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Paramyxoviruses lecture dwd

Morphology diseases and laboratory diagnosis

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Paramyxoviruses lecture dwd

  1. 1. • Paramyxoviridae contains a group of viruses; which are transmitted via the respiratory route following which : • They may cause localized respiratory infections in children e.g. respiratory syncytial virus & the parainfluenza viruses) or • They may disseminate throughout the body to cause highly contagious diseases of childhood such as mumps (parotid enlargement) & measles(rashes).
  2. 2. • Parainfluenza viruses resemble Orthomyxoviruses in morphology but are larger & pleomorphic. • Size : 100 – 300 nm, rarely 800nm, Rarely large filaments & giant forms seen. • Symmetry : Helical • Nucleocapsid : 18nm • Genome : Negative sense, linear, single stranded , non – segmented RNA
  3. 3. • Six structural Proteins : Which form capsid, polymerase, matrix protein ( underlies the envelop),& envelop glycoproteins. • Envelop : Nucleocapsid is surrounded by a host derived lipid envelop in which the following virus coded peplomers (glycoproteins ) are inserted.
  4. 4. • F – Glycoprotein : Present in all myxoviruses. Mediate membrane fusion. Also have hemolysin activity ( except in pneumoviruses). • Larger Glycoproteins – Help in attachment to the host cells. May be either H or HN or G type – 1. HN Glycoproteins – Have both haemagglutinin & neuraminidase activities e.g. in parainfluenza & mumps viruses 2. H Glycoproteins – Have only haemagglutinin activity e.g. in measles. 3. G Glycoproteins – No haemagglutinin & neuraminidase activities. Help in attachment e.g. in respiratory syncytial virus.
  5. 5. • Paramyxoviridae family - Divided into two subfamilies - Paramyxovirinae & Pneumovirinae. Subfamilies Paramyxovirinae Pneumovirinae Genera Respirovirus Rubulavirus Morbillivirus Henipavirus Pneumovirus Metapneumovirus Human Viruses Parainfluenza 1, 3 Mumps Parainfluenza 2, 4a, 4b Measles Hendra Nipah (Zoonotic) Respiratory Syncytial virus Human metapneumovirus
  6. 6. • Human parainfluenza viruses – one of the major causes of lower respiratory tract infections in young children. Has 5 serotypes. • Type 1 and 3 – Genus Respirovirus. • Type 2, 4a, 4b – Genus Rubulavirus.
  7. 7. • Transmission by respiratory route ( By direct salivary contact or by large – droplet aerosols). • Incubation Period – 5 to 6 days. • Virus multiplies locally and cause various respiratory manifestations. • Mild common cold syndrome like rhinitis, pharyngitis. • Laryngotracheobronchitis ( croup) – with type 1 & 2 viruses. • Bronchitis & Pneumonia • Reinfection.
  8. 8. • Worldwide in distribution • Type 3 – Most prevalent serotype & exists as endemic throughout the year with annual epidemics during spring. • Type 1 & Type 2 – Less common. Tend to cause epidemics during rainfall or winter. • Type 4a & 4b cause milder illness and are most difficult to isolate. • Parainfluenza viruses – Important cause of outbreaks in pediatric wards, day care centers & in schools.
  9. 9. • Antigen detection : Viral antigens in the infected exfoliated epithelial cells of nasopharynx – Detected by direct immunofluorescence by using specific monoclonal antibodies. It is rapid but less sensitive. • Viral isolation : 1. Specimens – Nasal washes, bronchoalveolar lavage fluid, lung tissue. Specimens to be inoculated as early as possible. 2. Tissue culture – Primary monkey kidney cell line – most sensitive. Other cell lines used – LLC – MK2. 3. Produce little or no cytopathic effects 4. Viral growth detected by performing haemadsorption using guinea pig erythrocytes or Ag detection by direct IF.
  10. 10. •Serum antibodies : Can be measured by neutralization test, haemagglutination inhibition test or ELISA. Presence of IgM or fourfold rise of IgG titer – Indicative of active infection. • Reverse transcriptase PCR : Highly specific & sensitive. But available only in limited settings.
  11. 11. • Most common cause of parotid gland enlargement in children. In severe cases, it can also cause orchitis & aseptic meningitis. • PATHOGENESIS :  Transmission – Through respiratory route via droplets, saliva, & fomites.  Primary replication – Occurs in the nasal mucosa or upper respiratory mucosa → infects mononuclear cells & regional lymph nodes→ spills over to blood stream resulting in viremia → dissemination.  Target sites – Mumps virus has special affinity for glandular epithelium. Classic sites – salivary glands, testes, pancreas, ovaries, mammary glands, & central nervous system.
