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D E R M A T O L O G Y
Candidiasis
 Candidiasis (or candidosis) refers to a diverse group of
infections caused by Candida albicans or by other
members of the genus Candida. These organisms
typically infect the skin, nails, mucous membranes, and
gastrointestinal tract, but they also may cause systemic
disease.
Etiology
 C. albicans is a dimorphic yeast that is responsible for 70
percent to 80 percent of all candidal infections, which
makes it the most common cause of superficial and
systemic candidiasis.
 Epidemiologic studies indicate that the relative preva
lence of C. albicans in clinical isolates is declining, and
other species such as C. glabrata, C. tropicalis, C. krusei,
C. dubliniensis and C. parapsilosis are increasingly
encountered as pathogens.
 The dif ferent species of Candida can be identified in the
laboratory by microscopic examination of yeast
morphology.
Factors predisposing to candida infections
 Mechanical factors- trauma, local occlusion,
moisture, maceration, dentures, obesity
 Nutritional factors- avitaminosis, iron deficiency,
generalized malnutrition
 Physiologic alterations- extremes of age,
pregnancy, menses
 Systemic illnesses- Down syndrome, endocrine
diseases, malignancy, uremia, immunodeficiency
 Iatrogenic causes- X-ray radiation, medications,
intravenous lines
Pathogenesis
 C. albicans is often found as a saprophyte and
colonizes the mucous membranes of warm blooded
animals.
 In up to 50 per cent of normal individuals, the
oropharynx is colonized.
 In addition, C. albicans exists as a commensal
organism in the vaginal mucosa of 20 percent to 25
per cent of asymptomatic, healthy women8 and up to
30 percent of pregnant women.
Clinical Manifestations
 The cutaneous and mucosal manifestations of
candidiasis can be divided into several distinct
clinical syndromes.
ORAL CANDIDIASIS
 Acute pseudomembranous
candidiasis or thrush is the
most common form of oral
candidiasis.
 Predisposing factors include
diabetes mellitus, systemic steroid
use, antibiotic use, pernicious
anemia, malignancies,
radiotherapy to head and neck, and
cell mediated immunodeficiency.
 Up to one third of patients infected
with human immunodeficiency
virus develop oral candidiasis, and
over 90 percent of patients with
acquired immunodeficiency
syndrome develop oral candidiasis
over the course of their disease.
 Oral candidiasis appears as discrete white patches that may become
confluent on the buccal mucosa, tongue, palate, and gingivae.
 This friable pseudomembrane resembles milk curds and consists of
desquamated epithelial cells, fun gal elements, inflammatory cells, fibrin,
and food debris.
 Scraping the patches exposes a brightly erythematous surface underneath.
 Microscopic examination of this material reveals masses of tangled
pseudohyphae and blastospores. In severe cases, the mucosal surface may
ulcerate.
 Acute atrophic candidiasis
(erythematous candidiasis)
commonly occurs after sloughing of
the thrush pseudomem brane.
 This condition is associated with
broad spectrum antibiotic therapy,
glucocorticoid use, and human immu
nodeficiency virus infections.
 The most common location is on the
dorsal surface of the tongue, where
there are patchy depapillated areas
with minimal pseudomembrane
formation.
 There is both an asymptomatic and
symptomatic variant, the later of
which is characterized by burning or
pain.
 Chronic atrophic candidiasis
(denture stomatitis) is a
common form of oral candidiasis
seen in 24 per- cent to 60 percent
of those wearing dentures.
 Female patients are affected more
commonly than males.
 Clinical findings of chronic
erythema and edema of the palatal
mucosa that contacts the dentures
as well as angular cheilitis are
present.
 Presumably, the chronic lowgrade
trauma and occlusion provided by
dentures predispose to candidal
colonization and subsequent
infection.
 Candidal cheilosis (angular
cheilitis), so-called
‘‘perleche’’, is characterized by
erythema, fissuring,
maceration, and soreness at the
angles of the mouth.
