Visceral leishmaniasis after allogeneic hematopoietic stem cell transplantation

Agteresch, Hendrik J.; Veer, Mars B. van ‘t; Cornelissen, Jan J.; Sluiters, J. F.

doi:10.1038/sj.bmt.1705728

Cited by 24 publications

(21 citation statements)

References 13 publications

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“…Reactivation of T. cruzi has been reported in HCT patients, but there are few reports of visceral leishmaniasis following HCT [519][520][521], and this case seemed to be acquired more than a year after transplantation, and not preexistent or transmitted by the stem cell product.…”

Section: Recommendations Regarding Trypanosoma Cruzi and Leishmaniamentioning

confidence: 99%

Guidelines for Preventing Infectious Complications among Hematopoietic Cell Transplantation Recipients: A Global Perspective

Tomblyn¹,

Chiller²,

Einsele³

et al. 2009

Biology of Blood and Marrow Transplantation

1,573

1,540

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Section: Recommendations Regarding Trypanosoma Cruzi and Leishmaniamentioning

confidence: 99%

Guidelines for Preventing Infectious Complications among Hematopoietic Cell Transplantation Recipients: A Global Perspective

Tomblyn¹,

Chiller²,

Einsele³

et al. 2009

Biology of Blood and Marrow Transplantation

1,573

1,540

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“…Leishmaniasis in HSCT recipients has been described in only 10 patients in the English literature ( Table 2). [69][70][71][72][73][74][75][76] Nine cases occurred following allogeneic HSCT and one after tandem autologous HSCT.…”

Section: Hematopoietic Stem Cell Transplant Recipientsmentioning

confidence: 99%

Leishmaniasis in solid organ and hematopoietic stem cell transplant recipients

Gajurel

Dhakal

Deresinski

2016

Clinical Transplantation

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Leishmaniasis occurs in <1% of solid organ and hematopoietic stem cell transplant recipients in endemic countries in which transplants are performed. Visceral leishmaniasis (VL) makes up the bulk of reported cases. The onset generally occurs months after transplantation and the mode of acquisition is often impossible to determine, but de novo vector-borne infection and reactivation of inapparent infection are thought to be the principal means. The potential role of clinically inapparent donor infection is uncertain and screening is not currently recommended, nor is it recommended for recipients from endemic areas, some of whom may have detectable circulating protozoan nucleic acid. While transplant recipients with VL often present with the non-specific findings of fever and cytopenia, the additional presence of hepatosplenomegaly in patients from endemic areas should lead to a directed diagnostic evaluation with bone marrow examination and PCR testing of marrow and peripheral blood having a high yield. Management may often be complicated by the presence of concomitant infections. A lipid formulation of amphotericin B is the preferred treatment, especially for VL, but the relapse rate in transplant recipients is approximately 25%. PCR monitoring of blood for either secondary prophylaxis or preemptive therapy requires further study.

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“…Three cases of LV in HSCT patients have been previously reported [7–9]. Two patients received allogenic, and one patient autologous, HSCT.…”

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confidence: 99%

“…Moreover, the number of cases of VL in endemic regions is significantly lower in HSCT recipients than in other immunocompromised patients, such as kidney transplant recipients [10]. The low rate of VL (and other infections, such as tuberculosis) in HSCT suggests that some unknown factor, other than the degree of cell‐mediated immunosuppression, may have a role in the pathogeny of opportunistic infections in transplant patients [7–9].…”

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confidence: 99%