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ENTEROVIRAL INFECTIONS

ENTEROVIRAL INFECTIONS. Dr.B.Boyle. ENTEROVIRAL INFECTIONS Contents of Lecture. ENTEROVIRUSES Also Discuss , Viruses that cause Gastroenteritis ROTAVIRUS SMALL ROUND STRUCTURED VIRUSES e.g Norwalk virus or Novovirus etc. ROTAVIRUS. Description Epidemiology Pathogenesis

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ENTEROVIRAL INFECTIONS

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  1. ENTEROVIRAL INFECTIONS Dr.B.Boyle

  2. ENTEROVIRAL INFECTIONSContents of Lecture • ENTEROVIRUSES • Also Discuss , Viruses that cause Gastroenteritis • ROTAVIRUS • SMALL ROUND STRUCTURED VIRUSES e.g Norwalk virus or Novovirus etc.

  3. ROTAVIRUS

  4. Description Epidemiology Pathogenesis Clinical Features Diagnosis Treatment The Future ROTAVIRUS

  5. ROTAVIRUS • First described in 1973 by electron microscopy from duodenal biopsy specimens • Causes 40-60% of cases of diarrhoea in cooler months in infants and children < 2 years

  6. Morphology-Rotaviruses • Reoviridae Family • Non-enveloped icosahedral structure, 70nm • EM: Wheel shape • Capsid: Outer(VP7 and 4) and Inner(VP6) proteins • Core encloses 11 segments of DS RNA Genome encoded Structural proteins VP1-7 and NSP 1-5, NSP4 has enterotoxinlike activity

  7. Epidemiology of Rotavirus • Incubation period : 2-4 days • Those affected :4-24 month old infants, infection before and reinfection after this usually asymptomatic (Breastfeeding results in milder disease) • Spread within families and institutions • Human to human, faecal-oral route • Found on fomites in childcare

  8. Epidemiology of Rotavirus • Main cause of severe diarrhoea in children < 5 years • 130 million episodes per year in the world • Between 600,000-870,000 deaths, mostly in the developing world • Rate of hospitalisation in developed world 2.5% • Seasonal pattern • Most persons infected by 3 years of age • Group A predominates

  9. Classfication-Rotavirus • Groups,Subgroups and serotypes depending on the antigenic properties of the capsid proteins • Group-VP6, seven exist A-G, 2 subgroups 1-2 • Groups A,B,C cause human infection

  10. Rotavirus-Pathogensis Infects Mature Enterocytes(on tips of Small Intestine villi) Villous Atrophy Compensatory Repopulation by immature Secretor cells and secondary hyperplasia Cell death because of villous ischaemia

  11. Mechanism of diarrhoea? Enteric nervous system stimulates Induction Of intestinal Water And electrolyte secretion Villous epithelium in relation To secretory capacity of Crypt cells Loss of permeability to Macromolecules e.g Lactose, Due to loss of disaccharideases

  12. Rotavirus Damage to Small Intestine

  13. Immune Response to Rotavirus • Localised Immune response protects against severe subsequent infections • NSP4 protein results in cell mediated immunity

  14. Outcome of Infection with Viruses • Lysis of cells e.g Influenza or polio • Persistent infection e.g. cell remains alive and continues to release virus particles e.g. Hepatitis B , CHRONIC CARRIER STATE • Latent Infection , no replication – Varicella Zoster or retrovirues , if triggered leads to lysis • Transformation of host cells e.g. warts or papovaviruses, HTLV 1 and 2

  15. Clinical Presentation-Rotavirus • Abrupt onset of vomiting followed within hours by watery, brown copious diarrhoea, often lasts 3-8 days • If Severe  Dehydration and death or hospitalisation

  16. DIAGNOSIS • Clinically • Latex agglutination Kit testing for Group A Rv antigen in stool Enzyme Immunoassay Group A Rv antigen in stool Less common EM and molecular methods Pos and neg

  17. TREATMENT • REHYRATE, oral and if severe parenteral • Some studies in immunocompromised persons showing the use of Human Immunoglobulin results in a reduction in the duration of symptoms and decreases viral sheeding • ISOLATION of patient in hospital with contact prescautions

  18. MANAGEMENT • In Home: Washing of surfaces with soap and water which may be contaminated with Rotavirus • 70% ethanol solution will kill the virus on environmental surfaces

  19. FAMILY: PICORNAVIRIDAE Cardiovirus Aphthousvirus etc RHINOVIRUS Type 1-100+ ENTEROVIRUSES Over 72+ POLIO virus type 1,2,3 COXSACKIE A virus type 1-22,24 COXSACKIE B virus type 1-6 E.C.H.O virus type 1-7,11-27,29-34 Numbered ENTEROVIRUSES type 68-71,73 Since 1967-all new ones are numbered E.C.H.O = enteric cytopathic human orphan

  20. Characteristics • VIRON= naked , small (25-30 nm) icosahedral capsid enclosing postive sense single stranded RNA • Enteroviruses are resistant to p H 3-9, Heat, Mild sewage treatment and detergents, conditions in GIT = FACILATES faecal oral spread

  21. Characteristics • Rhinovirus labile to acidic p H • Genome of Enteroviruses is m RNA • Naked genome is sufficient for infection • Replication in cytoplasm • Cytolytic viruses

  22. Neurological: e.g Poliomyelitis, Aseptic meningitis and encephalitis Neonate: neonatal sepsis EV 11 Non-specific febrile illness Hepatitis gi etc Haemorrhagic conjunctivitis, COX A24 and EV 71 Respiratory Symptoms e.g colds, herangina Skin Exanthem with meningitis Myocarditis Those associated with Coxsackie viruses Spread: Faecal oral route , respiratory route and peripartum mother to infant or fomite transmission IP: 3-6 DAYS Clinical Manifestations of EV Infections(Mostly Children)

