© 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd Transplant Infectious Disease, ISSN 1398-2273
Case report
Persistent parvovirus B19 infection resulting in red cell aplasia after allogeneic hematopoietic stem cell transplantation Y. Koda, T. Mori, J. Kato, S. Kohashi, T. Kikuchi, T. Mitsuhashi, M. Murata, T. Uemura, M. Handa, S. Okamoto. Persistent parvovirus B19 infection resulting in red cell aplasia after allogeneic hematopoietic stem cell transplantation. Transpl Infect Dis 2013: 15: E239–E242. All rights reserved Abstract: Persistent parvovirus B19 (PVB) infection has been reported sporadically in immunocompromised patients including hematopoietic stem cell and solid organ transplant recipients. However, the pathogenesis of persistent infection has yet to be fully elucidated. We report here a patient with multiple myeloma developing red cell aplasia during the hematopoietic recovery after allogeneic hematopoietic stem cell transplantation (HSCT) caused by PVB. The patient had already had PVB viremia before transplantation and remained asymptomatic. The route of PVB transmission was considered to be direct contact with the patient’s family member with primary PVB infection 1 month before transplantation. Treatment with intravenous immunoglobulin resulted in prompt resolution of anemia. These findings suggest that monitoring of PVB DNA is recommended for patients undergoing HSCT and having contact with individuals with documented PVB infection, even if they are asymptomatic.
Y. Koda1, T. Mori1, J. Kato1, S. Kohashi1, T. Kikuchi1, T. Mitsuhashi2, M. Murata2, T. Uemura3, M. Handa3, S. Okamoto1 1
Division of Hematology, Department of Medicine, Keio University School of Medicine, Tokyo, Japan, 2Department of Laboratory Medicine, Keio University School of Medicine, Tokyo, Japan, 3Department of Transfusion and Cell Therapy, Keio University Hospital, Tokyo, Japan Key words: parvovirus B19; persistent infection; red cell aplasia; allogeneic hematopoietic stem cell transplantation; multiple myeloma Correspondence to: Takehiko Mori, MD, PhD, Division of Hematology, Department of Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan Tel: +81 3 3353 1211 (ext. 62385) Fax: +81 3 3353 3515 e-mail: [email protected]
Received 13 April 2013, revised 25 June 2013, accepted for publication 6 September 2013 DOI: 10.1111/tid.12155 Transpl Infect Dis 2013: 15: E239–E242
Human parvovirus B19 (PVB), now termed erythrovirus, is a non-enveloped single-stranded DNA virus that has a strong tropism to erythroid progenitor cells. PVB is considered to infect erythroid progenitor cells through P-blood-group antigen as its receptor, and subsequent replication leads to the suppression of erythropoiesis (1). Therefore, PVB could cause red cell aplasia (RCA) in patients whose red blood cells have shortened survival times because of hemolytic disorders, pregnancy, or chemotherapy (1). In general, acute PVB infection is controlled and promptly cleared by the neutralizing antibodies. Therefore, persistent infection with PVD is considered rare. However,
sporadic cases of persistent PVB infection have been reported, mainly in immunocompromised patients (2–5). The pathogenesis and treatment of persistent PVB infection have yet to be fully evaluated. We experienced a case of RCA at the time of hematopoietic engraftment after allogeneic hematopoietic stem cell transplantation (HSCT), in which persistent PVB infection was found to have been preexisting from the pre-transplant period. We believe that this case could provide clinically useful insights into the pathogenesis and persistence of PVB infection and its impact on hematopoietic reconstitution after allogeneic HSCT.
