Poliomyelitis

Poliomyelitis is an acute viral infection of the anterior horn cells of the spinal cord caused by the poliovirus, classically producing asymmetric, flaccid, areflexic paralysis. For NEET PG, this is a "Community Medicine favourite" — the high-yield meat is the eradication programme, AFP surveillance, OPV vs IPV, VDPV, and India's 2014 polio-free certification.

Definition & the organism

Poliomyelitis ("polio" = grey, "myelos" = marrow) is an enteroviral infection that destroys the motor neurons of the anterior (ventral) horn of the spinal cord and the motor nuclei of the brainstem, producing lower motor neuron (LMN) flaccid paralysis.

• Agent: Poliovirus — an Enterovirus of family Picornaviridae; a small, non-enveloped, single-stranded RNA virus.
• Three antigenic types: Type 1 (Brunhilde), Type 2 (Lansing), Type 3 (Leon).
  • Type 1 — most paralytogenic, most epidemics, the type that persisted longest in the wild.
  • Type 2 — last wild case in 1999 (India, Aligarh, UP); wild type 2 declared eradicated in 2015.
  • Type 3 — last wild case Nov 2012 (Nigeria); declared eradicated in 2019.
• Reservoir: Man is the only reservoir (no animal reservoir, no long-term carrier) — a key reason polio is eradicable.

High-yield: Of the three wild types, only wild poliovirus type 1 (WPV1) still circulates (endemic in Pakistan and Afghanistan). WPV2 and WPV3 are globally eradicated.

Why polio is eradicable (mnemonic-worthy)

1. Man is the only reservoir; no animal/environmental reservoir.
2. An effective, cheap vaccine exists (OPV).
3. No long-term carrier state; subclinical infections are transient.
4. Survival of the virus outside the host is limited.

Epidemiology & transmission

Feature	Detail
Host	Humans only; children <5 yrs most affected
Source	Cases + subclinical (inapparent) infections (chief source — 90–95% infections are silent)
Route	Faeco-oral (predominant in developing countries) and droplet/pharyngeal (in developed)
Incubation period	7–14 days (range 3–35 days)
Communicability	7–10 days before & after onset of symptoms; virus in faeces up to 6 weeks or more
Site of multiplication	Pharynx and gut (Peyer's patches, lymphoid tissue) → viraemia → CNS

The ratio of inapparent to paralytic infection is roughly 1000:1 (about 1 paralytic case per 200–1000 infections). This silent transmission is exactly why surveillance of paralysis alone underestimates circulation, and why environmental (sewage) surveillance matters.

Pathophysiology

Poliovirus enters via the mouth → multiplies in the oropharyngeal and intestinal lymphoid tissue → spreads to regional lymph nodes → minor viraemia → most are contained here (abortive/inapparent). In a minority, a major viraemia seeds the CNS, where the virus has a tropism for motor neurons of the anterior horn and brainstem motor nuclei. Neuronal destruction → asymmetric, flaccid, areflexic paralysis with intact sensation.

Flow of disease: Ingestion → gut/pharyngeal replication → minor viraemia → (most stop here) → major viraemia → CNS invasion → anterior horn cell destruction → asymmetric LMN paralysis.

Clinical spectrum

Classic spectrum from inapparent to paralytic:

1. Inapparent (subclinical) infection — ~90–95%. No symptoms; only seroconversion.
2. Abortive polio (minor illness) — ~4–8%. Nonspecific fever, sore throat, malaise, GI upset; recovers fully, no CNS signs.
3. Non-paralytic polio (aseptic meningitis) — ~1%. Above + signs of meningeal irritation, neck/back stiffness.
4. Paralytic polio — <1% (~0.1–1%). Asymmetric flaccid paralysis.

Features of paralytic polio (exam pointers)

• Asymmetric, proximal > distal, lower limbs > upper limbs.
• Pure motor — sensation is intact (helps differentiate from GBS where sensory may be involved).
• Flaccid, areflexic (LMN); no sphincter/bladder involvement typically; no sensory loss.
• Biphasic ("dromedary/camel-back") fever — fever of minor illness, then a gap, then major illness.
• Bulbar polio — involves cranial nerve nuclei (IX, X) → dysphagia, respiratory difficulty; high mortality.
• Provocative factors for paralysis: intramuscular injections, intense exercise, trauma, tonsillectomy in the prodrome — the affected limb that received the injection ("provocation paralysis").

