Oral Medicine Seminar on Herpes Viruses

Seminar no: 09
Dr Sanjana Ravindra
Oral Medicine and radiology
Rajarajeswari Dental College
Bangalore

CONTENTS
VIRUS BASICS
 Introduction
 History
 General Characteristics
 Viral replication
 Pathogenesis
 Routes of entry
 Classification and
Nomenclature
 Antiviral Drugs
HERPES VIRUS
 Introduction
 History
 Morphology
 Classification
HERPES SIMPLEX
VIRUS
 Introduction
 Epidemiology
 Pathophysiology
 Clinical features
 Types
 Complications
 Diagnosis
 Differential Diagnosis
 Management
 Conclusion

TERMINOLOGIES
Lynch MA. Ulcerative, Vesicular, and Bullous Lesions. In: Lynch MA, Brightman VJ, Greenberg MS eds. Burket's Oral Medicine: Diagnosis
and Treatment. 8th ed. USA: JB Lippincott Company; 1984. 50-89
Vesicles. These are elevated blisters containing clear fluid
that are less than 1 cm in diameter
Bullae. These are elevated blisters containing clear fluid
that are greater than 1 cm in diameter
Erosions. These are red lesions often caused by the rupture
of vesicles or bullae or trauma and are generally moist on
the skin
Ulcers. These are well-circumscribed, often depressed
lesions with an epithelial defect that is covered by a fibrin
clot, causing a yellow-white appearance

INTRODUCTION
“Submicroscopic entities which reproduce within the specific
living cells”
. . .
The word virus in Latin refers to poison and other noxious substances.
Norrby E . Nobel Prizes and the emerging virus concept. Arch Virol 2008 153 (6): 1109–23.

HISTORY
Louis Pasteur and Edward Jenner developed the
first vaccines to protect against viral infections he
did not know that viruses existed.
The first evidence of the existence of
viruses came from experiments with filters
that had pores small enough to retain
bacteria.
In 1892, the Russian biologist Dmitry Ivanovsky (1864–
1920) used a Chamberland filter to study what is now
known as the tobacco mosaic virus. His experiments
showed that crushed leaf extracts from infected tobacco
plants remain infectious after filtration.
Oldstone MBA (2009). Viruses, Plagues, and History: Past, Present and Future. Oxford University Press, USA. p. 306.

HISTORY
.
THE FIRST ANIMAL VIRUSES
The second virus discovered was what is now
known as Foot and mouth disease virus
(FMDV) of farm and other animals, in 1898 by the
German scientists Friedrich Loeffler and Paul
Frosch
The FIRST HUMAN VIRUS
described was the agent which
causes yellow fever: this probably
originated in Africa, but was spread
along with its mosquito vector Aedes
aegyptii to the Americas and
neighbouring islands by the slave
trade.
Oldstone MBA (2009). Viruses, Plagues, and History: Past, Present and Future. Oxford University Press, USA. p. 306.

CHARACTERISTICS OF VIRUS
Samaranayake L. Virus and Prions. In: Essential Microbiology. 4th ed. Churchill livingstone.2011.P. 28-68.
Small, obligate, intracellular parasites.
Do not have a cellular organization.
Contain only one type of nucleic acid, either DNA or RNA but never both.
Cannot replicate on their own.
Must infect and take over a host cell in order to replicate.
Lack the enzymes necessary for protien & nucleic acid synthesis.
Multiply by a complex process and not by binary fission.
Unaffected by antibiotics

MORPHOLOGY
Size
• Much smaller than
bacteria
• Filterability: ability to
pass through filters
that can hold back
bacteria – thus known
as filterable virus
• Largest virus : pox
virus - 300nm
• Smallest virus :
parvovirus – 20nm
William Boyd A Textbook of Pathology- Structure and Function in Disease; 8th edition.

