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VIRAL EXANTHEMS

VIRAL EXANTHEMS. 21 Nov 2013 Danize Buemio Mary April Chan. MEASLES. Measles. Etiology Measles virus Single-stranded lipid enveloped RNA virus Family Paramyxoviridae , genus Morbilivirus 6 major structural proteins Hemagglutinin (H) protein

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VIRAL EXANTHEMS

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  1. VIRAL EXANTHEMS 21 Nov 2013 DanizeBuemio Mary April Chan

  2. MEASLES

  3. Measles • Etiology • Measles virus • Single-stranded lipid enveloped RNA virus • Family Paramyxoviridae, genus Morbilivirus • 6 major structural proteins • Hemagglutinin (H) protein • Fusion (F) protein – antibodies limit proliferation

  4. Measles • Transmission • Contact with large droplets or small droplet aerosols in which virus is suspended • Entry into respiratory tract or conjunctivae • Approx. 90% of exposed individuals develop measles • Face-fece contact is not necessary • Viable virus may be suspended in the air up to 1 hour

  5. Measles • Pathology • Necrosis of the respiratory tract epithelium with lymphocytic infiltrate • Small vessel vasculitison the skin and oral mucosa • Histological findings • Rash reveals intracellular edema and dyskeratosis • Epidermal syncytial giant cells with up to 26 nuclei • Lymphoid hyperplasia • Fusion of infected cells  multinucleated giant cells • Warthin-Finkeldey giant cells: pathognomonic for measles, up to 100 nuclei

  6. Measles

  7. Measles • Incubation period: 8-12 days • Virus migrates to regional lymph nodes • Primary viremia disseminates the virus to the reticuloendothelial system • Secondary viremia spreads virus to body surfaces

  8. Measles • Prodromal Phase: mild fever, Conjunctivitis with photophobia, Coryza, Cough • Enanthem: Koplik spots  pathognomonic • Appears 1-4 days before rash • Symptoms increase in intensity for 2-4 days until 1st day of the rash • Epithelial necrosis • Giant cell formation • Viral shedding • Viral replication

  9. Measles • Exanthem: maculopapular rash begins around forehead (hairline), behind the ears, upper neck  torso  extremities • Antibody production  viral replication and symptoms subside, rash fades over 7 days  desquamation • Infection of CD4 T cells  suppresion of immune response

  10. Inapparent Measles Infection • Subclinical form of measles • Individuals with passively acquired antibody • Infants, recepients of blood products • Rash may be indistinct, brief or absent • Do not shed measles virus or transmit infection

  11. Atypical measles • Original formalin-inactivated measles vaccine • More severe form • High onset of fever and headache • Maculopapular rash on the extremities  petechial and purpuric • Progress in centripetal direction • Frequently complicated by pneumonia and pleural effusion • Circulating immune complexes due to abnormal response to vaccine

  12. Diagnostics • CBC • Reduction in WBC count • Decrease in lymphocytes > neutrophils • ESR and C-protein normal • Serologic confirmation: IgM and IgG • IgM: appears 1-2 days after onset of rash, remains detectable for ~1month • IgG: 4-fold rise In specimens take 2-4 weeks later • Viral isolation and PCR

  13. Differential Diagnoses • Rubella • Adenoviruses • Epstein-Barr virus • Kawasaki Disease – presents with thrombocytosis, lacks Koplik spots and severe cough • Drug eruptions

  14. Treatment • Supportive • Goals of therapy: • Hydration, oxygenation, comfort • ORS, IV fluids • Airway humidification and supplemental O2 • Ventilatory support for croup or pneumonia • Antipyretics • Prophylactic antimicrobial tx is NOT indicated • Antiviral therapy is NOT effective in otherwise normal patients

  15. Treatment • Measles in immunocompromised is highly lethal • Ribavarin with or without intravenous gamma globulin

  16. Treatment • Vitamin A • Measles lowers serum retinol • Higher morbidity and mortality

  17. Complications • Morbidity and mortality are greatest in <5 years and >20 years • Crowding – larger inoculum dose • Severe malnutrition – suboptimal immune response • Measles in immunocompromised

  18. Complications • Dehydration • Fever, diarrhea, vomiting • Known to suppress PPD skin test responsiveness • May have an increased rate of PTB activation

  19. Complications • Pneumonia – most common cause of death • Giant cell pneumonia caused by virus • Superimposed bacterial infection • Final pathway: bronchiolitis obliterans • Croup, tracheitis • Otitis Media – most common complication • Sinusitis, mastoiditis, retropharygeal abscess • Encephalitis • Postinfectious immunologically mediated process • Seizures (56%), lethargy (45%), coma (28%), irritability (26%) • CSF: lymphocytic pleocytosis, elevated protein • Approx 15% death, 20-40% mental retardation, deafness, motor disabilities • Hemorrhagic or “black measles”: hemorrhagic skin eruption, fatal • Myocarditis: rare • SubacuteSclerosingParaencephalitis (SSPE)

  20. SubacuteSclerosingParaencephalitis (SSPE) • Rare disease • Results from a persistent infection with an altered measles virus harbored in CNS for years • After 7-10 years, virus regains virulence and attacks cells in CNS that offered the virus protection • Inflammation and cell death  neurodegenerative process

  21. SubacuteSclerosingParaencephalitis (SSPE) • Age of onset: <1 to <30 years • Usually in children in adolescents • Measles at an early age favors SSPE development • Males affected twice as often as females • Defective measles virus • Defective or immature immune system • Immature virus able to reside within neural cells for long periods

