels of circulating iodide. It is referred to as autoregulatory phenomenon and inhibits formation of thyroid hormones which, of course, is opposite of what you most likely are hoping to accomplish. High levels of intracellular iodide suppress some thyroid enzymes, and reduce synthesis of thyroxine. Wolff-Chaikoff effect can be used intentionally to shut down an overactive thyroid gland, but generally in 10 days it wears off.

In Robert Washabau, a diplomate in internal medicine on the faculty of the U. Penn vet school, is quoted as saying, “Routine hematology, serum biochemistry, and urinalysis should be performed in all cases to investigate possible secondary causes of megaesophagus (e.g., hypothyroidism, hypoadrenocorticism). …additional diagnostic tests… thyroid function test… dogs affected with hypothyroidism should be treated with levothyroxine.” Curiously, the same man hedged a little when as a co-author of another study, they did not sound as positive, saying, “this study did not reveal a clear association between hypothyroidism and acquired megaesophagus.” J Am Vet Med Assoc. 1997 Dec 1;211(11):1406-12. Risk factors for acquired megaesophagus in dogs. Gaynor AR, Shofer FS, Washabau RJ.
source.
Indeed, Wendy Brooks, DVM, is also at least as cautious in an article in : “Hypothyroidism may be associated with megaesophagus. It is easy to rule thyroid disease in or out with blood testing and it is important to treat a thyroid hormone deficiency; however, megaesophagus usually does not correct with thyroid replacement therapy. Whether or not hypothyroidism can truly cause megaesophagus is still being debated.” Washington State vet school, in said, “Less commonly recognized signs that may be seen in a small number of dogs with hypothyroidism include dilation of the esophagus (megaesophagus) …and abnormal ability to walk.”

A word about nutrition might be appropriate here. We know that dog food companies do a lot of blending, and geographic sources of ingredients would be impossible to report in an accurate and current manner. We also know that soil (and thus, grain and beef raised on it) varies considerably across the country in regard to such things as selenium content. Additionally, not all suppliers may be as convinced as some scientists about the need for a minimum amount of this mineral that is considered synergistic with vitamin E and other nutrients, so they may not adjust its level in their brands. Now, I fully realize that in 2008, an experimental program seemed to refute earlier claims of the benefits of vitamin E and selenium, but that study may have been flawed, and I still hold to other evidence that shows these are beneficial. The proponents of vitamin E and selenium supplementation (and I am one) will again have their day, I predict.
Here is the latest on that study: The National Cancer Institute, in 2008, cancelled a $120 million trial of 35,000 men taking selenium and vitamin E supplements as possible safeguards against prostate cancer. The trial ended four years into the projected 7-year period after scientists saw an unexpected increase in tumors among some of the men taking vitamin E, and a rise in adult-onset diabetes in some of those taking selenium. There could be other reasons for an apparent rise in incidence… one of many might be that some men taking such supplements have a false sense of security and reliance on the “miracle-vitamin”, and consequently do something stupid in some other diet or health-practice area, thinking they are invincible.

Such swings in opinion often are based on studies that are not all that well-designed in regard to eliminating other incidental causes for what results the investigators compile. For a recent example, cholesterol-lowering statin drugs were thought to yield better PSA tests in men, but lately it has been learned that they primarily reduce levels of a blood marker for prostate cancer, so it may be that they only mask the disease rather than actually lower the risk.

Another example: it seems that for a long time, every few years there is a back-or-forth reversal in whether or not chocolate, coffee, caffeine, or whatever is harmful to health. Over the years I have seen such claims and counterclaims come and go, with supposedly scientific evidence first showing one conclusion, then the opposite, then the original again, etc. The same thing has happened re saw palmetto, ginseng/ginger/gingko combinations, milk, how many cups of water one should drink each day, and many other things. If I keep to the Biblical admonition of “moderation in all things”, and the current scientific-journal evidence, plus my own observations, and balance all these, I should do OK, I think. So far, my philosophy on this has worked.

“Even mild selenium deficiency may contribute to the development and maintenance of autoimmune thyroid diseases” is a statement that comes from PubMed.gov, along with “In areas with severe selenium deficiency there is a higher incidence…” And, PubMed.gov also tells us, “Selenium deficiency produced up to a 14-fold decrease in hepatic T3 production from thyroxine (T4) in vitro.” In AvianWeb, we find Dr. Havashida’s study, Selenium Deficiency and Hypothyroidism. There are many more such works in the medical literature.

It must be acknowledged that there is no selenium in the thyroxine medication, and no reported level in the thyroid gland. Whether there is a direct connection or simply a beneficial effect on the whole body, or no real need for selenium in specific application to thyroid deficiency, is something that I do not think has been studied. We know that selenium is beneficial, and that Soloxine is a near-miracle drug for sick thyroids, but is there synergism or any connection? I think so, but I cannot state that as a fact backed up with scientific studies.

Complicating the picture is the apparent condition in some areas where diets contain adequate iodine but are selenium-deficient. High or normal T4 analysis may give a false sense of security, because T4 blood levels have been seen to rise when there is selenium deficiency, perhaps as a defensive reaction by the body. However, when this happens, it is often accompanied by depressed levels of T3, which is characteristic of those low-selenium, normal iodine regions.

T3 is converted by the body into T4 as needed, but it is very difficult for the dog owner to administer that without getting into toxic doses. It is much safer to give T4 and let the dog convert it internally. A few dogs are unable to do this, and these may require frequent medical monitoring by your vet. Some few dogs are able to get back to normal metabolism and do away with the need for thyroxine, but don’t count on it. If you follow up every couple of months, and see if dosage needs to be changed, long-term therapy can be very satisfactory. The good news is that Soloxine is cheap compared to most medicines, and your vet clinic visits can be spaced out further and further apart if the first months give good results.

If we learn nothing else, we should come away from a study of the endocrine system with the realization that not only do all the glands have effects on the others, but that there are many analogous biochemical interactions that teach us that the well-functioning body is a marvel of balances. Vitamins, minerals, vaccines, hormones, nutrition, medicines, genes, exercise activity — all are important to a healthy life, and in moderation, for the most part. The definition of homeostasis is appropriate here: The maintenance of steady states (you can call that “health”) in an organism by coordinated physiologic processes. Thus all organ systems are integrated by automatic adjustments to keep within narrow limits disturbances excited by, or directly resulting from, changes in the organism or its environments.

