Salud en el Labrador

Despite what may seem, the Labrador Retriever is one of the healthiest, most athletic, and robust breeds. All the diseases mentioned are found in many other breeds, but perhaps the success in Labrador breeding in Britain and the U.S., where it is one of the most popular breeds, has given us a better understanding of the potential diseases. It doesn’t mean they are more prevalent in this breed.

 

Hip Dysplasia

 

Hip dysplasia is the most commonly known hereditary disease among breeders and veterinarians, affecting many medium to large breeds. Affected animals show abnormal development of the hip joint, leading to premature wear of the joint cartilage. The disease’s etiology is polygenic multifactorial, involving various genes determining hip structure (genotype). Environmental factors, such as nutrition, exercise, and habitat, also influence the gene expression, resulting in a specific hip type (phenotype). Genetic and acquired causes contribute to the disease, making it challenging to create a reliable theoretical transmission model.

 

At birth, all Labrador Retriever puppies have healthy hips. During the growth phase, which is critical from 3 to 8 months, the animal is predisposed to hip dysplasia based on its genetic code. Environmental factors, especially nutrition and exercise, play crucial roles during this period. Obesity in puppies as young as 2 months has been shown to impact the disease’s onset negatively.

 

Labrador Retrievers have rapid growth, reaching adult height within a year. High metabolic requirements during growth make proper nutrition essential. Hypercaloric and hyperproteic diets leading to overweight should be avoided. Exercise also influences hip stability, with increased muscle mass stabilizing the joint and reducing hip subluxation.

 

The ideal scenario would involve a genetic diagnosis, but it is currently unattainable. Therefore, a combination of radiological diagnosis and other essential data, such as progeny information, is used. Symptoms vary from mild lameness to the inability to walk, and affected dogs may exhibit characteristic movements, such as short steps, back decompression, or rabbit-like jumps.

 

Treatment options for hip dysplasia range from anti-inflammatory drugs, diets, and alternative therapies to surgery, with triple pelvic osteotomy being a highly effective surgical procedure for young animals.

 

Elbow Dysplasia

 

Similar to hip dysplasia, elbow dysplasia has a genetic basis, manifesting as abnormalities during a puppy’s joint development. Two distinct pathological entities fall under elbow dysplasia: non-union of the anconeal process and fragmentation of the coronoid process. Both conditions stabilize around one year, with secondary osteoarthrosis processes appearing.

 

Genetic and environmental factors contributing to elbow dysplasia mirror those of hip dysplasia. Reproductive examinations, especially radiographs, are necessary for breeding specimens. Medical treatment involves exercise restriction, weight control, and anti-inflammatory therapy, while surgical interventions aim to remove detached cartilage or bone fragments to stabilize the joint.

 

Anterior Cruciate Ligament Rupture

 

Anterior cruciate ligament (ACL) rupture is not genetically based but stems from the breed’s conformation. Labrador Retriever knee joints, relying on ligaments and cartilage for stability, are prone to excessive biomechanical loads during activities like jumping or running. Diagnosis involves joint radiographs and physical tests, with surgical repair being the most effective treatment.

 

Exercise-Induced Collapse (EIC)

 

Exercise-Induced Collapse (EIC) is a neuromuscular disease that occurs in the Labrador Retriever and closely related breeds. So far, the mutation has been found in Labrador, Chesapeake-Bay, and Curly-Coated Retrievers. Recently, the research group led by Professor James Mickelson at the University of Minnesota has identified the responsible mutation in the DNM1 gene.

 

The initial symptoms of Exercise-Induced Collapse (EIC) include changes in the animal’s gait, limb stiffness, and an unsteady walk. Affected animals show muscle weakness and collapse 5-15 minutes after exercise (e.g., during training or after significant stress). In most dogs, the hind limbs are particularly affected, and in some cases, weakness in the front limbs may also occur, leaving the animal lying down. During the collapse, the animals remain conscious, but in severe cases, they may become disoriented or even lose consciousness.

 

EIC can go unnoticed for years if the animal does not experience strong or prolonged stress. The responsible mutation is located in the DNM1 gene and can be detected through DNA testing. The inheritance of EIC is autosomal recessive, meaning a dog only becomes affected when it inherits an affected gene from both the father and the mother. Therefore, both the sire and dam must carry the affected gene.

 

The carrier (an animal with a single affected gene) will rarely develop the disease but will pass the affected gene to its offspring with a 50% probability. A carrier should not be bred with another carrier. The inheritance of EIC has three genotypes:

 

  • Genotype N/N (healthy homozygote): This dog does not have the mutation and has a very low risk of EIC. It cannot pass the mutation to its offspring.

