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Viral Exanthems
Elise Christine D. Tompong, M.D. , PAPSHPI
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+ Chikungunya
A viral infection with symptoms similar to
dengue fever with an cute febrile phase
lasting two to five days followed by prolonged
athralgic phase affecting joints of the
extremities.
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Contorted posture of patients afflicted with severe joint pain

and arthritic symptoms is the reason why this is called
chikungunya from the local Makonde dialect, “that which
bends up”
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Pathophysiology

 human epithelial and endothelial cells primarily fibroblasts

and monocyte-derived macrophages

 Viral entry occurs through pH dependent endocytosis.

Infection is cytopathic and associated with the induction of
apoptosis in infected cell

 Infection is highly sensitive to antiviral activity of type 1 and

type 11 interferon.
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Clinical Presentation:

 Incubation period is from 1-12 days, symptoms start 3-7 days

after mosquito bite

 FEVER up to 40’C

 Petechial or maculopapular rash of trunk and occasionally the

limbs

 ARTHRALGIA affecting multiple joints

 Headache, nausea and vomiting, conjunctivitis

 Slight photophobia and partial loss of taste

 Most symptoms last for a week but in some, joint pains persist
for months.
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Cause:

 Chikungunya virus ( CHIKV)

Indigenous to tropical Africa and Asia

Transmitted via bite of infected mosquitoes of the Aedes.

CHIK fever is sustained by human-mosquito-human

transmission. The main virus reservoirs are monkeys .
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Differential Diagnosis:

 Dengue fever

 Measles

 Hand – Foot and Mouth disease

 Chicken pox
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Diagnosis:

 Virus isolation - The most definitive diagnosis. Exposing cell

lines to sanples from whole blood and identifying virus
specific responses.

 RT – PCR – used to amplify several CHIK specific genes from

whole blood

 Serlogical tests – ELISA assay to measure CHIK specific IgM

levels. False positives can occur.
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Treatment:

 No specific treatment

 Supportive only, but Chloroquine is gaining ground as

possbile treatment for the symptoms and as anti-
inflammatory to combat arthritis. Given at 250mg/day.

 No vaccines are available although clinical trials are

underway
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Prognosis:

 Recovery varies with age

 Younger patients within 5 – 15 days

 Middle aged in 1- 2.5 mos

 Recovery longer for the elderly

 Severity and duration is less in younger pxs and pregnant

women
 Information for vector control programs

+ Background
Mosquito-borne viral disease characterized by acute onset of fever and severe joint pain
Outbreaks have occurred in countries in Africa, Asia, Europe, and the Indian and Pacific Oceans
In late 2013, first local transmission in the Americas was reported on islands in the Caribbean

Vectors
Aedes aegypti and Aedes albopictus are the primary vectors
Both mosquitoes can be identified by the white stripes on their black bodies and legs
They are aggressive daytime biters, with crepuscular peak feeding activity
These mosquito species are present in many regions of the United States (see distribution maps below), which creates the
potential for emergence of chikungunya virus.

Aedes aegypti Aedes albopictus

An important vector in urban areas.
Closely associated with humans and their homes.
Adult mosquitoes are commonly found indoors.
Larval habitats are typically containers on the
household premises.
Approximate distribution of Aedes aegypti in
the United States*
More likely to play a larger role in transmission in the
United States due to its wide distribution.
Biting adults are found both indoors and outdoors, but
are most commonly found outdoors.
Larvae occur in peridomestic habitats as well as
surrounding natural habitats.
Approximate distribution of Aedes albopictus in
the United States*
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Hand-Foot-and-Mouth
Disease
An acute viral illness with a vesicular eruption
in the mouth and can also involve the hands,
feet, buttocks, and genitalia.
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Pathophysiology:

 fecal-oral route (stool)

 contact with skin lesions (blister fluid)

 and oral secretions ( saliva,sputum, nasal mucus)

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Epidemiology:

 generally occur in the summer but may be

sporadic

 mild self limited illness that resolves in 7-10 days

 serious complications rare

 no sexual predilection

 affects children less than 10yrs of age commonly

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Clinical Presentation:
 Incubation period lasts 1 week
 Starts with a fever (38-39F) for 2 days,poor appetite,malaise and sore
throat
 2 days after fever macular lesions on buccal mucosa, tongue and or
hard palate, progresses to vesicles that erode and become
surrounded by an erythematous halo HERPANGINA
 Skin rash develops over 1-2 days on palms, soles and may also
appear on the knees,elbows,buttocks or genital area.

