describes the etiopathogenesis , clinical features, investigations, differential diagnosis and management and prophylaxis of all important viral lesions affecting the oral cavity

2.  Introduction
 Classification
 Individual viruses: pathogenesis, c/f, o/m, diagnosis,
treatment.
 Conclusion
 References

3.  DEFINITION:
Luria & Darnell in 1978 defined viruses as “entities whose genomes are elements of nucleic acid
that replicate inside living cells , using the cellular synthetic machinery & causing the synthesis
of specialized elements that can transfer the viral genome to other cells.”
Since Dmitri Ivanovskys-1892 article a non-bacterial pathogen infecting tobacco plants,
and the discovery of the tobacco mosaic virus by Martinus Beijerinck in 1898, about
5,000 virus species have been described - millions of different types.
found in almost every ecosystem on Earth - most abundant type of biological entity.
The study of viruses - virology,a sub-speciality of microbiology.

4.  They are small, retaining infectivity after passage
through filters.
 They are totally dependent on living cells, either
eukaryotic or prokaryotic for replication and existence.
 They possess only one species of nucleic acid, either
DNA or RNA.
 They have a component – a receptor binding protein for
attaching to cells.

6. 1. Attachment of the virus to receptors on the host cell surface
2. Entry of the virus through the host cell membrane(viropexis or fusion)
3. Uncoating of viral nucleic acid
4. Replication
Transcription of mRNA from viral nucleic acid
Translation of mRNA into early proteins
Replication of viral nucleic acid
Synthesis of late structural proteins
5. Maturation of viral particles;
6. Release from the cell

7.  Antiviral drugs are most active when viruses are replicating
 Drugs can potentiallytarget any of thesteps
 But in many viral infectionsreplication of viruses peak at or
before manifestationofclinical symptoms.
 So to be effectivetherapy has to be started in theincubation
period ie. it has to be prophylactic

8.  First studied by Fenner using mousepox as the experimental model.
 Enters the skin

Multiplies initially-spread to regional
nodes thru lyphatics
Enters the bloodstream and
transported to central foci for
viral multiplication
Massive spillover to blood
stream-prodromal
symptoms
Reaches the target –
multiplication
produces lesion

9.  Significance of incubation period
 Represents time taken for virus to spread from the site of entry - organ of
multiplication - to the target organs for production of the lesions
 Influenced by relation between the sites of entry , multiplication and lesion
 When site of entry and site of lesion same- short incubation period-1 to 3 days
(respiratory viral infections)
 When virus enters thru respiratory tract and produces lesion in remote sites-
longer incubation period (chicken pox)

10.  Ability of pathogenic virus to lie dormant within a cell.
 Virus latency is not to be confused with clinical latency during the incubation
period when a virus is not dormant.
 Two types:
 Episomal latency
 Episomal latency refers to the use of genetic episomes during latency. viral
genes are stabilized floating in thecytoplasm or nucleus as distinct objects.
 Proviral latency:
 A provirus - virus genome integrated into the DNA of a host cell.
 automatic host cell division results in replication of the virus's genes-
nearly impossible to remove an integrated provirus from an infected cell
without killing the cell

11.  RNA Virus:
 Orthomyxovirus – Influenza
 Paramyxovirus – Measles
- Mumps
 Rhabdovirus
Rabies
Hemmorhagic fever
 Arenavirus
Lassa fever
Lymphocytic choriomeningitis
 Calicivirus – Hepatitis E
 Coronavirus – upper respiratory
infection
 Bunyavirus
 Picornavirus-Poliomyelitis
- Coxsackie diseases
- Foot & mouth disease
-Encephalomyocarditis
 Reovirus
 Togavirus – Rubella
- Yellow fever
- St. Louis encephalitis
 Retrovirus - HIV

12.  DNA virus:
 Herpes virus
- Herpes simplex I
- Herpes simplex II
- Varicella-zoster virus
- Epstein-Barr virus
- Cytomegalovirus
- Human herpes virus 6
- Human herpes virus 7
- Human herpes virus 8
- Simian herpes virus B
 Pox virus – Small pox
- Molluscum contagiosa
 Adenovirus
- Pharyngoconjunctival fever
- Epidemic keratoconjunctivitis
 Parvovirus
 Iridovirus
 Papovavirus
- Human warts / Papillomas
- Tumorigenic virus in animals

13.  80 known herpes viruses – 8 are known to cause infection
in humans.
 HSV-1&2- Herpes simplex Virus
 HHV-3- Varicella – zoster virus
 HH4-Epstein Barr virus
 HHV5-
 HHV6 and 7- Roseolovirus
 HHV 8- Kaposi’s sarcoma herpes virus(KSHV), also asso
with a small variety of lymphomas and castlemans
disease.

