Poliovirus immunisation for travellers

Poliovirus immunisation for travellers

Travel Medicine and Infectious Disease (2004) 2, 1–3 www.elsevierhealth.com/journals/tmid EDITORIAL Poliovirus immunisation for travellers Jane N. ...

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Travel Medicine and Infectious Disease (2004) 2, 1–3

www.elsevierhealth.com/journals/tmid

EDITORIAL

Poliovirus immunisation for travellers Jane N. Zuckerman* Academic Centre for Travel Medicine and Vaccines and the WHO Collaborating Centre for Reference, Research and Training in Travel Medicine, Royal Free and University College Medical School, University College London, Royal Free Campus, Rowland Hill Street, London NW3 2PF, UK Received 12 January 2004; accepted 12 January 2004

KEYWORDS Poliomyelitis; Poliovirus; Poliovaccine; Travellers

Summary Mass immunisation against poliomyelitis using principally oral live attenuated trivalent vaccine (OPV) has eradicated wild-type poliovirus transmission in the industrialised countries of the Western hemisphere and most other countries, and the global eradication of poliomyelitis is within reach. The risk of oral polio vaccine-associated poliomyelitis has been estimated by WHO at 0.5 –3.4 cases per million of susceptible children, and by the Centers for Disease Control and Prevention (USA) at 1 case per 2.4 million doses of OPV. This has led to the reintroduction and use of inactivated vaccine in the USA and a number of other countries. The current risk of poliomyelitis for travellers is reviewed together with the application of strategies for immunisation against these infections. q 2004 Elsevier Ltd. All rights reserved.

Introduction Poliovirus is a member of the enterovirus subgroup of the Picornaviridae (small RNA viruses) comprising five genera: enteroviruses, rhinoviruses, hepatoviruses, cardioviruses and aphthoviruses. Most infections with enteroviruses are inapparent, but some may cause serious infection of the central nervous system, heart, skeletal muscles, the liver and the pancreas. Sixty-six serotypes of enterovirus have been isolated from humans and can replicate in the epithelium of the nasopharynx, the gastrointestinal tract, lymphoid tissue, the reticuloendothelial system, and, in the case of hepatitis A virus, the liver. The virus may spread to other organs and may cause severe disease, for example, the central *Tel.: þ44-207-830-2999; fax: þ 44-207-830-2268. E-mail address: [email protected]

nervous system (polioviruses), the myocardium causing myocarditis (Coxsackie viruses) and others. Prevention by immunisation is limited so far to poliomyelitis, and hepatitis A. All the picornaviruses have similar morphology, molecular and structural properties and replication strategies. The enteroviruses are transient inhabitants of the gastrointestinal tract, stable at acid pH and rapidly inactivated by heat, formaldehyde, chloroforms and ultraviolet light. The virion is an icosahedral, unenveloped small particle measuring approximately 27 nm in diameter and containing a single positive-strand of RNA of approximately 7500 nucleotides. There are three serotypes of poliovirus. The virus enters the mouth and primary multiplication takes place in the pharynx and the gastrointestinal cells. The virus multiplies in the cytoplasm, and the RNA acts as a messenger to synthesize viral macromolecules. Viral RNA replicates in complex associated with the cytoplasmic

1477-8939/$ - see front matter q 2004 Elsevier Ltd. All rights reserved. doi:10.1016/j.tmaid.2004.01.007

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membranes. The virus then invades local lymphoid tissue, enters the blood stream and may invade the central nervous system spreading along nerves. Replication of poliovirus in motor neurons of the anterior horn cells of the spinal cord and the brain stem results in destruction of motor neurons. Virus is shed from the throat, and from the gastrointestinal tract in the faeces. Faecal shedding may continue for several weeks.1,2

Epidemiology The major route of transmission of poliovirus is faecal – oral where sanitation and standards of hygiene are poor. Pharyngeal spread is relatively more important in areas where sanitation is good and, in the past, during epidemics in industrialised countries. Poliomyelitis can affect all age groups. In areas with poor sanitation most infants were infected early in life and acquired active immunity while still protected by maternal antibodies. The infection occurred worldwide before the introduction of large-scale immunisation, and the highest incidence of clinical disease was in temperate zones and in the more developed countries, most commonly during summer and autumn. It is expected that poliomyelitis caused by wild-type virus will be eradicated from most (if not all) countries within the next decade, and wild poliovirus transmission has ceased in almost all industrialised countries and much of the developing world. It is likely that polioviruses found in nature will probably be derived from oral poliovirus vaccine strains. The incubation period is commonly 7 – 14 days for paralytic cases, with a reported range of 3 – 35 days. Cases are most infectious from 7 to 10 days before and after the onset of symptoms, and virus may be shed in the faeces for 6 weeks or longer. The reservoir of infection is man, most frequently persons with inapparent infection, especially children.

