Candidiasis

Etiology

Over 200 species of Candida have been identified, with approximately 20 known to cause human infections.[2] Candida albicans (C albicans) is the predominant species worldwide and tends to be susceptible to most of the limited number of widely used antifungal antibiotics. Please see StatPearls' companion resource, "Candidemia," for further information. Several Candida species other than Candida albicans cause human disease and hold growing clinical significance. These organisms pose multiple challenges, including difficulty in clinical and microbiologic differentiation from C albicans, reduced susceptibility to commonly prescribed antifungal agents, and an increasing prevalence worldwide.[3][4] Recognition of nonalbicans Candida species remains essential for accurate diagnosis and effective management. The most common Candida species other than Candida albicans responsible for infections include:

• C glabrata (Nakaseomyces glabratus)
• C parapsilosis
• C tropicalis
• C krusei (Pichia kudriavzevii)
• C auris
• C guilliermondii
• C lusitaniae
• C dubliniensis

Candidiasis can generally be divided into superficial localized and deep-tissue invasive infections. The pathophysiology, clinical characteristics, management, and prognosis differ significantly for each.

Common Localized Candida Infections

Intertrigo

Intertrigo is an inflammatory condition of the epidermis that often becomes secondarily infected by Candida (see Images. Candida Intertrigo and Candida-Associated Intertrigo). Warm, moist regions of the skin, including the axilla, underlying areas of the breast, groin, and buttock folds, are most commonly involved. Diaper dermatitis is a common form of intertrigo. Please see StatPearls' companion resource, "Intertrigo," for further information.

Thrush

Oropharyngeal candidiasis is commonly seen in infants, older adults who wear dentures, people treated with antibacterials, and those treated with immunosuppressants. Individuals with impaired cellular immunity, eg, those with AIDS, are also at risk. In addition, individuals who use inhaled glucocorticoids for asthma or rhinitis are also at risk (see Image. Oropharyngeal Candidiasis). Please see StatPearls' companion resource, "Fungal Infections of the Oral Mucosa," for further information.

Esophageal Candidiasis

Esophageal candidiasis most commonly occurs in individuals with impaired cellular immunity, eg, those with AIDS (see Images. Candida Esophagitis and Candida Esophagitis Photomicrograph). However, other risk factors include cancer, diabetes mellitus, the use of proton pump inhibitors, chemotherapy, glucocorticoid use, recent antibiotic use, alcohol use, smoking, and peptic ulcer disease.[5][6] Before the advent of highly active antiretroviral therapy, HIV infection represented a significant risk factor. In immunocompetent people, the use of proton pump inhibitors represents a common risk factor.[7] Please see StatPearls' companion resource, "Esophageal Candidiasis," for further information.

Candidal Balanitis

Balanitis is an inflammation of the glans and foreskin, and most commonly occurs in uncircumcised men (see Image. Candida Balanitis). Candida is the most common cause of balanitis. Candida intertrigo is a risk factor in neonates and incontinent older adults. Additionally, diabetes in adults is an associated risk factor. Sexual transmission is a common source.[8] Please see StatPearls' companion resource, "Balanitis," for further information.

Vulvovaginal Candidiasis

Vulvovaginal candidiasis can occur due to hormonal changes, eg, pregnancy, oral contraceptive use, and menopause, as well as the treatment of infections (eg, bacterial vaginosis and trichomoniasis), which disrupts the microbiome in the vagina, allowing for Candida to overgrow (see Image. Vulvovaginal Candida Infection). C albicans is the etiology of approximately 40% to 90% of the cases, with the remainder due to species other than Candida albicans.[9] The use of products, eg, vaginal sprays, spermicides, and douches, can also increase the risk for vulvovaginitis, as well as wearing tight-fitting, wet, or perspiration-soaked clothing.[10] Please see StatPearls' companion resource, "Vaginal Candidiasis," for further information.

Mastitis

The relationship between Candida and mastitis is highly controversial.[11][12] Recent data indicate that bacteria, not yeast, are responsible for the majority of the cases of nipple and breast pain that may occur in nursing mothers. Candida cultured from the inflamed nipple and areola tissue in nursing women most likely represent commensal organisms that are present in the infant's oral cavity. Please see StatPearls' companion resource, "Acute Mastitis," for further information.

