VIRAL DISEASES part II - A.T. Still University
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Transcript VIRAL DISEASES part II - A.T. Still University
VIRAL DISEASES
part II
Andrews’
p501-525
Molluscum contagiosum
Poxvirus
MCV-1 to -4 and variants
MCV-2 in HIV
Worldwide
Children, sexually active adults and
immunosuppressed
Direct contact
Lesions are smooth surfaced, firm and dome
shaped pearly papules
A central umbilication is characteristic
Clinical pattern depends on the group
affected
When restricted to only the genital area in a
child the possibility of sexual abuse must be
considered
Secondary infections may occur
Seen in 10-30 % of AIDS pts
Helper T-cell count of less than 100
Giant lesion may be confused with BCC
Henderson-Patterson bodies – basophilic
inclusion bodies
treatment
Topical tretinoin or imiquimod
Extraction
Light cryotherapy
Cantharadin
Curettage
podophyllotoxin
Human monkeypox
Rare
More than 90% of cases occur in children
under 15
Fatality rate of 11%
Disease is clinically similar to smallpox
Fever followed by vesiculopustular eruption
Develop following contact with wildlife
sources
Human to human transmission may occur
Picornavirus group
RNA
Only coxsackieviruses, the echoviruses, and
enterovirus type 71 are significant causes of
skin disease
Enterovirus infections
Person to person transmission occurs by the
intestinal-oral route and less commonly the
oral route
Usually the diagnosis is by clinical
characteristics
herpangina
Disease of children worldwide
Coxsackievirus and echovirus
Acute onset of fever, ha, sore throat,
dysphagia, anorexia, and sometimes a stiff
neck
Yellowish white, vesicles in the throat,
surrounded by an intense areola
Most frequently on the anterior faucial
pillars, tonsils, uvula, or soft palate
Lesions coalesce and ulcerate leaving a
shallow crater
Lesions disappear in 5-10 days
Treatment is supportive
Topical anesthetics or allopurinol mouthwash
Hand-Foot-and-Mouth Disease
Infection begins with a fever and sore mouth
90% have oral involvement
Lesions are small rapidly ulcerating vesicles
surrounded by a red areola
Buccal mucosa, tongue, soft palate, and
gingiva
Lesions on hands and feet
Red papules that quickly turn to gray vesicles
With a red halo
Typically lasts less than a week
Treatment is again supportive
Topical anesthetics
Coxsackievirus A-16
Distribution and presence of skin lesions
differentiates this from herpangina
Boston Exanthem Disease
Occurred as an epidemic in Boston
Caused by echovirus 16
Consisted of sparsely scattered pale red
macules and papules
Chiefly on the face chest and back
Now an uncommon cause of viral
exanthems
Eruptive pseudoangiomatosis
Young children during or immediately
following a viral illness develop red papules
that resemble angiomas
Face trunk and extremities
Resolve spontaneously within 10 days
Echoviruses 25 and 32 have been
implicated
PARAMYXOVIRUS GROUP
RNA viruses
Measles
Rubella
Measles
(rubeola, morbilli)
Worldwide disease
Commonly affects children under age of 15
months
Respiratory spread with an incubation of 912 days
Immunizations are highly effective
Prodrome- fever, malaise, conjunctivitis and
prominent upper respiratory symptoms
A macular or maculopapular eruption
appears after 1-7 days
Anterior scalp line and behind the ears
Quickly spreads over the face and involves
the entire body by day 3
Purpura may be present
Koplik’s spots are pathognomonic, appear
during the prodrome
Erythematous lesions
of the measles
exanthem
Pink macules with minimally elevated papules
with confluence
Koplik’s Spots
cluster of tiny bluish white papules with an
erythematous areola on buccal mucosa
opposite premolar teeth
complications
OM
Pneumonia
Encephalitis
Thrombocytopenic purpura
