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L Dijkshoorn

Publications and source records attributed to L Dijkshoorn.

At least 19 recordsLinked to original sources

Epidemiology of multiple Acinetobacter outbreaks in The Netherlands during the period 1999-2001.

An increase in the number of outbreaks of Acinetobacter infection was notified in The Netherlands during 1999-2001. The present study compared the outbreaks at the species and strain levels, and analysed the epidemiology and control measures at the different locations. For each institute, three representative isolates from three patients were identified to the species and strain levels by genotyping methods. A questionnaire investigated the impact of the outbreak, the control measures that were taken, and the possible effects of the measures. Seven outbreaks were associated with Acinetobacter baumannii (three outbreaks with a strain designated strain A, two outbreaks with a strain designated strain B, and one outbreak each with strains designated C and D). An additional outbreak was caused by genomic species 13TU, which is related closely to A. baumannii. Strains B and D were identified as European clones III and II, respectively. Except for two hospitals with outbreaks caused by strain A, there was no known epidemiological link between the participating hospitals. In all hospitals the outbreak occurred on one or several intensive care units, and spread to other departments was noted in two hospitals. The number of patients affected ranged from six to 66 over a period of 2-22 months. In most outbreaks, patients were the likely reservoir from which spread occurred. In all hospitals, a large panel of measures was required to bring the outbreak to an end. Extensive environmental sampling yielded numerous positive samples in most but not all hospitals.

Acinetobacter↗

Genotypic diversity and antibiotic susceptibility of Acinetobacter baumannii isolates in a Bulgarian hospital.

A set of 18 Acinetobacter baumannii isolates, collected prospectively in a Bulgarian hospital during episodes of increased A. baumannii occurrence during 2000-2002, was investigated for genotypic diversity and antibiotic susceptibility. Four genotypes were identified by amplified fragment length polymorphism genomic fingerprinting, one of which (type 1) accounted for 13 isolates, indicating that a specific strain was predominant. The single isolate allocated to type 2 was identified to European clone I. All isolates were resistant to multiple antibiotics, but most retained susceptibility to tobramycin and colistin, and all except one were susceptible to imipenem.

Acinetobacter Infections↗

High resolution DNA fingerprinting by AFLP to study the genetic variation among Oesophagostomum bifurcum (Nematoda) from human and non-human primates from Ghana.

An AFLP approach was established to investigate genetic diversity within Oesophagostomum bifurcum (order Strongylida) from human and non-human primates. Evaluation of different combinations of restriction enzymes (n = 8) and primers (n = 29) demonstrated that the use of HindIII/BglII digested templates and primers with the selective nucleotides + AG/ +AC, respectively, was the most effective for the analysis of O. bifurcum DNA. A total of 63 O. bifurcum adults from human, Patas monkey, Mona monkey and Olive baboon hosts from different geographical regions in Ghana were subjected to analysis using this method. Cluster analysis revealed 4 genetically distinct groups, namely O. bifurcum from the Patas monkey (I), from the Mona monkey (II), from humans (III) and from the Olive baboon (IV). These findings were concordant with those achieved previously using RAPD analysis and supports population genetic substructuring within O. bifurcum according to host species. The results demonstrated the effectiveness of the present AFLP method for establishing genetic variation within O. bifurcum, and indicates its applicability to other parasitic nematodes of human and/or veterinary health importance.

Animals↗

Prevalence of Acinetobacter baumannii and other Acinetobacter spp. in faecal samples from non-hospitalised individuals.

In total, 226 individuals from the community were investigated for faecal carriage of Acinetobacter spp. by broth enrichment culture, followed by growth on blood agar and/or Leeds Acinetobacter Medium (LAM). Acinetobacter baumannii was isolated on both LAM and blood agar from one of 100 specimens in the UK and one of 126 specimens in The Netherlands. The predominant species were Acinetobactor johnsonii and genomic sp. 11, which were cultured from 22 and five specimens, respectively. A. baumannii did not seem to be widespread in the faecal flora of individuals in the community.

Acinetobacter Infections↗

Outbreak of nosocomial meningitis caused by Acinetobacter baumannii in neurosurgical patients.

