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VIRAL
DISEASES




   Prepared by:
        Dr. Rea Corpuz
Viral Disease

 (1) Herpes Simplex

 (2) Varicella (Chicken Pox)

 (3) Herpes Zoster (Shingles)

 (4) Rubeola (Measles)

 (5) Epidemic Parotitis (Mumps)

 (6) Herpangina
Viral Disease

 (7) Infectious Mononucleosis
     (Kissing Disease)

 (8) Cytomegalic Inclusion
     Disease
(1) Herpes Simplex Virus

 2 types

   HSV-1

   HSV-2
(1)Herpes Simplex Virus-1

 spread predominantly
  through infected saliva or
  active perioral lesions

 adapted best + performs
  more efficiently in

    oral
    facial
    ocular area
(1)Herpes Simplex Virus-1


 pharynx
 intraoral sites    involved
 lips                 most
 eyes                frequently
 skin above waist
(1)Herpes Simplex Virus-1

 Clinical Features

    initial exposure to an
     individual without antibodies
     to virus is called primary
     infection

    typically occurs at a young age

    often asymptomatic
(1)Herpes Simplex Virus-1

 Clinical Features

    does not cause significant
     morbidity

    virus is taken up by sensory
     nerves

    transported to associated
     sensory or less frequently
     autonomic ganglia

      • virus remains in a latent state
(1)Herpes Simplex Virus-1

 Clinical Features

    all primary infections occur
     from contact with an
     infected person who is
     releasing the virus

    usual incubation period
     is 3-9 days
(1)Herpes Simplex Virus-1

 Clinical Features

    acquired from contact
     with contaminated:

      • saliva
      • active perioral lesions
      • crowding
      • poor oral hygiene
(1)Herpes Simplex Virus-1

 Clinical Features

    Acute Herpetic Gingivostomatitis
     (primary herpes)

      • most common pattern
       of symptomatic primary
       HSV infection

      • arise between ages of
       6 months and 5 years
(1)Herpes Simplex Virus-1

 Clinical Features

    Acute Herpetic Gingivostomatitis
     (primary herpes)

      • peak prevalence occurring
       between 2 and 3 years of
       age

      • onset is abrupt
(1)Herpes Simplex Virus-1

 Clinical Features

    Acute Herpetic Gingivostomatitis
     (primary herpes)

      • accompanied by:

          anterior cervical
           lymphadenopathy
          chills
          fever (103 to 105 F)
          nausea
(1)Herpes Simplex Virus-1

 Clinical Features

    Acute Herpetic Gingivostomatitis
     (primary herpes)

      • accompanied by:

          anoxeria
          irritability
          sore mouth lesions
(1)Herpes Simplex Virus-1

 Clinical Features

    Acute Herpetic Gingivostomatitis
     (primary herpes)

      • initially affected mucosa
       develops numerous pinhead
       vesicles, which rapidly collapse
       to form:

          small        lesions
          red
(1)Herpes Simplex Virus-1

 Clinical Features

    Acute Herpetic Gingivostomatitis
     (primary herpes)

      • both movable + attached
       oral mucosa can be affected

      • in all cases, gingiva is:

          enlarged
          painful
          extremely erythematous
(1)Herpes Simplex Virus-1

 Clinical Features

    Acute Herpetic Gingivostomatitis
     (primary herpes)

      • mild cases usually resolve
       within 5-7 days

      • severe cases may extend
       to 2 weeks
(1)Herpes Simplex Virus-2

 adapted best to the genital
  zones

 predominantly through
  sexual contact

 typically involves

   • genitalia
   • skin below waist
(1)Herpes Simplex Virus-2


 antibodies to HSV-1 decrease
  the chance of infection with
  HSV-2 or lessen severity
  of clinical manifestations
(1)Herpes Simplex Virus-2


 dramatic increase seen in
  HSV-2 due to:

    partly to lack of prior
     exposure to HSV-1

    increased sexual activity

    lack of barrier conception
Herpes Simplex Virus


 Treatment & Prognosis

   if infection is diagnosed
     early, antiviral medications
     can have significant influence
(2) Varicella (Chickenpox)


 similar to herpes simplex
  virus (HSV)

 chickenpox represents primary
  infection with VZV

 latency ensues, and recurrence
  is possible as herpes zoster
  often after many yesterday
(2) Varicella (Chickenpox)


 Etiology

    presumed to be spread
     through air droplets

    direct contact with
     active lesions

    arise between ages of
     5 and 9
(2) Varicella (Chickenpox)


 Clinical Features

    symptomatic phase usually
     begins with:

      • malaise
      • pahryngitis
      • rhinitis
(2) Varicella (Chickenpox)


 Clinical Features

    in older children + adults,
     additional symptoms:

