CANDIDIASIS
Salient
features
·
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.
Introduction
Virtually every individual in the
world experiences at least one episode of clinically apparent candidal disease
in his or her lifetime.
Yeasts are opportunistic pathogens that
require certain predisposing factors to trigger diseases. Yeast infections
therefore mainly affect people with a weakened immune system ("very young,
very old, and very sick").
Candida species are ubiquitous
yeast-like fungi that form true hyphae, pseudohyphae, and budding yeasts. This ability to simultaneously display several
morphological forms is known as polymorphism. Candidiasis (or candidosis) refers to
a various yeast infections caused by members of the genus Candida, and
predominantly by Candida albicans.
Candida yeasts
are found throughout the environment and are also found as common commensals in
the human skin, oropharyngs, upper respiratory tract, GI, and female
genital mucosa.
Candida species
are the most common cause of fungal infection in immunocompromised persons.
More than 90% of persons infected with HIV not receiving highly active
antiretroviral therapy (HAART) develop oropharyngeal candidiasis and 10% of
these patients develop oesophageal candidiasis.
EPIDEMIOLOGY AND
ETIOLOGY
Ecology
Gastro‐intestinal tract carriage
Candida
albicans is
a normal commensal of the gastro‐intestinal tract. Colonization with C.
albicans or another species may occur during birth directly from the birth
canal, at some time during infancy or perhaps later in life. Oropharyngeal
colonization with Candida is observed in up to 50% of healthy
individuals and may also be detected in 40%–65% of normal stool samples with
higher rates of carriage in women, smokers and antibiotic therapy. Candida resides particularly on the posterior
dorsum of the tongue
Vaginal carriage
C. albicans exists as a
commensal organism in the vaginal mucosa of 20%–25% of asymptomatic, healthy women; pregnancy,
oral contraception, and intrauterine devices increase the incidence of
carriage. Vulvovaginal
candidiasis (VC) is the second most common cause of vaginitis in women.
Cutaneous carriage
The skin is not a natural reservoir for Candida albicans or
for other species. However, in the skin
adjacent to the body orifices and the skin of the fingers, which are in
frequent contact with the mouth, often yield C. albicans and sometimes
other species, particularly C. parapsilosis and C. guilliermondii.
Candida may be a persistent colonizer of moist intertriginous sites in
individuals as well as the subungual space in patients with pre‐existing nail disease. Note
that this is colonization, not an infection, although the latter can manifest
relatively quickly when certain predisposing factors occur.
Pathogenesis
Candida
is dimorphic yeast that, under appropriate conditions, has the ability to
transform from a budding yeast phase to an invasive mycelial growth phase,
which is necessary for tissue invasion. Candida
species are facultatively pathogenic, opportunistic yeasts. The occurrence of
certain local and systemic conditions on the part of the host can be triggers
for the conversion of the commensal into the pathogenic form. Morphologically,
this step is characterized by the transition from the yeast phase to the
mycelium phase.
A healthy skin and a healthy mucous
membrane environment represent an effective barrier function against pathogens.
When
the local ecology is disturbed, or where there is an immune defect, Candida overgrowth
may lead to an opportunistic infection. Common predisposing factors for
superficial candidiasis include a warm, humid environment; hyperhidrosis;
occlusion of skin and hair follicles; extremes of age (neonates and adults >65
years of age); pregnancy; malnutrition; obesity; use of medication such as oral
contraceptive, antibiotic and systemic corticosteroid; diabetes mellitus; and
immunosuppression.
The most common cause of superficial
candidiasis is Candida albicans. Occasionally, other species such
as Candida glabrata, Candida tropicalis, Candida krusei, and Candida
parapsilosis can be pathogenic. Candidiasis is usually an endogenous
infection.
Factors
Predisposing to Candida Infections
Importantly, host defences
and iatrogenic causes both play a significant role in the development of
candidal infections. Associational and causal factors predisposing to Candida
infection are outlined:
|
MECHANICAL FACTORS ·
Dentures ·
Local occlusion (dressings or
garments), moisture, and/or maceration ·
Obesity ·
Trauma |
|
NUTRITIONAL FACTORS ·
Avitaminosis (vitamin A and C) ·
Generalized malnutrition ·
Iron deficiency (chronic mucocutaneous
candidiasis) ·
Parenteral hyperalimentation |
|
PHYSIOLOGIC ALTERATIONS ·
Extremes of age ·
Menses ·
Pregnancy |
|
SYSTEMIC ILLNESSES ·
Acrodermatitis enteropathica ·
Down syndrome ·
Endocrine disease ·
Cushing disease ·
Diabetes mellitus ·
Hypoadrenalism ·
Hypoparathyroidism ·
Hypothyroidism ·
Acute and chronic renal failure
(hemodialysis) ·
Bone marrow transplantation ·
Malignancy (especially hematologic,
thymoma) ·
Solid organ transplantation (liver,
kidney) ·
Immunodeficiency ·
Acquired immunodeficiency syndrome ·
Severe combined immunodeficiency
syndrome ·
Myeloperoxidase deficiency ·
Chédiak–Higashi syndrome ·
Hyperimmunoglobulinemia E syndrome ·
Chronic granulomatous disease ·
DiGeorge syndrome ·
Nezelof syndrome ·
Hypocomplementemia ·
Granulocytopenia |
|
IATROGENIC ·
Indwelling catheters and
intravenous lines ·
Prolonged hospitalizations ·
X-ray irradiation ·
Medications ·
Corticosteroids ·
Other immunosuppressive agents ·
Antibiotics (especially broad
spectrum, metronidazole) ·
Oral contraceptives (especially estrogen
dominant) ·
Phenylbutazone ·
Chemotherapy |
CLASSIFICATION
Candidosis of the
oral mucous membranes
·
Acute pseudomembranbous candidosis
·
Acute erythematous candidosis
·
Chronic pseudomembranous candidosis
·
Chronic erythematous candidosis
·
Chronic plaque‐like candidosis
·
Angular cheilitis
·
Median rhomboid glossitis
Candidosis of the
skin and genital mucous membranes
·
Candida intertrigo (flexural
candidosis)
·
Acute vulvo‐vaginal candidosis
·
Chronic vulvo‐vaginal candidosis
·
Candida balanitis
·
Perianal and scrotal candidosis
·
Perineal candidosis of infancy
Candidosis of the
nail and paronychium
·
Candida paronychium
·
Candida onychomycosis
Candidosis of oral mucous membranes
Pathophysiology
C albicans is
a dimorphic fungus that asymptomatically inhabits the mouths of almost 50% of
the population. Overgrowth of Candida is
protected against by local T cells and interleukin (IL)–17. Thus,
when immunity is compromised, growth proceeds unchecked and leads to
opportunistic infections.
