VIRAL EXANTHEMA

Dharmendra Mandal
 Viral Exanthema
 Viral exanthems are skin rashes or eruptions caused
by infections with certain types of viruses.
 The most common childhood viral exanthems include the
following:
 Measles (rubeola)
 Rubella (german measles)
 Varicella (or chickenpox)
 Fifth disease Erythema Infectiosum
 Roseola
 Measles
 Measles is highly contagious but owing to widespread
vaccination, endemic transmission has been interrupted in
the United States
 ETIOLOGY
 Measles virus is a single-stranded, lipid-enveloped RNA
virus in the family Paramyxoviridae and genus Morbillivirus..
 Humans are the only host of measles virus.
 Epidemiology
 Once worldwide in distribution, endemic transmission of
measles has been interrupted in many countries where there
is widespread vaccine coverage.
 Measles
 TRANSMISSION
 The portal of entry of measles virus is through
 the respiratory tract or
 conjunctivae following contact with large droplets or small-dropleta erosols in which the
virus is suspended
 Patients are infectious from 3 days before to up to 4-6 days after the onset of rash.
 PATHOLOGY
 Measles infection causes necrosis of the respiratory tract epithelium and an
accompanying lymphocytic infiltrate.
 Measles produces a small-vessel vasculitis on the skin and on the oral mucous
membranes.
 Histology of the rash and exanthem reveals intracellular edema and dyskeratosis
associated with formation of epidermal syncytial giant cells with up to 26 nuclei.
 the Warthin-Finkeldey giant cells that are pathognomonic for measles
 Measles
 PATHOGENESIS
 Measles consists of 4 phases:
 Incubation Period- 8-12 days,
 Prodromal Illness,
 Exanthematous Phase, And
 Recovery.
Incubation Period
Measles
 measles virus migrates to regional lymph nodes.
 A primary viremia disseminates the virus to the reticuloendothelial system.
 A secondary viremia spreads virus to body surfaces.

The prodromal
 After the secondary viremia
 Associated with epithelial necrosis and giant cell formation in body tissues.
 Cells are killed by cell-to-cell plasma membrane fusion associated with viral replication that
occurs in many body tissues, including cells of the central nervous system.
 Virus shedding begins in the prodromal phase.
Exanthematous Phase,
With onset of the rash, antibody production begins, and viral replication and symptoms begin to
subside.
 Recovery
 Measles
 Measles virus also infects CD4+ T cells, resulting in
suppression of the Th1 immune response and a
multitude of other immunosuppressive effects.
 Recent research has clarified the pathogenesis of
disease caused by measles virus
 attaches to specific cell receptors to infect host cells.
 . Unlike other Paramyxoviridae members that
utilize sialic acid molecules on the virus surface to
enter cells.
 Measles
 CLINICAL MANIFESTATIONS
 Measles is a serious infection characterized by
 High Fever
 An Enanthem,
 Cough,
 Coryza,
 Conjunctivitis, And
 A Prominent Exanthema.
 After An Incubation period of 8-12 days, the prodromal phase begins with a mild
fever followed by the onset of conjunctivitis with photophobia, coryza, a prominent
cough, and increasing fever.
 Koplik spots represent the enanthem and are the pathognomonic sign of measles,
 appearing 1-4 days prior to the onset of the rash .
Measles
 Measles
 Symptoms increase in intensity for 2-4 days until the 1st day
of the rash.
 The rash begins on the forehead (around the hairline), behind
the ears, and on the upper neck as a red maculopapular
eruption.
 It then spreads downward to the torso and extremities,
reaching the palms and soles in up to 50% of cases.
 With the onset of the rash, symptoms begin to subside.
 The rash fades over about 7 days
 The cough lasts the longest, often up to 10 days.
 Measles
 LABORATORY FINDINGS
 The diagnosis of measles is almost always based on clinical and epidemiologic findings.
 Acute phase include reduction in the total white blood cell count,
 with lymphocytes decreased more than neutrophils.
 Absolute neutropenia
 The erythrocyte sedimentation rate and C-reactive protein level are normal.
 