      • headache
      • myalgia
      • nausea
      • anorexia
      • vomiting
(2) Varicella (Chickenpox)

 Clinical Features

    rash begins on face +
     trunk followed by
     involvement of extremeties

    each lesion rapidly progresses
     through stages of:
      • erythema
      • vesicle
      • pustule
      • hardened crust
(2) Varicella (Chickenpox)

 Clinical Features

    lesions typically continue
     to erupt for 4 days

    some cases, exanthem’s
     arrival may extend to 7 or
     more days

    affected individuals are
     contagious from 2 days
     before exanthem until all
     lesions crust
(2) Varicella (Chickenpox)

 Clinical Features

    vermillion border of
     lips + palate are most
     common sites of
     involvement

    followed by buccal mucosa

    occasionally, gingival lesions
     resemble those with
     primary HSV infections
(2) Varicella (Chickenpox)

 Clinical Features

    lesions of varicella tend
     to be painless

    lesions begin as 3-to-4-mm
     white opaque vesicles

      • rupture to form
        1-to-3-mm ulcerations
(2) Varicella (Chickenpox)

 Clinical Features

    prevalence + number of
     oral lesions correlate
     with severity of extraoral
     infection
(2) Varicella (Chickenpox)

 Clinical Features

    mild cases: often only
    1 or 2 oral ulcers are evident

      • these heal within
       1-3 days

    severe cases: almost
     always have oral ulcerations
     upto 30 lesions

      • persist for 5-10 days
(2) Varicella (Chickenpox)

 Treatment & Prognosis

   warm bath with soap
     or baking soda

   application of calamine
     lotion

   systemic diphenhydramine

     • to relieve pruritus
(2) Varicella (Chickenpox)

 Treatment & Prognosis

   antipyretics should be
    given to reduce fever

   use of peroral antiviral
    medications such as:

     • acyclovir     been shown
     • valacyclovir   to reduce duration + severity
     • famciclovir if administered within first 24 hrs
                    of rash
(3) Herpes Zoster (Shingles)

 after initial infection with
  chickenpox, virus is transported
  up the sensory nerves

 presumably establishes
  latency in dorsal spinal
  ganglia

 occurs after reactivation
  of virus, with involvement
  of the distribution of affected
  sensory nerves
(3) Herpes Zoster (Shingles)

 predisposing factors for
  reactivation:

    immunosuppresion
    HIV-infection
    treatment with cytoxic or
     immunosuppresive drugs
    radiation
    presence of malignancies
    old age
    alcohol abuse
    stress (emotional or physical)
(3) Herpes Zoster (Shingles)

 Clinical Features

    can be grouped into 3
     phases:

      • (1) prodome
      • (2) acute
      • (3) chronic
(3) Herpes Zoster (Shingles)

 Clinical Features

    (1) Prodome

      • during initial viral replication
       active ganglionitis develops
       with resultant

          neuronal necrosis
          severe neuralgia
(3) Herpes Zoster (Shingles)

 Clinical Features

    (1) Prodome

      • inflammatory reaction
       is responsible for padromal
       symptoms of intense
       pain that precedes rash
       in more than 90% of
       cases
(3) Herpes Zoster (Shingles)

 Clinical Features

    (1) Prodome

      • as virus travels down the
       nerve, pain intensifies:

          burning
          tingling
          itching
         Boring
          prickly or knifelike
(3) Herpes Zoster (Shingles)

 Clinical Features

    (1) Prodome

      • pain develops in area of
       epithelium innervated by
       affected sensory nerve
       (dermatome)
(3) Herpes Zoster (Shingles)

 Clinical Features

    (1) Prodome

      • accompanied by:

          fever    normally present
          malaise   1-4 days before
          headache development of cutaneous
                      or mucosal lesions
(3) Herpes Zoster (Shingles)

 Clinical Features

    (2) Acute

      • begins as involved skin
        develops clusters of vesicles
        set on erythematous base

      • within 3-4 days, vesicles
        become pustular + ulcerate
        with crusts developing after
        7-10 days
(3) Herpes Zoster (Shingles)

 Clinical Features

    (2) Acute

      • oral lesions occur with
       trigeminal nerve involvement

      • may be present on movable
        or bound mucosa
(3) Herpes Zoster (Shingles)

 Clinical Features

    (2) Acute

      • lesions often extend to
       midline

      • frequently are present in
       conjunction with involvement
       of skin overlying affected
       quadrant
(3) Herpes Zoster (Shingles)

 Clinical Features

    (2) Acute

      • most cases, significant
       bone necrosis with loss of
       teeth in areas involved
       with herpes zoster
(3) Herpes Zoster (Shingles)

 Clinical Features

    (3) Chronic

      • approximately 15% of affected
       patients progress to chronic
       phase of herpes zoster

          characterized by pain
           (postherpetic neuralgia)
          persists longer than 3 months
           after initial presentation of acute rash
(3) Herpes Zoster (Shingles)

