Introduction

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The expanded immunisation programme in Zimbabwe started in 1981 and has a coverage of around 85% in most areas of the country.¹ The vaccination schedule is three doses of trivalent oral, live attenuated, poliomyelitis vaccine and diphtheria, tetanus, and pertussis vaccine at 3, 4, and 5 months of age, with a booster of diphtheria, tetanus, and pertussis vaccine at 18 months. In line with the World Health Organisation's goal of eradicating poliomyelitis by 2000,² children under 5 years old in Zimbabwe received two doses of oral vaccine, regardless of their vaccination history, during the national immunisation days in 1996.³ Most children infected with HIV live in developing countries, so the influence of HIV infection on vaccination against poliomyelitis is relevant. We describe a case of paralytic poliomyelitis in a child with HIV infection after vaccination with oral poliomyelitis vaccine.

	Case history

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A boy aged 41/2 years who was infected with HIV had been vaccinated with diphtheria, tetanus, and pertussis vaccine and oral poliomyelitis vaccine at the ages of 3, 4, and 5 months and had received a booster of diphtheria, tetanus, and pertussis vaccine at 24 months. On the national immunisation days of 1996 (7 August and 29 September) he received oral poliomyelitis vaccine, and a few days after the second immunisation he developed diarrhoea and fever. Two weeks later he developed weakness in his right leg. He was seen at a local primary healthcare clinic, but laboratory tests were not performed.

Three months later, in January 1997, he came to Parirenyatwa Teaching Hospital in Harare because of the persistent paralysis. On examination he was well nourished and had flaccid paralysis of his right leg, with diminished tone, power, and reflexes. Magnetic resonance imaging showed appreciable wasting of the muscles of his leg. His lymphocyte count was 2.1×10⁶/l, haemoglobin concentration 108 g/l, erythrocyte sedimentation rate 61 mm in the first hour, and total IgG concentration 29.3 g/l (normal value for children aged 5-7 years in Harare 8.0 (SD 3.2) g/l⁴). A serum sample contained no antibodies to tetanus or diphtheria toxin (both <0.01 IU/ml; toxin binding inhibition assay).

Poliovirus and poliovirus antibodies

HIV antibodies and CD4 counts

Maternal history

Follow up

	Discussion

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The results of physical examination and the presence of antibodies against poliomyelitis virus meet the criteria of the ninth revision of the international classification of diseases (ICD-9) for paralytic poliomyelitis, as the paralysis occurred within 4-30 days after vaccination.¹ Poliomyelitis was probably caused by the vaccine strain of poliovirus type 2. The presence of HIV antibodies meet the WHO's criteria for confirmed HIV infection,⁵ which was probably acquired perinatally.

Since 1990 no wild type poliovirus has been isolated in Zimbabwe (WHO Poliomyelitis Reference Laboratory, Harare, personal communication).¹ In the neighbouring country of Namibia, however, an outbreak of poliomyelitis caused by wild type poliovirus type 1 occurred in 1993.⁶ A review of hospital records during 1990-2 showed that three children under 15 years old developed acute flaccid paralysis in Zimbabwe.¹ Virus isolation and antibodies were not reported, so the infection may not have been caused by poliovirus. In 1995 acute flaccid paralysis was diagnosed in 39 children in Zimbabwe; poliovirus type 1 was isolated from stool samples in two children aged 5 and 6 years who did not remain paralysed. In 1996 among 20 children with acute flaccid paralysis poliovirus type 2 was isolated from one child aged 1 year who had residual paralysis (WHO, Poliomyelitis Reference Laboratory, Harare, personal communication). The HIV status of these last three children is not known.

Our patient probably had a humoral immune deficiency because after vaccination he did not develop antibodies against diphtheria toxin, tetanus toxin, or poliovirus types 1 and 3 and probably not against poliovirus type 2 after oral vaccination during infancy. This deficiency could be due to an altered immune state from his perinatally acquired HIV-1 infection. Interestingly, after infection with the vaccine strain he made antibodies against poliovirus type 2. Children infected with HIV-1 develop significantly less antibody than uninfected children in response to diphtheria toxoid, tetanus toxoid, and oral poliomyelitis vaccine. ^{7 8} Adults with HIV infection and low CD4 counts also form less antibody than do those with CD4 counts >300×10⁶/l in response to diphtheria toxoid, tetanus toxoid, and inactivated poliomyelitis vaccine.⁹