14.  Structural and behavioural characteristics
common among HHVs:
 Contain 4 layers
 Double –stranded DNA
 Protein capsid
 The tegument
 Lipid envelope
 Initial contact- primary infection-remains latent
within the nuclei of specific cells
 Site of latency differs among the members
 After rectivation-localised or disseminated recurrent
infections

15.  Human reservoirs only
 2 types – structurally similar , antigenically &
biologically different
 HSV-1: alpha-herpes virus is a ubiquitous virus
Above the waist – face, lips, oral cavity, upper body
skin, ocular areas, pharynx
 HSV-2: below the waist – genital lesions

16.  Humans- only natural hosts
 Sources- saliva,skin lesions,respiratory secretions
 Transmission- close contact
 Virus- enters through the defect in skin or OMM –multiplies locally-cell to cell
spread-
 Enters enter nerve fibers – intra-axonally to the ganglia
 Centrifugal migration-from ganglia to skin and mucosa-cutaneous and
mucosal lesions.
 Virus remain latent in ganglia-trigeminal(HSV-1)and sacral nerves(HSV-2)

17.  Trigerring factors:
 Fever
 UV light exposure
 Common cold
 Emotional stress
 Fatigue
 Trauma
 Oral cancer therapy
 Immunosuppression
 Oral& facial surgery
 Viral infection –HIV
 Gastrointestinal upset
 Pregnancy
 Menstruation
 Epidural morphine
 HSV – reactivated – newly
produced virions – anterograde
axoplasmic transport to
mucocutaneous sites – released
in saliva
 Factors:
 Prostaglandin E2 released at
mucocutaneous tissue
 CD4+ lymphocytes & CD8+ T
cells

18.  Acute herpetic gingovostomatitis:
 Most common pattern of symptomatic primary HSV
infection
 Incidence of primary HSV-1 increases after 6 months
of age
 Peak of inciudence- 2 and 3 years of age
 Incidence of HSV-2 does not increase until sexual
activity begins

19.  Many primary infections are subclinical
 Symptomatic disease preceded by prodromal-
fever, headache, malaise , nausea, vomiting and
LE
 Oral lesions –1-2 days after prodromals- 1-2mm
pinhead vesicles – collapse – numerous small red
lesions – enlarge – central area of ulceration with
yellow fibrin – ulcers coalesce – larger shallow
irregular ulcers – heal 10-14 days
 Satellite vesicles – perioral skin – common

20.  Gingiva:
 Self innoculation – fingers, eyes, genital areas
 Children – generalized initial –macular, later – purpuric cutaneous rash
 Adults – pharyngotonsillitis – sore throat, fever, malaise, headache –
initial symptoms. Numerous small vesicles – tonsils & posterior pharynx
– diffuse grayish yellow exudate over the ulcers.
 Mild cases resolve within 5 to 7 days—may extend upto 2 weeks
 Rare complications- keratocoinjunctivitis, oesophagitis,meningitis and
encephalitis

21.  Recurrent inf – site of 1* innoculation / adjacent areas of
epithellium – involved ganglion
 Recurrence of HSV1 –lips – herpes labialis
 Prodromal signs – 6 to 24 hrs before lesions develop – pain,
burning, itching, tingling, localized warmth, erythema of involved
epithellium
 Multiple, small erythematous papules – clusters of fluid-filled
vesicles – rupture – crust (2days) – healing (7-10 days)
 Variable intervals – months - years

22.  Immunocompetent patient – keratinized mucosa – attached
gingiva & hard palate& dorsum of the tongue
 Immunocompromised patients –at any site--’atypical’ more
extensive and /or aggressive , slow healing & extremely
painful
 If left untreated –more diseminated-more complications

23.  Herpetic whitlow (herpetic paronychia)
 Herpetic conjunctivitis: keratitis – swelling &
congestion (palpebral conjunctiva, keratitis) – corneal
ulceration. Recurrent lesions – corneal scarring –
blindness
 Herpes gladiatorum (Scrumpox)
 Herpetic meningioencephalitis: serious form

24.  Herpetic eczema (Kaposi varicelliform
eruption): epidermal form of infection
superimposed on pre-existing eczema & diffuse
typical umbilicated vesicular lesions of skin with
high fever
 Disseminated herpes simplex of newborn:
passage through birth canal of mother with
herpetic vulvovaginitis - fatal

25. 1. Herpetiform recurrent aphthous stomatitis
2. Coxsackie virus infection (hand-foot & mouth disease)
3. Herpangina
4. Herpes zoster virus infection:
5.Erythema multiforme (EM):.
6. Acute necrotizing ulcerative gingivitis

26.  Cell culture : gold standard test for HSV isolation
 Observe cytopathic effects of the cells inociulated with HSV
 Rate of CPE depends on type of host cell, type of virus , conc. Of virus
 Cytology: scrapings –base of lesion smeared onto glass slides. Stained –
Wright, Giemsa (Tzanck preparation) or Papanicolaou stain -
multinucleated giant cells / intranuclear inclusions like Lipschultz or
Cowdry type A
 PCR: most sensitive method-detection of viral DNA
 Doesnot require viable virus or infected cells for detection
 used to discriminate HSV typess

27.  Direct fluorescent antigen detection test:
 Specimen incubated with fluorescin isothiocyante-labeled HSV type-specific monoclonal
antibody-positive cells appear flourscent green
 Rapid diagnosis
 Sensitivity-80%,specificity-98%
 Serological methods: primary HSV – IgM titers followed several weeks later by
permanent IgG titers (seroconversion)
Recurrent infection - IgG antibody titer in acute & convalscent sera . Not reliable
tool
 Biopsy : not regularly done
 In immunocompromised pts, if biopsy revea;s features of HSV infectio, one
should rule co-infection of CMV via immunocytochemistry

