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VIRAL

EXANTHEMS

Viral Exanthem
General term for a rash caused by a
virus
Rashes can look similar
Symptoms and nature of rash provide
clues to the virus responsible
Usually needs supportive care
Generally appear red, blotchy, from
head to toe

Viral Exanthem
Accompanied by systemic
symptoms: fever, malaise,
headache
Reaction to viral toxin
Damage to skin by the virus

Rubeola

Measles, Morbilli

ETIOLOGY
Measles Virus
RNA Virus
Genus: Morbillivirus
Family: Paramyxoviridae
1 serotype known
During the prodromal period and a short
time after the rash appears, virus is shed in
the nasopharyngeal secretions, blood and
urine
Viable for 34 hours in room temperature

EPIDEMIOLOGY
Worldwide in distribution
Peak age incidence: 1-5 years
and at early school age
10 yrs of age: 90% infected
Adolescents or adults: 10%

TRANSMISSION
Highly contagious
Droplet spray during the prodromal
period (catarrhal stage)
Infants acquire immunity
transplacentally from mothers who have
had measles or measles immunization;
complete for the first 4-6 months and
wanes at variable rates

PATHOGENESIS
Essential lesion found in: skin, conjunctivae,
and other mucous membranes of the
nasopharynx, bronchi and intestinal tract
Hyperplasia of lymphoid tissue usually
occurs, particularly in the appendix, where
multinucleated giant cells (Warthin-Finkeldey
reticuloendothelial giant cells) may be found
Koplik spots: serous exudate and
proliferation of endothelial cells

Koplik spots
grayish
white dots
with slight
reddish
areolae
occur
opposite the
lower molars
but may
spread
irregularly
over the rest
of the buccal
mucosa
appear and
disappear
rapidly usually
within 12-18
hours

CLINICAL MANIFESTATIONS
3 Clinical Stages
1. Incubation Stage
Lasts approx 10-12 days to the first
prodromal symptoms and another 2-4
days to the appearance of the rash
Body temp increases 9-10 days from
the date of infection and subsides for
24 hours or so transmission can occur
by this time

CLINICAL MANIFESTATIONS
2. Prodromal Stage

Usually lasts 3-5 days


Low-grade to mod fever, dry cough,
coryza, conjunctivitis, photophobia
precede the appearance of Koplik
spots by 2-3 days

CLINICAL MANIFESTATIONS
3.Final Stage

Temp rises abruptly as the rash appears


Rash starts as faint macules: upper lateral
parts of the neck, behind the ears, along the
hairline and on the posterior parts of the cheek
Become maculopapular: entire face, neck,
upper arms, and upper part of chest within 24
hours
Succeeding 24 hours: back, abdomen, entire
arm and thighs
Reaches feet on the 2nd-3rd day: abrupt drop in
temp, symptoms subside

Rubeola Rash

CLINICAL MANIFESTATIONS
3. Final Stage

Desquamation and brownish discoloration


occur and disappear within 7-10 days
Cephalocaudal progression of rash
Generalized lymphadenopathy esp in the
posterior cervical area
Mesenteric lymphadenitis may cause
abdominal pain
Slight splenomegaly
Diarrhea: 50-60% of cases

MODIFIED MEASLES
Short prodrome, less severe rash
Occurs in partially immune host
Young infant with partial protection from
maternal antibodies
Immunized children with partial vaccine
failure

ATYPICAL MEASLES
Severe headache, severe abdominal
pain, vomiting, myalgia, pneumonia with
pleural effusion and an atypical rash
Atypical rash: first appears on the palms,
wrists, soles and ankles, and progresses
in centripetal direction; initially
maculopapular but become vesicular
Koplik spots rarely appear

DIAGNOSIS
Usually apparent from the clinical picture
Laboratory confirmation rarely needed
WBC count: low with relative
lymphocytosis
Testing for measles IgM
During prodromal stage, multinucleated
giant cells can be demonstrated in the
smears of nasal mucosa

TREATMENT
Entirely supportive
Antipyretics, bed rest, adequate oral
fluid intake
Vitamin A supplementation
Hyporetinemia present in more than 90%
of cases

