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Rubell ppt


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Rubell ppt

  2. 2. HISTORY - RUBELLA  The Teratogenic property of the infection was documented by an Australian ophthalmologist Norman McAlister Gregg, in 1941  The virus was isolated in 1962  An attenuated vaccine was developed in 1967
  3. 3.  The name is derived from the Latin, meaning little red.  Also called as three-day measles/German measles  The synonym "3-day measles" derives from the typical course of rubella exanthema that starts initially on the face and neck and spreads centrifugally to the trunk and extremities within 24 hours. Then begins to fade on the face on the second day and disappears throughout the body by the end of the third day.  Rubella is also known as German measles because the disease was first described by German physicians, Friedrich Hoffmann, in the mid-eighteenth century.  It is a generally mild disease caused by the rubella virus.  Congenital rubella syndrome (CRS) described by Gregg in 1941  Because of routine vaccination against rubella since 1970 , rubella is now rarely reported.
  4. 4. Rubella Epidemic United States, 1964-1965 12.5 million rubella cases 2,000 encephalitis cases 11,250 abortions (surgical/spontaneous) 2,100 neonatal deaths 30,000 CRS cases Deaf - 11,600 Blind - 3,580 Mentally retarded - 1,800 The largest rubella epidemic in the United States occurred in 1964- 1965, and resulted in the birth of an estimated 30,000 infants with congenital rubella syndrome. As many as 85% of pregnant women with clinical rubella delivered babies with congenital rubella. The highest percentage of congenital rubella occurred when the pregnant mothers had rubella during the first trimester
  5. 5. EPIDEMIOLOGICAL DETERMINANTS  Agent factors  Host factors  Environmental factors
  6. 6.  Causative agent: Rubella virus  ssRNA Virus of the Togaviridae Family  genus Rubivirus  One antigenic type  Diameter 50 – 70 nm  Enveloped Spherical  Virus carry hemagglutinin  Virus multiply in the cytoplasm of infected cell.  Highly sensitive to heat, extremes of pH & uv light.  At 4°C, virus is relatively stable for 24 hours.
  7. 7. Prevailing Genotypes 7
  8. 8. AGENT FACTORS cont.  CASES  Subclinical  Clinical  Congenital from infected pregnant women to fetus.  There is no known carrier state.  It probably extends from a week before symptoms to about a week after rash appears.  Infectivity is greatest when the rash is erupting. B- Source of infection C- Period of communicability
  9. 9. HOST FACTORS  Disease of childhood 3-10 yrs age group.  Following widespread immunization campaigns persons older than 15 yrs account for 70% cases in developed countries.  One attack results in life long immunity.  Infants of immune mothers are protected for 4-6 months.  In India, about 40% of child bearing age group women are susceptible to rubella. A- Age B- Immunity
  10. 10. Immunity - Rubella  Antibodies appear in serum as rash fades and antibody titers raise  Rapid raise in 1 – 3 weeks  Rash in association with detection of IgM indicates recent infection.  IgG antibodies persist for life
  11. 11. ENVIRONMENTAL FACTORS  Disease usually occurs in seasonal pattern, during the late winter & spring.  Epidemics every 4-9 years.
  12. 12.  Person to person- via respiratory route:-  Droplet from nose & throat  Droplet nuclei (aerosols)  Maintain in human population by chain transmission.  Acquired during pregnancy- vertical transmission:-  Virus can enter via the Placenta & infect the foetus in utero (Congenital Rubella Syndrome).
  13. 13.  Between 14-21 days
  14. 14. Rubella Pathogenesis  Respiratory transmission of virus  Replication in nasopharynx and regional lymph nodes  Viremia 5-7 days after exposure with spread to tissues  Placenta and fetus infected via hematogenous spread during viremia
  15. 15. Rubella Virus Developed in the nasopharynx Respiratory Tract Skin Lymph Nodes Joints Placenta or Fetus • Cough • Minor sore throat • Rashes • Lesions • Lymphadenopathy • Mild arthralgia • arthritis • Placentitis • Fetal Damage
  16. 16. Rubella virus Transmitted via respiratory droplets Infects cells in the upper respiratory tract Virus multipliesExtends in the regional lymph nodes Virus replicates in the nasopharynx Infection is established in the skin and other tissues including the respiratory tract Forchheimer’s Spot may develop Rashes develops, cough etc. Virus can be found in the skin, blood and respiratory tract
  17. 17. Diagnosis: doctor suspects whether patient has measles Virus culture/ blood test Recent infection With german measles vaccine Vaccination and proper interventions German Measles left untreated, it may cause complications: Rubella Arthritis, Encephalitis, Purpura bronchitis, abscesses in the ears and pneumonia
  18. 18.  Occurs worldwide  The virus tends to peak in countries with temperate climates  Common in children ages 5-10 years old  Human are only known reservoir.  Host -3-10 yrs  Source of infection – Respiratory secretion  Infants with CRS may shed virus for a year or more  Immunity –life long  Occurs round the year, peak in late winter and spring season  Transmission – droplet, vertical transmission  I.P – 2-3 weeks average 18 days  Rubella is world wide in distribution  Epidemics occur every 4-9 years.
