KRISHNADEVARAYA COLLEGE OF DENTAL SCIENCES

Affiliated to RGUHS, Krishnadevaraya Nagar, Hunasmaranahalli, International Airport, via Yelahanka

Bangalore-562157
2020-2021

DEPARTMENT OF PEDIATRIC AND PREVENTIVE

DENTISTRY

A Seminar Report
On
“ VIRAL & FUNGAL INFECTIONS ”
Submitted by
KEERTHI.S (18D0201) KCDS, Bangalore
 KRISHNADEVARAYA COLLEGE OF DENTAL SCIENCES
Hunasmaranahalli Bengaluru,Karnataka,India-562157
DEPARTMENT OF PEDIATRIC AND PREVENTIVE DENTISTRY
CERTIFICATE

This is to certify that seminar entitled “VIRAL & FUNGAL INFECTIONS” is submitted by KEERTHI.S
bearing ID 18D0201 on partial fulfillment of the requirements in the degree of Bachelor of Dental Sciences,
Rajiv Gandhi University of Health and Sciences, and Bangalore during the academic year 2020-2021,It is
certified that all corrections/suggestions initiated for the internal assessment have been incorporated in the
report deposited in departmental library.The seminar report has been approved as it satisfies the academic
requirements in prescribed for said degree.

Signature of the HOD

DR.PRIYA NAGAR
Dept.of Pediatric Dentistry
KCDS, Bangalore.
 ACKNOWLEDGEME
NT
• The satisfaction and euphoria that accompany the successful completion of any task would be
incomplete without complementing those made it possible,whose guidance and encouragement
made our efforts successful.
• My sincere thanks to highly esteemed institution KRISHNADEVARAYA COLLEGE OF
DENTAL SCIENCES,BANGALORE for grooming up me to be a dentist.
• I express our sincere thanks to Dr.PONNANNA AA. Principal KCDS Bangalore for providing the
required facility.
• I am grateful to my faculty Dr.RESHMA DODWAD, Dr. PALLAVI.URS, Dr.PUSHPAVENI
GOPAL who helped me to complete this seminar successfully by providing guidance,
encouragement.
Finally I am grateful to my parents Mr.SATISH GOWDA and Mrs. PUSHPA and express my sincere
thanks to my friends for their invaluable support guidance and encouragement.

KEERTHI.S
18D0201
VIRAL & FUNGAL

INFECTIONS
 VIRAL
CONTENTS
INFECTIONS
• Introduction
• Pox Virus
• Variola Virus
• Herpes Virus
• Varicella Zoster Virus C TS
S PE
• Epstein Barr Virus ALA
N IC
• Infectious Mononucleosis CL
I
NS
& TI O
• Cytomegalovirus RAL TA
E NE I FES E NT
• Papovavirus G
MAN G EM
• Retrovirus R AL A NA
O & M
• Measles SI S
O
• GN
Hepatitis DI A
 FUNGAL
CONTENTS
INFECTIONS

• Introduction
• Candidiasis
• Histoplasmosis CAL AS PE CTS
N I
CL I
• Blastomycosis NER A L &
STAT I ONS
GE E
ISF
• Rhinosporidiosis R ALM
AN
M E NT
O
NA GE
& MA
NOSIS
G
DIA
 VIRAL INFECTIONS
• Viruses are the smallest obligate intracellular
infective agents.They have no metabolic activity
outside the living cells.
• Viruses contain only one type of nucleic acid
(DNA/RNA) for protein & nuclei acid synthesis.
• They multiply by a complex process and not by
binary fission.
• They are unaffected by Antibiotics.
STRUCTURE
• The size of viruses range from 20 to 300 nm.
CLASSIFICATION OF VIRUSES