 This condition is commonly
encountered in habitual lip
lickers, usually in the young,
and in elderly patients with
sagging skin at the oral
commissures.
 Loss of dentition, poorly fitting
dentures, malocclusion, and
riboflavin deficiency may be
predisposing factors.
VAGINAL AND VULVOVAGINAL
CANDIDIASIS (VVC)
 Approximately three fourths of all
women will experi ence an episode of
vulvovaginal candidia sis (VVC) in
their lifetime.
 C. albicans causes 80 percent to 90
percent of cases of WC, and C.
glabrata is die next most common
species involved.
 Risk factors for VVC include diabetes
mellitus, steroid use, presence of an
intrauterine device, wearing of tight
fitting and synthetic clothing, and
immunosuppression. These factors
disrupt the vaginal lactobacilli that
nor mally inhibit overgrowth of
Candida
 Patients generally present with a thick vaginal
discharge associated with burning, itching, and
occasional dysuria.
 Examination shows whitish plaques on the
vaginal wall with underlying ery thema and
surrounding edema that can extend to the labia
and perineum.
 Recurrent VVC is defined as four or more
episodes per year. Recurrent VVC occurs in up
to 5 percent of women. Changes in the
hormonal environment, such as pregnancy and
the luteal phase of the menstrual cycle, can
induce a relapse of WC. Use of a genital
cleansing solution or douche is also associated
with recurrent candidiasis. The mechanism
may be an allergy or hypersensitivity
response that increases suscepti bility to
Candida. Frequent sexual intercourse may
predispose women to recurrent VVC.
CANDIDA OF MALE GENITALIA: BALANITIS
AND BALANOPOSTHITIS
 Candida cause 30 percent to 85
percent of infectious balanitis.
Factors predisposing to balanitis
include candidal vaginal infection in
sexual partners, diabetes mellitus,
and an uncircumcised state.
 C. albicans balanitis presents as
small papules or frag ile
papulopustules on the glans or in
the coronal sulcus.These break to
leave superficial erythematous
erosions with a collarette of whitish
scale. Infection may spread to the
scrotum and inguinal areas.
CUTANEOUS CANDIDIASIS
 Intertrigo is the most common
clinical presentation on glabrous
skin.
 Usual locations for in- tertrigo
include the genitocrural, axillary,
gluteal, interdigital, and
inframammary areas and between
folds of skin on the abdominal wall.
 Predisposing conditions include
obesity, wearing of occlusive
clothing, diabetes mellitus, and
occupational factors.
 Cutaneous candidiasis appears as pruritic,
erythematous, macerated skin in intertriginous areas
with satellite vesicopustules.
 These pustules break open, leaving an erythematous
base with a collarette of easily detachable necrotic
epidermis.
 Cutaneous candidal infection is diagnosed by the
typical appearance of skin lesions and the presence
of satellite vesi copustules.
 The clinical diagnosis should be confirmed by KOH
examination and culture of skin scrapings.
 Candidal diaper dermatitis
is caused by yeast colonization
from patients’ gastrointestinal
tracts.
 Chronic occlusion by wet
diapers furthers the infection.
 Lesions appear first in the
perianal area and spread to the
perineum and inguinal creases,
which show pronounced
erythema.
 Erosio interdigitalis
blastomycetica refers
to interdigital candidal
or polymicrobial
infection of the hands
or feet; because of
anatomic
considerations, it
usually affects the third
or fourth interspace.
 Candida miliaria
often affects the back in
bedridden patients.
Lesions start as isolated
vesicopustules that
contain yeast.
 Candida also can colonize
and infect the skin around
wounds covered by occlusive
dressings.
 Broadspectrum topical
antibiotics also con tribute
to Candida wound
infections.
 Candidal paronychia is
common in individuals whose
hands are habitually involved in
wet work (e.g., housekeep ers,
bakers, fishermen, bartenders).
