Oral Candidiasis also referred to as oral thrush is commonly encountered in a daily life of a dentist. An overview on this topic for undergraduate students.

2. CONTENTS
• INTRODUCTION
• CLASSIFICATION
• PREDISPOSING FACTORS
• PATHOGENESIS
• PRIMARY ORAL CANDIDIASIS
• SECONDARY ORAL CANDIDIASIS
• LABORATORY DIAGNOSIS
• TREATMENT
• REFERENCES

3. INTRODUCTION
• It was first described by the French paediatrician FrancoisValleix in 1838.
• Candidiasis is one of the most common fungal infections affecting human
beings. It occurs mainly as a secondary infection in patients with some
underlying immunosuppression and the primary form of disease is rare.
• It affects the skin, mucous membranes, nails gastrointestinal tract, vaginal
tract, urinary tract and internal organs.
• Oral involvement is the most common manifestation of human candida
infection.

4. CAUSATIVE ORGANISMS
• It is mainly caused by yeast-like fungus Candida albicans.
• Other candida species which cause candidiasis are :- Candida tropicalis,
Candida stellatoidea, Candida parapsillasis, Candida pseudotropicalis,
Candida rugosa, Candida krusei, Candida glabrata, Candida guilliermondi,
Candida dubliniensis and Candida viswanathii.
• It is present in three forms : yeast form, hyphal form and chlamydospore
form.
• It reproduces by asexual budding and form pseudo hyphae.
• These species grow rapidly at 25º - 37º c.
• It is relatively a common inhabitant of the oral cavity, gastrointestinal tract
and vagina of clinically normal persons.

5. CLASSIFICATION
CLASSIFICATIONOF
CANDIDIASIS
FIRST CLASSIFICATION
SECOND CLASSIFICATION
THIRD CLASSIFICATION

6. FIRST CLASSIFICATION
ACUTE CHRONIC
• Acute pseudomembranous candidiasis (thrush)
• Acute atrophic candidiasis
2) CHRONIC MUCOCUTANEOUSCANDIDIASIS
• FamilialCMC
• LocalizedCMC
• Diffuse CMC
• Candidiasis endocrinopathy syndrome
CHRONIC
a) Chronic atrophic candidiasis
• Denture stomatitis
• Median rhomboid glossitis
• Angular cheilitis
b) Id reaction
c) Chronic hyperplastic candidiasis
3) EXTRAORAL CANDIDIASIS
• Oral candidiasis associated with extraoral lesions,
orofacial and intertriginous sites ( candida
vulvovaginitis, intertriginous candidiasis.
• Gastrointestinal candidiasis
• Candida hypersensitivity syndrome
4) SYSTEMICCANDIDIASIS

7. SECOND CLASSIFICATION
• Classification of oral candidiasis [ as proposed by Samaranayake (1991) and
modified by Axéll et al (1997)]
• PRIMARY ORAL CANDIDIASIS
ACUTE FORMS CHRONIC FORMS CANDIDA –
ASSOCIATED LESIONS
KERATINIZED PRIMARY
LESIONS
SUPERINFECTEDWITH
CANDIDA
PSEUDOMEMBRANOUS HYPERPLASTIC DENTURE STOMATITIS LEUKOPLAKIA
ERYTHEMATOUS NODULAR ANGULAR CHELITIS LICHEN PLANUS
PLAQUE – LIKE MEDIAN RHOMBOID
GLOSSITIS
LUPUS ERYTHEMATOUS
ERYTHEMATOUS
PSEUDOMEMBRANOUS

8. SECONDARY ORAL CANDIDIASIS
FAMILIAL CHRONIC MUCOCUTANEOUS CANDIDIASIS
DIFFUSE CHRONIC MUCOCUTANEOUS CANDIDIASIS
CANDIDIASIS ENDOCRINOPATHY SYNDROME
FAMILIAL MUCOCUTANEOUS CANDIDIASIS
SEVERE COMBINED IMMUNODEFICIENCY
DiGEORGE SYNDROME
CHRONIC GRANULOMATOUS DISEASE
ACQUIRED IMMUNE DEFICIENCY SYNDROME (AIDS)

