We rigorously control the health of our Labradors. Below are some articles about common diseases in the breed.

Hip dysplasia is the most common hereditary orthopedic disease in dogs. It can occur in any breed but is more common in large or giant breeds, such as Labrador Retrievers, Shepherds, and Mastiffs, especially in animals that grow very fast.

This disease is characterized by the malformation of the hip joint, i.e., the connection of the hind limb to the pelvic girdle. The first symptoms usually appear around 4 to 7 months of age when the affected animal starts limping and experiencing pain when walking, especially on slippery surfaces. Due to the difficulty in walking, the dog may avoid using the limb, leading to muscle atrophy.

Hip dysplasia is genetically recessive, meaning both the male and female must have the disease, or at least the gene, for the offspring to inherit it. However, this deficiency has become more common as owners breed affected animals without considering transmission.

A dog with hip dysplasia can live a normal life but should not be used for breeding. Even if a puppy is normal but its parents are affected, it should not be used for reproduction, as its offspring may have problems.

To determine if a dog has hip dysplasia, a simple examination is made. The diagnosis is made through an X-ray, with the animal lying on its back and the hind legs stretched backward. Since dysplasia can cause severe pain and the most affected animals are large, anesthesia may be necessary. Usually, a short anesthesia lasting 10 to 20 minutes is administered to take X-rays. The veterinarian must be careful in positioning during the X-ray because poorly positioned X-rays are considered inappropriate for obtaining a diagnosis.

There are various categories of hip dysplasia, classified by severity.
The following chart outlines these categories:
Hip Dysplasia Categories:

Grade A: Normal Hip Joints (H.D. -) The femoral head and acetabulum are congruent. The cranial-lateral edge is pointed and slightly rounded. The joint space is narrow and regular. The acetabular angle, according to Norberg, is approximately 105° (as a reference). In excellent hip joints, the cranial-lateral edge surrounds the femoral head slightly more in the laterocaudal direction.

Grade B: Hip Joints Near Normal (H.D. +/-) The femoral head and acetabulum are slightly incongruent, and the acetabular angle, according to Norberg, is approximately 105° or the center of the femoral head is medially positioned to the dorsal acetabular edge, and the femoral head and acetabulum are congruent.

Grade C: Mild Hip Dysplasia (H.D. +) The femoral head and acetabulum are incongruent. The acetabular angle, according to Norberg, is approximately 100°, or there is a slight flattening of the cranial-lateral acetabular edge, or both. Irregularities or only small signs of osteoarthritic changes may be present in the cranial, caudal, or dorsal acetabular margin or in the femoral head and neck.

Grade D: Moderate Hip Dysplasia (H.D. ++) The incongruity between the femoral head and acetabulum is evident, with signs of subluxation. The acetabular angle, according to Norberg, is approximately 95° as a reference. Presence of flattening of the cranial-lateral edge or signs of osteoarthritis, or both.

Grade E: Severe Hip Dysplasia (H.D. +++) There are evident dysplastic changes in the hip joint, with signs of luxation or distinct subluxation. The Norberg angle is less than 90°. There is evident flattening of the cranial acetabular edge, deformation of the femoral head (mushroom shape, flattening), or other signs of osteoarthritis.

In Brazil, up to HD+ or grade C, a dog is accepted for breeding. However, an HD+ (grade C) animal should only mate with an HD- (grade A) one.
Radiographic report: The CBRV (Brazilian College of Veterinary Radiology) has adopted evaluation criteria from the Orthopedic Foundation for Animals (Offa) and the International Elbow Working Group (IEWG). It grades elbow joints based on signs of degenerative joint disease associated with the most common causes of elbow dysplasia. These include joint incongruity, fragmentation of the medial coronoid process of the ulna, non-union of the anconeal process of the ulna, osteochondrosis of the medial condyle of the humerus, and non-union of the medial epicondyle of the humerus.

Elbow Dysplasia Grades:
Grade 1: Slight bone proliferation on the anconeal process of the ulna (less than 3mm).
Grade 2: Bone proliferation in the anconeal process of the ulna (between 3 and 5mm) and sclerosis of the subchondral bone of the trochlear notch of the ulna.
Grade 3: Evident bone proliferation in the anconeal process of the ulna (above 5mm) and sclerosis of the subchondral bone of the trochlear notch of the ulna.

