During February and March of 1998, 12 sudden deaths were reported among residents of a high-Andean community in Ecuador. All 12 fatalities were members of the same extended family and some had apparent exposure to sick guinea-pigs. Following an initial investigation by public health officials, an additional death was reported in a nearby community in April, also associated with exposure to sick guinea-pigs. Blood samples from humans, dogs, and a rodent were tested for antibody to the F1 antigen of Yersinia pestis by passive haemagglutination assay. Tissue from rodents was subjected to direct fluorescent antibody staining using fluorescein-labelled monoclonal antibody to Y. pestis F1 antigen. Formalin-fixed specimens from the 2 autopsies were evaluated using a 2-step alkaline phosphatase immunoassay with a monoclonal antibody to Y. pestis F1 antigen, and tissues that had not been embedded in paraffin were tested for the presence of DNA encoding the F1 structural antigen by polymerase chain reaction. Serological evaluation of close contacts of the fatalities revealed positive titres to F1 antigen of Y. pestis, the aetiological agent of plague, in 3 contacts from the first community and 1 from the second. Immunohistochemical staining of tissues collected from 2 of the fatalities provided evidence that both had pneumonic plague. Five of 14 dogs found in the communities were seropositive for plague antibody, providing evidence of a recent epizootic plague in the area.

In 1990, researchers and health care professionals joined with members of several southwestern Native American communities to form an HIV/AIDS and substance abuse prevention partnership. Culturally sensitive approaches to theory-based interventions were developed into highly replicable, structured, school-based and community-based intervention programs. Process evaluations indicated high levels of program acceptance and fidelity. Outcome evaluations demonstrated significant positive preventive intervention effects among participants. This article reports how NAPPASA school prevention curricula were developed and discusses three critical processes in developing these successful curricula: 1) selection of integrative theory to address the multi-dimensional antecedents of HIV/AIDS and substance abuse among Native Americans, 2) use of ethnographic methodology to obtain intensive input from target groups and community members to ensure cultural and developmental sensitivity in the curriculum, and 3) use of process and outcome evaluations of pilot and field trials to develop an optimal curriculum.

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Osteosarcoma is a malignant bone-forming tumour that typically arises within the metaphysis of long bones. Extraskeletal osteosarcoma is a rare variant that usually arises in the deep soft tissues, especially in the legs. We report a 65-year-old white man with an ulcerated, nodular lesion of the forearm. Based on the histological features and immunohistochemical profile of the tumour, a diagnosis of osteoblastic osteosarcoma was made. Osteosarcoma arising in the skin is a rare condition that has seldom been reported in the English literature.

Myeloid and lymphoid neoplasms with fibroblastic growth factor receptor-1 (FGFR1) abnormalities originate from mutated pluripotent stem cells and have a heterogeneous clinical presentation. There are 12 identified partner genes commonly involved in FGFR1 translocation at an 8p11 breakpoint. In FGFR1-related neoplasms, T-lymphoblastic lymphoma with eosinophilia is the most common clinical scenario, whereas acute B-lymphoblastic leukemia/lymphoma (B-ALL/LBL) is rare. To date, only 7 cases of B-ALL/LBL with FGFR1 abnormalities have been reported. Here, we report an additional case of a 64-year-old gentleman with leukocytosis, eosinophilia and diffuse mediastinal and general lymphadenopathy. Bone marrow examination showed patchy infiltrates of immature precursors/blasts, along with myeloid/eosinophilic hyperplasia. Immunophenotyping confirmed increased B lymphoblasts (30-40%). Karyotyping revealed cytogenetic abnormalities, including t(8;13)(p11;q12)/ZMYM2 (ZNF198)-FGFR1 and trisomy 21. The patient did not respond to hyper-CVAD chemotherapy and within 4 months developed acute myelomonocytic leukemia and expired 11 months after the initial diagnosis. Similar cases from the literature are reviewed.