Sometimes, to restore or approach such homeostasis, we need to medicate. If you can accomplish it by careful breeding, all the better, but we live in an imperfect world, and sometimes we need a little help from our medical or chemical friends.

p.s. A typical testimonial, from GSD breeder Andrew Masia, May 2009: “It’s funny that you bring this up, because when I started breeding about 20 years ago, at the urging of Margaret Iaquinto and Al Stone, I put all my bitches on Soloxine starting about 1 month before their scheduled cycle and continuing on right up to their due date. All of the bitches were in estrus at about 16 to 20 days max with no incidents of a split heat cycle and the smallest litter that I had was 7 pups. It seems as though I have forgotten my past precautions over the last several years and I think that not so coincidentally I have recently seen more split heat cycles and smaller-sized litters. I will have to go back to the basics when my next bitch is nearing her heat. It will be interesting to see what the results will be.”
————————————————————————-
Copyright 2008 by Fred Lanting, All rights reserved, but reprinting allowed after permission. Please read his other articles: on SiriusDog.com and www.FredLanting.org, for example, or e-mail him at Mr.GSD [@] netscape.com for specific articles or to order his book on Canine Orthopedic Disorders or “The Total GSD”.

For a couple of decades, I have been taking small tour groups (one to three vehicles) on guided tours of Europe, with the Sieger Show as the centerpiece. For those reading about this for the first time, this show is the world’s largest single-breed dog show, and has competitors from various countries all around the globe. My background as an SV breed judge, combined with my lifetime of activity in the breed, species, and sport have enabled me to offer the best experience of this sort. I predict, explain, teach, guide, and introduce. If you would like to have fun and “save and see” along with a group of friendly fellow dog-lovers, contact me as soon as possible after the first of the year. Email Mr.GSD (@) netscape.com for details on my non-profit tours.

In 2009, the weather was great. A tremendous improvement over the cold rain in 2008. But the stadiums have overhanging roofs to keep spectators dry, and the GSD is a working dog that shrugs off weather anyway, so why shouldn’t its owners do the same? Even in the days after the 3-day show (that’s when I take my groups on visits to breeders, clubs, and regional attractions) we had balmy conditions. This year, it meant my folks could enjoy the ride up the mountain in open horse-drawn wagons to see the fabulous Neu Schwanstein castle in Bavaria that inspired the design of the smaller Disneyland one. Some of us climbed the 763 steps to the top of the world’s tallest church in Ulm during the weekend.

My group this year consisted of three from Uruguay (two had been on a previous tour, and I also knew them because I had judged in their country twice), and three from America. Three of the group had never been to a Sieger Show before. We flew into Munich, the land of lederhosen and spirit-lifting oom-pah-pah music, walked through part of the big park called “English Garden” and then watched the dancing figurines celebrate the striking of the hour in the tower of the immense, impressive Marienplatz building. Then we struck out for our hotel in Altenstadt, on the Iller River that forms the western border of Bavaria. Half an hour’s drive from the show, it was an economical and pleasant alternative to rooms in the city.

I’ll mention a little more about the tour before giving you the highlights of the show itself. This is just part of the difference between my reports (and tours) and others you will find on the `net, another being an SV judge’s perspective on the dogs and action. After this year’s competition, we dipped into a bit of Austria briefly and then toured one of the fantasy castles built by the free-spending Ludwig, the chief patron of Wagner, whose operatic themes are echoed everywhere in the Bavarian king’s opulent architectural creations. After that, we enjoyed the company of long-time successful breeders Martin and Maria Göbl of Wildsteiger Land kennel. Martin, who told me he was offering for sale most of his dogs in an attempt to retire, showed us his rooms full of trophies as well as his current dogs. One of these was the very handsome 3-year-old Yvo, who is one of those he might be willing to sell. Another is the excellent young untitled dog, Buffo.

That evening, after a typical Bavarian supper with wild venison and local specialty side-dishes, we enjoyed an evening with instrumental music and singing in the Bavarian style and language.

The following day, we visited the small kennels of Josef and Jürgen Erhard, who also have some truly beautiful dogs, including some outstanding puppies. Lunch with them was at a golf course that would rival some of the best country clubs in the States, but with the Alps as a backdrop. All of rural Germany is amazingly clean and beautiful, but the mountains in the distance add even more to the ambience. That evening we checked into the hotel near the airport. Because of the weakness of the dollar against the Euro this year, price inflation, and the relatively small group to divide my expenses amongst, I cut this year’s tour by one day. But we still had a super time with the show, the hosts, and the fellowship of the travelers. Next year the show is in Nürnberg (spelling corrupted by English and Americans as “Nuremberg”), and I’ll probably have my 2010 group fly into Frankfurt. As usual, I’ll have to brush up on my German and Spanish in the weeks leading up to the show. This year, I was struggling with switching between those languages and English to translate for everybody. Some of the people don’t speak English, most do not speak German, and it made for a lot of laughs.

And now for the show itself. If you have read my predictions on the `net, you will be aware that I was “darn close in my educated guesses” in spite of many absentees due to sale overseas (mostly China) or retirement. My prognostications are based both on my personal observation of gait & anatomy, and on how the dogs have performed in the past. For those who are breeders or prospective puppy buyers, I am listing the current hip rating (Zuchtwert) in parentheses behind dogs’ names. The lower, the better or safer. In the 70s is preferred, but close to 90 or above represents increased risk of dysplasia.

Entries and attendance were still down from many previous years because of the world economy, but Europe is better off than America in this regard, and is bouncing back earlier. The show was noticeably better than last year, and in a much better stadium.

Friday is the longest day, with lower-ranked dogs between 12 and 24 months’ age competing in four scattered rings, and the adults doing their protection qualification tests in the large stadium (divided by a screen so females and males, respectively, can’t see the bitework going on by the other). For those purists in the sport, and those who want to know the true performance in order to add that to the calculation of which dogs are better to breed to or linebreed on, this is the most important part of the competition. At smaller shows during the year, only the beauty-contest portion is seen, and that is not enough to base such decisions on.

But even in spite of this supposed safeguard for the integrity of the breed, many unworthy dogs sneak past this intended barrier, because the performance judges will frequently “pass” with a “Pronounced” rating some dogs that should fail or get a “Vorhanden” (passing but not very good). And the judges who are doing the individual conformation judging in a location far from the bitework (they are the ones that will rank the adults then and in the next two days) are not able to see the actual work. Therefore, they cannot consider a poor performance when they grade the dogs by beauty.

Last year, with only 155 adult males, there were 21 “working” (open, adult, titled) males who were either T2 “Vorhanden” (barely sufficient, but to place at the end of all the others if they stayed for that part of the show) or T3 “Nicht Genügend” (insufficient courage and not eligible to return for the beauty-&-gaiting competition). This year, there were 55 in those two categories combined, out of 237 presented. These figures have more meaning when you realize that in 2008, 14% of these males were T3 or T2, but in 2009, a whopping 23% “failed” (with both of these categories being failure in my demanding opinion). It was with a sickening feeling that most of the crowd watched and waited for decent performances. These statistics were somewhat offset by the larger numbers of working-line dogs entered, well-received by the crowd, and doing fairly well this year.