28. Primary infection:
PAIN CONTROL:
2% viscous lidocaine(swish and spit out 5ml 4-5times/d)
Liquid diphenhydramine(swish and spit out 5ml 4-5times/d)
Systemic analgesia
Benzydamine
Supportive care:
Hydration
Ice-chips
Soft bland diet
antipyretics

29.  Definitive therapy
 If presented within 24-48hrs after onset of vesicle
formation,antiviral medication help in reducing the healing
time:
 Acyclovir(Aceherpin) –inhibits viral replication
 Dosage: 200mg 5 times daily for 7 to 10 days/400mg TID for 7-10
days
 Valacyclovir(valcivir) and famciclovi(famtrex) is also available
–both has better bioavailability-hence fewer daily doses.
 Dosage: valacyclovir 1000mg BID for 7-10 days
famcilcovir 250 mg TID for 7-10 days

30.  Reducing trigger factors – sunscreen
 Topical antiviral medication:
1. 5% acyclovir cream -1 appl – every 4hr for 5 days
2. 3% penciclovir cream,
3. 10% docosanol cream – 3-6times/day (at first prodrome)
 Systemic therapy:
1. Tab.Zovirax (Acyclovir): 200mg 5times/day for 7 days
2. Tab.Valcivir (Valaciclovir):500-1000mg three times/day for 5 days.
3. Tab.Famtrex (Famciclovir):500-1000mg three times/day for 5-7 days
For patients –recureences asso with dental procedures,
2g valacyclovir BID on the day of procedure and 1g taken BID next day

31.  Resistance to anti-viral therapy develops in
immunocompromised –mutated thymine
kinase.
 Initial dose is repeated at elevated dose
 If this fails, IV foscarnet is administered
 If persists, IV cidofovir is recommended
 If all the above fails, vidarabine is recommended.

32.  Enveloped DNA virus – ALPHA, HHV-3
 Primary infection – Varicella (chicken pox)
 Latent – dorsal root ganglia/ganglia of cranial nerves
 Reactivation – Herpes zoster infection (shingles)
 Transmission: Air droplets/ direct contact with lesions.
 Children < 13 years
 Incubation period: 10-20 days.

33.  Chicken pox is an acute, ubiquitous, extremely contagious disease usually
occuring in children
 characterized by an exanthematous vesicular rash. It is most common in the
winter & spring months.
 Source of infection-chicken pox or zoster patients
 Portal of entry- conjunctiva or respiratory tract
 Incubation period of about 2 weeks
 Pt infectious during 2 before the exanthem starts until the lesions crusts

34. Clinical features:
 First 2 decades of life
 Begins with prodromals
 Intensely pruritic exanthema, maculopapular rash –followed by
vesicles-”dewdrop-like”-
 Turns cloudy and pustular , burst and scab with crst falling off
after 1 to 2 weeks)
 Begin on face & trunk – extremities(centrifugal spread)
 Typically continue to erupt for 4 days-may extend upto 7 or more
days
 Contagious from 2 days before eruoptions until all the lesions
crust

35.  Precede skin lesions-fairly common
 Most common sites vermillion border and palate-followed by
buccal mucosa
Gingival lesions may resemble Primary herpes
(varicella- painless)
 Blister-like lesions – initial raised vesicles(3-4mm) with
surrounding erythema – rupture – eroded ulcers
(1-3mm)

36.  In childhood, use of aspirin –
reyes syndrome
 Also secondary infections-
groupA,β-hemolytic streptococci
 In adults, increased
prevalence of complications,
 Varicella pneumonitis
 Encephalitis
 CNS involvement-
ataxia,convulsions , coma
 During pregnancy,
 Early involvemnt-abortion or
congenital defects
 Infection close to delivery,
 Severe fetal infection –lack of
maternal antibodies
 In immunocompromised,
 Extennsive cutaneous
involvement
 Hepatitis
 Pneumonitis
 Pancreatitis
 Encephalitis
 (7% mortality before advent of
antiviral therapy)

37.  History and clinical examination
 Confirmation : demonstration of viral cytopathic effects –cells
harvested from the vesicular fluid
 Further confirmatory tests:
 Viral isolation in cell culture- rapid diagnosis.
 Direct fluorescent antibody testing: fluorescin- conjugated VZV monoclonal
antibodies
 PCR: VZV DNA in CSF
 Serum investigation: acute stage & 14-28 days later – 4 fold
antibody titers to VZv

38.  Symptomatic:
 warm bath with soap(lipid envelope destroyed)
 Calamine lotion and systemic diphenhydramine-relieve pruritis
 Antipyretics other than aspirin: Acetaminophen.
 Systemic:
 To be administered within first 24 hours of the rash
 Reserved for pts at high risk for more severity
1. Acyclovir (Zovirax):adults-800 mg , 5 times/day for 7-10 days.
2. Valacyclovir (Valtrex):adults-1000 mg tid for 7-10 days
3. Famciclovir (Famvir): adult dose:500 mg tid for 7-10 days
 Immunocompromised:
 Purified VZVIg can be given to modify the clinical manifestations of the
infection. Within 96 hours of initial exposure

