One theory proposes that some of the dogs left the Asian steppes with the Goths, a confederation of German tribes. Some, (the Ostrogoths), went west and their dogs became the German poodle, called in German the poodle-hund or puddle-dog, that is, water-dog. Others, (the Visigoths), went south to fight the Romans, and their dogs became the Lion Dog, groomed in the traditional lion cut. In 413 CE, the Visigoths invaded Iberia and the dogs found their homeland before being settled in Aquitania north of the Pyrenees in 418 before extending their rule to most of Iberia after 470 CE.
A Portuguese Water Dog is first described in 1297 in a monk’s account of a drowning sailor who was pulled from the sea by a dog with a "black coat, the hair long and rough, cut to the first rib and with a tail tuft".
These theories explain how the Poodle and the Portuguese Water Dog may have developed from the same ancient genetic pool. At one time the Poodle was a longer-coated dog, as is one variety of the Portuguese Water Dog. The possibility also exists that some of the long-coated water dogs grew up with the ancient Iberians. In early times, Celtiberians migrated from lands which now belong to southwestern Germany. Swarming over the Pyrenees, circulating over the whole of western Europe, they established bases in Iberia, as well as in Ireland, Wales, and Brittany.
The PWD was a breed on the verge of extinction when, during the 1930s, Vasco Bensaude, a wealthy Portuguese shipping magnate, began to seek out fishermen's dogs and utilize them in a breeding program to re-establish the breed. Bensaude's kennel was named Algarbiorum, and his most famous dog was Leão (1931–1942), a very "type-y" (i.e., standard-conformant) fisherman's stud dog, who was bred to so many different females that about half of the pedigreed Portuguese Water Dogs in existence can trace their lineage back to him. Bensaude was aided by two Portuguese veterinarians, Dr. Francisco Pinto Soares and Dr. Manuel Fernandes Marques. His work was carried on by Conchita Cintron de Castelo Branco, to whom he gave his last 17 PWDs and all his archives.
Dr. António Cabral was the founder of the Avalade kennels in Portugal. Ch. Charlie de Avalade (Charlie), a brown-coated dog, and C. B. Baluarte de Avalade (Balu) were two of his many famous PWDs. He registered his first PWD in 1954, after Bensaude had pioneered the re-establishment of the breed in Portugal. Cabral worked with Carla Molinari, Deyanne Miller, Sonja Santos and others to establish PWDs in the US. The "Mark of Cabral" is a triangular shape of different color/textured hair, usually 2 to 3 inches (5 to 8 cm) from the base of the tail.
Deyanne Miller is the person most responsible for the rise of the PWD in America. In 1972, the Millers, along with 14 others, formed the Portuguese Water Dog Club of America, Inc. (PWDCA). She worked with dogs from both the Cintron and Cabral lineages to establish a stable genetic pool of PWDs in the US at her Farmion kennels. Another early US breeder of PWDs was the actor Raymond Burr.
As with all purebred dogs, PWDs are vulnerable to certain genetic defects. Due to the limited gene pool for this breed, conscientious breeders carefully study pedigrees and select dogs to minimize the chance of genetic disease and improper coat. Unfortunately, like many breeds, growing popularity has encouraged breeding by people not knowledgeable about the breed.
Like poodles, PWDs are vulnerable to hip dysplasia. However, the risk of a PWD developing hip dysplasia can be greatly reduced by thoroughly checking the pedigrees and health clearances in both the sire and dam of the dog. Hip dysplasia is a congenital and developmental problem with the hip joints.
Cataracts, PRA, and distichiasis
Cataracts and PRA (Progressive Retinal Atrophy) are two eye diseases found in PWDs. As with hip dysplasia, some lines carry these defects more frequently than others. PRA, which causes "night blindness", may lead to complete blindness. Fortunately this is a simple recessive gene. DNA testing is now available which can identify a dog carrying the gene for PRA. Known as "Optigen Testing" a "normal" or "A" dog does not carry the gene for PRA. A "carrier" or "B" dog carries one copy of the PRA gene and the dog will not express the disease but may or may not pass the gene to offspring. An "affected" or "C" dog has two copies of the PRA version of the gene and will probably express the disease as late onset Progressive Retinal Atrophy. A "B" or "C" dog should be bred only to an "A" dog to ensure that any offspring will not express the disease.
Ingrown eyelashes (distichiasis) occurs in some curly-coated breeds, but is not particularly common in PWDs. Ingrown eyelashes will rub the eye causing extensive corneal ulcerations. The condition is minor so long as it is not ignored, and can be surgically treated if necessary.
GM1 Storage Disease
GM1 Storage Disease, one of a family of conditions called GM1 gangliosidoses, is a recessive, genetic disorder that is inevitably fatal. It is caused by a deficiency of beta-galactosidase, with resulting abnormal storage of acidic lipid materials in cells of the central and peripheral nervous systems, but particularly in the nerve cells. Because PWDs are all rather closely related to one another and share a limited gene pool, PWDs who were GM1 Storage Disease carriers were able to be genetically identified, and the condition has now been almost entirely eliminated from the breed. All breeding stock should be tested for GM-1 storage disease or GM1 gangliosidoses, which is a fatal nerve disease that typically appears when a puppy is approximately six months of age. The affected puppy will show clinical signs of cerebellar dysfunction including ataxia, tremors, paresis, and seizures. The pet may also exhibit a change in temperament. Lesions of the retina and clouding of the cornea may occur. GM-1 storage disease is a recessive deficiency of betagalactosidase. The condition has been genetically identified and is no longer common.
Juvenile Dilated Cardiomyopathy
Juvenile Dilated Cardiomyopathy is a rare, fatal condition caused by an autosomal recessive gene. It affects young dogs, who succumb to heart failure before reaching adulthood. As a simple recessive gene, it had been difficult to identify and was particularly heartbreaking as seemingly healthy puppies would suddenly die, often shortly after joining their adopted families. Since a recessive gene is responsible, that means if at least one parent is homozygous dominant (that is, it does not carry a copy of the cardio version of the gene), its offspring can not contract the disease.
In 2007, a genetic linkage test became available which appears promising. This is not a test which confirms if a dog has, or does not have the disease; nor will it definitively predict the disease, as even if a dog is a JDC carrier this does not guarantee its offspring will suffer the disease. It only links certain strains of DNA as carriers of JDC. This is significant in that these strains can now largely be deselected for in the breeding process, as has been successful with GM1 Storage Disease (see above). The test is not yet complete for every bloodline, and why the identified strains are implicated is still unknown, and so in essence the cause of the condition remains a mystery to be solved