 DIAGNOSIS
 Confirmation of the clinical diagnosis .
 Serologic confirmation is most conveniently
 identification of immunoglobulin (Ig) M antibody in serum.
 IgM antibody appears 1-2 days after the onset of the rash and remains detectable for about 1 mo.

 Viral isolation from blood, urine, or respiratory secretions can be accomplished by culture
 Measles
 DIFFERENTIAL DIAGNOSIS
 Measles in the later stages or inapparent or subclinical infections
may be confused with a number of other exanthematous
 Rubella,
 Adenovirus infection,
 Enterovirus infection, and
 Epstein-Barr virus infection.
 Exanthem subitum (in infants) and erythema infectiosum (in older
children)
 Mycoplasma pneumoniae and group A streptococcus
 Kawasaki
 Drug eruptions.
 Measles
TREATMENT
 Management of measles is supportive.

 Antiviral therapy is not effective

 .Maintenance of hydration, oxygenation, and comfort are goals of therapy.

 Antipyretics for comfort and fever

 For patients with respiratory tract involvement, airway humidification and

supplemental oxygen may be of benefit.

 Respiratory failure from croup or pneumonia may require ventilatory support
 Oral rehydration is effective in most cases, but severe dehydration may require

intravenous therapy.
 Prophylactic antimicrobial therapy to prevent bacterial infection is not indicated.
 Measles infection in immunocompromised patients is highly lethal.
 Measles
 COMPLICATIONS
 Complications of measles are largely attributable to the pathogenic effects of the virus on the
respiratory tract and immune system .
 Morbidity and mortality from measles are greatest in patients younger than 5 yr of age
(especially <1 yr of age) and older than 20 yr of age.
 Pneumonia -most common cause of death in measles.
 Croup, tracheitis, and bronchiolitis are common complications in infants and toddlers with
measles.
 Acute otitis media is the most common complication of measles.
 Sinusitis and mastoiditis also occur as complications.
 Febrile seizures occur in <3% of children with measles.
 Encephalitis following measles is a long-associated complication.
 Myocarditis is a rare complication of measles.
 Subacute sclerosing panencephalitis (SSPE) is a chronic complication of measles with a
delayed onset and an outcome that is nearly always fatal.
 Measles
 PROGNOSIS
 In the early 20th century, deaths from measles in the United States varied about 10 deaths per 1,000

cases of measles
 With improvements in healthcare and antimicrobial therapy, better nutrition, and decreased
crowding, the death : case ratio fell to 1 per 1,000 cases.
 Pneumonia and encephalitis were complications in most of the fatal cases, and immunodeficiency
conditions were identified in 14-16% of deaths
PREVENTION
 Patients shed measles virus from 7 days after exposure to 4-6 days after the onset of rash. Exposure of

susceptible individuals to patients with measles should be avoided during this period.
 Immunocompromised patients with measles will shed virus for the duration of the illness, so
isolation should be maintained throughout the disease.
 Vaccine

Postexposure Prophylaxis
 Vaccine administration or immunization with immune globulin

 The vaccine is effective given within 72 hr of exposure

 Immune globulin e given up to 6 days after .

 Rubella (German measles or 3 day
measles
 is a mild, often exanthematous disease of infants and children.
 that is typically more severe and associated with more complications in adults
 Its major clinical significance is transplacental infection and fetal damage as
part of thecongenital rubella syndrome (CRS).
ETIOLOGY
 Rubella virus
 familyTogaviridae
 species of the genus Rubivirus.
 single-stranded RNA virus with a lipid envelope and 3
structural proteins,
 Humans are the only known host.
 .
Rubella


Biopsy or autopsy material from

cases of rubella revealed
only nonspecific findings of
lymphoreticular inflammation
and mononuclear perivascular
and meningeal infiltration.
The pathologic findings for CRS are
often severe and may involve
nearly every organ system.
 Rubella
PATHOGENESIS
 The viral mechanisms for cell injury and death in postnatal or congenital

rubella are not well understood.

 Following infection, the virus replicates in the respiratory epithelium and then
spreads to regional lymph nodes.
 Viremia ensues and is most intense from 10-17 days after infection.

