Joints: Patella Luxation
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Together with the femur and the tibia, the Patella, or kneecap, forms the knee joint. The Patella is held in place by the patella tendon. This tendon is attached to the tibia. In a healthy situation, the Patella will move up and down
in a groove, called the trochea that is located at the lower hand and frontside of the femur. When the trochea in the femur is too shallow, the attachement of the knee tendon is not in the right place or the position of the tibia in
relation to the femur deviates then the Patella could slip out of the trochea. This is called Patella Luxation.
In case of Lateral Patella Luxation (LPL), the Patella moves towards the outside of the leg. Often, this form of PL also involves arthritis and deformation of the tibia and/or the femur. In most of these cases, a surgical
operation is needed. Unilateral or bilateral (temporary) paralysis, swollen kneejoints, pain, unable/unwilling to walk and jump normally and bow-legs could be signs of LPL.
In case of Medial Patella Luxation (MPL), the most common form of LP, the tibia turns inwards and the Patella moves to the inside of the leg where it will lay against the inside of the tibia. The friction that is caused will damage the
smooth surface of the Patella. This will lead to arthritis.
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When the Patella is luxated, the muscle with which the Patella tendon merges, puts a rotational force on the tibia, which will increase the malformation with time and so will increase the problem. Regular luxation of the Patella
will make the Patella tendon looser with the result of increasing frequency of luxation. Due to the malformation the ligaments will be put under pressure. This can cause the ligaments to rupture.
A dog with a luxated Patella, depending on the severity, will try to spare his leg when walking. Until the Patella is in its place again, the leg can't be stretched. The dog may skip or hop, carry the leg or in the most extreme case
walk only on his front legs.
PL is heritary, however, it can also be caused by trauma. In the severe cases, PL is a very painful condition. Going up and down stairs and jumping can not cause PL.
When examining the knee, the depth of the groove, the placement of the Patella, the alignment of the tibia with regard to the femur and the curve of the tibia all must be checked. Behind the Patella lays a number of cruciate ligaments.
Because of the movement of the Patella, these may be damaged too. In the severe cases surgical correction may be needed.
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PL is graded from 1 to 4, in which 4 is the most severe case. Grade 1 can become a grade 4.
| Grade 1: | The Patella can be luxated manually and returns to the trochlea when released. Tibial rotation is minimal. Occasional luxation occurs but in general the dog won't feel inconvenienced. |
| Grade 2: | The Patella can be easily luxated manually and remains luxated until replaced. Luxation occurs frequently, causing the leg to be carried or used without full extension. Tibial rotation is present. |
| Grade 3: | The patella is permanently luxated, but can be replaced manually. The dog often uses the leg, but without full extension. Tibial rotation is marked. |
| Grade 4: | The patella is permanently luxated and can't be replaced manually. Extension of the leg is impossible. Tibial rotation is quite severe, resulting in a "bow
legged" appearance. Surgical correction generaly needed. |
Dogs with a grade 3 and 4 may have to deal with various degrees of paralysis. |
Disclaimer – The above article is not meant to serve as a substitute for Licensed Veterinarian care. The author and person/persons responsible for content
and posting are not responsible for any unsatisfactory occurrence as a result of this or any other article content posted on this website. |
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Joints: Legg Calve Perthes (LCP)
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The hip joint is formed by the femural head and the hip socket of the pelvic bone. The femural head is supplied with blood through 2 small arteries. LCP occurs when this blood supply is cut off. Due to the insufficient blood supply the femural head starts to die and disintegrate. The head will deform, causing pain, limping and eventually arthritis.
LCP can also be caused by trauma, in this article I concentrate on the inheriditery form.
LCP appears within 4-12 months of age. The reason why the
bloodflow is cut off is unknown. Lameness, limping and pain in the affected hip are first signs of LCP. Muscle atrophy, shorting of the affected leg and restricted joint movement are common physical signs. |
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LCP is thought of being polygenetic in nature. That means that more genes have to be present in the right combination to become affected. In most cases only one hip is affected, there are a few cases in which both hips were affected. LCP affects both dogs and bitches.
Diagnosis is confirmed by X-ray. In case of LCP in an early onset it will show decalcification of the joint, in a later stage deformation of the femural head. Recovering without interference is not (always) a possibility and treatment will
(often) exist of surgical removal of the head of the femur. The femur and the ligaments will form a new joint with the pelvis. If detected and operated early enough, the dog has the most chance of recovering without a limp.
After surgery the dog is free of pain, and maybe not even show a limp. In any case a dog diagnosed with LCP should not be used for breeding due to the degree of heritability. |
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The x-ray on the left shows the hip joints of a nine month old Chinese Crested bitch diagnosed with LCP. The deformed femoral head on the right of this image is clearly visible.