Candidiasis is seen in people
with altered local ecology, which in oral cases can be attributed to dental
appliances, xerostomia, antimicrobials, nasopharyngeal steroids, or oral
cancer. Impaired systemic immunity is another major cause of infection, notably
in patients who are on immunosuppressive therapy, infected by HIV, or have
diabetes.
C albicans is the
predominant causal organism of most candidiasis. Other species, such as Candida tropicalis and Candida stellatoidea,
more often appear in persons who are severely immunocompromised.
Secreted aspartyl proteinases
(SAPs) are proteins secreted by Candida that
contribute to virulence by facilitating invasion and inflammation. The
prevacuolar protein sorting gene, VPS4,
is required for extracellular secretion of SAPs, and it is a key component of
the virulence of Candida.
Additionally, studies have shown that women with vulvovaginal candidiasis have
higher levels of SAPs in their vaginal fluid.
In those with dental
devices, Candida,
upon attachment, can form a small subcolony of persister cells. These cells
have been shown to be highly resistant to antimicrobials, and they provide a
mechanism for the recurrent formation of biofilms.
Risk Factors
Candidiasis of oral mucosa is more likely to
develop when there is local or general immunosuppression. Immunosuppression is the most significant of these, and
it can be due to diabetes, antibiotics, immunosuppression, systemic steroid
use, and HIV infection, among others.
·
Immunocompromise: Increased
carriage rates are seen in several conditions, including HIV infection,
diabetes, systemic steroid use, aerosolized steroid use, immunosuppression, and
malignancy.
·
Hypo salivation: Increases
carriage of Candida and
can be due to drug effects (antipsychotics), Sjögren syndrome, radiotherapy, or
chemotherapy
·
Poor oral hygiene: Candida counts
increase during sleep but are reduced by eating and brushing the teeth
·
Dentures: Removal and
reinsertion of dentures cause increases in salivary candidal counts, suggesting
that plaque on the dentures harbours C
albicans
·
Missing teeth: Being edentulous
increases the overlap of skin at the corners of the mouth, increasing the risk
for angular cheilitis formation
·
Smoking: Increases Candida carriage by
30-70%
·
Antibiotic use: broad
spectrumantibiotic increases carriage of Candida
·
Vitamin deficiencies: Higher
association of candidiasis with vitamin B-12 and iron deficiency
Apart from systemic steroid therapy, local
applications of steroids in the form of steroid creams, mouthwashes and
lozenges for the treatment of aphthosis or lichen planus of the mouth may
predispose to candidosis.
Candida can secondarily invade other oral
conditions. In all cases, the removal of
Candida often speeds the recovery even though the yeast is only a contributory
cause.
Intraoral
candidosis
|
Type of candidosis |
Usual age at onset |
Predisposing factors * |
|
Acute
pseudomembranous candidosis (thrush) |
Any |
Local: dry mouth,
antimicrobials General:
corticosteroids, leukaemia, HIV |
|
Acute
atrophic candidosis (‘antibiotic mouth’; antibiotic sore mouth) |
Any |
Broad‐spectrum
antibiotics or corticosteroids |
|
Erythematous
candidosis |
|
Any,
HIV especially |
|
Chronic
atrophic candidosis (denture‐related stomatitis) |
Adults |
Denture
wearing, especially at night |
|
Chronic
hyperplastic candidosis (candidal leukoplakia)† |
Usually
middle aged or elderly |
Tobacco
smoking, denture wearing, immune defect |
|
Median
rhomboid glossitis |
Third
or later decades |
Tobacco
smoking, denture wearing, HIV |
|
|
|
|
*Immune defects can predispose to any form.
Acute
pseudomembranous candidiasis
Definition
The characteristic sign of this condition is
a sharply defined patch of creamy, crumbly, curd‐like, white pseudomembrane,
which, when removed, leaves an underlying erythematous base.
Predisposing factors
Healthy
neonates, who have yet to develop immunity to Candida species, may develop thrush;
preterm infant are especially susceptible. Apart from in neonatal oral
candidosis (as distinct from Candida carriage), acute pseudomembranous
candidosis is usually secondary to local or general predisposing factors,
notably diabetes mellitus, systemic steroid and broad spectrum
antibiotic use, xerostomia,
pernicious anemia, malignancy, radiation to head and neck and severe T‐cell mediated immunodeficiency. Thrush is a common and early feature of HIV
infection and may be a portent of developing AIDS.
Pathology
The pseudomembrane consists of desquamated
epithelial cells, fibrin, leukocytes, food debris and fungal mycelium that
attach it to the inflamed epithelium.
Clinical features
Acute
pseudomembranous candidiasis or thrush is the most common form of oral candidiasis. There may
be one or many patches. Thrush appears as sharply defined discrete soft creamy plaques of
white cheese or milk curds like pseudomembrane that may become confluent on the buccal
mucosa, the
gums or hard/soft
palate.
Removal
of the plaques with a dry gauze pad exposes a raw, brightly erythematous, and
sometimes bleeding base. Microscopic examination of this material reveals
masses of tangled pseudohyphae and blastospores. In immunocompromised patients, the
dorsum of tongue may be affected as well. In severe cases, extension to the
pharynx down into
esophagus
and
tracheobronchial tree (AIDS-defining conditions) may occur. In severe cases, the mucosal
surface may ulcerate. Oral candidosis is the most common secondary
infection in those with AIDS, and recurrent or more prolonged episodes are to
be expected in these patients. In general, the course of the disease
is often mild, with abnormal sensations (taste disorders, furry sensation) as leading
symptoms.
Acute atrophic
candidiasis (Acute erythematous candidiasis)
Definition
In this condition, there is marked soreness
and denuded, atrophic, erythematous mucous membranes, particularly on the
dorsum of the tongue. It may occur after sloughing of the thrush pseudomembrane,
when traces of the residual membrane will often be found.
Predisposing factors
It is
observed most often in the setting of broad-spectrum antibiotic or systemic or inhaled
steroids therapy and
HIV infection.