 Viral shedding from the nasopharynx

 10 days after infection and detected up to 2 wk following onset of the rash
 The period of highest communicability
 is from 5 days before to 6 days after the appearance of the rash.
 Risk factor for severe congenital defects
 stage of gestation at the time of infection.
 1st 8 wk of AOG  most severe and widespread defects.
 After 16 wk of gestation are uncommon
Rubella
 Rubella
CLINICAL MANIFESTATIONS
 Postnatal infection with rubella is a mild disease not easily discernible from other

viral infections, especially in children.

 Following an incubation period of 14-21 days,
 A prodrome consisting of
 Low-grade Fever,
 Sore Throat,
 Red Eyes With Or Without Eye Pain
 Headache,
 Malaise,
 Or Petechial Hemorrhages On The Soft Palate.
 The rash fades from the face as it extends to the rest of the body so that the whole
body may not be involved at any one time.
 The duration of the rash is generally 3 days, and it usually resolves without
desquamation.
 Rubella
LABORATORY FINDINGS
 (postnatal rubella)
 Leukopenia,
 neutropenia, and
 mild thrombocytopenia. 

DIAGNOSES
 A specific diagnosis of rubella is important:

 For epidemiologic reasons,

 For diagnosis of infection in pregnant women, and

 For confirmation of the diagnosis of congenital rubella.

 The most common diagnostic test is

 Rubella immunoglobulin (Ig) M enzyme immunosorbent assay.
 .Tests should be performed in the context of a supportive history of
exposure or consistent clinical findings.
 Rubella
DIFFERENTIAL DIAGNOSES
 Rubella may manifest as distinctive features suggesting the diagnosis.

 Measles. The absence of Koplik spots and a severe prodrome as well as a shorter course allow for
differentiation from measles. )
 Other infections caused by
 Adenoviruses,
 Parvovirus B19 (erythema infectiosum),
 Epstein-Barr virus,
 Enteroviruses, and Mycoplasma pneumonia.
COMPLICATIONS
 Complications following postnatal infection with rubella are infrequent and generally not

life-threatening.
 Postinfectious thrombocytopenia occurs in approximately 1 in 3,000 cases of rubella.

 Arthritis following rubella occurs more commonly among adults,especially women.

 Encephalitis is the most serious complication of postnatal rubella.

 Progressive rubella panencephalitis (PRP) is an extremely rare complication of either

acquired rubella or CRS.

 Rubella
 Congenital Rubella Syndrome
 Rubella
TREATMENT
 There is no specific treatment available for either acquired rubella or CRS.

SUPPORTIVE CARE
 Postnatal rubella mild illness no care beyond antipyretics and analgesics.

 Intravenous immunoglobulin or corticosteroids  for severe, nonremitting

thrombocytopenia.
 Management of children with CRS is more complex and requires pediatric,

cardiac, audiologic, ophthalmologic, and neurologic evaluation and follow-

up
PROGNOSIS
 Postnatal infection with rubella has an excellent prognosis.

 Long-term outcomes of CRS are less favorable and somewhat variable.

 Reinfection with wild virus occurs postnatally in both individuals who were

previously infected with wild-virus rubella and in vaccinated individuals

 Rubella
PREVENTION
 Patients with postnatal infection should be isolated from susceptible

individuals for 7 days after onset of the rash.

 Exposure of susceptible pregnant women poses a potential risk to the fetus,

 The routine use of immunoglobulin for susceptible pregnant women

exposed to rubella is not recommended.

VACCINATION
 Rubella vaccine (attenuated Wistar RA 27/3 strain ) combination with

measles and mumps (MMR) or also with varicella (MMRV) in a 2 dose

regimen at 12-15 mo and 4-6 yr of age.
 Vaccine should not be administered to severely immunocompromised.
 Varicella (or chickenpox)

 Chickenpox is a highly contagious disease caused by

the varicella-zoster virus (VZV).
 It can cause an itchy, blister-like rash.
 The rash appears first on the chest, back, and face,
and then spreads over the entire body.
 The primary infection is manifested as varicella
(chickenpox) and results in establishment of a
lifelong latent infection of sensory ganglion neurons.
, including proteins that are targets of cellular and
humoral immunity.
 Varicella (or chickenpox),