Another disappointment that I have voiced before, is the excusal from further competition, of dogs whose owners decide that their chances of making a big splash with a super placing have been diminished. This belief could be based on how the judge has placed the dog before, or comments made on this day, or other reason. The owner might feel it is better for stud-service reasons to pull the dog than to receive a placing further back than he believes the dog deserves. It used to be the rule that such a withdrawal from continued competition on the weekend required a veterinarian’s statement that the dog was sick or lame, but that route was so corrupted that it was misused or practically abandoned. On the other hand, there are many “working-lines” dogs whose owners just wanted their bitework to be seen by thousands of people, and who didn’t want to waste the time trying to get a show placing behind 150 other dogs.

This year, the crowd missed the chance to see the group gaiting and placing of such favorites as Furbo degli Achei (78), Ilbo Holtkämper See (78), Dax Intercanina (81), and Tiras Roten Feld (74), for whatever reasons that were given. Their absence after the bitework and “individuals” is one reason my forecast on placings was not quite as accurate as it could have been. Also, I do not keep up with who has been sold to China, or retired from competition. Still, I hit the mark pretty closely. Deducting the absentees, I had predicted this order: Vegas du Haut Mansard (85), Yerom Haus Salihin (88), Yukon Bastillie (86), and Kwantum Klostermoor (90), and I was “spot-on” with these first four. I also said that Tuareg Bad-Boll (73), the well-pigmented Schicco Freiheit Westerholt (92), Remo Fichtenschlag (71), Ustinov Römerland (82), Clinten Holtkämper See (75), Digger Elzmündungsraum (71), and Panjo Kirschental (90) would do especially well, and they indeed placed V14, VA6, VA7, V1, V8, and V10, respectively. VA means the top several of the V dogs, these letters standing for Vorzuglich (Excellent) and Vorzuglicht-Auslese (Excellent-Select).

Some dogs were not listed in the official tabulation as having been excused from competition. The slap-on-the-wrist “punishment” of not being allowed to compete for a few months is meaningless, because there are almost no shows in winter anyway. There are several reasons for their absence, not many being easy to discover. For example, the very nice-looking and good-working Tyson Köttersbusch only did the bitework and showed in his progeny group but, reportedly because of his size(?), the owner didn’t show him.

In females, I listed Alisha Eichenplatz (85), Viva Hopfenhalle (69!), Chayenne Karthäuser Löwentor (81), and Lea d’Ulmental (89) in that order, which was also close, as they finished VA2, VA9, V4, and VA7, respectively. You may remember that last year my group visited Chayenne at home after the show. Siegerin this year is the Vegas daughter Bella Kuckucksland (89). A couple of other bitches that caught my eye in the protection and gaiting were the Sirio daughter VA-10 Mega Holtkämper See (81), and the beautiful V6 Romina Piste Trophe (95).

Other than the dogs that completely lacked courage or those that failed to get a “pronounced” (ausgeprägt) and “lets out” (lässt ab — stops fighting on command or when struggle stops), there are other results with these codes: T1 = lässt nicht ab, ohne Bewertung TSB (doesn’t out in time, but no problem with the fighting drives); and T4 = abgebrochen wegen mangelnder Führigkeit, which means the dog failed to heel all the way to the point where the “bad guy” with the sleeve runs out from the blind to attack them. Many over-eager and less-trained dogs jump the gun, and they only have 3 tries to do it right. Unfortunately there were a few males who weren’t so controlled in that approach to the first blind, one of which was the strong-character dog we visited a few days later, Yvo Wildsteiger Land. This beautiful, well-constructed Odin son is pictured in the photo appendix to this article. And he has a Zuchtwert of 78, which is quite good. His problem this year was that he was too playful instead of serious about the bitework.

I already mentioned some of the top winners, and you can go to the SV websites for the official listing of all dogs shown, or any of the private sites that carry the whole results. However, in this report, I’d like to mention that I may have missed a few (one must visit the toilet once in a while!) and I wish to comment in detail on some others that may not have done as well as the top-placing dogs. So you will find here something more than just a catalog of winners. After each Sieger Show, I discuss with my group these additional observations.

In both the bitework and the younger classes, I paid more attention to the males, because they have more influence on the breed since they are bred so much more often, but I saw the work of a few females, too. Forgive me if I missed your favorite bitch. I would like to have seen lower ZW numbers in most of the top dogs, but it’s always a balancing act for breeders who want both good hips and super show results. Allow me to first mention some things about dogs with ZWs under 80 before commenting on some that may have placed higher in the show competition.

Remo Fichtenschlag (71), owned by Josephine Kao of Taiwan, got VA 7. Two places behind him was Paul Bierstadter Hof (77), a handsome Odin son with very good upper arm and chest development. V3 Paer Hasenborn (75) was not very convincing in the bites. V4 Clinten Holtkämper See (75) did not do good bitework, but got “ausgepragt” (pronounced) anyway. Peik Holtkämper Hof (75) was V11 this year, but watch for this great Ilbo/Roma son to make great strides in 2010, and I’d wager that he’ll have a great progeny class in 2011 if the Chinese don’t buy him too quickly. The Odin son V23 Ballack zu Worringer Rheinaue looked great and did very good protection routines. Yoe Haus Salihin (75) has a substantially lower ZW than his VA2 litter brother, did equally impressive protection work, and placed V27 in the beauty pageant. Also with a ZW of 75, the Esko Dänischen Hof son V34 Hero Annacarton (owned by Irishman Patrick Thomas) lived up to his name. Mr. T. also owns the great Ilbo Holtkämper See. V29 Chivas Bad-Boll (Odin son with a great ZW of 76) is promising in both the courage and beauty departments.

The Hill Farbenspiel son VA3 Yukon needs more training re the self-controlled “out”, but had very good hits on the “bad guy.” He also might be a little too deep in chest (and I noticed that in several of his sons this year). Dux Cuatro Flores might be a little better in that regard. The Vegas son VA8 Bojan Pendler (86) did very good work and looked very impressive in stance and gait. In Friday’s protection phase, one of the standouts was Puck Urbecke (96), who at (amazingly!) nearly ten years old, put on an impressive piece of work in the defense and attack. He never has placed high in the conformation competition, and was pulled after the bitework this year. The Arko Butjenter Land son V19 Bruno Vierhundert Hertz (81), a handsome dog with very dark mask, showed great courage and enthusiasm. Idol son V13 Taboo Nordteich (90) showed excellent work overall. A Dux Cuatro Flores son, Nexx Hartis Bohemis (79), did beautiful work with truly hard hits. He was one of several “showline” dogs given special recognition for excellent bitework, others being VA5 Ober Bad-Boll, V23 Ballack, V48 Filou Ducati, V40 Hillson Athaba, Sieger Vegas (did a truly great SchH routine), and V94 Untox Freiheit Westerholt.

