A two-year-old girl presented with sudden-onset of weakness of left lower limb of one month duration. The weakness was preceded by fever and cough for one day. Weakness progressed over the next month to involve right lower limb and weakness of left half of face. The parents gave a history of administration of first booster of OPV one- and-a-half month prior to onset of weakness in the child. There was no significant past illness requiring any hospitalization or prolonged antibiotics intake in child except recurrent fever, with cough and coryza over the previous four months. There was no significant family history.

Examination revealed stable vitals and mild pallor. Child was conscious and well oriented. The child was not able to close left eye and nasolabial fold of left side was less prominent. Muscles of lower limbs were flabby to touch (right> left) with wasting of right lower limb, with decreased power in both lower limbs (1/5 in right lower limb and 2/5 in left lower limb) and diminished reflexes in right lower limb. Rest of examination was unremarkable.

Routine hematological and biochemical investigations, including muscle enzymes, were within normal limits. Asymmetric motor sensory predominantly axonal polyneuropathy was found on nerve conduction velocity assessment of both lower limbs, and MRI dorsolumbar spine was normal. The child was investigated as a case of Acute flaccid paralysis.

The child’s weakness did not progress and she was started on intravenous immunoglobulin (IVIg)(400 mg/kg/day for 5 days). Her weakness improved over the next month. She was continued on monthly IVIg. Eight months after diagnosis, the excretion of polio virus continues to persist.

Aforementioned patient developed acute paralysis three months following booster dose of OPV. As the patient had underlying immunodeficiency, the vaccine virus likely reverted back to neurovirulence and resulted in development of paralysis. Kew, et al. [8] described a case of VDPP in a patient of common variable immunodeficiency, but this patient was a known case of CVID before paralysis onset, which occurred 6.9 years after vaccination and at least 2 years after diagnosis of CVID. This is unlike our case, where diagnosis of immunodeficiency was made after the isolation of vaccine polio virus. Type 2 vaccine virus is the predominant cause of VDPV worldwide, as well as in India [1].

Several strategies for eliminating poliovirus persistence in immunodeficient patients have been tried with equivocal results. Review of literature revealed that most persons with hypogammaglobulinemia who were fed OPV while receiving immunoglobulin replacement therapy cleared the infection within a few weeks [9]. In the present case, excretion of virus is persisting even months after monthly pulses of immunoglobulin.

This case further endorses the recommendation of the Government of India and WHO to switch from oral vaccine to inactivated vaccine to minimize the risk of paralysis, especially in immunocompromised children as screening for primary immunodeficiency is not possible prior to first dose of OPV. A step has already been taken in this direction with the introduction of one dose of IPV at 14 weeks of age in the National immunization program [10].

Acknowledgements: Prof Surjit Singh from PGI for carrying over detailed immunoprofile of the child. Dr Preeti Nigam, SMO NPSP for co-ordinating initial viral work up at NCDC, Civil Lines, Delhi. The advanced virology workup was done at ERC, Mumbai.

Contributors: SG: Analyzed the case, designed the work-up and helped in drafting the manuscript; VA: worked up the case and drafted the manuscript; PD: Helped to diagnose the disease and contributed in drafting the manuscript.

Funding: None; Competing interest: None stated.

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