 TENDER MACULES OR VESICLES ON AN ERYTHEMATOUS BASE

 HFMD caused by coxsackievirus strains rarely presents with

concomitant aseptic meningitis
 HFMD caused by EV-71 has a higher incidence of neurologic involvement,
including a poliolike syndrome, aseptic meningitis, encephalitis,
encephalomyelitis, acute cerebellar ataxia, acute transverse myelitis, Guillain-
Barré syndrome, opsomyoclonus syndrome, and benign intracranial hypertension.
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Causes:

 most commonly by coxsackie virus A16 but is also caused

coxsackie viruses A5, A7, A9, A10 B2, B5 and EV-71
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Differential Diagnosis:

 Herpes zoster

 Herpes simplex

 Kawasaki dse

 Pharyngitis, Viral
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Workup:

 Diagnosis is based on clinical grounds

 Laboratory studies usually unnecessary

 Virus can be isolated, identified via culture and

immunoassay from cutaneous and mucosal lesions or stool
samples. Oral is the best sample followed by
cutaneous
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Treatment:

 Treatment is supportive
 No vaccine available for prevention
 Prevention includes washing hands often, cleaning and
disinfecting frequently touched surfaces, avoid close
contact
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Herpes Zoster
o Common ,dermal and neurologic disorder caused
varicella-zoster virus
o Morphologically and antigenically similar to varicella
virus diiference lies on immune status of the patient
o Zoster results most often from failure of immune system
to contain latent varicella zoster virus replication
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Epidemiology:

 rarely fatal

 morbidity confined to pain which cen be severe and persist beyond the
duration of active disease (POSTHERPETIC NEURALGIA)

 Temporary or permanent decreased visual acuity or blindness ZOSTER

OPHTHALMICUS

 Secondary bacterial infection may add to morbidity

 Common among immunocompromised ,the elderly and those receiving

immunosuppressive drugs

 Can children have shingles?

 Can one have a second or third episode?

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Clinical Presentation:

 Prodromal symptoms:
 prodromal pain along 1 or more skin dermatome for 1 – 10 days (
toothachelike or muscle in origin) fever, anorexia, lassitude

 Onset of rash:
 patchy erythema with induration in dermatomal area
 regional lymphadenopathy
 GROUPED HERPETIFORM VESICLES ON ERYTHEMATOUS BASE ( BAND
OF ROSES FROM HELL) appearing unilaterally, only at the midline of
sensory coverage of dermatome. Vesicles are clear and then cloud,
rupture, crust and involute.
 After involution, scabs form in 7-10 days and clears up within 2-4 weeks
 scarring can occur
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Causes:

 Reactivation of varicella virus that has been dormant with

dorsal root ganglia after the patient’s initial exposure to the
virus in the form of varicella.

 Can shingles be passed on to another person?

 Triggering factors :
 external reexposure to the virus, acute or chronic disease
processes (particularly malignancies and infections), medications
of various types, and emotional stress.
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Differential Diagnosis:

 Folliculitis

 Ecthyma

 Insect bites

 Chicken pox

 Aphthous stomatitis

 ACD/ICD
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Work Up:

 general and systemic workups not usually necessary unless with

underlying diseases or complications

 Tzanck preparation is inexpensive but does not distinguish VZV

from HSV

 Viral culture

 Direct flourescence antibody of VZV in a scraping of cells from

the base of the lesion. Rapid,specific, and sensitive. Less
sensitive than PCR

 Polymerase Chain Reaction can be used to detect VZV DNA from

collected skin lesion specimen

 Skin Biopsy fr scrapings of cells

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Histologic findings:

 Multinucleated giant cells with accentutation of nuclear

material at the periphery of nuclei are characteristic
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Treatment:

 Systemic Acyclovir and derivatives ( Valacyclovir, Famciclovir,

Pencicylovir) shorten length and severity of ilness
 Initiate therapy within 72 hrs of onset of symptoms:
Acyclovir (Zovirax) 800mg PO every 4hrs for 7-10 days for acute
treatment.
Valacyclovir (Valtrex) 1g every 8 hrs for 7 days
 Systemic steroids at 40-60mg every morning for 1 wk and taper
over 1-2wks to prevent PHN
 Varicella zoster vaccine (VZV) recommended for 60yo or older to
prevent shingles:
Zostavax 0.65 ml SC upper arm as prophylaxis for 50 yrs and
older and persons with chronic medical conditions
Mevac-vari, V-Z Vax, Varilrix
 VZIG for immunocompromised patients
 Management of PHN
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Herpes Simplex
o Acute skin infection, GROUPED VESICLES ON
ERYTHEMATOUS BASE
o Rarely cause serious illness but can affect pregnancy by
harming fetus
o Recurrent and reappear at or near the same location
o HSV type 1- Herpes labialis, most common
o HSV type 2 – Herpes genitalis
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Pathophysiology:

 intimate contact bet susceptible person and affected person

via mucous memebranes or open or abraded skin.

