Fungi were found by Heinrich Anton de Bary in 1858. Most fungi cause skin or cosmetic infections while bacteria & viruses cause fatal diseases. Organ transplantation, Immunosuppressive drugs,Anticancer drugs, Broad-spectrum antimicrobials ,HIV-disease leads to Immunosuppression causing Opportunistic Fungal Infections

2. Fungal and Viral Diseases

3. Contents
Part A: Fungal Diseases
• Introduction to Fungal Diseases
• Fungi types
• Predisposing factors
• Candidiasis
• Aspergillosis
• Histoplasmosis
• Mucormycosis
• Blastomycosis
• Cryptococcosis
• References

4. Fungal infections of the oral cavity
• Fungi were found by Heinrich Anton de Bary in 1858.
• Most fungi cause skin or cosmetic infections while bacteria &
viruses cause fatal diseases.
• Organ transplantation, Immunosuppressive drugs,Anticancer
drugs, Broad-spectrum antimicrobials ,HIV-disease leads to
Immunosuppression causing Opportunistic Fungal Infections

5. • Fungi are eukaryotic i.e.
possess a true nucleus with
nuclear membrane &
mitochondria.
• Cell membrane have
ergosterol which is specific
target for antifungal agents
(cholestrol in mammalian
cells).

6. Fungi types- Based on morphology
1. Molds (filamentous fungi):
Most fungi are composed of
filamentous (tubular)
structures called hyphae.
May be septated OR
Aseptated.
Hyphae of Penicillium

7. 2. Yeasts Unicellular
(rounded or oval):
Reproduce by budding.
The only example of
pathogenic yeast is
Crptococcus
neoformans.
Saccharomyces cerevisiae, a
species of yeast

8. 3. Yeast-LikeUnicellular (rounded or oval):
• Reproduce by budding but buds fail to detach and may form
short chains of cells called pseudohyphae.
• Pseudohyphae are produced during infection and have
diagnostic value. Example: Candida

9. 4. Dimorphic Fungi:
• Able to grow in both mold and yeast form. This transition is
usually bought by change in temperature.
• As molds at room temperature and as yeasts on incubation at
37°C & during infection in body“ Mold in the cold, yeast in the
heat“
• Example: Histoplasma capsulatum

10. Predisposing factors for fungal
diseases
• Poor Oral Hygeine
• Immunocompromised
• Corticosteriod & Cytotoxic Antibiotic Use
• Medical Conditions Diabetes, Leukemia, Anemia,etc.
• Environmental Factors Humidity, Dry Mouth, Dental Appliance
• Hereditary Factors

11. Candidiasis
• Most commonly encountered opportunistic mycoses worldwide affecting the
oral mucosa.
• In the vast majority of cases, the lesions are caused by the yeast Candida
albicans.
• C. albicans is usually a weak pathogen, and candidiasis is said to affect the very
young, the very old, and the very sick. Most Candida infections only affect
mucosal linings, but the rare systemic manifestations may have a fatal course.
• Oral candidiasis is divided into primary and secondary infections. The primary
infections are restricted to the oral and perioral sites, whereas secondary
infections are accompanied by systemic mucocutaneous manifestations.

12. Candidiasis
Primary
Acute
Secondary
Chronic Candida Associated
Lesions
Keratinized lesions super
infected with Candida
•Hyperplastic
•Nodular
•Plaque like
•Erythematous
•Pseudomemb
ranous
•Denture
stomatitis
•Angular
cheilitis
•Median
rhomboid
glossitis
•Leukoplakia
•Lichen planus
•Lupus
erythematosus
Pseudomembr
anous
Erythematous

13. Pseudomembranous Candidiasis
• It is also known as thrush and is one of the most common
forms of the candidiasis.
• It may occur at any age, but is especially prone to occur in the
debilitated or the chronically ill patients or in infants.

14. Occurs either due to immune
suppression or because of
exposure to broad spectrum
antibiotics.
Characterized by the
appearance of soft, white,
slightly elevated plaques most
frequently occurring on the
buccal mucosa and tongue, but
also seen on the palate, gingiva,
and floor of
the mouth.
The elevated white contains tangled
masses of fungal hyphae and bacteria
with intermingled desquamated
epithelium, keratin, fibrin, necrotic
debris & leukocytes.