 Typ ically there is redness,
swelling, and ten derness of the
paronychial area with prominent
retraction of the cuticle to ward
the proximal nail fold.
 Occasionally, pus can be
expressed.
 Secondary nail changes include
onycholysis and transverse
depressions of the nail plate
(Beau’s lines) with a brownish or
green discoloration along the
lateral bor ders.
 Candidal paronychia
should be differentiated
from bacterial paronychia
or paronychia associated
with hypoparathyroidism,
celiac disease,
acrodermatitis
enteropathica, reactive
arthritis syndrome,
acrokeratosis
paraneoplastica, and
retinoid therapy.
DISSEMINATED CANDIDIASIS
 The incidence of disseminated
candidiasis is steadily rising as
more immunosuppressed
patients are living longer.
 The organisms responsible
include C. albicans, C. tropicalis,
C. glabrata, and C. parapsilasis.
These organisms may gain
hematogenous access from the
oropharynx or gastrointestinal
tract when the function of the
mucosal barrier rs
compromised (e.g., by mucosms
secondary to chemotherapy) or
through contaminated
intravenous catheters. Multiple
organs are involved.
 Skin lesions occur in some patients with
disseminated infection. The recognition
of such lesions may be important in
early diagnosis, because antemortem
blood culture results are negative in a
high percentage of patents with autopsy
proven systemic candidiasis.
 The characteristic skin lesions are
erythemamus papules with a
hemorrhagic or pustular center. The
eruption is located on the trunk and
extremities and has a varying number of
lesions.
 Associated findings include fever and
myalgias.Necrouccutaneous lesions also
have been encountered in these patients.
CHRONIC MUCOCUTANEOUS CANDIDIASIS
 Chronic mucocutaneous candidiasis
(CMC) consists of several clinical
syndromes characterized by chronic,
treatment resistant, superficial candidal
infections of the skin, nails, and
oropharynx.
 In general, the various syndromes may
be familial or sporadic.
 When rhey present in childhood, lesions
are detected before the age of 3 years.
 Oral lesions or diaper dermatitis appear
first, followed by angular cheilitis
(perleche), lip fissures, nail and
paronychial involvement, vulvovaginitis,
and cutaneous involvement. Cutaneous
lesions may appear with an
erythematous, serpiginous border or
areas of brownish desquamation on a
background of mild erythema.
 Nail involvement is
characterized by
markedly thickened and
dystrophic nail places
whose entire thickness is
invaded by Candida, The
paronychial areas are red
and edematous, there
may be pus, and the
fingertips are often
bulbous.
 There are multiple
conditions that have been
associated with CMC.
Most notably these
include candidal
esophagitis or laryngitis,
endocrinopathies (usually
hypoparathyroidism,
hypoadrenalism, and
hypothyroidism),
diabetes mellitus, vitiligo,
and iron deficiency.
LABORATORY FINDINGS
 In superficial candidal infections, the
diagnosis can be made by examining skin
scrapings and observing typical budding
yeasts with hyphae or pseudohyphae. C.
albicans grows readily on Sabouraud’s agar
with added antibiotics and is usually
recommended for isolation. Whitish mucoid
colonies grow within 2 to 5 days.
 In systemic candidiasis with skin lesions, the
diagnosis usually can be made from
histopathologic examination and culture of
appropriate skin biopsy specimens.
 Blood culture results often are negative in this
setting.
 Serologic studies using immunodiffusion,
counterimmunoelectrophoresis, and latex
agglutination methods may be somewhat
helpful in the diagnosis; however, false-
negative and false-positive reactions are
common.
Microscopic Studies
 Direct microscopic examination for
the presence of yeast provides rapid
evidence to support the clinical
diagnosis.
 Body fluids such as urine and
cerebrospinal fluid should be
centrifuged and the sediment
examined directly to increase the
probability of finding yeast.
 Sputum, surgical biopsy specimens,
and tissue scrapings must be treated
with a clearing agent such as 10
percent KOH and ink before the
material is examined.
