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INCUBATION PERIOD
CLINICAL MANIFESTATIONS OF INFECTION
Best estimates of the incubation period of poliomyelitis are 9 to 12 days (range, 5 to 35 days) measured from presumed contact until the onset of the prodromal symptoms, and 11 to 17 days (range, 8 to 36 days) until the onset of paralysis.26
The manifestations of infection by polioviruses range from unapparent illness to severe paralysis and death.
 
At least 95% of infections are asymptomatic or unapparent and can be recognized only by the isolation of poliovirus from feces or oropharynx or by a rise in antibody titer.
 
Abortive poliomyelitis, which occurs in 4% to 8% of infections, is characterized by a 2- to 3-day period of fever, which may be accompanied by headache, sore throat, listlessness, anorexia, vomiting, or abdominal pain. Because the neurologic exami- nation is normal, abortive poliomyelitis cannot be distinguished from other viral infections and can be clinically suspected only during an epidemic.
 
Nonparalytic poliomyelitis differs from abortive poliomyeli- tis by the presence of signs of meningeal irritation. The disease is identical to meningitis caused by other enteroviruses. The systemic manifestations of nonparalytic poliomyelitis are generally more severe than in abortive poliomyelitis.  


CLINICAL MANIFESTATIONS OF INFECTION
The manifestations of infection by polioviruses range from unapparent illness to severe paralysis and death. Usual estimates of the ratio of unapparent to clinically recognized polio infection, which vary by serotype, range from 60 to 1000 : 1.3,27 Figure 171-1 depicts the time course for the clinical manifestations of poliovirus infection. At least 95% of infections are asymptomatic or unapparent and can be recog- nized only by the isolation of poliovirus from feces or oropharynx or by a rise in antibody titer. Abortive poliomyelitis, which occurs in 4% to 8% of infections, is characterized by a 2- to 3-day period of fever, which may be accompanied by headache, sore throat, listlessness, anorexia, vomiting, or abdominal pain. Because the neurologic exami- nation is normal, abortive poliomyelitis cannot be distinguished from other viral infections and can be clinically suspected only during an epidemic. Nonparalytic poliomyelitis differs from abortive poliomyeli- tis by the presence of signs of meningeal irritation. The disease is identical to meningitis caused by other enteroviruses. The systemic manifestations of nonparalytic poliomyelitis are generally more severe than in abortive poliomyelitis.
Spinal Paralytic Poliomyelitis
Spinal Paralytic Poliomyelitis
Frank paralysis occurs in roughly 0.1% of all poliovirus infections. A biphasic course with minor and major illnesses is observed in approxi- mately one third of children with paralytic poliomyelitis. The minor illness, coinciding with viremia, corresponds to the symptoms of abor- tive poliomyelitis and lasts 1 to 3 days. The patient appears to be recovering and remains symptom-free for 2 to 5 days before the abrupt onset of the major illness, which is heralded by symptoms and signs of meningitis, including fever, chills, headache, fever, malaise, vomit- ing, neck stiffness, and cerebrospinal fluid (CSF) pleocytosis. Adults usually experience a single phase of illness, with a prolonged prodrome of symptoms preceding the gradual onset of paralysis.28,29 The major illness begins with severe myalgias and occasionally localized cutane- ous hyperesthesia, paresthesias, involuntary muscle spasm, or muscu- lar fasciculations. The meningismus and muscle pain are present for 1 to 2 days before frank weakness and paralysis ensue. The severity of the disease varies from weakness of a single portion of one muscle to complete quadriplegia. The paralysis is flaccid; deep tendon reflexes are initially hyperactive and then become absent. The most character- istic feature of the paralysis is its asymmetrical distribution, which affects some muscle groups while sparing others. Proximal muscles of the extremities tend to be more involved than distal muscles, the legs are more commonly involved than the arms, and the large muscle groups of the hand are at greater risk than the small ones. Any com- bination of limbs may be paralyzed, but the most common pattern is involvement of one leg, followed by one arm, or both legs and both arms. Quadriplegia is almost never observed in infants.29 Although occasional cases progress from the onset of weakness to complete quadriplegia and bulbar involvement in a few hours, more commonly the paralysis extends over 2 to 3 days. Progression of paralysis stops when the patient becomes afebrile.28 Paralysis of the bladder is usually associated with paralysis of the legs. It occurs in about 25% of adults but is uncommon in children. Sensory loss in poliomyelitis is very rare30 and its occurrence should strongly suggest some other diagnosis (e.g., Guillain-Barré syndrome).
Frank paralysis occurs in roughly 0.1% of all poliovirus infections. A biphasic course with minor and major illnesses is observed in approxi- mately one third of children with paralytic poliomyelitis. The minor illness, coinciding with viremia, corresponds to the symptoms of abor- tive poliomyelitis and lasts 1 to 3 days. The patient appears to be recovering and remains symptom-free for 2 to 5 days before the abrupt onset of the major illness, which is heralded by symptoms and signs of meningitis, including fever, chills, headache, fever, malaise, vomit- ing, neck stiffness, and cerebrospinal fluid (CSF) pleocytosis. Adults usually experience a single phase of illness, with a prolonged prodrome of symptoms preceding the gradual onset of paralysis.28,29 The major illness begins with severe myalgias and occasionally localized cutane- ous hyperesthesia, paresthesias, involuntary muscle spasm, or muscu- lar fasciculations. The meningismus and muscle pain are present for 1 to 2 days before frank weakness and paralysis ensue. The severity of the disease varies from weakness of a single portion of one muscle to complete quadriplegia. The paralysis is flaccid; deep tendon reflexes are initially hyperactive and then become absent. The most character- istic feature of the paralysis is its asymmetrical distribution, which affects some muscle groups while sparing others. Proximal muscles of the extremities tend to be more involved than distal muscles, the legs are more commonly involved than the arms, and the large muscle groups of the hand are at greater risk than the small ones. Any com- bination of limbs may be paralyzed, but the most common pattern is involvement of one leg, followed by one arm, or both legs and both arms. Quadriplegia is almost never observed in infants.29 Although occasional cases progress from the onset of weakness to complete quadriplegia and bulbar involvement in a few hours, more commonly the paralysis extends over 2 to 3 days. Progression of paralysis stops when the patient becomes afebrile.28 Paralysis of the bladder is usually associated with paralysis of the legs. It occurs in about 25% of adults but is uncommon in children. Sensory loss in poliomyelitis is very rare30 and its occurrence should strongly suggest some other diagnosis (e.g., Guillain-Barré syndrome).


