The Lagotto Romagnolo is a healthy breed, that easily can become 12 - 14 years. There are only a few health problems reported in some lines that are known to be inherited.
There are tests available to make sure that dogs used for breedig are healthy so the risk of producing sick puppies can be minimized. But no matter how many health tests we do and how carefully we select our breeding dogs, there always is a small percentage of risk left, because dogs are living creatures and mother nature sometimes has her own will...
Benign Familial Juvenile Epilepsy (JE)
Clinical studies indicated that the Lagotto Romagnolo can suffer from inherited benign juvenile epilepsy, which resembles idiopathic chiilepsy with benign outcomes in human.
Typical symptoms: tremor, loss of balance, uncoordinated movements and occasional falling.
Clinical and diagnostic evaluations of affected dogs including electromyography, electroencephalography, and other testing indicated that seizures in puppies begin at 5 to 9 weeks of age and usually resolve by 8 to 13 weeks. There are some adult-onset cases in the breed too. Dogs with the most severe seizures also have other neurologic signs such as generalized ataxia and hypermetria. Routine laboratory screenings of blood, urine, and cerebrospinal fluid did not reveal abnormalities. Electromyography, brainstem auditory-evoked potentials, and magnetic resonance imaging (MRI) remain normal in analyzed dogs. However, most affected puppies and adult cases revealed epileptiform activity in the electroencephalogram (EEG). Histopathologic examination shows cerebellar lesions in two studied lagottos. Pedigree analysis suggests an autosomal recessive mode of inheritance.
A laboratory in Finland has studied the genetics of the juvenile epilepsy in Lagottos and has identified one of the causative genes and now can perform a DNA test to verify if a dog is affected, even without showing any clinical signs.
If a dog carries one copy of the mutation, it can transfer the gene defect to approximately 50% of its offsprings. If the dog has two copies of the mutation it transfers the defect to all of its offsprings. It is recommended that dogs that are homozygous for the lagotto epilepsy mutation are withdrawn from breeding programs. Normal and carrier dogs can be used but it is advised to choose mutation-free partners for carriers.
There still is a second (or maybe even third) mutation causing Epilepsy in the breed with very similar symptoms that cannot be tested yet, but the laboratory is researching and hoping to find these mutations soon.
All our breeding stock is tested for JE. All our JE carriers will be breed only to mutation free partners to make sure that no sick puppies will get born.
Lyosomal Storage disease (LSD) and Cerebellar Ataxia (CA)
Recently, a new neurodegenerative storage disorder was identified in the Lagotto Romagnolo breed. The genetic background of the disease has been studied as a collaboration between the University of Helsinki and the University of Bern, Switzerland. A likely disease-causing mutation has now been found. Altogether 1300 Lagottos have been tested (using samples supplied for other purposes) as a part of the research. Out of all the tested dogs, 11% were carriers of the recessive mutation and 1% were affected.
The storage disorder is characterized by movement in-coordination, which is seen as a staggering, uncoordinated gait. Some affected dogs also suffered from involuntary eye movements (nystagmus) and behavioral changes, such as aggression. The onset of symptoms has varied from 4 months to 4 years. The condition is progressive and affected dogs deteriorate to the point where they need to be euthanized. On the pathological level, storage material accumulates to the affected dogs’ cerebellar neurons and other cells, causing dysfunction and cell death.
The results of genetic study indicate that the storage disorder in the Lagotto breed is inherited through a single gene, in an autosomal recessive manner. In recessive disorders, affected dogs have to inherit two copies of a disease-causing gene mutation. Those Lagotti that have a NORMAL result have inherited two normal copies of the disease gene; they do not pass the mutation down to their offspring. CARRIER dogs have inherited one normal copy and one with the mutation, they pass the mutation down to approximately half of their offspring. If a carrier dog is used for breeding, it should be mated with a dog that has been tested as normal. In carrier/carrier -matings, the resulting offspring can be either affected, carrier or normal, whereas in carrier/normal —matings, only carrier or normal dogs are born. AFFECTED dogs have inherited the mutation from both parents, and so they have two copies of the mutation. Their risk of developing the disease is very high.
In addition to the storage disorder, progressive cerebellar abiotrophy (CA) has been reported to occur in the Lagotto Romagnolo breed. The clinical signs and age of onset a similar between the different disorders, and therefore it is not possible to make a diagnosis based just on the dog’s symptoms. The genetic cause of the cerebellar abiotrophy has not been identified yet but ongoing research is aiming to shed light to this.
