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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.
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Viral Skin Infections Ziad Elnasser, MD, Ph.D
Skin rashes • World wide, Nonimmune, human reservoirs, respiratory tract. • Mumps, Measles, Rubella . • Erythemainfectiosum and Parvovirus B19. • RoseolaInfantum (Exantheme Subitum) and HHV6 and HHV7. • Poxviruses. • Herpes viruses.
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.
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 superinfectionin 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.
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 valvularstenosis. • Eye: Cataract, chorioretinitis, Glucoma, Coloboma, cloudy cornea, microophthalmia. • Sensorineural deafness, Liver, Spleen.
Thrombocytopenia, intrauterine growth. • CNS defects. • Late including DM, chronic thyroiditis, Subacutepanencephalitis (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.
Erythemainfectiosum • 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 (slapped-cheek), LNs, spleen, liver. • Thrombocytopenia, nephritis, encephalitis. • PCR, and serology.
RoseolaInfantum (ExanthemSubitum). • Sudden rash. • HHV6, HHV7. • EBV, Adenovirus, coxsakieviruses and echoviruses cause similar manifestations. • Faint macular rash.
Poxviruses • Birds, mammals, and insects. • DsDNA brick shaped, enveloped multiply in the cytoplasm, 100x200x300 nm. • Variola, Vaccinia, Moluscumcontagiosum, orf, cowpox, and pseudocowpox. • Variola major (smallpox), V. minor (alastrim). • Uniform papulovesicular rash, pustules with significant mortality.
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=2-8w, 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. • Icosahedralcapsid, 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, antiviralsdoesn,t work.
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.