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D A Caugant

Publications and source records attributed to D A Caugant.

At least 109 records · Page 6Linked to original sources

[Genotypes of Neisseria meningitidis strains isolated from patients in the Czech Republic].

A group of 75 strains of Neisseria meningitidis isolated from patients with meningococcal meningitis in the Czech Republic during 1980-1988 was characterized by assessment of serogroups, serotypes, serosubtypes and genotypes. Twelve strains belonged into serogroup A, 27 into serogroup B and 36 into serogroup C. The most frequently found serotype was 4, subserotype P1.2. The authors identified 48 different enzyme genotypes among which four genetically related groups were assessed. Strains of Neisseria meningitidis of the same genotype were found more frequently during the period of 1980-1984, when a rise of meningococcal meningitis in the Czech Republic was recorded. During this period 73% of the strains belonged into three genetically related groups, while during the subsequent period (1985-1988) these genetically related groups comprised only 47% of the strains. Only one strain of Neisseria meningitidis (878/85) represented a genetic clone ET-5 complex responsible for an epidemic of meningococcal meningitis in western European countries from the mid-seventies.

Genotype↗

Characterization of Neisseria meningitidis serogroup A strains from an outbreak in France by serotype, serosubtype, multilocus enzyme genotype and outer membrane protein pattern.

In an attempt to determine the epidemiological relationship between cases of infection caused by Neisseria meningitidis serogroup A in France between August 1987 and December 1988, and an outbreak which occurred in Mecca in August 1987, markers such as serotype, serosubtype, multilocus enzyme genotype and outer membrane protein (OMP) pattern were used to characterize the bacterial isolates. From a total of 28 cases, 20 strains were isolated. Sixteen isolates, including one which undoubtedly originated from the Mecca epidemic, were homogenous (serotype 4, serosubtype P1.9, multilocus enzyme genotype of clone III-1, identical OMP pattern). Four isolates had a different OMP pattern with little or no P1 protein, no P4 and no P6. Two of these isolates belonged to other clones (I.1 and group I) and they were considered to be unrelated to the Mecca epidemic strains. The origin of the remaining two isolates was not clear. It is concluded that the majority of the Neisseria meningitidis serogroup A strains recently isolated in France originate from the Mecca epidemic.

Adolescent↗

Genetic relationships among strains of Neisseria meningitidis causing disease in Italy, 1984-7.

Since 1984 a change in the epidemiological pattern of meningococcal disease in Italy has occurred with a predominance of Neisseria meningitidis of serogroup C (76%), serotype 2a and a high proportion of strains resistant to sulphonamides (71%). In order to understand better the epidemiology of the group C N. meningitidis strains responsible for the disease over the last years in Italy, we studied the genetic features of phenotypically closely related strains, by enzyme electrophoresis. The results showed that the genetic and the phenotypic characteristics of the 57 strains studied were similar, suggesting that spread of a single clone during recent years in our country. This result is in agreement with the circulation of strains typical of epidemic situations, despite the decreasing incidence of meningococcal disease in Italy.

Electrophoresis, Starch Gel↗

An epidemiologically valuable typing method for Neisseria meningitidis by analysis of restriction fragment length polymorphisms.

A restriction fragment length polymorphism (RFLP) typing method was developed for Neisseria meningitidis. A cloned EcoRI fragment from a Neisseria meningitidis Group B serotype 15P1.16 sulphonamide-resistant strain was used to probe Southern blots of total chromosomal DNA restriction fragments (enzyme AvaI). A group of 75 apparently unrelated organisms gave rise to 26 different restriction fragment length patterns and two different groups of epidemiologically related strains had RFLP patterns that were distinct for each group. The technique was highly reproducible and discriminatory. The RFLP data were compared with the results of serotyping and subtyping and isoenzyme electrophoretotyping. The RFLP data were consistent with those from the alternative typing methods; clones defined by isoenzyme analysis were subdivided by this technique. The use of RFLP typing by cloned probes should be of considerable epidemiological value.

Blotting, Southern↗

Emergence of a virulent clone of Neisseria meningitidis serotype 2a that is associated with meningococcal group C disease in Canada.

Multilocus enzyme electrophoresis was used to characterize 378 isolates of Neisseria meningitidis serogroup C recovered during a period of an increase in group C meningococcal disease in Canada. Thirty-four enzyme electrophoretic types were found among the isolates, which were predominantly (96.0%) serotype 2a. One clone (ET 15), characterized by a rarely occurring allele for the enzyme fumarase, was responsible for a focal outbreak in Ontario followed by the spread of group C disease across the province. This clone, which occurred infrequently among strains isolated in 1986, accounted for over 65% of group C strains associated with meningococcal disease in Canada in 1990.

