Clinical and Microbiological Diagnosis of Oral Candidiasis
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J Clin Exp Dent. 2013;5(5):e279-86. Diagnosis of oral candidiasis Journal section: Oral Medicine and Pathology d oi:10.4317/jced.51242 Publication Types: Review http://dx.doi.org/10.4317/jced.51242 Clinical and microbiological diagnosis of oral candidiasis Laura Coronado-Castellote 1, Yolanda Jiménez-Soriano 2 1 Dentistry. Master of Oral Medicine and Oral Surgery. Faculty of Medicine and Dentistry. University of Valencia. Spain 2 Associate Professor of the Department of Stomatology. Faculty of Medicine and Dentistry. University of Valencia. Spain Correspondence: C/ Gascó Oliag núm. 1 C.P: 46010, Valencia Spain [email protected] Coronado-Castellote L, Jiménez-Soriano Y. Clinical and microbiological diagnosis of oral candidiasis. J Clin Exp Dent. 2013;5(5):e279-86. http://www.medicinaoral.com/odo/volumenes/v5i5/jcedv5i5p279.pdf Article Number: 51242 http://www.medicinaoral.com/odo/indice.htm © Medicina Oral S. L. C.I.F. B 96689336 - eISSN: 1989-5488 Received: 04/08/2013 eMail: [email protected] Accepted: 26/09/2013 Indexed in: Scopus DOI® System Abstract Introduction: Candidiasis or oral candidiasis is the most frequent mucocutaneous mycosis of the oral cavity. It is produced by the genus Candida, which is found in the oral cavity of 53% of the general population as a common commensal organism. One hundred and fifty species have been isolated in the oral cavity, and 80% of the isolates correspond to Candida albicans, which can colonize the oral cavity alone or in combination with other species. Transformation from commensal organism to pathogen depends on the intervention of different predisposing fac- tors that modify the microenvironment of the oral cavity and favor the appearance of opportunistic infection. The present study offers a literature review on the diagnosis of oral candidiasis, with the purpose of establishing when complementary microbiological techniques for the diagnosis of oral candidiasis should be used, and which techniques are most commonly employed in routine clinical practice in order to establish a definitive diagnosis. Materials and methods: A Medline-PubMed, Scopus and Cochrane search was made covering the last 10 years. Results: The diagnosis of oral candidiasis is fundamentally clinical. Microbiological techniques are used when the clinical diagnosis needs to be confirmed, for establishing a differential diagnosis with other diseases, and in cases characterized by resistance to antifungal drugs. Biopsies in turn are indicated in patients with hyperplastic candidiasis. Staining (10% KOH) and culture (Sabouraud dextrose agar) are the methods most commonly used for diagnosing primary candidiasis. Identification of the individual species of Candida is usually carried out with CHROMagar Candida®. For the diagnosis of invasive candidiasis, and in cases requiring differentiation between C. albicans and C. dubliniensis, use is made of immunological and genetic techniques such as ELISA and PCR. Key words: Clinical, oral candidiasis, microbiology. e279 J Clin Exp Dent. 2013;5(5):e279-86. Diagnosis of oral candidiasis Introduction and immune disorders such as agranulocytosis (neu- Mycoses comprise a series of infectious diseases caused tropenia). Other predisposing conditions are malignant by the pathogenic action of fungi. Although most fungal diseases such as lymphomas or leukemias, aplastic ane- species are present as saprophytes in the environment mia, drug treatments (long-term administration of broad and in plants, where they play a key role in the natural spectrum antibiotics, corticosteroids, antidepressants, recycling of organic material, some of them are able to antineoplastic drugs and immunosuppressants)(9-11), cause disease in humans. Such conditions manifest as hyposialia (produced by disorders such as Sjögren’s di- allergic processes caused by the inhalation of spores, in- sease, drugs or radiotherapy), and terminal or end-stage toxication as a result of the ingestion of harmful substan- systemic diseases (10,12,13). The oral microenviron- ces (mycetismus or mushroom poisoning and mycotoxi- ment-modifying factors in turn include poorly fitting cosis), or infections, since some fungal species are able dentures (14-17), loss of vertical dimension, chronic to colonize, invade and multiply in different body tissues antiseptic use, prolonged dummy use in children, poor and organs, causing mycosis in a previously healthy host oral hygiene (16), smoking and alcoholism (10,18). The (primary pathogenic fungi) or in individuals with dimi- genus Candida is the most common of the many types nished defense mechanisms (opportunistic fungi). The of fungi found in the oral cavity. The species of Candida clinical profile of mycosis varies greatly