Infectious Disease Pathology
Case 1 -
Post-Transplant Lymphoproliferative Disorder, Burkitt lymphoma type
Children's Hospital of Pittsburgh
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In 1995, 6 year-old girl presented with a large left neck mass at the Children's
Hospital of Pittsburgh. Her past medical history was relevant for biliary cirrhosis secondary to
extrahepatic biliary obstruction (biliary atresia), treated with a Kasai procedure. At one year of age,
she underwent an orthotopic liver transplant (OLTx). At the time of her hospital admission, five years
after the liver transplant, relevant laboratory results included: , Hb= 12.2; Ht= 35.1; WBC= 7.6K/DL:
Plt.=296 K/dL; Neut.= 49%; Lymph.= 31%; Mon.= 9%; Eos.=10%; Bas./Band= 1%. SGTP/SGOT= 44/39 IU/L;
ALKP/GGTP= 157/22 IU/L. Renal function tests, electrolytes and glucose were within normal limits. Uric
acid= 3 mg/dL. The mass was removed and sent to pathology. Representative photomicrographs are
presented for discussion.
Case 1 - Figure 1
Imprint taken from the excised mass. Cells are monomorphous, mid-sized, with a small amount of cytoplasm, focally vacuolated. Nuclei reveal fine, granular chromatin, and several inconspicuous nucleoli. There are numerous apoptotic bodies due to increased cell turnover. Diff-Quik®, 40X
Case 1 - Figure 2
Low power photomicrograph (10X) showing the extensive effacement of the nodal architecture by a monotonous proliferation with a prominent "starry sky" pattern. The upper portion of the image shows partial preservation of the architecture.
Case 1 - Figure 3
Mid-power image (20X) featuring numerous macrophages with phagocytized cellular debris surrounded by a monomorphous proliferation of neoplastic lymphoid elements with intermediate size.
Case 1 - Figure 4
High-power photomicrograph (40X) revealing the very scanty cytoplasm, finely granular chromatin and multiple amphophilic nucleoli. Numerous apoptotic bodies and several mitotic figures are also shown.
Case 1 - Figure 5
Immunohistochemical staining is positive for CD20 in the proliferating lymphoid cells.
Case 1 - Figure 6
Immunohistochemistry for Ki67 is positive in essentially all lymphoid neoplastic elements.
Case 1 - Figure 7
Another low power view of the architectural effacement with a prominent starry sky pattern.
Case 1 - Figure 8
The numerous tingible body macrophages, imparting the classic "starry sky" pattern reflect a high level of cell apoptosis and turnover.
Case 1 - Figure 9
Additional detail on the scavenging macrophages.
Case 1 - Figure 10
Panoramic view of the touch imprint to show the high cellularity and monotony of the proliferating lymphoid cells.
Case 1 - Figure 11
Immunohistochemistry for CD10 is ++ positive in lymphoid elements.
Case 1 - Figure 12
Immunohistochemistry for BCL6 is +++ positive.
Pathological/Microscopic Findings and any Immunohistochemical or Other Studies:
The excised neck
mass, represented by two rubbery lymph nodes with associated fascial connective tissue, measuring in
total 4.5 x 2.5 x 1.5 cm was received in Pathology for examination. Histologically, the nodal
architecture reveals extensive effacement by a population of proliferating, mid-sized lymphoid elements
with scanty cytoplasm. The nuclear features include a finely granular, sometimes clumpy chromatin and
several inconspicuous nucleoli. The proliferating cells feature a brisk mitotic activity and multifocal
apoptosis. A prominent starry-sky pattern is evident, with numerous macrophages filled with cellular
debris. The capsule exhibits fibrosis, and the neoplastic elements extend into the surrounding adipose
tissue. The lymph node areas with architecture preservation show sinus histiocytosis and prominent
follicular hyperplasia, with focal necrosis and occasional neutrophil infiltration. Relevant
immunophenotyping shows ++++ positive staining for CD20, and λ restriction. CD3 and CD45RO (UCHL1)
immunohistochemical stains are negative in the proliferating cells. Studies directed to detect
Epstein-Barr virus (EBV) show positive staining with EBV-EZLF1 in multiple foci, and the in situ
hybridization for EBER is also positive in an overwhelming majority of cells. Retrospective analysis
performed in 2009, with additional immunohistochemical markers shows (+++) BCL6 staining, a +/++ positive
stain for CD10 in most areas of proliferating lymphoid elements, and Ki67 in essentially all lymphoid
cells within the areas of nodal involvement.
