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Lecture 2 On FUNGAL INFECTIONS

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DR.

AMIT GUPTA
READER
DEPARTMENT OF ORAL PATHOLOGY
OBJECTIVES
 To understand the causative micro-organisms,
clinical features, pathogenesis,
histopathological features of various fungal
infections.
NORTH AMERICAN
BLASTOMYCOSIS
(GILCHRIST’S DISEASE)
Diamorphic fungus
Blastomyces dermatitidis

Survives best in
1)Rich nutritive
2) Moist soil( moulds)
North American Disease
More common in male in
9:1 ratio
CLINICAL FEATURE
• The fungal spores reach alveoli of lung and grow as yeast at body
temperature.
• These fungal spores get disseminated, and get distributed to various organs
such as skin, bone, prostate, meninges, orophyrangeal mucosa and abdominal
organ.
• Cutaneous spread indicates infections from lungs
CLINICAL FEATURE

Acute phase

Clinically resembles pneumonia, characterized by high fever, chest


pain, malaise, night sweat and productive cough.

Chronic phase

-It mimics tuberculosis; both conditions are often as low grade fever,
night sweats and weight loss

-Calcification absent(radiographically)
HISTOPATHOLOGY
Broad attachment between budding
Acute inflammation daughter cell and parent cell

Granulatomatous inflammation Double refractile cell wall


PAS STAIN HISTOPATHOLOGY
TREATMENT
Acute phase
Systemic Amphoteracin B
a) seriously ill
b) not improving clinically
c) ill for more than 2-weeks

Itraclonazole is recommended for mild to moderate infection.

Ketoclonazole is less effective.


SOUTH AMERICAN
BLASTOMYCOSIS
Paracoccidioimycosis is a deep functional – Paracoccidiosis
brasiliensis
Caused by Blastomyces Brasiliensis

Prominent in South America

Male predominance- 25:1 (female hormones beta esterdiol


prevents transformation of fungal hyphae to pathogenic yeast
forms)
CLINICAL FEATURE
Initial appearance as pulmonary infections
which are generally self limiting.

Adrenal involvement often results


in hypoadrenocortism( Addisons disease)

Oral lesions
Granular, Erythematous, Mullberry like ulceration on alveolar mucosa
and gingiva. Involvement of lips, orophyranx, and buccal mucosa.
HISTOPATHOLOGIC
1)
FEATURE
Psuedoepitheliomatous hyperplasia
2) May be ulcerated
3) Granulomatous response (epitheloid like cell and multinucleated
giant cell)
4) PAS and Grocott Gomori stains positive.
5) Ears of Mickey Mouse pattern of yeast and spokes of marine wheel.
TREATMENT
Sulphonamide derivatives were used previously.

New antifungal derivative are used now days.

Cases are best treated by itraconazole, although therapy may


be needed for several month.

Ketoclonazole can also be used, although therapy may be used


for several month.
COCCCIDIOMYCOSIS
(SAN JOAQUIN VALLEY
FEVER)
Cocidiomycosis immitis
• Grows saprophitically in alkaline, semiarid, desert soil.

• Diamorphic

• Anthrospores- air borne- inhaled causes lungs

infection.
CLINICAL FEATURES
Acute phase
Flu like illness and pulmonary symtoms
Fatigue
Chest pain
Myalgias
Headache
Hypersenstivity reactions can be seen as erythema multiforme or
erythema nodusum.
Painful erythematous inflammatory nodules in subcutaneous tissue.
Chronic phase
Mimics tuberculosis ( persistent cough, heamopotosis, chest pain, low
grade fever).
CONT….
Disseminated type

• Spreads heamatogenously to extra pulmonary sites


• Rare condition
• Group of people are more susceptible
Patient taking large doses of systemic corticosteroids.
patients treated with cancer chemotherapy.
patients in end stages of chemotherapy.

Cutaneous lesions appear as papules, subcutaneous abscess,


verrucous plaques, granulomatous nodules
HISTOPATHOLOGY

Large numerous endospores ( 20 to 60 microns)

Host response is variable

1) Suppurative
2) Neutrophillic infilterate
3) Granulomatous inflammation
PAS Stain
GMS Stain
TREATMENT

Severity and extent


Patients immune status
Amphoteracin B is drug of choice

Some cases fluconazole is drug of choice, given in high


doses for extended period of time.
HISTOPLASMOSIS
(Darling’s disease)
 Caused by Histoplasma capsulatum, a
dimorphic fungus.
 It is a common systemic fungal infection mainly
in the USA, but has been noted worldwide.
 Humid areas with soil enriched by bird/bat
excretions are suitable for the growth of this
organism.
 Thus this infection is seen endemically in fertile
river valleys.
MODE OF TRANSMISSION:

It is mainly caused by inhalation of air-borne


spores which pass into the terminal passage
of the lungs & germinate.