 Clinical Features

    (3) Chronic

      • pain is described as:

          burning
          throbbing
          aching
          itching
          stabbing often with flares
           caused by light stroking of the area
           or from contact with adjacent clothing
(3) Herpes Zoster (Shingles)

 Treatment & Prognosis

   antipyretics

   antipruritics such as
     diphenhydramine

     • can be administered
      to decrease itching
(3) Herpes Zoster (Shingles)

 Treatment & Prognosis

   skin lesions should be kept
     dry + clean

     • prevent secondary infection

   antibiotics to treat secondary
     infections
(3) Herpes Zoster (Shingles)

 Treatment & Prognosis

   antiviral medications:

     • acyclovir    accelerate healing
     • valacyclovir of cutaneous + mucosal
     • famciclovir lesions;
                    reduce duration of
                    acute pain
                    effective if initiated within
                    72 hours after development
                     of 1st vesicle
(3) Herpes Zoster (Shingles)

 Treatment & Prognosis

   once skin lesions have healed,
     neuralgia become worst
     aspect of disease

     • often most difficult to
      resolve successfully

     • analgesics
     • narcotics
     • antidepresssants
     • anticonvulsants
(4) Rubeola (Measles)


 infection produced by a
  virus in the family
  Paramyxovirus, genus
  Morbillivirus
(4) Rubeola (Measles)


 Clinical Features

    most cases arise in winter

    spread though respiratory
     droplets

    incubation period is from
     10-12 days
(4) Rubeola (Measles)


 Clinical Features

    affected individuals are
     infectious from 2 days
     before becoming symptomatic
     until 4 days after appearance
     of associated rash
(4) Rubeola (Measles)


 Clinical Features

    virus is associated with
     significant lymphoid
     hyperplasia often involves
     sites such as:

      • lymph nodes
      • tonsils
      • adenoids
      • Peyer’s patches
(4) Rubeola (Measles)


 Clinical Features

    there are 3 stages of
     infection

    each stage lasting 3 days

    justifying designation
     nine-day measles
(4) Rubeola (Measles)


 Clinical Features

    First 3 days are dominated
     by 3 Cs:

      • Coryza (runny nose)

      • Cough (brassy + unconfortable)

      • Conjunctivitis (red, watery,
                photophobic eyes)
(4) Rubeola (Measles)


 Clinical Features

    fever typically accompanies
     these symptoms

    during initial stage, most
     distinctive oral manifestation

      • Koplik Spots
      • multiple areas of mucosal erythema
          visible on buccal + labial mucosa
(4) Rubeola (Measles)
(4) Rubeola (Measles)


 Clinical Features

    during initial stage, most
     distinctive oral manifestation

      • less often on soft palate
      • within these areas are numerous
        small, blue-white macules
(4) Rubeola (Measles)


 Clinical Features

    as second stage begins,

      • fever continues
      • Koplik spot’s fade
      • maculopapular + erythematous
       (morbilliform) rash begins
(4) Rubeola (Measles)


 Clinical Features

    as second stage begins,

      • face is involved first, with
       eventual downward spread
       to trunk + extremities
(4) Rubeola (Measles)


 Clinical Features

    as second stage begins,
(4) Rubeola (Measles)


 Clinical Features

    in third stage,

      • fever ends
      • rash begins to fade
      • demonstrate downward
       progression with
       replacement by a brown
       pigmentary staining
(4) Rubeola (Measles)
(4) Rubeola (Measles)


 Treatment & Prognosis

   good vaccination program

   in healthy patients with
     measles,

     • fluids
     • nonaspirin antipyretics
(5) Epidemic Parotitis (Mumps)


 infection caused by virus
  in the family Paramyxovirus,
  genus Rubulavirus

   • causes a diffuse disease of
     exocrine glands
(5) Epidemic Parotitis (Mumps)


 although salivary glands
  are best known sites of
  involvement

   • pancreas       frequently involved
   • choroid plexus exhibit edema +
   • mature ovaries lymphocytic
   • testes          infiltration
(5) Epidemic Parotitis (Mumps)


 Clinical Features

    symptomatic cases:

      • prodromal symptoms of
        low grade fever         arrive
      • headache                 first
      • malaise
      • anorexia
      • myalgia
(5) Epidemic Parotitis (Mumps)


 Clinical Features

    parotid gland is involved
     most frequently but
     sublingual + submandibular
     gland also can be affected
(5) Epidemic Parotitis (Mumps)


 Clinical Features

    discomfort + swelling develop
    in tissues surrounding
    lower half of external ear

    extending down along posterior
     inferior border of adjacent
     mandible
(5) Epidemic Parotitis (Mumps)


