Candida parapsilosis

Candida parapsilosis
Scientific classification
Kingdom: Fungi
Division: Ascomycota
Class: Saccharomycetes
Order: Saccharomycetales
Family: Saccharomycetaceae
Genus: Candida
Species:
C. parapsilosis
Binomial name
Candida parapsilosis
Langeron & Talice (1932)
Synonyms
  • Mycocandida parapsilosis C. W. Dodge (1935)
  • Mycotorula parapsilopsis Cif. & Redaelli (1943)
  • Candida quercus Montrocher & Claisse (1984)

Candida parapsilosis is a fungal species of yeast that has become a significant cause of sepsis and of wound and tissue infections in immunocompromised people. Unlike Candida albicans and Candida tropicalis, C. parapsilosis is not an obligate human pathogen, having been isolated from nonhuman sources such as domestic animals, insects and soil.[1] C. parapsilosis is also a normal human commensal and it is one of the fungi most frequently isolated from human hands.[1] There are several risk factors that can contribute to C. parapsilosis colonization. Immunocompromised individuals and surgical patients, particularly those undergoing surgery of the gastrointestinal tract, are at high risk for infection with C. parapsilosis.[1] There is currently no consensus on the treatment of invasive candidiasis caused by C. parapsilosis, although the therapeutic approach typically includes the removal of foreign bodies such as implanted prostheses and the administration of systemic antifungal therapy. Amphotericin B and Fluconazole are often used in the treatment of C. parapsilosis infection.[1]

History and taxonomy

Candida parapsilosis was discovered in Puerto Rico in 1928 by Ashford from a diarrheal stool. It was first named Monilia parapilosis and considered nonpathogenic.[1] It was later encountered as a causative agent of sepsis in an intravenous drug user in 1940.[1] It is now considered an important, emerging nosocomial pathogen.[2] C. parapsilosis is the most common non-C. albicans species of Candida[3] and the second most common pathogen in superficial candidiasis after C. albicans.[4]

Biology

Candida parapsilosis does not form true hyphae; it exists in either a yeast phase or pseudohyphal form.[1] It is white, creamy, and shiny in dextrose agar and its cell shape is oval, round, or cylindrical.[1] When C. parapsilosis is in yeast form, its phenotype is smooth or cratered. In contrast, the phenotype of the pseudohyphae form is wrinkled or concentric.[1] Recently found the formation of pseudohyphae is another significant factor that changes the morphology and phenotype of colonies which is related to citrulline.[1] C. parapsilosis is encountered more frequently in nature than other species Candida, likely because it is one of the few species of the genus not restricted to humans.[1] C. parapsilosis does not need prior colonization and is usually transmitted by external sources.[1] Invasive infection occurs very often in low-birth weight newborn babies in the United States, and bloodstream infection found in North America.[1] It is most commonly isolated from human skin[2] and is most frequently encountered in Asia and Latin America.[4] C. parapsilosis is considered a killer yeast and fungal antagonist based on its ability to produce chemicals that exert cytotoxic effects on the cells of other organisms.[5]

Disease

Endocarditis can be caused by C. parapsilosis in patients using prosthetic valves (57.4%), intravenous drug (20%), or having intravenous parenteral nutrition (6.9%), abdominal surgery (6.9%), immunosuppression (6.4%), treatment with broad-spectrum antibiotics (5.6%), and previous valvular disease (4.8%). Although the mortality rate is 41.7% to 61%, the treatment is still unknown.[1] Ocular infection caused by C. parapsilosis has been reported after cataract extraction and with corticosteroid eye drop use.[1] C. parapsilosis infection of the skin and gastrointestinal tract[1] can occur, in which the production of pseudohyphae is associated with the elicitation of an inflammatory response.[3] Candida parapsilosis is occasionally encountered in onychomycosis.[6][7][8]

Adhesion capacity and biofilm are important for C. parapsilosis, because C. parapilosis infection is mostly due to the use of in-dwelling devices.[9] Adhesion capacity is the ability of fungus to adhere to other organisms' cells or tissue, especially mucosal surfaces,[1] which is required for initial colonization.[10] C. parapsilosis is associated with thin, unstructured biofilms that consist of aggregated blastospores whose membranes contain more carbohydrate than protein.[10] The existence of the fungus in a biofilm contributes to its ability to resist antifungal treatment.[1][9] Thus, adhesion to abiotic and biotic surfaces is often a precursor to infection.[11] The risk of C. parapsilosis infection is increased in the setting of implanted medical devices, prostheses, and therapy with hyperalimentation solutions.[1] Also, low-birth weight infants are at higher risk of sepsis from this species.[12]