MORPHOLOGY
Structure and Shape
VIRAL
PARTICLE
COVERING
CAPSID(protein)
ENVELOPE (not
found in all
viruses)
INNER CORE
NUCLEIC ACID-
DNA/RNA
VARIOUS
PROTEINS
(enzymes)
Cann A.J. Particles. In: Principles of Molecular Virology. 4th ed. Elsevier Saunders, USA. 2005.

MORPHOLOGY
Structure and Shape
CAPSID
Virion consists of
mainly nucleic acid
surrounded by a
protein coat

MORPHOLOGY
Structure and Shape
CAPSID
Protect the nucleic acid
from inactivation by
nucleases and other
deleterious agents in the
environment
Introduce the viral genome
into host cells by adsorbing
readily to cell surface
FUNCTION

MORPHOLOGYStructure and Shape
CAPSID
ICOSAHEDRAL (CUBICAL)
Icosahedral  polygon with 12 vertices (corners), 20
facets (Sides)
Each facet is in shape of a equilateral triangle
Capsomeres in icosahedral symmetry are of two types
Pentagonal capsomeres at the vertices
Hexagonal capsomeres in the facets
HELICAL
Nucleic acid and capsomeres are wound together to form
a Helical tube
Rod like with capsid proteins winding around the core in
a spiral
COMPLEX
Polyhedral capsid attached to a helical tail.
Eg: Pox virus
.
.
.
Kapil A. Virology. In: Ananthanarayan and Paniker’s Textbook of Microbiology. 9th ed. United press, Hyderabad. P. 427-588.

MORPHOLOGYStructure and Shape
ENVELOPE
Enveloped
virus Non enveloped
( Naked Virus)
 Derived from host cell while budding
 Made up of lipoproteins
 Lipid from host + protein coded by virus
 Protein subunits projecting from the surface 
Peplomers
 Virus may carry more than one type of peplomers
 E.g – Influenza virus
 Triangular spike – Haemagglutinin spike
 Mushroom shaped structure –
Neuraminidase
 Envelope : Chemical , Antigenic & Biological
properties

ENVELOPE
Structure and Shape MORPHOLOGY

Chemical properties
NUCLEIC ACID
PROTEINS
LIPIDS

Resistance
Mostly heat labile
• Destroyed in seconds
@56°C
• Destroyed in minutes
@37°C
• Destroyed in days
@4°C
Stable at lower
temperatures
For long term
storage  store at
– 70°C
Better method –
Lyophilization/
freeze drying
Bordenave G . "Louis Pasteur (1822–1895)". Microbes and Infection / Institut Pasteur. 20035 (6): 553–60.

Resistance to acids – Vary
Susceptible to alkaline
conditions
Inactivated by Sunlight, UV
rays and ionizing radiation
More resistant to chemical
disinfectants – Some of
them act as preservatives
for virus
Killed by oxidizing agents
• Hydrogen peroxide
• Potassium permagnate
• hypochlorites
Formaldehyde & BPL are
actively virucidal
Ether, chloroform (Lipid
solvents) active on
enveloped viruses
Resistance
Bordenave G . "Louis Pasteur (1822–1895)". Microbes and Infection / Institut Pasteur. 20035 (6): 553–60.

VIRUS MULTIPLICATION
Adsorption /
Attachment
Penetration/Ent
ry
Replication
Assembly
Release

 Contact by random collision but
adsorption takes place only if
there is affinity between the two
 Cell surface contain specific
receptors for attachment of virus
ATTACHMENT/ADSORPTION PENETRATION/ ENTRY
• Bacteria have thick cell wall ,
viruses cannot penetrate so , only
nucleic acid is introduced
• Animal cells do not have rigid cell
walls so the whole virus gets in

 Virus DNA/RNA uses
ribosomes to make virus
proteins
 Virus proteins created by
transcription/ translation
REPLICATION ASSEMBLY
New virus proteins are
assembled in the cytoplasm

 Virus enzyme causes
cell membrane to
lyse (burst)
 Viruses are released
 Cycle repeats
RELEASE