An outbreak of nosocomial meningitis caused by Acinetobacter baumannii, which developed postoperatively in seven neurosurgical patients is described. The clinical isolates of A. baumannii were typed by biochemical profiles and antibiogram patterns, and by random amplified polymorphic DNA polymerase chain reaction (RAPD-PCR) and amplified fragment length polymorphism (AFLP) fingerprinting. The implicated strain was multi-drug resistant, however, susceptibility to imipenem and netilmicin was detected. An extensive search for the environmental source of the epidemic strain was carried out. Two of several isolates from hospital environment, corresponded to the A. baumannii outbreak strain, one being cultured from the suctioning equipment used in the care of these patients. The introduction of multiresistant epidemic A. baumannii into a neurosurgical unit is a severe risk factor for patients undergoing neurosurgical procedures. Genotypic typing methods are important for definitive identification of these strains in patients and their environment.

Acinetobacter Infections↗

A prevalent, multiresistant clone of Acinetobacter baumannii in Southeast England.

A multiresistant clone of Acinetobacter baumannii was identified in 24 hospitals in the UK, predominantly in the London area, over a period of three years. Isolates were characterized by distinctive ApaI macrorestriction profiles, as resolved by pulsed-field gel electrophoresis (PFGE), which all clustered within 80% similarity using a 1% band position tolerance setting. The first isolates identified were received by the reference laboratories in April 2000, and by June 2003, a total of 375 isolates with similar PFGE profiles from 310 patients from 24 hospitals had been received. The isolates originated mainly from sputum and wound specimens, with the majority from patients in intensive care units. Amplified fragment length polymorphism analysis of a subset of isolates showed that they clustered closely, supporting the PFGE results. All the isolates tested were highly resistant to ampicillin, piperacillin, piperacillin/tazobactam, ceftazidime, cefotaxime, gentamicin and ciprofloxacin, and most isolates were carbapenem resistant. Amikacin sensitivity varied from susceptible [minimum inhibitory concentration (MIC) 256 mg/L).

Acinetobacter Infections↗

Persistent Acinetobacter baumannii? Look inside your medical equipment.

Two outbreaks of multidrug-resistant Acinetobacter baumannii occurred in our hospital. The outbreak strains were eventually isolated from respiratory ventilators, an apparatus used to cool or warm patients, and four continuous veno-venous hemofiltration machines. Removing dust from the machines and replacing all dust filters brought the outbreaks to an end.

Acinetobacter Infections↗

Outbreak of a susceptible strain of Acinetobacter species 13 (sensu Tjernberg and Ursing) in an adult neurosurgical intensive care unit.

Between December 1999 and June 2000, an outbreak caused by Acinetobacter emerged on the neurosurgical intensive care unit of our hospital. It was shown using automated ribotyping using Eco RI and pulsed-field gel electrophoresis that the outbreak was caused by spread of a single strain, which was identified by ribotyping and amplified ribosomal DNA restriction analysis as Acinetobacter DNA group 13TU (sensu Tjernberg and Ursing). The outbreak strain, which showed no antibiotic resistance, was identified in 23 patients, five of whom developed an infection. The organism was also isolated from various environmental sites. Cross-transmission among patients continued despite contact isolation of colonized patients and reinforcement of basic disinfection procedures. Eventually, after implementation of additional stringent measures such as cohorting of positive patients and daily disinfection of the floor, the outbreak was brought under control. This study demonstrates that apart from Acinetobacter baumanii, Acinetobacter 13TU strains, even when they are fully susceptible, may cause outbreaks that are difficult to control. Correct identification to the species level of Acinetobacter by genotypic methods is necessary to get insight in the importance of the different Acinetobacter genomic species in hospital epidemiology.

Acinetobacter↗

Acinetobacter ursingii sp. nov. and Acinetobacter schindleri sp. nov., isolated from human clinical specimens.

The taxonomic status of two recently described phenetically distinctive groups within the genus Acinetobacter, designated phenon 1 and phenon 2, was investigated further. The study collection included 51 strains, mainly of clinical origin, from different European countries with properties of either phenon 1 (29 strains) or phenon 2 (22 strains). DNA-DNA hybridization studies and DNA polymorphism analysis by AFLP revealed that these phenons represented two new genomic species. Furthermore, 16S rRNA gene sequence analysis of three representatives of each phenon showed that they formed two distinct lineages within the genus Acinetobacter. The two phenons could be distinguished from each other and from all hitherto-described Acinetobacter (genomic) species by specific phenotypic features and amplified rDNA restriction analysis patterns. The names Acinetobacter ursingii sp. nov. (type strain LUH 3792T = NIPH 137T = LMG 19575T = CNCTC 6735T) and Acinetobacter schindleri sp. nov. (type strain LUH 5832T = NIPH 1034T = LMG 19576T = CNCTC 6736T) are proposed for phenon 1 and phenon 2, respectively. Clinical and epidemiological data indicate that A. ursingii has the capacity to cause bloodstream infections in hospitalized patients.

