Acute anterior poliomyelitis

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Acute anterior poliomyelitis, also known as poliomyelitis or Heine-Medin disease, is an epidemic summer virus. It is caused by non-enveloped ssRNA Poliovirus from the genus enteroviruses (Picornaviridae). Poliovirus has 3 antigen types without cross-immunity.

Incidence of poliomyelitis in the world, WHO, August 2015

Cave!!!.png Attention! Not to be confused with cerebral palsy!

Due to the fact that acute anterior poliomyelitis is already eradicated in the Czech Republic, it is possible to encounter so-called polio-like syndromes or poliomyelitis acquired abroad. Polio-like syndromes are manifested by peripheral paresis and muscle atrophy in the area of ​​one or two joints. Sensory disorders are not present, but pain may occur. EMG shows signs of an acute motoneuron lesion.[1]

Characteristics[edit | edit source]

The course of the disease is often silent and is limited to the gastrointestinal tract - water and food can be contaminated in this way. It is transmitted through the patient's stool. It selectively affects the anterior horns of the spinal cord and motor nuclei of the trunk. It has the same clinical picture as echoviruses and Coxsackie viruses.

Epidemiology[edit | edit source]

The incidence in the Czech Republic has been zero since 1957 (we are the first country in the world to do so). Poliovirus has 3 antigenic types – I, II, III and human is the only natural host of the virus. Only in small percentage viremia and CNS intrusion occur.

Eradication[2]

Poliovirus - life cycle

We divide regions into:

  • endemic: Afghanistan, Nigeria, Pakistan,
  • and non-endemic: Central African Republic, Chad, Ivory Coast, Democratic Republic of Congo, Ethiopia, Israel, West Bank, Gaza Strip, Kenya, Liberia, Mali, Niger, Somalia, Uganda.[3]

The European region was declared poliomyelitis free in June 2005. There is still a risk of poliomyelitis imports.

WHO polio eradication program [4]
  • Virological examination of patients with weak paresis.
  • Examination of contacts.
Enlargement in the world (2013)
  • Mandatory reporting of cases.
  • Professional analysis of isolates.

Pathology[edit | edit source]

Infiltration of lymphocytes and granulocytes around the stem motor nuclei and the cells of anterior horns of the spinal cord. Microglia proliferation.

Clinical signs[edit | edit source]

A man who has suffered from polio

Incubation period: 5–14 days[5] Flu-symptomes appear – fatigue, fever, sweating, headache, indigestion. Healing follows.

Only a fraction progresses to meningitis → headache, back pain, limbs, meningeal symptomes, muscle stiffness = preparalytic stage (or also meningeal). It progresses in the nervous system in about 2% = paralytic stage.

The course is most often asymptomatic. All stages leave immunity to the virus. The elimination it in the stool (3 months after the infection has subsided) helps to spread the virus.

Spinal form

It affects the anterior (sometimes lateral) corners of the spinal cord. Muscle fasciculations and pain occur. Paresis and vegetative manifestations develop within 24 hours. It can also affect the respiratory muscles.

Tribal form

It leads to paresis of the muscles of the pharynx, larynx, tongue, and facial expressions with possible spread to the respiratory muscles and to the heart. The improvement occurs one week after the development of nerve symptoms and continues within 1 year. It leaves serious lasting consequences. Residual peripheral paresis affecting various muscle groups of the limbs and torso, muscle contractures.

Complications

In acute stage: myocarditis, uroinfections, bronchopneumonia. In later stages: postpoliomyelitic syndrome.

Diagnosis[edit | edit source]

  • Clinical picture + cerebrospinal fluid examination (cytoprotein association).
  • Faecal isolation of faeces, rise of specific antibodies in cerebrospinal fluid and serum (confirmation of diagnostics).

Differential diagnostics[edit | edit source]

Other acute meningitis, polyradiculoneuritis, transverse myelitis.

Treatment and prevention[edit | edit source]

In the acute phase of the disease, physical rest and drinking are most important. Intensive care (ALV – mainly vacuum ventilation, using the so-called iron lung, artificial lung ventilation) is needed for severe forms (ascending Landry polio). It is a continuous long-term process. Interdisciplinary medical cooperation is important, as is cooperation with parents.

