oral microbiology - viral diseases

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OROFACIAL VIRAL
INFECTIONS
Dr. Saleem Shaikh
Introduction
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Viruses are some of the smallest microrganisms (100-300 nm).
Consist of a core [genome] containing either a DNA or a RNA surrounded
by a protein shell [caspid]
Many viruses have the property of latency and may reside in the tissue
asymptomatically for the entire life
Approximately 90% of the adults harbour viruses that have been acquired
as a result of infection during earlier life.
Oral tissues are a frequent site for viral lesions
Viral replication is a complex process comprising of a number of steps –
adsorption/penetration, uncoating, transcription, synthesis of viral
components, assembly and finally release of new virons.
Anti viral agents
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Relatively few antiviral drugs have been developed compared to the
number of antibacterial drugs, this is due to the intracellular nature of the
infection and the ability of the viruses to establish a latent form.
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Acyclovir was the first antiviral drug to be discovered
It enters into the viral infected cell and bibds to the viral DNA preventing
its further replication. Hence it should be given preferably within 48 hours
of onset of acute symptoms.
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Valaciclovir, penciclovir, famciclovir.
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Docosanol is an agent which alters the cell membrane to prevent the viral
entry and this is available as topical application for herpes simplex infection.
Laboratory diagnosis
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Electron microscopy can be used to provide identification of virus based on
morphological appearance but this has low specificity and requires
additional tests.
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Light microscopy in conjuction with immunofluorescence and monoclonal
antibodies can be used to give rapid and accurate results.
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Viruses can be grown in tissue culture, the swab of the lesion should be
carefully transported with addition of antibiotics and antifungals to prevent
the overgrowth of bacteria and fungus.
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Diagnosis can be confirmed retrospectively by detection of high rise in
antibody titre.
HUMAN HERPES VIRUS [HHV]
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HHV1 – Herpes simplex virus 1
HHV 2 - Herpes simplex virus 2
HHV 3 – Varicella zoster virus
HHV 4 – Epstein barr virus
HHV 5 – Cytomegalo virus
HHV 6
HHV 7
HHV 8 – Kaposi sarcoma virus
Herpes Simplex Virus
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It is a DNA virus, two types are seen - Type 1 & 2
HSV 1 is spread predominantly through the saliva or active perioral lesions
Seen more commonly on lips, eyes and skin above the waist
HSV 2 is seen more in genital areas and is transmitted predominantly
through sexual contact.
Clinical lesions produced by both types are identical
The initial exposure to an individual is called as primary infection, this is
seen at a very young age and is often asymptomatic.
The virus travels along the sensory nerves and reaches the associated
ganglion and becomes inactive [trigeminal ganglion in oral HSV infection]
Secondary [recurrent, recrudescent ] infection occurs by reactivation of
the virus.
Numerous conditions like old age, pregnancy, emotional stress, trauma,
allergy, systemic disease etc can cause reactivation of this virus
Herpes Simplex Virus
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Acute gingivostomatitis is the most common manifestation of symptomatic
primary HSV. symptoms like fever, nausea, chills etc are seen
Most of the acute herpetic gingivostomatitis arise between the ages of 6
months to 5 years.
Initially the affected mucosa develops small vesicles which enlarge slightly and
develop into ulcers.
When primary infection is seen in adults it usually results in pharyngotonsillitis.
Secondary or recurrent infections are seen either at the site of primary
inoculation or adjacent sites which are supplied by the involved ganglion.
The most common site of recurrence is the vermillion border of lips known as
– Herpes labialias .
Lesions on the oral mucosa are seen limited to the keratinized mucosa.
Herpetic whitlow
Herpes Gladiatorum.
Histological features
 Epithelial cells show achantholysis, nuclear clearing and nuclear enlargement
[Balooning degeneration]
 Tzank cells
 Intra nuclear inclusions – Lipshutz bodies
Lab diagnosis
Treatment – Acyclovir is the drug of choice, valacyclovir, famicyclovir
topical anesthetic
corticosteroids should not be prescribed to the patients.
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Varicella Infection
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Varicella zoster virus – VZV ; HHV 3
It also has a primary and secondary infection like HSV
Primary infection – Chicken pox
Secondary infection – Herpes Zoster
Chicken pox – this virus spreads by air droplets or direct contact
 Incubation period – 10 – 21 days
 Prodormal - Malaise, pharyngitis & rhinitis
 Rash begins on the face & spreads to the extremities.
 Each lesion progresses through the stages of Erythema – vesicle – pustule
– crust
 “Dewdrop on rose petal” is the classical presentation seen due to presence
of a vesicle with erythema.
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Oral lesion are seen on the palate and buccal mucosa frequently, oral
lesions look like HSV lesion but the most important distinguishing feature is
that the lesions of chicken pox are painless.
Complications- reye’s syndrome, encephalitis, pneumonia etc
Histologic features – Same as HSV
Treatment –
Warm baths with soap
Acyclovir, valacyclovir, famicyclovir
Herpes Zoster
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After initial infection, the virus becomes inactive and is present in the nerve
ganglion.
