Picornavirus

R.Varidianto Yudo T., dr.,MKes.

Lab. Mikrobiologi
Fakultas Kedokteran Universitas Hang Tuah
 TAXONOMY
Family: Picornaviridae
Enterovirus
Rhinovirus
Hepatovirus
Cardiovirus
Aphthovirus
Parechovirus
Erbovirus
Kobuvirus
Teschovirus
 CHARACTERISTIC
Virion: Icosahedral, 2830 nm in diameter,
contains 60 subunits
Composition: RNA (30%), protein (70%)
Genome: Single-stranded RNA, linear,
positive-sense, 7.28.4 kb in size, MW 2.5
million, infectious, contains genome-linked
protein (VPg)
Proteins: Four major polypeptides cleaved from a
large precursor polyprotein. Surface proteins
VP1 and VP3 are major antibody-binding
sites. Internal protein VP4 is associated with
viral RNA.
Envelope: None
Replication: Cytoplasm
Outstanding characteristics:Family is made up of
many enterovirus and rhinovirus types that
infect humans and lower animals, causing
various illnesses ranging from poliomyelitis to
aseptic meningitis to the common cold.
Polioviruses are 2430 nm in
size and cause poliomyelitis.
DISEASE
INFECTION CYCLE
 POLIOVIRUS
Limited to primates
Transmitted by Fecal-Oral route
Preferentially replicates in the motor
neuron located in the anterior horn of
spinal cord
Can prevented by both Killed vaccine
(Salk) and live attenuated vaccine (Sabin)
ABORTIVE POLIOMYELITIS
This is the most common form of the
disease.
The patient has only the minor illness,
characterized by fever, malaise, drowsiness,
headache, nausea, vomiting, constipation,
and sore throat in various combinations.
Recovery occurs in a few days.
NONPARALYTIC POLIOMYELITIS
(ASEPTIC MENINGITIS)
Stiffness and pain in the back and neck.
The disease lasts 210 days, and recovery is
rapid and complete.
In a small percentage of cases, the disease
advances to paralysis.
Poliovirus is only one of many viruses that
produce aseptic meningitis.
PARALYTIC POLIOMYELITIS
The predominating complaint is flaccid
paralysis resulting from lower motor neuron
damage.
Incoordination and life-threatening
respiratory paralysis secondary to brain
stem invasion.
The amount of damage varies greatly.
Maximal recovery usually occurs within 6
months, with residual paralysis lasting much
longer.
PROGRESSIVE POSTPOLIOMYELITIS
MUSCLE ATROPHY
Muscle wasting has been observed in
individuals decades after their experience with
paralytic poliomyelitis.
It is rare.
It does not appear to be a consequence of
persistent infection but rather a result of
physiologic and aging changes in paralytic
patients already burdened by loss of
neuromuscular functions.
Laboratory Diagnosis
The virus may be recovered from throat
swabs taken soon after onset of illness and
from rectal swabs or stool samples collected
over long periods.
No permanent carriers are known.
Poliovirus is uncommonly recovered from the
cerebrospinal fluidunlike some
coxsackieviruses and echoviruses.
 Specimens should be kept frozen during
transit to the laboratory.
Cultures of human or monkey cells are
inoculated, incubated, and observed.
Cytopathogenic effects appear in 36 days.
An isolated virus is identified and typed by
neutralization with specific antiserum.
Prevention & Control
Both live-virus and killed-virus vaccines are
available
Both killed-virus and live-virus vaccines induce
antibodies and protect the central nervous
system from subsequent invasion by wild virus.
However, the gut develops a far greater degree
of resistance after administration of live-virus
vaccine, a phenomenon that seems to be
dependent on the extent of virus multiplication
in the alimentary tract rather than on serum
antibody level.
 RHINOVIRUS
Usual symptoms in adults include
sneezing, nasal obstruction, nasal
discharge, and sore throat; other
symptoms may include headache, mild
cough, malaise, and a chilly sensation.
There is little or no fever.
The nasal and nasopharyngeal mucosa
become red and swollen, and the sense of
smell becomes less keen.
There are no distinctive clinical findings
that permit an etiologic diagnosis of colds
caused by rhinoviruses versus colds
caused by other viruses.
Secondary bacterial infection may produce
acute otitis media, sinusitis, bronchitis, or
pneumonitis, especially in children.
 COXSACKIEVIRUSES
NEUROLOGIC
Aseptic meningitis is caused by all types of
group B coxsackieviruses and by many group
A coxsackieviruses, most commonly A7 and A9.
Fever, malaise, headache, nausea, and
abdominal pain are common early symptoms.
The disease sometimes progresses to mild
muscle weakness suggestive of paralytic
poliomyelitis.
Patients almost always recover completely
from paresis.
SKIN AND MUCOSA
Herpangina is a severe febrile pharyngitis.
It is caused by certain group A viruses (26, 8,
10).
There is an abrupt onset of fever and sore
throat.
The pharynx is usually hyperemic, and
characteristic discrete vesicles occur on the
posterior half of the palate, pharynx, tonsils, or
tongue.
The illness is self-limited and most frequent in
small children.
 Hand-foot-and-mouth disease is
characterized by oral and pharyngeal
ulcerations and a vesicular rash of the palms
and soles that may spread to the arms and
legs.
Vesicles heal without crusting, which clinically
differentiates them from the vesicles of
herpesviruses and poxviruses.
This disease has been associated particularly
with coxsackievirus A16, but A5 and A10 have
also been implicated.
 Virus may be recovered not only from the
stool and pharyngeal secretions but also from
vesicular fluid.
It is not to be confused with foot-and-mouth
disease of cattle, caused by an unrelated
picornavirus that does not infect humans.
CARDIAC AND MUSCULAR DISEASE
Pleurodynia (also known as epidemic
myalgia or Bornholm disease) is caused by
group B viruses.
Fever and stabbing chest pain are usually
abrupt in onset but are sometimes preceded
by malaise, headache, and anorexia.
The chest pain may be located on either side
or substernally, is intensified by movement,
and may last from 2 days to 2 weeks.
Abdominal pain occurs in approximately half
of cases, and in children this may be the chief
complaint.
The illness is self-limited and recovery is
complete, though relapses are common.
 Myocarditis is a serious disease.
It is an acute inflammation of the heart or its
covering membranes (pericarditis).
Coxsackievirus B infections are a cause of
primary myocardial disease in adults as well
as children.
About 5% of all symptomatic coxsackievirus
infections induce heart disease.
Infections may be fatal in neonates or may
cause permanent heart damage at any age.
 Persistent viral infections of heart muscle may
occur, sustaining chronic inflammation.
There are suggestions that coxsackie B virus
infections may trigger host autoimmune
responses that lead to cardiomyopathies.
OCULAR
Acute hemorrhagic conjunctivitis was
recognized as a new disease in 1969.
It is usually caused by enterovirus 70, but
large outbreaks may also be caused by a
variant of the prototypical coxsackievirus A24.
 Referensi
Brooks G.F., Butel J.S., Morse S.A., 2001. Jawetz,
Melnick and Adelbergs Medical Microbiology (22nd ed.).
USA. Appleton & Lange
Levinson W, 2004. Medical Microbiology & Immunology:
Examination & Board Review, Eighth Edition. McGraw-
Hill Companies, Inc., USA