The Biology of Malassezia Organisms and Their Ability To Induce Immune Responses and Skin Disease (Pages 4-26)

Veterinary Dermatology 2005, 16, 426
Review
Blackwell Publishing, Ltd.
The biology of Malassezia organisms and their ability to induce

immune responses and skin disease
TAI-AN CHEN and PETER B. HILL
Division of Veterinary Clinical Studies, Royal (Dick) School of Veterinary Studies, The University of Edinburgh,
UK
(Received 9 December 2003; accepted 11 February 2004)
TABLE O F CONT E NT S
Introduction
History and taxonomy of the genus Malassezia
Biological characteristics of Malassezia organisms
Structure
Reproduction
Biochemistry
Distribution of Malassezia organisms on the host
Immunological and epidermal responses to
Malassezia organisms
The immune response to Malassezia organisms
Antigen release, penetration and presentation
Cell-mediated immune responses
IgG, IgM and IgA responses to Malassezia
organisms
IgE responses to Malassezia organisms
Mast cell responses
Epidermal responses associated with Malassezia
dermatitis
4
5
5
5
6
6
6
7
7
8
8
9
10
11
12
I N TRO D U CTI ON
The genus Malassezia is now known to include seven
species of yeast, many of which have been associated
with various diseases in humans and dogs. Malassezia
pachydermatis is a lipophilic budding yeast that colonizes the skin and mucosal sites of healthy dogs.1,2
Despite being part of the normal cutaneous microflora, it is now known that the yeast may become a
pathogen under certain circumstances. Malassezia dermatitis, an inflammatory dermatosis associated with
elevated populations of M. pachydermatis on the skin
of dogs, has been recognized with increasing frequency.
Correspondence: P. B. Hill, Division of Veterinary Clinical Studies,

Hospital for Small Animals, Royal (Dick) School of Veterinary
Studies, Easter Bush Veterinary Centre, Edinburgh EH25 9RG, UK.
E-mail: p.b.hill@ed.ac.uk
4
Malassezia organisms as pathogens in humans and

animals
Diseases associated with Malassezia spp. in humans
Pityriasis versicolor
Malassezia folliculitis
Seborrheic dermatitis and dandruff
Atopic dermatitis
Malassezia fungaemia
Diseases associated with Malassezia spp. in animals
Malassezia dermatitis in dogs
Predisposing factors for overgrowth of Malassezia
pachydermatis
Pathogenesis
Clinical features
Diagnosis
Treatment
Conclusions
References
13
13
13
13
14
14
14
15
15
15
16
16
17
18
19
19
Its importance in canine dermatology can be illustrated by the continuous rise in the number of articles
on this condition in the literature since it was first
described by Dufait in 1983.3
The interaction between Malassezia yeasts and their
host species has been studied extensively in humans but
less widely in dogs. In this article, we describe the basic
taxonomy and biology of Malassezia yeasts and review
current knowledge on the interplay between the organism and the skins protective responses. These include
cutaneous and systemic immune responses and the
protective barrier afforded by the epidermis. Failure of
these mechanisms to protect the host against proliferation of the organism can lead to pathogenicity and various disease states. In some cases, these responses are
actually deleterious and can lead to hypersensitivity
reactions or epidermal pathology. We end the review by
describing the clinical aspects of diseases associated
with Malassezia organisms in humans and animals and
2005 European Society of Veterinary Dermatology
The biology and cutaneous responses to Malassezia organisms

the current treatment options that are available for
these conditions.
H ISTO RY AND TA XONOM Y OF T H E

G EN U S MA L A SSE Z IA
The taxonomy and nomenclature of the yeasts currently classified within the genus Malassezia have been
controversial since the fungus was first described in
scales from lesions of pityriasis (tinea) versicolor by
Eichstedt in 1846.4 Because of the presence of filaments
associated with the yeasts, the organism was primarily
considered as a new species of dermatophyte and was
designated Microsporum furfur by Robin in 1853.5
Baillon renamed this filamentous fungus Malassezia
furfur in 1889.6,7 However, Malassez, in 1874, had
described ovoid-shaped cells without hyphae in scales
from humans with dandruff, and this organism was
named Pityrosporum malassezii by Sabouraud in 1904.
It was later referred to as Pityrosporum ovale by
Castellani and Chambers in 1913.8 These were initially
considered as two different organisms because hyphal
forms were rarely observed in cases of dandruff and
Pityrosporum did not produce hyphae in cultures.
The yeast and mycelial forms were later thought
to be related and were first classified into the same
genus by Panja in 1927.7 In 1951, Gordon9 cultured a
round-shaped organism from patients with pityriasis
versicolor, which he named Pityrosporum orbiculare.
By using a variety of culture conditions, induction of
P. ovale and P. orbiculare to produce hyphae was
demonstrated in the 1970s and the hyphae were indistinguishable from those seen in cases of pityriasis
versicolor.10,11 This confirmed the dimorphic nature of
Malassezia organisms and led to the suggestion that
round and oval yeast forms and hyphae represented
different stages of the life cycle.12 The two genera were
later unified with the acceptance of the species name
Malassezia furfur (including P. ovale, P. orbiculare, and
M. furfur) by the International Commission on the
Taxonomy of Fungi in 1986.13 Despite this, many
workers continued to differentiate strains on the basis
of cellular and colonial morphologies, and the names
P. ovale and P. orbiculare were still widely used in the
literature. Due to the heterogeneity of this organism,
Midgley14 maintained two species, P. ovale and P.
orbiculare, and subdivided the former into three forms
(P. ovale forms 13). Based on the serological differences determined by cell surface antigens, Cunningham et al.15 designated three serovars A, B and C
within the taxon M. furfur.
Malassezia pachydermatis was first identified in 1925
from scales on an Indian rhinoceros with exfoliative
dermatitis.16 Because of its resemblance to P. ovale but
its smaller size, Weidman16 proposed the name Pityrosporum pachydermatis for this organism. In 1955,
round or oval-shaped yeasts showing unipolar budding
were isolated from dogs with otitis externa by Gustafson,17 and he related them to the genus Pityrosporum.
In contrast to the lipid dependency of P. ovale and P.

orbiculare, these strains did not require lipid supplementation for growth. Gustafson therefore named his
isolates Pityrosporum canis. Nonlipid dependent yeasts
were also isolated from the ear canals of both healthy
dogs and dogs with otitis externa by Fraser;18 he
termed them P. pachydermatis because of the similarity
to the isolates described by Weidman.16 Subsequently,
all strains of Pityrosporum that were able to grow on
media without lipid supplementation were assigned to
a single species, P. pachydermatis, by Slooff.8 After unification of the two genera Pityrosporum and Malassezia in 1986,13 the name Malassezia pachydermatis
was adopted.
Since 1990, the use of genomic analysis has led to a
much clearer classification of the yeasts under the
genus Malassezia. Another lipid-dependent budding
yeast, Malassezia sympodialis, was defined by Simmons and Guho in 1990, based on the difference in
the percentage of guanine and cytosine in the DNA (%
GC) compared to M. furfur.19 Using genomic comparison and ribosomal large subunit sequencing, lipiddependent Malassezia yeasts were further classified
into six distinct taxa by Guho et al. in 1996, including
M. furfur, M. sympodialis and four new species, M. globosa, M. obtusa, M. restricta and M. slooffiae, resulting
in seven species under the genus Malassezia including
M. pachydermatis.20 Seven sequence types (named
sequevars IaIg) were also detected within the species
M. pachydermatis using ribosomal large subunit
sequencing.21
In addition to the currently accepted seven Malassezia species, two novel species have recently been
reported to be genetically different from existing species. Nell et al.22 isolated Malassezia yeasts from the
skin of healthy horses and they proposed the name
M. equi for a species that required lipid for growth on
Sabourauds dextrose agar, although further taxonomic studies are required to precisely identify this
organism. The other new species was found on the skin
of human patients with atopic dermatitis and the name
M. dermatis was proposed for the isolates.23 The clinical significance of this species is currently unknown.
B IO LO G IC A L C H A R AC T E R IST ICS
O F M A L A S S E Z IA O RG A N ISM S
Structure
The microscopic appearance of Malassezia organisms
is well known to veterinary dermatologists who visualize it regularly in samples obtained from clinical cases.
Malassezia pachydermatis is oval to peanut-shaped and
is approximately 23 m in width and 45 m in
length.1 Other species may differ slightly from this in
shape and size. A characteristic feature of the genus
Malassezia is its cell wall structure. Ultrastructurally,
the cell wall of Malassezia species is relatively thick (up
to 0.25 m) compared to other yeasts and is multilayered.2426 It constitutes 2637% of the cell volume.27
2005 European Society of Veterinary Dermatology, Veterinary Dermatology, 16, 426
T-A Chen and PB Hill
Around the cell wall there is an outer lamellar layer, the