The differential diagnosis is
relatively narrow, but includes a primary lymphoid neoplasm and a post-transplant lymphoproliferative
disorder (PTLD). Given the clinical history of OLTx, the second possibility is much more likely, and the
documentation of EBV militates strongly in favor of this option. The morphological and
immunophenotypical features of this proliferation are diagnostic of a Burkitt type PTLD.
Post-Transplant Lymphoproliferative Disorder, Burkitt lymphoma type.
PTLD is an entity with a wide spectrum ranging from atypical lymphoid or plasmacytoid proliferations
to malignant lymphomas. These growths arise as a consequence of immunosuppression in patients
transplanted with a solid organ, bone marrow, or stem cell allograft. Pediatric transplant recipients
are at increased risk of developing a PTLD because of their EBV-naïve status prior to transplantation (
many are EBV sero-negative at the time of transplantation), which makes them vulnerable to developing a
primary EBV infection while on potent immunosuppressive medications.
The morphological picture of PTLDs ranges from early EBV-associated infectious mononucleosis-type to
malignant lymphoma.  The majority of monomorphic PTLDs (M-PTLD) are composed of transformed B-cells that
fit the criteria of a non-Hodgkin Lymphoma (NHL), predominately of the diffuse large B-cell type (DLBCL)
and rarely as a Burkitt lymphoma (BL). While M-PTLDs have been thought to be histologically similar to
their lymphoma counterparts arising in the immunocompetent patient, new molecular evidence is emerging to
suggest that many of the B-cell M-PTLD are more closely related to other PTLDs rather than to B-cell
NHL.4 The gene expression profiles of these PTLDs appear to be related to memory or activated B-cells,
and share a non-germinal center phenotype. The exception is BL, which retains a germinal center
phenotype and does not cluster with the other PTLDs.
Burkitt lymphoma is an aggressive, mature B-cell lymphoma, composed of a monomorphous population of
small to intermediate-sized, non-cleaved lymphoid elements. It features high mitotic and proliferation
rates, and a characteristic "starry-sky" pattern, imparted from the scattered tingible body macrophages
engulfing apoptotic debris of the tumor. Ancillary immunophenotyping and cytogenetic analysis confirm
the diagnosis, separating it from a diffuse large B-cell lymphoma (DLBCL). A majority of cases feature
the classic translocation of the MYC gene, located at 8q24, to the 14q32
IG heavy chain region, although other, less common sites to which MYC translocates are the γ region at 22q11, or the κ region at
2p12. This translocation is a valuable adjunct in the diagnostic ancillary studies of BL using
fluorescent in situ hybridization, although up to 10% of cases may render
negative results by this methodology.  While the c-MYC
rearrangements are not specific, the combination of CD10 positive, bcl-2 negative B-cells is
considered diagnostic for BL.
Review of the literature and our own experience at CHP
Three main clinical variants of BL vary in their propensity to express EBV: Endemic predominately
occurring in children of equatorial Africa, is strongly associated with EBV infection;
Sporadic—presenting mainly in children and young adults less commonly expresses EBV (30%); and
Immunodeficiency-associated—primarily associated with HIV infection has an intermediate EBV expression
Case reports of BL occurring in the post-transplant setting seem to have an EBV expression
profile intermediate between the endemic and immunodeficiency-associated types of BL.
As a PTLD, BL typically occurs later than other PTLDs (average 4.5 years)
, presents at a higher
stage than other M-PTLDs, and must also be clinically treated more aggressively, as decreased
immunosuppression alone is inadequate therapy and immediate therapeutic regimens with alkylating
chemotherapy agents must be used.