9. THIRD CLASSIFICATION
ORAL MUCOSA CHRONIC ORAL
CANDIDIASIS
GASTROINTESTINAL
MUCOSA
ACUTE ORAL CANDIDIASIS CHRONIC ATROPHIC
CANDIDIASIS
PHARYNGEAL CANDIDIASIS
ACUTE
PSEUDOMEMBRANOUS
CANDIDIASIS
CHRONIC HYPERPLASTIC
CANDIDIASIS
ESOPHAGEAL CANDIDIASIS
ACUTE ATROPHIC
CANDIDIASIS
INTESTINAL CANDIDIASIS
1) CANDIDIASIS CONFINEDTOTHE MUCOSAE

10. CONFINEDTO MUCOCUTANEOUS
SURFACES - IN CONDITIONS WITH
MAJOR IMMUNOLOGIC DEFECT
IN CONDITIONS WITH MINOR
IMMUNOLOGIC DEFECT - CHRONIC
MUCOCUTANEOUS CANDIDIASIS
(CMC) SYNDROMES
CONFINEDTO MUCOCUTANEOUS
JUNCTIONS
SWISS –TYPE
AGAMMAGLOBULINEMIA
FAMILIAL MUCOCUTANEOUS
CANDIDIASIS
CANDIDAL ANGULAR CHELITIS
HEREDITARYTHYMIC DYSPLASIA CANDIDIASIS ENDOCRINOPATHY
SYNDROME
PERIANALCANDIDIASIS
DI GEORGE SYNDROME LOCALIZED CHRONIC
MUCOCUTANEOUS CANDIDIASIS
AIDS CHRONIC MUCOCUTANEOUS
CANDIDIASISASSOCIATEDWITH
THYMOMA
2) MUCOCUTANEOUS CANDIDIASIS

11. 3) CANDIDIASIS
CONFINED TO SKIN
4) CANDIDIASIS OF
NAILS AND SKIN
5) RESPIRATORY
MUCOSA
6) GENITOURINARY
MUCOSA
7) SYSTEMIC
CANDIDIASIS
INTERDIGITAL
CANDIDIASIS
CANDIDAL ONYCHIA BRONCHIAL
CANDIDIASIS
CANDIDAL
VULVOVAGINITIS
CANDIDAL
ENDOCARDITIS
INTERTRIGINOUS
CANDIDIASIS
CANDIDAL
PARONYCHIA
CANDIDAL
SEPTICEMIA
CANDIDIDS
(MONOLIDS)
CANDIDAL
MENINGITIS

13. PREDISPOSING FACTORS
LOCAL GENERAL
Denture wearing Immunosuppressive diseases
Smoking Impaired health status
Inhalation steroids Immunosuppressive drugs
Topical steroids Chemotherapy
Hyperkeratosis Endocrine disorders
Imbalance of oral microbial
flora
Hematinic deficiencies
Quality and quantity of saliva

14. PREDISPOSING FACTORS
1) CHANGES IN ORAL MICROBIAL FLORA
• Administration of antibiotics (broad-spectrum),
excessive use of antibacterial mouth rinses,
xerostomia secondary to anticholinergic agent or
salivary gland disease.
2) LOCAL IRRITANTS
• Chronic local irritant ( denture, orthodontic
appliance and heavy smoke).
3) DRUGTHERAPY
• Administration of corticosteroids, cytotoxic drugs,
immunosuppressive agents and radiation to head
and neck.

15. 4) ACUTE AND CHRONIC DISEASE
• Acute and chronic diseases such as leukaemia, lymphoma, diabetes
mellitus and tuberculosis.
5) MALNUTRITION STATES
• Malnutrition states such as low serum vitamin A, pyridoxine and iron levels.
6) AGE
• Infancy, pregnancy and old age, prolonged hospitalization and debilitating
diseases.
7) ENDOCRINOPATHY
• Endocrinopathies such as hypoparathyroidism, hypothyroidism and
Addison’s disease.

