Measles teaching


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Measles teaching

  1. 1. MEASLES basics Dr.T.V.Rao MD Dt.T.V.Rao MD 1
  2. 2. Early History of Measles• Reports of measles go back to at least 700 years, however, the first scientific description of the disease and its distinction from smallpox attributed to the Muslim physician Ibn Razi(Rhazes) 860-932 who published a book entitled "Smallpox and Measles" (in Arabic: Kitab fi al-jadari wa-al- hasbah). Dt.T.V.Rao MD 2
  3. 3. Serious disease as Per WHO. • It remains a leading cause of death among young children globally, despite the availability of a safe and effective vaccine. An estimated 197 000 people died from measles in 2007, mostly children under the age of five Dt.T.V.Rao MD 3
  4. 4. Measles - Paramyxoviridae• Measles is an infection of the respiratory system caused by a virus, specifically a Paramyxovirus of the genus Morbillivirus Morbilliviruses, like other paramyxovirus, are enveloped, single- stranded, negative-sense RNA viruses. Dt.T.V.Rao MD 4
  5. 5. Measles Virus• The measles virus is a spherical, nonsegmented, single- stranded RNA virus in the Morbillivirus family, closely related to the rinderpest and canine distemper viruses. It contains six structural proteins, three that are complexed to the RNA and three that are associated with the viral membrane envelope. Dt.T.V.Rao MD 5
  6. 6. Fusion Protein • The F (fusion) protein is responsible for fusion of virus and host cell membranes, viral penetration and haemolysis. The H (hem agglutinin) protein is responsible for adsorption of the virus to cells. • There is only one serotype of Measles virus and no subtypes have yet been recognized Dt.T.V.Rao MD 6
  7. 7. Measles • More than 20 million people worldwide are affected by measles each year. Measles outbreaks are common in many areas, including Europe. For many U.S. travellers and expatriates, the risk for exposure to measles can be high, but the illness can be prevented by a measles-containing vaccine Dt.T.V.Rao MD 7
  8. 8. Spread of Measles• Measles is spread through respiration (contact with fluids from an infected persons nose and mouth, either directly or through aerosol transmission), and is highly. The infection has an average incubation period of 14 days (range 6-19 days) and infectivity lasts from 2-4 days prior to 2-5 days following the onset of the rash. Dt.T.V.Rao MD 8
  9. 9. Measles threat to Developing World• In developing countries, measles affects 30 million children a year and causes 1 million deaths. Measles causes 15,000- 60,000 cases of blindness per year. Dt.T.V.Rao MD 9
  10. 10. Measles a Childhood Infection• Age-specific attack rates may be highest in susceptible infants younger than 12 months, school-aged children, or young adults, depending on local immunization practices and incidence of the disease. Dt.T.V.Rao MD 10
  11. 11. Prominent features andcomplications in Measles Dt.T.V.Rao MD 11
  12. 12. Patients on Physical examination• Patients tend to appear moderately ill and uncomfortable because of their viral prodromal symptoms.• The Koplik spots are 1-2 mm, blue-gray macules on an erythematous base.• The measles rash is a Maculopapular eythematous rash that involves the palms and soles.• Lesion density is greatest above the shoulders, where macular lesions may coalesce Dt.T.V.Rao MD 12
  13. 13. Early Symptoms in Measles• The incubation period from exposure to onset of symptoms ranges from 8-12 days. The prodromal phase is marked by malaise, fever, anorexia, and conjunctivitis, cough, and coryza (the "3 Cs"). The entire course of uncomplicated measles, from late prodrome to resolution of fever and rash, is 7-10 days. Cough may be the final symptom to appear MD Dt.T.V.Rao 13
  14. 14. Beginning of Illness in Measles• Approximately 10 days after the initial exposure to the virus, the classic viral prodrome occurs.• Fever• Non-productive cough• Coryza• Conjunctivitis• Additional prodromal symptoms may include malaise, myalgias, photophobia, and periorbital oedema. Dt.T.V.Rao MD 14
  15. 15. A rash is leading manifestations • Typically begins at the hairline and spreads caudally over the next 3 days as the prodromal symptoms resolve. • The rash lasts 4-6 days and then fades from the head downward. • Desquamation may be present but is generally not severe. • Complete recovery from the illness generally occurs within 7-10 days 15 Dt.T.V.Rao MD from the onset of the rash
  16. 16. Koplik Spots leading clue to Measles• With in 2-3 days, the pathognomonic Koplik spots typically arise on the buccal, gingival, and labial mucosa Dt.T.V.Rao MD 16
  17. 17. Rash is a Prominent Feature Dt.T.V.Rao MD 17
  18. 18. Risk factors for infection • Children with immunodeficiency due to HIV or acquired immunodeficiency syndrome (AIDS), leukaemia, alkylating agents, or corticosteroid therapy, regardless of immunization status Dt.T.V.Rao MD 18
