Viral Exanthems

Prepared By:
Hygeia Laurei M. Fernandez

DEFINITION
Exanthems are characterized by an acute generalized
eruption on skin.
Enanthem (enanthema) - An eruption upon a mucous
membrane
The most common presentation:
1. Morbilliform
2. Scarlatiniform

Description of Primary Skin Lesion

Macule: flat, colored lesion, <2cm in dm, not raise above the
surface of the surrounding skin. A freckle or ephelid is a
protypical pigmented macule.
Patch: A large, >2cm, flat lesion, with a color different from
the surrounding skin. This differs from a macule only by
size.
Papule: A small , solid lesion, <0.5 cm in dm, raised above
the surface of the surrounding skin and thus palpable (e.g.
comedone, or white-head, in acne)

Description of Primary Skin Lesion

Vesicle: A small, fluid-filled lesion, <0.5 cm in dm, raised

above the plane of surrounding skin. Fluid is often visible
and the lesions are translucent.
Pustule: A vesicle, filled with leukocytes.
Wheal: A raised, erythematous papule or plaque, usually
representing short lived vasodilation and vasopermeability

OVERVIEW
A. Macular and Maculopapular Rash
Rubeola (Measles)
Rubella (German Measles)
Roseola Infantum
Eyrthema Infectiosum
EpsteinBarr Virus

C. Papular Exanthems
Papular Acrodermatitis of
Childhood
Molluscum Contagiosum

B. Vesicular and Pustular Rashes

Varicella
Herpes Zoster
Eczema Herpeticum
HandFootMouth Disease
Acute Generalized Exanthematous
Pustulosis

D. Other Viral Exanthems

Papular Purpuric Glove & Socks Syndrome & Parvovirus-induced
Petechial Syndromes
Pityriasis Rosea
Erythema Multiforme
Unilateral Laterothoracic Exanthem
Nonspecific Viral Exanthem

MEASLES (RUBEOLA) 1st Disease

ETIOLOGY

Measles virus is a single-stranded, lipid-enveloped,

negative sense RNA virus.
Etiologic Agent: Family Paramyxoviridae Morbillivirus
genus
Humans are the only known host

MEASLES (RUBEOLA) 1st Disease

TRANSMISSION
Respiratory Droplet, Aerosol, Fluids, Secretion

INFECTIVITY
From 3 days before to up to 4-6 days after the onset of
rash.
Immunocompromised patients can be contagious for the
duration of the illness

MEASLES (RUBEOLA) 1st Disease

PATHOGENESIS
4 Phases of Measles:
Incubation

Prodromal

Exanthemous

Recovery

MEASLES (RUBEOLA) 1st Disease

INCUBATION PERIOD
Asymptomatic incubation period occurs 9-12 days
from initial exposure.
10 days to fever onset
14 days to rash onset
Migration to Regional Lymph Node
Primary Viremia
Secondary Viremia

MEASLES (RUBEOLA) 1st Disease

MEASLES (RUBEOLA) 1st Disease

PRODROMAL ILLNES
Begins AFTER secondary viremia
Warthin-Finkeldey giant cells
Virus shedding begins

MEASLES (RUBEOLA) 1st Disease

EXANTHEMOUS
With onset of the rash, antibody production begins
Viral replication and symptoms begin to subside
Measles virus also infects CD4+ T cells, resulting
in suppression of the Th1 immune response and a
multitude of other immunosuppressive effects.

MEASLES (RUBEOLA)

st
1

Disease

The rash usually appears about 14 days after a

person is exposed, which become confluent as the
rash spreads downward
Pattern of Spread: Cephalocaudal
Patients are considered to be contagious from 4 days
before to 4 days after the rash appears.

