Breeder/Exhibitor Ed, History
by Avi Marshak
The aim of this article is to try to cover as many aspects as possible which rise from the prohibition against showing cropped & docked Dobermanns in many countries around the world. To explore the past, to deal with the present and to try to foresee the future of our beloved breed, the Dobermann. It is funny to think that the future of our breed maybe lies between the two edges of the dog; the ear and the tail.
EARS
In our collective memory, we have and we shall have forever the mental image of a cropped and docked Dobermann. Even Dobermann clubs from countries that outlawed cropping such as Norway and Finland have on their clubs badges the image of a cropped Dobermann, interesting isn´t it?
Let us look back at the “good old days” when we had the freedom to crop anything that could be cropped. Ear cropping began centuries ago as a preventive measure because in those times, there were no antibiotics for infections or anaesthesias and no veterinary surgeons to repair cuts, wounds and infections.
The practical dog breeders learned to remove those portions of a puppy´s anatomy that had the tendency to tearing; they cropped ears, docked tails, and removed dewclaws. Looking at the photos of the early-cropped breeds we can see that all early ear crops were short and crude.
Today, thanks to the modern medicine, cropped ears are longer and it is very easy to crop but still it required the hand of the expert, for ears cropping is varied from one breed to another.
In the F.C.I. list of purebred dogs there are more than 100 breeds that are customarily cropped. Those who oppose the ear cropping claim that it is pure cosmetic surgery and it has nothing to do with the dog health.
Now let us try to answer the “one million dollars question” that people always ask and probably will ask in the future: why are Dobermann ears cropped? Well, I believe that Louis Dobermann the founder of the breed and many other early breeders had the vision of a breed with standing natural ears. If you can not get natural standing ears, the aim justifies the means; you achieve your desired goal by cropping. So they created a Dobermann with cropped ears, ears that prevent yeast infections and at the same time improve the silhouette of the new breed.
Cropped ears create an alert expression and menacing appearance that brought the Dobermann more fanciers. So we have learned that ear cropping was very popular in the early days and the Dobermann was no exception. If we take a look at the Bull Terrier history, a cropped breed that was created for fighting dog sport, once the breeders could get by selecting breeding small erect ears, they stopped cropping.
The late Herman Palmer “Von Fuerstenfeld” kennel told me many years ago that he played with the idea to cross the Dobermann with the ancient Pharaoh Hound breed (a breed with standing natural ears), and to create a Dobermann with natural standing ears, but as far as I know he has not done it.
Countries like England and all the Scandinavian countries have since the early years of the 20th century legislation prohibited cropping and docking of dogs; this legislation prohibits showing cropped and docked dogs in dog shows as well. Lately Holland joined these countries. Starting in 2002, showing cropped and docked dogs in dog shows in Germany will be prohibited. On the other hand an attempt to apply this legislation in Italy has failed.
I don´t believe that the following countries will join this prohibition : France, Portugal, Russia and rest of new republics in central Europe, and all South America countries.
TAILS
There are almost 100 breeds that are traditionally docked. Docking is done when the puppies are 2 – 4 days of age; it has been scientifically established that the nerves in the tail are not activated at that age and the puppies feel no pain what so ever.
To those people who claim that dog uses his tail for balance and communication, the answer is very simple. Puppies that have been docked have not encountered any problems with balance or communication…
The reason for docking Dobermann is very simple, the Dobermann used to be a police dog and service dog and by docking the tail we prevented the criminal from grabbing the dog by his tail during action.
In his book “The Dobermann Pinscher” 1959 edition, Philipp Gruennig disclosed that in the past there were Dobermanns born with “Bob Tails”: a natural short tail — however these blood lines were lost for those early Dobermann breeders concentrated their breeding efforts on improving the production of deep tan markings.
THE LEGAL SITUATION
The European Convention for Protection of Pet Animals, that was held in Strasbourg, France in 13.11.1987 calls for the prohibition against docking tails, cropping ears and removal of dew claws, it deals also with many other aspects of keeping and breeding of pet animals.
Although it calls for the prohibition against docking and cropping, it specifically recognizes the rights of nations which otherwise accept the Convention, to reserve their position on the issue.
Unfortunately, so far many governments ratified these Convention resolutions and the result is prohibition against docking, cropping and showing cropped and docked dogs.
In Britain the prestigious Royal College of Veterinary Surgeon decided not to press for Britain to sign up the controversial European Convention for the Protection of Pet Animals.
Today Europe and tomorrow? Any American, Canadian or Australian dog lovers believing they are safe from those seeking to ban tail docking or ears cropping, may be interested to know what their veterinary associations have to say on the matter.
In the USA, the Association of Veterinarians for Animal Rights opposes various surgeries done to meet “breed standards”.
In Canada, the Canadian Veterinary Medical Association also opposes surgical alteration of any animal, for cosmetic purposes.
In Australia, the Australian Veterinary Association calls on the states to ban cosmetic operations.
THE STANDARD
When the “flood” has started and more countries have adopted the anti cropping and docking legislation, the World Kennel Club, F.C.I initiated an elegant wise step to meet the new challenge.
The Standard Committee of the F.C.I stating published a circular :
“The fact that in more than a hundred breeds ears are either cropped or uncropped and tails docked or left their natural length should no longer influence the judgement at any exhibitions (National, International and World).
All shapes should be judged without distinction since the cropping of ears and docking of tails are in some countries legally prohibited.
The judgement, however takes into account w
hether the ears are well-cropped or not, whether the natural shapes and carriage of the ears in accordance with the standard and whether the tails are either correctly docked or the tails correctly carried.”
This circular is a preliminary step but it does not solve the many problems and questions that have been risen by the anti-cropping and docking legislation.
The F.C.I (Federation Cynological International) or the World Kennel Club customarily recognizes a breed’s standard that is recognized by the leading non-organizations (the AKC and the English Kennel Club).
Under the F.C.I jurisdiction, only the national club of the country of the origin has the authority to alter the breed standard.
The German Dobermann Club (Dobemann-Verein e.v.) – the standard-patron of the Dobermann, is the only organization that is authorized to alter the Dobermann standard.
Let see what changes have been inserted in the Dobermann standard re-ears and tails.
In the 1994 standard under the ears paragraph it is written:
“The ear, which is set high, is carried erect and cropped to a length in proportion to the head. In a country where cropping is not permitted the uncropped ear is equally recognized. (Medium size preferred and with the front edge lying close to the cheeks).
Here the standard provides us with reasonable answers in accordance with the spirit of the F.C.I standards committee circular.
Re-Tails it is written:
“It is high set and docked short whereby approximately two tail vertebrae remain visible. In countries where docking is legally not permitted the tail may remain natural“.
Here the standard also follows the spirit of the above-mentioned circular. However it does not disclose to us any specific details such as: what is natural, what is the desired length of the tail, what is the tail´s shape etc.
So far so good – the fact that cropped ears and docked tails are not included under the disqualifying fault paragraph gives us some hope for the future.
To conclude, let us all hope that docked tails and cropped ears will not be defined by the standard-patron, the German Dobermann Club, as disqualifying faults; this might be a “coup de grace” for the Dobermann breed.
BREEDING
If worst comes to worst, we shall have to put extreme efforts in breeding Dobermanns with small ears or we shall be forced to search for the natural standing ears.
Regarding tails, we don´t know yet what will be the shape, the length of the tails — shall we breed for the German Shepherd type tail? Than we shall have to look for a long slanted croup … or shall we breed for the curled tail that occurs in two basic varieties: single and double curl over the back with many variations? It is well known in the breeding field that ounce you try to improve something in the dog you may lose something else … this what happens in the sport of the purebred dogs.
As you are already aware of the many problems that lie ahead of us and I have not scratched yet the bottom of the “barrel”, let us be optimistic and face the future with a positive hope.
JUDGING & JUDGES
The fact that in many countries Dobermanns nowadays are being shown uncropped and undocked in the dog shows can affect the judging and the handling methods.
Natural ear changes the silhouette of the head; the head appears broader at the base of the skull, and less cone-shaped due to the natural hanging ears. When judging an uncropped Dobermann it is easier to see clearly the parallel lines in the head. While judging a cropped Dobermann, part of the skull between the ears remains invisible in profile because of the cropped ears.
The smart professional handler always lifts the natural ears up in order to emphasize the correct shape of skull and the parallel lines; by doing this it improves the expression as well.
Being a specialist Dobermann judge and F.C.I. International All Breeds Dog Judge, let me share with you my judging experiences.
My first overseas judging assignment was in South Africa, here most of the handlers lifted the ears in order to enable me to see the real shape of the head. Those who did not do so were requested kindly by me to lift up the ears.
So far I have judged many uncropped and undocked Dobermann in the Scandinavian countries. I know exactly what to look for but maybe the fact of being an All Breed Dog Judge who uses to various forms of silhouettes, ears shapes, etc, helps me to absorb the “new version” of the Dobermann silhouette.
To absorb the “new version” is necessary but this will never change my intimate mental image of the cropped and docked Dobermann with piercing expression that radiates alertness. In one of my Scandinavian shows I met an exhibitor who shoved the long tail into his jacket sleeve, but of course he could not run with it remaining there.
Training new judges to the breed can be a little complicated for these new judges may get, as a matter of course, the new image of the Dobermann and thus they may have the wrong idea of the correct Dobermann head.
Whenever I see my ” ideal Dobermann” in the ring or outside of the ring it is like having a “Mental orgasm”.
QUO VADIS ?
