The document covers mycotic infections of the oral cavity, focusing on the causes, pathogenesis, and specific types of candidiasis. It discusses the risk factors for developing fungal infections, the immune response, and various clinical manifestations of Candida and other fungal pathogens. Additionally, it highlights treatment options and provides insights into deep fungal infections, their diagnosis, and oral manifestations.

2. Presented by:
Dr.Prashant Munde
( MDS- I )
Guided by :
Dr. Mrs. SHUBHANGI KHANDEKAR
( PROFESSOR & GUIDE )
Dr. Mrs. ALKA DIVE
( PROFESSOR & H.O.D)
MYCOTIC INFECTIONS OF
THE ORAL CAVITY
SEMINAR

3. INTRODUCTION
• Mycotic infections are fungal infection of
animals, including humans.
• Mycotic infections are common and a variety of
environmental and physiological conditions can
contribute to the development of fungal
diseases.
• Inhalation of fungal spores or localized
colonization of the skin may initiate persistent
infections; therefore, Mycotic infections often
start in the lungs or on the skin.

4. The fungi that cause subcutaneous Mycotic
infections normally reside in soil or on
vegetation.
They enter the skin or subcutaneous tissue
by traumatic inoculation with contaminated
material.
In general, the lesions become granulomatous
and expand slowly from the area of
implantation to local lymph nodes.

5. Extension via the lymphatics draining the
lesion is slow except in sporotrichosis.
Mycotic infections are usually confined to
the subcutaneous tissues, but in rare
cases they become systemic and produce
life-threatening disease.

6. CAUSES
• People are at risk of fungal infections when
they are taking strong antibiotics for a long
period of time because antibiotics kill not only
damaging bacteria, but healthy bacteria as
well.
• This alters the balance of microorganisms in
the mouth, vagina, intestines and other places
in the body, and results in an overgrowth of
fungus.

7. Individuals with weakened immune systems
• with HIV/AIDS,
• under steroid treatments, and taking
chemotherapy.
• with diabetes also tend to develop fungal
infections.
• Very young and very old people, also, are
groups at risk.

8. PATHOGENESIS
• The response to infection with many fungi is
the formation of granulomas.
• Granulomas are produced in the major
systemic fungal diseases, e.g.,
coccidioidomycosis, histoplasmosis, and
blastomycosis, as well as several others.
• The cell-mediated immune response is
involved in granuloma formation.

9. • Activation of the cell-mediated immune
system results in a delayed hypersensitivity
skin test response to certain fungal antigens
injected intradermally.
• Acute suppuration( pyogenic response ),
characterized by the presence of neutrophils
in the exudate, also occurs in certain fungal
diseases such as aspergillosis and
sporotrichosis.

10. • Intact skin is an effective host defense
against certain fungi (e.g., Candida,
dermatophytes), but if the skin is damaged,
organisms can become established.
• The normal flora of the skin and mucous
membranes suppress fungi.
• When the normal flora is inhibited, e.g., by
antibiotics, overgrowth of fungi such as
C. albicans can occur.

11. CANDIDIASIS
(Candidosis,moniliasis,thrush)

12. CANDIDIASIS
(Candidosis,moniliasis,thrush)
• The fungal infections of the oral mucosa most
frequently occurred due to species of Candida,
Candida albicans.
• Infections can be short-lived, superficial skin
irritations to exaggerated , fatal systemic
diseases.
• Candida is present as a commensal organism in
the mouth of up to 40% of subjects with
clinically normal mouths.

13. • The number of organisms in the saliva of the
carrier increased with pregnancy, tobacco smoking
and with wearing of dentures.
• Account for 80% of nosocomial fungal
infections
• Candida is also present as a commensal
organism in throat ,lung, bowel and vagina.
• The primary oral reservoir for the organism in
carriers in the dorsum of the tongue .

14. • Isolation of the Candida from the mouth of an
adult is not confirmatory evidence of infection
and must be considered together with the clinical
findings .
• The histological sections must show the hyphae
but not spores alone to confirm the diagnosis.
• Budding cells of varying size that may form both
elongate pseudohyphae and true hyphae.
• Forms off-white, pasty colony with a yeasty odor.

15. • Both general and local predisposing
factors are important in the pathogenesis
of oral Candida infections for example;
debilitated patients , such as those
receiving antibiotic, steroid or cytotoxic
therapy are particularly susceptible to
Candida infections, with local factors
such as tobacco smoking ,trauma and
xerostomia.