39.  (WHO) recommends routine vaccination only if a country can keep more
than 80% of people vaccinated. Either one or two doses of the vaccine is
recommended
 In the United States two doses are recommended starting at twelve to fifteen
months of age as well as for all suspetible >13
 70% to 90% effective for preventing varicella and more than 95% effective for
preventing severe varicella.[
 follow-up evaluations in the US revealed protection for at least 11 years-
studies in Japan indicated protection for at least 20 years
 Combinig with MMR vaccine-MMRV vaccine –comparable effectiveness and safety

40.  Herpes zoster is an acute infectious viral disease of an
extremely painful & incapacitating nature - characterized by
inflammation of dorsal root ganglia, or extramedullary
cranial nerve ganglia-
 associated with vesicular eruptions of skin or mucous
membranes in areas supplied by the affected sensory nerves.

41.  Initial infection (VZV) – virus is transported up sensory
nerves – latency – dorsal spinal ganglia.
 Reactivation of virus – herpes zoster – affected sensory
nerve.
 Inflammation of peripheral nerves – demyelination &
wallerian degeneration + degeneration –dorsal horn cells
– spinal cord.
 Predisposing factors – immunosuppresed, cytotoxic
drugs, radiation, old age, alcohol abuse, malignancy or
tumor – dorsal root ganglia.

42.  Prodromal symptoms-intensepain, fever malaise, precedes the
rash in >90% cases.(1 to 4 days before exanthem)
 As the virus travels down the nerve- pain
intensifies(burning,tingling , itching,boring,knife-like)-area
innervated by the affected sensory nerves.
 Typically one dermatome is affected.
 Some case-no vesiculation of mucosa or skin-zoster sine
herpete
 Within 3 to 4 days the vesicles rupture to form clusters of
ulcers-crustates after 7 to 10 days-resolves within 2 to 3 weeks
in otherwise healthy
 Scaring on healing with hyper/hypo pigmentation.

43.  Trigeminal nerve involvement
 Movable / bound mucosa
 Lesion –extends upto midline, involvement of overlying skin
 Lesions – 1-4mm white opaque vesicles (painful) – buccal mucosa, tongue,
hard palate, gingiva,uvula, pharynx, larynx – rupture – shallow ulcerations –
coalasce – larger ulcers scalloped borders – heal (10-14 days)
 Devitalization of teeth
 HIV-resorption, exfoliation of teeth –osteonecrosis of jawbones

44.  Herpes simplex infection – lesions not limited
dermatome, moderate pain, fast healing, recurrence
 Blistering /ulcerative conditions – pemphigus/
pemphigoid – chronic progressive disease – not unilateral

45.  Viral culture – 24 hours. best way to confirm the diagnosis
 Cytologic smears – viral cytopathologic effects
 Serum investigations- transient rise in IgM & IgG
 Biopsy – multinucleated epithelial cells with viral inclusions
 PCR- VZV

46.  Post herpetic neuralgia is defined as pain that
lingers for 30 days or 120 days after the onset of the
acute rash or after an episode of zoster
 uncommon under the age of 50 –affects 50 % of ots older than
60
 Pain- burning, throbbing, aching, itching or stabbing
 Neuralgias – resolve within 1 year
 Clearance of pain reported within days after initiation of long-
term famciclovir
 Facial paralysis ass with herpes zoster of face or
external auditory meatus

47.  Hunt’s syndrome / James Ramsay
Hunt’s syndrome:
Special form of zoster infection of geniculate ganglion
with ipsilateral involvement – facial & auditory nerves
Facial paralysis (Bell’s palsy) + pain & vesicles – external
auditory meatus & pinna of ear + vesicular eruptions –
oral cavity & oropharynx – hoarseness + loss of taste
sensation – ant 2/3rd of tongue + tinnitus, vertigo, other
disturbances

48.  Symptomatic treatment- Skin lesions should be kept clean and dry to reduce the risk of bacterial
superinfection.
 Supportive care – hydration, soft bland diet.
 Specific treatment
Antiviral drugs
1. Acyclovir (Zovirax): adults-800 mg , 5 times/day for 7-10 days.
2. Valacyclovir (Valtrex):adults-1000 mg tid for 7-10 days
3. Famciclovir (Famvir): adult dose:500 mg tid for 7-10 days
4. Brivudin –dose of 125mg once daily for 7days.
5. Along with antiviral drugs, Prednisone 40-60mg daily for 1 to 2 weeks can be given
 Management of Post herpetic neuralgia
Gabapentin & 5% lidocaine patch –as first line of treatment

49.  Mono Glandular Fever, “Kissing disease”
 Exposure to Epstein-Barr virus (EBV) – HHV-4
 Burkitt’s lymphoma, Hodgkin’s disease, Oral hairy leukoplakia.
 Transmission:
 Intimate contact –once exposed –EBV remains
in host for life
 Children- contaminated saliva – finger , toys , other objects
 Adults – direct salivary transfer – shared straws , kissing

