Fungal Infections Of The Oral Mucosa

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Continuing Education Activity

Fungal infections are commonly encountered in the oral and maxillofacial regions. They may present clinically in the oral cavity as a primary infection or as a manifestation of the infection dissemination. Most oral fungal infections are opportunistic in nature. Physical examination is vital for diagnosis, especially in immunocompromised patients. Clinical assessment of oral lesions, recognition, correction of the underlying predisposing factors, and administration of appropriate antifungal agents by the dental professional is the cornerstone of managing oral mycoses. This activity describes the evaluation of fungal infections of the oral cavity and highlights the potential role of the dentist in frontline teams for early diagnosis and treatment of the condition.


  • Review the etiopathogenesis of oral mycoses, including candidiasis, aspergillosis, mucormycosis, histoplasmosis, blastomycosis, cryptococcosis, paracoccidioidomycosis, and geotrichosis.
  • Describe the epidemiology of oral mycoses: candidiasis, aspergillosis, mucormycosis, histoplasmosis, blastomycosis, cryptococcosis, paracoccidioidomycosis, and geotrichosis.
  • Outline the typical oral manifestation of fungal infections: candidiasis, aspergillosis, mucormycosis, histoplasmosis, blastomycosis, cryptococcosis, paracoccidioidomycosis, and geotrichosis.
  • Summarize the diagnosis and management of oral fungal infections: candidiasis, aspergillosis, mucormycosis, histoplasmosis, blastomycosis, cryptococcosis, paracoccidioidomycosis, and geotrichosis.


The oral cavity provides a unique ecological site that harbors a dynamic microbiota. Candida, Aspergillus, and Rhizopus are commensal oral fungi. However, they may become pathological and cause opportunistic infections under certain conditions. The incidence of fungal infections has been on the rise in recent years, especially in COVID 19 patients, due to several factors such as immunodeficiency, hyperglycemia caused by diabetes mellitus, prolonged hospitalizations, and prolonged use of steroids, and hematopoietic malignancies.[1][2] The advent of newer therapies for several diseases has also influenced the incidence of fungal infections.[3]

The diagnosis of oral fungal infections is mainly based on clinical presentation, cytology, and histopathology of the lesional tissue. The methods to detect fungal organisms have also evolved from culture to rapid molecular tests like polymerase chain reaction (PCR). Prompt evaluation of oral lesions is essential to establish the diagnosis, initiate therapy, and monitor clinical progress.

This article focuses on the epidemiology, patient history, risk factors, oral findings, diagnosis, and treatment of the oral cavity fungal infections, including oral candidiasis, aspergillosis, mucormycosis/zygomycosis, histoplasmosis, blastomycosis, cryptococcosis, paracoccidioidomycosis, and geotrichosis.


Oral Candidiasis

Candida albicans cause around 95% of oral candidiasis infections.[4] However, infections caused by antifungal-resistant, non-albicans species have increased in recent years, possibly due to age, malignancy, use of polyenes and azoles, indwelling catheters, and more advanced diagnostic methods.[5] 

Non-albicans species include C. glabrataC. tropicalis, C. parapsilosis, C. dubliniensis, C. guilliermondii, C. krusei, and C. kefyr. C. Besides C. AlbicansC. glabrata and C. dubliniensis are most commonly isolated from oral lesions in HIV patients.[6] Candida auris is an emerging multidrug-resistant strain causing outbreaks in healthcare settings, especially in post-COVID-19 patients.[7]


Aspergillosis is caused by Aspergillus species, saprophytes that grow on dead and decaying matter. Aspergillus fumigatus is the most common cause of invasive disease since the size of their conidia favors penetration into alveoli.[8] Aspergillus flavus can cause infections limited to the paranasal sinuses.[9]


Mucormycosis/Zygomycosis is caused by Zygomycetes, including RhizopusMucorAbsidia, and Rhizomucor speciesRhizopus accounts for 90% of rhinocerebral mucormycosis,[10] a rare opportunistic infection involving the brain, nasal cavity, oral cavity, and paranasal sinuses.[11] Rhizopus oryzaeRhizopus microsporus, and Absidia corymbifera are the commonly isolated species in patients with mucormycosis.[12]


Histoplasmosis is caused by Histoplasma capsulatum, a dimorphic environmental fungus that thrives in soil contaminated with bat or bird excreta.[13] There are two clinical entities of histoplasmosis in humans: the infection caused by H. capsulatum var. capsulatum, known as Darling’s disease, small form histoplasmosis, or American histoplasmosis; and the infection caused by H. capsulatum var. duboisii, referred to as large form histoplasmosis or African histoplasmosis.[14]


Blastomycosis is caused by Blastomyces dermatitidis, a spore-forming dimorphic fungus.[15] Blastomyces dermatitidis live in acidic, moist, and sandy soil. Blastomyces helicus and Blastomyces percursus are the other species recognized in blastomycosis.


