Oral Candidiasis: Dr. Ahmad Yusran, SPPD

ORAL CANDIDIASIS
Dr. Ahmad Yusran, SpPD

Risk factors. Clinical forms.
ORAL CANDIDIASIS
Diagnostic and Treatment
Candida spp. as commensal are

carried in the mouths of about 90% of
the population as a normal component
of the oral microbiota. Overgrowth is
prevented by other microorganisms.
This candidal carriage state is not
considered a disease, but when
Candida spp become pathogenic and
invade host tissues, oral candidiasis
can occur.
This change usually constitutes an
opportunistic infection of normally SOURCE
harmless micro-organisms because of http://www.helpyourautisticchildblog.com/category/candida/
local, or systemic factors altering host

immunity.
ORAL CANDIDIASIS
“ Candidiasis occurs in the very young, the very

old, or the very sick.
Candidiasis is a disease of the diseased ! ”
Prof. T. Djemileva
ORAL CANDIDIASIS
SPECIES
The causative organism is • C. tropicalis (1)

usually Candida albicans or
less commonly other • C. glabrata (2)
Candida species such as (in • C. parapsilosis (3)
decreasing order of
frequency: • C. krusei (4)
• C. dubliniensis (5)
• other
ORAL CANDIDIASIS
C. albicans 70-80% Highly virulent

(50%)
C. glabrata 5-10% HIV, leukaemia, elder patients, diabetic patients.
(10-15%)
C. Albicans and C. glabrata account for over 80% of cases

ORAL CANDIDIASIS
PATHOGENESIS
The host defenses against opportunistic infection of candida species are:
1.The oral epithelium, which acts both as a physical barrier preventing micro-
organisms from entering the tissues, and is the site of cell mediated immune
reactions.
2.Competition and inhibition interactions between Candida spp and other micro-
organisms in the mouth.
3.Saliva, which possesses both mechanical cleansing action and immunologic
action, including salivary IgAs antibodies, which aggregate candida organisms and
prevent them adhering to the epithelial surface; and enzymatic components such as
lysozyme, lactoperoxidase and antileukoprotease.
Disruption to any of these local and systemic host defense mechanisms
constitutes a potential susceptibility to oral candidiasis, which rarely occurs
without predisposing factors
ORAL CANDIDIASIS
PATHOGENESIS
Candidal carriage state is not • LOCAL FACTORS

considered a disease, but – Dentures;
when Candida spp become – Low рН of the saliva;
pathogenic and invade host – Neglected hygiene etc.
tissues, oral candidiasis can
occur: • SYSTEMIC FACTORS
– Systemic diseases;
The predisposing factors
– HIV/AIDS;
are:
– Immunosuppression
– Oncological treatment;
– Drugs misuse;
– Antibiotic treatment etc.
ORAL CANDIDIASIS
PATHOGENESIS. Macro-organism – systemic factors
Immunodeficiency/immunocompromise
• Acute pseudomembranous candidiasis occurs in about 5% of newborn

infants. Candida species are acquired from the mother's vaginal canal during
birth. At very young ages, the immune system is yet to develop fully and there
is no individual immune response to candida species, an infants antibodies to
the bacteria are normally supplied by the mother's breast milk.
• In non-infants, immunodeficiency is also a cause, e.g., as a result of AIDS/HIV
or chemotherapy.
• Topical or systemic corticosteroids, e.g., for treatment of asthma may also
result in oral candidiasis:
• Active cancer and oncological treatment, chemotherapy or radiotherapy
ORAL CANDIDIASIS
Diet
• Malnutrition, whether by malabsorption or poor diet, especially hematinic
deficiencies (iron, vitamin B12, folic acid) can predispose to oral candidiasis
by causing diminished host defense and epithelial integrity.
• For example, iron deficiency anemia is thought to cause depressed cell-
mediated immunity. Some sources state that deficiencies of vitamin A or
pyridoxine are also linked.
• There is evidence that a diet high in carbohydrates predisposes to oral
candidiasis.
• In vitro and studies show that Candidal growth, adhesion and biofilm
formation is enhanced by the presence of carbohydrates such as glucose,
galactose and sucrose.
ORAL CANDIDIASIS
Drug induced conditions