50.  Virus enters the pharyngeal epi cells via CD21 receptors
 Multiplies locally-invades the blood stream and infects B-lymphocytes
 Virus either become latent inside the B-lymphocytes(polyclonally
activated)/cause cell death and release of mature virions
 Inresponse to these b-cells, abnormally CD8+ T-lymphocytes are released by
host immune-Downey cells

52.  Hard / soft palate petechiae – transient –disappear 24-48
hrs
 Edema – soft palate & uvula
 Oropharyngeal tonsillar enlargement – diffuse surface
exudate , secondary tonsillar abcess
 ANUG – common-refractory to normal therapy should be
evaluated
 Oral ulcers – occasionally
 Oral hairy leukoplakia: most common EBV-related lesion
in HIV-faint whitess vertical streaks-thickened ,furrowed
areas of LK-lateral border of tongue- may become
extensive

53.  Increased WBC count with differetial count
showing relative lymphocytosis-2nd week of the
disease
 Exhibits downey cells –peripheral smear
 Classic serologic test-paul bunnel test-detect
heterophile antiodies titre- rise upto 1:4096
 Positive only in young adults
 For children younger than 4: ELISA or IDIFA confirms
EBV infections

54.  No specific treatment
 Course – 2-4 weeks
 Bed rest , adequate diet
 Antipyretics (non-aspirin)
 NSAIDs
 Antibiotics – avoided – allergic morbilliform skin rashes
 Corticosteroids – recommended in life threatening cases
COMPLICATIONS: Self limiting
CNS complications seen within 2 weeks
Acute hemiplegia and psychosis

55.  HHV-5 – B-herpes
 Double-stranded DNA virus
 Latent – salivary gland cells, endothelium, macrophages &
lymphocytes.
 salivary gland virus disease.
 Transmission:
 In utero transmission
 Sexual transmission
 Blood transfusion ,organ transplantation

56.  Entry into the host cell is achieved by attachment
of the viral glycoproteins to host receptors
 The hallmark of such infection appearance of atypical
lymphocytes in the peripheral blood; these cells are
predominantly activated CD8+ T lymphocytes

57.  90% - asymptomatic
 Neonatal inf:
 Hepatosplenomegaly , extra-medullary cutaneous erythropoiesis ,
encephalitis – mental retardation & motor retardation ,
thrombocytopenia – petechial haemmorhage
 Acute adult inf:
 = infectious mononucleosis
 Symptoms ranges from influenza-like to lethal multiorgan involvement
 Only 1/3rd of pts demonstarte pharyngitis and lympadenopathy
 Rarely, acute sialadenitis-xerostomia and enlargement of affected glands
 Unusual complicatios: myocarditis , pneumonitis, septic meningitis

58.  In immunocompromised, aggressive infection-
significant hepatitis, leukopenia,pneumonitis
 Common in AIDS pts- chorioretinitis and CMV
colitis

59.  Salivary gland involvement-all major and minor glands
 Chronic mucosal ulcerations-mostly single large ulcers – deep
penetrating –lips , tongue , pharynx , AIDS
 Gingival infection , gingivitis , gingival hyperplasia
 Co-infection – CMV + HSV(1/3rd cases)
 Neonatal CMV – developmental tooth defects – diffuse enamel
hypoplasia , attrition , enamel hypomaturation , yellow
discoloration – underlying dentin

60.  1. Herpes simplex and Varicella zoster viral infections
– CMV is often seen in association with HSV or VZV
 2. Squamous cell carcinoma –Single ulcers of acute onset
present for weeks or months
 3. Benign or malignant salivary gland tumours:
secondarily ulcerated from trauma.
 4. Traumatic ulcerative granuloma – Single ulcers on the
tongue may represent traumatic ulcerative granuloma.

61.  Biopsy : immunocompromised pt – chronic ulceration
Cellular changes – infection
Characteristic “owl eye” appearance of cellular inclusions
 Specific verification detection of viral antigens:
 By immunohistochemiostry and PCR
 Demonstrate viral antibody titers
 ELISA of CMV is recommended for any pts with an
unexplianed fever

62.  1.Prevention : By passive immunization with hyperimmune
gammaglobulin can be successful.
 2.Pain control : 2% viscous lidocaine Systemic analgesics.
 3.Supportive care: Hydration , Soft bland diet , Ice chips
 4. Definitive treatment:
 Cidofovir -5 mg/kg once a week for the initial 2 weeks and
then followed by maintenance regimens of 3–5 mg/kg every 2
weeks.
 Ganciclovir –500mg t.i.d for 7 days..

