Insights into the Microbiome of Breast Implants and Periprosthetic Tissue in Breast Implant-Associated Anaplastic Large Cell Lymphoma.

Though rare, breast implant-associated anaplastic large cell lymphoma (BIA-ALCL), a CD30+ T-cell lymphoma associated with textured breast implants, has adversely impacted our perception of the safety of breast implants. Its etiology unknown, one hypothesis suggests an initiating inflammatory stimulus, possibly infectious, triggers BIA-ALCL. We analyzed microbiota of breast, skin, implant and capsule in BIA-ALCL patients (n = 7), and controls via culturing methods, 16S rRNA microbiome sequencing, and immunohistochemistry. Alpha and beta diversity metrics and relative abundance of Gram-negative bacteria were calculated, and phylogenetic trees constructed. Staphylococcus spp., the most commonly cultured microbes, were identified in both the BIA-ALCL and contralateral control breast. The diversity of bacterial microbiota did not differ significantly between BIA-ALCL and controls for any material analyzed. Further, there were no significant differences in the relative abundance of Gram-negative bacteria between BIA-ALCL and control specimens. Heat maps suggested substantial diversity in the composition of the bacterial microbiota of the skin, breast, implant and capsule between patients with no clear trend to distinguish BIA-ALCL from controls. While we identified no consistent differences between patients with BIA-ALCL-affected and contralateral control breasts, this study provides insights into the composition of the breast microbiota in this population.

Bacterial Biofilm Infection Detected in Breast Implant-Associated Anaplastic Large-Cell Lymphoma.

BACKGROUND: A recent association between breast implants and the development of anaplastic large-cell lymphoma (ALCL) has been observed. The purpose of this study was to identify whether bacterial biofilm is present in breast implant-associated ALCL and, if so, to compare the bacterial microbiome to nontumor capsule samples from breast implants with contracture. METHODS: Twenty-six breast implant-associated ALCL samples were analyzed for the presence of biofilm by real-time quantitative polymerase chain reaction, next-generation sequencing, fluorescent in situ hybridization, and scanning electron microscopy, and compared to 62 nontumor capsule specimens. RESULTS: Both the breast implant-associated ALCL and nontumor capsule samples yielded high mean numbers of bacteria (breast implant-associated ALCL, 4.7 × 10 cells/mg of tissue; capsule, 4.9 × 10 cells/mg of tissue). Analysis of the microbiome in breast implant-associated ALCL specimens showed significant differences with species identified in nontumor capsule specimens. There was a significantly greater proportion of Ralstonia spp. present in ALCL specimens compared with nontumor capsule specimens (p < 0.05). In contrast, significantly more Staphylococcus spp. were found associated with nontumor capsule specimens compared with breast implant-associated ALCL specimens (p < 0.001). Bacterial biofilm was visualized both on scanning electron microscopy and fluorescent in situ hybridization. CONCLUSIONS: This novel finding of bacterial biofilm and a distinct microbiome in breast implant-associated ALCL samples points to a possible infectious contributing cause. Breast implants are widely used in both reconstructive and aesthetic surgery, and strategies to reduce their contamination should be more widely studied and practiced. CLINICAL QUESTION/LEVEL OF EVIDENCE: Risk, V.

Anaplastic large cell lymphoma and lepromatous leprosy: a rare coexistence.

Lepromatous leprosy (LL) has been reported in the literature with Non Hodgkin Lymphoma and rarely with Hodgkin Lymphoma. However, an extensive search of the literature shows no case report describing anaplastic large cell lymphoma (ALCL) in association with LL. We report a case of a young male with LL who was found to have ALCL. This is an interesting case of coexistence of an endemic infectious disease and a rare lymphoma involving the same lymph node, with a brief review of the literature.

Transmission of anaplastic large cell lymphoma via organ donation after cardiac death.

Recently, donation after cardiac death (DCD) has been encouraged in order to expand the donor pool. We present a case of anaplastic T-cell lymphoma transmitted to four recipients of solid organ transplants from a DCD donor suspected of having bacterial meningitis. On brain biopsy, the donor was found to have anaplastic central nervous system T-cell lymphoma, and the recipient of the donor's pancreas, liver and kidneys were found to have involvement of T-cell lymphoma. The transplanted kidneys and pancreas were excised from the respective recipients, and the kidney and pancreas recipients responded well to chemotherapy. The liver recipient underwent three cycles of chemotherapy, but later died due to complications of severe tumor burden. We recommend transplanting organs from donors with suspected bacterial meningitis only after identification of the infectious organism. In cases of lymphoma transmission, excision of the graft may be the only chance at long-term survival.