 Clinical Features

    enlargement typically
     peaks within 2-3 days

    pain is most intense during
     this period of maximal
     enlargement
(5) Epidemic Parotitis (Mumps)


 Clinical Features

    chewing movements of
     jaw or eating saliva-stimulating
     foods tends to increase pain

    enlargement of glands usually
     begins on one side

    followed by contralateral glandular
     changes within a few days
(5) Epidemic Parotitis (Mumps)


 Clinical Features

    unilateral involvement
     is most common

    most common oral manifestation
     is redness + enlargement of

      • Wharton’s     salivary gland
      • Stensen’s     duct openings
(5) Epidemic Parotitis (Mumps)


 Treatment & Prognosis

   palliative in nature

   nonaspirin analgesics

   antipyretics

   in attempt to minimize orchitis,
     bed rest is recommended for
     males until fever breaks
(5) Epidemic Parotitis (Mumps)


 Treatment & Prognosis

   avoid sour foods + drinks

     • helps decrease salivary
      gland discomfort

   as with measles + rubella,
     best results come from
     prior vaccination
(6) Herpangina


 begins with an acute onset
  of significant

    sore throat
    dysphagia
    fever
    ocassionally accompanied by
     cough
    rhinorrhea
    anorexia
(6) Herpangina


 begins with an acute onset
  of significant

    vomiting
    diarrhea
    myalgia
    headache
(6) Herpangina


 small number of oral lesions
  usually 2-6

   • develop in posterior areas
      of mouth
   • usually soft palate
   • tonsillar pillars
(6) Herpangina


 affected areas begin as
  red macules

   • form fragile vesicles
    that rapidly ulcerate

   • ulcerations average 2-4
     mm in diameter
(6) Herpangina


 systemic symptoms resolve
  within a few days

 ulcerations usually take
  7-10 days to heal
(7) Infectious Mononucleosis
   (Glandular Fever; Kissing
    Disease)
 symptomatic disease

 resulting from exposure to
  Epstein-Barr virus
  (EBV, HHV-4)

 infection usually occurs
  by intimate contact
(7) Infectious Mononucleosis
   (Glandular Fever; Kissing
    Disease)
 intrafamilial spread is common

 once a person is exposed, EBV
  remains in the host for life

 children usually become
  infected through contaminated
  saliva on fingers, toys or
  other objects
(7) Infectious Mononucleosis
   (Glandular Fever; Kissing
    Disease)
 adults usually contract virus
  through direct salivary
  transfer

    shared straws
    kissing
(7) Infectious Mononucleosis
   (Glandular Fever; Kissing
    Disease)
 Clinical Features

    most EBV infections in
     children are asymptomatic

    children younger than 4 years
     of age with symptoms
      • fever
      • lymphadenopathy
      • pharyngitis
      • hepatosplenomegaly
      • rhinitis or cough
(7) Infectious Mononucleosis
   (Glandular Fever; Kissing
    Disease)
 Clinical Features

    in young adult

      • prodomal fatigue
      • malaise
      • anorexia
      • body temperature may
       reach 104 F
          lasts from 2-14 days
(7) Infectious Mononucleosis
   (Glandular Fever; Kissing
    Disease)
 Clinical Features

    lingual tonsils can
     become hyperplastic

      • compromise airway

    lymphoid enlargement
(7) Infectious Mononucleosis
   (Glandular Fever; Kissing
    Disease)
 Clinical Features

    petechiae on hard or soft
     palate are present

      • transient
      • usually disappear within
        24-48 hours
(7) Infectious Mononucleosis
   (Glandular Fever; Kissing
    Disease)
 Treatment & Prognosis

   in most cases, resolves
     within 4-6 weeks

   non-aspirin-containing
     antipyretics + NSAIDs
(8) Cytomegalovirus


 (CMV, HHV-5)

 similar to other human herpes
  virus

    after initial infection

    latency is established

    reactivation is possible
    under conditions favorable to the virus
(8) Cytomegalovirus


 CMV can reside latently in:

    salivary glands cells

    endothelium

    macrophages

    lymphocytes
(8) Cytomegalovirus


 most clinically evident
  disease is found in neonates
  or immunosuppressed adults

 in infants, virus is contracted

    through placenta
    during pregnancy
    during breast-feeding
(8) Cytomegalovirus


 at any age, almost 90%
 of CMV infections are
 asymptomatic

 in clinical evident neonatal
  infection, infant appears
  ill within a few days
(8) Cytomegalovirus


 Typical Features

    hepatosplenomegaly

    extramedullary cutaneous
     erythropoiesis

    thrombocytopenia (often
     associated petechial hemorrhages)
(8) Cytomegalovirus


