Erysipelas is a bacterial disease caused by Erysipelothrix rhusiopathiae, which may infect swine as well as several other species of mammals and birds, including domestic fowl. In poultry, erysipelas may cause sudden high mortality due to septicemia. This communication describes the first isolation of E. rhusiopathiae from the haematophagous poultry red mite, Dermanyssus gallinae DeGeer (Acari: Dermanyssidae), that was collected on three farms where hen erysipelas was diagnosed. The bacteria were isolated from the integument as well as from the interior of the mites. Serotypes 1a and 1b of E. rhusiopathiae found in the mites corresponded with those isolated from the diseased birds. These findings imply that D. gallinae is a potential vector of E. rhusiopathiae. The current lack of effective measures to control D. gallinae causes recurring mite problems in poultry facilities once afflicted by this parasite. Consequently, mites containing E. rhusiopathiae may act as reservoir hosts of this bacterium, allowing it to persist in the poultry house between flock cycles as a source of infection for the replacement pullets. The zoonotic potentials of both E. rhusiopathiae and D. gallinae should also be considered.

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A major barrier for cancer immunotherapy is the presence of suppressive cell populations in cancer patients, such as myeloid-derived suppressor cells (MDSC) and tumor-associated macrophages (TAM), which contribute to the immunosuppressive microenvironment that promotes tumor growth and metastasis. Tasquinimod is a novel antitumor agent that is currently at an advanced stage of clinical development for treatment of castration-resistant prostate cancer. A target of tasquinimod is the inflammatory protein S100A9, which has been demonstrated to affect the accumulation and function of tumor-suppressive myeloid cells. Here, we report that tasquinimod provided a significant enhancement to the antitumor effects of two different immunotherapeutics in mouse models of cancer: a tumor vaccine (SurVaxM) for prostate cancer and a tumor-targeted superantigen (TTS) for melanoma. In the combination strategies, tasquinimod inhibited distinct MDSC populations and TAMs of the M2-polarized phenotype (CD206+). CD11b+ myeloid cells isolated from tumors of treated mice expressed lower levels of arginase-1 and higher levels of inducible nitric oxide synthase (iNOS), and were less immunosuppressive ex vivo, which translated into a significantly reduced tumor-promoting capacity in vivo when these cells were co-injected with tumor cells. Tumor-specific CD8+ T cells were increased markedly in the circulation and in tumors. Furthermore, T-cell effector functions, including cell-mediated cytotoxicity and IFNγ production, were potentiated. Taken together, these data suggest that pharmacologic targeting of suppressive myeloid cells by tasquinimod induces therapeutic benefit and provide the rationale for clinical testing of tasquinimod in combination with cancer immunotherapies.

Prophylactic treatment of paquinimod reduces synovial activation, osteophyte formation and cartilage damage in experimental OA with high synovial activation (CIOA) and ameliorates pathological effects of S100A9 in OA synovium ex vivo.

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