MEASLES (RUBEOLA) 1st Disease

Clinical Features

MEASLES (RUBEOLA)

st
1

Disease

Pathognomonic Enanthem
Kopliks spots:
appear as 1-2 mm blue-white spots on a bright
red background- just before rash onset
typically located on the buccal mucosa,
alongside the second molars
Appear during the prodromal period

MEASLES (RUBEOLA) 1st Disease

IMMUNITY
Hemagglutinin (H) protein
Fusion (F) protein
World Health Organization recognizes 8
clades, A-H, and 23 genotypes

MEASLES (RUBEOLA) 1st Disease

MEASLES (RUBEOLA) 1st Disease

Diagnosed clinically and epidemiologic wise
Confirmation by Serology: Anti-measles IgM and IgG,
Histologic evaluation of skin lesions or respiratory secretions
may show syncytial keratinocytic giant cells
Enzyme immunoassays
Viral Isolation in culture
PCR

MEASLES (RUBEOLA) 1st Disease

CBC
Reduce total WBC
Lymphocytes decreased more than neutrophils
Absolute neutropenia

Ancillary Tests
Normal ESR and CRP if measles are not complicated by
bacterial infection

MEASLES (RUBEOLA) 1st Disease

COMPLICATIONS
Pneumonia
Croup
Tracheitis
Bronchiolitis obliterans
Acute Otitis Media, Sinusitis, Mastoiditis
Dehydration 2 to Diarrhea and vomiting
Appendicitis
Febrile Seizure

MEASLES (RUBEOLA) 1st Disease

Black Measles
It manifested as a hemorrhagic skin eruption
Keratitis, appearing as multiple punctate epithelial
foci, resolved with recovery from the infection.
.

Subacute Sclerosing Panencephalitis

chronic complication of measles that results from a
persistent infection with an altered measles virus
harbored intracellularly in the CNS
Virus regains virulence after 7-10 yrs -> attack CNS
cells -> neurodegenerative process
Pathogenesis: virus isolated from rain tissue is missing
the matrix (M protein) -> immature virus resides &
propagate within neuron

Subacute Sclerosing Panencephalitis

Stage I
irritability, reduced attention span, temper outbursts

Stage II
massive myoclonus

Stage III
Choreoathetosis, immobility, dystonia, lead pipe rigidity

Stage IV
loss of critical centers that support breathing, heart rate, and
blood pressure

Subacute Sclerosing Panencephalitis

The diagnosis of SSPE: a compatible clinical course

and at least 1 of the following supporting findings:
(1) measles antibody detected in cerebrospinal fluid
(2) characteristic electroencephalographic findings,
and
(3) typical histologic findings in and/or isolation of
virus or viral antigen from brain tissue obtained by
biopsy or postmortem examination.

Subacute Sclerosing Panencephalitis

Cerebrospinal fluid analysis reveals normal cells
Elevated IgG and IgM antibody titers in dilutions >1 : 8.
Electroencephalographic patterns are normal in stage I,
but in the myoclonic phase, suppression burst episodes
are seen that are characteristic of, but not pathognomonic
for, SSPE.
Brain biopsy is no longer routinely indicated for diagnosis
of SSPE.

MEASLES (RUBEOLA) 1st Disease

MANAGEMENT
Supportive
1. Maintenance of hydration, oxygenation, and comfort are
goals of therapy.
2. Antipyretics for comfort and fever control are useful.

MEASLES (RUBEOLA) 1st Disease

VITAMIN A

50,000 IU is used for infants 1-6 months old

100,000 IU is recommended for infants 7-12 months old
200,000 IU for children >1 year old
A single dose is administered on two consecutive days
Transient vomiting and headache may be associated in the
administration of Vit. A

MEASLES (RUBEOLA)

st
1

Disease

PREVENTION
Live attenuated measles vaccine
Recommended age of first vaccination varies from 6-15 months
Measles vaccine has been available as the combination vaccine measlesmumps-rubella (MMR); this vaccine should be administered to children at
12-15 months of age.
(Vaccination at 12 months is preferred for infants whose mothers were
immunized against measles in childhood.)
A second dose of MMR vaccine is recommended for school-age children

GERMAN MEASLES (RUBELLA) - 3rd Disease

DEFINITION
Aka 3 Day Measles; 3rd Disease
A mild, often exanthematous disease of infants and
children that is typically more severe and
associated with more complications in adults.
Major clinical significance: Transplacental infection
and congenital rubella syndrome (CRS).