Invasive Candidiasis 

Invasive candidiasis is a life-threatening infection that includes candidemia and can involve many organ systems (see Images. Candida Endocarditis and Invasive Candida Infection of the Kidney.[13][3] Please see StatPearls' companion resource, "Candidemia," for further information.

Risk factors for invasive candidiasis include:

• Premature birth
• Admission to an intensive care unit (ICU)
• Vascular catheters
• Total parenteral nutrition
• Gastrointestinal perforation and anastomotic leak
• Use of broad-spectrum antibacterials
• Hyperglycemia
• Immunosuppression
• Immunodeficiencies
  • Hematologic malignancy
  • Solid organ or hematopoietic stem cell transplants
• Severe burns
• Major trauma

Epidemiology

Candida infections are most prevalent at the extremes of age. Approximately 45% of neonates, 45% to 65% of healthy children, 30% to 45% of healthy adults, and 50% to 65% of adults who wear removable dentures are colonized with C albicans in the oral cavity. The colonization rate is even higher in certain populations, eg, individuals living in acute and long-term care facilities (65% to 88%), individuals with acute leukemia undergoing chemotherapy (90%), and individuals living with HIV (95%).[14] In most cases, candidiasis occurs from a Candida strain that is a part of an individual's mycobiome. However, acquisition of new strains, eg, in the hospital environment, can also occur.[15] 

Superficial mucocutaneous Candida infections, eg, oropharyngeal candidiasis and diaper dermatitis, are prevalent in newborns, affecting approximately 10% to 20% of healthy infants at least once during the first few months of life.[16] Invasive infections are much less common, affecting neonates at a rate of approximately 5 to 10 cases per 100,000 live births.[17][18] Infections in neonates in the neonatal intensive care unit (NICU), particularly extremely low birth weight neonates, are more common.[19] C albicans accounts for approximately 50% to 60% of candidiasis in newborns, with C parapsilosis accounting for around 20% to 40% of cases.[20][21][22] Infections from other Candida species are less common. Infections caused by species other than Candida albicans tend to occur later in life and are more likely to be acquired in the hospital environment.[23]

Oral candidiasis develops in 9% to 31% of adults living with AIDS, and in 20% of individuals with cancer.[24] Up to 75% of women will have at least 1 episode of vulvovaginal candidiasis in their lifetime, with most episodes occurring during the reproductive years. Recurrent vulvovaginal candidiasis occurs in approximately 9% of women, with C albicans accounting for up to 90% of infections.[25] [9] 

Globally, an estimated 1.5 million people develop candidemia or invasive candidiasis annually.[26] Approximately 25,000 cases of candidemia occur in the United States every year, with an estimated incidence of 7 cases per 100,000 persons.[27] In one survey, C albicans accounted for 37% of cases, followed by C glabrata (30%), C parapsilosis (14%), C tropicalis (6%), and C auris (0.4%).[28] Invasive candidiasis is associated with longer hospitalizations and higher costs. The annual economic burden in the United States is approximately $1.8 billion.[3]

Pathophysiology

Candidiasis develops following overgrowth of Candida species associated with breakdown of host immune defenses or localized disruption of the microbiome. This overgrowth promotes pathogenicity through multiple virulence factors, including surface adhesion molecules that facilitate attachment to host cells. Tissue invasion occurs through several mechanisms, including the secretion of enzymes that facilitate tissue damage and enable deeper penetration, as well as switching from the yeast form to the hyphal form.[29]

Candida vulvovaginitis likely occurs from the migration of yeast from the rectum to the perineal region with subsequent vaginal colonization. Progression from asymptomatic colonization to symptomatic infection reflects a combination of factors, including organism overgrowth, penetration of the superficial epithelium, host inflammatory responses, and Candida virulence factors.[30]

