Labrador health

Despite what it may seem, the Labrador Retriever is one of the healthiest, athletic and healthy breeds. All diseases are going to see occur in many other races, but perhaps the success in
breeding Labrador in Britain and the US, where it is one of the most popular breeds, do we have a better understanding of the diseases that can suffer , Which does not mean that they are more
frequent in this breed.

Hip dysplasia

Hip dysplasia is the hereditary disease most commonly known by owners, breeders, and veterinarians, and affects a large number of medium and large breeds. Affected animals exhibit an
abnormal development of the coxofemoral joint, with an inadequate coaptation between the head of the femur and the acetabulum, which causes premature wear of the articular cartilage.
This defect in conformation triggers changes of the arthritic type that cause the symptomatic picture of the disease.
The etiology of the disease is polygenic multifactorial, there are several genes that will determine the structure of the hip (genotype), but these genes will be expressed to a greater or lesser extent depending on the influence of the environment (food, exercise, habitat, etc.). ), And from the interaction of these two factors (genotype and environment), we will obtain a specific type of hip (phenotype).
The first difficulties are in knowing what percentage of the disease is due to genetic causes (for most authors 70%) and that percentage to acquired causes. For an animal to be affected it is
imperative that it possesses altered genetics in a greater or lesser number of genes, and these genes are inherited by a complicated system of codominance and incomplete penetrance, which
prevents the creation of a reliable theoretical model of transmission.
At the time of birth all Labrador Retriever puppies have healthy hips, and it is during the growth phase when the animal is predisposed to suffer from dysplasia because it is written in its
genetic code and will develop the disease to a greater or lesser degree Depending on the environmental conditions. The most critical phase of growth is from 3 months to 8, although it has
been proven that obesity in puppies of only 2 months can be almost determinant for the onset of the disease. In this short time you have to take care of environmental factors, for example,
nutrition and exercise. Nutrition is the most important factor. Hypercaloric and hyperproteic diets that will produce overweight dogs should be avoided.
The Labrador Retriever is a fast-growing breed, reaching adult height by the year, therefore the metabolic requirements during the growth phase are very high, and any nutritional
decompensation, in both protein and energy and trace elements, can be crucial . These trace elements, which are found in small quantities in foods, are the cause of an adequate osmolarity of
the synovial fluid, which protects and lubricates the joints avoiding their wear, hence the importance of adequate intake of sodium, potassium, chlorine, phosphorus , Magnesium, etc.
Regarding exercise, there is a clear relationship between the development of dysplasia and the amount of muscle mass, the greater the musculature of the posterior third the more the joint is
stabilized and the lower the degree of subluxation of the hips.
Also, it is possible to emphasize other small variables, among others the type of habitat of the dog; Therefore, sliding floors favor joint laxity by preventing the dog from being stable. Also in dogs raised in kennels with a certain height, since they rise on their hind limbs in their search for any noise, a position that overloads the joints.
The ideal would be to establish a genetic diagnosis of the disease, but this possibility is not yet within reach, so there is a combination of radiological diagnosis along with other important
data, for example, progeny data.
The symptoms of the disease are very variable, ranging from slight lameness to impossibility to walk. Certain affected specimens present a characteristic type of movement with short steps
that involve little movement, since the hind limbs only move 45 º instead of the 110 º that travels the femur with respect to the hip in a normal animal; In addition a decomposition of the back occurs, losing the dorsal line that curves in an attempt to stretch the trunk to advance more without using the hind limbs, also can occur a hypertrophy of the musculature of the chest that will be overloaded when moving the dog Its center of gravity forward. Another type of characteristic movement is the jumps of rabbit, the animal moves pushing with both later extremities at the same time avoiding to realize the necessary impulses to move in the extremities of independent form.
The treatment of hip dysplasia is highly variable, with many effective anti-inflammatory drugs, diets, alternative therapies such as acupuncture and chiropractic, including surgeries with
excellent results. Perhaps the most effective surgical procedure is triple hip osteotomy, which must be performed in young animals, around eight or ten months of age, and that do not yet
present arthrosic degenerations in the joint, this being the last condition necessary to obtain good results.