63. Next presentaion will include:
Mumps,Measles
,Rubella,Coxsackie virus
infections,HIV

64.  Oral & maxillofacial pathology: Neville, 3rd
edition.
 Text book of oral medicine: Burkitts, 11th edition
 Shafer’s text book of oral pathology, 6th edition
 Ananthanarayanan and Panikers Textbook of
microbiology(7th edition)
 Journal articles(Den Clin Am 58(2014)281-297)
 Internet sources

65.  An acute, contagious, dermatrophic viral infection affecting
children produced by paramyxovirus family of genus
morbillivirus.
 RNA virus-linear single stranded RNA
TRANSMISSION:
 Direct contact with respiratory secretions and aerosols
Outbreak cycle: 2-3 years

66.  Infects skin, respiratory tract, viral replication in local
lymph nodes
 Spread of virus within leukocytes- RE cells
 Host cell necrosis
 Suppresion of cellular immunity. Sec viremia coryza
and cough

67.  Incubation period 10-12 days
 Infectious from 2 days before becoming symptomatic
until 4 days after appearance of asso rash.
 Lymphoid hyperplasia involving lymph nodes, tonsils,
adenoids, peyers patches
 3 STAGES: 9 DAY MEASLES

68. 1ST 3 DAYS:
 Cough
 Coryza
 C onjunctivitis
 Accompanied by fever
 KOPLIK’S SPOTS
 “GRAINS OF SALT IN
A RED
BACKGROUND”-
pathognomic

69. 2ND 3 DAYS:
 FEVER continues
 Koplik’s spots fade
 Maculopapular rash(morbiliform) begins-
erythematous – blanches on pressure
 Face involved 1st –spread to trunk and extremities
 Abdminal pain – sec to lymphatic involvement

70. 3rd STAGE:
 FEVER ends
 Rash begins to fade
 Downward progression -Replacement by brown
pigments
Complications:
 Young children: otitis media, pneumonia,persistent bronchiotis
and diarrhea
 Delayed complication: occurs in 1 in 100000 cases –sub –acute
panencephalitis(SSPE)-personality chnages seizure coma and
death-widespread vaccination eleminated SSPE
 Immunocompromised pts: more atypical rashes and severe
complications

71.  Apart from kopliks spots-candidiasis ,
ANUGand necrotising stomtitis can occur-
malnutrition
 Severe measles in children –affect
odontogenesis-pitted enamel hypoplasia.
 Enlargement of accessory lymphoids-lingual
and pharyngeal tonsils.

72.  Demonstration of multinucleated giant
lymphocytescells(wartin – Finkeldey cells) in giemsa
stained smears of nasal secretion- even before rashes
develop
 Desmonstration of rising serologic antibody titers-appear
within 1 to 3 days after exanthem- peaks in 3 to 4 weeks

73.  Isolation of patient
 Symptomatic treatment
 No specific drugs
 Antiviral drug –Ribavirin is effective against measles virus in vitro,
use in immunocompromised individuals.
 Cap. Ribavin 200mg QID Syr. Ribavin 50mg / 5ml – 15mg / kg
daily –2 divided doses.
 Vitamin A should be given - Vitamin A CHW-TAB – 50000 IU.
 Interferon : Vial Shanferon 3 MIU.

74.  MMR vaccine -Introduced in 1963
 Incidence decreased by 99%
 MMR vaccine:
MMR1- 1year ,
MMR2- 4-6 yrs.
 Passive immunization:
Human immunoglobulin (im)
<1 yr – 250mg ;
>1 yr – 500mg.

75.  Primarily in winter
 Toga virus-genus rubivirus
 TRANSMISSION: droplet infection, congenital rubella syndrome.-occurs in
winter
 Infection of the mother by Rubella virus during pregnancy can be serious-
Congenital rubella syndrome
 Spontaneous abortion occurs in up to 20% of cases
 "blueberry muffin lesions."

76.  Transmitted by the respiratory route and replicates
in the nasopharynx and lymph nodes.
 The virus is found in the blood 5 to 7 days after
infection and spreads throughout the body.
 Teratogenic properties.

77. INCUBATION PERIOD 14-21 DAYS
CONTAGIOUS-from 1 week before exanthem to about 5 days after
development of rashes
Large percentage remain asymptomatic
Prodromal symptoms-1 to 5 days before exanthem
Lymphadenopathy-persists for weekscervical, suboccipital , postauricular
Exanthematous rash- entire body within 3 days : 1st sign-pink macule-
papules-flaky desquamtion-resolves by day 3
Most common complication is arthritis. Rare : encephalitis and
thrombocytopenia

78. ORAL MANIFESTATIONS:
Forehheimer’s sign : 20 % cases 6 hrs after
1st symptom
 Dark red papules on soft palate, hard
palate along with rash
 Palatal petechiae
 1st month of pregnancy- hypoplasia,
caries, delayed eruption of deci teeth

79.  A fourfold rise in rubella IgG antibody titre between acute and
convalescent serum specimens.
 A positive serologic test for rubella-specific IgM antibody.
 A positive rubella culture (isolation of rubella virus).
 Serologic studies are best performed within 7 to 10 days after the
onset of the rash and should be repeated two to three weeks later

80.  No specific Rx-nonaspirin antipyretics and
antipruritics
Prevention: MMR vaccine, S.C inj
1st : around 1 year
2nd: 4-5 years.
Passive immunity : human rubella immunoglobulin.