Candida colonization in the neonate is typically a result of vertical transmission from the mother. Heavy maternal colonization with Candida or vulvovaginal candidiasis at the time of birth has been shown to increase the chance of neonatal colonization, particularly in the context of vaginal delivery or prolonged duration of premature rupture of membranes.[31] Horizontal transmission from either health care workers or the hospital environment has also been shown to play an important role in neonatal Candida colonization.[32][33]

Invasive candidiasis in children and adults develops after Candida species gain access to the bloodstream and disseminate to target organs. The 3 main routes by which Candida species gain access to the bloodstream are translocation across the gastrointestinal mucosal barrier, which represents the most frequent mechanism, especially among neutropenic patients and individuals in the ICU, colonization of medical devices, including intravascular catheters, which serves as another major source of candidemia, and localized infection (eg, one involving the urinary tract).[34][35]

Histopathology

When Candida species invade superficial tissues, histopathology of biopsied sections will show predominantly spongiotic changes in the epidermis, including irregular acanthosis, mild spongiosis, and inflammatory changes. The distinguishing feature of the superficial epidermis is the presence of neutrophils in the stratum corneum and upper layers of the epidermis. A small collection of neutrophils (spongiform pustulation) may form, which resembles impetigo or psoriasis.[36] 

C albicans grows partly as yeast and partly as elongated cells resembling hyphae, which form pseudomycelium (see Image. Candida Albicans Skin Scraping and Candida Albicans Yeast Form With Germ Tube). C albicans can be identified from other Candida species by growth characteristics, sugar assimilation, and fermentation tests. It produces germ tubes within 2 hours when incubated in human serum at 37 °C.

History and Physical

The clinical features of candidiasis vary based on the site of infection.

Intertrigo

Regions of the skin that are prone to friction and hyperhidrosis initially demonstrate erythema on both sides of the skin folds. Pruritus often leads to excoriations that evolve into macerated, crusting, and weeping patches (see Images. Chorioretinal Candida Lesion and Candida-Associated Intertrigo).

Thrush

Individuals with oropharyngeal candidiasis may lack symptoms. When symptoms are present, patients may experience a cotton-like feeling in the mouth, a loss of taste or unpleasant taste, and angular cheilitis. Denture stomatitis typically presents with erythema and swelling underneath the dentures, often appearing as a red or red-and-white patch on the palate, gums, or buccal mucosa. Individuals with denture stomatitis often will experience some pain, and those with Candida infection of the larynx may experience hoarseness. On physical exam, white plaques are often visualized on the tongue, palate, buccal mucosa, and oropharynx (see Image. Oropharyngeal Candidiasis).

Esophageal Candidiasis

Esophageal candidiasis typically causes dysphagia or odynophagia, most commonly over the retrosternum. Oropharyngeal candidiasis is often present on exam as well.

Candidal Balanitis

Balanitis is often associated with burning and itching of the distal shaft of the penis near the glans or foreskin and can also involve the thighs, buttocks, and scrotum. Diabetes is a risk factor. On exam, erythema, white patches, or white exudate can be present (see Image. Candida Balanitis). Inflammation of the foreskin can lead to constriction of the foreskin over the glans penis (phimosis), or trapping of the foreskin behind the glans penis (paraphimosis), which is a urologic emergency.[8] 

Vulvovaginal Candidiasis

Candida vulvovaginitis typically presents with vulvar itching, burning, and soreness. Dysuria and dyspareunia can also occur. Physical examination often reveals erythema of the vulva and vaginal mucosa. Excoriations and fissures of the vulva may be present. Vaginal discharge may be absent or copious, and when present, can range from thin and watery to white, thick, and clumpy (see Image. Vulvovaginal Candida Infection). 

Invasive Candidiasis

An appreciation of the risk factors for invasive candidiasis is very important when reviewing a patient's history. Signs and symptoms of candidemia and invasive candidiasis can include skin pustules due to cutaneous dissemination of the yeast, chorioretinitis resulting from ocular dissemination, sepsis, and multiorgan system failure (see Image. Chorioretinal Candida Lesion). 

Evaluation

Evaluation will vary based on the suspected site of infection.

Intertrigo

Intertriginous areas of skin characteristically include the skin folds between the buttocks, axillae, groin, and beneath the breasts. Erythema evolves into excoriated, macerated, and crusted patches. Diaper dermatitis is a common form of intertrigo.

