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Exanthematous Viral
Diseases
Leah T. Belazarian, Mayra E. Lorenzo,
Andrea L. Pearson, Susan M. Sweeney, &
Karen Wiss
EPSTEINBARR VIRUS
Oral hairy leukoplakia
Oral hairy leukoplakia is a manifestation of EBV
infection seen primarily in the HIV population.108 It
has also been noted in patients who are immunosuppressed for other reasons and rarely, in patients
who are not HIV-infected or immunosuppressed.
Unique to oral hairy leukoplakia is that the EBV replicates within the infected cells and expresses lytic
viral proteins.109,110 White or gray, verrucous plaques
with a corrugated appearance are observed on the
lateral sides of the tongue, either unilaterally or
bilaterally.83,109 Lesions cannot be scraped from the
tongue. Less commonly, there is involvement of
the dorsal or ventral tongue, buccal mucosa, or soft
palate.108 Most cases are asymptomatic, although
occasionally soreness or a burning sensation is
reported.109 Oral hairy leukoplakia is not a premalignant condition. It is, however, associated with
poorer prognosis in HIV disease.
Histologically, lesions demonstrate parakeratosis,
acanthosis, and little to no submucosal inflammation.111 There is association with candidiasis in
approximately 70% of cases. Intranuclear inclusions
may be seen in the stratum spinosum, and the
cytoplasm may show a ballooned or ground glass
appearance.
Clinical and histopathologic findings are suggestive of the diagnosis; however, the presence of EBV
must be demonstrated for definitive diagnosis.109
Accurate diagnosis is particularly important, as
oral hairy leukoplakia may be a clinical indicator
of immunosuppression, namely HIV disease. The
biopsy specimen may be used to identify EBV DNA
by in situ hybridization.109,112 Because a biopsy may
be contraindicated in certain patients (i.e., children
or those with a bleeding disorder), noninvasive
techniques for identification of EBV DNA have been
studied. Epithelial cells may be swabbed and evaluated via in situ hybridization with high sensitivity.112
Polymerase chain reaction (PCR) analysis of exfoliative cytology samples has been used but has a low
specificity.113
Differential diagnosis of oral hairy leukoplakia
includes entities such as candidiasis, lichen planus,
white sponge nevus, oral graft-versus-host disease,
and keratoses due to smoking or friction.109
Antiviral agents, topical vitamin A, topical podophyllin, antifungal therapy, cryotherapy, and
surgical excision have all been used as treatment
regimens; however, therapy in general is not indicated.109 In addition, lesions frequently recur after
therapy is discontinued.
HUMAN CYTOMEGALOVIRUS
Etiology and Pathogeneisis
HCMV, which corresponds to HHV-5, is a member
of the Herpesviridae family, and the prototype of
the -Herpesviridae subfamily. The 230-kbp virion
is composed of a double-stranded DNA linear
genome encapsulated in an icosahedral capsid
enclosed in a lipid bilayer membrane, which contains multiple membrane glycoproteins.142 HCMV
is distinguished by its salivary gland tropism, slow
growth, and species specificity.
The pathogenesis of skin manifestations associated with rotavirus is unknown, largely because there
have been few reports of associated skin findings
with varied morphologies.
Infection of cells results in cytomegaly and intracellular inclusions, hence the name cytomegalovirus. These protozoan cells were noted by Ribbert
in 1881 in organs of a stillborn. The disease later
became known as cytomegalic inclusion disease. In
1960, the term cytomegalovirus was proposed to
replace salivary gland virus and salivary inclusion
disease virus.148
ROTAVIRUS
Etiology and Pathogenesis
Rotaviruses belong to the family Reoviridae and the
genus Rotavirus.294 The virion structure resembles
a wheel, with short spokes radiating from a central
rim when examined with electron microscopy. The
rotavirus is named for this characteristic appearance (rota is derived from the Latin for wheel). The
virus measures 75 nm in diameter and is nonenveloped. A triple-layered, icosahedral capsid surrounds
a genome comprised of 11 segments of doublestranded RNA. Each of the RNA segments basically
encodes a single rotaviral protein.
Special Tests
Differential Diagnosis
The diagnosis of rotaviral infection is usually made
on clinical grounds in conjunction with identification of rotavirus as the etiologic agent. In general,
rotaviral infection is clinically indistinguishable
from other enteric viruses; however, diarrhea associated with rotavirus may be more severe and more
frequently involve vomiting and fever.289 Diagnoses
that may be considered include enterovirus, ES,
adenovirus, and rubella.
The pathogenesis of skin manifestations associated with rotavirus is unknown, largely because
there have been few reports of associated skin
findings with varied morphologies. Viremia may be
associated with rotaviral diarrhea at times295 and
was noted in up to 19.3% according to the results of