Clinical features
Erythematous
areas on the dorsum of the tongue, palate, or buccal mucosa are characteristic.
The most
common location is on the dorsal surface of the tongue, where depapillated,
smooth, shiny and red atrophic patches with minimal pseudomembrane formation
are noted. Angular
stomatitis may also be present. In those taking antimicrobials, a sore red
mouth, especially of the tongue, may be present. There are both asymptomatic and
symptomatic variants, the latter characterized by burning or pain.
Chronic pseudomembranous candidosis
This does not differ clinically from the
acute pseudomembranous variety but, as the name suggests, lesions are very
persistent. It occurs principally in immunocompromised patients.
Chronic atrophic
candidiasis (chronic erythematous candidiasis/denture stomatitis)
Definition
This common form of mild, chronic, atrophic oral
candidosis occurs only beneath a denture, usually a complete upper denture.
Epidemiology
Incidence
It is
seen in nearly
one‐quarter of all denture wearers.
Age and sex
It is a disease mainly of the middle‐aged or elderly and is more prevalent in women than men.
Patients appear otherwise healthy.
Predisposing factors
Dental appliances (mainly maxillary dentures),
especially when worn throughout the night, or with a dry mouth, are the major
predisposing factor. Diabetes, immunosuppressive therapy or a high‐carbohydrate diet occasionally predispose and HIV is a rare
underlying factor. Presumably, the chronic low-grade trauma and occlusion caused by
dentures predispose to candidal colonization and subsequent infection.
Pathology
Dentures
can produce a number of ecological changes, including the following:
·
Changes in the oral flora.
·
Plaque accumulation between the
mucosal surface of the denture and the palate.
·
Saliva present between the
maxillary denture and the mucosa may have a lower pH than usual.
·
Accumulation of microbial plaque
(bacteria and/or yeasts) on and in the fitting surface of the denture and the
underlying mucosa.
The
epithelium is often shiny and atrophic, and there may be marked edema. In late
cases, secondary papillary hyperplasia in the vault of the palate may occur.
Clinical features
The
characteristic presenting features of denture‐related stomatitis are:
·
Chronic erythema and edema of
the mucosa that contacts the fitting surface of the denture (usually a complete
upper denture). The condition is normally confined to the upper
denture-bearing area, gums and palatal mucosal surface in contact with the
dentures.
·
The mucosa below lower dentures
is rarely involved.
·
Erythema is restricted to the
denture‐bearing
area, fairly sharply defined at the margin of the denture.
·
Often associated with angular cheilitis, and
that is the feature that frequently brings the patient to seek dental or
medical advice, as there are no symptoms.
Clinical variants
The
lesions have been classified into three clinical types (Newton's types),
increasing in severity.
·
Type 1: a localized
inflammation or a pinpoint hyperemia.
·
Type 2: generalized erythema presenting as
more diffuse erythema involving a part of, or the entire, denture‐covered mucosa.
·
Type 3: a granular type (inflammatory
papillary hyperplasia) commonly involving the central part of the hard palate
and the alveolar ridge. Hyperplasia of oral mucosa can be seen.
Investigations
Denture‐related
stomatitis is a clinical diagnosis.
Management
Any
underlying systemic disease should be treated where possible. The oral biofilm must
be removed regularly. The denture plaque and fitting surface is infested,
usually with C.
albicans and dentures acts as a reservoir for microbial
colonization.
Therefore,
to treat (and prevent recurrence of) denture‐related stomatitis, dentures
should be removed from the mouth at night, cleaned and disinfected, and stored
in an antiseptic. Disinfection modalities, antifungal medications, antiseptic
mouthwashes, natural antimicrobial substances and photodynamic therapy could be
adjuncts or alternatives.
Cleansing
is crucial to therapeutic success. Microwave irradiation in combination with
soaking in denture cleanser and brushing effectively disinfects dentures and
removes denture biofilm. Microwave disinfection, at once per week for two
treatments, can be as effective as topical antifungal therapy for treating
denture stomatitis. Sodium hypochlorite 0.5% can help disinfect denture liners
and tissue conditioners. Hypochlorite is an effective anticandidal agent but
can turn chrome cobalt dentures black. The incorporation of nystatin in those
materials is also able to treat or prevent oral candidosis. Denture cleansers
also include chlorhexidine gluconate.
The
mucosal infection is eradicated by brushing the palate and using antifungals
for at least 4 weeks. Effective agents include miconazole gel or fluconazole
tablets, administered concurrently with an oral antiseptic such as
chlorhexidine, which itself have antifungal activity.
Surgery
may occasionally be needed to excise papillary hyperplasia.
Candidal Leukoplakia/ Chronic plaque‐like candidosis/ Chronic hyperplastic candidiasis
Definition
Very persistent, firm, single fixed, irregular
white plaque, occur commonly on the dorsum of tongue, buccal mucosa
or hard palate. Most patients are male and generally
over the age of 30 years.
Predisposing factors
Smokers appear to be particularly prone to
develop this form of oral candidosis.
Clinical features
Around the hyperplastic area, there may be a
margin of erythema. Unlike the acute pseudomembrane of oral thrush, this plaque
is more adherent and cannot be easily
removed or wiped off. The significance of this condition lies in the
fact that it must be differentiated from other types of leukoplakia as,
although the affected areas may undergo malignant change, it may eventually
clear with prolonged anti-Candida therapy.
Candidal cheilosis (angular cheilitis or perlèche)
Definition
Is characterized by erythema, fissuring,
maceration, and soreness at the angles of the mouth
extending outwards in the folds of the facial skin.
Pathophysiology
It is perhaps best considered as an
intertrigo in which different organisms may play a part. Both yeasts (candidal)
and bacteria (especially Staphylococcus
aureus) may be involved. Mechanical factors (e.g. the depth of the
fold), the presence of moisture from persistent salivation (drooling) or
licking the lips, particularly in children may also be important. The yeasts
involved clearly come from the mouth, and the association with denture
stomatitis is important. This condition is commonly encountered in edentulous and elderly
patients with sagging skin at the oral commissures. Poorly fitting dentures,
malocclusion, and riboflavin
deficiency also predispose one to cheilosis. Cheilosis is often associated with
chronic atrophic candidiasis in denture wearers.