Thrush

The diagnosis of oropharyngeal candidiasis is presumptively based on physical exam findings and risk factors. A definitive diagnosis is established by scraping the white plaques with a tongue depressor and performing a Gram stain or potassium hydroxide (KOH) preparation, which, on microscopy, reveals budding yeast with or without hyphae. Candida speciation, if needed, is determined by a fungal culture. 

Esophageal Candidiasis 

Esophageal candidiasis is typically diagnosed on upper endoscopy by visualization of white plaques attached to the mucosa. Microscopy of a biopsied sample will reveal yeast and hyphae invading mucosal cells (see Image. Candida Esophagitis Photomicrograph). Cultures can be performed on the biopsied tissue.

Candidal Balanitis

A presumptive diagnosis can often be made based on clinical appearance. Microscopic analysis of KOH or Gram stain smear of a skin scraping will reveal the typical yeast and pseudohyphal forms of Candida.

Vulvovaginal Candidiasis

In patients where Candida vulvovaginitis is clinically suspected, a sample of vaginal discharge can be collected for point-of-care testing with vaginal pH detection and microscopy. With Candida infections, vaginal pH is typically normal (4 to 4.5), which helps distinguish it from trichomoniasis and bacterial vaginosis, where the pH is typically greater than 4.5. Candida are often seen on a wet mount of the vaginal discharge after adding KOH, which destroys human cells and makes it easier to see budding yeast, pseudohyphae, and hyphae. However, microscopy is negative in up to 50% of patients with culture-confirmed Candida vulvovaginitis.[37] Alternatively, the vaginal discharge can be sent for a nucleic acid amplification test (NAAT), which is more sensitive than wet mount but has a longer turnaround time. In individuals with persistent or recurrent symptoms, cultures and antimicrobial sensitivity testing are indicated. Similar symptoms can result from a variety of etiologies, which should be considered among the differential diagnoses.[9] 

Invasive Candidiasis

Positive blood cultures and tissue biopsies establish a diagnosis of candidemia and invasive candidiasis, respectively. A positive Candida blood culture should never be interpreted as a contaminant. Blood cultures may be negative in 30% to 50% of individuals with disseminated candidiasis.[38][39] Growth in blood cultures can be slow, and the turnaround time is further delayed during species identification and analysis of antifungal susceptibilities. Certain species other than Candida albicans, eg, C glabrata, grow significantly more slowly in culture.[40] The absence of growth and the lag in identification contribute to delays in diagnosis and the initiation of therapy. Prior exposure to antifungals contributes to false-negative blood cultures. Thus, non-culture-based methods are increasingly being utilized.

Beta-D-glucan (BDG), a component of the Candida cell wall, can be detected in an assay of blood. BDG is also present in other fungi; the BDG assay has sensitivities of 70% to 80% and specificities of 55% to 80%, respectively.[41] A false positive BDG assay may result from a variety of causes, including bacterial infections, beta-lactam antibiotics, hemodialysis, immunoglobulin, albumin, bowel ischemia, mucositis, gauze bandages, extensive burns, uremia, and liver failure.[42] Matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF-MS) can reduce the time to speciate and obtain susceptibilities from positive blood cultures.[43] Peptide nucleic acid-fluorescence in situ hybridization (PNA-FISH) is capable of identifying Candida species directly from positive blood cultures within 1.5 hours.[44] Molecular methods, including NAAT and the T2Candida assay, are rapid, nonculture diagnostic technologies with high sensitivity and specificity.[45][46] Mouratidou et al provide an excellent, detailed discussion of diagnostic techniques.[47]

Treatment / Management

Intertrigo

Intertrigo treatment involves minimizing the causes of the skin irritation and inflammation. This may include the use of drying agents, loose clothing, anti-persperants, petrolatum ointment, and absorbent diapers. The use of topical and oral antifungal agents may be required in severe and recalcitrant cases. Please see StatPearls' companion resource, "Intertrigo," for further information.