depending on spp. isolated in the oral cavity are C. albicans, C. tro- the causal agent, the location of the infection, and the picalis, C. parapsilosis, C. krusei, C. guillermondii, C. predisposing factors of the patient. One of the most wi- glabrata and C. dubliniensis. Candida albicans posses- dely used practical classifications of mycoses is based ses pathogenicity factors that allow it to develop disea- on the location of the infection. In this sense, mycoses se more frequently than other species of Candida. The can be classified as superficial, cutaneous or mucocuta- formation of germinal tubes and the presence of certain neous, subcutaneous, and deep or systemic. Mucocuta- glycoproteins such as mannose and glucose in the fungal neous mycoses affect skin and mucosal membrane inte- wall facilitate adherence to cell membranes and recep- grity, and moreover produce inflammation. tors. At the same time, the presence of germinal tubes Candidiasis or oral candidiasis, produced by fungi of and the production of phospholipase C also facilitate fun- the genus Candida (Candida spp.), is the most frequent gal invasion. Some components of these yeasts alter the mucocutaneous mycosis of the oral cavity. Candida is host defense mechanisms (e.g., inhibiting phagocytosis). found in the oral cavity of 53% of the general population On the other hand, certain polysaccharides in the fun- as a common commensal organism. One hundred and gal wall induce suppressor T lymphocytes, and mannan fifty species of this genus have been isolated in the oral found in the wall can interfere with antigen presentation, cavity, and 80% of the isolates correspond to Candida inhibiting the immune defense response. Tissue damage albicans, which can colonize the cavity alone or in com- results from direct action of the microorganism but also bination Candida glabrata or Candida tropicalis (obser- from the host defenses developed against tissue inva- ved in 7% of all healthy people and in 80% of all patients sion, including IgE-mediated immune allergic reactions with candidiasis). Recently, Candida dubliniensis has against the fungal antigens and delayed hypersensitivi- been isolated in patients with human immunodeficiency ty reactions – as in chronic mucocutaneous candidiasis. virus (HIV) infection. This species is important, since Thus, in order for Candida to produce infection, it must it is associated with very severe candidiasic mucositis colonize, invade and multiply. of the oral cavity, esophagus and other locations, and is Candida is a rounded and oval-shaped yeast measuring moreover resistant to antifungal treatment. Despite the 3-30 µm in diameter. It reproduces asexually through a above observations, the prevalence of oral candidiasis is budding process in which protoplasmic protrusions or not well known, since in many cases these processes go buds (blastoconidia) emerge from the mother cell and undetected by the clinician. Nevertheless, the diagnosis grow until they finally detach to form a new cell. The of the disease is very important, since it may be the first daughter cells occasionally do not detach and form manifestation of a systemic disorder, including possible chains of cells called pseudohyphae, which can be mis- HIV infection (1). taken for hyphae. The latter are composed of a row of The pathogenesis of candidiasis combines three factors: elongated cells enveloped by a cell wall; they globally host, fungus and oral microenvironment-modifying fac- conform the mycelium (septate and ramified hyphae). In tors. The host predisposing factors include endocrine al- solid culture media, the yeast grows, giving rise to com- terations (diabetes mellitus, pregnancy, renal failure and pact colonies that are macroscopically visible after 24-48 hyperthyroidism)(2,3), immune depression (normally hours of incubation. Candida must be in the saprophytic associated to antineoplastic treatments or immunosu- phase in order to produce clinical lesions, though over ppression in transplant patients, as well as agammaglo- time nutritional and environmental variations modulate bulinemia or cellular immune defects)(1,4-8), acquired its conversion to the mycelial or invasive form. In this immunodeficiency syndrome (AIDS) or hematological phase the yeast keeps its previous virulence intact, and is e280 J Clin Exp Dent. 2013;5(5):e279-86. Diagnosis of oral candidiasis able to evade macrophage phagocytic action (19,26). ween primary oral candidiasis and secondary forms of The diagnosis of any of the forms of oral candidiasis is the disease, in which oral candidiasis merely constituted essentially clinical and is based on recognition of the le- one of the manifestations of mucocutaneous-systemic sions, which can be confirmed by the microscopic iden- candidiasic infection. At present, the most widely used tification