Angular cheilitis is not specific for mucosal
candidiasis. It can also be seen with vitamin B-12 or iron deficiency, Down
syndrome, orofacial granulomatosis, Crohn disease, HIV infection, or diabetes.
Clinical features
Although the condition may present acutely,
it is common to find a long history of soreness and cracking at the angles of
the mouth and a fluctuating course is typical. Obviously, the oral cavity
should be examined carefully in such cases and swabs taken from that site to
establish the presence of Candida carriage, as well as from the affected skin
at the angles of the mouth.
Median rhomboid glossitis
This red,
depapillated, rhomboidal, flat maculate or mamillated and raised benign lesion
is seen almost invariably in the midline of the dorsum of the tongue, just
anterior to the sulcus terminalis.
It is an
uncommon condition mainly seen in elderly patients.
Associated diseases
There is
a significant association between median rhomboid glossitis and Candida. Occasionally,
immune defects (including HIV) and diabetes predispose to this lesion.
Pathology
Histology
shows irregular pseudoepitheliomatous epithelial hyperplasia that may resemble
a carcinoma but it is not a malignant condition.
Clinical features
There is
typically a red central lesion of somewhat rhomboidal shape anterior to the
sulcus terminalis on the dorsum of the tongue sometimes with discomfort.
Occasionally, there is a nodular component. Multiple oral lesions may
occasionally be present, especially a ‘kissing’ lesion in the palatal vault.
There may also sometimes be a coexistent erythematous candidosis in the palate,
which some have termed ‘chronic oral multifocal candidosis’.
Investigations
Median
rhomboid glossitis is usually diagnosed on clinical grounds. Long disease
duration and no benefit from topical steroids are suggestive of this condition.
Since some lesions are nodular and may simulate a neoplasm or other pathology,
biopsy may be indicated.
Management
Median
rhomboid glossitis may respond to the use of antifungals. After antifungal
treatment, tongue pain disappears or improves markedly in most.
Candidosis of skin and genital mucous membranes
Superficial infections of skin
include intertrigo, diaper dermatitis, erosiointerdigitalis blastomycetica,
perianal dermatitis, and candidal balanitis. Candidal infections of the skin
have become more prevalent in recent years, principally because of the
increased numbers of immunocompromised patients. Candida species are not part of the
normal flora of the skin but may colonize fingers or body folds transiently.
Most cases of cutaneous candidosis occur in
the skin folds or where occlusion from clothing or medical dressings produces
abnormally moist conditions. Areas close to the body orifices and the fingers,
which are frequently contaminated with saliva, are also at risk.
CUTANEOUS CANDIDIASIS
Candida intertrigo (flexural
candidosis)
Definition
C. albicans has a
predilection for colonizing skin folds in which the local environment is moist
and warm. Any skin fold may be affected, especially in
the obese subject. Usual locations for candidal intertrigo include
the genitocrural, interdigital, intergluteal cleft, inframammary and beneath
the abdominal pannus and axillary areas.
Predisposing factors
Common predisposing factors are obesity, diabetes
mellitus, wearing of occlusive clothing and occupational factors.
Clinical features
Signs are typically erythema and a little
moist exudation starting deep in the fold. As the condition develops, it
spreads beyond the area of contact, usually developing the typical features of
candidosis. The pruritic eruption appears as macerated beefy-red
patches and thin
plaques with satellite papules and pustules at the periphery. These papules and
pustules on erythematous base become confluent and rupture leaving fairly
sharply demarcated, polycyclic, eroded patches on erythematous base with easily
detachable collarette-like scale at the margins of lesions.
Satellite lesions, pustular or papular, are classic.
Topical steroids, prescribed for relief of the latter symptoms, may modify the
inflammatory signs and cause diagnostic confusion.
Several clinical variants of Candida intertrigo deserve special
mention.
Interdigital candidiasis
It refers to interdigital
candidal or polymicrobial infection of the web spaces of the
fingers or toes, where
moisture trapping is thought to underlie the condition. It is most commonly seen in obese
elderly. Distribution: almost always seen between the middle and ring
fingers or the corresponding toes. One explanation is that this web space is
the least mobile in most patients, so that retention of sweat, soap, and water
leads to an irritant reaction and then secondary infection with C. albicans.
Typically, there is painful erthematous erosion surrounded by swollen macerated
thick,
white horny layer. It may be
associated with Candida paronychia. Patients
who have some abnormality, including wide, fat fingers, appears to predispose
to infection. Candida and Gram‐negative
bacteria are often co‐pathogens.
Similar
interdigital infections of the feet may occur in very hot climates,
particularly in those with heavy footwear, for example army personnel.
Candidal diaper dermatitis
Infants with oropharyngeal
candidiasis invariably harbor C
albicans in the intestine and feces (85-90%). Colonized stools
represent the most important focus for cutaneous infection. Moist macerated
skin due to chronic occlusion with wet diapers is
particularly susceptible to invasion by C
albicans. Additional factors that predispose infants to candidal
diaper dermatitis include local irritation of the skin by friction; ammonia
from bacterial breakdown of urea, intestinal enzymes, and stool; detergents;
and disinfectants.
The eruption with pronounced erythema
first appears in the perianal region and spreads to the perineum and inguinal
creases and,
in severe cases, the upper thighs, lower abdomen, and lower back. Maceration of
the anal mucosa and the perianal skin often is the first clinical
manifestation. Scaly papules merge to form well-defined, weeping, and eroded
lesions with a scalloped border. A collar of overhanging scales and an
erythematous base may be demonstrated. Satellite flaccid vesicopustules around
the primary intertriginous plaque also are characteristic and represent the
primary lesions.
Candida miliaria
Candida
miliaria
affects the back in bedridden patients. The eruption begins as isolated
vesiculopustules containing yeast, which spread over occluded regions on the
back. Candida also colonizes and infects skin around wounds covered with
occlusive dressings. Broad-spectrum topical antibiotics contribute to these Candida
wound infections.
Macerated
skin under rings and dressings may become infected with Candida.
Investigations
Cutaneous candidal infection is
diagnosed by the typical appearance of the eruption and confirmed by KOH
examination and, when necessary, culture. Bacterial
co-pathogens should be considered.