They may have associated oral lesions which


consists of chronic ulcers clinically resemble
a malignancy.
CLINICAL FEATURES:

3 main types:
 Acute Histoplasmosis

 Chronic Histoplasmosis

 Disseminated Histoplasmosis
Acute Histoplasmosis:
 It is a self limiting pulmonary infection that
probably develops in 1% of people who are
exposed to a low number of spores.
 These acute symptoms include fever,
headache, myalgia, non-productive cough,
anorexia. These features resemble that of
influenza.
 Patients are usually ill for 2 weeks.

 Calcification of the hilar lymph nodes may


be detected in chest radiographs years later.
Chronic Histoplasmosis:
 This primarily affects the lungs and is much
less common than the acute variant.
 It usually affects elderly individuals with
emphysema or immunosuppressed patients
i.e HIV infections.
 Clinically it is similar to tuberculosis with
persistent cough, weight loss, fever, chest
pain, hemoptysis, weakness & fatigue.
 Chest radiographs show upper-lobe
infiltration & cavitation.
Disseminated Histoplasmosis:

 Rare occurrence; 1 in 2000 patients.


 Characterised by progressive spread of the
infection to extrapulmonary sites.
 Occurs in older, debilitated patients &
patients with AIDS.
 Tissues affected could be spleen, liver, GIT,
CNS, kidneys, lymph nodes & oral mucosa.
Oral Manifestations:
 These occur primarily on the gingiva,
tongue, palate & buccal mucosa.
 The lesions are granulomatous, which appear
initially as a nodule & later ulcerate.
 The ulcers have raised, rolled borders &
induration of the surrounding tissues.
 This resembles ulcers of Tuberculosis or
Squamous Cell carcinoma.
Oral Manifestations (Contd..):
 On the gingiva, it appears as a diffuse
granulomatous process with underlying
alveolar bone loss & loosening of teeth.
 The ulcerated areas at times are covered by a
non-specific gray membrane.
HISTOPATHOLOGY:
 It is a granulomatous infection characterised
by formation of multiple, small, often small
granulomas composed of histiocytes, many
of which contain variable number of
organisms.
 Lymphocytes & plasma cells may be seen in
abundance.
 The organism is usually seen in it’s spore
form measuring 2-5 µ in diameter within
phagocytes & multinucleated giant cells.
 Stains used for demonstration are H & E,
DIAGNOSIS:
 Combination of data including clinical
evaluation, microscopic examination, culture,
serologic findings & histoplasmin skin test.
 The histoplasmin skin test uses inactivated
mycelia or yeast of the organism. It cannot be
used for detection in endemic areas.
 Most reliable test is the immunodiffusion test
which detects the patient serum antibody to
the H & M antigen of H.capsulatum.
 DNA probes are also available.
Treatment:

 Immunocompetant patients without CNS


involvement can be treated with
itraconazole or ketoconazole for 6 to 12
months.
 For disseminated forms, Amphotericin B
remains the drug of choice.
 In AIDS patients, there is recurrent
infection.
GEOTRICHOSIS
 Clinically similar to Candidiasis

 Causative agent: Geotrichum Sp

 Site: Mucosa and Lungs(Symptoms similar to bronchitis)

 H/F: Spores of 4-8µ

 Treatment: Non-specific
MUCORMYCOSIS
(Zygomycosis, Phycomycosis)
 Mucormycosis is an opportunistic infection
which grows mainly on decaying organic
material.
 Numerous spores may be liberated in the air
and may be inhaled by the human host.
 It may affect any part of the body but the
rhinocerebral form is most relevant to the
dentist.
 Seen in patients with immunocompromised
states or in uncontrolled diabetes.
Clinical Features:
 Nasal obstruction, bloody nasal discharge,
facial pain, headache, facial swelling /
cellulitis, visual disturbances are observed.
 Palsy may be seen associated with the cranial
nerve involvement.
 If it progresses in to the cranial vault it may
lead to blindness, lethargy, seizures and
ultimately death.
 If maxillary sinus is affected and untreated it
may lead to palatal ulceration which is black &
necrotic with massive tissue destruction.
Histopathology & Diagnosis:
 Extensive necrosis of lesional tissue with
numerous large branching, nonseptate
hyphae at the periphery. (6-30 µm in diameter).
 Hyphae tend to branch at 90 degree angles.
 Small blood vessels are affected leading to
infarction & necrosis.
 A neutrophilic infiltrate may be seen
predominantly if the patient is not
immunocompromised.
 Diagnosis is mainly done by culture &
treatment should begin immediately due to the
diseases grave consequences.
Treatment:
 Radical surgical debridement of the infected,
necrotic tissue & systemic administration of
high doses of amphotericin B.
 MRI of the head should be done to determine
the extent of the disease.
 Underlying diseases should be controlled.

 The massive tissue destruction affects the


patient functionally & esthetically. At times,
prosthetic obturation of palatal defects may be
necessary. PROGNOSIS IS POOR.
Commonly Asked Questions
 Histoplasmosis
References
Shafer, Hine,Levi. Textbook of Oral
Pathology; 5th Edition; Saunders Publications.
Neville BW, Damm DD, Allen CM, Bouquot
JE. Oral & Maxillofacial pathology. Second
ed, W.B Sounders Company, 2002

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