Prevention[edit | edit source]

Mortality reached up to 25% in the epidemic, the last in our country in 1960. A fundamental change was brought about by the introduction of active immunization in 1957, when vaccination with an inactivated vaccine (Salk) began. Since 1960, there has been vaccinated with a live oral vaccine (Sabin).

Since 2007, based on WHO recommendations, the Czech Republic has started vaccinating again with an inactivated vaccine, which is administered as part of a hexavaccine or as a monovaccine in five doses. The reason for switching to an inactivated vaccine is the fact that its use does not result in faecal excretion or virus mutations, so there is no risk of post-vaccination poliomyelitis.[6]

Prognosis[edit | edit source]

Good for all forms except paralytic. The lethality of the paralytic form is 5–15%, and the survivors no longer recover. Unusual fatigue, joint and muscle pain, further muscle weakness, probably due to overloading of functioning muscle groups.

Preference is given to placing the child in a normal group. Another option is the Jedlička Institute in Prague.

Motoneurons of the anterior horns of the spinal cord

Postpoliomyelitis syndrome[edit | edit source]

Usually 20 years of rest after stabilization of the clinical residue after the paralytic form of poliomyelitis. The cause is overload and dysfunction of the remaining motoneurons of the anterior horns.

Symptoms: increased fatigue, muscle weakness (even in previously unaffected segments), fasciculations, pain in the affected muscles and joints.

Therapy: non-specific, includes supportive orthoses and gentle rehabilitation.

Links[edit | edit source]

Related articles[edit | edit source]

External links[edit | edit source]

References[edit | edit source]

  • BENEŠ, Jiří. Infectious medicine. 1. edition. Praha : Galén, 2009. 651 pp. pp. 120. ISBN 978-80-7262-644-1.
  1. ↑ EHLER, E – DERĎÁKOVÁ, M – LATTA, J. Akutní polyradikuloneuritida – diferenciální diagnostika. Neurológia pre prax [online]. 2011, y. 12, vol. 3, p. 180-181, Available from <http://www.solen.sk/index.php?page=pdf_view&pdf_id=5109>. 
  2. ↑ ŽAMPACHOVÁ, Eva. Přednášky a materiály dr. Žampachové ke stažení [online]. [cit. 2012-01-27]. <http://mujweb.cz/?redirected=1521314685>.
  3. ↑ WHO. The Global Polio Eradication Initiative - Infected countries [online]. [cit. 2013-10-26]. <http://polioeradication.org/Infectedcountries/Importationcountries/Israel,WestBankandGaza.aspx>.
  4. ↑ ŽAMPACHOVÁ, Eva. Přednášky a materiály dr. Žampachové ke stažení [online]. [cit. 2012-01-27]. <http://mujweb.cz/?redirected=1521314685>.
  5. ↑ SEIDL, Zdeněk – OBENBERGER, Jiří. Neurologie pro studium i praxi. 1. edition. Praha : Grada Publishing, 2004. ISBN 80-247-0623-7. .
  6. ↑ STAŇKOVÁ, Marie – VANIŠTA, Jiří. Medicabáze.cz – Poliomyelitida [online]. ©2008. [cit. 6. 2. 2010]. <http://medicabaze.cz/?&sec=term_detail&termId=1619&tname=Poliomyelitida>.

References[edit | edit source]

  • SOSNA, A. – VAVŘÍK, P. – KRBEC, M.. Základy ortopedie. 1. edition. Praha : Triton, 2001. 152 pp. ISBN 80-7254-202-8.


  • DUNGL, P.. Ortopedie. 1. edition. Praha : Grada Publishing, 2005. ISBN 80-247-0550-8.


  • SEIDL, Zdeněk – OBENBERGER, Jiří. Neurologie pro studium i praxi. 1. edition. Praha : Grada Publishing, 2004. ISBN 80-247-0623-7.


  • NEVŠÍMALOVÁ, Soňa – RŮŽIČKA, Evžen – TICHÝ, Jiří. Neurologie. 1. edition. Praha : Galén, 2002, 2005. 368 pp. ISBN 80-7262-160-2.
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