Bazi Urbecke offspring (the adults) did very well in bitework and all looked very uniform in the progeny group. Outstanding among them were V98 Aslan Belle Amber (80), who showed excellent training, did not take re-bites or nibbles/chomping, and never turned to look over his shoulder; and V25 Frodo Langenbungert (89). One Bazi son, V67 Vigu (89) did not deserve the “ausgeprägt” he was given. Incidentally, his brother Valof just won V2 in Argentina’s Mar del Plata (Landesgruppen) show and “best attack” trophy. As expected, Hill Farbenspiel offspring did admirable work, such as Hillson (92), V89 Falco Bonne Patte (95), VA 3 Yukon, and V65 Urbano Urbecke (88).

Other miscellaneous comments on performance: The work by Panjo was good; that of Vegas son Cronos d’Ulmental (91) excellent (but he was then pulled); VA4 Kwantum (90) was a happy worker with great anatomy and reddish pigment. V1 Ustinov Römerland (82) did good work for a Quantum Arminius son (and half-brother to Sgr. Zamp). The Vegas son Arex Wilhelmswarte (84), bred by a SchH-trial judge and owned by a wealthy fancier, did poorly in the courage test yet got both “ausgeprägt” and V2; hopefully his performance will improve next year. The well-trained V49 Danish dog Karat’s Fedor (88) had wonderful attitude on the field and at ringside — his great parents are Aiko Goldenen Zweig and Karat’s Olly. Aiko also was sire of the good-working V69 Indro. V75 Xambo Roten Feld (72) was impressive in the work, as was Rüdiger Mai’s Dux Cuatro Flores son V43 Atlas Bierstadter Hof (96, unfortunately). We missed Godalis Tino this year because he tore a ligament in a rear leg.

As usual, the better performances were mostly done by the working-lines dogs, but they were also better represented in the progeny groups, kennel groups, and the show competition than previously. The ones that impressed me the most were V54 Javir v. Talka Marda (with a fabulous 70 ZW!) and his sons, V122 Zidane v. Kammberg (71), V124 Yack v. Kammberg (70), the dark sable and super worker V125 J.J. v. Trauntor (76), and daughter V118 Chini v. Ecke (70). There were many other, younger dogs in his progeny group, and all with happy, energetic temperaments. I suspect they will also prove to have admirable Zuchtwert numbers, too. Javir could be considered the star of Friday’s show. His intense and enthusiastic jumping straight up during the bark-and-hold, while barking in the face of the helper/attacker, excited the crowd. Good topline, though he could have taken some fewer steps in the gaiting. Zidane actually tore the sleeve off the attacker on the “long bite” (running attack down the field). Yack thrilled spectators with his incredibly long (and accurate) Malinois-like flying leap to hit the attacker on the long bite.

Other “working-line dogs” of note: SG1 Aik Ziegelbornschneise (76). The Olly Grauen sable son V74 Odin toten Niersarm (86) who had good enough structure that I would have moved him up many placings. The dark-B&T V130 Hutch kalten Hardt (74) was a quick, happy, excellent worker. Sable (the Germans call them “grey”) V135 Owen Klopferle (71) did impressive work. V91 Jakomos Längerts (71) was another sable that sped down the field eagerly. The bi-color V120 Hoogan Vorderhain (78) was big, fast, and did great bitework. Notice all those low ZWs? The “perennial” competitor V132 Gerry Waldesruh (82) at 6 years old did his usual excellent work. The super-working black V126 Alex schwarzen Seeperlen (84) showed expert training and drives. The American (Brookline, Massachusetts) V100 Azlan Petit Geant had very good training but a ZW of 91.

The judges recognized 20 males as having outstanding working drives, including Sieger Vegas, Aik Z, Untox Freiheit Westerholt, Yack and Zidane with their sire Javir, Ober, Ballack, Hutch, Nexx, Filou, and Hillson. Eight females were so honored, and included Chini and Lea whom I have mentioned.

As mentioned earlier, I concentrated my viewing on the adult males, but also saw some excellent younger dogs. One was the Irok son / Fritz Farbenspiel grandson from Pisa Italy, Taris dei Profeti. Owned by Giuliano Profeti, one of Italy’s premier breeders, Taris did not initially place high enough (in the “first group” in his very large class), so he was pulled before the final ranking. Maybe next year’s judge will like him better, Giuliano hopes. He has great strength in body and head, dark eyes and mask, and very good reach (a bit better than his action in the rear).

Winner of that 12-18 month male class was Sultan Jahnhohe (77), who stood out yards ahead of his nearest competition. This animated Vegas son has an excellent front assembly, good proportions though a bit stretched and long in second thigh, high withers, and a handsome head like his sire’s. Watch for this outstanding dog with VA potential next year, if the Chinese don’t get him first. In third place was another Vegas son, Marcus Ossmann’s Wegas Fichtenschlag (86) with excellence overall, but not a threat to the class leader this day. Also in that class was the very promising Bazi son, SG16 Yello Arminius (71), who could do with just a little more front angulation, but has everything else going for him. I like him very much. SG 2 was Nino v Tronje (97), another Irok son of high anatomical quality but a little lacking in desire by the time I spotted him. SG 22 Lux Valentinientis, a Nick Moorbeck son owned by Ernst Ruckert but not yet listed in the ZW statistics, has very good reach and drive, and good eye and mask pigment. SG4 was Sammo di Casa Beggiato (82), an Ober Bad-Boll son that Hans-Peter Rieker probably has great plans for. By the way, the ZW numbers of young dogs is more a calculation of their parents’ records than their own production because of their age (too young to produce X-rayed offspring themselves).

In Jugendklasse Rüden (12-18 months old males), I got to see a few very promising future stars. Uday Jani’s Godalis Tino son, Iceman Amur (78) was SG 5, and had very nice anatomy overall. Behind him in 6th position was another well-structured dog, the Zamp son Kratmosen’s Baroni. The Odin son, SG11 Ritzy Wustenberger-Land, owned by American Jeannette Kempkes, presented an outstanding outline and gait. Second, third, and fourth in that class were wonderful young dogs whose owners are from Italy, France, and Peru.

Whether your main interest is the enthralling beauty show, the sometimes-exciting courage tests at the show, shopping for a younger dog or a breeder, or to see an interesting part of Europe with an experienced judge-guide and friendly companions, you might wish to join my tour. Now, here’s the “commercial”: to prepare fully, I recommend that you get my book on The Total GSD (from me or from the publisher, Hoflin), and if you are breeding or curious, think about ordering my big HD & orthopedics book (direct from me).