16. Factors predisposing to oral
candidal infection.
*Local factors:
• Mucosal traumas
• Denture wearing
• Tobacco smoking
*Age:
• Extremes of age ;
• neonates ,infants, old age
*Drugs:
• Broad –spectrum antibiotics
• Steroids, Local systemic.
• Immunosuppressant

17. *Xerostomia
• Drugs, radiotherapy
• Sjogren syndrome
*Systemic disease
• Iron deficiency
• Megablastic anemia
• Acute leukemia
• Diabetes mellitus
• H.I.V infection.
• Immunodeficiency status

18. CLASSIFICATION OF ORAL CANDIDIOSIS
B- CHRONIC
*CHRONIC ATROPHIC
CANDIDIOSIS
(denture stomatitis)
*CHRONIC MUCOUTANOUS
CANDIDIOSIS
CHRONIC FAMILIAL
CHRONIC LOCALISED
CHRONIC DIFFUSED
*CHRONIC HYPERPLASTIC
CANDDOSIS
A-ACUTE
*ACUTE
PSEDOMEMBRANEOUS
ORAL CANDIDIOSIS
(THRUSH)
*ACUTE ATROPHIC ORAL
CANDIDIOSIS

19. ACUTE PSEDOMEMBRANEOUS
CANDIDOSIS
(THRUSH)

20. ACUTE PSEDOMEMBRANEOUS
CANDIDOSIS(THRUSH)
• Most common form of the candidosis
• Generally associated with local disturbance or
systemic illness
• Thrush occurs in up to 5% of new born
infants, which is probably associated with
immature antimicrobial defences, also its seen
in about 10% of elderly debilitated patient .

21. Acute Pseudomembranous Candidosis
(Thrush)
• Pain or burning
• Altered taste
• Predisposing:
– Xerostomia,
– Antibiotics
– Decreased host
resistance

22. Acute Pseudomembranous Candidosis (Thrush)
 presents clinically as a soft, thick white coating
slightly elevated plaques.
The white plaques on the affected mucosa, which
can be wiped away
to leave a red, or
normal appearing
mucosa .

23. The white plaques grossly resembling milk curds,
consists of tangled mass of fungal hyphae with
intermingled desquamatated epithelium,keratin
fibrin, necrotic debris, leukocytes, and bacteria.

24. Lesions may occurs on
any mucosal surface of
the mouth and vary in
size from small patches
to confluent lesions
covering a wide area.
Most frequently present
on buccal mucosa & tongue
but also seen on palate
,gingiva & floor of mouth.
In severe cases entire oral
cavity may be involved.

25. ACUTE ATROPHIC
CANDIDIOSIS

26. ACUTE ATROPHIC (ERYTHEMATOUS)
CANDIDIOSIS.
• Also known as ANTIBIOTIC SORE MOUTH
• Seen most commonly on the dorsum of the
tongue in patients undergoing prolonged
corticosteroid or antibiotic therapy.
• present as a red rather than
white and often painful area of
oral mucosa which resembles
thrush without the overlying
psedomembrane.

27. • Usually occurs as a
sequelae to a course of
broad spectrum
antibiotics.
• Generalized pain, burning,
erythema
• May occur at any site
• Red and consisistently
painful
Comes under category of Erythematous Candidosis
Includes
Central paipllary atrophy of the tongue
cheilocandidiasis

28. Central papillary atrophy of the tongue
Median Rhomboid Glossitis
• Asymptomatic, symmetric ,
erythematous lesion on dorsal
aspect of post. region of tongue,
Just anterior to foramen cecum.
• Red depapillated smooth or
fissured, due to loss of filiform
papillae
• Strong association with chronic
smoking
• Etiologic debate
– Developmental or chronic
candidal infection

29. CHRONIC ATROPHIC
CANDIDOSIS
( DENTURE STOMATITIS)

30. CHRONIC ATROPHIC CANDIDOSIS
( DENTURE STOMATITIS)
• This is common and usually symptomless
condition found in about 50% of denture
wearer ,more frequently in women than in man.
• Clinically there is chronic erythema and
oedema of the mucosa directly covered by the
denture.
• The palate is usually affected but it is very
unusual to see lesions related to lower
dentures.

31. CHRONIC ATROPHIC CANDIDOSIS
(denture stomatitis)
– May be asymptomatic
– Candida colonize the
denture surface
– Minimal or no candidal
invasion of mucosa
- Secondary infection by Candida in tissues
modified by continual wearing of dentures
 Poor denture hygiene
 High carbohydrate diet

32. Clinically ,patterns of inflammations
can be identified
1- Pin - point of erythema – localized
inflammation.
2- Diffuse area of erythema –
generalized inflammation.
3- Erythema associated with a
granular or multinodular mucosal
surface, chronic inflammatory
papillary hyperplasia.