The Dobermann has a rich and interesting past but the question is, does he have a future? Will the metamorphosis that the Dobermann is now undergoing affect the popularity of the breed? This is a “one million dollars question”.
What is a Dobermann? My answer is very simple; the Dobermann is everything that the individual expects him to be, whether he is cropped or uncropped, whether he is docked or undocked…
Breeder/Exhibitor Ed, History
Text and illustrations: Ria Hörter
Photos: Alice van Kempen
Karl Friedrich Louis Dobermann and his Dobermann Pinschers
Most dog breeds were developed after hundreds of years of evolution and lengthy selection by breeders. However, some breeds owe their existence to just one person, whose name they bear.
The double ‘n’ at the end of the family name more or less reveals the native country of the Dobermann’s creator, Mr Karl Friedrich Louis Dobermann. He was a German ‘tax officer, flayer and dog catcher’ whose name will be forever linked with a versatile working breed. Let’s become acquainted with the circumstances in which young Louis lived, in 19th-century Thuringia.
- Imperial Germany
- Karl Friedrich Louis Dobermann (Louis) was born in 1834 in the city of Apolda (Federal State of Thuringia). At that time, Germany was pided into 39 federal states. The French Occupation was over, but the Vienna Congress (1815) had not allowed Germany to unify. After the Constitution of 1849, the German federal states were united in a hereditary German Empire under Prussian leadership. In 1871, when Louis Dobermann was 37 years old, the first German Emperor stepped forward: William I of Prussia.
The federal states retained their own monarchs and governments, however. In Thuringia, for example, the royal families of Sachsen-Coburg-Gotha, Sachsen-Altenhausen and Sachsen-Weimar-Eisenach ran the show, with the government of Thuringia responsible for cultural and administrative affairs. In 1894, the year of Louis Dobermann’s death, Emperor William II was sitting on the throne for already 8 years. In a certain sense Dobermann was a typical exponent of Imperial Germany.
- ‘Tax collector and dog catcher’
- We know very little about the childhood of the man whose name is associated with one of the world’s most popular breeds. Writers and historians have different opinions even about the year of this birth (1834 is correct, but some say 1823 or 1824) and the year of his death (1894 and 1891 are reported). They agree, however, about Louis’ profession: “Justizangestellter im thüringischen Apolda und darüber hinaus Abdecker, Steuereintreiber und Hundefänger für das Ambt Niederrossla”. So many words for such a humble function: collector of dog tax, catcher of stray dogs and flayer for the region of Apolda, appointed by the judiciary in the Federal State of Thuringia. Aside from collection dog taxes, Louis Doberman had to catch and skin stray dogs. His second job was that of “Nachtpolizist” – a night watchman, traversing the city looking for unsavoury characters.
Dobermann would certainly have benefited from a dog’s protection as he collected taxes and patrolled at night. As a dogcatcher, he could choose the best dogs for his purposes. From the beginning, his dogs were known regionally as “Dobermann’s Hunde” (“Dobermann’s dogs”).
- Pinschers and Sheepdogs
- We know that Louis Dobermann crossed several types of dogs to get a “harsh dog”, but there are different opinions about the dogs he bred. The famous German dog writer Richard Strebel stated: “I very much doubt if we should place the Dobermann Pinscher in the Pinscher group. Maybe he belongs in the Sheepdog group.” Strebel claimed that the first dogs bred by Louis Dobermann were Pinscher/Sheepdog crossbreds. But he noted: “It is quite possible that other breeds contributed as well.”
- Breed origins
- In his book Die Deutschen Hunde (German Dog Breeds), published in 1904/05, Strebel wrote that the city’s “stray dogs catcher and dog skinner started breeding harsh dogs, together with two other men, a Turmwärter (tower guard) and a Fluhraufseher (a kind of county policeman).” For their first litters, the three men used stray dogs that were destined to be skinned! It must have been a peculiar trio, a tower guard, a county policeman and a catcher of stray dogs, walking the streets of Apolda, during the day as well as in the night. There was a certain similarity between the three men; all three preserved the law and were serving the community. Without a doubt, Dobermann’s profession impacted his decision to breed guard dogs. However, there were other reasons to breed this type of dog. The farmers in the Apolda region used guard dogs to deter intruders and tramps, and the dogs bred by Dobermann were also used for several jobs in the police force. At that time the dogs were called Gendarmen Hunde (Police dogs).
- “Schnuppe”
- It’s not easy to establish the origin of the Dobermann Pinscher. There are several stories, particularly about the first years. The version of Louis Dobermann’s contemporaries is that the first litters were bred from Dobermann’s favourite bitch, a mouse-grey smooth-coated Pinscher, named “Schnuppe”. The sire’s breed and name are unknown, but it could have been a Thuringer Sheepdog or Black and Tan Terrier. Looking at the photograph (circa 1870) of Louis Dobermann with two dogs, one must admit that these dogs show no similarity to the present Dobermann Pinscher. However, the 1903 drawing by Richard Strebel clearly shows two Dobermanns. In the intervening years, breeders had succeeded in developing a type immediately recognizable today.
- 1863 Dog Market
- The dogs bred by Louis Dobermann from the middle of the 19th century were certainly not mongrels! Both Strebel (1905) and Sleegers (a Dutch dog writer, 1912) argued that these dogs were very much the same as smooth-coated Pinschers, with perhaps a trace of sheepdog. Louis Dobermann, however, never showed great interest in the appearance of his dogs and didn’t keep stud books. His first requirement was to create a watchful, sharp, brave and intelligent dog. We know he succeeded. Several of his dogs were shot by hunters because they were too sharp and keen on game. In a way, this behaviour obstructed the breed’s popularity in its first years. Not infrequently, the life of such a dog ended on a chain. So in a certain sense, Louis Dob
ermann didn’t derive great pleasure from his dogs´ tremendous qualities as guard dogs and watchdogs. On the other hand, the presentation of Dobermann Pinschers at the first dog market in Apolda, in 1863, when Dobermann was 29 years old, was joyful and a success. This event became so important that it is officially recorded in the history of the city of Apolda.
- Otto Göller
- Reading the literature about Dobermann and his dogs, I almost come to the conclusion that his successor, Mr Otto Göller, hardly credited Louis Dobermann and his success. Göller owned a distillery in Apolda. He began buying quality Dobermanns and, by the turn of the 20th century, was keeping about 80 dogs (!) in his villa at Stegmann Strasse 33. A salesman with a good eye for a dog, Göller became a well-known promoter of the breed. Dogs from his kennel ‘von Thuringen’ were exported abroad. In The Netherlands, for example, the first Dobermann Pinscher entered as a separate breed was shown at the Nimrod Show in Amsterdam in 1901. Göller’s love for the breed was far reaching: he produced Echte Dobermanns Bitter (Real Dobermann Bitter) in his distillery.
- A different story
- Otto Göller tells a quite different story when it comes to the breed’s early history. He knew Louis Dobermann personally and in 1910 he wrote about him in Der Dobermannpinscher in Wort und Bild (The Dobermann Pinscher in Word and Picture). Göller reduced “Schnuppe” to “a cross bred between already existing dogs in Dobermann’s time in Apolda.” Nothing about a real Pinscher. According to Göller, “Schnuppe” had been mated to a “butcher’s dog”. He does not explain what a butcher’s dog was, but we can be reasonably certain that Göller was referring to the ancestor of the present-day Rottweiler (black and tan!) crossbred with a sheepdog. It is known that these types of dogs existed in Thuringia at that time. Göller further states that Pinschers and hunting dogs were also used, not purebred. At the end of his story, he wrote, Mr. Dobermann has bred with a mixture of these dogs in the years around 1870. As a token of admiration, Göller and his friends named these dogs after Louis Doberman…..
- Blue Great Danes?
- Göller had more to tell. He stated that the origin of the Dobermann Pinscher went back to the ancestors of the German Shepherd Dog, to Blue Great Danes, smooth-coated Pinschers and short-coated hunting dogs. His opinion is opposed by others, including the well-known Austrian scientist and dog fancier, Prof. Dr. Emil Hauck. The discussion continues today, the most important question being: Were Louis Dobermann’s foundation dogs purebred or was Otto Göller right about the mongrel “Schnuppe” and the ancestors of the German Shepherd? The Dutch author Seeghers (1912) wrote that Göller’s opinion was not valid and Strebel (1905) claimed that Louis Dobermann deserved all the credit.
However, there is one subject on which they all agreed: Otto Göller was the one who promoted the breed. It was he who, in 1899 and in cooperation with Oskar Vorwerk, founded the first breed club in Apolda. In the same year, the first Spezialzuchtschau (Specialty for Dobermanns) was organized, with an entry of 12 dogs. In 1905, Karl Meyer, a pharmacist in Apolda, published the breed’s first stud book.
- Hauck’s theory
- Prof. Dr. Emil Hauck’s view on the origin of the Dobermann Pinscher is important. In his opinion, the smooth-coated Pinscher was the breed’s most significant ancestor. If hunting dogs were used, they must have been hounds. He doubted the influence of sheepdogs, but admitted that Black and Tan Terriers could have contributed. There had been Dobermanns with Greyhound blood and, finally, Dr. Hauck believed that crossbreeding with Great Danes or Rottweilers was likely.
Perhaps Hauck’s opinion was based on the fact that Dobermanns are sometimes born tailless. The influence of the Rottweiler? From the beginning, Dobermann Pinschers had cropped ears and docked tails. Both are forbidden now in Germany and in most other European countries, Great Britain included.