Attachment
Entry
Replication
& Assembly
Release

PATHOGENESIS
OF VIRAL
INFECTION

PATHOGENESIS OF VIRAL INFECTION
Inapparent
infections
(subclinical)
Apparent (clinical)
infections which
may be acute,
subacute or chronic
Latent infections –
Recurrent, Persistent
RECURRENT
Clinical manifestations appear
after prolonged periods of
quiescence during which the
viruses remain hidden in the
nerve root ganglion
PERSISTENT
Occurs when the virus is
readily demonstrable in the
tissues of the host but neither
disease nor immune response
develops
Virus latency (or viral
latency) is the ability of a
pathogenic virus to lie
dormant (latent) within a
cell, denoted as the
lysogenic part of the viral
life cycle.
Latent viral infection is a type of persistent
viral infection which is distinguished from a
chronic viral infection.

ROUTES OF ENTRY
Sexual
Inhalation
Inoculation
Blood
Organ transplant
Ingestion
Congenital / vertical

CLASSIFICATION
AND
NOMENCLATURE
OF VIRUS

Either block viral entry into or
exit from the cell or be active
inside the host cell
Inhibit virus specific directed
nuclei rather than host cell
directed nucleic acid
Optimal efficacy- used as
prophylactic
Drugs can potentially target in the replication steps, so antiviral
drugs have to be specific for different viral mechanisms.
ANTIVIRAL DRUGS

NUCLEOSIDE REVERSE
TRANSCRIPTASE INHIBITORS
(NRTIS)
Zidovudine (AZT)
Didanosine
Stavudine,
Lamivudine
NONNUCLEOSIDE REVERSE
TRANSCRIPTASE INHIBITORS (NNRTIS)
Nevirapine
Delavirdine
PROTEASE INHIBITORS
Ritonavir
Indinavir
Nelfinavir
Lopinavir
Amantadine
Rimantadine
Ribavirin,
Lamivudine
Adefovir
Dipivoxil
Interferon A
Idoxuridine
Acyclovir
Valacyclovir
Famciclovir,
Ganciclovir
Foscarnet
Based on their
therapeutic use

INTRODUCTION
Characterised by ability to establish
latent infections, enabling the virus
to persist indefinetly within infected
hosts and to undergo periodic
reactivation

HISTORY
Hippocrates is known to have described the cutaneous
spreading of herpes simplex lesions
Scholars of greek civilization define the greek word "herpes"
to mean "to creep or crawl" in reference the spreading nature
of the herpetic skin lesions
1919- lowenstein confirmed experimentally the infectious
nature of HSV that shakespeare had only suspected.(It is
believed that shakespeare mentioned oral herpes in romeo and
juliet)
1920-1930: found that HSV not only infects the skin, but also
the central nervous system.
1930: the property of HSV - latency
More recent research has focused on antiviral research,
differences between HSV strains, and using HSV vectors for
use in vaccines.

MORPHOLOGY
The herpes virus capsid is
icosahedral, composed of
162 capsomere and
enclosing the core of linear
double stranded DNA
genome.
The envelope carries surface
spikes about 8nm long
Between envelope and the
capsid is an amorphous
structure called the
tegument, containing
several proteins.

Herpes Simplex Virus (HSV) Infection
• Human Simplex
Virus occurs naturally
only in humans
• Can produce
experimental
infection in many lab
animals
HSV-1 : usually located from lesions
in and around the mouth
Transmitted by direct contact or droplet
spread from cases/carrers
HSV-2 : majority of genital herpes
infections
Transmitted venereally
As a general rule,
HSV1 produces ‘above the waist’ and HSV2 ‘below the waist’

Primary infection
acquired in early childhood : 2-5 years of
age
Hosts - Humans
Source of infection: Saliva, Skin lesions or
Respiratory secretions

EPIDEMIOLOGY
 HSV has a worldwide distribution and is endemic in all human population groups
examined.
 The rate of infection and the timing of primary infection differs for hsv-1 and hsv-2,
reflecting the differences in the major modes of transmission of the two viruses.
 Overall prevalence of hsv-1 rates of 70% or lower are often reported among 30–40 year-
old adults
 The frequency of HSV-2 infection (up to 60%) is higher than that observed in HSV-1
 A single recurrence of ophthalmic infection is observed in 20–30% of atients within 2
years of the first infection
 The rate of recurrence is believed to be slightly higher in men than in women, with
rates of up to 2.7 and 1.9 episodes per 100 patient-days, respectively.