EPIDEMIOLOGY
 Before the introduction of varicella vaccine in 1996, varicella was an
almost universal communicable infection of childhood
 Most children were infected by 15 yr of age,
 Persons with varicella are contagious 24-48 hr before the rash is
evident and until vesicles are crusted, usually 3-7 days after onset of
rash.
 Varicella (or chickenpox),

PATHOGENESIs
 VZV is transmitted
oropharyngeal secretions and
The fluid of skin lesions of infected individuals,
either by airborne spread or through direct contact.
 Primary infection (varicella)
 results from inoculation of the virus onto the mucosa of the upper respiratory
tract and tonsillar lymphoid tissue.
 During the early part of the 10-21 day incubation period,
 virus replicates in the local lymphoid tissue, and then a brief subclinical viremia
spreads the virus to the reticuloendothelial system.
 Widespread cutaneous lesions occur during a
2nd viremic phase that lasts 3-7 days.
 Varicella (or chickenpox),

PATHOGENESIS
 Peripheral blood mononuclear cells carry infectious
virus, generating new crops of vesicles during this
period of viremia.
 VZV is also transported back to the mucosa of the
upper respiratory tract and oropharynx during the late
incubation
 Period. permitting spread to susceptible contacts 1-2
days before the appearance of rash. Host immune
responses limit viral replication and facilitate recovery
from infection
 Varicella (or chickenpox),
CLINICAL MANIFESTATIONS
 Varicella is an acute febrile rash illness that was common in children

before the universal childhood vaccination program.

Varicella in Unvaccinated Individuals
 The illness usually begins 14-16 days after exposure, ( incubation

period 10-21 days)

 Subclinical varicella is rare;
 All exposed, susceptible persons experience a

 Rash,
 Fever,
 Malaise,
 Anorexia, headache, and
 Occasionally mild abdominal pain may occur 24-48 hr before the rash appears.
 Varicella (or chickenpox),

 Fever and other systemic symptoms usually resolve within 2-4 days after the
onset of the rash. 
 Varicella lesions often appear first on the scalp, face, or trunk.
 The initial exanthem consists of intensely pruritic erythematous macules that
evolve through the papular stage to form clear, fluid-filled vesicles.
 Clouding and umbilication of the lesions begin in 24-48 hr.  
 While the initial lesions are crusting, new crops form on the trunk and then the
extremities; the simultaneous presence of lesions in various stages of evolution
is characteristic of varicella (Fig. 253-1).
 The distribution of the rash is predominantly central or centripetal with the
greatest concentration on the trunk and proximally on the extremities.
 Ulcerative lesions involving the mucosa of the oropharynx and vagina
 Varicella (or chickenpox),

Neonatal Varicella
 Mortality is particularly high in neonates born to

susceptible mothers who contracted varicella

around the time of delivery.
 Infants whose mothers demonstrate varicella in the
period from 5 days prior to delivery to 2 days
afterward are at high risk for severe varicella.
 The infant’s rash usually occurs toward the end of

the 1st wk to the early part of the 2nd wk of life

 Varicella (or chickenpox),
COMPLICATIONS
 The complications of VZV infection occur with varicella or with reactivation of infection, more commonly in

immunocompromised patients.
 Common but rarely clinically symptomatic.

 Mild thrombocytopenia
 Purpura, hemorrhagic vesicles
 hematuria,
 and gastrointestinal bleeding are rare complications that may have serious consequences
 Other complications of varicella,
 cerebellar ataxia,
 encephalitis,
 pneumonia, nephritis,
 nephrotic syndrome,
 hemolytic-uremic syndrome,
 arthritis,
 myocarditis,
 pericarditis, pancreatitis, orchitis, and acute retinal necrosis
 Varicella (or chickenpox),

DIAGNOSIS
 Varicella and herpes zoster have been diagnosed primarily by their clinical appearance.

 Laboratory evaluation has not been considered necessary for diagnosis or management

 laboratory diagnostic challenges.

