Viral diseases (3)
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Viral diseases (3) Presentation Transcript

  • 1. VIRALDISEASES 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
  • 59. (4) Rubeola (Measles)
  • 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
  • 65. (4) Rubeola (Measles)
  • 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)