 Candida appears as oval budding
cells, elongated filamentous cells
connected end to end
(pseudohyphae), or septate hyphae.
Pathology
 Organisms are seldom seen
within the pustule but can be
visualized in the stratum
corneum with the aid of a
periodic acid Schiff (PAS)
stain.
 The histologic examination
of a candidal granuloma
shows marked
papillomatosis and
hyperkeratosis and a dense
dermal infiltrate consisting
of lymphocytes,
granulocytes, plasma cells,
and multinucleated giant
cells.
TREATMENT
ORAL CANDIDIASIS
 In cases of uncomplicated oral candidiasis, nystatin
suspension or clotrimazole troches are effective.
However, in recurrent cases, oral azoles are proven
to be more effective.
CANDIDAL VULVOVAGINITIS AND BALANITIS
 Two therapeutic options exist when dealing with candidal vaginitis.
 There are many topical imidazoles that are effective, such as
butoconazole, miconazole, and clotrimazole, available over the
counter, and tioconazole, econazole, and terconazole available by
prescription. They may be used for 8 or 7 days.All these topical
agents are safe to use during pregnancy. Oral fluconazole,
itraconazole, and ketoconazole offer efficacy similar to that of
topical therapy.
 Prophylactic regimens can be used to prevent recurrent cases. A
weekly clotrimazole 500 mg tablet intravaginally or fluconazole 150
mg/week orally has been shown to prevent recurrences.
 The recommended treatment for candidal balanitis is topical
clotrimazole cream or a single 150 mg dose of fluconazoler
INTERTRIGO
 Intertrigo has been treated successfully with topical
antifungals in cluding nystatin and topical imidazole
creams. Miconazole powder can be use to dry moist
intertriginous areas.
CANDIDAL PARONYCHIA
 Chronic paronychia due to Candida is resistant to
therapy. All wet work should be minimized, and a
topical imidazole in solution form is the ideal
treaunent. Four percent thymol in chloroform or
absolute alcohol is drying and may be a suitable
alternative. Oral ketoconazole also may be used.
DISSEMINATED CANDIDIASIS
 Amphoteri cin B is available in newer lipid based
formulations. Also, caspofungin is available for
treating disseminated candidiasis.

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Candidiasis: Causes, Symptoms and Treatment

  • 1. D E R M A T O L O G Y Candidiasis
  • 2.  Candidiasis (or candidosis) refers to a diverse group of infections caused by Candida albicans or by other members of the genus Candida. These organisms typically infect the skin, nails, mucous membranes, and gastrointestinal tract, but they also may cause systemic disease.
  • 3. Etiology  C. albicans is a dimorphic yeast that is responsible for 70 percent to 80 percent of all candidal infections, which makes it the most common cause of superficial and systemic candidiasis.  Epidemiologic studies indicate that the relative preva lence of C. albicans in clinical isolates is declining, and other species such as C. glabrata, C. tropicalis, C. krusei, C. dubliniensis and C. parapsilosis are increasingly encountered as pathogens.  The dif ferent species of Candida can be identified in the laboratory by microscopic examination of yeast morphology.
  • 4. Factors predisposing to candida infections  Mechanical factors- trauma, local occlusion, moisture, maceration, dentures, obesity  Nutritional factors- avitaminosis, iron deficiency, generalized malnutrition  Physiologic alterations- extremes of age, pregnancy, menses  Systemic illnesses- Down syndrome, endocrine diseases, malignancy, uremia, immunodeficiency  Iatrogenic causes- X-ray radiation, medications, intravenous lines
  • 5. Pathogenesis  C. albicans is often found as a saprophyte and colonizes the mucous membranes of warm blooded animals.  In up to 50 per cent of normal individuals, the oropharynx is colonized.  In addition, C. albicans exists as a commensal organism in the vaginal mucosa of 20 percent to 25 per cent of asymptomatic, healthy women8 and up to 30 percent of pregnant women.