Pictures for this report are in a separate appendix, and both should be available on selected websites. If you did not find the photos, e-mail me for a URL where you can get them.
Fred Lanting, Mr.GSD@netscape.com

note: Author and worldwide consultant Fred Lanting is an internationally respected GSD specialty and all-breed judge for many registries, has judged numerous countries’ Sieger Shows and Landesgruppen events, and presents seminars on such topics as Structure, Orthopedic Disorders, Training Techniques, and the GSD. Fred invites all to join his annual non-profit Sieger Show and sightseeing tour. Articles can be found on http://siriusdog.com/sphider/search.php?query=lanting&search=1 , or by a Google search for his name. Request permission to reprint these copyright pieces and add this or a similar notice at the end.

For newcomers, it must be said that the international German Shepherd Dog “Sieger Show” is the main event for the breed held annually in Germany. It is the largest single-breed event in the world, although this year attendance in both the stands and the rings was down, due to the general economy entering near-depression in many countries including, most recently, those in Europe. When you read my abbreviated travelogue, think about being part of my group next year in Bavaria: lederhosen, yodeling, Alps, castles (including the one that inspired Disneyland’s little copy), and great food. I’ll start taking deposits in January. I offer expertise as an SV judge, plus knowledge of the geography, customs, breeders, competing dogs, and some familiarity with the language.

In spite of higher costs these days, it is still the experience of a lifetime for many, and will be more difficult to do if you put it off until later. Joining my non-profit tour is especially beneficial for newer people in the sport, but all in my group can benefit by sharing costs instead of trying to “go it alone”. You pay no fee; only a pro-rated share of my expenses in addition to your own. I find delightful, economical hotels that most people don’t discover. We visit breeders and sights you would otherwise miss. E-mail me with any questions.

The 2008 show was held in Aachen, on the border with southeastern Netherlands. My group of seven stayed in a marvelous hotel, a converted 18^th-Century monastery in Holland (portions still used by nuns and acolytes, though religion has almost disappeared from Europe). On the night that we all arrived, we went to a nearby training club, Alsdorf & Kellersberg, arranged by Hub Rutjens, watched members’ routines, and had our first local fare. European food is very heavy on the meat, very sparse on veggies, so I usually eat almost no meat for a week after returning home!

My group this year consisted of Philippe Rerat (France), Duncan Young (Canada), and Americans Wilma Aungst, Maren Friedhoff, Miguel Elguera, and Megan Streussnig. This was Miguel’s second time on my tour and Wilma’s first overseas trip. Philippe is a very successful Dobe breeder being “converted” to GSDs, and Maren is a German Texan who owns a couple of super dogs, one of which she got while on the tour.

After the three days of the show (Friday through Sunday), we resumed kennel and club visits. On Monday Sept. 15, we first did a little sightseeing in Köln (Cologne) and some of us climbed the many steps to the steeple top and looked over the Rhein River and surroundings. Then we went to the home of Bernd and Christine Klefisch, who with Herbert Zwettler co-own the wonderful 10-year-old Orbit v Tronje (ZW-75), as well as other super dogs. See http://www.orbitvontronje.homepage.t-online.de/ and http://vonjagenstadt.com/articles.html if my photos aren’t included with this copy.

Other dogs there included Quinci v Tronje (87) and the Madonna daughter by Opal Karanberg, this year’s V-16 Ornella v Satyr (85). At least one of my group put in an order for a pup from an upcoming litter out of Kevin Murrtal daughter Madonna Satyr (94) or Ornella. Madonna is just a tiny bit oversize and, under the new, more strictly-enforced size limits, would not have been placed well, anyway. The owners decided not to get the veterinary excuse that are being handed out like donuts at a Red Cross blood drive, so she was listed in the results as “U” (unsatisfactory), but let me assure you, she is a very nice bitch. The “U” means they cannot breed her for 6 months, but had not planned to, anyway.

Monday evening we enjoyed dinner (abend-essen) at SV judge Hans-Peter Fetten’s club, OG Rheydt, some distance to the north, where we saw some top-ranked dogs such as VA-11 Nando do their protection work. There were several working-lines dogs, too. While watching dogs practice their protection routines, one that especially caught my fancy was a substantial Ghandi Arlett son named Zito Steckenpferd (ZW-76), and V-57 in 2006, right behind Arex Herbramer-Wald in the ring. Magnificent in appearance, and terrific in bitework.

The Karthago working-lines kennel of Artur & Ursula Kemmer was our first stop on Tuesday. This is possibly the most famous in terms of turning out great Schutzdienst (working-trial) dogs since Busecker-Schloss (1920s through `80s), and both are featured in my GSD book (e-mail me for details on how to get a copy). Artur speaks no English, and his Deutsch is as fast as a machine-gun, so it’s always both fun and a challenge to converse and understand this great guy. He had only one bitch for sale, a dark sable that had just been bred a few days earlier. Get in touch with him or me immediately if you are interested, and are into top Schutzhund-competition lines.

We then drove another hour and more to Hemer, and had a light meal at the home club of Fritz Stenner’s Urbecke kennel. His translator-friend-associate Dietmar Papenberg showed us Lia, a lovely bitch he co-owns with Holtkaemper Hof. We watched training & met many dogs and people, as usual. This year we were fortunate to have many training clubs and a variety of techniques and dogs that my people could compare. Next year there will be more emphasis on sightseeing due to the location. But every year there is plenty of something for everybody in my tour groups.

Wednesday was a full day, thanks to Alfons Roerkohl, von Oasis kennel. Besides seeing his beautiful VA bitch Shalome again, we enjoyed watching members’ dogs practice at his club near Kamen, east of Dortmund. But before that, he took us on a tour of the famous Bochum Stadion, the most fantastic sports/entertainment stadium complex in the world. The whole football (soccer) field is in an immense, several-feet-deep “tub” that slides out of the stadium into the open for sun and rain most of the time, and back inside the gigantic covered-dome for sports events. The assembly is dragged on Teflon strips. Everything in this 7-year-old stadium looks like it was made just yesterday — I have never seen any public arena or facility kept in such immaculate condition! The roof slides open when weather allows, and when the football field is not indoors, there is additional room on “the floor” for seating and other uses.

Toward evening, with three of my people already on their ways home, the rest of us checked into the hotel at the DUS airport, turned in the van, settled the final bills (except for one who is giving me problems), and the next morning said goodbye. Two people bought dogs on this trip, everybody enjoyed the show and the visits, and several indicated they planned to join my Sieger Show tour again.

And now for the show itself. Entries and gate were down noticeably because of the world economy. In fact, inflation and the cost of the Euro cut my original group by two-thirds (from 21 to 7 by the time it all shook out on the day we got together). Still, those that remained enjoyed the experience, and for one, it was her first trip abroad.

