Portuguese Water Dogs
Recently chosen to be the First Dog of the United States, the once-obscure Portuguese Water Dog has gained new notoriety. President Obama and his family have chosen a Portuguese Water Dog to become the newest resident of 1600 Pennsylvania Ave in Washington, D.C.
Known to be a water-loving, affectionate, and loyal dog, the Portuguese Water Dog is intelligent and is an easily-trainable companion. A medium-sized dog, this particular breed is reported to be great with children and tends to play well with other doggy companions.
The Portuguese Water Dog comes in a variety of colors including solid black, white, brown, or parti-colored, which may include white coats with dark spots, black or brown coats with white markings, or even silver fox or gray is possible.
The coat of a Portuguese Water Dog is single-layered, non-shedding, and virtually hypo-allergenic. The coat may be curly or wavy. Although their hair grows slower than a poodle’s, they do require grooming. Traditionally one of two clips are used: The “lion clip,” in which the face and hindquarters are shaved, or the “retriever clip,” where the dog is scissor-trimmed to approximately a one-inch length all over.
Male dogs should be 20 to 22 inches in height while females should range from 17 to 20 inches. Males are typically 42 to 55 pounds with females being smaller at 35 to 49 pounds on average. Their life expectancy is from 10 to 14 years of age.
This breed was first developed as a working dog that aided Portuguese fishermen for centuries. In fact, the breed in Portugal was referred to as the “Cao de Agua,” or “Dog of Water.” The breed actually herded and caught fish by pulling out nets. They carried messages between ships and were used to retrieve anything that fell overboard. Once at port it was the Portuguese Water Dog that guarded the catch and the boat. In the past these dogs were considered to be so valuable that they were entitled to a share of the catch. Unfortunately by the 1930’s these dogs were almost entirely replaced by radios and other modern technologies. A wealthy shipping tycoon, Dr. Vasco Bensaude, saved the breed by creating a breeding program by the time they were nearly extinct.
In 1983 the breed was accepted by the AKC and is now a member of the working dog class.
Recognized problems seen with this breed include hip dysplasia, various eye problems, GM-1 storage disease, and Hypoadrenocorticism. Hip dysplasia is a congenital and developmental problem with the hip joints.
The two commonly seen eye problems with Portuguese Water dogs are Progressive Retinal Atrophy, or PRA, and distichiasis. With distichiasis, ingrown eyelashes will rub the eye causing extensive corneal ulcerations. The breed has risks for a PCR that may first lead to “night blindness” followed by total blindness.
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.
Portuguese Water Dogs, especially middle-aged female dogs, are prone to a heritable form of Addison’s Disease, or Hypoadrenocorticism. Hypoadrenocorticism occurs due to a lack of hormones produced by the adrenal glands. The most commonly seen clinical signs with this condition include sudden collapse, hypotension, diarrhea, and/or vomiting with progressive weakness.
Aiello, Susan, Ed. The Merck Veterinary Manual. 8th Edition. Merck and Co. Publishing. 1998. P. 908
Bruyette, David. “Managing Atypical and Critical Cases of Primary Hypoadrenocorticism in Dogs.” Veterinary Medicine. December 2008. Pp. 650-651.
Ettinger, Stephen and Edward Feldman. Textbook of Veterinary Internal Medicine. 5th Edition. Vol. 1. W.B. Saunders Co. 2000. P. 590.
Scott-Moncrieff C. “Update on the Diagnosis of Addison’s Disease. NAVC PROC. 2009. Pp. 409-412.