GERMAN MEASLES (RUBELLA) - 3rd Disease

ETIOLOGY
Member of the family Togaviridae
The only species of the genus Rubivirus.
Humans are the only known host

GERMAN MEASLES (RUBELLA) - 3rd Disease

TRANSMISSION
ACQUIRED RUBELLA: Via airborne droplet emission fro the upper respiratory
tract of active cases (can be passed along by the breath of people sick from
Rubella); The virus may also be present in the urine, feces. And on the skin
CONGENITAL RUBELLA SYNDROME: Maternal infection during the 1
week of gestation results in the most severe and widespread defects.

st

GERMAN MEASLES (RUBELLA) - 3rd Disease

Single-stranded RNA virus with a lipid envelope and 3
structural proteins
The structural proteins associated with rubella virus are
E1 and E2 (transmembrane envelope gycoproteins) and
C (the capsid protein that surrounds the viral RNA). Only
one serotype has been identified

GERMAN MEASLES (RUBELLA)

INCUBATION PERIOD: 2-3 weeks

INFECTIVITY: During this incubation period, the
patient is contagious typically for about one week
before he/she develops a rash and for about one
week thereafter

GERMAN MEASLES (RUBELLA) - 3rd Disease

CLINICAL MANIFESTATIONS

Foremost symptoms of acquired rubella include posterior

auricular, cervical and suboccipital lymphadenopathy, fever,

and rash
The rash often begins on the face and spreads down the
body.
Maculopapular but not confluent

GERMAN MEASLES (RUBELLA)

A petechial enanthem on the soft palate,

designated Forschheimer spots, may occur but is

not specific for rubella
Fever may be absent entirely or may be present
for only several days in the early phase of the
illness.

GERMAN MEASLES (RUBELLA) - 3rd Disease

GERMAN MEASLES (RUBELLA) - 3rd Disease

II. Congenital Rubella Syndrome
Cardiac, cerebral, ophthalmic, and auditory defects
May also cause prematurity, low birth weight, and
neonatal thrombocytopenia, anemia and hepatitis

GERMAN MEASLES (RUBELLA) - 3rd Disease

Clinical Problems Associated with CRS

GERMAN MEASLES (RUBELLA) - 3rd Disease

LABORATORY FINDINGS

Leukopenia, neutropenia, and mild thrombocytopenia

DIAGNOSIS
Clinical presentation
ELISA IgM IgG antibodies
PCR
Viral isolation very expensive

GERMAN MEASLES (RUBELLA) - 3rd Disease

COMPLICATIONS
Thrombocytopenia
Encephalitis
Arthritis
Progressive rubella panencephalitis (PRP)

GERMAN MEASLES (RUBELLA) - 3rd Disease

Nerve deafness : single most common
finding among infants with CRS.
Some degree of intrauterine growth
restriction.
Salt-and-pepper retinopathy are the most
common ocular abnormality but have little
early effect on
vision.
Unilateral or bilateral cataracts are the
most serious eye finding, occurring in about
a third of infants.

GERMAN MEASLES (RUBELLA) - 3rd Disease

TRANSIENT
Bony abnormalities
Cloudy cornea
Hemolytic anemia
Hepatitis
Hepatosplenomegaly
Jaundice
Low birth weight
Lymphadenopathy
Meningoencephalitis
Rubella viral pneumonia
Thrombocytopenic purpura

PERMANENT

Autism
Behavioral disorders
Congenital heart disease
Cryptorchidism
Deafness
Degenerative brain disease
DM
Glaucoma
Inguinal hernia
Mental retardation
Microcephaly
Myopia
Precocious puberty
Retinopathy
Seizures
Spastic diplegia
Thyroid disorders

GERMAN MEASLES (RUBELLA) - 3rd Disease

TREATMENT
There is no specific therapy for rubella
Symptom-based treatment is given for manifestations such as
fever, arthralgia, and arthritis
Treatment of newly born babies is focused on management of
the complications. Congenital heart defects and cataracts can
be corrected by direct surgery

GERMAN MEASLES (RUBELLA) - 3rd Disease

PREVENTION
The vaccine is now usually given as part of the MMR
vaccine
The WHO recommends the first dose is given at 12 to 18
months of age with a second dose at 36 months
Pregnant women are usually tested for immunity to rubella
early on
Women found to be susceptible are not vaccinated until
after the baby is born because the vaccine contains live
virus

GERMAN MEASLES (RUBELLA)

ERYTHEMA INFECTIOSUM 5th Disease

Disease in young children causing widespread red
rash
Aka Fifth Disease

ETIOLOGIC AGENT: Parvovirus B19

Parvoviruses are small, single-stranded DNA viruses, composed of
an icosahedral protein capsid without an envelope
B19 is a member of the genus Erythrovirus.

