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Biomedical subjects

C M Vandenbroucke-Grauls

Publications and source records attributed to C M Vandenbroucke-Grauls.

At least 19 recordsLinked to original sources

Herpes simplex virus type 1 and respiratory disease in critically-ill patients: Real pathogen or innocent bystander?

Herpes simplex virus type 1 (HSV-1) has been associated with pulmonary disease, mostly in severely immunocompromised patients. After reactivation and shedding in the oropharynx, the virus may reach the lower respiratory tract by aspiration or by contiguous spread. HSV-1 can be detected in clinical specimens by virus culture or quantitatively by nucleic acid amplification techniques. With these techniques, HSV-1 is often detected in the respiratory secretions of critically-ill patients. However, a clear diagnosis of HSV-1 pneumonia is difficult to establish because clinical criteria, radiological features and laboratory findings all lack specificity. Lower respiratory tract HSV-1 infections have not been associated with specific risk-factors. There is also an absence of consistent data concerning the effect of antiviral treatment on the outcome of critically-ill patients. Further studies are needed to better define the pathogenic role of HSV-1 in the lower respiratory tract of these patients, to improve the diagnosis, and, especially, to assess the need for antiviral treatment in the individual patient.

Antiviral Agents↗

Widely distributed and predominant CTX-M extended-spectrum beta-lactamases in Amsterdam, The Netherlands.

Three hundred sixty Enterobacteriaceae and nonfermenting gram-negative bacilli, isolated during one week in May 2004 at five hospitals in Amsterdam, The Netherlands, were evaluated for the presence of extended-spectrum beta-lactamases (ESBLs). A prevalence of 7.8% was found, in contrast to the 1% observed in 1997. CTX-M ESBLs dominated, and four types were identified in 18 isolates.

Anti-Bacterial Agents↗

[Vancomycin resistant enterococci in the Netherlands].

Enterococci (Enterococcus faecalis and Enterococcus faecium) are relatively avirulent enteric bacteria that usually only cause infections in immunocompromised patients. Antimicrobial treatment, however, is hampered as enterococci are intrinsically resistant to many antibiotics. For years, vancomycin was considered the last available antibiotic. Plasmid-mediated resistance against vancomycin among enterococci was first described in the nineteen-eighties and since then incidences of infection caused by vancomycin-resistant enterococci (VRE) have increased dramatically, especially in the United States. In 2000, three outbreaks of VRE occurred in hospitals in the Netherlands and a set of infection-control measures was proposed to limit further transmission. These measures were based on the simultaneous isolation of VRE from multiple patients. All three outbreaks were controlled by these measures and no new outbreaks in Dutch hospitals have been reported since then. Epidemiological studies have shown that hospital outbreaks on three continents were caused by a subpopulation of E. faecium, which is characterized by the presence of a potential virulence gene (variant esp) and resistance to amoxicillin. This 'hospital strain' of E. faecium has probably been prevalent within hospital settings for some time, but only became clinically relevant when it had acquired vancomycin-resistance. Current advice is to implement the set of infection control measures formulated in 2000, only in those patients colonized by amoxicillin-resistant VRE. The potential dangers of VRE were recently underlined by the proven transmission of the vancomycin-resistance gene from VRE to methicillin-resistant Staphylococcus aureus (MRSA) in two patients in the United States. It is in the interest of the patients that prevalence of VRE and MRSA in Dutch hospitals should be kept as low as possible.

Disease Outbreaks↗

[Enterobacter cloacae epidemic on a neonatal intensive care unit due to the use of contaminated thermometers].