 Typical Features

    significant encephalitis
     frequently leads to severe
     mental + motor retardation
(8) Cytomegalovirus

 common in patients with
  AIDS

 neonatal CMV infection also
  can produce developmental
  tooth defects

    exhibit diffuse enamel
     hypoplasia
    significant attrition
    enamel hypomaturation
    yellow coloration from underlying dentin
(8) Cytomegalovirus

 Treatment & Prognosis

   resolve spontaneously

   therapy is required in
     immunosuppressed patient

   antipyretic mediactions

   NSAIDs
(8) Cytomegalovirus

 Treatment & Prognosis

   Corticosteroids or IV
     gammaglobulins have been
     used in patients with
     hemolytic anemia or severe
     thrombocytopenia
References:
 Books
  Neville, et. al: Oral and Maxillofacial Pathology
        3rd Edition
        • (pages 240-264)

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Viral diseases (3)

  • 1. VIRAL DISEASES Prepared by: Dr. Rea Corpuz
  • 2. Viral Disease  (1) Herpes Simplex  (2) Varicella (Chicken Pox)  (3) Herpes Zoster (Shingles)  (4) Rubeola (Measles)  (5) Epidemic Parotitis (Mumps)  (6) Herpangina
  • 3. Viral Disease  (7) Infectious Mononucleosis (Kissing Disease)  (8) Cytomegalic Inclusion Disease
  • 4. (1) Herpes Simplex Virus  2 types  HSV-1  HSV-2
  • 5. (1)Herpes Simplex Virus-1  spread predominantly through infected saliva or active perioral lesions  adapted best + performs more efficiently in  oral  facial  ocular area
  • 6. (1)Herpes Simplex Virus-1  pharynx  intraoral sites involved  lips most  eyes frequently  skin above waist
  • 7. (1)Herpes Simplex Virus-1  Clinical Features  initial exposure to an individual without antibodies to virus is called primary infection  typically occurs at a young age  often asymptomatic
  • 8. (1)Herpes Simplex Virus-1  Clinical Features  does not cause significant morbidity  virus is taken up by sensory nerves  transported to associated sensory or less frequently autonomic ganglia • virus remains in a latent state
  • 9. (1)Herpes Simplex Virus-1  Clinical Features  all primary infections occur from contact with an infected person who is releasing the virus  usual incubation period is 3-9 days
  • 10. (1)Herpes Simplex Virus-1  Clinical Features  acquired from contact with contaminated: • saliva • active perioral lesions • crowding • poor oral hygiene
  • 11. (1)Herpes Simplex Virus-1  Clinical Features  Acute Herpetic Gingivostomatitis (primary herpes) • most common pattern of symptomatic primary HSV infection • arise between ages of 6 months and 5 years
  • 12. (1)Herpes Simplex Virus-1  Clinical Features  Acute Herpetic Gingivostomatitis (primary herpes) • peak prevalence occurring between 2 and 3 years of age • onset is abrupt
  • 13. (1)Herpes Simplex Virus-1  Clinical Features  Acute Herpetic Gingivostomatitis (primary herpes) • accompanied by:  anterior cervical lymphadenopathy  chills  fever (103 to 105 F)  nausea
  • 14. (1)Herpes Simplex Virus-1  Clinical Features  Acute Herpetic Gingivostomatitis (primary herpes) • accompanied by:  anoxeria  irritability  sore mouth lesions
  • 15. (1)Herpes Simplex Virus-1  Clinical Features  Acute Herpetic Gingivostomatitis (primary herpes) • initially affected mucosa develops numerous pinhead vesicles, which rapidly collapse to form:  small lesions  red
  • 16. (1)Herpes Simplex Virus-1  Clinical Features  Acute Herpetic Gingivostomatitis (primary herpes) • both movable + attached oral mucosa can be affected • in all cases, gingiva is:  enlarged  painful  extremely erythematous
  • 17. (1)Herpes Simplex Virus-1  Clinical Features  Acute Herpetic Gingivostomatitis (primary herpes) • mild cases usually resolve within 5-7 days • severe cases may extend to 2 weeks
  • 18. (1)Herpes Simplex Virus-2  adapted best to the genital zones  predominantly through sexual contact  typically involves • genitalia • skin below waist
  • 19. (1)Herpes Simplex Virus-2  antibodies to HSV-1 decrease the chance of infection with HSV-2 or lessen severity of clinical manifestations
  • 20. (1)Herpes Simplex Virus-2  dramatic increase seen in HSV-2 due to:  partly to lack of prior exposure to HSV-1  increased sexual activity  lack of barrier conception
  • 21. Herpes Simplex Virus  Treatment & Prognosis  if infection is diagnosed early, antiviral medications can have significant influence
  • 22. (2) Varicella (Chickenpox)  similar to herpes simplex virus (HSV)  chickenpox represents primary infection with VZV  latency ensues, and recurrence is possible as herpes zoster often after many yesterday