ERYTHEMA INFECTIOSUM 5th Disease

EPIDEMIOLOGY
most prevalent in school-aged children
70% of cases occurring in patients between 5 and 15 yr of age

TRANSMISSION
respiratory route, presumably via large droplet spread from
nasopharyngeal viral shedding
B19 is also transmissible in blood and blood products

ERYTHEMA INFECTIOSUM 5th Disease

INCUBATION PERIOD: 4-28 days (average 16-17 days).
INFECTIOUS PERIOD: up until onset of rash

ERYTHEMA INFECTIOSUM 5th Disease

PATHOGENESIS
Primary target: erythroid precursors near the pronormoblast
stage
Viral infection produces cell lysis erythrocyte P blood group
antigen, which is the primary cell receptor for the virus
Thrombocytopenia and neutropenia are often observed
clinically

ERYTHEMA INFECTIOSUM 5th Disease

CLINICAL MANIFESTATIONS
Prodromal phase is mild and consists of low-grade fever
in 15-30% of cases, headache, and symptoms of mild
upper respiratory tract infection
Adults, especially women, frequently experience acute
polyarthropathy with or without a rash

ERYTHEMA INFECTIOSUM 5th Disease

Hallmark of erythema infectiosum is the characteristic rash which
occurs in 3 stages that are not always distinguishable.
1st Stage: erythematous facial flushing, often described as a
slapped cheek appearance
2nd Stage: rash spreads rapidly or concurrently to the trunk and
proximal extremities as a diffuse macular erythema in the 2nd
stage
3rd Stage: Central clearing of macular lesions occurs promptly,
giving the rash a lacy, reticulated appearance rash tends to be
more prominent on extensor surfaces, sparing the palms and soles

1st Stage

2nd Stage

3rd Stage

ERYTHEMA INFECTIOSUM 5th Disease

OTHER CUTANEOUS MANIFESTATIONS
Papularpurpuricgloves-and-socks syndrome
(PPGSS)
PPGSS is characterized by fever, pruritus, and painful
edema and erythema localized to the distal extremities
in a distinct gloves-and-socks distribution, followed
by acral petechiae and oral lesions.
The syndrome is self-limited and resolves within a few
weeks.

Papularpurpuricgloves-and-socks Syndrome
(PPGSS)

ERYTHEMA INFECTIOSUM 5th Disease

DIAGNOSIS
Clinical presentation of the typical rash
Rarely requires virologic confirmation
Serologic tests for the diagnosis of B19 infection:
B19-specific IgM develops rapidly after infection and persists for 6-8 weeks
Anti-B19 IgG serves as a marker of past infection or immunity
anti-B19 IgM is the best marker of recent/acute infection on a single serum
sample

Diagnosis in immunocompromised persons requires methods to detect viral

DNA (polymerase chain reaction and nucleic acid hybridization)

ERYTHEMA INFECTIOSUM 5th Disease

Treatment
No specific antiviral therapy for B19 infection
IV Immunoglobulin used with some success in B19
related episodes of anemia and bone marrow failure in
immunocompromised children
Dosage 200 mg/kg/day for 5 to 10 days or 1g/kg/day for 3
days

B19 infected fetuses with anemia and hydrops

intrauterine RBC transfusions.

ERYTHEMA INFECTIOSUM 5th Disease

Prevention
Erythema infectiosum are not likely to be infectious at presentation (rash
and arthropathy represent immune mediated, post infections phenomena).
Isolation and exclusion from school are not necessary and ineffective after
diagnosis
Children with B 19 induced RBC aplasia infectious upon presentation
and demonstrate a more intense viremia
Isolated in the hospital to prevent spread. This should continue for at
least a weak until resolution of fever.
Pregnant women should avoid contact with these patient
No vaccine available

ERYTHEMA INFECTIOSUM 5th Disease

Complications
Arthralgias or arthritis in adolescent (may persist after resolution
of rash)
May rarely cause thrombocytopenic purpura
Neurologic complications
Aseptic meningitis
Encephalitis
Peripheral neuropathy
Increased incidence of stroke in children with sickle cell
disease following B19 induced aplastic crisis

ROSEOLA INFANTUM (Sixth Disease)

Exanthem subitum
Etiologic Agent: Human
herpesvirus 6 and 7
HHV-6 - responsible for the
majority of cases
Roseolovirus genus in the
Betaherpesvirinae subfamily
of human herpesviruses.