  12. 12. • CLINICAL MANIFESTATIONS : • Incubation period – 7 – 23 days (Average 19 days). • Inapparent infection – Half of the infected persons are either asymptomatic or present with non specific symptoms such as fever, myalgia, & anorexia( more common in adults). • Bilateral parotitis – Acute non – suppurative parotid gland enlargement, present in 70 – 90% cases. Rarely may be unilateral. • Epididymo – orchitis – Next most common presentation. 15 – 30 % cases. • Aseptic meningitis – Occurs in < 10% cases with a male predominance , self limiting • Oophoritis – In about 5% of females • Atypical mumps – Absent parotitis, directly presents as aseptic meningitis.
  13. 13. • EPIDEMIOLOGY – • Endemic worldwide. Peak in winter & spring. • Period of communicability – Pts are infectious from 1 wk. before to 1 wk. after the onset of symptoms. It is shed in saliva, respiratory droplets, & urine. • Source – Clinical & subclinical cases. No carrier state. • Reservoir – Humans are the only reservoir of infection. • Incidence – 100 – 1000 cases per 10000. • Age – 5 – 9 years. No age spared. • Immunity – One attack – lifelong immunity.
  14. 14. • LABORATORY DIAGNOSIS – • Specimens – Buccal or oral swab, CSF, Saliva, urine • Antigen detection – By direct IF test • Viral isolation – 1. Primary monkey kidney cells, 2. Shell viral technique. Cytopathic effect – cell rounding & giant cell formation. • Serum Abs – By ELISA, neutralization test, haemagglutination inhibition test. • RT – PCR – Detects viral RNA. • TREATMENT – • No specific antiviral drug. T/t – mostly symptomatic
  15. 15. • PROPHYLAXIS – • LIVE ATTENUATED VACCINE – From Jeryl Lynn or RIT 4385, or Urabe strain. It is prepared in chick embryo cell line. • MUMPS VACCINE IS AVAILABLE AS – 1. Trivalent MMR vaccine (Live attenuated Measles – Mumps – Rubella vaccine) or 2. Quadrivalent MMR – V vaccine ( contains additional live attenuated varicella vaccine) or 3. Monovalent mumps vaccine ( not commonly used) • Schedule – 2 doses of MMR is given by IM route at 1 yr. & 4 – 6 yr.(before starting school) • Efficacy – 90% after second dose.
  16. 16. • Measles is an acute, highly contagious childhood disease, characterized by fever, respiratory symptoms, followed by typical maculopapular rash. • PATHOGENESIS –  Transmission – Via respiratory route through droplet inhalation & aerosols.  Spread – Virus multiplies locally in the respiratory tract →Then spreads to regional lymph nodes → enters the blood stream in infected monocytes (primary viremia)→ further multiplies in reticuloendothelial system → spill over into blood ( secondary viremia)→ disseminates to various sites.  Target sites – Predominantly the virus is seeded in the epithelial surfaces of the body, including skin, respiratory tract & conjunctiva.
  17. 17. • CLINICAL MANIFESTATIONS – • Incubation period – 10 days to 3 wks. 1. PRODROMAL STAGE – lasts for 4 days. Characterized by – Fever – On day 1 i.e. 10th day of inf. • Koplik’s spots - are pathognomic of measles, appear on 12th day of inf. – 1 mm white to bluish spot surrounded by an erythema on buccal mucosa near 2nd lower molar. Rapidly spread to entire buccal mucosa & fades away on onset of rash. • Non specific symptoms – Cough, coryza, nasal discharge, redness of eye, diarrhea or vomiting.
  18. 18. • CLINICAL MANIFESTATIONS – 2. Eruptive stage – • Maculopapular dusky red rashes after 4 days of fever ( i.e. 14th day of infection). Typically appear first behind the ears→ spread to face, arm, trunk & legs→ then fade in the same order after 4 days of onset. 3. Post Measles Stage – • Characterized by weight loss, weakness ,disorientation , chronic illness.
  19. 19. • COMPLICATIONS – • Secondary bacterial infections – Otitis media, Bronchopneumonia. • Recurrence of fever or failure of fever to subside with rash. • Giant cell pneumonitis ( Hecht’s pneumonia) in Immunocompromised pts. Acute Laryngotracheobronchitis & diarrhoea. • CNS complications – 1. Post measles encephalomyelitis 2. Measles inclusion body encephalitis 3. Subacute sclerosing panencephelitis
  20. 20. • LABORATORY DIAGNOSIS : • Specimen – Nasopharyngeal swab • Antigen detection by using anti – nucleoprotein antibodies. • Virus isolation – 1. Monkey or human kidney cells or Vero / hSLAM cell line – produces CPE as multinucleated giant cells ( Warthin – Finkeledy cells. 2. Shell viral culture • Antibody detection – Against nucleoprotein Ag by ELISA or neutralization tests. • Reverse – transcriptase PCR – detects viral RNA.