structure of which varies depending on the lipid
sources in the medium. It is suggested that this lamellar
layer contains lipid and may play a role in the adhesion
process.26
The inner surface of the cell wall is corrugated,
which corresponds to invaginations of the closely
adherent plasma membrane.24,26,28 Cytoplasmic
organelles that have been described include a nucleus,
vacuoles containing lipid, and mitochondria.24,28 It has
been shown that the number of mitochondria possessed by round cells (P. orbiculare) is different from
that of oval cells (P. ovale). The former cells contain
approximately three mitochondria per cell, which
increase in volume rather than number during growth.
In contrast, there are approximately 23 mitochondria
in an oval cell and they increase in number rather than
size during growth.27 However, electron microscopic
observations do not reveal noticeable differences in
the mitochondrial appearance between P. ovale and
P. canis (M. pachydermatis).24
Reproduction
The proliferation of Malassezia yeasts is of clinical relevance because it is often overgrowth of the organism
that leads to disease. Yeasts of the genus Malassezia
reproduce by unipolar or sympodial (M. sympodialis)
budding and the budding process described for P.
ovale, P. orbiculare and M. pachydermatis is very similar.19,24,25,27 However, the budding base of M. pachydermatis (0.91.1 m in diameter) is broader than that
of P. ovale and P. orbiculare (0.50.7 m).25,27
Nishimura et al.25 precisely described the budding
process of M. pachydermatis in stages. The budding
yeast first forms an ear-like structure separating from
the cell wall. This structure grows outwards followed
by protrusion of the cytoplasm and dimpling of the cell
wall. The cell wall of the daughter cell then becomes
thicker, layered and serrated as it grows. When the
daughter cell is as long as the mother cell, a narrow
lumen forms in the cross-wall and fission takes place.
The bud is then completely released leaving the ear-like
structure as a bud scar.
Biochemistry
Lipid-dependent Malassezia species have been reported to elaborate a range of enzymes. These enzymes
have been the subject of recent interest because they
may be involved in the pathogenesis of clinical disease
states. Lipase activity has been demonstrated within
the cell wall and at the membrane sites of the yeast
in vitro using histochemical techniques and electron
microscopy. This suggests that this enzyme is synthesized intracellularly and exported to the cell surface.29
It has also been found that the fatty acid composition
of the cell varies depending on the lipid supplementation present in the medium, indicating that fatty acids
are required for membrane synthesis.30 The lipoxygenase activity of the yeast has been proposed to be
involved in the pathological changes associated with
pityriasis versicolor.31,32 Increased levels of lipoperoxides were detected in lipids from lesional but not nonlesional skin of patients with pityriasis versicolor.32
The by-products of lipoperoxidation induced by lipoxygenase activity of the yeast were considered to cause
damage to melanocytes, resulting in the hypopigmentation seen in pityriasis versicolor.31 In vitro, M. furfur
also produces phospholipases,33,34 the activity of which
was demonstrated to cause the release of arachidonic
acid from human epithelial cell lines, a mechanism by
which Malassezia organisms may trigger inflammation
in the skin.35 In addition to the enzymes described above,
Malassezia organisms produce azelaic acid in cultures
supplemented with oleic acid.36 Azelaic acid is an inhibitor of tyrosinase, an enzyme involved in the production of melanin, indicating that the production of azelaic
acid by Malassezia organisms may also play a role in
the pathological changes of pityriasis versicolor.36
M. pachydermatis has also been demonstrated to
produce various enzymes in vitro, including alkaline
and acid phosphatase, chondroitin-sulphatase,
esterase, esterase lipase, galactosidase, glucosidase,
hyaluronidase, leucine arylamidase, lipase, lecithinase,
peroxidase, phosphoamidase, phospholipase, phosphohydrolase, protease and urease.1,2,3740 Lipase was
found to be predominantly associated with the cell
membrane of M. pachydermatis, whereas protease is
secreted by the yeast.40 No significant difference was
found in the production of chondroitin-sulphatase,
hyaluronidase, phospholipase and protease by M.
pachydermatis strains isolated from dogs with otitis or
dermatitis.37 When cultured in liquid media, the activities of alkaline phosphatase and esterase lipase in the
culture supernatants from M. pachydermatis were significantly greater than that in the cell suspension. Furthermore, significantly greater activity of C4 esterase
was detected in cell suspensions of M. pachydermatis
strains obtained from healthy dogs compared to those
from dogs with dermatitis.2
D IST R IBU T IO N O F M A L A SS E Z IA
O RG A N IS M S O N T H E H O S T
Unlike many bacteria and other fungi, Malassezia
yeasts are rarely found in the environment.1,14 Their
habitat is primarily the skin and mucosae of mammals
and birds.1,14 Lipid-dependent Malassezia organisms
are frequently isolated from human skin. In a study
involving 200 healthy volunteers, Bandhaya41 isolated
Malassezia furfur from 10 different skin sites in every
individual, with the highest counts being on the head
and upper trunk. M. pachydermatis was only isolated
from 12% of the subjects.41
In healthy dogs, M. pachydermatis can be isolated
from the ear canal, anus, rectum, oral cavity and, less
commonly, the nose and vagina.4245 On normal canine
skin, carriage of the yeast is most common in the interdigital areas and around the mouth but uncommon
on the axilla, groin or dorsum.45,46 Interestingly, the

frequency of isolation and colony counts from the skin
and mucosal sites of Basset hounds, a breed predisposed to developing Malassezia dermatitis, are significantly higher than on other breeds.47 M. pachydermatis
is thought to adhere to the skin surface via trypsinsensitive protein adhesion molecules.48
In other species, Malassezia organisms have been
recovered from the skin of healthy cats, ferrets, foxes,
bears, pigs, horses, birds and rhinoceroses.1,4954
IMMU N O LOGI C A L AND

EPID ERMAL RE SP ONSE S TO
MALASSEZIA ORGANI SMS
The skin is continually challenged by a variety of environmental hazards. The first line of defence and protection is provided by the epidermis, the outermost skin
layer.55 The epidermis protects the body from water loss,
UV damage, mechanical injury, microbiological invasion, and immunological insults. The predominant cell
type of the epidermis, the keratinocyte, provides mechanical protection from parasites and micro-organisms,
and it also forms the first line of immunological
defence against environmental or microbiological antigens and allergens.56
The skin tends to respond to environmental insults
by activating the skin immune system and increasing
the thickness of the skin. The former mechanism
results in cutaneous inflammation; the latter results
from increased proliferation of cells in the basal layer
of the epidermis, leading to epidermal hyperplasia,
hyperkeratosis and lichenification. Inflammation and
lichenification are both generally seen in the skin of
dogs with Malassezia dermatitis, indicating that both
of these protective mechanisms are involved in the
disease process.
The immune response to Malassezia organisms

The skin immune system consists of cells residing in the
skin including keratinocytes, Langerhans cells, dermal
dendrocytes and mast cells, as well as skin-seeking T
lymphocytes and endothelial cells of cutaneous postcapillary venules.57 It functions in conjunction with
humoral substances, such as secretory immunoglobulins and cytokines, to deal with challenges from both
exogenous and endogenous antigens, to mount effector
responses of various types, and to balance the response
in order to minimize tissue damage whilst eliminating
the original insult.57 Defects in both innate and
acquired immune responses may lead to the development of skin diseases.
Based on information from existing immunological
literature related to other organisms or antigens, we
can formulate a hypothesis to explain the mechanisms
by which Malassezia pachydermatis might interact
with the cutaneous immune system in dogs (summarized in Fig. 1). In this scheme, it is postulated that M.
pachydermatis on the skin surface would produce antigens that could penetrate the skin and be captured by
epidermal Langerhans cells or dermal dendritic antigenpresenting cells. These cells would then migrate to
regional lymph nodes and present the antigen to a T
lymphocyte via a major histocompatibility complex
(MHC) class II molecule, which, in co-operation with
different environmental cytokines, would stimulate T
helper (Th) 0 precursor cells to differentiate into Th1
cells and/or Th2 cells. A cytokine environment dominated by IL-12 would favour Th1 cell development,
whereas IL-4 and IL-13 would stimulate the development of Th2 cells. T helper cells would activate B
lymphocytes and stimulate them to differentiate into
antibody-forming plasma cells. By secreting IL-2 and
IFN-, Th1 cells would promote IgG production,
whereas IL-4 and IL-13 from Th 2 cells would promote
Figure 1. Possible pathways for

immunological responses stimulated by
Malassezia organisms. Malassezia organisms
on the skin surface might release antigens
(Ag) that penetrate the skin and be captured
by an antigen-presenting cell (APC). The
APC would then present the antigens to a
T lymphocyte. The cytokines present in the
environment determine which T cell subset is
produced from Th0 cells. IL-12 stimulates
development of T helper 1 (Th1) cells. IL-4
and IL-13 favour the production of T helper
2 (Th2) cells. Th1 cells secrete IL-2 and IFN that induce IgG responses. Malasseziaspecific IgG might be protective or activate
complement, provoking inflammation.
Th2 cells secrete IL-4 and IL-13 that induce
allergen-specific IgE responses. The IgE
antibodies bind to mast cells (MC) and upon
subsequent encounter with allergens, trigger
degranulation leading to inflammation and
clinical features of Type I hypersensitivity
reactions.
immunoglobulin class switching to IgE. It is important

to remember that development of Th subsets into two
polarized subgroups with divergent cytokine responses
does not necessarily occur in immunological reactions
and both mechanisms can occur concurrently. The
production of Malassezia-specific IgG antibodies
could potentially provide a degree of protective immunity against Malassezia organisms. Alternatively, these
antibodies might activate the complement system causing epidermal damage and inflammation. The development of allergen-specific IgE antibodies could lead to
sensitization of cutaneous mast cells. Subsequent
exposure to Malassezia allergens could cross-link
surface-bound IgE and trigger the release of a variety of
inflammatory mediators, resulting in the clinical signs
of Type I hypersensitivity reactions (Fig. 1). To date,
only certain parts of the mechanisms described in the
above hypothesis have been investigated in dogs. These
include cell-mediated immune responses, humoral
immune responses, and mast cell responses to M. pachydermatis. The evidence in the literature to support various aspects of the proposed pathways described above
is reviewed in the following sections.
Antigen release, penetration and presentation

