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author:("bagnardi, J L")
1.  Nationwide laboratory-based surveillance of invasive beta-haemolytic streptococci in Denmark from 2005 to 2011 
Clinical Microbiology and Infection  2013;20(4):O216-O223.
The aim of this work was to describe national surveillance of invasive beta-haemolytic streptococci (BHS) in Denmark and to report overall trends and major findings by groups and types of BHS causing laboratory-confirmed disease from 2005 to 2011. A total of 3063 BHS isolates were received from 2872 patients. Based on confirmed cases the overall annual incidence increased from 6.2 to 8.9 per 100 000 persons between 2005 and 2011. In 2011 the incidences of group A, B, C and G streptococci were 3.1, 2.3, 0.9 and 2.6 per 100 000 persons, respectively. An increase was observed for all groups of BHS, but in particular for group G in men above 65 years of age. Among group A streptococci (GAS), five T-types (1, 28,12, 3,13,B3264 and B3264) represented 71% and five emm-types (1, 28, 3, 89 and 12) 76% of all isolates. Among group B streptococci (GBS) four types (III, Ia, V, Ib) represented 79% of the isolates. Potential coverage for future vaccines against GAS and GBS disease was 76% compared with the 26-valent GAS vaccine and 89% based on GBS serotypes Ia, Ib, II, III and V. The number of reported cases of invasive BHS disease increased in Denmark from 2005 to 2011. Nationwide laboratory-based surveillance of BHS is required to monitor epidemiological changes, explore potential outbreaks and determine potential vaccine coverage.
PMCID: PMC4232002  PMID: 24125634
Emm-type; group A B C and G streptococci; invasive disease; T-type; type; typing
2.  Factors associated with Pneumocystis carinii pneumonia in Wegener's granulomatosis. 
Annals of the Rheumatic Diseases  1995;54(12):991-994.
OBJECTIVE--To determine the factors associated with the occurrence of Pneumocystis carinii pneumonia (PCP) in Wegener's granulomatosis (WG). METHODS--We retrospectively compared a group of 12 patients with WG and PCP (PCP group), with 32 WG patients without PCP followed over the same period in the same centres (control group). RESULTS--The mean delay of onset of PCP after the start of the immunosuppressive therapy was 127 (SD 128) days. Before treatment, the clinical and biological features of the two groups were similar, except for the mean lymphocyte count which was lower in the PCP group than in the control group (1060/mm3 v 1426/mm3; p = 0.04). During treatment, both groups were lymphopenic. There was a significant difference between the lowest absolute lymphocyte count in each group (244/mm3 in the PCP group v 738/mm3 in the control group; p = 0.001). During the first three months of treatment, the lymphocyte count was less than 600/mm3 at least once in 10 of the 12 patients in the PCP group and in 11 of the 32 patients in the control group (p < 0.01). The mean cumulative dose of cyclophosphamide was greater in the PCP group than in the control group at the end of both the second (1.55 mg/kg/day v 0.99 mg/kg/day; p = 0.05) and the third (1.67 mg/kg/day v 0.97 mg/kg/day; p = 0.03) months. However, in multivariate analysis, the only two factors independently and significantly associated with the occurrence of PCP were the pretreatment lymphocyte count (p = 0.018) and the lymphocyte count three months after the start of the immunosuppressive treatment (p = 0.014). CONCLUSIONS--The severity of lymphocytopenia before and during immunosuppressive treatment is the factor best associated with PCP in WG.
PMCID: PMC1010066  PMID: 8546533
3.  Carbapenem resistance in a clinical isolate of Citrobacter freundii. 
Antimicrobial Agents and Chemotherapy  1997;41(11):2352-2354.
Carbapenem resistance was studied in two sets of Citrobacter freundii strains: (i) strain CFr950, resistant to imipenem (MIC, 16 microg/ml) and isolated in vivo during imipenem therapy, and strain CFr950-Rev, the spontaneous, imipenem-susceptible revertant of CFr950 selected in vitro, and (ii) strains CFr801 and CFr802, two imipenem-resistant mutants selected in vitro from the susceptible clinical isolate CFr800. In all strains, whether they were imipenem-susceptible or -resistant strains, production of the cephalosporinase was derepressed and their Km values for cephaloridine were in the range of 128 to 199 microM. No carbapenemase activity was detected in vitro. The role of cephalosporinase overproduction in the resistance was demonstrated after introduction of the ampD gene which decreased the level of production of cephalosporinase at least 250-fold and resulted in an 8- to 64-fold decrease in the MICs of the carbapenems. The role of reduced permeability in the resistance was suggested by the absence, in CFr950 and CFr802, of two outer membrane proteins (the 42- and 40-kDa putative porins whose levels were considerably decreased in CFr801) and the reappearance of the 42-kDa protein in imipenem-susceptible strain CFr950-Rev. This role was confirmed after introduction of the ompF gene of Escherichia coli into the CFr strains, which resulted in 8- to 16-fold decreases in the MICs of carbapenems for CFr802 and CFr950. We infer from these results that the association of reduced, porin-mediated permeability with high-level cephalosporinase production, observed previously in other gram-negative bacteria, may also confer carbapenem resistance on C. freundii.
