Download VIRAL EXANTHEM

VIRAL EXANTHEM
General Objectives: To discuss the general spectrum of infectious diseases in children particularly common viral infections
that produces exanthems or skin manifestations.
Specific Objectives: To know common viral infections seen in children and discuss the following:











Etiology
Incidence
Incubation period
Transmission
Pathogenesis
Clinical manifestations
Diagnosis
Complications
Management
Prevention
Prognosis
MEASLES (Rubeola)
acute communicable disease is characterized 3 stages:

Incubation stage- approximately 10-12 days with few, if any signs or symptoms

Prodromal stage- with an enanthem (Kopliks spot) on the buccal and pharyngeal mucosa,
slight to moderate fever, mild conjunctivitis, coryza and an increasingly severe cough.

Final stage- with a maculopapular rash erupting successively over the neck and face, body,
arms and legs and accompanied by high fever
ETIOLOGY
-
Measles is an RNA virus of the Family Paramyxoviridae, genus Morbilivirus
One antigenic type
During prodromal and short time after the rash appears the virus is found in the nasopharyngeal
secretions, blood and urine
It remained active for at least 34 hrs at room temperature
INFECTIVITY
EPIDEMIOLOGY
PATHOLOGY
-
maximal dissemination of the virus via droplet spray during the prodromal period
infected person becomes contagious by the 9yh-10th day after exposure (beginning of prodromal
phase), in some instances as early as the 7th day
isolation precaution should be maintained from the 7th day after exposure until 5 days after the rash
has appeared
Philippine statistics (DOH, 2001): 24,494 cases with rate of 31.4/100,000 population
essential lesion of measles is found in the skin, mucous membrane of nasopharynx, bronchi,
intestinal tract and conjunctivae.
There usually hyperplasia of the lymphoid tissue particularly in the appendix with multinucleated
giant cells (Warthin-Finkeldey reticuloendothelial cells)
CLINICAL MANIFESTATIONS
A.
INCUBATION PERIOD: approximately 10-12 days if the first prodromal symptom is selected as the time of
onset
14 days if the appearance of the rash is selected
B.
PRODROMAL PHASE: last 3-5 days, characterized with low to moderate grade fever, a hacking cough, coryza
and conjunctivitis
the 3 c’s nearly always preceed KOPLIK SPOTS – pathognomonic sign of measles by 2-3 days
KOPLIK SPOTS: an enanthem or red mottling is usually present on the hard and the soft palates. This
are slightly grayish white dots, usually as small as grains of snd, with slight, reddish areola,
occasional hemorrhagic. Located opposite the lower molars but may spread irregularly over the rest
of the buccal mucosa. They disappear within 12-18 hrs.
C.
Final stage/ appearance of rashes: temperature abruptly rises 40-40.5C
1
-
uncomplicated cases: when rash appears on the leg and the feet within 2 days, symptoms subside
rapidly.
Macular rashes appears on the lateral side of the neck, behind the ears, along hairline and the
posterior part of the cheek.
1st 24hrs: spread on the face neck, arms and upper part of the chest.
Succeeding 24 hrs: back, abdomen entire arms and thighs
2nd-3rd day: feet and begins to fade on the face
Rash is often slightly hemorrhagic, itching is generally slight
As the rash fades, BRANNY DESQUAMATION and brownish discoloration occurs and then disappears
within 7-10 days
MODIFIED MEASLES v.s. ATYPICAL MEASLES
Modified measles:
Atypical measles:
-
occurs in partially immune host; young infants with partial protection from maternal antibodies and
immunized children with partial vaccine failure
short prodrome, less severe rash; Koplik spot; diagnosis should not be made in the absence of cough
occurs in recipient of killed measles virus vaccine given until 1967 who came in contact with wild type
measles vaccine; few, less severe cases in children given live attenuated measles vaccine
sever headache, severe abdominal pain with vomiting, myalgia, pneumonia with pleural effusion and
an atypical rash that first appears on the palms, wrist, soles and ankle and progresses into centripetal
direction; maculopapular rashes can become vasicular later hemorrhagic. Koplik spots are rare.
DIAGNOSIS:
A. Clinical: characteristic clinical picture is the usual basis for diagnosis
B. Laboratory: rarely needed
a. Positive measles IgM antibody
b. Significant increases in measles IgG antibody in paired acute and convalescent sera
c. Isolation of measles virus from urine, blood and nasopharyngeal secretions
COMPLICATIONS
A. Otitis media
B. Laryngitis, laryngotrachietis, laryngotracheobronchitis
C. Pneumonia: most common complication and leading cause of death
a. Primary measles pneumonia
b. Pneumonia secondary to bacterial infection ( H. influenza, Streptococcus pyogenes, Streptococcus
pneumoniae)
D.
Encephalitis
a. More common in measles than any other viral exanthems (0.5-1/1000 cases)
b. Usually occurs 2-5 days after the rash
c. Early occurrence is the result of direct viral invasion: later occurrence is predominantly demyelinating.
E.
Subacute
a.
b.
c.
d.
e.
F.
G.
H.
I.
J.
K.
Sclerosing Panencephalitis (SSPE)- DAWSON ENCEPHALITIS
Rare degenerative CNS disease occurring years later (0.6-2.2/100,000 infection)
Due to persistent measles virus
Progressive behavioral and intellectual deterioration with seizures, mostly myoclonic jerks, motor
incoordination, visual and speech impairment.
Laboratory features: markedly elevated CSF globulin predominantly IgG, high serum measles
antibody titers and high CSF measles antibody titers
EEG: periodic suppression burst pattern
Exacerbation of an underlying Mycobacterium tuberculosis infection. A temporary loss of hypersensitivity
reaction to tuberculin occur 4-6 weeks (sate of anergy)
Myocarditis
Thrombocytopenic purpura
Severe conjunctivitis which may lead to corneal ulcerations and blindness
Dehydration
Malnutrition
TREATMENT:
A.
B.
specific: none
Non-specific
a. Supportive measures
2

