Fanconi anemia: myelodysplasia as a predictor of outcome.

The adverse potential of the development of myelodysplastic syndrome (MDS) in Fanconi anemia (FA) was examined in a retrospective study of 41 FA patients who had bone marrow morphology and chromosomes reviewed by a single group. Thirty-three patients had adequate cytogenetic studies, and 16 (48%) had one or more abnormal studies: nine initially, and seven more on follow-up. Cytogenetic clonal variation was frequent, including disappearance of clones, clonal evolution, and appearance of new clones. The estimated five-year survival with a cytogenetic clone is 0.40, compared to 0.94 without a clone. Morphologic myelodysplasia (MDS), independent of a cytogenetic clone, was found in 13/41 patients (32%). The estimated five-year survival with MDS is 0.09, versus 0.92 without MDS. Leukemia developed in three patients whose initial cytogenetic clones prior to leukemia were t(1;18), t(5;22) and monosomy 7; the one with t(1;18) also had MDS. Our results focus on marrow morphology, and suggest that morphologic MDS may be more important than classical cytogenetics in prediction of an adverse outcome.

Immunopathogenesis of canine angistrongylosis: pulmonary effects of infection.

Deposits of immunoglobulins, complement, and fibrinogen were localized in the lungs of Angiostrongylus vasorum-infected dogs. In acutely infected dogs, significant deposits of IgA, IgG and IgM, complement, and fibrinogen were seen. The predominant immunoglobulin noted in infections of longer duration was IgG. The continued presence of fibrinogen as the predominant protein deposited suggested a continuation of intravascular coagulation. This was borne out by demonstrating luminal deposits of fibrinogen in many blood vessels. Histopathologic examination of the large revealed lesions typical of angiostrongylosis, as well as eggs of the worm as early as 35 days postinfection. This is the earliest report of egg production by A. vasorum on record.

Phagocytic functions of pulmonary alveolar macrophages in genetically selected lean and obese swine and the effects of exogenous linolenic acid upon cell function.

Alveolar macrophages from genetically selected obese and lean swine were compared for in vitro phagocytic capabilities, using Fc (gamma)- and C3-mediated phagocytosis. Cells from obese pigs were significantly more effective at Fc (gamma)-mediated phagocytosis than those from lean pigs, both for percentage of total cells phagocytosing (P less than 0.044) and for the average number of opsonized sheep erythrocytes (SRBC) ingested per phagocyte (P less than 0.045). A seasonal interaction was noted for average number of SRBC ingested per phagocyte: the relative difference in macrophage responses between obese and lean groups became significantly more pronounced during winter and spring months (P less than 0.080). Macrophages from obese pigs also exhibited higher phagocytic activities at C3-mediated phagocytosis than did cells from lean pigs, but these differences were significant only for average number of SRBC ingested per phagocyte (P less than 0.080). Exogenous linolenic acid was added to selected cultures undergoing Fc (gamma)-mediated phagocytosis. Addition of the fatty acid frequently caused enhanced phagocytosis. Macrophages from obese pigs were stimulated by fatty acid treatment more frequently than cells from lean pigs (P less than 0.05). Relatively greater enhancement was also seen in cells from obese pigs, when compared with those from lean swine (P less than 0.025). These results suggest that genetically transferred factors are of primary importance in alveolar macrophage phagocytic responses and that linolenic acid can induce increased phagocytic activity by porcine alveolar macrophages in vitro.

Effects of Mycoplasma hyopneumoniae and Actinobacillus (Haemophilus) pleuropneumoniae infections on alveolar macrophage functions in swine.

Alveolar macrophages were collected at necropsy from pigs inoculated with Mycoplasma hyopneumoniae or Actinobacillus pleuropneumoniae or both and were tested for phagocytic capabilities, using in vitro techniques. Macrophages from noninoculated littermates were used as controls. Alveolar macrophages from pigs inoculated with either M hyopneumoniae or A pleuropneumoniae had significantly (P less than 0.05 to P less than 0.0025) higher phagocytic capacity than that of noninoculated controls. Macrophages from A pleuropneumoniae-inoculated pigs were comparatively more stimulated than were those from M hyopneumoniae-inoculated pigs. Pigs inoculated with M hyopneumoniae and then challenge-exposed with A pleuropneumoniae 2 and 4 weeks later had greatly reduced phagocytosis. Infection with M hyopneumoniae or A pleuropneumoniae caused stimulation of alveolar macrophage functions, and M hyopneumoniae infections may have suppressed phagocytic responses when pigs were challenge-exposed with a secondary pathogen (A pleuropneumoniae). This potential suppression may represent a prediposition of the host by M hyopneumoniae to secondary bacterial infections.