It has been suggested that entry through the skin is the
most likely mechanism by which Malassezia organisms
stimulate the immune system in human patients with
atopic dermatitis.58 A recent study demonstrated that
M. furfur was able to invade human keratinocytes
and resist phagolysosome fusion.59 It has also been
reported that the first cloned Malassezia allergen (Mal
s 1), a major allergen that is localized to the cell wall,
can be released into the culture medium when grown
in vitro.58 These findings support the hypothesis that
Malassezia organisms can penetrate the epidermal
barrier and probably release allergens in the skin,
where both whole organisms and allergenic components would come into contact with Langerhans cells
in the epidermis. Uptake of whole M. furfur yeast cells
and various allergenic components from the yeast,
including M. furfur extracts, recombinant M. furfur
allergen 5 (Mal f 5) and M. furfur mannan, has been
demonstrated in vitro using immature monocytederived dendritic cells (MDDCs), which reflect Langerhans cells in the skin.60 These results suggest that
sensitization of atopic patients to M. furfur can be
mediated by immature dendritic cells in the absence of
IgE in the skin. The internalization was shown to occur
via binding to the mannose receptor (other receptors
may also be involved) or pinocytosis.60 The presence
of M. furfur was also shown to induce maturation of
immature MDDCs by up-regulation of CD83 expression, and increase in expression of the costimulatory
molecules CD80 and CD86.61 Mature dendritic cells
are poor at antigen uptake, but excellent at presenting
antigens. They would therefore efficiently present antigen-derived peptides on MHC molecules to T cells.62
There is some evidence that suggests the interaction
between Malassezia antigen-bearing antigen-presenting
cells (APCs) and T cells takes place in the skin. An infiltration of CD4+ T cells has been detected at 24 h at
patch test sites in P. orbiculare patch test-positive,
atopic dermatitis patients, but was more pronounced at
72 h.63 The expression of intercelluar adhesion molecule (ICAM)-1 and human leucocyte antigen (HLA)DR in the dermis of these patients was also upregulated. At 24 h post-test, the former correlated with
the scale of the dermal CD3+ lymphocytic infiltrates,
with the majority being CD4+.63
To date, the release, penetration and presentation of
Malassezia antigens in the skin of dogs has not been
studied. However, it has been demonstrated that application of M. pachydermatis suspensions on healthy dog
skin can induce skin lesions similar to those observed
in naturally occurring Malassezia dermatitis.64 This
indicates that Malassezia antigens and/or organisms
may be able to penetrate into the skin, thus inducing
pathogenic effects. Also, there are some data providing
indirect evidence for a transepidermal route of antigen
penetration in dogs with atopic dermatitis. Higher
numbers of Langerhans cells have been detected in
lesional atopic skin compared to clinically normal
atopic or normal control canine skin.65,66 These cells
were present in clusters in lesional skin of dogs with
atopic dermatitis.67 Expression of surface IgE has also
been observed on epidermal Langerhans cells in
lesional atopic canine skin,66 and these cells are responsible for allergen capture and presentation.67 Moreover, eosinophils can be seen below the stratum
corneum in lesional atopic canine skin, but not in clinically normal atopic skin.68 Canine atopic skin also
exhibits hyperplasia of T lymphocytes expressing the
gamma-delta T-cell receptor.68 Furthermore, transepidermal penetration of staphylococcal antigens has
been demonstrated in dogs.69 Taken together, these
findings indicate it is likely that M. pachydermatis may
be able to release antigens that would penetrate the
skin of dogs, particularly those suffering from atopic
dermatitis, where they are captured by epidermal
APCs and thus initiate the process of antigen presentation to T cells and a cascade of immunological
responses.
Cell-mediated immune responses

T-cell-mediated immunity is important in the prevention and recovery from fungal infections.70 A
deficiency in cell-mediated responses could therefore
predispose the host to overgrowth of Malassezia
organisms.70 Cell-mediated immune responses to
Malassezia organisms have been investigated in both
humans and dogs using various assays. In order to gain
a clearer picture of cell-mediated immunity to M. furfur, Ashbee and Evans7 collated data from human subjects in various studies, ranging from 8 to 61 years of
age. They concluded that Malassezia organisms could
elicit significant cell-mediated immune responses in
healthy individuals as measured by lymphocyte transformation assays or a leucocyte migration inhibition
assay. Also, the responses were similar in different age

groups, suggesting that the level of cell-mediated
immunity to Malassezia organisms remains fairly
constant throughout life. In a recent study on cellmediated immunity to the mycelial phase of Malassezia organisms it was reported that positive responses
were detected in 75% of the healthy individuals studied, using a leucocyte migration inhibition assay.71 In
humans it has also been shown that immature MDDCs
preincubated with M. furfur induced a proliferative
response in autologous peripheral blood mononuclear
cells (PBMCs) in a dose-dependent manner.61
The proliferative response of PBMCs to Malassezia
organisms (P. orbiculare or P. ovale) in human patients
with atopic dermatitis was significantly higher than in
healthy individuals.7275 Furthermore, atopic patients
with specific IgE antibodies against P. orbiculare or
P. ovale were shown to have increased synthesis of
the Th2-related cytokines IL-4, IL-5 and IL-10 by
Pityrosporum-stimulated PBMCs.75,76 The results of
several studies investigating the correlation between
PBMC proliferation and skin test responses to Malassezia antigens are inconsistent. Some investigators
reported that a correlation was not found between the
PBMC proliferation and the skin prick test (SPT) or
atopy patch test (APT) in atopic dermatitis patients.63,72
In contrast, Johansson et al.77 showed a correlation
between PBMC proliferation in response to in vitro
stimulation with Malassezia extracts and M. furfur
APT reactions in atopic patients with positive SPT
reactions to the yeast. Additionally, both PBMC proliferation and APT reactions to Malassezia extracts
were also found to correlate with the production of the
Th2-related cytokines IL-4, IL-5 and IL-13 by PBMCs
in these patients. 77 In one study investigating Tlymphocyte clones isolated from lesional atopic skin, the
majority of the T cells that were reactive for P. orbiculare showed a Th2- or Th2/Th0-like cytokine profile.74
By examining T-cell receptor usage to determine whether
Malassezia organisms can act as superantigens, no
evidence has been found for superantigenic activity by
P. orbiculare in patients with atopic dermatitis.78
Bond et al.79 studied the cell-mediated immune
responses to M. pachydermatis in healthy dogs and
dogs with Malassezia dermatitis using a lymphocyte
proliferation assay. The PBMC proliferative responses
to M. pachydermatis antigens at a concentration of
500 g mL1 in seborrhoeic Basset hounds and Irish
setters with gluten-sensitive enteropathy were significantly lower than those in healthy Basset hounds.
There was no significant difference between the PBMC
responses of the first two groups and healthy beagles.
The responses to Malassezia antigens at 50 g mL1 in
the four groups of dogs, however, did not vary significantly. The reason for reduced PBMC responses to
M. pachydermatis in seborrhoeic Basset hounds, and
their relevance to the pathogenesis of the disease, is as
yet unclear.
The PBMC response to M. pachydermatis in atopic
dogs has also been studied recently. Atopic dogs with
cytological evidence of Malassezia overgrowth had
significantly higher PBMC responses to extracts of

M. pachydermatis than clinically normal dogs. Atopic
dogs without Malassezia overgrowth had PBMC
responses that fell between those of the above two
groups.80 A significant correlation was not found
between the PBMC proliferation and intradermal test
response to M. pachydermatis in atopic dogs in this
study.80 In another study, extracts from M. pachydermatis were shown to stimulate the proliferation of
canine PBMCs in both healthy and atopic dogs, with
or without evidence of Malassezia overgrowth, in a
dose-dependent fashion.81 In contrast to the study by
Morris et al.,80 there were no significant differences
between the various groups, suggesting that M. pachydermatis may be able to elaborate mitogens or superantigens. This would suggest that M. pachydermatis
could induce an inflammatory response in nonallergic
or nonsensitized dogs.81
IgG, IgM and IgA responses to Malassezia

organisms
Immunoglobulins specific to the yeast phase of Malassezia organisms have been studied in normal human
individuals with no history of skin disease at various
ages. Sohnle et al.82 measured IgM, IgG and IgA antibodies against Malassezia organisms by ELISA in sera
from 21 young subjects (aged 2344) and 20 elderly
subjects (aged 7088), none of whom had a history of
significant superficial fungal infections. It was found
that immunoglobulins of all three classes specific for
Malassezia organisms were present in both the young
and elderly groups, and the responses of the two groups
were very similar, except for the IgM response. The
level of Malassezia-specific IgM in the elderly group
was significantly lower than that in the young subjects.
In another study investigating Malassezia-specific IgG
in the sera of normal individuals aged between 29 and
81, the antibody titres were shown to decline with
increasing age, which paralleled the decreasing populations of Malassezia organisms detected on the skin of
elderly people.83 Lower titres of Malassezia-specific
IgG have also been reported in healthy children. Substantially lower levels of Malassezia-specific IgG were
detected in sera from five healthy 6-month-old children
compared to 10 healthy adults, but no statistical analysis was performed on the results in this study.84 Cunningham et al.85 studied IgM, IgG and IgA responses
to M. furfur serovars A, B and C in normal individuals
divided into five age groups: 23 years, 710 years, 20
24 years, 3340 years and 6064 years. There was no
significant difference in the titres of the three immunoglobulins between age groups as measured by
ELISA, except that the subjects aged between 60 and
64 had significantly lower Malassezia-specific IgM
titres than the others. The Malassezia-specific IgA level
was found to be low in all groups, suggesting that
mucosal sensitization by the yeast might not be important. Because of the difficulties in producing the mycelial phase of Malassezia organisms in vitro, very few
investigators have studied the humoral responses to the
10
mycelium of the yeast. One study reported that healthy