i. Antipyretics
ii. Adequate nutrition and fluid intake
b. Vitamin A supplementation:
i. < 6months – 12mons: 100,000 iu
ii. >12 months: 200,000 iu
dose should be repeated the next day and 4 weeks later if with ophthalmologic evidence of vitamin a
deficiency.
c. Antimicrobial therapy: not routinely given except in the presence of complication like otitis media or
pneumonia.
SUPPORTIVE MANAGEMENT:
A. isolation of hospitalized patients
B. Care of exposed persons
a. Active immunization: live measles vaccine given 72 hrs after exposure maybe protective in some
cases
b. Passive immunization: immunoglobulin may prevent or modify measles if given 6 days after
exposure.
c. Control measures: live measles vaccine immunization of infants 6-9 months and a second dose of at
12-15 months as MMR. A second dose of MMR given 4-6 years old.
RUBELLA ( German Measles/ Three-day measles)
-
common communicable disease in childhood characterized by mild constitutional symptoms, a rash
similar to mild rubeola, enlargement and tenderness of postoccipital, retroauricular and posterior
cervical lymphnodes
Rubella in early pregnancy may cause severe congenital anomalies ( Congenital Rubella Syndrome)
-
Rubella virus, an RNA virus under the family Togaviridae and genus Rubivirus
ETIOLOGY:
CLINICAL FORMS
A. Postnatal Rubella
a. Source:
i.
b.
c.
d.
e.
f.
g.
h.
During clinical illness the virus is present in the nasopharyngeal secretions, blood, feces
and urine of infected person including those with congenital rubella
Mode of transmission: direct of droplet contact from nasopharyngeal secretions
Period of communicability:
i. The virus can be recovered from the nasopharynx 7 days before the exanthema and 7-8
days after its disappearance.
Incubation period: 14-21 days
Clinical Picture:
i. Asymptomatic illness: account for 25-50% of cases
ii. Symptomatic illness
Manifestations:
i. Adenitis: enlargement of retroauricular, postcervical and suboccipital lymph nodes at least
24 hrs before the rash
ii. Forscheimer spots: discrete rose spots on the soft palte in 20% of patients before the rash
iii. Rash: maculopapular rashes on the face, rapidly becoming generalized within 24 hrs, with
minimal desquamation
iv. Mild conjunctivitis with photophobia, mild pharyngitis, slight splenomegaly, polyarthralgia/
polyarthritis
v. Fever is low grade or absent
Diagnosis
i. Clinical diagnosis is difficult because symptoms and rashes are similar to other viral
infections
ii. Laboratory diagnosis:
1. isolation of virus from nasal specimen, throat swab, blood, urine or CSF
2. Detection of antibodies
a. Rubella-specific IGM: recent postnatal infection
b. Rubella- specific IgG between acute and convalescent serum titters:
fourfold increase—INFECTION
Complications: rare
i. Encephalitis ( 1/6000 cases)
3
ii. Purpura: thrombocytopenic or non-thrombocytopenic
I. Treatment: supportive
B.
CONGENITAL RUBELLA
a. Pathogenesis
i. Transplacental infection of fetus with rubella virus occurs following primary maternal
viremia
ii. The time when rubella virus infection occurs during gestation is a critical factor that
determines the risk of fetal infection and disease severity:
Time of fetal infection
1st month of gestation
2nd month of gestation
3rd-4th month of gestation
b.
c.
d.
e.
f.
g.
h.
Risk of congenital defects
>/= 50%
20-30%
5%
Redbook 2003
Period of communicability:
i. As long as virus shedding occurs in nasopharyngeal secretions and urine; can last for 1
year or in more in a small number of patients
Clinical features:
i. Intrauterine growth retatardation: most common manifestation
ii. Ophthalmologic manifestations: cataract, retinopathy, congenital glaucoma
iii. Cardiac anomalies: PDA, peripheral pulmonary artery stenosis
iv. Auditory: sensorinueral deafness
v. Neurologic anomalies: behavioral disorders, meningoencephalitis, mental retardation
vi. “Blueberry muffin” skin lesions
vii. Hepatomegaly
viii. Persistent infection that may lead to pneumonia, hepatitis, bone luscencies,
thrombocytopenic purpura and anemia
Diagnosis:
i. Isolation of virus from nasopharyngeal secretions, urine, CSF and any tissue/organ in the
body
ii. Presence of specific rubella IgM antibodies in a newborn
Treatment: supportive
Isolation of patient
i. Droplet precaution in addition to standard precautions are recommended for 7 days after
the onset of rash
ii. Contact isolation is recommended in congenital rubella until at least 1 year old
Care of exposed persons:
i. Pregnant: tested for rubella antibody. If (+) rubella specific IgG antibody- likely IMMUNE.
If (-) test is repeated 2-3 weeks and then again, 6 weeks later, to note for seroconversion
which will indicative of infection
Control measures
i. Use of immunoglobulin for post exposure prophylaxis of rubella in early pregnancy is not
routine, but may be considered.
ii. Live rubella vaccine had not found to prevent infection after exposure but theoretically can
prevent the illness if given within 3 days after exposure
iii. MMR vaccine: 12-15 months (1st dose); 4-6 years old (2nd dose)
ERYTHEMA INFECTIOUSUM (Fifth Disease)
benign, self-limiting exanthematous lesions in childhood
it is fifth in the classification ( rubella, measles, scarlet fever and Filatov-Dukes disease- atypical
scarlet fever)
ETIOLOGY:
Parvo virus B19; small DNA contating virus under the family Parvoviridae
CLINICAL MANIFESTATION:
hallmark of EI is the characteristic rash but indistinguishable in the 3 stages