From December 1999 to March 2000 a nosocomial outbreak of multiresistant Enterobacter cloacae occurred in the neonatal intensive care unit (NICU) at the VU Medical Center, Amsterdam, the Netherlands. Twenty-six patients were infected or colonized with this strain resistant to third generation cephalosporins and with decreased sensitivity for aminoglycosides. Three neonates experienced sepsis with E. cloacae with serious clinical symptoms and two of them died. Comparison of the Enterobacter isolates by amplified-fragment length polymorphism indicated that this outbreak was caused by the spread of a single strain. Infection control precautions were initiated in order to stop further spread; barrier precautions, enforcement of hand disinfection and cohorting of colonized patients. A multidisciplinary crisis team coordinated these infection control precautions and informed all persons involved. Analysis of antibiotic usage in 1999 showed an increase in the use of third generation cephalosporins from November onwards. Due to the resistance pattern of the epidemic strain the use of third generation cephalosporins was discontinued in February 2000. At the end of February the NICU was temporarily closed. The epidemic strain of E. cloacae was isolated from one digital rectal thermometer. Patient use of thermometers and disposable coverings for rectal thermometers were introduced to eliminate this possible means of spread. No spread of multiresistant E. cloacae was found following the introduction of these interventions. Once all the neonates had been transferred, the NICU was disinfected and reopened in March.

Cephalosporin Resistance↗

[Periodontitis: a hidden chronic infection].

Periodontitis is a chronic inflammatory disease of the tooth supporting tissues which has a prevalence of 35% in the adult population. Risk factors are dental plaque, calculus, smoking, diabetes mellitus, stress and genetic traits. In parallel with chronic intestinal inflammatory diseases and stomach cancer, gene polymorphisms in the interleukin-I gene family are associated with severity of periodontitis. Periodontitis is usually painless. Symptoms of the disease are bleeding, redness and swelling of the gums, suppuration and migration of teeth. Halitosis may be present. Treatment of periodontitis involves supra- and subgingival mechanical debridement, oral hygiene instruction and surgical elimination of residual deepened and bleeding pockets on indication. Microbiological testing can be used to select patients who may benefit from additional systemic antimicrobial therapy. Periodontal lesions may act as a portal of entry for dissemination of periodontal bacteria into the blood stream, which may result in extraoral infections. For this reason it is recommended to include diagnosis of periodontitis in focal examination. Associations have been documented between periodontitis and cardiovascular diseases, arthritis and premature low birth weight infants.

Adult↗

Variant esp gene as a marker of a distinct genetic lineage of vancomycin-resistant Enterococcus faecium spreading in hospitals.

In the USA, vancomycin-resistant Enterococcus faecium (VREF) is endemic in hospitals, despite lack of carriage among healthy individuals. In Europe, however, hospital outbreaks are rare, but VREF carriage among healthy individuals and livestock is common. We used amplified fragment-length polymorphism analysis to genotype 120 VREF isolates associated with hospital outbreaks and 45 non-epidemic isolates from the USA, Europe, and Australia. We also looked for the esp virulence gene in these isolates and in 98 VREF from animals. A specific E. faecium subpopulation genetically distinct from non-epidemic VREF isolates was found to be the cause of the hospital epidemics in all three continents. This subpopulation contained a variant of the esp gene that was absent in all non-epidemic and animal isolates. Identification of the variant esp gene will be important in guiding infection-control strategies, and the Esp protein could be a new target for antibacterial therapy.

Bacterial Proteins↗

The role of Helicobacter pylori virulence factors in interleukin production by monocytic cells.

Helicobacter pylori infection results in chronic gastritis, which is initiated by the release of cytokines like interleukin (IL)-12 and IL-8 from mononuclear cells, and IL-8 from gastric epithelial cells. The severity of gastritis is influenced both by host factors and by bacterial factors such as the Cag proteins and the vacuolating cytotoxin VacA. Amounts of IL-12 and IL-8 produced by monocytic THP-1 cells differed considerably between the eight H. pylori isolates tested, but in contrast to H. pylori-induced IL-8 production by gastric epithelial cells, did not correlate to the Cag and VacA types of the strains. Apparently, in addition to Cag and VacA, other bacterial factors determine the extent in which H. pylori induced IL production in monocytes.

Antigens, Bacterial↗

Identification of environmental stress-regulated genes in Helicobacter pylori by a lacZ reporter gene fusion system.