Cryptococcus neoformans var. grubiiCryptococcus neoformans var. neoformansCryptococcus gattiiCryptococcus bacillisporusCryptococcus deuterogattiiCryptococcus tetragattii, and Cryptococcus decagattii are the Cryptococcus species known to be pathogenic. Cryptococcus neoformans is found in the excreta of birds like pigeons, environmental scavengers like amebas, and in tree hollows.[16]


Paracoccidiomycosis or South American Blastomycosis can be caused by Paracoccidioides brasiliensis complex, which comprises P. brasiliensis, P. americanaP. restrepiensis, and P. venezuelensis or Paracoccidiodes lutzii.[17]


Geotrichosis is a rare opportunistic fungal infection caused by Geotrichum candidum. Species like Geotrichum capitatum, and Geotrichum clavatum can affect the lungs.[18]


Oral Candidiasis

Oral candidiasis is the most common oral fungal infection. It is associated with extremes of age, newborns, and the elderly. Almost 5-7% of infants develop oral candidiasis.[19] Other risk factors include but are not limited to oral immunosuppression, diabetes mellitus, malnourishment, long-term steroid treatment, antibiotic treatment, and denture use.[20] The prevalence increases in patients with AIDS, cancer, and those undergoing radiotherapy or chemotherapy.[4]


Aspergillosis is the second most common oral mycosis. Primary invasive aspergillosis is uncommon in the oral cavity.[21] Dissemination from the nose or sinuses can result in oral aspergillosis. It frequently occurs in patients with uncontrolled diabetes mellitus, immunocompromising conditions, and those undergoing chemotherapy.[22] It has a male preference; the gingiva is most commonly affected, followed by the hard palate and maxillary sinus.


Mucormycosis is the third most common oral mycosis and a possibly fatal opportunistic fungal infection, notably in individuals with diabetes mellitus, hematological malignancies, and those under deferoxamine therapy.[23] It rarely occurs in healthy individuals. There has been a rise in the incidence of rhinomaxillary mucormycosis in COVID-19 patients due to poorly controlled diabetes, prolonged use of corticosteroids, cytokine storm, lymphopenia, endothelial damage, and iron dysregulation.[24] Oral mucormycosis commonly occur in the 4th to 6th decade of life.[25] Up to half of the patients with mucormycosis have diabetes.[26]


Histoplasmosis is the most common systemic fungal infection in the United States.[27] Histoplasmosis capsulati has a worldwide distribution, with the most significant prevalence in Central USA, whereas histoplasmosis duboisii is more common in West Africa.[14] 

Histoplasmosis mainly affects the lungs; although possible, oral lesions are rare. The oral cavity can be affected as part of disseminated histoplasmosis, as the initial presentation of disseminated form, as a localized lesion, or as the only manifestation. Oral histoplasmosis most frequently occurs in the tongue, palate, and lips and is more prevalent in men.[28]


Blastomycosis is endemic in Central and Southern North America, and, unlike histoplasmosis, it frequently affects immunocompetent individuals. Oral lesions present as a result of dissemination or local inoculation.[29] Blastomycosis is prevalent in men aged 20 to 50 years who work outdoors.


Cryptococcus neoformans causes infection in both immunocompromised and immunocompetent individuals, but Cryptococcus gattii infects immunocompetent hosts. Cryptococcus neoformans causes 95% of cryptococcal infections, whereas only 4% to 5% are caused by Cryptococcus gattii[16] HIV patients account for more than 80% of cryptococcosis cases.[16] The central nervous system and lungs are the most frequently affected areas; oral lesions occur rarely.


