Provocation poliomyelitis: vaccine associated paralytic poliomyelitis related to a rectal abscess in an infant

A. R. J. Bosley^, ^,^a, Gail Speirs^b and N. I. Markham^c

^a Department of Paediatrics, North Devon District Hospital, Raleigh Park, Barnstaple, North Devon, UK
^b Department of Microbiology, North Devon District Hospital, Raleigh Park, Barnstaple, North Devon, UK
^c Department of Surgery, North Devon District Hospital, Raleigh Park, Barnstaple, North Devon, UK

Accepted 12 January 2003. ; Available online 29 March 2003.

1. Introduction

Vaccination against poliomyelitis in the UK is with oral (Sabin) live attenuated virus and this remains the recommendation of the Department of Health. Cases of poliomyelitis due to the wild virus are now rare in the western world and in the last 10 years there has not been a confirmed case in the UK due to endogenous wild virus. Those cases of paralytic poliomyelitis that do occur are as a consequence of reversion of attenuating mutations in the gastrointestinal tract of the vaccinated host.[1] The incidence of such cases is very low––there are about 12 per year in the USA and 1–3 per year in the UK. The incidence of paralytic poliomyelitis is reported to be increased in those patients or contacts who have undergone a surgical procedure or had an injection in the incubation period of vaccine virus. Our case report illustrates a possible association with systemic illness in a recently immunised infant and raises questions about the policy of continued use of live attenuated virus in the absence of wild virus disease.

2. Case Report

A nine week old infant was seen by the out of hours service suffering from an area of left sided peri-anal inflammation. Six weeks previously, the infant had an inflammatory lesion on the right side of the per-anal area which spontaneously resolved. The peri-anal inflammation was reviewed the next day when he presented for routine immunisation which included oral poliomyelitis vaccine (OPV).

Three days after the immunizations the infant was admitted to hospital as an emergency with a left sided peri-anal abscess. This was incised, drained and packed under general anaesthesia and the infant was discharged the next day on treatment with co-amoxiclav.

Eight days later he was readmitted, unwell, with neck spasm, photophobia and a temperature of 39°C. A lumbar puncture (LP) was performed and the cerebrospinal fluid (csf) showed a pleocytosis with 470 white cells/mm³, (64% lymphocytes). No organisms were seen and the csf protein was 0.8 g/l. He was given intravenous (IV) cefotaxime (200 mg/kg/day) and IV acyclovir (30 mg/kg/day). A CT head scan showed changes consistent with posterior fossa cerebritis. Three days later he was markedly hypotonic with diminished reflexes. A repeat csf showed 80 white cells/mm³, (50% lymphocytes) and a raised protein of 1.6 g/l. An E.E.G. was normal. By day 5 he was apyrexial and had begun to show some spontaneous facial muscle movement. Oxygen saturation levels and blood gases remained normal. All biochemical tests performed were within normal limits.

The continued profound hypotonia and weakness raised the suspicion of paralytic poliomyelitis. A further LP at day 12 showed a fall in white cells to 12/mm³ (100% lymphocytes) and the protein was now 2.0 g/l. Polymerase Chain reaction (PCR) on the csf for meningococci, Herpes simplex, Varicella zoster and enteroviruses was negative. Serology against Mycoplasma, Coxiella, Chlamydia, Influenza A and B was negative. Enterovirus IgM (Coxsackie A B and Echovirus) antibody was negative, as were H. simplex and V. zoster complement fixation antibody titres. An enterovirus was isolated from faeces on days 1 and 9 and subsequently identified as Sabin-like polio virus type 1 and 3.

Detailed investigation of the infant's immune status was normal, both at the time of illness and six months later.

Infant and maternal antibody titres to polio viruses were studied and the infant had an antibody response to type 3 virus. The diagnosis was confirmed on the basis of aseptic meningitis, paralysis with areflexia, slow recovery and serology. A review of the child at 14 months of age showed him to have severe motor impairment.

3. Discussion

Wild poliovirus, a picornavirus, is transmitted via faecal oral contamination. The incubation period varies from 3–35 days with an average 10–14 days. Symptoms are non specific initially and include mild fever, malaise, headache, sore throat and gastrointestinal upset. Only 1–2% progress to paralytic disease. In paralytic cases where there is an aseptic meningitis, typically there is a pleocytosis and the cellular reaction precedes the rise in protein levels as was seen in this case. In paralytic illness, the weakness develops after the temperature settles and is associated with myalgia. Coxsackie B virus can cause paralysis which can be indistinguishable from paralytic poliomyelitis (PPM). Recovery from paralysis occurs mostly in the first six weeks. Guillain Barré should be considered but a cellular response in csf is atypical.

