Case report: Greater meningeal inflammation in lumbar than in ventricular region in human bacterial meningitis

Differences in the composition of ventricular and lumbar cerebrospinal fluid (CSF) based on single pairs of samples have previously been described. We describe a patient that developed post-surgical recurrent meningitis monitored by daily biochemical and bacteriological CSF analysis, simultaneously withdrawn from lumbar space and ventricles. A 20-year-old Caucasian man was admitted to the ICU after a resection of a chordoma that extended from the sphenoidal sinus to the anterior face of C2. CSF was continuously leaking into the pharyngeal cavity after surgery, and three episodes of recurrent meningitis, all due to Pseudomonas aeruginosa O12, occurred. Our case showed permanent ventricular-to-lumbar CSF gradients of leukocytes, protein and glucose that were increased during the acute phase of meningitis, with the greatest amplitude being observed when bacteria were present in both ventricular and lumbar CSF. This might suggest a greater extent of meningeal inflammation in the lumbar than in the ventricular region. Our case also showed that the increase in intravenous antibiotics (cefepim from 8 to 12 g/day and ciprofloxacine from 1.2 to 2.4 g/day) led to an increase in concentration in plasma but not in CSF

Local and systemic innate immune response to secondary human peritonitis. Influence of micro-organism.

International audienceINTRODUCTION: Our aim was to describe inflammatory cytokines response in the peritoneum and plasma of patients with peritonitis. We also tested the hypothesis that scenarios associated with worse outcome would result in different cytokine release patterns. Therefore, we compared cytokine responses according to the occurrence of septic shock, mortality, type of peritonitis and peritoneal microbiology. METHODS: Peritoneal and plasma cytokines (IL-1, tumour necrosis factor alpha [TNFalpha], IL-6, IL-10, and IFN) were measured in 66 patients with secondary peritonitis. RESULTS: The concentration ratio between peritoneal fluid and plasma cytokines varied from 5 [2 - 21] (IFN) to 1310 [145 - 3888] (IL-1). There was no correlation between plasma and peritoneal fluid concentration of any cytokine. In the plasma, TNFalpha, IL-6, IFN, and IL-10 were higher in patients with shock versus no shock, and in nonsurvivors versus survivors (p[less than or equal to]0.03). There was no differential plasma release for any cytokine between community-acquired and postoperative peritonitis. Presence of anaerobes or Enterococcus specie in peritoneal fluid was associated with higher plasma TNFalpha: 50 [37-106] vs 38 [29-66] and 45 [36 - 87] vs 39 [27 - 67] pg/ml, respectively (p=0.02). In the peritoneal compartment, occurrence of shock did not result in any difference in peritoneal cytokines. Peritoneal IL-10 was higher in patients who survived (1505 [450 to 3130] vs 102 [9 to 710] pg/ml; p=0.04). Presence of anaerobes and Enterococcus specie was associated with higher peritoneal IFN: 2 [1-6] vs 10 [5-28] and 7 [2-39] vs 2 [1-6], p=0.01 and 0.05 respectively). CONCLUSIONS: Peritonitis triggers an acute systemic and peritoneal innate immune response with a simultaneous release of pro and anti-inflammatory cytokines. Greater levels of all cytokines were observed in the plasma of patients with the most severe conditions (shock, non survivors), but this difference was not reflected in their peritoneal fluid. There was always a large gradient in cytokine concentration between peritoneal and plasma compartments highlighting the importance of compartmentalization of innate immune response in peritonitis

Additional file 4: of Reversal of neutrophil-to-lymphocyte count ratio in early versus late death from septic shock

Figure S4. In-ICU early death cumulative incidence of abdominal (n=99) and extra-abdominal (n=31) septic shock groups Figure S5. Cumulative incidence of death for patients alive at day 5 and still hospitalized in ICU according to the variation from Day 1-to-5 of NLCR. (DOC 21 kb

Additional file 2: Table S2. of Reversal of neutrophil-to-lymphocyte count ratio in early versus late death from septic shock

Area under the receiver operating characteristic (ROC) curve for cellular counts to predict death. (DOC 21 kb

Additional file 1: Table S1. of Reversal of neutrophil-to-lymphocyte count ratio in early versus late death from septic shock

p Values of the two-way ANOVA comparing cellular counts over time between survivors and nonsurvivors. (DOC 21 kb

Additional file 3: of Reversal of neutrophil-to-lymphocyte count ratio in early versus late death from septic shock

Table S3. Neutrophils, lymphocytes counts and NLCR variations according to the septic origin ( abdominal vs extra-abdominal) and death timing. (DOC 21 kb