Download Poliomyelitis

Poliomyelitis
Authors: Doctors David L. Heymann1 and R. Bruce Aylward
Creation date: August 2004
Scientific Editor: Professor Hermann Feldmeier
1
Polio Eradication Initiative WHO, Geneva 1211, Switzerland. [email protected]
Abstract
Key-words
Disease name/ synonyms
Definition/diagnostic criteria
Differential Diagnosis
Etiology
Clinical description
Diagnostic methods
Epidemiology
Management/treatment
Unresolved questions
References
Abstract
Poliomyelitis is a viral infection caused by any of three serotypes of human poliovirus and is most often
recognized by the acute onset of flaccid paralysis. It affects primarily children under the age of 5 years.
Transmission is primarily person-to-person spread, principally through the fecal-oral route. Usually the
infection is limited to the gastrointestinal tract and nasopharynx, and is often asymptomatic. The central
nervous system, primarily the spinal cord, may be affected, leading to rapidly progressive paralysis. Motor
neurons are primarily affected. Encephalitis may also occur. The virus replicates in the nervous system,
and may cause significant neuronal loss, most notably in the spinal cord. Poliomyelitis must be
distinguished from other paralytic conditions by isolation of virus from stool. Prevention is the only cure for
paralytic poliomyelitis. Both inactivated polio vaccine (IPV) and oral polio vaccine (OPV) are commercially
available. Progress in poliomyelitis eradication since its beginning in 1988 has been remarkable. In 1988,
125 countries were endemic for polio and an estimated 1,000 children were being paralyzed each day by
wild poliovirus. By the end of 2003, six polio-endemic countries remained (Afghanistan, Egypt, India,
Niger, Nigeria, Pakistan), and less than 3 children per day were being paralyzed by the poliovirus.
Interruption of human transmission of wild poliovirus worldwide is now targeted for the end of 2004.
Key-words
Poliomyelitis, acute flaccid paralysis, inactivated polio vaccine (IPV), oral polio vaccine (OPV)
Disease name/ synonyms
Acute poliomyelitis, Polio, Polioviral Fever,
Infantile Paralysis
Definition/diagnostic criteria
Poliomyelitis is a viral infection most often
recognized by the acute onset of flaccid
paralysis. Poliovirus infection occurs in the
gastrointestinal tract with spread to the regional
lymph nodes and, in a minority of cases, to the
central nervous system. Flaccid paralysis occurs
in less than 1% of poliovirus infections; aseptic
meningitis in another 1%; a minor illness with
symptoms including fever, malaise, headache,
nausea and vomiting in a further 10%, and the
remaining 88% of infections are asymptomatic.
Differential Diagnosis
The most frequent cause of acute flaccid
paralysis (AFP) that must be distinguished from
Heymann D and Aylward B. Poliomyelitis. Orphanet Encyclopedia. August 2004.
http://www.orpha.net/data/patho/GB/uk-Poliomyelitis.pdf
1
poliomyelitis is Guillain-Barré syndrome (GBS).
Paralysis in GBS is typically symmetrical and
may progress for periods as long as 10 days.
The fever, headache, nausea, vomiting and
pleocytosis characteristic of poliomyelitis are
usually absent in GBS; high protein and low cell
counts in the cerebrospinal fluid (CSF) and
sensory changes are seen in the majority of
GBS cases.
Other causes of AFP include transverse myelitis,
traumatic
neuritis,
infectious
and
toxic
neuropathies, tick paralysis, myasthenia gravis,
porphyria, botulism, insecticide poisoning,
polymyositis, trichinosis, central nervous system
schistosomiasis and periodic paralysis.
Differential diagnosis of acute nonparalytic
poliomyelitis also includes other forms of acute
nonbacterial meningitis, purulent meningitis,
brain
abscess,
tuberculous
meningitis,
leptospirosis,
lymphocytic
choriomeningitis,
infectious mononucleosis, the encephalitides,
neurosyphilis and toxic encephalopathies.
cause
an
illness
simulating
paralytic
poliomyelitis. Definitive laboratory diagnosis
requires isolation of the wild poliovirus from stool
samples, CSF or oropharyngeal secretions in
cell culture systems of human or monkey origin
(primate cells). Specialized laboratories can
differentiate “wild” virus strains from vaccine
virus strains.
Clinical description
Usually the infection is limited to the
gastrointestinal tract and nasopharynx, and is
often asymptomatic. The central nervous
system, primarily the spinal cord, may be
affected, leading to rapidly progressive paralysis.
Motor
neurons
are
primarily
affected.
Encephalitis may also occur. The virus replicates
in the nervous system, and may cause
significant neuronal loss, most notably in the
spinal cord.
The paralysis of poliomyelitis is usually
asymmetric, with fever present at the onset. The
maximum extent of paralysis is reached in a
short period, usually within 3–4 days. The site of
paralysis depends on the location of nerve cell
destruction in the spinal cord or brain stem. The
legs are affected more often than the arms.
Paralysis of the respiration and/or swallowing
muscles can be life-threatening. Some
improvement in paralysis may occur during
convalescence, but paralysis still present after
60 days is likely to be permanent.
Epidemiology
Accurate data on polio case counts are available
for 1996 to date from the World Health
Organization (WHO) website. As a result of
improved immunization worldwide and the global
initiative to eradicate poliomyelitis, the disease
may be on the verge of worldwide eradication; 6
countries remain endemic at mid-2004
(Afghanistan, Egypt, India, Niger, Nigeria,
Pakistan) with 440 cases reported to date.
Although wild poliovirus transmission has
ceased in the majority of countries, importation
remains a threat. A large outbreak of
poliomyelitis occurred in 1992–1993 in the
Netherlands among members of a religious
group that refuse immunization. The virus was
also found among members of a related religious
group in Canada, although no cases occurred.
