Viral diseases of the skin (Other)

Viral diseases of the skin
Cont.

Major Types of viruses thatMajor Types of viruses that
affect the skin:affect the skin:
 HUMAN PAPILLOMAVIRUSESHUMAN PAPILLOMAVIRUSES
 HUMAN HERPESVIRUSESHUMAN HERPESVIRUSES
 OTHER VIRAL DISEASESOTHER VIRAL DISEASES

Major Types of viruses thatMajor Types of viruses that
affect the skin:affect the skin:
 HUMAN PAPILLOMAVIRUSESHUMAN PAPILLOMAVIRUSES
 HUMAN HERPESVIRUSESHUMAN HERPESVIRUSES
 OTHER VIRAL DISEASESOTHER VIRAL DISEASES
1. Poxviruses
infections
2. Paramyxovirus:
Measles
3. Togaviridae:
German Measles
4. Parvovirus B19:
Erythema
Infectiosum
5. HFMD
6. Gianotti-Crosti
syndrome
7. Kawasaki
syndrome

Diseases caused by
poxviruses include:
1. Smallpox
2. Cowpox
3. Monkeypox
4. Tanapox
5. Vaccinia
6. Orf
7. Milker’s nodules
8. Molluscum contagiosum

Molluscum Contagiosum
Overview
 Self-limited epidermal viral infection
characterized by cytoplasmic replication.
 ETIOLOGY: dsDNA poxvirus. With the
eradication of smallpox, MC became the
most common & only remaining poxvirus
infection to specifically afflict humans.
 TYPES: MCV-1(90%) and MCV-2. result
in indistinguishable skin lesions.
 AGE:
1. Children;
2. Sexually active adults
 SEX: males > females.

Overview
 IP: 2wk-6m
 TRANSMISSION:
1. Direct skin-to-skin contact. spreads via
autoinoculation, scratching, or touching a lesion.
2. Indirect contact; fomites (less commonly)
3. Sexual contact with an affected partner

Overview
Classification by Risk Groups:
 Children; exposed skin sites. Child-to-child transmission
relatively low. Resolve spontaneously. Usually caused
by MCV-1.
 Sexually Active Adults; Occur in genital region. Virus
transmitted during sexual activity. Can Resolve
spontaneously.
 HIV-Infected Individuals; Most commonly occur on the
face, spread by shaving. Spontaneous regression
usually does not occur. Usually caused by MCV-2

C/P
 Most lesions are self-limiting and clear
spontaneously ranging from several months
to several years but usually within 6 to 9
months.
 Discrete firm, single or multiple skin-skin-
coloredcolored-white-white pearly papules.
 SITES: in children; most commonly on the
face, trunk, axillae, extremities, in adults in
the pubic and genital areas (STD).
 SURFACE: Smooth waxy surface with
umbilicated center.
 ON EXPRESSION  cheesy whitecheesy white
material.
 Unlike warts, the palms and soles are not
involved
 The disease is rare under the age of 1y.

C/P
Genital molluscum contagiosum may be a
manifestation of sexual abuse in children.

Inflammation of MC lesions can occur and
signals the development of a host immune
response
C/P

Inflamed molluscum (17%)
C/P
Furuncle-like presentation

Associated molluscum dermatitis is common especially in children with
atopic dermatitis.
C/P

C/P
 Increasing frequency in
immunocompromised
hosts, most notably HIV-
infected individuals.
 In HIV-infected individuals,
however, numerous large
mollusca often arise on the
face, causing significant
cosmetic disfigurement.
 Spontaneous regression
usually does not occur.

C/P - Dermatoscopy
The most salient feature is presence of polylobular
amorphous white to yellowish globules (which represent the
molluscum bodies)

1. Appendageal tumors (particularly syringoma)
2. Verrucae (particularly V.P, condylomata acuminata)
3. Basal cell carcinoma,
4. Juvenile xanthogranuloma,
5. Melanocytic nevi (especially Spitz nevi),
6. Papular granuloma annulare
7. Pyogenic granuloma.
8. Fordyce Spots
 In immunocompromised hosts, infectious processes such as
cryptococcosis or histoplasmosis.
 Inflammatory reactions to molluscum may resemble
staphylococcal furunculosis, Gianotti–Crosti syndrome.
DDx