- Breed Recognition
- The breed club was founded in the pub Zum Bergschlösschen during the Apolda Dog Market of August 1899. At the same time, breeding rules were determined. Around 1900, other breeds clubs were founded in Frankfort, Hamburg, Mannheim, Hanover and Berlin. Mr Goswin Tischler (kennel ‘Von Grönland’) arranged for the breed’s recognition in 1895. If Louis Dobermann had only lived one more year to see this!
It is said that the first Dobermann Pincher entry was at the dog show in Erfurt in 1897. But what about the Apolda Dog Market of 1863? Louis Dobermann presented his new ‘breed’ amidst all sorts of dogs. A romantic engraving shows market stalls with dozens of small and big dogs. Delighted children are looking at the dogs and the difference between lap dogs and working dogs is obvious. The strongest recommendation for buying Dobermann’s dogs could have been that they stood up for themselves. Although the Dobermann Pinscher is no longer a “harsh” guard dog and killer of game, the AKC breed standard states that the breed is “energetic, watchful, determined, alert, fearless, loyal and obedient”.
Louis Dobermann would no doubt be pleased to learn that his creation still possesses some of the characteristics he envisioned more than 100 years ago.
- The son of Apolda
- Louis Dobermann died in 1894, leaving four dogs in his legacy: “Rambo”, “Lux”, “Landgraf” and “Schnuppe”. If these names are correct, last mentioned is “Schnuppe 2”, because the first “Schnuppe” is pictured in the photo dating from about 1870.
In his home country of Germany, Louis Dobermann has not been forgotten. A bronze statue of three playing Dobermanns has been erected in Apolda. In addition, a street has been named after him and his birthplace is marked with a plaque – a salute to the son of Apolda whose name became known worldwide.
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Literature:
Handboek Kynologie<
/em>, Houten, 1991.
V. Knijff-Dermout, Ken uw Dobermann Pinscher, Amsterdam, 1977.
V. Knijff-Dermout, De Dobermann, Zutphen, 1985.
Geertje van Rheenen, De Dobermann, Zutphen, n.d.
L. Seeghers, Hondenrassen (two volumes), Amsterdam, 1912.
Richard Strebel, Die Deutschen Hunde (two volumes), Munich, 1904/05.
City of Apolda.
Breed Club Dobermann-Verein e.V Abteilung Apolda/Thüringen.
Breed Club Vereniging Dobermann Vrienden in Nederland.
Various websites.
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A breeder/exhibitor/judge and retired bookseller and publisher, Ria Hörter is a contributing editor of “Onze Hond”, leading dog magazine in The Netherlands. She also writes for “Dogs in Canada” and the Austrian dog magazine “Wuff”. (www.riahorter.com).
Alice van Kempen is an award winning dog photographer in The Netherlands. Her photos are published world wide (www.alicevankempen.com).
Illustrations:
Breeder/Exhibitor Ed, Health
Written by Dr. Alice Crook and taken from the Canine Inherited Disorders Database with permission
What is zinc-responsive dermatosis?
This disorder causes scaling and crusting of the skin. It is not due to a dietary deficiency of zinc; instead affected dogs appear to have a higher than normal requirement for zinc, perhaps due to abnormal intestinal absorption. As the name implies, the skin condition improves with zinc supplementation.
Young fast-growing puppies of large breeds such as Doberman Pinschers and Great Danes sometimes experience a similar condition due to a transient zinc deficiency.
How is zinc-responsive dermatosis inherited?
The mode of inheritance is unknown.
What breeds are affected by zinc-responsive dermatosis?
Alaskan Malamute, American Eskimo Dog, Samoyed, and Siberian Husky. Young rapidly growing Doberman Pinschers and Great Danes sometimes experience a similar condition due to a transient zinc deficiency.
For many breeds and many disorders, the studies to determine the mode of inheritance or the frequency in the breed have not been carried out, or are inconclusive. We have listed breeds for which there is a consensus among those investigating in this field and among veterinary practitioners, that the condition is significant in this breed.
What does zinc-responsive dermatosis mean to your dog & you?
Signs are usually first seen around puberty. There is reddening, scaling, crusting, and hair loss on the muzzle and around the eyes. The footpads as well as the area around the vulva and anus may be affected. The lesions are itchy in about half of dogs with this disorder, causing chewing of the feet or rubbing or pawing at the face.
How is zinc-responsive dermatosis diagnosed?
The diagnosis is made through a skin biopsy. This is a simple procedure done with local anesthetic, in which your veterinarian removes a small sample of your dog’s skin for examination by a veterinary pathologist. The biopsy will show changes characteristic of this condition.
How is zinc-responsive dermatosis treated?
Temporary zinc supplementation is effective in treating the transient zinc deficiency that may occur in young rapidly growing Great Danes and Doberman pinschers.
Affected dogs of the Northern breeds must receive dietary supplementation of zinc for life, or the signs will recur.
Breeding advice
Affected dogs and close relatives (parents, siblings) should not be bred.
FOR MORE INFORMATION ABOUT THIS DISORDER, PLEASE SEE YOUR VETERINARIAN.
Breeder/Exhibitor Ed, Health
- References available upon request
- Jessica J. Wilcock, DVM
`Wobbler´s Syndrome´ is the term used to refer to compression of the cervical spinal cord in Doberman Pinschers and Great Danes. This disorder has many names- it is also called cervical vertebral instability, cervical vertebral malarticulation/malformation, cervical vertebral stenotic myelopathy, and cervical spondylopathy – which is probably why most of us refer to it simply as `Wobbler´s.´
Wobbler´s is characterized by progressive neurological dysfunction of all four limbs, usually starting with the hind legs. Common symptoms are an abnormal `drunken´ or `wobbly´ gait, scuffing or dragging of the hind feet, a short, choppy gait of the front legs, neck pain, and holding the head and neck in a flexed (downward) position. Signs may progress to the point where the dog may not be able to walk or get up on its own.
Wobbler´s usually occurs in older Dobermans (3 to 8 years of age) although it has been reported in dogs less than two. The spinal cord compression occurs in the lower neck, most commonly in vertebrae C5, C6 and C7. Some dogs may have multiple areas where the spinal cord is compressed. The compression of the spinal cord can be caused by many things, the most common being:
1) Congenital malformation and/or malarticulation of the vertebrae- A misshapen vertebra, or one that doesn´t align properly with its neighbor can press on the spinal cord.
2) Instability of the vertebrae- usually due to malarticulation. This instability often results in hypertrophy (enlargement) of the ligaments associated with the vertebrae, which act to hold the vertebrae in their proper place. Both instability and hypertrophy of the ligaments can put pressure on the spinal cord.
3) Stenosis (narrowing) of the spinal cord canal- Stenosis can be caused by malformation of the vertebrae, or by hypertrophy of the ligaments associated with the vertebrae. This narrowing of the canal will cause compression of the spinal cord.
4) Protrusion of the intervertebral disks (`slipped disk´)- A disk can protrude from it´s place between the vertebrae and press on the spinal cord due to malarticulation or instability of the vertebrae. It should be noted that Dobermans with no malformation or malarticulation can also have slipped disks- that is not Wobbler´s Syndrome, that is a dog with Intervertebral Disk Disease.
As you can see, all of the above causes of spinal cord compression are inter- related; because of this, most dogs have more than one cause of compression- however, there usually is one cause that is responsible for the majority of the pressure on the spinal cord.
Treatment of Wobbler´s depends on the severity of the spinal cord compression. Milder cases may respond to rest and corticosteroid (i.e. cortisone) treatment to reduce the inflammation and swelling of the spinal cord. Acupuncture has also been shown to be helpful, especially in relieving pain. Chiropractic adjustment has also been suggested- however, in the case of a dog that has instability of it´s vertebrae, chiropractic adjustment has the potential to cause serious complications. In more severe cases, surgery is the only option. A myelogram or MRI must be done prior to surgery to determine where the compression is, whether there is more than one area of compression, and how severe the compression is. The type of surgery that is performed depends on the cause of the compression. Common surgical procedures performed are a dorsal laminectomy, a ventral slot procedure, a stabilization procedure or a combination of the above. Surgery usually carries a 75% success rate for either stopping the progression of the disease or improving clinical signs if the dog can still walk prior to surgery. The rate falls to 50% in dogs that can no longer walk prior to surgery.
The cause of Wobbler´s Syndrome is still unknown. Genetics, conformation of the neck, nutrition, injury- all have been theorized to play a part. Neck x-rays prior to breeding have been suggested, but since the malformation and malarticulation in an unsymptomatic dog can very subtle, they can be very difficult to interpret. Preventative breeding can be frustrating as most dogs do not show symptoms until they are past their prime breeding age. The best we can do at this point in time is to be aware of Wobbler´s in our pedigrees, and breed responsibly.
Breeder/Exhibitor Ed, Health
Written by Dr. Alice Crook and taken from the Canine Inherited Disorders Database with permission
related terms: Wobbler syndrome, cervical spondylomyelopathy, cervical vertebral deformity
What is cervical vertebral instability?
Anatomy of the vertebral column and spinal cord: The vertebral column, or backbone, is made up of a series of small bones, the vertebrae. These bones surround and protect the spinal cord, the large collection of nerves through which information is transmitted between the body and brain. The spinal cord must be intact and undamaged in order to feel sensations (including touch and pain), and for normal movement of the body and limbs. The individual vertebrae are separated by intervertebral disks. These soft tissue structures allow for normal movement between the vertebrae, and also act as shock absorbers.