81. Caused by paramyxovirus family , genus:Rubulavirus
Epidemiology markedly affected by MMR vaccine
Before vaccination, epidemics were seen evry 2 to 5 years- 90% before age 15
Post vaccintn, incidence reached an all time low in 1985(98% decrease)
Resurgence in 1986-mainly among 10 to 19 yr olds –due to loss of diligence
In 2006, oubreak in USA(IOWA)-49% had received atleats recommended 2 doses-proves only 90%
effective agenct mumps .
May lead to a recommendation for a third dose

82. Transmitted through urine saliva respiratory droplets
Incubation period – 16 to 18 days
Contagious from 1 before the clinical appearance to 14 days after its clinical
resolution
Best known site of involvement- salivary glands, pancreas, choroid plexus, mature
ovaries and testis.
One attack confers life long immunity

83.  infection and Proliferation of virus in upperResp tract
 Replication in resp epi
 Localisation in glandular & neural tissues
 Perivascular and interstitial mononuclear infiltrate,
necrosis- acinar cells

84.  CLINICAL FEATURES:
 30% subclinical
 5-15 YRS
 INCUBATION PERIOD: 2-4weeks
 Prodromal symptoms: pain below ear, headache,malaise,anorexia,myalgia
 Parotid gland is most commonly affected-Swelling 24-48 hrs accompanied by pain on mastication.
 Elevation of ear lobe
 25% unilateral. Starts off on one side and followed by contralateral involvemnt within a few days
 Oral mnifestation is redness and enlargemnt of Whartons and stensons ductal openings
COMPLICATIONS:
Orchitis, acute pancreatitis Rare: meningoencephalitiss

85.  Most frequently used confirmatory measure is demonstration mumps-
specific IgM or a 4-fold rise in IgG titers when measured during acute
phase and about 2 weeks later respectively
 Viral isolation from swabs obtained from salivary secretion of parotid
 Reverse-transcriptase – polymerase chain reaction testing- to detect viral
RNA

86.  palliative in nature
 Avoidance of sour foods and drinks helps to decrease the
salivary gland discomfort
 Application of intermittent ice
 Warm salt water gargles, soft foods, and extra fluids
Prevention:
 M-M-R (Measles, Mumps, and Rubella Virus Vaccine
Live)

87.  Cv – RNA virus- member of genus enterovirus and family
Picornaviridae-features common with poliovirus
 90% of infection by nonpolio enterovirus –asymptomatic or result in non-
specfic febrile illness
 CV type A -23 ,CVType B-6
 Transmission is through Feaco-oral route-some shedding occurs in upper
respiratory tract infection.
 In oral cavity CV causes
 Herpangina
 Hand foot and mouth disease
 Acute lymphonodular pharyngitis

88.  Vesicular eruption of the fauces & soft palate, fever sore
throat, pain on swallowing
 CV-A(serotypes 1-10,16 and 22)-isolated from this disease
 Age: <10 years
 Epidemic- summer
 Incubation period: 2-10 days
 Prodromal symptoms-(1 to 3 days)
 Fever 104F

89.  1st: Sore throat & pain on swallowing
 2nd: erythema irt soft palate, soft palate and
tonsillar pillars
 Red macules-fragile vesicles-ulcerates 24-48hrs
(grey base & inflamed periphery).
 Ulcers persists for 1 week.
Heal in 7-10 days
Permanent immunity develops rapidly- neutralising Ab
Lymphonodular pharygitis – variant of
herpangina(CVA10)-develop diffuse small nodules in the
oropharynx

90.  Tonsilitis/ pharyngitis : no vesicles/ ulcers.
purulent exudate , culture
 Chickenpox : skin lesions
 Primary herpetic gingivostomatitis: generalised
acute marginal gingivitis , not epidemic , anterior part of oral
cavity

91.  Viral isolation from cultures can be performed
 Analysis of stool specimens is the best technique
 Throst culture is positive during early acute phase
 Serologic demonstration of rising enteroviral antibody titres
between acute and convalscent stages
 PCR is replacing viral culture in diagnostic labs

92.  CV A16
 Skin and oral lesions with flu like symptoms
 Epidemic, seasonal
 High transmission rate

93.  6 month-5years
 Peak in summer
 Anorexia, low grade fever, lymphadenopathy, diarrhea
 Maculopapular exanthematous lesions on skin.
 Heal without crusting
 Borders of palms & soles, ventral surfaces, fingers &
toes.

94. O/M:
 Refusal to eat
 Oral lesions precede skin lesions
 Seen in hard palate, tongue, buccal mucosa
 Multiple vesicle(1-30)
 Resolve in 7 days
 Red and erythematous

95.  Culture: intra cytoplasmic viral inclusion
 Serology: CV A 16
 Skin biopsy: intraepidermal vesicles , degeneration -
epidermal cells , dermal edema , lymphocytic+
neutrophilic infiltrate , dermal vessels – eosinophilic
nuclear inclusions + intracytoplasmic picornavirus
particles

96. D/D:
 Herpetic gingivostomatitis: no hand , leg
involvement
 Varicella zoster infection: segmental distribution
 Herpangina: lesions –soft palate & faucial areas
 Allergic stomatitis: itching , noticeable erythema
 Chickenpox: exanthema – entire body
Treatment:
Self-limiting.therapy directed towards symptomatic relief.non-
aspirin antip[yretics and topical aneasthetica like dyclinine HCL

97.  RNA virus-(lentivirus subgroupretrovirus
family)-AIDS
 1st case reported in 1981 in US.
 Four recognised human retrovirus belong to 2
groups:
 Human T-lymphotrpic virus(HTLV-1 &2)
 HIV 1 &2(HIV-1 is more commonly asso with AIDS)
 Transmission: sexual route, blood product
exchange, mother-fetus. Organ transplantation,
artificial insemination.