 Molluscum contagiosum virus cannot be grown in tissue culture
I. Squash preparation: is microscopic
examination of cellular exudate. The cellular
material contained within the central
umbilication may be extracted manually,
flattened between 2 microscope slides, and
stained  the Henderson-Paterson bodies.
II.PCR
III.Electron microscopy: of the papule contents
IV.Histopathology
Dx

Histopathology

Histopathology
nucle
i

Histopathology
Molluscum contagiosum showing the epidermal invagination and
numerous eosinophilic viral inclusion bodies resembling a septate
tomato on scanner view

 AIMS OF THERAPY ARE:AIMS OF THERAPY ARE:
1) To remove the MC;
2) Not to produce scarring;
3) To induce lifelong immunity to prevent recurrence.
 Consider benign neglect:
- Eventual spontaneous involution in immunocompetent
patients.
- Risks of spread (especially in atopic patients), associated
dermatitis and pruritus.
 PREVENTIONPREVENTION: avoid direct, indirect or sexual contact (Genital
lesions in adults should be definitively treated) with known
patient.
 Treatment must be individualized.
Management

Management of MC
 MEDICAL TREATMENT “4”MEDICAL TREATMENT “4”
I. Topical agents
II. Systemic agents
III. Intralesional injections
IV. Alternative treatments

Management of MC
 SURGICAL (PHYSICAL) TREATMENT “5”SURGICAL (PHYSICAL) TREATMENT “5”
I. Cryotherapy
II. Manual extraction
III. Curettage
IV.Lasers.
V. Electrosurgery/
Electrodessiction

Management of MC
 MEDICAL TREATMENTMEDICAL TREATMENT
I. Topical agents
II. Systemic agents
1. Keratolytics (e.g. SSalicylic
and lactic acids)
2.2. TTrichloacetic acid (TCA)
3. Retinoids (e.g. TTretinoin)
4.4. PPodophyllotoxin 0.5%
5. Imiquimod 5% (Aldara)®
6.6. CCantharidin
7.7. CCidofovir (1-3% oint)idofovir (1-3% oint)
8.8. SSilver nitrate paste
9.9. PPotassium hydroxide
(KOH) 10% solution
10. Topical ccorticosteroid
(molluscum dermatitis)

Management of MC
I. Topical agents
II. Systemic agents
1. Cimetidine
2. Interferon-α, subcutaneous
3. Intravenous cidofovir (in
HIV-infected patients)
4. Antiretroviral therapy (in
HIV-infected patients)
5. Griseofulvin

Management of MC
I. Topical agents
II. Systemic agents
1. Interferon alpha (IFN-α)
2. Candida antigen

Management of MC
I. Topical agents
II. Systemic agents
IV. Alternative treatments Australian lemon myrtle

Orf (Ecthyma contagiosum)
 ETIOLOGY: poxvirus of the genus
Parapoxvirus
 HOST: Endemic in sheep and goats
presenting as nodules on the nose
and mouth.
 Most common in shepherds,
farmers, butchers & veterinarians

 C/P:
 Typically presents as a
papule/nodule on the
dorsal index finger.
 Progression through
several stages:
– maculopapular
– targetoid
– weeping nodule
– regenerative dry stage with black dots
– papillomatosis
– regression with a dry crust
 Other Findings; Ascending lymphangitis,
lymphadenopathy, malaise, and fever may occur.
 Bacterial superinfection may occur.
 Erythema multiforme occasionally occurs 10 to 14 ds. later

 COURSE: lesion resolves spontaneously in
4 to 6 weeks, healing without scar formation
 HISTOLOGIC FINDINGS: depend on stage of
the lesion and include epidermal necrosis,
vacuolated keratinocytes, a dense mixed
dermal infiltrate, and delicate finger-like
projections of the epidermis into the dermis;
eosinophilic inclusion bodies
(intracytoplasmic>intranuclear)
 MANAGEMENT:
1. Supportive;
2. Imiquimod may stimulate early regression.
3. Treat bacterial superinfection.
4. Manage pain.
 Antiviral agents are not effective.

Milker’s nodules
 ETIOLOGY: poxvirus of the genus
Parapoxvirus / Paravaccinia
 HOST: Cattle (Endemic), humans.
 Most common in shepherds, farmers, butchers &
veterinarians
 C/P:
 Papule develops at site of contact with lesions
on infected animals (e.g. muzzles of calves,
teats of cows)
• Often single lesions; favor hands and
forearms
• Cutaneous lesions virtually identical to orf
 DDx: orf (appearance of the nodules, number of
lesions and whether cows or sheep are being
mainly contacted is a guide)
 MANAGEMENT:
Supportive.

