Enterococci with high-level resistance to gentamicin account for 55% of clinical isolates of enterococci found in patients at the Ann Arbor Veterans Administration Medical Center. We prospectively studied cultures obtained from all 100 patients hospitalized from 1 December 1985 through 23 January 1986 on the surgical and thoracic intensive care units and a general medical floor. Ten patients' cultures grew colonies of gentamicin-resistant enterococci--six after admission to the intensive care units and four after hospitalization on the medical ward. The initial sites of colonization were the rectal and perineal areas in seven patients, sternal wound in one, urine in one, and the rectal and perineal areas as well as urine after Foley catheter insertion in one. Nine patients died and three of the deaths were associated with enterococcal infection. The acquisition of resistant strains was associated with previous and more frequent exposure to antimicrobial agents, and with geographic clustering of patients. Resistant enterococci were isolated from the hands of hospital personnel and were frequently isolated from environmental surfaces. Nosocomial acquisition and interhospital spread of gentamicin-resistant enterococci was shown to have occurred when plasmid content was used as an epidemiologic marker.
The detection of cryptococcal antigen by means of the agglutination of antibody-coated latex particles is an important aid in the diagnosis of cryptococcosis. A commercially available latex agglutination test (IBL kit) was compared with the latex agglutination test from the Center for Disease Control in regard to sensitivity, specificity, and height of antigen titer. Over a 13-month period, 335 specimens were tested with both kits. There was one false-positive reaction with both kits (0.4%) and one false-negative reaction only with the CDC kit, among 18 patients who had meningitis or disseminated infection due to Cryptococcus neoformans. Sera from patients who had localized pulmonary cryptococcosis showed negative results with both kits. The antigen titers measured by the two kits were the same or within two dilutions in 22 of 26 specimens of cerebrospinal fluid or serum from patients who had proved cryptococcosis. Overall, the IBL kit compared favorably with the CDC kit for the detection of cryptococcal antigen in cerebrospinal fluid or serum.
CD2 ('Ill; sheep erythrocyte receptor) is the surface component of an alternative, antigen-independent pathway of human T cell activation. The response to certain anti-CD2 antibodies is relatively independent of accessory cell signals and therefore provides a direct measurement of T cell function. The CD2 pathway may be important in the differentiation of thymocytes, on which the expression of CD2 precedes the appearance of the CD3-T cell receptor complex. In view of the impaired T cell regulation of immune responses in patients with systemic lupus erythematosus (SLE), we examined the activation of peripheral blood lymphocytes by anti-CD2 antibodies in 57 SIX patients and 32 normal control subjects. The CD2 pathway response was lower in the SLE patients (P < 0.0001); 18 of the 57 SLE patients had a lower response than any of the control subjects. The SI,E low-responder patients did not differ from the normal-responder patients in terms of disease activity or use of antiinflammatory and immunosuppressive medications. Low responses to anti-CD2 were corrected to normal by the coaddition of a submitogenic amount of phorbol myristate acetate (1 ng/ml). In some
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