Kandidiasis

AT-A-GLANCE

 Candida species produce a variety of inflammatory mucosal and cutaneous

manifestations.

 Favored areas of involvement include the oral mucosa and lips, fingers and nails,
intertriginous zones, and genitalia.

 A variety of conditions can predispose patients to chronic mucocutaneous

candidiasis with diffuse skin, mucosal, and nail involvement.

 Candida can cause invasive disease, including bloodstream infection, and is the most
common culprit in fatal fungal sepsis.

 Risk factors for infection include extremes of age, malnutrition, obesity, diabetes,
and immune deficiency.

 In mucocutaneous disease, morphology can be very helpful in making a clinical

diagnosis, although confirmatory testing with potassium hydroxide preparations,
culture, and histopathology (and in invasive disease, serology and polymerase chain
reaction) also may be helpful.

 Treatment includes topical imidazoles and nystatin, and in more-severe disease,

systemic agents, including oral azoles and echinocandins.

 EPIDEMIOLOGY
 Candida yeasts are found throughout the environment and are also common
commensals of the human skin, oropharyngeal, respiratory, GI, and genital mucosa.
Candidal colonization has been reported in the oral mucosa of more than 40% of
healthy adults, with higher rates of carriage in women and smokers.1 At least 15 of
the more than 200 Candidaspecies have been implicated in human disease.
Although Candida albicans is the most commonly implicated Candida species in
localized mucocutaneous candidiasis, an increasing number of other species have
been implicated in mucocutaneous disease, including Candida glabrata, Candida
tropicalis, Candida krusei, Candida parapsilosis, and Candida
dubliniensis. Additionally, while albicans is still the single most common species, non-
albicans species collectively now account for the majority of invasive candidiasis and
candidemia.2 Other specific risk factors for infection are described below (see section
“Risk Factors”).
 CLINICAL FEATURES
 CUTANEOUS FINDINGS
 Localized Candida infection in the skin classically presents as beefy-red patches and
plaques with satellite papules and pustules at the periphery (Fig. 161-1).
Intertriginous areas, particularly the axillae, inframammary folds, groin folds, and
infrapannus area, are frequently affected, and maceration may be an additional
feature in these sites (Fig. 161-2A, B). Candida also may be implicated in miliaria
arising on occluded skin surfaces, manifesting as small monomorphous vesicles (Fig.
161-3). On oropharyngeal mucosal surfaces, background erythema with adherent
whitish material may be seen, as in the pseudomembranous form of oropharyngeal
candidiasis (thrush) (Fig. 161-4A, D), however an erythematous form, characterized
by a shiny depapillated lingual surface, as in median rhomboid glossitis, also occurs,
and may be seen in those who wear dentures (Fig. 161-4B). Additionally, fissuring
and crusting at the oral commissures may be seen in angular cheilitis (also known as
perleche; Fig. 161-4C). In breastfeeding women, nipple candidiasis may present with
shiny erythema of the areola and nipple, which may be associated with flaking of the
skin, and thrush may concurrently be apparent in the infant’s mouth.3 On genital skin
and mucosa, including the vulva, glans penis, and prepuce, Candida may present
with patchy erythema or erythematous plaques with associated itching and burning
sensation. In patients with vulvovaginitis, a thick, white, curd-like discharge is typical.
Pustules are seen more frequently in balanitis and balanoposthitis than in vulvitis
(Fig. 161-5). In the diaper area, the classic presentation is beefy-red erythematous
plaques with satellite papules and pustules (Fig. 161-2C). In the interdigital spaces,
particularly the third webspace of the hands, a macerated whitish plaque on
erythematous background (erosio interdigitalis blastomycetica) may be seen,
especially in patients with chronic exposure to moisture from wet work (Fig. 161-2D).
 FIGURE 161-1
 Typical morphology of cutaneous candidiasis demonstrating erythematous papules
coalescing into plaques, with satellite papules and vesiculopustules.
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 FIGURE 161-2
 Examples of Candida intertrigo. A, Erythematous papules becoming confluent over
the inguinal area with prominent satellite papules (with scrotal involvement, in
contrast to tinea cruris). B, Erythematous plaques with erosion and satellite
papules. C, Diaper candidiasis demonstrated erythematous, partially eroded plaques,
and satellite papules. D, Erosio interdigitalis blastomycetica demonstrating an
erythematous plaque with prominent maceration in the interdigital webspace.
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 FIGURE 161-3
 Miliaria caused by Candida seen on the forehead of a diabetic patient who had
applied a partially occlusive dressing for headache symptoms.
