Granulomatous Pneumocystis jiroveci Pneumonia in a Patient with Chronic Lymphocytic Leukemia: A Literature Review and Hypothesis on Pathogenesis

Otahbachi, Mohammed; Nugent, Kenneth; Buscemi, Dolores

doi:10.1097/00000441-200702000-00014

Cited by 26 publications

(18 citation statements)

References 17 publications

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“…Cases with an SPN manifestation, as in our report, are rare [4]. Granulomatous PJP was reported in patients with various hematological malignancies, including chronic lymphocytic leukemia (CLL), small lymphocytic lymphoma (SLL), prolymphocytic leukemia (PLL) [3,5], non-Hodgkin’s lymphoma [4,7], Hodgkin’s lymphoma [5], multiple myeloma [1], and acute and chronic myeloid leukemia [1]. We reviewed the English literature and found no more than 14 such cases, including the present one.…”

Section: Discussionmentioning

confidence: 77%

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Granulomatous <i>Pneumocystis jiroveci </i>Pneumonia in a Patient with Diffuse Large B-Cell Lymphoma: Case Report and Review of the Literature

Chang

Shih

Wang³

et al. 2009

Acta Haematol

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Here we report a case of diffuse large B-cell lymphoma who developed granulomatous Pneumocystis jiroveci pneumonia (PJP) after rituximab and combination chemotherapy. The infection presented as a solitary pulmonary nodule (SPN) instead of the commonly seen diffuse ground-glass infiltrates. The diagnosis was made by wedge resection of the nodule. Both the CD4+ lymphocyte count and immunoglobulin level were low. A literature search revealed 14 granulomatous PJP patients with hematological neoplasms, including the present case, which was the first with diffuse large B-cell lymphoma and the only patient receiving rituximab before PJP development. In addition to our report, only one case had previously presented with an SPN. Our experience suggests that granulomatous PJP should be considered a possible etiology when immunocompromised patients develop fever and SPNs.

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Section: Discussionmentioning

confidence: 77%

“…However, some atypical manifestations, such as cavitary or granulomatous lesions, have also been reported [2,3]. Even for granulomatous PJP, most cases present with diffuse reticulonodular infiltrations.…”

Section: Discussionmentioning

confidence: 99%

Granulomatous <i>Pneumocystis jiroveci </i>Pneumonia in a Patient with Diffuse Large B-Cell Lymphoma: Case Report and Review of the Literature

Chang

Shih

Wang³

et al. 2009

Acta Haematol

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“…IRIS in the context of Pneumocystis infection has been described both in HIV-infected patients (21)(22)(23)(24) and for those with non-HIV immunosuppressive conditions (25,26). PCP-associated IRIS has been modeled in murine hosts using selective transfer of lymphocyte subsets (27), and depletion of regulatory T cells from these cell populations can exacerbate lung injury (28).…”

mentioning

confidence: 99%

Dectin Immunoadhesins and Pneumocystis Pneumonia

et al. 2013

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The opportunistic pathogen Pneumocystis jirovecii is a significant cause of disease in HIV-infected patients and others with immunosuppressive conditions. Pneumocystis can also cause complications in treatment following antiretroviral therapy or reversal of immunosuppressive therapy, as the newly reconstituted immune system can develop a pathological inflammatory response to remaining antigens or a previously undetected infection. To target ␤-(1,3)-glucan, a structural component of the Pneumocystis cell wall with immune-stimulating properties, we have developed immunoadhesins consisting of the carbohydrate binding domain of Dectin-1 fused to the Fc regions of the 4 subtypes of murine IgG (mIgG). These immunoadhesins bind ␤-glucan with high affinity, and precoating the surface of zymosan with Dectin-1:Fc can reduce cytokine production by macrophages in an in vitro stimulation assay. All Dectin-1:Fc variants showed specificity of binding to the asci of Pneumocystis murina, but effector activity of the fusion molecules varied depending on Fc subtype. Dectin-1:mIgG2a Fc was able to reduce the viability of P. murina in culture through a complement-dependent mechanism, whereas previous studies have shown the mIgG1 Fc fusion to increase macrophage-dependent killing. In an in vivo challenge model, systemic expression of Dectin-1:mIgG1 Fc significantly reduced ascus burden in the lung. When administered postinfection in a model of immune reconstitution inflammatory syndrome (IRIS), both Dectin-1:mIgG1 and Dectin-1:mIgG2a Fc reduced hypoxemia despite minimal effects on fungal burden in the lung. Taken together, these data indicate that molecules targeting ␤-glucan may provide a mechanism for treatment of fungal infection and for modulation of the inflammatory response to Pneumocystis and other pathogens.

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“…5 The mechanism for granuloma formation is not well understood but might be an inflammatory reaction after immune reconstitution in patients receiving immunosuppressive therapies. 6 The theory of immune reconstitution inflammatory syndrome is best described in the patients with acquired immunodeficiency syndromes, such as HIV. Patients experience increased CD4 1 lymphocyte function and a decrease in HIV plasma viral load after initiating antiretroviral therapy.…”

Section: Discussionmentioning

confidence: 99%