Child with polio sequelae

Picornaviruses


Classification
of
Picornaviruses
Genus
Species
Antigenic
types
Poliovirus

1,2,3

Coxsackievirus
Enterovirus

Coxsackie A
Coxsackie B

1-22,24
1-6

Echovirus

1-9,11-27,24-27

Enterovirus

68-71

Parechovirus

Parechovirus

1,2

Rhinovirus

Rhinovirus

1-113

Hepatovirus

Hepatitisvirus

Aphthovirus
Cardiovirus

Classification of Picornaviruses contd

Coxsackie A- type23 is now
classified as Echo 9
Echo 10 is classified as Reovirus-1
and Echo 28 as Rhino-1
Echo 22, 23 are classified as
Parechovirus types 1 and 2

Properties of
Picornaviruses
Property
Size (nm)
Capsid
form
Polypeptide
RNA type

Picornaviruses
22-30
Icosahedral
VP1, VP2, VP3,
VP4
SS-PS

Poliovirus

Morphology

Polioviruses
These viruses have affinity to
nervous tissue
Poliovirus is causative agent of
Poliomyelitis

Important Characteristics
Size: 27-30 nm
60 capsomeres in
icosahedral
symmetry
Each capsomere is
made up of four
virion proteins VP1,
VP2, VP3, and VP4
Type 1-3

Antigenic properties
On the basis of neutralisation tests
Three types 1,2 and 3
Type 1 most common and causes epidemics. Type
3 also causes epidemics but to a lesser extent
Type 2 commonly causes paralytic poliomyelitis
Each type contains C and D antigens
C antigen: Coreless antigen, cross-reactive in all
types.
D antigen: Dense antigen, also called Native (N)
antigen, type specific

Pathogenesis
1. Source of infection: Only man, apparent and
2.
3.
4.
5.

subclinical patients. Children are highly

susceptible.
Feco-oral transmission is common
Virus multiplies both in pharynx and
intestine, hence pharyngeal secretions may
also be the source of infection
Incubation: 7-14 days
Pathogenesis: Only much less than 0.1%
subjects exposed to polio virus form the
flaccid paralysis

Virus

Mouth
Multiplies in
lymphatic tissues of
oropharynx and intestine
Blood stream
Destroys the
Spinal cord and brain
anterior horn cells of
spinal cord

Clinical Syndromes
Asymptomatic illness: 90%
Abortive poliomyelitis, the minor illness: 5%
infected people
Nonparalytic poliomyelitis or aseptic
meningitis: 1%-2% of patients with poliovirus
infections.
Paralytic polio, the major illness: 0.1% to
2%of persons with poliovirus. Paralysis may
be classified as spinal, bulbar and bulbospinal

Immunity
sIgA and neutralizing antibody (IgG,
IgA, IgM) persist for life span

Lab Diagnosis
Specimens: stool (through out the
disease), CSF, Oropharyngeal secretions
(first 3-5 days), Spinal cord and Brain at
autopsy
Direct demonstration of virus in stool
can be done by electron or immune
electron microscopy.
Isolation of virus: Primary monkey
kidney cells and HeLa cells.
CPE in the form of rounding of cells is
usually evident within 36 hours

Lab Diagnosis contd

Serotyping is based on neutralization of
CPE by standardized antisera using
intersecting pool followed by specific
sera.
Serology: Four fold rise in antibody titre
ELISA
IFA

neutralizing Test
CFT

2 or 3 symptoms free intervening days

Meningeal irritation, asymmetric flaccid paralysis
with no significant sensory loss
Variable forms; in most serious forms all four limbs
may be completely paralyzed or the brain stem
may be attacked followed by paralysis of cranial
nerves and muscles of respiration (bulbar polio)
Temporarily damaged neurons regain their function
Recovery begins and may continue for 6 months
Paralysis persisting after this time is permanent

Prophylaxis
Two types of vaccines:
1.Oral polio vaccine(OPV) live attenuated,
(Sabin, 1957) and
2.Killed poliovirus vaccine(IPV)Salk, 1954
IPV is used for adult immunization and
Immunocompromised patients

Salks Killed Polio vaccine

Formalin inactivated vaccine of all three
types of polio virus grown in monkey
kidney cells.
Deep subcutaneous or IM injection.
Three doses given 4-6 weeks apart,
followed by booster dose after 6 months.
Boosters required every 3-5 years later to
maintain immunity.

Live Attenuated Oral Polio Vaccine

(Sabin Vaccine)
Live attenuated (Heat)strains of poliovirus types
1(10 lakh),2 (2 lakh) and 3 (3 lakh) grown in
monkey kidney cells and stabilised by MgCl2.