 HSV invades and replicates in neurons, epidermal and

dermal cells and become latent in dorsal root ganglion.
Recurrent outbreaks are induced bytauma, UVR, extremes in
temp, stress, immunosuppression or hormonal fluctuations.

 HSV 1 in trigeminal ganglia

 HSV 2 in lumbosacral ganglia

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Epidemiology:

 The risk of transmission of the virus to a neonate by a mother

who is infected is as high as 30-50% nearing the time of
delivery but before the third trimester it is less than 1%. It is
most commonly due to HSV 2
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Clinical Presentation:

 HSV 1 – Herpes labialis (cold sores, fever blisters)

 Occurs in childhood and is usually asymptomatic
 Primary Infection:
 prodrome fever, sorethroat, lymphadenopathy
 painful vesicles on the lips, gingiva, palate or tongue,
 assoc with eryhtema and edema
 lesions ulcerate and heal within 2-3 wks
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Recurrences:

 disease remains dormant then a reactivation in the trigeminal

sensory ganglia leads to recurrence pain, burning, itching
or paresthesia precedes recurrent vesicular lesions on
vermillion border that ulcerate or form a crust.

 lasts 1 week
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Clinical Presentation

 HSV 2- Genital herpes:

 Primary Infection:
 within 2 days – 2 wks after exposure and lasts 2-3 wks
 in men, painful, erythematous, vesicular lesions that ulcerate, commonly
on the penis, may occur on anus and perineum
 in women, vesicular/ ulcerated lesions on the cervix and painful on ext
genitalia bilaterally
 fever, malaise, edema, inguinal lymphadenopathy,dysuria
 vaginal or penile discharge
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Recurrences:

 virus may be latent for months to years

 recurrent outbreaks are milder and often preceded by

prodrome

 Individuals who are exposed to HSV and have asymptomatic

primary infections may experience an initial clinical episode
of genital herpes months to years after becoming infected.

 More than one half of individuals who are HSV-2 seropositive

do not experience clinically apparent outbreaks. However,
these individuals still have episodes of viral shedding and
can transmit the virus to their sexual partners.
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Other HSV Infections

 Kaposi varicelliform eruption – HSV 1

 Localized or disseminated eczema herpeticum
 Patients with AD, burns, inflammatory skin conditions
 Children commonly affected

 Herpes Whitlow – vesicular lesions on hands and digit HSV 1

 Children who suck thumbs increase in cases due to HSV 2
probably bec of digital-genital contact
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Other HSV infection (cont.)

 Herpes Gladiatorum
 HSV 1, on torsos of athletes involving close contact

 Neonatal HSV

 Disseminated HSV
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Differential Diagnosis:

 Chancroid

 Chickenpox

 HFMD

 Herpes zoster

 Erythema multiforme
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Workup:

 Polymerase Chain Reaction

 CSF (in newborns)

 stool, ruine, throat, nasopharynx, and conjunctivae

 Tzanck smear

 Direct Flourescent antibody

 ELISA, rapid HSV-2 POCKit test

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Histology:

 Ballooning and reticular epidermal degeneration

 intraepidermal vesicles

 intranuclear inclusion bodies

 steel grey nuclei

 multinucleate giant keratinocytes

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Treatment:

 Oral anitiviral ( Acyclovir,Valacyclovir, Famciclovir)-

 Topical antivirals – 5x daily for 4 days

 Intravenous antivirals for complicated HSV, neonatal HSV,

disseminated HSV

 IV Foscarnet and Cidofovir for recurrent HSV and

immunocompromised patients
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Rubella
German measles, 3 day measles
o Mild viral illness involving the skin, lymph nodes and
the joints.
o May cause a benign illness in pregnant females
causing Congenital Rubella Syndrome with chronic
fetal infection and malformation
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Epidemiology:

 Caused by an RNA virus

 affects young adults more than young children with the

advent of immunization

 transmission is via inhalation

 period of infectivity is from end of incubation to

disappearance of rash
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Clinical Presentation:

 Incubation period is from 14-21 days

 prodrome absent in children but present in adults and

adolescents (anorexia,malaise, conjunctivitis, headche, low
grade fever, mild URTI)

 pink macules and papules initially on forehead, to face,

trunk and extremities on the first day

 facial exanthem fades on the 2nd day

 exanthem fades completely without pigmentary change on

third day

 trunkal lesions become confluent,scarlatiniform eruption

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Clinical Presentation (cont.)

