Viral Infection

1. Dr. Arun Panwar
23/06/2020

2.  Introduction
 Classification
 Individual viruses:
Pathogenesis, Clinical Features, Oral Manifestations, Diagnosis,
Treatment.
 Conclusion
 References

3.  HSV - 1
 HSV - 2
 Varicella (Chicken Pox)
 Zoster (Shingles)
 Infectious Mononucleosis
 CMV
 Measles
 Rubella
 Mumps
 COVID 19

4. Found in almost every ecosystem on Earth - most abundant type of biological entity.
The study of viruses - virology.

5.  They are small (10 -200 millimicrons)
 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 receptor binding protein for attaching to cells.

7. Enters the skin
Multiplies initially then spread to
regional nodes through lymphatics
Enters the bloodstream and
transported to central foci for
viral multiplication
Massive spillover to blood stream–
appearance of prodromal symptoms
Reaches the target –
multiplication
produces lesion

8.  Orthomyxovirus – Influenza
 Paramyxovirus – Measles
- Mumps
 Rhabdovirus - Rabies
 Calicivirus – Hepatitis E
 Coronavirus – Upper respiratory
infection
 Picornavirus-Poliomyelitis
- Coxsackie diseases
- Foot & mouth disease
 Togavirus – Rubella
- Yellow fever
- St. Louis encephalitis
 Retrovirus - HIV

9.  Herpesvirus
- 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
 Pox virus – Small pox
- Molluscum contagiosa
 Adenovirus
- Pharyngoconjunctival fever
- Epidemic keratoconjunctivitis
 Papovavirus
- Human warts / Papillomas

10.  80 known herpes viruses – 8 are known to cause infection in
humans.
 HSV-1&2- Herpes simplex Virus
 HHV-3- Varicella – zoster virus
 HH4- CMV – Infective mononucleosis
 HHV5- EBV
 HHV6 and 7- Roseolovirus
 HHV 8- Kaposi’s sarcoma
 HSV 9 – Semian herpes virus

11.  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

12.  Sources- saliva,skin lesions,respiratory secretions
 Transmission- close contact
 Virus- enters through the defect in skin or oral mucous membrane –
multiplies locally- cell to cell spread.
 Enters nerve fibers – intra-axonally to the ganglia
 Centrifugal migration - from ganglia to skin and mucosa- cutaneous
tissue
 Virus remain latent in ganglia-trigeminal (HSV-1)and sacral nerves (HSV-2)

13.  Trigerring factors:
 Fever
 UV light exposure
 Common cold
 Emotional stress
 Fatigue
 Trauma
 Cancer therapy
 Immunosuppression
 Viral infection –HIV
 Pregnancy
 Menstruation

14.  Most common pattern of symptomatic primary HSV
infection
 Incidence of primary HSV-1 increases after 6 months
 Peak of incidence – b/w 2 and 3 years of age
 Incidence of HSV-2 does not increase until sexual
activity begins

15.  Many primary infections are subclinical
 Prodromal- fever, headache, malaise , nausea,
vomiting
 Oral lesions appear –1-2 days after prodromals
Numerous 1-2mm pinhead vesicles – collapse –
enlarge – central area of ulceration with yellow fibrin
– larger shallow irregular ulcers – heal 10-14 days
 Satellite vesicles – perioral skin – common
Clinical Features:

16.  Self innoculation – fingers, eyes, genital areas
 Children – gen. initial – macular, later – purpuric cutaneous rash
 Adults - pharyngotonsillitis – sore throat, fever, malaise, headache.
Numerous small vesicles – tonsils & posterior pharynx
Diffuse grayish yellow exudate over the ulcers.
 Mild cases resolve within 5 to 7 days.
 Rare complications- keratocoinjunctivitis, oesophagitis,meningitis and
encephalitis

17.  Recurrence of HSV1 –lips – recurrent 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

18.  Observe cytopathic effects of the cells inoculated 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 stain (Tzanck preparation) -
Multinucleated giant cells / intranuclear inclusions like Cowdry typeA
 PCR: most sensitive method-detection of viral DNA
 Does not require viable virus or infected cells for detection
 Used to distinguish HSV typess

19. Pain Control:
 2% viscous lidocaine (swish and spit out 5ml 4-5times/day)
 Systemic analgesics
Supportive care:
 Hydration
 Soft bland diet
 Antipyretics

