Transcript Chapter 36: Picornaviruses (Enterovirus & Rhinovirus Groups)

Picornaviruses

Represent a very large virus family with respect to the number of members

One of the smallest in terms of virion size and genetic complexity.

Include two major groups of human pathogens:
1- Enteroviruses : transient inhabitants of the human alimentary tract and may
be isolated from the throat or lower intestine.
2- Rhinoviruses : isolated chiefly from the nose and throat.

Enteroviruses are stable at acid pH (3.0–5.0) for 1–3 hours, whereas
rhinoviruses are acid-labile.

Many enteroviruses (polioviruses, echoviruses, some coxsackieviruses) can be
grown at 37°C in human and monkey cells. Most rhinovirus strains can be
recovered only in human cells at 33°C.
 However, subclinical infection is far more common than clinically manifest
disease.
 Diseases which are caused by many picornaviruses : severe paralysis,aseptic
meningitis, pleurodynia, myocarditis, vesicular and exanthematous skin lesions,
mucocutaneous lesions, respiratory illnesses, undifferentiated febrile illness,
conjunctivitis, and severe generalized disease of infants.
 The most serious disease caused by any enterovirus is poliomyelitis.
Members of the Picornaviridae Cause Many
Serious Diseases of Man and Animals
In geneneral : 9 genera
Genus Enterovirus (human)
- Poliovirus, 3 major types cause paralysis
- Coxsackievirus(A, B): pathogenic for newborn mice
- Echoviruse
Genus Rhinovirus (human)
- cause respiratory tract infections, acid labile, cause
colds in humans (,,, types).
Genus Hepatovirus (human)
- Hepatitis A, contagious liver infections.
Genus Cardiovirus
- Cause encephalomyocarditis in mouse
acid labile, source is a rodent reservoir.
Genus Apthovirus
- acid labile, foot and mouth disease, most destructive in Africa.
Genus Parcheovirus (human)
- similar to other enteroviruses, such as gastrointestinal and respiratory illness,
meningoencephalitis, otitis media, and neonatal diseases.
Poliomyelitis is an acute infectious disease that in its serious form affects the
central nervous system.
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Antigenic Properties
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There are three antigenic types of polioviruses.
Pathogenesis & Pathology:
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The mouth is the portal of entry of the virus, and primary multiplication takes
place in the oropharynx or intestine.
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It is believed that the virus first multiplies in the tonsils, the lymph nodes
of the neck, Peyer's patches, and the small intestine. The central nervous
system may then be invaded by way of the circulating blood.

The virus is regularly present in the throat and in the stools before the onset of
illness.

Antibodies to the virus appear early in the disease, usually before paralysis occurs.
Clinical Findings:
1. Mild Disease:
o This is the most common form of disease.
o The patient has only a minor illness, characterized by fever, headache,
nausea, vomiting, and sore throat in various combinations.
o Recovery occurs in a few days.
2. Nonparalytic Poliomyelitis (Aseptic Meningitis):
o In addition to the symptoms and signs listed in the preceding paragraph,
the patient with the nonparalytic form has stiffness and pain in the back and
neck.
3. Paralytic Poliomyelitis:
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The predominating complaint is flaccid paralysis resulting from lower motor neuron
damage.
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The changes that occur in peripheral nerves and voluntary muscles are secondary to the
destruction of nerve cells.
4.
Progressive Postpoliomyelitis Muscle Atrophy:
It is a specific syndrome and is rare. A result of physiologic and aging changes in
paralytic patients already burdened by loss of neuromuscular functions.
Laboratory Diagnosis:
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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.

Cytopathogenic effects appear in 3–6 days. An isolated virus is identified
and typed by neutralization with specific antiserum. Virus can also be
identified by polymerase chain reaction (PCR) assays.

Epidemiology:

Poliomyelitis has had three epidemiologic phases: endemic,
epidemic, and the vaccine era. The first two reflect prevaccine
patterns.

Before global eradication efforts began, poliomyelitis occurred
worldwide more during summer and fall.
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children are usually more susceptible than adults because of the
acquired immunity of the adult population.

The case fatality rate is variable. It is highest in the oldest
patients and may reach 5–10%.
 Prevention & Control:
Both live-virus and killed-virus vaccines are available.
 Formalinized vaccine (Salk) is prepared from virus grown in monkey kidney cultures.
Killed-virus vaccine induces humoral antibodies but does not induce local intestinal
immunity so that virus is still able to multiply in the gut.
 Oral vaccines contain live attenuated virus grown in primary monkey or human diploid cell
cultures. The vaccine produces not only IgM and IgG antibodies in the blood but also
secretory IgA antibodies in the intestine, which then becomes resistant to reinfection.
 Both killed-virus and live-virus vaccines induce antibodies and protect the central nervous
system from subsequent invasion by wild virus.
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The vaccine viruses—particularly types 2 and 3—may mutate in the
course of their multiplication in vaccinated children.
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Live-virus vaccine should not be administered to immunodeficient or
immunosuppressed individuals or their household contacts.

