Skip to main content

Detection and treatment of cerebral toxoplasmosis in an aplastic pediatric post-allogeneic hematopoietic cell transplant patient: a case report



Cerebral toxoplasmosis infection presents with non-specific neurologic symptoms in immunocompromised patients. With lack of measurable adaptive immune responses and reluctance to sample affected brain tissue, expedient diagnosis to guide directed treatment is often delayed.

Case presentation

We describe the use of cerebrospinal fluid polymerase chain reaction and plasma cell-free DNA technologies to supplement neuroimaging in the diagnosis of cerebral toxoplasmosis in an immunocompromised pediatric patient following allogeneic hematopoietic cell transplantation for idiopathic severe aplastic anemia. Successful cerebral toxoplasmosis treatment included antibiotic therapy for 1 year following restoration of cellular immunity with an allogeneic stem cell boost.


Plasma cell-free DNA technology provides a non-invasive method of rapid diagnosis, improving the likelihood of survival from often lethal opportunistic infection in a high risk, immunocompromised patient population.

Peer Review reports


Cerebral toxoplasmosis is a rare but serious complication of allogeneic hematopoietic cell transplantation (alloHCT). Caused by the protozoan parasite Toxoplasma gondii, toxoplasmosis most often results from reactivation of latent infection in immunocompromised patients [1]. It is one of the most common opportunistic infection of the central nervous system (CNS) [2], with greatest prevalence in those with acquired immunodeficiency syndrome (AIDS) [3]. The incidence of toxoplasmosis after alloHCT ranges from 0.3 to 9% [2, 4], with variation based on population seroprevalence. Although the incidence and treatment of toxoplasmosis in adult alloHCT patients has been reported extensively, few studies have focused specifically on cerebral toxoplasmosis in pediatric patients [5,6,7,8,9,10,11,12,13,14,15,16,17]. Furthermore, cerebral toxoplasmosis diagnosis is usually based on a combination of radiologic imaging abnormalities and clinical symptoms such as seizures, headaches, and altered mental status, non-specific findings contributing to delays in diagnosis and treatment [18]. This case reviews the successful management of cerebral toxoplasmosis in a pediatric alloHCT patient following diagnosis with the use of cerebrospinal fluid (CSF) polymerase chain reaction (PCR) and microbial cell free DNA (cfDNA) technology.

Case presentation

A 13-year-old male with idiopathic severe aplastic anemia was treated with a human leukocyte antigen (HLA)-matched unrelated donor alloHCT on an Institutional Review Board-approved protocol with parental consent. His transplant course was complicated by Epstein-Barr virus (EBV) viremia (day + 21, successfully treated with rituximab), immune-mediated cytopenias versus inadequate graft function (beginning at day + 100, refractory to granulocyte-colony stimulating factor (GCSF), corticosteroids, intravenous immunoglobulin (IVIG), plasmapheresis and bortezomib), and right cervical lymphadenopathy concerning for EBV-post-transplant lymphoproliferative disease (day + 188, surgically excised, negative for infection or malignancy). With persistent pancytopenia, he required blood product transfusions and prophylactic anti-infective agents (valacyclovir, itraconazole, and intravenous pentamidine). Eight months after alloHCT, he was hospitalized locally for a severe gastrointestinal hemorrhage requiring superior mesenteric artery branch embolization.

Nine months after alloHCT, he was readmitted to our hospital with refractory pancytopenia. He denied night sweats and weight loss, but endorsed 2 weeks of intermittent headaches. With no financial, cultural or social barriers to care, the patient was promptly evaluated. A bone marrow biopsy was hypocellular (5–10%), with 93% donor chimerism. On day 3 of hospitalization, his severe headache recurred, accompanied by somnolence, nausea, fever, and hypertension. Head computed tomography (CT) showed a curvilinear hyperdensity at the right parietal and occipital lobe junction. Brain magnetic resonance imaging (MRI), angiogram (MRA), and venogram (MRV) revealed numerous enhancing cerebellar and cerebral lesions with punctate microhemorrhages and surrounding vasogenic edema (Fig. 1). Compared to a previous brain MRI, third and 4th ventricle sizes were increased with accompanying ependymal enhancement concerning for possible hydrocephalus. Additionally, moderate stenosis of the distal transverse sinuses bilaterally raised concern for intracranial hypertension. Clinically, he had no focal neurological deficits and a normal ophthalmologic exam. Given his history, CNS EBV infection was initially suspected.

