Enteroviruses: Presented By: Andrea Dora J. Ortaliz MD-2

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ENTEROVIRUSES

Presented By:
Andrea Dora J. Ortaliz
MD-2
TERMS
 Bornholm disease: Contagious viral infection  Paralysis: The loss of motor function due to
 Cold-like symptoms: Symptoms similar to dysfunction of the spinal cord
the common cold.  Polio: Dangerous virus now rare due to
 Digestive Diseases: Diseases that affect the vaccination.
digestive system  Respiratory symptoms: Symptoms affecting
 Dilated cardiomyopathy: A rare chronic the breathing systems.
heart muscle condition where one or both  Paralysis: The loss of motor function due to
heart ventricles are dilated or have impaired dysfunction of the spinal cord
contractility.  Sudden Digestive Conditions: Various forms
 Encephalitis: Dangerous infection of the of sudden acute digestive upset.
brain  Vague symptoms: Vague, unclear, mild or
 Fever: Elevation of the body temperature non-specific symptoms
above the normal 37 degrees celsius  Viral diseases: Any disease that is caused by
 Flu-like symptoms: Symptoms similar to flu a virus
including fever  Viral gastroenteritis: Virus causing
 Myocarditis: Inflammation of the gastroenteritis of digestive tract.
myocardium (muscle walls of the heart)  Viral meningitis: Viral meningitis refers to
meningitis caused by a viral infection
INTRODUCTION
 Picornaviruses represent a very large virus family with respect to the number of
members but one of the smallest in terms of virion size and genetic complexity.
They include two major groups of human pathogens: enteroviruses and
rhinoviruses. Enteroviruses are transients of the human alimentary tract and may
be isolated from the throat or lower intestine.

 Many picornaviruses cause diseases in humans. Etiology is difficult to establish,


as different viruses may produce the same syndrome; as the same picornaviruses
may cause more than a single syndrome; and some clinical symptoms cannot be
distinguished from those caused by other types of viruses. The most serious
disease caused by any enterovirus is poliomyelitis.
INTRODUCTION
 Enteroviruses are a genus of the  At least 72 serotypes are known: divided
picornavirus family which replicate into 5 groups
mainly in the gut.
 Single stranded naked RNA virus with  Polioviruses
icosahedral symmetry  Coxsackie A viruses
 Unlike rhinoviruses, they are stable in
acid pH  Coxsackie B viruses
 Capsid has 60 copies each of 4 proteins,  Echoviruses
VP1, VP2, VP3 and VP4 arranged with
icosahedral symmetry around a positive  Enteroviruses (more recently, new
sense genome. enteroviruses subtype have been
allocated sequential numbers (68-
71))
INTRODUCTION
 Three serotypes comprise the polioviruses
 23 serotypes comprise coxsackievirus
group A
 6 serotypes comprise coxsackievirus group
B
 29 serotypes comprise the echoviruses.
ENTEROVIRUSES

Enterovirus Polio  Diseases of the human


Coxsackie A and B (and other) alimentary
Echo tract (e.g. polio virus)
Other enteroviruses
ENTEROVIRUSES
VIRUS FAMILY SEROTYPES

Polio 1-3

Coxsackie A 1-22, 24

Coxsackie B 1-6

Echovirus 1-9, 11-21, 25-26, 27, 29-33

Enteroviruses 68-71
Epidemiology
 Distributed worldwide
 Are influenced by season and climate
 Infections occur in summer and early fall in temperate
areas, while tropical and semitropical areas bear the
brunt all year.
 AHC occurs as epidemics in tropical countries during the
hot and rainy season.
 The worldwide prevalence of poliomyelitis has decreased
significantly because of improved economic conditions
and availability of vaccines
EPIDEMIOLOGY
 In 2008, 1,652 confirmed cases of paralytic polio were
reported worldwide. Polio is endemic in 4 countries:
Afghanistan, India, Nigeria, and Pakistan.

 3 epidemiologic phases of Poliomyelitis:


 Endemic
 Epidemic
 Vaccine era
 Occurs in all age group but children are more
susceptible  (“infantile paralysis”)
Epidemiology
 Direct correlation between poor hygiene, poor
sanitation, and overcrowded living condition  to the
acquisition of infection and antibodies at an early age

 MORTALITY/MORBIDITY
 >90% of infections caused by the nonpolio enteroviruses
---- asymptomatic or result in only an undifferentiated
febrile illness
 Myopericarditis carries a mortality rate of 0%-4%.
EPIDEMIOLOGY
 Prior to the vaccine era, the mortality rate in polio
epidemics was 5%-7%.

