Clinical Microbiology Fifth Year

1. VIRAL INFECTIONS OF MOUTH

2. Common Oral Conditions
• Acquired
• Developmental
• Congenital

3. Acquired Oral Conditions
• Infections:
Viral
Bacterial
Fungal -Candida
• Ulcers
• Autoimmune lesions
• Glossitis
• Discolored teethth

4. INFECTIOUS DISEASES
• DIAGNOSTIC CRITERIA
– Obtain medical history
– Obtain dental history
– Conduct complete clinical examination
– Obtain necessary laboratory and radiographic
studies.

5. Viruses causing oral lesions
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Human Herpes virus(HHV)
Human papilloma virus (HPV)
Coxasackie virus
Mumps virus
Measles virus
Rubella virus

6. Human Herpes virus(HHV)
• HHV infections are common in oral cavity
• 8 types of HHV have been linked with oral
disease
• HHV 1 – primary herpetic gingivostomatitis,
latent infections (common sore)
• HHV 2 – oral lesions clinically similar to HHV1
• HHV 3 ; Varicella –Zoster virus (VZV)Chicken
pox and Shingles

7. • HHV 4 ; Ebstein-Barr virus (EBV) - Oral hairy
leukoplakia, Infectious mononucleosis,
Nasopharyngeal ca, Burkitt’s lymphoma
• HHV 5; Cytomegalovirus (CMV)- primary
infection of salivary glands
• HHV 6&7 - Infects CD4 cells(Roseola infantum)
• HHV8 - Kaposi’s sarcoma

8. General features of Herpes viruses
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Herpen = To creep in crops
Enveloped, Icosahedral ds DNA viruses
Replicate in host cell nucleus.
TRANSMISSION – Saliva, direct , skin to skin,
skin to mucosal contact (oral genital)
• SPREAD – penetrate mucosal epithelial cells,
Cutaneous nerve fibers and sensory ganglia
• Remain LATENT in infected cells.
• Periodic reactivation

9. HERPETIC GINGIVOSTOMATITIS – HHV 1
• Primary lesions occur in children and adolescents
• Many infections are asymptomatic
• Lesions – small, multiple, clustered umbilicated
vesicles anywhere in and around oral cavity, peri
oral skin, pharynx, rupture to form large painful
ulcers,
• Recurrent herpes lesions – cold sores, keratinized
mucosa (lips, gingiva, hard palate)
• Other C/F – fever, malaise.

10. HERPETIC GINGIVOSTOMATITIS
• Diagnosis:
– Age: Young patients History
– First exposure to HSV
– Viral culture, serum antibody. EM, PCR,
Vesicle develop on the lips, tongue, gingival, palate

11. • Triggers for recurrence – sunlight exposure,
stress physical or emotional systemic illness,
trauma(dental procedures)
• Travel retrograde sensory neuron to local ganglion,
remain latent (trigeminal ,sacral, lumbar ganglion)
• Trigeminal neuralgia (HHV1).
• HHV-2 causes similar lesions
but less common

12. HHV3 (VARICELLA OR SHINGLES)
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Intra oral and pharyngeal vesicles may occur
Virus becomes latent in dorsal root ganglia
Recurrent Varicella (Herpes zoster or Shingles)
Usually affects single dermatome.
In mouth vesicles or ulcerations stop sharply
at midline
• Prodrome of pain, burning or itching that
mimics toothache may occur.

13. Human herpesvirus (HHV) type 3.
Intraoral herpes zoster closely
resembles recurrent HHV-1
infection, but the lesions generally
follow a dermatome and stop
sharply at the midline, as shown
here. However, the rules for
common sites of occurrence of HHV1 and HHV-3 often do not apply to
patients who are
immunocompromised.