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 FIGURE 161-4
 A, Oral candidiasis (pseudomembranous form, thrush). Typical white palatal patches
and plaques. B, Atrophic candidiasis demonstrating a shiny erythematous
depapillated areas under areas in contact with dentures. C, Angular cheilitis
(perleche) demonstrating fissured erythematous plaques at the bilateral oral
commissures. D, Hyperplastic candidiasis on the dorsal lingual surface.
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 FIGURE 161-5
 Balanoposthitis caused by Candida demonstrating pustules on the glans penis and
foreskin.
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 Candida also has been implicated in chronic paronychia, which presents with
erythema of the proximal nailfold area with loss of the cuticle and skin breakdown
(sometimes with associated onycholysis and nail dystrophy; Fig. 161-6A). More
recently, however, the Candida has been hypothesized to play a secondary role as a
colonizer with either chronic wet work leading to skin barrier breakdown or chronic
contact dermatitis being the primary insult.4 Candida, usually starting as paronychia,
can also directly invade the nail plate and produce onychomycosis (5% to 10% of
onychomycosis overall is caused by Candida; Fig. 161-6B), and is implicated in
several presentations, including a distal subungual presentation and total dystrophic
 onychomycosis.5,6 Candida onychomycosis is more often seen in the fingernails than
in the toenails, and is often associated with pain on pressure or movement of the
nail plate (both of these features are in contrast to dermatophytes), and more often
affects the dominant hand.6 Exposure to moisture and occupational wet work are
important risk factors.
 FIGURE 161-6
 A, Chronic paronychia caused by Candida albicans demonstrating erythematous,
edematous proximal nailfold with onycholysis and mild dystrophy. B, Severely
inflammatory candidal paronychia that has spread to the nail plate to produce
onychomycosis.
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 Patients with chronic mucocutaneous candidiasis may present with erythematous
plaques with overlying scale reminiscent of plaque psoriasis (Fig. 161-7). In patients
with candidemia, the presence of skin lesions, most typically discrete sparse lesions
ranging from erythematous papules with central pallor or necrosis to erythematous
nodules to (less commonly) plaques, may be an important clue to the diagnosis (Fig.
161-8).7 The distribution favors the trunk and proximal extremities although the
head and face may be involved. These classic skin lesions are reported to appear
approximately 10% to 30% of the time in candidemia, and are most commonly seen
in C. tropicalis infection.8
 FIGURE 161-7
 Patient with chronic mucocutaneous candidiasis. Sharply marginated erythematous
plaques with prominent scaling, reminiscent of plaque psoriasis.
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 FIGURE 161-8
 Disseminated candidiasis with candidemia. Neutropenic febrile patient with acute
myeloid leukemia demonstrating erythematous papules and nodules on the hand,
some with central pustulation. Biopsy demonstrated Candida organisms and blood
cultures were positive for Candida tropicalis.
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 NONCUTANEOUS FINDINGS
 In patients with candidemia, the classic clinical triad of fever, rash, and myalgia has
been described as a sufficient basis for initiation of empiric treatment for
presumptive invasive candidiasis in a hospitalized patient.9 The myalgia is the result
of hematogenous dissemination of Candida to muscle (usually in the lower
extremities) causing muscle abscesses, clinically presenting with a warm, sore muscle
and seen in up to 25% of patients with candidemia.10 Additionally, chorioretinitis,
vitreitis, and endophthalmitis may result from hematogenous spread in roughly 4%
to 7% of patients with candidemia.11,12 Although a majority of patients do complain
 of symptoms that include visual changes (if able to articulate symptoms),
ocular Candida is also detected in asymptomatic patients.11
 COMPLICATIONS
 Candida may cause multiorgan failure as a manifestation of septic shock, or may
hematogenously disseminate to any organ in the setting of candidemia, with the
liver, spleen, kidneys, heart (and heart valves), and meninges among the more
common. Retinal involvement may be painless and result in permanent visual loss.
 ETIOLOGY AND PATHOGENESIS
 Although typically a commensal organism, Candida does act as an opportunistic
pathogen under favorable circumstances, including alteration in normal flora or
immune function, a breach of skin, or a breach of mucosal integrity. A variety of
virulence factors assist it in establishing infection, including, importantly, the ability
to adhere to human epithelial cells.13 Candida infection elicits both innate and
