Journal of Clinical Pathology

Pasteurella species cause zoonotic infections in humans. Human pasteurella infections usually manifest as local skin or soft tissue infection following an animal bite or scratch. Systemic infections are less common and are limited to patients at the extremes of age or those who have serious underlying disorders, including cirrhosis. Most human pasteurella infections are caused by the multocida species. We report a case ofPasteurella dagmatisperitonitis and septicaemia in a patient with cirrhosis. The infection followed a scratch inflicted by a pet dog. Despite appropriate antibiotic treatment the infection proved fatal. Spontaneous bacterial peritonitis caused byP dagmatishas not been reported previously.Pasteurella dagmatisis a relatively recently described species, which is rarely reported as a human pathogen. This species may be misidentified unless commercial identification systems are supplemented by additional biochemical tests.

Eighteen strains ofStaph. pyogenes(nine penicillin-sensitive and nine penicillin-destroying) were passaged 40 to 50 times on Celbenin¹ditch plates.

All strains developed an increase in resistance to Celbenin and eight strains (four penicillin-sensitive and four penicillin-destroying) were able to grow in 100 μg/ml. or more Celbenin. Resistance was of the drug-tolerant type and none of the cultures inactivated Celbenin. There was an associated increase in tolerance to benzyl penicillin.

The highly Celbenin-resistant cultures isolated from penicillin-destroying staphylococci were in sharp contrast to those from penicillin-sensitive strains, as well as to penicillin G-tolerant staphylococci isolatedin vitro, because they retained the cultural characteristics, coagulase and haemolytic activity, and mouse virulence of the parent strains, and the degree of resistance remained stable after repeated passage in the absence of Celbenin.

Three naturally occurring Celbenin-resistant strains ofStaph. pyogenesisolated from infective processes were also studied. All three strains grew luxuriantly in concentrations of Celbenin up to 12·5 μg/ml. but very poorly in higher concentrations.

The possible significance of these findings is discussed.

Aims—To compare blood drug concentrations during life with postmortem drug concentrations measured from a peripheral site and a central site.

Methods—Coroner's cases from October 1990 to July 1997 were reviewed. Six cases had data on both antemortem and postmortem blood drug concentrations. The postmortem to antemortem ratio was compared with the postmortem central to peripheral ratio, using cardiac blood as a central site and femoral blood as a peripheral site.

Results—Drugs that have a high postmortem central to peripheral ratio; that is, drugs that exhibit considerable postmortem redistribution, also have high postmortem to antemortem ratios.

Conclusions—A large degree of error can arise from attempting to estimate antemortem drug concentrations and the ingested dose from postmortem measurements. The chosen site and technique for postmortem blood sampling can greatly influence the concentration of drug measured.

Chromosomal abnormalities and genomic instability are common features of, and possible driving forces in, tumorigenesis. Recently, several mitotic proteins that are critical to proper chromosome segregation have been identified. Members of the Aurora kinase family have been identified as having important roles in mitosis; overexpression induces multicellularity and fosters polyploidy. As aneuploidy is a common feature of malignant gliomas, particularly glioblastomas (GBMs), we examined 25 prospectively collected GBMs to assess the role that overexpression of one member of this family, Aurora B, might have in the clinical behaviour of GBMs. Aurora B expression levels were markedly correlated with a shortened survival. Aurora B expression was not directly related to age, tumour proliferation status or to several common molecular changes found in GBMs. These results suggest that Aurora B may be a prognostic feature of impaired survival and a novel therapeutic target in some patients.

Aims:To analyse the entity specific incidence and disease specific survival (DSS) of non-Hodgkin lymphomas (NHLs) in Tyrol/Austria, 1991–2000.

Methods:Data from 1307 NHLs (excluding primary cutaneous lymphomas and monoclonal gammopathies of undetermined significance) were obtained. Current status was available for all patients. Except for 29 cases of small lymphocytic (CLL/SLL), lymphoblastic leukaemia (ALL), and myeloma (MM), which were diagnosed cytologically, diagnoses were reclassified on paraffin wax embedded archival material according to new World Health Organisation criteria. Sex specific age adjusted standardised incidence rates were computed using Segi’s population weighting. Annual incidence changes were calculated by weighted least square regression analysis. Survival was estimated by the Kaplan–Meier method and compared by log rank test.

Results:NHL more frequently affected men (male/female ratio, 1.52). Mean age of occurrence was 61 and 66 years for men and women, respectively. The incidence rate of 14.3 remained constant. There was a significant increase in diffuse large B cell lymphoma (DLBCL) and decrease in CLL/SLL in men, and a decrease in MM in women. Overall DSS was 64% during the mean follow up (43 months). Age, T-NHL, λ light chain restriction in MM, and male sex in CLL/SLL were associated with poor prognosis. In B-NHL, DSS decreased in the following order: hairy cell leukaemia, marginal zone lymphoma, follicular lymphoma, Burkitt lymphoma, ALL, DLBCL, CLL, MM, and mantle cell lymphoma.

Conclusions:The incidence of NHL in Tyrol has changed in the past decade, with a significant increase in DLBCL, decrease in CLL/SLL in men, and decrease in MM in women.

The antigenic phenotype of human fetal osteoclasts was compared with that of human tissue macrophages and macrophage polykaryons in foreign body lesions using a large number of monoclonal antibodies directed against myeloid (granulocyte/mononuclear phagocyte) antigens. Osteoclasts expressed a restricted range of macrophage-associated antigens including CD13, CD15A, CD44, CD45, CD54, (ICAM-1), CD71 (transferrin receptor), and CD68. These antigens were also present on macrophages and macrophage polykaryons both of which also strongly expressed CD11a,b,c, CD18, (LFA family), CD14, CD31, CD36, CD37, CD39 and CD43 antigens. There was also weak and occasional expression of CD16 (FcRIII), CD25 (interleukin 2 receptor), CD32 (FcRII), CD35 (C3b receptor) and HLA-DR by macrophage polykaryons. The presence of some macrophage associated antigens on osteoclasts is consistent with their originating from cells of the mononuclear phagocyte system. The numerous differences in antigenic phenotype between osteoclasts and macrophage polykaryons, however, suggest that their pathways of development and differentiation are not identical. The differences discerned in antigenic phenotype should also permit distinction between these polykaryons (and possibly their mononuclear precursors) in normal and diseased tissues.