adults had detectable concentrations of IgM, IgG, IgG
subclasses and IgA to mycelial antigens of Malassezia
organisms in their sera, with the highest titres being
found for IgG.7
No significant difference in Malassezia-specific IgG
concentrations was found between adult patients with
atopic dermatitis and healthy individuals as measured
by in vitro serological tests.63,73 However, one study
reported significantly elevated Malassezia-specific IgG
concentrations in young adult patients with atopic
dermatitis aged between 16 and 21 years.86 The investigators proposed that this probably reflected increased
exposure to the organisms through atopic skin and a
tendency for IgG to follow IgE production. No correlation has been found between Malassezia-specific
serum IgG levels and APT responses to the yeast in
patients with atopic dermatitis.63 It is therefore considered that determination of Malassezia-specific IgG
concentrations has little value in the diagnosis of
Malassezia sensitization in atopic human patients.58,63
Bond et al.79 studied the humoral immune responses
to M. pachydermatis in healthy dogs and dogs with
Malassezia dermatitis using ELISA. Serum titres of
Malassezia-specific IgG and IgA in seborrhoeic Basset
hounds with high cutaneous populations of M. pachydermatis and affected dogs of various breeds were
found to be significantly greater than those of healthy
Basset hounds and healthy beagles. The investigators
concluded that high serum titres of IgG and IgA do not
prevent seborrhoeic dermatitis associated with M.
pachydermatis in either Basset hounds or other breeds.
Using western immunoblotting to detect IgG
responses to extracts of M. pachydermatis, four
proteins of 219, 110, 71 and 42 kDa were shown to be
recognized mainly by nonatopic dogs with Malassezia
dermatitis, compared to healthy dogs.87
Atopic dogs, with or without cytological evidence of
M. pachydermatis overgrowth, had significantly higher
serum titres of Malassezia-specific IgG than healthy
dogs as measured by ELISA.88 However, there was no
significant difference between atopic dogs with or without Malassezia overgrowth.88 By comparing the IgG
response to M. pachydermatis antigens using western
immunoblotting, a protein of 25 kDa was identified in
the majority of atopic dogs with Malassezia dermatitis,
but in only a few atopic dogs without Malassezia overgrowth and in none of the normal dogs, suggesting that
this protein may have some clinical relevance.89
In summary, it is clear that IgG responses to Malassezia yeasts are common in both healthy humans and
dogs. This probably reflects exposure of the immune
system to antigens produced by commensal organisms.
However, enhanced IgG responses can be seen in dogs
with Malassezia dermatitis and in humans and dogs
with atopic dermatitis. The role of this IgG response in
the pathogenesis of skin disease is currently unclear,
both in humans and dogs. IgG antibodies are known to
be able to act as opsonins coating micro-organisms and
to activate phagocytes, which in turn ingest and destroy
extracellular pathogens.90 This could in theory provide

protection for the host. However, as overgrowth with
Malassezia organisms does not appear to be a selfresolving condition, it seems likely that these antibodies
are not protective. Alternatively, IgG antibodies could
activate the complement system, as has been demonstrated with Pityrosporum ovale and P. orbiculare,91,92
and exacerbate the inflammatory response.90 A final
possibility is that IgG responses to the yeast are merely
an epiphenomenon and neither contribute to, nor
inhibit the ongoing disease process. Further studies are
therefore required to determine the precise role played
by these antibodies in Malassezia-induced skin disease.
IgE responses to Malassezia organisms

Using in vitro serological tests such as ELISA, the radioallergosorbent test (RAST) and western immunoblotting, Malassezia-specific IgE has been detected
in human atopic patients for over a decade. Krger
et al.76 studied the effect of Malassezia extracts on IgE
production by PBMCs in vitro. They found that IgE
synthesis by PBMCs from atopic dermatitis patients
with specific IgE for Malassezia organisms (RAST+)
was significantly higher than with RAST() atopic
dermatitis patients or normal controls as measured by
ELISA. Also, stimulation with Malassezia extracts
and IL-4 led to a dose-dependent increase in IgE synthesis from PBMCs only in RAST(+) atopic patients,
indicating a Th2-type skewed response towards Malassezia organisms in these patients.76 Several studies
comparing the titres of IgE specific to Malassezia
organisms have revealed similar results. Patients with
atopic dermatitis were found to have significantly
higher levels of Malassezia-specific IgE in their sera
compared to those with other atopic diseases or
healthy individuals.73,9395 Two studies investigating
IgE antibodies against Malassezia organisms in children and young adults (up to 21 years of age) also
showed that these antibodies were detected significantly more frequently in those with atopic dermatitis
than the other two groups.86,96 The Malassezia-specific
IgE, but not the total IgE in serum, has been found to
correlate with the degree of response to APT to Malassezia extracts at 48 h post-test in atopic dermatitis
patients.63
By using western immunoblotting to detect
Malassezia-specific IgE, and by using the criteria that
reaction of more than 50% of patients sera represents a major allergen, a number of major IgE-binding
proteins in the range of 9110 kDa have now been
documented in humans.97101 Some antigens defined as
major allergens in one study have been cited as minor
allergens by other investigators.7 This is likely to be
because of the disparity between methods and antigen
preparations used in different studies. Of the numerous
antigens documented, a limited number of antigens
have been further characterized. Nine allergens of
Malassezia furfur (Mal f 1Mal f 9) have recently been
sequenced and expressed as recombinant proteins.102106
However, the strain used in some of these studies has
11
Table 1. Three allergens of Malassezia furfur and six allergens of Malassezia sympodialis that have been sequenced and expressed as recombinant
proteins
Allergen name
MW
(kDa)
Percentage of AD
patients reacting
Mal s 1
37
70
Mal f 2
21
72
Mal f 3
20
70
Mal f 4
35
83
Mal s 5
Mal s 6
18.2
17.2
48
48
Mal s 7
Mal s 8
Mal s 9
16.2
19.2
14
40
40
24
Identity
No homology to known proteins
Membrane or secreted cell wall protein
Homology to peroxisomal membrane proteins of
Candida boidinii and Aspergillus fumigatus (Asp f 3)
Homology to peroxisomal membrane proteins of
Candida boidinii and Aspergillus fumigatus (Asp f 3)
Showing 57% homology to mitochondria malate
dehydrogenase from Saccharomyces cerevisiae
Showing 82% homology to cyclophilin from
Schizosaccharomyces pombe
AD, atopic dermatitis.
now been re-assigned to the species M. sympodialis,58

and the current nomenclature of purified Malassezia
allergens is summarized in Table 1. It is important to
note that many of the studies described above were
performed using the old classification of Malassezia
species, and therefore might reflect the characteristics
of other, more recently described Malassezia species. A
study investigating IgE binding components in five of
the seven species currently classified under the Malassezia genus, including Malassezia furfur, M. globosa,
M. restricta, M. slooffiae, and M. sympodialis, showed
that both species-specific and common antigenic components were present between species. The molecular
weights of bands most frequently recognized using the
sera of AD patients were 6772 (28%), 4550 (80%),
3540 (39%), 4346 (20%) and 1922 kDa (43%),
respectively.107 Zargari et al.108 also showed that seven
Malassezia species shared allergenic determinants to a
great extent, but also contained species-specific allergens, by measuring species-specific IgE antibodies and
performing inhibition immunoblotting. It is likely that
further studies comparing different species and the use
of molecular techniques will define more precisely the
identity of major allergens of Malassezia species.
Recently, specific IgE antibodies to M. pachydermatis in dogs have been investigated. Significantly higher
concentrations of Malassezia-specific IgE, measured
by ELISA, were detected in atopic dogs with or without Malassezia dermatitis and/or otitis than either
healthy dogs or nonatopic dogs with clinical evidence
of Malassezia overgrowth in the skin and/or ear
canals.88 However, the difference between the atopic
groups was not significant.88 By using western immunoblotting, proteins from M. pachydermatis with
molecular weights of 45, 52, 56, and 63 kDa were demonstrated to be major allergens, recognized by IgE in
more than 50% of the sera from atopic dogs with
Malassezia overgrowth.109
Hence, as with IgG responses, humans and dogs
with atopic dermatitis can develop enhanced IgE
responses to allergens derived from the yeast. The

Malassezia-specific IgE antibodies in human and
canine atopic patients could play a key role in enhancement of immune responses. In addition to their role
in mast cell-mediated inflammation (see below), the
allergen-specific IgE antibodies could bind to Langerhans cells in the skin, thus enhancing their allergen
capturing and presentation capacity upon a second
encounter with the allergen.110,111
Mast cell responses

