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Malassezia
dermatitis (Malasseziasis)
- a research extract
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Malassezia pachydermatis (previously known as Pityrosporum
canis) is a commensal lipophilic yeast (Guillot & Bond,
1999) found on the majority of external ear canals on the canine
species (Mason et al, 1996). M. pachydermatis has been found
on the human scalp, without clinical signs of infection (Harding
et al, 2002); it has also been isolated from equine skin, in the
groin region, although its clinical significance is currently unknown
(Nell et al, 2002).
Pathogenic invasion may occur in the superficial epidermal layers
if changes in the microclimate arise, this may be caused by increased
sebum production, moist maceration of the skin, trauma, allergies
or bacterial infection (Patterson, 1998). The invasion of M.
pachydermatis
can lead to secondary ear and skin infections (Mason et al, 1996)
such as otitis externa and seborrheic dermatitis (Lloyd, 1993).
As found in human dandruff sufferers, cutaneous sensitivity was
increased. This may be due to an impaired barrier function in the
scalp caused by a combination of reduced free fatty acids, cholesterol
and ceramides, which form a critical part of the epidermal water
barrier. This weakened barrier allowed the invasion of M.
pachydermatis
(Harding et al, 2002).
Resistance to fungal infections can be natural or acquired. Natural
resistance mechanisms such as phagocytic cells can engulf fungi,
particularly where they invade around the hair follicle and the
secretion of sebum containing fatty acids has an inhibitory effect
on fungi proliferation (Hay, 1993). However the fatty acid residues
that inhibit dermatophytes often support the growth of Malassezia
yeast (Hay, 1993).
With acquired resistance to superficial mycoses, elevated levels
of immunoglobulin E (IgE) have been associated with chronic infections
as they can trigger a rapid release of histamine (Tizard, 2000).
Patients with seborrheic dermatitis were found to have higher titres
of IgG and IgM against antigens of M.
pachydermatis
isolates. However, no correlation has been found between the development
of an antibody response and the recovery of dermatophytosis (Hay,
1993).
M.
pachydermatis
can cause a type I atopic hypersensitivity reaction in those sensitive
to its presence. Kroger et al (1996) and Chen et al (2002) suggested
that an IgE mediated immune response might be clinically important
in the pathogenesis of disease, as animals suffering with a M. pachydermatis
infection showed a greater IgE response than non infected animals.
Bond et al (1998) demonstrated that high densities of M.
pachydermatis
were not associated with serum IgA deficiency. However, dogs with
M.
pachydermatis
associated skin disorders frequently developed high serum titres
of M.
pachydermatis
-specific IgG and
modest increases of IgA in comparison to healthy dogs. Although,
high serum IgG and IgA do not prevent M.
pachydermatis-related
skin disease as chronic disease development can still occur in the
presence of these titres.
Certain healthy and also affected individuals can develop cell-mediated
immune responses to the antigens associated with this commensal
yeast. Lower stimulation indices in affected Basset Hounds indicate
that their lymphocytes were less responsive to this antigen, a difference
that may be of significance in the development of disease. However,
it was not clear whether the lower stimulation indices were a cause
or an effect of the microbial skin infection (Bond et al, 1998).
Breed predisposition to M.
pachydermatis
is thought to be due to the presence of skin folds (Guaguere &
Prelaud, 1996), with susceptible breeds including West Highland
White Terriers, Basset Hounds and Cocker Spaniels (Patterson, 1998;
Bond et al, 1998).
As the predisposing factors are general problems, M.
pachydermatis
may appear as a secondary disease, which could make diagnosis difficult.
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