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Overview

Many cases of poliomyelitis result in only temporary paralysis. After an interval of 30–40 years, 25%–40% of persons who contracted paralytic poliomyelitis in childhood experience new muscle pain and exacerbation of existing weakness, or develop new weakness or paralysis. This disease entity is referred to as pos-tpolio syndrome. 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.

Natural History

Poliovirus enters the body through the mouth, infecting nearby cells, such as those of the oral mucosa, nose and throat. The incubation period is considered the time between the assumed time of infection, and symptom onset. The incubation period often ranges from 7 to 14 days, however, it may vary from 5 to 35 days.[1][2]


Many cases of poliomyelitis result in only temporary paralysis.[3] Nerve impulses return to the formerly paralyzed muscle within a month, and recovery is usually complete in six to eight months. 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.[4] Paralysis remaining after one year is likely to be permanent, although modest recoveries of muscle strength are possible 12 to 18 months after infection.

One mechanism involved in recovery is nerve terminal sprouting, in which remaining brainstem and spinal cord motor neurons develop new branches, or axonal sprouts.[5] These sprouts can reinnervate orphaned muscle fibers that have been denervated by acute polio infection,[6] restoring the fibers' capacity to contract and improving strength.[7] Terminal sprouting may generate a few significantly enlarged motor neurons doing work previously performed by as many as four or five units: [8] 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.[6][9]

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.

Complications

Potential complications of poliomyelitis may include:[10][11][12][13][14][15][16][17]

Complications Description
Respiratory compromise
Myocarditis
  • Inflammatory infiltration in cardiac muscle
Gastrointestinal
Musculo-Skeletal
Postpoliomyelitis Syndrome
  • Occurs in 20-30% of patients with history of paralytic poliomyelitis (25-35 years before), who have made a partial or full recovery
  • Commonly involves previously affected muscles
  • New onset of:
  • Gradual symptom progression
  • Possible cause:
  • Attrition of motor nerves that innervate previously affected muscles

