HTLV-I-associated myelopathy following allogeneic bone marrow transplantation.

A 39-year-old polytransfused patient with aplastic anemia acquired transfusion-associated HTLV-I infection shortly before transplantation. The patient underwent allogeneic bone marrow transplantation and developed HTLV-I associated myelopathy 3 years later. Clinical abnormalities and a host of atypical findings are presented in the context of previous reports describing uncommon features of the disease.

Murine IL-10 fails to reduce GVHD despite inhibition of alloreactivity in vitro.

Graft-versus-host disease (GVHD) is a serious complication following allogeneic bone marrow transplantation (BMT). Initial immunologic events that are thought to lead to clinical GVHD include allogeneic antigen presentation, CD4+ T cell proliferation and eventually generation of specific cytotoxic lymphocytes. Interleukin-10 (IL-10) has been shown to inhibit the function of antigen presenting cells (APC) and to reduce lymphocyte proliferation. In this study we investigated the possible role of recombinant murine IL-10 (rmIL-10) as prophylactic treatment of GVHD in a murine BMT model involving B10.BR donor mice (H-2k) and AKR recipients (H-2k). In particular, we wished to determine whether early post-BMT administration of IL-10 would suppress GVHD by interfering with macrophage function and inflammatory cytokine production during the proposed "afferent' phase of GVHD. In MLR assays, rmIL-10 significantly inhibited the proliferation of donor spleen cells when stimulated by irradiated recipient spleen cells in a dose-dependent manner. In murine BMT, rmIL-10 was administered exogenously by intraperitoneal injection of 100 U daily in two different dosage schedules, on days-1, 0, 1, 2, 3, 6 to target the early post-BMT phase, and days-1, 0, 3, 5, 7, 10 after BMT, to administer the same total dose throughout the engraftment period. IL-10 injected mice had lower plasma IL-1 alpha levels on day 3 (12 pg/ml vs 64 pg/ml in controls, P < 0.05), suggesting that both macrophage function and inflammatory cytokine production were inhibited. In contrast to the MLR data, no significant improvement in morbidity and mortality from GVHD was observed. Therefore, IL-10 does not appear to be useful in GVHD prophylaxis.

Leptospirosis complicated by a Jarisch-Herxheimer reaction and adult respiratory distress syndrome: case report.

Leptospirosis, severe infection due to Leptospira interrogans, is a potentially lethal disease that causes multiple organ failure. In addition to hepatic, renal, and CNS involvement, which are classic complications of leptospirosis, the disease may also be complicated by adult respiratory distress syndrome. Treatment with penicillin may precipitate a severe Jarisch-Herxheimer reaction. The mechanisms of Leptospira-induced toxicity remain obscure. We report a near-fatal case of leptospirosis in a patient who developed a JHR and respiratory failure immediately after initiation of therapy.

Trimethoprim, sulphamethoxazole, bacterial adhesion and polymorphonuclear leucocyte function.

Culturing Escherichia coli, Proteus mirabilis and Klebsiella pneumoniae in the presence of subinhibitory concentrations (1/4 MIC) of trimethoprim, sulphamethoxazole or their combination, resulted in reduced adherence of all the above strains. The number of phagocytosed bacteria pre-exposed to subinhibitory concentrations of the above antibiotics was not significantly changed, but a significant increase of bactericidal activity of the polymorphonuclear leucocytes was observed. Furthermore, filtrates of K. pneumoniae and P. mirabilis grown in the presence of trimethoprim alone or in combination with sulphamethoxazole induced an increased chemotactic response of human polymorphonuclear leucocytes.