Viral Skin Infections
Ziad Elnasser, MD, Ph.D
Skin rashes

World wide, Nonimmune, human reservoirs,
respiratory tract.
 Mumps, Measles, Rubella .
 Erythema infectiosum and Parvovirus B19.
 Roseola Infantum (Exantheme Subitum) and
HHV6 and HHV7.
Poxviruses.
 Herpes viruses.

Mumps
Mumps
Paramyxovirus one antigenic type.
 NA, HA on envelope.
 Parotitis, aseptic meningitis in children.
 Acute orchitis in adults.
 Communicable 7days before to 9 days
after.
 Late winter to spring.

Local replication, viremia, salivary glands
and CNS, second viremia then organs.
 Kidneys.
 Cell necrosis and inflamation.
 IgM, then IgG, CMI might contribute.
 Permanent immunity.
 IP=12 to 29 days ave. 16-18 days.
 Unilateral or Bilateral.
 Meningitis, encephalitis, transverse
myelitis, Pancreatitis, orchitis, Oophoritis.
 Myocarditis, nephritis, arthritis, thyroiditis,
sensorineural deafness.

Saliva, CSF, Pharynx.
 Primary monolayer of Monkey kidney cell
culture.
 Cyncytial giant cells, viral agglutination.
 Serology.
 No specific therapy, only MMR one or two
doses.

Measles (Rubeola)
Paramyxovirus (Mobillivirus).
 H, F proteins, CD46 receptor.
 Fever, rash and immunesuppression.
 More than 6 months of age.
 Late winter and early spring.
 95% infectivity, 3-5 days before to 4 days
after the disappearance of the rash.

Exanthemes and enanthemes
Pathogenesis
URT, intense infection, inclusion bodies in
the nucleus and the cytoplasm.
 Viremia.
 B and T cells, PMN’s, CMI and humoral
immunity effect, superinfection.
 Warthin-Finkeldey cells.
 Vasculitis and skin rash, exantheme and
enantheme (Koplik’s spots).
 CNS involvement.

CMI suppression.
 Humoral peaks in 2-3 weeks, persist at
low level.
 Life long immunity.
 5 day measles, IP=7-18 days, URT
symptoms, conjunctivitis, fever, Kopkik’s
spots, skin rash, LNs.
 Mortality could reach 15-25%.
 Bacterial superinfection in 5-15% (URT,
pneumonia, encephalitis,
thrombocytopenic purpora,
 SSPE and evidence.

Clinical Diagnosis.
 Viral isolation from oropharynx or urine.
 Multinucleated giant cells.
 Serology.
 Treat complications.
 MMR, once (12 to 15 months)or twice (4-6
years or 10-12 years), contraindications.

Rubella (German measles)
Mild benign childhood exantheme.
 Profound effects on developing fetuses.
 Togavirus, only in humans.
 Agglutinates chicks RBC’s, Trypsin treated
O RBC’s.
 Winter and spring, only 30-60% develop
clinical apparent disease.
 Contagious 7 days before to 7 days after.
 Infected babies spread the virus 6 M after
birth.

Rubella Virus
URT, LNs, Viremia up to 8 days before
rash to 2 days after.
 CMI and Immune complexes, rash,
arthritis.
 Maternal viremia, placenta, fetus and
congenital infection, vasculitis, impaired
oxygenation and chromosomal breakage.
 Shedding prolonged, IgM and IgG for 4 Y.
 Mononuclear cell infiltration, Ca++
deposition is delayed (Celery stalk).
 Life long immunity.

Three day measles.
 IP=14 – 21 days (16 average), fever, URT
symptoms, LNs.
 Macular rash, faint, arthralgia, arthritis.
 Risk for fetal damage is up to 80% in 2w, 6
– 10% by 14th, 20-30% over all.
 Cardiac: PDA, Pulmonary valvular
stenosis.
 Eye: Cataract, chorioretinitis, Glucoma,
Coloboma, cloudy cornea,
microophthalmia.
 Sensorineural deafness, Liver, Spleen.

Thrombocytopenia, intrauterine growth.
 CNS defects.
 Late including DM, chronic thyroiditis,
Subacute panencephalitis (SPE).
 Diagnosis: Clinically is not enough.

Respiratory secretions, Urine.
 Cell culture.
 PCR.
 Serology, IgM significance.