33. ANGULAR CHEILITIS
• Multifactorial disease of
infectious origin
• Fungal or bacterial or
combined
– Candida or Staph aureus
or Streptoccocci
• Mainly in denture wearers
– 30% of patient with
denture stomatitis have
anguar cheilitis

34.  Clinically characterized by
soreness, erythema ,Cracks,
crusts, pain and fissuring at the
corners of mouth.
– Loss of vertical dimension
– Deep folds of skin at angles of
mouth
– Nutritional deficiencies
Iron ,folic acid , B12

35. CHRONIC HYPERPLASTIC
CANDIDOSIS
(candidal leukoplakia)

36. CHRONIC HYPERPLASTIC CANDIDOSIS.
(candidal leukoplakia)
• Commonly referred to as candidal leukoplakia,
presents clinically as a persistent firm,
adherent white plaques on the oral mucosa
which is indistinguishable from leukoplakia.
• They cannot be removed by scraping but
fragments may be detached and identification
of hyphae in smears of such material assists
in diagnosis.

37. Chronic Hyperplastic Candidosis
(Candidal Leukoplakia)
• The lesions present as
dense ,opaque white
patches of irregular
thickness with a rough
or nodular surface.
• Most frequent
location:
• Lips , tongue,
buccal mucosa at
commissures

38. • It is considered to be a premalignant lesion
and epithelial dysplasia is seen in about 50%
of cases.
• It is not been conclusively shown whether
chronic hyperplastic candidosis is primarily
leukoplakia with a secondary candidal
infection or whether its primarily a chronic
candidal infection which in time leads to
epithelial hyperplasia and acanthosis.

39. • According to Cawson and Binnie , there is a
definite relationship between chronic
candidiasis and oral epidermoid carcinoma
basing on this , chronic candidiosis itself is a
cause of leukoplakia and thus must be regarded
as having possible premalignant potential.
• Roed -peterson and his associates have
reported a high incidence of candida organisms
and occurance of cytological epithelial atypia in
the biopsied lesions of leukoplakia.

40. CHRONIC MUCOCUTANOUS
CANDIDOSIS

41. • This is a group of disorders characterized
by persistent superficial candidal infections
of the skin, scalp, nails & mucous membranes
• Oral mucosa involved in most cases
• similar to chronic hyperplastic
candidiasis and occur in same
intraoral locations.
CHRONIC MUCOCUTANOUS
CANDIDOSIS

42. • Oral manifestations occur in numerous
forms of candidiasis and these have been
categorised and modified by Lehner, and
includes the -
o CHRONIC LOCALISED MUCOCUTANEOUS
CANDIDIASIS
o CHRONIC DIFFUSE MUCOCUTANEOUS
CANDIDIASIS
o CANDIDASIS ENDOCRINOPATHY SYNDROME

43. FEATURESSUBGROUP
Severe form occuring in early life, no
genetic transmission,Widespread skin
involvement and granulomatous and
horny masses on scalp, nail and face.
CHRONIC LOCALISED
MUCOCUTANEOUS
CANDIDIASIS
Least common form, of late onset
Severe skin and oral lesions raised
crusty sheets involving groin,limbs,
face , scalp, shoulder, nails, and mouth.
CHRONIC DIFFUSE
MUCOCUTANEOUS
CANDIDIASIS
Genetically transmitted (AR)
Mildmoderate oral and skin lesions
Hypoparathyrodism,Addison's disease
,D.M or ovarian insufficiency.
CANDIDASIS
ENDOCRINOPATHY
SYNDROME
CHRONIC MUCOCUTANOUS CANDIDOSIS

44. DEEP FUNGAL
INFECTIONS

45. ETIOLOGY AND PATHOGENESIS
Deep fungal infections are characterized by
primary involvement of the lungs.
 Infections may disseminate from this focus to
involve other organs.
 Oral infections typically follow implantation of
infected sputum in oral mucos or may also follow
hematogenous spread of fungus from another site
such as the lung.

46. Oral manifestation of deep
fungal infections
• Oral lesions are relatively
uncommon presenting most
frequently as non-specific
ulceration or as nodular
granulomatous lesion.