 

  • Genotype N/EIC (carrier homozygote): This dog has one copy of the mutated gene. It has a very low risk of EIC but will pass the mutation to its offspring with a 50% probability. This animal should only be bred with another EIC-free animal.

 

  • Genotype EIC/EIC (affected homozygote): This animal has two copies of the mutated gene and has a very high risk of EIC. It will pass the mutation to its offspring with a 100% probability and should only be bred with an EIC-free animal.

 

Over 80% of dogs with the EIC/EIC genotype show typical EIC symptoms by the age of 3 and have experienced at least one collapse. Dogs with the N/EIC or N/N genotypes may also suffer similar symptoms, primarily caused by other reasons. For example, this can be due to centronuclear myopathy (CNM, HMLR), which produces muscle weakness and stiffness, verifiable through the HMLR genetic test.

 

DNA testing allows the direct detection of the responsible mutation. The DNA analysis is independent of the animal’s age and can be performed on puppies. It not only distinguishes between animals with or without the mutation but also identifies healthy animals, which is crucial for breeding. To maximize test reliability, each sample is independently analyzed twice.

 

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, resulting in chronic irritation and inflammation of the skin on the nose.

 

Symptoms of this disorder typically appear between 6 and 12 months of age. Affected dogs develop dry, rough noses with gray to brown crusts on the surface and edge of the nose. In some cases, painful cracks may form around and on the tip of the nose, potentially leading to superficial bacterial infections if left untreated. Over time, the nose often begins to depigment, changing the skin color from dark to light.

 

Although the disorder is not lethal, continuous care is required throughout the dog’s life to reduce the recurrence of excessive nasal crust formation.

 

Since HNPK is a recessive disorder, a dog must have two copies of the mutation for the disease to manifest. This means a dog can have one copy of the mutation and show no signs or symptoms of HNPK; this dog would be known as a carrier. The carrier can then pass either the normal gene or the mutated gene to any offspring. If two carriers are bred, there is a 25% chance of producing a dog that receives two mutated copies of the gene and would be affected by HNPK:

 

  • HNPK/HNPK: The dog carries two copies of the mutated gene and is homozygous for HNPK. This dog will be affected and will always transmit the defective gene to its offspring.

 

  • HNPK/N: Normal and mutated gene copies detected. The dog is a carrier of the SUV39H2 mutation and can pass a copy of the defective gene to its offspring 50% of the time.

 

  • N/N: Negative results for the SUV39H2 gene mutation and will not pass the defective gene to its offspring.

Tail Myopathy:

Also known as “wet tail,” this is another condition that, although not exclusive to Labrador Retrievers, occurs in them with some frequency. Although it lacks significance or great importance, it is causing some concern among owners of specimens of this breed. This anomaly consists of the flaccid paralysis of the tail and draws attention because if there is something continuously in motion in the Labrador, it is its tail.

The causes can be various: intense hunting or training sessions, baths in cold water or baths before an exhibition, inadequate resting areas (dogs confined in transport crates without being accustomed or for too long), etc.

It manifests as a lack of tail mobility, with its inability to surpass the dorsal line, and there is pain when palpating the muscles at the base of the tail. The prognosis is always good; rest and anti-inflammatory treatment are usually sufficient for a complete recovery. It only has one problem: it usually manifests on the day of an exhibition, just before leaving the ring, and unfortunately, it does not resolve in ten minutes.

 

Ocular Defects:

Writing about the most common eye diseases in 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 in this breed than others and should be observed by breeders, veterinarians, and owners as soon as possible to separate these animals from any breeding program and thus prevent the spread of these pathologies. Better known in the Retriever, given the large number of specimens in England and the United States, which are widely tested for specimens. The importance of early diagnosis of some of these diseases lies in their genetic basis and hereditary nature.

 

Genetic base:

The clearest example is progressive retinal atrophy, a disease that is transmitted in a simple recessive form: the genotype RR will be that of a healthy animal, and the genotype rr will be that of an affected animal; Dominating the R gene over r. The case of Rr animals is that of so-called carriers; Healthy animals potentially transmitting the disease and producing affected offspring only if paired with rr and rr genotypes, so they can only be identified through progeny tests; By examining the offspring, we will know that the parents are affected by an abnormality in this gene and are carriers of the disease. On the other hand, if we pair an Rr carrier 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 determine if an animal is a carrier or healthy. It is very difficult to carry out these tests due to the high economic cost and the long duration in terms of time. Another form of inheritance is cases of multiple or polygenic transmission, most commonly known as entropion and retinal dysplasia. In this mode of inheritance, several genes and external conditions are involved, making the inheritance pattern completely unrecognizable.