In cervical vertebral instability, there is compression of the spinal cord in the neck (cervical) region. There are seven vertebrae in the neck which surround and protect the spinal cord. Movement between these bones allows normal movement of the neck. With this condition, there are abnormalities in the structure of the vertebrae, of the ligaments that connect them, and/or of the disks between them. The reasons for these abnormalities are not clear; inheritance is a factor, and overfeeding in rapidly-growing large breed dogs is also thought to play a role.
The result is instability between adjacent vertebrae, narrowing (stenosis) of the spinal canal, and pressure on the spinal cord. The consequences of compression of the spinal cord in the neck region are weakness and incoordination in all 4 legs – hence the name “wobbler”.
How is cervical vertebral instability inherited?
Unknown. It has been suggested to be autosomal recessive in the Great Dane, Doberman Pinscher, and borzoi.
What breeds are affected by cervical vertebral instability?
This disease is most common in the Great Dane, where the signs are first seen between 3 and 18 months of age, and the Doberman pinscher, where problems develop later, between 3 to 9 years. Cervical vertebral instability is also seen in most other large breed dogs, including the St. Bernard, Weimaraner, Labrador Retriever, German Shepherd, Boxer, Rhodesian Ridgeback, Dalmatian, Samoyed, Old English Sheepdog, Bull Mastiff, Borzoi, Rottweiler, Chow Chow, Golden Retriever, Irish Setter, Irish Wolfhound, and Great Pyrenees, and in the Basset Hound, Fox Terrier, and Beagle.
For many breeds and many disorders, the studies to determine the mode of inheritance or the frequency in the breed have not been carried out, or are inconclusive. We have listed breeds for which there is a consensus among those investigating in this field and among veterinary practitioners, that the condition is significant in this breed.
What does cervical vertebral instability mean to your dog and you?
The main signs with this disease are weakness and incoordination (ataxia); these signs begin insidiously and worsen slowly over several months. It may look like your dog doesn’t know where his or her feet are. This will be most obvious when s/he is rising from lying down, or negotiating a turn or stairs. Over time, your dog may develop a stiff, high-stepping, exaggerated gait that gradually worsens.
The signs are bilateral and symmetrical (meaning they occur equally on both sides). All 4 legs are eventually affected, with the hind legs affected first, and more severely. Sometimes there is a sudden change for the worse as a result of minor trauma. Doberman pinschers often experience severe neck pain (as a result of disk herniation- see intervertebral disk disease) and may develop rigid front legs.
This is a chronic, progressive disease (i.e.. it gets worse with time). Without treatment, your dog’s condition will gradually deteriorate. With therapy (either medical management or surgery) the prospect for recovery remains guarded.
How is cervical vertebral instability diagnosed?
Your veterinarian will suspect this disease if your large-breed dog displays the characteristic clinical signs: slowly progressive, bilateral, symmetrical hind leg weakness and ataxia. The front legs are affected after the hind legs, and usually less severely. Your dog´s neck may be painful, and may be held flexed slightly downward. Plain x-rays are taken to show structural abnormalities in the vertebrae, but myelography is necessary to determine if there is spinal cord compression. In order to do a myelogram, your dog is anesthetized, dye is injected into the spinal canal, and x-rays are taken which will show the exact location(s) of spinal cord compression. This information is essential in considering treatment options, especially if surgical repair is to be attempted. Other imaging techniques, such as CT scans and MRI, may also be used. Your veterinarian may refer you to a veterinary referral centre for these specialized radiographic techniques, and for potential surgery.
For the veterinarian: The two most commonly affected breeds have characteristic lesions; older Doberman pinschers frequently show ventral spinal cord compression, while young Great Danes show dorsal spinal cord compression. Lesions are more common at the more caudal cervical segments (C5-6 and C6-7). Underlying systemic or metabolic diseases may also be present. “Traction” myelograms can be used to demonstrate the dynamic component of this disease (instability between vertebrae). Forced extension of the neck may exacerbate spinal cord compression.
How is cervical vertebral instability treated?
The type of treatment chosen for this condition will depend on a number of factors, including the severity and duration of your dog´s signs, and the extent of spinal cord compression apparent on radiography. The goals of medical management are to minimize neck movement (through confinement and use of a neck brace) and use anti-inflammatory medications to prevent further damage to the spinal cord. Medical management may be effective for weeks to years, although it does not address the underlying problem of spinal cord compression. A variety of surgical techniques have been developed (and more are being developed) which attempt to both alleviate the spinal cord compression and stabilize the vertebrae. Surgery is not without risk, including a variety of potentially severe postoperative complications. Ultimately, the prospects for recovery depend on a number of factors, including duration and severity of clinical signs, and whether the spinal cord is compressed at a single site or at multiple sites.
Because of the requirement for both specialized radiographic and surgical techniques in treating this condition, your veterinarian may provide initial neck stabilization and anti-inflammatory therapy for your dog, and then refer you to a veterinary referral centre for further treatment.
Breeding advice
Although the exact mechanism of inheritance is not known, dogs with cervical vertebral instability should not be bred. (Unfortunately, because this condition often has a later onset, dogs may be bred before any problems appear). It is best to avoid breeding their parents or siblings as well, who are considered potential carriers of the trait.
The best ways to avoid this condition in a large breed dog are to inquire before purchase if there is any family history of vertebral instability, to refrain from providing mineral supplements to the diet, and to feed several small meals daily (rather than ad libitum feeding).
FOR MORE INFORMATION ABOUT THIS DISORDER, PLEASE SEE YOUR VETERINARIAN.
Resources
LeCouteur RA, Child G. 1995. Diseases of the spinal cord. In EJ Ettinger and EC Feldman (eds) Textbook of Veter
inary Internal Medicine, p. 629-696. WB Saunders Co, Toronto.
Breeder/Exhibitor Ed, Health
- Jessica J. Wilcock, DVM,
- Talent Dobermans, USA
1. What is the life cycle of Whipworms?
The dog ingests soil that has whipworm eggs in it (i.e.. where a previous dog has pooped that has whipworms), the larvae hatch and establish themselves in the cecum, a part of the intestine after the small intestine and before the large intestine/colon. There is no intermediate host.
2. What do they do?
Cause inflammation at the area where they attach, frequently causing bloody, mucousy diarrhea.
- 3. What is the cheapest treatment (if you do multiple dogs)?
- Panacur
- 4. Does it take Multiple wormings?
- More than likely. The eggs can survive for 4-5 years in the soil.
- 5. Can pregnant bitches be wormed?
- I don’t usually recommend worming pregnant bitches. However, pregnant bitches can be given Interceptor.
- 6. Do pups subjected to an ‘area’ where a dog has been diagnosed with it get wormed? Is puppy worming ok?
- I would check a fecal sample first, but puppies can be wormed with Panacur. I can’t remember how old they have to be before they can get Interceptor. I think it’s eight weeks.
- 7. Is there any way to rid soil of eggs/worm reinfestation?
- Other than moving or scorching the place- it’s *very* difficult. Interceptor works well though!
8. Now seriously, if a pregnant bitch has whips, will the worms cross placenta into pups? - I’m honestly not sure on this one – I would guess not, but if she has them, it’s likely that the pups will pick them up too.
- 9. If pups get whips from the soil and are treated, how do you prevent reinfestation ,if you are unable to move then to “perceived” clear soil?
- Keep them on Interceptor.
- 10. When wormed do you see Whip worms expelled in feces? If not, Why do we see some worm types expelled that way, and not others?
- I doubt it- whip worms are very small, fine thread-like worms. Round worms and tape worms are the most frequently seen passed in the stool due to their size (large).
Note: There are apparently really only three ways to eliminate whip worms…
1. Give your dogs a preventative such as Interceptor and let nature take its course – i.e. in one end and out the other
2. dig up 8 inches of your top soil and replace it or
3. use copper sulphate and kill everything in your yard
Breeder/Exhibitor Ed, Health
Vitamin C and its role in Stress Management, Bone Metabolism and its influence on the skin and coat of the dog
By Melvyn John BHS. IT.
VYDEX ANIMAL HEALTH LTD.
In recent years major advances have been achieved in our understanding of the metabolism and the importance of vitamin C in domestic animals (*Wegger et al., 1984). Numerous studies have shown that the synthesis and the consumption of vitamin C depend on many factors. In various nutritional deficiencies and in many diseases of domestic animals the synthesis of vitamin C is reduced and its concentration in the blood plasma drops.
Owing to a concurrent reduction in the concentration of vitamin C in the cells, the rates of various biochemical reactions are reduced and the performance of various cell types impaired. Administration of vitamin C has been found beneficial in dealing with various infectious diseases, hip displasia, bone development, protein metabolism and stress of domestic animals. The list of biochemical function that vitamin C is involved in is much more extensive, I have highlighted those that are relevant to this article.
Of particular interest in veterinary medicine are cases of scurvy which were characterized by painful swellings of joints being reported in young dogs. In such cases insufficient synthesis or insufficient uptake of vitamin C has been indicated as the cause.
Various studies have shown that adding small amounts of vitamin C to the food have a beneficial effect on growth and on improved performance of the immune system.
The following is intended to provide an understanding of the role of vitamin C and the basics of physiological stress and ways of using this knowledge in practical situations, the influence vitamin C has on the immune system, the influence vitamin C has on Vitamin D3 and bone metabolism and the importance of vitamin C for skin and coat.
Much confusion exists as to what stress is, and is not. Consequently, management practices may result in stress responses often creating situations which aggravate the initial reaction to the stressor. In order to avoid this we must first understand what ‘physiological’ stress really is. Physiological stress is not psychological stress, (the pressures we feel in our daily lives). Physiological stress is the nonspecific response to any external demand which calls upon the animal to adapt to a new situation. Life is a constant set of adjustments.