Friday is the longest of the 3-day event, and important to those who want to see for themselves the true performance in the courage test that is required (for those over 2 years old) to pass in order to compete in the show ring. This year, it seemed there was not quite the percentage that failed this prerequisite. Twenty-one males and 28 females were either “vorhanden” (barely sufficient, but to place at the end of all the others) or “nicht genugend” (insufficient courage; not eligible to return for the beauty-&-gaiting competition). These are still uncomfortably high percentages for the purist GSD fancier, but better than most recent years. There were only 155 adult males and 143 females at the end, after weeding out those that failed the test, and deducting the many that got that too-easy “veterinary excuse” when the owners found out the initial placings in the line-up was not to their liking, the dogs that failed to heel all the way to the first blind in the preliminary courage test, and the few who were rated “SG/very-good” or “Insufficient” (re structure).

I paid more attention to the males, because they have more influence on the breed since they are bred so much more often, but saw the work of a few females, too. Forgive me if I missed your favorite bitch. I give in parentheses the latest Zuchtwert (ZW) hip ratings. Remember, the lower numbers are best, and anything over the low 80s should make potential buyers a little nervous.

The Sieger this year was Vegas du Haut Mansard (ZW-85), whom I described in past “Impressions”, and anybody who bet against that outcome would have felt his wallet shrink immediately upon seeing Vegas’ photo in the 2008 logo on the cover of the catalogs, the T-shirts and jackets being sold, and other goods being sold. The Niedergassels were riding high on “Cloud Nine” this year, with the next three dogs all from that family’s breeding program. VA2 was Odin Holtkämper Hof (89), who looked better to me than the Sieger. Following the tradition of his sire Yak and grandsire Hoss, he did very good bitework as well. VA4 was another Yak son, Ilbo Holtkämper See (83), who also performed well in the test. In 2007, I had taken my group to the Niedergassel kennels and got up-close-and-personal with many wonderful dogs and their human families. Combined, the Holtkämper operations are among the premier large kennels in all of Europe.

VA3 this year was Negus Holtkämper See (85). Neither he nor his sire have been consistently convincing in the protection qualification in the past. If you keep copies of previous years’ reports, you will note that I had said in 2007, “V3 Negus should be stronger in character, which observation might be expected if one looks at the sire line (Sgr Zamp/ Quantum Arminius/ Dux della Valcuvia), as there is a slight weakness in character there.” Something I had warned about in 2006 as well. Negus is now owned by a fancier in Japan. He should do well there, and if he doesn’t stay in Germany for another try for the Sieger title in 2009, he’ll probably soon leave for the land of the rising sun. Last year’s female Jugendklasse winner Paula Gut Lethe (Negus daughter) was not in competition this year because of weakness in character, according to very reliable sources. Genes often speak loudly and clearly!

Ingodds Agassi (86), a Ghandi son, came in VA5, showing to me once again the producing ability of dogs whose offspring are noticeably better than themselves. I never cared much for Ghandi, but many of his sons are super! Agassi performed very well in the protection phase. VA6 this year was Budiman Salihin’s handsome Yerom Haus Salihin (86), son of the terrific Mark Schwalmbergtal, who was killed by enemies of the owner about a year ago — great loss, but Yerom and others may fill his footprints in the sands of time. Littermate Yoe was V-39. VA7 Yukon Bastillie (82) almost seems to have come from nowhere, without much fame in past years; he is a Hill Farbenspiel son, and it is considered important to keep this line active for now.

Quantum Fiemereck (76) was VA8. This Ando grandson and Rocky Haus Tepferd son (half-brother to a dog I own) again did his bitework admirably and presents a very attractive picture standing and trotting. The vociferous Italian contingent in the stands were justifiably excited about “their” Furbo degli Achei (78) being placed VA9. This Quenn Löwer Weg son has an outstanding sidegait and is very handsome in stance. He also did a very good courage/protection routine. The only drawback I could see, and it may have been a temporary quirk, is that he could look a little “cleaner” coming at you (though he is still considerably better in that view than is the Sieger). VA-11 (down from VA6 in 2007) was Nando Gollerweiher (92). His bitework was OK, as it was when we saw him at his home club on Monday, but for some reason his star is declining. My 2007 forecast or guess was not borne out, when I had said then, “Only 3.5 years old this year, he will probably be at his peak next year in Aachen.” He apparently wasn’t, in the judge’s eyes, and it was the same judge as then.

Now, for the question that was the buzz all weekend and more: Why did 2007’s VA2 Quenn not show up? Perhaps several reasons. “Word on the street” has it that there was an understanding that if he did show up, he would certainly not go ahead of Vegas. For one thing, Quenn does not have a Sieger for a sire. Less likely is the subtle but repeated rumor that there was reluctance to give the big award to a British Indian. I tend to reject that explanation, as I know both the owner and the judge. More credible is that if Uday expected his 2007 winner of the 18-24-mo. class, the Quenn son Godalis Tino (73), to get a VA this year, he’d better pull Quenn… not enough room for two VA’s from that one owner. Who knows for sure? Whatever the reasons, Tino indeed got VA-10. Running right behind his half-brother Furbo, spectators could see the latter has a little better ground-covering stride length and a bit stronger-looking head, but Tino is still a terrific dog who should and will be used often and well.

It was surprising that there were so many VA awards in both males and females, considering the lower total number of dogs in competition. If it is an official message with the meaning that quality has intensified, there are plenty of us who are not convinced. On the other hand, it makes one wonder if there is a truly good reason for even having a VA category, especially when so many VA dogs in recent years have had little to almost nothing to brag about in progeny displayed. You may say that since the bitches do not have a progeny class to “help” them get a VA rating, it is not necessary for males, either. But that could be argued, because stud dogs have a far greater and faster influence on the breed. Many of us feel that VA males should have substantial evidence of breed value in the progeny group and in the placings of those offspring in their classes, especially the adult, titled, Gebrauchshund (open) classes.

There were many exciting dogs in the line-up below the VA dogs, some of whom have much promise to advance considerably next year. These include a Zamp son V2 Kwantum Klostermoor (86); the Quantum Arminius son V4 Panjo Kirschental (91) who had won the 12-18-mo. Jugendklasse in 2007; Idol son V9 Clinten Holtkämper See (76) who did very nice bitework (I predict a great future for him); and more. V-1 was Uran Wilhelmswarte (79) who moved up from V5 last year and again showed the good bitework of so many of Dux Cuatro Flores sons.

Other than the noise from the Italian cheering section, the most crowd enthusiasm was again for Gerd Dexel’s sable Timo Berrekasten son, Arex Herbramer-Wald (unfortunately, only a 91ZW). This dog with the most sparkling personality you could imagine (happily barking in the ring as if to say “Let’s run!”, and happily meeting admirers outside the ring) got a bit more recognition this year, moving up by leaps and bounds to wind up in V-21 place (last year it was V-28). I reported last year about his “great front reach, ground-covering powerful gait off-leash while leaving others in the dust, a tremendously handsome masculine head, [and] nice overall anatomy”. If he had had a progeny class, that might have given him an additional boost, but there is still too much anti-grey prejudice in Germany’s hochtzuchtlinie breeding circles, so he has not been used as much as perhaps he should have. Since he is almost 7 years old, this was undoubtedly his last fling at the Sieger Show, even though he acted as spry as a 2- or 3-year-old. His bitework was also excellent, as always.