High-yield: Polio paralysis is asymmetric, descending, pure motor, with intact sensation and intact bladder. This triad of "asymmetric + flaccid + no sensory loss" separates it from Guillain–Barré syndrome.

Diagnosis & investigation of choice

• Stool virology is the diagnostic gold standard. Collect two stool specimens, 24–48 hours apart, within 14 days of onset of paralysis, maintain reverse cold chain, send to a WHO-accredited lab.
• Virus isolation in cell culture + intratypic differentiation (ITD) by RT-PCR distinguishes:
  • Wild poliovirus (WPV)
  • Sabin-like (vaccine) virus
  • Vaccine-derived poliovirus (VDPV)
• CSF: shows aseptic-meningitis picture (lymphocytic pleocytosis, mildly raised protein, normal sugar) — supportive, not diagnostic.

High-yield: The investigation of choice for confirming polio is virus isolation from stool (two samples, 24–48 h apart, within 14 days of onset). Serology/CSF are only supportive.

AFP surveillance — the cornerstone of eradication

Because paralytic polio is rare and clinically mimicked by other conditions, the WHO strategy is to investigate every case of acute flaccid paralysis.

Definition of AFP: Any child <15 years with acute (sudden onset, <4 weeks evolution) flaccid paralysis, OR paralytic illness in a person of any age in whom polio is suspected.

Key AFP surveillance indicators

Indicator	Standard / target
Non-polio AFP rate	≥1 (now ≥2) per 100,000 children <15 yrs/year (sensitivity of system)
Adequate stool specimens	≥80% of AFP cases with 2 stool samples, 24–48 h apart, within 14 days of onset
Specimens reaching lab in reverse cold chain	≥80% in good condition
60-day follow-up	Examine for residual paralysis at 60 days

A high non-polio AFP rate is desirable — it shows the system is sensitive enough to detect even the rarer true polio case.

High-yield: A non-polio AFP rate of ≥2/100,000 children under 15 with ≥80% adequate stool specimen collection indicates a sensitive, well-performing surveillance system. AFP surveillance — not vaccination alone — is the cornerstone of eradication, because it proves absence of circulation.

Environmental (sewage) surveillance

Testing sewage/sewerage samples for poliovirus detects silent circulation even when there are no paralytic cases (remember the 1000:1 silent:paralytic ratio). India uses environmental surveillance at sentinel sites (e.g., Mumbai, Delhi, Kolkata, Patna, Hyderabad) as an early warning system to detect imported WPV or VDPV before a clinical case appears.

The vaccines — OPV vs IPV

Two vaccines exist: OPV (Sabin, live attenuated, oral) and IPV (Salk, killed/inactivated, injectable).

Feature	OPV (Sabin)	IPV (Salk)
Nature	Live attenuated	Killed / inactivated
Route	Oral	Intramuscular / subcutaneous
Immunity produced	Humoral + intestinal (mucosal/IgA)	Humoral only (poor gut immunity)
Herd immunity / secondary spread	Yes (vaccine virus spreads to contacts)	No
Risk of VAPP / VDPV	Yes	No (cannot revert)
Cold chain	Most heat-labile EPI vaccine	More stable
Cost	Cheap	Costlier
Use in immunodeficiency	Contraindicated	Safe
Stabiliser	Magnesium chloride (MgCl₂)	—

High-yield: OPV gives intestinal (mucosal) immunity and interrupts faeco-oral transmission → ideal for eradication. IPV gives only humoral immunity but carries no risk of VAPP or VDPV → ideal once eradication is near. India therefore now uses both.

VVM (vaccine vial monitor): OPV is the most heat-sensitive vaccine in the cold chain. Potency is judged by the VVM and by colour — manufacturers add a VVM and OPV must be stored at –20°C (long term) / +2 to +8°C (in use). OPV is the most sensitive marker of cold-chain integrity.