47. A. North american blastomycosis
(gilchrist’s disease)
B. South american blastomycosis
(paracoccidioidomycosis)
C. Histoplasmosis
( darling’s disease)
D. Coccidioidomycosis:
(san joaquin valley fever)
E. Cryptococcosis
F. Phycomycosis
G. Sporotrichosis

48. North American
Blastomycosis
(Gilchrist’s disease)

49. North American Blastomycosis
(Gilchrist’s disease)
• Blastomyces dermatitidis- causes blastomycosis
• Free-living species distributed in soil of a large
section of the north U.S.
• Inhaled 10-100 conidia convert to yeasts and
multiply in lungs.
• Affects mainly lungs and nearly 50% of those
infected show cough and fever or no symptom.
• It may spread to other parts of the body,
skin is involved in 20% to 40% of cases.

50. Cutaneous features
Skin lesions are common on the face, neck and
the extremities as the infection spreads from
the lungs to other parts of the body.
Lesions begin as papules, pustules or as
subcutaneous nodule. Within weeks to months,
the lesions develop into ulcers and form crusty
sores.

51. Clinically, the chronic, non healing oral ulcers
may resemble those of epidermoid carcinoms
and cervicofacial actinomycosis.
Over a period of months to years, lesions
grow larger and heal to form raised wart-like
scars.
Lesions may cover much of the face causing
severe disfigurement.

52. Figure 2-25 Blastomycosis showing granuloma (macrophages) with a central abscess.
The basic inflammatory response in a deep fungal infection is
granulomatous.
In the presence of these microorganisms, macrophages and
multinucleated giant cells dominate the histologic picture .
Peculiar to blastomycosis is pseudoepitheliomatous
hyperplasia, associated with superficial infections in which
ulceration has not yet occurred.

53. Histologic freatures:-
Inflammed connective tissue shows giant cells and
macrophages and typical round budding organisms with
doubly refractile capsule measuring between 5 to 15
microns in diameter.

54. TREATMENT
• Those suffering from mild symptoms require
no treatment as symptoms are usually self-
limiting and the infection clears
spontaneously
• When other organs or skin are involved,
sponteneous resolution does not occur
• Itraconazole – oral
• Amphotericin B – intravenous

55. South American
Blastomycosis
(Paracoccidioidomycosis)

56. South American Blastomycosis
(Paracoccidioidomycosis)
• Paracoccidioides brasiliensis
• Distributed in Central and South America
• Lung infection occurs through inhalation or
inoculation of spores.
• Systemic lesions are similar to those of North
American Blastomycosis

57. • The organisms enter the body
through periodontal tissues and
subsequently reach the regional lymph
nodes, producing lymphadenopathy,
• Papillary lesions & Widespread
ulcerations of the oral cavity

58.  The difference between north and South American
Blastomycosis is in size of micro organisms.
 South American Blastomycosis 10 to 60 microns in
diameter
 North American Blastomycosis 5 to 15 microns in
diameter.
South American Blastomycosis North American Blastomycosis

59. Diagnosis and Treatment
• Presumptive diagnosis made if budding yeast
cells and pseudohyphae are found.
• Growth on selective, differential media
differentiates Candida species
• Topical antifungals for superficial infections,
amphotericin B and fluconazole for systemics

60. HISTOPLASMOSIS
( Darling’s Disease)
Ohio Valley Fever

61. HISTOPLASMOSIS ( Darling’s Disease)
Ohio Valley Fever
Caused by Histoplasma capsulatum ,
worldwide in distribution, although it is
endemic in the northestern United States.
The organism multiplies in soil enriched with
the droppings of birds and bats and the
spores remain viable for years.
Infection is by inhalation of infected dust
containing spores of fungus excreta of birds ,
such as pigeons, starlings and blackbirds.

62. HISTOPLASMOSIS- PATHOLOGY
• The parasite in its yeast phase multiplies in
the monocytes and macrophages and
produces areas of necrosis where parasites
may abound.
• From these foci the blood stream may be
invaded producing metastatic lesions in the
liver, spleen and lymph nodes.
• Pulmonary histoplasmosis may produce
changes similar to those of tuberculosis.

63.  The ulcerated areas are covered by
nonspecific grey membrane and are indurated.
 They appear as nodular ,ulcerative , or
vegetative lesions on the buccal mucosa, gingiva ,
tongue, palate , or lips.
Figure 2-23 Histoplasmosis-caused chronic ulcers.