Antimicrobial therapy in the presence of


OM or pneumonia

COMPLICATIONS
Chief complications: Otitis Media, Pneumonia,
and Encephalitis
Most common in young children
Pneumonia: common and leading cause of death
Encephalitis: usually occurs by 2-5 days after the
rash
Neurologic complications (Subacute Sclerosing
Panencephalitis) more common in measles than
in any of the other viral exanthems
Gestational measles may induce premature
delivery, stillbirths or abortion but is hardly
teratogenic

PROGNOSIS
Case Fatality Rate: 1-3/ 1000 cases
Cause: pneumonia or secondary
viral infection

PREVENTION
Vaccine
Measles vaccine at 9 m0 of age
MMR vaccine at 12-15 mo of age;
2nd dose at 4-6 yrs of age (at
least 4 wks from 1st dose)

PREVENTION

Post exposure prophylaxis


Immune globulin: effective for prevention and attenuation
within 6 days of exposure
Ig (0.25 mL/kg; max. 15 mL) IM ASAP within 5 days for:
Susceptible contacts < 12 mo of age, Pregnant persons
Immunocompromised persons: Ig (0.5 mL/kg; max. 15 mL)
IM regardless of immunization status
Infants <= 6 mo born to non-immune mothers should
receive Ig
Susceptible children 6-12 mo should be vaccinated (does
not count as one of the 2 required)
Susceptible children >= 12 mo should receive vaccine
alone within 72 hours

Rubella

German Measles

ETIOLOGY
Rubella Virus
An RNA virus
Genus: Rubivirus
Family: Togaviridae

EPIDEMIOLOGY
Humans are the only natural host
Spread: oral droplet or transplacentally
During clinical illness, virus shed in:
nasopharyngeal secretions, blood, feces
and urine
Recovered from the nasopharynx 7 days
before exanthem and 7-8 days after its
disappearance (period of
communicability)

PATHOGENESIS
Not well understood
Risk for congenital defects and
disease is greatest with primary
maternal infection during the 1st
trimester (90% when before the 11th
week AOG)

CLINICAL MANIFESTATIONS
Incubation Period: 14-21 days
Prodromal Phase: mild catarrhal
symptoms, shorter than that of measles and
may be so mild that it goes unnoticed
Retroauricular, posterior cervical and
postoccipital lymphadenopathy (tender,
enlarged): most characteristic sign
Forchheimer spots: discrete rose-colored
spots on the soft palate that may coalesce
into a red blush and extend over the fauces

CLINICAL MANIFESTATIONS
Exanthem more variable than rubeola
Maculopapular rash begins on the face and
spreads quickly; so rapid that the rash may
be fading on the face by the time it appears
on the trunk
During 2nd day, the rash assume a pinpoint
appearance esp on the trunk
Mild itching may occur
Eruption clears by the 3rd day
Desquamation minimal

Rubella Rash

CLINICAL MANIFESTATIONS
No photophobia
Fever low grade or absent during the
rash and persists for 1-3 days
Polyarthritis may occur with
arthralgia, swelling, tenderness, and
effusion but usually without any
residuum

DIAGNOSIS
Apparent from the clinical symptoms and
physical examination
Usually confirmed by serology or virus culture
Spleen: slightly enlarged
WBC count: N or slightly reduced,
thrombocytopenia rare
IgM detectable in the first few days of illness:
considered diagnostic
Virus can be cultured from the nasopharynx
and blood

TREATMENT
No specific antiviral therapy
Entirely supportive
Antipyretics indicated for fever

COMPLICATION
Relatively uncommon
Encephalitis: 1/6000 cases
(Progressive Rubella Panencephalitis)
Most important consequence in
pregnant women: Congenital Rubella
Syndrome

PREVENTION
Vaccine
Derived from the RA 27/3 strain of rubella virus,
attenuated
Initial rubella immunization, as MMR:12-15 mo
of age
2nd immunization, as MMR: 4-6 years of age
Esp important for girls to have immunity to
rubella before they reach childbearing age
Pregnant women should not be given live
rubella virus vaccine and should avoid getting
pregnant for 3 mo after vaccination

Roseola Infantum

Exanthem Subitum, Sixth


Disease

ETIOLOGY
HHV6: 2/3 of cases (types A and B-more
than 99%)
HHV 7: of cases
Others: echovirus 16
HHV-6 and HHV-7: B-herpesvirus subfamily
of herpesviruses (includes CMV)
Large double-stranded DNA, nucleocapsid,
established period of latency