 Forchheimer spots –petechiae on soft palate during

prodrome

 Lymphadenopathy

 Spleen may be enlarged

 Arthritis in adults
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Differential Diagnosis:

 Drug eruptions

 Rubeola

 Kawasaki

 Scarlet fever
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Workup:

 diagnosis is made on clinical basis and lab work up is usually

not necessary
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Treatment:

 usually self-limited, no specific treatment

 immunization is highly effective for prevention

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Rubeola
Morbili, Measles
highly contagious, characterized by fever, coryza,
cough, conjunctivitis, Koplik’s spots, exanthem
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Epidemiology:

 spread via respiratory droplets

 infected patients contagious several days before onset of

rash to 5 days after rash appears
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Clinical Presentation:

 Incubation period 10-15 days

 prodromal symptoms

 discrete erythematous macules and papules becoming

confluent appearing on forehead at hairline then spreading
centrifugally then inferiorly reaching the feet on the third
day

 lesions fade in order of appearance with faint desquamation

resolves in 4-6 days

 KOPLIK’S SPOTS- cluster of tiny bluish white spots on

erythematous base appearing on 2nd day of fever on buccal
mucosa opposite premolar teeth
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Differential Diagnosis:

 other viral exanthems

 drug eruptions
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Workup:

 diagnosis based on clinical findings

 PCR, serology, culture

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Treatment

 self- limited

 supportive treatment

 immunization for prevention

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Varicella
Chickenpox
Highly contagious primary infection by varicella zoster virus
Successive crops of of pruritic vesicles ,becomes pustular,
crusts and sometime scars
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Epidemiology:

 90% of cases occur in children less than 10 yrs

 transmission via respiratory droplet,direct contact with

blisters or through contact with infected items

 Incubation period is 7 to 21 days after exposure

 Infectious a day or two before lesions appear and until last

crop of lesions or until the lesions are dry and scabbed over
(5 to 6 days after onset of rash) or crusted.
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Pathophysiology:

 acquired via respiratory droplets

 viral proliferation in lymph nodes of URT for 2-4 days

 primary viremia on days 4-6

 secondary viremia on days 14-16 in internal organs (liver and

spleen) char by diffuse viral invasion of capillaries and
epidermis, inetr and intracellular edema resultung in vesicles
thus Primary infection

 from mucosal and epidermal lesions, they spread to sensory

nerves

 becoming latent in the dorsal root ganlion of sensory nerve for

reacticavation thus Herpes zoster
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Clinical Presentation:

 prodrome is absent or mild in children more common in

adults

 exanthem appears after 2-3 days of prodrome,appears in

crops, characterized as papules or wheals evolving to
vesicles, superficial and thin walled with surrounding
erythema

 DROPS OF WATER OR DEWDROPS ON A ROSE PETAL

 vesicles become umbilicated, becomes pustules and crusts

in 8-12 hrs
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Clinical Presentation (cont.)

 Lesions begin on face and scalp spreading inferiorly

 Abundant in areas with least pressure

 Crusts fall off in 1-3 wks with a pink depressed base

 Maternal varicella during first trimester of pregnancy may

result in Fetal Varicella Syndrome ( limb hypoplasia, eye and
brain damage, skin lesions)

 In children, Reye’s syndrome and encephalitis and

bacteremia are common complications
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Differential diagnosis;

 Other viral exanthems, bullous diseases

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Workup:

 diagnosis based on clincal findings

 Tzanck smear

 DFA

 Culture

 serology
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Treatment:

 Acyclovir 20mg/kg QID for 5days, should be administered

within 24 hrs

 Immunization- may be sued to prevent or attenuate illness if

given to susceptible contacts within 5 days(preferrably
72hrs) of first exposure

 VZIG 625 units IM within 10 days (ideally 4 days) then

considr a second 3 wks after initial administration

 calamine lotion, tepid bathing or cool compresses

 oral anithistamines

 topical anitbiotics for superinfections

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