The first sign of something wrong presented as difficulty and pain when she would try to stand up from a lying down position. Shortly after the first signs of distress this x-ray was taken. The same week the x-ray was taken the bitch had surgery. The femoral head was successfully removed and within a very short time the bitch was back up on all fours with no sign of pain or limp. |
Disclaimer – The above article is not meant to serve as a substitute for Licensed Veterinarian care. The author and person/persons responsible for content
and posting are not responsible for any unsatisfactory occurrence as a result of this or any other article content posted on this website. |
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Look into the eyeball: Cataract
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The lens is a clear, transparent body in the eye. The lens does not contain bloodvessels and so for its metabolism it depends on the surrounding fluids, mainly consists of water and proteine.
In a healthy eye incoming light falls through the lens onto the retina, light is then transfered in nerve signals and sent to the brain which create images. To get clear images the lens should be completely clear. When the proteine in the
lens clot together the lens will become clouded and the amount of light reflected on the retina will decrease. These cloudiness will lead to loss of eyesight, the images will be blurred.
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When the cataract is small the cloudiness will only affect part of the lens. There will be little signs of sightloss. Cataracts do grow and in time the conditions will worsten and finally every incomming vision will be projected
blurred. At the point that the whole lens is infected, there will be no vision left with that eye.
Cataracts can be inherited but also accur due to aging, trauma, nutrition deficiency, diabetes and poisening. A cataract can also lead to Lens Luxation and Glaucoma.
Cataracts can be surgically removed but if such an operation is meaningful depends on the amount of growth and amount of sightloss.
Dogs with Cataracts should not be used for breeding. In most cases cataracts will occur early in life so affected dogs can be pulled out of the breedingprogram. It would be advisable to not use the parents/second generation for breeding for they are/ can be affected/carrier of this fault gene. Yearly testing by a licensed ophtalmologist ought to be done to reduce the chance of breeding with an affected dog. |
Disclaimer – The above article is not meant to serve as a substitute for Licensed Veterinarian care. The author and person/persons responsible for content
and posting are not responsible for any unsatisfactory occurrence as a result of this or any other article content posted on this website. |
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Look into the eyeball: Glaucoma
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The eyeball is filled with a vitreous fluid that is, in a healthy situation, supplied and discharged continuously. The amount of vitreous fluid determines the inner pressure and the shape
of the eyeball. Glaucoma is caused by an increase in this pressure. In most cases this is caused by the drainage canal being blocked, however the input of fresh fluid continues. This will cause the eye to deform and is extremely painful.
Due to the increased pressure in the eyeball, also the optic nerve at the back of the eye will be pressured. The optic nerve sends signals to the brain to form
images. When too much pressure is exerted on the optic nerve, it loses its ability to function properly and the eyesight fails. |
Glaucoma can be caused by heredity, trauma, inflammation, eyetumor and Lens Luxation. If the Glaucoma is the result of heredity, both eyes could become affected. Glaucoma is generally diagnosed in one eye initially. It may not appear in the second eye for 5 months, up to 2 years.
Glaucoma can cause acute blindness within 24 hours. However, it can also take weeks/months before blindness occurs. It depends totally on how rapidly the increased pressure in the eye damages the optic nerve. This is why it is so important that you consult your vet immediately, when any signs of eye problems/injuries occur. If the pressure can be decreased within 24 hours of onset, there is a chance the vision may be saved in the affected eye. However, even if the pressure has been present for a considerable time and vision has been lost, the pain caused by the increased pressure is still severe.
Glaucoma in early stages can be recognised by a mild eye infection, excessive tearing, pain to the eye, squinting of the eye, sensitivity to light and cloudiness of the cornea. Glaucoma in a later stage can be recognized by the reddish color of the white (sclera) of the eye, an increase in the size of the eye or eyelids that do not close completely. In almost all cases, this is the stage glaucoma is diagnosed. Medication/surgery will be necessary to relieve the dog of this extreme pain. The vision cannot be restored in the affected eye.
Dogs with glaucoma should not be used for breeding. Unfortunately, the hereditary form usually does not occur until a later age. By this time, most dogs have already been used and already have offspring. Therefore, it is advisable not to use the second generation for breeding. The probability will be high that the offspring are either affected or a carrier of the responsible gene. Yearly testing by a licensed ophtalmologist will greatly reduce the chances of using an affected dog for breeding. |
Disclaimer – The above article is not meant to serve as a substitute for Licensed Veterinarian care. The author and person/persons responsible for content
and posting are not responsible for any unsatisfactory occurrence as a result of this or any other article content posted on this website. |
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Look into the eyeball: Lens Luxation
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The lens of the eye is located behind the iris and a part of it is visible through the opening of the pupil. In a normal situation the lens is kept in place by small fibers called zonules.