Energy is needed to make these adjustments. Whether the adjustment is either great or small, physiological stress provides the energy to accomplish the adjustment through nonspecific responses. For every external demand, or ‘stressor’ (a situation that causes stress), there is both a specific response and a nonspecific response. The specific response is unique for each stressor but the nonspecific response is essentially the same for every stressor. Since the presence of stressors is constant, by definition the absence of stress would be death. We cannot totally avoid stress, we must manage it.
The concept of physiological stress was first developed by a scientist named *Selye (1936,1973), who termed his observations General Adaptation Syndrome (GAS). Selye observed that most chronically ill individuals exhibited similar symptoms. There are three stages in the ‘General Adaptation Syndrome’. The first is the alarm reaction or the so-called ‘fight or flight’ reaction.
At this stage a sudden biochemical reaction takes place, (characterized by huge releases of adrenaline and similar hormones from the sympathetic nervous system). These compounds cause rapid release of glucose from body reserves (primarily from glycogen). This produces available energy to elude a stressor. The animal quickly enters the stage of resistance. This is the period when glucose is formed from less available reserves such as lipids and proteins.
The important aspect of the stage of resistance is that it will continue until recovery from the stressor occurs or the animal enters the stage of fatigue and dies. The animal dies from either the depletion of reserves or adrenocortical exhaustion. That is when the adrenal cortex (the source of corticosteroids) depletes the survival functions which include regulation of heat loss, blood flow and respiration etc. so that they can no longer be supported. The time course of the three stages of the ‘General Adaptation Syndrome’ depends upon the severity of the stressor. A chronic stressor requires small changes over a long period of time.
The adaptation to warmer weather that takes place over several weeks during the start of summer is an example. An acute stressor requires immediate life-saving adaptations to survive. The sudden onset of very hot weather creates such a situation. The animal has not had sufficient time to adapt to the hot weather. In the latter case an alarm reaction is followed by a resistance stage. If the adreal-cortex is depleted before the stressor is removed, then death will occur.
Although they may seem unlikely, growth and reproduction both call upon the body to constantly change, and are by definition stressors. With a seemingly endless myriad of stressors, the challenge for modern animal management is to modify or manage physiological stress. Ascorbic acid (vitamin C) supplementation has been shown to reduce heat stress related mortality in birds (*Pardue, 1983). One of the most difficult concepts of physiological stress to understand is suppression of the immune system. The immune reaction consumes considerable quantities of metabolic reserves. Additionally, aberrant reactions such as allergic reactions can be harmful and should be suppressed. Vitamin C has been shown to modify the immune response, *Pardue (1983). Vitamin C has also been shown to improve reproductive efficiency.
In infectious diseases the food uptake is often reduced and the concentration of glucose in the blood plasma drops. Under these circumstances the extent of synthesis of vitamin C in the liver of mammals drops. At the same time the consumption of vitamin C increases because of the increase in secretion of glucocorticosteroids. Various investigations on domestic animals suffering from certain infections have shown a reduction in the content of vitamin C in the blood plasma or serum.
In dogs suffering from distemper, administration of vitamin C at high levels for three days or longer usually results in improvement in the clinical condition and rapid recovery, especially if this treatment is used at an early stage (*Leveque, 1969). As a rule, an optimal supply level can be achieved by oral administration of 300 to 500mg vitamin C daily. Studies conducted by *Brehm (1964) indicate insufficient synthesis of vitamin C in dogs suffering from various diseases.
These studies indicate that vitamin C levels of less than 0.4 mg/dl in a dog’s blood plasma are evidence of insufficient synthesis. Supplementary administration of vitamin C is also advisable after surgery because it promotes the formation of collagen by the fibroblasts, osteoblasts and osteocytes. Topical administration of vitamin C into the region of bone fractures stimulates the healing process (*Pataky et al., 1963).
Parasitic infestation of the liver leads to a reduction in the synthesis of vitamin C which, in mammals, takes place in this organ.
Many investigations have shown that in diseases of domestic animals displaying higher than normal temperature and reduced food uptake, the concentration of vitamin C in the blood plasma drops considerably for some time. In view of the great importance of vitamin C for immune defense and for regeneration of tiss
ue, administration of vitamin C in daily dosages of 200 to 300mg for small animals and of 2 to 3g for large animals is advisable.
Scury-like symptoms in dogs are likely to be due to congenital inability to synthesise vitamin C. In such cases the concentration of vitamin C in the blood plasma is below 0.1mg/dl.
Results of recent trials show that Vitamin C influences bone development and strength through its effects on the production of vitamin D metabolites and calcium-binding protein.
Vitamin D3 supplied in a feed supplement is transported to the kidneys for conversion to the active metabolite form. Latest studies show that vitamin C is required to achieve optimum conversion of vitamin D3 into these active metabolites. Improvements in bone synthesis appear to be directly related to an increase in the conversion of vitamin D3 to the active metabolite and to the increase of calcium-binding protein through the influence of supplemented vitamin C in the diet.
At times of stress unfortunately absorption of vitamin C from the gut may not be fully effective, therefore daily supplementation is recommended.
In large breeds of dogs, hip dysplasia, long considered to be an inherited birth defect, may be an easily controlled biochemical condition. The lesion in hip dysplasia appears to merely poor quality, low strength collagen in the affected ligaments. In litters from dysplastic German Shepherd parents or parents that produced dysplastic offspring, there have been no signs of hip dysplasia when the bitches were given higher than normal doses of vitamin C during pregnancy and the pups were given daily doses of vitamin C until they reached young adulthood.
In potentially dysplastic pups of large breeds, the first year or two of life is a high stress period. The demands on the body are great, the demands for large quantities of vitamin C even greater. The laxity of the hip ligament and changes in the pectineus muscle and tendon, consequent upon lack of high quality collagen is evident. The weak collagen in the ligaments causes them to stretch or loosen, resulting in joint laxity, which allows the young femoral head to separate from the hip socket.
After separation of the femoral head from the acetabulum, an inflammatory process (arthritis) ensues. Varying amounts of scar tissue form in the acetabulum, preventing the head of the femur from returning to its normal position. This results in coxofemoral subluxation (hip dysplasia). Simultaneously, the poor quality of collagen in the pectineous muscles and ligaments retards their growth and development. The impaired growth and development of tendon and muscle, together with the rapid growth of the femur, contributes further to the cause of the dislocation.
In trials conducted over a five-year period using eight litters of German Shepherd puppies from dysplastic parents, or parents known to have produced dysplastic offspring, none of these pups which have been maintained on high doses of vitamin C have, to date, shown dysplasia. The regime consists of giving the pregnant bitch high doses of vitamin C in the ration daily. At birth, the pups are given 50 to 200mg of vitamin C orally.
When the pups reach three weeks of age, the daily amount increased to 500mg until the pups are four months old. At that time, the dosage is increased to 1 or 2g daily and maintained at that level until the pups were 18 months to two years of age. This program was so successful that, when selling puppies, breeders in America involved now incorporate into their sales agreements a clause stating that the pups are guaranteed dysplasia free only if they are kept on the prescribed regime of vitamin C.
The skin and the coat fulfill many functions:
Physiological functions such as protection, storage, excretion and the sensory function.
Social functions which partly control their relationships with other dogs (identification, territorial demarcation, sexual behavior).
Finally, in view of the current role of the dog (and of pet animals in general), functions related to acceptance in human society.
These aesthetic functions are probably of the greatest concern to most dog owners.
Skin disorders are particularly frequent in the dog and may be due to a wide variety of causes.
For example:
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Infectious dermatitis;
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Allergic or contact dermatitis;
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Alopecias of hormonal origin, other skin changes, thyroid deficiency; Ectoparasites and their direct or secondary consequences (demodectic mange);
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Disorders of dietary or nutritional origin; for example, liver and kidney disorders or overloads, or deficiency conditions.
Despite this list the relationships between diet and the condition of the skin and coat are often considered self-evident, not only by breeders and owners, but also by veterinarians. The skin and the coat may show primary lesions caused directly by specific nutritional deficiencies or excesses, but similar effects may appear as secondary symptoms of disorders of the gastrointestinal tract, the liver or the kidneys.
Vitamin C has a direct influence on the lustre of the coat through its influence on the efficient metabolism of other key micronutrients like amino acids, B complex and vitamin E.
Where diets are deficient in vitamin C metabolism of sulphur-containing amino acids will be impaired. As the coat in mainly made up of these amino acids the coat can never reach its full potential. A reduction in fur growth, possible irregularity in growth pattern, reduction in pigmentation and the activity of the hair follicles and potential loss of fur. The amino acid lysine is a vital component in the metabolism of muscle tissue-this amino acid is also dependent on vitamin C.
Vitamin C appears to be involved with the absorption of iron from the gut. It is also required for the synthesis of hemoglobin and is necessary for the development collagen in skin. Vitamin C plays an important role in the healing process of wounds.
Summary
Under conditions of acute stress, animal can not synthesise sufficient vitamin C to alleviate many detrimental effects associated with stress. Due to the vital link of vitamin C and bone metabolism and the development of collagen in teeth, bone, skin cartilage and amino acids and the improvement in the immune system response to disease challenge. Supplementation of vitamin C should become part of standard management procedure and increased particularly when known stressors are to be imposed.