20.  Within 24-48hrs, antiviral medication help in reducing the
healing time:
 Acyclovir ( Tab. Aciherpin) –inhibits viral replication
 Dosage: 200mg 5 times daily for 7 to 10 days or
 400mg TID for 7-10 days
 Valacyclovir (Tab. valcivir) and famciclovi(Tab. famtrex)
–Better bioavailability, hence fewer daily doses.
Valacyclovir 1000mg BID for 7-10 days
Famcilcovir 250 mg TID for 7-10 days

21.  Topical antiviral medication:
5% acyclovir cream - every 4hr for 5 days
3% penciclovir cream - 3-6 times/day for 5 days
 Systemic therapy:
Tab.Zovirax (Acyclovir): 200mg 5times/day for 7 days
Tab.Valcivir (Valaciclovir):500-1000mg three times/day for 5 days.
Tab.Famtrex (Famciclovir):500-1000mg three times/day for 5-7 days

22.  Enveloped DNA virus – 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 withlesions.
 Children < 13 years
 Incubation period: 10-20 days.

23.  Chicken pox is an acute, ubiquitous, extremely contagious disease usually
occuring in children
 Characterized by an exanthematous vesicular rash.
 Source of infection-chicken pox or zoster patients
 Portal of entry- conjunctiva or respiratory tract
 Incubation period of about 2 weeks

24. Clinical features:
 First 2 decades of life
 Begins with prodromals
 Maculopapular rash appear –followed by vesicles-”dewdrop-like“
 Burst and scab with crust falling off after 1 to 2 weeks
 Centrifugal spread
 Typically continue to erupt for 4 - 7 days
 Contagious from 2 days before eruptions until all the lesions crust

25.  Commonly precede skin lesions
 Most common sites - vermillion border, palate, buccal mucosa
Gingival lesions may resemble Primary herpes.
 Initial raised vesicles (3-4mm) with surrounding erythema
 Rupture and form eroded ulcers (1-3mm)

26.  History and clinical examination
 Confirmation : demonstration of viral cytopathic effects in
cells harvested from the vesicular fluid
 Further confirmatory tests:
 Viral isolation in cell culture- rapid diagnosis.
 Direct fluorescent antibody testing: VZV monoclonal antibodies
 PCR: VZV DNA in CSF

27.  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
 For pts at high risk or more severity
1. Acyclovir (Tab Zovirax) 800 mg 5 times/day for 7-10 days.
2. Valacyclovir (Tab Valtrex) 1000 mg tid for 7-10 days
3. Famciclovir (Tab Famvir) 500 mg tid for 7-10 days
 Immunocompromised:
 Purified VZV Ig can be given to modify the clinical manifestations of
the infection.
 Within 96 hours of initial exposure

28.  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.

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

30.  Prodromal symptoms precede rash in >90% cases (1 to 4 days before
exanthem)
 As the virus travels down the nerve- pain intensifies(burning,tingling ,
itching) in the area innervated by the affected sensory nerves.
 Rarely - zoster sine herpete
 Within 3 to 4 days the vesicles rupture to form clusters of ulcers-
Crustates after 7 to 10 days - resolve within 2 to 3 weeks normally.
 Scaring on healing with hyper/hypo pigmentation.

31. 


Trigeminal nerve involved
Lesion –extends upto midline, involvement of overlying skin
Lesions – 1-4mm white opaque vesicles (painful) – buccal mucosa, hard palate,
gingiva,uvula, pharynx – rupture and form shallow ulcers

32. Cytologic smears – viral cytopathologic effects
Serum investigations- transient rise in IgM & IgG
Biopsy – multinucleated epithelial cells with viral inclusions

33. Commonly affects paients olderthan 60 yrs
 Pain- burning, throbbing, aching, itching orstabbing
 Neuralgias – resolve within 1 year
 Pain subsides after initiation of long- term (Tab. famciclovir)
Facial paralysis associated with herpes zoster of faceor external
auditory meatus

34. Special form of zoster infection of geniculate ganglion
with ipsilateral involvement – facial & auditory nerves
Facial paralysis (Bell’s palsy) + pain + unilateral vesicles over
External auditory meatus & pinna of ear, Oral cavity & pharynx
Hoarseness of voice, loss of taste sensation – ant 2/3rd of tongue

35.  Supportive care – hydration, soft bland diet.
 Specific treatment
Antiviral drugs
Acyclovir (Tab. Zovirax): 800 mg 5 times/day for 7-10 days
Valacyclovir (Tab. Valtrex):1000 mg tid for 7-10 days
Famciclovir (Tab. Famvir): 500 mg tid for 7-10 days
 Management of Post herpetic neuralgia
Gabapentin & 5% lidocaine patch –as first line of treatment

