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== Diagnosis ==
A laboratory diagnosis of poliomyelitis is usually made based on recovery of poliovirus from the stool or pharynx. Neutralizing antibodies to poliovirus can be diagnostic and are generally detected in the blood of infected patients early in the course of infection. Analysis of the patient's cerebrospinal fluid (CSF), which is collected by a lumbar puncture ("spinal tap") reveals an increased number of white blood cells (primarily lymphocytes) and a mildly elevated protein level. Detection of virus from the CSF is diagnostic of paralytic polio, but rarely occurs.
If poliovirus is isolated from a patient experiencing acute flaccid paralysis it is further tested, using oligonucleotide mapping (genetic fingerprinting), or more recently by PCR amplification, to determine if the virus is “wild type” (that is, the virus encountered in nature) or vaccine type (is derived from a strain of poliovirus used to produce polio vaccine). For each reported case of paralytic polio caused by wild poliovirus, it is estimated that another 200 to 3,000 contagious asymptomatic carriers exist. Therefore, isolation of wild poliovirus constitutes a public health emergency, and appropriate efforts to control the spread of the disease must be initiated immediately.


== Treatment ==
== Treatment ==

Revision as of 16:37, 10 October 2012

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]



Treatment

A modern negative pressure ventilator (iron lung)

No cure for polio exists, and the focus of modern polio treatment has been on increasing comfort, speeding recovery and preventing complications. Supportive measures include: antibiotics to prevent infections in weakened muscles, analgesics for pain, moderate exercise and a nutritious diet. Treatment of polio also often requires long-term rehabilitation including physical therapy, braces, corrective shoes and, in some cases, orthopedic surgery.

Portable ventilators may be required to support breathing. Historically, a noninvasive negative-pressure ventilator (more commonly called an iron lung) was used to artificially maintain respiration during an acute polio infection until a person could breathe independently; generally about one to two weeks. Today many polio survivors with permanent respiratory paralysis use modern jacket-type negative-pressure ventilators that are worn over the chest and abdomen.

Other historical treatments for polio have included hydrotherapy, electrotherapy and surgical treatments such as tendon lengthening and nerve grafting. The use of devices such as rigid braces and body casts—which tended to cause muscle atrophy due to the limited movement of the user—were also touted as effective treatments. Massage, passive motion exercises, and vitamin C were also used to treat polio victims, with varying degrees of success.

Primary Prevention

Passive immunization

In 1950, William Hammon at the University of Pittsburgh purified the gamma globulin component of the blood plasma of polio survivors.[1] Hammon proposed that the gamma globulin, which contained antibodies to poliovirus, could be used to halt poliovirus infection, prevent disease, and reduce the severity of disease in other patients who had contracted polio. The results of a large clinical trial were promising; the gamma globulin was shown to be about 80% effective in preventing the development of paralytic poliomyelitis.[2] It was also shown to reduce the severity of the disease in patients that developed polio.[1] The gamma globulin approach was later deemed impractical for widespread use, however, due in large part to the limited supply of blood plasma, and the medical community turned its focus to the development of a polio vaccine.[3]

A child receives oral polio vaccine

Antibody serum

In 1950 William Hammon at the University of Pittsburgh isolated a serum from the blood of polio survivors. Hammon proposed that the serum, which contained antibodies to poliovirus, could be used to halt poliovirus infection, prevent disease, and reduce the severity of disease in other patients who had contracted polio. The results of a large clinical trial were promising; the serum was shown to be about 80% effective in preventing the development of paralytic poliomyelitis. The serum was also shown to reduce the severity of the disease in patients that developed polio. The antibody approach was later deemed impractical for widespread use, however, due in large part to the limited supply of blood plasma, and the medical community turned its focus to the development of a polio vaccine.

Vaccine

Polio vaccine

Two polio vaccines are used throughout the world to combat polio. Both vaccines induce immunity to polio, efficiently blocking person-to-person transmission of wild poliovirus, thereby protecting both individual vaccine recipients and the wider community (so-called herd immunity).

