Herpes simplex

Fever blister
Cold sores
herpetic gingivostomatitis
Herpetic stomatitis

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 Introduction
• Acute infectious disease
• Most common viral disease (except common cold)
• Affected tissue are derived from ectoderm:
 Skin; Mucous membrane; Eyes; CNS

Incubation period: 1 – 26 days

Two types of Herpes Simplex Virus:
• HSV 1- predominantly affects upper half of body
• HSV 2- predominantly affects lower half of body
• Transmission by close contact

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Classification of Herpes Simplex Virus Infection

Primary infection
• Infection in persons not having antibodies
• People with no exposure to virus

Recurrent/secondary infection
• Infection in persons having antibodies
• People already exposed to virus
• Reactivation of dormant virus

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 Pathogenesis
Primary infection
• Entry of virus through abraded skin and mucous membrane
• Replication of virus in the epidermal cells
• Lysis of cells and formation of vesicles
• It enters into sensory, autonomic nerve endings and remains
latent in ganglia.
Recurrent infection
• Virus replicates
• Virus spreads to skin and mucosal surfaces by centrifugal
distribution of virions through peripheral nerves.
• The spread involves wider and larger surface area.

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 Precipitating factors
Sunshine
Fever
GIT upset
Trauma
Allergy
Stress
Types of herpes simplex infection
• Herpes genitalis
• Herpes meningoencephelitis
• Herpes conjuctivitis
• Disseminated herpes simplex of the new born
• Herpetic whitlow- occurs in finger due to auto-inoculation
• Herpes gladiataram- occurs in wrestlers

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Herpetic stomatitis

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 Primary herpetic stomatitis
Clinical features:
• Affects children and young adults
• Stomatitis, Fever, Irritability, Headache, Pain on swallowing
• Regional lymphadenopathy
• Gingiva is edematous and erythematous
• Yellowish fluid-filled vesicles develop
• They rupture and form shallow, ragged extremely painful
ulcers covered by a grey membrane and surrounded by an
erythematous halo.
• The ulcers vary considerable in size, ranging from very tiny
lesions to several centimeters.
• They heal spontaneously within 7-14 days and leave no scar.

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 Recurrent herpetic stomatitis
• The HSV once entered in to the body, resides dormant in the regional
ganglia, and when reactivation is triggered, spread along the nerves to sites
on oral mucosa and skin where they destroy the epithelial cells and induce
the typical inflammatory response with the characteristic lesions of
recurrent infection.

• Lesions may develop at site of primary inoculation or in the adjacent area

supplied by the involved ganglia.
• Lesions are preceded by a burning or tingling sensation and a feeling of
tautness.
• The vesicles subsequently formed.
• These vesicles are generally small (1 mm or less in diameter)
• They occur in localized clusters.
• May coalesce to form larger lesions.

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 Histologic features
• The herpetic vesicle is an intra-epithelial blister filled with
fluid.
• Ballooning degeneration- The infected cells are swollen and
have pale eosinophillic cytoplasm and large vesicular nuclei.
• Lipschutz bodies- intranuclear inclusion bodies. They are
eosinophilic, ovoid, homogeneous structures within the
nucleus.
• They push the nucleolus and nuclear chromatin peripherally.
• The connective tissue is usually infiltrated by inflammatory
cells.

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 Diagnosis
• Case history
• Clinical features
• Scraping of cells from base of the lesion, stained with Wright’s
stain, Geimsa stain, PAP stain. Slide shows balloon
degeneration, multinucleated giant cells, intranuclear
inclusions.
• Tissue culture tests
• Serological tests
• PCR

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 Treatment

• Hydration
• Analgesic mouthwash
• Antiviral drugs
• Antibiotic therapy for secondary infections
• NSAIDS and topical anesthetics for pain.

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 Measles
Rubeola
Acute, contagious viral infection
Primarily affecting children
Occurs many times as an epidemic

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 Etiology
• Paramyxovirus
• RNA virus
• Spread of the disease occurs by direct contact with an
affected person or by droplet infection
• The portal of entry being the respiratory tract

Pathogenesis
• Once entering the respiratory epithelium
• It reaches reticuloendothelial system through blood stream
and thereby infect skin, respiratory tract and other organs.
• Viremia develops

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 Clinical features
• Incubation period of 8 – 10 days
• Onset of fever.
• Malaise
• Cough
• Conjuntivitis, photophobia, lacrimation
• Skin eruptions
• Begin on face, in the hair line and behind ear
• Spread to neck, chest, back and extremities
• They appear as tiny red macules or papules
• They may coalesce to become larger lesions which blanch on
pressure
• They fade away in 4-5 days

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 Oral manifestations
• Oral lesions are prodromal (occur before the skin lesions)
• They occur 2-3 days before the cutaneous rash
• The intra oral lesions are called Koplik’s spots

Koplik’s spots

• Generally occur on buccal mucosa

• They are small, irregular bluish white specks with a bright red
margin.
• The macular lesions increase in number and may coalesce
• The spots disappear after the onset of rash.