Paracoccidiomycosis is endemic in Latin America.[30] Male predilection is seen. The conversion of hyphal to yeast form is prevented by beta-estradiol present in female hormones; hence, the lesser prevalence in females.[31]


Geotrichosis is rare in the nails, skin, and oral cavity. Pulmonary infection is the most common form of the disease.[32]


Oral Candidiasis

Candida albicans are commensal fungi in the oral cavity. Commensal microorganisms reside in the external surface of the body or mucosa without affecting human health. However, they may become pathological under appropriate conditions, causing superficial to invasive disseminated infections. 

In its commensal yeast state, Candida reversibly attaches to the oral epithelial cells through electrostatic interactions.[4] The attachment is mediated by cell-wall receptors like the agglutinin-like sequence family of glycoproteins.[4] The yeasts change their morphology to filamentous hyphal form whenever the host defense mechanism is impaired, known as phenotypic switching - critical for the invasion of the host tissue.[4] 

Extracellular hydrolytic enzymes like secreted aspartyl proteinases and secreted phospholipases produced by C. albicans mediate the destruction of host tissue and subsequent invasion.[4] C. albicans can form biofilms on denture bases, thereby increasing virulence and decreasing antifungal susceptibility.[33]


The fungal conidia enter the respiratory tract by inhalation but are removed by the alveolar macrophages in healthy people. Conidia that escape macrophage surveillance are encountered by the neutrophils. In patients with underlying risk factors, the conidia germinate and disseminate by vascular invasion and spread to the skin, orbits, and palate. After Aspergillus has inoculated the oral cavity, it can invade the host tissues by releasing toxins, e.g., aflatoxin, proteases, phospholipases, hemolysin, gliotoxin, and phthioic acid.[21]

Spores can also enter the sinuses during dental procedures like root canal treatment or tooth extraction and become pathological.[34] In hospital settings, rotten leaves or insufficient cleaning of dust may increase the risk of aspergillosis in vulnerable patients.[35] The infection's clinical manifestation depends on the organism's pathogenicity and the host's immune response.


Spores of Zygomycetes enter the host by inhalation of dust or air from air conditioners. Neutrophils and phagocytes play a central role in the host defense mechanism. This explains the prevalence of mucormycosis in patients with diabetes mellitus and neutropenia. 

The infection usually starts in the nasal cavity, where the humid environment favors fungal growth. Oral infection usually spreads through the paranasal sinuses via the nose or direct wound contamination. The palate is affected if the infection spreads through the sinuses. Wound contamination can affect any part of the oral cavity. Implantation of the organism into the maxilla can occur during any oral surgical procedure.[25] 

The fungal organism invades the small blood vessels and forms thrombi within them, reducing the tissue vascularity and causing necrosis. Interaction of spore-coat protein (CotH) on the fungal surface and glucose regulator protein (GRP78) on the endothelium facilitates the organism's attachment to the blood vessels.

Patients with diabetic ketoacidosis or patients under deferoxamine therapy are at increased risk of developing zygomycosis. Increased serum iron levels are observed in diabetic ketoacidosis as acidosis causes the release of iron from iron-binding proteins like transferrin. Fungal hyphae produce rhizoferrin, which binds to iron and facilitates iron uptake by the fungus. Iron enhances the growth of Zygomycetes.[36]


Histoplasma capsulatum thrives in the soil rich in bird or bat excrement. Upon entry into the host through inhalation, the mycelium form transforms into yeast form.[27] After passing through the mucosal barriers in the terminal passage of the lungs, the yeasts are phagocyted by macrophages, and the host defense mechanism usually destroys them. Dectin-1 is a macrophage receptor that recognizes β-glucan present in the cell wall of Histoplasma. To evade this host response, Histoplasma produces α-linked glucans to surround and conceal β-glucans.

The heat shock protein, Hsp60, present on the cell wall of the yeasts, facilitates their entry into the macrophage by interacting with the CR3 receptor present on the host macrophage without triggering inflammation. When the immunity is low, the fungus multiplies within the macrophages and disseminates to other organs. In some cases, the macrophages surround and confine the fungi, which reactivate at a later stage.[13]


Following inhalation, Blastomyces dermatitidis conidia are phagocyted by alveolar macrophages, neutrophils, and monocytes. Conidia that survive phagocytosis undergo a morphological shift to the yeast form, which is resistant to phagocytosis due to a thick capsule.[15]

The conversion of conidia to yeast form in response to a change in temperature from 22 to 37 degrees C is essential for its pathogenicity, which is mediated by virulence factors: dimorphism-regulating kinase-1 and blastomyces adhesion-1 (BAD1).