15. A. Classic “curdled milk” appearance of the oral lesions
of pseudomembranous candidiasis.
B. the pseudomembranous plaques can be removed by scrapping with
a dry gauge, which may reveal normal mucosa or erythematous
mucosal surface (arrow)

16. • The plaques are characteristically distributed on the buccal
mucosa, palate and dorsal tongue.
• Symptoms, if present at all, are usually relatively mild,
consisting of a burning sensation of the oral mucosa or an
unpleasant taste in the mouth, variably described as salty or
bitter.

17. Erythematous Candisiasis
• Also known as antibiotic sore mouth.
• occurs as a sequela to a course of broad spectrum antibiotics,
corticosteroids or any disease which suppresses the immune
system, more commonly HIV disease.
• Patients often complain that the mouth feels as if a hot
beverage had scalded it

18. • The lesions in this form of
the disease appear red or
erythematous rather than
white, thus resembling the
pseudomembranous type in
which the white membrane
has been wiped off.
• The redness is due to
increased vascularity. The patchy, denuded areas (not the white
areas) of the dorsal tongue represent
erythematous candidiasis

19. • The redness is distinguished
from erythroplakia by its
diffuse border wherein
erythroplakia the borders
are sharp and well
demarcated
• This is the only candidiasis
which is constantly painful.
Erythematous candidosis caused
by inhalation steroids.

20. Patients often complain that the mouth feels as
if a hot beverage had scalded it. This burning
sensation is usually accompanied by a diffuse loss
of the filiform papillae of the dorsal tongue,
resulting in a reddened, “bald” appearance of the
tongue .
Burning mouth syndrome frequently manifests
with a scalded sensation of the tongue; however,
the tongue appears normal in that condition.

21. • Other forms of erythematous
candidiasis are usually
asymptomatic and chronic.
Included in this category is the
condition known as central
papillary atrophy of the tongue,
or median rhomboid glossitis.
• Clinically, central papillary atrophy
appears as a well-demarcated
erythematous zone that affects
the midline, posterior dorsal
tongue and often is asymptomatic.
Erythematous candidiasis.
A. Severe presentation of central papillary
atrophy. In this
patient the lesion was asymptomatic.
B. Marked regeneration of the dorsal tongue
papillae occurred 2 weeks after antifungal
therapy with fluconazole.

22. • Sometimes a concurrent
erythematous lesion may be
observed in the palatal
mucosa also known as
kissing lesions. The lesion
does not entail any
increased risk for malignant
transformation.

23. CHRONIC HYPERPLASTIC CANDIDIASIS
(CANDIDAL LEUKOPLAKIA) and NODULAR CANDIDIASIS
• The oral lesions in this form consist
of firm, white persistent plaques,
usually on the lips, tongue, and
cheeks and appear similar to
leukoplakia
• A positive correlation between oral
candidiasis and moderate to severe
epithelial dysplasia has been
observed in both the chronic
plaque-type and nodular candidiasis
The White patch typically cannot
be removed by scrapping

24. Denture Stomatitis
(Chronic atrophic candidiasis)
• It is a diffuse erythema and
edema of the denture-bearing
area.
• Usually asymptomatic except
for the soreness and the
presenting complaint may be
angular stomatitis.
• Mandibular mucosa is rarely
affected

25. Angular Cheilitis
• Angular cheilitis is infected
fissures of the commissures of
the mouth, often surrounded
by erythema.
• The lesions are frequently
coinfected with bothCandida
and Staphylococcus aureus.
• Vitamin B12 & iron
deficiencies have been
associated to this disorder

26. Oral Candidiasis Associated with HIV.
• More than 90% of AIDS patients have
had oral candidiasis during the course
of their HIV infection, and the infection
is considered a portent of AIDS
development . The most common types
of oral candidiasis in conjunction with
HIV are pseudomembranous
candidiasis, erythematous candidiasis,
angular cheilitis, and chronic
hyperplastic candidiasis. As a result of
the highly active antiretroviral therapy
(HAART), the prevalence of oral
candidiasis has decreased substantially.
Erythematous candidiasis at the
central part of the tongue in
an AIDS patient. Hairy leukoplakia
can be seen at the right lateral
border.

27. Management
1. Before starting antifungal medication, it is necessary to identify any
predisposing factor. Local factors are often easy to identify but
sometimes not possible to reduce or eradicate.
2. Antifungal drugs have a primary role in such cases. Polyenes such as
nystatin and amphotericin B are the first alternatives in treatment of
primary oral candidiasis and are well tolerated. They exert the action
through a negative effect on the production of ergosterol,
which is critical for the Candida cell membrane integrity.
Polyenes can also affect the adherence of the fungi.