EPIDEMIOLOGY
Primary HHV-6 infection occurs early in life:
6-15 mo of age
Infection: rare before 3 mo & after 4 yrs of age
Incubation period: averages 10 days (5-15
days)
Most adults excrete HHV-6 and HHV-7 in saliva
and may serve as primary sources for virus
transmission to children

CLINICAL MANIFESTATIONS
Prodromal period: usually asymptomatic
but may include mild upper respiratory tract
signs (minimal rhinorrhea, slight pharyngeal
inflamm, and mild conjunctival redness)
Clinical illness heralded by high
temperature (37.9- 40 deg Celsius)
Febrile stage: irritability, anorexia, but
most behave normally despite high temp,
seizures (5-10%); persists for 3-5 days then
typically resolves rather abruptly
Rash: appears within 12-24 hours of fever
resolution

PATHOGENESIS
Little is known
Virus is probably acquired from saliva of
healthy persons and enters the host through
the oral, nasal, or conjunctival mucosa
HHV-6: CD46 receptors
HHV-7: CD4 receptors
Replication at an unknown site produces
viremia and then latency develops
Basis for the unique pattern of rash after
resolution of fever has not been established

Roseola Rash

rose-colored
fairly distinctive
Blanches on
pressure
begins as a
discrete, small,
slightly raised pink
lesions on the trunk
and usually spreads
to the neck, face,
and proximal
extremities
not pruritic, no
vesicles, or
pustules
rash fades after
1-3 days

CLINICAL MANIFESTATIONS
Infrequent complaints: rhinorrhea, sore
throat, abd pain, vomiting, diarrhea
Nagayama spots: erythematous papules
ulcers at the uvulopalatoglossal junction

DIAGNOSIS
establishing the diagnosis: differentiate
this generally mild illness from other
potentially more serious childhood rash
illnesses
on the basis of age, history and clinical
findings
WBC count: 8000-9000 /uL at 1st few
days of fever
w/ presence of exanthem: the WBC falls
to 4000-6000 /uL with a relative
lymphocytosis (70-90%)

TREATMENT
Generally benign nature
Essentially supportive: adequate fluid
intake, antipyretics
PROGNOSIS: excellent
PREVENTION: no specific
recommendations, no vaccine developed

Erythema Infectiosum

Fifth Disease

ETIOLOGY

Parvovirus B19
Genus Erythrovirus
Family Parvoviridae
Small DNA viruses
B19: only parvovirus that is pathogenic in
humans; does not infect other animals;
single-stranded DNA, relatively heat and
solvent resistant; only 1 known serotype
Animal parvoviruses do not infect
humans

EPIDEMIOLOGY
Most prevalent in school-aged children
70% occurring between 5-15 years of
age
Transmission: respiratory route via large
droplet spread from nasopharyngeal
viral shedding; may be transmissible by
blood and blood products

PATHOGENESIS
Primary target of B19: erythroid cell line,
specifically erythroid precursors near the
pronormoblast stage
Viral infection produces lysis of these
cells, leading to progressive depletion
and a transient arrest of erythropoiesis
Thrombocytopenia and neutropenia
observed clinically but their
pathogenesis is unexplained

PATHOGENESIS

Normal immunologic response to PV-B19


Immunocompetent Host
Th-1-mediated cellular response
Production of IgM, then
immunocomplexes
Signs and symptoms as a result of
deposition of the immune complexes in
the skin and joints; not from the
circulating virus

CLINICAL MANIFESTATIONS
Incubation period: 4-28 days (ave, 16-17
days)
Prodromal phase: mild, consists of lowgrade fever, headache, and symptoms
of mild upper respiratory tract infection
Hallmark: characteristic rash which
occurs in 3 stages that are not always
distinguishable

CLINICAL MANIFESTATIONS
Initial stage: erythematous facial
flushing or slapped-cheek appearance
Second stage: spreads rapid to the
trunk and proximal extremities as a
diffuse macular erythema
Third stage: central clearing of macular
lesions occur promptly, giving the rash
a lacy, reticulated appearance

