Human Parvovirus B19

Abstract

American Journal of TransplantationVolume 4, Issue s10 p. 92-94 Free Access Human Parvovirus B19 First published: 25 October 2004 https://doi.org/10.1111/j.1600-6135.2004.00731.xCitations: 1AboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Epidemiology Parvovirus B19 is a single-stranded DNA virus. Because replication only occurs in human erythrocyte precursors, this virus is classified as a member of the Erythrovirus genus of the Parvoviridae family. Parvovirus B19 is a common cause of infection in children with the usual time of acquisition being during the school-age time period. Serologic evidence of past infection increases substantially between the ages of 5 and 15, by adulthood, to 30–60% of people are seropositive. Infection appears to confer lifelong immunity to immunocompetent hosts (1). Most infections of immunocompetent children are asymptomatic or result in a mild illness known as erythema infectiosum, characterized by a ‘slapped cheek’ rash with or without a lacy erythematous exanthem involving the extremities (1). Infection with Parvovirus B19 has also been associated with a variety of other clinical syndromes including mild respiratory tract illness without a rash. Arthritis has also been associated with Parvovirus B19 infection though this is seen more commonly in adult females (1). Parvovirus B19 has a predilection for erythroid precursors. Because infection may be prolonged in immunosuppressed patients, Parvovirus B19 infection may lead to depletion of these erythroid precursors resulting in severe, areticulocytotic anemia. Similarly, in patients with shortened redcell lifespans (e.g. hemolytic anemias), Parvovirus B19 infections can also result in severe anemia. This has been seen after solid organ and bone marrow transplantation. In solid organ transplant recipients, Parvovirus B19 most typically presents as a pure red cell aplasia with an extremely low or absent reticulocyte count (2-4). Although large, prospective surveillance studies are lacking, it has been estimated that ∼1–2% of unselected, organ transplant recipients experience symptomatic Parvovirus B19 infections (5). This rate may be higher in children as a result of their lower degree of preexisting immunity, but prospective data confirming this speculation are lacking. Parvovirus B19-associated anemia has only been infrequently described after bone marrow transplantation (6-8). The low-level incidence in this population has been ascribed to the potential prophylactic effect of intravenous immunoglobulin (IVIG) which is commonly used after bone marrow transplantation (5). Infection with Parvovirus B19 in the immunocompromised patient has also been associated with fever, rashes, and less frequently pancytopenia and hepatitis. Transmission Community-acquired acquisition via exposure to infectious respiratory secretions is the most common route of transmission in both immunocompetent and immunocompromised individuals. Transmission can also occur via exposure to blood or blood products. However, transmission via this route is rare as blood and blood product donors tend to be older and are therefore at very low risk of acquiring (and hence transmitting) infection. It is worth noting that by the time that immunocompetent patients develop the rash of erythema infectiousum they are no longer infectious. In contrast, immunosuppressed patients with Parvovirus B19 may shed the virus in respiratory secretions for prolonged periods of time (6). This observation may explain a nosocomial outbreak of three cases of Parvovirus B19 infection reported in a renal transplant unit (6). For this reason, droplet precautions in addition to standard precautions are recommended for individuals caring for hospitalized children with aplastic crisis or immunosuppressed patients with chronic infection and anemia for the duration of the hospitalization. Pregnant health care personnel should be informed of the potential risks to the fetus from Parvovirus B19 infections and about preventative measures that may reduce the risk (e.g. attention to strict infection control procedures). Some experts have recommended that pregnant women should avoid caring for immunocompromised patients with evidence of chronic parvovirus infection or those with Parvovirus B19-associated aplastic crises to avoid exposure to this potentially highly contagious disease. Diagnosis Parvovirus B19 infection can be diagnosed by serology, bone marrow histology or detection of viral DNA using a polymerase chain reaction (PCR) assay. In the immunocompetent host, detection of serum Parvovirus B19 IgM antibody indicates that infection probably occurred within the previous 2–4 months. However, persistence of IgM antibody against Parvovirus B19 has been found in symptomatic transplant recipients and likely is a marker of on-going infection. The presence of IgG antibody alone is most consistent with remote infection in both immunocompetent and immunocompromised patients. One concern with the use of serologies for making the diagnosis is the potential for passive acquisition