References *
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Animal Nutrition (McDonal, Edwards, and Greenhalgh)
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Vitamins in Animal Nutrition (arbeitgemeinschaft Wirkstoffe Tierernahrunge (AWT) (Wegger et al.) 1984; (Selye) 1936, 1973; (Pataky et al.) 1963; (Pardue) 1983; (Leveque) 1969.
The above article was taken from the The Service Dog magazine published by the British Police and Services Canine Association.
Reprinted with permission from the U.S.P.C.A.
Breeder/Exhibitor Ed, Health
Vitamin E:
Vitamin E is an important nutrient which has been shown to have a number of physiologic and pharmacologic effects. It in a potent antioxidant and reduces fat oxidation and increases the production of HDL cholesterol. At higher doses, it also reduces cyclooxygenase and lipooxygenase activities, decreasing production of prostaglandins and leukotreines. As such, it is a potent anti-inflammatory drug. It will reduce platelet function and prolong the bleeding time slightly in healthy individuals. There is no known side-effects to vitamin E at levels less than 4000-6000 IU per day. I recommend that vitamin E be given to all dogs. For dogs under 2 years of age, give 400 IU of vitamin E daily. For dogs over 2 years of age, give 800 IU of vitamin E daily.
Vitamin C:
Vitamin C works with vitamin E and helps regenerate vitamin E, potentiating its antioxidant effect. Vitamin C supplementation does no harm, since the excess is excreted through the kidney. While dogs produce vitamin C in their bodies (unlike human beings and guinea pigs who must have it in their diet), under stress or disease, they may need vitamin C in excess of their manufacturing capacity. In excessive dose, vitamin C can cause flatulence and diarrhea. This intestinal tolerance level varies among dogs, but is generally around 3000 mg per day in an adult German Shepherd. I recommend this be given to all dogs. For dogs under 2 years of age, give 250 mg vitamin C twice a day. For dogs over 2 years of age, give 500 mg of vitamin C twice a day.
Breeder/Exhibitor Ed, Health
Written by Dr. Alice Crook and taken from the Canine Inherited Disorders Database with permission
What is von Willebrand’s disease?
Von Willebrand’s disease (vWD) is a common, usually mild, inherited bleeding disorder in people and in dogs. It is caused by a lack of von Willebrand factor (vWF), which plays an essential role in the blood clotting process.
Normally the body responds to an injury causing bleeding through a complex defense system. This consists of local changes in the damaged blood vessels, activation of blood cells called platelets, and the coagulation process. A reduction in von Willebrand factor leads to abnormal platelet function and prolonged bleeding times. Affected dogs are prone to bleeding episodes such as nose bleeds, and generally experience increased bleeding with trauma or a surgical procedure.
Three forms of the disease are distinguished based on vWF concentration and function. Dogs with Type I vWD (by far the most common) have mild to moderate bleeding abnormalities, depending on the level of vWF. The much rarer types II and III vWD cause severe bleeding disorders.
How is von Willebrand’s disease inherited?
The most common form (Type I vWD) is thought to be an autosomal trait with incomplete dominance. This means offspring may inherit the disorder if either parent carries the gene, but not all offspring will be affected to the same extent. Dogs with type I disease have reduced but measurable levels of Von Willebrand factor (1 to 60 per cent). Animals that inherit the gene for type I vWD from both parents (homozygotes) die before birth or shortly thereafter.
Type III vWD is relatively rare. This form is autosomal recessive. Animals are only affected if they inherit the abnormal gene from both parents, who are clinically unaffected carriers. Affected dogs have zero levels of vWF, while carrier parents have 15 to 60 per cent of normal levels.
Type II vWD is very rare. It is an autosomal recessive trait.
Bleeding abnormalities are severe in dogs with Types II and III von Willebrand’s disease.
What breeds are affected by von Willebrand’s disease?
Type I vWD: This is by far the most common form. The gene for the condition is widespread in the Doberman Pinscher population, and is also relatively common in the Scottish Terrier and Shetland Sheep Dog. There is an increased risk of the disorder in the Golden Retriever, Standard and Miniature Poodle, Welsh Pembroke Corgi, Miniature Schnauzer, Basset Hound, German Shepherd, Rottweiler, Manchester Terrier, Keeshond, and Standard and Miniature Dachshund. This disease occurs in most other breeds and in mixed-breed dogs as well.
Type III vWD: rare, occurs in the Scottish terrier, Shetland sheepdog, and very sporadically, in the Chesapeake Bay Retriever
Type II: extremely rare, German Short-haired Pointer
For many breeds and many disorders, the studies to determine the mode of inheritance or the frequency in the breed have not been carried out, or are inconclusive. We have listed breeds for which there is a general consensus among those investigating in this field and among veterinary practitioners, that the condition is significant in this breed.
What does von Willebrand’s disease mean to your dog & you?
Although many dogs are affected by vWD, only a small proportion have severe problems. Dogs with vWD are prone to nose bleeds, bleeding from the gums, and prolonged bleeding during heat or after whelping. There may be prolonged bleeding from the umbilical cord at birth or when your pup sheds its baby teeth. Excessive bleeding after surgery or trauma is common, and may be the first sign of this condition in your dog. You may see blood in your dog’s urine or stool.
Most dogs with vWD can lead normal lives, with occasional bleeding episodes that may go unnoticed or can be treated appropriately. Other illnesses, or physical or emotional stress may worsen bleeding episodes. In affected dogs, it is best to consult your veterinarian before using any over-the-counter medications. Drugs such as aspirin for example, alter the function of platelets, and should be avoided in dogs with bleeding disorders.
How is von Willebrand’s disease diagnosed?
Because the severity of bleeding with von Willebrand’s disease is quite variable, often the disease is not diagnosed until the dog is 3 to 5 years old. Your veterinarian may suspect vWD because of a history of abnormal bleeding in your dog, such as unexplained nosebleeds, or there may be heavy bleeding during surgery. Stillbirths or pups that die shortly after birth (“fading puppies”) may be a result of both parents being carriers of the gene for von Willebrand’s disease.
There are specialized tests available to make the diagnosis of von Willebrand’s disease. One is a genetic test and the other measures blood levels of von Willebrand factor.
FOR THE VETERINARIAN: Mucosal bleeding time is the best screening test for a potential defect in platelet function, and is prolonged in dogs with a deficiency in vWF. However the test is non-specific for vWD because it is also prolonged in dogs with thrombocytopenia or functional platelet defects. (Bleeding times are normal in animals with warfarin toxicity, hemophilia A or B, or a deficiency of Factor VII.)
Specific diagnosis of vWD requires either genetic testing in those breeds in which it is available, or vWF measurement. The genetic test is performed by submitting a sample (such as a mucosal scraping) to a genetic testing laboratory. The results are reliable at any age. Measurement of vWF:Ag levels is done by electroimmunoassay or enzyme-linked immunoabsorbent assay (ELISA). Samples for testing must be submitted to the diagnostic laboratory very fresh in a citrate tube (within 1 to 2 hours of collection). Where this isn’t possible, the blood sample should be separated immediately after collection and the plasma submitted frozen. It is best to check with your diagnostic laboratory for shipping instructions. VWF levels vary between breeds and with respect to age.
Because of the possible link with hypothyroidism, thyroid status should be evaluated.
How is von Willebrand’s disease treated?
This condition cannot be cured but it can be managed. Your veterinarian will discuss this with you when the diagnosis is made.
You will likely be able to control mild bleeding yourself by applying prolonged pressure. In other circumstances, veterinary care such as cautery or sutures may be required. Severe bleeding episodes are treated by administering a source of von Willebrand factor through a transfusion. If your dog requires surgery, your veterinarian may recommend a transfusion pre-operatively as a precaution, depending on the severity of the bleeding disorder, and the type of surgery.
Thyroid supplements may help to control bleeding, if your veterinarian determines that your dog is hypothyroid.
FOR THE VETERINARIAN: Exogenous vWF may be supplied through administration of fresh whole blood, fresh or fresh-frozen plasma, or cryoprecipitate (treatment of choice).
Where possible, avoid the use of drugs that have been known to cause thrombocytopenia or otherwise affect platelets. Such drugs include NSAIDs (aspirin, phenylbutazone, ibuprofen, indomethacin), some antibiotics (penicillin, sulfonamides, ampicillin, chloramphenical), antihistamines, phenothiazines, theophylline,heparin, and estrogen.
Some studies have shown that thyroid supplementation in euthyroid dogs can reduce bleeding, but other studies have contradicted this.
Genetic counseling
The trait for von Willebrand’s disease is w
idespread, particularly in Doberman Pinschers but also in several other breeds. An accurate genetic test has been developed for the Doberman Pinscher, Scottish Terrier, Shetland Sheepdog, Manchester Terrier, Poodle, and Pembroke Welsh Corgi. Testing can reliably identify dogs with vWD, dogs that are carriers, or dogs that are clear (see reference below for information on testing).
In breeds where specific genetic tests are not yet available, carriers of the trait can still be identified through the blood test for von Willebrand factor. These dogs have reduced levels of vWF (25 to 60 per cent) but do not have bleeding problems. Levels vary with age and between breeds. Where a bleeding disorder has been identified, breeders are advised to test breeding stock. Dogs with von Willebrand’s disease and those who are carriers should not be used for breeding.
Where to find more information?
deGopegui, R.R. and Feldman, B.F. 1998.Acquired and inherited platelet dysfunction in small animals. Compendium on Continuing Education for the Practicing Veterinarian 20:1039.