SEX
 The male-to-female ratio of myopericarditis is 2:1. The
risk of cardiac involvement is higher during pregnancy
and immediately postpartum.
 The prevalence of polio infection is equal in boys and
girls, although paralysis is more common in boys.
Among adults, women are at increased risk of infection
and the postpolio syndrome
Epidemiology
 Aseptic meningitis is approximately twice as common in
males as in females.

AGE
 Enteroviral infections are most common in young
children.
 Herpangina primarily affects children aged 3 months to
16 years.
 Poliomyelitis is observed in children younger than 15
years.
Epidemiology
 Aseptic meningitis due to enteroviral infection is more
common in infants than in adults. Most cases of
pleurodynia occur in children and adults younger than
30 years.
 Myopericarditis is most prevalent in young adults,
especially those who are physically active. AHC is most
prevalent in adults aged 20-50 years.
 Neonates are at high risk for severe sepsis due to
enterovirus infections
INCIDENCE (ANNUAL) OF
ENTEROVIRUSES
 estimated 10-15 million cases East Timor 37,472 1,019,252²
annually in USA
Indonesia 8,766,652 238,452,952²
Extrapolation of Incidence Rate for
Enteroviruses to Countries and Laos 223,092 6,068,117²
Regions
Enteroviruses in Southeastern Asia Malaysia 864,797 23,522,482²
(Extrapolated Statistics)
Philippines 3,170,650 86,241,697²

Singapore 160,069 4,353,893²

Thailand 2,384,761 64,865,523²

Vietnam 3,039,073 82,662,800²


About prevalence and incidence
statistics in general for Enteroviruses:
 ‘prevalence’ of Enteroviruses usually means the
estimated population of people who are managing
Enteroviruses at any given time (i.e. people with
Enteroviruses).

 ‘incidence’ of Enteroviruses means the annual diagnosis


rate, or the number of new cases of Enteroviruses
diagnosed each year (i.e. getting Enteroviruses).
INCIDENCE RATE/PREVALENCE
 Incidence Rate of Enteroviruses: approx 1 in 27 or
3.68% or 10 million people in USA.
 
 Prevalance of Enteroviruses: Non-polio enteroviruses
are second only to the "common cold" viruses, the
rhinoviruses, as the most common viral infectious
agents in humans. The enteroviruses cause an
estimated 10-15 million or more symptomatic infections
a year in the United States.
Paralytic poliomyelitis
3 types (1-3) Aseptic meningitis
Poliovirus Febrile illness
Aseptic meningitis
23 types (A1-22, A24) Herpangina
Coxsackie group A Febrile illness
Conjunctivitis
Hand, foot and mouth disease
Aseptic meningitis
6 types (B1-6) Severe neonatal disease
Coxsackie group B Myopericarditis
Bornholm disease
Encephalitis
Febrile illness

Echovirus Aseptic meningitis


31 types (1-9, 11-27) Ras
Febrile illness
Conjunctivitis
Severe generalized neonatal disease

Enterovirus Polio-like illness


4 types (68-71) Aseptic meningitis
Hand, foot and mouth (E71)
Epidemic conjunctivitis (E70)
INFECTIOUS DISEASE
PROCESS
 POLIOMYELITIS  COXSACKIE GROUP A
AGENT: poliovirus AGENT: coxsackievirus A
RESERVOIR: Human RESERVOIR: Human
PORTAL OF ENTRY/EXIT: Fecal- PORTAL OF ENTRY/EXIT: Fecal-oral
oral INCUBATION PERIOD: 2-9/2-10
INCUBATION PERIOD: 7-14days; days
may range from 3-35 days MODE OF TRANSMISSION: Fecal-
MODE OF TRANSMISSION: Fecal- oral; person-to-person direct
oral; person-to-person direct contact, droplet/respiratory
contact, droplet/respiratory secretions, contaminated objects
secretions, contaminated objects SUSCEPTIBLE HOST: Children 3-10
SUSCEPTIBLE HOST: infants; years old
younger children
INFECTIOUS DISEASE
PROCESS
 COXSACKIE GROUP B  ECHOVIRUS (ENTERIC
AGENT: coxsackievirus B CYTOPATHIC HUMAN ORPHAN
VIRUSES)
RESERVOIR: Human  Nonpolio enterovirus infection
PORTAL OF ENTRY/EXIT: Fecal-oral AGENT: echovirus
INCUBATION PERIOD: 2-9/2-10 RESERVOIR: Human
days PORTAL OF ENTRY/EXIT: Fecal-oral
MODE OF TRANSMISSION: Fecal- INCUBATION PERIOD: 2-7 days
oral; person-to-person direct MODE OF TRANSMISSION: Fecal-oral;
contact, droplet/respiratory (airborne) air to other hosts 1–3 weeks
secretions, contaminated objects after infection and can spread through
SUSCEPTIBLE HOST: below 1-year- feces to other hosts eight weeks after
old; older children infection
SUSCEPTIBLE HOST: Infants; young
children
INFECTIOUS DISEASE
PROCESS