Bacterial Typing Techniques↗

Characterization of serogroup A and B strains of Neisseria meningitidis with serotype 4 and 21 monoclonal antibodies and by multilocus enzyme electrophoresis.

The reactions of serogroup A strains of Neisseria meningitidis with one monoclonal antibody specific for serotype 21 and three different monoclonal antibodies specific for serotype 4 were compared with those of serogroup B strains previously assigned to serotype 4. Antibody binding was studied by enzyme-linked immunosorbent assay (ELISA), dot blotting, and immunoblotting. Characterization of the isolates by the electrophoretic mobilities of 14 metabolic enzymes showed 50 multilocus enzyme genotypes. All except two genotypes fell into three distinct clusters: I, IIa and IIb. The enzyme genotypes of serogroup B strains were mainly in cluster I, and 88% of the serogroup A strains had genotypes in clusters IIa and IIb. Serogroup B strains generally reacted with all three serotype 4 monoclonal antibodies in ELISA and dot blotting but with only two in immunoblots. Serogroup A strains showed two different reactions in the blotting methods: either binding of the serotype 21 antibody only or binding of this and two of the three serotype 4 monoclonal antibodies. Strains of the first pattern were in clusters I and IIa, whereas all but two strains in cluster IIb were of the second pattern. In ELISA, an additional reaction of two of the serotype 4 monoclonal antibodies with serogroup A isolates was observed. The different binding of these two monoclonal antibodies in ELISA and the blotting methods appeared to result from heat inactivation of the meningococcal cells and use of detergent-containing reagents in ELISA. The results show that the serotype of serogroup A strains is distinct from serotype 4 of serogroup B strains.

Antibodies, Monoclonal↗

Clones of serogroup B Neisseria meningitidis causing systemic disease in The Netherlands, 1958-1986.

Serogroup B isolates of Neisseria meningitidis recovered from 278 patients with systemic disease in the Netherlands between 1958 and 1986 were analyzed with respect to serotype and multilocus enzyme genotype. Of the isolates, 28% were serotype 2b and 53% were neither serotypeable nor serosubtypeable. There were 145 distinct multilocus genotypes (electrophoretic types, ETs), with up to 31 isolates belonging to the same ET. Temporal changes in the genotypic composition of meningococcal populations in the Netherlands were demonstrated by the recent occurrence of disease caused by three clone lineages, I, III, and VI, that were not found before 1975. The epidemic of 1966-1967 and the hyperendemic wave of 1972 were caused, in large part, by two closely related but distinct clones of serotype 2b isolates, ET-11 and ET-17, respectively. Deviations in male-to-female ratio and age distribution of patients were observed for disease caused by isolates of individual clone lineages.

Adolescent↗

Differentiation between Actinobacillus (Haemophilus) actinomycetemcomitans, Haemophilus aphrophilus and Haemophilus paraphrophilus by multilocus enzyme electrophoresis.

Genetic relationships among isolates assigned to Actinobacillus actinomycetemcomitans, Haemophilus aphrophilus and H. paraphrophilus were determined by analysis of electrophoretically demonstrable allelic variation in 14 structural genes encoding metabolic enzymes. Among the 51 isolates analysed there were 25 electrophoretic types (ETs), among which mean genetic diversity per locus was 0.753. Cluster analysis of ETs demonstrated one well-defined group of 11 ETs representing solely the genotypes of all 17 isolates assigned to A. actinomycetemcomitans. The remaining 14 ETs represented the genotypes of the 34 isolates of H. aphrophilus and H. paraphrophilus. With the exception of ATCC 13252, all strains of H. aphrophilus were closely related, whereas strains assigned to H. paraphrophilus included distantly related lineages, some of which were similar to those of H. aphrophilus and should be assigned to this species. Thus, the study showed that there is no significant overall genetic similarity between A. actinomycetemcomitans and the two Haemophilus spp.

Actinobacillus↗

Characterization of epidemic and nonepidemic Neisseria meningitidis serogroup A strains from Sudan and Sweden.