Fig. 1

Resolution of cerebral toxoplasmosis with combined antibiotics and restoration of cellular immunity. Radiologic improvements in right posterior temporal and left occipital toxoplasmosis over time (axial fluid-attenuated inversion recovery 1.5 (16.5 months) or 3-T (all other) brain MRI images, are shown with a timeline of Toxoplasma directed antibiotics, interventions for presumed immune-mediated cytopenias, CD34 + PBSC boost, and blood laboratory findings (CD4 + lymphocyte count, platelet count, and absolute neutrophil count)

A lumbar puncture (LP) on hospital day 5 (alloHCT day + 304) revealed an elevated opening pressure of 38 cm H2O (normal 10–20) and CSF with 6 WBC/microliter (54% lymphocytes, 46% monocytes/macrophages), 8 RBC/microliter, glucose 39 mg/dL, and protein 112 mg/dL. Toxoplasma gondii was identified by CSF PCR and plasma cfDNA testing (5081 DNA molecules per microliter; Karius assay, Redwood City, CA), while serologies for Toxoplasma were negative. Given concurrent cytopenias and suspicion for alternative etiology, Toxoplasma therapy began only after these positive results (cfDNA testing returning in 2 days, CSF PCR in 4 days). Oral therapy with high dose pyrimethamine (200 mg loading dose followed by 75 mg once daily) with leucovorin rescue (50 mg daily) and sulfadiazine (1500 mg every 6 h daily) was initiated. While the patient was already on stress dosing hydrocortisone, three days of neuroprotective dexamethasone was provided within initiation of Toxoplasma therapy. Repeat Toxoplasma CSF PCR and plasma cfDNA testing was negative 2 weeks into treatment and remained so on future evaluations.

During the 3rd week of toxoplasmosis therapy, the patient required intensive care including 18 days of intubation/ventilation for an acute increase in somnolence and hypertension. While head CT and ophthalmologic exams were unchanged, his LP opening pressure was again elevated at 55 cm H2O. Improvement in mental status/alertness following the LP (closing pressure of 26.5) prompted initiation of acetazolamide and serial therapeutic LPs (16 times over 58 days). Atovaquone (1500 mg twice daily) was added when an MRI at 4 weeks of therapy (day + 337 post-alloHCT) showed decreased cerebral edema but unchanged toxoplasmosis lesions.

In the context of persistent cytopenias and poor graft function despite multi-modal therapy (Fig. 1), the patient received 4 days of immunosuppressive fludarabine followed by a CD34 + selected peripheral blood stem cell boost from his previous bone marrow donor (day + 349 after alloHCT). After 6 weeks of toxoplasmosis treatment showing both clinical and radiologic response, and to avoid bone marrow suppression after his stem cell boost, sulfadiazine was transitioned to oral clindamycin 600 mg 3 times/day for chronic maintenance therapy. One month after the stem cell boost, peripheral blood donor chimerism was 100% in the CD33 + myeloid compartment and 87% in the CD3 + lymphoid compartment. Transfusion independence was achieved at 42 days, eltrombopag discontinued at 60 days, and GCSF discontinued at 100 days. Fifty-five days following his stem cell boost—3 months of hospitalization—he was discharged on maintenance pyrimethamine and clindamycin. Adherence to oral therapies was monitored by nursing while inpatient and by the patient’s mother while outpatient. The patient himself reported no intolerance or adverse toxicities.

After 5 months of cerebral toxoplasmosis therapy, comprehensive neuropsychologic evaluations were completed. Compared to pre-alloHCT 14 months earlier, he displayed fine motor speed, dexterity and visuomotor integration deficiencies. From 6 to 12 months following cerebral toxoplasmosis diagnosis, his course was complicated by a single 30 s partial seizure. A brain MRI at 12.5 months of therapy revealed residual hypointense right posterior temporal lesions, resolution of associated vasogenic edema, and no new lesions. A bone marrow evaluation at that time was remarkable for 30–40% cellularity, trilineage hematopoiesis with no dysplasia and 98% donor contribution. With reassuring MRI findings and a CD4 count > 400 cells/microliter, toxoplasmosis therapy was discontinued. A 4 month off-therapy brain MRI was stable with no new lesions and interval improvement in mild ventriculomegaly.

