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The role of lymphocyte apoptosis in septic shock remains a controversial issue. Using Annexin V and flow cytometry analysis on freshly isolated cells, we evaluated circulating lymphocyte apoptosis in 23 septic shock, 25 sepsis without shock, 7 nonseptic critically ill, and 25 control patients. In patients with sepsis, we compared day 1 lymphocyte apoptosis (i.e., within 3 days of the onset of infection) with that observed 5-7 days after (day 6) according to shock state, mortality, and seventy factors. At day 1, patients in septic shock exhibited higher lymphocyte apoptosis than that present in controls (16.5% +/- 3.5% vs. 3% +/- 0.5%, respectively, P = 0.0001). At day 6, patients with sepsis without shock restored undamaged CD4+ T and CD8+ T lymphocyte counts, whereas patients in septic shock increased only CD4+ T cells. Similarly, survivors restored undamaged lymphocyte count at day 6 (+70%, P < 0.001), whereas nonsurvivors did not. Day 6 undamaged lymphocyte count negatively correlated with day 1 SAPS II, day 6 LOD score, mechanical ventilation, and ICU stay duration. We observed no apoptotic effect of septic shock plasma or septic shock circulating mononuclear cells on target lymphoid cell lines. We found no alteration in any death receptors Fas, TRAIL-R1, TRAIL-R2, or in their ligands on circulating blood cells. Catecholamines and interleukin 10 levels significantly increased in patients with septic shock, but did not correlate with apoptosis levels. We conclude that lymphocyte apoptosis is rapidly increased in blood of patients in septic shock and that lymphocyte apoptosis leads to a profound and persistent lymphopenia associated with poor outcome. These results suggest that lymphocyte apoptosis is one of the main components of human septic shock immune dysfunction and could be related more to microcirculatory disturbance than to circulating factors.

Monocyte deactivation has been identified as a major factor of immunosuppression in sepsis and is associated with a loss of surface human leukocyte antigen-DR (HLA-DR) expression on circulating monocytes. Using flow cytometry, quantitative reverse transcription-polymerase chain reaction, we investigated this phenomenon in septic patients. We confirmed the early loss of monocyte HLA-DR expression in all infected patients and demonstrated that this persistent lowered expression at Day 6 correlated with severity scores, secondary infection, and death. This phenomenon occurred at a transcriptional level via a decrease in the class II transactivator A (CIITA) transcription. Furthermore, these abnormalities correlated with the high cortisol levels observed in sepsis and not with those of other putative factors such as catecholamines or interleukin-10. Finally, in vitro studies evidenced that glucocorticoids decrease HLA-DR expression at a transcriptional level via a decrease in CIITA mRNA levels, mainly by down modulating its isoforms I and III. We conclude that in human sepsis, the loss of HLA-DR expression on circulating monocytes is associated with a poor outcome. We suggest that the high endogenous cortisol level observed in septic shock may be a possible new factor involved in the loss of HLA-DR expression on monocytes via its effect on HLA-DR and CIITA transcription.

Acquired infections were substantially reduced by mupirocin/chlorhexidine plus polymyxin/tobramycin, whereas each regimen given alone was ineffective. Whether both regimens could increase Candida infections deserves further investigation.

SAPS II score higher than 46, duration of symptoms prior to ICU admission longer than 5 days and intubation were associated with increased mortality. Initiation of fluoroquinolone therapy within 8 h of ICU admission significantly reduced mortality.

Older patients are more susceptible to severe Epstein-Barr virus (EBV)-related infectious mononucleosis (IM). This condition may increase in industrialized countries where primary EBV infection occurs later in life.Between 1990 and 2004, 38 patients were admitted to our department with EBV-related IM. Two patients died. The annual incidence increased significantly (r ‫؍‬ 0.623; P ‫؍‬ 0.013).Primary Epstein-Barr virus (EBV) infection during childhood is usually subclinical, whereas infection of adolescents or adults results in infectious mononucleosis (IM) in 30 to 70% of cases and can prove severe (1,2,5,6,8). We recently noticed a sharp increase in the incidence of EBV-related IM that required hospitalization.Pontchaillou is a university-affiliated hospital which serves as a referral center for patients more than 15 years old in our area. EBV-related IM was defined as IM with at least one serological marker of acute EBV infection among the following: (i) the presence of immunoglobulin M antibodies to viral capsid antigen in the absence of antibodies to EBV nuclear antigen (EBNA), (ii) the presence of heterophile antibodies (Monospot or Paul-Bunnell Davidsohn test), and/or (iii) a positive PCR for EBV DNA. Patients previously known as immunocompromised were excluded. Linear trends over time were analyzed by a nonparametric Spearman rank order correlation analysis, using years as the independent variable. P values were based on two-tailed tests of significance (P Ͻ 0.05). Statistical analysis was performed using SPSS software version 11.5 (SPSS).Between 1990 and 2004, 38 patients (15 male, 23 female) were admitted to our department with EBV-related IM. The mean age was 22.6 years (standard deviation, 9.2 years; range, 16 to 53 years).

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Coxsackievirus A-16 (CVA-16) is the agent of hand, foot, and mouth disease in children. We report a case of fatal pneumonitis in an adult due to a CVA-16 strain with a low (78.6%) rate of sequence homology with the reference strain. A modified, more virulent, strain of CVA-16 could be emerging.