When the zonules tear off the lens can become detached. The lens can now slide through the opening into the anterior chamber or moves backwards in the vitreous body. (If the zonules tear off partly we speak of lens subluxation).
When the lens will come in contact with the cornea it can cause much damage. The lens will also block the flow of the aqueous fluid in the eye. The pressure in the eye will increase. As a result of this a Glaucoma will occur.
Lens Luxation can be inherited yet can be caused by a trauma, inflammation and Glaucoma as well.
Treatment of LL depends on where the lens is located (this can be either in the anterior chamber or in the vitreous body), the presence of Glaucoma and the visibility of the affected eye. With an early diagnosis vision in the affected eye could be saved by removing the lens out of the anterior chamber. But in most cases the eye can't be saved and maybe then it's better to remove the affected eye.
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When the lens is located in the vitreous body the option could be to give eyedrops (lifelong) that will keep the pupil small and so the lens should stay behind it. This type of LL should not be painful for the dog and it should even be possible to see with the affected eye.
With heredity LL both eyes will be affected. In some cases the lenses of both eyes will get loose at the same time but in most cases there will be a time between the loosening of the first lens and the second. This can be weeks,
months or even years.
The signals of LL can vary between minor to extreme pain to the eye, red coloring of the white of the eyeball, cloudyness of the cornea, tearing and blindness. Don't wait with contacting your vet!
Allready after only a few hours too much damage could be done to save the vision/eye.
Dogs with LL should not be used for breeding. However, this condition will mostly occur at a later age and most dogs used for breeding will already have
produced offspring. Caution should be used if using a likely carrier (parent,sibling,close relative of an affected) for breeding. Yearly testing by a licensed ophtalmologist ought to be done to reduce the chance of breeding with an affected dog. |
Disclaimer – The above article is not meant to serve as a substitute for Licensed Veterinarian care. The author and person/persons responsible for content
and posting are not responsible for any unsatisfactory occurrence as a result of this or any other article content posted on this website. |
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Look into the Eyeball: Progressive Retinal Atrophy (PRA)
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The Cornea of the eye contains special cells called rods and cones. The rods are responsible for seeing in dim light, the cones make it possible to see in daylight and distinguish colors.
The part of the Cornea that is located
directly behind the lens, called the fovea, contains only cones. Outside this section the amount of cones decreases and the number of rods increases. The area outside the fovea is used to see in dim light. Light intensity can be
distinguished but because of the absence of cones not so many colors.
These rods and cones catch the light that falls through the lens and send signals through the optic nerve to the brain which will convert the signals into images. PRA is a genetic disorder which affects the rods and cones. In it's
early stages only the rods will be affected; the dog will become night-blind first. In a later stage the cones also will be affected with the result that also daytime-vision and color-discrimination will dissapear. |
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PRA in most cases expresses itself at an age between 3-5 years. The rods can already be affected from 5 months of age on but can remain undetected for a long time.
Because of the gradualness of PRA, the infected dog can adapt to his decreasing eye-sight. If his environment is not changed, he will learn his way.
To receive more incoming light to be able to see something, the lens will be set wide open. This will cause a noticable shine to the eye. The lens doesn't contract anymore when (bright) light falls in, which is what it would do in normal cases. The chances are high a Cataract will develop.
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PRA in Cresteds is a recessive gene. That means that a dog, to become affected by PRA, must get the PRA gene from both of his parents. PRA affects both eyes
(in both dogs and bitches) so an affected dog will become totally blind. When only one of the parents carries the PRA-gene and gives it to its offspring, this offspring will not encounter any problems. However, this offspring is then a
carrier of the PRA-gene. A breeding with another carrier will result in offspring that could be carrier/affected with PRA. A breeding between 2 affected dogs will result in offspring that are all affected.
In 2006 the search for the DNA-marker for PRCD-PRA in Cresteds was succesful. By means of a bloodtest it's now possible to find out whether a Crested is clear, carrier or affected for PRCD-PRA. Such a bloodtest can be done early in life.
More information about this bloodtest can be found at www.optigen.com.
There this breed has to deal with 2 types of PRA yearly examination by a licensed ophtalmologist is still necessary.
Dogs with PRA should not be used for breeding. However, this condition will mostly occur at a later age and most dogs used for breeding will already have produced offspring. Caution should be used if using a likely carrier
(parent,sibling,close relative of an affected) for breeding. Yearly testing by a licensed ophtalmologist ought to be done to reduce the chance of breeding with an affected dog.