Discussion and conclusions

This case demonstrates the successful diagnosis and management of cerebral toxoplasmosis in a pediatric alloHCT patient. While seroprevalence of Toxoplasma exceeds 50% in some regions of the world, in both the United States and China (where this patient resided for 3 years), Toxoplasma is less common (~ 10%) [19, 20]. As such, surveillance for Toxoplasma is not routine prior to alloHCT at our institution and the serostatus of this patient was unknown. Risk factors for opportunistic reactivation included 4–6 months of preceding cytopenias and medication-associated immunosuppression from graft-versus-host disease prophylaxis, EBV treatment, and immune-mediated cytopenia therapies. Notably, routine prophylaxis against Pneumocystis jirovecii pneumonia with trimethoprim-sulfamethoxazole (TMP-SMX) until at least 1 year post-alloHCT and recovery of CD4 + lymphocyte count to > 200 cell/mm3 additionally protects against Toxoplasma reactivation and infection. However, to avoid further myelosuppression from TMP-SMX in this patient with concurrent cytopenias, his Pneumocystis jirovecii pneumonia prophylaxis had been transitioned to pentamidine, an agent with no activity against Toxoplasma [21]. Without standard alloHCT population recommendations, toxoplasmosis treatment and duration was based on U.S. Department of Health and Human Services “Guidelines for prevention and treatment of opportunistic infection in adults and adolescents with HIV” (available at https://aidsinfo.nih.gov2019).

PCR as a diagnostic tool for CSF samples of immunocompromised patients with suspected cerebral toxoplasmosis demonstrates wide variability in sensitivity [22,23,24,25,26,27]. Variations are attributable to laboratory variability, sample processing efficiency, and patient level differences in CSF protein and cellularity [27,28,29]. Regardless, CSF PCR remains less invasive than brain biopsy and provides rapid detection of parasite DNA. Moreover, CSF PCR expanded gene targets to detect Toxoplasma DNA [17, 28] are increasing accuracy of this methodology.

Microbial cfDNA sequencing technology provides a novel, non-invasive approach to the diagnosis of thousands of infectious organisms [30], including detection of opportunistic infection in immunocompromised hosts [31, 32]. However, cfDNA studies to date are limited by small sample sizes, lack of control groups, and cohort heterogeneity. Clinical indications for this novel approach remain to be clearly established. There is no published medical literature reporting the use of cfDNA to identify cerebral toxoplasmosis in an immunocompromised host. Prior to CSF PCR and plasma cfDNA sequencing results, the infectious differential diagnosis for our teenage alloHCT patient’s brain lesions included a broad group of neurotropic viruses, fungi and parasites. In our case, cfDNA sequencing provided rapid evidence of cerebral toxoplasmosis despite negative blood serologies and ophthalmologic examination. Thus, cfDNA sequencing emerges as a useful adjunct to diagnosis for toxoplasmosis, particularly when tissue diagnosis is not feasible [33].

Of note, while Toxoplasma serologies are often useful to assess for prior or current immune response to infection, they are unreliable before adequate immune reconstitution after alloHCT. This particularly patient was profoundly immune suppressed from treatment of immune mediated cytopenias after alloHCT and had recently undergone plasmapheresis, further reducing the likelihood of production of circulating antibodies. Interpretation of positive serologies, had they been found, would also be challenging as he had recently received IVIG.

While mortality of cerebral toxoplasmosis in post-alloHCT patients is reported from 38 to 67% [34], little is known about long term sequelae in adult or pediatric survivors [14]. While promptly initiated on antibiotics, our patient only displayed definitive clinical improvement after a CD34 + stem cell boost restored the cellular immunity essential for Toxoplasma clearance. Clinical and radiographic signs of recovery persisted at follow-up 4 months following completion of maintenance antibiotics. Future studies exploring the incidence and outcomes of cerebral toxoplasmosis in pediatric post-alloHCT patients are needed.

Patient perspective

Fortunately during the time I was most ill as a patient I don’t really remember how I felt in the hospital and only have hazy memories. However, as I began to heal I do have memories of some nurses that especially helped me laugh during this time. I also remember enjoying integrative healing therapies in the form of music, aromatherapy, and massages. I am currently doing great, finishing my Freshman year of high school, playing in fantasy sports leagues, and also relieved to not be on clindamycin anymore.