Infection in pregnant patients is associated
with fetal death
DX
Clinical- high fever, Koplik’s spots,
conjunctivitis, upper respiratory symptoms, rash
course and prognosis
maximum intensity of rash reached in 3 days
rash fades 5-10 days
self limited
death 1 in 3000
chronic complication, subacute sclerosing
panencephalitis
RUBEOLA
management
Acute
Vitamin A
decreases morbidity and mortality
given to severe measles even if no nutritional
deficit is suspected
vaccine
MMR given at 12-15 months, and 4-6 years
measles
Rubella
German measles, 3-day measles
benign contagious viral disease
etiology
transmission
Togavirus
inhalation of aerosolized respiratory droplets
incubation
12-23 days
Vaccination gives lifelong immunity
RUBELLA
clinical manifestations
Prodrome- 1-5 days
mild symptoms of malaise, headache, sore
throat, eye pain, and moderate temperature
elevation
Pain on lateral and upward eye movement is
characteristic
precedes eruption by a few hours to a day
children are usually asymptomatic
RUBELLA
clinical manifestations
Eruptive phase
begins on neck or face
spreads to trunk and extremities in hours
lesions are pinpoint to 1 cm, round or oval,
pinkish or rosy red, macules or maculopapules
(purplish lesions of measles and fine punctate
yellow-red lesions of scarlet fever)
discrete, grouped or coalesced
arthritis of phalangeal joints may be seen in
women
RUBELLA
Diagnosis
course and prognosis
Clinical, posterior cervical, suboccipital, and
postauricular lymphadenitis occurs in more than half
can be confirmed with serology
typically mild, requiring only symptomatic treatment
lesions last 24 -48 hours, followed by desquamation
prevention
MMR given at 12-15 months, and 4-6 years
rubella
RUBELLA
Forchheimer Spots
red palatal lesions start
with onset of rash
Congenital Rubella Syndrome
Infants born to mothers who have had rubella
during the first trimester of pregnancy
transplacental transmission as high as 80% in the
first trimester
Typical anomalies include IUGR, deafness, mental
retardation, cataracts, retinopathy, cardiac defects,
and “blueberry muffin” rash.
Prior to pregnancy antibody titer should be
verified. Immunization is contraindicated in
pregnancy.
Asymmetric Periflexural
Exanthem of Childhood (APEC)
AKA unilateral laterothoracic exanthem
Children 8 mo to 10 yrs
Cause is unknown
Viral origin has been proposed
Symptoms of mild upper respiratory or
gastrointestinal infection usually precede
the eruption
Erythematous macules
and papules involving
the axilla, lateral trunk
and flank.
In this patient the
exanthem progressed
to bilateral distribution
but maintained leftsided predominance
Erythematous papules coalesce to form
poorly marginated morbilliform plaques
Mild pruritis
Lesions begin unilaterally, close to a
flexural area, usually the axilla
Centrifugal spread to adjacent trunk and
extremity
The contralateral side is involved in 70% of
cases, asymmetrical nature is maintained
Lymphadenopathy is seen in 70%
Last 2-6 weeks on average
Resolves spontaneously
Topical steroids or oral antibiotic are of no
benefit
Oral antihistamines
PARVOVIRUS GROUP
Erythema Infectiosum
(Fifth Disease)
Worldwide benign infectious exanthem
Parvovirus B19
Spread by respiratory droplets
Viral shedding has stopped by the time the
exanthem has appeared
Incubation 4-14 days
prodrome
pruritus, low-grade fever, sore throat, malaise
seen in 10% of cases
Three distinct overlapping stages
facial erythema. Red papules on the
cheeks that rapidly coalesce. Resembles
erysipelas. “slapped cheek.”
net pattern erythema. Fishnet like pattern,
begins on extremities then extends to trunk
recurrent phase. Eruption may reappear
following emotional upset or sunlight
exposure over next 2-3 weeks.
