Poliomyelitis

Poliomyelitis is an acute viral infection caused by poliovirus, an enterovirus transmitted via the faecal oral route. Most infections are asymptomatic. A minority cause a non specific febrile illness. In a small proportion, the virus invades the central nervous system and destroys anterior horn motor neurons, producing acute flaccid paralysis.

Global eradication efforts have eliminated wild type virus from all but a small number of endemic regions. Vaccine derived poliovirus and the ongoing risk of reintroduction into under immunised populations maintain the clinical and public health relevance of the disease.

Pathophysiology

After faecal oral transmission, the virus replicates initially within the gastrointestinal tract and associated lymphoid tissue. A minor viraemia occurs in most infected individuals.

A small proportion progress to a major viraemia with central nervous system invasion. The virus selectively destroys anterior horn cells within the spinal cord and, less commonly, motor neurons within the brainstem. The result is asymmetric, predominantly lower motor neuron flaccid paralysis without sensory involvement.

The large majority of infections (estimated at ninety to ninety five percent) are entirely asymptomatic.

A further proportion (approximately four to eight percent) produce only a non specific, self limiting febrile illness with malaise, headache, sore throat and gastrointestinal upset. It resolves without neurological involvement and is termed abortive poliomyelitis.

Non paralytic (aseptic meningitis) poliomyelitis occurs in a smaller proportion. It presents with fever, headache, neck stiffness and photophobia, and resolves completely without residual weakness.

Paralytic poliomyelitis occurs in less than one percent of infected individuals. It presents with acute onset asymmetric flaccid weakness, most commonly affecting the lower limbs, developing over a period of hours to a few days. It typically follows a several day interval after resolution of the initial febrile prodromal illness.

Deep tendon reflexes are reduced or absent. There is no sensory loss, which distinguishes it from Guillain Barré syndrome and other causes of acute flaccid paralysis.

Bulbar poliomyelitis involves the brainstem motor nuclei. It produces dysphagia, dysarthria and, most critically, respiratory muscle weakness with the potential for life threatening respiratory failure requiring ventilatory support. It is the most severe and immediately dangerous manifestation.

Report and investigate any case of acute flaccid paralysis in a child under fifteen years as suspected poliomyelitis, regardless of the ultimate confirmed cause. Public health surveillance is critical for maintaining global eradication efforts.

The standard diagnostic approach is viral isolation by culture, or detection by reverse transcriptase polymerase chain reaction, from two stool specimens collected at least twenty four hours apart within fourteen days of symptom onset. Genomic sequencing of any isolated virus distinguishes wild type from vaccine derived strains, a distinction with different public health implications.

Cerebrospinal fluid analysis typically shows a mild lymphocytic pleocytosis with normal or mildly elevated protein, supporting central nervous system involvement. Electromyography can help confirm the anterior horn cell pattern of motor neuron involvement and exclude alternative diagnoses where the clinical picture is atypical.

There is no specific antiviral treatment for poliomyelitis. Management is entirely supportive. It focuses on symptom relief during the acute illness and full rehabilitation to maximise functional recovery from any resulting paralysis.

Bed rest and avoidance of physical exertion are recommended during the acute febrile and early paralytic phase. Historical evidence suggests that intramuscular injections and strenuous activity during this period may be associated with more severe subsequent paralysis, though this rests on older observational evidence.

Bulbar poliomyelitis with respiratory muscle involvement requires respiratory support, including non invasive or invasive mechanical ventilation. Manage it in an intensive care setting with close monitoring of respiratory function, swallowing safety (given aspiration risk with bulbar involvement) and airway protection.

Acute management has these components:

• Analgesia for the significant muscle pain that frequently accompanies the acute paralytic phase: paracetamol and, where required, opioid analgesia titrated to effect
• Careful positioning and physiotherapy from the earliest appropriate stage, to prevent contracture and support subsequent functional recovery

Rehabilitation is prolonged and essential. It includes physiotherapy, occupational therapy and, where required, orthotic support or surgical intervention for established deformity. Recovery of strength, where it occurs, continues over months following the acute illness.

A proportion of patients are left with permanent residual weakness. Some experience post polio syndrome, a delayed further decline in strength occurring decades after the original illness. It requires its own specific supportive and rehabilitative management.

Prevention through vaccination remains the cornerstone of global disease control. Oral live attenuated vaccine and inactivated injectable vaccine are both used according to national programme schedules and epidemiological context. Any suspected case triggers urgent public health notification and outbreak investigation, given the implications for ongoing global eradication efforts.