Everyone is at risk. Infants, children, and


adolescents are more likely to be
susceptibleto infection and illness from
these viruses, but adults can also
become infected and ill if they do not
have immunity to a specific enterovirus.
Syndrome Polio Cox A Cox B Echo

Paralytic disease + + + +

Meningitis- + + + +
encephalitis
Carditis + + + +

Neonatal disease - - + +

Pleurodynia - - + -

Herpangina - + - -
Syndrome Polio Cox A Cox B Echo

Rash disease - + + +

Respiratory + + + +
Infections

Undifferentiated + + + +
fever

Diabetes/ - - + -
pancreatitis

Disease in + + - +
immunocomp.
CLINICAL
FINDINGS/MANIFESTATIONS
 Most patients infected with an enterovirus

 remain asymptomatic but in small children benign fevers


caused by unidentified enteroviruses are relatively common
(non-specific febrile illness).
 Many outbreaks of febrile illness accompanied by rashes are
also caused by enteroviruses.
 
CLINICAL
FINDINGS/MANIFESTATIONS
 Poliomyelitis  Approximately 95% of these
are subclinical infections, which
Alternate Names : Infantile may go unnoticed.
Paralysis, Polio
 Clinical poliomyelitis affects the
central nervous system (brain
 Three basic patterns of and spinal cord) and is divided
polio infection: into nonparalytic and paralytic
forms. It may occur after
 subclinical infections recovery from a subclinical
infection.
 Nonparalytic
 Paralytic
CLINICAL
FINDINGS/MANIFESTATIONS
 Clinical poliomyelitis affects the  possible outcomes following
central nervous system (brain poliovirus infection:
and spinal cord);  Subclinical infection (90 - 95%) -
inapparent subclinical infection
account for the vast majority of
 DIVIDED into : poliovirus infections.
 no symptoms, or symptoms
 nonparalytic lasting 72 hours or less
 paralytic forms  slight fever
 It may occur after recovery from a  headache
subclinical infection.
 general discomfort or uneasiness
(malaise)
 sore throat
 red throat
 vomiting
CLINICAL
FINDINGS/MANIFESTATIONS
 Poliomyelitis
 Abortive infection (4 - 8%)  may be accompanied by
aseptic meningitis - similar
 influenza-like symptoms to the meningitis caused
such as fever, malaise, by other enteroviruses
drowsiness, headache,
nausea, vomiting,  resolve without sequelae
constipation and sore within 2 - 10 days.
throat  may be accompanied by
 Recovery within few days aseptic meningitis - similar
and the diagnosis can only to the meningitis caused
be made by the laboratory by other enteroviruses
 may be accompanied by  resolve without sequelae
aseptic meningitis - similar within 2 - 10 days.
to the meningitis caused
by other enteroviruses
CLINICAL
FINDINGS/MANIFESTATIONS
 Major illness
(POLIOMYELITIS)  Painful muscle spasms and
 (1 - 2%) - may present 2 - incoordination of non-
3 days following the minor paralysed muscles may
illness occur
 without evidence of any  Involvement of the
preceding minor illness medulla may lead to
respiratory paralysis and
 Signs of aseptic meningitis death
are common  The paralysis usually
 Involvement of the develops over several days
anterior horn cells lead to and some recovery may
flaccid paralysis take place
 Painful muscle spasms and  Any effects persisting for
incoordination of non- more than 6 months are
paralysed muscles may usually permanent.
occur
CLINICAL
FINDINGS/MANIFESTATIONS
 Major illness  moderate fever
 Nonparalytic  headache
Poliomyelitis (Aseptic  stiff neck
Meningitis)  vomiting
 Stiffness and pain in the  diarrhea
back and neck  excessive tiredness, fatigue
 Lasts 2 – 10 days 
recovery is rapid and
complete
 May advance to
paralysis
 symptoms last 1 to 2 weeks
CLINICAL
FINDINGS/MANIFESTATIONS
 Major illness
 Nonparalytic Poliomyelitis (Aseptic Meningitis)
 irritability
 pain or stiffness of the back, arms, legs, abdomen
 muscle tenderness and spasm in any area of the body
 neck pain
 pain front part of neck
 neck stiffness
 back pain or backache
 leg pain (calf muscles)
 skin rash or lesion with pain
 muscle stiffness
CLINICAL
FINDINGS/MANIFESTATIONS
 Paralytic
Poliomyelitis  Maximal recovery within 9 months 
 Predominating residual paralysis last much longer
complaint is flaccid  fever, occurring 5 to 7 days before
paralysis  LMN other symptoms
damage  headache
 Incoordination  stiff neck and back
secondary to brainstem
invasion and painful
 muscle weakness, asymmetrical
spasms of nonparalyzed  rapid onset
muscles  progresses to paralysis
 Maximal recovery  location depends on where the spinal
within 9 months  cord is affected
residual paralysis last
much longer
CLINICAL
FINDINGS/MANIFESTATIONS
Paralytic Poliomyelitis
 muscle pain
 abnormal sensations (but not
loss of sensation) of an area  muscle contractions or
 sensitivity to touch, mild touch muscle spasms, particularly in the
may be painful calf, neck, or back
 difficulty beginning to urinate  drooling
 constipation  breathing difficulty
 bloated feeling of abdomen  irritability or poor temper control
 swallowing difficulty
 positive Babinski's reflex
CLINICAL
FINDINGS/MANIFESTATIONS
 Progressive
Postpoliomyelitis
Muscle Atrophy