28. 3. Topical treatment with azoles such as miconazole is the treatment of
choice in angular cheilitis often infected by both S. aureus and Candida.
This drug has a biostatic effect on S. aureus in addition to the fungistatic
effect to Candida.
4. Systemic azoles may be used for deeply seated primary candidiasis, such as
as chronic hyperplastic candidiasis, denture stomatitis, and median
rhomboid glossitis with a granular appearance, and for therapy-resistant
infections, mostly related to compliance failure.
5. The prognosis of oral candidiasis is good given that predisposing factors
associated with the infection are reduced or eliminated.

29. Aspergillosis
• Aspergillosis is a fungal disease that is characterized by
noninvasive and invasive forms.
• Noninvasive aspergillosis usually affects a normal host,
appearing either as an allergic reaction or a cluster of fungal
hyphae. Localized invasive infection of damaged tissue may be
seen in a normal host, but a more extensive invasive infection
is often evident in the immunocompromised patient.

30. • Normally, the various species of the Aspergillus genus
reside worldwide as saprobic organisms in soil, water, or
decaying organic debris. Resistant spores are released into
the air and inhaled by the human host, resulting in
opportunistic fungal infection second in frequency only to
candidiasis.
• Aspergillus fumigatus and Aspergillus flavus are primarily
responsible for systemic infections

31. • Transmitted by air borne light spores.
• The clinical manifestations of aspergillosis vary, depending on the
host immune status and the presence or absence of tissue damage.
In the normal host, the disease may appear as an allergy affecting
either the sinuses (allergic fungal sinusitis) or the
bronchopulmonary tract. It can lead to asthma, rhinitis,
bronchopulmonary aspergillosis and invasive aspergillosis.

32. • It is encountered by the oral health care provider especially
after tooth extraction or endodontic treatment, especially in
the maxillary posterior segments. Presumably, tissue damage
predisposes the sinus to infection, resulting in symptoms of
localized pain and tenderness accompanied by nasal
discharge.
• Susceptible to oral aspergillosis, and some investigators have
suggested that the portal of entry may be the marginal gingiva
and gingival sulcus.

33. • Painful gingival ulcerations are
initially noted, and
peripherally the mucosa and
soft tissue develops diffuse
swelling with a gray or
violaceous hue.
• If the disease is not treated,
extensive necrosis, seen
clinically as a yellow or black
ulcer, and facial swelling
evolve.

34. • Disseminated aspergillosis occurs principally
immunocompromised patients, particularly in those who have
leukemia or who are taking high daily doses of corticosteroids.
• Such patients usually exhibit symptoms related to the primary site
of inoculation; the lungs.
• The patient typically has chest pain, cough, and fever, but such
symptoms are vague. Therefore, obtaining an early, accurate
diagnosis may be difficult.

35. Diagnosis
• Ideally, the diagnosis should be supported by culture of the
organism from the lesion; however, from a practical
standpoint, treatment may need to be initiated immediately
to prevent the patient’s demise.
• Culture specimens of sputum and blood are of limited value
because they are often negative despite disseminated
disease.

36. Treatment
Depending on the clinical presentation, following treatment
options can be preferred:
• For immunocompetent patients with a noninvasive aspergilloma,
surgical débridement may be all that is necessary. Patients who
have allergic fungal sinusitis are treated with débridement and
corticosteroid drugs.
• For localized invasive aspergillosis in the immunocompetent host,
débridement followed by antifungal medication is indicated. Recent
studies have shown that voriconazole, a triazole antifungal agent, is
more effective for treating these patients. Itraconazole has also
been approved as an alternative therapy.

37. • Immunocompromised patients who have invasive aspergillosis
should be treated by aggressive débridement of necrotic
tissue, combined with systemic antifungal therapy as
described previously.
• The prognosis for immunocompromised patients is much
worse compared with immunocompetent individuals,
particularly if the infection is disseminated. Even with
appropriate therapy, only about one third of these patients
survive.

38. • Because aspergillosis in the immunocompromised patient
usually develops while the individual is hospitalized, particular
attention should be given to the ventilation system in the
hospital to prevent patient exposure to the airborne spores of
Aspergillus spp.

39. Contents

40. HISTOPLASMOSIS
• Histoplasmosis is a generalized fungal infection caused by the
dimorphic fungus Histoplasma capsulatum.
• Usually acquired by inhalation of dust containing spores of the
fungus, the contamination probably occurring from excreta of
birds such as pigeons, starlings, and blackbirds.
• Infection ensues when microconidiae or hyphae are inhaled
into the lung and develop into yeast or when old foci of
infection are reactivated. AIDS patients are particularly at risk
due to impairment of cellular immunity.