Thrush

The topical agents, nystatin, clotrimazole, and miconazole, are recommended for mild cases of oropharyngeal candidiasis. For moderate-to-severe cases, oral fluconazole is recommended. Itraconazole oral solution, posaconazole suspension, voriconazole, and isavuconazole are used to treat fluconazole-resistant Candida. Amphotericin B oral suspension has been used to treat azole-resistant infections. The echinocandins are an option for severe and recalcitrant thrush.

The choice of antifungal agent and the duration of therapy should be based on pharmacologic principles that consider potential drug interactions, pregnancy and lactation, cost, and the patient's immune status.[48] Please see StatPearls' companion resource, "Antifungal Agents," for further information on antifungal therapies. Inhaled glucocorticoids are a risk factor for thrush, and patients should be instructed to rinse with water immediately after use.[49] Dentures should be properly fitted and disinfected after use.[50] Please see StatPearls' companion resource, "Fungal Infections of the Oral Mucosa," for further information.(B3)

Esophageal Candidiasis

Treatment requires systemic antifungals. If tolerated, oral fluconazole is preferred and is generally given daily for 14 to 21 days. For patients unable to take oral medications, intravenous administration is required. In cases of fluconazole resistance or a recalcitrant infection, other azoles, echinocandins, and amphotericin B are alternative options. As noted above, the choice of therapy should be individualized and based on sound pharmacologic principles. When possible, efforts to minimize exposure to antibacterials and immunosuppressants should be attempted.[51]

Candidal Balanitis

Either topical or oral antifungals are recommended for treatment. A single oral dose of fluconazole was found to be equivalent to a 7-day multiple-dose regimen of clotrimazole ointment.[52] The single-dose strategy led to improved compliance and overall response. Proper hygiene should be encouraged. In recalcitrant cases, consideration should be given to the presence of fluconazole-resistant Candida, and antifungal therapy should be modified on that basis.

Vulvovaginal Candidiasis

Both topical and oral azole antifungal agents are equally efficacious in the treatment of uncomplicated vulvovaginal candidiasis.[53] A 3-day course of topical treatment is recommended. Oral azole antifungals should be avoided in pregnancy due to concerns about teratogenicity, whereas topical azoles are safe to use. Approximately 10% of women who have had an episode of vulvovaginal candidiasis will experience a recurrence, and more than 50% of that population will experience additional recurrences after completing courses of maintenance therapy.(B3)

Confirming that their symptoms are, in fact, due to Candida and obtaining antifungal sensitivities is key to management. Infections due to non-albicans Candida are increasing in frequency. Fluconazole is commonly used in this setting, and long-term suppressive therapy lasting several months is recommended. Oteseconazole is a new azole that is indicated for recurrent Candida vulvovaginitis.[54] This medication has a half-life of 138 days, retains activity against many fluconazole-resistant Candida species, and may be a preferred azole agent in this setting. Ibrexafungerp, a new oral beta-D-glucan synthase inhibitor, has been approved for treatment.[55] This medication achieves high vaginal concentrations, is active against fluconazole-resistant Candida, and is effective in treating recurrences; however, Ibrexafungerp is not approved for treatment in pregnant women. Please see StatPearls' companion resource, "Vaginal Candidiasis," for further information.

Invasive Candidiasis

Detailed treatment recommendations are beyond the scope of this article due to the variety of Candida species, their antifungal susceptibility profiles, the diverse characteristics of the host, the source of the Candida, and the varying complexities of the infection. Excellent, published treatment guidelines are recommended.[56][57][58] While C albicans is the predominant species of infection in many parts of the world, non-albicans Candida can predominate in several geographic regions; they are increasing in prevalence worldwide and vary in their antifungal susceptibilities. Adding to the complexity of treatment are the cumulative delays associated with Candida growth in culture (assuming they grow in the first place), speciation, and antifungal susceptibilities. (Please refer to the Evaluation section for more information on Candida culture.)(A1)

In general, several strategies are designed to initiate treatment as promptly as possible, including antifungal prophylaxis for high-risk patients, empiric therapy administered before Candida is identified, and targeted therapy once the organism and its susceptibility are confirmed.[58] Please see StatPearls' companion resource, "Antifungal Agents," "Candidemia," "Candida auris," "Febrile Neutropenia," "Fungal Endopthalmitis," "Fungal Endocarditis," "Renal Abscess," and "Splenic Abscess," for further information.