When a female has elbow dysplasia, or the chances of the puppy having it are high, some precautions can be taken to prevent the condition from getting worse:

It is essential to be aware and take care of animals from a young age to prevent such problems. A healthy animal that visits the vet regularly is more likely to have a long and problem-free life. When buying a puppy, especially of susceptible breeds, ask the owner to provide the parents' dysplasia certificate to ensure your puppy does not have this problem. If you already have a dog at home, consult your vet to perform this simple examination and prevent the disease from spreading.

Dr. Cristina Jorge
Veterinarian - Campinas - SP


Progressive Retinal Atrophy (PRA or PRCD) in the form of prcd (progressive rod-cone degeneration) is a hereditary eye disease. In affected English Cocker Spaniels, there is a progressive and irreversible degeneration of both cone and rod cells in both eyes, leading slowly to complete blindness. PRA prcd occurs after the normal development of photoreceptors. Various dog breeds, including mixed breeds (SRD - Sem Raça Definida), can be affected by this disease.

Rod cells degenerate first. Affected dogs experience night blindness, meaning they can't see well in low-light environments. This is often the first symptom recognized by owners. Dogs typically lose their sense of direction and may bump into objects while walking. The pupil dilates significantly when exposed to light. Later, cone cells begin to degenerate. The final symptoms of the disease are total blindness and possibly cataracts.

The timeframe for total blindness varies considerably from dog to dog and from breed to breed. In English Cocker Spaniels, there are cases where the disease appears around four years of age. In most cases, the average age of prcd PRA onset is around eight years. A dog at this age is still active, and blindness can significantly impact its life.

PRA prcd is a recessive hereditary disease, so both the father and the mother must have the recessive PRA gene to transmitte the disease to the offspring. PRA manifests only in dogs with a P/P genotype, called Affected (homozygous affected). Dogs with an N/P genotype are considered carriers of the disease (heterozygous). Dogs with an N/N genotype are considered normal (homozygous normal). Other terminologies are also used for these definitions:
Homozygous normal (N/N) PRA Normal/Clear - healthy non-carriers
(will not develop the disease and will not produce affected offspring).
Heterozygous (N/P) PRA Carrier - healthy carriers
(will not develop the disease but may produce affected offspring, depending on the mating) Homozygous affected (P/P) PRA Affected - affected
(will eventually develop the disease if they live long enough)

Recommended breedings are those that avoid the appearance of affected dogs (P/P). It is advised that at least one parent be Normal/Clear (N/N). Other breedings have a high risk of producing affected dogs (P/P) with an extreme likelihood of developing prcd PRA during their lives. The disease cannot be cured, but it can be eliminated through genetic testing for the prcd form of PRA and the correct choice of breedings. It's not necessary, nor desirable, to remove good dogs from a breeding program. However, when selecting dogs for reproduction, the gradual selection of genetically healthy dogs is important. Tests can be performed only once during the dog's life since the genotype does not change over time.
(Sire or Dam) (Sire or Dam)

Normal/Clear (N/N) Carrier (N/C) Affected (C/C)

Normal/Clear (N/N) All = Normal/Clear 1/2 = Normal/Clear

1/2 = Carrier All = Carrier
Carrier (N/C) 1/2 = Normal/Clear
 1/2 = Carrier 1/4 = Normal/Clear
1/2 = Carrier

1/4 = Affected 1/2 = Carrier
1/2 = Affected

Affected (C/C) All = Carrier 1/2 = Carrier

1/2 = Affected All = Affected

In red are breedings that should be avoided. For example, it would not be advisable to breed an Affected dog (C/C) with a Carrier (N/C) as it may generate affected dogs.


Exercise-Induced Collapse (EIC) is a hereditary condition characterized by muscle weakness, difficulty in movement, and collapse after intense physical activity. This autosomal recessive disorder primarily affects young Labrador Retrievers and is caused by the c.767G>T mutation in the dynamin 1 (DNM1) protein-encoding gene. This report aims to document the first case of EIC in a Labrador Retriever in Brazil.

Molecular testing to detect the EIC-causing mutation confirmed the clinical diagnosis in a Labrador Retriever with a history of muscle weakness and collapse after exercise. Once diagnosed in Brazil, it is emphasized that EIC should be considered in the differential diagnosis of neuromuscular disorders in Labrador Retrievers. Molecular diagnosis is recommended to guide breeding practices. Exercise-Induced Collapse (EIC) is an autosomal recessive hereditary disorder diagnosed more frequently in Labrador Retrievers (TAYLOR et al., 2008; MINOR et al., 2011), considered the most common cause of exercise intolerance in young dogs of this breed in the United States (TAYLOR et al., 2008).