41. Histoplasmosis
Acute Chronic Disseminated

42. • Acute histoplasmosis is a self-limited pulmonary infection that
probably develops in only about 1% of people who are exposed to a
low number of spores.
• With a high concentration of spores, as many as 50% to 100% of
individuals may experience acute symptoms.
• These symptoms includes fever, headache, myalgia, nonproductive
cough, anorexia results in a clinical picture similar to that of
influenza.
• Patients are usually ill for 2 weeks, although calcification of the
hilar lymph nodes may be detected as an incidental finding on chest
radiographs years later.

43. • Chronic histoplasmosis also primarily affects the lungs,
although it is much less common than acute histoplasmosis.
The chronic form usually affects immunosuppressed patients.
• Patients typically exhibit cough, weight loss, fever,
• dyspnea, chest pain, hemoptysis, weakness, and fatigue.
• Chest radiograph show supper-lobe infiltrates and cavitation.

44. • Disseminated histoplasmosis usually occurs in either older,
debilitated, or immunosuppressed patients.
• This condition is characterized by the progressive spread of the
infection to extrapulmonary sites.
• Tissues that may be affected include the spleen, adrenal glands,
liver, lymph nodes, gastrointestinal tract, central nervous system
(CNS), kidneys,and oral mucosa.
• Most oral lesions of histoplasmosis occur with the disseminated
form of the disease.

45. • The most commonly affected
sites are the tongue, palate,
and buccal mucosa.
• The condition usually appears
as a solitary, variably painful
ulceration of several weeks’
duration; however, some
lesions may appear
erythematous or white with
an irregular surface.
This chronic ulceration of the
ventral and lateral tongue represents an
oral lesion of
histoplasmosis that had disseminated
from the lungs. The
lesion clinically resembles carcinoma;
because of this highrisk
site, biopsy is mandatory.

46. • Disseminated variant can also
be seen in patients suffering
from AIDS.
• The ulcerated lesions have
firm, rolled margins, and they
may be indistinguishable
clinically from a malignancy
This ulcerated granular lesion
involves the maxillary buccal
vestibule and is easily mistaken
clinically for carcinoma. Biopsy
established the diagnosis.

47. DIAGNOSIS
• The diagnosis of histoplasmosis can be made by
histopathologic identification of the organism in tissue
sections or by culture.
• Other helpful diagnostic studies include serologic testing in
which antibodies directed against H. capsulatum are
demonstrated and antigen produced by the yeast is identified.

48. Management
• Acute histoplasmosis, because it is a self-limited process,
generally warrants no specific treatment other than
supportive care with analgesic and antipyretic agents.
• Often the disease is not treated because the symptoms are so
nonspecific and the diagnosis is not readily evident.

49. • Patients with chronic histoplasmosis require treatment, despite the
fact that up to half of them may recover spontaneously.
• Amphotericin B administered intravenously is the first-choice drug,
especially in severe cases.
• However, significant kidney damage can result from this therapy;
therefore, Itraconazole may be used in nonimmunosuppressed
patients because it is associated with fewer side effects, but this
medication requires daily dosing for at least 3 months.
• Ketoconazole and Fluconazole appear to be less effective than
itraconazole and less likely to produce a desired therapeutic
response.

50. • Since Disseminated histoplasmosis is a very serious condition that
results in death in 80% to 90% of patients if they remain untreated,
Amphotericin B is usually indicated for such patients; once the life-
threatening phase of the disease is under control, daily itraconazole
is necessary for 6 to 18 months.
• Despite therapy, however, a mortality rate of 7% to 23% is
observed. Itraconazole alone may be used if the patient is
nonimmunocompromised and has relatively mild to moderate
disease; however, the response rate is slower than for patients
receiving amphotericin B, and the relapse rate may be higher.

51. Mucormycosis (Zygomycosis,
Phycomycosis)
• The term mucormycosis refers to a distinctive group of diseases
caused by saprophytic fungi of the order,
Mucorales:Rhizopus, Mucor, Rhizomucor, Cunninghamella,
and Absidia. The organisms are common inhabitants of soil and may
be found in the nasal cavities of healthy individuals.
• Infection arises by inhalation of spores that are deposited in
pulmonary alveoli. Other modes of infection include contamination
of traumatized tissues and direct inoculation.

