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Chapter 192

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.

Kikuchi histiocytic necrotizing


lymphadenitis
Kikuchi histiocytic necrotizing lymphadenitis, or
Kikuchi disease, is a worldwide, self-limited disease
that primarily affects women 2030 years old.125
Patients typically have unilateral lymph node
enlargement, most often in the posterior cervical chain, which may be accompanied by fevers,
chills, myalgias, malaise, diarrhea, nausea, vomiting,
hepatosplenomegaly, or generalized lymphadenopathy.125,126 Abnormal laboratory values may
include leukopenia and atypical lymphocytes.126
The etiology is not known, but it is thought that
Kikuchi disease occurs in response to an infectious
agent. EBV has been implicated as one causative
agent. Skin findings have been noted in up to 40%
of patients with Kikuchi disease. Cutaneous findings are nonspecific and may include erythematous
macules, papules, plaques, nodules, facial erythema
or ulcers of the gingivae.125,127,128 Diagnosis is by
biopsy of the affected lymph node, which typically
shows histiocytic aggregates, atypical lymphoid
cells, karyorrhectic debris, and patchy necrosis as
well as absence of neutrophils or a granulomatous
reaction.123 Pathology of the skin lesions is similar to
that of lymph nodes. The disease typically resolves
spontaneously after 16 months without treatment.126

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

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294 Chapter 192: Exanthematous Viral Diseases

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.

one Chinese study.296 Those with viremia were more


likely to experience extraintestinal involvement
after rotaviral infection (p <0.05), including skin
involvement.

Humans are the only known reservoir for HCMV,


and transmission occurs from person to person.
Close contact is required as the virion is labile to
heat and drying.142 Transmission can also occur via
saliva, fomites, sexual activity, blood transfusions,
organ transplantation, intrauterine perinatal exposure, and breast milk.142,145

The pathogenesis of skin manifestations associated with rotavirus is unknown, largely because there
have been few reports of associated skin findings
with varied morphologies.

The virus disseminates throughout the body in


leukocytes via the bloodstream. It can infect various organs depending on the age of the host.143 As
with other herpesviruses, HCMV establishes latency
in the host after recovery from acute primary
infection. HCMV remains latent in CD34+ myeloid
progenitor cells in bone marrow.146 Productive
infection can result in cell lysis, but organ dysfunction during symptomatic infection is a combination
of infected cell dysfunction and the inflammatory
response to the infection.147

Originally, electron microscopy was used to detect


viral particles in stool. However, this method however, is less sensitive compared with other available
techniques.304 Rotavirus can be cultivated from
stool samples in cell culture but this tends to be
difficult and laborious.305 ELISA and latex agglutination assay are currently the most common methods
used to identify rotavirus in stool samples305 and
are both sensitive and specific in detecting rotaviral
particles.307 Polyacrylamide gel electrophoresis to
detect rotavirus antigens in fecal samples207 and
PCR308 are other methods used to detect rotavirus
in the stool.

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

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