  19. 19. Spread of Virus• The highly contagious virus is spread by coughing and sneezing, close personal contact or direct contact with infected nasal or throat secretion Dt.T.V.Rao MD 19
  20. 20. Risk factors for severe measles• Malnutrition• Underlying immunodeficienc y• Pregnancy• Vitamin A deficiency Dt.T.V.Rao MD 20
  21. 21. Mortality Rate in Measles • The mortality rate associated with uncomplicated measles in immunocompetent, well nourished children is low but raises rapidly with malnourishment (marked in African children ), in immunocompromised, and to lesser extent with age. Dt.T.V.Rao MD 21
  22. 22. Modified Measles• Modified measles occurs in children who have received serum immunoglobulin after their exposure to measles. The measles symptom complex may still occur, but the incubation period is as long as 21 days, with the same symptoms as measles but milder. Dt.T.V.Rao MD 22
  23. 23. Atypical Measles• Atypical measles occurs in individuals who were previously immunized with the killed measles vaccine between 1963 and 1967 and who have incomplete immunity. Dt.T.V.Rao MD 23
  24. 24. Sub acute sclerosing panencephalitis SSPE• SSPE is a neurodegenerative disease caused by persistent infection of the brain by an altered form of the measles virus. Neither the biology underlying the viral persistence nor the triggering mechanism for viral reactivation is well understood. In most cases, infected children remain symptom-free for 6-15 years after acute measles infection[ Dt.T.V.Rao MD 24
  25. 25. Sub acute sclerosing panencephalitis• Subacute sclerosing panencephalitis (SSPE) 1 in 100,000 people infected with measles develop SSPE. SSPE is incurable but the condition can be managed by medication if treatment is started at an early stage. Dt.T.V.Rao MD 25
  26. 26. Clinical Presentation of SSPE• Characterized by a history of primary measles infection usually before the age of 2 years, followed by several asymptomatic years (6–15 on average), and then gradual, progressive psycho neurological deterioration, consisting of personality change, seizures, myoclonus, ataxia, photosensitivity, ocular abnormalities, spasticity, and coma. Dt.T.V.Rao MD 26
  27. 27. Diagnosis of Measles• Most cases of Measles are diagnosed clinically, usually in patient’s home or in General practice• Direct Virological confirmation is difficult in most of the Developing countries Dt.T.V.Rao MD 27
  28. 28. Diagnosis withImmunofluorescence Direct and indirect immunofluores cence have been used extensively to demonstrate MV antigens in cells from NPS specimens. Dt.T.V.Rao MD 28
  29. 29. Diagnosis by Viral Isolation• Measles virus can be isolated form a variety of sources, e.g. throat or conjunctival washings, sputum, urinary sediment cells and lymphocytes. Primary human kidney (HEK) cells are the best, although primary monkey kidney can be used as well. Continuous cell lines such as Vero cells can also be used Dt.T.V.Rao MD 29
  30. 30. Diagnosis by Serology • Diagnosis of measles infection can be made if the antibody titres rise by 4 fold between the acute and the convalescent phase or if measles- specific IgM is found. The methods that can be used include HAI, CF, neutralization and ELISA tests. Dt.T.V.Rao MD 30
  31. 31. Diagnosis of SSPE• The presence of measles specific antibodies in the CSF is the most reliable means of laboratory diagnosis of SSPE. Demonstration of MV- specific antibodies in the CSF may be sufficient with, Dt.T.V.Rao MD 31
  32. 32. Epidemiological Trends • Measles epidemics occur every 2 year in developed countries in the absence of widespread use of vaccine • Poverty and overcrowding increases epidemics Dt.T.V.Rao MD 32
  33. 33. Treatment• Severe complications from measles can be avoided though supportive care that ensures good nutrition, adequate fluid intake and treatment Antibiotics should be prescribed to treat eye and ear infections, and pneumonia. Dt.T.V.Rao MD 33
  34. 34. VACCINATION• The Vaccines are Live attenuated containing Edmonston B or Schwartz strains which will give seroconversion rate of 90%.• The immunity produce may be life long. Dt.T.V.Rao MD 34
  35. 35. Measles vaccine is given as MMR Vaccine • The measles vaccine is often incorporated with rubella and/or mumps vaccines in countries where these illnesses are problems. It is equally effective in the single or combined form. • The combination proved to be effective and safe Dt.T.V.Rao MD 35
  36. 36. Two doses of Measles Vaccine• Continued progress depends on ensuring that all children receive two doses of measles vaccine including one dose by their first birthday, strengthening disease surveillance systems, and providing effective treatment for Dt.T.V.Rao MD 36 measles.
  37. 37. Changing trends for a Booster Dose • About 15% of vaccinated children fail to develop immunity from the first dose. Dt.T.V.Rao MD 37
  38. 38. For topics current Interest on Infectious diseases follow me on.. Dt.T.V.Rao MD 38
  39. 39. Created for Medical andparamedical students in Developing world Email Dt.T.V.Rao MD 39