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Koda et al: Parvovirus-induced red cell aplasia
Case report A 44-year-old Japanese man with immunoglobulin (Ig) G-j type multiple myeloma (MM) received combination chemotherapy followed by high-dose melphalan (200 mg/m2) supported by autologus peripheral blood SCT. The maximum response to the therapy was a partial response, and 3 courses of lenalidomide in combination with dexamethasone were given. Because of the poor response to this series of chemotherapy, allogeneic HSCT was planned. Four weeks before HSCT, his 5-year-old daughter developed erythema infectiosum and the patient had contact with her. The patient was free from fever and skin rash and remained asymptomatic after the exposure, and the laboratory examinations did not reveal relevant abnormalities suggesting PVB infection. Allogeneic bone marrow transplantation from an ABOmatched, human leukocyte antigen-mismatched unrelated donor was performed as scheduled. Preparative regimen consisted of fludarabine (125 mg/m2) and melphalan (140 mg/m2), and anti-thymocyte globulin (2.5 mg/kg). Tacrolimus and short-term methotrexate were given for the prophylaxis of graft-versus-host disease. Except for mild-to-moderate mucositis as regimen-related toxicity, his post transplant course was unremarkable until the neutrophil and platelet engraftments, which were achieved on days 14 and 16 post transplant, respectively. In contrast to the prompt recovery of neutrophil and platelet, reticulocytopenia persisted and he remained red blood cell transfusion-dependent. On day 28, bone marrow examination revealed erythroid cell hypoplasia (erythroid cells: 1.6%) with giant proerythroblasts and with normal differentiation in myeloid lineage cells and megakaryocytes (Fig. 1). PVB was detected in the serum by polymerase chain reaction (PCR), and anti-PVB IgG and IgM antibodies were to be found positive on day 30 post transplant (Table 1). PCR to detect PVB was not performed using the bone marrow. The serum samples that had been stored 162 and 18 days before transplantation were available for further analyses. The serum stored 162 days before transplantation was positive for antiPVB IgG antibody but negative for PVB by PCR and anti-PVB IgM antibody (Table 1). The serum stored 18 days before transplantation was positive for PVB by PCR and anti-PVB IgG antibody but negative for antiPVB IgM antibody (Table 1). In total, 3 doses of intravenous immunoglobulin (IVIg) (100 mg/kg of body weight for each) were given after HSCT, one of which was given empirically for febrile neutropenia. Reticulocyte count began to
E240
Fig. 1. Bone marrow smear at the diagnosis of red cell aplasia. Marked hypoplasia in erythroid cells and giant proerythroblasts (arrow) were observed.
Detection of parvovirus B19 (PVB) and antibodies against PVB 162 days before transplantation
18 days before transplantation
30 days after transplantation
Anti-PVB antibodies IgG
Positive
Positive
Positive
IgM
Negative
Negative
Positive
PVB DNA
Negative
Positive
Positive
Ig, immunoglobulin.
Table 1
increase 10 days after the first dose of IVIg, and he became transfusion independent. After recovery, PCR to detect PVB was not performed. On day 90, bone marrow did not reveal any significant morphological abnormalities. RCA did not recur thereafter, although a series of combination chemotherapies was given for MM relapsing 3 months after the transplantation.
Discussion The patient in the case presented here developed RCA caused by PVB at the time of hematopoietic recovery after allogeneic HSCT. Prominent RCA was considered unusual at 28 days after allogeneic HSCT from an ABOmatched donor, as the reported time to red blood cell transfusion independence was 12–24 days after transplantation (6). In addition, the identification of giant
Transplant Infectious Disease 2013: 15: E239–E242
Koda et al: Parvovirus-induced red cell aplasia
proerythroblasts in the bone marrow prompted us to evaluate the effects of PVB infection. It is notable that PVB infection had been present since the pre-transplant period and persisted until hematopoietic recovery after allogeneic HSCT. To the best of our knowledge, this is the first reported case in which erythroid engraftment after HSCT was not achieved because of RCA caused by the preexisting persistent PVB infection. In general, primary PVB infection causes transient selflimited manifestations, namely erythema infectiosum, commonly occurring in children. The natural course of primary PVB infection in immunocompetent individuals is characterized by the prompt clearance of viremia within 1 week by neutralizing antibodies (7). Primary infection causes RCA in the specific conditions where red blood cell survival time is shortened; however, the duration between the primary infection and development of RCA has not been demonstrated. Those conditions include hemolytic disorders, pregnancy, and hematopoietic recovery phase after anti-cancer chemotherapy (1, 8, 9). In contrast, it has been reported that persistent PVB infection could be established in immunosuppressed conditions where the ability to constitute effective antiviral immunity is severely impaired. These conditions include human