Lacy, reticulated skin
eruption over the arm
during the second
stage of the exanthem
Papular Purpuric Stocking and
Glove Syndrome
Occurs in teenagers and young adults
Pruritis, edema, and erythema of the hands
and feet, and a fever is present
Lesions are sharply cut off at the wrists and
ankles
Mild erythema of the cheeks, elbows, knees
and groin
Syndrome resolves within 2 weeks
Erythematous patches with petechiae on
the palms
Serovonversion for parvovirus B19 has been
found
Complications are uncommon and age
dependent
Arthritis and arthralgias occur in 60% of
adult women
Aplastic crises may result in the sickle cell pt
In primarily infected pregnant women, fetal
death can result from hydrops fetalis as a
result of intrauterine anemia, esp. first 20
weeks
ARBOVIRUS GROUP
Comprise the numerous arthropod-borne
RNA viruses
West Nile Fever
A maculopapular eruption accompanied by
lymphadenopathy and fever characterize
this disease
The Culex mosquito is the vector
Disease seen in the Middle East
Sandfly Fever
AKA phlebotomus fever and pappataci fever
Small pruritic papules appear after the bite of a
sandfly
Fever, ha, malaise, nausea, conjunctival
injection, stiff neck, and abdominal pains
suddenly develop
Recovery is slow, with recurring bouts of fever
No specific treatment is available
Dengue
(break-bone fever)
A common disease of tropical regions
throughout the world
Spread by Aedes aegypti mosquito
Disease begins with a sudden high fever, ha,
back ache, retroorbital pain, bone and joint
pain, weakness, depression and malaise
A scarlatiniform or morbilliform exanthem,
especially on the thorax and joint flexors
may be seen
Patient may recover fully at this stage
In 1-7% of cases dengue hemorrhagic fever
develops, bleeding, thrombocytopenia, and
hemoconcentration develop
Mortality 1-15%
Alphavirus
Sindbis virus infection
Seen in Finland
Transmitted by the mosquito
Multiple erythematous papules with a
surrounding halo associated with a fever
and prominent arthralgias
Symptoms resolve over a few weeks
PAPOVAVIRUS GROUP
DS, DNA viruses
Slow growing
Replicate within the nucleus
Verruca
Human papillomaviruses include more than
80 types
Most types cause specific types of warts and
favor certain anatomic locations
Infections are described as clinical,
subclinical and latent
Verruca vulgaris
Commonly HPV 2
5% prevalence in children
Frequent emersion of hands in water is a
risk factor
Natural history is for spontaneous
resolution, half by 1 year and two thirds by
2 years
Usually located on the hands
Present as elevated, rough, grayish papules
Verruca vulgaris.
Note the characteristic
features of ‘church spire’ papillomatosis heaped with orthoand parakeratosis, acanthosis and koilocytosis.
Diagnostic clue- warts do not have
dermatoglyphics
Occur anywhere on skin
Spread by autoinnoculation
Digitate or filiform warts on the face and
scalp
Verruca plana
HPV 3
Children and young adults
Flat-topped papules that are slightly
erythematous or brown
Generally multiple and grouped
Face, neck, dorsa of hands, wrists and knees
Men who shave and women who shave their
legs
Koebnerization
Highest rate of spontaneous remission
Verruca plantaris
HPV type 1
Appear at pressure points on the ball of the
foot
Frequently several lesions are seen
Mosaic wart
May be confused with callous, no black dots
Myrmecia type- occurs as smooth surfaced,
deep, often inflamed and tender papules or
plaques- may be confused with mucinous cyst
Myrmecial wart
Verrucae plantares
Photo after the
shaving of the
hyperkeratotic
surface
HPV-60
Ridged wart
Persistence of dermatoglyphics
This type also causes plantar verrucous
cysts
treatment
Depends on the type of wart and the age of
the patient
Allow 2-3 months of therapy
Do not abandon any treatment too quickly
TX-flat warts
Frequently undergo spontaneous remission
Cryotherapy
Topical salicylic acid preparations
topical tretinoin
5-FU
anthralin
TX-common warts
Two basic approaches
Destruction and Induction of local immune
reactions
Cryotherapy, salicylic acid preparations,
canthrone, bleomycin, surgical ablation,
laser, high dose cimetidine, heat treatment,
isotretinoin, hypnotic suggestion, DNCB
TX-plantar warts
Salicylic acid preparations
Cryotherapy
Cantharadin
Bleomycin, laser, and DNCB
Genital warts
The most common sexually transmitted
disease
Lifetime risk in sexually active young
adults may be as high as 80%
A large portion of genital HPV is either
subclinical or latent
Infection is closely linked with cancer of the
cervix, glans penis, anus, vulvovaginal area,
and periungal skin
Transition zones of cervix and anus
Numerous HPV types are associated with
genital warts
Those producing benign lesions- low risk
Those associated with cancer- high risk or
oncogenic type
Most common are HPV-6 and HPV-11
most common HPV-16 and HPV-18
Virtually all condylomata are caused by
types –6 and –11
Condylomata acuminata
Appear as lobulated papules that are
frequently multifocal
Intraurethral condylomata may present with
terminal hematuria, altered urinary stream,
or urethral bleeding
Numerous genital warts may appear during
pregnancy
Other sexually transmitted disease may be
present
Bowenoid papulosis and HPVinduced genital dysplasias
Characterized by flat, often hyperpigmented
papules
Singly or in multiples
HPV-16may behave similar to other genital
warts
May progress to invasive SCC
Bowenoid papulosis
of the anus positive
for high-risk HPV
in a homosexual
male
Erythroplasia of Queyrat.