The inhaled spores enter the lungs, where they activate alveolar macrophages. The macrophages, in turn, recruit other immune cells to elicit helper T cell responses. 

The yeast can be latent within the phagolysosome in thoracic lymph nodes for many years. The prominent mucopolysaccharide capsule and other virulence factors (melanin production, phospholipase, and urease activity) protect the fungi against the host defense, enabling them to survive within the macrophages. The fungi produce mucin, causing the macrophages to burst, ultimately leading to granulomatous inflammation.[37]

The infection may become symptomatic or disseminated without a granulomatous reaction. In immunodeficient states, the yeast proliferates and spreads through the blood to the brain by crossing the blood-brain barrier.[38]


Paracoccidioides enter the lungs through inhalation, transform into yeast form, and then disseminate. Sometimes the organism can directly enter the mucosa without affecting the lungs.[17]


Geotrichum is a part of the normal oral flora. It is not pathogenic in immunocompetent individuals.[32]

History and Physical

Oral Candidiasis

Patients with oral candidiasis often complain of a burning sensation or unpleasant taste lasting for weeks, months, or even years. There are several clinical forms of oral candidiasis.[19]

Pseudomembranous candidiasis, commonly known as thrush, presents as white plaques in the buccal mucosa, tongue, and palate, which can be removed by scraping or rubbing, exposing an underlying erythematous mucosa. The acute form is commonly observed in infants, which can be attributed to their underdeveloped immune systems. It can also occur with the use of steroid inhalers, rinses, gels, and ointments. Xerostomia may also be a contributing factor.[20]

Erythematous candidiasis manifests as erythematous areas with depapillation on the dorsum of the tongue.[19] The acute form of erythematous candidiasis, previously known as 'antibiotic sore mouth,' occurs due to the long-term use of broad-spectrum antibiotics. A chronic, atrophic form of erythematous candidiasis is common in the palate in HIV patients.

Chronic hyperplastic candidiasis, previously referred to as candidal leukoplakia, presents as non-scrapable white plaques, mostly in the buccal mucosa. This form of candidiasis has the potential for malignant transformation.[39]

Candida-associated lesions are angular cheilitis, denture stomatitis, and median rhomboid glossitis. Denture stomatitis is a form of chronic atrophic erythematous candidiasis. It is commonly seen in the palate of the denture-wearers as erythema.[39] Irregularities of acrylic denture base and denture-relining materials serve as a reservoir for Candida species. Angular cheilitis presents as erythema, fissuring, and crusting of the oral commissures.[40]

It is common in denture-wearers with decreased vertical occlusal dimension and may be associated with denture stomatitis. Median rhomboid glossitis or central papillary atrophy presents as the erythematous area in the midline of the posterior dorsum of the tongue.[40]

Chronic Mucocutaneous Candidiasis refers to candidiasis seen in a rare group of immunologic disorders. Patients may present with candida infections of the oral cavity, skin, and nails during the first few years of life. Autoimmune polyendocrinopathy-candidiasis-ectodermal dysplasia (APECED) syndrome is a syndrome characterized by the development of chronic mucocutaneous candidiasis, adrenocortical failure (Addison disease), and hypoparathyroidism. It is an inherited disorder caused by mutations in the autoimmune regulator (AIRE) gene.

The patients with APECED syndrome have multi-organ autoimmunity and ectodermal dystrophy and develop endocrinal disturbances like Addison's disease, hypoparathyroidism, hypothyroidism, and diabetes mellitus months or years after the onset of candidiasis. Enamel defects can also be observed in these patients.[41] There is an increased propensity for these patients to develop oral squamous cell carcinoma.


Clinical presentation of aspergillosis depends on the immune status of the patient. Non-invasive infection can occur in an immunocompetent host and may present as allergic sinusitis.[42] A low-grade, non-invasive infection of the maxillary sinus is called aspergilloma. Tissue damage following extraction or endodontic treatment of posterior maxillary teeth predisposes the sinus to infection, presenting as pain and nasal discharge.