Erythema Infectiosum Rash

CLINICAL MANIFESTATIONS
Palms and soles are spared, and rash tends
to be more prominent on extensor surfaces
Affected children: afebrile and not illappearing
Mild pruritus
Rash resolves spontaneously without
desquamation but tends to wax and wane
over 1-3 weeks
Can recur with exposure to sunlight, heat,
exercise, and stress
Arthropathy: arthritis and arthralgia

DIAGNOSIS
Usually based on clinical presentation of
the typical rash
B19-specific IgM
Virus cannot be isolated by culture

TREATMENT
No specific antiviral therapy
Essentially supportive

COMPLICATIONS
Often accompanied by arthralgias or
arthritis in adolescents and adults which
may persist after resolution of the rash
B19 may cause thrombocytopenic
purpura and rarely aseptic meningitis

PREVENTION
Not likely to be infectious at
presentation because the rash and
arthropathy represent immunemediated, post-infectious phenomena
Isolation and exclusion from school are
unnecessary and ineffective after
diagnosis
Essentially supportive

Measles
(rubeola)

Paramyxovirus

Discrete lesions that become


confluent as rash spreads from
hairline downward, sparing
palms and soles, lasts> 3 days,
Kopliks spots

Cough,
conjunctivitis,
coryza, rash
accompanied
by fever.

German
measles
(rubella)

Togavirus

Spreads from hairline


downward, clearing as it
spreads, Forscheimer spots

Adenopathy,
arthritis

Erythema
Infectiosum

Human
Parvovirus B19

bright-red slapped cheek


appearance followed by diffuse
lacy reticular rash, sparing of
palms and soles

Mild fever,
arthritis in
adults

Diffuse maculopapular
eruption, sparing face, resolves
within 2 days

Rash following
resolution of
fever

Exanthem HHV6
subitum
(roseola
infantum)

Varicella
Chickenpox

ETIOLOGY
Varicella-Zoster Virus (VZV)
Neurotropic human a-herpesvirus
Double stranded DNA

EPIDEMIOLOGY
Man is the only source of infection
May occur in any age including the
neonate with the peak between 5-10
years old
Contagious from 24-48 hours before the
rash appears and until vesicles crusted,
usually 3-7 days after onset of rash

PATHOGENESIS
Transmission: respiratory secretions and
in the fluid of skin lesions either by
airborne spread or through direct
contact
Primary infection: results from the resp
inoculation of the virus (early part of the
10-21 day incubation period) followed by
a brief subclinical viremia

PATHOGENESIS
Second viremic phase: widespread
cutaneous lesions occur
Late incubation period: VZV transported
back to resp mucosal sites, permitting
spread to susceptible contacts prior to
the appearance of the rash

CLINICAL MANIFESTATIONS
Incubation period: 10-21 days
Illness usually begins 14-16 days after
exposure
Prodromal symptoms: may be present
Fever, malaise, anorexia, headache, and
occ mild abd pain may occur 24-48
hours before the rash appears
Temp elevation usually moderate

CLINICAL MANIFESTATIONS
Varicella lesions: appear first on the
scalp, face, or trunk
Initial exanthem: intensely pruritic
erythematous macules
Papular stage: macules evolve to clear
fluid-filled vesicles; clouding and
umbilication begin in 24-48 hours
While the initial lesions are crusting, new
crops form on the trunk and then
extremities

Varicella
Lesions
the
simultaneous
presence of
lesions in
various stages
of evolution is
characteristic
of varicella

Varicella

TREATMENT
Directed in avoiding known
complications
Hygiene is important to prevent
secondary infection
Antipruritic drugs
Acetaminophen- to avoid risk of Reyes
syndrome
Tx with steroids and acyclovir not
recommended

PREVENTION
Active immunization
Varicella vaccine; 1 dose SC for children 12
yo and younger
2 doses 4-8 weeks apart for those older
than 12 yo

Passive immunization- not available


locally

Herpes Zoster
Shingles, Acute Posterior
Ganglionitis

EPIDEMIOLOGY
Herpes zoster occurring in a partially
immune individual due to a previous
varicella infection
Common in older children and adults
Uncommon under 10 years old