• Broad-spectrum antibiotics eliminate the competing bacteria and
disrupt the normally balanced ecology of oral micro-organisms. Acute
oral candidiasis occurring due to medication with corticosteroids or
broad-spectrum antibiotics (e.g., tetracycline).
Smoking
• Smoking, especially heavy smoking, is an important predisposing
factor but the reasons for this relationship are unknown. One
hypothesis is that cigarette smoke contains nutritional factors for C.
albicans, or that local epithelial alterations occur that facilitate
colonization of candida species
ORAL CANDIDIASIS
PATHOGENESIS. Macro-organism – localfactors
ALTERED BARRIER FUNCTION OF THE ORAL MUCOSA
• Presence of certain mucosal lesions, especially those that cause

hyperkeratosis and/or dysplasia, e.g., lichen planus. Such changes in the
mucosa predispose it to secondary infection with candidiasis.
• Other physical mucosal alterations are sometimes associated with candida

overgrowth, such as Fissured tongue (rarely) or Tongue piercing.
ORAL CANDIDIASIS
QUANTITY AND QUALITY OF SALIVA
• Both the quantity and quality of saliva are important oral defenses against
Candida spp.
• Decreased salivary flow rate or a change in the composition of saliva,
collectively termed salivary hypofunction or hyposalivation is an important
predisposing factor.
• Xerostomia is frequently listed as a cause of candidiasis, but xerostomia can
be subjective or objective, i.e., a symptom present with or without actual
changes in the saliva consistency or flow rate.
ORAL CANDIDIASIS
IMBALANCE OF THE ORAL MICROBIOTA
• Broad-spectrum antibiotics which eliminate the competing bacteria and disrupt

the normally balanced ecology of oral micro-biota. Acute oral candidiasis
occurring due to medication with corticosteroids or broad-spectrum antibiotics.
• Denture wearing, and poor denture hygiene, particularly wearing the denture
continually rather than removing them during sleep, is another risk factor, both
for candidal carriage and for oral candidiasis. Dentures provide a relative
acidic, moist and anaerobic environment because the mucosa covered by the
denture is sheltered from oxygen and saliva. Loose, poorly fitting dentures
may also cause minor trauma to the mucosa,which is thought to increase the
permeability of the mucosa and increase the ability of C. albicans to invade
the tissues
ORAL CANDIDIASIS
PATHOGENESIS. Candida’s pathogenicfactors
Pathogenesis 1
• Adhesion is an important determinant of Candida’s virulence
– Candida produces a large number of adhesins that mediate adherence to host

epithelial and endothelial cells
– Strains with faulty adhesins are avirulent

ORAL CANDIDIASIS
Pathogenesis 2
• Candida produces many enzymes that contribute to its pathogenicity
– Produces 9 proteinases involved in invasion of tissues by degradation of

extracellular matrix proteins
– Produces adenosine which blocks neutrophil degranulation, thus impairing

phagocytosis
ORAL CANDIDIASIS
Pathogenesis 3
• Candida adapts rapidly to changes in host environment
– Shifts between phenotypes in a reversible and random fashion
– Produces genetically altered variants at a high rate
– This adaptation makes it difficult for host defenses to attack and eliminate
infection
ORAL CANDIDIASIS
Head&Neck radiotherapy – acute mucositis.

ORAL CANDIDIASIS
Head&Neck radiotherapy –
severe xerostomia
ORAL CANDIDIASIS
Head&Neck radiotherapy – severe xerostomia (0.1ml saliva for 5min.), decreased

рН (6.4) and low buffer capacity. Saliva is viscous and sticky.
ORAL CANDIDIASIS
Neutropenia after Acute pseudomembranous candidiasis

chemotherapy in the same patient
ORAL CANDIDIASIS
External stigmas of advanced diabetes.

