candidiasis and its clinical management with laboratory diagnosis and importance in dentistry

1. CANDIDIASIS
Ashok kumar A
1st year PG
Dept of Orthodontics

2. CONTENTS
• Introduction
• History of Candidiasis
• Morphology
• Predisposing factors
• Pathogenesis & Classification
• Laboratory diagnosis
• Treatment & prevention

3. INTRODUCTION
• Candidiasis (moniliasis) is an infection of the skin,
mucosa, and rarely of the internal organs, caused by a
yeast-like fungus Candida albicans, and occasionally
by other Candida species.
• The most opportunistic infection in the world.

4. • The descriptions oral thrush go back to the time
of Hippocrates .
• Vulvovaginal candidiasis was first described in 1849 by
Wilkinson.
• In 1875, Haussmann demonstrated the causative organism in
both vulvovaginal and oral candidiasis is the same.
• With the advent of antibiotics following World War II, the rates
of candidiasis increased. The rates then decreased in the 1950s
following the development of nystatin .
HISTORY

5. SPECIES OF CANDIDA
Important species of Candida found in man are:
(i) C. albicans;
(ii) C. stellatoidea;
(iii) C. tropicalis;
(iv) C. krusei;
(v) C. guilliermondii;
(vi) C. parapsilosis;
(vii) C. glabrata,
(viii) C. viswanathii

6. Ovoid/Spherical
3-5 µm diameter
25–37°C
Asexual budding
1)Pseudohyphae,
2)Yeast,
3)Chlamydospore
MORPHOLOGY

7. Predisposing factors

8. PATHOGENESIS
Superficial candidiasis
Mucocutaneous Lesions
• Oral thrush
• Vulvovaginitis
• Balanitis.
• Conjunctivitis.
• Keratitis
Skin and Nail Infections
• Intertriginous Infection
• Interdigital Involvement
• Onychomycosis
• Napkin Dermatitis
Chronic Mucocutaneous Candidiasis
Systemic candidiasis.
• Septicemia
• Endocarditis
• Meningitis
• Kidney infections
• Urinary tract infections &
• Intestinal candidiais

9. Classication of oral candidiasis [as proposed by
Samaranayake (1991) and modifed by Axell et al (1997)]

11. LABORATORY TESTS
DIRECT MICROSCOPY
Gram stained smears & KOH mounts from lesion of skin,
nail or mucous membrane shows budding gram positive yeast
cells .

12. CULTURE
• Cultures are obtained on Sabouraud’s dextrose agar (SDA) and
on ordinary bacteriological culture media, e.g. blood agar at
room temperature or at 37°C.
• Colonies are creamy white,
smooth and with a yeast odour.
• Gram stained smear from colonies
shows gram-positive budding
yeast cells.

13. IDENTIFICATION
• Germ tube test: C. albicans has ability to form germ tubes
within two hours when incubated in human serum at 37°C
(Reynolds-Braude phenomenon)

14. • CHLAMYDOSPORES
Chlamydospores develop
in a nutritionally deficient
medium such as cornmeal agar
at 20°C. They can be seen at the
end of pseudohyphae

15. SEROLOGY
• Agglutinins appear in the sera of patients but as they are
frequent in normal persons also, they are not helpful in
diagnosis.
• The detection of circulating cell wall mannan, using a latex
agglutination test or an enzyme
immunoassay, is much more specific,
but the test lacks sensitivity.

16. BIOPSY
• A biopsy of affected tissue may be indicated,
especially when candidiasis is suspected in conjunction with
some concurrent pathology, such as candidal
leukoplakia,epithelial dysplasia, squamous cell carcinoma, or
lichen planus.
• The sections should be stained with PAS or Gridley’s or
Gomori methenamine silver (GMS), because Candida species
stain poorly by hematoxylin and eosin.

17. SKIN TEST
• Delayed hypersensitivity to Candida is so universal that skin
testing with Candida extracts is used as an indicator of the
functional integrity of cell mediated immunity

18. IMPRINT CULTURE TECHNIQUE
• This technique uses a sterile plastic foam pad of known size
(2.5×2.5 cm) dipped in Sabouraud’s broth and placed on the suspect
mucosal surface for 60 seconds. Then the plastic foam is placed
directly on Sabouraud’s or Pagano-Levin agar.
• Candida density at each site is determined by a Gallenkamp
colony counter and expressed as colony-forming units (CFU) per
mm2.
≥30 CFU cm2 of mucosa in the dentate
≥ 49 CFU cm2 in denture wearers.

19. ORAL RINSE TECHNIQUE
• Here the patient is asked to rinse the mouth for 60 seconds
with 10 ml of sterile phosphate buffered saline or sterile water.
The oral rinse is centrifuged at 1,700 g for 10 minutes and the
deposit resuspended in 1 ml of sterile PBS.
• The concentrated oral rinse is now inoculated
on appropriate media to assess CFU per mm of
rinse sample using a spiral plater prior
to incubation.

20. SALIVARY CULTURE TECHNIQUE
• This involves patients 2 ml of mixed unstimulated saliva into a
sterile, universal container.
• The number of Candida expressed as CFU per mm of saliva is
estimated by counting the resultant growth on Sabouraud’s
agar.