Oral aspergillosis presents as painful gingival ulcers with diffuse swelling, which may undergo necrosis. Invasive aspergillosis can affect the paranasal sinuses of immunocompromised individuals. Dissemination is common in the lungs.[22] Invasive aspergillosis in the oral cavity presents as a painful necrotic lesion covered by a yellow slough.[21]


Six clinical variants of mucormycosis have been observed: rhinocerebral, pulmonary, gastrointestinal, cutaneous, disseminated, and uncommon site infections. Rhinocerebral is the most common form, which manifests clinically as nasal obstruction, nasal discharge, facial pain, and swelling. It may present as a fatal rhino-orbito-cerebral form or less fatal rhino-maxillary form.

In the oral cavity, the palate is commonly affected due to the involvement of sphenopalatine and greater palatine arteries, resulting in thrombosis of the turbinate and palatal necrosis. Initially, intra-oral swelling of the maxilla is evident, which may later present as a black, necrotic ulcer and palatal perforation.[43]


Three clinical forms of histoplasmosis exist, primary acute pulmonary, chronic pulmonary, and disseminated. Patients with acute histoplasmosis are usually asymptomatic but may present with pulmonary symptoms like nonproductive cough accompanied by fever and headache. The chronic form is common in immunocompromised individuals. Oral lesions are frequently associated with chronic disseminated histoplasmosis and typically present as painful ulcers with rolled margins and irregular surfaces.[44] Oral histoplasmosis may also manifest as vegetative, granulomatous, or plaque-like lesions.[28]


Pulmonary infection can be asymptomatic or symptomatic with fever, malaise, hemoptysis, cough, chest pain, and dyspnea. Blastomycosis in the oral cavity manifest as intraoral pain, progressively growing verrucous or papular growth or ulcers with rolled borders. These lesions may develop in any area of the oral cavity.[44] The ulcers mimic squamous cell carcinoma.[44]

Bone involvement may present as non-healing extraction sockets. Osteomyelitis results from the direct spread of infection from contiguous sites. These lesions may develop in any area of the oral cavity.[44] But, the gingiva, alveolar mucosa, and buccal mucosa are most commonly affected.[29]


Cryptococcosis infection is usually asymptomatic in immunocompetent individuals. Meningoencephalitis may present as headache, fever, and pulmonary cryptococcosis may present as productive cough, chest pain, weight loss, and fever. Oral cryptococcosis may present as a non-healing ulcer, draining sinuses, erythematous plaques, or granuloma.[1] The ulceration usually develops in the palate, gingival tissue, or tonsillar pillar.[44]


The oral cavity may be the first site of manifestation and may present as mulberry-like ulcers with a granular appearance.[45]


The clinical manifestation of oral geotrichosis is similar to oral candidiasis. It may present as pseudomembranous white plaques, hyperplastic lesions, or palatal ulcers.[32]



In patients with suspected oral candidiasis, it is essential to identify the predisposing factor. Predisposing factors can be local, e.g., topical steroid use, salivary hypofunction, the uninterrupted wearing of dentures, and tobacco use. Systemic factors include immunodeficiency, nutritional deficiency, and chronic corticosteroid or antibiotic therapy.[19]

The diagnosis of oral candidiasis is mainly based on clinical features. A swab or smear obtained from the lesion may reveal Candidal hyphae when stained with the periodic acid-Schiff method. A biopsy is required in chronic hyperplastic candidiasis cases to rule out malignancy.[39]

Histopathology of the lesional tissue reveals the increased thickness of the parakeratin layer with Candidal hyphae embedded in it, micro abscess in the superficial spinous cell layer, and elongated rete ridges. The underlying connective tissue contains chronic inflammatory infiltrate.[46] 

Antifungal susceptibility testing is essential in patients who relapse or do not respond to conventional antifungals.[5] CHROMagar culture media can be used to isolate and identify the species of Candida. Production of germ tubes in the germ tube test indicates the presence of C. albicans or C. dubliniensis. Immunological methods to detect mannan antigen and anti-mannan antibodies, antimycelial antibodies, or β-D-glucan can be employed in immunocompromised patients when it is challenging to obtain deep samples. Matrix-assisted laser desorption ionization-time of flight (MALDI-TOF) mass spectrometry reduces the culture time and is helpful in the identification of candidal species.[47]