Prognosis

  • The mortality rate from poliomyelitis is referred to the period during which the disease was epidemic. During that period, acute paralytic poliomyelitis had a mortality rate of 5-10%, however, this number was higher in the case of bulbar poliomyelitis.[18]
  • Patients with abortive poliomyelitis often have a full recovery.[19]
  • Patients who develop aseptic meningitis, can expect symptoms to persist for 2-10 days, followed by complete recovery.[20]
  • Spinal poliomyelitis is rarely fatal.[21]
  • Muscle paralysis usually lasts 1-3 days, and in some cases up to 1 week.[22] Persistent weakness occurs in two thirds of patients with the paralytic form of the disease.
  • Patients with severe form of paralytic poliomyelitis, and those who require mechanical ventilation have less probability to recover.[23]
  • 5 to 10% of patients with paralytic poliomyelitis die due to the paralysis of respiratory muscles. The mortality rate varies with age: 2-5% in children, 15-30% in adult. In the presence of support, bulbar poliomyelitis has a mortality rate of 25-75%, depending on the patient's age.[24] When positive pressure ventilators are available, the mortality can be reduced to 15%.[25]
  • Permanent sequelae is uncommon in patients who have survived bulbar poliomyelitis.[26]

References

  1. ↑ 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. doi:10.1016/j.virusres.2005.04.008. PMID 15885840.
  2. ↑ Mandell, Gerald (2010). Mandell, Douglas, and Bennett's principles and practice of infectious diseases. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0443068399.
  3. ↑ Frauenthal HWA, Manning JVV (1914). Manual of infantile paralysis, with modern methods of treatment.. Philadelphia Davis, 79–101. OCLC 2078290
  4. ↑ 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.
  5. ↑ 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.
  6. ↑ 6.0 6.1 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.
  7. ↑ Trojan DA, Cashman NR (2005). "Post-poliomyelitis syndrome". Muscle Nerve. 31 (1): 6–19. PMID 15599928.
  8. ↑ 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.
  9. ↑ 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.
  10. ↑ Mandell, Gerald (2010). Mandell, Douglas, and Bennett's principles and practice of infectious diseases. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0443068399.
  11. ↑ WEINSTEIN L (1957). "Cardiovascular disturbances in poliomyelitis". Circulation. 15 (5): 735–56. PMID 13427128.
  12. ↑ GALPINE JF, WILSON WC (1959). "Occurrence of myocarditis in paralytic poliomyelitis". Br Med J. 2 (5163): 1379–81. PMC 1990933. PMID 13826196.
  13. ↑ 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)
  14. ↑ 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.
  15. ↑ Dalakas MC, Sever JL, Madden DL, Papadopoulos NM, Shekarchi IC, Albrecht P; et al. (1984). "Late postpoliomyelitis muscular atrophy: clinical, virologic, and immunologic studies". Rev Infect Dis. 6 Suppl 2: S562–7. PMID 6330854.
  16. ↑ Dalakas MC, Elder G, Hallett M, Ravits J, Baker M, Papadopoulos N; et al. (1986). "A long-term follow-up study of patients with post-poliomyelitis neuromuscular symptoms". N Engl J Med. 314 (15): 959–63. doi:10.1056/NEJM198604103141505. PMID 3007983.
  17. ↑ Johnson RT (1984). "Late progression of poliomyelitis paralysis: discussion of pathogenesis". Rev Infect Dis. 6 Suppl 2: S568–70. PMID 6330855.
  18. ↑ FERRIS BG, AULD PA, CRONKHITE L, KAUFMANN HJ, KEARSLEY RB, PRIZER M; et al. (1960). "Life-threatening poliomyelitis, Boston, 1955". N Engl J Med. 262: 371–80. doi:10.1056/NEJM196002252620801. PMID 13822503.
  19. ↑ Mandell, Gerald (2010). Mandell, Douglas, and Bennett's principles and practice of infectious diseases. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0443068399.
  20. ↑ 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.
  21. ↑ Silverstein A, Silverstein V, Nunn LS (2001). Polio, Diseases and People. Berkeley Heights, NJ: Enslow Publishers, 12. ISBN 0-7660-1592-0.
  22. ↑ Ritchie Russell, W.; Fischer-Williams, M. (1954). "RECOVERY OF MUSCULAR STRENGTH AFTER POLIOMYELITIS". The Lancet. 263 (6807): 330–333. doi:10.1016/S0140-6736(54)91084-3. ISSN 0140-6736.
  23. ↑ Mandell, Gerald (2010). Mandell, Douglas, and Bennett's principles and practice of infectious diseases. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0443068399.
  24. ↑ Miller AH, Buck LS (1950). "Tracheotomy in bulbar poliomyelitis". California medicine. 72 (1): 34–6. PMID 15398892.
  25. ↑ Template:Cite paper
  26. ↑ Mandell, Gerald (2010). Mandell, Douglas, and Bennett's principles and practice of infectious diseases. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0443068399.

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