100.  1. acute infection:
 Within 3-6 weeks of infection
 50%-experience mononucleosis like symptoms
 Spontaneous resolution occurs withion week
 HIV antibody may be negative at the onset-become positive during course- seroconversion
 2. Latent infection:
 Last upto several years
 Positive HIV antibody test –infectious
 Doens not mean microbiological latency-replication continues
 Host immune response –can only limit the virus load.
 CD4+ decreses from 1000 per microlitre to about 500
 3.persistent lymphadenopathy:
 Enlarged lymph nodes at leats 1 cm –persist for atleast 3 months
 4. AIDS related complex(ARC): (CD4+-50-200per uL)
 Considerable immunodeficiency with constitutional symptoms and
minor opportunistic symptomse
 Progress to AIDS in a few months

101. 4. AIDS:
 End stage representing
complete breakdown of
immune defence mechanism
 Leaving the pt prey to
progressive opportunistic
infections and malignancies.
 Clinical findings in HIV
infection can be
categorised as:
 Cardinal finmdings
 Kaposis sarcoma
 Pneumocytis carinii
pneumonia
 Toxoplasmosis
 CMV retintis
 Oesophageal candidiasis
 Characteristic findings:
 Oral thrush
 OHL
 Extrapulmonary and
pulmonary TB
 Crypotococcla meningitis
 Associated findings
 Weight loss more than 10%
 Fever more than one month
 Diarrhea more than one
month
 Generalised extra-inguinal
lymphoadenopathy
 Skin infections
 Persistent cough

102.  Revised classification by European
Community Clearing House:
 Group 1lesions strongly asso with
HIV infection
 Candidiasis (pseudomembranous and
erythematous)
 Hairy leukoplakia
 Kaposis sarcoma
 Non hodgkins lymphoma
 Periodontal disease(anug,anup)
 Group 2 lesions less commonly
asso with HIV infection
 Bacterial infection(m.tuberculosis,m.
avium)
 Melanotic hyperpigmentation
 Necrotising ulcerative stomatitis
 Salivary gland disease
 Thrombocytopenia purpura
 Viral infections(HSV,HPV,VZV,HZV)
 Group 3 lesions seen in HIV
infection:
 Bacterial infections:
(a.israeli,E.coli,Kliebsiella)
 Cat-scratch disease
 Drug reactions(EM,lichenoid,Toxci
epidermolysis)
 Fungal other than candidiasis
 Neurologic disturbances
 Facial palsy
 TN
 Recurrent aphthous stomatitis
 Viral
 CMV
 Molluscum contagiosum

103. VIRUS BASED TESTS:
 Viral culture: directly detects virus. Positive
even in window period and terminal phase
 PCR for viral RNA in plasma & DNA in host
cell
 P 24 Ag capture assay: in window period & late
phase. Not routine.
 Saliva & GCF

104.  Ab to HIV appears in serum by 4-6 weeks after infection.
 ELISA: If +ve, western blot not required. It is –ve in window period.
 Western blot test: specific Ab
discrete band formation , -ve in window period( infection-seroconversion)
IMMUNOLOGICAL TESTS:
 CD4+ T cell count, percent & ratio
 Gradual decrease in count- disease progression
SALIVARY TESTS: saliva & GCF
 HIV IgG Ab capture assay:

105.  Aimed at managing the conditions arising out of imunosuppression and opportunistic
infection, and the virus itself
 Managemnt of the viral infection:(Antiretro-viral therapy)s
 Instituted in pts with AIDS regardless of CD4+ count and in asymptomatics with
count less than 200 cells/mm3
 Four groups of drugs can be used .
 Fusion inhibitors(enfuviride)
 Nucleoside reverse transcriptase inhibitors(lamivudine,zidovudine)
 Non-nucleoside reverse transcriptase inhibitors(nevirapine,efavirenz)
 Protease inhibitors(indinavir,ritonavir)
 A combination of these drugs may be used –regimens referred to as highly active
retro-viral therapy(HAART):
 1NNRTI +2NRTI
 1 OR 2 PI+2 NRTI
 TRIPLE NRTI

106.  SIDE EFFTECTS OF HAART:
 IRIS(immune reconstitution inflammatory
syndrome)
 Other SEs:
bone marrow suppression
bleeding disorders
Hapato and renal toxicity
HSRs and EMs

108.  Oral & maxillofacial pathology: Neville, 3rd
edition.
 Text book of oral medicine: Burkitts, 11th edition
 Shafer’s text book of oral pathology, 6th edition
 Ananthanarayanan and Panikers Textbook of
microbiology(7th edition)
 Journal articles(Den Clin Am 58(2014)281-297)
 Internet sources