Exanthem - acute generalized eruptions on

skin.
Enanthem - eruption upon a mucous
membrane
The most common presentation:
Morbilliform
Scarlatiniform
 MORBILLIFORM SCARLATINIFORM

presents as tiny, sometimes infiltrated macules

rash consists of erythematous macules that converging rapidly to form broad expanses of
tend to merge and are separated by bright or dark red skin with rare patches of
patches of non pruriginous, healthy skin healthy skin in between, particularly in the skin
folds ; it is rarely pruriginous
 Macule: flat, colored lesion, <2cm in cm, not raise
above the surface of the surrounding skin.

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.
 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
 1st Disease Measles or Rubeola
2nd Disease Scarlet Fever
3rd Disease Rubella or German Measles
4th Disease Filatovs or Dukes Disease
5th Disease Erythema Infectiosum
6th Disease Exanthem Subitum or Roseola Infantum
1st Disease
 Family Paramyxoviridae-Morbillivirus genus
Single-stranded, lipid-enveloped RNA virus

Humans are the only known host

 Dramatically declined after introduction of
measles vaccine in 1963
Measles was a real battle in the Philippines in
2014 with the final measles tally on the
archipelago at 58,010 cases, according to
the World Health Organization (WHO).
Mortality of 110.
 Transmission: Entry through respiratory
tract or conjunctivae after contact of
droplets, aerosol, fluids or secretions

Infectivity: From 3 days before to up to 4-

6 days after the onset of rash.
4 PHASES of MEASLES

Incubation Prodromal Exanthematous Recovery

 Asymptomatic incubation period occurs 9-12
days from initial exposure.
10 days to fever onset
14 days to rash onset
Migration to Regional Lymph Nodes
Primary Viremia dissemination of the virus to
the reticuloendothelial system
Secondary Viremia spread to body surfaces
Begins AFTER secondary viremia
Associated with epithelial necrosis and giant
cell formation in body tissues
Warthin-Finkeldey giant cells fusion of
epidermal syncytial giant cells with up to 100
nuclei and intracytoplasmic and intranucelar
inclusions
Viral shedding begins
 With onset of the rash, antibody production
begins
Measles virus also infects CD4+ T cells,
resulting in suppression of the Th1 immune
response and a multitude of other
immunosuppressive effects.
Primarily targets alveolar macrophages,
dendritic cells and lymphocytes
 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.
 Incubation Period of 8-12 days
No clinical symptoms yet

Prodromal Phase
High fever with conjunctivitis; photophobia, coryza, prominent cough and
increasing fever, apperance of Kopliks Spots

Exanthematous Phase
Appearance of rash, other symptoms subside
 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, 1-4 days
prior to onset of rash
In 50-70% of measles cases
 Diagnosed clinically and epidemiologic wise
Confirmation by Serology: Anti-measles IgM
and IgG
Histologic evaluation of skin lesions or
respiratory secretions
Enzyme immunoassays
Viral Isolation in culture
PCR
 CBC
Reduced total WBC
Lymphocytes decreased more than neutrophils
Absolute neutropenia
Ancillary Tests
Normal ESR and CRP if measles are not
complicated by bacterial infection
 Pneumonia giant cell pneumonia
Bronchiolitis obliterans
Croup, Tracheitis
Acute Otitis Media, Sinusitis, Mastoiditis
Encephalitis
Dehydration due to Diarrhea and vomiting
Appendicitis
Febrile Seizure
 Black Measles
Manifest as a hemorrhagic skin eruption
Keratitis, appearing as multiple punctate
epithelial foci, resolved with recovery from the
infection.
Atypical Measles
 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
 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
Primarily supportive

Maintenance of hydration, oxygenation, and

comfort are goals of therapy.