EIC results from the c.767G>T mutation in the dynamin 1 (DNM1) protein-encoding gene (PATTERSON et al., 2008), responsible for recycling synaptic vesicles in nerve terminals during persistent and high-frequency stimulation (FERGUSON et al., 2007). This mutation leads to the substitution of arginine with leucine, causing abnormal synaptic transmission due to decreased correct translation of dynamin 1 protein, affecting the normal function of the nervous system (FERGUSON et al., 2007; PATTERSON et al., 2008). The mutation responsible for EIC has also been observed in dogs of related breeds, such as Chesapeake Bay Retrievers and Curly-Coated Retrievers (PATTERSON et al., 2008). Additionally, other breeds, including Boykin Spaniel, Pembroke Welsh Corgi, and mixed Labrador Retrievers, have been reported to carry the mutation associated with EIC (MINOR et al., 2011). Homozygous Labradors for the c.767G>T mutation in the DNM1 gene are clinically normal at rest but experience collapse after 5 to 20 minutes of intense exercise (PATTERSON et al., 2008; TAYLOR et al., 2009; MINOR et al., 2011). In a study by TAYLOR et al. (2008), seven out of 335 dogs died during collapse episodes. The diagnosis of EIC is suggested by excluding other diseases related to collapse and exercise intolerance (TAYLOR et al., 2008).

However, specific diagnosis of EIC is only possible through the detection of the mutation in molecular tests (MINOR et al., 2011). Given that EIC is commonly diagnosed in Labrador Retrievers in other countries, the aim of this report is to document the first case of this disease in Brazil and alert veterinarians and breeders about the importance of performing molecular tests for this condition in animals of this breed used in breeding programs. A yellow male Labrador Retriever, two years old, was referred to the Veterinary Hospital of the Faculty of Veterinary Medicine and Zootechnics of Botucatu, Unesp, with a history of weakness in the hind limbs during intense walking activities.

The dog had experienced four similar crises, with the first episode occurring at approximately one year of age when the dog started training activities. All episodes were similar, involving progressive weakness in the hind limbs leading to an inability to walk. The symptoms appeared after approximately 20 minutes of physical exercise, more frequently on warmer days. During the crises, the dog showed no changes in consciousness. After the collapse, the dog rested and recovered within a few hours. The dog was in good overall condition, and no additional complaints were reported during the anamnesis.

Physical examination parameters were within normal ranges. Orthopedic and neurological examinations revealed no abnormalities. Moreover, at the time of evaluation, the dog ran and jumped normally, without paresis, ataxia, or signs of joint pain. Complete blood count and biochemical analyses (urea, creatinine, total protein, albumin, globulin, GGT, alkaline phosphatase, ALT) showed normal results. The final diagnosis of EIC was confirmed by the Molecular Biology Laboratory of the Department of Veterinary Clinic, FMVZ - Unesp -Botucatu. DNA extraction from blood was performed using the Illustra Blood GenomicPrep Mini Spin Kit (GE Healthcare).

DNA concentration and purity were assessed by spectrophotometry using the Nanodrop® 2000 (Thermo ScientificTM). PCR was performed using primers previously described by PATTERSON et al. (2008), amplifying a 337-base pair fragment, including the entire exon 6 of the DNM1 gene. Negative controls of the reaction were performed using water. PCR products with the correct estimated size after electrophoresis on 1.5% agarose gel stained with Gelred® (Biotium®) were subjected to direct sequencing using BigDye® Terminator v3.1 Cycle Sequencing (Applied BiosystemsTM). Sequences and electropherograms were analyzed in the SequencherTM 5.1 program (Gene Codes©) and aligned and compared to the normal Canis lupus familiaris dynamin 1 (DNM1) mRNA sequence with the tool available at

The genetic test confirmed that the dog had the mutated allele in homozygosity. After the diagnosis, no drug treatment was prescribed. The owner was advised to reduce the intensity of exercises, avoid exercising during the hottest parts of the day, and stop physical activity at the first signs of motor incoordination. Cases of exercise-induced collapse are commonly observed in other countries (TAYLOR et al., 2008; MINOR et al., 2011), with studies describing up to 4.5% of homozygotes (PATTERSON et al., 2008; TAKANOSU et al., 2012). Like the dog in this report, most dogs with the syndrome show the first clinical signs before four years of age (MINOR et al., 2011). Although the disease occurred in a yellow male, EIC does not show a preference for sex or coat color (TAYLOR et al., 2008). Intense exercise, accompanied by excitement and agitation, appears to facilitate the onset of collapse (TAYLOR et al., 2009).

