FUNGAL INFECTIONS OF ORAL CAVITY

CONTENT FUNGAL
S INFECTIONS
Candidiasis
Blastomycosis
Histoplasmosis
Coccodiomycosis
Cryptococcosis
Phycomycosis
Sporotrichosis
Rhinoporidiosis
Cysticercosis
Aspergillosis
Toxoplasmosis
Oral myiasis
 CANDIDIASIS
Refers to infection with yeast like fungal organism.
Most common oral fungal infection.
It is a component of normal oral flora.
Can occur in persons who are debilitated by other diseases or
in otherwise healthy individuals also.
PREDISPOSING FACTORS: -
a) Local Factors :
- Mucosal trauma
- Denture wearers
- Denture hygiene
- Tobacco smoking
- Carbohydrate rich diet
- Drugs (Broad spectrum antibiotics, steroids,
immunosuppressant cytotoxic agents)
- Xerostomia
b) Systemic factors :
- Iron deficiency anaemia
- Megaloblastic anaemia
- Acute leukaemia
- Diabetes mellitus
- HIV infection
- Other immunodeficiency states
 CLASSIFICATION OF CANDIDIASIS: -
Group 1 (Conditions confined to the oral mucosa):
Acute -
- Acute pseudomembranous candidiasis
- Acute atrophic candidiasis
Chronic -
- Chronic atrophic candidiasis
- Candida associated angular cheilitis
- Chronic hyperplastic candidiasis

Group 2 (oral manifestations of generalized candidiasis)

- Chronic mucocutaneous candidiasis
ACUTE PSEUDOMEMBRANEOUS CANDIDIASIS
(THRUSH )

Best recognized form of candidiasis.

Characterized by development of white plaques that can be
scraped off with tongue blade.
Can be initiated by broad spectrum antibiotics or immune
dysfunction.
Occurs characteristically on buccal
mucosa, palate and dorsal tongue.
Usually asymptomatic or patients may
c/o burning sensation of mucosa or
unpleasant taste in mouth.
Can occur in infants also.
ATROPHIC CANDIDIASIS
(Erythematous candidiasis)

Several presentations seen

1. Acute atrophic candidiasis
2. Median rhomboid glossitis
3. Chronic multifocal candidiasis
4. Angular cheilitis
5. Chronic atrophic (denture sore mouth)
candidiasis
1. ACUTE ATROPHIC
CANDIDIASIS: -
Also called antibiotic sore mouth, as it
follows course of broad spectrum
antibiotics.
Patients c/o burning sensation of mucosae.
Seen as diffuse loss of filliform papillae
resulting in a bald appearance of tongue.
2. MEDIAN RHOMBOID GLOSSITIS:

Also called central papillary atrophy of tongue.

Well demarcated erythematous zone affecting midline of
dorsum of tongue.
Often asymptomatic.
Erythema due to loss of filliform papillae.
Sometimes, other areas of oral cavity like hard palate and
angles of mouth also show lesions (Chronic multifocal
candidiasis).
3. CHRONIC ATROPHIC
CANDIDIASIS: -
Characterized by varying degrees of
erythema in denture bearing areas of usually
maxillary prostheses.
Usually asymptomatic.
Patients give h/o wearing denture
continuously.
4. ANGULAR CHEILITIS: -

Also called perleche.

Characterized by erythema, fissuring and
scaling of corners of mouth.
Typically occurs either along with multifocal
candidiasis or in old patients with reduced
vertical dimension.
Saliva pools in these areas, keeping them moist
and thus favoring fungal infection
5. CHRONIC HYPERPLASTIC CANDIDIASIS:

Least common of all types.

