Malassezia pachydermatis, a lipophilic, unipolar-budding yeast is a commensal on
canine skin and it can be isolated from the skin and ear canals of healthy dogs. A
dermatitis associated with elevated cutaneous populations of M. pachydermatis has
been increasingly recognised in the last two decades and one of the most common
underlying causes of Malassezia overgrowth in dogs is atopic dermatitis. The aim of
these studies was to investigate two aspects of the host's protective responses against
the organism - activation of a humoral immune response and thickening of the skin
by epidermal hyperplasia.
The interaction between M. pachydermatis and the host's immune system has not
been widely studied either in normal or atopic dogs. To investigate antibody
responses to M. pachydermatis, Western blotting techniques were used to detect
Malassezia-specific IgG and IgE binding proteins from M. pachydermatis in atopic
dogs with or without Malassezia dermatitis and normal dogs. By comparing the
binding activity on the immunoblots, atopic dogs with Malassezia dermatitis showed
much greater IgG and IgE responses to M. pachydermatis than normal dogs. The IgG
in sera from the majority of the atopic dogs with Malassezia dermatitis recognised a
25 kDa protein, which was only seen in less than 25 % of the atopic dogs without
Malassezia dermatitis and none of the normal dogs. Proteins of 45, 52, 56, and 63
kDa were recognised by IgE in more than 50 % of the atopic dogs with Malassezia
dermatitis, but only recognised by a minority of normal dog sera, and therefore
represented major allergens. These results suggest that Malassezia dermatitis in
atopic dogs is associated with an IgG and IgE response to the organism, with the
above proteins being most relevant in the immunological reaction.
In addition to mounting immunological responses, the skin also undergoes biological
changes in response to environmental insults. Epidermal hyperplasia is one of the
major characteristics of skin biopsies from dogs with Malassezia dermatitis. The
mechanisms by which M. pachydermatis induces epidermal lesions are not fully
understood. To investigate the role of M. pachydermatis in the pathogenesis of
epidermal hyperplasia associated with Malassezia dermatitis, a colourimetric cell
proliferation assay was developed to evaluate the effect of extracts and culture
supernatants from M. pachydermatis on proliferation of canine keratinocytes in vitro.
Malassezia extracts, either with or without protease inhibitors, and culture
supernatants from the yeast, did not affect the proliferation of normal canine
keratinocytes in vitro. To further investigate the response of a direct interaction
between canine keratinocytes and live Malassezia organisms, an in vitro co-culture
system was developed. The proliferative response of the keratinocytes was assessed
using direct manual counting and immunohistochemistry techniques. Malassezia
organisms did not cause keratinocyte proliferation, but they induced keratinocyte
detachment from the substratum and cell death. These results suggest that the
epidermal hyperplasia seen in dogs with Malassezia dermatitis is unlikely to be
caused by a direct effect of the organism on the keratinocyte cell cycle, but is likely
to involve other mechanisms.
These studies provide further information regarding the host response to M.
pachydermatis, and suggest possible mechanisms by which overgrowth of
Malassezia organisms causes pathological changes in the skin of dogs.