adaptive host immune responses largely through the interleukin-17 (IL-17) pathway,
and defects in this pathway, including in genes such as STAT1, STAT3, IL17F,
IL17RA, among many others, are associated with susceptibility to chronic
mucocutaneous candidiasis.14,15 Recent research also has identified that mutations in
caspase recruitment domain-containing protein 9 (CARD9), a molecule necessary for
the induction of T-helper-17 cells, result in a specific defect in the ability of
neutrophils to kill Candida, resulting in vulnerability to
invasive Candida infections.16Interestingly, the importance of the IL-17 pathway
to Candida susceptibility is borne out in patients taking the increasingly prevalent IL-
17–blocking medications, with early evidence suggesting an increase
in Candida infections in psoriasis and psoriatic arthritis patients taking the new anti–
IL-17 medications brodalumab, secukinumab, and ixekizumab.17
 RISK FACTORS
 Risk factors for localized/superficial Candida infections include extremes of age;
diabetes; obesity; pregnancy; HIV/AIDS (although prevalence has decreased
significantly in the era of highly active antiretroviral therapy)18; and use of broad-
spectrum antibiotics, corticosteroids, or immunosuppressive medications,
specifically anti–IL-17-blocking medications as discussed above. Risk factors for oral
candidiasis include xerostomia; wearing of dentures or other oral hardware; inhaled
and systemic corticosteroids; vitamin deficiencies; radiation therapy to the
head/neck; and hypothyroidism.1 Risk factors for invasive candidiasis/candidemia
include neutropenia and neutrophil dysfunction (including CARD9 mutations);
hematologic malignancy; stem cell transplantation; indwelling intravascular
catheters (including patients on hemodialysis); intensive care unit placement; and
immunosuppressive medications.19
 DIAGNOSIS
 Figure 161-9 is an algorithm summarizing current recommendations for diagnosing
cutaneous candidiasis.
 FIGURE 161-9
 Diagnostic algorithm for cutaneous candidiasis. H&E, hematoxylin and eosin; KOH,
potassium hydroxide; PCR, polymerase chain reaction.
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 SUPPORTIVE STUDIES
 The morphology may be distinctive and sufficient to make a clinical diagnosis in
many cases of superficial Candida skin infection. Rapid confirmation may be
achieved with bedside potassium hydroxide (KOH) preparation (either from a
scraping from an intact pustule, or a touch preparation from a punch biopsy
specimen) demonstrating pseudohyphae and budding yeast (Fig. 161-10).
 FIGURE 161-10
 Potassium hydroxide (KOH) preparation demonstrating Candida forms including
pseudohyphae and budding yeasts.
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 LABORATORY TESTING
 Definitive diagnosis and speciation can be achieved via either swab culture (taken
from an intact pustule if possible) or tissue culture from biopsy specimens taken
from affected areas. In patients suspected of having candidemia, positive blood
cultures are still considered the “gold standard” however with poor sensitivity
(approximately 50%), adjunctive techniques such as β-D-glucan assay and
polymerase chain reaction may be helpful.20
 PATHOLOGY
 Skin biopsies are of variable yield in making the diagnosis. While in localized
mucocutaneous candidiasis, organisms may sometimes be readily seen in the
epithelium with Grocott methenamine silver or periodic acid–Schiff staining, in
patients with disseminated candidiasis, organisms (sometimes forming
 microabscesses) are more likely to be found in and around the dermal blood vessels,
although sometimes only a mononuclear inflammatory infiltrate is seen.21
 DIFFERENTIAL DIAGNOSIS
 Table 161-1 summarizes the differential diagnosis for cutaneous candidiasis.
 TABLE 161-1Differential Diagnosis for Cutaneous Candidiasis
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 CLINICAL COURSE AND PROGNOSIS
 While most localized mucocutaneous Candida infections cause minor symptoms and
respond readily to treatment, in patients with underlying risk factors (see “Risk
Factors” before) infection may be recurrent and chronic, contributing to varying
degrees of morbidity although not life-threatening. By contrast, mortality in patients
with candidemia is significant, at 35% over 12 weeks in one larger study2; in some
case series, the mortality exceeds 80%.8
 MANAGEMENT
 Table 161-2 summarizes the management of cutaneous candidiasis. The Infectious
Diseases Society of America guidelines were most recently updated in 2016 (as of
this writing) and provide clinicians with comprehensive guidance in the treatment of
localized and disseminated Candida infections,22 as summarized below, and may be
consulted for further detailed recommendations. Areas not covered by these
guidelines include the treatment of localized cutaneous candidiasis, chronic
mucocutaneous candidiasis, paronychia, and onychomycosis, for which other
