Enteroviral Diseases

Enteroviruses
• Picornaviridae family- lincked
taxonomically with rhinoviruses, also RNA
viruses
• Polioviruses
• Coxackieviruses
• Echoviruses (enteric cytopathic human
orphan)
• Enteroviruses type 68 to 71 which have
growth and host characteristics that
overlap with coxackieviruses and
echoviruses
– Entrovirus 72-HAV
 Biology and Epidemiology
of Enteroviruses
• Named so as they are primary
replicating in enteral mucosa where
from viremia originated, and end-
organ disease may develop
• They have been isolated from oral
secretions, stool, blood and CSF
 Poliomyelitis
• Acute infection caused be poliovirus,
producing non-specific minor illness,
aseptic meningitis(nonparalytic
poliomyelitis), and flaccid weakness of
various muscle groups(paralytic
poliomyelitis)
• Asymetric flaccid limb paralysis or
bulbar palsies without sensory loss
during an acute febrile illness in a child or
young adult indicates poliomyelitis
 Poliomyelitis –
epidemiology
• Humans are the only natural host
• Infection occurs through direct contact
and is highly contagious
• The ratio of inaparent infections to
clinical cases is > 100:1
• In sanitation poor countries the virus is
circulating extensivelly and there are no
epidemics, infection and immunity are
acguired early , in first few years of life,
and 90% of paralyitic cases occur in
children < 5 yr.
Poliomyelitis-pathology and
pathogenesis
• Virus enters the mouth, and primary
multiplication occurs in lyphoid tissue in the
oropharinx and GI tract(ileum)
• Someviruses reach the blood and are extensive
replication occures.
• carried to other sites in the RES, where
Secondary virmia is followed by CNS invasion.
• With symptomes onset viremia disappears while
antibodies have already develop; virus persits in
throat few weeks , and >3 to 6 weeks in feces
after symptom onset.
 Pathogenesis
• Significnt virlal pathology occures
only in spinal cord and brain
• Involving motor neurons of the
anterior horn of the spinal cord, the
medulla, and to lesser degree other
parts of the brain, including
cerebellum,and the motor cortex
 Pathogenesis
• Damage to the
neurons by the
virus, the primary
event,elicts an
intense
inflamatory
respons and
eventualy
neuropathology
 Symptoms and Signs
• Minor poliomyelitis
occurs in 80 to 90% of symptomatic
infections, chiefly in young children
CNS is not ivolved
Fever,malaise, sore throat, headache,
vomiting, which occure 3 to 5 days after
exposure
Recovery occurs in 24 to 72 h.
 Symptoms and Signs
• Major poliomyelitis
may have preceding minor illness
Incubation isusualy 7 to 14 days
Fever, severe headache, stiff neck and back,
deep muscle pain, and sometimes paresthesia
may occure.
During active myelitis, urinary retntion and
muscle spasm are common
Loss of certain tendon reflex and asymmetric
weakness orparalysis of muscle groups may
develop, depending on the location of lesions in
spinal cord or medulla
Respiratory failure...
 Diagnosis
• Asymetric flaccid limb paralysis...

• The causative virus can be identified by

laboratory tests like isolation of the virus from
the troat or feces,and demonstrtion of rise in
specific antibody titer.

• Ather enteroviruses,coxackie A7, and

enterovirus type 71 may cuse paralysis that can
not be clinically differentiated from parlytic
poliomyelitis
Hand, foot and mouth disease
• Hand, foot and mouth disease, usually
caused by Coxsackie A16 (occasionally
by A5 and A10) is characterized by small,
lax vesicles within an erythematous
margin on the hands and feet together
with vesicles within the oral cavity. It is
usually seen in children under 10 years
old and is accompanied by fever and sore
throat. Less commonly, there is an
associated maculopapular rash on the
buttocks and thighs.
 Herpangina
• An acute febrile illness caused by
numerous group A coxackieviruses, and
occasionally other entroviruses,
characterized by vesiculoulcerative
mucosal lessions.
• Herpangina tend to occur in epidmics in
ifants and children
• Diagnosis is based on symptoms,and
characteristic oral lessions
 Herpangina
• Sudden onset of fever, sore throat, headache,
anorexia, pain in the neck, abdomen, and
extremites.
• Vomiting and convulsions may occur in infants
• Within 2 days after onset few small grayish
papulovesiculr lessions with erythematous
areolae appera on the tonsillar pillars, on the
soft palate, uvula and tonsils.
• During 24h lessions become shallow ulcers, and
heal in 1 to 5 days.
• Diferential diagnosis:lymphonodular pharyngitis,
herpetic stomatitis
 Myocarditis and
Pericarditis
• Myocarditis neonatorum, and myocrditis and
pericrditis in dults and children may be due to
group A or B coxackievirus or an echovirus
• In older children and adults symptoms and signs
are usually localized to the myocardium or
pericardium, while in new borns CNS, hepatic,
pancreatic, adrenal lesions may be concomitant.
• Diagnosis is made by isolating the virus or
determing the antibody titer.
• PCR to detect viral DNA in biopsy specimens.
• Treatment is symptomatic and include bed rest
and control of hart failure and arrhytmias
 Epidemic plerodinia
• May occur at any age, but is most
common in children
• Sudden onset of pleuritic pain, fever, sore
throat, and malaise
• Local chest muscle tenderness, muscle
swelling, hyperestesia, and myalgias of
the trunk and extremities may occur.
• The disease usually subsides in 2 to 4
days, but it may relapse and symptoms
continue for several weeks
 Epidemic plerodinia
• Up to 5% of cases are complicated by aseptic
meningitis,or less common by fibrinous pleuritis
and peicarditis
• The diagnosis my be mistaken for spontaneous
pneumothorax, acute appendicitis pancreatitis,
MI
• Laboratory diagnosis consists of demonstrating
a rise in specific neutralizing antibody titers, or
isolating the virus on throat or stool culture
• Prognosis is good
• Symptomatic treatment
 Aseptic meningitis
• Onset of the meningeal syndome may bea abrupt
or preceded by prodromal fever, malaise,
anorexia and vomiting.
• Symptoms subsides by the end of first week
• CSF finding consists of normal or slightly
elevated protein level, a normal sugar level, and
cell count usually less then 500/mm3
• Neutrophils predominate initially, but
lymphocytes are more common in 1 to 2 days
• Encephalitis signs occsionlly develop and may
be severe
 Aseptic meningitis
• Acute meningitis due to entroviruses is
impossible to differentiate from other viral
meningitides
• Occasionaly a patient presents with CSF
hypoglicorrachia and neutrophil predominance,
suggesting bacterial meningitis.
• The diagnosis is made by isolating the virus from
the throat, stool specimens, or CSF
• Prognosis is generally good
• Patients with agammaglobulinemia may develop
chronic meningitis
 Rash
• Enteroviruses may cause
epidemic,occasionaly sporadic rash,
particularly in infants and children
• The rash is generally discrete, non-
pruritic,and nondesquamative
• Usually confind to the face, neck, and
chest
• Maculopapular or morbilliform,
occasionaly hemorrhagic, petechial or
vesicular
• Benign course
 Respiratory Disease
• In infants and children enteroviruses
may cause respiratory disease
characterized by fever, coryza,
pharyngitis, sometimes with
diarrhea and vomiting
• Bronchitis and interstitial
pneumonia have occasionally
occured in infants
• Treatment is symptomatic
 Gastroenteritis
• Enteroviruses are occasionally
isolated from the stool of newborns
with acute diarrhea and from
immunocompromisd patients with
protracted diarrhea, but their
caustive role is questionable