52. • These fungus are angioinvasive and preferentially erodes arteries,
resulting in thrombosis with subsequent necrosis of the
surrounding tissues.
• Traditional risk factors that increase the chances of acquiring
mucormycosis include diabetes mellitus, haematological
malignancies, stem cell transplant, organ transplant, iron overload,
treatment with deferoxamine, malnutrition, burns, extensive use of
broad-spectrum antibiotics, critical care admissions. It is also
commonly associated with HIV positive patients.

53. Mucormycosis
Superficial
Involves External
ear, skin and
fingernails
Visceral
Rhinocerebral Pulmonary Gastrointestinal

54. • Rhino-orbital-cerebral mucormycosis is the most commonly
observed manifestation, followed by cutaneous and
pulmonary mucormycosis.
• the rhinocerebral variant is of greatest interest to the dental
profession.
• The infection apparently enters the tissues through the nasal
mucosa and extends to the paranasal sinuses, pharynx,
palate, orbit, and brain.

55. • One early clinical
manifestation of the disease
is the appearance of a
reddish-black nasal
turbinate and septum with a
nasal discharge.
• The necrosis may extend to
the paranasal sinuses and
orbital cavity, with the
development of sinus tracts
and sloughing of tissue.
Whitish spongy secretions are present in
the nasal cavities (A) and in the oral
cavity (B)
A 50 year old patient with uncontrolled
diabetes. On exam, he has periorbital swelling
and rhinorrhea. There is a black eschar over his
nares and palate.

56. • Cases of phycomycosis
involving the maxillary sinus
may present clinically as a
mass in the maxilla,
resembling carcinoma of the
antrum, and radiographs may
support the latter diagnosis.
• Surgical exploration will reveal
masses of necrotic tissue in
which the organisms can be
demonstrated histologically.
Mucormycosis involving the
maxillary antrum.

57. Management
• The main purpose of the therapy is to correct any predisposing risk
factors, an aggressive surgery to eliminate the disease and a rapid
antifungal treatment.
• Surgical debridement must be as aggressive as possible.
• Treatment with antifungal with intravenous amphotericin B should be
started as quickly as possible. Liposomal formulations of amphotericin B
are preferred because they are more tolerable in these already
systemically compromised patients and have less side effect profiles.
• Other studies showed that posaconazole and isavuconazole as a second
line agent could be used as salvage therapy in no response cases

58. BLASTOMYCOSIS
• Blastomycosis is a relatively uncommon disease caused by the
dimorphic fungus known as Blastomyces dermatitidis.
• It is a deep mycotic infection and presents as either pulmonary,
disseminated, or localized cutaneous lesions. As in aspergillosis, the
fungal spores are found in the soil and may initiate the disease
when inhaled.
• Although most cases of blastomycosis are either asymptomatic or
produce only very mild symptoms, patients who do experience
symptoms usually have pulmonary complaints.

59. • Acute blastomycosis resembles pneumonia, characterized by high
fever, chest pain, malaise, night sweats, and productive cough with
mucopurulent sputum.
• Chronic blastomycosis is more common than the acute form, and it
may mimic tuberculosis; both conditions are often characterized by
low-grade fever, night sweats, weight loss, and productive cough.
Unlike the situation with tuberculosis and histoplasmosis,
calcification is not typically present.

60. • Cutaneous lesions usually
represent the spread of
infection from the lungs,
although occasionally they are
the only sign of disease. Such
lesions begin as erythematous
nodules that enlarge,
becoming verrucous or
ulcerated
granular erythematous
plaque of cutaneous blastomycosis
Severe cutaneous infection

61. • Oral lesions of blastomycosis may
result from either extrapulmonary
dissemination or local inoculation
with the organism.
• These lesions may have an
irregular, erythematous or white
intact surface, or they may appear
as ulcerations with irregular rolled
borders and varying degrees of
pain.
• Biopsy and histopathologic
examination are required as they
resemble SCC clinically.
Granular exophytic and indurated
mass on the buccal mucosa.
These irregular ulcerations of the
tongue represent blastomycosis.

62. Diagnosis
• Rapid diagnosis of blastomycosis can be performed by
microscopic examination of either histopathologic sections or
an alcohol-fixed cytologic preparation.
• The most accurate method of identifying B. dermatitidis is by
obtaining a culture specimen from sputum or fresh biopsy
material and growing the organism on Sabouraud’s agar.