Viral exanthems
 An exanthem is defined as a skin eruption
occurring as a sign of a general disease.
 Nonspecific viral exanthems are the most
common type of exanthem seen in children.

Nonspecific viral exanthems
 These eruptions lack distinctive features
such as specific lesional morphologies,
distribution patterns, natural histories, or
enanthems (eruption on the mucous
membranes). They most often present with
blanchable erythematous papules and
macules in a widespread distribution on the
trunk and extremities, and less often the face.
Associated symptoms such as a low-grade
fever, myalgia, headache, rhinorrhea or
gastrointestinal complaints may be present.

Exanthems were previously consecutively
numbered according to their historical appearance
# Consecutive number Exanthematous disease
Causative
organism
1 First disease Measles Measles virus
2 Second disease Scarlet fever Streptococci (The
Only Bacterial)
3 Third disease Rubella (German measles) Rubella virus
4 Fourth disease Dukes' disease Probably
coxsackie virus or
echovirus
5 Fifth disease Erythema infectiosum Parvovirus B19
6 Sixth disease Roseola infantum HHV-6/HHV-7

MEASLES (Rubeola / Morbilli /
First disease)
 Measles is a highly contagious
childhood viral infection.
 Significant morbidity and
mortality occur in acute and
chronic course.
 Epidemic disease; worldwide
distribution
 ETIOLOGY: Morbillivirus
Paramyxovirus (RNA)
 HOST/RESERVOIR: humans
 TRANSMISSION: respiratory
droplets.
 IP: 10-14 days

MEASLES
C/P
 CLINICAL COURSE;
Prodrome + Exanthem
PRODROME ; Fever, malaise,
3 “C’s”; Cough, Coryza,
Conjunctivitis,
 Koplik spots;
(Pathognomonic enanthem)
Cluster of tiny gray–whitegray–white
papules on the buccal
mucosa on red background
on buccal mucosa opposite
premolar teeth. They fade
with the onset of rash.

EXANTHEM ; Generalized erythematous macules
and papules
 Appears over 2-4 days
 Cephalocaudad spread from the forehead and
behind the ears to the trunk and extremities.
 Fades on day 5 in the same cephalocaudad
direction
 More severe disease in immunocompromised or
malnourished individuals.
MEASLES
C/P

Measles. Evolution of the signs
and symptoms.

MEASLES
Dx
 RT-PCR (Reverse Transcription- PCR): virus
RNA detection in nasopharyngeal secretions
(or urine)
 Serologic assays for measles-specific
antibodies (IgM or IgG).

MEASLES
Rx
 There is no specific antiviral therapy for
measles.
 Prevention of measles by vaccination is the
most effective way to reduce measles
morbidity and mortality.
 Childhood immunization by combined MMR
vaccine:
- initial dose of vaccine at 12–15 months
- second dose at 4–6 years of age
l Supportive care such as hydration
and administration of antipyretics.
l Vitamin A (WHO) recommendation
l Immune globulin, IM or IV (within 6
days)
l Measles vaccine (within 3 days)
l Antibiotics: to treat 2ry infections

German measles (RUBELLA)
 3-day measles.
 Epidemic disease; worldwide distribution.
 ETIOLOGY: is an enveloped RNA
Rubella virus in the Togaviridae family
 TRANSMISSION: respiratory droplets.
 IP: about 18 days

German measles
C/P
 In children, many cases are
subclinical.
 PRODROME; Short: fever,
headache and upper respiratory
symptoms.
 EXANTHEM; of rose-pink macules
and papules with cephalocaudad
spread pink macular rash, which
fades, first on the turnk over the
course of few days.
 Tender lymphadenopathy of
cervical, occipital, & postauricular
glands.
 Joint involvement common

CONGENITAL RUBELLA
SYNDROME
 Occurs when nonimmune pregnant woman
transfers the virus to the fetus during the first trimester carries
high risk of miscarriage, stillbirth and fetal malformations
(microcephaly, congenital heart disease /PDA & VSD,
deafness, cataracts).
 “Blueberry muffin baby” presentation may be observed
 TORCH infections

German measles
Dx
 RT-PCR (Reverse Transcription- PCR): virus
RNA detection in nasopharyngeal secretions
(or urine)
 Serologic assays for german measles-
specific antibodies (anti-rubella IgM or IgG
antibodies).