relevant sources are provided.
 TABLE 161-2Candidiasis Treatment Algorithm
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 CUTANEOUS CANDIDIASIS
 First-line treatment of localized disease includes topical formulations of imidazoles
(ketoconazole, clotrimazole, miconazole, econazole) in various formulations, which
may include creams or powders. Nystatin topical is also effective. More severe cases
typically require short courses of oral antifungals such as fluconazole 150 mg for
several doses.
 ORAL CANDIDIASIS
 Clotrimazole 10-mg troches 5 times daily or miconazole 50-mg buccal tablets for 1 to
2 weeks is first-line treatment, with nystatin suspension 100,000 units/mL, 4 to 6 mL
4 times daily for 1 to 2 weeks as an alternative. Moderate and severe cases may
require fluconazole 100 to 200 mg oral daily for 1 to 2 weeks.
Itraconazole, posaconazole, voriconazole, and amphotericin B solutions and
suspensions are alternatives for refractory or resistant disease. For denture wearers,
disinfection of dentures is an important adjunctive step to prevent reinfection; the
most effective methods for removal of Candida include soaking with commercially
available effervescent denture tablets or a dilute bleach concentration of 1:32 or
higher.23,24 For HIV-positive patients, initiation of highly active antiretroviral therapy
is recommended to decrease chances of recurrence. For patients with recurrent
disease, chronic suppressive dosing of fluconazole 150 mg orally 3 times weekly can
be helpful.
 PARONYCHIA AND ONYCHOMYCOSIS
 First-line treatment of Candida onychomycosis is itraconazole given orally as pulsed
dosing at 400 mg daily for 1 week monthly or 200 mg daily continuous dosing, for a
 total minimum duration of 4 weeks for fingernail and 12 weeks for toenail disease.
Fluconazole is considered equally effective and can be given at 50 mg daily or 300 mg
weekly dosing for similar durations. Although terbinafine has lower efficacy, cure
rates are improved by longer courses of 250 mg daily for 4 months or longer, which
makes compliance a potential concern.6
 For chronic paronychia, avoidance of wet work or wearing of gloves to keep the skin
dry is recommended. Given recent evidence that Candida colonization may play a
secondary role, with the primary insult being skin barrier breakdown resulting from
wet work and possible contact dermatitis,4 a role for topical corticosteroids has been
demonstrated. In a randomized trial, topical corticosteroids were shown to yield a
higher cure rate than systemic antifungals.25 Topical tacrolimus also is
effective.26 Topical imidazole solutions, as well as thymol 40% compounded in
ethanol or dilute acetic acid soaks, also have been used adjunctively in the treatment
of chronic paronychia.
 VULVOVAGINITIS AND BALANITIS
 Topical antifungals such miconazole and clotrimazole are first-line treatment
for Candidavulvovaginitis. Oral fluconazole (usually 150 mg in a single dose) is an
alternative. Two to 3 doses 72 hours apart are recommended for more-severe cases,
and even longer courses for recurrent cases. For balanitis and balanoposthitis,
topical antifungal creams, in some cases in conjunction with low- to mid-potency
topical corticosteroids, are employed.
 CHRONIC MUCOCUTANEOUS CANDIDIASIS
 Given the high likelihood of recurrence, prolonged courses of oral imidazoles or
newer triazoles (including voriconazole and posaconazole) are first-line treatment.
Because of the development of resistance, echinocandins, liposomal amphotericin,
or flucytosine is sometimes required.27
 DISSEMINATED CANDIDIASIS
 Treatment of patients with invasive candidiasis should be undertaken with the
assistance of an infectious disease specialist. Either an echinocandin
(caspofungin, micafungin, or anidulafungin) or fluconazole is a first-line treatment
recommended in hemodynamically stable immunocompetent patients.
 Neutropenic patients should be started on empiric echinocandin and switched to
fluconazole once stable.22 Resistance to azoles and echinocandins is a potential
concern, particularly in non–Candida albicans species disease and in patients with
prior exposure to these medications. Lipid formulation amphotericin B is an
alternative in situations of resistance to first-line agents. Followup blood cultures
and ophthalmologic examination are recommended for all patients with candidemia.
kandidiasis adalah infeksi jamur yang disebabkan oleh jamur Candida albicans. Infeksi jamur
ini biasanya terjadi di kulit, mulut, dan organ intim. Jika tidak mendapatkan penanganan,
infeksi akibat jamur ini bisa menyebar ke bagian tubuh lain, seperti usus, ginjal, jantung, dan
otak.
Candidiasis dapat dialami oleh siapa saja. Namun, orang dengan sistem kekebalan tubuh
yang lemah lebih berisiko terkena infeksi ini. Beberapa penyakit yang bisa menyebabkan
turunnya kekebalan tubuh adalah diabetes, kanker, dan HIV/AIDS.