63. Management
• Most patients with blastomycosis require no treatment.
• Even in the case of symptomatic acute blastomycosis,
administration of systemic amphotericin B is indicated only if
one or more of the following is noted:
I. Patient is seriously ill (AIDS, organ transplant recipient,
other immune suppression disorder)
II. Patient is not improving clinically
III. Patient is ill for more than 2 or 3 weeks

64. • Patients with chronic blastomycosis or extrapulmonary lesions
need treatment.
• Itraconazole is generally recommended, particularly if the
infection is mild or moderate. Although ketoconazole and
fluconazole are active against B. dermatitidis, these drugs
have been shown to be less effective than itraconazole.
• Amphotericin B is reserved for patients who are severely ill or
show no response to itraconazole.

65. Cryptococcsis
• Cryptococcosis is a relatively uncommon fungal disease
caused by the yeast Cryptococcus neoformans.
• This organism normally causes no problem in
immunocompetent people, but it can be devastating to
the immunocompromised patient. The incidence of
cryptococcosis increased dramatically during the 1990s,
primarily because of the AIDS epidemic.

66. • The disease has a worldwide distribution because of its association
with the pigeon with the organism living in the deposits of excreta
left by the birds.
• The disease is acquired by inhalation of C. neoformans spores into
the lungs, resulting in an immediate influx of neutrophils, which
destroys most of the yeasts. Macrophages soon follow, although
resolution of infection in the immunocompetent host ultimately
depends on an intact cell-mediated immune system.
• Primary cryptococcal infection of the lungs is often asymptomatic;
however, a mild flulike illness may develop. Patients complain of
productive cough, chest pain, fever, and malaise.

67. • Most patients with a diagnosis of cryptococcosis have a signifi cant
underlying medical problem related to immune suppression (e.g.,
systemic corticosteroid therapy, cancer chemotherapy, malignancy,
AIDS).
• Dissemination of the infection is common in these
immunocompromised patients, and the most frequent site of
involvement is the meninges, followed by skin, bone, and the
prostate gland.
• Cryptococcal meningitis is characterized by headache, fever,
vomiting, and neck stiffness.

68. • Cutaneous lesions often
involves the skin of the head
and neck.
• The lesions appear as
erythematous papules or
pustules that may ulcerate,
discharging a puslike material
rich in cryptococcal organisms
These papules of the facial skin
represent disseminated cryptococcal
infection in a patient
infected with human immunodefi ciency
virus (HIV)

69. • Oral mucosal lesions of
cryptococcosis are extremely
rare and have been mainly
reported in AIDS patients who
suffered of disseminated
infection.
• Oral lesions have been
described either as craterlike,
nonhealing ulcers that are
tender on palpation, as
hyperplastic tissue or as friable
papillary erythematous
plaques.
Gingival enlargements with erythematous
color, granular texture, and micro-ulcerations
covered by serous secretions and some
bleeding

70. Management
• Management of cryptococcal infections can be very difficult
because most of the affected patients have an underlying medical
problem.
• For cryptococcal meningitis, a combination of systemic
amphotericin B and flucytosine is used initially for 2 weeks in most
cases.
• Then, either fluconazole or itraconazole is given for an additional
minimal period of 10 weeks.
• For relatively mild cases of pulmonary cryptococcosis, only
fluconazole or itraconazole may be used.

72. References
• B.Sivapathasundharam Shaefer’s. Textbook of Oral Pathology.Elsevier. 7th Edition; 2012,
Page no. 367-380.
• Blyth, Christopher & Palasanthiran, Pamela & O'Brien, Tracey. (2007). Antifungal
Therapy in Children With Invasive Fungal Infections: A Systematic Review. Pediatrics.
119. 772-84. 10.1542/peds.2006-2931.
• Brad W. Neville, Douglas D. Damm, Carl M. Allen, Jerry E. Bouquot. Oral and
Maxillofacial Pathology. Elsevier. 3rd Edition;2008,Page no. 213-239.
• Delgado W (2017) Oral Cryptococcosis. JSM Tropical Medicine Research 2(1): 1015.

73. • Galletti, Bruno & Francesco, Gazia & Galletti, Cosimo & Perani, Fulvio &
Ciodaro, Francesco & Freni, Francesco & Galletti, Francesco. (2019).
Rhinocerebral mucormycosis with dissemination to pontine area in a
diabetic patient: Treatment and management. Clinical Case Reports. 7.
10.1002/ccr3.2255
• Greenberg S. (2008) Burket’s oral medicine. 11th Edition, BC Decker Inc,
Hamilton
• Martin S. Greenberg, Michael Glick, Jonathan A. Ship. Burket’s Oral
Medicine. B.C. Decker. 11th Edition; 2008, Page no. 77-106