On the inside of the eye lies a reflective layer, the Tapetum Lucidum. This layer is using the (dim)light in a most optimal way so the dog can see in dim light. We see this layer as a green, blue or yellow glow in the eye in dim light
and also in photographs taken with a flash. When a dog lacks this layer, he is nightblind. The glow will then be red which is caused by the reflection of light on the bloodvessels in the eye. Because night blindness is the first sign of
PRA, we have to be careful not to confuse these 2 disorders. |
Disclaimer – The above article is not meant to serve as a substitute for Licensed Veterinarian care. The author and person/persons responsible for content
and posting are not responsible for any unsatisfactory occurrence as a result of this or any other article content posted on this website. |
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Genetics: Introduction to Genetics
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The basic principles of genetics will be explained by text and images. In all crosses mentioned on this page, it doesn't matter which of the two dogs involved is the male or the female.
The results 'on paper' are just an indication of what the crossing could result into and doesn't say anything about the number of offspring and the dividing of the given gene combinations.
Each trait in a body is written by genes located on the chromosomes. A chromosome can be seen as a pair of strings divided in compartments, the loci (singular: locus) shown on the left (1).
In every locus lays an allele (half part of a gene) which makes up a certain trait of the animal. Color, size, hairless or coated, all traits are written by these genes. One string is received from the sire, the other from the dam.
To make it easier writing down crossings on paper each allele is given a letter. One letter (allele) is received from the sire, the other from the dam. |
2a. Homozygote dominant (HH)
2b. Homozygote recessive (hh)
2c. Heterozygote (Hh) |
A capital letter in genetics means this gene is dominant. Dominant means that the gene will show itself in the appearance of the dog (the phenotype).
A small letter means it is a recessive gene. Recessive means that the gene is surpressed in the presence of a dominant gene. It won't show up in the phenotype but lays hidden in the genotype. (In some cases recessive genes show up even in the presence of a dominant gene. We won't discuss this here).
Only one thing left to add to this list. As explained above each trait is made by a gene made up from 2 alleles, so two letters on paper. The dominant letter is always put first. The recessive, if present, always last. So if we take the gene H for example we can make 3 combinations: HH, Hh and hh.
When the 2 alleles are alike in case of the HH (2a) and hh (2b) we call that homozygote. When the 2 alleles are not alike, so Hh (2c) it is called heterozygote. |
 | Lets look at the inheritance of a trait. In this fictional case we will look at how the color grey (G) and blue (g) will inherit. We start with 2 homozygote dogs (so GG for the grey dog and gg for the blue dog). To make it easy on paper we use a so called crossing scheme.
Each parent gives 1 allele to each offspring. In this case the grey parent (GG) can only give a G allele where the blue parent (gg) can only give the g. The genotypic result of this breeding then is Gg, Gg, Gg and Gg which we can see in the scheme. The phenotype shows 100% grey offspring which all carry the allele for blue with them.
For the second breeding we breed two of this offspring. Gg x Gg
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Result: GG : Gg : gg = 1: 2 : 1.
So three of the offspring will be grey (GG and Gg) and one will be blue (gg).
It should be understandable now that the mating GG x GG will only resolve in 100% homozygote dominant grey offspring and gg x gg in 100% homozygote recessive offspring.
© Wendy van Goolen June 2007 |
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Genetics: Breeding in the Dark
Would it be possible in the future to have build a wide genepool without inheritable diseases and abnormalities like Legg Calve Perthes, Monorchidism, Lens luxation, PRA and other related health issues?
It may not be impossible with genetests that hopefully will become available in the future but until then it is up to the breeders to make the percentage of affected dogs (and carriers as well) as low as possible. To achieve this minimal risk the breed in total should be mapped and tracked, breeding stock as well as those dogs placed as pets which can still carry inheritable abnormalities given by their parents still used for breeding. Breeders being open about their findings when it comes to their dogs health is a pre, or even a must.
The sooner this is done, the less chance there is that these abnormalities spread throughout the entire breed that is widening as time passes.
So what is the chance of spreading an unwanted gene in say 5 (untested) generations which in dogs could take around 9 years of time on average? Without testing this is a huge risk. Without a genetest it's allready hard if not impossible to tell which dog is clear and which is carrier of a defect without having to breed it. In case of an affected dog it may even take a while before the unwanted disorder shows itself and by that time chances are high it has allready been used for breeding. In the best case scenario it was bred to a clear dog and it only produced 100% carriers (1a). In the worst case scenario the other dog was a carrier as well (1b) or even affected (1c) and a whole new high risk generation has been produced.
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 = Clear. No unwanted gene to pass on.
 = Carrier. Hidden gene that can be passed on to the offspring.
 = Affected. The disorder could show up sooner or later and the gene will be passed on to every offspring.
* Hypothetical outcome; The number of offspring and the dividing of the
given gene combinations in the offspring can differ from reality.
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1a. Clear x Affected breeding | 
1b. Carrier x Affected breeding* |
1c. Affected x Affected breeding |
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So in case of an affected dog, no matter what it was bred to, there isn't a single clear to be found in its offspring.
