Poliomyelitis

Original Editor -Chrysolite Jyothi Kommu

Top Contributors - Chrysolite Jyothi Kommu, Stacy Schiurring, Nikhil Benhur Abburi, Jess Bell, Momina Khalid, Simisola Ajeyalemi and Kim Jackson

Aetiology

Poliomyelitis (also known as Polio) is an acute infectious disease caused by poliovirus. Humans are the only natural reservoir for poliovirus, and transmission occurs primarily through the faecal-oral route, with respiratory transmission being less commonly encountered. There are three serotypes (variations) of poliovirus.

Serotype 1 (PV1) is the most paralytogenic (likely to cause paralysis) and used to be the most common cause of epidemics. PV1 is the most common form encountered in nature and as of March 2020, wild PV1 is highly localised to regions in Pakistan and Afghanistan.

Serotype 2 (PV2) has been successfully eradicated. Certification of the eradication of indigenous transmission of wild PV2 occurred in September 2015, after last being detected in 1999.

Serotype 3 (PV3) was also eradicated, with eradication certified in October 2019 for wild PV3, after last being detected in 2012.

Multiple risk factors increase susceptibility to polio infection, including pregnancy, extreme age (very young or very old), immune deficiency, and malnutrition. The disease primarily affects children younger than 5 years in countries with poor water, sanitation, and hygiene infrastructure. Unvaccinated individuals under 15 years are at increased risk, with those under 5 being most susceptible. Environmental and social factors that contribute to transmission include high population density, poor health service infrastructure, poor sanitation, high incidence of diarrhoeal diseases, and low oral polio vaccine coverage. Improper sanitation facilities and a lack of personal hygiene have been identified as the most important contributory factors, leading to exposure at ages when maternal antibody protection has waned.

Epidemiology

Evidence indicates that polio is an ancient disease, dating back to ancient Egypt (1570–1342 BCE). However, polio epidemics did not begin to occur until the latter part of the 19th century.

The epidemic form of this disease was first reported by Medin in 1890, after an epidemic of 44 cases in Stockholm in the summer of 1887. The first known polio epidemic in the United States occurred in Vermont in 1894. There were cycles of epidemics from 1900, each cycle seeming to get stronger and more disastrous, affecting mostly children. The disease reached its peak devastation in the mid-20th century.

The turning point came with vaccine development. In the early 1950s, the first successful vaccine was created by US physician Jonas Salk. The vaccine was found to be 80-90% effective against paralytic polio, and the US government licensed Salk's vaccine in 1955. Subsequently, in 1962, an oral polio vaccine was developed by researcher Albert Sabin, using an attenuated live polio virus, which was easier to administer and greatly facilitated distribution. Soon after the introduction of effective vaccines in the 1950s and 1960s, polio was brought under control and practically eliminated as a public health problem in developed countries. This success laid the foundation for the global eradication initiative that continues today.

Poliomyelitis has had a dramatic epidemiological transformation since the launch of the Global Polio Eradication Initiative in 1988. Wild poliovirus cases have decreased by over 99% since 1988, from an estimated 350,000 cases in more than 125 endemic countries to historically low levels. Currently, Afghanistan and Pakistan are the only two remaining polio endemic countries in the world. Additionally, circulating vaccine-derived poliovirus outbreaks continue to emerge in multiple regions globally, primarily in Africa. These outbreaks are driven by inadequate vaccination coverage. Despite these challenges, the global epidemiological picture demonstrates that the world stands on the threshold of eradicating a human disease globally for only the second time in history, after smallpox in 1980. However, failure to stop polio in these last remaining areas could result in global resurgence of the disease.

Pathogenesis

The pathogenesis of poliomyelitis follows three distinct phases (alimentary, viremic, neurologic) that progress from initial infection to potential neurological complications.

Alimentary phase: polio is an enterovirus that is ingested and travels through the gastrointestinal tract where infection can be initiated. It begins when the virus multiplies in the alimentary mucosa, and possibly in the tonsils and Peyer's patches.

Viremic phase: there is viral spread through both the lymphatic system and the bloodstream. The virus invades local lymphoid tissue and subsequently moves into the bloodstream. The poliovirus is able to survive and multiply within the blood and lymphatics for long periods of time, sometimes as long as 17 weeks.