 Leukopenia is typical during the 1st 72 hr after onset of rash;
 it isfollowed by a relative and absolute lymphocytosis
 Results of liver function tests are also usually (75%) mildly elevated.  
 Rapid laboratory diagnosis of VZV is often important in high-risk patients and can be important
for infection control
 VZV can be identifiedquickly by
 Direct fluorescence assay of cells from cutaneous lesions (vesicular fluid) in 15-20 min,
 By PCR amplification testing (vesicular fluid, crusts) in hours to days, and
 By rapid culture with specific immunofluorescence staining (shell vial technique) in 48-72 hr
 Serologic tests are not useful for the initial diagnosis of herpes zoster, but a large rise in IgG titer
in convalescent titer in the presence of an atypical zoster rash is confirmatory.
 clinical judgment to decide on the best course of therapy
 Varicella (or chickenpox),
TREATMENT
 Antiviral treatment modifies the course of both varicella and herpes zoster.

 Antiviral drug resistance is rare

 HIV infection and
 other immunocompromising conditions (where frequent relapse of VZV infections has resulted in multiple courses of antiviral therapy.)
 Foscarnet and cidofovir may be useful for the treatment of acyclovir-resistant VZV infections
Varicella
 The only antiviral drug available for pediatric use is
 Acyclovir.
 Oral therapy with acyclovir (
 20mg/kg/dose; maximum: 800 mg/dose) given as 4 doses/day for 5 days most effective, treatment
should be initiated as early as possible,
 preferably within 24 hr of the onset of the exanthem.
 Intravenous therapy
 for severe disease and
 for varicella in immunocompromised patients.
 Acyclovir-resistant VZV has been identified primarily in children infected with HIV.
 intravenous foscarnet (120 mg/kg/day divided every 8 hr for up to 3 wk
 Varicella (or chickenpox),
PROGNOSIS
 Primary varicella has a mortality rate of 2-3 per 100,000 cases,

 withthe lowest case fatality rates among children 1-9 yr of age (~1
death per 100,000 cases).
 Compared with these age groups, infants have a 4times greater risk

of dying and adults have a 25 times greater risk of

 dying.

 The most common complications

 pneumonia,
 central nervous system complications,
 secondary infections, and
 hemorrhagic conditions.
 Varicella (or chickenpox),
PREVENTION
 VZV transmission is difficult to prevent,

 because a person with varicella is contagious for 24-48 hr before the rash is apparent.
 Infection control practices
 isolation rooms with filtered air systems, of

Vaccine
 Varicella is a vaccine-preventable disease.

 live, attenuated VZV (Oka strain)

 subcutaneous administration.
 2 dose regimen tat ages 12-15 mo and 4-6 yr.
Postexposure Prophylaxis
 3 or 5 days after exposure (as soon as possible is preferred) is effective in preventing or modifying varicella.

 Varicella vaccine is now recommended for postexposure use

 and for outbreak control.

 Oral acyclovir administered late in the incubation period may modify subsequent varicella in the healthy

child;
 Erythema Infectiosum Or Fifth
Disease
 Fifth disease is a mild rash illness caused by parvovirus B19.
 It is more common in children than adults.
 There are now 4 different types of parvoviruses known to infect
humans:
 The dependoviruses also called adeno-associated viruses (AAVs),
 parvovirus B19 (B19),
 human bocaviruses (HBoV), and
 parvovirus 4

 B19 and HBoV (pathogenic in humans.)

 Erythema Infectiosum Or Fifth
Disease
EPIDEMIOLOGY
 Parvovirus B19

 Infections with B19 are common and occur worldwide.

 Clinically apparent infections, such as the rash illness

of erythema infectiosum and transient aplastic crisis,
are most prevalent in school-age children (70% of
cases occur in patients between 5 and 15 yr of age).
 Seasonal peaks occur in the late winter and spring,

with sporadic infections throughout the year.