Appears as non scrapable white patch resembling
leukoplakia (candidal leukoplakia)
Believed that it represents candidiasis
superimposed on pre-existing leukoplakia.
Diagnosis confirmed by demonstration of
candidal hyphae within the lesion and resolution
of lesion after antifungal therapy.
CHRONIC MUCOCUTANEOUS
CANDIDIASIS: -

Severe oral candidiasis can also occur as a

component of a rare immunological disorder called
mucocutaneous candidiasis.
Autosomal recessive disorder.
Immune dysfunction becomes evident in early life
patient develops candidiasis of mouth, nails, skin
and other mucosae.
Oral lesions appear as thick, white non scrapable
patches.
HISTOLOGICAL FEATURES:

Biopsy specimen show hyperparakeratinization,

elongation of rete ridges, chronic inflammatory
cell infiltration of underlying CT and small
microabscesses collection of PMNLs) within
parakeratin layer.
Candidal hyphae can be seen embedded in
parakeratin layer and superficial spinous layer.
EXFOLIATIVE CYTOLOGY: -
Candidal hyphae can also be demonstrated by exfoliative cytology by PAS stain.
Hyphae are stained magenta color by the PAS stain.

RAPID DIAGNOSTIC TEST: -

A 10% - 20% KOH preparation used for rapid diagnosis.
KOH lyses background of epithelial cells allowing yeast and hyphae to be seen.

TREATMENT:
Specific antifungal agent like Nyastatin.
Other drugs of value are clotrimazole, amphotericin B and
miconazole
 Blastomycosis
1. North American Blastomycosis:
Mycotic infection caused by Blastomyces Dermatitidis
Occur in cutaneous form or systemic form involving bones, liver, lungs,
subcutaneous tissues and other organs.

CLINICAL FEATURES:
Common in men than women
Middle age
Skin lesions begin as papules which gradually increase in size and form tiny
miliary abscess or pustules which may ulcerate to discharge the pus through
a tiny sinus.
Exhibit indurated and elevated borders.
Infection spreads through subcutaneous tissue into the blood stream.
Systemic disease is characterized by fever, sudden weight loss, productive
cough in case of lung involvement with other symptoms of pulmonary TB
ORAL MANIFESTATIONS:
Tiny ulcers may be the chief complaint.
May resemble actinomycosis.
Sometimes they bore resemblance to epidermoid carcinoma.

HISTOPATHOLOGIC FEATURES:
Similar to other chronic granulomatous infections.
Inflamed connective tissue shows occasional giant cells and macrophages and typical round organisms,
often budding, which appear to have a doubly refractile capsule.
Microorganisms are commonly found within giant cells.
Micro abscess are frequently found.
If lesion is not ulcerated, overlying pseudoepitheliomatous hyperplasia may be prominent.
Microabscess
formation
2. South American blastomycosis:
Caused by blastomyces brasileinsis.
Systemic lesions similar to North American blastomycosis.

ORAL MANIFESTATIONS:
Organisms enter through periodontal tissues and reach regional lymph nodes producing
lymphadenopathy.
Organisms were cultivated from both periodontal tissues and periapical granuloma.
Shown to penetrate tissues and establish infection after extraction of teeth, producing papillary lesions
of oral mucosa.
Widespread oral ulceration is also common.

Chief difference between NAB and SAB is in size of causative organism.

Fungus of SAB varies between 10 to 60 in diameter, beig considerably larger
than NAB organism.
HISTOPLASMOSIS
Caused by Histoplasma capsulatum.
Dimorphic in nature, growing as a yeast at body temperature in
human body and as a mold in its natural environment.
Air borne spores of organisms are inhaled, pass into the terminal
passages of lungs and germinate.