Shelf life of OPV is four months at 4-8 C but 2

years at -20C
Characters of attenuated strains:
Should not be neurovirulent
Able to set up intestinal infection and induce
immune response
Should not acquire neurovirulence after serial
passage
Should possess stable genetic markers

Genetic markers
Marker

Property

Wild
strain

Vaccine
strain

d
marker

Growth in low
levels of
bicarbonate

Good

Poor

rct 40

Growth at
40C

Good

Poor

MS

Growth in
Good
Monkey kidney
cell line

Poor

OPV
Advantages
Effectiveness
Lifelong immunity
Induction of secretory antibody response
similar to that of natural infection
Possibility of attenuated virus circulating in
community by spread to contacts (indirect
immunization)(herd immunity)
Ease of administration
Lack of need for repeated boosters

Disadvantages
Risk of vaccine-associated poliomyelitis in
vaccine recipients or contacts
Unsafe administration for immunodeficient
patients

IPV
Advantages
Good stability during transport and in
storage
Safe administration in immunodeficient
patients
No risk of vaccine-related disease
Disadvantages
Lack of induction of local (gut) immunity
Need for booster vaccine for lifelong
immunity
Fact that higher community immunization
levels are needed than with live vaccine

Eradication of Polio
Poliomyelitis can be eradicated as
o man is the only host.
o a long-term carrier state is not
known
o appropriate and effective vaccine
available

Pulse Polio Immunisation

Simultaneous administration of OPV to
all the children below 5 years in a region
on the same day is known as pulse polio
immunisation.
Live attenuated virus multiplying in the
gut helps in interrupting the
transmission of wild virus by displacing
it from intestine.

COXSACKIE VIRUSES

Introduction
Coxsackievirus are distinguished from other
Enteroviruses by their pathogenecity for suckling
rather than adult mice. They are divided into 2
groups on the basis of the lesions observed in
suckling mice.

Group A viruses produce a diffuse myositis with

acute inflammation and necrosis of fibers of
voluntary muscles.

Group B viruses produce focal areas of

degeneration in the brain, necrosis in the
skeletal muscles, and inflammatory changes in
the dorsal fat pads, the pancreas and
occasionally the myocardium.

Features of coxsackievirus
infection in the labortory
Types

Growth in MK
cell culture

Effect in
sucking

mice
Coxsackie A virus
Paralysis
Coxsackie B virus
Spasticity

1-24
1-6

+ (7 & 9)
+

MK , monkey kidney
*
Coxsackievirus A23 now classified as echovirus 9

Features of coxsackievirus
infection in man
Coxsackievirus A 1-24

Aseptic meningitis
Herpangina (Vesicular pharyngitis)
Hand-foot-and-mouth disease
Coxsackievirus B 1-6

Epidemic myalgia (Bornholm disease)

Neonatal disease
Myocarditis and Pericarditis
Aseptic Meningitis
Juvenile diabetes

Aseptic meningitis: caused by most

group A and all group B viruses.
Clinically resembles paralytic
poliomyelitis.
Herpangina: caused by types
2,4,5,6,8,and 10. abrupt onset of fever
pharyngitis, usually seen in children.
Hand-foot and mouth disease: caused
bt type 5 and 16. vesicular lesions
involving mouth hands and feet.

HAND/FOOT/MOUTH

Epidemic myalgia: Fever and stitch like pain in

the chest. Epidemics may occur.
Myocarditis and pericarditis: Fatal disease in
newborn.
Juvenile diabetes: Type B4 is associated with
disease.
Neonatal infections: Transplacental passage
results in disseminated disease like hepatitis,
myocarditis, meningo-encephalitis and adrenal
failure
Post viral fatigue syndrome: Not clearly defined

Laboratory diagnosis
Specimens: feaces, and from site of
lesion.
Virus isolation: Suckling mice are
inoculated and observed for disease.
Tissue culture: Monkey kidney cell

ECHO Viruses
Enteric Cytopathic Human Orphan viruses
Orphan viruses: Thought to be unrelated to
any particular disease.
32 antigenic types
Inhabit alimentary tract and spread by
faeco-oral route
Causes: 1. Aseptic meningitis
2. Rash
3.Conjunctivits
4. Upper Respiratory Tract Infection

Enteroviruses 68-71
Serotype
68
69
70
71

Disease
Pneumoniae and bronchitis
Acute hemorrhagic
conjunctivitis
Meningitis and encephalitis

Acute hemorrhagic conjunctivitis: Pandemic

forms,
Incubation period is 24 hrs. Sub-conjuntival
Hge is characteristic feature

Rhinoviruses (Rhine: nose)

Causative agents of common cold.
Habitat mainly nose and throat not
intestine.
Properties:
Acid lability: Hence cannot infect GIT.
Grow at temperature of 33C
113 antigenic types

Cultivation:
Human or Monkey cell cultures.
Classified as:
M (Monkey) strains: can grow in both
human and monkey cells
H (Human) strains: grow only in human
cells.
O strains: can grow only in nasal or
tracheal ciliated epithelium.

Pathogenesis
Man is the only natural host.
Cause common cold. Infection transmitted
by droplets. Patient develops profuse
watery discharge with nasal obstruction,
sneezing, fever headache etc.
Other viruses causing common cold:

i. Corona viruses
ii. Respiratory syncitial virus
iii.Parainfluenza viruses
iv.Adenoviruses
v. ECHO viruses