  • 23. (2) Varicella (Chickenpox)  Etiology  presumed to be spread through air droplets  direct contact with active lesions  arise between ages of 5 and 9
  • 24. (2) Varicella (Chickenpox)  Clinical Features  symptomatic phase usually begins with: • malaise • pahryngitis • rhinitis
  • 25. (2) Varicella (Chickenpox)  Clinical Features  in older children + adults, additional symptoms: • headache • myalgia • nausea • anorexia • vomiting
  • 26. (2) Varicella (Chickenpox)  Clinical Features  rash begins on face + trunk followed by involvement of extremeties  each lesion rapidly progresses through stages of: • erythema • vesicle • pustule • hardened crust
  • 27. (2) Varicella (Chickenpox)  Clinical Features  lesions typically continue to erupt for 4 days  some cases, exanthem’s arrival may extend to 7 or more days  affected individuals are contagious from 2 days before exanthem until all lesions crust
  • 28. (2) Varicella (Chickenpox)  Clinical Features  vermillion border of lips + palate are most common sites of involvement  followed by buccal mucosa  occasionally, gingival lesions resemble those with primary HSV infections
  • 29. (2) Varicella (Chickenpox)  Clinical Features  lesions of varicella tend to be painless  lesions begin as 3-to-4-mm white opaque vesicles • rupture to form 1-to-3-mm ulcerations
  • 30. (2) Varicella (Chickenpox)  Clinical Features  prevalence + number of oral lesions correlate with severity of extraoral infection
  • 31. (2) Varicella (Chickenpox)  Clinical Features  mild cases: often only 1 or 2 oral ulcers are evident • these heal within 1-3 days  severe cases: almost always have oral ulcerations upto 30 lesions • persist for 5-10 days
  • 32. (2) Varicella (Chickenpox)  Treatment & Prognosis  warm bath with soap or baking soda  application of calamine lotion  systemic diphenhydramine • to relieve pruritus
  • 33. (2) Varicella (Chickenpox)  Treatment & Prognosis  antipyretics should be given to reduce fever  use of peroral antiviral medications such as: • acyclovir been shown • valacyclovir to reduce duration + severity • famciclovir if administered within first 24 hrs of rash
  • 34. (3) Herpes Zoster (Shingles)  after initial infection with chickenpox, virus is transported up the sensory nerves  presumably establishes latency in dorsal spinal ganglia  occurs after reactivation of virus, with involvement of the distribution of affected sensory nerves
  • 35. (3) Herpes Zoster (Shingles)  predisposing factors for reactivation:  immunosuppresion  HIV-infection  treatment with cytoxic or immunosuppresive drugs  radiation  presence of malignancies  old age  alcohol abuse  stress (emotional or physical)
  • 36. (3) Herpes Zoster (Shingles)  Clinical Features  can be grouped into 3 phases: • (1) prodome • (2) acute • (3) chronic
  • 37. (3) Herpes Zoster (Shingles)  Clinical Features  (1) Prodome • during initial viral replication active ganglionitis develops with resultant  neuronal necrosis  severe neuralgia
  • 38. (3) Herpes Zoster (Shingles)  Clinical Features  (1) Prodome • inflammatory reaction is responsible for padromal symptoms of intense pain that precedes rash in more than 90% of cases
  • 39. (3) Herpes Zoster (Shingles)  Clinical Features  (1) Prodome • as virus travels down the nerve, pain intensifies:  burning  tingling  itching Boring  prickly or knifelike
  • 40. (3) Herpes Zoster (Shingles)  Clinical Features  (1) Prodome • pain develops in area of epithelium innervated by affected sensory nerve (dermatome)
  • 41. (3) Herpes Zoster (Shingles)  Clinical Features  (1) Prodome • accompanied by:  fever normally present  malaise 1-4 days before  headache development of cutaneous or mucosal lesions
  • 42. (3) Herpes Zoster (Shingles)  Clinical Features  (2) Acute • begins as involved skin develops clusters of vesicles set on erythematous base • within 3-4 days, vesicles become pustular + ulcerate with crusts developing after 7-10 days
  • 43. (3) Herpes Zoster (Shingles)  Clinical Features  (2) Acute • oral lesions occur with trigeminal nerve involvement • may be present on movable or bound mucosa
  • 44. (3) Herpes Zoster (Shingles)  Clinical Features  (2) Acute • lesions often extend to midline • frequently are present in conjunction with involvement of skin overlying affected quadrant
  • 45. (3) Herpes Zoster (Shingles)  Clinical Features  (2) Acute • most cases, significant bone necrosis with loss of teeth in areas involved with herpes zoster
  • 46. (3) Herpes Zoster (Shingles)  Clinical Features  (3) Chronic • approximately 15% of affected patients progress to chronic phase of herpes zoster  characterized by pain (postherpetic neuralgia)  persists longer than 3 months after initial presentation of acute rash