Diagnosis is mainly based on clinical, microbiological, and histopathological features. Histopathology of aspergillosis reveals septate hyphae, branching at acute angles, of size 3 to 4 µm.[48] In addition to necrosis, granulomatous inflammation is noted in immunocompetent individuals. Histopathology of aspergilloma reveals a tangled mass of hypha without any evidence of tissue invasion. Allergic sinusitis reveals pools of eosinophils and lymphocytes.[49] 

Special stains like Grocott-Gomori's methenamine silver stain and galactomannan can be employed to confirm the diagnosis. Galactomannan is a fungal cell wall marker relatively specific for aspergillus, which can be identified in the serum.[23]


Mucormycosis is an opportunistic infection in patients with underlying diseases like uncontrolled diabetes mellitus, AIDS, leukemia, and lymphoma. Other systemic risk factors include burns, bone marrow transplant patients, and those taking deferoxamine. History of tooth extraction, periodontal surgery, and abscess drainage can be local risk factors for mucormycosis.

Radiographs reveal opacification of the sinuses and effacement of the sinus walls. Scrapings examined with 10 to 20% potassium hydroxide shows non-septate fungal organisms. The final diagnosis is confirmed by pathologic examination, which reveals necrosis and non-septate fungal hyphae of size 6 to 30 µm branching at 90 degrees. Culturing on Sabouraud's glucose agar can identify mucor.[25] Real-time quantitative PCR is a rapid, sensitive, and accurate method to detect 18S or 28S ribosomal RNA genes of Mucorales.


Diagnosis is based on clinical presentation, histopathology, and cultures. Histopathology reveals diffuse lymphohistiocytic infiltrate with fungal elements of size 1 to 2 µm within the cytoplasm of histiocytes. A well-formed granuloma with macrophages and multinucleated giant cells is a rare observation. Stains like Periodic acid- Schiff and Grocott-Gomori methenamine silver can be used to highlight the cell wall of Histoplasma capsulatum. The cytoplasm retracts from the thick cell wall giving a classic "halo" appearance.[28] Diagnosis by fungal culture is the gold standard method for identification of the organism, which can be employed in chronic pulmonary or disseminated histoplasmosis.


Many methods can be used to visualize Blastomyces, including 10% potassium hydroxide, calcofluor white, Gomori methenamine silver, and periodic acid-Schiff. The diagnostic feature is yeast cells of size 8 to 20 µm with double-refractive capsules and broad bud attachment to the parent cell. Histopathology reveals pseudoepitheliomatous hyperplasia with granulomatous reaction and acute inflammation.[50] Culture can aid in making the definitive diagnosis but may take two to three weeks. Enzyme immunoassay can be used to detect BAD1 protein.


India ink is a rapid method to visualize encapsulated yeast cells in cerebrospinal fluid, but false negative results are common.[37] Cryptococcal polysaccharide antigen can be detected in the serum or cerebrospinal fluid. Histopathology shows granulomatous inflammation with multinucleated giant cells containing organisms of 4 to 6 µm surrounded by a clear halo representing the capsule. The capsule can be demonstrated by staining with mucicarmine. Fontana–Masson stain can be used to identify melanin in the cell walls and Calcofluor to stain fungal chitin.[51]


Histopathology reveals pesudoepitheliomatous hyperplasia associated with connective tissue containing epithelioid macrophages and multinucleated giant cells. The organisms may be seen as parent cells with multiple offshoots (daughter buds) resembling 'Mickey mouse ears,' giving a steering-wheel appearance.[52]


Multiple hyphae with rectangular anthroconidia long with acute inflammatory cells are evident in the histopathological section. It is also characterized by rectangular anthroconidia with rounded borders called clavata cells in KOH mounts. Culture is essential for diagnosis.[53]

Treatment / Management

Oral Candidiasis

Management of candidiasis involves maintaining proper oral and denture hygiene, evaluating and correcting predisposing factors, and selecting an appropriate antifungal agent.

Topical clotrimazole is the first line of treatment for candidiasis in adults. Nystatin suspension is most commonly used for infants.[54] In disseminated infections, systemic administration of fluconazole or itraconazole may be necessary. Posaconazole oral solution can be used in patients with immunosuppression and drug resistance.[19]


Surgical debridement alone is sufficient for treating non-invasive aspergilloma in immunocompetent individuals. Surgical debridement and corticosteroid therapy is the treatment for allergic fungal sinusitis. Debridement followed by administration of voriconazole is the treatment for immunocompetent individuals with localized aspergillosis. Aggressive debridement and systemic antifungal therapy with voriconazole, itraconazole, or amphotericin B can be given for immunosuppressed patients with invasive aspergillosis.[55]


Management involves surgical debridement of the necrotic tissue followed by administration of systemic antifungals like liposomal amphotericin B. Prosthetic obturator, or surgical closure, is the treatment for oronasal communication.[56] Supportive measures like hyperbaric oxygen can promote neovascularization of tissue and reduce acidosis.