Polio-free countries remain at risk of polio as
long as the wild poliovirus continues to transmit
from human to human; countries that do not
maintain high immunity levels among all
segments of population are at greatest risk.
Historically, in endemic areas, cases of
poliomyelitis occurred both sporadically and as
epidemics each year in tropical countries during
the rainy season. Poliomyelitis is today primarily
a disease of infants and children under the age
of five years.
Transmission is primarily person-to-person
spread, principally through the fecal-oral route.
In rare instances, milk, foodstuffs and other
materials contaminated with feces have been
incriminated as vehicles; water and sewage are
rarely implicated. The period of incubation is
commonly 7–14 days for paralytic cases. Virus
typically persists in the throat for approximately 1
week and in feces for 3–6 weeks after infection,
with transmission greatest during the days
before and after onset of symptoms.
Type-specific immunity, apparently of lifelong
duration, follows both clinically recognizable and
unapparent infections. Intramuscular injections,
trauma or surgery during the incubation period or
prodromal illness may provoke paralysis in the
affected extremity.
Diagnostic methods
Poliomyelitis must be distinguished from other
paralytic conditions by isolation of virus from
stool. Other enteroviruses (notably types 70 and
71), echoviruses and coxsackieviruses can
Management/treatment
Prevention is the only cure for paralytic
poliomyelitis. Both a trivalent live, attenuated
oral poliovirus vaccine (OPV) and an injectable,
inactivated poliovirus vaccine (IPV) are
Etiology
Poliomyelitis is caused by any of the three
serotypes
of
human
Poliovirus
(genus
Enterovirus). Type 1 is isolated from paralytic
cases most often and type 3 less so. Circulating
wild type 2 poliovirus has not been detected
since October 1999. Type 1 most frequently
causes epidemics.
Heymann D and Aylward B. Poliomyelitis. Orphanet Encyclopedia. August 2004.
http://www.orpha.net/data/patho/GB/uk-Poliomyelitis.pdf
2
commercially available. OPV simulates natural
infection by inducing both circulating antibody
and resistance to infection of the pharynx and
intestine, and also immunizes some susceptible
contacts through secondary spread. WHO
recommends the use of OPV alone for
immunization programs in developing countries
because of its superior capacity to provide
population immunity through community spread.
IPV likewise provides excellent individual
protection by inducing circulating antibody that
blocks the spread of virus to the CNS. IPV does
not induce intestinal immunity of the level
induced by OPV.
There are no risks associated with IPV. OPV,
however, is associated with two risks: vaccinerelated paralytic polio (VAPP) and outbreaks
caused by circulating vaccine-derived poliovirus
(cVDPV). VAPP occurs in vaccine recipients or
their healthy contacts at a rate of approximately
one in every 800 000 first vaccinations.
Circulating VDPV are recombinants with other
neurovirulent enteric viruses capable of
spreading through populations. The extent of the
cVDPV problem is currently being evaluated.
There is no curative antiviral for poliomyelitis.
Treatment during acute illness is for the
complications of paralysis and requires expert
knowledge and equipment, especially for
patients in need of respiratory assistance.
Physical therapy is used to attain maximum
function after paralytic poliomyelitis and can
prevent many deformities that are late
manifestations of the illness.
Unresolved questions
Infrequently, recurrence of muscle weakness
following recovery may occur many years after
the original infection has resolved (“postpolio
syndrome”); this is not believed to be related to
persistence of the virus itself, but little is known
of the biological mechanism that causes this
syndrome.
References
Circulating
Vaccine-Derived
Poliovirus-Philippines, Morbidity and mortality weekly
report, 2001, 50:874–5.
Expanded Programme on Immunization. Field
guide for supplemental activities aimed at
achieving polio eradication. WHO/EPI/GEN 95.1.
Heymann DL, Rodier GR. Hot spots in a wired
world. Lancet Infectious Diseases 2001, 1: 345353.
Kew OM, Morris-Glasgow V, Landaverde M,
Burns C, Shaw J. et al. Outbreak of poliomyelitis
in Hispaniola associated with circulating type 1
vaccine-derived poliovirus. Science 2002, 296:
356-359.
Kew OM, Wright PE, Agol VL, Delpeyroux F, et
al. Circulating vaccine-derived polioviruses:
current knowledge. Bulletin of the World Health
Organization, 2004, 82:1:16-23
Mulders MN, Reimerink JHJ, Koopmans MPG,
van Loon AM, van der Avoort HGAM. Genetic
analysis of wild type poliovirus importation into
the Netherlands (1979-1995). Journal of
Infectious Diseases 1997;176:617-24.
Rousset D et al. Recombinant vaccine-derived
poliovirus in Madagascar. Emerging Infectious
Diseases, 2003, 9:885–887.
Smith J, Leke R, Adams A, Tangermann RH.
Certification of polio eradication:process and
lessons learned. Bulletin of the World Health
Organization, 2004, 82:1:24-29.
WHO global action plan for laboratory
containment of wild polioviruses. Second
Edition. WHO/V&B/03.11.
World Health Organization. Guidelines for the
safe production and quality control of IPV
manufactured from wild polioviruses. Geneva:
World Health Organization; (in press) for latest
publication
information
visit:
http://www.who.int/biologicals
Yang C-F et al. Circulation of endemic type 2
vaccine-derived poliovirus in Egypt from 1983 to
1993. Journal of virology, 2003, 77:8366–8377.
Heymann D and Aylward B. Poliomyelitis. Orphanet Encyclopedia. August 2004.
http://www.orpha.net/data/patho/GB/uk-Poliomyelitis.pdf
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