CLINICAL FEATURES
Cutaneous infections
Cheeks
Chin
Around the
mouth
Forehead
buttocks in
infants
(napkin
rash)
Typical lesion – ‘fever blister’
or ‘herpes febrilis’
(caused by viral reactivation
in febrile patients)
In some sensitive persons,
very minor stimuli, like the
common cold, exposure to
sun or stress
Eczema
herpeticum:
Generalized
eruption caused
by herpes infection
in children
suffering from
eczema

Herpetic whitlows, can infect patients and have led to
outbreaks of infection in hospitals and among patients in
dental practices.
Now that gloves are universally worn when giving dental
treatment, such cross-infections should no longer
happen.
In immunodeficient patients, such infections can be
dangerous but aciclovir has dramatically improved the
prognosis in such cases and may be given on suspicion.
Mothers applying antiherpetic drugs to children's lesions
should wear gloves.
HERPETIC CROSS-INFECTIONS
Herpetic whitlow
Cutaneous infections

CLINICAL FEATURES
Mucosal infections
Buccal mucosa is most commonly
affected site followed by hard
palate, gingiva, dorsum surface of
tongue
Acute gingivostomatitis is a
selflimiting disease and resolution
begins abruptly. The lesions
become painless and inflammation
subsides.
In young children the skin around
the mouth is frequently involved
Hard palate Attached
gingiva
Tongue

GENITAL
In men, the lesions occur mainly on the urethra causing
urethritis
In women, the cervix, vagina, vulva and perineum are affected
When only cervix is involved, the infection is usually
asymptomatic
The primary infection is usually more serious, accompanied
by systemic features like fever and malaise
Both types of HSV may cause genital lesions, though
HSV2 is responsible more frequently and causes more
recurrences

PRIMARY HERPES SIMPLEX INFECTION
 Acute herpetic gingivo-stomatitis
 Herpes labialis
 Fever blister
 Cold sore
 Infectious stomatitis
Occurs in patients with HSV-1
HSV reaches nerve ganglion supplying the affected area, along
nerve pathways and remains latent until reactivated
Usual ganglion involved – trigeminal for HSV-1 and lumbosacral
for HSV-2

Primary Herpes Simplex Infection
AGE
Develops in both, children and young adults
INCUBATION PERIOD
5-7 days
PRODORMAL SYMPTOMS
Precede local lesion by 1 to 2 days and includes fever, headache,
malaise, nausea, vomiting and subsequently painful
Irritability, pain upon swallowing and regional lymphadenopathy Hard palate Attached
gingiva
Tongue Skin
LOCATION

APPEARANCE
• Small
vesicles- thin
walled -
surrounded
by
inflammatory
base
• They rupture
quickly
leaving small,
shallow, oval
shaped
discrete ulcers
SIZE
• Individual
ulcer : 2-6
mm
• As disease
progresses,
several lesions
may coalesce-
forming
larger,
irregular
lesions
BASE
• Grayish white
or yellow
plaque
MARGINS
• Uneven and
are
accentuated
by bright red
rimmed, well
demarcated,
inflammatory
halos

LIPS: In severe cases, excoriation
involving the lips may become
hemorrhagic and matted with
serosanguinous fibrin- like exudate and
parting of the lips during mastication
and speech may become difficult
ACUTE MARGINAL GINGIVITIS : entire
gingiva is edematous and swollen
Small gingival ulcers are seen
PHARYNX: inflammation causing
difficulty in swallowing
LYMPH NODES: cervical and
submandibular
HEALING: self limiting- begin healing 7-10 days- leave no scar

Histopathological Findings
Lipschutz bodies,
Presence of multinucleated
gaint cells, ballooning
degeneration of cells.