Gejala Candidiasis
Penderita candidiasis memiliki gejala yang berbeda-beda, tergantung pada lokasi infeksinya.
Berikut adalah beberapa gejala candidiasis yang dibagi berdasarkan bagian tubuh yang
terserang:
Candidiasis mulut (thrush)

 Bercak putih atau kuning di lidah, bibir, gusi, langit-langit mulut, dan pipi bagian
dalam
 Kemerahan di mulut dan tenggorokan
 Kulit pecah-pecah di sudut mulut
 Rasa nyeri saat menelan

Candidiasis vulvovaginal
  Rasa gatal yang ekstrem di vagina
 Rasa nyeri dan terbakar saat buang air kecil
 Rasa tidak nyaman selama berhubungan seks
 Pembengkakan pada vagina dan vulva
 Keputihan yang menggumpal

Candidiasis kulit (cutaneous candidiasis)

 Ruam yang gatal di lipatan kulit, seperti ketiak, selangkangan, sela jari, atau di bawah
payudara
 Kulit yang kering dan pecah-pecah
 jika terjadi infeksi sekunder (infeksi kuman lain termasuk bakteri pada area kulit)

Kapan harus ke dokter

Lakukan pemeriksaan ke dokter jika Anda mengalami keluhan dan gejala yang disebutkan di
atas. Anda juga harus melakukan kontrol ke dokter jika memiliki faktor risiko yang bisa
meningkatkan terjadinya candidiasis, seperti menderita HIV, kanker, atau diabetes.
Jika Anda sudah didiagnosis mengalami candidiasis, lakukan kontrol sesuai jadwal yang
disarankan oleh dokter. Selain untuk memantau terapi, hal ini juga bertujuan mencegah
komplikasi.

Penyebab dan Faktor Risiko Candidiasis

Pada keadaan normal, jamur candida memang hidup di kulit dan beberapa bagian tubuh,
seperti mulut, tenggorokan, saluran cerna, dan vagina, tanpa menyebabkan gangguan
kesehatan.
Namun, jika jamur candida berkembang biak tanpa terkontrol atau masuk aliran darah,
ginjal, jantung, dan otak, hal ini dapat berbahaya bagi tubuh.
Pertumbuhan dan perkembangan jamur candida yang tidak terkendali paling sering
disebabkan oleh sistem kekebalan tubuh yang lemah. Beberapa kondisi yang bisa
melemahkan daya tahan tubuh adalah:

 Menderita diabetes, HIV/AIDS, kanker, atau menjalani kemoterapi

 Menggunakan obat kortikosteroid dalam jangka yang lama
 Menggunakan antibiotik dalam jangka waktu yang lama
 Menderita obesitas atau malnutrisi

Selain itu, beberapa faktor berikut juga bisa meningkatkan risiko terjadinya candidiasis pada
kulit dan area kelamin:

 Cuaca yang hangat dan lembap

 Kebiasaan jarang mengganti pakaian dalam
 Kebiasaan menggunakan pakaian yang tidak menyerap keringat
 Kebersihan pribadi yang buruk
Diagnosis Candidiasis
Dokter akan menanyakan seputar keluhan dan gejala yang dialami pasien, serta riwayat
kesehatan dan obat-obatan yang sedang dikonsumsinya. Dokter juga akan melakukan
pemeriksaan fisik menyeluruh, termasuk pemeriksaan pada kulit untuk melihat ruam yang
timbul.
Untuk memastikan diagnosis, dokter akan melakukan beberapa pemeriksaan penunjang,
seperti:

 Tes KOH, dengan mengambil sampel kerokan kulit untuk melihat jenis jamur yang
tumbuh di kulit
 Tes darah, dengan mengambil sampel darah untuk mendeteksi infeksi di tubuh
 Kultur jamur, dengan mengambil sampel dari darah dan jaringan tubuh untuk
mendeteksi jenis jamur yang menginfeksi tubuh
 Tes cairan vagina, dengan mengambil sampel cairan keputihan di vagina untuk
mendeteksi adanya pertumbuhan jamur dan jenis jamur yang menyebabkan infeksi
di vagina
 Tes urine, dengan mengambil sampel urine untuk mendeteksi adanya pertumbuhan
jamur candida di sampel urine.

Pengobatan dan Pencegahan Candidiasis

Tujuan pengobatan candidiasis adalah untuk mengatasi infeksi dan mencegah terjadinya
komplikasi. Saat sudah didiagnosis mengalami candidiasis, dokter akan memberikan
obat antijamur, sesuai dengan lokasi dan tingkat keparahan infeksi. Obat antijamur yang
dapat digunakan adalah:

 Amphotericin B
 Butoconazole
 Caspofungin
 Clotrimazole
 Flukonazol
 Miconazole
 Micafungin
 Nystatin
 Tioconale
 Vorikonazol

Komplikasi Candidiasis 
Candidiasis di kulit biasanya akan menimbulkan rasa tidak nyaman dan mengganggu
kepercayaan diri penderitanya. Jika infeksi menyebar ke aliran darah dan organ tubuh lain,
dapat terjadi komplikasi berupa sepsis dan gangguan pada organ yang terinfeksi.
Pada kasus tertentu, penyebaran candida ke selaput pembungkus otak (meningen) akan
menyebabkan meningitis.
Pencegahan Candidiasis
Candidiasis dapat dicegah dengan menjaga kebersihan pribadi dan sistem kekebalan tubuh.
Beberapa cara yang bisa dilakukan adalah:

 Jaga kebersihan mulut dan gigi dengan rutin menggosok gigi dan melakukan
pemeriksaan ke dokter gigi minimal 6 bulan sekali
 Hentikan kebiasaan merokok.
 Gunakan pakaian yang nyaman dan menyerap keringat
 Ganti pakaian, pakaian dalam, dan kaos kaku, secara teratur.
 Ganti pembalut secara rutin saat menstruasi.
 Konsumsi makanan bergizi seimbang dan probiotik.
 Bersihkan area vagina dengan air mengalir, serta hindari penggunaan panty liner dan
sabun pembersih kewanitaan tanpa anjuran dokter.
 Lakukan kontrol rutin ke dokter, jika Anda menderita penyakit yang bisa
melemahkan sistem kekebalan tubuh, seperti diabetes, kanker, atau HIV/AIDS.
 Kontrol rutin juga perlu dilakukan bila Anda menjalani kemoterapi atau
menggunakan obat kortikosteroid untuk waktu yang lama.
 Jangan menggunakan obat kortikosteroid dan antibiotik di luar anjuran dokter.