Elbow Dysplasia

As in the case of the hip, it is a disease with a genetic basis in which anomalies occur during the development of the pup that affect the elbow joint, although this designation includes two
distinct pathological entities:

  • Non-union of the ancóneo process
  • Fragmentation of the coronoid process

Both pathologies are primary lesions that stabilize towards the year of age, resulting secondary to the appearance of osteoarthrosis processes in the elbow joint.
The genetic cause and environmental factors are the same as for hip dysplasia; Consequently the methods for the eradication and control of the disease will also be the same, that is why the
need for radiographic examination of the specimens intended for reproduction. In the case of the elbow, the number of individuals suffering from the disease and may be asymptomatic is even
greater than for the hip, hence the need for complementary examinations.
Treatment will depend on the severity of the lesions and their nature. Medical treatment includes exercise restriction, weight control and anti-inflammatory therapy, with good results. Surgical treatment consists of extracting fragments of detached cartilage or bone and stabilizing the joint to avoid pain.
The dissecting osteochondritis of the humeral scapula joint could also be encompassed here, although the genetic cause of it is not clear. In this case a cartilage flap is formed as a
consequence of the abnormal development of the subchondral bone. This cartilaginous flap can not be nourished or healed by being detached and falls within the joint, creating the
consequent lameness due to the high process.
Other osteochondritis may occur in the knee joint, affecting the femoral condyle, and even in the joint of the tarsus creating the respective cases of osteoarthritis.

Anterior Cruciate Ligament rupture

There is no genetic basis in this pathology but a predisposition of the race due to its conformation. The knee joint is not overly rigid and depends on a large number of ligaments and cartilage to keep it stable. This joint is used both in the jump and in the propulsion, and given the weight and morphology of the Labrador, the biomechanical loads that suffer the knees can be excessive in a jump with displacement or in a rotation in race with too much inertia, in which case Is the anterior cruciate ligament that breaks causing a sudden onset lameness.
X-rays of the affected joint are performed for diagnosis, and the drainage test is performed, showing the excessive displacement of the femur over the tibia in the absence of ligamentous
attachment. Surgical repair is the treatment that gives the best results.

Tail myopathyl

Also called wet tail, this is another pathology that although not exclusive to the Labrador Retriever, does occur in them with some assiduity. Although without transcendence, or too much
importance, it is causing some scares among the owners of the specimens of this breed. This anomaly consists of flaccid paralysis of the tail, and draws attention because if there is
something in continuous movement in the Labrador, it is its tail.
The causes can be several: hunting sessions or intense training, baths in cold water or baths before an exhibition, areas of inadequate rest (dogs confined in boxes of transport without being
accustomed, or for too long), etc.
It manifests as a lack of mobility of the tail, with its inability to overcome the dorsal line, and there is pain at the palpation of the muscles at the base of the tail; The prognosis is always good, it is enough with rest and treatment with anti-inflammatory in some occasions to achieve a total recovery. It only has one problem: it usually manifests itself the day of an exhibition, just before leaving the ring, and unfortunately it is not resolved in ten minutes.

Eye defects

Writing about the most frequent eye diseases of this breed does not mean that the Labrador Retriever is more likely than other breeds to become blind in the near future.
However, some ocular alterations are more frequent than others in this breed and should be observed by breeders, veterinarians and owners as soon as possible in order to separate these
animals from any breeding program and thus avoid the dissemination of these Pathologies Perhaps the eye diseases are better known in the Retriever, given the great number of specimens in
England and the United States, both of which are extensively tested for specimens. The importance of early diagnosis of some of these diseases lies in their genetic basis and hereditary


The clearest example is progressive retinal atrophy, a disease that is transmitted in a simple recessive form: the RR genotype will be that of a healthy animal, and the rr genotype will be that of an affected animal; Dominating the R gene over r. The case of animals Rr is that of the so-called carriers; Healthy animals that are potentially transmitters of the disease and that will only produce affected children if they are paired with rr and rr genotypes, in such a way that they can only be identified by progeny tests; When examining the children we will know that the parents are affected by an abnormality in this gene and are transmitters of the disease. On the other hand if we couple an Rr bearer with a healthy RR animal, we will never get affected animals.
Reproductive tests are the most efficient way to detect carriers, but a great knowledge of pedigrees and up to seven generations is necessary to be able to determine if an animal is a carrier or healthy; It is very difficult to carry out these tests given the high economic costs and their long duration in terms of time.
Another form of inheritance is multiple or polygenic transmission cases most commonly known are entropion and retinal dysplasia. In this mode of inheritance several genes and also the
external conditions participate, so that the inheritance pattern becomes totally unrecognizable.