Diagnosis:

This diagnostic method has gained adherents in recent years. It is a test performed with a blood sample that must be sent to reference laboratories (Optigen or Vetgen), where genetic markers detect the existence or absence of alleles that cause progressive retinal atrophy (PRA) in the Labrador Retriever. The advantages of this test are early diagnosis of affected or carrier animals of PRA; Tests can even be done on Labrador Retriever puppies as young as three months old. The other key advantage is that genetic tests are valid for a lifetime.

Disadvantages include its high economic cost, lesion specificity (this test is not valid for detecting other ocular abnormalities), and the existence of certain false positives that can occur when there is a mutant allele, a question that seems to be improving with a new update of the test markers. DNA analyses for any test can be of two types: specific and linkage. In specific tests, the analysis is done directly on the gene involved in the disease, and thus, the molecular nature of the mutation has been previously identified. In other cases where the causative gene has not been isolated or is unknown, linkage tests are used. In these tests, the animal’s phenotype is determined for a second easily identifiable gene used as a marker, and it is known from previous genetic studies to be in the same chromosomal region as the main gene (the one involved in the disease) and very close to it. The closer the gene and the marker involved, the more reliable the results will be by reducing the possibility of recombination between these genes. Linkage tests are performed by Optigen. The results of these tests categorize animals into three groups:

 

  • Optigen A: free APR.
  • Optigen B: Animal carrying the defective allele and therefore carrying APR.
  • Optigen C: Animal affected by APR when carrying two defective alleles.

 

This diagnostic method can also be performed using DNA obtained from frozen semen samples, so it can be determined if a deceased stallion may be suitable for use in our breeding program. In the near future, several tests for different genetic diseases, including narcolepsy, will be launched. The information provided by genetic tests should be used with caution by Breed Clubs and Associations if they decide to initiate an improvement program to eliminate or reduce the incidence of a disease in a particular breed, as the breeding program must consider maintaining the genetic diversity of the breed. A radical breeding program, such as crossing only normal homozygotes (RR, in our case), would likely lead to the loss of important genetic characteristics for the breed.

 

In an ocular test, the following anomalies can be distinguished:

 

Microphthalmia

Reduced size of the eyeball, housed in the lower part of the orbit; It may be accompanied by mucopurulent conjunctivitis and tearing. The hereditary nature of the breed has not been proven.

 

Entropion

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

 

Ectropion

Eversion of the margin of the lower eyelid that exposes more surface of the conjunctiva of the eyeball, causing frequent conjunctivitis; Like entropion, surgical correction is definitive and is transmitted in the same way. Most cases of ectropion are generally due to an untreated or poorly healed injury on the margin of the eyelid.

 

Corneal Lipidosis

Deposition of lipids on the cornea manifested as whitish spots on the front of the eye that allow the passage of some light; They are generally associated with high-fat diets.

 

Hereditary Cataracts

Opacity of the lens affecting the animal from birth and causing total blindness; It can manifest from the moment the dog opens its eyes until two years of age, transmitted by a dominant gene.

 

Retinal Dysplasia

It is a congenital anomaly present at birth, where there is a lack of development of the retinal epithelium with disorganization of the outer layers, which can even lead to retinal detachments. Affected animals are detected as blind at 6-7 weeks of age, with dilated pupils that do not respond to changes in light. It may be associated with microphthalmia.

 

Progressive Retinal Atrophy (APR)

It is currently called progressive degeneration of cones and rods, the most common hereditary condition in the dog’s retina. In this disease, there is an enzymatic failure in the photoreceptors of the retina, which, if it affects the rods first, will produce a loss of night vision; On the other hand, the loss of daytime vision will occur first by affecting the cones. The injured retina will show pigmented areas, so it is classified as central APR if it affects the center of the retina and as generalized APR when pigmented areas are distributed everywhere. Central APR is the one that generally affects the Labrador Retriever, is transmitted in a simple recessive way, and usually manifests with a gradual and slow loss of vision that begins around three years of age. Since fundus alterations usually do not produce pain, there are times when the owner is not aware of the disease until well advanced, hence the importance of routine exams for early diagnosis. The first manifestations are usually a loss of the central visual field, so the dog perfectly observes lateral movements, but not central ones. These are the dogs that come to their master’s call zigzagging, so as not to lose sight of him, or hunting animals that in the field are able to follow a shot bird to the ground but then on the ground are unable to locate it. In cases of central APR, the vision that is altered more rapidly is daytime, with a higher density of cones in the center of the retina, and this part is 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 well. Other disorders, such as multifocal retinal dysplasia, caused by abnormal differentiation of the retina during the embryonic period and abnormal pigmentary deposits of melanin in various parts of the eye, are still under study, so they have not yet been classified as breed abnormalities

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