  • 47. (3) Herpes Zoster (Shingles)  Clinical Features  (3) Chronic • pain is described as:  burning  throbbing  aching  itching  stabbing often with flares caused by light stroking of the area or from contact with adjacent clothing
  • 48. (3) Herpes Zoster (Shingles)  Treatment & Prognosis  antipyretics  antipruritics such as diphenhydramine • can be administered to decrease itching
  • 49. (3) Herpes Zoster (Shingles)  Treatment & Prognosis  skin lesions should be kept dry + clean • prevent secondary infection  antibiotics to treat secondary infections
  • 50. (3) Herpes Zoster (Shingles)  Treatment & Prognosis  antiviral medications: • acyclovir accelerate healing • valacyclovir of cutaneous + mucosal • famciclovir lesions; reduce duration of acute pain effective if initiated within 72 hours after development of 1st vesicle
  • 51. (3) Herpes Zoster (Shingles)  Treatment & Prognosis  once skin lesions have healed, neuralgia become worst aspect of disease • often most difficult to resolve successfully • analgesics • narcotics • antidepresssants • anticonvulsants
  • 52. (4) Rubeola (Measles)  infection produced by a virus in the family Paramyxovirus, genus Morbillivirus
  • 53. (4) Rubeola (Measles)  Clinical Features  most cases arise in winter  spread though respiratory droplets  incubation period is from 10-12 days
  • 54. (4) Rubeola (Measles)  Clinical Features  affected individuals are infectious from 2 days before becoming symptomatic until 4 days after appearance of associated rash
  • 55. (4) Rubeola (Measles)  Clinical Features  virus is associated with significant lymphoid hyperplasia often involves sites such as: • lymph nodes • tonsils • adenoids • Peyer’s patches
  • 56. (4) Rubeola (Measles)  Clinical Features  there are 3 stages of infection  each stage lasting 3 days  justifying designation nine-day measles
  • 57. (4) Rubeola (Measles)  Clinical Features  First 3 days are dominated by 3 Cs: • Coryza (runny nose) • Cough (brassy + unconfortable) • Conjunctivitis (red, watery, photophobic eyes)
  • 58. (4) Rubeola (Measles)  Clinical Features  fever typically accompanies these symptoms  during initial stage, most distinctive oral manifestation • Koplik Spots • multiple areas of mucosal erythema  visible on buccal + labial mucosa
  • 60. (4) Rubeola (Measles)  Clinical Features  during initial stage, most distinctive oral manifestation • less often on soft palate • within these areas are numerous small, blue-white macules
  • 61. (4) Rubeola (Measles)  Clinical Features  as second stage begins, • fever continues • Koplik spot’s fade • maculopapular + erythematous (morbilliform) rash begins
  • 62. (4) Rubeola (Measles)  Clinical Features  as second stage begins, • face is involved first, with eventual downward spread to trunk + extremities
  • 63. (4) Rubeola (Measles)  Clinical Features  as second stage begins,
  • 64. (4) Rubeola (Measles)  Clinical Features  in third stage, • fever ends • rash begins to fade • demonstrate downward progression with replacement by a brown pigmentary staining
  • 66. (4) Rubeola (Measles)  Treatment & Prognosis  good vaccination program  in healthy patients with measles, • fluids • nonaspirin antipyretics
  • 67. (5) Epidemic Parotitis (Mumps)  infection caused by virus in the family Paramyxovirus, genus Rubulavirus • causes a diffuse disease of exocrine glands
  • 68. (5) Epidemic Parotitis (Mumps)  although salivary glands are best known sites of involvement • pancreas frequently involved • choroid plexus exhibit edema + • mature ovaries lymphocytic • testes infiltration
  • 69. (5) Epidemic Parotitis (Mumps)  Clinical Features  symptomatic cases: • prodromal symptoms of low grade fever arrive • headache first • malaise • anorexia • myalgia
  • 70. (5) Epidemic Parotitis (Mumps)  Clinical Features  parotid gland is involved most frequently but sublingual + submandibular gland also can be affected
  • 71. (5) Epidemic Parotitis (Mumps)  Clinical Features  discomfort + swelling develop in tissues surrounding lower half of external ear  extending down along posterior inferior border of adjacent mandible
  • 72. (5) Epidemic Parotitis (Mumps)  Clinical Features  enlargement typically peaks within 2-3 days  pain is most intense during this period of maximal enlargement
  • 73. (5) Epidemic Parotitis (Mumps)  Clinical Features  chewing movements of jaw or eating saliva-stimulating foods tends to increase pain  enlargement of glands usually begins on one side  followed by contralateral glandular changes within a few days