The clinical signs presented by this Labrador in this case are consistent with those described in the literature. Animals affected by the syndrome are normal at rest, but after 5 to 20 minutes of intense physical activity, they develop non-painful flaccid paraparesis, which may progress to collapse (TAYLOR et al., 2009). As observed in this report, the recovery after a collapse in the vast majority of cases is gradual, occurring over 5 to 45 minutes (TAYLOR et al., 2008). However, some animals may die during the crisis (TAYLOR et al., 2008; FURROW et al., 2013). Most affected dogs do not show changes in consciousness during the collapse; however, in the study by TAYLOR et al. (2008), owners observed some degree of mental alteration in 23% of affected dogs.

These authors emphasize the clinical importance of this syndrome, as 3% of the observed cases were fatal. According to STEISS et al. (2004), there is a possibility that the increase in body temperature and respiratory alkalosis after exercise in competition dogs of the Labrador Retriever breed may be related to triggering the collapse. There is a hypothesis that high body temperatures reached during intense exercise may contribute to dysfunction in the mutant protein, thus causing failures in synaptic transmission, triggering the signs of the disease (MATWICHUK et al., 1999; TAYLOR et al., 2009). The animal in this report was not evaluated during the collapse, so there is no data on its body temperature or possible metabolic changes at that time. Since restricting intense physical exercises drastically reduced the episodes of collapse or even led to the complete disappearance of these episodes in most animals (TAYLOR et al., 2008), and in the absence of specific treatment for the disease, the owner of the animal in this report was only advised to decrease the frequency of crises, avoid exercising during the hottest times of the day, and suspend physical activity as soon as the first signs of motor incoordination become apparent.

The molecular diagnosis of the mutation responsible for EIC has already been performed using PCR associated with restriction enzymes (PATTERSON et al., 2008) and allele-specific PCR (TAKANOSU et al., 2012). In this report, we opted for direct sequencing of PCR products using primers previously described by PATTERSON et al. (2008). This methodology, in addition to being cost-effective, proved to be efficient for diagnosis. The molecular confirmation of the mutation responsible for EIC in this case points to the need to include this disease among the differential diagnoses of neuromuscular diseases in Labrador Retrievers in Brazil. Additionally, it reinforces the importance for breeders of this breed to assess whether the mutation is present in their dogs for breeding guidance.


Brucellosis is a disease that affects dogs, with sexual contact being its primary mode of transmission. The most common symptoms include abortion and infertility. It is caused by bacteria of the genus Brucella, with B. canis being the primary agent. Puppies are the main hosts for this bacterium.

In addition to infected semen, transmission can occur through ingestion or inhalation of aerosols from aborted material (fetus and placenta), secretions from abortions, urine, and contaminated materials. The most significant entry point for the agent appears to be the oral mucosa; however, infection can also occur through the nasal, conjunctival (inner eyelids), and genital mucosa, damaged skin, and placenta. In females, the main symptoms include early embryonic death, abortion in the final third of gestation, and high rates of stillbirths (fetuses expelled dead at the time of delivery).

Males may exhibit infertility, epididymitis, orchitis, and scrotal dermatitis (all inflammations in the reproductive system) as a result of semen alterations. There are also reports of uveitis (intraocular inflammation), spondylitic discospondylitis (vertebral changes), meningitis (inflammation of the meninges), glomerulonephritis (kidney infection), and pyogranulomatous dermatitis (skin infection).

Diagnosis is based on the animal's clinical history, accompanied by serology (a specific blood serum test). The procedure that confirms the presence of Brucella, once the animal is seropositive (serological test positive for brucellosis), is the isolation of this agent in organic secretions or tissues.

Treatment can be carried out using antibiotics specifically indicated for the disease. It should always be remembered that brucellosis is a zoonosis and can be transmitted to humans. The first step in disease prevention and control is confirming the presence of Brucella in kennel animals or your dog. Before any mating occurs, both dogs should be tested for brucellosis. They should only mate if both have negative serological test results. This ensures that the animals are not infected during mating.

When a dog is identified as positive in the serological test, it should be isolated and treated until the infection is eliminated. Tests should be conducted every four months for identification and elimination of positive animals, which is the only effective method of prevention and control in kennels, as sanitary measures and antibiotic therapy do not prevent transmission to non-infected animals.

If you choose to treat a seropositive animal for brucellosis, it should be isolated from others during treatment until it tests seronegative (negative serological test). Consult your veterinarian for information on precautions and risks. Remember that brucellosis can be transmitted to humans.


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