immunodeficiency virus infection, hematological diseases, HSCT, and solid organ transplantation (2–5, 8, 9). In addition to our case, only one case of MM has been reported in which persistent PVB infection was documented and caused RCA (10). In MM, humoral immunity is profoundly impaired not only by the disease itself but also by the treatment. It is plausible that patients with MM could be susceptible to persistent PVB infection and at high risk for developing persistent PVB infection. Prevention of exposure to PVB is the most effective method for the management of PVB infection. One of the possible routes of PVB infection is direct contact with individuals infected with PVB. In this case, PVB was considered to be transmitted from the patient’s young daughter with documented PVB infection. Although the patient had remained free from any symptoms suggesting PVB infection, asymptomatic persistent PVB infection had been established. Therefore, it is considered that monitoring of PVB DNA in blood by PCR is required if susceptible patients had contact with individuals with documented PVB infection, even though they did not subsequently develop any symptoms associated with PVB infection. In addition, identification of asymptomatic patients with PVB infection, could further prevent the intra-institutional expansion of PVB to other susceptible individuals. The other possible route of PVB infection is through blood transfusions. Recently, persistent PVB infection
(viremia) in immunocompetent individuals has been documented by detecting PVB DNA in blood products donated from volunteer donors (11, 12). This route is also reinforced by the higher seropositivity of PVB in patients receiving blood transfusions (5). Therefore, screening of PVB DNA in blood products is also required, especially for immunosuppressed patients requiring multiple blood transfusions, such as HSCT and solid organ transplant recipients. The standard treatment for PVB infection in immunocompromised patients has yet to be established; however, evidence has been accumulating for the efficacy of IVIg (4, 8, 10, 13). IVIg treatment makes sense because humoral immunity plays a crucial role in the protection against PVB infection, and available immunoglobulin formulations universally contain antiPVB IgG. Indeed, recovery of reticulocytes was also observed shortly after IVIg administration in our case, which strongly suggests its efficacy against PVB infection. Regarding the doses of immunoglobulin, our patient responded well with a relatively lower dose (in total 300 mg/kg) compared with the previously reported doses ranging between 1500 and 4000 mg/kg (4, 8, 10, 13). Because of the high cost of high-dose IVIg administration, the efficacy of lower doses should be investigated by accumulating the outcomes of patients treated with lower doses. It is notable that anti-PVB IgM antibody turned out to be positive even at a very early post transplant period (day 30 after HSCT) in our case, which had been negative before HSCT. This finding suggested that antiPVB IgM antibody was produced by donor-derived immune cells and could have contributed to the eradication of PVB cooperatively with passively administered immunoglobulin. In conclusion, persistent PVB infection is rare, but could be established in immunocompromised patients. Therefore, even though they remain asymptomatic, the detection of PVB by PCR in immunocompromised patients is strongly recommended when patients have contact with an individual with documented PVB infection, and IVIg should be promptly given before proceeding to further treatments, such as HSCT and solid organ transplantation.
References 1. Servant-Delmas A, Lefrere JJ, Morinet F, Pillet S. Advances in human B19 erythrovirus biology. J Virol 2010; 84 (19): 9658–9665. 2. Frickhofen N, Abkowitz JL, Safford M, et al. Persistent B19 parvovirus infection in patients infected with human
Transplant Infectious Disease 2013: 15: E239–E242
E241
Koda et al: Parvovirus-induced red cell aplasia
3.
4.
5.
6.
7. 8.
immunodeficiency virus type 1 (HIV-1): a treatable cause of anemia in AIDS. Ann Intern Med 1990; 113 (12): 926–933. LaMonte AC, Paul ME, Read JS, et al.; Women and Infants Transmission Study. Persistent parvovirus B19 infection without the development of chronic anemia in HIV-infected and -uninfected children: the Women and Infants Transmission Study. J Infect Dis 2004 189 (5): 847–851. Eid AJ, Brown RA, Patel R, Razonable RR. Parvovirus B19 infection after transplantation: a review of 98 cases. Clin Infect Dis 2006; 43 (1): 40–48. Flunker G, Peters A, Wiersbitzky S, Modrow S, Seidel W. Persistent parvovirus B19 infections in immunocompromised children. Med Microbiol Immunol 1998; 186 (4): 189–194. Pavletic ZS, Bishop MR, Tarantolo SR, et al. Hematopoietic recovery after allogeneic blood stem-cell transplantation compared with bone marrow transplantation in patients with hematologic malignancies. J Clin Oncol 1997; 15 (4): 1608–1616. Anderson MJ, Higgins PG, Davis LR, et al. Experimental parvoviral infection in humans. J Infect Dis 1985; 152 (2): 257–265. Katragadda L, Shahid Z, Restrepo A, Muzaffar J, Alapat D, Anaissie E. Preemptive intravenous immunoglobulin allows safe
E242
9.