Antipyretics for comfort and fever control are

useful
VITAMIN A

50,000 IU is used for infants 1-6 month sold

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

 Live attenuated measles vaccine

Recommended age of first vaccination varies from 6-15

months

Measles vaccine has been available as the combination

vaccine measles-mumps-rubella (MMR)

A second dose of MMR vaccine is recommended for

school-age children
 Vaccine to be given within 72 hours of exposure

Immune globulin up to 6 days after exposure to prevent

or modify infection
Indicated for susceptible household contact
Infants <6mo old, pregnant women, immunocompromised host

Immunocompetent children 0.25 mL/kg IM

Immunocompromised children 0.5 mL/kg

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).
 Member of the family Togaviridae

The only species of the genus Rubivirus

Humans are the only known host

 Decreased dramatically with the introduction of the
vaccine

Occurred more frequently in persons >19 years of age

 ACQUIRED RUBELLA: Via airborne droplet emission from
the upper respiratory tract of active cases; the virus may
also be present in the urine, feces and skin

CONGENITAL RUBELLA SYNDROME: Maternal infection

during the 1st 8 weeks of gestation results in the most
severe and widespread defects.
 INCUBATION PERIOD: 2-3 weeks

INFECTIVITY: 5-7 days before development of the

rash and for about 6-7 days thereafter
 Following infection, virus replicates in the respiratory
epithelium, then spreads to the regional lymph nodes

Viremia ensues and is most intense 10-17 days after

infection
 Incubation Period of 14-21 days

No apparent symptoms yet

Prodromal/Exanthematous Phase
Rash, Low-grade fever, sore throat, red eyes with or without
eye pain, headache, malaise, anorexia, lymphadenopathy
 Rash variable, not distinctive, begins in the face and neck as small,
irregular pink macules that coalesce and spread centrifugally to the
torso and extremities
 Forschheimer spots -
petechial enanthem on the
soft palate may occur but is
not specific for rubella
 Cardiac, cerebral,
ophthalmic, and auditory
defects

May also cause prematurity,

low birth weight, and
neonatal thrombocytopenia,
anemia and hepatitis
 Stage of gestation at the time of infection
Defects occurring after 16 weeks of gestation
are uncommon
Tissue necrosis due to vascular insufficiency
Reduced cellular multiplication time
Chromosomal breaks
Mitotic arresting protein
 Nerve deafness : single most common finding
Some degree of intrauterine growth restriction.
Salt-and-pepper retinopathy
Unilateral or bilateral cataracts
 TRANSIENT PERMANENT

Bony abnormalities Autism

Cloudy cornea Behavioral disorders
Hemolytic anemia Congenital heart disease
Hepatitis Cryptorchidism
Hepatosplenomegaly Deafness
Jaundice Degenerative brain disease
Low birth weight DM
Lymphadenopathy Glaucoma
Meningoencephalitis Inguinal hernia
Rubella viral pneumonia Mental retardation
Thrombocytopenic purpura Microcephaly
Myopia
Precocious puberty
Retinopathy
Seizures
Spastic diplegia
Thyroid disorders
 LABORATORY FINDINGS
Leukopenia, neutropenia, and mild
thrombocytopenia

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

Arthritis

Post-infectious Encephalitis

Progressive rubella panencephalitis(PRP)

 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
 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

Women found to be susceptible are not

vaccinated
5th disease
 Disease in young children causing widespread red rash

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.

 Common and occur worldwide

70% of patients in 5 and 15 years of age

Seasonal peaks in late winter and spring with

sporadic infections throughout
 respiratory route, presumably via large droplet
spread from nasopharyngeal viral shedding

B19 is also transmissible in blood and blood

products
 INCUBATION PERIOD: 4-28 days (average 16-17
days)

INFECTIOUS PERIOD: up until onset of rash

 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
 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

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
 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
 Arthropathy
Transient Aplastic Crisis
Immunocompromised Persons
Fetal Infection
Myocarditis
 Papular purpuric gloves-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.
 Clinical presentation of the typical rash
Rarely requires virologic confirmation
Serologic tests for the diagnosis of B19
infection:
B19-specific IgM
Anti-B19 IgG
anti-B19 IgM
 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

B19 infected fetuses with anemia and hydrops

intrauterine RBC transfusions.
 Erythema infectiosum are not likely to be infectious at
presentation (rash and arthropathy represent immune
mediated, post infections phenomena).