The Yanox son, V8 Tuareg Bad-Boll (74), who had done well in the summer season, showed great protection work and joyful show-ring attitude. Some dogs further down the line did excellent protection routines, such as fast-as-a-bulletV-132 Hutch kalten Hardt (73), Yak son V97 Tim Holtkämper Hof (85), the Esko Dänischen Hof son V-18 Nesch Grafwenburg-Ost (92), the Quenn sons V36 Drago Langenbungert (82) and V-90 Samson Urbecke (75), the sable V-115 Gerry Waldesruh (82), another sable, V-126 Charly v Matrix (74), SG-3 Enzo Grauen v Monstab (79), V-11 Digger Elmündungsraum (87), (whose former kennelmate the promising Ken Elmündungsraum recently died from torsion), V35 Merlin Osterbergerland (87), and some black dogs such as V-110 Woody Dreisbachtal (87),V-128 Hoss Dellwiger Grenze (80), and SG2 Magic Kraichgauer Wald (77). Some of these might be looked down on by the show-only crowd because they are from “working lines”, but they deserve recognition, too. The sport is about more than beauty.

Although I could not pay as much attention to the work of the females, which was going on in the adjoining ring, a few stood out for me. Pakros daughter VA6 Schiwa Osterberger-Land (79) and Zamp dau. VA5 Chanel degli Achei (87) did very good work, as did VA2 Zambia Milewo (85) and V-19 Ziegerkamp Arwen (91), two of many very nice offspring of Arko Butjenter Land. I believe the excellent work of so many of Arko’s offspring can be attributed greatly to his dam as much as to his sire Flipp Arlett. Two of Esko Dänischen Hof’s daughters, V-119 Dina Friesenblick and (one of the best TSB examples) the Irish-owned entry V-25 Dani Dänischen Hof () again proved he could produce excellent character, too. VA4 Anika Herdersfarm () did very good work, better than her sire Euro v Media usually did. Another Pakros dau, V61 Yuka Simonhof, the Yoker dau V92 Karat’s Mündi, and Agassi dau V46 Bonny Fuchsbachtal pleased the crowd with their work. Excellent performances were given by the Parko d’U./Benny d’U. dau VA8 Lea d’Ulmental (90), V-129 Cimbaly alten Laibach-Telch, and the Odin dau V-120 Neele Winnloh.

While most females will not be seen again (they will be busy with the whelping-box duties), their bloodlines should be recognized if they perform well in either conformation or performance (hopefully both). Also, an explanation as to why I have not reported all females’ Zuchtwert numbers: they will not be bred as often. If you are interested in getting a pup, then indeed you should look up its mother’s and ancestors’ ZW numbers.

As mentioned above, next year the tour will again be centered in the Ulm-and-Bavaria (southern) region of Germany, and if you want great scenery, food, and fun as well as looking at great dogs, think about joining my 2009 group. If you would like to be guided by an SV breed judge who has trained many dogs to Schutzhund titles and is familiar with most of Germany, and want to experience those cultural and natural attractions, let me know as soon as you can. You would see more and save money by going with me rather than doing a trip alone; and I do not charge a fee, only a prorated share of expenses.

Fred Lanting, Mr.GSD@netscape.com

editor’s note: Fred is a superannuated SV Zuchtrichter (breed judge) and author of several books, among them are The Total GSD, and the monumental work on Orthopedic Disorders. You can get autographed books directly from the author and schedule judging or lectures by e-mailing him.

]]> http://www.fredlanting.org/2009/08/2008-sieger-show-impressions/feed/ 0 http://www.fredlanting.org/2009/07/canine-digestive-tract-disorders-in-several-breeds-part-4/ http://www.fredlanting.org/2009/07/canine-digestive-tract-disorders-in-several-breeds-part-4/#comments Mon, 20 Jul 2009 22:08:04 +0000 admin http://www.fredlanting.org/?p=59

OTHER DISORDERS

Intussusception — In very young pups (and other animals including humans) the intestine can invaginate (one part slips inside another). The condition, also referred to as “telescoping intestines”, also occurs in adults, but not as frequently. Most common immediate causes include worms, obstruction by indigestible materials, garbage, or toxic substances. The German Shepherd Dog seems to experience a relatively high incidence of this disorder and I believe there is a genetic propensity, a familial trait, in certain bloodlines.

Diarrhea and soft stool — Diarrhea can be a symptom of any number of disorders from cancer to overeating, but is most often associated with disease or parasitism of the small intestine. Diarrhea or loose stool is quite common in the German Shepherd Dog, even when no physiological disease has been identified. However, since this is not a normal condition, the owner should make a sincere attempt to find and attack the cause. Some of the causative factors in true diarrhea are: pancreatic insufficiency, chemical or mechanical irritation of intestinal linings, parasites, microorganisms, and a psychosomatic condition related to the “high-strung,” emotional make-up of the German Shepherd Dog. Foods that can cause loose stool include milk (if suddenly introduced into the diet), excessive liver, fats, and those with a high fiber content. However, simple overeating is perhaps the most frequent culprit. Most people overfeed their dogs.

Soft to runny stools may be an indication of a general inflammation of the stomach and intestines known as eosinophilic gastroenteritis. It is treated symptomatically with something to coat the lining, plus perhaps a steroid and Kaopectate, until the dog “heals itself.” Many veterinarians and owners administer Pepto-Bismol, also. In the case of very young puppies with watery stool or repeated diarrhea, rush to your veterinary clinic with the pup and the stool samples. Most of the time the cause of diarrhea in a young puppy is serious, such as parvo or coccidiosis, perhaps with hookworm as well. The Campylobacter bacteria cause some cases of acute or chronic diarrhea, and most labs would have no trouble identifying this infection. Generally, watery diarrhea is not an indicator of “campy”, but more often has a different cause. Erythromycin antibiotic is 90% effective against that organism, although resistant strains may be evolving.

