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Symptoms and Signs
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Candidiasis (Invasive)(Candidosis; Moniliasis)

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(See also See also Fungal Skin Infections: Candidiasis (Mucocutaneous), see also Vaginitis, Cervicitis, and Pelvic Inflammatory Disease (PID): Candidal Vaginitis, and see also Immunodeficiency Disorders: Chronic Mucocutaneous Candidiasis.)

Candidiasis is infection by Candida sp (most often C. albicans), manifested by mucocutaneous lesions, fungemia, and sometimes focal infection of multiple sites. Symptoms depend on the site of infection and include dysphagia, skin and mucosal lesions, blindness, vaginal symptoms (itching, burning, discharge), fever, shock, oliguria, renal shutdown, and disseminated intravascular coagulation. Diagnosis is confirmed by histopathology and cultures from normally sterile sites. Treatment is with amphotericin B, fluconazole, echinocandins, voriconazole, or posaconazole.

(See also the Infectious Diseases Society of America's Guidelines for Treatment of Candidiasis.)

Candida sp are commensal organisms that inhabit the GI tract and sometimes the skin (see Fungal Skin Infections: Etiology). Unlike other systemic mycoses, candidiasis results from endogenous organisms. Most infections are caused by C. albicans or C. tropicalis; however, C. glabrata (formerly Torulopsis glabrata) is increasingly involved in fungemia, UTIs, and, occasionally, pneumonia or other focal disease.

Candida sp account for about 80% of major systemic fungal infections and are the most common cause of fungal infections in immunocompromised patients. Candidal infections are one of the most common hospital-acquired infections.

Photographs

Candidiasis (Oral)

Candidiasis (Oral)
Photographs

Candidiasis (Esophageal)

Candidiasis (Esophageal)

Candidiasis involving the mouth and esophagus is a defining opportunistic infection in AIDS. Although mucocutaneous candidiasis is frequently present in HIV-infected patients, hematogenous dissemination is unusual until immunosuppression becomes profound. Neutropenic patients (eg, those receiving cancer chemotherapy) are at high risk of developing life-threatening disseminated candidiasis.

Candidemia may occur in nonneutropenic patients during prolonged hospitalization. This bloodstream infection is often related to one or more of the following:

  • Multiple trauma
  • Surgical procedures
  • Multiple courses of broad-spectrum antibacterial therapy
  • IV hyperalimentation

IV lines and the GI tract are the usual portals of entry. Candidemia often prolongs hospitalization and increases mortality due to concurrent disorders. Prolonged or untreated candidemia may lead to endocarditis or meningitis as well as to focal involvement of skin, subcutaneous tissues, bones, joints, liver, spleen, kidneys, eyes, and other tissues. Endocarditis is commonly related to IV drug abuse, valve replacement, or intravascular trauma induced by indwelling IV catheters.

All forms of disseminated candidiasis should be considered serious, progressive, and potentially fatal.

Symptoms and Signs

Esophagitis is most often manifested by dysphagia. Symptoms of respiratory tract infections (eg, cough) are nonspecific.

Candidemia usually causes fever, but no symptoms are specific. Some patients develop a syndrome resembling bacterial sepsis, with a fulminating course that may include shock, oliguria, renal shutdown, and disseminated intravascular coagulation.

Candidal endophthalmitis starts as white retinal lesions that are initially asymptomatic but can progress, opacifying the vitreous and causing potentially irreversible scarring and blindness. In neutropenic patients, retinal hemorrhages occasionally also occur, but actual infection of the eye is rare.

Papulonodular skin lesions may also develop, especially in neutropenic patients, in whom they indicate widespread hematogenous dissemination to other organs. Symptoms of other focal infection depend on the organ involved.

Diagnosis

  • Histopathology and fungal cultures

Because Candida spp are commensal, their culture from sputum, the mouth, the vagina, urine, stool, or skin does not necessarily signify an invasive, progressive infection. A characteristic clinical lesion must also be present, histopathologic evidence of tissue invasion (eg, yeasts, pseudohyphae, or hyphae in tissue specimens) must be documented, and other etiologies must be excluded. Positive cultures of blood, CSF, pericardium or pericardial fluid or tissue biopsy specimens provide definitive evidence that systemic therapy is needed.

Serologic assays do not have sufficient specificity or sensitivity to be useful.

Photographs

Candida albicans

Candida albicans

Treatment

  • Amphotericin BSome Trade Names
    ABELCET
    AMBISOME
    AMPHOCIN
    AMPHOTEC
    Click for Drug Monograph
    for severe illness, otherwise an echinocandin or azole

Predisposing conditions (eg, neutropenia, immunosuppression, use of broad-spectrum antibacterial antibiotics, hyperalimentation, presence of indwelling lines) should be reversed or controlled if possible. IV amphotericin BSome Trade Names
ABELCET
AMBISOME
AMPHOCIN
AMPHOTEC
Click for Drug Monograph
is recommended for most severely ill patients, especially those who are immunosuppressed. Echinocandins are an alternative to amphotericin BSome Trade Names
ABELCET
AMBISOME
AMPHOCIN
AMPHOTEC
Click for Drug Monograph
in adults with or without neutropenia. FluconazoleSome Trade Names
DIFLUCAN
Click for Drug Monograph
400 to 800 mg po once/day is also considered a first-line drug (unless C. krusei or C. glabrata is involved) for nonneutropenic patients and may be effective in patients with neutropenia.

Esophageal candidiasis is treated with fluconazoleSome Trade Names
DIFLUCAN
Click for Drug Monograph
200 to 400 mg po or IV once/day or itraconazoleSome Trade Names
SPORANOX
Click for Drug Monograph
200 mg po once/day. If these drugs are ineffective or if infection is severe, voriconazoleSome Trade Names
VFEND
Click for Drug Monograph
4 mg/kg po or IV bid, posaconazoleSome Trade Names
NOXAFIL
Click for Drug Monograph
400 mg po bid, or one of the echinocandins may be used. These drugs are also effective for bloodstream and other hematogenously disseminated infections.

Last full review/revision April 2009 by Alan M. Sugar, MD

Content last modified February 2012

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