Poliomyelitis

Background

Neurotropic enterovirus
Extremely rare in developed world, targeted for global eradication by WHO
Still endemic in Pakistan, Afghanistan, and Nigeria
Fecal-oral transmission, virus enters through GI tract then reproduces in GI lymphoid tissues
If virus reaches critical concentration, can spread to motor nuclei of spinal cord, brainstem, and reticular formation → loss of infected neurons→ cycle of muscle denervation/reinnervation→ loss of muscle function

>90% of infections are asymptomatic
Minor (abortive) polio:
- Fever
- Diarrhea
- Headache
- Sore throat
Non-paralytic polio:
- Fever
- Headache
- Meningismus
- Muscle spasms without paralysis
Paralytic (spinal) polio (~1-2% of polio infections)
- Neuro symptoms may manifest after resolution of initial febrile illness
- Maximal paralysis at around 5 days, muscle wasting after several weeks, with most patients' paralysis resolving after about 1 year
- Flaccid muscle weakness/paralysis
- Fasciculations
- Absent or decreased reflexes
- Autonomic dysfunction (e.g. sweating disturbances, urinary retention, constipation
- Neuropathic pain, paresthesias, though usually no sensory deficits on exam
- Bulbar dysfunction in about 20% of spinal polio (dysphagia, dysarthria, facial weakness)
- Encephalitis: can cause reticular formation disturbances, resulting in dysrhythmias, BP lability, hypoxia, and hypercarbia
Post-polio syndrome
- Occurs sometime after complete resolution of initial acute symptoms
- Can involve same muscle groups affected during patient's acute illness, as well as those not affected during initial viral infection
- Symptoms include muscle weakness, atrophy, fasciculations, fatigue, insomnia, joint pain, bulbar dysfunction, respiratory dysfunction

Evaluate for other causes of symptoms
PCR: virus can be identified in throat washings (early), CSF (early), and stool/rectal swab (highest yield)
CSF: Pleocytosis (PMN predominance initially, then mostly lymphocytes), usually ~normal opening pressure, protein, and glucose.