VAPP and VDPV — the dark side of OPV

• VAPP (Vaccine-Associated Paralytic Polio): Paralysis caused by the vaccine (Sabin) virus reverting to neurovirulence in the vaccinee or a close contact. Risk ~1 in 2.7 million doses (highest with the first dose). Type 2 and type 3 Sabin strains revert most readily; type 2 was the commonest cause of VAPP — a major reason for dropping type 2 from OPV.
• VDPV (Vaccine-Derived Poliovirus): Sabin virus that has circulated long enough in under-immunised populations to acquire wild-like neurovirulence and transmissibility (genetic divergence — historically >1% for types 1/3, >0.6% for type 2 from the parent Sabin strain).

VDPV category	Meaning
cVDPV	Circulating VDPV — community spread; behaves like wild virus; needs outbreak response
iVDPV	Immunodeficiency-associated — prolonged excretion in B-cell immunodeficient individuals
aVDPV	Ambiguous — isolate from a person/sewage, source unclear

High-yield: cVDPV2 (circulating vaccine-derived poliovirus type 2) is now the commonest cause of polio outbreaks worldwide since wild virus retreated. This paradox — the vaccine virus causing outbreaks — drives the endgame switch from OPV to IPV. nOPV2 (novel OPV type 2), genetically stabilised against reversion, is the newer tool against cVDPV2 outbreaks.

The tOPV → bOPV "switch" and why type 2 was removed

• tOPV = trivalent OPV (types 1, 2, 3).
• bOPV = bivalent OPV (types 1 and 3 only).

Rationale for the switch (April 2016, "the Switch"):

1. Wild poliovirus type 2 was eradicated (last case 1999; declared eradicated Sept 2015) — so keeping type 2 in OPV gave no benefit against wild virus.
2. Type 2 Sabin component caused the majority of VAPP and most cVDPV outbreaks.
3. Removing type 2 from OPV removes ongoing exposure to the most troublesome strain.

To cover the lost type 2 immunity after the switch, ≥1 dose of IPV (which contains all three types) was introduced into routine immunisation.

The switch flow: Wild type 2 eradicated → type 2 OPV is now net harmful → remove type 2 from OPV (tOPV → bOPV, April 2016) → introduce IPV to maintain type 2 humoral immunity.

High-yield: The globally synchronised tOPV → bOPV switch occurred in April 2016, accompanied by introduction of at least one dose of IPV in routine immunisation worldwide.

India's immunisation schedule for polio (UIP)

• OPV: Birth dose (zero dose) + 6, 10, 14 weeks (primary) + booster at 16–24 months + at 5 years. Plus bOPV in Pulse Polio (NIDs/SNIDs).
• IPV: Introduced into UIP; given as fractional IPV (fIPV) — two fractional intradermal doses at 6 and 14 weeks (0.1 mL ID), a dose-sparing strategy.

Pulse Polio Immunisation (PPI): Began in 1995 in India. Mass campaigns giving bOPV to all children <5 years on National Immunisation Days (NIDs) regardless of prior immunisation status, to rapidly raise herd/intestinal immunity and interrupt transmission.

Eradication milestones

Year	Milestone
1988	Global Polio Eradication Initiative (GPEI) launched (WHO, UNICEF, Rotary, CDC)
1995	India launches Pulse Polio Immunisation
1999	Last wild poliovirus type 2 case (Aligarh, India)
2011 (13 Jan)	India's last wild polio case — a girl in Howrah, West Bengal (type 1)
2012 (Nov)	Last wild type 3 case (Nigeria)
2014 (27 Mar)	WHO South-East Asia Region (incl. India) certified polio-free
2015	WPV2 declared eradicated
2016 (Apr)	Global tOPV → bOPV switch + IPV introduction
2019	WPV3 declared eradicated

High-yield: India's last wild polio case was 13 January 2011 (Howrah, West Bengal); the WHO South-East Asia Region was certified polio-free on 27 March 2014. Remaining endemic countries for WPV1: Pakistan and Afghanistan.

Management

There is no specific antiviral treatment for poliomyelitis — management is supportive.

• Acute phase: Bed rest, analgesics, hot moist packs for muscle pain; avoid IM injections and overexertion (provocation). Respiratory support/ventilation for bulbar/respiratory polio.
• Convalescent/rehabilitation phase: Physiotherapy, prevention of contractures, orthopaedic correction of deformities, callipers/orthoses, rehabilitation.
• Prevention is the mainstay: OPV + IPV, surveillance, outbreak response. Post-Polio Syndrome (new weakness decades later) is managed symptomatically.