This diagnostic method is gaining adherents during the last years. It is a test that is performed with a blood sample that should be sent to the reference laboratories (Optigen or Vetgen), where genetic markers detect the existence or not of alleles that cause progressive retinal atrophy (APR ) In the Labrador Retriever. The advantages of this test are an early diagnosis of affected animals or carriers of APR; The tests can be done even to puppies of Labrador Retriever of only three months of age. The other key advantage is that genetic testing is valid for life.
As a disadvantage, it is worth mentioning its high economic cost, its specificity of injury (this test is not valid to detect the rest of ocular abnormalities) and the existence of certain false positives that can occur when there is a mutant allele, a question that seems to go Be improved with a new update of the test markers.
DNA analyzes for any test can be of two types: specific and binding. In the specific tests the analysis is done directly on the gene involved in the disease and, therefore, the molecular nature of the mutation has been previously identified. In other cases it is not possible to perform the direct test because the causative gene has not been isolated or unknown, then linkage tests are used, in which the animal’s phenotype is determined for a second, easily identifiable gene And which is used as a marker, and which by previous genetic studies is known to be located on the same chromosome region as the main gene (the one involved in the disease), and very close to it. The closer the involved gene and marker are, the more reliable the results will be by
decreasing the possibility of recombination between these genes. The linkage tests are those performed by Optigen.
The results of this test categorize the animals into three groups:

  • Optigen A: Free APR.
  • Optigen B: Animal carrying the defective allele and therefore carrying APR
  • Optigen C: Affected animal of APR when carrying two defective alleles.

This diagnostic method can also be performed from DNA obtained from frozen semen samples, so that it can be known whether a stallion already deceased may be suitable for use in our
reproductive program.
In the near future several tests for different genetic diseases, including narcolepsy, will be launched on the market.
The information provided by the genetic tests must be used with caution by the Breeders’ Clubs and Associations if they decide to initiate a breeding program to eliminate or reduce the
incidence of a disease in a particular breed, since the breeding program Must take into account that the genetic diversity of the breed must be maintained. A program of radical crosses, such
as crossing only normal homozygotes (RR, in our case), would most likely lead to the loss of genetic characteristics important to the breed.


Smaller size of the eyeball, which is lodged at the bottom of the orbit; May be accompanied by mucopurulent conjunctivitis and lacrimation. The hereditary character in the breed has not been


It involves the inversion of all or part of the eyelid margin, and may affect the upper, lower eyelid or both. It is caused by alterations in the tension of the orbicularis muscles and is influenced by factors such as the conformation of the skull, orbit size and facial folds. It causes pain and irritation with continuous tearing by the rubbing of the eyelid against the cornea and its correction by surgery is easy. Form of inheritance by multiple transmission.


Eversion of the margin of the lower eyelid that exposes more surface of the conjunctiva of the due, reason why frequent conjuntivitis occur; As in entropion, the surgical correction is definitive, and is transmitted in the same way. Most cases of ectropion are usually due to some poorly healed injury or injury to the eyelid margin.

Corneal lipidosis

Lipid deposit in the cornea that manifests as spots of whitish color in the front of the eye and that allow the passage of part of the light; Are generally associated with high fat diets.

Hereditary Cataracts

Opacity of the lens that affects the animal from birth and causes total blindness; Can manifest itself from the time the dog opens its eyes until two years of age, is transmitted by a dominant

Retinal dysplasia

Currently called progressive degeneration of cones and canes, it is the most frequent hereditary condition in the retina of the dog. In this disease, an enzymatic failure occurs in the retinal
photo receptors, which, if it first affects the rods, will produce a loss in the nocturnal vision; On the other hand, loss of daytime vision will occur first by affecting the cones. The injured retina will show zones of pigmentation, so that it is classified as central APR if they affect the center of the retina and as generalized APR when the pigmented zones are distributed all over.
The central APR is the one that usually affects the Labrador Retriever, is transmitted in a simple recessive way and usually manifests with a gradual loss and slow of vision that begins towards the three years of age. Since fundus alterations do not usually produce pain, there are times when the owner is not aware of the disease until well advanced, hence the importance of routine examinations for an early diagnosis. The first manifestations are usually a loss of the central visual field, so that the dog perfectly observes the lateral movements, but not the central ones.
These are dogs that come to the call of his master come zigzagging, so as not to lose sight of him, or game animals that in the field are able to follow a bird shot down to land but then on the ground are unable To locate it. In the cases of central APR, the vision that is most rapidly altered is diurnal, with a higher density of cones in the center of the retina and this part being affected.
If we find an affected animal we will know that the parents are carriers of the gene and should not be used for reproduction, and siblings have more than a 50% chance of carrying the gene as
Other alterations, such as multifocal retinal dysplasia, caused by abnormal differentiation of the retina during the embryonic period, and abnormal pigment deposits of melanin in various parts
of the eye are still under study, so that they have not yet been classified as alterations of the breed.