BACKGROUND: Helicobacter pylori persists in the human stomach for decades. This requires an efficient adaptation of H. pylori to the gastric niche and involves the regulation of bacterial genes in response to environmental stress. Efficient molecular tools to identify regulated H. pylori genes are scarce, therefore we developed a genomic lacZ reporter gene fusion system in H. pylori to screen for stress-regulated genes. MATERIALS AND METHODS: The integration vector pBW was constructed and used to generate random genomic lacZ fusions in H. pylori. Two-hundred-and-fifty H. pylori transformants were selected from this library, replica-plated and screened for differential lacZ expression after exposure to two environmental stress conditions: increased temperature (42 degrees C), and iron-limitation. RESULTS: From a library of H. pylori transformants with random genomic transcriptional lacZ fusions, two stress-regulated H. pylori loci were identified. The transcription of a gene of unknown function (designated hsp12) was increased by incubation at 42 degrees C. The transcription of a locus, consisting of the three fumarate reductase subunit genes (frdCAB) and the HP0190 gene from H. pylori strain 26695, was decreased under iron-limitation. CONCLUSIONS: This is the first time that a genomic transcriptional lacZ reporter gene H. pylori library has been used as a tool for the fast and efficient identification of environmental stress-regulated H. pylori genes.

Bacterial Proteins↗

H(+),K(+)-atpase (proton pump) is the target autoantigen of Th1-type cytotoxic T cells in autoimmune gastritis.

BACKGROUND & AIMS: The proton pump H(+),K(+)-adenosine triphosphatase (H(+),K(+)-ATPase) of parietal cells is the major humoral autoantigen in both human and experimental autoimmune gastritis (AIG) characterized by an inflammatory infiltrate in the gastric mucosa and loss of parietal cells. The aim of this study was to detect H(+),K(+)-ATPase-specific T cells in the gastric mucosa of patients with AIG and to define their functional properties. METHODS: In vivo-activated T cells from the infiltrates of the gastric mucosa of 5 patients with AIG were isolated and cloned. The ability of gastric T-cell clones to proliferate and to produce cytokines in response to H(+),K(+)-ATPase, as well as their expression of B-cell help, perforin-mediated cytotoxicity, and Fas-Fas ligand-mediated apoptosis in target cells, were assessed. RESULTS: A proportion (25%) of the CD4(+) clones from the gastric corpus of AIG patients proliferated in response to porcine H(+),K(+)-ATPase. Most of these clones (88%) showed a Th1 profile, whereas a few secreted both Th1 and Th2 cytokines. Virtually all of the H(+),K(+)-ATPase-specific clones produced tumor necrosis factor alpha and provided substantial help for B-cell immunoglobulin production, and most of them expressed perforin-mediated cytotoxicity against antigen-presenting cells and induced Fas-Fas ligand-mediated apoptosis in target cells. CONCLUSIONS: Activation of proton pump-specific Th1 cytotoxic/proapoptotic T cells in the gastric mucosa can represent an effector mechanism for the target cell destruction in AIG.

Adult↗

The bacterial flora in inflammatory bowel disease: current insights in pathogenesis and the influence of antibiotics and probiotics.