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 Histologic features
• Pathognomic multinucleated giant cells called Warthin
Finkildey giant cells.

Complications

• Bronchial pneumonia
• Encephalitis
• Otitis media
• Noma
• Delay in wound healing

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 Vaccination

• Measles is seldom given as individual vaccine nowadays and is

often given in combination with mumps and rubella.
• Mumps Measles Rubella vaccine, live attenuated (MMR)

• Age of vaccination is 9 months

• Second dose at 15-18 months.

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 Small pox
• Acute viral disease
History
• Was epidemic in nature
• Caused millions of deaths
• 4,00,000 people died every year in Europe in 18th century
• In 1967 WHO initiated a program to eradicate small pox
On 9 / 12 / 1979, WHO declared
 Small pox eradication has been achieved
 There is no evidence that small pox will return as an endemic
disease
• Small pox vaccine was the first successful vaccine developed.
• Introduced by Edward Jenner

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 Clinical features
Caused by pox virus
Incubation period of 7-10 days
• High fever, chills
• Nausea, Vomiting, Headache
• The patient is extremely ill and may become comatose during this
period.
• Skin lesions begin as small macules and papules
• They appear first on face and rapidly spread to cover whole body
• In few days papules develop into vesicles which become pustular.
• Pustules are small, elevated and yellowish green with inflamed
border
• They become secondarily infected and heamorrhagic
• Healing phase begins with desquamation

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 Chicken pox
(Varicella)
• Acute, extremely contagious infection
• More common in winters and springs
• The disease results in a characteristic skin rash that
forms small, itchy blisters, which eventually scab over.
• Chicken pox is a primary lesion and a reactivated lesion is
known as herpes zoster.
Etiology
• Varicella zoster virus Incubation period 2 weeks
• DNA virus
• Mode of transmission- airborne droplets or direct contact
with infected lesions.

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 Clinical features
• Headache, Nasopharyngitis, Anorexia
• Maculopapular or vesicular eruptions of skin
• Fever
• These eruptions begin on trunk and spread to involve face
and extremities.
• The lesions of the skin eventually rupture, form a superficial
crust and heal by desquamation.
• The disease lasts for 7-10 days.
• Seldom leaving after effects

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 Complications
• Encephalitis
• Guillain – Barre syndrome
• Reye’s syndrome
• Pheumonia
• Myocarditis
• Nephritis
• Arthritis
Treatment
• Sponge bath with warm water
• Antipyretics
• Anti-viral for severe cases

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 Herpes zoster
(Shingles)

• Acute infectious viral disease

• Extremely painful
• Inflammation of dorsal root ganglia, or cranial root ganglia
• Associated with vesicular eruptions of skin supplied by the
affected sensory nerve

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 Etiology
• Varicella zoster virus
• Same which causes chicken pox
• It caused by reactivation of the latent varicella zoster virus
which has been acquired during previous attack of chicken
pox.
• It is not a primary exogenous infection
Triggering factors
• Trauma
• Malignancy
• X-ray radiation
• Immunosuppressive therapy
• Immuno-compromised patients

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 Clinical features
• More common in adults
• Fever
• Malaise
• Pain and tenderness along the course of the involved sensory
nerve, usually unilateral.
• Often the trunk is involved
• Within few days patient has linear papules or vesicular
eruptions of the skin supplied by the affected nerve

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 Oral manifestations
• Herpes zoster that involve the face by infection of trigeminal nerve
• Extremely painful vesicles
• They generally rupture to leave an area of erosion
• Typically the lesions will extend up to the midline and abruptly stop.

James Ramsey Hunt syndrome

• Herpes zoster infection of the geniculate ganglion, with the
involvement of external ear and oral mucosa.

Clinical features:
• Facial paralysis
• Ear pain
• Hoarseness of voice
• Vesicular eruptions in the oral cavity
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 Mumps
(Epidemic parotitis)

• Acute contagious viral infection

• Characterized by unilateral or bilateral salivary gland swelling
(usually parotid)

Etiology

• Paramyxovirus
Incubation period of 2-3 weeks
• Transmitted through respiratory route

• Once infected a person develops a life long immunity

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 Pathogenesis

Transmitted through droplets

• Virus replicates in respiratory epithelium
• It spreads to local lymph nodes and develops viremia
• The affected area shows inflammatory infiltrate with edema
• Necrosis of acini and epithelial duct is seen in salivary glands

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 Clinical features
• Headache; Chills; Fever; Vomiting; Pain below ear
Followed by:
• Firm rubbery swelling of salivary glands causing elevation
of ear
• Salivary gland involvement causes pain in mastication
• Pain and tenderness may be severe
• The swelling rapidly enlarges, reaches its maximum in 3
days, stabilizes for 2-3 days then gradually subsides.
• Submandibular and sublingual salivary glands may also
be involved.
• Papilla of the opening of parotid gland may be puffy and
reddened.

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 Vaccination

• Mumps Measles Rubella vaccine, live attenuated (MMR)

• Age of vaccination is 9 months

• Second dose at 15-18 months.