CLINICAL FEATURES:
Expression of disease depends on quantity of spores inhaled, immune
status of host and strain of H. Capsulatum.
Most individuals who are exposed to spores are relatively healthy.
They may have no symptoms or they may have mild flu like illness for
1-2 weeks. Immunity develops inn 2-3 weeks and antibodies directed
against the organisms appear several weeks later.
 ACUTE HISTOPLASMOSIS
Self limiting pulmonary infection.
Acute symptoms like fever, headache, myalgia, non
productive cough, anorexia develop with exposure to high
concentration of spores.
Symptoms result in clinical picture similar to influenza.
Pts usually ill for 2 weeks, calcification of hilar lymph nodes
may be detected as an accidental finding on chest
radiographs.
 Chronic histoplasmosis
Primarily affects lungs.
Much less common than acute form
Usually affects older, emphysematous, white men or
immunosuppressed patients.
Clinically similar to TB.
Pts exhibit cough, weight loss, fever, dyspnea, chest pain,
hemoptysis, weakness and fatigue.
Chest radiographs shows upper lobe infiltrates and
cavitation.
DISSEMINATED HISTOPLASMOSIS
Less common than acute and chronic form.
Characterized by progressive spread of infection to extrapulmonary
sites, occurs in older, debilitated or immunosuppressed patients
specially AIDS patients.
Tissues that may be affected include the spleen, adrenal glands, liver,
lymph nodes, GIT, CNS, kidneys and oral mucosa.
Adrenal involvement may produce hypoadrenocorticism (Addisons
disease)
Most affected sites in oral cavity are tongue, palate and buccal
mucosa.
Condition appears as a solitary, variably painful ulceration of several
weeks duration.
Some lesions may appear erythematous or white with irregular
surface.
Ulcerated lesion have rolled margins and may be indistinguishable
clinically from malignancy.
 Histopathology
Lesional tissue shows either diffuse infiltrate of
macrophages or collection of macrophages to form
granuloma.
Multinucleated giant cells are seen wit granuloma
inflammation.
Special stains such as PAS and Gomori methenamine silver
method readily demonstrate yeasts of H.Capsulatum.

DIAGNOSIS:
Tissue culture.
Other helpful techniques include serologic testing in which
antibodies directed against H.Capsulatum are
demonstrated and antigen produced by yeast is identified.
Granuloma
formation and
spherule
formation
 Treatment
Acute histoplasmosis: self limiting, no specific treatment apart
from supportive care with analgesics and antipyretics.

Chronic histoplasmosis: half of them may resolve

spontaneously. Pulmonary damage is progressive if left
untreated. Treatment of choice is IV Amphotericin B in severe
cases. Itraconazole may be used in non-immunocompromised
pts with daily dozing for 3 months.

Disseminated histoplasmosis: very serious disease, results in

death in 80-90% patients if left untreated. Amphotericin B is
indicated for such pts, once life threatening phase is under
control, daily itraconazole is necessary for 6-18 months.
Itraconazole may be alone used if patient is non-
immunocompromised and has relatively mild to moderate
disease.
Coccidioidomycosis
Causative organism is coccidioides immitis, disease appears to
be transmitted by inhalation of dust containing spores.

CLINICAL FEATURES:
2 basic forms of disease
1. Primary non-disseminated: develop manifestations of
respiratory disease like cough, pleural pain, head ache and
anorexia. 20% pts may develop skin lesions either erythema
nodosum or erythema multiforme. Disease is self limiting,
subsides in 10-14 days.
2. Progressive disseminated: usually runs a rapid course and
dissemination extends from lungs to various viscera, bones,
joints, skin and to CNS where meningitis may cause death.
Dissemination to bone results in osteomyelitis.
Oral manifestations
Proliferative granulomatous and ulcerated lesions appear on
skin and oral mucosa.
Heals by hyalinization and scar.
Marked chronicity is often a feature of these lesions.

HISTOPATHOLOGY:
Large mononuclear cells, lymphocytes and plasma cells
predominate.
Foci of coagulation necrosis in centre of small granuloma, MNGC
are scattered throughout the lesion.
Organisms often found in cytoplasm of giant cells.

TREATMENT:
Amphotericin B provide effective chemotherapeutic control.
Foci of
coagulation
necrosis
surrounded by
MNGCs
 Cryptococcosis
Chronic fungal infection caused by Cryptococcus neoformans and
Cryptococcus bacillispora, cause widespread lesions in skin, oral
mucosa, subcutaneous tissues, lungs, joints and particularly
meninges.
Organisms appear to harbour in pigeons but actual infection results
due to inhalation of air borne microorganisms.