 Erythema Infectiosum Or Fifth
Disease
PATHOGENESIS
 Parvovirus B19
The primary target of B19 infection is the erythroid cell line, specifically
erythroid precursors near the pronormoblast stage

Viral infection produces cell lysis,

leading to a progressive depletion of erythroid precursors and a transient arrest

of erythropoiesis.
 Erythema Infectiosum Or Fifth
Disease
 The virus Experimental infection of normal volunteers with B19
revealed abiphasic illness.
 From 7-11 days after inoculation, subjects had viremia and
nasopharyngeal viral shedding with fever, malaise, and
rhinorrhea.
 Reticulocyte counts dropped to undetectable
 Several subjects experienced a rash associated with arthralgia
17-18 days after inoculation.
 . Skin biopsy of patients with erythema infectiosum reveals
edema in the epidermis and a perivascular mononuclear
infiltrate compatible with an immune-mediated process
 Erythema Infectiosum Or Fifth
CLINICAL MANIFESTATIONS Disease
 The incubation period 4-28 days (average: 16-17 days).
 The prodromal phase
 mild and consists of low-grade fever in 15-30% of cases,
 headache, and
 symptoms of mild upper respiratory tract infection.
 The hallmark of erythema infectiosum is the characteristic rash, which occurs in 3 stages
 The initial stage is an erythematous facial flushing, a “slapped-cheek” appearance .
 The rash spreads rapidly or concurrently to the trunk and proximal extremities as a diffuse
macular erythema in the 2nd stage.
 Central clearing of macular lesions occurs promptly, giving the rash a lacy, reticulated
appearance (Fig. 251-2).
 The rash tends to be more prominent on extensor surfaces, sparing the palms and soles.
 The rash resolves spontaneously without desquamation,
Erythema Infectiosum Or Fifth
Disease
 Erythema Infectiosum Or Fifth
 CLINICAL MANIFESTATIONS Disease
 Arthropathy
Arthritisand arthralgia may occur in isolation or with other symptoms.
Joint symptoms ( Females > males)
Transient Aplastic Crisis

Immunocompromised Persons:
 Chronic anemia is the most common manifestation, sometimes accompanied by neutropenia, thrombocytopenia, or

 complete marrow suppression.

Fetal Infection
 Primary maternal infection is associated with nonimmune fetal hydrops and intrauterine fetal demise, with the risk

for fetal loss after infection estimated at <5%.

 Myocarditis

 B19 infection has been associated with myocarditis in fetuses, infants, children, and a few adults.

Other Cutaneous Manifestations

 A variety of atypical skin eruptions have been reported with B19 infection.

 . Among these rashes, the papularpurpuric

 “gloves-and-socks” syndrome (PPGSS) is well established in the dermatologic literature as distinctly associated with

B19 infection
 Erythema Infectiosum Or Fifth
Disease
 DIAGNOSIS
 clinical presentation of the typical rash and
 Rarely requires virologic confirmation.
 B19- specific IgM develops rapidly after infection and
persists for 6-8 wk.
 Anti-B19 IgG serves as a marker of past infection or
immunity
 Serologic diagnosis is unreliable in
immunocompromised persons
 Erythema Infectiosum Or Fifth
 TREATMENT
Disease
 no specific antiviral therapy
 Commercial lots of intravenous immunoglobulin (IVIG) have been used with some success
to treat B19-related episodes of anemia and bone marrow failure in immunocompromised
children.
 In patients whose immune status is not likely to improve
 B19-infected fetuses with anemia and hydrops have been managed successfully with
intrauterine RBC transfusions, but this procedure has significant attendant risks.
 
COMPLICATIONS
 Arthralgias or arthritis in adolescents and adults that may persist after resolution of the rash.

 Thrombocytopenic purpura –rare

 Neurologic conditions, including aseptic meningitis, encephalitis, and peripheral

neuropathy,
 Roseola infantum
 Roseola infantum is a common disease of childhood caused by a
primary infection with human herpesvirus 6 (HHV-6) and less
frequently, by human herpesvirus 7 (HHV-7).
 This disease, also known as exanthema subitum and sixth disease,
 Presents in children ages six to 12 months with 90% of cases occurring
in children younger than two years.
 Caused by the B variant of HHV-6,
 Patients with the virus classically present with an acute onset of a
high-grade fever up to 40 C (104 F) for three to five days.
 The child will experience a rapid defervescence of the fever with
accompanying nonpruritic, pink papular rash that begins on the trunk.
 Roseola infantum
ETIOLOGY
 HHV-6A, HHV-6B, and HHV-7 are the sole members of the