Treatment
Candida intertrigo requires specific topical azole
creams (e.g., clotrimazole,
econazole,
ciclopirox,
miconazole,
ketoconazole)
usually continued for about 2 weeks, but treatment may be required for longer
periods, and is likely to fail if attention is not given to drying the affected
area. Powder preparations also keep dry otherwise moist environments can
facilitate candidal infections. In some patients with moist Candida intertrigo,
potassium permanganate soaks are more effective. Attention should be given to
treating concomitant bacteria; once again, potassium permanganate is useful for
this purpose. In finger or toe web infections, topical antifungal therapy,
combined with the use of open footwear in the case of infections of the feet,
is appropriate. Oral antifungal therapy is recommended for extensive cutaneous
infections.
GENITAL CANDIDIASIS
It occurs on the non keratlnized genital
mucosa.
• Vulva and vagina.
• Preputial sac of the penis.
• Usually represents overgrowth of Candida in
mucocutaneous microbiome.
Vulvovaginal Candidiasis
Epidemiology and predisposing factors
Most vaginal candidiasis occurs in the healthy population. Seventy-five percent of women experience at least one episode; 40 to 45% experience two or more episodes. Vaginal candidiasis is often associated with vulvar candidiasis, i.e., vulvovaginal candidiasis. C. albicans causes 80%–90% of VVC and is followed by C. glabrata in frequency. Risk factors are presence of an intrauterine device, wearing of tight-fitting and synthetic clothing, and immunosuppression. These factors disrupt vaginal flora of lactobacilli that serve to inhibit overgrowth of Candida.
Recurrent VC, defined as four or more episodes per year, occurs in up to
10% of women
and in around 5% of women it becomes a chronic condition. Changes
in hormone levels during pregnancy and the luteal phase of the menstrual cycle in the
non-pregnant may induce relapses. Use of genital cleansing
solutions or douche may elicit a hypersensitivity response and increase
susceptibility to Candida. Frequent sexual intercourse, resulting in
vaginal abrasions and involving semen allergy, may also predispose women to
recurrent VVC. When none of the above mentioned factors is involved in VVC, one
should consider use of broad spectrum antibiotics, immunosuppression, or
diabetes mellitus as potential contributors.
Clinical features
This common condition in women presents with a vaginal discharge
associated with vulvar itching, burning, and occasional dysuria or
dyspareunia. Although most candidal
infections occur more frequently with advancing age, vulvovaginitis is unusual
in older women. It is most prevalent in women aged 25-34 years. In the absence
of oestrogen stimulation, the vaginal mucosa becomes thin and atrophic,
producing less glycogen. Candidal colonization of vaginal mucosa is oestrogen dependent
and subsequently decreases sharply after menopause. The widespread use of
hormone replacement for reduction of osteoporosis and heart disease may cause
an increasing trend in candidal vulvovaginitis among older women.
Onset is often
abrupt, usually the week before menstruation. Symptoms may recur before each
menstruation. Typically,
there is dusky red erythema of the epithelium of vagina and the vulva, with
curdy white flecks of discharge, but on occasions the only sign is erythema. Vaginal examination shows thick curd-like
whitish plaques on the vaginal wall with underlying erythema and surrounding edema. Erythema may extend
onto the perineum and into the groins. The perianal area is often affected. In
extensive cases, subcorneal pustules may be seen peripherally. The cervix is normal upon
speculum examination. In chronic cases, the vaginal mucosa may
become glazed and atrophic.
In pregnancy, the picture is modified by
marked physiological leukorrhoea.
A patient presenting with symptoms of vulvovaginitis with
identification of yeasts in the vaginal discharge has a diagnosis of
candidiasis.
Treatment
For acute vulvovaginitis, two therapeutic
approaches exist. Topical imidazole preparations (pessary or ovule) available
over the counter, such as butoconazole,
miconazole,
and clotrimazole,
as well as those available by prescription, including tioconazole,
econazole,
and terconazole
are easy to use and effective over 3–7 days of treatment. These agents are also
safe to use during pregnancy. If there is coexistent involvement of the skin, a
topically applied cream should also be used. However, single‐day oral therapy with
fluconazole 150 mg is both effective and convenient; itraconazole 600 mg is an
alternative. Efficacy is similar to that seen with topical drugs. Prophylactic
regimens to prevent recurrences include weekly clotrimazole 500-mg tablet used
intravaginally or fluconazole 150 mg/week orally.
In recurrent candidal
vulvovaginitis, precipitating factors must be
identified. Sexual transmission may be
an important factor in recurrent candidiasis and, therefore, treatment of both
partners may be justified. Possible regimens for recurrent disease include oral fluconazole 150 mg weekly for 6 months,
clotrimazole 500 mg vaginal tablet weekly for 6 months, or itraconazole 200 mg
BID orally once monthly for 6 months.
Balanitis and Balanoposthitis
Factors
predisposing to candidal balanitis include diabetes mellitus, an uncircumcised
state, and candidal vaginal infection in sexual partners.
The
skin of the glans penis, especially in the uncircumcised, may sometimes be
colonized by Candida asymptomatically. When Candida balanitis develops, it is
usual to find either abundant vaginal Candida carriage or frank vulvovaginitis
in the sexual partner.
Clinical features
In men, balanitis or balanoposthitis, or rarely, widespread
involvement of the perianal area, perineum, and groin is seen. Balanitis is
more common in the uncircumcised man. Occasionally, patients with balanitis complain of
transient erythema and burning occurring shortly after intercourse. The
eruption involving the penis is pruritic. Physical findings include white
patches on the glans or prepuce. Multiple discrete small papules or fragile
pustules on the glans, along the coronal sulcus and inner aspect of the
foreskin break to leave erythematous erosions with a collarette of whitish
scale. Infection may spread to the scrotum, gluteal folds, buttocks, and
thighs.
It
is wise to consider diabetes in cases of genital yeast infections, as florid
persistent lesions spreading beyond the genitalia seem most likely to be
associated with that condition. Although the large majority of patients with
genital candidosis will not have diabetes, it is appropriate to test for
glycosuria in persistent or recurrent cases. Edema, ulcerations, and
fissuring of prepuce are usually seen in diabetic men. All these
may prevent retraction of the foreskin.
Treatment
Balanitis and balanoposthitis,
usually responds satisfactorily to topical antifungal creams, in some
cases in conjunction with low- to mid-potency topical corticosteroids, but if
there is a source of infection in the sexual partner this should be treated
appropriately, and diabetes, if discovered, obviously requires management. A
single oral 150-mg dose of fluconazole is used for refractory cases.