CLINICAL FEATURES:
Respiratory tract colonization or visceral lesions to be the primary
site, skin lesions occurring secondary.
Skin lesion appears as multiple brown papules which ulcerate.
Lesions of lungs produce non specific pneuminitis, meningeal lesions
produce a variety neurologic signs and symptoms associated with
increased intracranial pressure.
It has been reported in pts suffering from some form of malignant
lymphoma.
ORAL MANIFESTATIONS:
The oral lesions appeared as simply non specific, single or multiple
ulcers. Sometimes confused with patient known to have leukemiadue
to their inability to react to mild, non specific bacterial infection.

HISTOPATHOLOGY:
Causative organism covered with extremely thick capsule.
Microorganism appears as a small organism with a large clear halo
described as tissue microcyst.
Capsule is stained with PAS and cultured on Sabourauds glucose agar.
Focal necrosis is absent, epitheloid cell proliferation is minimal.
MNGC are organisms with characteristic halos found singly or in
groups scattered throughout granuloma.

TREATMENT:
Amphotericin B gives excellent results.
Organism covered by
thick capsule, formation
of microcyst.
 PHYCOMYCOSIS/ MUCORMYCOSIS
Caused by mucorales and endomophthorales.
Organism occurs in soil, manure, fruits and decaying matter.
These organisms are present in nasal passages and oral cavity of
normal persons.
It is an opportunistic infection associated with debilitation especially
with any malignant lymphomas, renal failure, organ transplant, AIDS
and cirrhosis. Common in pts wit DM especially diabetes
ketoacidosis.

CLINICAL FEATURES:
2 types- superficial (localized) and visceral (disseminated).
Superficial type includes involvement of external ear, fingernails and
skin.
Visceral form has 3 main types- pulmonary, gastrointestinal and
rhinocerebral.
 Infections of head by these organism is characterized by classical
syndrome of DM, opthalmoplegia and meningoencephalitis.
Infections enters through nasal mucosa extends into paranasal
sinuses, pharynx, palate, orbit and brain.
Early manifestation is appearance of reddish black nasal turbinate ad
septum with nasal discharge. Necrosis may extend to paranasal
sinuses an orbital cavity with development of sinus tract and
sloughing of tissue.
Max. sinus may present clinically as a mass of maxilla, resembling Ca.
of antrum. Surgical exploration reveals mass of necrotic tissue with
demonstration of organism histologically.

HISTOPATHOLOGY:
Organism appear as large, non septate hyphae with branching at
obtuse angle.
Round or ovoid sporangia frequently seen.
 Histopathologically mucormycosis must be differentiated from
aspergillosis in which former has obtuse angled branched hyphae
and latter has acute angulating branched hyphae of smaller width.
Grocotts silver methanamine stain is used to confirm the diagnosis.

TREATMENT:
Control of predisposing factors such as DM, surgical excision if
lesion is localized, administration of Amphotericin B as its the only
drug with proven efficacy.
 SPOROTRICHOSIS
Caused by sporotrichum schenckii.
Reported to occur after
1. Exposure to wide variety of animals.
2. Accidental injury from thorns
3. Accidental lab or clinical inoculation of hospital workers.

CLINICAL FEATURES:
Involves skin, subcutaneous tissues and oral, nasal and pharyngeal
mucosa.
Disseminated visceral involvement rarely occurs.
Skin lesions referred to as sporotrichotic chancres appear at site of
infection as firm, red to purple nodules which ilcerate.

ORAL MANIFESTATIONS:
Non-specific ulcer of oral, nasal and pharyngeal mucosa associated
with regional lymphadenopathy.
 Lesions are described as healing by soft, pliable scar even though
organism may still be present in the tissues.

