impaginato piccolo - Società Italiana di Parassitologia (SoIPa)

Parassitologia 50: 65-67, 2008
The Pathogenesis of Malassezia Yeasts
C. Cafarchia, D. Otranto
Dipartimento di Sanità Pubblica e Zootecnia, Facoltà di Medicina Veterinaria, Università di Bari, Bari, Italy.
Introduction
Abstract. The genus Malassezia includes twelve species of yeast, many of which have been mainly associated
with human and canine diseases. Malassezia pachydermatis colonizes the skin and mucosal sites of
healthy dogs and cats. Despite being part of the normal cutaneous microflora, Malassezia spp. yeast may
become pathogenic under certain circumstances. This article reviews the factors related to both host and
yeast which affect the pathogenical or commensal phenotypes of Malassezia yeasts.
Key words: Malassezia pachydermatis, pathogenicity, host defence, virulence factors.
Malassezia spp. are lipophilic yeasts belonging to the
normal cutaneous microflora of most warm-blooded
animals and sometimes act as opportunistic pathogens
(Batra et al, 2005). The lipid-dependent species are frequently
associated with human skin disorders, while
the non-lipid dependent Malassezia pachydermatis is
considered to be an opportunistic pathogen growing on
skin surface and ear canal of dogs and cats (Guillot and
Bond, 1999; Chen and Hill, 2005). Malassezia dermatitis
may presents with pruritus, inflammation and
epidermal hyperplasia (Chen and Hill, 2005) and the
pathogenic role of Malassezia yeasts in the occurrence
of lesions may be related to host immune system as well
to yeast virulence factors. The aim of this article was to
review and discuss the scientific literature available on
the pathogenesis of Malassezia spp.
Host predisposing factors
The proliferation of Malassezia yeasts is likely to be a
preliminary step toward dermatitis and/or otitis
(Nardoni et al, 2005; Cafarchia et al, 2005a;
Cafarchia et al, 2005b). The yeast overgrowth may be
caused by changes in the cutaneous microenvironment
and/or alterations in host defence mechanisms
(Chen and Hill, 2005). Under the above circumstances,
hypersensitivity diseases (e.g. atopic dermatitis)
(Nardoni et al, 2007), parasitic infestation (e.g.
Otodectes, Sarcoptes, Demodex mites -Radi, 2004;
Anane et al, 2007), keratinization disorders (e.g. seborrheic
dermatitis), alterations in host immune system
by endocrine diseases (diabetes mellitus in dogs), FIV,
Felv infections (Sierra et al, 2000; Peikes et al, 2001)
and antibiotic and/or glucocorticoid treatment
restricting microbial colonization of the skin (Chen
Correspondence: Domenico Otranto
Department of Veterinary Public Health,
Faculty of Veterinary Medicine, University of Bari,
Str. prov.le per Casamassima Km 3, 70010,Valenzano, Bari (Italy)
Tel/Fax: +39 080 467 9839,
e-mail: d.otranto@veterinaria.uniba.it
and Hill, 2005), predispose to Malassezia overgrowth.
The value of pH and humidity of the skin surface
also may bias the growth of Malassezia yeasts:
the higher is the cutaneous pH level the higher the
release of Malassezia sympodialis allergens leading to
inflammation (Selander et al, 2006) while a low pH
inhibits M. pachydermatis growth (Matousek et al,
2003). Furthermore, Malassezia yeast growth may be
also affected by skin humidity being this infection
more common in warm, humid climates and seasons,
and in certain anatomic sites such as skin folds
(Bergbrant, 1995).
In animals with otitis a larger population size of
Malassezia yeasts was observed in male cats and dogs,
in cats over one year of age and in dogs under one year
of age, in autumn for cats and in winter for dogs
(Cafarchia et al, 2005a; Nardoni et al, 2005).
The chemical composition of the skin may play a role
in selection of Malassezia genetic population
(Cafarchia et al, 2008b). In fact, the distribution pattern
of a particular genotypes (Cafarchia et al, 2007c,
Cafarchia et al, 2007d) of M. pachydermatis on the
skin of dogs is related to the affinity of the yeast to a
particular skin site and to the presence of lesions
(Cafarchia et al, 2008b).
In hosts Malassezia yeasts produce antigens that could
penetrate the animal skin being captured by epidermal
Langerhans’ cells and stimulating Th1cells and/or Th2
cells to produce IgG and/or IgE immunoglobulin (in
Chen and Hill, 2005). Consequently, the production of
Malassezia-specific IgG antibodies might activate the
complement system causing epidermal damage and
inflammation and allergen-specific IgE antibodies
could lead to a Type I hypersensitivity reactions (Chen
and Hill, 2005).
Malassezia yeast virulence factors
Malassezia yeasts are also per se pathogenic to animals.
For example, the zymogen pro-enzyme of the yeast cell
wall may activate the complement system resulting in
damage of keratinocyte integrity and thus epidermal
spongiosis, inflammation and pruritus (Belew et al,
1980). Malassezia yeasts produce esterase, lipase,
phosphatase acid, lipossigenase and protease