A patient with anaplastic large cell lymphoma (Ki-1 lymphoma) showing clonal integration of HTLV-1 proviral DNA.

We encountered a patient with anaplastic large cell lymphoma (Ki-1 lymphoma) that originated in the stomach and showed histiocytic lymphoma-like morphology. CD43 antigen was positive, and rearrangement of TCR-beta gene was observed. The lymphoma was the T-cell type. Though no atypical lymphocytes or histological images specific to adult T-cell leukemia were observed, clonal integration of HTLV-1 proviral DNA was noted. Viruses such as HTLV-1 appear to be involved in the development of some anaplastic large cell lymphomas.

Cutaneous manifestations of Epstein-Barr virus-associated T-cell lymphoma.

BACKGROUND: In addition to human T-lymphotropic virus (HTLV-I), the Epstein-Barr virus (EBV) has recently been demonstrated to be associated with cutaneous T-cell lymphoma (CTCL). OBJECTIVE: Our purpose was to investigate characteristic clinicopathologic features of the cutaneous lesions of EBV-associated T-cell malignancies. METHODS: Clinical records, laboratory data, and histopathologic sections were reviewed. Freshly frozen tumor tissues were immunophenotyped. Southern blot and in situ hybridization studies were performed to detect the EBV genomes. RESULTS: Ten of 35 CTCL biopsy specimens collected between 1985 and 1992 were found to be EBV-associated. Clonotypic proliferation of EBV genomes was demonstrated in each case, and the atypical T lymphoid cells contained EBV genomes. The cutaneous eruptions of these patients included multiple violaceous papules or nodules, chronic ulcers, and tumors on the trunk or extremities. Three distinct clinicopathologic subgroups could be recognized. The most consistent was the angiocentric T-cell lymphoma or lymphomatoid granulomatosis (type III CTCL) (four cases), presenting with chronic ulcers or violaceous papules. The second group was the T large-cell lymphoma (type II CTCL), Ki-1 antigen (CD30) (positive or negative) (four cases). Three patients with Ki-1- lymphoma had fulminant disease, whereas the remaining Ki-1+ case had a benign course. The third group was the secondary type CTCL (type V CTCL) (two cases), representing systemic EBV-associated T-cell lymphoma. The prognosis was grave. The common features of these EBV-associated CTCLs are resistance to conventional chemotherapy, poor prognosis, and the terminal manifestation of a hemophagocytic syndrome. No EBV genome could be detected in 12 cases of classic CTCL/mycosis fungoides (type I CTCL), or in three cases of HTLV-I-associated adult T-cell lymphoma (type IV CTCL). CONCLUSION: Three distinct clinicopathologic subtypes of EBV-associated CTCL were recognized, including one additional type of virus-associated CTCL.

CD30 (Ki-1) positive anaplastic large cell lymphomas in individuals infected with the human immunodeficiency virus.

BACKGROUND: CD30 (Ki-1) positive anaplastic large cell lymphoma (ALCL) has been only rarely described in HIV-positive patients. METHODS: The clinicopathologic features of eight ALCLs occurring in four AIDS and four HIV-positive patients were investigated. The phenotype of each neoplasm was determined by immunohistochemical methods. In three cases fresh tissue was available for molecular analysis. RESULTS: The ALCLs are a clinically heterogeneous group of T (4), B (1) and indeterminate (3) cell malignant lymphomas which presented in the skin (4), liver (1), lung (1), nasal cavity (1; also with bone marrow involvement) and peritoneal fluid (1). While most of the patients had aggressive disease, dying in a median of three months, two patients had either localized or regressing skin lesions. Molecular studies showed that two ALCLs, one of B cell and one of indeterminate cell lineage, contained clonal Epstein-Barr virus sequences. None of the ALCLs examined contained evidence of HTLV-1 or HIV integration nor did they exhibit c-myc or bcl-2 proto-oncogene rearrangements. No mutations or deletions of the p53 tumor suppressor gene were identified in the three cases studied. CONCLUSIONS: HIV-related ALCL represents a clinically heterogeneous group of T cell, B cell and null cell malignant lymphomas, distinct from the previously described categories of AIDS-associated NHL, that may expand the spectrum of lymphoid neoplasms associated with HIV-infection. Identification and investigation of other cases of HIV-associated ALCL is important to determine the nature of the relationship between HIV infection and the development of ALCL.