Prodromal phase: mild, low grade fever, headache and mild AURI. The rash during this
stage erythematous facial flushing“slapped- cheek” appearance

Second stage: rashes spread rapidly to the trunk and proximal extremities as a diffuse
macular erythema

3rd stage: central clearing of macular lesions giving a lacy reticulated appearance

Palms and soles are spared and rashes more prominent on extensor surface
DIAGNOSIS:
4
A.
B.
Laboratory:
a. Not routinely done
b. Virus cannot be isolated
Based on clinical observation of the rash
TREATMENT: no specific antiviral treatment
ROSEOLA INFANTUM (Exanthem subitum or Sixth disease)
ETIOLOGY:
EPIDEMIOLOGY:
-
INCIDENCE:
-
Human herpes virus 6: common
Human herpes virus 7 and Echo virus 16: less frequent
HHV 6/7: beta- heper virus under subfamily of herpes virus
Double stranded DNA
6-15 months: peak of roseola which also correspond to peak age of acquisition of HHV 6 infection
Can develop in children year round

Mode of transmission: most adults excrete the virus in saliva and may serve as the primary
source of virus transmission in children

Saliva of healthy persons and enter the host oral, nasal and conjunctival mucosa
less then 3 years old: 95% with peak at 6-15 months.
Transplacental antibodies likely to protect most infants until 6 months.
MANIFESTATIONS:
Prodromal period: asymptomatic but may include mild upper respiratory signs ( rhinorrhea, slight
pharyngeal irritations, mild conjuctival redness)
Mild cervical or less frequent occipital lymphaenopathy
High grade fever ( 37.9-40C)
CHILDREN BEHAVE NORMALLY DESPITE HIGH TEMPERATURE
NAGAYAMA SPOTS: seen in asian children, ulcers at the uvulopalatoglossal junction.
Fever persist for 3-5 days and resolved abruptly
RASHES: appears 12-24 hrs after resolution of fever

Rose colored

Discrete, non-pruritic, small (2-5mm), slightly raised pink lesion on the trunk and spread
neck, face, and proximal extremities- CENTRIFUGAL

1-3 days rashes fades
DIAGNOSIS
based mainly on age, history and clinical findings to differentiate with other potentially serious viral
exanthems
laboratory: serology, virus culture, antigen detection and PCR
D/Dx:
-
-
Rubella: mild prodromal period