16. 8) IMMUNODEFICIENCY STATES
• Primary and acquired immunodeficiency
states such as AIDS and
hypogammaglobinemia
9) OTHERS
• Tight and close – fitting garments encourage
the growth of candida.
• Use of intravenous tubes, catheters, heart
valves and poorly maintained dentures and
heavy smoking.

17. PATHOGENESIS
• Candida albicans causes thrush when normal host immunity or normal host flora is
disrupted, hence it is called ‘opportunistic infection’.
Salivary IgA affects the adherence of candida to the
mucosal cells
Overgrowth of yeast on the oral mucosa leads to
desquamation of epithelial cells and accumulation
of bacteria, keratin, necrotic tissue and debris to
form pseudo membrane
Specific and Non- specific factors like anticandidal factors and
anti adherence factors have a role in the development of
candidiasis

18. T-cells and neutrophils play a role in preventing and
clearing the infection
Following fungal penetration, these cells exhibits
phagocytic and candidacidal activity, which involves
myeloperoxidase and superoxide or cationic
proteins
Other factors of less significant role are
complement, transferrin, lactoferrin, vitamin A and
C1 – serum antibody
The membrane shows extensive areas of oedema, ulceration and
necrosis of the underlying mucosa

19. PRIMARY ORAL CANDIDIASIS
PSEUDOMEMBRANOUSCANDIDIASIS
• It is a prototype of oral infection caused by yeast – like fungus.
• It is also known as ‘thrush’ and is one of the most common forms of
candidiasis.

20. CLINICAL FEATURES : IN INFANTS
AGE
• In neonates, oral lesions start between the 6th and 10th day after birth.
CAUSE
• Infection is contracted from the maternal vaginal canal where Candida
albicans flourishes during pregnancy.
APPEARENCE
• Soft white or bluish white, adherent patches on the oral mucosa, which may
extend to circumoral tissue.
SYMPTOMS
• They are painless and noticed on careful examination.They may be
removed with little difficulty.

22. CLINICAL FEATURES : INADULTS
AGE
• Occurs at any age, but is especially prone to occur in the debilitated or
chronically ill patients.
• Occurrence of this lesion in a healthy individual indicates the presence of
immune suppression, especially HIV patients..
SITE
• Buccal mucosa, roof of the mouth, retromolar area, tongue, gingiva, floor of
the mouth and mucobuccal fold.
SEX
• Female predilection

23. CAUSE
• Initiated by exposure of patient to broad- spectrum antibiotics and patients
receiving corticosteroids.
SYMPTOMS
• Rapid onset of unpleasant taste and spicy food will cause discomfort.
• Patients may complain of burning sensation.
APPEARENCE
• Soft, pearly, white or bluish white plaques are present on the oral mucosa.
They resemble ‘ cottage cheese’ or milk curds. Adjacent mucosa appears red
and moderately swollen.
COMPOSITON OF PLAQUES
• It is composed of tangled mass of fungal hyphae with intermingled
desquamated epithelium, keratin, fibrin, necrotic debris, leucocytes and
bacteria.

24. WIPING OFTHE
PATCHES
• White patches are easily wiped out with a wet gauze, which leaves either a
normal or erythematous area or atrophic area.This area may be painful.
• Deeper invasion by the organism leaves an ulcerative lesion upon the
removal of the patch.
MALIGNANT
ASSOCIATION
• It is occasionally associated with dysplastic or carcinomatous change.
• In severe cases, there is concomitant involvement of oral cavity and
oesophagus, which is common in HIV patients.