 Prevention by vaccination with the
combined MMR vaccine
 Prophylaxis via administration of IM/IVIg to
rubella susceptible women exposed to
confirmed rubella early in pregnancy
German measles
Rx

ERYTHEMA INFECTIOSUM
(FIFTH DISEASE/SLAPPED
CHEEK DISEASE)

Erythemainfectiosum
/5th
disease
 Small outbreaks in spring & autumn.
 Children mainly 2-10 years & One infection
→ life long immunity.
 TRANSMISSION:
1. Via respiratory secretions.
2. Blood products.
3. Vertically from a mother to her fetus.
 IP: 4-14 days
 ETIOLOGY: is caused by the
parvovirus B19.

Asymptomatic infection is common.
PRODROM: usually mild or absent (e.g. low-grade fever,
myalgias, headache, chills) may occur 7–10 days before the
characteristic exanthem appears.
EXANTHEM:
 Commonly develops suddenly
 There are 3 distinct,
overlapping stages.
 THE INITIAL STAGE (FACIALTHE INITIAL STAGE (FACIAL
ERYTHEMA)ERYTHEMA) of the exanthem
consists of bright red macular erythema of the
cheeks, with sparing of the nasal bridge and circumoral
regions giving a ‘slapped cheek’ appearance.
Erythemainfectiosum
C/P

Erythemainfectiosum
C/P
 THE SECOND STAGE (RETICULAR ERYTHEMA)THE SECOND STAGE (RETICULAR ERYTHEMA) appears one
to 4 days later in the form of erythematous macules and
papules on the extremities and (to a lesser extent) the trunk,
progressing to a lacy, reticulated pattern. The palms and soles
may be involved and acral lesions may be petechial
 THE RECURRENT STAGETHE RECURRENT STAGE
wax & wane over 7-14 days.
 This exanthem typically lasts from
1 to 3 weeks (occasionally longer)
but fluctuates in intensity during
this time, often with
exacerbations upon exposure
to sunlight or overheating.

CONDITIONS ASSOCIATED
WITH PARVOVIRUS B19
1. Asymptomatic infection.
2. Erythema infectiosum (MC).
3. Arthropathy.
4. Hydrops fetalis.
5. Papular-purpuric gloves and socks syndrome.
6. Petechial eruptions
7. Degos-like lesions.
8. Transient aplastic crises in at-risk individuals.
9. Chronic anemia.
10. Thrombocytopenic purpura.
11. Hepatitis.

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 wk

1. Serology: Detection of serum anti-B19 IgM
antibody its presence indicates infection
within the previous 2–4 months.
2. PCR-based assays are especially useful for
diagnosing infection in the
immunocompromised host.
3. Electron microscopy: can detected the
virus in the serum
4. CBC: leukocytosis (During the early stages)
& Relative lymphopenia.
Erythemainfectiosum
Dx

 Require no treatment.
Erythemainfectiosum
Rx

Hand-Foot-and-Mouth Disease
 Coxsackievirus A-16
 Infection begins with a fever and
sore mouth
 90% have oral involvement
 Lesions are small rapidly
ulcerating vesicles surrounded
by a red halo
 Buccal mucosa, tongue, soft
palate, and gingiva
 Lesions on hands and feet
 Red papules that quickly turn to
gray vesicles on an erythematous
base

Hand-Foot-and-Mouth Disease
 Typically lasts less than a week
 If no cutaneous lesions - herpangina
 TREATMENT:
1. Supportive
2. Topical anesthetics

GIANOTTI-CROSTI SYNDROME
(Papular acrodermatitis of childhood)
 ETIOLOGY: self-limited
cutaneous response to various
infections. Historically
associated with hepatitis B
infection, but now more often
triggered by Epstein-Barr virus.
 The exanthem occurs in young
children 1 to 6 years old,
 Histopathologic findings are
nonspecific variety of histologic
findings reflecting the diversity of
agents that may cause the
condition.

C/P presenting as abrupt discrete non-
pruritic, skin-colored to pink–red,
edematous monomorphic dome-
shaped or flat-topped papules
symmetrically distributed on face,
buttocks and extensor extremities.
 The trunk usually spared.
 Lesions tend to be asymptomatic & may
occasionally be vesicular or purpuric.
 Systemic manifestations include
o low-grade fever
o LAD (mainly inguinal & axillary)
o hepatomegaly (occur less often)
o splenomegaly (occur less often).