The first polio vaccine was developed in 1952 by Jonas Salk at the University of Pittsburgh, and announced to the world on April 12, 1955. The Salk vaccine, or inactivated poliovirus vaccine (IPV), is based on poliovirus grown in a type of monkey kidney tissue culture (Vero cell line), which is chemically-inactivated with formalin. After two doses of IPV, ninety percent or more of individuals develop protective antibody to all three serotypes of poliovirus, and at least 99% are immune to poliovirus following three doses. IPV is currently the vaccine of choice in most countries.

Eight years after Salk's success, Albert Sabin developed an oral polio vaccine (OPV) using live but weakened (attenuated) virus, produced by the repeated passage of the virus through non-human cells at sub-physiological temperatures. Human trials of Sabin's vaccine began in 1957 and it was licensed in 1962. The attenuated poliovirus in the Sabin vaccine replicates very efficiently in the gut, the primary site of wild poliovirus infection and replication, but the vaccine strain is unable to replicate efficiently within nervous system tissue. OPV produces excellent immunity in the intestine, which helps prevent infection with wild virus in areas where the virus is endemic. A single dose of oral polio vaccince produces immunity to all three poliovirus serotypes in approximately 50% of recipients. Three doses of live-attenuated OPV produce protective antibody to all three poliovirus types in more than 95% of recipients.

Prognosis

Patients with abortive polio infections recover completely. In those that develop only aseptic meningitis, the symptoms can be expected to persist for two to ten days, followed by complete recovery.[4] In cases of spinal polio, if the affected nerve cells are completely destroyed, paralysis will be permanent; cells that are not destroyed but lose function temporarily may recover within four to six weeks after onset.[4] Half the patients with spinal polio recover fully, one quarter recover with mild disability and the remaining quarter are left with severe disability.[5] The degree of both acute paralysis and residual paralysis is likely to be proportional to the degree of viremia, and inversely proportional to the degree of immunity.[6]. Spinal polio is rarely fatal.[7]

A child with a deformity of her right leg due to polio

Without respiratory support, consequences of poliomyelitis with respiratory involvement include suffocation or pneumonia from aspiration of secretions.[8] Overall, 5–10% of patients with paralytic polio die due to the paralysis of muscles used for breathing. The mortality rate varies by age: 2–5% of children and up to 15–30% of adults die.[9] Bulbar polio often causes death if respiratory support is not provided;[10] with support, its mortality rate ranges from 25 to 75%, depending on the age of the patient.[9][11] When positive pressure ventilators are available, the mortality can be reduced to 15%.[12]

Recovery

Many cases of poliomyelitis result in only temporary paralysis.[13] Nerve impulses return to the formerly paralyzed muscle within a month, and recovery is usually complete in six to eight months.[4] The neurophysiological processes involved in recovery following acute paralytic poliomyelitis are quite effective; muscles are able to retain normal strength even if half the original motor neurons have been lost.[14] Paralysis remaining after one year is likely to be permanent, although modest recoveries of muscle strength are possible 12 to 18 months after infection.[4]

One mechanism involved in recovery is nerve terminal sprouting, in which remaining brainstem and spinal cord motor neurons develop new branches, or axonal sprouts.[15] These sprouts can reinnervate orphaned muscle fibers that have been denervated by acute polio infection,[16] restoring the fibers' capacity to contract and improving strength.[17] Terminal sprouting may generate a few significantly enlarged motor neurons doing work previously performed by as many as four or five units: [18] a single motor neuron that once controlled 200 muscle cells might control 800 to 1000 cells. Other mechanisms that occur during the rehabilitation phase, and contribute to muscle strength restoration, include myofiber hypertrophy—enlargement of muscle fibers through exercise and activity—and transformation of type II muscle fibers to type I muscle fibers.[16][19]