Availability of data and materials

Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study. All relevant data are herein included.



Allogeneic hematopoietic cell transplantation


Central nervous system


Acquired immunodeficiency syndrome


Cerebrospinal fluid


Polymerase chain reaction


Human leukocyte antigen


Epstein-Barr virus


Granulocyte colony stimulating factor


Intravenous immunoglobulin


Computed tomography


Magnetic resonance imaging


Lumbar puncture




Cell free DNA




  1. 1.

    Martino R, Cordonnier C, European Group for B, Marrow Transplantation Infectious Diseases Working P. Toxoplasmosis following allogeneic hematopoietic stem cell transplantation. Bone Marrow Transpl. 2003;31(7):617–8.

    Article  Google Scholar 

  2. 2.

    Maschke M, Dietrich U, Prumbaum M, Kastrup O, Turowski B, Schaefer UW, et al. Opportunistic CNS infection after bone marrow transplantation. Bone Marrow Transpl. 1999;23(11):1167–76.

    CAS  Article  Google Scholar 

  3. 3.

    Belanger F, Derouin F, Grangeot-Keros L, Meyer L. Incidence and risk factors of toxoplasmosis in a cohort of human immunodeficiency virus-infected patients: 1988–1995. HEMOCO and SEROCO Study Groups. Clin Infect Dis. 1999;28(3):575–81.

    CAS  Article  Google Scholar 

  4. 4.

    Martino R, Bretagne S, Rovira M, Ullmann AJ, Maertens J, Held T, et al. Toxoplasmosis after hematopoietic stem transplantation. Report of a 5-year survey from the Infectious Diseases Working Party of the European Group for Blood and Marrow Transplantation. Bone Marrow Transpl. 2000;25(10):1111–4.

    CAS  Article  Google Scholar 

  5. 5.

    Hirsch R, Burke BA, Kersey JH. Toxoplasmosis in bone marrow transplant recipients. J Pediatr. 1984;105(3):426–8.

    CAS  Article  Google Scholar 

  6. 6.

    Jurges E, Young Y, Eltumi M, Holliman RE, Vellodi A, Rogers TR, et al. Transmission of toxoplasmosis by bone marrow transplant associated with Campath-1G. Bone Marrow Transpl. 1992;9(1):65–6.

    CAS  Google Scholar 

  7. 7.

    Slavin MA, Meyers JD, Remington JS, Hackman RC. Toxoplasma gondii infection in marrow transplant recipients: a 20 year experience. Bone Marrow Transpl. 1994;13(5):549–57.

    CAS  Google Scholar 

  8. 8.

    Duzovali O, Choroszy MS, Chan KW. Hyponatremia as the presenting feature of cerebral toxoplasmosis. Bone Marrow Transpl. 2005;35(12):1221–2.

    CAS  Article  Google Scholar 

  9. 9.

    Goebel WS, Conway JH, Faught P, Vakili ST, Haut PR. Disseminated toxoplasmosis resulting in graft failure in a cord blood stem cell transplant recipient. Pediatr Blood Cancer. 2007;48(2):222–6.

    Article  Google Scholar 

  10. 10.

    Megged O, Shalit I, Yaniv I, Stein J, Fisher S, Levy I. Breakthrough cerebral toxoplasmosis in a patient receiving atovaquone prophylaxis after a hematopoietic stem cell transplantation. Pediatr Transpl. 2008;12(8):902–5.

    Article  Google Scholar 

  11. 11.

    Fricker-Hidalgo H, Bulabois CE, Brenier-Pinchart MP, Hamidfar R, Garban F, Brion JP, et al. Diagnosis of toxoplasmosis after allogeneic stem cell transplantation: results of DNA detection and serological techniques. Clin Infect Dis. 2009;48(2):e9–15.

    Article  Google Scholar 

  12. 12.

    Caselli D, Andreoli E, Paolicchi O, Savelli S, Guidi S, Pecile P, et al. Acute encephalopathy in the immune-compromised child: never forget toxoplasmosis. J Pediatr Hematol Oncol. 2012;34(5):383–6.

    Article  Google Scholar 

  13. 13.

    Bautista G, Ramos A, Fores R, Regidor C, Ruiz E, de Laiglesia A, et al. Toxoplasmosis in cord blood transplantation recipients. Transpl Infectious Dis: Off J Transpl Soc. 2012;14(5):496–501.