26. DIAGNOSISAND DIFFERENTIAL
DIAGNOSIS
DIAGNOSIS
• Clinical Diagnosis :
Pseudomembranous lesion
which can be scrapped off
will diagnose candidiasis.
DIFFERENTIAL DIAGNOSIS
• Plaque form of Lichen planus
• Leukoplakia
• Geno dermatoses
• Gangrenous stomatitis
• Chemical burns

27. ACUTE ATROPHIC CANDIDIASIS
• Synonyms : Erythematous candidiasis, Antibiotic sore
mouth
• It is also called ‘antibiotic sore mouth’ and it includes
central papillary atrophy of tongue and cheilo
candidiasis.
• CAUSE : It may arise in acute pseudomembranous
candidiasis after the white plaques are shed.
• It occurs as a sequelae to a course of broad-spectrum
antibiotics, corticosteroids or any immunosuppressive
diseases, more commonly HIV infection.

28. CLINICAL FEATURES :
SITE
• It can occur in any site but it usually involves the tongue and tissue
underlying the prosthesis.
SYMPTOMS
• Patient usually describes a vague pain or a burning sensation.
• It is the only variety of oral candidiasis which is ‘painful’

29. SIGNS
• Careful examination reveals a few white thickened foci that rub off leaving a
painful surface.
APPEARENCE
• The lesion appears as red or erythematous, rather than white, thus
resembling the pseudo membranous type in which white membrane has
wiped off.The redness is due to increased vascularity.
• The borders are diffuse.
• Central papillary atrophy of tongue is an asymptomatic symmetric
erythematous lesion on dorsal aspect in posterior region.
• Some patients with central papillary atrophy may also exhibit signs of oral
mucosal candida infection at other sites.This presentation of erythematous
candidiasis is been termed as ‘chronic multifocal candidiasis’.
• The palatal lesion contacts with the dorsal tongue lesion when tongue is at
rest – Kissing lesion.

31. DIAGNOSISAND DIFFERENTIAL
DIAGNOSIS
DIAGNOSIS
• Clinical diagnosis :
Erythematous area with
condition causing diminished
host resistance will diagnose
acute atrophic candidiasis.
DIFFERENTIAL DIAGNOSIS
•Chemical burn
•Drug reaction
•Syphilitic mucus patches
•Necrotic ulcer and
gangrenous stomatitis
•Traumatic ulcer

32. CHRONIC HYPERPLASTIC CANDIDIASIS
• Synonyms : Candidal leukoplakia, Chronic-
plaque type, Nodular candidiasis
• It is also called ‘ candida leukoplakia’
because of its presentation as firm and
adherent white patches occurring in the oral
mucosa which appear similar to leukoplakia.
• It is the least common form of candidiasis.
• Causon and Binnie have presented data
based on their finding that chronic
candidiasis itself is a cause of leukoplakia
and thus must be regarded as having a
possible premalignant potential.

33. CLINICAL FEATURES :
AGE AND SEX
• Predominantly occurs in men of middle age or above.
• Majority of these patients are heavy smokers.
SITE
• Cheeks, tongue and lips.
Symptoms
• Lesions may persist without any symptoms for years.

34. SIGNS
• It does not rub off with lateral pressure.
• Lesions range from slightly white to dense white with cracks and fissures
occasionally present.
• The borders are often vague which mimic the appearance of epithelial
dysplasia.
APPEARENCE
• Oral lesions consist of firm, white and leathery plaque.
• These lesions may be homogenous or speckled.

35. DIAGNOSISAND DIFFERENTIAL
DIAGNOSIS
DIAGNOSIS
• A firm white leathery
appearance which cannot
be rubbed off
DIFFERENTIAL DIAGNOSIS
•Hairy Leukoplakia
•Lichen Planus
•Superficial bacterial
infection

36. CANDIDA – ASSOCIATED LESIONS
• DENTURE STOMATITS
• MEDIAN RHOMBOID GLOSSITIS
• ANGULAR CHEILITIS

37. DENTURE STOMATITIS (CHRONIC
ATROPHIC CANDIDIASIS)
• Denture stomatitis is now considered synonymous with the condition
better known as denture sore mouth, a diffuse erythema and oedema of
the denture-bearing area.
• TYPES :
• TYPE I – Localized to minor erythematous sites caused by trauma from
denture
• TYPE II – Affects major part of denture covering mucosa
• TYPE III – Granular mucosa in the central part of the palate

38. CLINICAL FEATURES :
AGE AND SEX
• No apparent age limit
• Female predilection
SITE
• Usually found under the complete denture or partial denture mainly on the
palate.
Symptoms
• Asymptomatic; Soreness and dryness of mouth and presenting complaint
may be angular stomatitis.

