Fatal outcome of first case of Streptococcus sinensis in infective endocarditis in the Netherlands: a case report.

BACKGROUND: Infective endocarditis is a relatively common disease in a cardiologist's daily practice. Nowadays more detailed information about pathogens is provided to us by diagnostics such as MALDI Biotyper Massa Spectrometer. We present a case of endocarditis lenta in which Streptococcus sinensis was identified in the Netherlands for the first time. CASE SUMMARY: A 58-year-old man was admitted with high suspicion of endocarditis lenta complicated by severe kidney dysfunction and anaemia. He was treated with penicillin and gentamycin. Transthoracic echocardiogram revealed a large vegetation at the mitral valve and MALDI Biotyper Massa Spectrometer (Microflex) revealed S. sinensis as the pathogen. The patient refused to receive blood transfusions or surgery. Due to cerebral infarction with haemorrhagic transformation, the patient died 8 days after admission. DISCUSSION: Streptococcus sinensis was described in Hong Kong for the first time and is associated with endocarditis in rheumatic heart disease. To our knowledge, this is the first case reporting a fatal outcome of endocarditis due to this bacterium in the acute phase. In this case, late discovery, disease severity, and under treatment all contributed to the poor outcome. We want to share the knowledge on the existence of this bacteria.

Phylogeographic Distribution of Human and Hare Francisella Tularensis Subsp. Holarctica Strains in the Netherlands and Its Pathology in European Brown Hares (Lepus Europaeus).

Sequence-based typing of Francisella tularensis has led to insights in the evolutionary developments of tularemia. In Europe, two major basal clades of F. tularensis subsp. holarctica exist, with a distinct geographical distribution. Basal clade B.6 is primarily found in Western Europe, while basal clade B.12 occurs predominantly in the central and eastern parts of Europe. There are indications that tularemia is geographically expanding and that strains from the two clades might differ in pathogenicity, with basal clade B.6 strains being potentially more virulent than basal clade B.12. This study provides information on genotypes detected in the Netherlands during 2011-2017. Data are presented for seven autochthonous human cases and for 29 European brown hares (Lepus europaeus) with laboratory confirmed tularemia. Associated disease patterns are described for 25 European brown hares which underwent post-mortem examination. The basal clades B.6 and B.12 are present both in humans and in European brown hares in the Netherlands, with a patchy geographical distribution. For both genotypes the main pathological findings in hares associated with tularemia were severe (sub)acute necrotizing hepatitis and splenitis as well as necrotizing lesions and hemorrhages in several other organs. Pneumonia was significantly more common in the B.6 than in the B.12 cases. In conclusion, the two major basal clades present in different parts in Europe are both present in the Netherlands. In hares found dead, both genotypes were associated with severe acute disease affecting multiple organs. Hepatitis and splenitis were common pathological findings in hares infected with either genotype, but pneumonia occurred significantly more frequently in hares infected with the B.6 genotype compared to hares infected with the B.12 genotype.

Development of cystic periventricular leukomalacia in newborn infants after rotavirus infection.

We describe 5 preterm and 3 term infants who presented with seizures during rotavirus infection within 6 weeks after birth. Six of these infants developed late-onset cystic periventricular leukomalacia. Four of the preterm infants had neurodevelopmental delay, and 4 (near) term infants had normal early outcome.

Cytomegalovirus and Chlamydia pneumoniae as predictors for adverse events and angina pectoris after percutaneous coronary intervention.

BACKGROUND: The aim of our study was to investigate the influence of prior cytomegalovirus (CMV) or Chlamydia pneumoniae (CP) infection on prognosis after percutaneous coronary intervention (PCI). METHODS: Using the enzyme-linked immunosorbent assay technique preprocedural anti-CMV immunoglobulin G and anti-CP immunoglobulin A (CP IgA), immunoglobulin M, and immunoglobulin G antibodies were measured. Repeat anginal complaints and major adverse clinical events (MACE), including PCI, coronary artery bypass grafting, myocardial infarction, and death, were recorded at 8-month follow-up. RESULTS: Six hundred consecutive patients were included after successful PCI. Sixty-four percent of the patients were stented. The mean age was 61.6 years, and 68.9% were male. The rate of seropositivity for CP IgA in patients with MACE as compared with patients without MACE was 50.9% versus 35.4% (P =.0276). In patients with repeat anginal complaints, CP IgA seropositivity was 41.6% versus 34.6% in patients without repeat angina (P =.1057). The negative effect of CP on prognosis was confirmed after calculating the odds ratios for MACE (1.9, 95% CI 1.1-3.3). The rates of seropositivity for anti-CMV immunoglobulin G were not significantly different between both groups, although we found an association between infectious burden and repeat angina pectoris (odds ratio 1.8, 95% CI 1.1-3.0). CONCLUSIONS: We conclude that preprocedural seropositivity of CP IgA is a risk factor for MACE and angina pectoris after PCI. Although no such relation was found for CMV alone, the cumulative infectious burden was also related to these clinical manifestations of restenosis.

Azithromycin inhibits interleukin-6 but not fibrinogen production in hepatocytes infected with cytomegalovirus and chlamydia pneumoniae.

