ENTEROVIRAL INFECTIONS
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ENTEROVIRAL INFECTIONSENTEROVIRAL INFECTIONS
Dr.B.Boyle
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ENTEROVIRAL INFECTIONSENTEROVIRAL INFECTIONSContents of LectureContents of Lecture
ENTEROVIRUSESAlso Discuss , Viruses that cause
GastroenteritisROTAVIRUSSMALL ROUND STRUCTURED
VIRUSES e.g Norwalk virus or Novovirus etc.
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ROTAVIRUSROTAVIRUS
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ROTAVIRUSROTAVIRUS
Description Epidemiology Pathogenesis Clinical Features Diagnosis Treatment The Future
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ROTAVIRUSROTAVIRUS
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
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Morphology-RotavirusesMorphology-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 RNAGenome encoded Structural
proteins VP1-7 and NSP 1-5, NSP4 has enterotoxinlike activity
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Epidemiology of RotavirusEpidemiology 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 routeFound on fomites in childcare
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Epidemiology of RotavirusEpidemiology 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
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Classfication-RotavirusClassfication-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
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Rotavirus-PathogensisRotavirus-Pathogensis
Mature Enterocytes(on tips of Small Intestine villi)
Infects
Villous Atrophy
Compensatory Repopulation by immature Secretor cells and secondary hyperplasia
Cell death because of villous ischaemia
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Mechanism of diarrhoea?Mechanism of diarrhoea?
Villous epithelium in relation To secretory capacity of
Crypt cells
Loss of permeability to Macromolecules e.g Lactose,
Due to loss of disaccharideases
Enteric nervous system stimulates InductionOf intestinal Water
And electrolyte secretion
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Rotavirus Damage to Small Rotavirus Damage to Small IntestineIntestine
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Immune Response to Immune Response to RotavirusRotavirus
Localised Immune response protects against severe subsequent infections
NSP4 protein results in cell mediated immunity
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Outcome of Infection with Outcome of Infection with VirusesViruses
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
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Clinical Presentation-Clinical Presentation-RotavirusRotavirus
Abrupt onset of vomiting followed within hours by watery, brown copious diarrhoea, often lasts 3-8 days
If Severe Dehydration and death or hospitalisation
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DIAGNOSISDIAGNOSIS
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 Pos and neg
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TREATMENTTREATMENT
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
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MANAGEMENTMANAGEMENT
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
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FAMILY: PICORNAVIRIDAEFAMILY: PICORNAVIRIDAE
ENTEROVIRUSESOver 72+
RHINOVIRUSType 1-100+
POLIO virus type 1,2,3COXSACKIE A virus type 1-22,24
COXSACKIE B virus type 1-6E.C.H.O virus type 1-7,11-27,29-34
Numbered ENTEROVIRUSES type 68-71,73
Since 1967-all new ones are numbered
CardiovirusAphthousvirusetc
E.C.H.O = enteric cytopathic human orphan
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CharacteristicsCharacteristics
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
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CharacteristicsCharacteristics
Rhinovirus labile to acidic p H
Genome of Enteroviruses is m RNA
Naked genome is sufficient for infection
Replication in cytoplasm Cytolytic viruses
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Clinical Manifestations of EV Clinical Manifestations of EV Infections(Mostly Children)Infections(Mostly Children)
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
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COXSACKIE VIRUSESCOXSACKIE VIRUSES
29+ immunogenic typesDivided into A and B on the basis of
different pathogenic potential for miceResult in a number of different clinical
presentations
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COXSACKIE VIRUSESCOXSACKIE VIRUSES
Herangina Summer minor
illness Aseptic meningitis Neonatal Disease Colds
Hand , Foot and mouth illness
Myocarditis ? Diabetes mellitus Epidemic myalgia
(Bornholm Disease)
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HAND/FOOT/MOUTHHAND/FOOT/MOUTH
Coxsackie Coxsackie A16A16
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H/F/MH/F/M
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ECHO VirusesECHO Viruses
General properties similar to other enteroviruses
30+ antigenic typesResults in: - 1. Aseptic meningitis 2. Rash 3.Conjunctivits 4. Upper Respiratory Tract
Infection
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ENTEROVIRUS 71ENTEROVIRUS 71
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ManagementManagement 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
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POLIO VIRUSPOLIO VIRUS
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PoliovirusesPolioviruses
are RNA , ENTEROVIRUSES
3 Serotypes 1, 2 ,3 Major cause of paralytic