DDx
1. Drug eruption,
2. Papular urticaria,
3. Other viral exanthems,
4. Erythema multiforme
5. Molluscum contagiosum.

Rx
 Spontaneous resolution usually occurs within 3–4 weeks,
although the eruption may occasionally persist for up to 8 weeks
Supportive
Topical corticosteroids are often of little
benefit.
Antihistaminics if pruritus present

KAWASAKI DISEASE
(MUCOCUTANEOUS LYMPH
NODE SYNDROME)

KAWASAKI DISEASE
 Vasculitis of unknown etiology
 Multisystem involvement and inflammation of
small and medium sized arteries with
aneurysm formation
 More common among children of Asian decent
 Usually children <5 years; peak 2-3 years
 The condition is 1.5 times more common in boys
than in girls
 Represents the most common cause of acquired
heart disease in children in the US

KAWASAKI DISEASE
C/P
 3 phases:
I.I. ACUTE PHASEACUTE PHASE (1-2 weeks)
 Sudden onset of high fever followed by;
 conjunctival erythema,
 mucosal changes,
 cervical adenopathy,
 swelling of hands and feet
 Irritability
 Abdominal pain, hydrops of gall bladder
 Arthritis

II.II. SUBACUTE PHASESUBACUTE PHASE
 Lasts up to 4th
week
 Resolution of fever and other symptoms
 Desquamation of fingers and toes
 Elevation of platelet count
 Coronary artery aneurysms
II.II. CONVALESCENT PHASECONVALESCENT PHASE
 Disappearance of clinical symptoms
 6-8 weeks after initial symptoms
KAWASAKI DISEASE
C/P

KAWASAKI DISEASE
Diagnostic Criteria
 Fever for at least 5 days
 At least 4 of the following 5
features:
1. Changes in the peripheral
extremities: edema, erythema,
followed by desquamation
2. Polymorphous exanthem: usually
trunkal often with early perineal
involvement.
3. Conjunctival injection bilateral
non-purulent.
4. Oropharyngeal changes: diffuse
hyperemia, strawberry tongue
dryness & fissuring of lips.
5. Cervical lymphadenopathy:
(usually unilateral)

Trager, J. D. N Engl J Med 333(21): 1391. 1995.

Characteristic early cutaneous finding is
erythema of the perineum, which often
desquamates within 48 hours

1. Viral exanthems …..
2. Scarlet fever.
3. Toxic shock syndrome.
4. Staphylococcal scalded skin syndrome (SSSS).
5. Erythema multiforme (EM).
6. Drug eruption.
KAWASAKI DISEASE
DDx

KAWASAKI DISEASE
COMPLICATIONS
1.1. Coronary artery thrombosisCoronary artery thrombosis
&/or aneurysm&/or aneurysm
2.2. Myocardial infarction (MI)Myocardial infarction (MI)
3.3. MyopericarditisMyopericarditis
4.4. Pericardial effusionsPericardial effusions
5.5. CongestiveCongestive heartheart failurefailure(CHF)(CHF)
6.6. Hepatic dysfunction,Hepatic dysfunction,
7.7. Obstructive jaundice,Obstructive jaundice,
8.8. Hydrops of gall bladderHydrops of gall bladder
9.9. Aseptic meningitisAseptic meningitis
10.10. ArthritisArthritis
11.11. Sterile pyuriaSterile pyuria
12.12. UrethritisUrethritis
13.13. ThrombocytosisThrombocytosis
14.14. DiarrheaDiarrhea
15.15. PancreatitisPancreatitis
16.16. Peripheral gangrenePeripheral gangrene

KAWASAKI DISEASE
Rx
I. IVIg
 first-line therapy
 mechanism unknown
 Single dose of 2 g/kg over 12 hours
 Rapid defervescence and symptom resolution
 Reduces incidence of coronary artery aneurysm
I. Aspirin
 80-100 mg/kg/day q 6 hours for 48 hours then reduce by ½
 Continue for 6-8 weeks until cardiac ECHO shows no
evidence of cardiac pathology
III. Corticosteroids (refractory KD)
IV. Infliximab (refractory KD)

References
 DR. Ali El-ethawi
 Bolognia 3rd
ed.
 Dr.B.BALAGOBI

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