    CAS  Article  Google Scholar 

  14. 14.

    Kerl K, Ehlert K, Brentrup A, Schiborr M, Keyvani K, Becker K, et al. Cerebral toxoplasmosis in an adolescent post allogeneic hematopoietic stem cell transplantation: successful outcome by antiprotozoal chemotherapy and CD4+ T-lymphocyte recovery. Transpl Infectious Dis: Off J Transpl Soc. 2015;17(1):119–24.

    CAS  Article  Google Scholar 

  15. 15.

    Decembrino N, Comelli A, Genco F, Vitullo A, Recupero S, Zecca M, et al. Toxoplasmosis disease in paediatric hematopoietic stem cell transplantation: do not forget it still exists. Bone Marrow Transpl. 2017;52(9):1326–9.

    CAS  Article  Google Scholar 

  16. 16.

    Czyzewski K, Fraczkiewicz J, Salamonowicz M, Pieczonka A, Zajac-Spychala O, Zaucha-Prazmo A, et al. Low seroprevalence and low incidence of infection with Toxoplasma gondii (Nicolle et Manceaux, 1908) in pediatric hematopoietic cell transplantation donors and recipients: polish nationwide study. Folia Parasitol (Praha). 2019;66.

  17. 17.

    Zaucha-Prazmo A, Samardakiewicz M, Dubelt J, Kowalczyk JR. Cerebral toxoplasmosis after haematopoietic stem cell transplantation. Ann Agric Environ Med. 2017;24(2):237–9.

    Article  Google Scholar 

  18. 18.

    Hakko E, Ozkan HA, Karaman K, Gulbas Z. Analysis of cerebral toxoplasmosis in a series of 170 allogeneic hematopoietic stem cell transplant patients. Transpl Infectious Dis: Off J Transpl Soc. 2013;15(6):575–80.

    CAS  Article  Google Scholar 

  19. 19.

    Pappas G, Roussos N, Falagas ME. Toxoplasmosis snapshots: global status of Toxoplasma gondii seroprevalence and implications for pregnancy and congenital toxoplasmosis. Int J Parasitol. 2009;39(12):1385–94.

    Article  Google Scholar 

  20. 20.

    Wang T, Han Y, Pan Z, Wang H, Yuan M, Lin H. Seroprevalence of Toxoplasma gondii infection in blood donors in mainland China: a systematic review and meta-analysis. Parasite. 2018;25:36.

    Article  Google Scholar 

  21. 21.

    Bozzette SA, Finkelstein DM, Spector SA, Frame P, Powderly WG, He W, et al. A randomized trial of three antipneumocystis agents in patients with advanced human immunodeficiency virus infection. NIAID AIDS Clinical Trials Group. N Engl J Med. 1995;332(11):693–9.

    CAS  Article  Google Scholar 

  22. 22.

    Costa JM, Pautas C, Ernault P, Foulet F, Cordonnier C, Bretagne S. Real-time PCR for diagnosis and follow-up of Toxoplasma reactivation after allogeneic stem cell transplantation using fluorescence resonance energy transfer hybridization probes. J Clin Microbiol. 2000;38(8):2929–32.

    CAS  Article  Google Scholar 

  23. 23.

    Buchbinder S, Blatz R, Rodloff AC. Comparison of real-time PCR detection methods for B1 and P30 genes of Toxoplasma gondii. Diagn Microbiol Infect Dis. 2003;45(4):269–71.

    CAS  Article  Google Scholar 

  24. 24.

    Hierl T, Reischl U, Lang P, Hebart H, Stark M, Kyme P, et al. Preliminary evaluation of one conventional nested and two real-time PCR assays for the detection of Toxoplasma gondii in immunocompromised patients. J Med Microbiol. 2004;53(Pt 7):629–32.

    CAS  Article  Google Scholar 

  25. 25.

    Edvinsson B, Lappalainen M, Evengard B. Toxoplasmosis ESGf. real-time PCR targeting a 529-bp repeat element for diagnosis of toxoplasmosis. Clin Microbiol Infect. 2006;12(2):131–6.

    CAS  Article  Google Scholar 

  26. 26.

    Brenier-Pinchart MP, Morand-Bui V, Fricker-Hidalgo H, Equy V, Marlu R, Pelloux H. Adapting a conventional PCR assay for Toxoplasma gondii detection to real-time quantitative PCR including a competitive internal control. Parasite. 2007;14(2):149–54.