While cerebellar ataxia can be caused by tumors or brain infections, it's most commonly passed down through families as a genetic illness. In cases of hereditary cerebellar ataxia, some or all of the cells of the cerebellum deteriorate. The cerebellum is a vital portion of your dog's brain, responsible for coordinating movement. As the cerebellum deteriorates, motor coordination decreases, and sometimes cognitive impairment also occurs.
Cerebellar ataxia is a progressive canine disease that causes symptoms to appear in a certain order. Initial symptoms typically include clumsiness and slight swaying. As your dog's condition worsens, he will fail to keep his balance and begin falling down frequently. Your dog's head and eyes may begin to move rapidly and at random. Your dog will have trouble walking and may lose weight.
Vets do not completely understand how cerebellar ataxia occurs or how it progresses. In some dogs, symptoms appear slowly and cause only mild disability for up to five years. In other dogs, symptoms progress swiftly and cause rapid, serious impairment. Symptoms usually appear in dogs older than two years of age.
All our breeding stock is tested for LSD. All our LSD carriers will be breed only to mutation free partners to make sure that no sick puppies will get born.
Unfortunately there is no test yet for the CA, but so far we haven't had any cases in our breeding program or the lines we use.
Hip Dysplasia is a genetic disease of various degrees of arthritis (also called degenerative joint disease, arthrosis, osteoarthrosis), it can lead to pain and debilitation.
The very first step in the development of arthritis is articular cartilage (the type of cartilage lining the joint) damage due to the inherited bad biomechanics of an abnormally developed hip joint. Traumatic articular fracture through the joint surface is another way cartilage is damaged. With cartilage damage, lots of degradative enzymes are released into the joint. These enzymes degrade and decrease the synthesis of important constituent molecules that form hyaline cartilage called proteoglycans. This causes the cartilage to lose its thickness and elasticity, which are important in absorbing mechanical loads placed across the joint during movement. Eventually, more debris and enzymes spill into the joint fluid and destroy molecules called glycosaminoglycan and hyaluronate which are important precursors that form the cartilage proteoglycans. The joint's lubrication and ability to block inflammatory cells are lost and the debris-tainted joint fluid loses its ability to properly nourish the cartilage through impairment of nutrient-waste exchange across the joint cartilage cells. The damage then spreads to the synovial membrane lining the joint capsule and more degradative enzymes and inflammatory cells stream into the joint. Full thickness loss of cartilage allows the synovial fluid to contact nerve endings in the subchondral bone, resulting in pain. In an attempt to stabilize the joint to decrease the pain, the animal's body produces new bone at the edges of the joint surface, joint capsule, ligament and muscle attachments (bone spurs). The joint capsule also eventually thickens and the joint's range of motion decreases. However it is very important to distinguish between radiographic hip dysplasia (where the x-ray plates shown noticeable joint changes but the dog shows no sign of the condition) and clinical hip dysplasia (where the dog becomes stiff, lame and in obvious discomfort with arthritis setting in at an early age.) Many dogs with radiographic hip dysplasia will never show any signs of the disease even in old age. Others with genetically better hips will develop the condition. The main factor in the development of clinical hip dysplasia is environment not genetic inheritance (which is generally thought to be about 30-35%). Overweight and over exercise plus poor diet will vastly increase the chances of a dog developing hip dysplasia particularly in big heavy breeds with slow bone growth. Lagotti as a breed are not predisposed to hip dysplasia. They are fast growing, sturdy but agile puppies with lightish bone for their size. If reared correctly there is little chance of them developing clinical hip dysplasia but dogs always should be checked for HD before used in breeding.
All our breedings stock is tested for HD and has a passing hip score.
Eye Cataract and PRA
Like a camera, eyes have a clear lens inside them that is used for focusing. A cataract is any opacity within a lens. The opacity can be very small (incipient cataract) and not interfere with vision. It can involve more of the lens (immature cataract) and cause blurred vision. Eventually, the entire lens can become cloudy, and all functional vision lost. This is called a mature cataract.
Cataracts may be primary (where the condition is probably inherited) or secondary e.g. the cataract occurs as a result of inflammation; metabolic disease; congenital anomalies; trauma. Some cataracts may be detected at an early age; others develop later, may occur in different part of the lens and may progress at different rates. Some mature cataracts will transform over time into hypermature cataracts. Hypermature cataracts usually are reduced in size due to loss of water and proteins from the lens. This causes the lens to shrivel and the lens capsule to wrinkle—similar to a grape turning into a raisin. Hypermature cataracts vary in how cloudy they are. Some are completely cloudy, and others have clear areas that can allow some vision IF the rest of the eye is functional. Depending on the dog’s age and breed, it can take several months to years for a mature cataract to turn into a hypermature cataract.