of antibody against parvovirus. However, since it is highly unlikely that the presence of IgM antibody against parvovirus will be passively acquired, this should not really impact on the ability to make a serologic diagnosis. The sensitivity of a serologic diagnosis may be lowered by the inability of the immunosuppressed transplant recipient to mount an antibody response against Parvovirus B19 (5). Stereotypical histologic findings of giant pronormoblasts in the bone marrow of affected patients on marrow smears or electron microscopy is also suggestive of Parvovirus B19 infection (2). PCR detection of Parvovirus B19 in the blood or serum may be the optimal method of diagnosing this infection in immunocompromised patients (1, 4). Unfortunately, Parvovirus B19 DNA can be detected by PCR in serum for up to 9 months after the viremic phase of infection in some patients. Thus, a positive DNA PCR for parvovirus does not necessarily indicate acute infection. However, the positive predictive value of a DNA PCR in an immunocompromised host with red cell aplasia is high. Treatment There is no specific antiviral chemotherapeutic agent available for the treatment of Parvovirus B19. However, IVIG has been shown to resolve the symptoms and anemia associated with this in immunocompromised patients including transplant recipients (2-4, 9-12) (AII). Unfortunately, the optimal dosing regimen and duration of IVIG for the treatment of Parvovirus B19 infection use in these patients has not been established. In addition, the mechanism of IVIG activity against Parvovirus B19 is unknown. Several groups have reported the potential for relapse of red cell aplasia associated with recurrent presence of Parvovirus B19 DNA (detected by PCR) in the blood of HIV infected patients. One review of the published experience with recurrence of Parvovirus B19 infection in transplant recipients identified a 10% recurrence rate among 22 published cases of red cell aplasia due to Parvovirus B19 treated with IVIG (13). Such cases might be identified by serial monitoring of their blood for the presence of Parvovirus B19 DNA. However, given the relative infrequency of relapse, it would seem more prudent to simply follow serial hemoglobin measurement and consider obtaining parvovirus DNA PCRs for those patients developing anemia. Retreatment with IVIG would seem reasonable in such patients. Prevention No proven specific preventive strategy against Parvovirus B19 infection is available; however, some authors suggest that IVIG may be effective in preventing development of this infection (14). Anecdotal experience in bone marrow transplant recipients has demonstrated an absence of Parvovirus B19 disease in cohorts of patients who received prophylactic IVIG for other reasons (8) (CIII). However, comparative studies evaluating the frequency of this complication in BMT recipients who did not receive IVIG are not available. Routine screening of donor and recipient serostatus for Parvovirus B19 is not routinely recommended. Recommendations aimed at avoiding exposure of transplant recipients to children or adults with Parvovirus B19 have not been offered by any advisory groups. While it would seem logical to avoid contact with patients who may be experiencing parvovirus infection during its infectious stage, such a policy is not helpful since immunocompetent individuals are infectious prior to the time that classic symptoms of clinical disease are present and once immunocompetent patients manifest these symptoms they are no longer contagious. Further, there are no specific guidelines at present suggesting avoidance of populations at risk of developing parvovirus infection which could represent a source of exposures for transplant recipients (e.g. avoiding occupations with frequent exposures to children). The relative rarity of this diagnosis in transplant recipients, particularly among pediatric transplant recipients, does not support the introduction of such a policy. Finally, preliminary research is underway to identify potential candidate Parvovirus B19 vaccines. However, data determining which of these vaccines might be licensed and what their immunogenicity would be in immunosuppressed transplant recipients are not available at this time. Future studies Multicenter trials to establish the most effective regimen and trials to determine the best monitoring for response to therapy or for potential relapse. References 1 Anderson LJ . Human parvoviruses . J Infect Dis 1990 ; 161 : 603 – 608 . 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DOI: 10.1034/j.1399-0012.2000.140612.x Wiley Online LibraryCASPubMedWeb of Science®Google Scholar 14 Ang HA , Apperley JF , Ward KN . Persistence of antibody to human Parvovirus B19 after allogeneic bone marrow transplantation: role of prior recipient immunity . Blood 1997 ; 89 : 4646 – 4651 . CASPubMedWeb of Science®Google Scholar Citing Literature Volume4, Issues10October 2004Pages 92-94 AST and ASTS members - please log in via your Society website for full journal access.AST Members >> ASTS Members >> ReferencesRelatedInformation