Recurrent or Secondary Herpes Simplex Infection
Herpes Simplex Virus may be latent in epithelium-
main cause
HSV reactivated at the latent site it moves
centrally to the mucosa
When reactivation is triggered, they spread along
the nerves to different sites on the oral mucosa and
skin
Destroy the epithelial cells and induce the typical
inflammatory response

TYPES
Recurrent
Herpes Labialis
Recurrent
intraoral herpes
simplex infection

SURGERY
• Which involve trigeminal ganglion, recurrent infections with herpes can occur
(since herpes remains latent in T.ganglion)
IMMUNITY
• Low serum IgA, decreased cell mediated immunity, decreased anti-herpes activity
and depression of Antibody dependent cellular cytotoxicity and interleukin-2
caused by prostaglandin release in skin can precipitate the attack
TRAUMA
• Trauma to lips, dental extraction
INFECTION
• Upper respiratory tract infection can trigger the herpes infection
OTHERS
• Fever, emotional upset, sunburns, fatigue, menstruation, pregnancy and allergy
may precipitate
Precipitating Factor

Clinical Features
OCCURANCE
Every month in
some patients to
about once a pear
or even less than
that
PRODOMALSYMPTOMS
Lesion is
preceded by
tingling and
burning
sensation and
feeling of
tautness, swelling
or slight soreness
subsequent to
development of
vesicles
SIGNS
Edema at the site
of lesion,
followed by
formation of
clusters of small
vesicles

Clinical Features
RECURRENT HERPES LABIALIS
These gray or white vesicles rupture
quickly leaving small red ulcerations
Slightly erythematous halo on lip covered
by brownish crust on lips
Sizes: 1-3mm to 1-2 cm
Sometimes large enough to cause
disfigurement
RECURRENT INTRAORAL HERPES
Vesicles break rapidly to form small red
ulcerations, sometimes erythematous
halo
Size: 1-2 mm in diameter
Site: gingivae, tongue, palate and
alveolar region

Clinical Features
COMPLICATIONS:
Extra-genital lesions
CNS complications
Vaginal fungal super
infections
HEALING:
within 7-10
days and leaves
no scars

Herpes Simplex Virus in Immunocompromised Patient
Appears mainly as herpes labialis and recurrent intraoral herpes
HERPES LABIALIS:
vesicles on an
erythematous base that
heals within 7-10 days
RECURRENT
INTRAORAL HERPES:
more widespread as
compared to lesions in
non HIV patients
TREATMENT: systemic acyclovir 30mg/kg/day
In acyclovir resistant patient- Foscarnet is advised

HERPES AND PREGNANCY
Pregnant women who are infected with
either herpes simplex virus 2 (HSV-2) or
herpes simplex virus 1 (HSV-1)
genital herpes have a higher risk for
miscarriage, premature labor, retarded
fetal growth, or transmission of the
herpes infection to the infant while in the
uterus or at the time of delivery.
Herpes in newborn babies (neonatals) can
be a very serious condition.

The reported incidence of neonatal herpes varies from extremes of 1 case in 2500 live births
(Alabama, USA; Whitley, 1993) to 1.65 per 100 000 live births reported in a UK survey (Tookey
and Peckham, 1996).
Most commonly, infection is acquired during
passage through an infected birth canal and
disease is evident 3–21 days (mean 12 days) post-
delivery.
Infection can also occur as a result of
transmission of oral herpes from the mother, her
relatives or hospital staff in the immediate post-
delivery period.
In this situation disease may appear up to 28
days post-partum.
NEONATAL HERPES
Symptoms at presentation
can range from the very
severe, associated with high
mortality, to the relatively
mild, which nonetheless can
be a cause of significant
residual morbidity