The pathogenesis of inflammatory bowel disease (IBD) remains unknown, although in recent years more data have become available. The contribution of genetic and environmental factors is evident, and the luminal bacterial flora plays a major role in the initiation and perpetuation of chronic IBD. Animal models of IBD have shown that colitis does not occur in a germ-free environment. In human IBD, inflammation is present in parts of the gut containing the highest bacterial concentrations. Moreover, the terminal ileum, caecum and rectum are areas of relative stasis, providing prolonged mucosal contact with luminal contents. Enhanced mucosal permeability may play a pivotal role in maintaining a chronic inflammatory state, due to a genetic predisposition or as a result of direct contact with bacteria or their products. A detective epithelial barrier may cause a loss of tolerance to the normal enteric flora. Furthermore, an increased mucosal absorption of viable bacteria and bacterial products is found in IBD. Serum and secreted antibodies are increased and mucosal T-lymphocytes that recognize luminal bacteria are present. However, there is evidence that the immune system reacts over aggressively towards the normal luminal flora rather than the flora being altered in IBD. Several approaches have been used in attempts to discover a specific microbial agent in the cause of IBD. These include demonstration of the presence of organisms or specific antigens in affected tissues, culture of microbes firm the affected tissues, demonstration of serological responses to several agents, and localization and detection of individual pathogen-specific nucleic acid sequences in affected tissue by in situ hybridization and polymerase chain reaction. So far, no specific micro-organism has been directly associated with the pathogenesis of IBD. Analysis of the luminal enteric flora, however, has revealed differences in the composition of this flora compared to healthy controls. In Crohn disease, concentrations of Bacteroides, Eubacteria and Peptostreptococcus are increased, whereas Bifidobacteria numbers are significantly reduced. Furthermore, in ulcerative colitis, concentrations of facultative anaerobic bacteria are increased. The arrival of new molecular techniques qualifying and quantifying the complex intestinal flora has induced a revival of interest in this microflora. Therapeutic approaches geared towards changing the environment at the mucosal border have been attempted by the use of elemental diets, total parenteral nutrition, surgical diversion of the faecal stream and antibiotics. Over the past few years, the use of probiotics in IBD and other intestinal disorders has gained attention. Strengthened by promising experimental data and commercial interests, research in this field is rapidly expanding. Manipulation of the colonic bacteria with antibiotic drugs and probiotic agents may prove to be more effective and better tolerated than immunosuppressants in the future.

Anti-Bacterial Agents↗

Antibiotic resistance is a major risk factor for epidemic behavior of Acinetobacter baumannii.

OBJECTIVE: To study the presence of bacterial factors in clinical isolates of Acinetobacter species in order to identify markers of epidemic potential. DESIGN: Case-control study. METHODS: Forty-six isolates of Acinetobacter species, including 23 epidemic and 23 sporadic strains from different outbreaks in nine European countries, were compared for the presence of the following factors: hemagglutination, presence of capsules and fimbriae, binding to salivary mucins, resistance to drying, and antibiogram typing. Genotyping of all strains was performed by amplified fragment-length polymorphism (AFLP). RESULTS: All outbreak strains except two (91%) were identified as Acinetobacter baumannii. Binding to salivary mucins and resistance to antibiotics were significantly associated with epidemic behavior. Antibiogram typing showed clustering of predominantly A baumannii strains within one group, and these strains were significantly more resistant to antibiotics than sporadic strains. AFLP genotyping revealed a great heterogeneity among the different European Acinetobacter strains. Cluster analysis of AFLP fingerprints showed several small clusters of different A baumannii outbreak strains. AFLP genotyping could not identify a common epidemic marker within the strains studied. CONCLUSIONS: Antibiogram typing can be used in routine clinical laboratories as a screening method to recognize potentially epidemic A baumannii strains. Several other factors were found, both in different outbreaks as well as in sporadic Acinetobacter isolates. These characteristics were unable to predict epidemic behavior and therefore cannot be used as discriminative epidemic markers. AFLP genotyping demonstrated no common clonal origin of European epidemic A baumannii strains. This indicates that any clinical A baumannii isolate with resistance to multiple antibiotics can be a potential nosocomial outbreak strain.

Acinetobacter↗

Nickel-responsive induction of urease expression in Helicobacter pylori is mediated at the transcriptional level.

