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

ROTAVIRUS 
     

Description Epidemiology Pathogenesis Clinical Features Diagnosis Treatment The Future

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

70nm  EM: Wheel shape  Capsid: Outer(VP7 and 4) and Inner(VP6) proteins  Core encloses 11 segments of DS RNA Genome encoded Structural proteins VP17 and NSP 1-5.MorphologyMorphology-Rotaviruses Reoviridae Family  Non-enveloped icosahedral structure. NSP4 has enterotoxinlike activity  .

faecal-oral route  Found on fomites in childcare .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.

000-870.5% Seasonal pattern Most persons infected by 3 years of age Group A predominates .Epidemiology of Rotavirus        Main cause of severe diarrhoea in children < 5 years 130 million episodes per year in the world Between 600.000 deaths. mostly in the developing world Rate of hospitalisation in developed world 2.

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

RotavirusRotavirus-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 .

Due to loss of disaccharideases .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.

Rotavirus Damage to Small Intestine .

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

.

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

brown copious diarrhoea.Clinical PresentationPresentationRotavirus   Abrupt onset of vomiting followed within hours by watery. often lasts 3-8 days If Severe Dehydration and death or hospitalisation .

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 .

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 .TREATMENT  REHYRATE.

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 .

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

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

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

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

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 .

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

HAND/FOOT/MOUTH Coxsackie A16 .

H/F/M .

Aseptic meningitis 2.1.Conjunctivits 4. Upper Respiratory Tract Infection . Rash 3.ECHO Viruses  General properties similar to other enteroviruses  30+ antigenic types  Results in: .

ENTEROVIRUS 71 .

good oral bioavailibility This compound binds to the floor of a VP1 and VP3 canyon floor . those who have deficiencies (congenital ±or acquired)are given Intravenous Immunoglobulin . broad spectrum.Management      Supportive Capsid function inhibitors: Pleconaril. potent to Rhino and enteroviruses. 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.

POLIO VIRUS .

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

but risk of paralytic disease increases with age No indigeous wild type polio in U. 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 .S since 1979.EPIDEMIOLOGY      Human host Spread: Faecal oral or Respiratory routes More common in infants and young children.

5 million doses.EPIDEMIOLOGY  Risk of VAPP is one case per 2. greatest risk with first dose  If using OPV strict hygiene after nappy changing or toileting should be observed for 6 weeks .

1 month BCG Usually in maternity hospitals *At 2 months Diphtheria Whooping Cough Tetanus Hib Inactivated Polio + Meningococcal C Diphtheria Whooping Cough Tetanus Hib Inactivated Polio + Meningococcal C 5-in-1(G.PRESENT VACCINE SCHEDULE At birth.P) *At 4 months 5-in-1(G.P) .

15 months Measles Mumps Rubella.P) *At 12. Hib1 MMR Hib1 .PRESENT SCHEDULE *At 6 months Diphtheria Whooping Cough Tetanus Hib Inactivated Polio + Meningococcal C 5-in-1(G.

PRESENT SCHEDULE **4-5 YEARS Diphtheria Whooping Cough Tetanus Inactivated Polio + Measles Mumps Rubella Measles Mumps Rubella 4-in-1 MMR **11-12 YEARS MMR Omit if 2 previous doses have been given .

PRESENT SCHEDULE **11-14 years Tetanus Diphtheria (low dose) Td **10-14 years if not protected(immune) BCG2 (AN INTERVAL OF 4 WEEKS AFTER MMR) Meningococcal C Under 23 years(Colleges etc) ‡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 .

95% of infections are ASYMPTOMATIC Minor illness in 4-8% of lowgrade fever.Clinical Presentations of Poliovirus Infection       Approx.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 . sore throat Aseptic Meninigits in 1-5% Asymmetrical acute flaccid paralysis with areflexia of limbs involved in 0.

Poliomyelitis .

Poliomyelitis .

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

.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.

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 .

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

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

Global Eradication programme .

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  .SLV-NLV-NovovirusSLV-NLV-NovovirusCalciviruses Family: Calciviridae  Single Stranded RNA.

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

NO LONG TERM PROTECTION Accounts for >85% of non-bacterial outbreaks of gastroenteritis .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.

Institutions and hospitals Spread: Person to person via faecal oral route or through contaminated food or water or fomites Incubation Period: 12-72 hours Vomitus /Faeces infectious . hotels.EPIDEMIOLOGY      Sporadic cases however causes epidemic outbreaks Examples: on cruise ships.

myalgia and abdominal cramps Symptoms last 1 day to 70 hours usually Virus excreted 5 to 7 days after the onset of symptoms in half of people although may last 13 days .CLINICAL FEATURES      DIARRHOEA VOMITING Commonly accompanied by fever. malaise.

can have a result in a few hours Not labour intensive Evaluation of kits must be carried out for sensitivity/specificity      Reverse Transcriptase Polymerase chain reaction (RT-PCR)  Used in outbreaks as large numbers can be processed efficiently  .Diagnosis(sample: stool) Electron Microscopy Labour intense Relatively insensitive Used in Sporadacic cases EIA Stool tested.

Treatment  Supportive therapy: rehydration. electrolyte replacement  Isolation of Hospitalised patient  Control Measures: Standard and Contact precautions  No Vaccine .

difficile and other viruses .Suspect an outbreak in hospital if  Projectile vomiting in >50% of cases  Duration of illness 12-60 hours  Incubation period 15-48 hours  Staff and patients ill  Stools negative for bacterial pathogens and C.

Control Measures in Hospital Outbreaks        Isolation or Cohort Contact Precautionsdisposable plastic apron/ gloves.1%) used to disinfect surfaces Cohort Staff Limit Movement Ward not reopened until 72 hours after last new case or after last vomiting/diarrhoea Terminal cleaning . Hand Hygiene Close Ward to Admissions Non-essential personnel excluded Avoid Transfers If Staff unwell not return to work until free from symptoms 48 hours Increase frequency of ward cleaning       Vomit/Faeces to be cleaned and disinfected promptly Hypochlorite(0.

The Future  Plasmidic DNA and Antigen Vaccines  Interrrupt Transmission  Supportive Therapy .

Sign up to vote on this title
UsefulNot useful