OPHTHALMIC
The normal course of the disease is 3 weeks but if ulcers are large, healing can be slow.
Mild systemic disturbances, blepharitis and circumocular herpetic dermatitis are commonly
present during the primary infection.
Most common cause of corneal
blindness
There are several forms of
recurrent ophthalmic infection
that may occur in combination.
Dendritic or larger ‘geographic’
ulcers are usually the first
manifestation of recurrence,
with the patient complaining of
ocular irritation, lacrimation,
photophobia and sometimes
blurring of vision.
Infection is usually confined to
the superficial layers of the
cornea and stromal
involvement is absent or only
relatively mild
Days or weeks after the
recurrent infection, the corneal
epithelium may ulcerate to
form a nondescript ovoid ulcer,
known as post-infectious or
metaherpetic keratitis
The early symptoms of herpes
keratitis are of a unilateral or
bilateral conjunctivitis, with
pre-auricular
lymphadenopathy.
Acute keratoconjunctivitis may
occur by itself or by extension
from facial herpes
Acute retinal necrosis caused
by HSV-1, or less commonly by
HSV-2, is a severe ocular
inflammatory syndrome
associated with a poor (visual)
prognosis.

Ophthalmic disease associated
with intrauterine and neonatal
infection with HSV can present
as keratoconjunctivitis or later
as chorioretinitis.

VISCERAL
HSV esophagitis may
cause dysphagia,
substernal pain and
weight loss
It may involve the
respiratory tract, causing
tracheobronchitis and
pneumonitis

NERVOUS SYSTEM
HSV
encephalitis HSV
meningitis
HSV encephalitis –
rare – is most
common sporadic
acute viral
encephalitis in most
parts of the world
It has an acute onset,
with fever and focal
neurological
symptoms
HSV meningitis is a self limiting disease,
usually resolving in about a week
HSV can cause sacral
autonomic dysfunction
and also rarely transverse
myelitis or the Guillian-
Barre syndrome
HSV has been implicated in the causation of Bell’s palsy

Herpes Simplex Dermatitis; Zosteriform Herpes Simplex; Herpes
Gladiatorum
HERPETIC
DERMATITIS is a
complication of primary
infection. Perioral or
periorbital herpes simplex
regularly accompanies
more severe primary
gingivostomatitis or
primary/initial herpes
keratitis.
A distinct form of
cutaneous infection,
‘ZOSTERIFORM
HERPES simplex’, is an
infrequent presentation of
herpes simplex but is
recognised when the
distribution of HSV
lesions accords with a
dermatome and otherwise
resembles zoster.
HERPES
GLADIATORUM and
‘scrum pox’ are conditions
spread among wrestlers
through bites or ‘mat
burns’, and among rugby
players through bites and
facial scraping. The
appearance of herpetic
vesicles at ‘unusual’ sites
can sometimes be
explained by an inquiry
into the individual’s
athletic pursuits!

DIAGNOSIS
History
Typical C/F
Microscopy
Serology
Virus isolation

DIAGNOSIS
Negative past history of recurrent
herpes labialis and a positive history
of close contact with a patient with
primary or recurrent HSV
Generalised symptoms followed by
eruption of oral vesicles and acute
marginal gingivitis and does not
have history of recurrent herpes
HISTORY TYPICAL CLINICAL FEATURES
Serological methods are useful in
diagnosis of primary infection
Antibodies developed within a few
days of infection and rise in titre of
antibodies may be demonstrated by
ELISA, neutralisation or
complement fixation test
In recurrent or re-infection herpes,
there may be little change in titre
SEROLOGY

VIRUS ISOLATION
1. Primary cells - Monkey Kidney
2. Semi-continuous cells - Human embryonic kidney and skin
fibroblasts
3. Continuous cells - HeLa, Vero, Hep2, LLC-MK2, MDCK
Primary cell culture are widely acknowledged as the best cell culture
systems available since they support the widest range of viruses.
However, they are very expensive and it is often difficult to obtain a
reliable supply. Continuous cells are the most easy to handle but the
range of viruses supported is often limited.