10.
11.
12.
13.
and timely administration of antineoplastic therapies in patients with multiple myeloma and parvovirus B19 disease. Transpl Infect Dis 2013; 15 (4): 354–360. Jitschin R, Peters O, Plentz A, Turowski P, Segerer H, Modrow S. Impact of parvovirus B19 infection on paediatric patients with haematological and/or oncological disorders. Clin Microbiol Infect 2011; 17 (9): 1336–1342. Muslimani AA, Kundranda MN, Daw HA. Chronic anemia due to parvovirus B19 infection in a patient with multiple myeloma. Clin Adv Hematol Oncol 2007; 5 (1): 48–49. Lefrere JJ, Servant-Delmas A, Candotti D, et al. Persistent B19 infection in immunocompetent individuals: implications for transfusion safety. Blood 2005; 106 (8): 2890–2895. Tsukada Y, Yokoyama K, Ishida A, et al. Erythroid crisis caused by parvovirus B19 transmitted via red blood cell transfusion. Intern Med 2011; 50 (20): 2379–2382. Kurtzman G, Frickhofen N, Kimball J, Jenkins DW, Nienhuis AW, Young NS. Pure red-cell aplasia of 10 years’ duration due to persistent parvovirus B19 infection and its cure with immunoglobulin therapy. N Engl J Med 1989; 321 (8): 519–553.
Transplant Infectious Disease 2013: 15: E239–E242
Copyright of Transplant Infectious Disease is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
Case report
Persistent parvovirus B19 infection resulting in red cell aplasia after allogeneic hematopoietic stem cell transplantation Y. Koda, T. Mori, J. Kato, S. Kohashi, T. Kikuchi, T. Mitsuhashi, M. Murata, T. Uemura, M. Handa, S. Okamoto. Persistent parvovirus B19 infection resulting in red cell aplasia after allogeneic hematopoietic stem cell transplantation. Transpl Infect Dis 2013: 15: E239–E242. All rights reserved Abstract: Persistent parvovirus B19 (PVB) infection has been reported sporadically in immunocompromised patients including hematopoietic stem cell and solid organ transplant recipients. However, the pathogenesis of persistent infection has yet to be fully elucidated. We report here a patient with multiple myeloma developing red cell aplasia during the hematopoietic recovery after allogeneic hematopoietic stem cell transplantation (HSCT) caused by PVB. The patient had already had PVB viremia before transplantation and remained asymptomatic. The route of PVB transmission was considered to be direct contact with the patient’s family member with primary PVB infection 1 month before transplantation. Treatment with intravenous immunoglobulin resulted in prompt resolution of anemia. These findings suggest that monitoring of PVB DNA is recommended for patients undergoing HSCT and having contact with individuals with documented PVB infection, even if they are asymptomatic.