21. CANDIDIASIS IN
CLINICALS

22. ACUTE PSEUDOMEMBRANOUS CANDIDIASIS
Prevalence (approximate): Uncommon.
Age mainly affected: Neonates and adults.
Gender : M = F.
Etiopathogenesis: Candida albicans is a harmless commensal yeast in the
mouths of nearly 50% of the population (carriers).
Oropharyngeal candidosis may be seen in healthy neonates as they
have yet to acquire immunity.
Local ecological changes (e.g. by antibiotics, xerostomia),
Decrease in immune defences (e.g. by immunosuppressive treatment or
immune defects (HIV/AIDS, leukemias, lymphomas, cancer, diabetes)

23. DIAGNOSTIC FEATURES
Oral: Candidosis presents anywhere but especially in the upper
buccal vestibule and the palate .
White or creamy plaques that can be wiped off to leave
a red base are typical
Extraoral: Other mucosae, nails and skin may be affected if the
cause is generalized, such as an immune defect.
Differential diagnosis: Lichen planus,
hairy leukoplakia, leukoplakia,

24. CHRONIC HYPERPLASTIC CANDIDOSIS
(CANDIDAL LEUKOPLAKIA)
Prevalence (approximate): Uncommon.
Age : Middle‐age and older.
Gender : M = F.
Etiopathogenesis:
Candida albicans can produce nitrosamines
and can induce epithelial proliferation and dysplasia. Co‐factors,
such as smoking, vitamin deficiency and immune suppression,
may contribute.

25. Diagnostic features
Oral: A tough adherent white leukoplakia‐like plaque. The plaque
is variable in thickness and often rough or irregular in texture,
or nodular with an erythematous background (speckled
leukoplakia).
The usual sites are the dorsum of the tongue or the
post‐commissural buccal mucosa.
Differential diagnosis: Thrush,
leukoplakia, keratosis.

26. CHRONIC MUCOCUTANEOUS CANDIDOSIS
(CMC)
Prevalence (approximate): Rare.
Age :From early pre‐school childhood.
Gender :M = F.

27. Etiopathogenesis :
• Various, usually congenital, cellular immune defects underly CMC
• Decreased interleukin 2 (IL‐2) and interferon‐gamma (TH 1
cytokines) and increased IL‐10 may be implicated.
• Hypoparathyroidism (with dental defects), diabetes,
hypoadrenocorticism, and hypothyroidism may be seen in one
variant – candidosis‐endocrinopathy syndrome (CES).
• In thymoma (thymus tumor) and diseases such as myasthenia
gravis, myositis, aplastic anemia, neutropenia and
hypogammaglobulinemia, CMC may develop in adult life.

28. Diagnostic features
Oral: White plaques which become widespread, thick and
adherent.
Oral carcinoma may occasionally supervene.
Extraoral: Candidal infections of nails (paronychia and
onychomycosis), scalp, trunk, hands and feet.
Differential diagnosis: lichen planus, leukoplakia.

29. ACUTE ATROPHIC CANDIDIASIS
Etiopathogenesis
• It may be squeal of pseudomembranous candidiasis after white patch has
been shed off
• Prolonged drug therapy ,topical steroid ,broad spectrum antibiotics ,denture
wearers
Clinical feature
• Any site but mainly involves tongue
or area facing prosthesis
• Red or erythematous
• Vague pain or burning sensation .

30. MEDIAN RHOMBOID GLOSSITIS
It is a form of chronic atrophic candidiasis characterized by
an asymptomatic, elongated, erythematous patch of atrophic
mucosa of the posterior mid-dorsal surface of the tongue due to
a chronic Candida infection .
A concurrent ‘kissing lesion’ of the palate is sometimes noted.

31. ROLE OF CANDIDA IN ORAL CARCINOGENESIS
• Candidal leukoplakias may develop into carcinoma .
• The Candida species may be involved in carcinogenesis by
elaborating nitrosamine compounds, which act either directly
on the oral mucosa or interact with other chemical carcinogens
to activate specified protooncogenes and thereby initiate oral
carcinoma.

33. PREVENTION
• Try using yogurt or acidophilus capsules when you take antibiotics.
• Treat any vaginal yeast infections that develop during pregnancy as
soon as possible.
• Quit smoking
• Dental checkup regularly at least every six to 12 months. especially
if you have diabetes or wear dentures.
• Brush and floss your teeth as often as your dentist recommends.
• Try limiting the amount of sugar and yeast-containing foods you eat,
including bread, beer and wine. These may encourage the growth of
Candida.

34. Evaluation of Candida Albicans Biofilm Formation
on Various Dental Restorative Material Surfaces

35. Conclusion: This finding emphasizes the use of glass ionomer
restorative cements and amalgam to reduce C. albicans adhesion to dental
restorative materials especially in people with weakened immune systems,
neutropenia, and cancer.

36. Candida albicans Adherence to Surface-Modified
Denture Resin Surfaces
• Three groups were tested
Group 1: control, pure poly(methyl methacrylate) (PMMA)
Group 2: modified PMMA(mPMMA) with 16% methacrylic acid
Group 3: pure PMMA coated with self-bonding polymer (SBP)

37. The effects of orthodontic appliances on Candida in
the human mouth.
No healthy patients developed Candida infection from the
orthodontic appliances. However, there seems to be a trend that some non-
Candida carriers converted to Candida carriers following the insertion of
the appliances by unknown mechanism. This may indicate a more cautious
approach when providing orthodontic
treatments to immuno compromised
children concerning the possible
increased risk of candidal infection.

38. REFERENCE
• Shafer’s Textbook of Oral Pathology, 6th
edition
• Textbook of Oral medicine, Anil Govindrao
Ghoom, 2nd edition
• Burkitt’s Oral medicine, 11th edition