We used four criteria to define true bloodstream infections after isolation of coagulase-negative staphylococci (CNS) from Isolator (Wampole Laboratories, Cranbury, NJ) blood cultures: (1) the patient's temperature was > or = 38 degrees C, (2) appropriate treatment was administered, (3) the physician diagnosed bloodstream infection or criteria for nosocomial bloodstream infection were met, and (4) at least one clinical sign or laboratory value was consistent with infection. Sixty (26.4%) of 227 episodes met these four criteria. By logistic regression, variables associated with meeting the definition of infection were admission to a service other than the surgical intensive care unit, the biotype of the Staphylococcus epidermidis isolates, the log of the weighted average of the total number of bacteria per milliliter of blood in all positive cultures, resistance to at least six antimicrobial agents, and the positivity of a BACTEC blood culture specimen that was drawn with the first positive Isolator culture specimen. In a high-risk population, 26% of Isolator blood cultures positive for CNS represented infections, a rate two to four times greater than that reported in the literature. Information regarding the species, biotype, antibiogram, and number of organisms per milliliter of blood might help physicians distinguish between CNS bloodstream infections and contamination.

Different mechanisms may contribute to early T cell reconstitution in HIV-1-infected children and adolescents during ART: decreased activation-induced apoptosis leading to increased survival of circulating primed/memory T cells; decreased activation-induced naive-to-memory shift increasing the frequency of circulating resting/naive T cells; increased input of haematopoietic progenitor cells from the bone marrow into the thymus and decreased intrathymic T cell death leading to an increased thymic output of naive T cells.

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We evaluated the use of a whole-blood assay that measures spontaneous and activation-induced CD69 expression on peripheral blood T-cells in vitro for assessment of T-cell function in HIV-1-infected paediatric patients. Heparinized venous blood from 28 HIV-1 positive children and adolescents and 23 healthy controls was incubated for 4 h with or without 5 microg/ml phytohaemagglutinin (PHA). Thereafter, analysis of CD69 expression on CD4+ and CD8+ T-cells was done by flow cytometry; simultaneously we determined CD4+ T-cell counts and plasma HIV-1 viral load. Neither spontaneous nor PHA-induced CD69 expression differed significantly between HIV-1 positive patients and healthy controls. However, T-cells from HIV-1 positive patients with plasma HIV-1 viral load levels above 70x10(3) copies/ml showed a higher spontaneous CD69 expression than T-cells from patients with lower plasma viral load levels in different stages of the disease. Antiretroviral treatment in four patients reduced spontaneous CD69 expression in CD4+ T-cells and PHA-induced CD69 expression in CD4+ and CD8+ T-cells significantly after 8 weeks of therapy. Conclusion Spontaneous and activation-induced expression of the early (activation) antigen CD69 on peripheral blood T-cells does not distinguish HIV-1 positive patients from HIV-1 negative healthy controls and is not correlated with peripheral blood CD4+ T-cell counts. This test may not be a reliable marker for functional T-cell deficiency during early stages of HIV disease. Increased spontaneous as well as PHA-induced CD69 expression on T-cells from HIV-1-infected children and adolescents in vitro may rather reflect HIV-induced pre-activation of T-cells in vivo.

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