14. Ramsay- Hunt syndrome
• Seen when HHV3 emerges from latency in
geniculate ganglion
• Facial nerve (VII) is involved.
• C/F – paralysis of facial muscles, levator palati,
loss of secretory function, vertigo, tinnitus,
pain, vesicles in pharynx eardrum.
• Persistent facial nerve weakness or deafness
may follow.

15. HHV 4 (EBV)
• Primary infection - Infectious mononucleosis
• Infected saliva (kissing disease) Subclinical, young
adulthood.
• Spreads to B and salivary glands and multiplies
• T lymphocytes (If the patient is immunocompetent, cytotoxic T cells
become activated and a characteristic lymphadenopathy posterior cervical
nodes accompanies tonsillitis and hepatosplenomegaly.)
• Latent infection in B cells

16. •
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Infectious mononucleosis
Nasopharyngeal ca
African Burkitt's lymphoma
Oral hairy leukoplakia

17. A 21-year-old
woman with
infectious
mononucleosis
presents with a
petechial lesion
on her palate.
Infectious mononucleosis

18. Oral Hairy leukoplakia (HHV4)
• White patches in the mouth
• Benign lesion in Immunocompromised adults
• Asymptomatic white lesions on the dorsal or
ventral,sides of tongue and rarely on buccal
mucosa.
• Lesions- Greyish white, corrugated, linear
appearance, granular or nodular or may have hair
like projections.
• May be the first manifestation of IC status (HIV)
other conditions

19. • OHL can look like thrush (CANDIDA),
• Thrush usually comes off when it is lightly
scraped with a toothbrush, whereas OHL does
not.
• Patches do not usually cause discomfort and
generally do not affect the taste of foods or
liquids.

21. HHV 8 (Kaposi’s Sarcoma
associated Herpes virus KSHV)
• Seen commonly in IC or IS patients, rarely in
children.
• The lesion may appear as a red, purple or
dusky patch that enlarges into a plaque and
later progresses into a tumorous mass.
• Palate is initial site of intra oral KS, others
include gingiva, tongue and Tonsillar area.

22. HHV-Diagnosis and treatment
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Most of the times Clinical findings alone
Smear of intact vesicle for HHV 1,2 & 3
Direct immunofluorescence(DIFAT)
Culture - Cell cultures, Embryonated egg.
Biopsy for confirmation of KSHV and others.
Molecular methods- PCR,

23. HHV-MANAGEMENT
• HHV1,2 - Analgesics, Acyclovir IN EARLY stages
• HHV3 - Acyclovir WITHIN 48-72 hrs,
Valcyclovir or Famciclovir better in reducing
pain and lessening post herpetic neuralgia,
Vaccine (live attenuated)12 months onwards.
• EBV – conservative approach for oral hairy
leukoplakia (topical PODOPHYLLIN, TRETINOIN
less useful, systemic antivirals rarely)

24. HHV 8 (KSHV) MANAGEMENT
• Referred to expert, improve systemic immune
status, low dose radiation therapy when
lesions are confined to mouth, intra lesional
injections of Vinblastine and/or sodium tetra
decyl sulfate, and/or interferonalfa(IFN-A)
• Regular follow up for immune status

25. HUMAN PAPILLOMA VIRUS
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Papovaviridae family
PA PO VA = PApillma, POlyoma, VAcuolisation.
Small icosahedral, NE, circular dsDNA virus.
Transmission - close skin to skin contact, sexual,
oro-genital contact.
• Penetrates the mucosal epithelium & invades the
cells of basal layer.
• Rate of HPV carriage in oral cavity of healthy
adults is 5-80%.