VAPP is reported from countries using oral attenuated live virus vaccine. VAPP is rare but 1–3 cases occur per year in the UK. A study from the USA showed the greatest risk is in recipients of the first dose (1 in 520000 doses) compared to those receiving subsequent doses (1 in 12.6 million doses).[2] In the U.K. during 1985–1991 there were 21 cases of PPM, of which 13 were vaccine associated (9 recipient and 4 contact). [3] Other cases were imported and the remaining three were unknown. No case of wild virus disease was identified. The risk of PPM was 1.46 per million for the first dose and 0.49 per million for the second dose. The risk was zero for subsequent doses. [3]

VAPP is a result of reversion of the vaccine virus by mutation in the gut of the vaccinated individual.[4] It is usually associated with polio virus type 2 and 3, but rarely type 1, as the former two types (and particularly type 3) have the least mutations to undergo to revert to virulence. This case showed a high antibody titre to poliovirus type 3 and the mother had a low serum titre to type 3––this is most likely to reflect infection rather than vaccine induced immunity. The mechanism of VAPP is not completely clear. Unimmunised household and close contacts are at risk but the greater incidence has been reported in India [5] and Romania [6] associated with intramuscular injections at the time of, or shortly after, immunization. In India the cases have a much greater risk of being caused by wild virus––66.3% of cases being unimmunised at the time of illness. The risk factors identified for provocation poliomyelitis were the unimmunised state and multiple intramuscular injections in the preparalytic phase. [4]

The reason for the connection between paralysis and intramuscular injections may lie in the tissue reaction to the injected material. In India the paralysis rate is increased by a factor of 25 following multiple intramuscular injections, such as may be given for syphills and yaws.[7 and 5] Wyatt has proposed that the virus gains entry to the csf by the inflammatory reasction at sites of tissue damage during the viraemic period; the inflammatory reaction enhancing the transport of the virus into the peripheral nerves. [8] Differences in incubation periods before paralysis are explained by the length of the peripheral nerves involved.

There was no evidence of an immune deficiency in this patient but evidence from the USA indicates that about 14% of VAPP occurs in immunocompromised subjects.[2] Inflamed tissue related to the rectal abscess would, in itself, increase the likelihood of VAPP. [6]

The Department of Health Guidelines on Immunisation Against Infectious Disease gives advice on surgery and immunisation: `Surgery is not a contraindication, nor is immunization a contraindication to anaesthesia or surgery'.[9] In situations where there is a coexisting acute infection the advice is: `If an individual is suffering from an acute illness, the immunization should be postponed until recovery has occurred. Minor infections without fever or systemic upset are not reasons to postpone immunisation'. [10]

The immunisation policy in the United Kingdom remains that of using live attenuated virus.

This policy may need review in the light of serious cases of VAPP. In Sweden the policy is to immunize with inactivated Salk vaccine and there have been no cases of VAPP reported. A combined policy of the first dose being Salk and subsequent doses being oral Sabin vaccines would reduce the risk of VAPP and could be advocated on the basis of the few serious cases of VAPP.[11]

The UK urgently needs to review the current immunization policy for poliomyelitis. The cost of two serious cases of VAPP per year is cumulatively substantial in terms of long term care. These cases could be prevented by a change in the immunization policy and in relation to other expenditures the cost would appear to be small.

References

1. F. Freiderich, Neurologic complications associated with oral poliovirus vaccine and genomic variability of the vaccine strains after multiplication in humans. Acta Virol 42 (1998), pp. 187–195.

2. B.M. Nkowane, S.G.F. Wassilak, W.A. Orenstein et al., Vaccine-associated paralytic poliomyelitis. JAMA 257 (1987), pp. 1335–1340.

3. R. Joce, D. Wood, D. Brown and N. Begg, Paralytic poliomyelitis in England and Wales. BMJ 305 (1992), pp. 69–70.

4. M. Gromier and E. Wimmer, Mechanism of injury-provoked poliomyelitis. J Virol 72 (1998), pp. 5056–5060.

5. S. Mahadevan, S. Ananthakrihnan, S. Srinivasan et al., Poliomyelitis: 20 years––the Pondicherry experience. J Trop Med Hyg 92 (1989), pp. 416–421.

6. P.M. Strebel, N. Ion-Nedelcu, A.L. Baughman, R.W. Sutter and S.L. Cochi, Intramuscular injections within 30 days of immunization with oral poliovirus vaccine––a risk factor for vaccine associated paralytic poliomyelitis. N EJM 332 (1995), pp. 500–506.

7. H.V. Wyatt, Provocation of poliomyelitis by multiple injections. Trans R Soc Trop Med Hyg 79 (1985), pp. 355–358.

8. H.V. Wyatt, Provocation poliomyelitis and entry of poliovirus to the CNS. Med Hypothesis 2 (1976), pp. 269–274.

9. D.M. Salisbury and N.T. Begg, Editors, 1996 Immunisation against Infectious Disease, HMSO, London (1996), p. 26.

10. D.M. Salisbury and N.T. Begg, Editors, 1996 Immunisation against Infectious Disease, HMSO, London (1996), p. 20.

11. A. Finn and F. Bell, Polio vaccine: is it time for a change?. Arch Dis Child 78 (1998), pp. 571–574.

Your use of this service is governed by Terms and Conditions. Please review our Privacy Policy for details on how we protect information that you supply.

	This Document
		SummaryPlus
		Full Text + Links
		PDF (67 K)

	Actions
		E-mail Article

Abstract

Article Outline

1. Introduction

2. Case Report

3. Discussion

References