So what can breeders do until the markers for (at least some) genetic disorders are found?
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2a. Clear x Clear breeding | 
2b. Clear x Carrier breeding* |
2c. Carrier x Carrier breeding* |
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Avoid breeding affected dogs whenever possible and be careful breeding with known carriers (2c). To achieve a safe foundation for todays and future breeders (2a and 2b) todays breeders rely on testresults, wether that is a patella examination, CERF or ECVO eye test or OFA.
Mapping the breed or breeding in the dark.
© Wendy van Goolen June 2007 |
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FCI Breed Standard
| Origin | China |
| Patronage | Great Britain |
| Date of pub. | 24.06.1987 |
| Utilization | Toy dog |
| Class. FCI | Group 9 Companion and Toy Dogs
Section 4 Hairless Dogs
Without working trial |
| General appearance | A small, active and graceful dog; medium-to fine-boned, smooth hairless body, with hair on feet, head and tail only; or covered with a soft veil of hair. Two distinct types of this breed : Deer type, racy and fine-boned, and Cobby type, heavier in body and bone. |
| Behavior & temperament | Happy, never vicious. |
| Head | Smooth, without excess wrinkles. Distance from base of skull to stop equal to distance from stop to tip of nose. Head presenting graceful appearance with alert expression. |
| Cranial Region |
| Skull | Slightly rounded and elongated. |
| Stop | Slightly pronounced, but not extreme. |
| Facial Region |
| Nose | A prominent feature, narrow in keeping with muzzle. Any colour nose acceptable. |
| Muzzle | Tapering slightly but never pointed, lean without flews. |
| Lips | Tight and thin. |
| Jaws/Teeth | Jaws strong, with perfect, regular scissor bite, i.e. the upper teeth closely overlapping the lower teeth and set square to the jaws. |
| Cheeks | Cleanly chiselled, lean and flat, tapering into muzzle. |
| Crest | Ideally beginning at stop tapering off down neck. A long and flowing crest preferred, but sparse acceptable. |
| Eyes | So dark as to appear black. Little or no white showing. Medium size. Set wide apart. |
| Ears | Set low : highest point of base of ear level with outside corner of eye. Large and erect, with or without fringe, except in Powder Puffs where drop ears are permissible. |
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| Neck | Lean, free from throatiness, long and sloping gracefully into strong shoulders. When moving, carried high and slightly arched. |
| Body | Medium to long, supple. |
| Back | Level. |
| Loin | Taut. |
| Croup | Well rounded and muscular. |
| Chest | Rather broad and deep, not barrel-ribbed. Breast bone not prominent. Brisket extending to elbows. |
| Underline | Moderate tuck-up. |
| Tail | Set high, carried up or out when in motion. Long and tapering, fairly straight, not curled or twisted to either side, falling naturally when at rest. Plume long and flowing, confined to lower two-thirds of tail. Sparse plume acceptable. |
| Forquarters | Legs long and slender, set well under body. |
| Shoulder | Clean, narrow and well laid back. |
| Elbows | Held close to body. |
| Pasterns | Fine, strong, nearly vertical. |
| Hindquarters | Hindlegs set wide apart. Angulation of the rear limb must be such as to produce a level back. |
| Stifles | Firm and long, sweeping smoothly into hock. |
| Hocks | Well let down |
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| Feet | Extreme hare-foot, narrow and very long, with unique elongation of small bones between joints, especially in forefeet, which almost appear to possess an extra joint. Nails any colour, moderately long. Socks ideally confined to toes, but not extending above top of pastern. Feet and toes turning neither in nor out. |
| Gait/movement | Long, flowing and elegant with good reach and plenty of drive. |
| Coat |
| Hair | No large patches of hair anywhere on body. Skin fine-grained, smooth, warm to the touch. In Powder Puffs coat consists of an undercoat with soft veil of long hair, veil coat a feature. |
| Colour | Any colour or combination of colours. |
| Size |
| Ideal height dogs | 28-33 cm (11-13 ins) at withers. |
| Bitches | 23-30 cm ( 9-12 ins) at withers. |
| Weight | Weight varies considerably, but should not be over 5 1/2 kgs (12 lbs). |
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| Faults | Any departure from the foregoing points should be considered a fault and the seriousness with which the fault should be regarded should be in exact proportion to its degree and its effect upon the health and welfare of the dog.