The mast cell response to Malassezia antigens has been
investigated with intradermal tests (IDT) or skin prick
tests (SPT) in human atopic patients. One study comparing the two test methods with Malassezia extracts
showed that a higher percentage of patients with atopic
dermatitis reacted positively in IDT than in SPT.95
However, positive IDT reactions to Malassezia
extracts were also seen in some patients with other
atopic diseases, whereas all the atopic controls gave
negative results in SPT.95 Studies using SPT to detect
hypersensitivity to Malassezia organisms have shown
an increased sensitivity in patients with generalized
atopic dermatitis72,86,95 or those with lesions predominantly on the head and neck.100,112,113 The SPT results
have also been found to correlate with levels of
Malassezia-specific IgE in the serum,86,114 and with
results of basophil histamine release tests,112 but not
with the severity of atopic dermatitis.114
Positive IDT results to Malassezia extracts have also
been reported in atopic dogs. Immediate hypersensitivity responses to intradermal injections of M. pachydermatis extracts at concentrations which caused no
reaction in healthy dogs have been observed in atopic
dogs with Malassezia dermatitis, although they were
also seen in some atopic dogs without Malassezia dermatitis.115 Nevertheless, the reactivity to the extracts in
atopic dogs with cytological evidence of Malassezia
overgrowth was significantly higher than that in
atopic dogs without.115 Bond et al.116 investigated the
12
Figure 2. Possible mechanisms for the

formation of epidermal hyperplasia in
Malassezia dermatitis. Malassezia organisms
might secrete proteins or interact with
keratinocytes, which could have a direct
effect on their proliferation (upper pathway).
Alternatively, M. pachydermatis might be an
indirect factor in the proliferation of
keratinocytes. In this case, the formation of
epidermal hyperplasia could be induced by
immune responses stimulated by the
organism, or inflammation and self-trauma
caused by other underlying diseases
commonly associated with Malassezia
dermatitis.
frequency of IDT reactivity to M. pachydermatis extracts

in atopic dogs and reported similar results. In this
study, atopic dogs were not grouped according to their
cytological findings of Malassezia populations. However, the frequency of positive reactivity to the extract
in atopic dogs was found to be significantly greater
than in healthy beagles.116 In contrast, the frequency of
immediate hypersensitivity responses to M. pachydermatis extracts in nonatopic dogs with Malassezia
dermatitis is low. One recent study investigating IDT
reactivity to M. pachydermatis in eight healthy basset
hounds, 17 basset hounds with Malassezia dermatitis,
and 19 healthy beagles, reported that only two affected
basset hounds and one healthy beagle showed immediate hypersensitivity reactions.117 Additionally, a recent
report has demonstrated positive immediate hypersensitivity reactions to extracts from M. pachydermatis
using PrausnitzKstner tests.118 Clinically normal dogs
received pooled sera from atopic dogs with Malassezia
dermatitis that were IDT positive to Malassezia extracts and serum from an atopic dog with Malassezia
dermatitis exhibiting high levels of anti-Malassezia
IgE on an ELISA assay. Positive IDT responses were
observed in the recipients following subsequent injection of the yeast extract, indicating that antiMalassezia IgE antibodies are functional in Type I
hypersensitivity reactions.118 Taken together, these
findings suggest that mast cell-mediated hypersensitivity responses to M. pachydermatis allergens may be
involved in the pathogenesis, and contribute to the clinical signs, in some cases of canine atopic dermatitis.
Epidermal responses associated with Malassezia

dermatitis
The skin acts as a barrier to prevent invasion of microorganisms and its barrier function is largely provided
by the epidermis. The process by which the stratum
corneum is continually renewed by keratinization of
the epidermal cells provides a defence against cutaneous micro-organisms, including superficial fungi. The
renewing process results in continuous shedding of

the stratum corneum, which may remove fungal
micro-organisms.119
Similar to other chronic inflammatory dermatoses,
Malassezia dermatitis is often associated with epidermal hyperplasia, which is a protective mechanism seen
in the skin in response to a variety of environmental
insults. Mild epidermal hyperplasia has also been
observed at the sites of application of Malassezia
organisms to the skin surface of laboratory beagles.64
The mechanism by which epidermal hyperplasia
occurs in Malassezia dermatitis is however not completely understood. A number of hypotheses can be
drawn up to explain the hyperplasia and lichenification
seen in clinical cases of skin disease (Fig. 2). The
organism could secrete proteins capable of acting as
growth factors, and/or interact with surface molecules
of keratinocytes, which could convey signals to stimulate their proliferation. Alternatively, the organism
might play an indirect role and the epidermal hyperplasia could be caused by immune responses stimulated
by the yeast or other underlying diseases commonly
associated with Malassezia dermatitis. Many of these
underlying diseases can cause inflammation and selftrauma, which could then lead to the formation of
epidermal hyperplasia (Fig. 2).
Little is known about the direct interaction between
Malassezia organisms and keratinocytes, either in
humans or in dogs. In a preliminary report, a significant increase in a cellular proliferation marker was
demonstrated in canine keratinocytes cocultured with
M. pachydermatis compared to control cells in vitro.120
This could indicate that Malassezia organisms might
be able to activate the proliferative cell cycle of canine
keratinocytes. Recently, the epidermal dysplasia in two
West Highland white terriers with cytological evidence
of Malassezia overgrowth was reported to be reversible
after antifungal therapy,121 suggesting a possible pathogenic role of M. pachydermatis in the epidermal hyperplasia associated with Malassezia dermatitis. However,
13
in a study published more recently, we have shown that

extracts or culture supernatants from M. pachydermatis failed to stimulate the proliferation of canine keratinocytes in vitro, regardless of whether or not protease
inhibitors were present.122 We have also shown that
coculture of whole, viable M. pachydermatis organisms
with cultured canine keratinocytes in vitro did not
induce the cells to proliferate.123 These results suggest
that M. pachydermatis has no direct effect on keratinocyte proliferation (upper pathway in Fig. 2). However,
it must be borne in mind that these were in vitro studies
in which the keratinocytes were isolated from their normal environment. It is possible that M. pachydermatis
might be able to stimulate keratinocyte proliferation
directly in a living epidermis that had a blood supply
and a functional immune system. An alternative possibility is that M. pachydermatis has no direct effect on
keratinocyte proliferation either in vitro or in vivo, and
the epidermal hyperplasia seen in Malassezia dermatitis is a result of the inflammatory response stimulated
by the organism itself or the underlying diseases (lower
pathway in Fig. 2).123 Future studies using living epidermis (skin explants) or experimental dogs are therefore required to further investigate the mechanisms by
which overgrowth of M. pachydermatis might cause
epidermal hyperplasia in dogs.
MALASSEZIA ORGANI SMS AS

PATH O G ENS I N HUM A NS AND
AN IMALS
Although Malassezia organisms can be found on normal human skin, they have been implicated in a range
of both cutaneous and systemic diseases. They are
most frequently associated with pityriasis (tinea) versicolor, which is one of the most common disorders of
pigmentation seen in human dermatological clinics
worldwide. Diseases associated with Malassezia spp. in
animals have also been widely reported. In dogs, a dermatitis caused by overgrowth of M. pachydermatis on
the skin surface is recognized with increasing frequency. The pathogenic role of Malassezia spp. in various diseases is therefore a continued topic of interest in
human and veterinary medical literature.
Diseases associated with Malassezia spp. in

humans
Pityriasis versicolor. Pityriasis versicolor is a chronic
superficial fungal infection of the skin caused by
Malassezia spp. organisms.124,125 Since the differentiation of the new Malassezia species, several studies on
the mycology of pityriasis versicolor have been documented. The species that have been isolated from
patients with pityriasis versicolor include M. furfur, M.
globosa, M. restricta, M. slooffiae and M. sympodialis,
and more than one species can be found in some
patients.126129 Although some investigators have suggested that M. globosa was the causative agent of
Figure 3. Pityriasis versicolor in an adult human. Note the

multifocal patches of hypopigmentation over the trunk. Photograph
courtesy of Dr Gina Kavanagh, University of Edinburgh.
pityriasis versicolor because of its predominant presence in populations of affected patients,127 it remains to
be determined whether M. globosa is also the predominant species in the lesions of individuals. Pityriasis
versicolor most often occurs on the trunk, neck and
proximal extremities. It is characterized by scaly hypoor hyperpigmented macules and patches with minimal
pruritus (Fig. 3).130 The diagnosis can be made by
potassium hydroxide preparations of skin scrapings
or tape strippings, which reveal typical clusters of
yeasts with hyphae.124,125 There are several therapeutic
options for treating pityriasis versicolor, such as
topical treatment with lotions or creams containing
selenium, sodium thiosulphate or specific antifungal
agents, or oral medication with ketoconazole, fluconazole or itraconazole. However, relapse is very common
and prophylactic treatment may be required.125
Malassezia folliculitis. Malassezia folliculitis is characterized by follicular papules and pustules localized to
the trunk, upper arms, neck, and, less often, the face
(Fig. 4). These lesions are generally pruritic.124 Diagnosis is based on clinical signs, cytology and culture in
combination with histopathology. Budding yeasts and,
rarely, hyphae can be found in cytological samples and
14
Figure 4. Malassezia folliculitis on the upper back of an adult

human. Note the multiple papules and pustules. Malassezia
organisms can be found on cytological specimens. Photograph
courtesy of Dr Gina Kavanagh, University of Edinburgh.
Figure 6. Atopic dermatitis on the flexural surface of the elbow in an

adult human. These lesions can be colonized by Malassezia
organisms, resulting in a hypersensitivity response to allergens from
the yeast.
organisms and the severity of the diseases.135,136 The

species that have been isolated from patients with seborrheic dermatitis include M. furfur, M. globosa and
M. sympodialis, with the first two species showing
higher frequency.129 Seborrhoeic dermatitis can be
treated with topical antifungal agents, which can also
be used prophylactically to reduce the recurrence
rate.124,133
Figure 5. Seborrhoeic dermatitis on the neck of an adult human.