Exercise-induced collapse (EIC)

Exercise-induced collapse (EIC) is a neuromuscular disease, occurring in the Labrador Retriever and closely related breeds. So far mutation has been found in the Labrador, Chesapeake-Bayand Curly-Coated Retriever breeds. Recently, the research group of Professor James Mickelson of the University of Minnesota has found the mutation responsible in the DNM1 gene.
The first symptoms of exercise-induced collapse (EIC) are changes in the gait of the animal, with limb stiffness and gait when walking. Sick animals show muscle weakness and collapse 5-15
minutes after exercise (eg in training or after significant stress).
In most dogs are affected especially the hind limbs, in some cases comes weakness to the previous limbs, leaving the animal lying down. During the collapse the animals remain conscious,
but in severe cases of disease they may even find themselves disoriented and even without knowledge.
EIC may remain undiscovered for years if the animal does not undergo strong stress or high stress.
The mutation responsible is found in the DNM1 gene and can be detected by DNA testing.
EIC disease is inherited in an autosomal recessive manner. This means that a dog will only get sick when it has a gene affected by the father and the mother. Therefore, both the father and the
mother must have the affected gene.
The carrier (that animal with only one affected gene) will get sick on rare occasion, but will give the offspring the affected gene with a probability of 50%. In mating between two carriers is the risk that the offspring will be affected by the disease. Therefore, a carrier should not be crossed with another carrier.
EIC disease has autosomal recessive inheritance. There are three genotypes:

  • Genotype N / N (healthy homozygote): This dog does not have the mutation and has a very low risk of EIC disease. He can not transmit the mutation to his offspring.
  • Genotype N / EIC (Heterocidote carrier): This dog has a copy of the mutated gene. He has a very low risk of DIC, but will transmit the mutation to his offspring with a probability of 50%. This animal should be paired only with another animal free of the EIC mutation.
  • EIC / EIC genotype (homozygous affected): This animal has two copies of the mutated gene, and has a very high risk of CIE disease. It will transmit the mutation to its offspring with a 100% probability, and should only be paired with an EIC free animal.

More than 80% of dogs with the EIC / EIC genotype show typical symptoms of EIC at the age of 3 and have had at least one collapse. Also dogs with the N / EIC or N / N genotype may suffer
similar symptoms, although these are mostly produced for other reasons. For example, this can be caused by centronuclear myopathy (CNM, HMLR) that produces muscle weakness and
hardness, which can be verified by the genetic test HMLR.
A DNA test enables the direct detection of the responsible mutation. DNA analysis is independent of the age of the animal and can be done in puppies. Not only is it possible to differentiate
between the animals that have the mutation or not, but also that healthy animals can be detected, which is of great importance for breeding. To maximize the safety of the test, each sample is
analyzed in duplicate independently.

Hereditary nasal parakeratosis (HNPK)

Hereditary nasal parakeratosis (HNPK) is an autosomal recessive hereditary disorder in the Labrador Retriever. A T> G mutation in the SUV39H2 gene causes the nose to dry out resulting in
chronic irritation and inflammation of the skin noses.
Symptoms of this disorder usually appear around 6 to 12 months of age. Affected dogs develop dry, rough; Gray to brown crusts on the surface and the edge of the nose. In some cases,
painful cracks around and at the tip of the nose develop and if untreated to develop superficial bacterial infections. Over time, the nose often begins to depigmentate changing the skin color
from darkness to light in color. Although the disorder is non-life threatening, continuous care to reduce the recurrence of excessive nasal crust formation is required throughout the dog’s life.
Because HNPK is a recessive disorder, a dog must have two copies of the mutation for the disease to manifest itself. This means that a dog may have a copy of the mutation and not
experience any sign or symptom of HNPK, this dog would be known as a carrier. The carrier can then transmit the normal gene or the mutated gene to any offspring. If two carriers are raised,
there is a 25% probability of raising a dog that receives two mutated copies of the gene and would be affected by HNPK:

  • HNPK / HNPK SICK The dog carries two copies of the mutant gene and SUV39H2 is homozygous for HNPK. This dog will be affected and will always transmit the defective gene so that of
    the offspring
  • HNPK / N CARRIER Both normal and mutant copies of the gene detected. The dog is a carrier of the SUV39H2 mutation and can pass on a copy of the defective gene to its offspring 50%
    of the time
  • N / N FREE Dog were negative to the mutation of the SUV39H2 gene and did not transmit the defective gene to their offspring