References

  1. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 David Trofa, Attila Gácser, Joshua D. Nosanchuk (2008). "Candida parapsilosis, an Emerging Fungal Pathogen". Clin Microbiol Rev. 21 (4): 606–025. doi:10.1128/CMR.00013-08. PMC 2570155. PMID 18854483.{{cite journal}}: CS1 maint: uses authors parameter (link)
  2. 1 2 M. de Toro, M. J. Torres, Ruiz Maite, J. Aznar (2010). "Characterization of Candida parapsilosis complex isolates". Clinical Microbiology and Infection. 17 (3): 418–424. doi:10.1111/j.1469-0691.2010.03302.x. PMID 20636431.{{cite journal}}: CS1 maint: uses authors parameter (link)
  3. 1 2 Adél Tóth, Erik Zajta, Katalin Csonka, Csaba Vágvölgyi, Mihai G. Netea, Attila Gácser (2017). "Specific pathways mediating inflammasome activation by Candida parapsilosis". Scientific Reports. 7: 43129. Bibcode:2017NatSR...743129T. doi:10.1038/srep43129. PMC 5320503. PMID 28225025.{{cite journal}}: CS1 maint: uses authors parameter (link)
  4. 1 2 Xiaobo Feng, Bo Ling, Guimei Yang, Xia Yu, Daming Ren, Zhirong Yao (2012). "Prevalence and Distribution Profiles of Candida parapsilosis, Candida orthopsilosis and Candida metapsilosis Responsible for Superficial Candidiasis in a Chinese University Hospital". Mycopathologia. 173 (4): 229–234. doi:10.1007/s11046-011-9496-5. PMID 22102007. S2CID 18867907.{{cite journal}}: CS1 maint: uses authors parameter (link)
  5. ↑ Efrén Robledo-Leal, Mariana Elizondo-Zertuche, Licet Villarreal-Treviño, Rogelio de J. Treviño-Rangel, Nancy García-Maldonado, Juan M. Adame-Rodríguez, Gloria M. González (2014). "Killer behavior within the Candida parapsilosis complex". Folia Microbiologica. 59 (6): 503–506. doi:10.1007/s12223-014-0327-1. PMID 24898174. S2CID 884540.{{cite journal}}: CS1 maint: uses authors parameter (link)
  6. ↑ Segal R, Kritzman A, Cividalli L, Samra Z, David M, Tiqva P (1996). "Treatment of Candida nail infection with terbinafine". Journal of the American Academy of Dermatology. 35 (6): 958–961. doi:10.1016/s0190-9622(96)90120-6. PMID 8959955.{{cite journal}}: CS1 maint: uses authors parameter (link)
  7. ↑ Supram Hosuru Subramanya, Deependra Hamal, Niranjan Nayak, Shishir Gokhale (2016). "Onychomycosis due to Candida parapsilosis in a Child with Ventricular Septal Defect: An Unusual Predisposition". Case Reports in Pediatrics. 2016: 1–4. doi:10.1155/2016/7026068. PMC 4852352. PMID 27195165.{{cite journal}}: CS1 maint: uses authors parameter (link)
  8. ↑ Different toenail onychomycosis due to Rhodotorula mucilaginosa and Candida parapsilosis in an immunocompetent young adult, Gai Ge,a Dongmei Li,b Huan Mei,c Guixia Lu,c Hailin Zheng,c Weida Liu,c and Dongmei Shid,∗
  9. 1 2 Duncan M. Kuhn, Pranab K. Mukherjee, Thomas A. Clark, Claude Pujol, Jyotsna Chandra, Rana A. Hajjeh, David W. Warnock, David R. Soll, Mahmoud A. Ghannoum (2004). "Candida parapsilosis Characterization in an Outbreak Setting". Emerging Infectious Diseases. 10 (6): 1074–1081. doi:10.3201/eid1006.030873. PMC 3323144. PMID 15207060.{{cite journal}}: CS1 maint: uses authors parameter (link)
  10. 1 2 Sonia Silva, Melyssa Negri, Mariana Henriques, Rosario Oliveira, David W. Williams, Joana Azeredo (2012). "Candida glabrata, Candida parapsilosis and Candida tropicalis: biology, epidemiology, pathogenicityand antifungal resistance". FEMS Microbiology Letters. 36 (2): 288–305. doi:10.1111/j.1574-6976.2011.00278.x. PMID 21569057.{{cite journal}}: CS1 maint: uses authors parameter (link)
  11. ↑ Alessia Bertini, Flavia De Bernardis, Lambert A.M. Hensgens, Silvia Sandini, Sonia Senesi, Arianna Tavanti (2013). "Comparison of Candida parapsilosis, Candida orthopsilosis, and Candida metapsilosis adhesive properties and pathogenicity". International Journal of Medical Microbiology. 303 (2): 98–103. doi:10.1016/j.ijmm.2012.12.006. PMID 23403338.{{cite journal}}: CS1 maint: uses authors parameter (link)
  12. ↑ Itzhak Levy, Lorry G. Rubin, Sanjeev Vasishtha, Victor Tucci, Sunil K. Sood (1998). "Emergence of Candida parapsilosis as the Predominant Species Causing Candidemia in Children". Clinical Infectious Diseases. 26 (5): 1086–1088. doi:10.1086/520277. PMID 9597232.{{cite journal}}: CS1 maint: uses authors parameter (link)
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