Note the erythema and scaling around the hair margin. Malassezia
organisms were found on stained tape strips.
in dilated follicles of biopsy sections.6,124 Although it

has been suggested that follicular occlusion was the
primary cause of Malassezia folliculitis with overgrowth of Malassezia organisms as a secondary
event,131 colonization of normal pilosebaceous units
by these yeasts can also be heavy.132 The exact role of
Malassezia organisms in Malassezia folliculitis therefore awaits further elucidation. Malassezia folliculitis
responds rapidly to antifungal therapy. It can be
treated with topical antifungal agents or with oral
azole antifungal drugs for patients who do not respond
to topical treatment. As with pityriasis versicolor,
recurrence tends to be a common problem.133
Seborrheic dermatitis and dandruff. Seborrheic dermatitis is characterized by inflammation and desquamation in areas that are rich in sebaceous glands such
as the scalp, face and upper trunk (Fig. 5), whereas
dandruff is a noninflammatory scaling condition of the
scalp. It is now generally considered that the latter is
the mildest form or a variant of seborrheic dermatitis.124,133,134 The importance of Malassezia organisms
in these two conditions has been supported by studies
demonstrating parallel decreases in the number of
Atopic dermatitis. Atopic dermatitis is a chronic,

multifactorial, inflammatory skin disease associated
with abnormal immunological regulation (Fig. 6). As
discussed in detail above, allergens from Malassezia
organisms have been implicated in its pathogenesis.58,137 The IgE response to the organism has been
investigated extensively using several diagnostic methods such as the intradermal test, skin prick test, and
ELISA. Six Malassezia species have been isolated from
patients with atopic dermatitis, including M. furfur, M.
globosa, M. restricta, M. slooffiae, M. sympodialis
and M. dermatis. However, the most frequently isolated species reported varies with different investigators.128,129,138 The respective pathogenic role of
different Malassezia spp. in atopic dermatitis remains
to be clarified. For atopic patients with a hypersensitivity response to Malassezia spp., antifungal therapy
should be included in the treatment regime.124
Malassezia fungaemia. Systemic bloodstream infection with Malassezia organisms has been recognized
for about two decades. It is related to administration of
lipids through intravenous catheters, especially to
infants in intensive care units. M. furfur and M. pachydermatis are the only two species that have been
reported to cause systemic disease, and the latter is
considered to be transferred from a household pet as it
is rarely isolated from normal human skin.139142 However, other Malassezia spp. might also be involved but
were not recognized before the new taxonomy was
adopted. Many blood culture systems do not effectively
15
support the growth of lipid-dependent Malassezia

spp. and this may also hinder the identification.143 The
catheter has to be removed if antifungal therapy is
unsuccessful, possibly because of incomplete penetration of drugs to organisms that are embedded in the
catheter.4,7
In addition to the diseases described above, the isolation of Malassezia spp. from a range of other human
skin conditions including psoriasis, otitis and acne has
also been reported.7,143,144
Diseases associated with Malassezia spp. in

animals
An Indian rhinoceros with exfoliative dermatitis was
the first case of skin disease that was reported to be
associated with M. pachydermatis.16 More recently,
similar lesions have been observed in a southern white
rhinoceros.145 Malassezia organisms have also been
found in a variety of other animals with diseases.
Nonlipid-dependent Malassezia yeasts were recently
isolated from a horse showing an erythematous patch
of alopecia on the face, which responded well to a miconazole/chlorhexidine shampoo.146 M. pachydermatisassociated dermatitis has also been reported in sea
lions.147,148 In addition to dogs and cats, otitis externa
caused by M. pachydermatis has been described in ferrets, fennecs, pigs and dromedaries.1,149 In contrast, the
species that have been isolated from cattle with otitis
are M. globosa, M. sympodialis, M. furfur and M.
slooffiae, with higher frequencies seen with the first two
species.150,151 A case of noncutaneous disease has been
documented in a macaw with an ulcer in the crop from
which M. pachydermatis was isolated.152
In contrast to dogs, in which Malassezia dermatitis
and otitis are frequently diagnosed, these conditions
are less common in cats. The clinical signs in cats
include pruritus, erythema, self-excoriation, and less
commonly lichenification (Fig. 7).153 M. pachydermatis has also been associated with feline chin acne.154
Three lipid-dependent Malassezia spp. (M. furfur, M.
globosa and M. sympodialis) have been isolated from
healthy cats4952 to date, and M. sympodialis and M.
pachydermatis have been reported to be associated with
otitis externa in cats.155,156 Malassezia overgrowth has
also been reported in cats with thymoma-associated
dermatitis and paraneoplastic alopecia.157159
Malassezia dermatitis in dogs. Malassezia dermatitis
in dogs was first reported in 1983 by Dufait.3 To date,
the potentially important role of M. pachydermatis in
this condition has gained widespread acceptance due
to the consistent recovery of elevated populations of
M. pachydermatis from the skin of affected dogs and
the favourable therapeutic response that occurs to antifungal therapy.
Predisposing factors for overgrowth of Malassezia
pachydermatis. The predisposing factors for Malassezia overgrowth on the skin of dogs are still a focus of
research and debate. Two mechanisms that have been
Figure 7. (a) Malassezia overgrowth in a cat at the site of extension

flap surgery, used to close a wound. The area was inflamed, pruritic
and exudative. Large numbers of Malassezia organisms were seen on
stained tape strips. (b) The same area after 7 days of topical
antifungal therapy with 2% chlorhexidene/2% miconazole shampoo
(Malaseb, Leo Animal Health, Denmark). The small ulcer at the
centre of the picture is an area of granulation tissue surrounding a
suture.
suggested to trigger overgrowth of the yeast are alterations in host defence mechanisms and changes in the
cutaneous microenvironment.70,160 By causing these
changes, various diseases have been suggested as
underlying causes of Malassezia dermatitis.
As described earlier, a disrupted epidermal barrier
renders the skin more prone to bacterial and yeast
infections. Diseases that can cause a decrease in cutaneous barrier function and are commonly associated
with Malassezia dermatitis are hypersensitivity diseases (especially atopic dermatitis), parasite infestation
and keratinization disorders.160,161 Alterations in the
immune system caused by hypersensitivity and endocrine diseases are also thought to predispose to Malassezia dermatitis.160
The cutaneous microenvironment is generally
considered to be important in controlling Malassezia
populations. Malassezia dermatitis seems to be more
common in warm, humid climates and seasons, and in
certain anatomic sites such as skin folds, suggesting
that increased cutaneous humidity favours yeast
growth.161 Additionally, changes in lipids on the skin
surface, resulting in increased availability of nutrients
and growth factors for Malassezia organisms, may promote their proliferation. The diseases that can cause
changes in sebum production and that are associated
16
with Malassezia dermatitis include endocrine diseases,

bacterial skin diseases (in which the bacteria could
release lipase), and keratinization disorders such as
seborrheic dermatitis.160162
Genetic predisposition appears to be important in
certain breeds, especially West Highland white terriers,
Basset hounds, dachshunds, cocker spaniels, Shih
Tzus, and English setters.161163 Furthermore, the use
of certain medications such as long-term glucocorticoid therapy may also be predisposing factors.161 Some
investigators have suggested that antibiotic treatment
is associated with increased Malassezia populations,162
whereas others do not support this point of view.160
Pathogenesis. The pathogenesis of Malassezia dermatitis in dogs has not been fully elucidated. In addition
to the immunological factors described earlier in this
review, there are several other mechanisms by which
M. pachydermatis might cause pathological changes
in the skin of dogs. Zymogen (an inactive pro-enzyme)
in the yeast cell wall is capable of activating the
complement system. This could result in damage to
keratinocyte integrity, leading to epidermal spongiosis,
inflammation and pruritus. A defective epidermal
water barrier, caused either by direct keratinocyte damage or by underlying atopic dermatitis, could lead to an
increase in humidity on the skin surface, thus favouring
yeast proliferation.70 Additionally, the disrupted epidermal barrier could permit the skin immune system to
be exposed to Malassezia antigens and products, eliciting inflammatory and/or hypersensitivity reactions.161
As proteases are believed to be the mediator of itch
at free nerve endings in the skin, the proteases released
by Malassezia organisms could also contribute to pruritus.164 Malassezia organisms also produce lipases,
which alter sebum production and produce free fatty
acids on the skin surface. Released lipids can be used
by yeasts for nutrition, and free fatty acids would provide protection by inhibiting other organisms.165
Clinical features. Malassezia dermatitis occurs in dogs
of any age, sex and breed, but is more often diagnosed
in dogs between 1 and 3 years of age.166 Some breeds
also appear to be predisposed (listed above). The dermatitis often begins in the summer or in humid
months, which also corresponds to the allergy season,
and then persists into winter. There is a second spike of
cases in early spring.70,161
Skin lesions may be localized or generalized.
Regional dermatitis commonly occurs in the external
ear canal (Fig. 8), or on the face, ventral neck (Fig. 9),
axillae (Fig. 10), groin, interdigital skin or intertriginous areas. Skin lesions are characterized by erythema,
alopecia, greasy exudation and varying degrees of scaling. Chronic cases can have marked hyperpigmentation and lichenification (Fig. 11). Pruritus varies from
mild to extremely severe. Dogs with generalized lesions
often have an offensive, rancid or yeasty odour. Malassezia paronychia may occur with or without more generalized Malassezia dermatitis. In these cases, there is
Figure 8. Malassezia otitis in a Golden retriever secondary to

underlying atopic dermatitis. Note the typical brown and waxy
discharge.
Figure 9. Malassezia dermatitis on the ventral neck of a Basset

hound. The skin is erythematous and the hair is stained by a brown
discoloration. This is a predilection site in a predisposed breed.
reddish-brown staining of the claws or hair, with

inflammation of the surrounding soft tissue (Fig. 12).
In some cases, a localized area of Malassezia overgrowth can occur following persistent licking (Fig. 13).
Most dogs with Malassezia dermatitis have concurrent
dermatoses, especially hypersensitivity disorders,
ectoparasitic infestation, bacterial pyoderma, endocrinopathies, or keratinization defects.70,153,161,166,167
Figure 10. Malassezia dermatitis in the axilla of a West Highland

white terrier, secondary to underlying atopic dermatitis. Note the
erythema, scaling, lichenification and hyperpigmentation, indicating
chronicity. The papular eruption indicates concurrent
staphylococcal infection.
Figure 11. Severe and chronic Malassezia dermatitis on the ventral

neck of a Shar pei. Note the extreme lichenification and
hyperpigmentation.
Figure 12. Brown staining of the proximal claws in a dog with