Histoplasmosis is self-limited in immunocompetent patients. Intravenous amphotericin B is given for treating pulmonary histoplasmosis in immunosuppressed patients. Itraconazole can be given for localized infection, mild to moderate cases, and relapse prevention.[13]


Itraconazole is the first-line therapy in non-life-threatening conditions. Systemic administration of amphotericin B may be essential only in patients with immunosuppression.[15]


Localized cryptococcosis infection without any underlying systemic immunodeficiency can be treated with oral fluconazole. Cryptococcal meningitis is treated with amphotericin B and flucytosine in three phases: induction, consolidation, and maintenance.[57]


Patients with oral paracoccidioidomycosis are treated with oral itraconazole or ketoconazole.[30]


Treatment of oral Geotrichosis is similar to that of oral candidiasis.[53]

Differential Diagnosis

Oral candidiasis

White coated tongue, leukoplakia, lichenoid reactions, and secondary syphilis may mimic pseudomembranous candidiasis. The differential diagnosis for erythematous candidiasis includes thermal burns, erythroplakia, anemia, and oral mucositis.[4]


Histologically, granulomatous inflammation observed in aspergillosis can be similar to that seen in tuberculosis, syphilis, Wegener's granulomatosis, or leprosy.[58]


Palatal necrosis can be seen in other conditions like bacterial infection (actinomycosis), viral infection (herpes zoster), radiation, and trauma. Mucormycosis and aspergillosis often pose a diagnostic challenge that can be solved by evaluating the histopathological appearance of the fungal hyphae.[25]


Chronic histoplasmosis primarily affects the lungs causing clinical manifestations similar to tuberculosis: fever, weight loss, cough, dyspnea, and chest pain. Oral histoplasmosis is clinically indistinguishable from malignancy.[28]


Blastomycosis lesions resemble oral carcinoma both clinically and histopathologically. Hence careful histological demonstration of yeasts is essential.[29] The clinical course may also mimic bacterial infections like syphilis, tuberculosis actinomycosis, or autoimmune diseases like Crohn's disease and systemic lupus erythematosus.


Clinically oral cryptococcosis appears similar to histoplasmosis, paracoccidioidomycosis, tuberculosis, and malignancy.[59]


Oral lesions mimic malignancies and other granulomatous lesions.[30]


Oral geotrichosis resembles oral candidiasis.[32]


Oral Candidiasis

Oral candidiasis has a good prognosis when treated appropriately.[40] Recurrences may occur due to poor patient compliance or if the underlying predisposing factor is unresolved.


The prognosis of disseminated aspergillosis is poor for immunocompromised patients.[60] The mortality rate of invasive aspergillosis is almost 58%.[21]


Mucormycosis has a poor prognosis and is fatal in almost all cases of immunocompromised patients if dissemination occurs.[60] Prophylactic administration of oral posaconazole can be given to neutropenic patients or patients with graft-versus-host disease.


Prognosis is dependent on the immune status of the patient. HIV patients presenting with severe pulmonary and renal impairment have a poor prognosis. Disseminated histoplasmosis can be fatal if not treated.[13]


The mortality rate is approximately 2 to 6%. It is higher in patients with disseminated disease. Immunocompromised patients have a poor prognosis.[61]


Cryptococcosis can be life-threatening in patients with AIDS. Prognosis in HIV patients depends on antiretroviral therapy. Treatment with antiretrovirals during antifungal therapy can cause cryptococcal immune reconstitution inflammatory syndrome. Cryptococcal meningitis has a poor prognosis and a high mortality rate.[57]


The prognosis depends on the severity of the disease.[30]


Oral geotrichosis responds well to treatment.[32]


Oral Candidiasis

If not treated, oral candidiasis can lead to chronic persistent infection or invasive candidiasis, necrotizing ulcerative mucositis, and oropharyngeal and esophageal candidiasis. It may further progress to cause bronchitis, pneumonia, and endocarditis.[4]