  23. COXSACKIE VIRUSES • 29+ immunogenic types • Divided into A and B on the basis of different pathogenic potential for mice • Result in a number of different clinical presentations

  24. Herangina Summer minor illness Aseptic meningitis Neonatal Disease Colds Hand , Foot and mouth illness Myocarditis ? Diabetes mellitus Epidemic myalgia (Bornholm Disease) COXSACKIE VIRUSES

  25. HAND/FOOT/MOUTH Coxsackie A16

  26. H/F/M

  27. ECHO Viruses • General properties similar to other enteroviruses • 30+ antigenic types • Results in: - 1. Aseptic meningitis 2. Rash 3.Conjunctivits 4. Upper Respiratory Tract Infection

  28. ENTEROVIRUS 71

  29. Management • Supportive • Capsid function inhibitors: Pleconaril, broad spectrum, potent to Rhino and enteroviruses, good oral bioavailibility • This compound binds to the floor of a VP1 and VP3 canyon floor , prevents binding to receptor on cells • Used in cases of meningoencephalitis shown to be effective • As humoral immunity is the body`s defence for enteroviruses, those who have deficiencies (congenital –or acquired)are given Intravenous Immunoglobulin

  30. POLIO VIRUS

  31. Polioviruses • are RNA , ENTEROVIRUSES • 3 Serotypes 1, 2 ,3 • Major cause of paralytic poliomyelitis and now seeing post polio syndrome • Global Eradication Programme of WHO

  32. EPIDEMIOLOGY • Human host • Spread: Faecal oral or Respiratory routes • More common in infants and young children, but risk of paralytic disease increases with age • No indigeous wild type polio in U.S since 1979, imported in 1993, last wild type case in Ireland 1984 • Vaccine Associated Paralytic Polio(VAPP) WHEN ORAL POLIO VACCINE (OPV) was in use( Reversion to wild type) now inactivated polio vaccine used(IPV) used in Ireland since 2001

  33. EPIDEMIOLOGY • Risk of VAPP is one case per 2.5 million doses, greatest risk with first dose • If using OPV strict hygiene after nappy changing or toileting should be observed for 6 weeks

  34. PRESENT VACCINE SCHEDULE

  35. PRESENT SCHEDULE

  36. PRESENT SCHEDULE

  37. PRESENT SCHEDULE • From Family Doctor • 1: A single dose of Hib vaccine if child presents after 13 months and has no previous Hib vaccine • 2: Only those known to be tuberculin negative and have no previous BCG • **These immunizations are generally administered in schools by Health Boards

  38. Clinical Presentations of Poliovirus Infection • Approx. 95% of infections are ASYMPTOMATIC • Minor illness in 4-8% of lowgrade fever, sore throat • Aseptic Meninigits in 1-5% • Asymmetrical acute flaccid paralysis with areflexia of limbs involved in 0.1%-2% of infections (Respiratory Muscles may be involved) • Residual Paralytic Diease in 2/3 of these • Some develop Post-Polio syndrome 30-40 years post infection with return of muscle pain and weakness

  39. Poliomyelitis

  40. Poliomyelitis

  41. Pathogenesis of Enteroviral Infection Evades Virus Replicates in Nasopharnyx Binds Enterocytes Receptor coded by Ch 19 Acidic PH Minor Viraemia, Replication in organs Endocytosed , replication in Peyer`s patches Anterior Motor Neuron horn cells To CNS* Major Viraemia + Trophism + Virulence Skeletal Muscle Neuromuscular Endplate Ascends along Motor Nerves *Spinal, Bulbar, Medullary Red=specifc for polio

  42. Communciability • This is greatest shortly before and after onset of clinical illness when virus in the throat and it is excreted in high concentrations in faeces • For OPV RECIPIENTS, VIRUS IN THE THROAT 1-2 WEEKS AND FAECES FOR SEVERAL WEEKS USUALLY MAX 6-8 WEEKS IN NORMAL IMMUNOCOMPOTENT INDIVIDUAL.

  43. Surveillance • For Acute flaccid paralysis • Since September 1998 • Two faecal specimens 24-48 hours apart for viral culture as soon as possible after onset of acute flaccid paralysis • Faeces most likely to yield virus

  44. Diagnosis • Clinical Presentation • Laboratory Diagnosis • Faecal, Throat (2 or more samples), CSF(Culture and RT-PCR)

  45. TREATMENT/PREVENTION • Supportive • Prevention is by Vaccination. • Global Eradiation Programme • Part of Routine immunisation schedule and travellers to endemic areas should be vaccinated

  46. Global Eradication programme

  47. SLV-NLV-Novovirus-Calciviruses • Family: Calciviridae • Single Stranded RNA, ps • Consists of Single Structural Capsid protein with icosahedric symmetry but has 32 cup-shaped depressions on the axes of the Icosahedron hence the name calyx • Multiple antigenic types

  48. Epidemiology • Genotype 1,11 and 4 are associated with outbreaks • Often affecting institutions • Commonest cause of gastroenteritis outbreaks in 2nd quarter 2005, with 32 outbreaks and 675 persons ill, 72% of cases • Present circulating genotype in Ireland since 2004 is Genotype 11.4 JAM strain • Review: Lopman et al Lancet Feb 2004

  49. Pathogenesis of Disease • Not fully understood although some evidence suggesting it may be simliar to Rotavirus • Causes delayed gastric emptying • Immunity: infection induces specific IG G/A/M even if there is previous exposure • 2 weeks post infection there is ⇧ in jejunal Ig A , resistance to reinfection lasts 4-6 months, • NO LONG TERM PROTECTION • Accounts for >85% of non-bacterial outbreaks of gastroenteritis

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