Poliomyelitis vs. Guillain-Barré syndrome: A comparative analysis of etiology, symptoms, prognosis and treatment
Both poliomyelitis and Guillain-Barré syndrome (GBS) cause acute flaccid paralysis (Yuki & Hartung, 2012). However, polio has been nearly eradicated, worldwide, making GBS a leading cause of acute flaccid paralysis (Yuki & Hartung, 2012). Poliomyelitis and GBS are comparable with regard to some of the symptoms exhibited by the patients (Papadakis & McPheee, 2013); however, both of these diseases differ remarkably in the causative agent, pathophysiology, prognosis and treatment regime (Papadakis & McPheee, 2013).
Epidemiology and etiology
Poliomyelitis is caused by Poliovirus, an enterovirus. The route of disease transmission is fecal-oral, usually by a hand-to-hand-to-mouth route (Nathanson & Kew, 2010). The excreta and the pharyngeal fluids form the major source of the virus (Papadakis & McPheee, 2013). The earliest outbreaks of poliomyelitis were recorded in Europe in the 19th century. The most vulnerable group is children aged five years and under (Nathanson & Kew, 2010). Even though poliomyelitis is a disorder of acute flaccid paralysis, only 1 in 200 patients suffer from irreversible paralysis. Poliomyelitis is fatal if the paralysis occurs in the respiratory muscles and has been found to occur in 5-10% of the cases. The discovery of polio vaccine in the mid 1950s helped bring down the polio cases by 99% within three decades (Centers for Disease Control and Prevention [CDC], 2015). There are three types of wild poliovirus (WPV 1-3), of which type-1 is responsible for 80% of the paralytic polio (Nathanson & Kew, 2010).
Unlike polio, which occurs because of a viral infection, GBS is a post-infection autoimmune disorder. That is, GBS usually occurs a few weeks after an infection, typically caused by Campylobacter jejuni, a bacterium (Pithadia & Kakadia, 2010). Infectious agents such as Mycoplasma pneumoniae, Epstein-Barr virus and Haemophilus influenzae have also been associated with the development of GBS. Such a preceding infection has been observed in two-thirds of the patients, with fever, cough and sore throat being the most common symptoms. Antibodies against self- axon gangliosides cause GBS (Papadakis & McPheee, 2013). GBS is characterized by albuminocytologic dissociation in 50% of the patients in the first week and 75% of the cases within the third week. Poliomyelitis, also shows albuminocytologic dissociation but only during the late phases (Yuki & Hartung, 2012). The annual worldwide incidence of GBS in the Western countries has been found to be between 0.89 and 1.89 for 100,000 person years. Men are nearly twice more likely to be affected by GBS than women (Yuki & Hartung, 2012). Though such a gender disparity is not seen in poliomyelitis, age disparity is prevalent. C. jejuni accounts for about 30% of the infections that result in GBA, followed by cytomegalovirus that causes 10% of the infection preceding GBS (Yuki & Hartung, 2012).
Signs and symptoms
72% of the patients with poliovirus infections are asymptomatic while the rest show symptoms such as fever, sore throat, muscle spasms and stiffness of the neck and limbs (CDC, 2015). There are four types of poliomyelitis, namely, abortive, non-paralytic, paralytic spinal and paralytic bulbar poliomyelitis. Abortive poliomyelitis is characterized by fever, diarrhea, constipation, vomiting and headache, which clears up within a week. Non-paralytic poliomyelitis is characterized by symptoms of abortive poliomyelitis along with muscle spasms and pain during lifting of legs and heads that last for a maximum of 10 days followed by complete recovery (CDC, 2015). Paralytic spinal poliomyelitis, which is common in children, is characterized by paralysis of the shoulder, diaphragm, intercostal and chest muscles. Permanent paralysis occurs in the lower extremities. Paralytic bulbar poliomyelitis is common in adults, which is characterized by respiratory paralysis, regurgitation of fluids from the nasal passage, inability to swallow and facial weakness and is fatal (Papadakis & McPheee, 2013). Unlike GBS, numbness is not a sign associated with poliomyelitis (CDC, 2015).