    CAS  Article  Google Scholar 

  27. 27.

    Anselmo LM, Vilar FC, Lima JE, Yamamoto AY, Bollela VR, Takayanagui OM. Usefulness and limitations of polymerase chain reaction in the etiologic diagnosis of neurotoxoplasmosis in immunocompromised patients. J Neurol Sci. 2014;346(1–2):231–4.

    Article  Google Scholar 

  28. 28.

    Robert-Gangneux F, Belaz S. Molecular diagnosis of toxoplasmosis in immunocompromised patients. Curr Opin Infect Dis. 2016;29(4):330–9.

    Article  Google Scholar 

  29. 29.

    Correia CC, Melo HR, Costa VM. Influence of neurotoxoplasmosis characteristics on real-time PCR sensitivity among AIDS patients in Brazil. Trans R Soc Trop Med Hyg. 2010;104(1):24–8.

    Article  Google Scholar 

  30. 30.

    Blauwkamp TA, Thair S, Rosen MJ, Blair L, Lindner MS, Vilfan ID, et al. Analytical and clinical validation of a microbial cell-free DNA sequencing test for infectious disease. Nat Microbiol. 2019;4(4):663–74.

    CAS  Article  Google Scholar 

  31. 31.

    Camargo JF, Ahmed AA, Lindner MS, Morris MI, Anjan S, Anderson AD, et al. Next-generation sequencing of microbial cell-free DNA for rapid noninvasive diagnosis of infectious diseases in immunocompromised hosts. F1000Res. 2019;8:1194.

    Article  Google Scholar 

  32. 32.

    Armstrong AE, Rossoff J, Hollemon D, Hong DK, Muller WJ, Chaudhury S. Cell-free DNA next-generation sequencing successfully detects infectious pathogens in pediatric oncology and hematopoietic stem cell transplant patients at risk for invasive fungal disease. Pediatr Blood Cancer. 2019;66(7):e27734.

    Article  Google Scholar 

  33. 33.

    Hong DK, Blauwkamp TA, Kertesz M, Bercovici S, Truong C, Banaei N. Liquid biopsy for infectious diseases: sequencing of cell-free plasma to detect pathogen DNA in patients with invasive fungal disease. Diagn Microbiol Infect Dis. 2018;92(3):210–3.

    CAS  Article  Google Scholar 

  34. 34.

    Gajurel K, Dhakal R, Montoya JG. Toxoplasma prophylaxis in haematopoietic cell transplant recipients: a review of the literature and recommendations. Curr Opin Infect Dis. 2015;28(4):283–92.

    CAS  Article  Google Scholar 

Download references


We thank our patient and his family for their patience and perseverance during his complicated alloHCT and cerebral toxoplasmosis course.


This research was supported by the National Institutes of Health’s National Center for Advancing Translational Sciences, Grants KL2TR002492, funding research effort for CLE. The content is the sole responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health’s National Center for Advancing Translational Sciences which had no role in study design, data collection, analysis, interpretation or writing of the manuscript.

Author information




DB and CLE contributed to conception of the report and drafted the manuscript, DB, MLM, SIN, MRS, JY, and CLE all contributed to data analysis and critical revision of the manuscript, CLE interpreted data and created the figure. All authors read and approved the final manuscript.

Corresponding author

Correspondence to Christen L. Ebens.

Ethics declarations

Ethics approval and consent to participate

The patient’s care was provided on a University of Minnesota IRB approved allogeneic hematopoietic cell transplant protocol.

Consent for publication

Verbal and written consent for publication of de-identified clinical data was obtained from the patient’s parent with the patient’s assent.

Competing interests

The authors report no competing interests.

Additional information

Publisher's Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and Permissions

About this article

Verify currency and authenticity via CrossMark

Cite this article

Brewer, D., MacMillan, M.L., Schleiss, M.R. et al. Detection and treatment of cerebral toxoplasmosis in an aplastic pediatric post-allogeneic hematopoietic cell transplant patient: a case report. BMC Infect Dis 21, 941 (2021).

Download citation


  • Toxoplasmosis
  • Allogeneic hematopoietic cell transplantation
  • Severe aplastic anemia
  • Immune mediated cytopenia
  • Cell-free DNA
  • Case report