  19. 19. Rubella Clinical Features  Incubation period 18 days (range 14-21 days)  Prodrome of low grade fever  Lymphadenopathy in second week  Maculopapular rash 14-17 days after exposure
  20. 20. SIGNS AND SYMPTOMS  RASH- After an incubation period of 14-21 days, the primary symptom of rubella virus infection is the appearance of a rash (exanthema) on the face which spreads to the trunk and limbs and usually fades after three days with no staining or peeling of the skin.The skin manifestations are called "blueberry muffin lesions."  LYMPH NODE- Tender lymphadenopathy (particularly posterior auricular and suboccipital lymph nodes) persist for up to a week.  TEMPERATURE-Fever rarely rises above 38 oC(100.4 oF) 20
  21. 21.  Eye pain on lateral and upward eye movement (a particularly troublesome complaint)  Conjunctivitis  Sore throat  Headache  General body aches  Low-grade fever  Chills  Anorexia  Nausea  Forchheimer sign
  22. 22. Other manifestations & complications  May produce transient Arthritis, particular in women.  Serious complications are-  Thrombocytopenia Purpura  Encephalitis
  23. 23. Rubella Rashes
  24. 24. Rubella Rashes
  25. 25. Image in a 4-year-old girl with a 4-day history of low-grade fever, symptoms of an upper respiratory tract infection, and rash. Courtesy of Pamela L. Dyne, MD.
  26. 26. Posterior auricular tender lymphadenopathy
  27. 27. Forchheimer’s Spot  Fleeting enanthema  Pinpoint or larger petechiae that usually occur on the soft palate in 20% of patients  Similar spots can be seen in measles and scarlet fever.
  28. 28. Systemic events of Rubella Infection 28
  29. 29. Main Clinical Events During Pregnancy The clinical events occurring in the neonatal age is more important and divided into two major groups-  1 Congenital Rubella  2 Post Natal Rubella
  30. 30.  Occurs during the first trimester of pregnancy.  Affects the development of the fetus.  may lead to several birth defects.  Infection may affect all organs.  May lead to fetal death or premature delivery.  Severity of damage to fetus depends gestational age.  Infants: virus is isolated from urine and feces.
  31. 31. Rubella infection – At various trimesters  Ist trimester infections lead to abnormalities in 85 % of cases. and greater damage to organs  2nd trimester infections lead to defects in 16 %  > 20 weeks of pregnancy fetal defects are uncommon  However Rubella infection can also lead to fetal deaths, and spontaneous abortion.  The intrauterine infections lead to viral excretion in various secretion in newborn up to 12-18 months.
  32. 32. Rubella infection & Chance of CRS  0–28 days before conception - 43% chance  0–12 weeks after conception - 51% chance  13–26 weeks after conception - 23% chance  Infants are not generally affected if rubella is contracted during the third trimester
  33. 33.  Sensorineural hearing loss – 58%  Ocular abnormalities including cataract, infantile glaucoma, micro- ophthalmia and pigmentary retinopathy occur in approximately 43%.  Congenital heart disease including patent ductus arteriosus (pda) and pulmonary artery stenosis - 50%.  Bone lesions  Psychiatric disorder  Diabetes mellitus type 1  Hypogammaglobulinemia  Generalized lymphadenopathy  Intrauterine growth restriction  Liver and spleen damage  Hepatosplenomegaly,, hepatitis, jaundice, thrombocytopenic purpura, with petechiae and "blueberry muffin" lesions  Central nervous system  Retardation, microcephaly  Motor delay, behavioural disorders, autism  Intellectual disability (13%)  A rare complication of pan encephalitis can occur in second decade with congenital rubella syndrome may progress to death  Problems in balance
  34. 34. Classical Triad of congenital Rubella  Cataract  Cardiac abnormalities  Deafness
  35. 35. Salt and pepper retinopathy
  36. 36. Post natal Rubella  Occurs in Neonates and Childhood  Adult infection occurs through mucosa of the upper respiratory tract spread to cervical lymph nodes  Viremia develops after 7 – 9 day  Lasts for 13 – 15 days  Leads to development of antibodies  The appearance of antibodies coincides the appearance of suggestive immulogic basis for the rash  In 20 – 50 % cases of primary infections are subclinical.