Prophylactic antifungal treatment

Prophylaxis is recommended for newborns weighing less than 1000 g, patients experiencing prolonged neutropenia, critically ill patients with gastrointestinal perforation or anastomotic leak, and solid organ and hematopoietic transplant patients. In low-weight neonates, fluconazole prophylaxis is recommended. Patients receiving cytoreductive chemotherapy are at risk of invasive candidiasis due to drug-induced mucosal damage as well as the presence of central vascular access catheters. Prophylaxis with either fluconazole or voriconazole is recommended during the duration of neutropenia. 

Antifungal prophylaxis is recommended for critically ill patients in the intensive care unit (ICU) who have any of the following: gastrointestinal perforation, anastomotic leak, solid organ transplant, or hematopoietic transplant.[47] Fluconazole prophylaxis is recommended unless there has been recent exposure or high rates of azole resistance in the ICU, in which case echinocandins should be used.

Empiric therapy

Empiric therapy is initiated in high-risk patients with suspected candidemia while awaiting culture results. Patients with neutropenia who remain persistently febrile despite receiving prophylactic azoles and broad-spectrum antibacterials should receive an echinocandin. Liposomal amphotericin B is an alternative if echinocandins are unavailable or not tolerated. High-risk, critically ill nonneutropenic patients should be carefully assessed for surrogate markers of invasive candidiasis, including yeast colonization and the BDG assay.

In the presence of unexplained fever or sepsis despite broad-spectrum antibacterial therapy, echinocandin antifungal therapy should be considered because of its broad antifungal activity and safety profile.[59][57] Fluconazole is an acceptable alternative if the patient has not received recent azole therapy and when the prevalence of azole-resistant Candida is low. Liposomal amphotericin B is an acceptable alternative when echinocandins are unavailable or not tolerated. Clinicians should note that, currently, no studies have demonstrated a definite mortality benefit in the cohort of critically ill patients who receive preemptive antifungal therapy. Clinical risk prediction scores are being assessed in an effort to identify patients most likely to benefit from empiric and preemptive therapy.[60][61](A1)

Targeted therapy 

In neonates with invasive candidiasis, amphotericin B deoxycholate is recommended as initial treatment. Fluconazole is an alternative for neonates who have not received azole prophylaxis. Neonates with candidemia should have an ophthalmic exam and a lumbar puncture. For the treatment of neonatal central nervous system Candida infections, either amphotericin B deoxycholate or liposomal amphotericin B is recommended as initial therapy. Fluconazole can be administered as step-down therapy should azole-sensitive Candida be identified.[57](A1)

In neutropenic patients with candidemia, echinocandins are recommended. Liposomal amphotericin B is an acceptable alternative, although comparatively higher rates of toxicity should be anticipated. In patients who have not received azole prophylaxis and when the prevalence of azole resistance is low, fluconazole is an acceptable alternative. A transition from echinocandins or liposomal amphotericin B to fluconazole can be made if the candidemia is subsequently found to be susceptible and blood cultures have turned negative.[57] Central vascular catheters should be removed as soon as feasible if they are considered a potential source of infection. (A1)

Echinocandins should be considered first-line therapy in nonneutropenic patients with candidemia and invasive candidiasis. Liposomal amphotericin B is an acceptable alternative if the Candida is likely to be resistant to echinocandins and azoles. The transition from an echinocandin or liposomal amphotericin B to fluconazole should be considered if the Candida is susceptible and follow-up blood cultures are negative. A central vascular catheter should be removed if the catheter is likely to be the source of the infection. Patients with candidemia should receive an ophthalmologic examination. Follow-up blood cultures should be obtained either daily or every other day until negative. Should fungemia persist after removal of the vascular catheter and while on antifungal therapy, a search for metastatic foci of infection should be undertaken. Common sites of metastatic infection include the eye, heart valves, kidney, liver, spleen, and osteoarticular structures. 