Such a patients are prone to develop
different fungal infections
ORAL CANDIDIASIS
• Erythematous candidiasis usually occurs on the dorsum of the tongue in persons who use
corticosteroid inhalators due to asthma treatment
• In individuals who have developed candidiasis secondary to the use of inhaled steroids, rinsing
out the mouth with water after taking the steroid, and using a spacer device to reduce the contact
with the oral mucosa (particularly the dorsal tongue) may be beneficial
ORAL CANDIDIASIS
Imbalance of the oral microbiota. Broad-spectrum antibiotics, which eliminate the competing
bacteria and disrupt the normally balanced ecology of oral micro-organisms..
Lingua nigra villosa and antibiotic sore tongue after oral intake of suspension of Augmentin
ORAL CANDIDIASIS
TONGUE piercing Microbiological sampling and Candida albicans grown in the

laboratory
ORAL CANDIDIASIS
Presence of certain mucosal alterations are sometimes

associated with Candida spp overgrowth, such as Epulis
fissuratum
ORAL CANDIDIASIS
Presence of certain mucosal alterations are sometimes associated with Candida spp
overgrowth, such as fissured tongue (Lingua plicata)
ORAL CANDIDIASIS
Good denture hygiene involves regular cleaning of the dentures, and leaving them out of the mouth
during sleep. This gives the mucosa a chance to recover. In oral candidiasis, the dentures may act as
a reservoir of Candida species
ORAL CANDIDIASIS
CLASSIFICATION of the clinical forms
Acute • Pseudomembranous candidiasis (oral thrush)

candidiasis • Erythematous (atrophic) candidiasis
Chronic • Erythematous (atrophic) candidiasis

candidiasis • Hyperplastic candidiasis (Candida leukoplakia)
• Candida-associated lesions in oral cavity
- Angular cheilitis
- Denture related stomatitis
- Median rhomboid glossitis
- Linear gingival erythema (?)
SOURCE: Scully, Crispian (2008). Oral and maxillofacial medicine: the basis of
diagnosis and treatment (2nd ed.). Edinburgh: Churchill Livingstone. pp. 191–199
ORAL CANDIDIASIS
CLINICAL CHARACTERISTICS
Acute Pseudomembranous Candidiasis (Thrush)

• Acute pseudomembranous candidiasis is a classic form of oral candidiasis. Overall, this
is one of the most common type of oral candidiasis, accounting for about 35% of oral
candidiasis cases
• It is characterized by a coating or individual patches of pseudomembranous white
slough that can be easily wiped away to reveal erythematous, and sometimes minimally
bleeding mucosa beneath. These areas of pseudomembrane are sometimes described
as "curdled milk". The white material is made up of debris, fibrin, and desquamated
epithelium that has been invaded by yeast cells and hyphae that invade to the depth of
the stratum spinosum.
ORAL CANDIDIASIS
• Due to the fact that an erythematous surface is revealed beneath the

pseudomembranes, some consider pseudomembranous candidiasis and
erythematous candidiasis stages of the same entity.
• Pseudomembraneous candidiasis can involve any part of the mouth, but usually it
appears on the tongue, buccal mucosae or palate.
ORAL CANDIDIASIS
• It is classically an acute condition, appearing in infants, people taking

antibiotics or immunosuppressant medications, or immunocompromising
diseases.
• However, sometimes it can be chronic and intermittent, even lasting for many
years. Chronicity of this subtype generally occurs in immunocompromised
states, (e.g., leukemia, HIV) or in persons who use corticosteroids topically or
by aerosol.
ORAL CANDIDIASIS
• White, cheesy, creamy, loose patches that can be easily rubbed off
• Underlying mucosa is erythematous and easily bleeds
• Disturbed taste sensations (disgeusia)

ORAL CANDIDIASIS
Acute Pseudomembranous Candidiasis

ORAL CANDIDIASIS

ORAL CANDIDIASIS

ORAL CANDIDIASIS
Acute Pseudomembranous Candidiasis I usually observed

in:
• Newly born (first weeks after birth)