36.  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

37.  Multiplies locally - invades the blood stream and infects B-lymphocytes
 Virus either become latent inside the B-lymphocytes
cause cell death and lead to release of mature virions
 In response to these b-cells, abnormal CD8+ T-lymphocytes are released by
host immune - Downey cells

39.  Hard / soft palate petechiae – transient –disappear 24-48 hrs
 Oropharyngeal tonsillar enlargement -- 2o to tonsillar abcess
 ANUG – common - refractory to normal therapy
 Oral ulcers – occasionally
 OHL: most common EBV related lesion in HIV

40. Classic serologic test-
Paul bunnel test – detect heterophile antiodies
Titre above 100 suggestive of infection
 Positive only in young adults
 For children younger than 4: ELISA can confirm EBV
infections

41.  No specific treatment
 Self limiting, 2-4 weeks
 Bed rest , adequate diet
 Antipyretics (non-aspirin)
 NSAIDs
 Antibiotics – avoided – may cause skin rashes
 Corticosteroids – recommended in life threatening cases

42.  HHV-5 – B-herpes
 Double-stranded DNAvirus
 Latent – salivary gland cells, endothelium, macrophages &
lymphocytes.
 Salivary gland lymphoma.
 Transmission:
 In utero transmission
 Sexual transmission
 Blood transfusion ,organ transplantation

43.  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

44.  90% - asymptomatic
 Neonatal infection:
 Hepatosplenomegaly , extra-medullary cutaneous erythropoiesis,
mental retardation & motor retardation , thrombocytopenia
 Acute adult infection:
 Symptoms ranges from influenza -like to lethal multiorgan involvement
 Only 1/3rd of pts demonstarte pharyngitis and lymphadenopathy
 Rarely, acute sialadenitis-xerostomia and enlargement of affected glands

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

46.  Biopsy :
Characteristic “owl eye” appearance of cellular inclusions
 Specific verification by detection of viral antigens:
 By immunohistochemiostry and PCR
 Demonstrate viral antibody titers
 ELISA of CMV is recommended for any pts with an
unexplianed fever

47.  Prevention : By passive immunization with hyperimmune
gammaglobulin can be successfully prevented
 Pain control : 2% viscous lidocaine, Systemic analgesics.
 Supportive care: Hydration , Soft bland diet
 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..

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

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

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

51.  Cough
 Coryza
 C onjunctivitis
 Accompanied by fever
 Koplik’s Spots – buccal mucosa
 “Grains Of Salt In A Red Background”-
Pathognomic

52.  Fever continues
 Koplik’s spots fade
 Morbiliform rash begins - blanches on pressure
 Face is involved 1st then spread to trunk andextremities
 Abdominal pain – secondary to lymphatic involvement

53.  Fever ends
 Rash begins to fade
 Downward progression -Replacement by brown pigments
Complications:
 Young children: otitis media, pneumonia,persistent bronchitis and diarrhea
 Immunocompromised pts: more atypical rashes

54. -
 Apart from koplik spots-
Candidiasis, ANUG and necrotising
stomatitis can occur
 Severe measles in children –affect
odontogenesis-pitted enamel hypoplasia.
 Enlargement of tonsils.

55. Desmonstration of rising serologic antibody titers-
appear within 1 to 3 days after exanthem- peaks in 3
to 4 weeks

56.  No specific drugs
 Antiviral drug –Ribavirin is effective against measles.
 Cap. Ribavin 200mg QID
Syrup Ribavin 5ml daily –2 divided doses.
 VitaminA should be given - VitaminA Chewable TAB – 50000 IU.
.

57.  MMR vaccine -Introduced in 1963
 Incidence decreased by 99%
 MMR vaccine:
MMR 1 - 1year
MMR 2 - 4-6yrs.
 Passive immunization: Human immunoglobulin (im)
<1 yr – 250mg ;
>1 yr – 500mg.

58.  Primarily in winter
 Toga virus
 Transmission: droplet infection, congenital
rubella syndrome
 Infection of the mother by Rubella virus
during pregnancy can be serious
 Spontaneous abortion occurs in up to 20%
of cases
 "Blueberry muffin lesions."

59.  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.