HISTOPATHOLOGY:
Fungus is small, ovoid branching organism with septate hyphae,
showing budding forms.
Cultured on Sabourauds medium.
Tissue reaction is a granulomatous one with epitheloid cells, MNGC
of Langhans type and lymphocytes, surrounding a central area of
purulent caseous necrosis.
PMNLs are prominent in some cases.
Asteroid bodies radiate formations around the fungal spores in
tissues commonly found.
Pseudoepitheliomatous hyperplasia of overlying epithelium of skin
or mucosal lesions is almost present.

TREATMENT:
No specific treatment , remissions and relapses are common.
Langhans type giant
cells and areas of
caseous necrosis
 RHINOSPORIDIOSIS
Chronic granulomatous disease caused by rhinosporidium seeberi.
Chiefly affects oropharynx and nasopharynx as well as larynx, skin,
eyes and genital mucosa.

CLINICAL FEATURES:
Nasal mucosa most involved site.
Appears as small verrucae or warts, becomes pedunculated.
Genital lesions resemble condylomas.

ORAL MANIFESTATIONS:
Oropharyngeal lesions accompanied by mucoid discharge.
Appear as soft, red polypoid growths of tumour like nature, spreads to
pharynx and larynx.
 Lesions are vascular, bleeds readily.
Soft palate most frequent site intra orally.

HISTOPATHOLOGY:
Appear as sporangia containing large no. of round or ovoid spores.
In smear preparation or tissue sections, these sporangia are the
characteristic feature.
Surrounding tissue reaction is non specific, consisting of vascular
granulation tissue with focal abscess formation and MNGC.
Acute and Chronic inflammatory cells are present.

TREATMENT:
Surgical removal of growth is treatment of choice.
Formation of sporangia
 CYSTICERCOSIS
Caused by cysticercus.
Among varoius species, larval form of tapeworm, taenia solium or
cysticercus cellulosae infests human beings.
Consumption of inadequately cooked pork is primary cause since pigs serve
as intermediate host.
Other causes include consumption of fecally contaminated vegetables, food
or water, self contamination bye reflux from intestine into stomach or by
contaminated hands.
Intraorally, it involves lips, cheeks and tongue.
Most cases present as a solitary or multiple, painless, well circumscribed,
fluctuant swellings and mimic mucoceles.

HISTOPATHOLOGY:
Appears as fibrous capsule around the organism.
Bladder wall of larvae appears lightly eosinophilic wavy membrane with
multiple tiny ovoid nuclei in stroma.
Due to chemotherapy organism dies but it disintegrates or gets calcified
with residual fibrous scar.
Fibrous capsule around
micro organism
 ASPERGILLOSIS
Non invasive and invasive forms.
Non invasive usually affects normal host appearing either as an
allergic reaction or a cluster of fungal hyphae.
Localised invasive infection of damaged tissue may be seen in normal
host but more extensive invasive infection is evident in
immunocompromised patients.
2 most common encountered species are A.flavus and A.fumigatus
with A.fumigatus responsible for 90% of cases.

CLINICAL FEATURES:
Normal host: disease may appear as an allergy affecting either
sinuses or bronchopulmonary tract. An asthma attack may be
triggered by inhalation of spores in susceptible person.
Low grade infection becomes established in maxillary sinus resulting
in mass of fungal hyphae called aspergilloma.
 Tissue damage predisposes the sinus to infection resulting in
symptoms of localized pain and tenderness accompanied by nasal
discharge.
Portal of entry may be marginal gingiva and gingival sulcus.
Painful gingival ulcerations noted initially, peripherally the mucosa
and soft tissue develops diffuse swelling with gray or violaceous hue.
If not treated, extensive necrosis may lead to yellow or black ulcer
with facial swelling.

Disseminated aspergillosis: occurs in immunocompromised pts,

primary site of inoculation is lungs.
Pt typically has chest pain, cough and fever.
Once fungal organism enters the blood stream, infection spreads to
sites as CNS, eyes, skin, liver, GIT, bone and thyroid gland.