Roseolovirusm genus in the Betaherpes virinae subfamily of

human herpesviruses.
EPIDEMIOLOGY
 Primary infection with HHV-6B is acquired rapidly by

essentially all children following the loss of maternal

antibodies in the 1st few mo of infancy, 95% of children
being infected with HHV-6 by 2 yr of age.
 The peak age of primary HHV-6B infection is 6-9 mo of life.
 Roseola infantum
CLINICAL MANIFESTATIONS
 An acute, self-limited disease of infancy and early childhood.

 It is characterized by
 The abrupt onset of high fever, which may be accompanied by fussiness.
 The fever usually resolves acutely after 72 hr (“crisis”) but may
gradually fade over a day (“lysis”) coincident with the appearance of a
faint pink or rose-colored, nonpruritic, 2-3 mm morbilliform rash on the
trunk .
 The rash usually lasts 1-3 days butspreading from the trunk to the face
and extremities.
 Associated signs are few but can include mild injection of the pharynx,
palpebral conjunctivae, or tympanic membranes and enlarged
suboccipital nodes.
 Roseola infantum
 CLINICAL MANIFESTATIONS
 In Asian countries, ulcers at the uvulopalatoglossal junction
(Nagayama spots) are commonly reported in infants with roseola.
 High fever (mean: 39.7°C [103.5°F]) is the most consistent finding
associated with primary HHV-6B infection.
 Additional symptoms and signs include irritability, inflamed
tympanic membranes, rhinorrhea and congestion, gastrointestinal
complaints, and encephalopathy.
 The mean duration of illness caused by primary HHV-6B infection
is 6 days, with 15% of children having fever for 6 or more days
Roseola infantum
 Roseola infantum
LABORATORY FINDINGS
 The most characteristic laboratory findings noted
 lower mean numbers of total white blood cells (8,900/μL),
 lymphocytes (3,400/μL), and neutrophils (4,500/μL),
 Thrombocytopenia,
 Elevated serum transaminase values, and
 Atypical lymphocytes
 Results of CSF analyses reported in patients with encephalitis only minimal CSF pleocytosis with mild
elevations of protein

DIAGNOSIS.
 A history of 3 days of high fever in an otherwise nontoxic 10 mo old infant with a blanching maculopapular rash on the trunk

 Specific diagnosis of HHV-6 is not usually necessary .

 Primary infection with either HHV-6 or HHV-7 is confirmed by demonstrating the presence of actively replicating virus in the

patient’s blood sample coupled with seroconversion.

 Viral culture is the gold standard method to document active viral replication.

 Detection of viral DNA by PCR on acellular

 Serologic methods including indirect immunofluorescence assays, enzyme-linked immunosorbent assays, neutralization

assays, and immunoblot have been described for the measurement of concentrations of antibodies to HHV-6 and HHV-7 in
serum or plasma
 Roseola infantum
 TREATMENT
 Supportive care is usually all that is needed for infants with
roseola.
 Parents should be advised to maintain hydration and may use
antipyretics if the child is especially uncomfortable with the fever.
 Specific antiviral therapy is not recommended for routine cases
 Ganciclovir, foscarnet, and cidofovir all demonstrate inhibitory
activity against HHV-6 in vitro similar to their activity against
cytomegalovirus.
 Roseola infantum
COMPLICATIONS
 Convulsions are the most common complication of

roseola and are recognized in up to one third of patients.

 Seizures are also the most common complication of

children with primary HHV-6B infection, occurring in

approximately 15%, with a peak age of 12-15 mo.
 Partial seizures, prolonged seizures, postictal paralysis,

and repeated seizures than are children with febrile

seizures sequelae
 Roseola
PROGNOSIS
 Roseola is generally a self-limited illness associated with

complete recovery.
 seizures are a common complication of primary infection

with HHV-6B and HHV-7,

PREVENTION
 Primary infections with HHV-6 and HHV-7 are

widespread throughout the human population with no

current means of interrupting transmission.
Thank you =)