39. SIGNS
• Palatal tissue is bright red, oedematous and granular.
• Red patches may be erythematous or speckled.
• The multiple pinpoint foci of hyperaemia usually involving the
maxilla frequently occurs.
APPEARENCE
• Patchy distribution often associated with speckled curd-like
white lesion.

40. DIAGNOSISAND DIFFERENTIAL
DIAGNOSIS
DIAGNOSIS
• Clinical Diagnosis : An
erythematous area under the
complete denture.
DIFFERENTIAL DIAGNOSIS
•Allergic reaction due to
denture base
•Erosive lichen planus
•Dermatitis herpetiformis

41. MEDIAN RHOMBOID GLOSSITIS
• It is also called ‘central papillary atrophy of
tongue’.
• The area of erythema results from the atrophy
of filiform papilla.
• It is a benign lesion of the tongue,
characterized by rhomboid or oval in shape,
changes occur in the tongue mucosa in the
midline, just anterior to the foramen cecum.
• Candida albicans is many times found in this
lesion.This type of lesion is called as posterior
midline atrophy candidiasis.

42. ANGULAR CHEILITIS
• It is also called as ‘Perleche’, ‘Angular
Cheilosis’, ‘Cheilocandidiasis’.
• Causes mainly include Candida albicans,
Staphylococci, Streptococci and other
factors.
• Mainly seen in old edentulous patients
with denture non – bearer.
• It presents as a rough triangular area of
erythema and oedema at one or more;
commonly both the corners of the mouth.
• Chronic atrophic candidiasis occur with
angular cheilitis.

43. SECONDARYORAL CANDIDIASIS

44. CHRONIC MUCOCUTANEOUS
CANDIDIASIS
• Chronic mucocutaneous candidiasis is a group of different forms of the
infection, dome of which may have multiple features in common although
they can usually be separated as entities.
• It is characterized by chronic candida involvement of the skin, scalp, nails
and mucous membranes.
• It is caused by defect in the cellular immunity impaired cell-mediated
immunity. Isolated IgA deficiency and reduced serum candidacidal activity.
• Other factors responsible are diabetes, steroid therapy and in some cases
of pregnancy.

45. TYPES
Chronic familial mucocutaneous candidiasis
Chronic mucocutaneous candidiasis in
association with thymoma
Chronic localized mucocutaneous
candidiasis
Endocrinopathy candidiasis syndrome
Chronic diffuse mucocutaneous candidiasis

46. ID REACTION
• It is a hypersensitivity reaction to
candida antigen, which manifests as
vesicular and papular rash on the skin
of patients with chronic candidiasis.
• A person with chronic candida
infection may develop secondarily
response characterized by localized or
generalized sterile vesicopapular rash
that is believed to be an allergic
response to candida antigen (also
called monolids).

47. LABORATORY DIAGNOSIS
• The candida organism can be seen microscopically in either an exfoliative
cytologic preparator or tissue sections.
• Fragments of the plaque material may be smeared on a microscopic slide,
macerated with 20% potassium hydroxide (KOH) and examined for typical
hyphae.
• Organisms can be cultured in a variety of media including blood agar,
cornmeal agar and sabouraud’s broth.
• Histologic sections of a biopsy from a lesion of oral candidiasis can show
the presence of the yeast cells and hyphae or mycelia.