26. • At least 106 types of HPV- High risk (16, 18,
33, 35) and Low risk types(1,2, 3,4, 27, 29,
etc…)
• HPV 16 associated with dysplasia and
carcinoma in oral cavity, cervix.
• HPV lesions are more common in IC (HIV)
patients
• Play role in oral pre malignancy and
malignancies (Squamous cell carcinoma)

27. Common lesions
• Verrucca vulgaris or Common warts (HPV
types 2, 4)
• Condyloma acuminata 0R Genital warts
(HPV types 6,11)
• Focal epithlial hyperplasia or Heck’s
disease(HPV types 13, 32)

28. A mnemonic for remembering
the microscopic and clinical
shapes of verruciform oral
lesions:
• Verruca vulgaris is
shaped like a series of
inverted V's.
• Condyloma acuminata
are shaped like a series of
C's placed on their sides.
• Papillomas are
pedunculated like the letter P.

29. VERRUCCA VULGARIS or COMMON
WARTS (HPV2, 4)
• The name "verruca" is Latin for wart
• A local growth of the outer layer of the skin
caused by a virus
• White, sessile, verrucous, solitary or multiple
elevated lesions with discrete borders.
• Common on skin(lips, hard palate or gingiva)
• In patients with oral infection, commonly
seen on digits.

30. • Human papillomavirus (HPV).
Verruca vulgaris on the lateral
border of the tongue exhibits the
multiple, sharp-tipped, white,
verrucous appearance, which is
classic for this lesion in the oral
cavity. Not all verrucae are so
clinically diagnostic.
• This verruca on the retromolar
pad shows much less
keratinization and a broader base.
• Verrucae and papillomas may be
difficult to differentiate, but both
are usually surgically excised.

31. This is a verruca vulgaris
of the anterior maxillary
gingiva in a healthy
young male. He had
recently resolved a wart
on his finger.
These small papillomas
on the lateral tongue of a
young woman showed
histologic evidence of
HPV in the form of
extensive koilocytosis.

32. Condyloma acuminata or Genital
warts (HPV types 6,11)
• Can affect oral mucosa, cerebriform, pink,
sessile, solitary or multiple.
• Occur commonly on non keratinised
mucosa(genital area)
Condylomata on the lower
lip

33. Focal epithlial hyperplasia or Heck’s
disease(13, 32) –
Epidemic in young adults.
• Multiple smooth sessile nodules and
mucosal surface of lower lip or
buccal mucosa.
•

34. Laboratory diagnosis
• Immunohistochemical detection of HPV
structural proteins
• Enzyme immunoassays – very sensitive
• PCR DNA amplification – excisional biopsy
• Histologic findings –koilocytosis, dark
shrunken nuclei and cytoplasmic
vacuolisation.

35. Management
• Oral lesions are treated with excisional biopsy
• Topical agents are used – Cidofovir antiviral
• Intralesional injections – Bleomycin (cytotoxic
polypeptide that inhibits DNA
synthesis in cells and viruses.
• IFN-A - Naturally occurring cytokine with antiviral,
antibacterial, anticancer and immunmodulatory
• Systemic agents – Retinoids or systemic vitamin A
anologs
• Imiquimod 5% - toll like receptor 7 activator
• Vaccine – oral HPV related disease is not yet known.

36. Coxsackie virus
• PicoRNAviridae family, Enterovirus genus
• Enteroviruses 4 subgroups – Polio viruses,
Coxsackievirus group A,B and ECHO viruses.
• Infect humans via fecal-oral route.
• Attach to mucosal epithelium in pharynx to
ileum.
• Spreads to regional lymph nodes cervical and
mesenteric – viraemia.
• Most infections subclinical, IP 3-5 days

37. • Hand Foot and Mouth disease – vesicular,
eryhematous lesions in mouth(tongue, buccal
mucosa, soft palate) hands and fingers, feet
and toes.
• Herpangina – sudden onset of sore throat,
fever and painful swallowing, vesicles on soft
palate.
• Acute lymphonodular pharyngitis – variant of
herpangina, lesions remain papular without
progressing to vesicles and ulcers.