64. Histoplasmosis
Figure 2-24 Histoplasmosis showing macrophages
with cytoplasmic microorganisms.

65. HISTOPLASMOSIS-
MANAGEMENT
• Only symptomatic acute pulmonary
histoplasmosis, chronic histoplasmosis and
acute disseminated histoplasmosis require
therapy.
• Itraconazole or ketoconazole are indicated
for moderate disease. Severe infection is
treated with intravenous amphotericin B to a
total dose of 1.5 g followed by itraconazole.

66. Coccidioidomycosis
San Joaquin Valley Fever

67. Coccidioidomycosis:
San Joaquin Valley Fever
• Coccidioides immitis - causes coccidioidomycosis
• Distinctive morphology – blocklike arthroconidia
in the free-living stage and spherules containing
endospores in the lungs.
• Lives in alkaline soils in semiarid, hot climates and
is endemic to southwestern U.S.

68. • Arthrospores inhaled from dust,
creates spherules and nodules in the
lungs.
• A skin eruption resembling erythema
multiforme occasionally appears
concomitantly with coccidioidomycosis
infection
• Amphotericin B treatment

69. Cryptococcosis

70. CRYPTOCOCCOSIS
• Cryptococcus neoformans causes
cryptococcosis.
• A widespread encapsulated yeast that
inhabits soil around pigeon roosts
• Common infection of AIDS, cancer or
diabetes patients.

71. • Infection of lungs leads to cough,
fever, and lung nodules
• Dissemination to meninges and brain
can cause severe neurological
disturbance and death.

72. Diagnosis and Treatment
• Negative stain demonstrating
encapsulated budding yeast
• Biochemical tests, serological testing
• Systemic infection requires
amphotericin B and fluconazole.

73. PHYCOMYCOSIS/
ZYCOMYCOSIS

74. • Phycomycosis, also known as mucormycosis,
fungal infections caused by the genera Mucor
and Rhizopus.
• Organisms in this family of fungi, which
normally are found in bread mold or decaying
fruit and vegetables, are opportunistic,
infecting humans when systemic health is
compromised.
PHYCOMYCOSIS/ ZYCOMYCOSIS

75. • In the head and neck, lesions are most likely to occur in
the nasal cavity, paranasal sinuses, and oropharynx.
Pain and swelling precede ulceration.
• Tissue necrosis result in perforation of palate. Extension
into the orbit or brain is a common complication.
• The fungus has a predilection for arterial wall invasion,
which may lead to infarction.

76. PHYCOMYCOSIS/ Zycomycosis
Microscopically, an acute and chronic inflammatory infiltrate
is seen in response to the fungus .
The organism is usually readily identified in hematoxylin and
eosin-stained sections in areas of tissue necrosis.
Characteristic necrotic vessel walls containing thrombi and
fungi may be evident.
Microscopically, the
fungus consists of large,
pale-staining, nonseptate
hyphae that tend to
branch at obtuse angles.
Round or ovoid sporangia
are also frequently seen
in tissue sections.

77. SPOROTRICHOSIS

78. SPOROTRICHOSIS
Caused by Sporothrix schenckii lives as a
saprophyte on plants in many areas of the
world.
In which portal of entry is not entirely
understood.
Reported to occur after-
Exposure to animals
Accidental injury to thorns of plants
Lab. or clinical inoculation of hospital
workers

79. Etiology and Pathogenesis
Subcutaneous Fungal Infections affect primarily
subcutaneous tissues results from inoculation of
the skin or mucosa by contaminated soil or
thorny plants.
After an incubation period of several weeks,
subcutaneous nodules, which frequently become
ulcerated, develop.
Systemic involvement is rare but may occur in
individuals with suppressed immune responses.

80. Clinical Manifestations
Involve skin, subcutaneous tissue,oral, nasal and
pharangeal mucosa.
Skin lesions appear as red papule often described as
“Sporotrichotic chancres “forms at the site of
inoculation.
Oral lesions are described as nonspecific ulcerations
healing by soft pliable scars.
Over the next several weeks, similar nodules form
along proximal lymphatic channels.
The nodules intermittently discharge small amounts
of pus and ulceration may occur.

81. SPOROTRICHOSIS-
Diagnosis
• Culture of pus, joint fluid, sputum, or
a skin biopsy specimen is preferred.
• In skin lesions, the organisms are
hard to find because of small size of
fungus 3-5 microns.
• It can be cultered on SDA

82. LABORATORY
DIAGNOSIS

83. LABORATORY DIAGNOSIS
• There are four approaches to the
laboratory diagnosis of fungal diseases:
(1) DIRECT MICROSCOPIC EXAMINATION,
(2) CULTURE OF THE ORGANISM,
(3) DNA PROBE TESTS, AND
(4) SEROLOGIC TESTS.