Specific syndrome
Recrudescence of
paralysis and muscle
wasting
Not a consequence but a
result of physiologic and
aging changes
burdened by loss of
neuromuscular functions
CLINICAL
FINDINGS/MANIFESTATIONS
 Coxsackieviruses
 Aseptic meningitis
 Caused by Cox A and B
 Fever, malaise, headache, nausea and abdominal pain  early
symptoms
 May progress to mild paresis  recover completely
 Herpangina
 Severe febrile pharyngitis
 Cox A (2 – 6, 8, 10)
 Abrupt onset of fever and sore throat
 Pharynx is hyperemic with vesicles on the posterior half of the
pharynx, tonsils or tongue
CLINICAL
FINDINGS/MANIFESTATIONS
 Hand-foot-and-mouth  Virus may be recovered in
the blister fluid, stool and
disease pharyngeal swab.
(Coxsackievirus)  Must not be confused with
 Oral and pharyngeal foot-and-mouth disease of
ulcerations the cattle  unrelated
 Vesicular rash of the palms  Pleurodynia
and soles  may spread to
arms and legs
 Bornholm disease (Epidemic
myalgia)
 Vesicles heal without
crusting
 Cox B
 Particularly associated with  Sudden onset of fever,
Cox A16, A 5 and A10 myalgia, HA, anorexia
and stabbing chest pain
Enteroviruses. This is the skin of a young boy after 3 days of an
echovirus type 9 infection; treated at New York
Presbyterian Hospital.
CLINICAL
FINDINGS/MANIFESTATIONS
 Pleurodynia
 Chest pain maybe on either
side or substernal,  May cause permanent heart
intensified by movement and damage
lasts for 2 to 14 days  Persistent viral infections of
 Abdominal pain – children the heart muscle may occur
 Self-limited with complete  sustaining chronic
recovery; relapses are infection
common  May trigger host
 Myocarditis autoimmune response
responses that lead to
 Severe / serious / fatal  cardiomyopathies
adults and children
 Cox B
CLINICAL
FINDINGS/MANIFESTATIONS
 Acute Hemorrhagic  neurological complications may
occur  polio-like paralytic
conjunctivitis illness
 coxsackie A24 B2 (Echo 7 and  neurological involvement may
11, and enterovirus 70) develop 2 or more weeks after
 isolated from the conjunctiva the onset of conjunctivitis
in sporadic cases
 majority of the epidemics are
due to enterovirus 70
 OTHERS
 generally localized to the eye
and there is characteristic  Respiratory infection 
subconjunctival hemorrhage,
either petechial or larger common colds
"blotches", and transient  Cox A21, A24, B1 and B3
keratitis -5
 Gastrointestinal
symptoms  diarrhea
CLINICAL
FINDINGS/MANIFESTATIONS
 Neonatal Infection/
Generalized disease of  May be transmitted during the
birth process or in postnatally
infants via the mother or other virus-
 coxsackie B and echoviruses infected infants in the hospital
 severe and often fatal infection  may develop illness at 3 - 7
in newborn infants. days of age which may range
 Simultaneous viral infections from a mild febrile illness to a
 multiple organ infection severe fulminating
 may be transmitted multisystem disease and death
transplacentally in late  virus can be recovered from
pregnancy, with the infant the feces, brain, spinal cord
developing heart failure and myocardium
following delivery from a
severe myocarditis, hepatitis,
pneumonia or a
meningoencephalitis
CLINICAL
FINDINGS/MANIFESTATIONS
 Diabetes and  Postviral Fatigue
pancreatitis Syndrome
 Aka. myalgic
encehalomyelitis (ME)
 occurs as both sporadic
 Coxsackie B particularly and epidemic cases
B4  poorly characterized
 juvenile onset IDDM illness  cardinal feature
being excess fatigability of
 30% of children with the skeletal muscles,
IDDM have IgM muscle pain, headache,
antibodies to coxsackie B inability to concentrate,
viruses compared to 5 - paresthesiae, impairment
8% for matched controls of short term memory and
poor visual
accommodation
CLINICAL
FINDINGS/MANIFESTATIONS
Postviral Fatigue  ECHOVIRUS
