POLIOVIRUS VACCINE STRAINS IN SEWAGE AND RIVER WATER IN SOUTH AFRICA 

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CHAPTER 2 LITERATURE REVIEW

Introduction

Poliomyelitis, or polio, is a life-threatening acute paralytic disease caused by poliovirus (PV), a member of the genus Enterovirus in the family Picornaviridae (Melnick, 1996a; Hovi et al., 2004). Like other ribonucleic acid (RNA) viruses, PVs exist as mixtures of microvariants, called quasispecies (Mulders et al., 1999). This is caused by the error-prone, virus-encoded RNA polymerase, which lacks proof-reading activity, resulting in a rapid accumulation of mutations upon replication (Mulders et al., 1999; Hovi et al., 2004). An additional mode of generating divergence among PVs and other enteroviruses (EVs) is their ability to recombine with other serotypes (intertypic recombinants) or with another genome of the same serotype (intratypic recombinants) (Mulders et al., 1999; Hovi et al., 2004). During replication in humans and upon transmission between hosts, some of the mutations are enriched, which has resulted in numerous genetic lineages within each serotype of PV that co-circulate worldwide (Mulders et al., 1999).
To date, there are three PV serotypes, designated type 1, type 2 and type 3, that were originally distinguished from the other EVs by neutralisation with serotype-specific antisera and the propensity to cause paralytic illness (Bodian et al., 1949; Georgopoulou et al., 2000). Furthermore, PVs have been associated with seasonal undifferentiated febrile illness, particularly during summer outbreaks and enteroviral meningitis (Melnick, 1996a; Georgopoulou et al., 2000).
Protective immunity against poliomyelitis is conferred through immunisation or natural PV infection (Ghendon and Robertson, 1994; Wood et al., 2000; Centers for Disease Control and Prevention [CDC], 2002a). The use of highly efficacious PV vaccines, the oral live attenuated vaccine made from the Sabin strains (oral poliovirus vaccine [OPV]) and the inactivated Salk vaccine (inactivated poliovirus vaccine [IPV]), has resulted in a dramatic global decrease in the circulation of wild-type PVs (Wood et al., 2000; Cherkasova et al., 2002). Due to the ability of OPV to induce a higher level of intestinal immunity (providing long-term protection against polio through durable humoral immunity), the ability to spread and immunise unvaccinated contacts of vaccine recipients (increasing the impact of OPV), plus the advantages of oral administration and lower costs, made OPV the vaccine of choice for the poliomyelitis eradication initiative (PEI) (Wood et al., 2000; Kew et al., 2004).
Immunisation with OPV has been so effective that the global eradication of wild-type PV seems a realistic goal for the foreseeable future (Cherkasova et al., 2002). Since the PEI was launched in 1988, extraordinary progress has been made to stop transmission of wild-type PV and to achieve global certification of eradication by 2005 (World Health Organization [WHO], 2004). By the end of 2002, the number of wild-type polio cases decreased from 350 000 to less than 500 and the number of polio endemic countries declined from more than 125 to 7 (Wood and Thorley, 2003; WHO, 2004). Poliomyelitis transmission has been interrupted in the American, European and Western Pacific Regions, and by the end of 2002 more than 180 countries and territories were declared as polio-free (Wood and Thorley, 2003; WHO, 2004). The last case of polio, caused by a wild-type PV in South Africa occurred in 1989 (CDC, 2003). However, this global initiative may be jeopardised due to recent outbreaks of polio in several African countries such as Botswana, Guinea, Mali and Sudan (ProMED-mail, 2004a). The current eradication strategies recommended by the WHO include: (1) high, routine infant immunisation coverage with at least three doses of OPV plus a dose at birth in polio-endemic countries; (2) national immunisation days (NIDs) targeting all children <5 years; acute flaccid paralysis (AFP) surveillance and laboratory investigations; and (4) mop-up immunisation campaigns with OPV to interrupt final chains of transmission (WHO, 2004).
However, the success of the OPV was tempered by its genetic lability, because mutations at critical sites of the live attenuated PV during genomic replication have resulted in loss of attenuation and concomitant increase in neurovirulence (Wood and Thorley, 2003; Kew et al., 2004). If these mutations lead to poliomyelitis in a vaccine recipient or a close contact, it is defined as vaccine-associated paralytic poliomyelitis (VAPP) (Wood and Thorley, 2003). Long-term persistence (in some instances up to several years) of vaccine-derived polioviruses (VDPVs) in immunodeficient individuals and the ability of the evolved variants to cause paralytic disease are well-established phenomena (Kew et al., 1998; Bellmunt et al., 1999; Martin et al., 2000; Cherkasova et al., 2002). Outbreaks of poliomyelitis in Belarus (1965-1966), Egypt (1988-1993), Hispaniola (2000-2001), the Philippines (2001) and Madagascar (2001-2002) associated with circulating VDPVs (cVDPVs), support the notion that there is a significant risk of prolonged circulation of the PV vaccine strains in populations with low immunity level, as well as their conversion into epidemic strains (Cherkasova et al., 2002; Kew et al., 2004). Highly evolved VDPVs have been isolated from environmental samples (such as sewage and river water) even in the absence of apparent cases of paralytic poliomyelitis (Shulman et al., 2000; Cherkasova et al., 2002; Horie et al., 2002; Yoshida et al., 2002; Blomqvist et al., 2004).
The purpose of this study was, firstly, to isolate OPV strains from the environment (such as selected sewage and river water samples) and from stool specimens of children infected with human immunodeficiency virus (HIV) (including those with acquired immunodeficiency syndrome [AIDS] indicator condition according to the CDC classification) at Kalafong Hospital, South Africa. Secondly, this study aimed to determine the presence of mutations in the OPV genomes (associated with reversion of attenuation to increased neurovirulence) and to determine the prevalence of VDPVs in the stool specimens of the immunodeficient children studied as well as the environment.