What is not a cataract?
All geriatric dogs (usually beginning at 6 years of age) develop a hardening of the lens (Nuclear Sclerosis) that causes the lens to have a grayish appearance. The grayish-blue haze increases as the dog ages. Nuclear sclerosis is NOT a cataract, and does not usually interfere with vision. The photo to the right shows a normal geriatric dog eye with normal nuclear sclerosis. Nuclear sclerosis also occurs in humans, and the hardening of the lens with age results in reduced near-vision in people; this is why people in their 40’s and older need reading glasses—because their lenses no longer are soft enough to easily change shape to allow for near vision. Another name for this is presbyopia, which means “old eye”. Dogs do not have good near-vision to begin with (compared to people), so nuclear sclerosis does not significantly interfere with their near-vision
How do you tell the difference between nuclear sclerosis and cataract in your dog? The answer is that you can’t. You can start with having your family veterinarian evaluate your dog’s eyes, but often it is difficult for a doctor who is not an ophthalmologist to differentiate between the two conditions. However, veterinary ophthalmologists can tell the difference between nuclear sclerosis and cataract, using specialized equipment and their expertise. Also keep in mind that dogs can develop BOTH nuclear sclerosis AND cataract—many geriatric dogs do develop cataracts. If your geriatric dog has cloudy eyes but still appears to see well, this does not mean that they do not have cataracts—dogs can see fairly well if their cataracts are small. Dogs also can adapt well if one eye is blind from cataract and the other is not. Often, they adapt so well that the owner does not realize that the dog cannot see out of one eye. Dogs can also adapt well—up to a point—if both eyes gradually develop severe cataracts; dogs can develop a “memory map” as to where things are in their familiar environment. Dogs with poor vision do not let their owners know that they have a vision problem until it is severe in both eyes.
Progressive Retinal Atrophy (PRA) is an inherited disease of the retina (the “film in the camera”) in dogs, in which the rod cells in the retina are programmed to die. PRA occurs in both eyes simultaneously and is nonpainful. There are many different types of inherited retinal degenerative diseases in purebred dogs, and discussing these are beyond the scope of this article. PRA occurs in most breeds of dogs and also occurs in mixed breeds. It is recessively inherited in all breeds studied, with the following exceptions: PRA is dominantly inherited in Old English Mastiffs and Bullmastiffs, and is sex-linked and found primarily in male dogs in Siberian Husky and Samoyed breeds. Because PRA makes rods die, and rods are responsible for vision in dim light (“night vision”), the first clinical signs that the owner often notices are night-blindness (poor vision in dim light) and that the pupils are dilated; owners often notice a “glow” and increased “eye shine” from the eyes. Clinical signs in dogs with PRA vary from the dog first becoming night blind in the early stage of PRA, to the entire visual field in all light levels becoming affected in advanced PRA. In the final stage of PRA, the dog is completely blind. The natural course of the disease, if specific daily antioxidant supplementation is not given, is that all dogs with PRA will develop blindness within one year.
PRA is a blinding disease in most affected dogs, but in the opinion of many veterinary ophthalmologists, including Dr. McCalla, PRA is no longer a hopeless disease. New insight into the mechanisms of retinal damage from oxidative stress has resulted in much more hope for prolonging the vision of affected dogs. Typical PRA is a disease caused by a mutation in the rod photoreceptors (rods are responsible for night vision/ vision in dim light) leading to their death. Cones are responsible for daytime vision/ vision in bright light, and also for color vision (dogs do see color, but not as well as humans do). The dog retina has about 120 million rods and cones; of these, only 5% are cones (6 million). Thus, PRA kills 95% of the photoreceptors!
When the rods die, there is a lot of “left-over”, excessive oxygen delivered to the retina that the dead rods can’t use anymore. Cone death subsequently occurs due to excessive oxygen exposure in the face of rod death from damaging oxidative stress mechanisms. After the rods die, the excessive “left-over” oxygen is toxic, causing oxidative damage and ultimate death of cones.
It is important to understand that most dogs with PRA are happy dogs with an acceptable quality of life. The retinal damage is not painful, and dogs usually adjust very well to their slow loss of vision.
Unfortunately there are no genetic tests yet for PRA and cataract, but all our breeding dogs are tested for genetic eye diseases on a regular basis by a specialist.