A random selection of 25 strains isolated during an epidemic caused by serogroup A Neisseria meningitidis in Sudan (1988), 3 preepidemic meningococcal strains (1985), and 26 serogroup A strains isolated from sporadic cases of meningitis in Sweden (1973 to 1987) were assessed for multilocus enzyme genotypes (ETs), DNA restriction enzyme patterns, outer membrane proteins, lipopolysaccharides, pilus formation, and antibiograms. All of the 25 Sudanese epidemic isolates and 22 of the Swedish strains were of the same or closely related ETs (ETs 3, 4, and 5), corresponding to clone III-1, which has been responsible for two pandemic waves in the last three decades. The earlier pandemic involved Scandinavia, and the last one caused an outbreak during the pilgrimage to Mecca, Saudi Arabia (August 1987), spreading to Sudan, Chad, and Ethiopia. The three Sudanese preepidemic isolates (1985) were clone IV-1 (sulfonamide susceptible), which has been resident in the African meningitis belt for the last 25 years. The uniformity of clone III-1 strains (all sulfonamide resistant) from Sudan and Sweden was confirmed by DNA restriction enzyme patterns. ETs 3, 4, and 5 from Sudan and Sweden had 86 to 100% similarity to a Swedish clone III-1 reference strain, whereas ETs 1, 2, 6, and 7 showed 50 to 80% similarity. Class 1 protein for clone III-1 showed serosubtype antigens P1.9 and P1.x, whereas ET6 strains (clone IV-1) had serosubtype P1.7. Lipopolysaccharides were variable in the Sudanese and Swedish strains. Pili were expressed in all clone III-1 isolates from Sudan and Sweden but in none of the clone IV-1 isolates (Sudan, 1985).

Antigenic Variation↗

Characteristics of serogroup A Neisseria meningitidis responsible for an epidemic in Ethiopia, 1988-89.

In September 1988, an epidemic of meningococcal disease started in Ethiopia. 21 Neisseria meningitidis isolates recovered from patients in Addis Ababa and towns 200 km south of the capital were characterized by serogrouping, serotyping, testing of susceptibility to antibiotics, restriction endonuclease fingerprinting, and multilocus enzyme electrophoresis. The 21 isolates were essentially homogeneous for all properties tested and belonged to clone III-1 of serogroup A N. meningitidis, which was also responsible for the epidemics in Saudi Arabia in 1987 and in Sudan and Chad in 1988.

Adolescent↗

Serogroup A Neisseria meningitidis of clone III-1 present in western Norway as early as 1969-73.

A clone of serogroup A Neisseria meningitidis recognized by multilocus enzyme electrophoresis and designated as clone III-1, has caused major epidemics of meningococcal disease in various parts of the world since the 1970s. In Norway, serogroup B meningococci have been responsible for an epidemic since the mid-1970s. We have studied a sample of 53 meningococci isolated from patients in western Norway prior to the serogroup B epidemic. 22/35 meningococcal isolates collected 1969-73 represented clone III-1, whereas this clone was not found in the 18 isolates from 1962-68. It has been speculated that the epidemic of meningococcal disease in Finland caused by clone III-1 in 1973-75 had spread from an epidemic in USSR that began in 1969. Our findings demonstrate, however, that the clone III-1 was present in Scandinavia in 1969.

Clone Cells↗

Genetic diversity of penicillin G-resistant Neisseria meningitidis from Spain.

Genotypic and phenotypic diversity among 16 penicillin G-resistant (Penr) isolates of Neisseria meningitidis recovered from human blood or cerebrospinal fluid in Spain was compared with that among 12 penicillin-susceptible (Pens) isolates by the use of multilocus enzyme electrophoresis, serotyping, auxotroph testing in chemically defined media, and sodium dodecyl sulfate-polyacrylamide gel electrophoresis of penicillin-binding proteins (PBPs). Thirteen distinctive multilocus enzyme genotypes (electrophoretic types [ETs] ) were identified among the 28 isolates. There was slightly less genetic diversity among the eight ETs of Penr isolates (H = 0.385) than among the eight ETs of Pens isolates (H = 0.431). Cluster analysis demonstrated two distinctive complexes of ETs and one ET that was not closely related to either complex. The possibility of a singular clonal origin of penicillin G-resistant isolates was excluded by the observations that resistance occurred in isolates of each of the two distantly related complexes of ETs, that three of the four ETs represented by multiple isolates included both susceptible and resistant strains, and that serotypes and growth requirements were not associated with the resistance phenotype. The 28 isolates showed a relatively homogeneous pattern of four PBPs, with apparently reduced penicillin G binding by PBP 3 of the Penr isolates.

Bacterial Proteins↗

Clonal diversity and relationships among strains of Yersinia enterocolitica.

Allelic variation in the chromosomal genome of 81 isolates of Yersinia enterocolitica and single isolates of Yersinia intermedia, Yersinia frederiksenii, Yersinia mollaretii, and Yersinia kristensenii was assessed by analysis of electrophoretically demonstrable polymorphism in 21 genes encoding metabolic enzymes. Eighteen distinctive multilocus genotypes (electrophoretic types [ETs]) were identified. Clustering of the ETs from a matrix of pairwise genetic distances, based on the 21 enzyme loci, confirmed the genetic distinctness of serogroup 3 isolates of Y. intermedia, Y. frederiksenii, Y. mollaretii, and Y. kristensenii and identified another serogroup 3 isolate that was also not a member of Y. enterocolitica. The 13 ETs of Y. enterocolitica clustered into two groups: cluster A, which included eight ETs represented by isolates of serogroups 1; 2; 3; 5,27; and 9, and cluster B, which included four ETs represented by isolates of serogroups 8, 13, and 21. Clones of cluster A were found to be distributed worldwide, but those of cluster B were largely restricted to North America. Isolates of genotypes belonging to cluster B were lethal to mice, whereas those of cluster A were not, suggesting an influence of the chromosomal background on the virulence of Y. enterocolitica.

