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Parvovirus B19 (B19) is common worldwide, with antibody studies indicating that more than 50% of people are infected during childhood. The highest rates reported have been among children in tropical areas.1,2 Outbreaks occurring at 3–6-year intervals have been described.2,3 The most common manifestation of acute B19 infection is erythema infectosum, or Fifth disease, a self-limiting febrile illness, although many other disease manifestations may occur. After initial contact with B19, specific IgM antibody is produced at approximately day 9.4 IgM usually becomes undetectable after 2–4 months depending on the initial level of response,5 although persistence of up to 9 months has been reported.6 B19-specific IgG becomes detectable around day 13 and usually persists for life. Recently B19 infection has recently been found to contribute to cases of severe anemia among young children in the Maprik area of Papua New Guinea.7 In this report, we present the results of a serosurvey of IgG and IgM antibodies to B19 among children in the East Sepik Province of Papua New Guinea.
In connection with a series of malariologic surveys in the Maprik to Pagwi area, East Sepik Province, Papua New Guinea, we surveyed children less than 10 years of age in 15 villages for evidence of past and concurrent parvovirus infections (Figure 1
). After consultation with community leaders, 3 villages in the vicinity of each of the 5 health centers serving the area were selected from 125 villages in the study area. The surveys were household-based and consisted of a social and health questionnaire, a check for splenic enlargement, and collection of finger prick blood from each individual. The survey methods and sampling strategies for the malarial surveys have been described elsewhere.8 In addition, the type of house was noted and socioeconomic status of families was determined through counting common household possessions. Families that owned no more than 5 items (21.8%) were categorized as having low socioeconomic status. Hemoglobin was measured at the time of sample collection using the HemoCue® system (HemoCue AB, Ångelholm, Sweden), a blood slide for malaria was made, and 50–500 µL of blood were collected in a numbered tube containing anticoagulant. These samples were subsequently centrifuged and the cell pellet was separated from the plasma.
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The chi-square test and Fisher’s exact test were used to test for association of IgM and IgG positivity with individual explanatory variables. Logistic regression was used for multivariate analyses. Mean hemoglobin values were compared using the t-test. All analyses were done with STATA version 8.0 statistical software (Stata Corporation, College Station, TX). Ethical approval for this study was obtained from the Papua New Guinea Medical Research Advisory Committee and the University of Sydney Human Ethics Committee.
Of the 904 specimens tested for IgG and IgM antibodies to parvovirus B19, 484 (53.5%) were IgG positive, 385 (42.6%) were IgG negative, and 35(3.9%) were IgG equivocal; 13 (1.4%) were IgM positive, 869 (96.2%) were IgM negative, and 22 (2.4%) were IgM equivocal. Equivocal samples were considered negative in all further analyses.
Overall prevalence of IgG was found to gradually increase with age from 14% in children less than 1 year of age to 73–83% in children 6–10 years of age (Table 1). No clear age dependence was observed among IgM-positive children, with IgM prevalence ranging from 0.0% to 3.2%. Significant differences in prevalence of IgG (
2 = 56.2, degrees of freedom = 4, P < 0.001) but not in prevalence of IgM (P = 0.5, by Fisher’s exact test) were observed between different regions within the study area. Overall IgG prevalence was highest (70.9%) in villages near Ulupu, followed by those near Ilaita (65.2%), and the Burkham health center (50.0%), with the lowest prevalence rates observed in areas near the Sepik River (i.e., Wombisa (42.2%) and Burui (40.0%) (Table 2). Despite these large overall differences, IgG prevalence showed comparable (linear) increases with age in all regions (Figure 2) (2 = 5.37, degrees of freedom = 4, P = 0.25, by likelihood ratio test).