84. • Direct microscopic examination of clinical
specimens such as sputum, lung biopsy material,
and skin scrapings depends on finding
characteristic asexual spores, hyphae, or yeasts
in the light microscope.
• The specimen is either treated with 10% KOH to
dissolve tissue material, leaving the alkali-
resistant fungi intact, or stained with special
fungal stains.
DIRECT MICROSCOPIC
EXAMINATION

85. Some examples of diagnostically important
findings made by direct examination are
(1) spherules of C. immitis and
(2)wide capsule of Cryptococcus neoformans
seen in India ink preparations of spinal fluid.
Calcofluor white is a fluorescent dye that binds
to fungal cell walls and is useful in the
identification of fungi in tissue specimens.
Methenamine-silver stain is also useful in the
microscopic diagnosis of fungi in tissue.

86. Smear preperation

89. PAS stain

90. PAS stain modified for fungi

91. • Fungi are frequently cultured on Sabouraud's
agar, which facilitates the appearance of the
slow-growing fungi by inhibiting the growth of
bacteria in the specimen.
Inhibition of bacterial growth is due to :
• low pH of the medium
• chloramphenicol
• cycloheximide.
• The appearance of the mycelium and the
nature of the asexual spores are frequently
sufficient to identify the organism.
SABOURAUD'S AGAR

92. DNA TECHNIQUES
• Tests involving DNA probes can identify colonies
growing in culture at an earlier stage of growth than
can tests based on visual detection of the colonies.
• As a result, the diagnosis can be made more rapidly.
• At present, DNA probe tests are available for
1. Coccidioides,
2. Histoplasma,
3. Blastomyces,
4. Cryptococcus.

93. • A significant rise in the antibody titer must be
observed to confirm a diagnosis.
• The complement fixation test is most frequently
used in suspected cases of coccidioidomycosis,
histoplasmosis, and blastomycosis.
• In cryptococcal meningitis, the presence of the
polysaccharide capsular antigens of C.
neoformans in the spinal fluid can be detected by
the latex agglutination test.
SEROLOGY

94. ANTIFUNGAL THERAPY

95. ANTIFUNGAL THERAPY
• The most effective antifungal drugs, amphotericin B
and the various azoles, exploit the presence of
ergosterol in fungal cell membranes that is not found
in bacterial or human cell membranes.
• Amphotericin B disrupts fungal cell membranes at
the site of ergosterol and azole drugs inhibit the
synthesis of ergosterol, which is an essential
component of fungal membranes.
• Another antifungal drug, caspofungin (Cancidas),
inhibits the synthesis of -glucan, which is found in
fungal cell walls but not in bacterial cell walls. Human
cells do not have a cell wall.

96. TREATMENT MODELATIES
• Look for underlying cause and treat it
• If antibiotics or corticosteroids are
the cause, reduce the dose or change
the treatment
• Intermittent or prolonged topical
antifungal may be necessary when the
underlying cause is unavoidable
• Denture cleansing is necessary

97. ANTIFUNGAL AGENTS
• Amphotericin B is an effective
treatment for all forms of oral fungal
infection
• Other agents that are less cytotoxic
may also be effective
• Azoles are considered better but
expensive
• Newer azoles may be required in
invasive or resistant infections

98. Antifungal agents..
• Flucytosine Active against Candida
and Cryptococcus species
• Fluconazole has been active against
oral candidosis in HIV disease
• Nystatin is oftenly used for
Candidosis

99. COMPLICATIONS
• Drug resistance
• Drug interactions and adverse
effects
• Structural defects or loss of function
(eg, resulting from fungal destruction
of the maxilla, orbit, and/or cranial
base)

100. PROGNOSIS
• Most fungal infections in healthy individuals
are self-limiting and have a good prognosis
• If a deep fungal oral lesion develops, the
lesion likely represents a potentially serious
underlying infection
• Although most deep fungal infections
respond to aggressive antifungal therapy,
infections can be fatal

101. CONCLUSION
• Most deep fungal infections have their
primary foci in the lungs, therefore
those presenting with distant organs or
skin involvement should be managed
aggressively as untreated or severe
disease can lead to severe scarring,
disfigurement and even death

102. REFFERENCE
Regezi: Oral Pathology: Clinical
Pathologic Correlations, 5th ed.
Shafer’s Textbook of oral pathology,
5 th edition.
Color Atlas of Clinical Oral Pathology,
2nd Edition

103. THANK YOU!