In addition to these physiological processes, the body possesses a number of compensatory mechanisms to maintain function in the presence of residual paralysis. These include the use of weaker muscles at a higher than usual intensity relative to the muscle's maximal capacity, enhancing athletic development of previously little-used muscles, and using ligaments for stability, which enables greater mobility.[19]

Complications

Residual complications of paralytic polio often occur following the initial recovery process. [20] Muscle paresis and paralysis can sometimes result in skeletal deformities, tightening of the joints and movement disability. Once the muscles in the limb become flaccid, they may interfere with the function of other muscles. A typical manifestation of this problem is equinus foot (similar to club foot). This deformity develops when the muscles that pull the toes downward are working, but those that pull it upward are not, and the foot naturally tends to drop toward the ground. If the problem is left untreated, the Achilles tendons at the back of the foot retract and the foot cannot take on a normal position. Polio victims that develop equinus foot cannot walk properly because they cannot put their heel on the ground. A similar situation can develop if the arms become paralyzed.[21] In some cases the growth of an affected leg is slowed by polio, while the other leg continues to grow normally. The result is that one leg is shorter than the other and the person limps and leans to one side, in turn leading to deformities of the spine (such as scoliosis).[21] Osteoporosis and increased likelihood of bone fractures may occur. Extended use of braces or wheelchairs may cause compression neuropathy, as well as a loss of proper function of the veins in the legs, due to pooling of blood in paralyzed lower limbs.[22][10] Complications from prolonged immobility involving the lungs, kidneys and heart include pulmonary edema, aspiration pneumonia, urinary tract infections, kidney stones, paralytic ileus, myocarditis and cor pulmonale.[22][10]

Post-polio syndrome

Main article: Post-polio syndrome

Around a quarter of individuals who survive paralytic polio in childhood develop additional symptoms decades after recovering from the acute infection, notably muscle weakness, extreme fatigue, or paralysis. This condition is known as post-polio syndrome (PPS).[23] The symptoms of PPS are thought to involve a failure of the over-sized motor units created during recovery from paralytic disease.[24][25] Factors that increase the risk of PPS include the length of time since acute poliovirus infection, the presence of permanent residual impairment after recovery from the acute illness, and both overuse and disuse of neurons.[23] Post-polio syndrome is not an infectious process, and persons experiencing the syndrome do not shed poliovirus.[9]