• Old patients (marasmus)
• Leukemia
• Chemotherapy/radiotherapy
• Severe xerostomia
• Local application of corticosteroids
• Immunosuppression e.g. HIV/AIDS
ORAL CANDIDIASIS
SOURCE SOURCE
Martin S. Spiller, D.M.D. courtesy of Dr. Ed Cataldo © DermNetNZ
http://doctorspiller.com/candidiasis.htm http://www.dermnetnz.org/fungal/oral-candidiasis.html
Oral candidiasis in an infant. At very young ages, the immune system is yet to develop fully
ORAL CANDIDIASIS
Acute erythematous (atrophic) candidiasis
• Erythematous (atrophic) candidiasis is where

the condition appears as a red, raw-looking
lesion.
• It may precede the formation of a
pseudomembrane, be left when the
membrane is removed, or arise de novo.
ORAL CANDIDIASIS
Acute erythematous (atrophic) candidiasis
• The erythematous candidiasis accounts for 60% of oral candidiasis cases. Where it
is associated with inhalation steroids, erythematous candidiasis commonly appears
on the palate or the dorsum of the tongue
• Some authors consider denture-related stomatitis, angular stomatitis, median

rhombiod glossitis, and antiobiotic-induced stomatitis as subtypes of erythematous
candidiasis, since these lesions are commonly erythematous/atrophic
ORAL CANDIDIASIS
Atrophic (Erythematous) Candidiasis

• Acute erythematous candidiasis usually occurs
on the dorsum of the tongue in persons taking
long term corticosteroids or antibiotics, but
occasionally it can occur after only a few days of
using a topical antibiotic.This is usually termed
"antibiotic induced stomatitis" because it is
commonly painful as well as red.
• Chronic erythematous candidiasis is more

usually associated with denture wearing
ORAL CANDIDIASIS
Atrophic (Erythematous) Candidiasis
Erythematous candidiasis can mimic

geographic tongue. Erythematous
candidiasis usually has a diffuse border
that helps distinguish it from erythroplakia,
which normally has a sharply defined
border.
geographic tongue
ORAL CANDIDIASIS
Candida-associated denture induced stomatitis

• The major risk factor for the development of this condition is
wearing an upper complete denture, particularly when it is not
removed during sleep and cleaned regularly. Older dentures are
more likely to be involved. Other factors include xerostomia (dry
mouth), diabetes or a high carbohydrate diet
• The local environment under a denture is more acidic and less
exposed to the cleansing action of saliva, which favors high
Candida enzymatic activity and may cause inflammation in the
mucosa
• Poorly fitting dentures may cause pressure on the mucosa and
mechanical irritation
ORAL CANDIDIASIS
• Denture-related stomatitis is usually painless and asymptomatic.

• The appearance of the involved mucosa is erythematous (red)
and edematous (swollen), sometimes with petechial hemorrhage.
• This usually occurs beneath an upper denture. Sometimes
angular cheilitis can coexist, which is inflammation of the corners
of the mouth, also often associated with Candida albicans.
• The affected mucosa is often sharply defined, in the shape of the
covering denture.
• Stomatitis rarely develops under a lower denture.
ORAL CANDIDIASIS

The Newton classification divides denture-related stomatitis into three types
based on severity.
• Type 1 - Localized inflammation or pinpoint hyperemia

• Type 2 - More diffuse erythema (redness) involving part or all of the
mucosa which is covered by the denture
• Type 3 - Inflammatory nodular/papillary hyperplasia usually on the
central hard palate and the alveolar ridge
Type one may represent an early stage of the condition, whilst type two is
the most common and type three is uncommon.
ORAL CANDIDIASIS
Type 1 - Localized inflammation or pinpoint hyperemia

ORAL CANDIDIASIS
Type 2 - More diffuse erythema (redness) involving part or all of

the mucosa which is covered by the denture
ORAL CANDIDIASIS
Type 3 - Inflammatory nodular/papillary hyperplasia usually on the central hard palate and the
alveolar ridge
ORAL CANDIDIASIS
Type 3 - Inflammatory nodular/papillary hyperplasia usually on the central hard palate and the
alveolar ridge
ORAL CANDIDIASIS
CLINICAL CHARACTERIASTICS
Glossitis rhombica mediana
• Median rhomboid glossitis is a

condition characterized by an
area of redness and loss of
lingual papillae, situated on the
dorsum of the tongue in the
midline immediately in front of
the circumvallate papillae
• Median rhomboid glossitis is
thought to be related to a chronic
fungal infection
ORAL CANDIDIASIS
• Apart from the appearance of the lesion, there