ROSEOLA INFANTUM (Sixth Disease)

ETIOLOGY
HHV-6 and HHV-7- Within the nucleocapsid- large, linear, double-stranded
DNA genomes that encode >80 unique proteins.

HHV-6- Two variants- can be distinguished by restriction fragment length

polymorphisms, reactivity with monoclonal antibodies, differential growth in
tissue culture cell lines, and epidemiology
Variant A- detected in children from Africa
Variant B- predominant strain in both normal and
immunocompromised hosts (culture and PCR)

ROSEOLA INFANTUM (Sixth Disease)

Incubation period: 9 days

Infectious period: Virus is intermittently
shed into saliva throughout life;
asymptomatic infection
At risk: 6-36 months
Season: Sporadic

ROSEOLA INFANTUM (Sixth Disease)

CLINICAL MANIFESTATIONS:
High Fever for 3-4 days
Abrupt defervescence with appearance of rash
Diffuse maculopapular eruption over trunk and neck
In Asian countries, ulcers at the uvulopalatoglossal junction (Nagayama
spots) are commonly reported in infants with roseola.

Febrile seizures may occur

Associated with other diseases, including infectious mononucleiosis,
encephalitis, especially in immunocompromised hosts.
Most postnatally infected children develop symptoms: fever, fussiness,
and diarrhea.

ROSEOLA INFANTUM (Sixth Disease)

Resolves within 2 days

Varicella- Zoster Virus

ETIOLOGIC AGENT:
Varicella Zoster Virus is a member of the family
Herpesviridae, double-stranded DNA
INCUBATION PERIOD:
Usually 14-17 days with a range of 10-21 days
TRANSMISSION
VZV is transmitted by contact with oropharyngeal secretions and the
fluid of skin lesions of infected individuals, either by airborne spread
or through direct contact.

Varicella- Zoster Virus

Varicella-zoster virus (VZV) causes two distinct clinical
entities:
Chickenpox, a ubiquitous and extremely contagious
infection, is usually a benign illness of childhood
characterized by an exanthematous vesicular rash.
With reactivation of latent VZV (which is most common
after the sixth decade of life), herpes zoster presents
as a dermatomal vesicular rash, usually associated with
severe pain.

Varicella- Zoster Virus

The period of communicability extends from 1
to 2 days before the onset of rash until lesions
have formed crusts.
Vaccinated persons with varicella may develop
lesions that do not crust (macules and papules
only).

Varicella- Zoster Virus

Humans are the only known reservoir for VZV.
Chickenpox is highly contagious, with an attack rate of at
least 90% among susceptible (seronegative) individuals.
Season: Late winter and early spring in the temperate zone
At risk: Children 59 years old are most commonly affected
and account for 50% of all cases. Most other cases involve
children 14 and 1014 years old.

Varicella- Zoster Virus

Viremia in patients with chickenpox
is reflected in the diffuse and
scattered nature of the skin lesions
Vesicles involve the corium and
dermis, with degenerative changes
characterized by ballooning, the
presence of multinucleated giant
cells, and eosinophilic intranuclear
inclusions.

Varicella- Zoster Virus

Infection may involve localized blood
vessels of the skin, resulting in necrosis
and epidermal hemorrhage.
With the evolution of disease, the
vesicular fluid becomes cloudy because
of the recruitment of polymorphonuclear
leukocytes and the presence of
degenerated cells and fibrin.
Ultimately, the vesicles either rupture
and release their fluid (which includes
infectious virus) or are gradually
reabsorbed.

Varicella- Zoster Virus

Varicella lesions at various
stages of evolution:
1. vesicles on an
erythematous base,
2. umbilical vesicles
3. crusts.