Perianal
and scrotal candidosis
Perianal
and scrotal candidosis may occur with, or independently of, genital
involvement. Although usually starting around the anal margin with nonspecific
erythema, soreness and irritation, subsequent spread along the natal cleft is
common, with classical features of sheet like erythema and fissuring develops
as it extends. The inguinal-scrotal fold is a
frequent site of involvement, and here, in addition to the erythema, the skin
focally may appear white due to maceration of the accompanying scale. Satellite
lesions, including pustules, are often seen.
Involvement of the scrotum is usually in the
form of a nondescript erythema and sub corneal pustules are rarely seen.
Candidosis must be included in the differential diagnosis of unexplained
erythema of scrotal skin.
Napkin candidosis (diaper candidiasis).
Definition
Candida albicans is
commonly isolated from the moist skin of the buttocks and genitalia of the
infant but is more prevalent where the skin is affected by napkin rash. Candidal diaper dermatitis
results from yeast colonization of the gastrointestinal tract and chronic
occlusion with wet diapers.
Pathophysiology
Steroid creams applied to this site not only
modify the clinical features but they are probably advantageous to Candida.
Moreover, if the bacterial flora has been suppressed by a topical antibiotic,
this will also favor yeast growth. All these factors should be considered in
any napkin rash.
Clinical features
Erythema first appears in the
perianal region and spreads to the perineum and inguinal creases. The classic
presentation is beefy red, partially eroded plaques with collarette-like
scaling at the margins of lesions,
and “satellite pustules” in the area covered by a diaper are the usual
findings.
Differential diagnosis
In acrodermatitis enteropathica, in which
zinc deficiency plays a central role, there may be a secondary Candida
infection, particularly of the napkin area.
Investigations
In all cases of napkin eruption, a moistened
swab or a scraping should be taken to discover whether or not Candida is
present on the affected skin. If Candida is present, particularly in large
numbers, even if the features are non‐specific, a trial of anti‐Candida therapy is
generally indicated.
Treatment
In infants, rashes in the napkin area should
be investigated for Candida and, if present, this can be treated topically. The
topically antifungal should be combined with a general regimen for napkin
dermatitis, with frequent nappy changes. In seborrheic dermatitis, a weak
topical steroid is appropriate for the disseminated dry lesions, but steroids
should be avoided on the napkin area itself.
Candidosis of the nail and paronychium
Candidal Paronychia
Salient features
• Associated with damage to the cuticle,
mechanical or chemical.
• At risk: Adult women, food handlers, and
house cleaners.
• Chronic dermatitis of proximal nail fold
and matrix: chronic inflammation (eczema, psoriasis) with loss of cuticle,
separation of nail plate from proximal nail fold.
• Predisposing factors:
1. Dermatosis:
Psoriasis, dermatitis [atopic. irritant (occupational), allergic contact], and
lichen planus.
2. Drugs:
oral retinoids ( isotretinoin, acitretin), indinavir.
3. Foreign
body: Hair, bristle, and wood splinters.
• Manifestations: First, second, and third
fingers of the dominant hand; proximal and lateral nail folds erythematous and
swollen; cuticle absent
• Secondary infection/colonization: Candida
spp., Pseudomonas aeruginosa, or Staphylococcus aureus. Nail plate may become discolored;
green under surface with Pseudomonas. Infection associated with painful acute
inflammation.
• Management
1. Protection.
2. Treat
the dermatitis with glucocorticoid: topical, intralesional triamcinolone, or a
short course of prednisone.
3. Treat
secondary infection.
Definition
Candida paronychium is a Candida infection of
the nail fold.
Pathophysiology
Candida species, not always C. albicans, can
be isolated from the majority of cases of chronic paronychia. The yeast is
thought to have an etiological role in this condition, but bacteria and
irritant or allergic contact dermatitis also play a part. 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.
Predisposing factors
Often there is chronic damage to the cuticle,
either through manipulation or who habitually immerse their hands in water
(i.e., housekeepers, bakers, fishermen, and bartenders),
but in chefs and pastry cooks the presence of organic debris such as flour and
other carbohydrates may be equally important.
The disease is more common in patients with
diabetes. Toenail folds are not usually affected.
Clinical features
Typically, several fingers are chronically
infected, but one or all may be involved. Redness,
swelling and tenderness of the proximal and lateral nail folds,
and there is loss of the cuticle, and detachment of the proximal nail fold from
the dorsal surface of the nail plate, leading to pocketing. Occasionally, thick
white pus may discharge; often force is needed to express it. The patient
usually has marked tenderness, and spontaneous pain is an occasional feature. Candidal paronychia
should be differentiated from acute bacterial paronychia, which
is caused by Staphylococcus
aureus and presents with proximal abscess formation. Nail
dystrophy with buckling of the nail plate and some discoloration and
onycholysis around the lateral nail fold frequently occur, but massive
destruction of the nail plate is rare. Many patients, particularly those who
are resistant to treatment, appear to have a poor peripheral circulation. If
there is secondary bacterial co-infection with Pseudomonas, there will be a green discoloration under the nail. A
potassium hydroxide (KOH) preparation is helpful and is likely to show yeast
organisms.
Treatment
Chronic paronychia due to Candida is often
resistant to therapy. The most important aspects of therapy include minimizing
contributing factors such as water exposures, as well as trauma. Topical
imidazole in solution form should be considered initially for a prolonged
period with frequent applications. Four percent thymol in ethyl alcohol
(compounded by the pharmacy, as it is not commercially available) or dilute
acetic acid soaks may be a suitable alternative. Oral itraconazole or
fluconazole may also be used in otherwise refractory cases. Whatever anti‐Candida regimen is
chosen, it must be followed by general measures such as ensuring adequate
drying of the hands. Even so relapse is common in many patients, particularly
in the chronic phases of paronychia. The role of Candida is more controversial
and other factors such as irritant or allergic contact dermatitis may play a
part in the ongoing inflammatory response. For this reason, in chronic cases,
the addition of a topical corticosteroid is a logical approach. In a randomized
trial, topical corticosteroids were shown to yield a higher cure rate than
systemic antifungals. Topical tacrolimus also is effective.