Neurologic phase: the most critical stage where the virus can infect the cells of the central nervous system (CNS). Within the CNS, the poliovirus can replicate within the spinal cord, brain stem, or motor cortex. This causes the selective destruction of motor neurons, which leads to temporary or permanent paralysis. This neuroinvasive phase occurs in less than 1% of infections, but represents the most devastating manifestation of poliovirus symptoms.

Clinical Presentation

The clinical progression of paralytic poliomyelitis follows four distinct stages, from initial symptoms through to long-term recovery.

During the pre-paralytic (or prodromal) stage, early signs and symptoms are present, including fever, headache, muscle pain, and general malaise. This stage may last several days before the onset of paralysis and it can be mistaken for other viral illnesses.

The acute phase is the most critical period. During this phase, the virus affects the CNS, causing symptoms, such as loss of reflexes, severe muscle aches or spasms, and flaccid paralysis. These symptoms are often worse on one side of the body, and typically develop within a week of the neurologic phase of disease pathogenesis.

The convalescent stage begins as the acute inflammatory process subsides. It is during this stage that the extent of permanent damage becomes apparent—patients begin to stabilise and present with neurological deficits.

The recovery stage is the prolonged rehabilitation period where affected muscles can be strengthened to their maximum capacity. Recovery can occur for up to 2 years, with maximal improvement typically occurring in the first 6 months after infection. Approximately 60% of polio survivors continue to have permanent neuromotor deficits.

Table 1. Signs and Symptoms of Poliomyelitis by Clinical Presentation

Clinical Presentation	Prevalence	Common Signs and Symptoms
Asymptomatic Infection	70-95% of all cases	Most people with a normal immune system have an asymptomatic poliovirus infection
Abortive Poliomyelitis	24% of symptomatic cases	Fever (up to 103°F or 39.4°C) Decreased appetite Nausea and/or vomiting Sore throat Malaise Constipation Abdominal pain NO CNS involvement Complete recovery occurring within one or two weeks
Nonparalytic Poliomyelitis	1-5% of infections	Represents aseptic meningitis with CNS involvement but WITHOUT paralysis Flu-like symptoms that include: fever, fatigue, sore throat, headache Digestive issues: nausea and vomiting, diarrhoea, constipation, stomach pain Signs of brain and spinal cord swelling: severe headache, sensitivity to light or touch, neck stiffness Nervous system effects: pain or pins-and-needles sensations Complete recovery typically occurs within 2-10 days
Paralytic Poliomyelitis	<1% of infections	Initial symptoms: fever, fatigue, headache, vomiting, neck stiffness and pain in the limbs In the preparalytic period (24-48 hours prior to paralysis): fever, headache, nausea, vomiting, malaise, and sore throat Secondary symptoms: deep muscle pain, hyperaesthesias, paraesthesias; during active myelitis: urinary retention and muscle spasms Asymmetric flaccid paralysis that may develop and progress over 2 to 3 days Irreversible paralysis (usually in the legs) occurs in 1 in 200 infections; 5-10% of patients have affected muscles of respiration Different presentations of paralytic poliomyelitis: Spinal type is the most frequent presentation. It is characterised by flaccid paralysis of muscles innervated by the motor neurons of the spinal cord, with asymmetric paralysis that most often involves the legs. There are often flexion contractures of the hip and knee, and equinus deformity of the ankle. Bulbar type affects the glossopharyngeal nerve (cranial nerve VIII). Bulbar involvement causes dysphagia, dysarthria, and difficulty managing secretions. Spinobulbar type is a combination of both spinal and bulbar type. Approximately 19% of all paralytic polio cases have both bulbar and spinal symptoms. Postencephalic type occurs in rare cases. It is characterised by confusion, changes in mental status, headaches, fever, and, less commonly, seizures and spastic paralysis, and symptoms similar to meningitis (i.e., headache, vomiting, neck stiffness)
Post-Polio Syndrome	25-40% of persons with Polio after 15-40 years	New muscle pain and exacerbation of existing weakness or development of new weakness or paralysis

Diagnosis

The diagnosis of poliomyelitis relies primarily on laboratory testing. Testing works by isolating the virus in cell culture or by detecting the virus by polymerase chain reaction (PCR). Virus isolation in culture is the most sensitive method of diagnosis. PCR testing of poliovirus isolates can identify the serotype and whether it is a wild or vaccine-derived version of the virus.