  21. 21. • PROPHYLAXIS – • Live attenuated vaccine – Strains used – Edmonston strain, Schwartz strain , Edmonston - Zagreb strain , Moraten strain. • Vaccine is prepared in chick embryo cell line. • Vaccine available in lyophilized form & has to be reconstituted with distilled water & to be used within 4 hours. Stored at -200 C • Dose – One dose (0.5ml) containing > 100 infective viral units & is administered subcutaneously.
  22. 22. • PROPHYLAXIS – • Combined vaccines – MMR or MMR – V vaccines • Contacts – Measles immunoglobulin – 0.25 mg / kg/body wt.
  23. 23. • EPIDEMIOLOGY – • Source – Cases are only source of infection. • Reservoir – Humans only • Infective material – Virus shed in secretions of nose, throat, & respiratory tract of cases of measles. • Period of communicability - Pts. Are infectious from 4 days before to 4 days after the onset of rash. • Secondary attack rate – high • Age – Children 6 months to 3 years in developing countries & older children > 5 yrs. In developed countries.
  24. 24. • RSV is a major respiratory pathogen of young children & is the most common cause of LRTI ( Bronchiolitis & pneumonia) in infants. • PATHOGENESIS – • Transmission – Direct contact( contaminated fingers, fomites, self inoculation onto conjunctiva or anterior nares or by large droplets. • Spread – It replicates locally in the epithelial cells of nasopharynx  spread to LRT  cause bronchiolitis & pneumonia • Pathology – Peribronchiolar infiltration by lymphocytes. Submucosal edema, Necrosis of bronchiolar epithelium & formation of plugs consisting of mucus, cellular debris & fibrin which occlude the smaller bronchioles.
  25. 25. • CLINICAL MANIFESTATIONS – • I.P. – 3 – 5 days . Most common cause of LRTI in infants < 1 yr. • Symptoms – Running nose, fever, accompanied by cough, wheezing, & dyspnoea. • In Adults – RSV produces influenza like URTI. Occasionally can cause LRTI • Recurrent infection – Common both in children & adults.
  26. 26. • LABORATORY DIAGNOSIS – • Ag Detection – Direct IF test detecting virus on exfoliated cells & ELISA detecting Ag in nasopharyngeal secretions. • Virus Isolation – HeLa & HEp – 2 cell lines for RSV isolation . Characteristic CPE – Syncytium formation. • Antibody Detection – IF, neutralization tests, ELISA. • Reverse Transcriptase PCR – Viral RNA.
  27. 27. • Not a myxovirus . Also c/a German measles. • MORPHOLOGY - Belongs to Togaviridae family & is the only member under genus Rubivirus. It is enveloped, SS RNA virus measuring 50 – 70 nm. Envelop contains two types of spike – like glycoproteins E1 & E2. Only one serotype. Humans only reservoir. • Types of infections – Post natal or congenital • Transmission – spreads from person to person by respiratory droplets via upper respiratory mucosa. • Spread – Replicates locally in nasopharynx  L.N.  viremia after 7 – 9 days  Rash
  28. 28. • CLINICAL FEATURES – • I.P. – 14 days . Infection subclinical in 20% • Rash – generalized & maculopapular in nature. • Lymphadenopathy • Forchheimer spots – Pin head sized petechie on soft palate & uvula. • Complications – Arthralgia and Arthritis.
  29. 29. • LABORATORY DIAGNOSIS – • Specimens – Nasopharyngeal & Throat swab. • Virus Isolation – In monkey or rabbit origin cell lines & then growth detected by viral interference. Shell viral technique. • Antibody Detection – By HAI or ELISA • CONGENITAL RUBELLA SYNDROME – Has teratogenic effect. Transmission to fetus if mother is infected during first trimester . • Causes ear defect, ocular defect, cardiac defect & CNS defects.
  30. 30. • VACCINATION – • RA 27/3 is live attenuated vaccine for rubella prepared from human diploid fibroblast cell line. Available singly or in combination of mumps & measles – MMR. • Schedule – Single dose (0.5 ml) of vaccine is administered subcutaneously.

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