PMCID: PMC164127  PMID: 9371332
4.  Synergistic effect of amoxicillin and cefotaxime against Enterococcus faecalis. 
The antibacterial efficacy of the combination of amoxicillin and cefotaxime was assessed against 50 clinical strains of Enterococcus faecalis. For 48 of 50 strains, the MIC of amoxicillin that inhibited 50% of isolates tested decreased from 0.5 microgram/ml (range, 0.25 to 1 microgram/ml) to 0.06 microgram/ml (range, 0.01 to 0.25 microgram/ml) in the presence of only 4 micrograms of cefotaxime per ml. Alternatively, the MIC of cefotaxime that inhibited 50% of isolates tested decreased from 256 micrograms/ml (range, 8 to 512 micrograms/ml) to 1 micrograms/ml (range, 0.5 to 16 micrograms/ml) in the presence of only 0.06 microgram of amoxicillin per ml. For JH2-2, a reference strain of E. faecalis, the MICs of amoxicillin, cefotaxime, and amoxicillin in the presence of cefotaxime (4 micrograms/ml) were 0.5, 512, and 0.06 microgram/ml, respectively. By using a penicillin-binding protein (PBP) competition assay, it was shown that with cefotaxime, 50% saturation of PBPs 2 and 3 was obtained at very low concentrations (< 1 microgram/ml), while 50% saturation of PBPs 1, 4, and 5 was obtained with > or = 128 micrograms/ml. With amoxicillin, 50% saturation of PBPs 4 and 5 was obtained at 0.12 and 0.5 microgram/ml, respectively. Therefore, the partial saturation of PBPs 4 and 5 by amoxicillin combined with the total saturation of PBPs 2 and 3 by cefotaxime could be responsible for the observed synergy between these two compounds.
PMCID: PMC162868  PMID: 8540703
5.  Influence of antimicrobial therapy on kinetics of tumor necrosis factor levels in experimental endocarditis caused by Klebsiella pneumoniae. 
The kinetics of tumor necrosis factor (TNF) levels in serum during therapy with cell wall-active agents (ceftriaxone, imipenem) and gentamicin were investigated in rabbits with experimental endocarditis caused by an isogenic pair of Klebsiella pneumoniae strains: a TEM-3 beta-lactamase-producing strain (KpR) or its susceptible variant (KpS). In vitro, KpR was resistant to ceftriaxone and was susceptible to gentamicin and imipenem, while KpS was susceptible to all three antibiotics. Serum TNF levels were determined in control rabbits hourly after bacterial inoculation and then daily; they were determined in treated animals hourly after the first antibiotic injection and then daily during a 4-day therapy with either imipenem (60 mg/kg of body weight four times daily), ceftriaxone (75 mg/kg once daily), or gentamicin (4 mg/kg once daily) alone or in combination with ceftriaxone. After a transient peak (10.2 +/- 3.1 ng/ml) at 90 min following bacterial challenge, serum TNF levels remained low and stable in control animals. The peak in the serum TNF levels occurred 4 h after the first antibiotic injection and with ceftriaxone was significantly higher (P < 0.05) against KpS (1.99 +/- 0.52 ng/ml) than against KpR (1.40 +/- 0.17 ng/ml). Against the KpR strain, the levels observed with ceftriaxone were significantly higher (P < 0.05) than those obtained with the other therapeutic regimens (0.70 to 0.80 ng/ml). On the day of sacrifice, effective regimens were associated with low TNF levels. We concluded that TNF production depends on (i) the antiobiotic's mechanism of action and the susceptibility of the strain at the early phase of therapy, without any effect of the rapidity of bacterial killing, and (ii) the final reduction of the bacterial count at a later stage of therapy.
PMCID: PMC188143  PMID: 8067731

Results 1-5 (5)