Varicella- Zoster Virus

A mild prodrome may precede the onset of a rash. Adults may
have 1 to 2 days of fever and malaise prior to rash onset, but in
children the rash is often the first sign of disease.
The rash is generalized and pruritic and progresses rapidly from
macules to papules to vesicular lesions before crusting.
The rash usually appears first on the head, then on the trunk,
and then the extremities; the highest concentration of lesions is
on the trunk.

Varicella- Zoster Virus

Lesions also can occur on mucous membranes of the
oropharynx, respiratory tract, vagina, conjunctiva, and the
cornea.
Lesions are usually 1 to 4 mm in diameter.
The vesicles are superficial and delicate and contain clear fluid
on an erythematous base.
Vesicles may rupture or become purulent before they dry and
crust.

Varicella- Zoster Virus

Successive crops appear over several
days, with lesions present in several
stages of development. For example,
macular lesions may be observed in the
same area of skin as mature vesicles.
Healthy children usually have 200 to 500
lesions in 2 to 4 successive crops.

Varicella- Zoster Virus

Varicella Complications
Bacterial infection of skin lesions
Pneumonia (viral or bacterial)
Central nervous system manifestations
Reye syndrome
Hospitalization: 2-3 per 1,000 cases (children)
Death: 1 per 60,000 cases

Varicella- Zoster Virus

Isolation of varicella virus from clinical specimen
Rapid varicella virus identification using realtime PCR (preferred, if available) or DFA
Significant rise in varicella IgG by any standard
serologic assay

Varicella- Zoster Virus

TREATMENT

Oral therapy with acyclovir (20 mg/kg/dose; maximum: 800 mg/dose)

given as 4 doses/day for 5 days can be used to treat uncomplicated
varicella in individuals at increased risk for moderate to severe
varicella

Some experts recommend the use of famciclovir or valacyclovir in older

children who can swallow tablets. These drugs are highly active against VZV
by the same mechanism as acyclovir and are better absorbed by the oral
route than acyclovir. Valacyclovir (20 mg/kg/dose; maximum: 1,000 mg/dose,
administered 3 times daily for 5 days) is licensed for treatment of varicella in
children 2 to <18 yr of age,

Hand-Foot-and-Mouth Disease
Coxsackievirus A16

Hand-Foot-and-Mouth Disease
ETIOLOGIC AGENT:
1. Coxsackievirus A16:
2. Enterovirus 71 (EV-71) is the
second-most common cause
Picornaviridae family
Enterovirus Genus
Enteroviruses are nonenveloped, singlestranded, positive-sense
viruses in the Picornaviridae

Hand-Foot-and-Mouth Disease
TRANSMISSION
The viruses that cause HFMD are spread through
direct contact with the mucus, saliva, or feces of an
infected person.
HFMD often occurs in small epidemics in nursery
schools or kindergartens, usually during the summer
or autumn months.

Hand-Foot-and-Mouth Disease
Mild illness with or without fever
Inflamed oropharynx
Vesicles tongue, buccal mucosa,
posterior pharynx, palate, gingiva,
lips
Maculopapular, vesicular, and/or
pustular hands, fingers, feet,
buttocks, groin

Hand-Foot-and-Mouth Disease

DIAGNOSIS
Viral Culture Gold standard for confirmation
Clues to enterovirus:
Characteristic findings
Consistent seasonality
Known community outbreak
Exposure to enterovirus-compatible disease

Hand-Foot-and-Mouth Disease
TREATMENT
Supportive care
Immune globulin
PREVENTION
Hygiene
Handwashing to prevent fecal-oral and respiratory spread
Avoidance of sharing fomites
Disinfection

Hand-Foot-and-Mouth Disease
Health complications from hand, foot, and mouth disease are not common.
Viral or "aseptic" meningitis can occur with hand, foot, and mouth disease, but
it is rare. It causes fever, headache, stiff neck, or back pain and may require
the infected person to be hospitalized for a few days.
Encephalitis (inflammation of the brain) or polio-like paralysis can occur, but
this is even rarer.
Fingernail and toenail loss have been reported, occurring mostly in children
within a few weeks after having hand, foot, and mouth disease. At this time, it
is not known whether nail loss was a result of the disease in reported cases.
However, in the reports reviewed, the nail loss was temporary, and the nail
grew back without medical treatment.