There are three subtypes of GBS, namely, acute motor axonal neuropathy (AMAN), acute motor and sensory axonal neuropathy (AMSAN) and Miller-Fischer syndrome (which resembles paralytic bulbar poliomyelitis) (Papadakis & McPheee, 2013). After an unremarkable infection, the first signs of GBS appear in the form of numbness, ‘pins and needles’ sensation in the legs that spread upwards to the face along with pain and weakness of the extremities and absence of reflexes in the legs and arms with subsequent progression to paralysis of all the four limbs. The weakness is bilateral and symmetric, which is a distinguishing feature of GBS as poliomyelitis-associated paralysis is typically asymmetric (Yuki & Hartung, 2012; CDC, 2015). Electrodiagnostic test findings include high protein content in the cerebrospinal fluid (CSF) with normal cell numbers and demyelination. In poliomyelitis, protein in CSF is normal or only slightly elevated (Papadakis & McPheee, 2013). Fifty percent of the patients reach the clinical lowest point by 2 weeks while 95% of the cases reach nadir by week 4. A third of the patients suffer respiratory paralysis and 20% of the mechanically ventilated patients die of GBS. While recovery of muscle function is better in GBS when compared to poliomyelitis, 20-30% of the patients with GBS experience permanent disability. Heart rate and blood pressure fluctuations are serious implications of GBS. Patients who cannot walk and are typically bedridden can experience deep vein thrombosis (Meena et al., 2011).
Poliovirus enters through the mouth and multiplies in the gastrointestinal tract and pharynx. The virus is shed through the mouth and stool even before the onset of the disease. The virus incubates for an average of 10 days (Nathanson & Kew, 2010). The virus enters the bloodstream, invades the lymphoid tissues and cells of the central nervous system and destroys motor neurons that leads to paralysis and other symptoms of poliomyelitis (CDC, 2015).
Following an infection such as C. jejuni, the body commences production of self-antibodies against the axon gangliosides such as GM1, GM1b, GD1a, and GalNAc-GD1a. C. jejuni has been found to have structural similarities to the ganglioside present in humans. Therefore, the antibodies produced against C. jejuni end up attacking not only the bacterium but also the self-gangliosides. This mechanism of molecular mimicry and cross-reactivity is thought to cause demyelination and axonal damage, thereby resulting in GBS (Pithadia & Kakadia, 2010).
Prevention and treatment
There is no treatment for poliomyelitis and prevention by immunization is the only way to avoid poliovirus infection. Inactivated poliovirus vaccine (IPV) was the first vaccine against polio. Trivalent oral polio vaccine (OPV) contains live attenuated virus strains. In the late 1980s, an improved potency IPV was developed, which replaced the use of OPV in some countries (CDC, 2015). Clinical management during poliomyelitis includes immediate hospitalization, bed rest to reduce paralysis, use of polio beds to rotate patient's position, treating fecal impaction and urine retention owing to muscle paralysis of the pelvis, alleviating weakened respiratory ability and psychological support regarding the possible reduced quality of life owing to lifelong disability (Papadakis & McPheee, 2013).
Just like poliomyelitis, the effects of GBS can only be alleviated to a certain extent but not cured. Plasmapheresis or plasma exchange (PE) and intravenous immunoglobulin (IVIg) are some of the effective treatment regimens for managing GBS (Meena et al, 2011; (Papadakis & McPheee, 2013). PE (5 sessions of 50ml/kg over 2 weeks) is usually the first line of treatment and very effective for patients with mild to severe GBS. IVIg (400 mg/kg/d for 5 days) is a good option for those with cardiovascular complications.
When comparing data on the two diseases, it can be concluded that polio is associated with symptoms such as asymmetric paralysis, normal CSF protein levels, viral in origin, working sensory neurons, increased childhood prevalence and late phase albumincytologic dissociation. GBS is associated with numbness, symmetric and ascending paralysis, elevated CSF protein, post-infection disorder, prevalent in adults, especially men and shows an early phase albumincytologic dissociation. Both polio and GBS have the ability to confer permanent disability. Both the diseases are associated with a certain level of mortality. While there is no treatment for polio, it can be prevented through IPV and OPV. GBS cannot be prevented but can be managed for full recovery using PE and IVIg.
Centers for Disease Control and Prevention. (2015). Epidemiology and Prevention of Vaccine-Preventable Diseases (13th ed.). Hamborsky J, Kroger A, Wolfe S (Eds.). Washington D.C.: Public Health Foundation.
Meena, A. K., Khadilkar, S. V., & Murthy, J. M. K. (2011). Treatment guidelines for Guillain–Barré syndrome. Annals of Indian Academy of Neurology, 14(Suppl1), S73.
Nathanson, N., & Kew, O. M. (2010). From emergence to eradication: the epidemiology of poliomyelitis deconstructed. American journal of epidemiology, 1-17.
Papadakis, M. A. & McPhee, S. J. (Eds.). (2013). Current Medical Diagnosis & Treatment 2013. McGraw-Hill Medical.
Pithadia, A. B., & Kakadia, N. (2010). Guillain-Barré syndrome (GBS). Pharmacological Reports, 62(2), 220-232.
Yuki, N., & Hartung, H. P. (2012). Guillain–Barré syndrome. New England Journal of Medicine, 366(24), 2294-2304.