Therapeutic ladder
First line
Azole solution twice daily for 2–4 months
depending on clinical response
Plus in chronic cases a medium strength
topical steroid applied to the nail fold skin once daily
Or
Itraconazole 100 mg daily for 1–2 months
Fluconazole 100 mg daily for 1–2 months
Second line
4% thymol solution
Dilute acetic acid soaks
Candida onychomycosis
Definition
Candida onychomycosis is an infection of the
nail plate caused by Candida species. Candida, usually starting as a
paronychia, can also directly invade the nail plate and produce onychomycosis
(5-10% of onychomycosis overall is caused by candida) and is implicated in
several presentations.
Predisposing factors
Two important predisposing conditions are
Raynaud phenomenon or disease and Cushing syndrome.
Causative organism
The main clues that the yeast is a
significant pathogen are erosion of the distal nail plate, the presence of
yeasts and hyphae in the nail on direct microscopy and the isolation of C.
albicans.
Clinical features
Candidal onychomycosis is more often seen in
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. Exposure to moisture
and occupational wet work are important risk factors. There are three main
manifestations of Candida infection of the nail apparatus. The most common is
distal and lateral subungual onychomycosis (DLSO) associated with paronychia.
In addition to these conditions, erosion of the distal and lateral nail plate
of the fingernails, not usually progressing to total nail dystrophy, has been
associated with C. albicans invasion of the nail, most often seen in women.
Investigations
To detect organism in chronic paronychia, a
platinum loop introduced into the nail fold may be more valuable than a swab
for this. When nail plate involvement is suspected, clippings should be taken.
Treatment
Oral itraconazole
or fluconazole
appear to be most efficacious for candidal onychomycosis. Two treatment
regimens are available: the daily dose or pulsed-dose regimen. Itraconazole may
be administered at 200 mg daily for 6 weeks for fingernails and for 12 weeks
for toenails. It may also be administered in pulse therapy, 200 mg twice daily
for 1 week per month, for a total of two pulses for fingernails and three
pulses for toenails.
Laboratory Findings of mucocutaneous candidiasis
What
are Hyphae?
Hyphae
are defined as elongated, tubular, and branching filaments that form the
mycelium (vegetative part of a fungus consisting of numerous filaments) of a
fungus. Hyphae may or may not contain septa. Hyphae with septa are called
as septate hyphae and, on the other hand, hyphae without septa
are called as aseptate hyphae.
What
are Pseudohyphae?
Pseudohyphae are a type of filaments
that form pseudomycelia mostly in polymorphic fungi like Candida spp.
It is composed of ellipsoidal and elongated yeast like cells. These cells
remain connected as a chain with constrictions at the site where septa found.
Pseudohyphae form during the cell division and newly divided cells through
budding remained adhered as chains and branches. Some scientists consider
pseudohyphae as an intermediate state between yeast like cells and true hyphae.
Candida albicans (organism that causes candidiasis) is an example of
fungi with pseudohyphae.
What
is the difference between Hyphae and Pesudohypahe?
•
Both hyphae and pseudohyphae are filaments that composed of fungal cells
arranged next to each other as a chain.
•
Hyphae may or may not contain septa, whereas pseudohyphae always contain septa.
•
There is no constriction at the place where septa found in hyphae, whereas it
is found in pseudohyphae.
•
Hyphae do not show budding whereas pseudohyphae do show budding through which
it grows continuously.
Candida
albicans is a human
opportunist pathogen that can grow as yeast, pseudohyphae, or true hyphae in vitro and in vivo, depending on
environmental conditions.
C. albicans has three distinct morphological
forms. It forms:
1.
a budding
yeast,
2.
pseudohyphae
,and
3. filamentous hyphae
The three morphological forms of Candida albicans. Yeasts
(1) are small, round cells that divide by conventional cell division. Pseudohyphae
(2) are less elongated hyphae which are more constricted at septa than
true hyphae. True hyphae (3) are elongated cells that do not separate following
cell division and are separated by specialised septa that allow passage of
cytoplasm and other components between compartments.
The ability to switch between these
forms is controlled by a highly complex genetic network and is
dependent on a number of environmental factors. Hyphae are thought
to be more virulent since expression of toxins, including the recently
discovered Candidalysin, is associated with this morphology. Candidalysin is a
toxin secreted by hyphae that damages epithelial cells, and thus may
allow C. albicans to penetrate barrier tissues and establish
infections.
Pseudohyphae are formed by a
wide variety of yeast species including most pathogenic Candida species.
Amongst the Candida species,
true hyphae are normally formed only by C.
albicans and C.
dubliniensis.
The morphology of skin lesions
may be distinctive and sufficient to make a clinical diagnosis in many cases of
superficial mucocutaneous candidiasis. Rapid confirmation may be achieved with bedside
potassium hydroxide (KOH) preparation (either scraping from an intact pustule
or a touch preparation form a punch biopsy specimen) demonstrating pseudohyphae
and budding yeast.
KOH
preparation is the easiest and most cost-effective method for diagnosing
mucocutaneous candidiasis. Application of 10% KOH and
applying gentle heat lyses host cells and allows for visualization of the organism.
Definite diagnosis and species identification can be achieved
via either swab culture (taken from an intact pustule if possible) or tissue
culture from biopsy specimens taken from affected areas.
As C. albicans is a
common commensal, the interpretation of cultural findings has to be related to
the clinical appearances. A scanty growth of C. albicans from the skin or from a
mucocutaneous site may be meaningless without evidence of infection from a
positive direct microscopy.
Cultures from affected nails may help
identify the etiologic agent responsible for onychomycosis (dermatophyte vs.
yeast). One should use Sabouraud's agar medium, incubate the culture at 37
degree C, and check it after 24-48 hours. C. albicans readily produce smooth
whit colonies, usually < 5mm in diameter.
Pathology
Skin biopsies are of variable yield in making
the diagnosis. Superficial candidiasis is characterized by sub corneal pustules.
Organisms are seldom seen within the pustules. Fungal elements are almost always restricted to the outer
layers of epithelium, including the stratum corneum that can be highlighted
with Grocott methenamine silver or periodic acid-Schiff (PAS)
staining in a skin biopsy specimen. The
presence of pseudomycelia in tissue suggests C. albicans and is pathogenic. On the skin, particularly in acute
infections, mycelium may be very sparse, and indeed yeast forms may be present
in only small numbers.
Apart from the
presence of the fungus, acute oral candidosis is characterized by inflammatory
changes with the formation of a pseudomembrane of epithelial and inflammatory
cells. In the oral epithelium and cutaneous epidermis, the inflammatory
infiltrate consists predominantly of polymorphs, which may form micro abscesses
or sub corneal pustules.