18] While PTLD and BL are independently more commonly seen
in children, BL as a PTLD is a rare entity within the pediatric transplant population. In the available
medical literature, there are only a handful of case reports describing BL-in the post-transplant
19] and in large transplant studies there is a low incidence of BL-PTLD
, ranging from 0.3 to 0.7% in heart and liver transplant patients.
BL-PTLD is emerging as a distinct form of PTLD that needs to be more fully characterized in
the pediatric population.
At the Children's Hospital of Pittsburgh, we have identified over a
28-year period, 10 cases that fit the diagnostic criteria of BL-PTLD, representing one of the largest
series available (study approved by the University of Pittsburgh Institutional Review Board, number
PRO09100103). Age at transplant ranged from 5 months to 16 years (median 3 y); 7 patients were boys
(Table 1). Four patients had liver transplants [two of these had a second transplant (at 26 mo -case 6-
and 20 mo -case 7) status post BL-PTLD diagnosis]; others included heart transplants (n=4), small bowel
transplant (n=1), and kidney transplant (n=1, with a second kidney transplant 66 mo after BL-PTLD
diagnosis). The BL-PTLD diagnosis was made 6 to 107 months after transplant (median 60 mo). The most
frequent signs and symptoms included rapidly enlarging masses (abdominal masses; adenopathy) and
abdominal pain. One case developed the BL-PTLD within the graft (case 10); the sites of involvement were
the head and neck (n=4), and abdomen (n=4), including the small bowel; one case occurred in the kidney.
Table 1. BL-PTLD at Children's Hospital of Pittsburgh. Clinical data.
| ||Sex ||Age at Tx ||Tx organ ||Site BL-PTLD ||TX-PTLD ||PTLD-outcome ||EBV donor ||EBV Pre-tx ||EBV @ PTLD ||Disease free (mo), Outcome|
|BL-1 ||M ||7 mo ||heart ||Mandible, lymph node capsule, skull base, GI tract ||56 ||127 ||POS ||NEG ||POS ||127, Alive, no disease|
|BL-2 ||F ||1 ||liver ||Neck lymph node ||63 ||168 ||na ||na ||POS ||168, Alive, no disease|
|BL-3 ||M ||5 mo ||heart ||Kidney-right; *Kidney-bilateral ||76 ||60 ||na ||NEG ||POS ||60, Dead, complication of therapy, no disease at autopsy|
|BL-4 ||F ||3 ||heart ||Abdominal mass ||107 ||14 ||Equivocal ||NEG ||POS ||14, Alive, no disease|
|BL-5 ||M ||10 ||small bowel ||Neck lymph node ||34 ||16 ||POS ||NEG ||POS ||16, Alive, no disease|
|BL-6 ||M ||16 ||liver/liver ||Small bowel ||6 ||134 ||na ||na ||na ||134, Dead, infection|
|BL-7 ||F ||2 ||liver/liver ||Neck lymph node ||101 ||199 ||na ||POS ||POS ||199, Alive, no disease|
|BL-8 ||M ||8 ||kidney/kidney ||Small bowel, abdominal mass ||47 ||178 ||POS|
|NEG ||POS ||178, Alive, no disease|
|BL-9 ||M ||9 mo ||heart ||Abdominal mass ||29 ||86 ||NEG ||NEG ||POS ||86, Alive, no disease|
|BL-10 ||M ||10.5 ||liver ||Liver allograft, widespread metastasis ||100 ||3 ||NEG ||NEG ||POS ||3, Dead, graft failure and cardiac arrest|
TX-PTLD indicates months from transplant to BL-PTLD; PTLD-outcome indicates months from initial PTLD
to recurrence or last follow-up; *Recurrence; LRD=living related donor; LN=lymph node. Index case is BL-2
In all cases, the allograft biopsies immediately preceding the presentation of the BL-PTLD ranged from
no rejection to mild cellular rejection. Donor EBV status was known in three cases (positive: cases 5
and 8; negative: case 10). Pre-transplantation EBV serology and/or titers were negative in 6 of 8
patients (75%) and were positive, post-transplant, for all known tested cases (9/9). Pre-transplant CMV
serology and/or titers were negative in 6 of 9 tested patients.