A well demarcated
velvety plaque of the prepuce positive for high-risk
HPV
Giant condyloma acuminatum
(Buschke-Löwenstein tumor)
A rare, aggressive wart-like growth that is a
verrucous carcinoma
HPV-6
Most often occurs on the glans penis or
prepuce of an uncircumcised male
May invade deeply, and uncommonly
metastases
Complete surgical excision
Buschke-
Löwenstein
Tumor
Cauliflower-like
deeply infiltrating
giant condyloma
acuminata
Diagnosis of genital warts
Inspection
Acetowhitening may help in the
differentiation of certain genital papules
Bowenoid papulosis may require Bx
Treatment of genital warts
Recurrence is frequent
Not proven to reduce transmission to sexual
partners nor to prevent progression to
dysplasia or cancer
Subclinical of the external genitalia should
not be sought or treated
Bleeding genital warts may increase the
sexual transmission of HIV and hepatitis B
and C
Treatment of genital warts
Podophyllin 4-8 hrs, weekly application
Purified podophyllotoxin 0.5% sln
Aldara, 3 alternate days per week
TCA (safe in pregnancy)
Cryotherapy (also safe in pregnancy)
Electrofulgeration or electrocauterization
CO2 laser
Any surgical method that generates a smoke
plume is potentially infectious to the
surgeon
5-FU 5% cream, esp. bowenoid papulosis
Systemic and intralesional interferon alfa
CDC no longer recommends
Genital warts in children
Children can acquire genital warts through
vertical transmission perinatally, digital
inoculation or autoinoculation, fomite or
social nonsexual contact, or through sexual
abuse
HPV typing has demonstrated that most
warts in the genital area of children are
“genital” HPV type
And most children with them have family
members with them as well
Finding of a nongenital type does not exclude
abuse
The risk for sexual abuse is highest for
children older than 3 yrs of age
Case-by-case management
Should screen for other STDs
Podophyllotoxin, imiquimod, light
cryotherapy
Recurrent respiratory (laryngeal)
papillomatosis
HPV associated papillomas may occur
throughout the respiratory tract, from the
nose to the lungs
Bimodal distribution- children under 5 and
after 15
Affected young children were born to
mothers with genital condylomata and
present with hoarseness
HPV-6 HPV-11
Carcinoma that is often fatal develops in 14%
Heck’s disease
Linked to HPV-13
AKA focal epithelia hyperplasia
Small white to pinkish papules occur
diffusely in the oral cavity
Epidermodysplasia verruciformis
A rare inherited disorder characterized by
widespread HPV infection and cutaneous
SCCs
Most commonly inherited as and AR trait
HPV-3, HPV-10 and many other “unique”
types
Pathogenesis is unknown
Presents in childhood and continues
throughout life
Skin lesions include flat, wartlike lesions of
the dorsal hands, extremities, and face
SCCs develop in 30-60% of pts, most often
on sun exposed areas,-5,-8,-47
Actinic background
Surgery, radiation is contraindicated
Strict sun avoidance
Warts in immunosuppressed
patients
Predisposing conditions include organ
transplantation, immunosuppressive
medication, congenital immunodeficiency
diseases, lymphoma and HIV infection
By 5 yrs posttransplant 90% of pts have warts
Regular dermatologic examinations
Standard methods of treatment, efficacy is
reduced
RETROVIRUSES
Contain RNA which is converted by a
virally coded reverse transcriptase to DNA
in the host cell
The target cell population is primarily
CD4+ lymphocytes
Transmission by sexual intercourse, blood
products/intravenous drug use, and from
mother to child during childbirth or
breastfeeding
HTLV-1
Endemic in Japan, subSaharan Africa and
southeastern US
Responsible for several clinical syndromes
1% will develop adult T-cell leukemialymphoma
Four forms: smoldering, chronic, acute, and
lymphomatous, usually progressing in that
order
Skin lesions in ATLL include erythematous
papules or nodules
Infected patients may develop various forms
of dermatitis mimicking other skin diseases