Y. Koda1, T. Mori1, J. Kato1, S. Kohashi1, T. Kikuchi1, T. Mitsuhashi2, M. Murata2, T. Uemura3, M. Handa3, S. Okamoto1 1
Division of Hematology, Department of Medicine, Keio University School of Medicine, Tokyo, Japan, 2Department of Laboratory Medicine, Keio University School of Medicine, Tokyo, Japan, 3Department of Transfusion and Cell Therapy, Keio University Hospital, Tokyo, Japan Key words: parvovirus B19; persistent infection; red cell aplasia; allogeneic hematopoietic stem cell transplantation; multiple myeloma Correspondence to: Takehiko Mori, MD, PhD, Division of Hematology, Department of Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan Tel: +81 3 3353 1211 (ext. 62385) Fax: +81 3 3353 3515 e-mail: [email protected]
Received 13 April 2013, revised 25 June 2013, accepted for publication 6 September 2013 DOI: 10.1111/tid.12155 Transpl Infect Dis 2013: 15: E239–E242
Human parvovirus B19 (PVB), now termed erythrovirus, is a non-enveloped single-stranded DNA virus that has a strong tropism to erythroid progenitor cells. PVB is considered to infect erythroid progenitor cells through P-blood-group antigen as its receptor, and subsequent replication leads to the suppression of erythropoiesis (1). Therefore, PVB could cause red cell aplasia (RCA) in patients whose red blood cells have shortened survival times because of hemolytic disorders, pregnancy, or chemotherapy (1). In general, acute PVB infection is controlled and promptly cleared by the neutralizing antibodies. Therefore, persistent infection with PVD is considered rare. However,
sporadic cases of persistent PVB infection have been reported, mainly in immunocompromised patients (2–5). The pathogenesis and treatment of persistent PVB infection have yet to be fully evaluated. We experienced a case of RCA at the time of hematopoietic engraftment after allogeneic hematopoietic stem cell transplantation (HSCT), in which persistent PVB infection was found to have been preexisting from the pre-transplant period. We believe that this case could provide clinically useful insights into the pathogenesis and persistence of PVB infection and its impact on hematopoietic reconstitution after allogeneic HSCT.
E239
Koda et al: Parvovirus-induced red cell aplasia
Case report A 44-year-old Japanese man with immunoglobulin (Ig) G-j type multiple myeloma (MM) received combination chemotherapy followed by high-dose melphalan (200 mg/m2) supported by autologus peripheral blood SCT. The maximum response to the therapy was a partial response, and 3 courses of lenalidomide in combination with dexamethasone were given. Because of the poor response to this series of chemotherapy, allogeneic HSCT was planned. Four weeks before HSCT, his 5-year-old daughter developed erythema infectiosum and the patient had contact with her. The patient was free from fever and skin rash and remained asymptomatic after the exposure, and the laboratory examinations did not reveal relevant abnormalities suggesting PVB infection. Allogeneic bone marrow transplantation from an ABOmatched, human leukocyte antigen-mismatched unrelated donor was performed as scheduled. Preparative regimen consisted of fludarabine (125 mg/m2) and melphalan (140 mg/m2), and anti-thymocyte globulin (2.5 mg/kg). Tacrolimus and short-term methotrexate were given for the prophylaxis of graft-versus-host disease. Except for mild-to-moderate mucositis as regimen-related toxicity, his post transplant course was unremarkable until the neutrophil and platelet engraftments, which were achieved on days 14 and 16 post transplant, respectively. In contrast to the prompt recovery of neutrophil and platelet, reticulocytopenia persisted and he remained red blood cell transfusion-dependent. On day 28, bone marrow examination revealed erythroid cell hypoplasia (erythroid cells: 1.6%) with giant proerythroblasts and with normal differentiation in myeloid lineage cells and megakaryocytes (Fig. 1). PVB was detected in the serum by polymerase chain reaction (PCR), and anti-PVB IgG and IgM antibodies were to be found positive on day 30 post transplant (Table 1). PCR to detect PVB was not performed using the bone marrow. The serum samples that had been stored 162 and 18 days before transplantation were available for further analyses. The serum stored 162 days before transplantation was positive for antiPVB IgG antibody but negative for PVB by PCR and anti-PVB IgM antibody (Table 1). The serum stored 18 days before transplantation was positive for PVB by PCR and anti-PVB IgG antibody but negative for antiPVB IgM antibody (Table 1). In total, 3 doses of intravenous immunoglobulin (IVIg) (100 mg/kg of body weight for each) were given after HSCT, one of which was given empirically for febrile neutropenia. Reticulocyte count began to
E240
Fig. 1. Bone marrow smear at the diagnosis of red cell aplasia. Marked hypoplasia in erythroid cells and giant proerythroblasts (arrow) were observed.