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HIV

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 Introduction
• AIDS, the acquired immuno-deficiency syndrome is a fatal
illness caused by a retrovirus known as the human immuno-
deficiency virus (HIV) which breaks down the body’s immune
system.

• Person get infected for life

• The term AIDS refers only to the last stage of the HIV
infection.
• Recognized as an emerging disease only in the early 1980.

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 Structure
• Icosahedral structure
• two copies of positive single-stranded RNA
• It has 2 major envelop proteins:
 External gp120
 Transmembrane gp41
• Viral protein p25
• Nucleocapsid proteins p7
• Core protein p17 found outside viral nucleoid and forms the
matrix of the virion.
• GP-41 and GP-120 make a snug attachment on CD4 receptors.
• CD4 receptors are present on T4 lymphocytes.

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 Modes of transmission
1. Sexual intercourse.
2. HIV-infected mother to fetus/infant before, during or after
birth.
3. Blood, blood products, transplanted organs or tissues, use
of syringes or needles infected with HIV positive blood are
all likely to transmit HIV.

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 Viral replication

1) The HIV has a special affinity for cells which bear CD4
receptors. The gp120 of the HIV binds to the CD4 receptors.
2) The virus gains entry into the T4 cell by action of the HIV
protease.
3) The viral RNA changes to viral DNA by reverse transcription.
4) The viral DNA enters the host cell nucleus and gets integrated
into the host DNA by action of integrase.
5) The host is forced to code for the viral proteins and viral
assembly takes place within the T4 cell. The new virions bud
out of the T4 cell to attack a new host.

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• HIV infects macrophages and lymphocytes (they possess CD 4
receptor site).
• With in a few days virus migrates to regional lymph nodes and then
enters the circulation system.
• This results in widespread dissemination – primary HIV syndrome
or seroconversion syndrome.

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 Pathophysiology
• After infection there is a rapid rise in viremia.
1. Initial infection
Acute illness-

• General mild illness; Fever; Sore throat; Rash

• Some may remain asymptomatic
• The acute symptoms last for few days to more than 10 weeks.
• The severity and duration of illness may have prognostic
implications. Severe and prolonged symptoms are correlated with
rapid disease progression.
• After the initial rise there is a marked reduction from the peak
viremia to a steady state level of viral replication.
• The decrease in the viral load is due to immune response that limit
viral replication.

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• Within 6-12 weeks, antibodies to HIV are detectable in the
blood.
• At this stage patients are confirmed as HIV positive.
• Window period - HIV antibodies usually take about 2 – 12
weeks to appear in the blood stream.
• During this period the person tests negative for standard
antibody test for HIV.
• The window period is the time between initial HIV infection
and the time when the body has produced enough HIV
antibodies to e detected by an HIV antibody test.

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2. Asymptomatic carrier state – CD4 count >500/cu.mm.
• Following infection, the virus often enters a dormant stage
lasting for 2-15 years.
• Patients develop antibodies, but no overt signs of disease
except persistent generalised lymphadenopathy.
• It may lasts for few months to 10 years.
3. AIDS related complex CD4 count 200-500/cu.mm.
• Person shows symptoms caused by damage to the immune
system, but without opportunistic infection and cancer.
Symptoms seen are:
• Unexplained diarrhoea; Fatigue, malaise; Loss of wgt more
than 10%; Fever, night sweats; Mild opportunistic infections
4. AIDS CD4 count < 200 cu.mm.
• end stage of HIV infection
• Death is due to uncontrolled infection
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 Oral lesions in HIV infection
• Oral lesions are often clearly visible and several can be
diagnosed accurately on clinical features alone.
• Oral lesions associated with HIV are important, as they not
only affect the quality of life of the patient but also are useful
markers of disease progression and immuno-suppression.
Group I
lesion strongly associated with HIV infection Group III
• Candidiasis lesion seen in HIV infection
• Hairy leukoplakia • Bacterial infections
• Kaposi sarcoma
• Drug reactions
• Non-Hodgkins lymphoma
• Periodontal diseases • Bacillary angiomatosis
– Linear gingival eruthema • Fungal infections other than
– Necrotizing ulcerative gingivitis candidiasis
– Necrotizing ulcerative periodontitis • Neurological disturbances
Group II – Facial palsy
lesion less commonly associated with HIV infection – Trigeminal neuralgia
• Bacterial infections • Recurrent aphthous stomatitis
• Tuberculosis • Viral infections
• Melanotic hyperpigmentation
• Necrotizing ulcerative stomatitis Shvndr 40
 Treatment
1. Reverse- transcriptase 2. Non-Nucleoside analogue
inhibitors- NRTI RT inhibitors (NNRTI)
i) Zidovudine i) Nevirapine
ii) Didanosine 3. Protease inhibitors
a) Saquinavir
b) Ritonavir

Post-exposure prophylaxis
A COMBINATION DRUG THERAPY is recommended for 4 weeks
for accidental exposure from a known HIV patient.

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