Infective dermatitis, children present with a
chronic eczema of the scalp, axilla, groin,
external auditory canal, retroauricular area,
eyelid margins, paranasal areas and neck
Chronic nasal discharge
Cultures positive for S. aureus
Human Immunodeficiency Virus
(HIV, HTLV III)
Cutaneous manifestations are prominent
Affecting up to 90% of HIV-infected persons
Many have multiple skin lesions of different
types
Skin lesions can be classified into three broad
categories: infections, inflammatory
dermatoses, and neoplasms
Skin lesions tend to appear at a specific stage
of disease, making them useful markers
Seborrheic dermatitis , pruritis ani,
psoriasis, Reiter’s syndrome, atopic
dermatitis, herpes zoster, acne rosacea, oral
hairy leukoplakia, onychomycosis, warts,
recurrent S. aureus folliculitis and
mucocutaneous candidiasis- helper T-cell
counts 200-500
With counts < 200, pt defined as AIDS
Opportunistic infections: chronic herpes
simplex, MC, bacillary angiomatosis,
systemic fungal infections and
mycobacterial infections
Hyperreactive skin is also seen: eosinophilic
folliculitis, GA, drug reactions,
photodermatitis
Eosinophilic
folliculitis (right)
Bacillary angiomatosis
(below)
T-cell count < 50 = advanced AIDS
Unusual presentations of opportunistic
infection
Treatment is difficult
Combination cocktails, (HAART), highly
active antiretroviral therapy
About half of HIV patients respond
Opportunistic infections no longer occur and
mortality decreases
Eosinophilic folliculitis and drug eruptions
may become more frequent and severe
Primary HIV infection
(Acute seroconversion syndrome)
An acute illness develops several weeks
after infection
Clinical syndrome resembles Ebstein-Barr
infection
Fever, sore throat, cervical adenopathy,
rash, and oral and genital and rectal
ulceration
Dysphagia may be prominent
Oral candidiasis or Pneumocystis carinii may
develop
Suspect DX in at risk individuals
Direct measurement if HIV load will confirm
Prompt combination antiviral therapy
HIV-Associated pruritis
Not caused by HIV disease itself but related to
its associated inflammatory dermatoses
“papular pruritic eruption”- a wastebasket
diagnosis
Follicular eruptions are more common
Eosinophilic folliculitis is the most common
pruritic follicular eruption, helper T-cell <200
Urticarial follicular papules on the upper
trunk, face, scalp, and neck
90% of lesions occur above the nipple line
Disease wanes and wanes and may
spontaneously clear, only to flare
unpredictably
Peripheral eosinophilia may be present
Topical steroids and antihistamines
Phototherapy or itraconazole
isotretinoin
HIV-Associated Neoplasia
Kaposi’s sarcoma
Superficial BCC
SCC
Genital HPV-induced SCC
Extranodal B-cell and T-cell lymphoma
BCC’s behave in the same manner, receive
standard management
SCC’s, standard management, excision is
recommended
SCC in sun-exposed skin can be very
aggressive
Genital SCC, associated with “high-risk”
HPV types (-16, -18)
Extranodal B-cell and T-cell
lymphoma
Associated with advanced
immunosuppression of AIDS
Present as violaceous or plum-colored
papules, nodules or tumors
MF can also be seen in patients with HIV
infection
Melanoma
Occasionally seen in HIV patients
Prognosis is unknown
It has been suggested that the risk of
metastasis is increased
AIDS and Kaposi’s Sarcoma
HHV-8
Patients with AIDS present with
symmetrical widespread lesions, that are
often numerous
Any mucocutaneous surface may be
involved
Favors hard palate, trunk, penis, lower legs
and soles
DX by biopsy
Red-violet papules on the palate
in addition to oral candidiasis
Treatment depends on the extent and
aggressiveness of the disease
Effective HAART after about 6 months is
associated with involution of KS lesions
Initial treatment for fewer than 50 lesions
Intralesional vinblastine
Cryotherapy
Irradiation therapy
Systemic therapy in aggressive disease
Interferon alfa
Vinca alkaloids
Bleomycin
Liposomal doxyrubicin