Microscopy
TZANCKSMEAR
Smears are taken from
base of vesicle
Stained with 1% aqueous
solution of toluidine blue
– 15 sec
Multinucleated gaint cells
with faceted nuclei and
homogeneously stained
‘ground glass’ chromatin
“Tzanck cells” constitute
positive smear
GIEMSA-STAINEDSMEARS
Intranuclear type A
inclusion bodies
FLUROSCENTANTIBODY
TECHNIQUE
Fluorescent
antibody test
on brain
biopsy
specimen
provides
reliable and
speedy
diagnosis in
encephalitis

Differential Diagnosis
RECURRENT HERPES SIMPLEX
INFECTION
HERPES ZOSTER
Prodomal symptoms: tension,
burning, itching
Prodomal symptoms: fatigue,
hyperesthesia, pain
Development: vesiculoerosive lesion in
crops and clusters, but not limited to
dermatome
Development: edema and erythema,
papulovesicular then vesiculopapular
lesions and erosions
Crosses midline Does not crosses midline
Moderate pain Severe pain
Fast healing without any consequences Longer course- post zoster neuralgia
Recurrent appearances No recurrences

Differential Diagnosis
HAND- FOOT AND MOUTH
DISEASE
Not clustered
Gingiva is not affected
Prominently seen on feet and hand
HERPANGINA
Oropharyngeal and soft palate
involvement is more prominent
Affects children in late summar and
early monsoon
CHRONIC RECURRING APHTHAE
No stomatitis
No general systemic symptoms and
lesions
Less numerous
More often seen in adults

Management
Primary herpes simplex infection
Symptomatic
PAIN CONTROL
MEASURES
• Topical
anesthetics like
2% lidocaine
• 0.1% diclonine
hydrochloride
• 0.5% benzocaine
hydrocholride
TOPICAL ANTI-
INFECTIVE
AGENTS
Given to prevent
secondary infection
0.2% chlorhexidine
gluconate
Tetracycline
mouthwash /
diphenylhydramine
SUPPORTIVE CARE
• Fluid is given to
maintain proper
hydration and
electrolyte
balance
• Antipyretics can
be given to
control fever
GOOD ORAL
HYGIENE
To avoid any
secondary infection

Management
Primary herpes simplex infection
Specific
ACYCLOVIR
• It inhibits DNA
replication in HSV
infected cells reducing
the duration of illness
but with few side-effects
• 1000-1600 mg daily for 7-
10 days
• 15mg/kg 5 times a day
VALACYCLOVIR
• Prodrug of acyclovir
• Better biocompatibility
than acyclovir
• Should be used in
combination with
famicyclovir

Management
Recurrent Herpes Simplex Infection
MINIMIZEDOBVIOUS
TRIGGER
Applying
sunscreen lotion
to lip
TOPICALANTIVIRAL
MEDICATION
5% acyclovir
cream
3% penciclovir
cream
10% docosanol
cream
3-6 times daily
SYSTEMICANTIVIRAL
MEDICATION
Valacyclovir /
Famiclovir(500-
1000 mg 3 times
daily)
TOPICALCARBON
OXOLONE
In herpetic
gingivostomatitis

Management
Herpes Simplex Infection in Immunocompromised patients
The primary pathogen for herpes encephalitis and herpes pneumonitis is HSV-1
For patients undergoing hematopoietic stem cell transplantation, antiviral therapy
at suppressive doses should be initiated for all patients who are HSV seropositive.
A cyclovir and valacyclovir suppress HSV reactivation in such patients.
Acyclovir-resistant HSV is most frequently seen in this group of patients, where
the virally derived thymidine kinase that activates acyclovir is mutated.
In such cases, foscarnet is the drug of choice.
The dosage of the acyclovir family of drugs should be adjusted for age and renal
health.

1. Oldstone MBA (2009). Viruses, Plagues, and History: Past, Present and Future. Oxford University Press,
USA. p. 306.
2. Norrby E (2008). "Nobel Prizes and the emerging virus concept". Archives of Virology. 153 (6): 1109–
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