Management
General principles of management
In the treatment of candidiasis it
is important to alter both localized and general susceptibility factors. In the
mouth, for instance, this involves frequent toilet in the seriously ill, and
denture hygiene in other patients, whereas in Candida infections
affecting the skin, careful drying of the affected sites is important. In many
cases, topical antifungal therapy alone is sufficient to produce a response,
but in immunocompromised patients with oro‐pharyngeal candidosis, oral systemic therapy may be
necessary to treat concomitant esophageal infection as well as being the most
effective treatment for oral candidosis in AIDS patients.
Therapeutic agents
The
important group of agents effective against Candida is the imidazoles.
Clotrimazole and miconazole are the best known in topical use, and significant
resistance to them has not developed in Candida species. Contact
allergy, although reported, seems to be almost as rare. The most useful oral
treatments are the two triazoles, fluconazole and itraconazole, that are also
effective in these conditions and have the additional advantage that
hepatotoxicity, seen with ketoconazole, is exceptionally rare with both drugs.
The usual daily doses are fluconazole 100–400 mg and itraconazole 100–200 mg. In
addition, fluconazole can be given for systemic candidosis as an intravenous
compound. Resistance to fluconazole has been reported in HIV, AIDS or CMC
patients receiving long‐term
therapy with the drug. Other azoles active against Candida species
include voriconazole and posaconazole. Both have been used for severe oro‐pharyngeal and oesophageal infection.
In infants, miconazole solution applied
several times a day is usually adequate for treating oral thrush. In the adult
patient, removal of dentures at night and disinfection of the dentures are important adjuvant steps to prevent
reinfection; the most effective methods to remove candida include soaking with
commercially available effervescent denture tablets or a dilute bleach
concentration of 1:32 or higher. Miconazole muco adhesive tablets are effective
in non‐immunocompromised
patients. The duration of the treatment varies with the condition: 10–14 days
may be enough in acute cases. For treatment of unresponsive and chronic cases,
such as those with hyperplastic candidosis, the responses to topical therapy are
often poor, and either fluconazole (100–200 mg/day) or itraconazole (100–200
mg/day) are more effective. Voriconazole or posaconazole are alternatives. In
patients with chronic oral candidosis, a biopsy may be justified to exclude
leukoplakia. Angular stomatitis usually responds to treatment of the primary
oral condition, although a topical antifungal applied to the area may speed
recovery.
Oral candidosis in patients with AIDS by
contrast, frequently fails to respond to topical therapy. In these conditions,
the best approach is to use itraconazole or fluconazole. If possible, therapy
should be given for short courses because of the risk of resistance developing
with continuous therapy. Treatment is usually given until there is symptomatic
recovery, which is usually quicker with fluconazole than the capsule
formulation of itraconazole. A solution of itraconazole is an alternative to
the capsule form and a new and better absorbed itraconazole formulation
(Lozanoc) is available in some countries. Posaconazole or voriconazole are
alternative treatments for these patients too.
Candidal
onychomycosis can be treated with the oral fluconazole or itraconazole regimens
described for tinea unguium.
|
TREATMENT OF
MUCOCUTANEOUS CANDIDA INFECTIONS |
|
|
Type of infection |
Treatment regimen (adult doses unless
otherwise indicated) |
|
Oropharyngeal candidiasis |
1.
Nystatin* 100 000 units/ml suspension: Children and adults
– 4–6 ml swish and swallow four times daily 1.
Infants – 2 ml
(1 ml inside each cheek) four times daily 2.
3.
Clotrimazole* 10 mg troche five times daily 4.
5.
Fluconazole† 200 mg po on day 1, then 100–200 mg
po daily 6.
7.
Continue treatment for 7–14 days after clinical
resolution |
|
Esophageal candidiasis |
1.
Fluconazole* 200–400 mg po on day 1, then
100–400 mg daily 2.
3.
Itraconazole 200 mg po daily 4.
5.
Voriconazole 200 mg po or iv BID 6.
7.
Posaconazole 400 mg po BID 8.
9.
Caspofungin 50 mg po iv daily Continue treatment
for 7–14 days following resolution of symptoms, for a minimum of 21 days
total |
|
Candidal vulvovaginitis§ |
1.
Fluconazole* 150 mg po single dose or (for severe
disease or an immunosuppressed patient) three doses at 3-day intervals 2.
3.
Butoconazole 2% vaginal cream, 5 g daily for 1–3 days 4.
5.
Clotrimazole*,‡ -1% vaginal cream (or other topical
formulation), 5 g daily for 7–14 days -Vaginal
suppositories: 100 mg daily for 7 days or 200 mg daily for 3 days 6.
7.
Miconazole*,‡ ·
2% cream, 5 g daily for 7 days ·
Vaginal suppositories: 100 mg daily for 7
days, 200 mg daily for 3 days, or 1200 mg single dose 8.
9.
Tioconazole* 6.5% cream, 5 g single dose Terconazole* ·
0.4% or 0.8% cream, 5 g daily for 7 or 3
days, respectively ·
80 mg vaginal suppository daily for 3 days
Fluconazole 150 mg weekly
for 6 months 1.
2.
Clotrimazole vaginal suppository, 200 mg twice weekly or
500 mg weekly for 6 months |
|
|
|
|
Candidal intertrigo or balanitis§ |
Topical imidazole or ciclopirox cream or lotion twice daily for 1–2
weeks or until resolved¶ 1.
Fluconazole ·
50 to 100 mg po daily for 14 days ·
150 mg po weekly for 2–4 weeks 2.
3.
Itraconazole 200 mg po twice daily for 14 days |
* Recommended as first-line treatment for immunocompetent
individuals.
† Recommended as first-line treatment for HIV-infected
patients (or other immunosuppressed individuals) with moderate to severe
disease, recurrent infection, or a CD4 count of <200 cells/mcl.
‡ Preferred treatments (with 7-day regimens) for pregnant
patients.
§ In cases of recurrent vulvovaginitis, treatment of the
patient's sexual partner is controversial; in contrast, for recurrent
balanitis, eradication of Candida from
the sexual partner's genital tract is generally recommended.
¶ After clinical resolution, topical treatments may be
continued twice weekly to prevent recurrence.