are usually no other signs or symptoms.
• Rarely is any soreness associated with the
condition.
• The typical appearance of the lesion is an oval

or rhomboid shaped area located in the midline
of the dorsal surface of the tongue, just anterior
of the sulcus terminalis.
ORAL CANDIDIASIS
• The lesion is usually symmetric, well

demarcated, erythematous and depapillated,
which has a smooth, shiny surface.
• Less typically, the lesion may be hyperplastic or

lobulated and exophytic.
• The lesion is typically 2 – 3 cm in its longest

dimension.
ORAL CANDIDIASIS
Sometimes an approximating erythematous lesion is present on the palate as tongue

touches the palate frequently - a "kissing lesions"
ORAL CANDIDIASIS
Sometimes an approximating erythematous lesion is present on the palate as tongue

touches the palate frequently - a "kissing lesions"
ORAL CANDIDIASIS
Angular cheilitis
• Angular cheilitis is inflammation at the corners

(angles) of the mouth, very commonly involving
Candida species
• Candida spp alone are responsible for about
20% of cases, and a mixed infection of C.
albicans and Staphylococcus aureus for about
60% of cases
• Signs and symptoms include soreness,
erythema (redness), and fissuring of one, or
more commonly both the angles of the mouth,
with edema seen intraorally on the commisures
ORAL CANDIDIASIS
• Angular cheilitis is generally occurs in elderly people and is associated with denture related
stomatitis.
• Sometimes dentures become very worn, or they have been constructed to allow insufficient lower
facial height (occlusal vertical dimension), leading to over-closure of the mouth. This causes
pronouncement of the skin folds at the corners of the mouth, in effect creating an intertriginous
areas where angular cheilitis can develop.
ORAL CANDIDIASIS
Chronic Hyperplastic Candidiasis
• The most common appearance of hyperplastic candidiasis is a persistent white

plaque that does not rub off.
• The lesion may be rough or nodular in texture.
• Hyperplastic candidiasis is uncommon, accounting for about 5% of oral candidiasis
cases, and is usually chronic and found in adults.
• The most common site of involvement is the commisural region of the buccal mucosa,
usually on both sides of the mouth.
ORAL CANDIDIASIS
• Another term for hyperplastic candidiasis is "candidal leukoplakia". This term is a

largely historical synonym for this subtype of candidiasis, rather than a true
leukoplakia. Indeed it can be clinically indistinguishable from true leukoplakia, but
tissue biopsy shows candidal hyphae invading the epithelium.
• Some sources use this term to describe leukoplakia lesions that become colonized
secondarily by Candida species, thereby distinguishing it from hyperplastic
candidiasis.
ORAL CANDIDIASIS
• White plaque that does not rub off
• Commonly found on buccal mucosa along occlusal line in V-shape and widening
as it approaches commissure
• Biopsy is conditional
ORAL CANDIDIASIS
ORAL CANDIDIASIS AND HIV/AIDS
• The oral candidiasis may occasionally be a herald of a more

sinister undiagnosed pathology, such as HIV/AIDS.
• Oral candidiasis is rare if CD4 counts are above 500.

Outbreaks are more common as the count drops to 100, when
it may be harder to treat.
ORAL CANDIDIASIS
Esophageal candidiasis
• A more serious condition of the throat and

windpipe, called esophageal candidiasis, is
on the list of AIDS defining illnesses, affecting
up to 1 in 5 of people with AIDS.
• It often occurs together with oral candidiasis.
• Symptoms include chest pain, nausea and

painful or difficult swallowing, causing
patients to not want to eat
ORAL CANDIDIASIS
Pseudomembranous Candidiasis
SOURCE:
Classification of oral diseases of HIV- associated immune suppression
(ODHIS) Glick M, Abel SN, Flaitz CM, Migliorati CA, Patton LL, Phelan
JA, Reznik DA (ODHIS Workshop Group-USA, Dental Alliance for
AIDS/HIV CARE – DAAC)
ORAL CANDIDIASIS
Oesophageal Candidiasis
SOURCE:
ORAL CANDIDIASIS
ORAL CANDIDIASIS AND