MMR: RA 27/3 human diploid fibroblast
cell culture, female adults, hospital staff at
risk, contraindications.
Erythema infectiosum
Parvovirus B19.
 SSDNA, cultured in BM cells, fetal liver
cells.
 Blood group P as a receptor.
 Anemia, and aplastic crises.
 Indurated rash on the face (slappedcheek), LNs, spleen, liver.
 Thrombocytopenia, nephritis, encephalitis.
 PCR, and serology.

Parvovirus B19

Roseola Infantum (Exanthem Subitum).
Sudden rash.
 HHV6, HHV7.
 EBV, Adenovirus, coxsakieviruses and
echoviruses cause similar manifestations.
 Faint macular rash.

Roseola infantum
Poxviruses
Birds, mammals, and insects.
 DsDNA brick shaped, enveloped multiply
in the cytoplasm, 100x200x300 nm.
 Variola, Vaccinia, Moluscum contagiosum,
orf, cowpox, and pseudocowpox.
 Variola major (smallpox), V. minor
(alastrim).
 Uniform papulovesicular rash, pustules
with significant mortality.

poxviruses
Survives well in the extracellular milieu.
 Highly contagious, saliva, skin, articles
and fomites.
 Eradicated in 1977. Only humans, no
carriers.
 Concern for recurrence?
 Cell lysis, eosinophilic inclusions
Guarnieri’s bodies.
 IP=12-14 days, can be short to 4-5 days.
 Fever, chills, myalgia, rash 3-4 days later.
 Firm papulovesicles, pustular in 10-12 day
 All in the same stage of evolution

Hemorrhagic rash (sledge hammer).
 Diagnosis by taking vesicular scraping,
culture, electron microscopy, PCR.
 Bacterial superinfection leads to death.
 Edward Jenner, Vaccinia virus, combination,
 Vaccination resembles real infection.
 Vaccinia virus is used as a vector for vaccines
 Molluscum contagiosum: Direct contact, IP=28w, pearl-like cheesy painless nodule,
curettage, eosinophilic inclusions (molluscum
bodies).
 Orf, milkers nodules and cowpox.

Herpesviruses
Enveloped, DsDNA, painfull skin ulcers,
chickenpox, and encephalitis.
 8 types:HSV1,2, CMV, VZV, EBV, HHV6,
HHV7, HHV8, alpha, beta and gamma.
 Icosahedral capsid, large genome, cross
similarity.
 Latency and reactivation.
 Replication, IE, E, and L, role of TK,
polymerase, in antiviral effect.

Herpes simplex
dsDNA , linear, 50% similarity.
 Recurrent ulcers in skin and mm, above
and below the waist, latency.
 Humans only, 90% +ve abs for type1, type
2 sexual 15-30%. Cervix in 5-12%.
 Acute infection, multinucleated giant cells,
latent infection of sensory and autonomic
nerve ganglion.
 Latent infection, trigeminal, superior
cervical and vagal nerve ganglion, S2,S3
for HSV-2, antivirals doesn,t work.

Herpes simplex type 2
Asymptomatic or mild illness in secondary
infection.
 Both Humoral and CMI are important,
ADCC mechanism.
 Single vesicular legions, pustular, coalese
then ulcerate, ectoderm origin.
 Cold sores, fever blisters, herpetic whitlow,
 Corneal damage and blindness.
 Encephalitis.
 Primary and recurrent genital herpes
infection.
 Neonatal herpes.

Tissue culture and CPE.
 Tzanck test.
 PCR.
 Serology is of less value.
 Acyclovir is used Foscarnet if R.
 Valacyclovir, and Famciclovir.
 Safe sex.
 C-section.

Varicella-Zoster
Similar to HSV differ in the glycoproteins.
 Human diploid cell culture.
 Chickenpox and shingles.
 90% get the disease before 10.
 Spread via the respiratory tract, highly
contagious, winter and spring, 1-2 days
before the rash to 3-4 days into the rash.
 URTI, LNs, viremia, RES, viremia, skin.
 Chickenpox and zoster sensory Nerve root
ganglion. Dermatomes.

CMI and humoral are important. Reactivation
is more severe in Immunesuppressed.
 Generalized vesicular rash, different stage of
evolution.
 Progressive varicella and high mortality (20%)
 CNS, pneumonia, hepatitis, nephritis.
 Post herpetic neuralgia.
 Fetal embryopathy in pregnant women,
microcephaly, cataract, chorioretinitis,
microphthalmia.
 Diagnosis: clinical, IF, serological, PCR.
 Treatment: Acyclovir, Famciclovir, valacyclovir

High titer Immunoglobulins within 96hrs.
 Not effective in shingles, or if rash has
evolved.
 Alive attenuated vaccine after 12 M, health
care workers.