Detection of parvovirus B19 (PVB) and antibodies against PVB 162 days before transplantation
18 days before transplantation
30 days after transplantation
Anti-PVB antibodies IgG
Positive
Positive
Positive
IgM
Negative
Negative
Positive
PVB DNA
Negative
Positive
Positive
Ig, immunoglobulin.
Table 1
increase 10 days after the first dose of IVIg, and he became transfusion independent. After recovery, PCR to detect PVB was not performed. On day 90, bone marrow did not reveal any significant morphological abnormalities. RCA did not recur thereafter, although a series of combination chemotherapies was given for MM relapsing 3 months after the transplantation.
Discussion The patient in the case presented here developed RCA caused by PVB at the time of hematopoietic recovery after allogeneic HSCT. Prominent RCA was considered unusual at 28 days after allogeneic HSCT from an ABOmatched donor, as the reported time to red blood cell transfusion independence was 12–24 days after transplantation (6). In addition, the identification of giant
Transplant Infectious Disease 2013: 15: E239–E242
Koda et al: Parvovirus-induced red cell aplasia
proerythroblasts in the bone marrow prompted us to evaluate the effects of PVB infection. It is notable that PVB infection had been present since the pre-transplant period and persisted until hematopoietic recovery after allogeneic HSCT. To the best of our knowledge, this is the first reported case in which erythroid engraftment after HSCT was not achieved because of RCA caused by the preexisting persistent PVB infection. In general, primary PVB infection causes transient selflimited manifestations, namely erythema infectiosum, commonly occurring in children. The natural course of primary PVB infection in immunocompetent individuals is characterized by the prompt clearance of viremia within 1 week by neutralizing antibodies (7). Primary infection causes RCA in the specific conditions where red blood cell survival time is shortened; however, the duration between the primary infection and development of RCA has not been demonstrated. Those conditions include hemolytic disorders, pregnancy, and hematopoietic recovery phase after anti-cancer chemotherapy (1, 8, 9). In contrast, it has been reported that persistent PVB infection could be established in immunosuppressed conditions where the ability to constitute effective antiviral immunity is severely impaired. These conditions include human immunodeficiency virus infection, hematological diseases, HSCT, and solid organ transplantation (2–5, 8, 9). In addition to our case, only one case of MM has been reported in which persistent PVB infection was documented and caused RCA (10). In MM, humoral immunity is profoundly impaired not only by the disease itself but also by the treatment. It is plausible that patients with MM could be susceptible to persistent PVB infection and at high risk for developing persistent PVB infection. Prevention of exposure to PVB is the most effective method for the management of PVB infection. One of the possible routes of PVB infection is direct contact with individuals infected with PVB. In this case, PVB was considered to be transmitted from the patient’s young daughter with documented PVB infection. Although the patient had remained free from any symptoms suggesting PVB infection, asymptomatic persistent PVB infection had been established. Therefore, it is considered that monitoring of PVB DNA in blood by PCR is required if susceptible patients had contact with individuals with documented PVB infection, even though they did not subsequently develop any symptoms associated with PVB infection. In addition, identification of asymptomatic patients with PVB infection, could further prevent the intra-institutional expansion of PVB to other susceptible individuals. The other possible route of PVB infection is through blood transfusions. Recently, persistent PVB infection
(viremia) in immunocompetent individuals has been documented by detecting PVB DNA in blood products donated from volunteer donors (11, 12). This route is also reinforced by the higher seropositivity of PVB in patients receiving blood transfusions (5). Therefore, screening of PVB DNA in blood products is also required, especially for immunosuppressed patients requiring multiple blood transfusions, such as HSCT and solid organ transplant recipients. The standard treatment for PVB infection in immunocompromised patients has yet to be established; however, evidence has been accumulating for the efficacy of IVIg (4, 8, 10, 13). IVIg treatment makes sense because humoral immunity plays a crucial role in the protection against PVB infection, and available immunoglobulin formulations universally contain antiPVB IgG. Indeed, recovery of reticulocytes was also observed shortly after IVIg administration in our case, which strongly suggests its efficacy against PVB infection. Regarding the doses of immunoglobulin, our patient responded well with a relatively lower dose (in total 300 mg/kg) compared with the previously reported doses ranging between 1500 and 4000 mg/kg (4, 8, 10, 13). Because of the high cost of high-dose IVIg administration, the efficacy of lower doses should be investigated by accumulating the outcomes of patients treated with lower doses. It is notable that anti-PVB IgM antibody turned out to be positive even at a very early post transplant period (day 30 after HSCT) in our case, which had been negative before HSCT. This finding suggested that antiPVB IgM antibody was produced by donor-derived immune cells and could have contributed to the eradication of PVB cooperatively with passively administered immunoglobulin. In conclusion, persistent PVB infection is rare, but could be established in immunocompromised patients. Therefore, even though they remain asymptomatic, the detection of PVB by PCR in immunocompromised patients is strongly recommended when patients have contact with an individual with documented PVB infection, and IVIg should be promptly given before proceeding to further treatments, such as HSCT and solid organ transplantation.