HISTOPATHOLOGY:
Invasive form: These hyphae tend to branch at acute angle and
invade adjacent blood vessels.
 Occlusion of vessels often results in characteristic pattern of necrosis
associated with the disease.
Inflammatory response is weak or absent leading to extensive tissue
destruction.

Non invasive form: h/p differ from invasive form.

Allergic fungal sinusitis exhibits large pools of eosinophilic mucin
with interspersed sheet like collection of lymphocytes and
eosinophils.

DIAGNOSIS:
Diagnosis is supported by culture of organism from lesion.
Culture specimen of sputum and blood.
TREATMENT:
Non invasive: pts with allergic fungal sinusitis treated with
debridement and corticosteroid therapy.
Localised invasive: debridement followed by anti fungal
medications.
Obtuse angled
fungal hyphae
 TOXOPLASMOSIS
Caused by toxoplasma gondii.
Disease can be devastating for developing fetus or
immunocompromised patient.
Cats are considered to be the definitive host. This microorganism
multiplies in the intestinal tract of cats by means of sexual cycle,
discharging numerous oocytes in their feces.
When human ingest these oocytes, results in disease.

CLINICAL FEATURES:
In normal person, infection is asymptomatic. If symptoms develop
they are mild and resemble IM (low grade fever, cervical
lymphadenopathy, fatigue, muscle or joint pain). Symptoms last for
few days to months but host recovers without therapy.
In immunocompromised pts, it may represent a new, primary
infection or more frequently reactivation of previously encysted
organisms.
 Principal groups at risk are AIDS, transplant pts and cancer pts.
Manifestations may include necrotizing encephalitis, pneumonia,
myositis or myocarditis.
CNS involvement is seen in AIDS pts. Its a serious condition, pt may
complain of headache, lethargy, disorientation and hemiparesis.
Congenital toxoplasmosis occurs when a non immune mother
contracts the disease during her pregnancy and organism crosses the
placental barrier infecting the fetus.
The potential effects are blindness, mental retardation and delayed
psychomotor development are most severe if infection occurs during
1st trimester of pregnancy.

HISTOPATHOLOGY:
Lymph node obtained from pt of active toxoplasmosis shows
characteristic reactive germinal centers exhibiting accumulation of
eosinophilic macrophages.
Macrophages encroach the germinal centers and accumulate within
subcapsular and sinusoidal regions of lymPh nodes.
 DIAGNOSIS:
Established by rising serum antibody titres of T.Gondii within 10-14 days of
infection.
Biopsy of involved lymph node may suggest diagnosis.
Causative organism may be detected by IHC using antibodies directed
against T.gondii specific antigens.
Diagnosis should also be confirmed by serologic studies.

TREATMENT
Most patients require no specific treatment because symptoms are mild
and self limiting.
Pregnant women should avoid situations that may place them at risk like
handling or eating raw meat or cleaning of cat litter.
If exposure during pregnancy is suspected, combination of sulphadiazine
and pyrimethamine prevents transmission of T.gondii to fetus.
Most cases of toxoplasmosis in AIDS represent reactivation of encysted
organisms, prophylactic administration of trimethoprim and
sulfamethoxazole is generally recommended.
Reactive germinal centre
exhibiting accumulation of
eosinophilic macrophages
 ORAL MYIASIS
A condition in which soft tissues f different parts of oral cavity are
invaded by parasitic larvae of flies.
These larvae known as maggots are of 2 winged flies, the diptera.
Myiasis mainly occurs in tropic and associated with poor oral hygiene.
Female fly infests ova in open wounds, dead tissue or natural body
cavities like ears, nostrils and oral cavity.
The flies lay eggs directly on disease tissue. These eggs hatch and
they get their nourishment from soft tissue.
It is a rare condition but cases have ben reported in gingiva, palate
and extracted wounds.
The usual presenting symptoms are painful growth with ulceration
and itching due to crawling movement of larvae.
Treatment is aimed at removal of larvae from affected area and
flushing of arear with normal saline and antiseptics.