Giardia

Even Giardia can be quite dangerous, if the pup is young and has been exposed to other challenges, such as being wormy, stressed, or otherwise weakened. Giardiasis is marked by watery diarrhea with a uniquely acrid “bloody” odor, that experienced breeders can identify quite easily even before a stool sample is analyzed. Giardia is a protozoan disease; i.e., it is caused by a single-celled “animal” flagellate parasite, so-called because it is highly motile, having a tail. The Merck Veterinary Manual describes it: “Transmission occurs in the cyst stage by the fecal-oral route. Incubation and pre-patent periods are generally 5 to 14 days. Giardia cysts survive in the environment and thus are a source of infection and reinfection for animals, particularly those in crowded conditions… prompt removal of feces from cages, runs, and yards will limit environmental contamination. Cysts contaminating the hair of dogs and cats may be a source of reinfection.” Regarding treatment, the manual says, “Flagyl ™ (metronidazole) is about 65% effective” (in removing cysts from feces) and if administered “for 3 days, effectively removes Giardia cysts from feces of dogs; no side effects are reported.” By the way, these oocysts are much smaller than worm eggs, and require much higher magnification to find them; still, they are not shed every day, so it may be wise to start treatment and then wait for a three-to-five-day combined stool sample to be checked by your vet. Despite the “low” rate or ridding the body of cysts, many vets prefer Flagyl. The success rate is reportedly declining as Giardia is now demonstrating resistance to the drug. In addition, it may be a little hard on young puppies, with some neurological side effects. I prefer the use of Albon™ to control concomitant bacterial infections in weakened pups, with or without Flagyl for the protozoa, as mentioned below.

Panacur (fenbendazole) is relatively pricey and seems to be sold only in large-volume jars from the usual vet supply catalogs. For Giardia, Panacur is considered a static drug, 100% effective in clearing cysts from feces in 3 days (the cysts are the infective part), with no side effects reported, and is safe for pregnant and lactating animals. In the lab, Giardia did not develop resistance to fenbendazole. It does not have a repelling taste. A field representative for Intervet, the company that manufactures Panacur, admitted that Flagyl may be preferable for the occasional dog that has general stomach distress. With either one, a 5-day dose has been reported by some to be effective when the 3-day regime was not.

I would also recommend that you ask your vet about Albon™ (sulfamethoxine) which is much more effective, although for a different reason, and should be given for 15 to 21 days. The sulfa drugs do nothing to the Giardia organism itself, but they do combat the secondary bacterial infections that are probably the real killers of puppies. Such an approach allows the pup to regain enough health to withstand the protozoan, even though it may be retained in the body for a while. It is more readily available, probably lower in cost, and in widespread use. A disadvantage in any sulfa drug is a number of adverse side-effects, but I have not had any problems, probably because I do not keep dogs on the medication longer than recommended, and have genetically strong breeding stock.

There are a few less-often used: Valbazen (albendazole) is about 90% effective in removing cysts but has been implicated in birth defects, suppression of the immune system, and destruction of red blood cells. Atabrine (quinacrine) also has unpleasant side effects. Some have recommended a Giardia lamblia vaccine for dogs with persistent or repeated cases.

Toxic gut syndrome (TGS) — This disorder has been identified as a specific syndrome, with some similarities to other disorders such as intestinal volvulus, which may have been blamed for death when TGS was the real villain. Dr. Chuck Kruger, a Corgi and GSD breeder in Washington State, has been an intensive observer of this syndrome, and has given up private practice to market his line of nutritional supplements. Chronic intestinal disease, called overgrowth of intestinal bacteria in the UK, and probably the same thing that Kruger dubbed “toxic gut syndrome”, is also being studied in Britain, and has been found to be a particular problem in younger dogs. Treatment with high dosage of antibiotics over a long term has been claimed to have a good success rate there. Kruger pioneered much work in the problem because of so much found in certain American GSD lines. See <http:\\www.dockruger.com>

The German Shepherd Dog has a higher packed cell volume (number of blood cells per unit of blood) than do most other breeds, with 50 to 60 percent “solids” compared with 40 to 45 percent. When such a dog becomes dehydrated, thickened and/or lessened blood supply to the small intestine apparently increases growth of bacteria that are always present there. These Clostridium and E. coli bacteria produce such quantities of toxins that the dog is unable to get rid of them fast enough, and death by poisoning occurs. By the time owners see symptoms such as discomfort when the abdomen is touched, attempts to vomit, and excessive salivation, it is probably too late. Prevention may be accomplished through dietary means (feeding Lactobacillus acidophilus, yogurt, or cultured buttermilk), or by the same toxoid vaccine that is given to lambs to prevent Clostridium perfringens types C and D. As research is done on this recently defined syndrome, more will become known as to the best treatment.

Vomiting and gastritis — Vomiting comes easily to dogs. Grass eating and subsequent vomiting give rise to all sorts of explanations, the most popular being that the dog was sick and ate the grass to help him throw up. Actually, excess grass is more likely the reason for the reflex action. Dogs mostly eat grass because they like the taste of it, just as with the case of garbage, but it does appear that individuals learn that too much can cause vomiting, so the intentional eating of grass to induce vomiting seems to come after experience. Gastritis, an inflammation of the stomach lining, can be caused by the ingestion of too much grass, garbage, or indigestible materials. It can also be caused by viral or bacterial invasion, but much more common, especially in pups, is the presence of endoparasites: tapeworms, roundworms, hookworms, whipworms, and coccidia. Actually, tapeworms or roundworms can fill up the belly to the extent that they back up and cause vomiting from sheer bulk. The initial treatment for gastritis or vomiting may be the withholding of food and administration of Kaopectate™ every four hours.

Ulcers — Ulcers have been diagnosed all too frequently in German Shepherds and may be related to pancreatic problems or other causes: it’s difficult to tell, when several conditions exist at once, whether one is the cause or effect of another. Necrotic bowel syndrome, a disorder of unknown cause, is diagnosed usually on autopsy, when part of the intestine is found to be dead and rotting away. This condition may be synonymous with or overlap intussusception or other diseases. It takes a small toll, mostly among heavily linebred German Shepherd Dogs with “American lines”. Eosinophilic ulcerative colitis syndrome is most common in Cocker Spaniels and German Shepherd Dogs. If your pup or adult has intermittent to constant diarrhea, with or without blood, and does not respond to treatments for the more common disorders, this disease may be the cause. Initial treatment may include corticosteroids, antibiotics, and antispasmodics to see if the symptoms can be halted.

Irritable colon — Also known as spastic colon, this disorder with mucus in or on the surface of soft or frequent stools may be the result of stress. The best “cure” is prevention — breed stable temperaments and build confidence in puppies.

Polyps — Rectal polyps are little round or teardrop-shaped, red to purplish, blood-filled balls hanging on the lining of the rectum. Sometimes they are clustered like tiny grapes, and are found very close to the anal opening or further inside the rectum. They should be surgically removed, since they rupture easily and are a potential site for infection. A drop of bright red blood recurring on the end of stools is a sign that you should have the dog examined for polyps. They are similar to hemorrhoids in humans in that respect.

****************************************************

The author is a long-time breeder, a teacher & lecturer in canine topics, and a dog show judge. Order his book, Canine HD and Other Orthopedic Disorders, directly from the author. The Total German Shepherd Dog is also available from him, and he can be contacted at Mr.GSD@netscape.com . Info on books and dogs, plus other articles, can be found on www.angelfire.com/de3/jagenstadt/vonsalixHome.html, siriusdog.com, and others.