Immune globulin can provide protection for a few weeks against the
paralytic disease but does not prevent subclinical infection. Immune
globulin is effective only if given shortly before infection; it is of no
value after clinical symptoms develop.
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Divided into two groups, A and B
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Group A: Herpangina (vesicular pharyngitis), hand-foot-and-mouth disease, and acute
hemorrhagic conjunctivitis
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Group B: pleurodynia (epidemic myalgia), myocarditis, pericarditis, and severe
generalized disease of infants.
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More pathogenic than the echoviruses.
Clinical Findings:
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Aseptic meningitis: Caused by all types of group B and by many group A viruses (A7
and A9). Fever, malaise, headache, nausea, and abdominal pain are common early
symptoms.
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Herpangina: Caused by certain group A viruses. There is an abrupt onset of fever and
sore throat with discrete vesicles on the posterior half of the palate, pharynx, tonsils,
or tongue.
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Hand-foot-and-mouth disease: Associated particularly with coxsackievirus A16.
characterized by oral and pharyngeal ulcerations and a vesicular rash of the palms
and soles that may spread to the arms and legs
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Pleurodynia: (epidemic myalgia) Caused by group B viruses.
Fever and stabbing chest pain are usually abrupt in onset but are sometimes
preceded by malaise, headache, and anorexia.
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Myocarditis: 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.
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Generalized disease of infants: Caused by group B coxsackieviruses.
An extremely serious disease in which the infant is overwhelmed by simultaneous
viral infections of multiple organs, including heart, liver, and brain.
 Laboratory
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Nucleic Acid Detection
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Serology
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diagnosis:
Epidemiology:
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Found in all over the world
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Isolated more in summer and early fall.
 Control:
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No vaccines or antiviral drugs available for prevention or treatment of diseases
caused by coxsackieviruses
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Echoviruses infect the human enteric tract
Cause aseptic meningitis, encephalitis, febrile illnesses with or without rash,
common colds, and ocular disease
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Epidemiology:

Similar to that of other enteroviruses
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Occur in all parts of the globe
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More found in the young than in the old.

Control:

No antivirals or vaccines (other than polio vaccines) available for the treatment or
prevention of any enterovirus diseases.
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Laboratory diagnosis:
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Nucleic Acid Detection
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Serology
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Rhinoviruses are the common cold viruses.

They are usually isolated from nasal secretions but may also be found in throat and
oral secretions.

These viruses—as well as coronaviruses, adenoviruses, enteroviruses,
parainfluenza viruses, and influenza viruses—cause upper respiratory tract
infections, including the common cold syndrome.
Classification:
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Human rhinoviruses can be divided into major and minor receptor groups.
I.
The major group: use intercellular adhesion molecule-1 (ICAM-1) as receptor
II.
The minor group: bind members of the low-density lipoprotein receptor (LDLR)
family.
Properties of the Virus:
General Properties:
 They are more thermostable than enteroviruses
 These viruses are infectious only for humans, gibbons, and chimpanzees
 They can be grown in a number of human cell lines, including the WI-38 and
MRC-5 lines
.
Pathogenesis & Pathology:
 There is a direct correlation between the amount of virus in secretions and the
severity of illness.
 Replication is limited to the surface epithelium of the nasal mucosa.
Clinical Findings:
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The incubation period is brief from 2 to 4 days
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The acute illness usually lasts for 7 days

Usual symptoms in adults include sneezing, nasal obstruction, nasal
discharge, and sore throat, etc.
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Secondary bacterial infection may produce acute otitis media, sinusitis,
bronchitis, or pneumonitis, especially in children.
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Antibody develops 7–21 days after infection
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They be transmitted through close contact, by means of viruscontaminated respiratory secretions
Treatment & Control:
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No vaccine: - difficulty in growing rhinoviruses to high titer in culture
- The multiplicity of serotypes causing colds
a hundred days of foot and mouth
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It may be transmitted to humans by contact or ingestion
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In humans, the disease is characterized by fever, salivation, and
vesiculation of the mucous membranes of the oropharynx and of the skin
of the palms, soles, fingers, and toes.
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Highly contagious disease of domestic and wild ruminants and pigs.

In the early stages of infection when viremia is present and when vesicles
in the mouth and on the feet rupture and liberate large amounts of virus.
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can be fatal in young animals – myocarditis
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not usually fatal in adults but causes economic losses (trade implications)