Differential Diagnosis

Intertigo

Differential diagnoses that should be considered along with intertigo include:

• Other infectious causes 
  • bacteria
  • viruses
  • dermatophytes 
    • tinea, trichophyton, microsporum, and epidermophyon
• Seborrheic dermatitis
• Irritant or allergic contact dermatitis
• Atopic dermatitis
• Inverse psoriasis
• Pemphigus
• Scabies
• Metabolic derangements
• Malignancies

Thrush

Differential diagnoses that have similar clinical features to thrush include:

• Oral mucositis
• Erythroplakia
• Thermal burns
• Erythema migrans
• Anemia
• Leucoplakia
• Angioedema
• Apthus stomatitis
• Herpes gingivostomatitis
• Measles (Koplik spots)
• Perioral dermatitis
• Stevens-Johnson syndrome
• Histiocytosis
• Blastomycosis
• Lymphohistiocytosis
• Diphtheria
• Syphilis
• Streptococcal pharyngitis

Esophageal Candidiasis

Differential diagnoses that should be considered along with esophageal candidiasis:

• Other causes of odynophagia
  • Esophageal stricture
  • Neoplasia
  • Eosinophilic esophagitis
  • Achalasia
  • Medication-induced esophagitis
  • Radiation-induced esophagitis
  • Bacterial, viral, other fungi, and parasitic causes of esophagitis 

Candidal Balanitis

Differential diagnoses that have similar clinical features to balanitis include:

• Bacteria
• Other fungi
• Viruses
• Scabies
• Contact dermatitis
• Drug allergy
• Lichen planus
• Lichen sclerosis
• Psoriasis
• Eczema
• Edema
• Neoplasia
• Chemical irritants
• Trauma

Vulvovaginal Candidiasis 

Differential diagnoses that have similar clinical features to vaginal candidiasis include:

• Allergic reaction
• Atopic dermatitis
• Lichen sclerosis
• Lichen simplex chronicus
• Neoplasm
• Paget disease
• Physiologic leukorrhea
• Psoriasis
• Sexual abuse
• Vulvodynia
• Bacterial vaginosis
• Trichomoniasis

Invasive Candidiasis

The differential diagnosis is extensive and includes all the causes of fever, sepsis, septic shock, and multiorgan system failure. 

Prognosis

Intertrigo

The prognosis is excellent when the underlying risk factors, eg, diabetes, hyperhidrosis, and obesity, are addressed.

Thrush

The prognosis is excellent with proper management.

Esophageal Candidiasis

The prognosis is excellent when the underlying risk factors, eg, immunocompromised states, are treated.

Candidal Balanitis

The prognosis is excellent when the underlying risk factors, eg, diabetes, incontinence, poor hygiene, immunosuppression, and a tight foreskin, are addressed.

Vulvovaginal Candidiasis 

Recurrences are common and can be caused by endogenous relapse of persisting organisms, exogenous reinfection with the same Candida strain, or by a new exogenous strain.

Invasive Candidiasis

Mortality rates range from 35% to 70%. Factors that negatively affect survival rates include delays in initiating antifungal therapy, poor underlying health, lack of source control, and infections caused by species other than Candida albicans species, eg, C auris and C tropicalis.

Complications

Intertrigo

If left untreated, Candida intertrigo can become secondarily infected by bacteria and progress to cellulitis. On rare occasions, topical antifungals can cause contact dermatitis.

Thrush

In immunocompromised hosts, thrush can progress to esophageal candidiasis.

Esophageal Candidiasis

Complications that are associated with esophageal candidiasis include:

• Ulcerations
• Perforation
• Malnourishment
• Candidemia
• Stricture
• Bronchial fistula

Candidal Balanitis

Complications associated with balanitis include phimosis.

Vulvovaginal Candidiasis 

Complications associated with vulvovaginal candidiasis include:

• Chronic and recurrent vulvovaginal candidiasis 
• Dyspaerunia 

Invasive Candidiasis

Candidemia and invasive candidiasis can potentially involve every organ system and result in sepsis syndrome and multiorgan system failure.