HIV/AIDS
Hyperplastic Candidiasis
SOURCE:
Classification of oral
diseases of HIV-
associated immune
suppression (ODHIS)
Glick M, Abel SN,
Flaitz CM, Migliorati
CA, Patton LL,Phelan
JA, Reznik DA
(ODHIS Workshop
Group-USA, Dental
Alliance for AIDS/HIV
CARE – DAAC)
ORAL CANDIDIASIS
Erythematous Candidiasis
SOURCE:
ORAL CANDIDIASIS

This is a localized or
generalized, linear
band of erythematous
gingivitis. It was first
observed in HIV
infected individuals
and termed "HIV-
gingivitis", but the
condition is not
confined to this group.
Candida species are
involved, and in some
cases the lesion
responds to antifungal
therapy.
SOURCE:
Classification of oral diseases of HIV- associated
immune suppression (ODHIS) Glick M, Abel SN,
Linear Gingival Erythema
Flaitz CM, Migliorati CA, Patton LL, Phelan JA,
Reznik DA (ODHIS Workshop Group-USA,Dental
Alliance for AIDS/HIV CARE – DAAC)
ORAL CANDIDIASIS
Angular cheilitis associated with Candidiasis

SOURCE:
Classification of oral diseases of HIV- associated immune
suppression (ODHIS) Glick M, Abel SN, Flaitz CM, Migliorati CA,
Patton LL, Phelan JA, Reznik DA (ODHIS Workshop Group-
USA, Dental Alliance for AIDS/HIV CARE – DAAC)
ORAL CANDIDIASIS
Kaposi sarcoma associated with Candidiasis
SOURCE
Sol Silverman, Jr., D.D.S., University of California, San Francisco
http://hardinmd.lib.uiowa.edu/cdc/6058.html
ORAL CANDIDIASIS
DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS

• The diagnosis can typically be made from the clinical appearance alone, but not always.
• As candidiasis can be variable in appearance, and present with white, red or combined
white and red lesions, the differential diagnosis can be extensive.
• In general Candida spp are grown in the laboratory on solid growth media or in liquid
broths
• Special investigations to detect the presence of candida species include oral swabs,
oral rinse or oral smears.
• Molecular diagnosis of Candida spp using real-time polymerase chain reaction (RT -
PCR), Monoclonal Antibody and Rapid Latex Agglutination (RLA)
• If candidal leukoplakia is suspected, a biopsy may be indicated. Smears and biopsies

are usually stained with Periodic acid-Schiff, which stains cabohydrate in fungal cell
walls magenta
ORAL CANDIDIASIS
In pseudomembraneous candidiasis, the membranous slough can be wiped away to reveal

an erythematous surface underneath. This is helpful in distinguishing pseudomembraneous
candidiasis from other white lesions in the mouth that cannot be wiped away, such as lichen
planus, oral leukoplakia etc
ORAL CANDIDIASIS
In general Candida spp are grown in the laboratory on solid

growth media or in liquid broths
• Candida albicans growing on Sabouraud agar
• Candida appears as large, round, white or cream colonies with a yeasty odor
on agar plates at room temperature.
ORAL CANDIDIASIS
DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS
• Smears are collected by gentle scraping of the lesion with a

spatula or tongue blade and the resulting debris directly applied to
a glass slide.
• Oral swabs are taken if culture is required. Some recommend that

swabs be taken from 3 different oral sites.
• Oral rinse involves rinsing the mouth with phosphate-buffered

saline for 1 minute and then spitting the solution into a vessel that
examined in a pathology laboratory. Oral rinse technique can
distinguish between commensal candidal carriage and candidiasis.
• Gram staining is also used as Candida stains strongly Gram(+).