Any dog clearly showing physical or behavioural abnormalities shall be disqualified. |
| N.B. | Male animals should have two apparently normal testicles fully descended into the scrotum. |
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Poisonous stuff
| Name | English | Nederlands | Français | Deutsch | Poisonous parts |
| VEGETABLES & FRUITS |
| Allium cepa | Onion | Ui | Oignon | Zwiebel | All parts |
| Allium porrum | Leek | Prei | Poireau | Lauch | All parts |
| Allium sativum | Garlic | Knoflook | Ail cultivé | Knoblauch | All parts |
| All. schoenoprasum | Chives | Bieslook | Ciboulette | Schnittlauch | All parts |
| Asparagus | Asparagus | Asperge | Asperge | Spargel | All parts |
| Beans (raw) | Brown/white | Boon | Haricot | Bohne | Pods and seeds |
| Juglans regia | Walnut | Walnoot | Noix | Walnuß | Shell |
| Lycopersicum | Tomato | Tomaat | Tomate | Tomate | Green parts |
| Mac. Integrifolia | Macadamia Nut | Macadamia | Macadamia | Macadamia | All parts |
| Malus | Apple | Appel | Pomme | Apfel | Stem, seed, leaf |
| Momordica charantia | Bitter melon | Balsempeer | Margose | Balsambirne | Fresh juice |
| Myristica fragrans | Nutmeg | Nootmuskaat | Muscadier | Muskatnuss | Seed |
| Persea americana | Avocado | Avocado | Avocatier | Avocado | Green and pith |
| Prunus | Cherry | Kers | Cerise | Kirsche | Stem, seed, leaf |
| Prunus armeniaca | Apricot | Abrikoos | Abricot | Aprikose | Stem, seed, leaf |
| Prunus domestica | Plum | Pruim | Prunier | Pflaume | Seed |
| Prunus dulcis | Almond | Amandel | Amandier | Mandel | Seed |
| Prunus persica | Peach | Perzik | Pêche | Pfirsich | Seed |
| Solanum tuberosum | Potato | Aardappel | Pomme de terre | Kartoffel | Sprouts, peel (raw) |
| Spiraea stachys | Woundwort | Andorn | Epiaire | Ziest | Seeds |
| Vitis vinifera | Grape / raisin | Druif / rozijn | Raisin (sec) | Weintraube / Rosine | All parts |
| PLANTS & BUSHES |
| Abrus precatorius | Jequirity | Paternosterboontje | Paternoster | Paternostererbse | Seeds |
| Aconitum napellus | Monkshood | Monnikskap | Aconit napel | Blauer Eisenhut | All parts |
| Adonis vernalis | Yellow Pheas. Eye | Voorjaarsadonis | Adonis de printemps | Frühl.-Adonisröschen | All parts |
| Aesculus hippocastanum | Horse Chestnut | Paardenkastanje | Marronnier d' Inde | Roßkastanie | Nuts, foliage |
| Aethusa cynapium | Hondspeterselie | Hondspeterselie | Petite ciguë | Hundspetersilie | All parts |
| Agrostemma githago | Corn Cockle | Bolderik | Nielle des blés | Kornrade | All parts |
| Anagallis arvensis | Pimpernel | Guichelheil | Mouron | Gauchheil | All parts |
| Andromeda polifolia | Bog-rosemary | Lavendelheide | Andromède | Rosmarinheide | All parts |
| Araceae | Philodendron | Philodendron | Philodendron | Philodendron | All parts |
| Aristolochia | Birthwort | Pijpbloem | Aristoloche clématite | Osterluzei | All parts |
| Armoracia rusticana | Horseradish | Mierikswortel | Raifort | Meerrettich | Green parts |
| Arum | Lords-and-ladies | Aronskelk | Gouet | Aronstab | All parts |
| Aquilegia | Columbine | Akelei | Ancolie | Akelei | All parts |
| Atropa bella-donna | Deadly nightshade | Wolfskers | Belladone | Schwarze Tollkirsche | All parts |
| Buxus Sempervirens | Common Box | Palmboompje | Buis commun | Buchsbaum | Foliage, twig |
| Caltha palustris | Kingcup | Dotterbloem | Populage des marais | Sumpfdotterblume | All parts |
| Cannabis sativa | Marijuana | Wiet | Cannabis | Hanf | Flower, leaves |
| Cicuta virosa | Cowbane | Waterscheerling | Ciguë aquatique | Wasserschierling | All parts |
| Chelidonium majus | Greater celandine | Stinkende gouwe | Chélidoine | Schöllkraut | All parts |
| Clematis | Clematis | Clematis | Clématite | Waldreben | All parts |
| Colchicum autumnale | Autumn crocus | Herfsttijloos | Herbstzeitlose | Colchique d'automne | Tuber |
