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Reactivation of Multiple Infectious Pathogens after Hematopoietic Stem Cell Transplantation

cluding human, the oocytes will infect intestinal epithelium and from there disseminate throughout the body. The parasite can encyst in any nucleated cell and remain dormant in tissues for the… Click to show full abstract

cluding human, the oocytes will infect intestinal epithelium and from there disseminate throughout the body. The parasite can encyst in any nucleated cell and remain dormant in tissues for the life of the host. In humans, CNS lesions often present as ring-enhancing brain abscesses [3] . Human infection occurs most frequently via ingestion of infectious oocytes from contaminated water, soil, and also from eating uncooked or undercooked meats. Primary infection is asymptomatic, and reactivation occurs with immunosuppression such as transplantation. In HSCT, toxoplasma is a devastating complication with attributable mortality up to 43.5% [4] . As many as 87% of the HSCT recipients are seropositive prior to transplant, antibiotics prophylaxis is not always provided against toxoplasmosis after transplant. The loss of prior immunity to toxoplasmosis from transplant increases the risk of reactivation. CD8+ T cells specific to the organisms are crucial in order to control reactivation. In subjects treated with alemtuzumab, loss of T cells increases the risk of such reactivation. BKV reactivates after HSCT regardless of alemtuzumab use. BKV infection is the leading infectious complications after HSCT in some studies [5] . Serious consequences of BKV HC include considerable blood loss, extreme pain, and potential renal failure when BKV nephropathy occurs concurrently. There is currently no effective antiviral therapy against BKV. Thus, clinical care of patients with BKV HC is limited to supportive care with blood transfusion and pain control. Studies have examined factors associated with BKV reactivation after HSCT and found the presence of BK IgG prior to transIn the article by Schneidewind et al. [1] , the authors examined a retrospective collection of data from a single center. Over a 4-year period, they studied 64 adults with their first hematopoietic stem cell transplantation (HSCT) and collected follow-up data for up to 2 years. Similar to all transplant centers, this cohort of heterogeneous patients had different hematological malignancies requiring transplant and received several different conditioning regimens. All of these patients, however, received alemtuzumab as prophylaxis against graft-versus-host disease. The authors found that 27 patients (41.5%) had CMV reactivation, 10 (15.6%) had BK virus (BKV)-associated hemorrhagic cystitis (BKV HC), and 3 (4.6%) had toxoplasmosis. On analysis, there was a significant association of BKV HC and toxoplasmosis, and BKV and JC virus (JCV) reactivations with toxoplasmosis. These findings suggested the association of alemtuzumab and opportunistic infections after transplant. Specifically, these findings raised the question of whether there is an association between the reactivations of 2 human polyomaviruses and toxoplasmosis. Is there an association between the polyomaviruses and toxoplasmosis and alemtuzumab? Toxoplasma gondii is a protozoan that resides intracellularly and causes infection worldwide. There are at 3 genotypes: genotype II is predominant in Europe (where this study was conducted), and genotypes I and II are most prevalent in North America [2] . Seroprevalence in the general population can range from 9% in the USA to 78% in Brazil. Felines are the only animals that can complete a life cycle, where infectious oocytes can be shed in their stool. When oocytes are ingested by other mammals, inReceived: April 4, 2017 Accepted after revision: May 16, 2017 Published online: June 9, 2017

Keywords: bkv; toxoplasmosis; reactivation; transplantation; hematopoietic stem; cell

Journal Title: Acta Haematologica
Year Published: 2017

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