In reply

We would like to make a contribution toward the recent publication in TRANSFUSION by Mestra and coworkers. Firstly, the authors said that this is the first report of transfusion-transmitted leishmaniasis in an immunocompromised patient in Colombia. However, identification of the Leishmania infection was demonstrated neither in transfused blood components nor in blood donors. Antibodies against Leishmania spp. were detected in the patient’s serum samples as part of a study to rule out renal transplant-transmitted visceral leishmaniasis. However, it is not clear if the serologic Leishmaniapositive result of the patient’s serum corresponded to a sample taken before or after receiving transfusions. To our understanding, if no data related to the patient’s infection status before the transfusions have been clearly provided and, additionally, as Leishmania infection in transfused blood components and/or blood donors has not been demonstrated by the authors, it is very difficult to agree that this certainly represents a case of transfusiontransmitted visceral leishmaniasis. From the transfusion point of view it would have been interesting to know whether or not the transfused blood components were leukoreduced and, if so, when the leukoreduction was performed, that is, before storage or at the bedside, since various studies have been published on the efficacy of whole blood, fresh plasma, and red blood cell filters used for leukoreduction in reducing the number of Leishmania spp. parasites in blood components and thereby minimizing the potential risk of Leishmania transmission through blood transfusions. This information could have thrown light on the probability of the parasite being transmitted to the patient through the transfusion of a contaminated blood component taken from an asymptomatic donor. This case was also published in 2006 as allograft kidney dysfunction associated with infection with amastigotes of Trypanosoma cruzi. However, neither polymerase chain reaction (PCR) nor any other antigen detection technique was performed to demonstrate that the amastigotes in the renal parenchymal corresponded to T. cruzi. To distinguish Chagas disease from Leishmania infection, it would have been helpful to perform Leishmaniaand T. cruzi– specific PCRs on the renal biopsy since it is difficult to differentiate the amastigotes from these two genera by direct microscopic examination. This observation has implications related to the article being commented on because it would explain the patient’s clinical symptoms showing after the renal transplant and immediately before initiating the transfusions. Nifurtimox was given to treat Chagas disease. This may have also contributed to delaying the diagnosis of visceral leishmaniasis, since this medication is partially effective against Leishmania spp. as in vivo studies have shown. All these aspects could also be compatible with the reactivation of a latent Leishmania infection by immunosuppression. We believe that this is a very interesting report concerning a case of visceral leishmaniasis caused by L. (L.) mexicana in an immunocompromised patient in Colombia. This is already in itself a very remarkable contribution made by the authors because, as mentioned in the article, L. (L.) mexicana is a species that has been associated mainly with cutaneous leishmaniasis. There are, however, various aspects that might support the fact that this case was due to the reactivation of a latent Leishmania infection, that is, the patient’s clinical symptoms, the lack of data related to the patient’s infection status before the transfusion, the blood components transfused, and their donors. Similarly, other aspects, which are primarily based on ruling out the transmission of visceral leishmaniasis through solid-organ transplantation, and the fact that the patient’s medical interview did not reveal any prior exposure to Leishmania, all support the hypothesis that the visceral leishmaniasis was transmitted through blood transfusion. Since there are arguments both for and against the two options, we would suggest that this report be considered as a possible case of transfusion-transmitted visceral leishmaniasis.

[1]  R. Weiskopf,et al.  Transfusion-related acute lung injury: incidence and risk factors. , 2012, Blood.

[2]  R. Nieuwland,et al.  Accumulation of bioactive lipids during storage of blood products is not cell but plasma derived and temperature dependent , 2011, Transfusion.

[3]  C. Muskus,et al.  Transfusion‐transmitted visceral leishmaniasis caused by Leishmania (Leishmania) mexicana in an immunocompromised patient: a case report , 2011, Transfusion.

[4]  B. Gathof,et al.  Generation of neutrophil priming activity by cell‐containing blood components treated with pathogen reduction technology and stored in platelet additive solutions , 2011, Transfusion.

[5]  C. Silliman,et al.  Identification of lipids that accumulate during the routine storage of prestorage leukoreduced red blood cells and cause acute lung injury , 2011, Transfusion.

[6]  J. Korevaar,et al.  The incidence, risk factors, and outcome of transfusion-related acute lung injury in a cohort of cardiac surgery patients: a prospective nested case-control study. , 2011, Blood.

[7]  M. Kersten,et al.  The divergent clinical presentations of transfusion-related acute lung injury illustrated by two case reports. , 2010, Medical science monitor : international medical journal of experimental and clinical research.

[8]  R. Nieuwland,et al.  Supernatant of Aged Erythrocytes Causes Lung Inflammation and Coagulopathy in a “Two-Hit” In Vivo Syngeneic Transfusion Model , 2010, Anesthesiology.

[9]  Y. Yatomi,et al.  Impact of fresh‐frozen plasma from male‐only donors versus mixed‐sex donors on postoperative respiratory function in surgical patients: a prospective case‐controlled study , 2009, Transfusion.

[10]  E. Moore,et al.  Plasma from stored packed red blood cells and MHC class I antibodies causes acute lung injury in a 2-event in vivo rat model. , 2009, Blood.

[11]  C. Homma,et al.  Reduction in adverse reactions to platelets by the removal of plasma supernatant and resuspension in a new additive solution (M‐sol) , 2009, Transfusion.

[12]  J. Hirayama,et al.  Maintenance of platelet in vitro properties during 7‐day storage in M‐sol with a 30‐hour interruption of agitation , 2008, Transfusion.

[13]  C. Homma,et al.  Storage of platelets in a novel additive solution (M‐sol), which is prepared by mixing solutions approved for clinical use that are not especially for platelet storage , 2007, Transfusion.

[14]  N. Voelkel,et al.  Plasma and lipids from stored platelets cause acute lung injury in an animal model , 2003, Transfusion.

[15]  C. Silliman,et al.  Transfusion-related acute lung injury: epidemiology and a prospective analysis of etiologic factors. , 2003, Blood.

[16]  S. Murphy,et al.  The effect of the interruption of agitation on plateletquality during storage for transfusion , 2001, Transfusion.

[17]  N. Voelkel,et al.  Plasma and lipids from stored packed red blood cells cause acute lung injury in an animal model. , 1998, The Journal of clinical investigation.

[18]  G. Moroff,et al.  The maintenance of platelet properties upon limited discontinuation of agitation during storage , 1990, Transfusion.