DNA VIRUSES RNA VIRUSES

1. POX VIRUS 1. ORTHOMYXO VIRUS
2. HERPES VIRUS 2. PARAMYXO VIRUS
3. ADENO VIRUS 3. PICORNA VIRUS
4. PAPOVA VIRUS 4. RHABDO VIRUS
5. TOGA VIRUS
6. FLAVI VIRUS
7. RETRO VIRUS
8. CORONA VIRUS
 POX VIRUSES
• Pox viruses belongs to the family POXVIRIDAE and causes number of
human diseases
• Pox viruses are brick shaped, largest viruses measuring 300-100 nm.
• CULTIVATION:-tissue cultures of monkey kidney, chick embryo cells can
be used to grow.
• VIRUSES CAUSING HUMAN INFECTIONS :-
1. VARIOLA
2. VACCINIA
3. COWPOX
4. HUMAN MONKEYPOX
5. MILERS’S NODE
 VARIOLA
• Variola viruses causes small pox .
• The name variola major was given to the
virus causing classical smallpox and
variola minor was given to other virus
causing alastrim.
• In 1967, WHO embarked on a Small pox
eradication camping.
• It is now a disease of only historical
interest
 HERPES VIRUSES
• Herpes viruses are included in the family
herpesviridae
• Herpes virus is 100-200nm in diameter.
• It contains an icosahedral capsid
composed of 162 capsomers,double
stranded DNA genome surrounded by
lipid envelope containing peplomers.
• Between capsid and envelope tegument
is present
CLASSIFICATION OF HUMAN HERPES
VIRUS
 HERPES SIMPLEX VIRUS
(Human herpes virus 1 and 2 )
• HSV-1 and HSV-2 can be differentiated by serotyping, DNA homology and to some
extent by clinical disease pattern.
• The infections caused by HSV can be divided into primary infection, latent infection,
reactivation and recrudescence.
• PRIMARY INFECTIONS : There is an incubation period of 2-20 days, depending
upon INFECTIONS
the infected site and the infecting strain
caused by HSV-1
pf virus. The lesions include:
INFECTIONS caused by HSV-2
1. Acute Gingivostomatitis 1. Genital Herpes
2. Herpetic whitlow 2. Aseptic meningitis
3. Keratoconjuctivitis 3. Neonatal infections
4. Eczema herpeticum
5. Encephalitis
6. Generalized infection
 HSV-1 PRIMARY INFECTIONS

ACUTE GINGIVOSTOMATITIS ECZEMA HERPTIUM

KERATOCONJUCTIVITIS

HERPETIC WHITLOW ENCEPHALITIS

 RECURRENT INFECTIONS

• Recurrence of HSV entails activation of the non

infectious form of the latent virus residing in the
neurons of either trigeminal ganglion or sacral
ganglia.
• Reactivation is provoked by menstruation, stress,
sunlight, local trauma etc.
• The lesions tend to recur at the site of the primary
lesion. HERPES LABIALIS
Recurrence of facial herpes infection due
to reactivation of latent virus in
trigeminal ganglion
 EPIDEMIOLOGY
• Humans are the only reservoir for HSV-1 & HSV-2.
• As the virus is highly labile most primary infections are
acquired through direct contact.
• HSV-1 causes orofacial lesions and is acquired early in life
whereas HSV-2 causes genital herpes and appears after
onset of sexual activity.

DIAGNOSIS
• Direct demonstration of viral antigens in vesicular
fluid/scrapings by electron microscopy or
immunofluorescence
• Demonstration of characteristic multinuclear giant cells
• Propagation of virus in tissue culture.
 PREVENTION & TREATMENT

• Control is difficult because of • The course of primary infection

high frequency of asymptomatic
infection.
• It is important to avoid contact
with acute herpetic lesions and
contaminated body fluid.
• No vaccine is available.
can be altered significantly with
drugs that interfere with viral
DNA synthesis such as,
ACYCLOVOIR and VIDARABINE
 VARICELA-ZOSTER VIRUS
(Human herpesvirus-3)
• This organism causes both Varicella(chicken pox) and Herpes
Zoster(Shingles) – two different diseases due to an identical
organism.
• Chickenpox is the primary infection, and zoster the reactivation of
illness.
• Chickenpox is one of the commonest childhood exanthemata.
• The virus enters through respiratory route.
• The source of infection is a chickenpox/zoster patient.
• It is a highly infectious disease characterised by vesicular rash
mostly on the trunk.
 CLINICAL DISEASE OF VARICELA-ZOSTER
ZOSTER
• The disease usually affects the adults and the virus is
reactivated despite circulating antibodies.
• Zoster is triggered by trauma, drugs, neoplastic disease
or immunosuppression.
VARICELA • Ramsay Hunt Syndrome is a are manifestation of
zoster,with a vesicular rash.
• After a 2 week incubation period, fever
develops followed by a popular rash of the
skin and mucous membrane, including oral
mucosa
• Rash progress as papule,vesicle,pustle and
scab.
• The rash is centripetal in distribution.
EPIDEMIOLOGY: TREATMENT:
• Shingles is a primarily a disease of • Chickenpox is self-limiting and
older adults and immunocompromised requires symptomatic treatment
persons, rare in children.
• Highly contagious infection in a host
• Disseminated zoster in
not previously exposed to virus. immunocompromised patients
require Antiviral Drugs
• Transmission occurs by direct contact
with skin lesions or droplet infection.