The nickel-containing enzyme urease is an essential colonization factor of the gastric pathogen Helicobacter pylori, as it allows the bacterium to survive the acidic conditions in the gastric mucosa. Although urease can represents up to 10% of the total protein content of H. pylori, expression of urease genes is thought to be constitutive. Here it is demonstrated that H. pylori regulates the expression and activity of its urease enzyme as a function of the availability of the cofactor nickel. Supplementation of brucella growth medium with 1 or 100 microM NiCl(2) resulted in up to 3.5-fold-increased expression of the urease subunit proteins UreA and UreB and up to 12-fold-increased urease enzyme activity. The induction was specific for nickel, since the addition of cadmium, cobalt, copper, iron, manganese, or zinc did not affect the expression of urease. Both Northern hybridization studies and a transcriptional ureA::lacZ fusion demonstrated that the observed nickel-responsive regulation of urease is mediated at the transcriptional level. Mutation of the HP1027 gene, encoding the ferric uptake regulator (Fur), did not affect the expression of urease in unsupplemented medium but reduced the nickel induction of urease expression to only twofold. This indicates that Fur is involved in the modulation of urease expression in response to nickel. These data demonstrate nickel-responsive regulation of H. pylori urease, a phenomenon likely to be of importance during the colonization and persistence of H. pylori in the gastric mucosa.

Bacterial Proteins↗

Identification of epidemic strains of Acinetobacter baumannii by integrase gene PCR.

Forty-eight clinical Acinetobacter isolates with different epidemic behavior were investigated for the presence of integrons and plasmids and for antibiotic susceptibility. Integrons were demonstrated in 50% of the strains by an integrase gene PCR. Epidemic strains of Acinetobacter baumannii were found to contain significantly more integrons than nonepidemic strains. Also, the presence of integrons was significantly correlated with simultaneous resistance to several antibiotics. Plasmids were detected in 42% of the strains. However, there was no significant correlation between the numbers of plasmids and integrons in Acinetobacter species strains, no significant difference in the number of plasmids between epidemic and nonepidemic A. baumannii strains, and no significant correlation between the presence of plasmids and antibiotic resistance. Hence, it is likely that integrons play an important role in antibiotic resistance and thereby in the epidemic behavior of A. baumannii. Because the integrase gene PCR identified almost three-quarters of the epidemic A. baumannii isolates (17 of 23), this seems to be a rapid and simple technique for the routine screening and identification of clinical A. baumannii isolates with epidemic potential.

Acinetobacter↗

[What is to be done with vancomycin-resistant enterococcal infections?].

Recently, three epidemics in Dutch hospitals were caused by vancomycin-resistant enterococci (VRE). Although the number of infections was small, spread of colonization was extensive and many infection control measures were necessary to prevent further spread. VRE are relatively avirulent bacteria. However, few, if any, antibiotics are available for treatment of infections caused by VRE and the genetic code for resistance may be transferable to other, more virulent, bacteria, such as methicillin-resistant Staphylococcus aureus (MRSA). Although colonization and infection with MRSA have become endemic in many surrounding countries, such a situation has been prevented in the Netherlands by employing an aggressive 'search and destroy' policy. Although many questions regarding the optimal approach of VRE remain unanswered, a similar policy as employed for MRSA will not be possible. In contrast to MRSA, colonization with VRE occurs in the open population, no populations with increased risk for colonization appear to be definable and colonization cannot be eradicated. Based on common sense, a differentiated approach seems indicated in which extensive infection control measures should only be implemented when spread of a single genotype has been demonstrated. A reference laboratory should be created for uniform genotyping.

Anti-Bacterial Agents↗

Identification of loci essential for the growth of Helicobacter pylori under acidic conditions.

To persist in the hostile acidic environment of the stomach, Helicobacter pylori must survive acid shock and grow at acidic pH. Of a library of 1250 random mutants screened for isolates unable to grow at low pH, 10 mutants were detected that were unable to grow at pH 4.8. However, all 10 mutants were resistant to acid shock. Four mutants had an insertion in genes of unknown function. One mutant was affected in lepA, an orthologue of a membrane GTPase. Three mutants were disrupted in loci involved in the transport of H(+) ions or other cations (FRaseI, czcA, and aldo-keto reductase). Two mutants were affected in loci that contribute to acid resistance in other microorganisms (uvrA and atpF'). Thus, at least 10 loci not related to urease are essential for the growth of H. pylori under acidic conditions and should be critical for lifelong infection by this pathogen.

Chromosome Mapping↗