  • 74. (5) Epidemic Parotitis (Mumps)  Clinical Features  unilateral involvement is most common  most common oral manifestation is redness + enlargement of • Wharton’s salivary gland • Stensen’s duct openings
  • 75. (5) Epidemic Parotitis (Mumps)  Treatment & Prognosis  palliative in nature  nonaspirin analgesics  antipyretics  in attempt to minimize orchitis, bed rest is recommended for males until fever breaks
  • 76. (5) Epidemic Parotitis (Mumps)  Treatment & Prognosis  avoid sour foods + drinks • helps decrease salivary gland discomfort  as with measles + rubella, best results come from prior vaccination
  • 77. (6) Herpangina  begins with an acute onset of significant  sore throat  dysphagia  fever  ocassionally accompanied by cough  rhinorrhea  anorexia
  • 78. (6) Herpangina  begins with an acute onset of significant  vomiting  diarrhea  myalgia  headache
  • 79. (6) Herpangina  small number of oral lesions usually 2-6 • develop in posterior areas of mouth • usually soft palate • tonsillar pillars
  • 80. (6) Herpangina  affected areas begin as red macules • form fragile vesicles that rapidly ulcerate • ulcerations average 2-4 mm in diameter
  • 81. (6) Herpangina  systemic symptoms resolve within a few days  ulcerations usually take 7-10 days to heal
  • 82. (7) Infectious Mononucleosis (Glandular Fever; Kissing Disease)  symptomatic disease  resulting from exposure to Epstein-Barr virus (EBV, HHV-4)  infection usually occurs by intimate contact
  • 83. (7) Infectious Mononucleosis (Glandular Fever; Kissing Disease)  intrafamilial spread is common  once a person is exposed, EBV remains in the host for life  children usually become infected through contaminated saliva on fingers, toys or other objects
  • 84. (7) Infectious Mononucleosis (Glandular Fever; Kissing Disease)  adults usually contract virus through direct salivary transfer  shared straws  kissing
  • 85. (7) Infectious Mononucleosis (Glandular Fever; Kissing Disease)  Clinical Features  most EBV infections in children are asymptomatic  children younger than 4 years of age with symptoms • fever • lymphadenopathy • pharyngitis • hepatosplenomegaly • rhinitis or cough
  • 86. (7) Infectious Mononucleosis (Glandular Fever; Kissing Disease)  Clinical Features  in young adult • prodomal fatigue • malaise • anorexia • body temperature may reach 104 F  lasts from 2-14 days
  • 87. (7) Infectious Mononucleosis (Glandular Fever; Kissing Disease)  Clinical Features  lingual tonsils can become hyperplastic • compromise airway  lymphoid enlargement
  • 88. (7) Infectious Mononucleosis (Glandular Fever; Kissing Disease)  Clinical Features  petechiae on hard or soft palate are present • transient • usually disappear within 24-48 hours
  • 89. (7) Infectious Mononucleosis (Glandular Fever; Kissing Disease)  Treatment & Prognosis  in most cases, resolves within 4-6 weeks  non-aspirin-containing antipyretics + NSAIDs
  • 90. (8) Cytomegalovirus  (CMV, HHV-5)  similar to other human herpes virus  after initial infection  latency is established  reactivation is possible under conditions favorable to the virus
  • 91. (8) Cytomegalovirus  CMV can reside latently in:  salivary glands cells  endothelium  macrophages  lymphocytes
  • 92. (8) Cytomegalovirus  most clinically evident disease is found in neonates or immunosuppressed adults  in infants, virus is contracted  through placenta  during pregnancy  during breast-feeding
  • 93. (8) Cytomegalovirus  at any age, almost 90% of CMV infections are asymptomatic  in clinical evident neonatal infection, infant appears ill within a few days
  • 94. (8) Cytomegalovirus  Typical Features  hepatosplenomegaly  extramedullary cutaneous erythropoiesis  thrombocytopenia (often associated petechial hemorrhages)
  • 95. (8) Cytomegalovirus  Typical Features  significant encephalitis frequently leads to severe mental + motor retardation
  • 96. (8) Cytomegalovirus  common in patients with AIDS  neonatal CMV infection also can produce developmental tooth defects  exhibit diffuse enamel hypoplasia  significant attrition  enamel hypomaturation  yellow coloration from underlying dentin
  • 97. (8) Cytomegalovirus  Treatment & Prognosis  resolve spontaneously  therapy is required in immunosuppressed patient  antipyretic mediactions  NSAIDs
  • 98. (8) Cytomegalovirus  Treatment & Prognosis  Corticosteroids or IV gammaglobulins have been used in patients with hemolytic anemia or severe thrombocytopenia
  • 99. References:  Books Neville, et. al: Oral and Maxillofacial Pathology 3rd Edition • (pages 240-264)