The document discusses several viral diseases including herpes simplex virus types 1 and 2, varicella (chickenpox), herpes zoster (shingles), rubeola (measles), and epidemic parotitis (mumps). It provides details on the etiology, clinical features, treatment, and prognosis of each disease. The diseases are spread through respiratory droplets, contact with lesions, or sexual contact. Clinical features may include lesions, rashes, fever, and lymphadenopathy. Treatment involves antivirals, analgesics, and supportive care.
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
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
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
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
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
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
98. (8) Cytomegalovirus
Treatment & Prognosis
Corticosteroids or IV
gammaglobulins have been
used in patients with
hemolytic anemia or severe
thrombocytopenia