PREVENTION :
• Passive immunization with varicella-zoster immune
globulin may be indicated for persons at high risk of
severe infection.
 EPSTEIN-BARR VIRUS
(Human Herpes virus-4)

• Epstein-Barr virus is widespread in humans, most adults have antibody to

virus
• Latent EBV infection is common in population
• It is the aetiological agent of number of diseases:
1. Infectious Mononucleosis (glandular fever)
2. Burkitts’s lymphoma and other B-cell lymphoma
3. Oral hairy Leucoplakia
4. Nasopharyngeal carcinoma
5. Post-transplant lymphoproliferative diseases.
INFECTIOUS MONONUCLEOSIS
• An acute infection affecting
lymphoid tissue throughout the
body.
• Commonly seen in teenagers
(peak of incidence 15-20 years)
• Organism is present in saliva
and is postulated to be
transmitted during kissing-
hence called ‘Kissing Disease’.
• INCUBATION PERIOD: 4-7
weeks
SIGNS & SYMPTOMS
 HAIRY LEUKOPLAKIA:
• The term ‘hairy leucoplakia’ is
given to rasied,white areas
thickening, particularly on lateral
border of tongue
• Seen in HIV patients & other
immunosuppressed patients

BURKITTS’S
LYMPHOMA:
NASOPHARYNGEAL
• Highly malignant tumour,
CARCINOMA: spreads rapidly with
• A tumour with racial widespread metastases
distribution • Particularly common in
African children.
• Particularly most common
among the southern Chinese • Associated with chronic
co-infections with malaria
 EPIDEMIOLOGY, DIAGNOSIS &
TREATMENT EBV
EPIDEMIOLOGY
• Virus is ubiquitous and
human are only known host.
• Spread of EBV is via
respiratory secretions, oral
contact.
DIAGNOSIS
• Indirect Immunofluorescence is used
to detect specific IgM antibody TREATMENT
• Haematology: a blood film is useful • Infectious
in demonstrating atypical mononucleosis is
generally mild &
lymphocytosis in infectious
self limiting.
mononucleosis. • Hence therapy is
• Heterophile antibody: infectious usually
mononucleosis is characterised by asymptomatic.
appearance of heterophile
antibodies in patient’s serum.
 CYTOMEGALOVIRUS
• Congenital infection
• Symptomless infection
• Route of infection: Sexually transmitted, blood
transfusion, Organ transplantation, mother-child.
• Diagnosis: Cytomegalic cells demonstration,
Tissue culture, antigen detection, PCR, Serology
can done
• Treatment: there is no proven regimens therapy and
prevention for CMV Infections.
 PAPOVAVIRUS
• Non-enveloped
• Double stranded DNA genome
• Cutaneous warts, genital warts, oral papillomatosis,
cervical cancer common diseases.
• Route of infection: sexual contact.
• Diagnosis: virus particles can be seen by electron
microscope, PCR, tissue culture.
 RETROVIRUSES
• These are the RNA Viruses belong to family
Retroviridae.
• Members of this family posses reverse transcriptase
enzyme and this is characteristic feature.
• Enveloped
• Single stranded RNA genome
• 90-12-nm diameter.
• Virus: HUMAN IMMUNODEFICIENCY VIRUS
(HIV)
• Mode of transmission: Sexual contact, Blood
transfusion, Needle stick injury, Perinatal
transmission.
CLINICAL FEATURES
 ORAL MANIFESTATIONS FOR HIV
• Patients with AIDS are at greater risk for
bacterial, viral, fungal infections of mouth.
• Dental caries and Gingivitis may occur.
• ANUG may act as indicator that patient have
AIDS.
• Herpes simplex viral infections may be present
as multiple, deeper, more painful oral lesions
in patients with AIDS.
 LABORATORY DIAGNOSIS
SPECIFIC TESTS NON-SPECIFIC TESTS
i. Antigen detection i. Total and differential leucocyte count
ii. Virus isolation ii. T-lymphocyte subset assays
iii. Detection of viral nucleic acid
iv. Antibody reaction