Acinetobacter↗

O-antigen diversity among Acinetobacter baumannii strains from the Czech Republic and Northwestern Europe, as determined by lipopolysaccharide-specific monoclonal antibodies.

O-antigen-specific monoclonal antibodies (MAbs) are currently being generated to develop an O-serotyping scheme for the genus Acinetobacter and to provide potent tools to study the diversity of O-antigens among Acinetobacter strains. In this report, Acinetobacter baumannii strains from the Czech Republic and from two clonal groups identified in Northwestern Europe (termed clones I and II) were investigated for their reactivity with a panel of O-antigen-specific MAbs generated against Acinetobacter strains from various species. The bacteria were characterized for their ribotype, biotype, and antibiotic susceptibility and the presence of the 8.7-kb plasmid pAN1. By using the combination of these typing profiles, the Czech strains could be classified into four previously defined groups (A. Nemec, L. Janda, O. Melter, and L. Dijkshoorn, J. Med. Microbiol. 48:287-296, 1999): two relatively homogeneous groups of multiresistant strains (termed groups A and B), a heterogeneous group of other multiresistant strains, and a group of susceptible strains. O-antigen reactivity was observed primarily with MAbs generated against Acinetobacter calcoaceticus and Acinetobacter baumannii strains. A comparison of reaction patterns confirmed the previously hypothesized clonal relationship between group A and clone I strains, which are also similar in other properties. The results show that there is limited O-antigen variability among strains with similar geno- and phenotypic characteristics and are suggestive of a high prevalence of certain A. baumannii serotypes in the clinical environment. It is also shown that O-antigen-specific MAbs are useful for the follow-up of strains causing outbreaks in hospitals.

Acinetobacter↗

Epidemiologic typing of Escherichia coli using RAPD analysis, ribotyping and serotyping.

OBJECTIVE: To compare random amplified polymorphic DNA (RAPD) analysis and ribotyping with serotyping for epidemiologic typing of Escherichia coli. METHODS: Thirty-two epidemiologically unrelated strains, nine cerebrospinal fluid isolates with the O7K1 serotype from nine patients, and nine sets of epidemiologically related E. coli isolates from nine patients were typed by RAPD analysis, ribotyping and serotyping. RESULTS: Among the 32 epidemiologically unrelated E. coli isolates, 29 types were distinguished by RAPD analysis, 25 by ribotyping and 27 by serotyping. Indistinguishable patterns were obtained by RAPD analysis and ribotyping within the collection of nine cerebrospinal fluid isolates. For the epidemiologically related isolates, intrapatient variation was only found by RAPD analysis among the isolates of one set and by ribotyping among the isolates of two sets. No interpatient variation was observed between three sets of isolates. With serotyping, the epidemiologically related isolates yielded similar typing relationships to those obtained by RAPD analysis and ribotyping. CONCLUSIONS: RAPD analysis had the highest discriminatory capacity for typing E. coli isolates. RAPD analysis, ribotyping and serotyping can all be used for assessment of strain relationships.

Adult↗

Distribution and in-vitro transfer of tetracycline resistance determinants in clinical and aquatic Acinetobacter strains.

Following characterisation by phenotypic tests and amplified ribosomal DNA restriction analysis (ARDRA), 50 tetracycline-resistant (MIC > or = 16 mg/L) Acinetobacter strains from clinical (n = 35) and aquatic (n = 15) samples were analysed by PCR for tetracycline resistance (Tet) determinants of classes A-E. All the clinical strains were A. baumannii; most (33 of 35) had Tet A (n = 16) or B (n = 17) determinants, and only two did not yield amplicons with primers for any of the five tetracycline resistance determinants. The aquatic strains belonged to genomic species other than A. baumannii, and most (12 of 15) did not contain determinants Tet A-E. Strains negative for Tet A-E were also negative for Tet G and M; further analysis of two aquatic strains with specific primers for Tet O and Tet Y and degenerate primers for Tet M-S-O-P(B)-Q also showed negative results. Transfer of tetracycline resistance was tested for 20 strains with three aquatic Acinetobacter strains and Escherichia coli K-12 as recipients. Transfer of resistance was demonstrated between aquatic strains from distinct ecological niches, but not from clinical to aquatic strains, nor from any Acinetobacter strain to E. coli K-12. Most transconjugants acquired multiple relatively small plasmids (<36 kb). Transfer did not occur when DNA from the donor strains was added to the recipient cultures and was not affected by deoxyribonuclease I, suggesting a conjugative mechanism. It is concluded that Tet A and B are widespread among tetracycline-resistant A. baumannii strains of clinical origin, but unknown genetic determinants are responsible for most tetracycline resistance among aquatic Acinetobacter spp. These differences, together with the inability of clinical strains to transfer tetracycline resistance in vitro to aquatic strains, contra-indicate any important flow of tetracycline resistance genes between clinical and aquatic acinetobacter populations.