References

  1. ↑ 1.0 1.1 Hammon W (1955). "Passive immunization against poliomyelitis". Monogr Ser World Health Organ. 26: 357–70. PMID 14374581.
  2. ↑ Hammon W, Coriell L, Ludwig E; et al. (1954). "Evaluation of Red Cross gamma globulin as a prophylactic agent for poliomyelitis. 5. Reanalysis of results based on laboratory-confirmed cases". J Am Med Assoc. 156 (1): 21–7. PMID 13183798.
  3. ↑ Rinaldo C (2005). "Passive immunization against poliomyelitis: the Hammon gamma globulin field trials, 1951–1953". Am J Public Health. 95 (5): 790–9. PMID 15855454.
  4. ↑ 4.0 4.1 4.2 4.3 Neumann D (2004). "Polio: its impact on the people of the United States and the emerging profession of physical therapy" (PDF). The Journal of orthopaedic and sports physical therapy. 34 (8): 479–92. PMID 15373011. Reproduced online with permission by Post-Polio Health International; retrieved on 2007-11-10.
  5. ↑ Cuccurullo SJ (2004). Physical Medicine and Rehabilitation Board Review. Demos Medical Publishing. ISBN 1-888799-45-5.
  6. ↑ Mueller S, Wimmer E, Cello J (2005). "Poliovirus and poliomyelitis: a tale of guts, brains, and an accidental event". Virus Res 111 (2): 175–93. PMID 15885840
  7. ↑ Silverstein A, Silverstein V, Nunn LS (2001). Polio, Diseases and People. Berkeley Heights, NJ: Enslow Publishers, 12. ISBN 0-7660-1592-0.
  8. ↑ Goldberg A (2002). "Noninvasive mechanical ventilation at home: building upon the tradition". Chest. 121 (2): 321–4. PMID 11834636.
  9. ↑ 9.0 9.1 9.2
  10. ↑ 10.0 10.1 10.2 Hoyt, William Graves; Miller, Neil; Walsh, Frank (2005). Walsh and Hoyt's clinical neuro-ophthalmology. Hagerstown, MD: Lippincott Williams & Wilkins. pp. 3264–65. ISBN 0-7817-4814-3.
  11. ↑ Miller AH, Buck LS (1950). "Tracheotomy in bulbar poliomyelitis". California medicine. 72 (1): 34–6. PMID 15398892.
  12. ↑ Template:Cite paper
  13. ↑ Frauenthal HWA, Manning JVV (1914). Manual of infantile paralysis, with modern methods of treatment.. Philadelphia Davis, 79–101. OCLC 2078290
  14. ↑ Sandberg A, Hansson B, Stålberg E (1999). "Comparison between concentric needle EMG and macro EMG in patients with a history of polio". Clinical Neurophysiology. 110 (11): 1900–8. PMID 10576485.
  15. ↑ Cashman NR, Covault J, Wollman RL, Sanes JR (1987). "Neural cell adhesion molecule in normal, denervated, and myopathic human muscle". Ann. Neurol. 21 (5): 481–9. PMID 3296947.
  16. ↑ 16.0 16.1 Agre JC, Rodríquez AA, Tafel JA (1991). "Late effects of polio: critical review of the literature on neuromuscular function". Archives of physical medicine and rehabilitation. 72 (11): 923–31. PMID 1929813.
  17. ↑ Trojan DA, Cashman NR (2005). "Post-poliomyelitis syndrome". Muscle Nerve. 31 (1): 6–19. PMID 15599928.
  18. ↑ Gawne AC, Halstead LS (1995). "Post-polio syndrome: pathophysiology and clinical management". Critical Review in Physical Medicine and Rehabilitation 7: 147–88. Reproduced online with permission by Lincolnshire Post-Polio Library; retrieved on 2007-11-10.
  19. ↑ 19.0 19.1 Grimby G, Einarsson G, Hedberg M, Aniansson A (1989). "Muscle adaptive changes in post-polio subjects". Scandinavian journal of rehabilitation medicine. 21 (1): 19–26. PMID 2711135.
  20. ↑ Leboeuf C (1992). The late effects of Polio: Information For Health Care Providers. (PDF), Commonwealth Department of Community Services and Health. ISBN 1-875412-05-0. Retrieved on 2007-11-10.
  21. ↑ 21.0 21.1 Sanofi Pasteur. "Poliomyelitis virus (picornavirus, enterovirus), after-effects of the polio, paralysis, deformations". Polio Eradication. Retrieved 2007-07-31.
  22. ↑ 22.0 22.1 Mayo Clinic Staff (2005-05-19). "Polio: Complications". Mayo Foundation for Medical Education and Research (MFMER). Retrieved 2007-02-26. Check date values in: |date= (help)
  23. ↑ 23.0 23.1 Trojan D, Cashman N (2005). "Post-poliomyelitis syndrome". Muscle Nerve. 31 (1): 6–19. PMID 15599928.
  24. ↑ Ramlow J, Alexander M, LaPorte R, Kaufmann C, Kuller L (1992). "Epidemiology of the post-polio syndrome". Am. J. Epidemiol. 136 (7): 769–86. PMID 1442743.
  25. ↑ Lin K, Lim Y (2005). "Post-poliomyelitis syndrome: case report and review of the literature" (PDF). Ann Acad Med Singapore. 34 (7): 447–9. PMID 16123820.


Further reading

Acknowledgements

The content on this page was first contributed by: C. Michael Gibson, M.S., M.D.

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