The summary of Pathology results is shown in Table 2.
Table 2. Summary of Pathology results.
| ||Histology ||Immunophenotype ||EBER ||Cytogenetics ||Previous PTLD|
|BL-1 ||SNC-BL, vacuolated cytoplasm ||CD20,10,79a, 43, bcl-6,cK; neg: TdT ||POS ||25.8% of cells c-MYC - RA (BAP) |
|BL-2 ||SNC-BL ||CD20, Lambda, bcl6 ||POS ||NA ||yes; Mono-like|
|BL-3 ||atypical cells with hi N/C ratio, apoptotic bodies ||*CD20,19,22,10,79a,bcl6,DR,cK; negTdT ||POS;|
|BL-4 ||SNC-BL ||CD20,79a, CD10,bcl-6; neg:TdT ||POS ||NA |
|BL-5 ||Medium-large atypical lymphoid cells, with GC-type BL phenotype ||CD20,19,10,bcl-6; neg:TdT ||NEG; |
|NEG c-Myc/IgH; 200/201 Neg (1-8q24+) ||yes;P-PTLD|
|BL-6 ||Diffuse NHL B-cells ||NA ||NA ||NA |
|BL-7 ||Monomorphic Large lymphoid cells; malignant lymphoma ||IgM,K,L, rare bcl6 ||POS ||t(8:14), complex karyotype ||yes;P-PTLD|
|BL-8 ||Monomorphous, BL-vacuoles, starry sky ||IgM kappa, bcl6 ||POS ||t(8:14) and +c-myc |
|BL-9 ||Monomorphic, BL morphology-vacuoles, apoptosis, necrosis ||CD79a,10,bcl6,cK+; neg Tdt ||POS (50-80%) ||t(8;14) ||yes;Monolike|
|BL-10 ||intermediate non-cleaved-BL, TBM, apoptosis,mitosis ||*CD20,19,10,79a,bcl-6,38,cK,DR+; neg: TdT ||NEG (rpt) ||t(8;14) and c-myc |
SNC=small noncleaved cell; *Immunophenotype from concurrent Bone Marrow. RA= rearrangement; BAP=
Index case is BL-2.
At our institution, BL-PTLD represented 15% of PTLD for pediatric heart, lung, heart/lung transplants
from 1982-present (1.1% incidence-unpublished data); 14% of all pediatric renal PTLD cases from 1989-1995
(1.6% incidence-unpublished data); and 6% of all liver PTLD cases from 1989-1991 (0.76%
Our case-series showed that 78% (7/9) of cases were EBV+, which is similar to
the frequency of BL-PTLD (72%) that we extracted from case series for both pediatric and adult cases in
This frequency is similar to EBV expression in other PTLDs
but is higher than the one shown by both sporadic and immunodeficiency-associated BL (primarily
The majority of our cases (75%) had negative EBV serology and/or titers
prior to transplant but all cases were positive post-transplant, prior to or at the diagnosis of the
BL-PTLD. EBV seronegative recipient status is the single most important risk factor in the development
of PTLD and appears to also be important in BL-PTLD, despite its later onset and more
aggressive clinical presentation, as compared to other PTLDs.
The relationship of EBV infection/expression with PTLD and BL is intriguing in regards to the
interplay between this virus and the oncogenic transformation furnished by the MYC gene. While endemic BL has a high expression of EBV, sporadic and
immunodeficiency-BLs have a much lower EBV prevalence. The role of EBV in the pathogenesis of BL is not
as well understood as it is in PTLD, in which virally infected resting B-lymphocytes become immortalized
by the interaction of the virus with cell cycle control and the bcl-2 gene
to prevent apoptosis. 