| Conium maculatum | Poison hemlock | Gevlekte scheerling | Grande ciguë | Gefleckter Schierling | All parts |
| Convallarla majalis | Lily of the Valley | Lelietje van dalen | Muguet de mai | Maiglöckchen | All parts |
| Cycas revoluta | Sago Cycad | Cycaspalm | Cycas du Japon | Japanischer Palmfarn | All parts |
| Cyclamen persicum | Cyclamen | Cyclaam | Cyclamen | Alpenveilchen | Tuber |
| Cytisus scoparius | Scotch Broom | Bezembrem | Genêt à balais | Besenginster | All parts |
| Daphne mezereum | Mezereon | Peperboompje | Bois-gentil | Seidelbast | All parts |
| Datura stramonium | Thorn Apple | Doornappel | Datura stramoine | Gemeiner Stechapfel | All parts |
| Delphinium ajacis | Common Larkspur | Ridderspoor | Ackerrittersporn | Pied d'alouette | All parts |
| Dieffenbachia | Dumbcane | Dieffenbachia | Dieffenbachia | Dieffenbachien | All parts |
| Digitalis purpurea | Common Foxglove | Vingerhoedskruid | Digitale pourpre | Roter Fingerhut | All parts |
| Ecballium elaterium | Squirting cucumber | Springkomkommer | Concombre d'âne | Spritzgurke | Fruits |
| Eranthis | Winter aconite | Winterakoniet | Hellébore d'hiver | Winterling | All parts |
| Euonymus europaea | European spindle | Kardinaalsmuts | Fusain d'Europe | Gewöhnl. Spindelstr. | All parts |
| Euphorbiaceae | Spurge family | Wolfsmelkfamilie | f. des Euphorbiacées | Wolfsmilchgewächse | Juice |
| Ficus elastica | Rubber fig | Rubberboom | Caoutchouc | Gummibaum | Juice |
| Ficus macraphylla | Common Fig | Vijgenboom | Figuier commun | Echte Feige | Juice |
| Galanthus nivalis | Snowdrop | Sneeuwklokje | Perce Neige | Schneeglöckchen | Bulb, foliage |
| Gelsemium sempervirens | Carolina Jasmine | Gele jasmijn | Jasmin de Caroline | Carolina-Jasmin | All parts |
| Glyceria maxima | Reed Sweet Grass | Liesgras | Glycérie aquatique | Große Schwaden | All parts |
| Gratiola officinalis | Hedge hyssop | Genadekruid | Gratiole officinale | Gottes-Gnadenkraut | All parts |
| Hedera helix | Ivy | Klimop | Lierre | Efeu | Berries, foliage |
| Helleborus foetidus | Bear's foot | Stinkend nieskruid | Hellébore fétide | Stinkende Nieswurz | All parts |
| Helleborus niger | Christmas Rose | Kerstroos | Rose de Noël | Schneerose | All parts |
| Heracleum sphondylium | Common hogweed | Berenklauw | Berce | Wiesen-Bärenklau | Sap |
| Hyacinthus orientalis | Hyacinth | Hyacint | Hyacinthus | Hyazinthen | All parts |
| Hydrangea | Hortensia | Hortensia | Hortensia | Hortensien | All parts |
| Hyoscyamus niger | Black Henbane | Bilzekruid | Jusquiame noire | Sch. Bilsenkraut | All parts |
| Ilex aquifolium | Holly | Hulst | Ilex | Stechpalmen | Berries |
| Iris pseudacorus | Yellow iris | Gele lis | Iris des marais | Sumpf-Schwertlilie | Leaves, stems |
| Jacobaea vulgaris | Ragwort | Jakobskruiskruid | Séneçon de Jacob | Jakobs-Greiskraut | All parts |
| Juniperus sabina | Savin Juniper | Zevenboom | Genévrier sabine | Sadebaum | All parts |
| Laburnum anagyroides | Laburnum | Goudenregen | Cytise | Goldregen | All parts |
| Lactuca virosa | Wild Lettuce | Gifsla | Laitue vireuse | Gift-Lattich | All parts |
| Lantana camara | Spanish Flag | Wisselbloem | Thé de Gambie | Wandelröschen | Berries |
| Lathyrus | Lathyrus | Lathyrus | Gesse | Platterbsen | Stems, seeds |
| Laurus nobilis | Bay Laurel | Laurier | Laurier sauce | Echter Lorbeer | All parts |
| Ligustrum vulgare | Common Privet | Wilde liguster | Troène commun | Gewöhnliche Liguster | All parts |
| Liliaceae | Lily Family | Leliefamilie | Liliacées | Liliengewächse | All parts |
| Lonicera | Honeysuckle | Kamperfoelie | Chèvrefeuille | Heckenkirschen | Berries |
| Lupinus | Lupin | Lupine | Lupin | Lupinen | All parts |
| Melilotus | Sweet Clover | Honingklaver | Mélilot | Steinklee | All parts |
| Mercurialis perennis | Dog's Mercury | Bosbingelkruid | Mercuriale des bois | Wald-Bingelkraut | All parts |