Acinetobacter↗

Strain, clone and species: comments on three basic concepts of bacteriology.

Different aspects of the terms strain, clone and species are discussed. The term strain is commonly used to denote a pure culture - here called 'the strain in the taxonomic sense' - but does also refer to a natural concept closely related to the clone. The term clone on the other hand is used both in a general and in a more restricted sense, the latter indicating a low degree of genetic exchange. The important distinction between the definition of a species and the criteria for a species is emphasised and the main kinds of criteria are considered.

Animals↗

Recognition of two novel phenons of the genus Acinetobacter among non-glucose-acidifying isolates from human specimens.

Genomic species diversity among 147 Acinetobacter clinical isolates not belonging to the A. calcoaceticus- A. baumannii (ACB) complex was investigated by phenotypic and genotypic identification methods. The isolates were obtained between 1991 and 1999 from numerous diagnostic laboratories in the Czech Republic and were studied by numerical probabilistic identification using two biochemical frequency matrices and amplified rDNA restriction analysis (ARDRA). Their final identification was derived from the combined phenotypic and ARDRA results. In total, 102 isolates were unambiguously (n = 89) or presumptively (n = 13) identified as A. lwoffii (n = 63), genomic species 13BJ/14TU (n = 9), A. johnsonii (n = 7), A. haemolyticus (n = 6), A. junii (n = 5), and other genomic species (n < 5 isolates each). Forty-five isolates could not be identified as belonging to any described species. Among the unidentified isolates two large groups of non-glucose-acidifying, nonhemolytic, and non-gelatinase-producing isolates were distinguished. These groups, designated phenon 1 (n = 17) and phenon 2 (n = 15), had distinctive phenotypic features and novel ARDRA profiles, which suggests that they represent hitherto undescribed Acinetobacter species. Phenon 2 included mainly clinically insignificant isolates from outpatients, while phenon 1 comprised clinically relevant isolates mostly from the blood of hospitalized patients, and its precise taxonomic definition may therefore be of medical importance. Overall, the development of practical methods for identification required for the elucidation of the biological significance of the (genomic) species within the genus Acinetobacter remains a challenging task.

Acinetobacter↗

Performance of phenotypic and genotypic methods to determine the clinical relevance of serial blood isolates of staphylococcus epidermidis in patients with septicemia.

Five typing methods, including biotyping (API ID32; BioMérieux, Marcy l'Etoile, France), quantitative antibiogram typing based on actual zone sizes, plasmid typing, randomly amplified polymorphic DNA (RAPD) analysis (with primer M13 and primer set ERIC-2-1026), and pulsed-field gel electrophoresis (PFGE), were compared with a previously performed method of DNA fingerprinting by AFLP (amplified fragment length polymorphism analysis) for their performance in the typing of blood isolates of Staphylococcus epidermidis. Sixteen epidemiologically unrelated strains and 11 sets of four blood culture isolates from 11 patients with septicemia were used. The stabilities and reproducibilities of the patterns, the discriminatory capacities of the methods, and the ability to apply the methods to blood culture isolates were used as performance criteria. All strains tested were typeable by each method, and the patterns were stable and reproducible. The numbers of different types within the collection of 16 epidemiologically different isolates were 5 by biotyping, 14 by antibiogram typing, 4 by plasmid typing, 9 by the RAPD assay (combination of results with primer M13 and primer set ERIC-2-1026), and 16 by PFGE. Within the 11 sets of four blood culture isolates the types found by quantitative antibiogram typing, plasmid typing, and PFGE were unique for each set, whereas by biotyping and RAPD analysis some types were observed in more than one set. The results of biotyping did not correspond with the results of the other methods or the results of AFLP. For 6 of the 11 sets, the results of all methods except those of biotyping corresponded completely. Quantitative antibiogram typing, PFGE, and AFLP proved to be the most accurate of the six typing methods tested.

Bacteremia↗