Syndrome  (ENTERIC CYTOPATHIC
 focal neurological signs HUMAN ORPHAN VIRUSES)
are rare
 nonspecific viral illness  ECHO viruses cause a wide
and some variety of conditions. Symptoms
lymphadenopathy may be depend on the type of disease:
present
 Routine laboratory
 Aseptic meningitis
investigations are usually  Croup
normal
 Recovery usually takes
 Encephalitis
place within a few weeks  Mouth sores (herpangina)
or months but the illness  Myocarditis
may persists in some
patients with periods of
 Pericarditis
remission and relapse.
CLINICAL
FINDINGS/MANIFESTATIONS
 ECHOVIRUS
 Pneumonia
 Skin rashes
 Upper respiratory infection
 Viral pharyngitis
DIAGNOSIS/DIAGNOSTIC TESTS
 Laboratory Diagnosis (Enteroviruses):
 Virus/Viral Isolation
 Viral cultures – throat washing, stool, or CSF
 Throat swabs after onset of illness/Throat culture
 Rectal swabs of stool samples
 Rectal culture
 PCR/RT-PCR Assays
 CSF Analysis/Spinal fluid culture
 Microneatralization Test
 Serology
DIAGNOSIS/DIAGNOSTIC TESTS
 Imaging Studies  Diagnosis/Diagnostics Tests
(Enteroviruses):  Differential Diagnosis
 Adenoviruses
 Chest radiography
 MyocardialInfarction
 Botulism
 Echocardiography  Pharyngitis,
 BacterialEhrlichiosisPharyngitis,
 Other Tests  ViralHand-Foot-and-MouthDisease
(Enteroviruses):  Pleurodynia
 Herpangina
 ECG  Rocky Mountain
 Electroencephalography
 SpottedFever
 Herpes Simplex
 Ophthalmic slit-lamp examination  VaricellaZoster Virus
 Lyme Disease
TREATMENT
 Polio management is supportive  Medications, such as
in nature. bethanechol, may reduce urinary
 The goal of treatment is to control retention. Analgesics are used to
symptoms while the infection runs reduce headache, muscle pain,
its course. and spasms. Narcotics are not
 Lifesaving measures, particularly usually given because they
assistance with breathing, may be increase the risk of
necessary in severe cases. breathing difficulty.
 Symptoms are treated according
 Moist heat (heating pads, warm
to their presence and severity. towels, etc.) may reduce muscle
pain and spasm.
Antibiotics may be used to treat
urinary tract infections.  Physical therapy, braces or
corrective shoes, orthopedic
surgery, or similar interventions
may eventually be necessary to
maximize recovery of muscle
strength and function.
TREATMENT
 Abortive polio: Treatment with bed rest  Align the body in a neutral position to
and minimal exertion may be done at minimize deformity. Patients should
home. Supportive treatment with start physical therapy soon after the
analgesics and sedatives may be resolution of pain. Physical therapy
used. should include both active and
 Nonparalytic polio: Management is passive exercises.
similar to that of abortive polio.  Mechanical ventilation may be
Combine analgesic therapy with hot required if respiratory muscles are
packs for pain relief. affected.
 Paralytic polio: In contrast to abortive  Postural drainage and suction should
and nonparalytic polio, which can be be implemented in mild bulbar polio.
managed at home, patients with  Patients with weakness or paralysis of
paralytic polio require hospitalization. the bladder may be treated with
 Bed rest is required during the early cholinergic agents, the sound of
stages of the disease because running water, or catheterization.
exertion may worsen the paralysis.
 Applying hot packs to affected
muscles may alleviate pain.
TREATMENT
 Pleurodynia: Treatment is symptomatic,
using analgesics and heat application for  Bed rest is important since exercise
pain relief. Severe pain may require opiate can increase the degree of
analgesics. myocardial necrosis.
 Aseptic meningitis: Treatment is  Intravenous immunoglobulin (IVIG)
symptomatic, with analgesics for therapy has shown some benefit in