  • 6. Clinical Manifestations  The cutaneous and mucosal manifestations of candidiasis can be divided into several distinct clinical syndromes.
  • 7. ORAL CANDIDIASIS  Acute pseudomembranous candidiasis or thrush is the most common form of oral candidiasis.  Predisposing factors include diabetes mellitus, systemic steroid use, antibiotic use, pernicious anemia, malignancies, radiotherapy to head and neck, and cell mediated immunodeficiency.  Up to one third of patients infected with human immunodeficiency virus develop oral candidiasis, and over 90 percent of patients with acquired immunodeficiency syndrome develop oral candidiasis over the course of their disease.
  • 8.  Oral candidiasis appears as discrete white patches that may become confluent on the buccal mucosa, tongue, palate, and gingivae.  This friable pseudomembrane resembles milk curds and consists of desquamated epithelial cells, fun gal elements, inflammatory cells, fibrin, and food debris.  Scraping the patches exposes a brightly erythematous surface underneath.  Microscopic examination of this material reveals masses of tangled pseudohyphae and blastospores. In severe cases, the mucosal surface may ulcerate.
  • 9.  Acute atrophic candidiasis (erythematous candidiasis) commonly occurs after sloughing of the thrush pseudomem brane.  This condition is associated with broad spectrum antibiotic therapy, glucocorticoid use, and human immu nodeficiency virus infections.  The most common location is on the dorsal surface of the tongue, where there are patchy depapillated areas with minimal pseudomembrane formation.  There is both an asymptomatic and symptomatic variant, the later of which is characterized by burning or pain.
  • 10.  Chronic atrophic candidiasis (denture stomatitis) is a common form of oral candidiasis seen in 24 per- cent to 60 percent of those wearing dentures.  Female patients are affected more commonly than males.  Clinical findings of chronic erythema and edema of the palatal mucosa that contacts the dentures as well as angular cheilitis are present.  Presumably, the chronic lowgrade trauma and occlusion provided by dentures predispose to candidal colonization and subsequent infection.
  • 11.  Candidal cheilosis (angular cheilitis), so-called ‘‘perleche’’, is characterized by erythema, fissuring, maceration, and soreness at the angles of the mouth.  This condition is commonly encountered in habitual lip lickers, usually in the young, and in elderly patients with sagging skin at the oral commissures.  Loss of dentition, poorly fitting dentures, malocclusion, and riboflavin deficiency may be predisposing factors.
  • 12. VAGINAL AND VULVOVAGINAL CANDIDIASIS (VVC)  Approximately three fourths of all women will experi ence an episode of vulvovaginal candidia sis (VVC) in their lifetime.  C. albicans causes 80 percent to 90 percent of cases of WC, and C. glabrata is die next most common species involved.  Risk factors for VVC include diabetes mellitus, steroid use, presence of an intrauterine device, wearing of tight fitting and synthetic clothing, and immunosuppression. These factors disrupt the vaginal lactobacilli that nor mally inhibit overgrowth of Candida
  • 13.  Patients generally present with a thick vaginal discharge associated with burning, itching, and occasional dysuria.  Examination shows whitish plaques on the vaginal wall with underlying ery thema and surrounding edema that can extend to the labia and perineum.  Recurrent VVC is defined as four or more episodes per year. Recurrent VVC occurs in up to 5 percent of women. Changes in the hormonal environment, such as pregnancy and the luteal phase of the menstrual cycle, can induce a relapse of WC. Use of a genital cleansing solution or douche is also associated with recurrent candidiasis. The mechanism may be an allergy or hypersensitivity response that increases suscepti bility to Candida. Frequent sexual intercourse may predispose women to recurrent VVC.
  • 14. CANDIDA OF MALE GENITALIA: BALANITIS AND BALANOPOSTHITIS  Candida cause 30 percent to 85 percent of infectious balanitis. Factors predisposing to balanitis include candidal vaginal infection in sexual partners, diabetes mellitus, and an uncircumcised state.  C. albicans balanitis presents as small papules or frag ile papulopustules on the glans or in the coronal sulcus.These break to leave superficial erythematous erosions with a collarette of whitish scale. Infection may spread to the scrotum and inguinal areas.