  22. SubacuteSclerosingParaencephalitis (SSPE) • Symptoms begin 7-13 years after primary measles infection • 1st stage: Subtle changes in behavior • Irritability, reduced attention span, temper outbursts • Fever, headache, signs of encephalitis are absent • 2nd stage: massive myoclonus • Extension of inflammatory process to deeper brain structures including basal ganglia • 3rd stage: choreoathetosis, immobility, dystonia, lead pipe rigidity • Sensorium deteriorates: dementia  stupor  coma • involuntary movements disappear • 4th stage • Loss of centers supporting breathing, heart rate, BP • Death

  23. MUMPS

  24. Mumps • Etiology • Mumps virus • Single-stranded pleomorphic RNA virus • Family Paramyxoviridae, Genus Rubulavirus • Encapsulated in a lipoprotein envelope • 7 structural proteins • Hemagglutin-neuraminidase (HN) • Fusion (F) • Humans are the only natural host

  25. Mumps • Transmission • Spread from person-person via respiratory droplets • Virus appears in saliva 7 days before and 7 days after the onset of parotid swelling • Period of maximum infectiousness: 1-2 days before to 5 days after parotid swelling

  26. Mumps • Pathology • Targets the salivary glands, CNS, pancreas, testes • Thyroid, ovaries, heart, kidneys, liver, joint synovia • Initial viral replication in the upper respiratory tract • Spread to adjacent lymph nodes target tissues • Necrosis of infected cells • Salivary gland ducts are lined with necrotic epithelium, interstitium lined with lymphocytes

  27. Mumps • Incubation Period: 12-25 days, usu. 16-18

  28. Mumps • Prodrome: 1-2 days • Fever, headache, vomiting, achiness

  29. Mumps • Parotid swelling appears • May be unilateral initially, but becomes bilateral 70% • Peaks in 3 days, subsides over 7 days • Submandibular glands may also be involved

  30. Mumps • Parotid gland is tender • May be preceeded by ear pain • Angle of jaw is obscured • Earlobe lifted upward and outward • Sour or acidic food may enhance pain • Morbiliform rash is rarely seen

  31. Mumps • Fever resolves in 3-5 days along with other systemic symptoms

  32. Diagnostics • History of exposure to mumps infection • Clinical findings • Elevated amylase level • Relative lymphocytosis • Serologic testing • Increase in mumps IgG, IgM • IgG may cross react with antibodies to parainfluenza virus • Isolation of the virus in cell culture, PCR, immunofluorescence

  33. Treatment • No specific antiviral therapy is available for mumps • Pain control • Adequate hydration • Antipyretics for fever

  34. Complications • Encephalitis, meningitis, meningoencephalitis • Usually manifests 5 days after parotid swelling • Infants, young children: fever, malaise, lethargy • Older children: headache, meningeal signs • Pancreatitis • Epigastric pain, vomiting • Orchitis • 2nd to parotitis as a common finding • After puberty, occurs 30-40% • High fever, chills, pain and swelling of testes • Oophoritis • Uncommon in postpubertal females • Severe pain

  35. Prognosis • Excellent • Some fatal cases of encephalitis were reported

  36. Prevention • 2 dose MMR vaccine • MMR1: 12-15 mos • MMR2: 4-6 years

  37. ROSEOLA

  38. RoseolaInfantum • Exanthemsubitum or Sixth disease • Mild febrile exanthematous illness • Occurs almost exclusively during infancy • >95% occur in children younger than 3, peak at 6-15 mos • Etiology • Human herpesvirus (HHV) types 6 and 7 • Genus: Roseolovirus • Subfamily: Betaherpesvirinae • Transmission • Droplet • From saliva of healthy persons, enters host through oral, nasal or conjunctival mucosa

  39. RoseolaInfantum • Prodrome • Usually asymptomatic • Mild URTI signs: minimal rhinorrhea, slight pharyngeal inflammation, mild conjunctival redness • Mild cervical or occipital lymphadenoathy • Mild palpebral edema

  40. RoseolaInfantum • High fever (average: 39C), lasts for 3-5 days • Rhinorrhea, sore throat, abdominal pain, vomiting, diarrhea • Nagayama spots: ulcers at uvulopalatoglossal junction • Rash appears within 12-24 hours of fever lysis • Rose-colored, discrete, 2-5mm, slightly raised lesions on trunk  neck  face  proximal ext • Usu. Non-pruritic, no vesicles or pustules • Fades after 1-3 days

  41. Clinical Manifestation

  42. Diagnostics • Clinical presentation • Serology • Virus culture • PCR

  43. Treatment • Supportive therapy • HHV-6 inhibit by ganciclovir, cidofovir, foscarnet (but not acyclovir) • HHV-7 inhibited by cidovir and foscarnet • No approved treatment • Treatment is warranted for immunocompromised children with severe disease • Gangciclovir, cidofovirfor 2-3 weeks

  44. RUBELLA

  45. Rubella • German measles • Three-day measles

  46. Rash similar to that of mild rubeola or scarlet fever • Enlargement and tenderness of the postoccipital, retroauricular, and posterior cervical lymph nodes

  47. Rubella in early pregnancy may cause the congenital rubella syndrome

  48. Etiology • RNA virus • Genus Rubivirus • Family Togaviridae

  49. Epidemiology • Humans are the only natural host of rubella virus • Distributed worldwide, affects both sexes equally • Spread by: • Oral droplet • Transplacentally to the fetus

  50. Epidemiology • Peak incidence: 5-14 years of age • In closed populations, such as institutions and military barracks, almost 100% of susceptible individuals may become infected. • In family settings, 50-60% of susceptible family members acquire the disease.

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