J.N. Zuckerman

asymmetric. Case fatality rates in paralytic cases vary from 2 to 10% in different epidemics and increase dramatically with age. Differential clinical diagnosis includes postinfectious polyneuritis, Guillain – Barre syndrome and other causes of paralysis. The differential diagnosis of acute non-paralytic poliomyelitis includes asceptic meningitis, bacterial meningitis, brain abscess and encephalitis. Laboratory diagnosis is based on viral isolation from faecal samples 24 – 48 h apart, and type identification based on molecular techniques. Faecal samples should also be obtained from household and other close contacts. It should be noted that other enteroviruses, particularly Coxsackie virus A7 and enterovirus 71, occasionally cause poliomyelitis-like illness.1

Poliovirus vaccines Inactivated (Salk) poliovirus vaccine referred to as IPV has been in use since 1955. Live attenuated (Sabin) trivalent poliovirus vaccine or OPV has been the vaccine of choice in most countries since 1963. Mass immunisation has been most successful, and wild-type poliovirus transmission has been eradicated from North America and most industrialised countries in the Western hemisphere in 1991.3,4 Global eradication of poliomyelitis is within reach and is likely to be attained within the next decade.3 The risk of oral polio vaccine-associated poliomyelitis has been estimated by the World Health Organisation at between 0.5 and 3.4 cases per million of susceptible children,3 and this has reestablished a role for the use of the inactivated vaccine and a new strategy for immunisation with IPV in the USA and elsewhere.4

Inactivated poliovirus vaccine (IPV) Clinical features and diagnosis Most infections are asymptomatic or range in severity from non-paralytic fever, headache, nausea, gastrointestinal symptoms to asceptic meningitis and paralysis. Most clinical illnesses resolve without paralysis. The clinical syndrome may be biphasic, with a minor illness followed by remission, which subsequently develops into a major severe illness. Paralysis of respiratory muscles and swallowing usually threatens life. Paralysis is typically

The three serotypes of poliovirus are grown in monkey kidney tissue culture and inactivated with formaldehyde. The vaccine contains 2-phenoxyethanol and a trace amount of neomycin, streptomycin and polymyxin B. The vaccine is inoculated subcutaneously or intramuscularly. Three spaced doses are recommended at monthly intervals. Ninety-percent or more of vaccine recipients develop protective antibodies to all three poliovirus serotypes and at least 99% develop immunity after three doses. Protection is likely to be many years.4

Poliovirus immunisation for travellers

Oral poliovirus vaccine (OPV) This is a trivalent vaccine containing live attenuated strains of all three poliovirus serotypes grown in monkey kidney cell culture. The vaccine contains trace amounts of streptomycin and neomycin. The vaccine, given by mouth and three doses at monthly intervals produces immunity to all three poliovirus serotypes in over 95% of recipients. Immunity is probably lifelong. Live attenuated polioviruses multiply in the intestinal mucosa and the regional lymph nodes. Vaccine strains are excreted in the faeces of the vaccinated person for up to 6 weeks after each dose of the vaccine, and may spread to contacts. Vaccine-associated paralytic poliomyelitis occurs for every 1 – 3 million does of OPV administered due to reversion of the vaccine virus towards neurovirulence. The resulting paralysis is identical to that caused by the wild-type virus. Vaccine-associated paralytic poliomyelitis is more likely to occur in adults, in immunodeficient states and in children who are not immunocompetent. Since July 1999, only the inactivated polio vaccine (IPV) is used in the USA,4 and a similar policy is being adopted elsewhere. This is reinforced by the occurrence of outbreaks of vaccine-derived poliovirus type 1 in the Dominican Republic and Haiti in the year 2000 and in the Philippines in 2001.

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travellers may-reintroduce wild-type virus into poliomyelitis free zones.3,4 Persons are considered to be fully immunised if they have received in the past a primary course of three doses of IPV or OPV, or four doses of any combination of IPV and OPV. Infants and children, depending on local policy, should be immunised with four doses of IPV or three doses of OPV. Unvaccinated older children and adults should be immunised with four doses of IPV. IPV is used in the USA and in several European countries where adults who are travelling to polioendemic areas and are unvaccinated or whose immunisation history is not known to receive two doses of IPV at intervals of 4 – 8 weeks and a third dose 6 –12 months after the second dose. Accelerated courses of three doses at least 4 weeks apart are also used. IPV is the vaccine of choice for travellers with no history of the use of OPV, and in the immunocomprimised and their contacts and family members.3 Other countries recommend IPV or OPV for unvaccinated travellers, but IPV has the advantage of avoiding vaccine-associated paralytic poliomyelitis. Travellers to polio-endemic areas who last received a complete course of three or more doses of OPV or IPV in the past, should receive another single lifetime booster dose of IPV 4 weeks before departure.

References Risk for travellers Most of the world’s remaining poliovirus transmission occurs in five countries: Afghanistan, India, Pakistan, Nigeria and Niger,3 but may occur elsewhere for example the Eastern Mediterranean.4 Travellers to countries where the infection is epidemic or still endemic should be fully immunised since the consequences of infection are life threatening or paralysis, and in addition infected

1. Minor PD, Morgan-Capner M, Muir P. Enteroviruses. In: Zuckerman AJ, Banatvala JE, Pattison JR, editors. Principals and Practice of Clinical Virology, 4th ed. Chichester: Wiley; 2000. p. 427—49. 2. Salisbury DM, Begg NT, editors. Poliomyelitis. Immunisation against infectious disease, London: HMSO; 1996. p. 173—82. 3. World Health Organisation. International Travel and Health. Vaccine-preventable diseases: Poliomyelitis; 2003. www. who.int/ith 4. Centers for Disease Control and Prevention. Health Topics: Poliomyelitis; 2003. www.cdc.gov/health