References 1. Servant-Delmas A, Lefrere JJ, Morinet F, Pillet S. Advances in human B19 erythrovirus biology. J Virol 2010; 84 (19): 9658–9665. 2. Frickhofen N, Abkowitz JL, Safford M, et al. Persistent B19 parvovirus infection in patients infected with human
Transplant Infectious Disease 2013: 15: E239–E242
E241
Koda et al: Parvovirus-induced red cell aplasia
3.
4.
5.
6.
7. 8.
immunodeficiency virus type 1 (HIV-1): a treatable cause of anemia in AIDS. Ann Intern Med 1990; 113 (12): 926–933. LaMonte AC, Paul ME, Read JS, et al.; Women and Infants Transmission Study. Persistent parvovirus B19 infection without the development of chronic anemia in HIV-infected and -uninfected children: the Women and Infants Transmission Study. J Infect Dis 2004 189 (5): 847–851. Eid AJ, Brown RA, Patel R, Razonable RR. Parvovirus B19 infection after transplantation: a review of 98 cases. Clin Infect Dis 2006; 43 (1): 40–48. Flunker G, Peters A, Wiersbitzky S, Modrow S, Seidel W. Persistent parvovirus B19 infections in immunocompromised children. Med Microbiol Immunol 1998; 186 (4): 189–194. Pavletic ZS, Bishop MR, Tarantolo SR, et al. Hematopoietic recovery after allogeneic blood stem-cell transplantation compared with bone marrow transplantation in patients with hematologic malignancies. J Clin Oncol 1997; 15 (4): 1608–1616. Anderson MJ, Higgins PG, Davis LR, et al. Experimental parvoviral infection in humans. J Infect Dis 1985; 152 (2): 257–265. Katragadda L, Shahid Z, Restrepo A, Muzaffar J, Alapat D, Anaissie E. Preemptive intravenous immunoglobulin allows safe
E242
9.
10.
11.
12.
13.
and timely administration of antineoplastic therapies in patients with multiple myeloma and parvovirus B19 disease. Transpl Infect Dis 2013; 15 (4): 354–360. Jitschin R, Peters O, Plentz A, Turowski P, Segerer H, Modrow S. Impact of parvovirus B19 infection on paediatric patients with haematological and/or oncological disorders. Clin Microbiol Infect 2011; 17 (9): 1336–1342. Muslimani AA, Kundranda MN, Daw HA. Chronic anemia due to parvovirus B19 infection in a patient with multiple myeloma. Clin Adv Hematol Oncol 2007; 5 (1): 48–49. Lefrere JJ, Servant-Delmas A, Candotti D, et al. Persistent B19 infection in immunocompetent individuals: implications for transfusion safety. Blood 2005; 106 (8): 2890–2895. Tsukada Y, Yokoyama K, Ishida A, et al. Erythroid crisis caused by parvovirus B19 transmitted via red blood cell transfusion. Intern Med 2011; 50 (20): 2379–2382. Kurtzman G, Frickhofen N, Kimball J, Jenkins DW, Nienhuis AW, Young NS. Pure red-cell aplasia of 10 years’ duration due to persistent parvovirus B19 infection and its cure with immunoglobulin therapy. N Engl J Med 1989; 321 (8): 519–553.
Transplant Infectious Disease 2013: 15: E239–E242
Copyright of Transplant Infectious Disease is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