SCREENING TESTS: SUPPLEMENTAL TESTS

 ELISA  Western blot test
 Rapid tests  Indirect immunofluorescence test
PREVENTIVE & PROPHYLAXIS
Measures recommended;
o All blood and products has to
be screened for HIV
o Safe sexual contact
o Contaminated needles should
not be shared
o Control of infection
o No effective vaccine has yet
been found out.
o Specific treatment with
ART(antiviral therapy) is the
mainstay in management of
HIV
 MEASLES ( Rubeola )
• Caused by Paramyxovirus
• Spread through droplets
• Incubation period ; 10-12 days
• Prodromal symptoms include fever, malaise, runny
nose, conjunctivitis, cough
• Rashes develop & lasts for 4-7 days
• Face is the first sight & rashes spread downwards to
involve trunk & extremities
ORAL MANISFESTATIONS:
• Koplik’s spots
• Multiple areas of mucosal
erythema are visible on buccal &
labial mucosa
TREATMENT:
• MMR Vaccine
• Fluid & antipyretics
• Immunocompromised
patients- Ribavirin,
immunoglobulins etc.,
HEPATITIS VIRUSES
• Viral hepatitis is a systemic disease with
primary inflammation in liver
• Till now 6 hepatitis virus i.e. Hepatitis
A,B,C,D,E,G
• Hepatitis B is DNA Virus while others are
RNA genome
COMPARISION
 FUNGAL INFECTIONS
• Fungi are eukaryotic organisms.
• Obligate or facultative anaerobe.
• They either exists as saprophytes, parasites or commensals.
• Fungi possess rigid cell walls.
• The cytoplasmic membrane contains sterols.
• Cytoplasm contains true nuclei with nuclear membrane,
mitochondria and endoplasmic reticulum.
• Fungi may be unicellular or multicellular.
• They divide by asexually, sexually or by both processes.
 CLASSIFICATION OF FUNGI
YEASTS YEAST LIKE FUNGI MOULDS DIMORPHIC FUNGI

• Round to oval unicellular • They grow partly as yeast • Grow as branching • They exist as yeast in host
fungi, reproduce by and partly as chains of filaments- Hyphae. tissue and in culture at
budding. budding cells forming 37C, and in hyphae forms
pseudohyphae. in soil at 22-25C.

• Example:CRYPTOCOCUS • Example: CANDIDA • Example; ASPERGILLUS, • Example: HISTOPLASMA

NEOFORMANS ALBICANS PENICILLIUM. CAPSULATUM
CLASSIFICATION OF FUNGAL DISEASES
SUPERFICIAL SUBCUTANEOUS SYSTEMIC MYCOSES OPPORTUNISTIC
MYCOSES MYCOSES FUNGI

• Involves skin, hair • Involves subcutaneous • Involves internal • Cause infections in