Brooks, M. 1996. Emergency management of canine von Willebrand’s disease. A.C.V.I.M. Proceedings of the 14th Annual Vet. Medical Forum.34.
http://www.vetgen.com – information on genetic testing available
Breeder/Exhibitor Ed, Health
By Nancy Morris DVM, Diplomate ACVIM Cardiology
Rapid, erratic, heart beats known as Ventricular Tachycardia (VT) account for 25-30% of Dobermans with Cardiomyopathy that die suddenly prior to the onset of fluid in the lungs, or congestive heart failure. (1-3) Ventricular tachycardia may also occur when the heart dilates and the left ventricular function worsens. Sustained Ventricular Tachycardia at fast heart rates can cause acute worsening of heart function rapidly over days to weeks if it remains untreated. This can precipitate the acute onset of coughing and fluid in the lungs or pulmonary edema, as dilated cardiomyopathy (DCM) worsens.
Doberman Cardiomyopathy: What is Ventricular Tachycardia?
The heart has an electrical generator system, conduit, and electrical switching station, within it. When an electrical impulse is transmitted this causes the heart to beat or contract. When the ventricles of the heart are diseased, the electrical impulse that causes the heart muscle to contract is transmitted abnormally and it results in an electrical waveform recording on either EKG or 24 hour Holter monitor that is usually faster than the baseline heart beats. The erratic heart beats arising from the diseased ventricles do not behave like normal heart beats. They may be very fast or in strings of ventricular premature beats, called ventricular tachycardia. Tachycardia means a heart rate that is faster than normal.
Singular ventricular premature beats (VPC´s) are Singular VPC considered abnormal if there are more than 50 to 100 of them recorded during a 24 hour holter monitor study. An EKG is a short recording of the electrical activity of the heart but it only records up to 2 minutes out of a 24 hour period. If the EKG is normal, the 24 hour holter monitor recording may be abnormal because of the prolonged recording time. EKG´s are generally a poor means of identifying ventricular premature beats in Doberman Pinschers unless the abnormal ventricular beats are frequent or severe. Singular VPC´s when, compared with couplets, triplets or runs of ventricular tachycardia, are not as dangerous as the latter. The risk for sudden death from erratic ventricular heart beats increases as the numbers of couplets, triplets or runs of ventricular tachycardia increase on a 24 hour holter study. These abnormal heart beats may be sustained and occur at rates that are so fast that the pumping of the heart is ineffective and oxygen is not carried to the dogs brain adequately. When this occurs the dog will faint or experience syncope, when he exerts. If the abnormally fast heart beats slow down, the dog will wake up or experience aborted sudden death. If the fast and abnormal rhythm continues for just a few minutes continuously, the dog will die.
Ventricular Tachycardia
There are many medicines that may be used to treat ventricular tachycardia with the goal being to improve the abnormal beats and revert the heart rhythm to more normal and regular beating. The second reason to treat erratic ventricular heart beats, or ventricular arrhythmias is to try to prevent sudden death from lethal arrhythmias. A famous medical scientific study performed in people in the 1980´s called the Cardiac Arrhythmia Suppression Trial (CAST) demonstrated that some of the drugs used to treat ventricular arrhythmias could actually worsen the arrhythmias and the trial was stopped because people receiving certain medications had a higher incidence of sudden death than those not receiving medications. The CAST study spawned a series of studies on these drugs and the findings showed that it was not possible to predict which person will benefit from which medicine to treat abnormal heart beats. Further research in people has lead to knowledge of which medications are most likely to result in improvement in specific patient populations such as patients with arrhythmia and dilated cardiomyopathy (DCM). Most antiarrhythmic medications have the ability to cause “proarrhythmias” or worsening of the arrhythmias they are being used to treat. The same drug that causes proarrhythmia in one person may not in another person. Another important finding of all of these studies, in people, is that no drug used to treat ventricular tachycardia has been shown to prevent sudden death, even if it improves symptoms of syncope or fainting and even if the ventricular arrhythmias are markedly improved on the medication. To complicate matters even more, none of these kinds of studies have been performed in dogs. Dogs are similar to people but they sometimes do not react to medication as a person would.
For the reason´s cited above, treatment of ventricular tachycardia with medications is generally reserved for dogs experiencing many couplets, short runs of fast ventricular tachycardia or sustained ventricular tachycardia. Dogs that are experiencing symptoms or fainting are always put on medications to try to improve these symptoms. Monitoring of arrhythmias after treatment is advisable to ensure that medications are helping and not worsening the heart rhythms. Follow-up 24 hour holter monitoring is the best way to achieve this goal. Generally, singular VPC´s even relatively high numbers on a 24 hr holter study are not treated with medications. We do not know if medications to treat ventricular tachycardia in dogs results in a decrease in the incidence of sudden death. In addition, the natural day to day variation in numbers of VPC´s and severity of ventricular arrhythmias without treatment remains unknown in Doberman Pinschers. The 24 hour holter monitoring study is typically used to determine drug efficacy. All veterinary cardiologists make the assumption that if the holter study is improved on medications, the medication is responsible for the improvement. However, we do not know if this is actually the case. With the support and help of Doberman Pinscher owner/breeders we will know shortly.
Mass Veterinary Cardiology Services of Pembroke, MA and Dr. Nancy Morris are performing a study, now in Dobermans with known ventricular arrhythmias, to determine the day to day variation in abnormal heart beats without treatment. The study involves Doberman Pinschers with known abnormal holter results, that are receiving no antiarrhythmic medications, but maybe receiving other cardiac medications. Each dog has 7 days of continuous holter recordings performed. Five Dobermans have participated and completed the study to date. Our goal is to enroll 7 more dogs for this study before March 2007. Findings from this study may provide the foundation to determine which drugs are best used in Dobermans, and which drugs if any decrease the incidence of sudden death. Preliminary results will be presented in the next issue of Doberman Digest. Please consider volunteering your dog for this study, if you know that your dog has an abnormal holter test result. Contact Susan Krom, Director of Cardiology Services, at 413-530-6819 or email SueKrom@comcast.net for more information.
References
1. Calvert CA, Wall M: Results of ambulatory electrocardiography in overtly healthy Doberman Pinschers with equivocal echocardiographic evidence of dilated cardiomyopathy. J Am Vet Med Assoc. 2001 Sept 15;219 (6): 782-784.
Breeder/Exhibitor Ed, Health
The following is taken from the April/May Newsletter of the Senior Dogs Project:
Vaccinations: All Veterinary Schools in North America Changing Vaccination Protocols
Recent editions of the Senior Dogs Project’s newsletter have reported on the ever-broadening trend of eliminating vaccinations for adult dogs, except for rabies, where required by state law. We have now had a report that all 27 veterinary schools in North America are in the process of changing their protocols for vaccinating dogs and cats. Here, in a nutshell, are the new guidelines under consideration: “Dogs and cats immune systems mature fully at 6 months. If a modified live virus (MLV) vaccine is given after 6 months of age, it produces immunity, which is good for the life of the pet (i.e., canine distemper, parvo, feline distemper). If another MLV vaccine is given a year later, the antibodies from the first vaccine neutralize the antigens of the second vaccine and there is little or no effect. The titer is not ‘boosted’ nor are more memory cells induced.
“Not only are annual boosters for parvo and distemper unnecessary, they subject the pet to potential risks of allergic reactions and immune-mediated hemolytic anemia. There is no scientific documentation to back up label claims for annual administration of MLV vaccines. Puppies receive antibodies through their mothers milk. This natural protection can last 8-14 weeks. Puppies and kittens should NOT be vaccinated at LESS than 8 weeks. Maternal immunity will neutralize the vaccine and little protection (0-38%) will be produced. Vaccination at 6 weeks will, however, delay the timing of the first highly effective vaccine. Vaccinations given 2 weeks apart suppress rather than stimulate the immune system. A series of vaccinations is given starting at 8 weeks and given 3-4 weeks apart up to 16 weeks of age. Another vaccination given sometime after 6 months of age (usually at 1 year 4 months) will provide lifetime immunity.”
An article on Fort Dodge Vaccines is available for download in Adobe Acrobat PDF format Vaccination Protocol (pdf).
Breeder/Exhibitor Ed, Health
Dr. W. Jean Dodd’s vaccination protocol is now being adopted by ALL 27 North American veterinary schools. I highly recommend that you read this. Copy and save it to your files. Print it and pass it out at dog fairs, cat shows, kennel club meetings, dog parks, give a copy to your veterinarian and groomer, etc., etc.*
Get the word out.
VACCINATION NEWS FLASH
*I would like to make you aware that all 27 veterinary schools in North America are in the process of changing their protocols for vaccinating dogs and cats. Some of this information will present an ethical &economic challenge to vets, and there will be skeptics.
Some organizations have come up with a political compromise suggesting vaccinations every 3 years to appease those who fear loss of income vs. those concerned about potential side effects. Politics, traditions, or the doctor’s economic well being should not be a factor in medical decision.
NEW PRINCIPLES OF IMMUNOLOGY
“Dogs and cats immune systems mature fully at 6 months. If a modified live virus vaccine is given after 6 months of age, it produces an immunity which is good for the life of the pet (ie: canine distemper,parvo, feline distemper). If another MLV vaccine is given a year later, the antibodies from the first vaccine neutralize the antigens of the second vaccine and there is little or no effect. The titer is not “boosted” nor are more memory cells induced.” Not only are annual boosters for parvo and distemper unnecessary, they subject the pet to potential risks of allergic reactions and immune-mediated hemolytic anemia. “There is no scientific documentation to back up label claims for annual administration of MLV vaccines.” Puppies receive antibodies through their mothers milk. This natural protection can last 8-14weeks. Puppies & kittens should NOT be vaccinated at LESS than 8weeks. Maternal immunity will neutralize the vaccine and little protection (0-38%) will be produced. Vaccination at 6 weeks will, however, delay the timing of the first highly effective vaccine. Vaccinations given 2 weeks apart suppress rather than stimulate the immune system. A series of vaccinations is given starting at 8 weeks and given 3-4 weeks apart up to 16 weeks of age.Another vaccination given sometime after 6 months of age (usually at 1 year 4mo) will provide lifetime immunity.
