Evaluation of the VIDAS hepatitis E IgM test in a nonendemic region.

Hepatitis E virus (HEV) causes worldwide more than 20 million new hepatitis cases yearly. These infections can take on fulminant forms or cause severe extrahepatic manifestations, and integration into hepatitis differential diagnosis is recommended. In developed countries, genotypes 3 and 4 are most common, mainly through zoonotic transmission. HEV diagnosis is usually first approached with serological methods, sometimes completed with PCR. In this study, we tested the VIDAS anti-HEV immunoglobulin M assay for its specificity on 181 serum samples from patients infected with selected pathogens possibly causing comparable symptoms or false-positive hepatitis E IgM, such as cytomegalovirus, enterovirus, or other hepatitis viruses. Additionally, serum samples were included from 29 patients who tested positive for autoantibodies in immune-mediated liver disease. We report 8 false-positives (specificity 96%), predominantly for hepatitis A, Epstein-Barr virus, and cytomegalovirus, with numbers that are generally lower than reported for comparable assays. A small sensitivity study showed that its use is limited in immunocompromised patients, for whom molecular detection is recommended as first-line test.

A case of a surgical-site infection with Staphylococcus condimenti.

INTRODUCTION: Coagulase-negative staphylococci (CNS) are considered to have a medium or low pathogenic capacity when compared to S. aureus. Among the more harmless, CNS are those that are used in the food industry, represented by S. carnosus, whose genome has extensively been studied. Its genome was found to contain several genomic sequences that have a virulent function in the pathogenic S. aureus. Even though these genes are probably not virulent in S. carnosus, their presence might indicate a more virulent potential. We report the third clinical case associated with a surgical-site infection with S. condimenti, which belongs to these food industry related CNS. It corresponds to a blood stream infection, secondary to a surgical-site infection. RESULTS: Antibiotic susceptibility testing indicated a resistance to erythromycin and rifampicin, which was partly confirmed by the presence of a macrolide resistance gene by PCR screening for S. aureus virulence factors. Although no other putative virulence factors were detected, this organism managed to cause a severe post-operative wound infection. CONCLUSION: This case shows that CNS that are currently used in the food industry may play a role in human infection. With technologies such as MALDI-TOF, pathogens that are regarded non-pathogenic could be identified more often. Therefore, the risk of different Staphylococcus strains used in the food industry must be better assessed.

Heterozygous FGA p.Asp473Ter (fibrinogen Nieuwegein) presenting as antepartum cerebral thrombosis.

INTRODUCTION: The propositus - a two-week-old boy - was transferred to our university hospital for investigation of increased head circumference and full fontanel. On ultrasound, thrombosis of the right internal cerebral vein and intraventricular haemorrhage was diagnosed, confirmed by MRI. Family history revealed a bleeding history in the mother. A haemostatic work-up in both mother and child was performed in order to rule out congenital coagulopathy. AIM: We document a clinical case of congenital dysfibrinogenemia, caused by heterozygosity for the mutation FGA p.Asp473Ter, previously reported as fibrinogen Nieuwegein in homozygosity in an asymptomatic patient. METHODS: Fibrinogen activity in plasma was determined by functional Clauss assay, and immunological fibrinogen concentration by nephelometry. In vitro fibrin clot investigations and genetic analysis of the fibrinogen gene were performed. Complete haemostatic work-up was done by conventional methods. RESULTS AND DISCUSSION: After full laboratory work-up, dysfibrinogenemia was diagnosed, based on fibrinogen activity:antigen ratio, thrombin time, and reptilase time. Molecular analysis showed a frameshift mutation in exon 5 of FGA: c.1415_1416 insC, leading to a termination codon immediately after the insertion (CCT GAT>CCC TGA) and resulting in a truncated αC-domain. This mutation has been reported earlier as fibrinogen Nieuwegein. Further in vitro investigations revealed an abnormally tight clot structure, prolonged clot lysis time and affected polymerization, suggesting a thrombotic phenotype. Cerebral imaging revealed thrombosis, most likely developed in the antenatal period, leading to extensive intraventricular haemorrhage and posthaemorrhagic ventricular dilatation. CONCLUSION: We highlight the combined thrombotic and haemorrhagic phenotype linked to heterozygous fibrinogen Nieuwegein, in contrast to the previously reported asymptomatic homozygous case.