In our patient humoral immune deficiency, especially the absence of polio antibodies, might have contributed to the dissemination of the virus after vaccination with oral vaccine during the national immunisation days, thus causing infection of the central nervous system. The prevalence of paralytic poliomyelitis associated with oral poliomyelitis vaccine is low: one case per 2.5 million doses. In addition, 18% of those who developed this complication were immunocompromised, predominantly young children with hypogammaglobulinaemia or agammaglobulinaemia. ^{3 10 11} Children infected with HIV are potentially at risk of this and other complications after vaccination with live attenuated micro-organisms. ^{3 7 8} We believe that only one case of paralytic paralysis associated with oral poliomyelitis vaccine has been reported in a child with HIV infection from Romania.¹² Thus oral poliomyelitis vaccine seems to be safe when given during the first year of life. ^{1 7 10 13} To our knowledge, our case is the first report of poliomyelitis associated with poliomyelitis vaccination in a child infected with HIV from Africa. In countries where HIV infection is endemic and the risk of infection with wild type poliomyelitis virus is high, the benefits of immunisation outweigh the apparently low risk of paralysis due to vaccination with oral poliomyelitis vaccine.

	Acknowledgments

We thank Dr E N Sibanda, Department of Immunology, University of Zimbabwe, Harare, for his help.

Contributors: IC and RvF are both responsible for all aspects of this paper and are guarantors for the study.

	Footnotes

Funding: None.

Competing interests: None declared.

	References

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1. Anonymous. Acute flaccid paralysis surveillance, 1992, Zimbabwe. Wkly Epidemiol Rec 1993; 68: 264-266[Medline].
2. Wright PF, Kim-Farley RJ, de Quadros CA, Robertson SE, Scott RM, Ward NA, et al. Strategies for the global eradication of poliomyelitis by the year 2000. N Engl J Med 1992; 325: 1774-1779[Medline].
3. Robertson SE. The immunological basis for immunization. VI. Poliomyelitis. WHO/EPI/GEN 1993;16:1-24. (Available from WHO Geneva.)
4. Gomo Z, Sikunda D. The immunoglobulin levels in infants attending a routine health clinic at Mbare polyclinic. Central African Journal of Medicine 1992; 38: 281-286.
5. Anonymous. WHO case definitions for AIDS surveillance in adults and adolescents Wkly Epidemiol Rec 1994; 69: 273-275[Medline]
6. Van Niekerk ABW, Schoub BD, Chezzi C, Blackburn NK, Vries JB, Baard J. Outbreak of poliomyelitis in Namibia. Lancet 1994; 343: 51[Medline].
7. Ryder RW, Oxtoby MJ, Mvula M, Batter V, Baende E, Nsa W, et al. Safety and immunogenicity of bacille Calmette-Guérin, diphtheria-tetanus-pertussis, and oral polio vaccines in newborn children in Zaire infected with human immunodeficiency virus type 1. J Pediatr 1993; 122: 697-702[Medline].
8. Barbi M, Biffi MR, Binda S, Clerici-Schoeller M, Ferraris G, Luraschi C, et al. Immunization in children with HIV seropositivity at birth: antibody response to polio vaccine and tetanus toxoid. AIDS 1992; 6: 1465-1469[Medline].
9. Kroon FP, van Dissel JT, Labadie J, van Loon AM, van Furth R. Antibody response to diphtheria, tetanus, and poliomyelitis vaccines in relation to the number of CD4+ T lymphocytes in adults infected with human immunodeficiency virus. Clin Infect Dis 1995; 21: 1197-1203[Medline].
10. Nikowane BM, Wassilak SGF, Orenstein WA, Bart KJ, Schonberger LB, Hinman AR, et al. Vaccine-associated paralytic poliomyelitis: 1973 through 1984. JAMA 1987; 257: 1335-1340[Abstract/Free Full Text].
11. Strebel PM, Sutter RW, Cochi SL, Biellik RJ, Brink EW, Kew OM, et al. Epidemiology of poliomyelitis in the United States one decade after the last reported case of indigenous wild virus-assosiated disease Clin Infect Dis 1992; 14: 568-579[Medline].
12. Ion-Nedelcu N, Dobrescu A, Strebel PM, Sutter RW. Vaccine-associated paralytic poliomyelitis and HIV infection. Lancet 1994; 343: 51-52.
13. McLaughlin M, Thomas P, Onorato I, Oleske J, Nicholas S, Krasinski K, et al. Live virus vaccines in human immunodeficiency virus-infected children: a retrospective survey. Pediatrics 1988; 82: 229-233[Abstract/Free Full Text].

(Accepted 16 April 1998)