CURRENT RECOMMENDATIONS FOR DOGS
Distemper & Parvo * “According to Dr. Schultz, AVMA, 8-15-95, when a vaccinations series given at 2, 3 & 4 months a nd again at 1 year with a MLV, puppies and kitten program memory cells that survive for life, providing lifelong immunity.” Dr. Carmichael at Cornell and Dr. Schultz have studies showing immunity against challenge at 2-10 years for canine distemper & 4 years for parvovirus. Studies for longer duration are pending. “There are no new strains of parvovirus as one mfg. would like to suggest. Parvovirus vaccination provides cross immunity for all types.” Hepatitis (Adenovirus) is one of the agents known to be a cause of kennel cough. Only vaccines wi th CAV-2 should be used asCAV-1 vaccines carry the risk of “hepatitis blue-eye” reactions & kidney damage.**Bordetella Parainfluenza: Commonly called “Kennel cough” Recommended only for those dogs boarded, groomed, taken to dog shows, or for any reason housed where exposed to a lot of dogs. The intranasal vaccine provides more complete and more rapid onset of immunity with less chance
of reaction. Immunity requires 72 hours and does not protect from every cause of kennel cough. Immunity is of short duration (4 to 6 months).*
*RABIES There have been no reported cases of rabid dogs or cats in Harris, Montogomery or Ft. Bend Counties [Texas], there have been rabid skunks and bats so the potential exists. / It is a killed vaccineand must be given every year./*//
*Lyme disease_is a tick born disease which can cause lameness, kidney failure and heart disease in dogs. Ticks can also transmit the disease to humans. The original Ft. Dodge killed bacteria has proven to be the most effective vaccine. Lyme disease prevention should emphasize early removal of ticks. Amitraz collars are more effective than Top Spot, as amitraz paralyzes the tick’s mouthparts preventing transmission of disease.
**VACCINATIONS NOT RECOMMENDED**
Multiple components in vaccines compete with each other for the immune system and result in lesser immunity for each individual disease as well as increasing the risk of a reaction. Canine Corona Virus is only a disease of puppies. It is rare, self limiting (dogs get well in 3 days without treatment). Cornell & Texas A&M have only diagnosed one case each in the last 7 years. Corona virus does not cause disease in adult dogs.*
*Leptospirosis vaccine is a common cause of adverse reactions in dogs. Most of the clinical cases of lepto reported in dogs in the US are caused by serovaars (or types) grippotyphosa and bratsilvia. The vaccines contain different serovaars eanicola and ictohemorrhagica. Cross protection is not provided and protection is short lived. Lepto vaccine is immuno-supressive to puppies less than 16 weeks.
/NEW RECOMMENDATIONS FOR CATS
Feline vaccine related Fibrosarcoma is a type of terminal cancer related in inflammation caused by rabies & leukemia vaccines. This cancer is thought to affect 1 in 10,000 cats vaccinated. Vaccines with aluminum adjuvant, an ingredient included to stimulate the immune system, have been implicated as a higher risk. We now
recommend anon-adjuvanted rabies vaccine for cats. Testing by Dr. Macy, Colorado State , has shown this vaccine to have the lowest tissu e reaction and although there is no guarantee that a vaccine induced sarcoma will not develop, the risk will be much lower than with other vaccines.*
*Program injectable 6 mo flea prevention for cats has been shown to be very tissue reactive & therefore has the potential of inducing an injection site fiborsarcoma. If your cats develops a lump at the site of a vaccination, we recommend that it be removed ASAP, within 3-12 weeks.*
*Feline Leukemia Virus Vaccine This virus is the leading viral killer of cats. The individuals most at risk of infection are young outdoor cats, indoor/outdoor cats and cats exposed to such individuals. Indoor only cats with no exposure to potentially infected cats are unlikely to become infected. All cats should be tested prior to vaccination. /Cats over one year of age are naturally immune to Fel.V whether they are vaccinated or not, so annual vaccination of adult cats is NOT necessary. The incubation period of Feline leukemia can be over 3 years, so if your cat is in the incubation state of the disease prior to vaccination, the vaccine will not
prevent the disease. *
/Feline Panleukopenia Virus Vaccine. Also called feline distemper is a highly contagious and deadly viral disease of kittens. It’s extremely hardy and is resistant to extremes in temperature and to most available disinfectants. Although an effective treatment protocol is available, it is expensive to treat because of the serious nature of the disease and the continued presence of virus in the environment, vaccination is highly recommended for all kittens. Cats vaccinated at 6 month or older with either killed or MLV vaccine will produce an immunity good for life. Adult cats do NOT need this vaccine./*
*/Feline Calicivirus/ He
rpesvirus Vaccine. Responsible for 80-90% of infectious feline upper respiratory tract diseases. The currently available injectable vaccines will minimize the severity of upper respiratory infections, although none will prevent disease in all situations.* *Intranasal vaccines are more effective at preventing the disease entirely. Don’t worry about normal sneezing for a couple of days. Because intranasal vaccines produce an immunity of shorter durations, annual vaccination is recommended.
VACCINES NOT RECOMMENDED
Chlamydia or pneumonitis. The vaccine produces on a short (2 month)duration of immunity and accounts for less than 5% of upper respiratory infections in cats. The risks outweigh the benefits.*
**
*Feline Infectious Peritonitis. A controversial vaccine. Most kittens that contract FIP become infected during the first 3 months of life. The vaccine is labeled foruse at 16 weeks. All 27 vet schools do not recommend the vaccine.*
Bordetella A new vaccine for feline bordetella has been introduced. Dr. Wolfe of Texas A&M says that bordetella is a normal flora and does not cause disease in adult cats. Dr. Lappin of Colorado State says that a review of the Colorado State medical records reveals not one case diagnosed in 10 years.
NEW DEVELOPMENTS: Giardia is the most common intestinal parasite of humans in North America, 30% or more of all dogs & cats are infected with giardia. It has now been demonstrated that humans can transmit giardiato dogs & cats & vice versa. *
Heartworm preventative must be given year-round in Houston .
*VACCINES BADLY NEEDED New vaccines in development include: Feline Immunodeficiency Virus and cat scratch fever vaccine for cats and Ehrlichia [one of the other tick diseases, much worse than Lymes] for dogs.
THE VIEW FROM THE TRENCHES; BUSINESS ASPECTS
Most vets recommend annual boosters and most kennel operators require them. For years the pricing structure of vets has misled clients into thinking that the inherent value of an annual office visit was in the “shots” they failed to emphasize the importance of a physical exam for early detection of treatable disea ses. It is my hope that you will continue to require rabies & Kennel cough and emphasize the importance of a recent vet exam. I also hope you will accept the new protocols and honor these pets as currently vaccinated. Those in the boarding business who will honor the new vaccine protocols can gain new customers who were turned away from vet owned boarding facilities reluctant to change.
CONCLUSION
Dogs & cats no longer need to be vaccinated against distemper, parvo, & feline leukemia every year. Once the initial series of puppy or kitten vaccinations and first annual vaccinations are completed, i mmunity from MLV vaccines persists for life. It has been shown that cats over 1 year of age are immune to Feline Leukemia whether they have been vaccinated or not. Imagine the money you will save, not to mention less risks from side effects. PCR rabies vaccine, because it is not adjuvanted, will mean less risk of mediated hemolytic anemia and allergic reactions are reduced by less frequent use of vaccines as well as by avoiding unnecessary vaccines such as K-9 Corona virus and chlamydia for cats, as well as ineffective vaccines such as Leptospirosis and FIP. Intranasal vaccine for Rhiotracheitis and Calici virus, two upper respiratory viruses of cats provide more complete protection than injectable vaccines with less risk of serious reactions.
The AAHA and all 27 veterinary schools of North America are our biggest endorsement for these new protocols.*
*Dr. Bob Rogers* Please consider as current on all vaccinations for boarding purposes.
DOGS Initial series of puppy vaccines
1. distemper, hepatitis, parvo, parinfluenze – 3 sets one month apart concluding at 16 weeks of age.*
2. Rabies at 16 weeks of age (later is better)
3. Bordetella within last 4-6 months First annual (usually at 1 year and4 months of age)*
1. DHP, Parvo, Rabies
2. Bordetella within last 4-6 months 2 years or older
1. Rabies with in last year
2. Bordetella within last 4-6 months
3. DHP & Parvo given anytime over 6 months of age , but not necessarily within the last year.
Recommended: Physical exam for transmissible diseases and health risks.
*CATS Initial kitten series
1. Distemper [PLP], Rhino Calicivirus, Feline Leukemia Vaccine – 3 sets given one month apart concluding at 16weeks.
2. Rabies at 16 weeks
First Annual [usually at 1 year and 4 months of age]
1. Distemper (PLP), Rhino Calicivirus, Rabies 2 years or older
1. Rabies within the last year
2. Rhino Calicivirus within last year
3. Distemper and FelV given anytime after 6 months of age, but not necessarily with the last year.
Recommended: Physical exam, FeLV/FIV testing, fecal exam for giardia.