Malassezia paronychia. Malassezia organisms can often be found in
scrapings of this material.
However, it is important to remember that in some

cases, especially in predisposed breeds, there is no identifiable underlying cause and the dogs skin disease
resolves completely with antifungal therapy.
17
Figure 13. Localized area of Malassezia dermatitis following

persistent licking. The dog had started to lick the medial thigh
following stifle surgery. Large numbers of Malassezia organisms
were found on stained tape strips and the condition responded
completely to topical antifungal therapy.
Diagnosis. The criteria required for the diagnosis of

Malassezia dermatitis have not been definitively established. It has been proposed that a diagnosis of Malassezia dermatitis is appropriate when a dog with
elevated M. pachydermatis populations on lesional
skin shows a good clinical and mycological response to
appropriate antifungal therapy.47 The diagnostic tools
used to identify elevated populations of Malassezia
yeasts on the skin include cytological, cultural and
histopathological techniques.
Cytological examination is the most useful technique that allows Malassezia populations to be rapidly
assessed. A variety of methods have been used to
collect cytological samples for the evaluation of the
organisms. These include pressing a piece of clear acetate tape onto lesional skin several times, vigorously
rubbing a cotton swab on the skin surface, performing
a superficial skin scraping, and directly pressing a glass
slide onto lesional skin.70,161 In many clinicians hands,
the acetate tape technique appears to be the most useful clinically, especially for sampling between the toes
or dry or greasy areas of skin. Cotton swabs are typically used to obtain material from the ear canal. Direct
impression with a glass slide is possible if the skin surface is flat and greasy.153,160,161 It is difficult to determine which sampling method is the best as each has its
own benefits and disadvantages. It has been shown that
swabs, skin scrapings and impression smears gave similar results in normal dogs.46 Using dogs with elevated
cutaneous Malassezia populations, Bond and Sant168
observed relatively higher numbers of Malassezia
organisms using tape stripping and dry scraping than
with damp swabs. Some investigators have reported
that direct impression with a glass slide was the most
reliable technique for producing uniform cytological
preparations.162
The samples collected are transferred to a glass slide
and stained with a suitable cytological stain such
as Diff-Quik (Dade AG, Dudingen, Switzerland),
18
Figure 14. Cytological examination of a Diff-Quik-stained tape

strip obtained from the skin of a dog with Malassezia dermatitis
(1000). Numerous round to oval or peanut-shaped budding yeasts
are present.
Giemsa, or methylene blue.160 The slides should be

examined under high power (400) or preferably with
an oil immersion lens (1000) on a light microscope.
Microscopic examination reveals round to oval yeasts
with monopolar budding (Fig. 14). Yeasts are often
seen in clusters or adhered to keratinocytes.161 As M.
pachydermatis can be found in a small number on
healthy dog skin, it is difficult to define the amount of
yeast that is pathogenic. It has been suggested that
populations should be considered elevated if the yeast
is readily identified.167 Some investigators have also
suggested that an elevated population is more likely
when a certain number of yeasts are found.161 The various criteria proposed include greater than 10 organisms in 15 randomly chosen oil-immersion microscopic
fields (1000) using tape stripping samples; an average
of greater than or equal to four organisms per oilimmersion microscopic field; an average of greater
than or equal to one organism per field in 10 oilimmersion microscopic fields; and greater than two
organisms per high power field (400) with specimens
obtained using any of the commonly used sampling
techniques. In view of the conflicting data, the authors
would recommend, as a general guide, that finding one
organism per oil-immersion field in the presence of
clinical signs can usually be taken to indicate an overgrowth of M. pachydermatis.
Four methods have been described to culture
Malassezia organisms from the skin including cotton
swabs,45,169 adhesive tapes,46,169,170 contact plates171
and detergent scrubs.172 M. pachydermatis grows well
on both Sabourauds dextrose agar and modified
Dixons agar at 3237 C. However, an atmosphere
containing 510% carbon dioxide significantly
increases the frequency of isolation and colony counts
on Sabourauds dextrose agar, but not on modified
Dixons agar.173 Nevertheless, modified Dixons agar, a
lipid-supplemented medium, may be advantageous for
diagnostic purposes because it supports the growth of
more lipid-dependent variants of M. pachydermatis174
and the lipid-dependent Malassezia spp. that may be
found on cats.4952 As Malassezia spp. are commensal

organisms and as elevated populations can be readily
found on cytology, culturing is not usually necessary
and rarely used by most clinicians.160,161 However,
quantitative culture has been reported to have diagnostic value by some authors.171,172
Malassezia organisms may also be demonstrated by
microscopic examination of skin biopsy specimens
(Fig. 15). The yeasts are typically located in the stratum corneum and are occasionally seen in the follicular
infundibulum. Because of the possible loss or disruption of the stratum corneum during processing, skin
biopsy is generally considered to be less sensitive and
reliable than other diagnostic tools. There are several
characteristic histological features in skin biopsy
samples from dogs with Malassezia dermatitis, although
none of these are pathognomonic.121,161,175178 The epidermis is characterized by marked irregular hyperplasia with formation of deep rete ridges (Fig. 15a).
Hyperplasia can also be seen in the follicular infundibula. Orthokeratotic hyperkeratosis with focal parakeratosis is frequently observed. Spongiosis is marked in
active lesions (Fig. 15b). The dermal inflammation is
usually superficial perivascular to interstitial with
lymphocyte exocytosis and focal accumulations of
neutrophils. Eosinophils are present occasionally. Linear
alignment of mast cells at the dermoepidermal junction can also be observed in some affected dogs.178,179
Scott and Miller175 described a hyperplastic dermatosis
associated with secondary M. pachydermatis infection
in West Highland white terriers. They proposed a term,
epidermal dysplasia, to describe the epidermal hyperplasia with round-bottomed rete ridges in these dogs.
Treatment. The treatment of canine Malassezia dermatitis is currently based on the use of topical and systemic antifungal therapy.153 A combination of topical
and systemic therapy may speed resolution of the disease and increase efficacy160,161 although, in the UK,
topical therapy alone would be the initial treatment of
choice. Topical agents that can be used for Malassezia
dermatitis include chlorhexidine, clotrimazole, enilconazole, ketoconazole, miconazole, nystatin and selenium sulphide.70,161 It has been reported that M.
pachydermatis showed sensitivity, in decreasing order
of efficacy, to ketoconazole, econazole, clotrimazole,
miconazole and nystatin in vitro,180 although the methods used in this study could be questioned because they
did not take into account the diffusion properties of
the various drugs on the media. These agents are used
in various forms of topical antifungal products such as
sprays, ointments and shampoos. A double-blinded
study demonstrated that a shampoo containing 2%
chlorhexidine and 2% miconazole (Sebolyse Medicated Foam, Dermcare-Vet, Australia), when used
every 3 days for 3 weeks, was effective for treating
Malassezia dermatitis in dogs. This was because of its
degreasing, anti-Malassezia and antibacterial properties.181 The commonly used systemic agents for Malassezia dermatitis in dogs are the azoles. Ketoconazole or
19
itraconazole are usually given at 510 mg kg1 per day

per os for 2130 days.153,160 However, adverse effects
including anorexia, vomiting, diarrhoea and hepatotoxicity have been reported.153 A recent study demonstrated that itraconazole given at 5 mg kg1 every 24 h
per os on 2 consecutive days per week for 3 weeks
(pulse administration) was as effective as when given at
5 mg kg1 every 24 h on a daily basis for 21 days in
treating canine Malassezia dermatitis.182
Clinical improvement usually occurs within 7
14 days after the start of antifungal therapy. As Malassezia dermatitis in dogs is often associated with an
underlying disorder, the dog should be evaluated for
concurrent diseases in order to prevent frequent
relapses. For frequently recurring cases, either due to
primary disease or uncontrollable underlying factors,
shampoo therapy or pulse oral medication may be used
prophylactically.153,161,167
C O N C LU SIO N S
Advances in molecular techniques have led to a clearer
classification of Malassezia yeasts. Certain species
within the genus Malassezia have been associated with
skin diseases, both in humans and animals. Current
research has revealed that Malassezia organisms can
induce immunological responses in normal and atopic
individuals. The identification of several major allergens of Malassezia organisms in atopic humans and
dogs has provided the potential for future development
of immunotherapy for chronically affected patients.
Although the characteristics of the dermatoses associated with Malassezia spp. such as greasy scales and
epidermal hyperplasia have been well recognized, the
interaction between Malassezia organisms and the epidermis remains incompletely understood. Future studies aiming to identify important factors which mediate
the initiation of inflammation or the formation of epidermal hyperplasia seen in Malassezia dermatitis, such
as cytokines and adhesion molecules, might also lead
to novel approaches to prevent or better control
Malassezia dermatitis in humans and dogs.
A D D IT IO NA L N O T E
Figure 15. Histopathology of canine Malassezia dermatitis.
(a) Irregular epidermal hyperplasia and hyperkeratosis (40).
(b) The epidermis shows marked spongiosis and orthokeratotic
hyperkeratosis with focal parakeratosis (250). Malassezia yeasts are
visible in the stratum corneum (thin arrow). Some keratinocytes
show multiple nucleoli, indicating mitotic activity (bold arrows).
(c) Budding yeasts showing characteristic morphology of Malassezia
spp. (thin arrows, 400). Scale bars for (a), (b) and (c) are 100, 10 and
10 m, respectively. H&E stain. Section courtesy of Dr S. Rhind,
University of Edinburgh.
A new species of Malassezia has recently been