nail and mucosa. tissue. organs. immunocompromised
• Disease: • Disease: MYCETOMA • Disease: individuals.
DERMATOPHYTOSIS HISTOPLASMOSIS • Disease:
CANDIDIASIS
OPPORTUNISTIC MYCOTIC INFECTIONS
(CANDIDIASIS)
• Caused by yeast like fungus Candida albicans.
• C.albicans is an ovoid/spherical budding yeast cell,
show dimorphism.
• Other names- Moniliasis, Oral thrush.
• Three factors determine candida infection:
a. Immune status of host
b. Oral mucosal environment
c. Strain of C.albicans
 CLINICAL TYPES
1. PSEUDOMEMBRANOUS CANDIDIASIS:
• Most common form also known as THRUSH.
• Presence of white plaques resembling cottage
cheese or curdy white appearance.
• Scrapable masses, underlying base
erythematous.
2. ERYTHEMATOUS CANDIDIASIS: 3. MEDIAL RHOMBOID
GLOSSITIS:
• Don’t show white flecks, Red patch
appearance • Asymptomatic erythematous lesion
• Loss of filiform papillae-bald appearance • Erythema is due to loss of filiform
papillae.
• Antibiotic sore mouth
• Symmetrical lesion
4. ANGULAR CHEILITIS:
• Lesion of corner of mouth.
• Chronic multifocal candidiasis
5. DENTURE STOMATITS:
• Localized to denture bearing areas
• These dentures show heavy
colonization of candida organisms
• Bad denture hygiene
6. CANDIDAL LEUKOPLAKIA:
• Non-scrapable white patch
• Increase epithelial dysplasia
• Speckled leucoplakia
• Usually anterior buccal mucosa
7. MUCO-CUTANEOUS CANDIDIASIS:
• Associated with immunological disorders
• Involves mouth, nails, skin and other
mucosal surfaces
• Oral lesions resembles chronic hyperplastic
candidiasis & cannot be rubbed off easily
 LABORATORY DIAGNOSIS
• PAS preparation of exfoliative cytology
specimen/tissue sections
• KOH preparation
• Culture of organism in Sabouraud’s Agar
• Latest techniques include PCR, ELISA,
Tissue Array
 TREATMENT
• 7 Days of treatment
• Oral symptoms disappears in 2-5 days
• Removal of causative factors; - ill fitting denture,
proper cleaning of denture, withdrawal/change of
antibiotics
• TOPICAL: Amphotericin B , Nystatin,
Clotrimazole
• SYSTEMIC: Ketoconazole, Itraconazole
• LATEST DRUGS: Fluconazole oral rinses
 HISTOPLASMOSIS
• Caused by Histoplasma Capsulatum.
• Most common systemic fungal infection in USA
• Histoplasmosis is endemic in certain geographic
regions of India including Assam, Bihar, Punjab
etc.,
• Dimorphic fungi
• Airborne – spores
• Other name- Darling Disease
 CLINICAL FEATURES
ACUTE HISTOPLASMOSIS CHRONIC DISSEMINATED
HISTOPLASMOSIS HISTOPLASMOSIS
• Self limited pulmonary  Less common • Much less than acute &
infection  Lungs involved chronic forms
• Acute symptoms – fever,  Symptoms: cough, weight • Seen in 2-10% AIDS
anorexia, flu like symptoms loss, chest pain, fever, patients
for 1-2 weeks weakness, fatigue • Organs involved – spleen,
oral mucosa, liver, GIT,
lymph nodes
• Oral lesions appear solitary
ulcers roller borders
DIAGNOSIS:
• Made by histopathological
examination
• Isolation by organism culture
• Serological test
TREATMENT:
• Acute Histoplasmosis: doesn’t
require treatment
• Chronic Histoplasmosis: require
treatment to avoid pulmonary
damage & death-50% recovery
• Disseminated Histoplasmosis: fatal
and kills 90% of people.
Amphotericin B is indicated.
 BLASTOMYCOSIS
• Blastomyces dermatitdis – dimorphic fungi
• M:F = 9:1
• Many case series – Male predilection
• India – Sporadic (Africa, Europe)
• Seen in rich moist soil
• CLINICAL FEATURES: acquired by inhalation of
spores
1. Acute Blastomycosis: resembles pneumonia, high
fever, chest pain
2. Chronic Blastomycosis: more common than acute,
mimics TB, Low grade fever, night sweats, weight loss
HISTOPATHOLOGY: TREATMENT:
• Acute & granulomatous • No treatment required
inflammation around the • Seriously ill
yeast cells • Mild moderate cases –
• Doubly retractile cell Ketoconazole,
wall DIAGNOSIS: Itraconazole
• Broad attachment • Severe ill – I.V
1. Cytologic fixed Amphotericin B
between budding cells &
daughter cells
preparation
2. KOH preparation
3. Culture(sputum) –
Sabouraud’s Agar :
3-4 weeks
 RHINOSPORIDIASIS
• Chronic granulomatous mycosis caused by
RHINOSPORIDIUM SEEBERI
• First described by Seeber in 1990 in patient from
Argentina
• Endemic in India, Srilanka, S.America, Africa
• R.seeberi cannot be grown in artificial culture
medium
SPREAD OF INFECTION:
1. Auto-inoculation
2. Haematogenous spread
CLINICAL SYMPTOMS:
3. Lymphatic spread
• Vascular friable polyps arise from:
- Nasal mucosa, Nasopharynx, Soft palate,
Larynx, Conjunctiva, Ear, genitalia
• Bleed readily
• Painless
• Chronic lesions- persist for several years
RHINOSPORIDIUM DEVELOPMENTAL STAGES
LAB DIAGNOSIS:
• Clinical specimen: - Biopsy from
lesion
- Tissue sections are stained by
H&E stain TREATMENT:
- Sporangia of different stages can • Surgical excision
be observed • Pentavalent antimony
compounds(intravenous)
 CONCLUSION
1. Infection control:
Since these viral and fungal infections are life threatening a
proper infection control is very important in health care
profession.
 Health care professionals, who do not practice proper infection control allow
themselves become susceptible to number of infections.
- Strategy to achieve Infection control;
i. All the patients must be screened
ii. Usage of barriers for personal protection
iii. Careful aseptic techniques
iv. Disposal of contaminated waste safely
 2. Patient Management:

• This is a descriptive of interaction, from intake to completion of treatment which takes place
between the patient & the health care team.
• It includes communication, empathy, examination, evaluation, diagnosis & prognosis, treatment
 REFERENCES
 Textbook of Pedodontics~ Nikhil Marwah
 Textbook of Microbiology for Dental students ~ Dr. C.P Baveja
 Essential Microbiology for Dentistry ~L.P Samaranayake
 Textbook of Microbiology for Dental Students ~ D.R. Arora
 Shafer’s Textbook of Oral Pathology