38. HFMD - vesicular eruption in the mouth

39. HERPANGINA =
Painful mouth and
throat ulcers

40. Diagnosis and Management
• Diagnosed mainly on clinical grounds.
• Confirmed by Virus isolation(cell culture, most
widely used), PCR, serological testing.
• Treatment not required usually, prevent
secondary infections, topical anesthetics and
coating agents, analgesics paracetamol.

41. Rubella (German measles)
• RNA virus, Family Togaviridae, genus Rubi
virus
• Unstable virus killed by lipid solvents trypsin,
formalin, UV light and extreme Ph.
• Acute exanthematous viral infection similar to
Measles infection.
• Spread – droplet (Inhalation), replicates in
nasopharynx and lymph nodes

42. Clinical features
• Lymphadenopathy (major manifestation)- post
auricular, post cervical and sub occipital
lymph nodes.
• Intraorally (Forchheimer sign) – dark red
papules on soft palate, arise at onset of rash,
enanthem consisting petechial lesions,
seen in 20% of cases.

43. Forchheimer sign- Petechial lesions in mouth

44. Diagnosis and management
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Clinical evaluation
Virus isolation
ELISA for IgM, IgG antibodies.
Vaccine – live attenuated vaccine available
(MMR)

45. Mumps
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Paramyxoviridae family, genus Rubula virus
Endemic through out the world.
Transmission- droplets, direct contact, fomites
URT & Regional lymph nodes.
Viraemia – glandular and neural tissues.
Epidemic parotitis , acute generalized
infection in children 5-15 years.

46. Clinical features – Parotitis
• Low grade fever, malaise, headache, earache
tenderness of parotid glands simoultaneously
on both sides.
• Recurrent acute and chronic sialadenitis are
complications.
• Earlobes on affected side lifted upwards and
outwards
• Trismus – difficulty in eating and speaking
• Intraorally enlargement and redness of
opening of Stensen’s duct.

48. Complications
• CNS – Aseptic meningitis(asymptomatic 60%),
headache, neck stiffness in 15%
• Orchitis (testicular inflammation) 20-50%
post pubertal males, atrophy in 50% , sterility
is uncommon.
• Pancreatitis - uncommon complication
• Deafness - acquired sensory neural deafness

49. Diagnosis and management
• Clinical diagnosis
• Supportive – analgesics, liqid diet, isolation,
bed rest
• Prevention – Live attenuated vaccine( Jeryl –
Lynn strain) given with Measles and Rubella,
at least 2 doses before 4-6 years, life long
immunity.

50. Measles (Rubeola)
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Family Paramyxoviridae, genus Morbillivirus
Acute, highly contagious disease in children
Spread – droplets from respiratory secretions
Initial site of infection is upper respiratory
tract epithelium, lymph nodes  primary
viraemia  Reticulo Endothelial System.
• Secondary viraemia after breakdown and
necrosis of RES cells

51. Clinical features
• IP 10-14 days, Exanthematous fever, and
cough, coryza,
• Rash – erythematous, maculopapular
spreading from head to toe direction.
• Koplik’s spots pathognomonic for measles.
• Located on buccal mucosa in premolar and
molar area, bluish grey pecks against
Erythematous background (rains of sand)
• Plaque like or nodular and oval or round

52. Koplik spots in measles.
They are small, white
spots (often on a
reddened background)
that occur on the inside of
the cheeks early in the
course of measles.

53. Diagnosis and Management
• Virus isolation- blood, urine, nasopharyngeal
• Serology – IgM detection.
• Histology - Warthin- Finkeldy cells MNG cells,
neutrophils in koplik spots
• PCR
• Antibiotics for secondary bacterial infections,
Vit A, Ribavirin in Immunocompromised
• Prevention – MMR vaccine(EdmonstonEnders strain)

54. Complications
• No oral complications have been reported.
• Diarrhea, otitis media, pneumonia are
common.
• Sub acute sclerosing pan encephalitis (SSPE)
– CNS disease years after primary infection,
progressive deterioration of higher functions,
seizures, motor functions eventually death.