Complications

• Respiratory failure (bulbar/spinal involvement of intercostals & diaphragm) — leading cause of acute death.
• Bulbar palsy — dysphagia, aspiration, circulatory collapse.
• Permanent residual paralysis & limb deformities, contractures, growth retardation of the limb, scoliosis.
• Post-Polio Syndrome (PPS): New muscle weakness, fatigue, pain appearing 15–40 years after the acute illness in previously affected survivors.

Key differentials of AFP

Condition	Distinguishing features vs polio
Guillain–Barré syndrome (GBS)	Symmetric, ascending, sensory involvement possible, albumino-cytological dissociation in CSF; bilateral
Traumatic neuritis	History of IM injection; paralysis confined to that limb; usually less severe
Transverse myelitis	Symmetric, sensory level, bladder/bowel involvement (sphincters affected)
Non-polio enterovirus / acute flaccid myelitis	Enterovirus D68/A71; needs stool/lab differentiation

High-yield: GBS is symmetric & ascending with sensory features and CSF albumino-cytological dissociation; polio is asymmetric, pure motor with intact sensation and intact sphincters. This is the single most-tested differentiation.

Recently asked / exam angle

• Cornerstone of polio eradication = AFP surveillance (with environmental/sewage surveillance as adjunct). Frequently asked as "best indicator of surveillance sensitivity = non-polio AFP rate."
• Commonest cause of current polio outbreaks = cVDPV2, not wild virus — a recurring conceptual MCQ.
• Why was type 2 removed from OPV? → wild type 2 eradicated + type 2 Sabin = most VAPP/VDPV.
• OPV gives intestinal immunity; IPV gives only humoral immunity — classic one-liner pairing.
• India polio-free certification = 2014 (SEAR); last wild case = Jan 2011, Howrah, WB.
• fIPV = two intradermal fractional doses at 6 & 14 weeks — newer schedule MCQ.
• OPV is the most heat-sensitive vaccine (cold-chain question), stabiliser MgCl₂, stored at –20°C.
• Stool sample protocol: 2 samples, 24–48 h apart, within 14 days of paralysis onset — frequently tested verbatim.
• VVM and 60-day follow-up examination of AFP cases.
• Remaining endemic countries: Pakistan & Afghanistan.

Rapid revision

1. Poliovirus = ssRNA Picornavirus (Enterovirus); 3 types — Type 1 (Brunhilde) most paralytogenic; man is the only reservoir.
2. 90–95% infections are inapparent; paralytic disease in <1%; silent:paralytic ratio ~1000:1.
3. Paralysis is asymmetric, flaccid, pure motor, sensation intact, sphincters spared — opposite of transverse myelitis; differs from symmetric ascending GBS.
4. IM injection in the prodrome = provocation paralysis.
5. Diagnosis = virus isolation from stool: 2 samples, 24–48 h apart, within 14 days of onset, reverse cold chain.
6. AFP = acute flaccid paralysis in child <15 yrs; cornerstone of eradication; target non-polio AFP rate ≥2/100,000 <15 yrs with ≥80% adequate stool collection; 60-day follow-up.
7. Environmental (sewage) surveillance = early warning for silent circulation.
8. OPV (Sabin, live, oral) = humoral + intestinal immunity, herd effect, but risk of VAPP & VDPV; most heat-labile vaccine; stabiliser MgCl₂.
9. IPV (Salk, killed, IM) = humoral only, no VAPP/VDPV, safe in immunodeficiency; India uses fIPV (2 ID doses at 6 & 14 wks).
10. tOPV → bOPV switch in April 2016 (dropped type 2) + IPV introduction; type 2 removed because WPV2 eradicated & type 2 caused most VAPP/cVDPV.
11. cVDPV2 = commonest cause of current outbreaks; nOPV2 = stabilised vaccine against it.
12. India's last wild case = 13 Jan 2011 (Howrah, WB); SEAR certified polio-free = 27 March 2014; WPV1 still endemic in Pakistan & Afghanistan.