  • 15. CUTANEOUS CANDIDIASIS  Intertrigo is the most common clinical presentation on glabrous skin.  Usual locations for in- tertrigo include the genitocrural, axillary, gluteal, interdigital, and inframammary areas and between folds of skin on the abdominal wall.  Predisposing conditions include obesity, wearing of occlusive clothing, diabetes mellitus, and occupational factors.
  • 16.  Cutaneous candidiasis appears as pruritic, erythematous, macerated skin in intertriginous areas with satellite vesicopustules.  These pustules break open, leaving an erythematous base with a collarette of easily detachable necrotic epidermis.  Cutaneous candidal infection is diagnosed by the typical appearance of skin lesions and the presence of satellite vesi copustules.  The clinical diagnosis should be confirmed by KOH examination and culture of skin scrapings.
  • 17.  Candidal diaper dermatitis is caused by yeast colonization from patients’ gastrointestinal tracts.  Chronic occlusion by wet diapers furthers the infection.  Lesions appear first in the perianal area and spread to the perineum and inguinal creases, which show pronounced erythema.
  • 18.  Erosio interdigitalis blastomycetica refers to interdigital candidal or polymicrobial infection of the hands or feet; because of anatomic considerations, it usually affects the third or fourth interspace.
  • 19.  Candida miliaria often affects the back in bedridden patients. Lesions start as isolated vesicopustules that contain yeast.
  • 20.  Candida also can colonize and infect the skin around wounds covered by occlusive dressings.  Broadspectrum topical antibiotics also con tribute to Candida wound infections.
  • 21.  Candidal paronychia is common in individuals whose hands are habitually involved in wet work (e.g., housekeep ers, bakers, fishermen, bartenders).  Typ ically there is redness, swelling, and ten derness of the paronychial area with prominent retraction of the cuticle to ward the proximal nail fold.  Occasionally, pus can be expressed.  Secondary nail changes include onycholysis and transverse depressions of the nail plate (Beau’s lines) with a brownish or green discoloration along the lateral bor ders.
  • 22.  Candidal paronychia should be differentiated from bacterial paronychia or paronychia associated with hypoparathyroidism, celiac disease, acrodermatitis enteropathica, reactive arthritis syndrome, acrokeratosis paraneoplastica, and retinoid therapy.
  • 23. DISSEMINATED CANDIDIASIS  The incidence of disseminated candidiasis is steadily rising as more immunosuppressed patients are living longer.  The organisms responsible include C. albicans, C. tropicalis, C. glabrata, and C. parapsilasis. These organisms may gain hematogenous access from the oropharynx or gastrointestinal tract when the function of the mucosal barrier rs compromised (e.g., by mucosms secondary to chemotherapy) or through contaminated intravenous catheters. Multiple organs are involved.
  • 24.  Skin lesions occur in some patients with disseminated infection. The recognition of such lesions may be important in early diagnosis, because antemortem blood culture results are negative in a high percentage of patents with autopsy proven systemic candidiasis.  The characteristic skin lesions are erythemamus papules with a hemorrhagic or pustular center. The eruption is located on the trunk and extremities and has a varying number of lesions.  Associated findings include fever and myalgias.Necrouccutaneous lesions also have been encountered in these patients.
  • 25. CHRONIC MUCOCUTANEOUS CANDIDIASIS  Chronic mucocutaneous candidiasis (CMC) consists of several clinical syndromes characterized by chronic, treatment resistant, superficial candidal infections of the skin, nails, and oropharynx.  In general, the various syndromes may be familial or sporadic.  When rhey present in childhood, lesions are detected before the age of 3 years.  Oral lesions or diaper dermatitis appear first, followed by angular cheilitis (perleche), lip fissures, nail and paronychial involvement, vulvovaginitis, and cutaneous involvement. Cutaneous lesions may appear with an erythematous, serpiginous border or areas of brownish desquamation on a background of mild erythema.