| Mycelia | Mushrooms | Paddestoelen | Champignon de cult. | Pilze | All parts/species |
| Narcissus | Narcissus | Narcis | Narcisse | Narzissen | All parts |
| Nerium oleander | Oleander | Oleander | Laurier rose | Rosenlorbeer | All parts |
| Nicotiana tabacum | Common Tobacco | Tabaksplant | Tabac commun | virginischer Tabak | All parts |
| Oenanthe aquatica | Water-dropwort | Watertorkruid | Fenouil aquatique | Wasserfenchel | All parts |
| Ornithogalum umbellatum | Star-of-Bethlehem | Vogelmelk | Dame d'onze heures | Dolden-Milchstern | All parts |
| Papaveraceae | Papaveraceae | Papaverfamilie | f. des Papavéracées | Mohngewächse | Unripe seeds |
| Paris quadrifolia | Herb Paris | Eenbes | Parisette à 4 feuilles | Einbeere | All parts |
| Parthenocissus | Creeper | Wingerd | Vigne vierge | Jungfernrebe | Berries |
| Petunia | Petunia | Petunia | Pétunia | Petunien | All parts |
| Phytocala americana | Pokeweed | Karmozijnbes | Phytolacca | Kermesbeeren | All parts |
| Platycladus orientalis | Chinese Arborvitae | Oost. Levensboom | Thuya de Chine | Morgenl. Lebensbaum | All parts |
| Polygonatum multiflorum | Solomon's Seal | Salomonszegel | Sceau de Salomon | Vielblütige Weißwurz | Berries |
| Prunus laurocerasus | Cherry-laurel | Laurierkers | Laurier-cerise | Lorbeerkirsche | All parts |
| Rhamnus cathartica | Buckthorn | Wegedoorn | Nerprun purgatif | Kreuzdorn | Bark, fruits |
| Rhododendron | Rhododendron | Rododendron | Rhododendron | Rhododendron | Foliage, flower |
| Ricinus communis | Castor oil plant | Wonderboom | Ricin commun | Wunderbaum | Seeds |
| Robinia pseudoacacia | Locust tree | Witte acacia | Robinier faux-acacia | Robinie | All parts |
| Rosa | Rose | Roos | Rose | Rosier | Rose hip |
| Saintpaulia | African violet | Kaaps viooltje | Saintpaulia | Usambaraveilchen | All parts |
| Sambucus ebulus | Danewort | Kruidvlier | Sureau hièble | Attich | All parts |
| Sedum acre | Biting Stonecrop | Muurpeper | Orpin âcre | Scharfer Mauerpfeffer | Green parts |
| Sinapis arvensis | Charlock | Herik | Moutarde des champs | Ackersenf | Seeds, green |
| Solanum | Solanum | Nachtschade | Solanum | Nachtschatten | All parts |
| Solanum dulcamara | Woody Nightshade | Bitterzoet | Douce-amère | Bittersüßer N.schatten | Fruits |
| Strychnos | Strychnos | Braaknotenboom | Strychnos | Strychnos | Sap |
| Symphoricarpus albus | Snowberry | Sneeuwbes | Symphorine | Schneebeere | Beries |
| Tamus communis | Black Bryony | Spekwortel | Tamier | Schmerwurz | All parts |
| Taxaceae | Yew family | Taxusfamilie | Fam. des Taxacées | Eibengewächse | All parts |
| Tuberhybrida | Begonia | Bégonia | Begonia | Begonia | All parts |
| Tulipa | Tulip | Tulp | Tulipe | Tulpen | Bulbs |
| Viburnum opulus | Guelder-rose | Gelderse roos | Viorne obier | Gewöhnl. Schneeball | Berries |
| Vincetoxicum hirundinaria | Swallow-wort | Witte engbloem | Dompte-venin | Weiße Schwalbenwurz | All parts |
| Viscum album | Mistletoe | Maretak | Gui | Weißbeerige Mistel | Berries |
| Wisteria | Wisteria | Blauweregen | Glycine | Blauregen | All parts |
| OTHER |
| Acetaminophen | Paracetamol | Paracetamol | Paracétamol | Paracetamol | Minimal dosis |
| Cyanophyta | Blue-green algae | Blauwalgen | Algues bleues | Blaualgen | All parts |
| Etheenglycol | Antifreeze | Antivries | Refroidissement | Frostschutzmittel | Minimal dosis |
| Herbiciden | Herbicide | Onkruidbestrijder | Désherbant | Unkrautbekämpfungsm. | Minimal dosis |
| Methaldehyde | Snail bait | Slakkengif | Anti-limaces | Schneckenkorn | Minimal dosis |
| Sinapis alba | Mustard | Mosterd | Moutarde | Senf | All parts |
| Theobroma cacao | Chocolate | Chocolade | Cacao | Kakao | All products |
| Warfarine | Rodenticide | Rattengif | Raticide | Rodentizid | Minimal dosis | |
|