described and named Malassezia nana (nana is Latin
for a female dwarf, so named because of the organisms
comparatively small cells). The organism was isolated
from the skin of a cat and from the ear canal of cows.183
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Rsum Le genre Malassezia comporte sept espces de levures, dont la plupart a t associe ) des maladies
varies chez lhomme et chez le chien. Malassezia pachydermatis est une levure lipophile, bourgeonnante, qui colonise la peau les muqueuses des chiens sains. Bien quil sagisse dun lment normal de microflore cutane, cette
levure peut dans certaines circonstances devenir pathogne. La dermatite Malassezia est une dermatose inflammatoire associe la prsence de population leves de M. pachydermatis sur la peau du chien, reconnue de plus
en plus frquemment. Son importance en dermatologie canine peut tre illustre par laugmentation continue
du nombre darticles publis sur cette maladie depuis sa premire description par Dufait en 1983.
Les interactions entre les levures Malassezia et leur hte ont t tudies de faon approfondie chez lhomme,
moins chez le chien. Dans cet article, nous dcrivons la taxonomie et la biologique des levures Malassezia ainsi
que les lments connus actuellement concernant les interactions entre le microorganisme et les moyens de dfense
de la peau. Ces derniers incluent les rponses immunitaires cutanes et systmiques, et la barrire pidermique.
Lincapacit de ces mcanismes de dfense ) protger lhte contre la prolifration des levures peut provoquer
leur pathognicit et lapparition dune dermatose. Dans certains cas, ces rponses peuvent mme tre dltres
et provoquer des ractions dhypersensibilit ou une anomalie pidermique. Nous terminons cette revue en
dcrivant les aspects cliniques des maladies associes Malassezia chez lhomme et lanimal et les moyens
thrapeutiques disponibles pour traiter ces maladies.
Resumen El gnero Malassezia incluye siete especies de levadura, muchas de las cuales se han asociado a enfermedades en humanos y perros. La Malassezia pachydermatis es una levadura lipoflica que se reproduce por
gemacin, que coloniza piel y mucosas de perros sanos.1,2 A pesar de formar parte de la microflora cutnea normal, actualmente se sabe que esta levadura puede comportarse como patgeno bajo ciertas circunstancias. La
dermatitis por Malassezia, una dermatosis inflamatoria asociada a una elevada poblacin de M. pachydermatis
en la piel del perro, se describe con frecuencia creciente. Puede ilustrarse su importancia en la dermatologa canina observando el continuo aumento en el nmero de artculos sobre esta presentacin en la bibliografa desde
que se describi por primera vez por Dufait en 1983.3
Se ha estudiado ampliamente la interaccin entre las levaduras de Malassezia y sus especies husped en el caso
de los humanos, pero menos en el perro. En este artculo, describimos la taxonoma bsica y biologa de las
levaduras Malassezia y presentamos una revisin de los conocimientos actuales sobre la interaccin entre el
organismo y las respuestas protectoras de la piel. stas incluyen las respuestas inmunitarias cutneas y sistmicas
y la barrera protectora proporcionada por la epidermis. Cuando estos mecanismos dejan de proteger el husped
contra la proliferacin del organismo, puede producirse patogenicidad y diferentes presentaciones clnicas. En
algunos casos, estas respuestas son en realidad perjudiciales y pueden llevar a reacciones de hipersensibilidad o
a patologa epidrmica. Finalizamos la revisin describiendo aspectos clnicos de enfermedades asociadas a
organismos del gnero Malassezia en humanos y animales, y las diferentes opciones teraputicas actuales para
el tratamiento de estas presentaciones.
Zusammenfassung Die Gattung Malassezia beinhaltet bekannterweise sieben Species von Hefepilzen, von
denen viele mit verschiedenen Erkrankungen beim Menschen und Hund assoziiert sind. Malassezia pachydermatis ist eine lipophile sprossende Hefe, die die Haut und die Schleimhute gesunder Hunde kolonisiert. Obwohl
sie Teil der normalen cutanen Mikroflora ist, wei man jetzt, dass die Hefe unter gewissen Umstnden Krankheitserreger werden kann. Malassezia-Dermatitis, eine entzndliche Dermatose, die mit erhhter Population von M.
pachydermatis auf der Haut von Hunden verbunden ist, wurde mit zunehmender Hufigkeit diagnostiziert. Ihre
Bedeutung in caniner Dermatologie wird durch den kontinuierlichen Anstieg der Anzahl an Artikeln zu dieser
Erkrankung in der Literatur seit ihrer ersten Beschreibung durch Dufait 1983 verdeutlicht.
Die Interaktion zwischen Malassezia-Hefen und ihrer Wirtsart wurde beim Menschen ausgiebig, beim Hund
jedoch in geringerem Umfang studiert. In diesem Artikel beschreiben wir die grundstzliche Taxonomie und Biologie
von Malassezia-Hefepilzen und den augenblicklichen Wissenstand bezglich des Wechselspiels zwischen dem
26

Organismus und den Schutzmechanismen der Haut. Diese umfassen cutane und systemische Immunantworten
und Schutzbarrieren durch die Epidermis. Ein Scheitern dieser Mechanismen beim Schutz des Wirtes gegen die
Proliferation der Organismen kann zu Pathogenitt und verschiedenen Krankheiten fhren. In einigen Fllen
sind diese Immunantworten sogar schdlich und knnen zu Hypersensitivittsreaktionen oder epidermalen
pathologischen Vernderungen fhren. Wir beenden diesen bersichtsartikel mit einer Beschreibung der klinischen Aspekte von Erkrankungen, die mit Malassezia-Organismen beim Menschen und Hund verbunden sind
und die aktuellen Behandlungsoptionen, die fr die Behandlung dieser Erkrankungen verfgbar sind.

The Biology of Malassezia Organisms and Their Ability To Induce Immune Responses and Skin Disease (Pages 4-26)

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Veterinary Dermatology 2005, 16, 426

Blackwell Publishing, Ltd.

The biology of Malassezia organisms and their ability to induce

Correspondence: P. B. Hill, Division of Veterinary Clinical Studies,

Malassezia organisms as pathogens in humans and

The biology and cutaneous responses to Malassezia organisms

H ISTO RY AND TA XONOM Y OF T H E

In contrast to the lipid dependency of P. ovale and P.

2005 European Society of Veterinary Dermatology, Veterinary Dermatology, 16, 426

T-A Chen and PB Hill

Around the cell wall there is an outer lamellar layer, the

2005 European Society of Veterinary Dermatology, Veterinary Dermatology, 16, 426

The biology and cutaneous responses to Malassezia organisms

IMMU N O LOGI C A L AND

The immune response to Malassezia organisms

Figure 1. Possible pathways for

T-A Chen and PB Hill

immunoglobulin class switching to IgE. It is important

Antigen release, penetration and presentation

Cell-mediated immune responses

2005 European Society of Veterinary Dermatology, Veterinary Dermatology, 16, 426

The biology and cutaneous responses to Malassezia organisms

significantly higher PBMC responses to extracts of

IgG, IgM and IgA responses to Malassezia

2005 European Society of Veterinary Dermatology, Veterinary Dermatology, 16, 426

T-A Chen and PB Hill

mycelium of the yeast. One study reported that healthy

extracellular pathogens.90 This could in theory provide

IgE responses to Malassezia organisms

2005 European Society of Veterinary Dermatology, Veterinary Dermatology, 16, 426

The biology and cutaneous responses to Malassezia organisms

AD, atopic dermatitis.

now been re-assigned to the species M. sympodialis,58

responses to allergens derived from the yeast. The

Mast cell responses

2005 European Society of Veterinary Dermatology, Veterinary Dermatology, 16, 426

T-A Chen and PB Hill

Figure 2. Possible mechanisms for the

frequency of IDT reactivity to M. pachydermatis extracts

Epidermal responses associated with Malassezia

renewing process results in continuous shedding of

2005 European Society of Veterinary Dermatology, Veterinary Dermatology, 16, 426

The biology and cutaneous responses to Malassezia organisms

in a study published more recently, we have shown that

MALASSEZIA ORGANI SMS AS

Diseases associated with Malassezia spp. in

Figure 3. Pityriasis versicolor in an adult human. Note the

2005 European Society of Veterinary Dermatology, Veterinary Dermatology, 16, 426

T-A Chen and PB Hill

Figure 4. Malassezia folliculitis on the upper back of an adult

Figure 6. Atopic dermatitis on the flexural surface of the elbow in an

organisms and the severity of the diseases.135,136 The

Figure 5. Seborrhoeic dermatitis on the neck of an adult human.

in dilated follicles of biopsy sections.6,124 Although it

Atopic dermatitis. Atopic dermatitis is a chronic,

2005 European Society of Veterinary Dermatology, Veterinary Dermatology, 16, 426

The biology and cutaneous responses to Malassezia organisms

support the growth of lipid-dependent Malassezia

Diseases associated with Malassezia spp. in

Figure 7. (a) Malassezia overgrowth in a cat at the site of extension

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T-A Chen and PB Hill

with Malassezia dermatitis include endocrine diseases,