Picornaviruses — Poliovirus, Coxsackie A and B, Echovirus and Enterovirus Syndromes

Picornaviridae are very small (15–30 nm) RNA viruses — pico + RNA. The capsid is icosahedral and non-enveloped, and the genome is positive-sense single-stranded RNA of about 7,400 nucleotides. Translation starts from an internal ribosomal entry site (IRES) instead of a 5' cap. Without a lipid envelope, the enteroviruses can survive the acid of the stomach.

The genus Enterovirus is divided into 12 species (enteroviruses A–J and rhinoviruses A–C) with more than 200 serotypes. It contains poliovirus, coxsackieviruses, echoviruses and rhinoviruses. Poliovirus belongs to enterovirus C; coxsackie B to enterovirus B.

• Enterovirus C, family Picornaviridae; non-enveloped, acid-resistant, positive-sense ssRNA.
• Three wild serotypes: 1, 2 and 3 (WPV1–3), each with a slightly different capsid protein. Infection gives lifelong immunity only to the infecting serotype.
• Humans (and some great apes) are the only natural hosts; there is no animal reservoir.
• Spread is mainly faeco-oral, less often oral-oral by respiratory secretions. More than 90% of household contacts seroconvert.
• Incubation is usually 7–10 days (range 4–35 days). Children under 5 are at greatest risk.
• WPV2 was declared eradicated in 2015 and WPV3 in October 2019; only WPV1 still circulates (Pakistan and Afghanistan).

After ingestion the virus replicates in the oropharynx and gastrointestinal lymphoid tissue. Antibodies usually confine it there. Without antibodies a typically silent viraemia follows, and in a small minority the virus reaches the CNS across the blood-brain barrier or by retrograde axonal transport. It destroys alpha motor neurons in the anterior horn of the spinal cord, and the motor nuclei of the medulla, pons and midbrain. The result is a lower motor neuron paralysis with no sensory loss.

In paralytic disease fever returns 1–3 days after apparent recovery with severe muscle pain, fasciculations and spasms. Weakness is asymmetric, proximal to distal and mostly in the lower limbs; it peaks within 2–4 days and rarely progresses once fever settles. Paralytic polio kills about 10% (up to 20% quoted) mainly through bulbar involvement. Roughly 60% of survivors keep permanent deficits.

• Stool is the preferred specimen for culture or RT-PCR. The CDC advises two specimens at least 24 hours apart within 14 days of paralysis onset, kept at −20 °C.
• Virus is shed in stool for 3–6 weeks and in the nasopharynx for up to 2 weeks — even in asymptomatic people. Peak shedding starts 2–3 days before symptoms.
• CSF isolation is uncommon and a negative CSF does not exclude polio. Serology is not helpful because of high background immunity.
• After culture, RT-PCR/sequencing distinguishes wild virus from vaccine-derived virus.
• MRI may show typical anterior horn changes and exclude cord infarction.
• No antiviral therapy exists. Care is supportive — fever control, prevention of chest infection, ventilation for respiratory paralysis, splints and physiotherapy; later orthopaedic surgery for contractures and deformity. Pocapavir is available on compassionate use for immunodeficient patients who cannot clear the virus.

WHO schedules advise at least 3 doses of IPV (IPV-only) or at least 3 doses of bivalent OPV plus at least 2 doses of IPV in countries where polio risk persists. The oral vaccine is live attenuated; the injectable vaccine is inactivated. Mucosal immunity after infection or OPV reduces viral replication and excretion, which is why OPV is valuable for interrupting transmission.

Link this with the immunisation timetable in national immunisation schedule and the storage rules in cold chain and vaccine storage.

Coxsackie A mainly causes skin and mucosal disease (HFMD, herpangina); coxsackie B has 6 serotypes (CVB1–6) with tropism for the heart, pancreas and liver. Viral entry into cardiac muscle uses the coxsackie-adenovirus receptor (CAR), concentrated at the intercalated discs, and decay-accelerating factor (DAF). Incubation is 2–6 days. Coxsackie B in neonates can cause severe multi-organ disease with sepsis-like illness.

For other viral rashes compare viral exanthems and viral skin infections; for cardiac involvement see pericarditis.

HFMD is a viral exanthem of infants and young children, mostly under 5 years. It is caused most often by coxsackie A16 and enterovirus A71; coxsackie A6 and A10 are also implicated. Incubation is 3–6 days and patients are most infectious in the first week.

• Starts with low-grade fever, reduced appetite and malaise; mouth or throat pain from the enanthem is the commonest presenting symptom.
• Oral vesicles with a thin red halo rupture into shallow ulcers with a grey-yellow base (buccal mucosa, tongue, soft palate).
• Skin lesions are 2–6 mm macules, papules or vesicles on the hands, feet, buttocks, legs and arms; non-pruritic, usually painless and heal without scarring in about 10 days.
• Diagnosis is clinical; RT-PCR on a lesion swab confirms. Treatment is supportive (analgesia, hydration); steroids were associated with severe disease.
• EV-A71 is the strain notorious for CNS involvement — meningitis, encephalitis, polio-like illness, transverse myelitis and GBS.
• A late complication is nail shedding (onychomadesis) and Beau's lines weeks after the illness, because of transient arrest of the nail matrix. See nail disorders and signs.

• RT-PCR is the primary test: on blood, CSF, pericardial fluid or tissue it is diagnostic; on respiratory secretions it is highly suggestive; stool positivity may mean carriage or recent shedding.
• Culture is slower and only 65–75% sensitive, now used mainly for surveillance. Serology needs acute and convalescent sera and is retrospective.
• Most infections are self-limiting, so a clinical diagnosis is enough; testing is reserved for severe disease (myocarditis, meningitis, encephalitis, neonatal infection, immunocompromised hosts).
• Treatment is supportive. No antiviral is approved; pleconaril is investigational. Poliovirus is the only enterovirus with an effective vaccine.