poliomylitis.pdf

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About This Presentation

polio virus


Slide Content

POLIOVIRUSES

Dr /Eman Ahmed

Lecturer of Medical Microbiology
&lmmunology

Poliomyelitis

« Poliomyelitis is an acute infectious disease
that in its serious form affects the central
nervous system (CNS). The destruction of
motor neurons in the spinal cord results in
flaccid paralysis. However, most poliovirus

infections are subclinical.

Poliomyelitis

Causative agent :Polio virus

* It is an icosahedral non-
enveloped virus, the
genome is a_ positive
sense single stranded |
RNA, 25-30 nm in
diameter.

Mode of transmission

* Poliovirus is transmitted by fecal-oral contact

Children can contract poliovirus by touching
contaminated objects and putting their hands
in their mouths

Properties of the virus

* There are 3 antigenic types.

¢ They are inactivated when heated at 55°C for
30 minutes

+ Chlorine are used to disinfect sewage
containing virus .

* The virus infects only primates, e.g. man and

monkeys as they possess specific receptors for
viral attachment.

Properties of the virus

+ Stable at acidic pH (pH 3.0)
(CAN BE TRANSIMITTED BY
INGESTION)

+ Optimal temperature for
growth 37 (°C)

Replication cycle

Poliovirus

Pg acts as a
primer for RNA
replication

Genomic

Assembly of new poliovirus particle
containing a +ssRNA and viral proteins

Release during
host cell lysis

2 Life Cycle of a Poliovirus
Dt

2 Nerve cell receptors auch to the vi

rg

Replication cycle

Replication begins by attachment to specific
receptors on the cell membrane and entry into the
cell, this is followed by uncoating.

The genome RNA functions as mRNA and is
translated into one large polypeptide, which is
cleaved by virus encoded protease into structural
proteins and enzymes.

Replication of the genome occurs by synthesis of
a complementary negative strand, which then
serves as the template for the positive strands.

Assembly then occurs and the virus accumulates
in the cytoplasm and is released by cell lysis.

Pathogenesis of poliomyelitis

Hypothesis of
pathogenesis

A. Virus is
ingested
by mouth’

. Only if amount of

¡gested virus is

very large is there

primary infection of

‘oropharyngeal mucosa. D. Varying
amounts of
virus enter
bloodstream.

€. In most instances
virus is swallowed
and passes through
Stomach into
intestine, where it
multiplies rapidly and
invades aggregated lymph
nodules of intestinal

wall (Peyer patches).

AR

Medulla oblongata

suscept
extraneural

issues

tissues, including oropharynx, are
then frequently secondarily ‘cal
fected via bloodstream, and Spiral cord

virus also multiplies there. F. From sites of multiplication in intestine,
oropharynx, and other extraneural tissues, virus
reaches central nervous system, probably via
regional afferent neural pathways, first into.
motor neurons of spinal cord (primary spinal
paralysis) or medulla (primary bulbar paralysis).
Further axonal spread of virus then occurs alon;
insulated tracts to distal neurons elsewhere in
central nervous system, and also by contiguity
to adjacent motor neurons.

in feces, by which
it is disseminated.

Pathogenesis and Pathology

* Infection occurs by the ingestion of food or drink
contaminated by stools of cases or carriers.

¢ Incubation period is 7-14 days. The organism
multiplies in the oropharynx and in the intestine
and is excreted in stools. Infection may stop at

this stage i.e. inapparent infection.

Pathogenesis and Pathology

* Infection may continue and the virus passes to the
deep cervical and deep mesenteric lymph nodes. Then
it invades the blood stream Viraemia is associated with
mild symptoms of fever, malaise, headache,
nausea,(FAHM) and vomiting. The disease may be

stopped at this stage i.e. abortive infection.

Pathogenesis and Pathology

¢ Aseptic meningitis (non-paralytic poliomyelitis)
may occur and manifests by stiffness and pain in
the back and neck. It usually recovers but it may

progress to paralysis.

Pathogenesis and Pathology

» Paralytic poliomyelitis occurs only in 0.1-1%
of cases. The virus affects the anterior horn
cells of the spinal cord leading to flaccid
paralysis. In severe cases, it may affect the
posterior horn cells, the vestibular nuclei and
motor cortex. Death may occur due to
respiratory paralysis.

Pathogenesis and Pathology

The CNS may then be invaded by
* way of the circulating blood.