Children with B 19 induced RBC aplasia are

infectious upon presentation and demonstrate a more
intense viremia

No vaccine available
 Arthralgias or arthritis in adolescent (may persist after
resolution of rash)
May rarely cause thrombocytopenic purpura
Aseptic meningitis
Encephalitis
Peripheral neuropathy
Increased incidence of stroke in children with sickle cell
disease following B19 induced aplastic crisis
Exanthema Subitum (6th Disease)
 Exanthem subitum
Etiologic Agent: Human
herpesvirus 6 and 7
HHV-6 -responsible for the
majority of cases
Roseolovirus genus in the
Beta herpes virinae
subfamily of human herpes
viruses.
 95% of children being infected HHV-6 by 2
years of age
Peak age of HHV-6 infection is 6-9 mo of life,
occuring sporadically and with seasonal
predilection
HHV-7 is also widespread but occurs later in
childhood and at a slower rate
Congenital
 Incubation period: 9 days

Infectious period: Virus is intermittently shed

into saliva throughout life; asymptomatic
infection
 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
Most postnatally infected children develop symptoms:
fever, fussiness, and diarrhea.
Resolves within 2 days
 Inflammed tympanic membranes
Rhinorrhea and congestion
GI complaints
Encephalopathy
Cough
 Methods
Gold standard: viral culture

Laboratory Findings
Lower mean numbers of total white bloods,
lymphocytes, and neutrophils
Thrombocytopenia, elevated serum transaminase
values, atypical lymphocytes
Convulsions, seizures

Encephalitis
 Supportive Care
Maintain hydration
Use of antipyretics
Ganciclovir, foscarnet, and cidofovir
for Encephalitis
 Widespread throughout the human population
with no current means of interrupting
transmission
 Varicella Zoster Virus is a member of the
family Herpesviridae, double-stranded DNA
 Widespread before introduction of the vaccine in 1995
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.
 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.
 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 (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.
 diffuse and scattered skin
lesions

Vesicles involve the corium

and dermis, with
degenerative changes
 Infection may involve localized
blood vessels of the skin

The vesicular fluid becomes

cloudy because of the
recruitment of
polymorphonuclear leukocytes
and the presence of
degenerated cells and fibrin.

The vesicles either rupture and

release their fluid or are
gradually reabsorbed.
Varicella lesions at
various stages of
evolution:
1. vesicles on an
erythematous base,
2. umbilical vesicles
3. crusts
 A mild prodrome may precede the onset of a rash. 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.
 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.
 Successive crops appear over
several days, 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.
 Breakthrough Varicella

Progressive Varicella

Neonatal Varicella

Congenital Varicella Syndrome

 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
 Isolation of varicella virus from clinical specimen

Rapid varicella virus identification using real-time

PCR (preferred, if available) or DFA

Significant rise in varicella IgG by any standard

serologic assay
 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. 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
 1.CoxsackievirusA16
2.Enterovirus 71 (EV-71); the second-most common cause

Picornaviridae family
Enterovirus Genus
Enteroviruses are nonenveloped, single-stranded,
positive-sense viruses in the Picornaviridae
 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.
 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
 Viral Culture Gold standard for confirmation
Clues to enterovirus:
Characteristic findings
Consistent seasonality
Known community outbreak
Exposure to enterovirus-compatible disease
 Supportive care
Immunoglobulin
Hygiene
Handwashing to prevent fecal-oral and respiratory
spread
Avoidance of sharing fomites
Disinfection
Health complications from hand, foot, and mouth
disease are not common.

Viral or "aseptic" meningitis

Encephalitis (inflammation of the brain) or polio-like
paralysis
Temporary fingernail and toenail loss