48. CANDIDA ISOLATION INTHE CLINICAND
QUANTIFICATION FROM ORAL SAMPLES
METHOD MAIN STEPS ADVANTAGES DISADVANTAGES
Smear Scrapping, smearing
directly onto slide
Simple and quick Low Sensitivity
Swab Taken by rubbing cotton-
tipped swabs over lesional
tissue
Relatively simple Selecting sampling sites
critical
Imprint culture Sterile plastic, foam pads
dipped into Sabouraud
(Sab) broth, placed on
lesion for 60 s; pad
pressed on Sab agar plate
and incubated; colony –
counter used
Sensitive and reliable; can
discriminate between
infected and carrier states
Reading above 50
CFU/cm² can be
inaccurate; selection of
sites difficult if no clinical
signs present

49. METHOD MAIN STEPS ADVANTAGES DISADVANTAGES
Impression culture Maxillary and mandibular
alginate impressions;
casting in agar fortified
with Sab broth;
incubation
Useful to determine
relative distributions of
the yeasts on oral
surfaces
Useful mostly as a
research tool
Salivary culture Patient expectorates 2
mL saliva into sterile
container; vibration;
culture on Sab agar by
spiral plating; counting
As useful as imprint
culture
Considerable chairside
time; not useful for
xerostomics; cannot
identify site of infection
Oral rinse Subject rinses for 60 s
with PBS at pH 7.2, 0.1 M,
and returns it to the
original container;
concentrated by
centrifugation; cultured
and counted as previous
methods
Comparable in sensitivity
with imprint method;
better results if CFU
>50/cm²; simple method
Recommended for
surveillance cultures in
the absence of focal
lesions; cannot identify
site of infection

50. TREATMENT OF ORAL
CANDIDIASIS
• Oral Candidiasis may be treated either
topically or systematically.
• Treatment should be maintained for 7 days.
• To identify and eliminate predisposing or
precipitating factors;
• Replacement of the denture and thorough
cleaning regularly should be done.
• Withdrawal or change of antibiotics can be
done if feasible.

51. TOPICALTREATMENT
CLOTRIMAZOLE (Primary drug of choice) NYSTATIN
Oral Suspension – 5 mL 3 -4 times daily for 2
weeks
Oral Suspension- 400,000 – 600,000 units 4 –
5 times daily (swish and swallow) for 7 – 21
days
Troche – 10 mg. Slowly dissolve in mouth,
apply 5 times daily to affected area bid for 7
days
Cream and Ointment – 100,000 U/g. Apply to
affected area 4-5 times/day. Powder – 50
million U. Sprinkle on tissue contact area of
denture
Cream – 1% cream, 2-3 times daily for 3-4
weeks
Nystatin tablets ( 1 tablet, 100,000 units,
dissolved in mouth 3 times a day).
Oral pastille (200,000 unit) 5 times a day

52. TOPICALTREATMENT
AMPHOTERICIN B MICONAZOLE AND
KETOCONAZOLE
MYCOSTATIN
Oral suspension – 100 mg/
mL 3 -4 times after food for 2
weeks
Cream – 2% Miconazole/
Ketoconazole gently into the
affected area 1-2 times daily.
Cream – 100,000 unit or
lactose containing tablet
kept under the tongue.
Troche – 10 mg; slowly
dissolve in mouth; apply 3 – 4
times daily to affected area
for 2 weeks.
Used as a rinse for 7-10 days;
3-4 times a day.

53. SYSTEMICTHERAPY
Tab. Ketoconazole – 200 – 400 mg/day as single dose for 7 -14 days.
Cap. Fluconazole – 200 mg on day 1 then 100 mg daily for 7 – 14 days ( 1st drug of choice)
Cap. Itraconazole – 100 mg tablets once daily (if not responding to Fluconazole)
Cap. Posaconazole – 400 mg bid for 7 – 14 days (if not responding to Itraconazole)

54. REFERENCES
• Burket’s Oral Medicine (12th Edition) – Michael Glick
• Shafer’s textbook of Oral Pathology (8th Edition)
• Textbook of Oral Medicine (3rd Edition) – Anil Govindrao Ghom
• Textbook of Oral Medicine and Oral Radiology – Peeyush Shivhare