* Poliovirus can spread along axons of
peripheral nerves to the CNS

Pathogenesis and Pathology

¢ The primary targets of poliovirus infection in
the CNS are anterior horn motor neurons of
the spinal cord

Pathogenesis and Pathology
* Poliovirus does not multiply in muscle in vivo.

¢ The changes that occur in peripheral nerves
and voluntary muscles are secondary to the
destruction of nerve cells.

Apoliovirusap- ¿y
proaches a nerve

cell through the La o

bloodstream.

The poliovirus releases
genetic material into
the nerve cell and forms
more polioviruses.

a
de
ye 'elhost cell swells and
8 ursts, releasing thou-
S&S sands of new viruses back
into the bloodstream.

Pathogenesis and Pathology

¢ No permanent carrier state occurs, but virus
excretion in stools can occur for several
months. Immunity is permanent to the type
of poliovirus causing the infection

Clinical pictures of Poliomyelitis

1) inapparent ( 95% ): the organism multiply at oropharynx &
intestine and excreted in stool

2) abortive ( 4-8% ) : the organism reach blood > viremia >
FAHM + VOMITING)

3) aseptic meningitis ( 1% ) ( non paralytic polio ) : stiffness of
back of neck
4) paralytic polio ( 0.1 - 1%) : involve the following forms :

a- Spinal poliomyelitis : affection of AHC > flaccid paralysis ,
intact sensations

b- Bulbar poliomyelitis : more serious , affect brain stem
c- Bulbo-spinal poliomyelitis : very poor prognosis
d- Encephalitis : very rare

Lab Diagnosis of poliomyelitis

Sample :stool or CSF and serum for detection of
Ab

1) Direct : > virus itself by immunoelectro
microscope

> viral Ag by ELISA, RIA

> genetic material by PCR, probe

2) Indirect : tissue culture > CPE

3) Serology : specific IgM , raising IgG , C.F

Prophylaxis

1) Active :Active immunization: There are two
vaccines that contain the three types of virus
and produce neutralizing antibodies and prevent
CNS infection.

2) Passive:Gamma globulins given early to
susceptible unimmunized contacts may be
effective in preventing paralytic poliomyelitis.

A) Active immunization

1) Sabin living attenuated oral polio-vaccine
(OPV):
It is a living attenuated vaccine prepared from

non-paralytogenic mutants of the three types
of poliovirus grown.

Four doses are given orally at the age of 2, 4
and 6 months and a booster dose is given at 4-
6 years.

A)Active immunization

Advantages of Sabin :

a- easily administration " orally "

b- multiplies locally in intestine > local immunity
IgA , interferons and also stimulate production of
IgG , IgM.

c- Herd immunity :- (VIP)

Vaccine strains pass with stool & are disseminated
in the environment & can be transmitted to non

immunized children by feco-oral route >
eradication of polio virus

Disadvantages of Sabin
a- failure of vaccination due to:

> loss of potency (Atel!) due to improper refrigeration
during storage

> interference with replication of virus in intestine by
another enterovirus

b- vaccine may cause paralytic disease in
immunodeficient

c- VAPP " vaccine associated paralytic poliomyelitis "
due to reversion of the attenuated virus to virulent state

2)Salk vaccine : It is a formalin killed vaccine
prepared from the three types of the virus
grown in monkey kidney cell cultures. It is given
in 4 subcutaneous doses at 2, 4 and 6 months

and a booster injection is given at 4-6 years.

2)Salk vaccine

Disadvantages:

The vaccine produces neutralizing antibodies
(IgG and IgM) and prevents infection of the CNS.
However, it does not prevent virus replication
in the intestine. So, the vaccine protects against
paralytic poliomyelitis but not against non-
paralytic forms of infection.

2)Salk vaccine

Advantages

The vaccine can be safely given to
immunosuppressed children and pregnant
mothers, in whom Sabin vaccine is
contraindicated.

Salk Sabin
Type of vaccine Formalin Live

killed attenuated
Rout of vaccine administration S.C Oral
Prevents paralytic disease Yes Yes
Prevent non-paralytic forms of infection. No Yes
Induces humoral IgG Yes Yes
Induces intestinal IgA ¡No Yes
prodoce herd immunity No Yes
Prevents replication of wild strain in the gut No Yes
May revert to virulent No Yes
Coinfection with other enteroviruses may
impair immunization No Yes
Requires refrigeration No Yes
Can cause disease in the immunocompromised No Yes
Route of administration Injection Oral
Duration of immunity Shorter Longer
Used in Egypt No Yes
[Used in USA Yes No