herpes simplex viral infection - dr sanjana ravindra

Seminar no: 09

Dr Sanjana RavindraOral Medicine and radiologyRajarajeswari Dental CollegeBangalore

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

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

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

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.

https://en.wikipedia.org/wiki/Louis_Pasteur

https://en.wikipedia.org/wiki/Edward_Jenner

https://en.wikipedia.org/wiki/Vaccine

https://en.wikipedia.org/wiki/Dmitry_Ivanovsky

https://en.wikipedia.org/wiki/Tobacco_mosaic_virus

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 Aedesaegyptii 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.

GENERAL

CHARACTERISTICS

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

CAPSIDICOSAHEDRAL (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.

MORPHOLOGY

Structure and Shape

VIRAL PARTICLE

COVERING

CAPSID(protein)


viruses)

INNER CORE




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


MORPHOLOGY

Structure and Shape

VIRAL PARTICLE

COVERING

CAPSID(protein)


viruses)

INNER CORE




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 – VarySusceptible 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 REPLICATION

VIRUS MULTIPLICATION

Adsorption / Attachment

Penetration/Entry

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

Inapparentinfections

(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

ROUTES OF ENTRY

Sexual

Inhalation

Inoculation

BloodOrgan transplant

Ingestion

Congenital / vertical

CLASSIFICATION

AND

NOMENCLATURE

OF VIRUS

ANTIVIRAL

DRUGS

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)

DidanosineStavudine,

Lamivudine

NONNUCLEOSIDE REVERSE TRANSCRIPTASE INHIBITORS (NNRTIS)

NevirapineDelavirdine

PROTEASE INHIBITORSRitonavirIndinavirNelfinavirLopinavir

AmantadineRimantadine

Ribavirin, Lamivudine

AdefovirDipivoxil

Interferon A

Idoxuridine

Acyclovir

Valacyclovir

Famciclovir,

Ganciclovir

Foscarnet

Based on their therapeutic use

HERPES VIRUS

INTRODUCTION

INTRODUCTION

Characterised by ability to establish latent infections, enabling the virus to persist indefinetly within infected

hosts and to undergo periodic reactivation

HISTORY

HISTORYHippocrates 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

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.

CLASSIFICATION

HERPES SIMPLEX

INFECTION

INTRODUCTION

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 mouthTransmitted by direct contact or droplet

spread from cases/carrers

HSV-2 : majority of genital herpes

infectionsTransmitted 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

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.

PATHOPHYSIOLOGY

CLINICAL

FEATURES

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


AP

PE

AR

AN

CE

• Small vesicles- thin walled -surrounded by inflammatory base

• They rupture quickly leaving small, shallow, oval shaped discrete ulcers

SIZ

E

• Individual ulcer : 2-6 mm

• As disease progresses, several lesions may coalesce-forming larger, irregular lesions

BA

SE

• Grayish white or yellow plaque M

AR

GIN

S

• 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

OC

CU

RA

NC

E

Every month in some patients to about once a pear or even less than that

PR

OD

OM

AL

SY

MP

TO

MS

Lesion is preceded by tingling and burning sensation and feeling of tautness, swelling or slight soreness subsequent to development of vesicles

SIG

NS

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 lesionsCNS 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/dayIn acyclovir resistant patient- Foscarnet is advised

COMPLICATIONS

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

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 culturesystems available since they support the widest range of viruses.However, they are very expensive and it is often difficult to obtain areliable supply. Continuous cells are the most easy to handle but therange of viruses supported is often limited.

MicroscopyT

ZA

NC

K S

ME

AR

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

GIE

MS

A-

ST

AIN

ED

SM

EA

RS

Intranuclear type A inclusion bodies

FL

UR

OS

CE

NT

AN

TIB

OD

Y

TE

CH

NIQ

UE

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 vesiculopapularlesions 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


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

Management

Primary herpes simplex infection

Symptomatic

PAIN CONTROL MEASURES

• Topical anesthetics like 2% lidocaine

• 0.1% dicloninehydrochloride

• 0.5% benzocaine hydrocholride

TOPICAL ANTI-INFECTIVE

AGENTS

Given to prevent secondary infection

0.2% chlorhexidinegluconate

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

MIN

IMIZ

ED

OB

VIO

US

T

RIG

GE

R Applying sunscreen lotion to lip

TO

PIC

AL

AN

TIV

IRA

L

ME

DIC

AT

ION

5% acyclovir cream

3% penciclovircream

10% docosanolcream

3-6 times daily

SY

ST

EM

IC A

NT

IVIR

AL

M

ED

ICA

TIO

N

Valacyclovir / Famiclovir(500-1000 mg 3 times daily)

TO

PIC

AL

CA

RB

ON

O

XO

LO

NE

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.

CONCLUSION

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