In the post-transplant immunosuppressed host, cytotoxic T-lymphocytes (CTL) are
inhibited in order to prevent cellular rejection, impairing their ability to kill the EBV-infected
B-lymphocytes. These EBV infected cells continue proliferating and can then manifest as an early,
polymorphous, or a monomorphous PTLD.  The interplay between EBV and the MYC oncogene in BL-PTLD may occur by the virus contributing to the dysfunction of
the MYC gene altering specific breakpoint patterns
 Existing data show that certain MYC
breakpoint locations (in which the c-MYC regulatory region remains intact)
are more common in EBV+ than in EBV(-) BL. This suggests that EBV proteins may influence the regulatory
regions of the c-MYC gene and thus could play a specific pathogenic role in
certain types of EBV+ BL, including BL-PTLD. 
While there is a low incidence of BL-PTLD in the literature, it appears to be different than other
PTLDs, both in clinical presentation and through molecular studies. BL in the post-transplant setting is
a more aggressive type of PTLD since it does not respond to decreased immunosuppression alone, requiring
In this pediatric population, the time from transplant to the initial development of BL-PTLD was also
much longer than other types of pediatric PTLD. In our case-series, the median time to presentation was
about 60 months post-transplant, compared to about 10.2 to 23 months for other PTLD in pediatric liver
and heart patients, respectively.
Our reported time interval is similar to other
published pediatric case reports for BL-PTLD, ranging from 24-72 months post-transplant.
One hypothesis to explain this longer lag time in BL-PTLD points towards a more complex pathophysiology
or an increased number of alterations needed to induce the genetic dysregulation of the MYC oncogene that accumulates over time, in contrast to the immediate CTL
immunosuppression and subsequent EBV B-cell proliferation for other PTLDs. Four cases did have some type
of PTLD proliferation prior to the BL-PTLD presentation; however, no real conclusion can be made as to
whether an early-type or polymorphous PTLD predisposes or impacts the development of BL-PTLD, as there
was a wide time range both in the initial PTLD and subsequent BL-PLTD presentations.
Lastly, gene expression data suggest that many of the M-PTLD are more related to other early and
P-PTLD than to their NHL counterparts, with the exception of BL and a minority of DLBCL, which retain a
germinal center phenoptype.
Capello et al. suggests that there are many PTLD with a
non-germinal center phenotype that have a nonfunctional IgVH or IgVL, crippling
gene rearrangements that lead to B-cell receptor (BCR) loss; however, rescue from apoptosis may occur
through EBV-LMP1 antigen expression that induces bcl-2 expression. It may be suggested that BL-PTLD,
through its c-MYC dysregulation and persistence of a GC-phenotype, has a
singular molecular profile that is more genetically similar to its immunocompetent counterpart than other
BL-PTLD is an emerging, aggressive subtype of M-PTLD that needs to be recognized and
accurately diagnosed as such in order to establish immediate therapy, not only decreasing
immunosuppression, but also administering alkylating agents. It shares some features of other PTLDs,
like high expression of EBV, which likely plays an additional role in the pathogenesis of MYC
dysregulation. However, features such as a more aggressive clinical presentation with higher stage,
longer interval between transplant and presentation, and a GC-phenotype, segregate BL from other M-PTLDs.
Awareness of BL as a PTLD is necessary because a different clinical management is needed for proper
treatment. Further work to understand the genetic expression profile of this PTLD subtype is needed to
fully characterize its biology, since only a handful of cases have been studied with current molecular
methods, only a minority of them in pediatric patients. The patient discussed here is currently
20-years-old and continues in good health, with no evidence of rejection or PTLD. Acknowledgements: I
want to thank specially Dr. Jennifer Picarsic, YPG3 of the AP/CP program at UPMC, for her excellent job
in reviewing the data and preparing the manuscript draft on which much of this presentation is based. I
also thank my colleague, Ron Jaffe, for sharing with us cases collected by him through many years.
Finally, I thank Drs. George Mazariegos, Steve Weber, Michael Green and Demetrius Ellis, our clinical
colleagues at CHP, for providing clinical information derived from their transplant patients.
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