CLINICAL MANIFESTATIONS
Rash with the same progression as that
in varicella and generally follows a
dermatome
Characterized by severe pain and
tenderness localized to the area
Starts with burning, itching and pain
then erythematous patches appear,
followed by crops of vesicles along the
course of involved dermatomes
Lesions may last 1-2 wks

Herpes Zoster

DIAGNOSIS
There is usually a history of previous
varicella

PROGNOSIS: good
TREATMENT:
Postherpetic neuralgia in children is rare
Some would not treat with antiviral agents
Oral acyclovir (20mg/kg/dose, max
800mg/dose) to shorten duration of illness
Corticosteroids not recommended

Herpes Zoster
Smallpox

GENERALITIES
Etiology: Variola virus
Epidemiology: eradicated
Transmission: direct contact through
fomites and other contaminated articles
Incubation period: 1-3 wks

CLINICAL MANIFESTATIONS
2-4 days hyperpyrexia, weakness and
backache
At the 3rd day, rash appears on the face,
wrists, ankles, spreads to the extremities
and often in areas of pressure and tight skin
Rashes are shotty, discrete and centripetal
in distribution
Eruptions lasts about 1-2 weeks
Similar lesions may occur in the buccal
mucosa and cornea

Smallpox

DIAGNOSIS
Done clinically
Laboratories: leukopenia and increased
large lymphocytes, Guarnieri bodies are
identified in the vesicle fluid
Positive Pauls test

TREATMENT
Symptomatic
No specific cure
Antibiotics are indicated only for
secondary bacterial infection
PREVENTION
Smallpox vaccination
Presently no longer routinely done
disease eradicated

Differentiating Points from


Varicella
Prodromal period is prolonged and
severe
Systemic manifestations are more
pronounced
Lesions are uniformly of 1 stage in any 1
area
Centripetal distribution of rash

Herpes Zoster
Hand, Foot and Mouth Disease

Etiology
Enterovirus genus
Picornaviridae family
coxsackievirus A16

enterovirus 71
Sporadic Cases:
coxsackievirus types A4-A7, A9, A10, B1B3, and B5

Epidemiology
Epidemics tend to occur every 3 years in
the United States
Worldwide occurrence
seasonal pattern in temperate climates
peak in late summer and early fall
children younger than 10 years

Morbidity/Mortality
more severe in infants and children than
adults
Rarely, disease recurs
Infection in the first trimester may lead
to spontaneous abortion or intrauterine
growth retardation

Transmission
incubation period averages 3-6 days
highly contagious
horizontal transmission from child to
child and from mother to fetus
direct contact with nasal and/or oral
secretions, fecal material, or aerosolized
droplets in a fecal-oral or oral-oral route

Pathophysiology
Initial viral implantation in the buccal
and ileal mucosa
spread to lymph nodes within 24 hours
Viremia
spread to the oral mucosa and skin
neutralizing antibody levels increase by
day 7
virus is eliminated

Clinical Manifestations
brief prodrome, 12-36 hours

Low-grade fever, ave. 38.3C, 2-3 days


Anorexia
Malaise
Abdominal pain
Sore mouth
Cough

Clinical Manifestations
Occasionally, patients have high fever,
marked malaise, diarrhea, and
arthralgias
Oral lesions begin as erythematous
macules that evolve into 2-3 mm
vesicles on an erythematous base
vesicles rarely observed; rapidly become
ulcerated

Clinical Manifestations
vesicles may involve the palate, buccal
mucosa, gingiva, and tongue
Cutaneous lesions are characteristic and
are present in two-thirds of patients
hands, feet, and buttocks are involved.
Hands often than the feet, dorsal aspect of
the hands and sides of the fingers more
than the palmar surfaces.

Clinical Manifestations
Each lesion begins as a 2-10 mm
erythematous macule on which a
central, gray, oval vesicle develops.
lesions are elliptical; their long axis
parallels the skin lines.
asymptomatic and resolve in 3-7 days as
a result of fluid resorption.

Clinical Manifestations
enanthem usually precedes the
exanthem but both may occur
simultaneously.
lesions on the hands and feet are
present for 5-10 days
mucosal and cutaneous lesions heal
spontaneously in 5-7 days.

Lesions in Hand Foot and Mouth


Disease

Complications
neurological complications
Encephalitis
Meningitis
acute flaccid paralysis

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