Malassezia pachydermatis
| Malassezia pachydermatis | |
|---|---|
Scientific classification 
| |
| Domain: | Eukaryota |
| Kingdom: | Fungi |
| Division: | Basidiomycota |
| Class: | Malasseziomycetes |
| Order: | Malasseziales |
| Family: | Malasseziaceae |
| Genus: | Malassezia |
| Species: | M. pachydermatis
|
| Binomial name | |
| Malassezia pachydermatis (Weidman)
C.W.Dodge (1935)[1] | |
| Synonyms | |
| |
Malassezia pachydermatis is a zoophilic
Description
Malassezia pachydermatis is a bottle-shaped,
Optimal growth occurs at 30–37 °C (86–99 °F) with maturation occurring in five days.[9] It is the only species of Malassezia capable of growing without the presence of fatty acids.[5] Although it is not lipid-dependent, its growth is enhanced by the presence of lipids.[10] Its DNA is characterized by a 56% guanine-cytosine content.[11]
Pathogenicity
Within infected tissues, this yeast produces several enzymes such as
Malassezia pachydermatis in its pathogenic form can be found colonizing a variety of animals such as rhinoceroses,[2] sea lions,[12] black bears[3] and domesticated cats.[13] It is however most commonly associated with canine ear and skin infections.[7][9][10]
Canine infection
Malessezia pachydermatis is an important pathogen in veterinary medicine.[14] It has been known to become pathogenic to its host causing otitis and seborrhoeic dermatitis.[4] First associated with canine otitis externa in 1955 by Benght A. Gustafson, this yeast has since become an important pathogen especially in the study of small animal medicine. Symptoms include excessive scratching, head shaking, odour, and reddish-brown waxy deposits within the ear canal.[3] Malassezia pachydermatis caused canine seborrhoeic dermatitis was first discovered by Dufait in 1975 and may be characterized by symptoms ranging from dandruff to scaly lesions. At infection sites sebaceous secretions are increased.[3] Differences to susceptibility can be seen across breeds for example, increased infection among the West Highland White Terrier has been attributed to a genetic abnormality.[3]
Low pH environments have been associated with antimicrobial activity and dogs have among the highest skin pH levels of any domesticated animal. Malassezia pachydermatis is most commonly isolated from areas of the skin and ears with higher pH levels. Therefore canine colonization may occur more readily due to the skins increased alkalinity.[14] Samples have been collected from the ears, skin, vagina, and anal sacs.[9] Canine infection often co-occurs with atopy and other allergic disorders.[13][15] In contrast, felines are rarely infected by M. pachydermatis but when Malassezia spp. dermatitis does occur, it is not typically associated with any other conditions.[13]
Human infection
Infections are relatively rare in humans, with some studies reporting only about 2% prevalence on individuals with
Detection
Malassezia pachydermatis can be distinguished from other species in the genus by its ability to grow on Sabouraud agar.[8] Cotton ear swabs, adhesive tape methods, skin scrapings, and biopsy can be used to collect samples that are analysed via microscopy or culturing techniques, however, under-diagnoses may occur due to an increase in the number of days culture may require to develop and discrepancies in laboratory techniques.[3]
While M. pachydermatis is routinely detected by swabbing of external areas of canine ears, its presence within the deeper portions of the ear canal is associated with infection.[3]
Treatment
Antifungal medications such as imidazole, nystatin and natamycin may be used to treat infections. The former functions by weakening the fungal cell wall, while the latter two disrupt permeability of the plasma membrane. In canine infection causing otitis externa the ear canal may be cleaned using an ear cleansing solution often paired with the removal of surrounding hair.[3]
Separation of biotypes as well as treatment has proven successful using killer yeast strains such as Pichia anomala.[15] In these studies by Coutinho et al., M. pachydermatis was isolated from canine skin swabs and otic secretions which were then exposed to toxin producing killer yeast strains that inhibited M. pachydermatis growth.[15]
References
- ^ Rippon, J.W. (1988). Medical Mycology (3rd ed.). Philadelphia: WB Saunders. p. 797.
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