60. Incubation Period 14-21 Days
Contagious - from 1 week before exanthem to about
5 days after development of rashes
Mostly asymptomatic
Prodromal symptoms-1 to 5 days before exanthem
Lymphadenopathy-persists for weeks - cervical, postauricular
Exanthematous rash- entire body within 3 days : 1st sign-pink macule-
papules-flaky desquamtion-resolves by day 3
Most common complication is arthritis

61. 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 decidous teeth

62.  A four fold rise in rubella IgG antibody titre between acute
and convalescent serum specimens.
 A positive serologic test for rubella-specific IgMantibody.
 A positive rubella culture (isolation of rubellavirus).
 Serologic studies are best performed within 7 to 10 days afterthe
onset of the rash and should be repeated two to three weekslater

63. No specific Rx- non aspirin antipyretics and antipruritics
Prevention: MMR vaccine, sub cutaneous inj.
1st around 1 year
2nd: 4-5 years.
Passive immunity : human rubella immunoglobulin.

64.  Caused by paramyxovirus family , genus:Rubulavirus
 Epidemiology markedly affected by MMR vaccine
 Before vaccination, epidemics were seen every 2 to 5 years- 90% before age 15
 Post vaccination, 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

65.  Transmitted through urine, saliva, respiratory droplets
 Incubation period – 15 to 18 days
 Contagious from 1 day before the clinical appearance to 14 days
after itsclinical resolution
 Site of involvement- salivary glands, pancreas, choroid plexus,mature
ovaries and testis.
 One attack confers life long immunity

66.  Infection and Proliferation of virus in upper Resp tract
 Replication in respiratory epithelium
 Localisation in glandular & neural tissues
 Perivascular and interstitial mononuclear infiltrate,
necrosis- acinar cells

67.  30% subclinical
 5-15 YRS
 Incubation Period: 2-4weeks
 Prodromal symptoms: pain below ear, headache,malaise,myalgia
 Parotid gland is most commonly affected-Swelling occurs within 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 manifestation is redness and enlargemnt of Whartons and stensons ductal
openings

68.  Most frequently used confirmatory measure is demonstration of
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

69.  Palliative in nature
 Avoidance of sour foods and more liquid helps to decrease the
salivary gland discomfort
 Application of intermittent ice
 Warm saline gargles, soft foods, and extra fluids
Prevention:
 M-M-R (Measles, Mumps, and Rubella Virus Vaccine
Live)

70.  First identified in 1937, in birds that had the potential to devastate
poultry stocks.
 Evidence of human coronaviruses found in the 1960s, in the noses of
people with the common cold.
 Human coronaviruses that are particularly prevalent include 229E,
NL63, OC43, and HKU1.
 The name “coronavirus” comes from the crown-like projections on their
surfaces.
 “Corona” in Latin means “halo” or “crown.”

71.  Common in animals worldwide, rarely affects humans.
 WHO used the term 2019 novel coronavirus to refer to a coronavirus that
affected the lower respiratory tract of patients with pneumonia in Wuhan,
China on 29 December 2019.
 WHO named 2019 novel coronavirus as coronavirus disease (COVID-19)
 Current reference name for the virus is severe acute respiratory syndrome
coronavirus 2 (SARS-CoV-2).
 Highly transmissible than the SARS-CoV.
 Incubation duration ranges from 7 to 14 days
 Most people who get COVID-19 will have a mild form of the disease.
 According to WHO, around 80% of people who get COVID-19 will recover
without needing hospitalization.
 Remaining 20% become seriously ill and develop difficulty breathing.

72.  Most common symptoms: Fever, dry cough. tiredness.
 Less common symptoms:
Aches and pains, sore throat, diarrhea, Conjunctivitis,
headache, loss of taste and smell, a rash on skin.
 Serious symptoms: Difficulty breathing or shortness of
breath.
 Chest pain or pressure.

73.  Multiple ulcers with an erythematous halo and symmetric distribution
on the right hard palate
 Blisters on the inner lip mucosa

74. Currently, no definite cure has been found.

75.  The most common reason for oral ulcerations and blisters
is viral infections.
 Major challenge in the diagnosis of oral viral infections is
due to complex clinical presentations
 Early recognition of oral viral infections will reduce the
morbidity, comorbidity, and the clinical care cost.
 Hence, diagnosing oral lesions with presence of systemic
manifestations will serve as a useful tool in clinical
situation.

76.  Oral & maxillofacial pathology: Neville, 3rd
edition.
 Text book of oral medicine: Burkitts, 11th edition
 Shafer’s text book of oral pathology, 6th edition


77. Thank You :)