History of poliomyelitis

Sporadic cases of paralytic poliomyelitis have been occurring for at least as long as human history has been recorded (Melnick, 1996a). In 1920, the former United States president F.D. Roosevelt developed a febrile illness during his summer vacation that was followed by paralysis (Zaoutis and Klein, 1998). However, the first evidence of any human disease being attributed to a PV infection was a funerary stele from Middle Kingdom Egypt, dated at ~1300 BC, which depicted the priest Rom with the classical withered limb and down-flexed foot that is a well-known characteristic of poliomyelitis (Minor, 1999). Since ancient times and into the late 1800s, PVs were widely distributed in most of the world’s populations, surviving in an endemic fashion by continuously infecting susceptible infants newly born into the community (Melnick, 1996a).
Although records from antiquity mention crippling diseases compatible with poliomyelitis, it was Michael Underwood from Britain who, in 1789, first described debility of the lower extremities in children that was recognisable as poliomyelitis (CDC, 2002a). The first outbreaks of paralytic poliomyelitis were reported in Europe (initially in Sweden) and North America in the early 19th century (CDC, 2002a). These epidemics became increasingly severe, more frequent, more widespread and the average age of persons affected rose (CDC, 2002a). Cases of infantile paralysis began to be observed in adolescents and in young adults (Melnick, 1996a; Minor, 1999). This was primarily due to improved sanitation, so that children were older when they were first exposed to PV infection and therefore, no longer protected by the antibodies that they had passively acquired from their mothers (Minor, 1999).
Large epidemics of poliomyelitis spread across the world in the first half of the 20th century (Melnick, 1996a). In the United States in the summer of 1916, over 27 000 persons were reported to have been paralysed, with 6 000 deaths (Melnick, 1996a). In New York alone, more than 9 000 cases and more than 2 000 deaths were recorded (Melnick, 1996a). In 1952, over 21 000 paralytic cases were reported in the United States (Melnick, 1996a; CDC, 2002a).
Polio incidence, however, fell rapidly across the world following the introduction of effective vaccines and the global WHO-sponsored PEI (Muir et al., 1998; CDC, 2002a). The last case of wild-type PV acquired in the United States was reported in the year 1979, whereas the last case of polio associated with a wild-type PV in South Africa occurred in 1989 (CDC, 2002a; CDC, 2003).

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Clinical manifestations of poliovirus infections

A specific protein receptor on susceptible human cells allows the attachment and entry of PV in the human body (Melnick, 1996a). As the virus travels from the portal of entry (the mouth), implantation and multiplication take place in the oropharynx from where the PV enters the blood stream and infects other susceptible tissues, such as lymph nodes and the central nervous system (CNS) (Melnick, 1996a). The incubation period is between 7 and 14 days but may range from 2 to 35 days (Melnick, 1996a). Infected persons without symptoms shed PVs in faeces and are able to transmit PVs to other people (Melnick, 1996a; CDC, 2002a).
The response to PV infection is variable and has been categorised based on the severity of clinical presentation (CDC, 2002a). Ninety percent or more of wild-type PV infections are asymptomatic or unapparent (Rotbart, 1997). Three clinical syndromes are attributed to PV infection, namely abortive poliomyelitis, aseptic meningitis and paralytic poliomyelitis (Melnick, 1996a; Zaoutis and Klein, 1998). As the infection progresses, a minor illness may be followed by a major, severe illness (Melnick, 1996a; Rotbart, 1997). However, such biphasic course is more common in young children and infants than in adults (Melnick, 1996a; Rotbart, 1997).
Approximately 4% – 8% of PV infections are characterised by a minor, non-specific illness without clinical or laboratory evidence of CNS invasion (CDC, 2002a). This syndrome is known as abortive poliomyelitis and results in upper respiratory infection (sore throat and fever), gastrointestinal disturbances (nausea, vomiting, abdominal pain, constipation or diarrhoea) as well as influenza-like illness (CDC, 2002a). Nearly 10% of patients with abortive poliomyelitis will develop aseptic meningitis (non-paralytic poliomyelitis) indistinguishable from the minor illness due to non-polio enteroviruses (NPEVs) (Rotbart, 1997). Typically, symptoms (stiffness of the neck, back and legs) will last from 2 to 10 days, followed by a complete recovery (Rotbart, 1997; CDC, 2002a).
Less than 2% of all polio infections result in flaccid paralysis, which begins with a minor febrile illness followed by a short asymptomatic period of 2 to 3 days (Zaoutis and Klein, 1998). A sudden onset of asymmetric flaccid paralysis with no significant sensory loss is the characteristic finding of paralytic disease (Zaoutis and Klein, 1998). Paralysis is presented by severe myalgia in the involved limb resulting from involvement of single or multiple muscle groups (Rotbart, 1997). Motor and sensory disturbances may be observed in the same affected muscle groups (Rotbart, 1997).
Paralytic polio is classified into three types (spinal, bulbar and bulbospinal polio) depending on the level of involvement (CDC, 2002a). Spinal polio is characterised by asymmetric paralysis mostly of the legs (CDC, 2002a). Cranial nerve involvement may result in bulbar paralysis, which leads to difficulties in breathing, speech, swallowing, eye movement and facial muscle involvement (Rotbart, 1997). Bulbospinal polio accounted for 19% of cases in the United States during the period of 1969 to 1979 and was due to a combination of bulbar and spinal paralysis (Melnick, 1996a; Rotbart, 1997; CDC, 2002a).