ORAL CANDIDIASIS
Routine diagnostic of Candida spp – DIRECT MICROSCOPY

ORAL CANDIDIASIS
BIOCHEMIC IDENTIFICATION
• C. albicans ferments glucose and maltose to acid and

gas, sucrose to acid, and does not ferment lactose,
which help to distinguish it from other Candida species
• API test at 20°C
ORAL CANDIDIASIS
SEROLOGICAL TESTS
• Whole cell agglutination

• Immunofluorescence
• immunoenzyme analysis for detection of IgG antibodies against Candida spp
• Radio-immunological analysis
ИЗТОЧНИК ИЗТОЧНИК
CDC/Maxine Jalbert, Dr. LeoKaufman ELI.H.A Candida
http://www.microbiologybook.org/mycology/ http://www.elitechgroup.com/corporate/products
/market-segment/microbiology/mycology/
ORAL CANDIDIASIS
Molecular diagnosis of Candida spp using real-time polymerase chain

reaction (RT - PCR)
Real-time PCR detection of Candida DNA

from samples may aid in diagnosis of oral
candidiasis in high risk populations. This
assay's ability to discriminate between C.
albicans and non-C. albicans species,
including C. glabrata, C. krusei, and C.
parapsilosis, may allow for implementation
of species-specific therapies, when
SOURCE
necessary. PCR-based gene targeting in Candida albicans
http://www.nature.com/nprot/journal/v3/n9/fig_tab/nprot.2008.137_F1.html
ORAL CANDIDIASIS
TREATMENT – common recommendations
• Treatment of co-existing
systematic diseases
• Proper diet, probiotics
• The candida load in the mouth

can be reduced by improving
oral hygiene measures, such as
regular toothbrushing and use of
anti-microbial mouthwashes
ORAL CANDIDIASIS
Treatment with ANTI-FUNGAL drugs
• Oral candidiasis can be treated with topical anti-fungal

drugs, such as nystatin, miconazole, gentian violet or
amphotericin B. Topical treatment is recommended for
patients with normal immune function
• Patients who are immunocompromised, either with

HIV/AIDS or as a result of chemotherapy, may require
systemic treatment with oral anti-fungals
ORAL CANDIDIASIS
SYSTEMIC TREATMENT of acute oral candidiasis
• Fluconazole
50 – 150mg/daily for 7-14 days
• Itraconazole
2x 100 mg/daily for 7-14 days
• Posaconazole (Noxafil)
200 mg/first day. 100 mg/daily for the rest 7-14 days.
Systemic treatment is advocated in case of relapse

ORAL CANDIDIASIS
TREATMENT of acute pseudomembranous candidiasis
Before treatment After treatment

ORAL CANDIDIASIS
TREATMENT of acute pseudomembranous candidiasis
Before treatment After treatment

ORAL CANDIDIASIS
LOCAL TREATMENT of erythematous candidiasis
• Nystatin (100000 IU/ml - 50 ml)

4-6x/daily for 7-14 days
• Natamycin (10mg)
4-6x/daily for 7-14 days. It is not absorbed in GIT
• Miconazole (Dactarin oral gel 2%)

4-6x/daily for 7-14 days.
ORAL CANDIDIASIS
TREATMENT MODALITIES FOR DENTURE-RELATED

STOMATITIS
• The most important aspect of treatment is improving denture

hygiene, i.e. removing the denture at night, cleaning and
disinfecting it, and storing it overnight in an antiseptic solution.
This is important as the denture is usually infected with C.
albicans which will cause re-infection if it is not removed.
• Substances which are used include solutions of alkaline
peroxides, acids (e.g. benzoic acid), yeast lytic enzymes and
proteolytic enzymes (e.g. alcalase protease).
• The other aspect of treatment involves resolution of the
mucosal infection, for which topical antifungal medications are
used (e.g. nystatin, amphotericin, miconazole, fluconazole or
itraconazole).
• Often an antimicrobial mouthwash such as chlorhexidine is
concurrently prescribed.
ORAL CANDIDIASIS
Candida-associated denture induced stomatitis - Type 2
Before treatment After denture removal

ORAL CANDIDIASIS
Candida-associated denture induced stomatitis - Type 2
Alkalizing and Dactarin gel applications Two weeks after treatment