Chlamydia pneumoniae and cytomegalovirus (CMV) have been associated with the development of atherosclerosis. Inflammatory stimuli initiate the biosynthesis of fibrinogen, interleukin (IL)-6 and plasminogen activator inhibitor (PAI)-1 in the liver. Chronic infection may perpetuate the inflammatory status. We hypothesized that infection of human hepatocytes with the intracellular pathogens C pneumoniae and CMV accelerates biosynthesis of fibrinogen, IL-6, and PAI-1 but that this biosynthesis can be reduced with the use of azithromycin. HepG2 human hepatocytes were infected with C pneumoniae and CMV in vitro in the presence of 0, 0.016, 0.125, or 1 microg/mL azithromycin. We measured IL-6, PAI-1, and fibrinogen after 24, 48, 72, and 96 hours. C pneumoniae-infected hepatocytes produce IL-6 (2667 +/- 309 pg/mL vs 137 +/- 120 pg/mL in uninfected cells after 96 hours. Incubation with 0.016 microg/mL azithromycin decreased IL-6 levels to a mean of 1516 +/- 402 pg/mL, and incubation with 0.125 and 1 microg/mL azithromycin decreased IL-6 to 871 +/- 364 and 752 +/- 403 pg/mL, respectively. C pneumoniae-induced IL-6 production was time- and dose-dependent. The interaction of C pneumoniae with azithromycin treatment was significant, indicating an inhibitory effect of azithromycin on C pneumoniae-induced IL-6 production. CMV infection did not lead to IL-6 production by hepatocytes. C pneumoniae and CMV infection did not induce any changes in PAI-1 production. Fibrinogen production was increased by CMV infection after 72 hours (838 +/- 88 ng/mL; P <.01) and after 96 hours by infection with both C pneumoniae and CMV (765 +/- 100 and 846 +/- 123 ng/mL, respectively; P <.05). Azithromycin did not suppress CMV- or C pneumoniae-induced fibrinogen production. Moreover, we could not confirm an antiinflammatory effect of azithromycin in experiments with cross-titrations of azithromycin against either IL-1 or IL-6 (P >.05). Azithromycin reduces C pneumoniae-induced IL-6 production, but not fibrinogen production, by human hepatocytes. This is a result of the antimicrobial properties of azithromycin and not a direct antiinflammatory effect.

Preprocedural serum levels of acute-phase reactants and prognosis after percutaneous coronary intervention.

OBJECTIVE: In this study we evaluate the value of baseline concentrations of acute-phase reactants on prognosis after percutaneous coronary intervention (PCI). METHODS: Blood samples were drawn immediately before PCI to measure baseline concentrations of C-reactive protein (CRP), interleukin-6 (IL-6), lipoprotein(a) (Lp(a)), and fibrinogen. Follow-up data were collected at 8 months. Repeat PCI, CABG, myocardial infarction, and death were recorded as major adverse clinical events (MACE). Furthermore the recurrence of angina pectoris was noted. RESULTS: The study included 600 consecutive patients after a successful PCI. Sixty-four percent of the patients were stented. The mean age was 61.6 years and 68.9% were male. CRP levels were significantly higher in patients who were to have repeat angina as compared with those who were not (P=0.0322). IL-6 levels were not correlated with angina or MACE. Lp(a) and fibrinogen concentrations were both significantly related to MACE (P=0.0337 and P=0.0253, respectively). CONCLUSION: Our study clearly supports the role of inflammation in restenosis after PCI as measured in statistically higher levels of Lp(a) and fibrinogen in patients with MACE and CRP in patients with repeat angina.

Genotyping of clinical methicillin-susceptible Staphylococcus aureus isolates in a Dutch teaching hospital.

Methicillin-susceptible Staphylococcus aureus isolates, recovered from 204 patients in our hospital in a 22-month period, were characterized by pulsed-field gel electrophoresis. Among the multiple S. aureus types six clonal lineages dominated, comprising isolates from 158 patients. Despite the limited genetic variation, cross-transmission was made plausible only sporadically.

Survival of Chlamydia pneumoniae following contact with various surfaces.

OBJECTIVE: In this study, the survival and recovery of Chlamydia pneumoniae (Cp) strains TW-183, AR-39, AR-388 and CWL-029 were measured after inoculation on glass, stainless steel, FormicaR laminate, paper, fabric and human skin. METHODS: Inoculum in throat washes from healthy volunteers was applied to each surface. Samples were taken immediately after inoculum application and at specified intervals thereafter to determine infectivity. RESULTS: Infectious Cp was recovered from glass for up to 4 h, from paper and fabric for up to 3 h, from FormicaR laminate for up to 2 h, from stainless steel for up to 60 min and from human skin for up to 30 min. Drying of the inoculated area had no significant effect on the recovery of infectious Cp. Further experiments demonstrated that infectious Cp could be transferred to hands by touching these contaminated surfaces and could be recovered from these hands for up to 3 min. Addition of albumin, surfactant or phosphatidylcholine had no significant effect on the survival of Cp. CONCLUSIONS: These results suggest that contact with contaminated surfaces may be a potential mode of transmission of Cp.