Update On Sebaceous Adenitis
Poodle Club of America, June, 2006

Some 20 years after veterinary literature first described sebaceous adenitis, SA remains quite a mystery to Standard Poodle breeders. For example, consider Michael, born in 1990 as part of the sebaceous adenitis test litter. Michael developed clinical SA when he began losing hair at about age 2 and for the next few years had a very sparse coat. With regular oil baths, however, he had no scales, thickened skin or odor. Oil baths stopped at age 6 when he was put on a topical flea preventive, and Michael then surprised his family by re-growing coat that was soft and yet appeared normal for the rest of his 14 years.

Consider also the Poodles that develop clinical SA well before reaching their second birthday, contrasted with those that test "affected" in routine SA screening but never show clinical signs of disease. Or consider anecdotes of affected dogs re-growing hair after an upgrade in diet or other environmental change. Then there's the invasive and expensive skin-punch test that can miss lesions and yield a false-negative result. Yet that screening test is the best tool breeders have, augmented by pedigree study and risk-assessment strategies, when making breeding decisions.

Things may change soon. Robert Dunstan, DVM, MS, DACVP, a respected dermatopathologist well known in the Poodle world, was among the first researchers using DNA technology to investigate SA. Early pedigree data and the Standard Poodle test-litter breeding suggested a simple autosomal recessive inheritance, in which puppies receiving the defective gene from both parents will be affected with the disorder.

"The biggest problem with this disease, as everybody found out, is that SA almost follows a clear autosomal recessive pattern, but not quite," Dr. Dunstan says. "So some other factor is determining the severity or initial expression that nobody has figured out—either one gene with another factor, or more than one gene associated with the disease. Other factors, even environment, are clearly at work. It's not just that you have it or you don't."

Early SA gene-mapping studies made little headway, Dr. Dunstan notes, but he is optimistic that dramatic advances being made in DNA technology will allow researchers to solve the puzzle of SA genetics. A more complete map of the entire canine genome, reported in the December 8, 2005 issue of the journal Nature, was an exciting step. New gene-sleuthing tools based on that map are becoming available and may even allow scientists to close in on the multiple genes involved in polygenic disorders such as hip dysplasia.

At least two research teams are using this evolving technology to study SA. In Germany, a group is looking at SA in Akitas. In the United Kingdom, researchers with the Animal Health Trust are studying Poodles in a project supported by the Standard Poodle Club.

Pending progress in gene mapping, skin-punch evaluation for inflamed sebaceous glands remains the gold standard as a screening and diagnostic test (procedure at OFA). Early studies looking at levels of certain lipids (fats) in ear sebum to detect signs of SA were discontinued. Dr. Dunstan's current research includes studies of human sebaceous glands using lipid-analysis techniques that--like DNA technology--have advanced dramatically. He thinks development of an SA test using this approach would now be possible.

In the treatment realm, a recent study found that long-term cyclosporine therapy in dogs with SA could reduce inflammation (Journal of the AVMA, January 1, 2005). Regular oil baths, however, appear to help most Poodles with clinical SA and remain the most commonly used treatment after any skin infection is cleared with antibiotics. You can find an example of oil bath methods on the Versatility in Poodles web site.