headache relief. Headache is often severe small case-control studies.
and prolonged in adults; potent analgesics Nevertheless, most reports lack
should be administered, when necessary. statistical significance, and
randomized trials are needed.53,54
 Myopericarditis  Capsid-binding inhibitors belong to
 Treatment is mainly supportive in a class of drugs that have shown
nature and involves management of benefit in some immunosuppressed
pericardial pain, pericardial effusion, patients with myocarditis. However,
arrhythmias, and heart failure. these drugs are not available for
use in the United States.
 Corticosteroids
TREATMENT
 Herpangina and hand-foot-
 Acute hemorrhagic and-mouth disease
conjunctivitis  Symptomatic treatment for sore
throat is the mainstay of treatment,
 Treatment is primarily including analgesics, topical
symptomatic in nature. anesthetics, mouth wash, and saline
 Antimicrobial agents are not rinses.
indicated unless bacterial  Viscous lidocaine (2% solution) may
superinfection occurs. be helpful.
Corticosteroids are  ECHO virus infections tend to
contraindicated. clear up on their own. No specific
 Cold compresses may be used, antiviral medications are
along with available.
antihistamine/decongestant eye  An immune booster called IVIG
drops may help patients with severe
ECHO virus infections who have
a compromised immune system.
TREATMENT
 Surgical Care  Consultation with a cardiovascular
surgeon may be required for the
management of complicated pericardial
 Cardiac transplantation may be required in effusions and in some cases for cardiac
severe cases of dilated cardiomyopathy transplantation.
due to enteroviral infection.  Consultation with an ophthalmologist is
appropriate for AHC.
 Consultation with a neurologist is
 Consultations recommended in cases of paralytic polio.
 Consultation with a physiatrist is helpful  Physical and occupational therapists help
to plan specific exercise programs, to patients with polio to establish a safe
direct physical therapy, and to provide exercise program, to adapt the home
adaptive equipment for patients with environment, and to use mechanical aids
paralytic polio. (eg, grab bars).
 Consultation with a cardiologist may be  Consultation with an infectious disease
requested in myopericarditis for specialist may be useful in cases of
management of arrhythmias. unexplained aseptic meningitis or
myopericarditis.
TREATMENT
 Diet  Activity
 Patients with paralytic polio should be  Bed rest is required for patients in the
encouraged to maintain a high fluid early stages of paralytic polio. Physical
intake. therapy should begin as soon as possible
 The application of hot packs leads to after the resolution of pain. Isometric
sweating, meaning that fluids need to exercises for select muscle groups can
be replenished. help increase muscle strength. Muscle
 High fluid intake protects against capacity can also be increased with
bracing and orthotics.
nephrocalcinosis and urinary tract
infections due to prolonged
immobilization.  Medications
 A diet rich in L-carnitine is under
 Management is supportive and addresses
research as a treatment for postpolio symptoms. No antiviral medications are
syndrome. currently approved for the treatment of
 Patients with herpangina should
enterovirus infections.
consume soft bland foods and fluids
and avoid pain-inducing salty foods
and citrus fruits.
TREATMENT
 Medications  Latest Treatments for
 Management is supportive and addresses Enteroviruses
symptoms. No antiviral medications are
currently approved for the treatment of
enterovirus infections.  Naloxone
 Inpatient & Outpatient  Thiamine
Medications  Glucose
 Pleconaril  Mannitol
 Immunoglobulins – used therapeutically