Sinus infection is often invasive, involving the bone. The fungi invade the blood vessel wall resulting in thrombosis, hemorrhagic necrosis, and fatal bleeding. Hematogeneous spread to distant sites like eyes, brain, skin, and gastrointestinal tract can occur.[60]


The infection from the nasal cavity rapidly spreads to the paranasal sinuses and then to the orbit. Visual impairment and facial paralysis due to cranial nerve involvement can occur. If left untreated, the infection may spread to the brain through ethmoidal sinuses and orbit, resulting in death.[60]


A pathological fracture can occur as a result of progressive bone destruction. The infection may get disseminated to extrapulmonary sites like the adrenal gland, spleen, liver lymph nodes, and gastrointestinal tract.[13]


Dissemination occurs commonly on the skin. Other sites include bone, prostate, testicles, and central nervous system.[61]


Dissemination is common in immunocompromised patients and can occur in the skin, prostate, eyes, and bone. The infection may rarely spread to salivary glands.[57]


The oral lesion may precede the pulmonary infection. Hence lung evaluation is essential even in patients without pulmonary symptoms.[52]

Deterrence and Patient Education

Oral Candidiasis

The candidal load can be reduced in the oral cavity through proper oral hygiene practices and antimicrobial mouthwash. Denture-wearing patients must be instructed to remove their dentures at night, wash and place them in 0.2% chlorhexidine solution. Patients must also be counseled to quit the use of tobacco. Patients using inhaled steroids should be instructed to rinse the mouth with water every time after use.[33] Patients are advised to report to the dentist periodically for oral cavity examination and to check dentures' retention, fit, and stability. [4]


Patients at high risk of inhaling fungal spores like construction workers should wear protective masks, preferably an N95/P2 respirator. Patients with active sinus infections should avoid air travel since high altitude can worsen the pre-existing hypoxemia.[62]


Nonhealing of extraction sockets, especially in patients with diabetes or immunodeficiency, should raise high suspicion for mucormycosis.[56] Patients surviving the disease have severe maxillary or orbital destruction. Hence, rehabilitation of the defect is essential to restore the patient's quality of life.


Patients with oral histoplasmosis may subsequently develop disseminated disease. Hence there is a need for periodic evaluation of these patients.[28]


People involved in outdoor activities like hunting or fishing in wooded areas have an increased chance of acquiring the disease. Hence to prevent the disease, the soil should not be disturbed.[62]


Screening for cryptococcal polysaccharide antigen and preemptive therapy is vital in immunocompromised patients.[57] Following up with patients with oral cryptococcosis is essential to promptly recognize CNS infection or dissemination.[37]


Patient follow-up is essential to monitor the side effects of ketoconazole on liver function.[52]

Enhancing Healthcare Team Outcomes

To successfully manage oral fungal infections and eradicate underlying systemic disease, interprofessional healthcare team effort is required. Dentists play an important role in the early diagnosis of fungal infections and in referring patients appropriately to manage underlying conditions. Patient compliance is pivotal for preventing a recurrence. Hence, dentists, dental therapists, and dental hygienists should educate patients about oral health care. Pharmacists should emphasize compliance with the antimicrobial regimen, alert patients about antimicrobial resistance, and verify the appropriateness of the chosen agent for the pathogen.

Oral manifestation may be the first sign of systemic infections. Hence the primary health care provider must look out for oral lesions, especially in immunocompromised patients and those with uncontrolled diabetes. Nurses should provide the patients with appropriate counseling for tobacco cessation and ensure regular monitoring of blood sugar levels for patients with diabetes.

Attention should be given to the ventilation system in the hospital to prevent exposure to airborne fungal spores and thereby prevent nosocomial infections. Consultation with ENT surgeons, infectious disease specialists, thoracic surgeons, pulmonologists, and oncologists is indispensable in cancer patients undergoing radiotherapy and chemotherapy and infected with immunodeficiency viruses at increased risk of developing oral mycoses.

All interprofessional team members must be able to communicate with other team members regarding any patient status changes or concerns, and every interaction or intervention must be accurately recorded in the patient's medical record. Interprofessional coordination will drive optimal patient outcomes. [Level 5]

Article Details

Article Author

Divya Bose

Article Editor:

Melina Brizuela


3/19/2023 2:00:56 PM



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