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The results in this study show that parvovirus B19 infection is common among young children in the East Sepik Province of Papua New Guinea, with more than 60% of children having been infected by the age of six years. Our results are similar to those from other tropical areas such as Brazil, where 35% of children 0–4 years of age and approximately 80% of children 11–15 years of age had IgG against B19,13 Malawi, where 50% of children 1–10 years of age had IgG against B19,14 and Eritrea, where 83% of children less than one year of age and 56% of children 1–5 years of age had IgG against B19 detected on blood sampling.15 The prevalence of IgG antibody to B19 is lower among children in temperate regions.2
Data on the prevalence of B19 IgM in tropical children are limited. Studies of adult blood donors in the United States indicate a B19 IgM prevalence of approximately 1%.9 The present study found a similar prevalence of B19 IgM (1.5%) in this population. The IgG studies indicate that B19 infection is more common in children in tropical areas.2 Thus, it may have been expected that the IgM prevalence in this population would be higher. However, it should be remembered that in other areas B19 transmission has been seen to occur in outbreaks every 3–6 years. It is thus possible that the timing of this serosurvey corresponded to a period of relatively low transmission of B19 in at least some of the villages sampled.
Taken as a single population, the steady increase in prevalence of B19 IgG with age is suggestive of an endemic mode of transmission in the study area. The observed difference in overall IgG prevalence between regions within the study area, the low IgM prevalence, and the fact that no children less than two years of age were positive for IgG in the Burui region indicate that B19 transmission levels vary substantially between neighboring villages and regions. Alternatively, transmission may be characterized by small, very localized outbreaks of B19 infections that affected only a few villages or hamlets at a time, rather than the entire study population. Nevertheless, it is clear that B19 infection occurs frequently in children less than two years of age in this area. For this reason, any preventive measures such as a vaccine will need to be targeted at the very young, probably in the first year of life. High levels of B19 in young children are of particular concern because B19 infection as been associated with an increased risk for severe anemia in this region.7 Because the etiology of anemia is multifactoral (parvovirus, malarial, and hook worm infections and iron deficiency all contribute significantly to the high burden of anemia in our study population), longitudinal studies that follow hemoglobin levels over time are needed to properly assess the proportion of anemias that are associated with parvovirus infection.
Received August 21, 2006. Accepted for publication February 12, 2007.
Acknowledgments: We thank the participants and the staff of the Papua New Guinea Institute of Medical Research in Goroka and Maprik and the staff of the Department of Infectious Diseases, University of Sydney for their participation in the study. We also thank Lawrence Rare, Simone Widmer, Daniela Michel, and the health center surveillance nurses for collecting samples.
Financial support: Travel to the field for James Wildig was supported by the University of Sydney.
* Address correspondence to Yvonne Cossart, Department of Infectious Diseases and Immunology, University of Sydney, Room 604, D06 Blackburn Building, Sydney, New South Wales 2006, Australia. E-mail: ycossart{at}infdis.usyd.edu.au 
Authors’ addresses: James Wildig and Yvonne Cossart, Department of Infectious Diseases and Immunology, University of Sydney, Level 6, D06 Blackburn Building, Sydney, New South Wales 2006, Australia, Telephone: 61-2-9351-2412 and 61-2-9351-2900, Fax: 61-2-9351-4731, E-mail: ycossart{at}infdis.usyd.edu.au. Ivo Mueller, Malaria Epidemiology, Papua New Guinea Institute of Medical Research. PO Box 60, Goroka, EHP 441, Papua New Guinea, Telephone: 675-732-2800, Fax: 675-732-1998. Benson Kiniboro and Seri Maraga, Papua New Guinea Institute of Medical Research, Maprik Branch, PO Box 400, Maprik ESP 533, Papua New Guinea, Telephone: 675-858-1294, Fax: 675-858-1257, E-mail: sepik{at}pngimr.org.pg. Peter Siba, Microbiology/Immunology, Papua New Guinea Institute of Medical Research PO Box 60, Goroka, EHP 441, Papua New Guinea, Telephone: 675-732-2800, Fax: 675-732-1998.
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