and prophylactically for enteroviral CNS
 Dilantin
infections in neonates and  Phenobarbital
immunocompromised hosts. Pre-exposure  Steroids
prophylaxis with immunoglobulins –
known to reduce the risk of paralysis in  Acyclovir
patients with poliovirus infections.  Ganciclovir
 Diazepam
Control and Prevention Strategies
 Hygienic measures such as adequate
disposal of infected secretions and waste  Poliovirus will replicate readily in cell
disposal help prevent the spread of cultures derived from non-nervous tissue
enteroviral infections.
 Viremia is essential for the pathogenesis
of paralytic poliomyelitis so that serum
 POLIOMYELITIS: antibodies MUST interrupt the viremia
 Prevention
 No specific treatment except supportive  2 vaccines available:
measures in paralytic poliomyelitis
 it is possible to prevent the disease 1) inactivated Salk vaccine
through active immunization 2) attenuated Sabin vaccine.
 3 major discoveries responsible for the
development of successful vaccines:
 Protection is required against all 3 types
of poliovirus.
Control and Prevention Strategies
 Inactivated Salk Vaccine  Live Attenuated Vaccine (Sabine
 formalin inactivated intramuscular polio vaccine)
vaccine (IPV) - high potency and purity  live attenuated oral polio vaccine (OPV)
 safe and effective  advantages over IPV
 does not induce local IgA mediated  induces long lasting immunity – similar to
immunity to polioviruses in the gut natural infection
 induces IgA formation - local immunity
 had been shown to confer herd immunity against reinfection in the pharynx and gut
against poliovirus  not seen in IPV
 reduce pharyngeal, and fecal shedding of  regarded as the crucial argument in favor
of OPV
the virus in vaccinated individuals who  mucosal immunity is not life-long and
have been infected by poliovirus in the gut reinfection is possible within a few months
although excretion is short-lived
 Recent small outbreak - type 3 strain  greater herd immunity based on 2 factors;
(1) stimulation of mucosal immunity and
resultant curtailment of spread of wild
virus (2) displacement of wild virus in the
community by vaccine related strains.
 inexpensive mass immunization without
the need for expensive sterile equipment
Control and Prevention Strategies
 1988 WHO established the year
2000 for achieving global  2005:Stop poliovirus
poliomyelitis eradication transmission
 1994, the Americas were certified as
polio-free
 2006:End supplementary
 All other regions are making steady vaccination
progress towards the goal of global  2007:Complete laboratory
eradication, which is now scheduled containment
for  2008:Certify global eradication
 2008  reversal to neurovirulence by
the strains of virus used in OPV
 2009 onwards:Long term
immunization policy
 response rate to OPV may be poor in
developing countries with a warm
climate
Control and Prevention Strategies
 The spread of AHC is The Universal Standard
prevented by hand washing and Precaution and
using separate towels.
preventive measure…
 Patient Education
 HFMD is very contagious,
especially during the first week
HANDWASHING
of the illness. The virus can still
be spread weeks after symptoms
have resolved. As a preventive Is the best !!!
measure, close contact with
affected individuals should be
avoided
JOURNAL

Fatal Case of Enterovirus 71 Infection, France,


2007

Abstract
A fatal case of enterovirus 71 infection with pulmonary edema and rhombencephalitis occurred in Brest, France, in April
2007. The virus was identified as subgenogroup C2. This highly neurotropic enterovirus merits specific surveillance outside
the Asia-Pacific region.

EID Journal Home > Volume 15, Number 11–November 2009


Volume 15, Number 11–November 2009

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