poliomyelitis and now seeing post polio syndrome
Global Eradication Programme of WHO
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EPIDEMIOLOGYEPIDEMIOLOGY 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
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EPIDEMIOLOGYEPIDEMIOLOGY
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
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PRESENT VACCINE PRESENT VACCINE SCHEDULESCHEDULE
At birth- 1 month BCG Usually in maternity hospitals
*At 2 months Diphtheria
Whooping Cough
Tetanus
Hib
Inactivated Polio
+
Meningococcal C
5-in-1(G.P)
*At 4 months Diphtheria
Whooping Cough
Tetanus
Hib
Inactivated Polio
+
Meningococcal C
5-in-1(G.P)
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PRESENT SCHEDULEPRESENT SCHEDULE
*At 6 months Diphtheria
Whooping Cough
Tetanus
Hib
Inactivated Polio
+
Meningococcal C
5-in-1(G.P)
*At 12- 15 months Measles
Mumps
Rubella,
Hib1
MMR
Hib1
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PRESENT SCHEDULEPRESENT SCHEDULE
**4-5 YEARS Diphtheria
Whooping Cough
Tetanus
Inactivated Polio
+
Measles
Mumps
Rubella
4-in-1
MMR
**11-12 YEARS Measles
Mumps
Rubella MMR
Omit if 2 previous doses have been given
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PRESENT SCHEDULEPRESENT SCHEDULE
**11-14 years Tetanus
Diphtheria (low dose)Td
**10-14 years if not protected(immune)
Under 23 years(Colleges etc)
BCG2
(AN INTERVAL OF 4 WEEKS AFTER MMR)
Meningococcal C
•From Family Doctor1: A single dose of Hib vaccine if child presents after 13 months and has no previous Hib vaccine2: Only those known to be tuberculin negative and have no previous BCG**These immunizations are generally administered in schools by Health Boards
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Clinical Presentations of Clinical Presentations of Poliovirus Infection 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
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PoliomyelitisPoliomyelitis
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PoliomyelitisPoliomyelitis
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Pathogenesis of Enteroviral Pathogenesis of Enteroviral InfectionInfection
Virus Replicates in Nasopharnyx
Binds Enterocytes Receptor coded by Ch 19
Evades
Acidic PH
Endocytosed , replication inPeyer`s patches
Minor Viraemia,Replication in organs
Major Viraemia+ Trophism+ Virulence
Skeletal MuscleNeuromuscular
Endplate
Ascends alongMotor Nerves
Anterior MotorNeuron horn
cellsTo CNS*
*Spinal, Bulbar, Medullary Red=specifc for polio
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CommunciabilityCommunciability
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.
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Surveillance Surveillance
For Acute flaccid paralysisSince September 1998Two 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
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DiagnosisDiagnosis
Clinical Presentation Laboratory
Diagnosis Faecal, Throat (2 or
more samples), CSF(Culture and RT-PCR)
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TREATMENT/PREVENTIONTREATMENT/PREVENTION
Supportive Prevention is by Vaccination.Global Eradiation ProgrammePart of Routine immunisation schedule
and travellers to endemic areas should be vaccinated
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Global Eradication programmeGlobal Eradication programme
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SLV-NLV-Novovirus-SLV-NLV-Novovirus-CalcivirusesCalciviruses
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
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EpidemiologyEpidemiology
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
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Pathogenesis of DiseasePathogenesis 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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EPIDEMIOLOGYEPIDEMIOLOGY Sporadic cases however
causes epidemic outbreaks Examples: on cruise ships,
hotels, 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
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CLINICAL FEATURESCLINICAL FEATURES
DIARRHOEA VOMITING Commonly accompanied
by fever, malaise, 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
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Diagnosis(sample: stool)Diagnosis(sample: stool)
Electron Microscopy Labour intense Relatively insensitive Used in Sporadacic cases EIAStool tested, can have a
result in a few hoursNot labour intensiveEvaluation 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
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TreatmentTreatment
Supportive therapy: rehydration, electrolyte replacement
Isolation of Hospitalised patientControl Measures: Standard and
Contact precautionsNo Vaccine
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Suspect an outbreak in hospital Suspect an outbreak in hospital ifif
Projectile vomiting in >50% of casesDuration of illness 12-60 hoursIncubation period 15-48 hoursStaff and patients illStools negative for bacterial pathogens and C.difficile and other viruses
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Control Measures in Control Measures in Hospital OutbreaksHospital Outbreaks
Isolation or Cohort Contact Precautions-
disposable plastic apron/ gloves, 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(0.1%) 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
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The FutureThe Future
Plasmidic DNA and Antigen VaccinesInterrrupt TransmissionSupportive Therapy