Acknowledgements
SUMMARY 
OPSOMMING 
LIST OF ABBREVIATIONS 
LIST OF TABLES 
LIST OF FIGURES 
LIST OF PUBLICATIONS AND CONFERENCE CONTRIBUTIONS 
CHAPTER 1: INTRODUCTION 
CHAPTER 2: LITERATURE REVIEW 
2.1 Introduction
2.2 History of poliomyelitis
2.3 Clinical manifestations of poliovirus infections
2.4 Genomic characterisation of poliovirus
2.5 Mode of transmission of poliovirus
2.6 Survival of poliovirus in nature
2.7 Poliovirus vaccines
2.7.1 Inactivated poliovirus vaccine
2.7.2 Oral poliovirus vaccine
2.8 Genetic basis for the attenuation of Sabin vaccine strains of live attenuated poliovirus
2.9 Complications resulting from the use of oral poliovirus vaccine
2.10 Molecular changes of poliovirus vaccine strains in vaccine recipients
2.10.1 Mutations in Sabin poliovirus vaccine strains
2.10.2 Recombination in Sabin poliovirus vaccine strains
2.11 Vaccine-associated paralytic poliomyelitis and immunodeficiency
2.12 Vaccine-derived polioviruses
2.12.1 Immunodeficient vaccine-derived polioviruses
2.12.2 Circulating vaccine-derived polioviruses
2.13 Environmental surveillance of poliovirus circulation
2.14 Isolation and identification of polioviruses
2.14.1 Recommended cell lines for the isolation of polioviruses
2.14.2 Serological diagnosis of poliovirus infection
2.14.3 Molecular techniques for the detection of polioviruses
2.14.3.1 Reverse transcription multiplex PCR
2.14.3.2 Sabin specific RT-triplex PCR
2.14.3.3 Restriction fragment length polymorphism
2.14.3.4 Nucleotide sequencing of the enteroviral genomes
2.14.4 Intratypic differentiation methods recommended by the WHO
2.15 Eradication of poliomyelitis: Progress and Challenges
2.16 Summary
2.17 References
CHAPTER 3: POLIOVIRUS VACCINE STRAINS IN SEWAGE AND RIVER WATER IN SOUTH AFRICA 
3.1 Abstract
3.2 Introduction
3.3 Materials and methods
3.4 Results and discussion
3.5 Conclusions
3.6 References
CHAPTER 4: ISOLATION OF POLIOVIRUS VACCINE STRAINS FROM STOOL SPECIMENS OF IMMUNODEFICIENT CHILDREN IN SOUTH AFRICA 
4.1 Abstract
4.2 Introduction
4.3 Materials and methods
4.4 Results and discussion
4.5 Conclusions
4.6 References
CHAPTER 5: PREVALENCE OF VACCINE-DERIVED POLIOVIRUSES IN SEWAGE AND RIVER WATER IN SOUTH AFRICA
5.1 Abstract
5.2 Introduction
5.3 Materials and methods
5.4 Results and discussion
5.5 Conclusions
5.6 References
CHAPTER 6: PREVALENCE OF VACCINE-DERIVED POLIOVIRUSES IN STOOLS OF IMMUNODEFICIENT CHILDREN IN SOUTH AFRICA 
6.1 Abstract
6.2 Introduction
6.3 Materials and methods
6.4 Results and discussion
6.5 Conclusions
6.6 References
CHAPTER 7: GENERAL DISCUSSION 
APPENDIX
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