(+) prominent occipital and postauricular lymphadenopathy

Low grade fever which coincides with the exanthema

More extensive rashes

(+) exposure to person with Rubella
Measles: exanthems at the height of fever

3Cs (+) Koplik spot
TREATMENT:
-
SUPPORTIVE
HHV 6: gancyclovir
VARICELLA
- disease spectrum encompasses:
- primary infection (varicella/chicken pox),
- latent infection ( latent infection on sensory ganglia)
- recurrent infection (herpes zoster/ shingles)
ETIOLOGY
-
Varicella-zoster virus: neurotropic human herpesvirus
Alpha-herpes virus; double stranded DNA
EPIDENMIOLOGY
5
PATHOGENESIS
-
-
contagious from 24-48 hours before the rash appears and until the vesicles are crusted, usually 3-7
days after onset of rash
“ Breakthrough varicella”: mild manifestation; varicella among immunized children
Hepes zoster: due to reactivation of latent VZV; uncommon in childhood (~45 year old)
transmission via respiratory secretions and in the fluid of skin lesions either by airborne spread of
through direct contact
Primary Infection (VARICELLA): respiratory inoculation of the virus

IP: 10-21 days- the virus replicate in the respiratory tract followed by brief subclinical
viremia

Second viremic phase: wide spread cutaneous lesions
Latent infection: VZV establishes in the sensory ganglia cells in all individual who experienced primary
infection
Herpes zoster infection: subsequent reactivation of latent virus

Vesicular rashes that usually located dermatomal in distribution – posterior nerve roots,
more frequently on the trunk (dorsal root0, shoulder, arms and neck (second to fourth
cervical ganglia)
CLINICAL MANIFESTATION
A.
VARICELLA (PRIMARY INFECTION)
begins 14-16 days after exposure
fever, malaise, anorexia, headache, mild abdominal pain- 24-48 hrs before the appearance of rashes
starts to appear on the scalp, face, trunk
erythematous pruritic macule  popular stage vesicle with clear filled fluidlesions become cloudy
and umbilicated 24-48 hrs crusting.
While other lesions are crusting, new crops form on the trunk and extremities simultaneous
presence of lesions on various stages of evolution is the characteristic picture of varicella crusting
(“celestial map”)
Rash distribution is predominantly central that goes distally (difference from small pox – rashes starts
at the face and distal extremities)
B.
BREAKTHROUGH VARICELLA
vaccination of varicella vaccine can prevent 95% of having a typical varicella and 70-90% preventing
all disease
varicella in a child vaccinated more than 42 days before onset of rash and is due to wild type VZV
rash occurring within first 2 weeks of vaccination is most commonly wild type VZV.
Rash occurring 2-6 weeks after vaccination could be due to either wild or vaccine strains
Rash: atypical, maculopapular, vesicles are uncommon.
C.
NEONATAL VARICELLA
birth within 1 week before or after the onset of maternal varicella frequently result in the newborn
developing varicella which maybe severe
if there was 1 week or greater interval between maternal varicella and parturition, it is likely that the
newborn received sufficient transplacental antibody to VZV to ameliorate neonatal infection
if less than 1 week, the newborn will be unlikely to have protective VZV antibody and neonatal
varicella may be exceptionally severe.
D.
CONGENITAL VARICELLA SYNDROME
Embryopathy: affects the skin, eye, brain and limbs

2% of fetuses affected if mother had varicella on the first 20 weeks of pregnancy

6-12 weeks: maximum interruption on limb development

16-20 weeks: affects the eye and brain development
CICATRIX: characteristic cutaneous lesion; zigzag scarring pften dermatomal in distribution
Shortened and malformed extremities, cataract, extensive aplasia of the entire brain
Stigmata of VZV infection
A. Damage to sensory nerves
cicatricial skin lesion
hypopigmentation
B. Damage to optic stalk and lens vesicle
microphthalmia
cataract
chorioretinitis
optic atropy
6
C.
D.
E.
Damage
Damage
-
to brain and encephalitis
microcephaly
hydrocephalus
calcifications
aplasia of brain
to cervical and lumbosacral cord
hypolpasia of extremities
motor and sensory deficit
absent deep tendon reflex
anisocoria
horner’s syndrome
anal/urinary sphincter dysfunction
Herpes zoster: vesicular lesion clustered within one or less common 2 adjacent dermatome
i. Children: less common. Less painful, low grade fever
1. Complete resolution within 1-2 weeks
ii. 2nd episode is common. 3rd is rare
DIAGNOSIS
b.
c.
COMPLICATIONS
d.
e.
f.
g.
h.
i.
j.
determination of VZ antibody titer
demonstration of VZ virus by electron microscopic examination of vesicular fluid
not common in children
secondary bacterial infection
encephalitis or meningitis
pneumonia
Reye syndrome ( associated with aspirin administration)
Congenital varicella
Glomerulonephritis
TREATMENT:
k.
l.
SPECIFIC: none except those who are immunocompromised, >12 year old, with chronic skin disease,
persons using long term salicylate and those person under treatment of corticosteroids
Acyclovir: 15-30 mkday IV in 3 divided dose or 200-400 tablet orally every 4hrs minus the midnight
dose for 5 days.
7