Microsoft word - sebaceaous adenitis 16 02 06.doc
“Sebaceaous Adenitis” – a mysterious skin disease
Sebaceous adenitis (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, Hovawart, Vizsla and Samojede is known.
The following part explains the actual status of scientific investigations/knowledge.
As already mentioned, the sebaceaous glands have a central meaning in SA. The
sebaceous glands (Glandulae sebaceae) are localized superficially in the hairy skin
of dogs. They have an execution way to the skin surface, the epidermis. Via this
connection (duct) the glands empty the sebum (2).
The oily sebum can be found on the surface of the skin and hair. This emulsion
ordinarily serves not only for regularization of the humidity of the skin, but trains a
physically chemical barrier against potential pathogens. Furthermore the sebum
consists of inorganic salts and proteins, as well as interferons and immunoglobulines.
This comprehensive protection mechanism guarantee against external causes.
Additionally, this function is supported by many released fatty acids.
It was found that the number and size of the sebaceous glands vary over the body
regions of a dog. Especially large sebaceaous glands are localized at the chin. In the
neck and in the region of tale also a high number of sebaceaous glands were
However, in the toes and soles bale, nipples and in the nasal mirror there were no
sebaceaous glands found.
Today only one skin disease, coupled with attacked sebaceaous glands, was
described in veterinary medicine literature: "The sebaceous adenitis " Sebaceous Adenitis
The Sebaceaous Adenistis is a primary, selective inflammation reaction against the
sebaceaous glands. Although the disease has been reported in more than 50 other
breeds, cats and rabbits (1,2.3). This illness can lead to the entire loss of the glands.
The loss of the secretion does not seem to impair the hair growth. In more chronic
cases the hair coat may become thin. The remaining hairs tend to have an adhered
cast of follicular debris around the root.
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 sebaceaous glands the inflammation intensity decreases.
Clinically the skin seems dry and scaly combined with many hairless places.
In general, the coat is dull, dry and fragile. In addition the smell of the dogs’ changes:
They smell like “three days carried socks ".
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 sebaceaous
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.
The hair follicles themselves seem to be not involved in the process. In the final stage
of the disease all above mentioned immune cells have destroyed the sebaceous
glands and microscopically no more gland-structure was recognizable (1). Young
adult to middle-aged dogs are most commonly affected and no sex predisposition
has been noted. Fig: 1
Anatomy of the sebaceaous gland
The first signs of the disease may be 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. Fig.: 2
Clump of hairs (2)
The reason why sebaceous glands are attacked, is actually unknown. In any case,
no viruses, bacteria or other pathogens are observed as a primary cause.
As shown in poodles SA follows an autosomal recessive inheritance *1
, a so
called genodermatose *2
(3). Furthermore it is supposed that also stress situations
can trigger SA. However, cases of glucocorticoide medication seems to be also
relevant for SA.
In addition 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 timespan of 2 months. On contrary, individuals were
monitored with a destruction of the glands for many years, similar to a creeping
process. The disease has a very individual character (3). In some cases all cells of a
gland were destroyed, and regeneration became impossible. But in advanced SA
there are no gland-cell reminants.
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
For the etiology of the disease microscopic investigations showed cells or other
components of the immune system participate 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 belonging to
body of the dog.
Interesting in this context was that, immunsuppressive drugs (Cylosporin=
Glucocorticoids *3 ) switched off the autoimmune attack and the disease delayed. On
contrary when the drug was set down, the SA-dog falls back and the disease
What causes exactly the false control of the immune system?
Until now the research has shown that SA positive dogs have changes in the
which we cannot assign. In the blood many components of the immune
system are transported. Finally these components can be found again later in the
sebaceous glands, so the question is:
1. What sort of connections exists between the immune system / blood and the
2. What sort of genetic background triggers 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 the search for causes is multi-layered. But to find the key and
the connections to the genetically triggered reasons, lots of investigations are necessary. Without 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.
Linek M, Boss C, Haemmerling R, Hewicker-Trautwein M, Mecklenburg L.:
“Effects of cyclosporine A on clinical and histologic abnormalities in dogs with sebaceous adenitis”.
J Am Vet Med Assoc. 2005
Jan 1;226(1):59-64 (2)
Sousa CA.: „Sebaceous adenitis“.
Vet Clin North Am Small Anim Pract. 2006
Reichler IM, Hauser B, Schiller I, Dunstan RW, Credille KM, Binder H, Glaus T, Arnold S.:”
Sebaceous adenitis in the Akita: clinical observations, histopathology and heredity”
Vet Dermatol. 2001
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.
A skin condition of genetic origin. *3 :
Glucocorticoids are a class of steroid hormones characterised by an ability to bind with the cortisol receptor and trigger similar effects. Glucocorticoids are distinguished from mineralocorticoids and sex steroids by the specific receptors, target cells, and effects. Technically, the term corticosteroid refers to both glucocorticoids and mineralocorticoids, but is often used as a synonym for glucocorticoid. The name glucocorticoid derives from early observations that these hormones were involved in glucose metabolism. In the fasted state, cortisol stimulates several processes that collectively serve to increase and maintain normal concentrations of glucose in blood.
Glucocorticoids have potent anti-inflammatory and immunosuppressive properties
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