ORAL CANDIDIASIS
TREATMENT of angular cheilitis associated with C. albicans
Treatment of the infection and inflammation of the lesions with topical antifungal medication,
such as clotrimazole, amphotericin B, ketoconazole, or nystatin cream is recommended.
Some antifungal creams are combined with corticosteroids such as hydrocortisoneor
triamcinolone to reduce inflammation, and some antifungals such as miconazole cream also
have some antibacterial action.
ORAL CANDIDIASIS
PROGNOSIS of angular cheilitis associated with C. albicans
• Most cases of angular cheilitis respond quickly

when antifungal treatment is used.
• In more long standing cases, the severity of

the condition often follows a relapsing and
remitting course over time.
• The condition can be difficult to treat and can

be prolonged.
ORAL CANDIDIASIS
PROGNOSIS • The prognosis of oral candidiasis is

usually excellent after the application
of topical or systemic treatments.
• However, oral candidiasis can be

recurrent. Individuals continue to be at
risk of the condition if underlying
factors such as reduced salivary flow
rate or immunosuppression are not
rectifiable.
• Candidiasis can be a marker for

underlying disease, so the overall
prognosis may also be dependent
upon this.

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ORAL CANDIDIASIS

Dr. Ahmad Yusran, SpPD

Candida spp. as commensal are

local, or systemic factors altering host

“ Candidiasis occurs in the very young, the very

The causative organism is • C. tropicalis (1)

C. albicans 70-80% Highly virulent

C. Albicans and C. glabrata account for over 80% of cases

Candidal carriage state is not • LOCAL FACTORS

PATHOGENESIS. Macro-organism – systemic factors

• Acute pseudomembranous candidiasis occurs in about 5% of newborn

PATHOGENESIS. Macro-organism – systemic factors

PATHOGENESIS. Macro-organism – systemic factors

Drug induced conditions

PATHOGENESIS. Macro-organism – localfactors

ALTERED BARRIER FUNCTION OF THE ORAL MUCOSA

• Presence of certain mucosal lesions, especially those that cause

• Other physical mucosal alterations are sometimes associated with candida

PATHOGENESIS. Macro-organism – localfactors

QUANTITY AND QUALITY OF SALIVA

PATHOGENESIS. Macro-organism – localfactors

IMBALANCE OF THE ORAL MICROBIOTA

• Broad-spectrum antibiotics which eliminate the competing bacteria and disrupt

PATHOGENESIS. Candida’s pathogenicfactors

• Adhesion is an important determinant of Candida’s virulence

– Candida produces a large number of adhesins that mediate adherence to host

– Strains with faulty adhesins are avirulent

PATHOGENESIS. Candida’s pathogenicfactors

• Candida produces many enzymes that contribute to its pathogenicity

– Produces 9 proteinases involved in invasion of tissues by degradation of

– Produces adenosine which blocks neutrophil degranulation, thus impairing

PATHOGENESIS. Candida’s pathogenicfactors

• Candida adapts rapidly to changes in host environment

– Shifts between phenotypes in a reversible and random fashion

– Produces genetically altered variants at a high rate

Head&Neck radiotherapy – acute mucositis.

Head&Neck radiotherapy – severe xerostomia (0.1ml saliva for 5min.), decreased

Neutropenia after Acute pseudomembranous candidiasis

External stigmas of advanced diabetes.

TONGUE piercing Microbiological sampling and Candida albicans grown in the

Presence of certain mucosal alterations are sometimes

CLASSIFICATION of the clinical forms

Acute • Pseudomembranous candidiasis (oral thrush)

Chronic • Erythematous (atrophic) candidiasis

Acute Pseudomembranous Candidiasis (Thrush)

Acute Pseudomembranous Candidiasis (Thrush)

• Due to the fact that an erythematous surface is revealed beneath the

Acute Pseudomembranous Candidiasis (Thrush)

• It is classically an acute condition, appearing in infants, people taking

• Underlying mucosa is erythematous and easily bleeds

• Disturbed taste sensations (disgeusia)

Acute Pseudomembranous Candidiasis

Acute Pseudomembranous Candidiasis

Acute Pseudomembranous Candidiasis

Acute Pseudomembranous Candidiasis I usually observed

• Newly born (first weeks after birth)

Acute erythematous (atrophic) candidiasis

• Erythematous (atrophic) candidiasis is where