Alleles↗

Comparison of epidemiological marker methods for identification of Salmonella typhimurium isolates from an outbreak caused by contaminated chocolate.

Plasmid profile analysis, restriction endonuclease analysis, and multilocus enzyme electrophoresis were used in conjunction with serotyping, bacteriophage typing, and biochemical fingerprinting to trace epidemiologically related isolates of Salmonella typhimurium from an outbreak caused by contaminated chocolate products in Norway and Finland. To evaluate the efficiency of the epidemiological marker methods, isolates from the outbreak were compared with five groups of control isolates not known to be associated with the outbreak. Both plasmid profile analysis and phage typing provided further discrimination over that produced by serotyping and biochemical fingerprinting. Plasmid profile analysis and phage typing were equally reliable in differentiating the outbreak isolates from the epidemiologically unrelated controls and were significantly more effective than multilocus enzyme electrophoresis and restriction enzyme analysis of total DNA. The greatest differentiation was achieved when plasmid profile analysis and phage typing were combined to complement serotyping and biochemical fingerprinting. However, none of the methods employed, including restriction enzyme analysis of plasmid DNA, were able to distinguish the outbreak isolates from five isolates recovered in Norway and Finland over a period of years from dead passerine birds and a calf.

Animals↗

Sulfonamide resistance in Neisseria meningitidis isolates of clones of the ET-5 complex.

A distinctive group of genetically closely related clones, as determined by multilocus enzyme electrophoresis, the ET-5 complex, has been responsible for an epidemic of meningococcal disease in Norway since the mid-1970's. Most isolates of the ET-5 complex from Norway are sulfonamide-resistant, serogroup B, and serotype 15:P1.16. Clones of the ET-5 complex that have been identified as the causative agents of recent outbreaks and epidemics in many other parts of the world show, outside Northern Europe, different associations of serotype protein antigens. We here report the analysis of sulfonamide susceptibility of isolates of the ET-5 complex from various geographic sources. There was no difference in resistance according to geographic source, serogroup, or serotype of the isolates, demonstrating that, in contrast to serotype and serogroup, sulfonamide resistance is an essentially invariant property of clones of the ET-5 complex.

Drug Resistance, Microbial↗

Clonal diversity of Neisseria meningitidis from a population of asymptomatic carriers.

Genetic diversity and relationships among 109 isolates of Neisseria meningitidis obtained from throat cultures of healthy individuals in Norway in 1984 were assessed by analyzing electrophoretically demonstrable allelic variation at 15 enzyme-encoding chromosomal genes. Seventy-eight distinctive electrophoretic types (ETs), representing multilocus genotypes, were identified. The mean genetic diversity per locus among the 78 ETs (0.538) was equivalent to that among 19 ETs represented by 66 isolates collected from patients with meningococcal disease in Norway in the first 5 months of 1984. The clonal composition of the collection of carrier strains was, however, quite different from that of strains from patients. The two groups of clones, the ET-5 complex and the ET-37 complex, that were responsible for 91% of the cases of systemic disease in Norway in 1984 were identified in only 7 and 9%, respectively, of the throat cultures from healthy individuals, and their frequencies in the human population sampled were only 0.7% for clones of the ET-5 complex and 0.9% for those of the ET-37 complex. The complex of clones that was most frequently represented by isolates from carriers (19%) has never been recovered from patients with meningococcal disease in Norway or elsewhere, which suggests that these clones have a low virulence potential. Children attending the same day care center or school seldom harbored the same clone in their throats.

Age Factors↗

Multilocus genotypes of two strains of Neisseria meningitidis and their presumed variants obtained upon subcultivation.

Loss of sulfonamide resistance and endotoxin liberation have been described in two strains of Neisseria meningitidis serogroup B, upon subcultivation every 1 to 2 months over an 18-month period. Subsequently, the two laboratory variants, designated 270E- and 840E-, were also found to differ from the parent strains, 270E+ and 840E+, in serotype, outer membrane protein pattern, and virulence in mice. We report here the multilocus genotypes determined by enzyme electrophoresis, of the four isolates 270E+, 270E-, 840E+, and 840E-, and demonstrate that 270E- and 840E- strains could not have originated from subcultivation of 270E+ and 840E+, respectively, but that a mix-up of strains has occurred.

Alleles↗