Reactivation of the virus can occur due to various reasons, but unlike HSV
multiple recurrences are seen in herpes zoster infection.
Clinical features: the infection has three phases – Prodrome, acute and
chronic
Severe neuralgia is the most common prodromal symptom, the pain is
severe – burning or stabbing type. Fever, malaise and headache may also be
seen.
The acute phase is characterized by appearance of vesicles on an
etythematous base, in 3-4 days the vesicles become pustular, ulcerate and
crust. The lesions tend to occur along the course of the nerve and
terminate at the midline. Oral lesions are also seen along with the skin
involvement.
If pain persists for mare than 3 months after the initial presentation it is
chronic phase and is called as ‘postherpetic neuralgia’
Herpes Zoster
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James Ramsay Hunt syndrome: facial nerve paralysis, deafness, vertigo, and
pain. Due to infection of the geniculate ganglion.
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Zoster sine herpete – some patients may develop the neuralgic pain but
the lesions are not seen. This condition is very difficult to diagnose and
maybe misdiagnosed as dental problem, migraine, myocardial infarction or
appendicitis depending on the involved dermatome.
Infectious Mononucleosis
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Caused by Epstein-barr virus –HHV 4
This is known to spread through intimate contact.
Infection in children is asymptomatic. In adults fever, lympadenopathy,
tonsillitis, pharyngitis. The fever may reach 1040 F
Oral lesions include petichae on the hard and soft palate. Necrotizing
ulcerative gingivitis may also be seen.
Oropharyngeal tonsillar enlargement is seen, parotid gland enlargement
with facial nerve palsy is also reported.
Classic serological test for infectious mononucleosis is the “Paul-bunnell
test”
Cytomegalovirus –HHV 5
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Primary infection followed by secondary infection due to
reactivation
Establishes latency in salivary gland cells, endothelium,
macrophages & lymphocytes
Almost 90% of cases are asymptomatic
Adult clinical infection resembles infectious mononucleosis
Oral lesions are seen in AIDS (mucosal ulcers)
Neonatal – hypoplasia, attrition, yellow coloration of dentin
Histologic features: infected cells are enlarged and have
prominent nucleoli - “owl eye” alteration.
Coxsakie Virus
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Belongs to group of enterovirus
Herpangina – A1-6,8,10,22
Hand foot & mouth – A16
Acute lymphonodular pharyngitis – A10
Measles (Rubeola)
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Paramyxovirus
Incubation period of 10 days, patient becomes infectious 2 days before
becoming symptomatic and untill 4 days after appearance of rash
Prodormal symptoms are followed by a rash – face is involved first
Complications like otitis, pneumonia, diarrhea
Oral manifestations – “Koplik’s spots” are the most distinctive oral
manifestation. Areas of erythema with small bluish white macules
Enamel hypoplasia of the pitted type is also seen
Enlargement of lingual and pharyngeal tonsils
Histologic features: large number of neutrophils and lymphocytes. Large
multinucleated Warthin – Finkeldey giant cells are seen.
Mumps
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Paramyxovirus infection that primarily affects salivary gland
Incubation period of 16 -18 days
Spreads through saliva, respiratory droplets
Contagious from 1 day before appearance to 14 days after clinical
resolution of the infection
Low grade prodormal symptoms of 1 day followed by salivary gland
changes, Parotid gland is most common, discomfort and swelling are seen in
the region around the ear.
Enlargement peaks within 2-3 days and is most painful during this period.
Enlargement of the glands usually begins on one side and is followed by
contralateral gland enlargement.
The second most common finding is epididymoorchitis – testicle exhibits
rapid swelling with pain and tenderness.
Oophoritis & mastitis are also seen
Redness and enlargement of stensons and whartons duct
MMR vaccine
Treatment of mumps is pallative in nature
Acquired Immunodeficiency Syndrome
[AIDS]
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Caused by human immunodeficiency virus – HIV
The primary target of HIV is CD4+ helper T cells
HIV infection is may be asymptomatic or an acute viral response may be
seen .
The acute viral response develops within 1-6 weeks after the exposure, the
symptoms resemble infectious mononucleosis, oral changes include
mucosal erythema and focal ulcerations.
This acute phase clears within a few weeks, followed by a variable
asymptomatic period. Some patients develop a phase of chronic fever,
weight loss, diarrhea, oral candidiasis, herpes zoster, oral hairy leukoplakiathis has been termed as AIDS related complex [ARC]
This is followed by development of overt AIDS, the presentation is highly
variable. The signs and symptoms of ARC are all seen along with increasing
number of opportunistic infections and neoplastic processes.
Oral manifestations of AIDS
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Group 1 – (Strongly associated)
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Candidiasis
Hairy leukoplakia
Kaposi’s sarcoma
Non hodgkins lymphoma
Periodontal disease
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Linear gingival erythema
NUG
NUP
Oral manifestations of AIDS
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Group 2 – (commonly associated)
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Bacterial infections
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Tuberculosis
Melanotic hyperpigmentation
Necrotizing stomatitis
Group 3 – (seen)
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Apthous ulcerations
Verruca vulgaris; squamous papollioma
Histoplasmosis
Thrombocytopenia
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