  • 26.  Nail involvement is characterized by markedly thickened and dystrophic nail places whose entire thickness is invaded by Candida, The paronychial areas are red and edematous, there may be pus, and the fingertips are often bulbous.
  • 27.  There are multiple conditions that have been associated with CMC. Most notably these include candidal esophagitis or laryngitis, endocrinopathies (usually hypoparathyroidism, hypoadrenalism, and hypothyroidism), diabetes mellitus, vitiligo, and iron deficiency.
  • 28. LABORATORY FINDINGS  In superficial candidal infections, the diagnosis can be made by examining skin scrapings and observing typical budding yeasts with hyphae or pseudohyphae. C. albicans grows readily on Sabouraud’s agar with added antibiotics and is usually recommended for isolation. Whitish mucoid colonies grow within 2 to 5 days.  In systemic candidiasis with skin lesions, the diagnosis usually can be made from histopathologic examination and culture of appropriate skin biopsy specimens.  Blood culture results often are negative in this setting.  Serologic studies using immunodiffusion, counterimmunoelectrophoresis, and latex agglutination methods may be somewhat helpful in the diagnosis; however, false- negative and false-positive reactions are common.
  • 29. Microscopic Studies  Direct microscopic examination for the presence of yeast provides rapid evidence to support the clinical diagnosis.  Body fluids such as urine and cerebrospinal fluid should be centrifuged and the sediment examined directly to increase the probability of finding yeast.  Sputum, surgical biopsy specimens, and tissue scrapings must be treated with a clearing agent such as 10 percent KOH and ink before the material is examined.  Candida appears as oval budding cells, elongated filamentous cells connected end to end (pseudohyphae), or septate hyphae.
  • 30. Pathology  Organisms are seldom seen within the pustule but can be visualized in the stratum corneum with the aid of a periodic acid Schiff (PAS) stain.  The histologic examination of a candidal granuloma shows marked papillomatosis and hyperkeratosis and a dense dermal infiltrate consisting of lymphocytes, granulocytes, plasma cells, and multinucleated giant cells.
  • 31. TREATMENT ORAL CANDIDIASIS  In cases of uncomplicated oral candidiasis, nystatin suspension or clotrimazole troches are effective. However, in recurrent cases, oral azoles are proven to be more effective.
  • 32. CANDIDAL VULVOVAGINITIS AND BALANITIS  Two therapeutic options exist when dealing with candidal vaginitis.  There are many topical imidazoles that are effective, such as butoconazole, miconazole, and clotrimazole, available over the counter, and tioconazole, econazole, and terconazole available by prescription. They may be used for 8 or 7 days.All these topical agents are safe to use during pregnancy. Oral fluconazole, itraconazole, and ketoconazole offer efficacy similar to that of topical therapy.  Prophylactic regimens can be used to prevent recurrent cases. A weekly clotrimazole 500 mg tablet intravaginally or fluconazole 150 mg/week orally has been shown to prevent recurrences.  The recommended treatment for candidal balanitis is topical clotrimazole cream or a single 150 mg dose of fluconazoler
  • 33. INTERTRIGO  Intertrigo has been treated successfully with topical antifungals in cluding nystatin and topical imidazole creams. Miconazole powder can be use to dry moist intertriginous areas.
  • 34. CANDIDAL PARONYCHIA  Chronic paronychia due to Candida is resistant to therapy. All wet work should be minimized, and a topical imidazole in solution form is the ideal treaunent. Four percent thymol in chloroform or absolute alcohol is drying and may be a suitable alternative. Oral ketoconazole also may be used.
  • 35. DISSEMINATED CANDIDIASIS  Amphoteri cin B is available in newer lipid based formulations. Also, caspofungin is available for treating disseminated candidiasis.