The preferred diagnostic method is via stool sample due to the ease of sample collection and testing availability. Two stool specimens (quarter-sized amounts each) are ideally collected separately (24 hours apart) within 14 days of symptom onset.

Medical Treatment Considerations

There is no specific antiviral treatment for poliomyelitis, and management focuses on supportive care, including relief of symptoms, speeding recovery and preventing complications.

During the initial recovery phase, treatment may include resting in bed, pain management, nutritional support, and gentle range of motion. In severe paralytic cases which affect the respiratory muscles, mechanical ventilation support becomes critical, historically through iron lungs and currently with mechanical ventilation.

Preventative options: prevention through vaccination is the cornerstone of polio control. Vaccination is ideally started in childhood, with children receiving four doses of inactivated polio vaccine (IPV) for best protection. The polio vaccine has been shown to be safe and effective with more than 99% of all children who complete the four recommended doses being protected from serious infection. Adults who are known or suspected to be unvaccinated, or incompletely vaccinated against polio should receive and complete the polio vaccination series with IPV. Adults who completed their polio vaccination but are at increased risk of exposure may receive one lifetime IPV booster. Additional preventative measures include avoiding travel to countries where cases and outbreaks of wild-type and vaccine-derived polio are occurring.

Rehabilitation Treatment Considerations

Rehabilitation treatment for people with poliomyelitis must be carefully staged according to disease progression, with distinct considerations for each phase of recovery.

During the acute stage, muscle tenderness is the most important sign—the patient should not be over-handled, with treatment including complete bed rest, and careful observation. Patients presenting with muscle paralysis benefit from frequent passive range of motion (PROM) and splinting of joints to prevent contracture and joint ankylosis. Chest physiotherapy (CPT) helps to prevent pulmonary complications, such as atelectasis, in patients with bulbar involvement. As recovery progresses, PROM should be continued and progressed as muscle strength returns. Historically, massage has been contraindicated during the acute phase. However, there is a lack of evidence in support of or against massage at this stage. Massage is recommended for patients in the post-polio syndrome stage.

During the convalescent and recovery phases, strengthening exercises should be initiated to return muscles to their maximum capacity (typically within the first 2-years post-infection). The use of orthotic braces may be required to support patient mobility.

For long-term management and post-polio syndrome, treatments should be individualised and take into consideration each patient's pattern of fatigue and functional limitations while maximising independence and preventing secondary complications. Examples of appropriate exercise interventions include aerobic exercise, aquatic therapy, strength training, range of motion and stretching exercises.

Aerobic/cardiovascular exercise: people with poliomyelitis benefit from regular, moderate aerobic exercise, especially less strenuous activities, such as swimming or water aerobics. These can be performed every other day at a relaxed pace.

Aquatic therapy: one of the best forms of exercise for polio survivors due to reduced gravity and buoyancy. Aquatic therapy programmes may include a combination of range of motion, strengthening and aerobic exercises, stretching, and relaxation. Aquatic therapy has a positive impact on pain and muscle function, making it particularly beneficial for people with post-polio syndrome who need joint support during exercise.

Strength training: vigorous strength training is not recommended as it may damage weakened muscles. Gentle muscle strengthening programmes should focus on building functional strength and not cause pain.

Range of motion and stretching: range of motion exercises are crucial for maintaining joint flexibility, preventing contractures and developing secondary complications.

Exercise precautions and modifications: patients with severe fatigue should adapt their daily exercise routine to their specific case. Patients who experience marked pain or fatigue following any exercise should hold off that exercise until they have contacted their healthcare provider. Exercise programmess must be carefully monitored and individualised to prevent overuse of already compromised motor units.

Additional Resources

The following video provides a simple but thorough overview of Poliomyelitis etiology and clinical presentation.