W.U.A.C. World Union of Akita Clubs

Sebaceous Adenitis – Realities in Akita dogs

W.U.A.C. Meeting 2007 Wiesbaden
By Ina Pfeiffer, Tina Roth and Robin Wellmann

In 1985 the first report about Sebaceous Adenitis (SA) was published.

SA is an uncommon inflammatory disease centred on the destruction of the sebaceous glands. The disease has been reported in many different dog breeds and also in mixed breeds. Nevertheless, a predisposition of Akita, Poodles, Hovawart, Vizsla and Samojede is known. In the United States SA affected dogs were collected in a database administrated by the Orthopedic Foundation of America.

Today only one skin disease, coupled with attacked glands was described in veterinary medicine literature: "Sebaceous Adenitis"

The following part explains the actual situation of the scientific investigations / knowledge.

Sebaceous Adenitis

In general, typical outer signs of Sebaceous Adenitis are, the coat is dull, dry and fragile like moth-eaten and the odor of the dog changes: They smell like “three days worn socks ".

The first signs of the disease are subtile and appear at the head, the ears and in the trunk. The hair seems thinner, almost "similarly to moth damage". In some cases the coat-colour changes.

SA is normally nonpruritic unless there is a secondary staphyloccal skin infection and even furunculosis may develop.

As already mentioned, different inflammation degrees of the skin can be ascertained by microscopic investigations. At the beginning of the disease, histopathologic findings demonstrate different cell-types of the immune system in the sebaceous glands. The cells were described as perifollicular granulomes (aggregations of many cells). The aggregations consist of defensive cells, macrophages, lymphocytes, plasma cells and neutrophile granulocytes.

As microscopic investigations (histological examinations) of skin biopsies pointed out, the inflammation character of SA goes through several different stages. Only after complete loss of the sebaceous glands the inflammation intensity decreases.

The etiology of microscopic investigations showed cells or other components of the immune system participating massively in the destruction process. However, no bacteria, viruses or other pathogens are proven to be the cause of the disease, but all autoimmune reactions are focused against self substances/cells.

As demonstrated by several statistical calculations (Segregation Analysis) our new investigations have shown that SA in Akitas follows an autosomal recessive inheritance (*1), a so called genodermatose.

In this context we check lots of pedigrees available from affected and non affected dogs and their relatives. Nevertheless we can exclude environmental factors as the main cause of the disease.

Beside this SA can be triggered by stress: eg. pregnancy, changes in the ownership.

Additionally no significant relations can be derived between the duration of the disease and the degree of SA. It has turned out, that it is very difficult to find out in which stage of the disease a SA-dog actually is. There are dogs with a nearly complete destruction of all glands after a time-span of 2 months. On contrary, individuals were monitored with a destruction of the glands for many years eg. 8-9 years, similar to a slowly creeping process. Typical for the disease is a very “individual character” in each case.

The reason for the destruction of the sebaceous glands, is actually unknown. In any case, no viruses, bacteria or other pathogens are observed as a primary cause.

From this point of view the scope of SA-research is actually focused on mechanisms triggering the destruction of the cells by the immune system and what kind of genetic reason(s) plays a key role.

Research

Due to the etiology of the disease microscopic investigations showed cells or other components of the immune system participating massively in the destruction process. However, no bacteria, viruses or other pathogens are proven as a cause of the disease, but the autoimmune reactions run against substances/cells of the dog.

What causes exactly the “false control” of the immune system?

Until today, the research has shown that SA positive dogs have “changes” in the blood, which we cannot assign. In the blood many components of the immune system are located. Finally these components can be found later in the sebaceous glands,- so the question is:

1. What kind of connecting links/cross-reactions exists between the immune system / blood and the sebaceous glands?
2. What kind of genetic background is responsible this process?

At the moment both questions were investigated by different methodical attempts. The organisation of immune system is very complicated and a huge number of interactions run off, so our search is multi-layered. But to observe the key and the connections to the triggered reasons, lots of investigations are necessary.

Actually we investigate a so called “Hot Spot” on genetic level, because this mutation seems to be very prominent in affected dogs. But we need more EDTA-blood samples from affected dogs to undertake a “risk calculation”.

Furthermore we need pedigrees from affected dogs with their relatives to investigate the mendelian inheritance of the disease. This pedigree information we will incorporate into our segregation matrices (statistical calculations) to generate powerful results.

But without the support of engaged breeders and Akita-friends the progress of the SA-research would not be conceivable and we thank to all who help us.

PD Dr. Ina Pfeiffer
Dipl Biol. Tina Roth
Dipl. Mathem. Robin Wellmann
Insitut for Biologie
University of Kassel
Heinrich – Plett Strasse 40
34109 Kassel
Tel 0561 804 4775
email: Dr.Ina Pfeiffer

Explanations:

*1: Autosomal recessive Inheritance:

An abnormal gene on one of the chromosomes from each parent is required to cause the disease. Dogs with only one abnormal gene in the gene pair are called carriers, but since the gene is recessive they do not exhibit the disease. In other words, the normal gene of the pair can supply the function of the gene so that the abnormal gene is described as acting in a recessive manner. BOTH parents must be carriers in order for a child to have symptoms of the disease; a child who inherits the gene from one parent will be a carrier.

*2 : Genodermatosis:
A skin condition of genetic origin.

Here you will find the publications and preliminary results of the SA-research (.pdf oder .ppt):

Sebaceous Adenitis (SA) research Wiesbaden 2007

Interim Findings Helsinki 2006

Power Point Presentation Oktober 2005

Interim Findings of the Research Project on SA 2004

Interim Findings October 2003 - February 2004