  37. 37. Diagnosis of Rubella in Adults Clinical Diagnosis is unreliable Many viral infections mimic Rubella Specific diagnosis of infection with- 1 Isolation of virus 2 Evidence of seroconversion
  38. 38. Isolation and Identification of virus  Nasopharyngeal or throat swabs taken 6 days prior or after appearance of rash is a good source of Rubella virus  Using cell cultured in shell vial antigens can be detected by Immunofluresecente methods
  39. 39. Culturing the Virus  The virus can be cultured and adopted to continuous cell lines Rabbit kidney cells (RK 13 ) and Vero cells
  40. 40. Serology In Rubella  Haemagglutination inhibition test for Rubella is of Diagnostic significance  ELISA tests are greater importance  A raise in Antibody titers must be demonstrated between two serum samples taken at least 10 days apart.  Or Detection of Rubella specific IgM must be detected in a single specimen.
  41. 41. Diagnosis of acute rubella in mother  Fourfold rise in IgG titer between acute and convalescent serum specimens  Obtained within 7 to 10 days after onset of rash  Repeated 2 to 3 weeks later  Presence of rubella specific IgM  Positive rubella culture  Can be isolated from nasal, blood, throat, urine, or cerebrospinal fluid  Generally isolated from pharynx one week before to two weeks after rash.
  42. 42. Diagnosis in infant  Isolation of rubella virus  Most frequently isolated from nasopharyngeal secretions  Can be cultured from blood, urine, CSF, lens tissue, etc.  Serial rubella-specific IgG levels at 3, 6, and 12 months  Rubella-specific IgG antibodies that persist at higher concentration or longer duration than expected from passive transfer of maternal antibody  Maternal rubella antibody- half-life= 1 month, should decrease by 4 to 8 fold by 3 months of age and should disappear by 6 to 12 months  Can delay diagnosis  Presence of rubella-specific haemagglutination inhibition (HAI) after nine months of age  Demonstration of rubella-specific IgM antibodies  Demonstration of Rubella antibodies of IgM in a new born is diagnostic value. As IgM group do not cross the placenta and they are produce in the infected fetus.  Most useful in infants younger than 2 months, but may persist for up to 12 months  False- negative-20% of infected infants tested for rubella IgM may not detectable titers before 1 month.  If clinically consistent and test negative after birth, should be retested at 1 month  False- positive- rheumatoid factor, viral infections (EBV, IM, parvovirus), and heterophile antibodies
  43. 43.  Rubella is a mild self limited illness.  No specific treatment or Antiviral treatment is indicated.  Isolation and quarantine  Increase fluid intake  Encourage the patient to rest  Good ventilation  Encourage the patient to drink either lemon or orange juice  Provide health teaching about Rubella (cause, immunizations)
  44. 44. Treatment for acute maternal rubella infection  Acetaminophen for symptomatic relief  IgG- controversial, CDC recommends limiting use of immune globulin to women with known rubella exposure who decline pregnancy termination.  Glucocorticoids, platelet transfusion, and other supportive measures for complications.  Should be counselled about maternal-fetal transmission and offered pregnancy termination, especially prior to 16 wks. Gestation.  After 20 wks. gestation- individualized management.
  45. 45. Recommendations  Screening at first post-conceptual appointment, first-trimester screening  Routine screening of child-bearing age women not recommended  Routine vaccination of all women of childbearing age not recommended
  46. 46.  Rubella vaccine is given to children at 15 months of age as a part of the MMR (measles-mumps-rubella) immunization.  The vaccine is live and attenuated and confers lifelong immunity.  Given to children 12 and 15 months and again between 3-6 years of age
  47. 47. Treatment, Prevention, Control in childbearing age women  No specific treatment is available  CRS can be prevented by effective immunization of the young children and teenage girls, remain the best option to prevent Congenital Rubella Syndrome.  The component of Rubella in MMR vaccine protects the vaccinated
  48. 48. MMR Vaccine  The MMR vaccine is a mixture of three live attenuated viruses, administered via injection for immunization against measles, mumps and rubella virus strain RA 27/3 . It is generally administered to children around the age of one year, with a second dose before starting school (i.e. age 4/5). The second dose is not a booster; it is a dose to produce immunity in the small number of persons (2-5%) who fail to develop measles immunity after the first dose, the vaccine was licensed in 1963 and the second dose was introduced in the mid 1990s. It is widely used.  Contraindications= immunodeficiency disorder, history of anaphylaxis to neomycin, and pregnancy  Side effects- arthritis, arthralgia, rash, adinopathy, or fever. 48
  49. 49. THANK YOU