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Background: The increase in smartphone use and mobile health applications (apps) holds potential to use apps to reduce and detect healthcare-associated infections (HAIs) in clinical practice., Aim: To obtain an overview of available apps for HAI prevention, by selecting the clinically relevant apps and scoring functionality, quality and usefulness., Methods: This scoping review of available apps in the iOS and Android app stores uses an in-house-developed tool (scraper https://holtder.github.io/talos) to systematically aggregate available apps relevant for HAI prevention. The apps are evaluated on functionality, assessed on quality using the 'Mobile Application Rating Scale' (MARS), and assessed on potential use in clinical infection prevention., Findings: Using the scraper with CDC HAI topics through 146 search terms resulted in 92,726 potentially relevant apps, of which 28 apps met the inclusion criteria. The majority of these apps have the functionality to inform (27 of 28 apps) or to instruct (20/28). MARS scores for the 28 apps were high in the following domains: functionality (4.19/5), aesthetics (3.49/5), and information (3.74/5), with relatively low scores in engagement (2.97/5), resulting in a good average score (3.57/5)., Conclusion: Low engagement scores restrict apps that intend to inform or instruct, possibly explained by the often-academic nature of the development of these apps. Although the number of HAI prevention apps increased by 60% in 5 years, the proportion of clinically relevant apps is limited. The variation in HAI app quality and lack of user engagement, could be improved by co-creation and development in the clinical setting., (Copyright © 2021 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

An increase in B:15:P1.12 meningococci among isolates from patients with Neisseria meningitidis infection in Norway in recent years led to further characterization of such strains. Between 1987 and 1992, B:15:P1.12 strains constituted 9.8% (24 strains) of B:15 isolates. The B:15:P1.12 strains belonged to the electrophoretic type 5 (ET-5) complex, but 17 (71%) strains were a new clone (ET-5c) not found elsewhere in the world. All but one strain of ET-5c were responsible for a localized outbreak of systemic meningococcal disease in western Norway. A novel monoclonal antibody (202,G-12), developed against the unknown variable region 2 on the class 1 protein of one of these strains, bound to 19 of the 15:P1.12 strains, 4 strains bound the subtype P1.13 reference monoclonal antibody MN24H10.75, and the remaining strain showed no reaction. Sequencing of porA genes demonstrated a series of nine threonine residues in the deduced variable region 2 of the latter strain, while four and five threonine residues were found in the corresponding regions of strains reacting with the monoclonal antibodies 202,G-12 and MN24H10.75, respectively. Epitope mapping with synthetic peptides showed that 202,G-12 bound to a sequence of 11 amino acids which included the four threonine residues specific for subtype P1.13a. Immunoglobulin G antibodies against the P1.7,16 subtype protein, induced in volunteers after vaccination with the Norwegian meningococcal vaccine, did not cross-react on immunoblots with the subtype protein of clone ET-5c. Thus, postvaccination class 1 protein antibodies, assumed to be protective, may not be effective against infection with the new clone.

For more than 15 years, Norway has had the highest incidence of meningococcal disease in northern Europe, with 80% of cases being due to serogroup B meningococci. The case-fatality has remained high, at about 10%. In this study, an outer membrane vaccine, which had previously been shown to induce an increase in bactericidal antibodies to the parent strain, was assessed in a large-scale, randomised, double-blind trial. From October, 1988, 171,800 students in secondary schools volunteered to take part in a double-blind, placebo-controlled, efficacy trial with school as the randomisation unit. Hospitals and clinics that routinely receive patients with infectious disease were asked to report urgently all cases of suspected meningitis and/or septicaemia in 13-21-year-old students in Norway. These cases were registered and further investigated according to a detailed protocol. 89 out of the 221 cases investigated by June 3, 1991, were shown to be severe systemic disease due to group B meningococci. 36 cases in 35 schools took part in the trial (11 schools with vaccinated students and 24 with students given placebo). The calculated rate of protection was thus 57.2% (p = 0.012, one-sided test). The findings suggest that, although the vaccine conferred protection against group B meningococcal disease, the effect was insufficient to justify a public vaccination programme.

Thirteen systemic strains, i e strains isolated from systemic infections, and 77 carrier isolates of Neisseria meningitidis were serogrouped by agglutination and analyzed by gas chromatography (GC) of phenol extracts. For systemic strains the sugar patterns were in accordance with their group-specific capsular polysaccharides (CPS). Some carrier isolates revealed unexpected GC profiles. Upon immunological retesting with new sera, GC results were generally confirmed. Occasional isolates initially serogrouped as B or Y completely lacked neuraminic acid. Some non-groupable isolates were shown by ultracentrifugation and GC to have significant amounts of this sugar likely to originate from CPS of known composition or from unknown polysaccharides. One such originally non-groupable isolate showed a weak agglutination reaction specifically with group B antiserum when reexamined. Generally, carrier isolates had lower amounts of CPS than systemic strains of the same group. Five successive isolates from one carrier were first serogrouped as X, Z or non-groupable, but they had high amounts of galactosamine and 2-keto-3-deoxy octonate, sugars characterizing CPS of serogroup 29E. These isolates were confirmed by agglutination with recently available group 29E antiserum to be of this serogroup, which has not been reported before in Norway. Ultracentrifugation revealed the presence of unknown polysaccharides containing glucose, galactose or glucosamine, but further purification of these polymers is required to determine their composition and immunological importance.

Activities corresponding to the enzymes glucokinase, glucose 6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, malate dehydrogenase, pyridine nucleotide independent malate dehydrogenase, and glutamate dehydrogenase were found in cell free extracts from Neisseria elongata subsp. gkcolytica. Activities corresponding to 6-phosphogluconate dehydrase and 2-keto-3-deoxy-6-phosphogluconate aldolase were not found. Glucose was catabolized only vira the pentose phosphate pathway. The radiorespirometric findings suggest an extensive recycling of the triose and fructose phosphates. There was no evidence for formation of pyruvate from glucose. Glutamate was oxidized via the tricarboxylic acid cycle. Pyruvate and acetate were obviously catabolized by the glyoxylic and tricarboxylic acid cycles, as in N. elongata.

A combined serogroup B capsular polysaccharide and serotype 2a outer membrane complex meningococcal vaccine and a placebo preparation were tested double-blindly in 55 adult, male volunteers. The vaccine gave twofold increased binding antibodies, measured by ELISA, against non-capsular outer membrane antigen in 85 per cent of those vaccinated. Bactericidal antibodies towards a meningococcal serogroup C serotype 2a strain also increased fourfold or more among 85% vaccinated. New acquisition of meningococcal carriage was associated with antibody increase in one person from the placebo group.

Patient and carrier strains of Neisseria meningitidis from 2 different periods were compared with respect to serogroups, serotypes and sensitivity to sulphadiazine. The majority of 249 patient strains were resistant to sulphadiazine, and belonged to the groups A, B or C. The group B and C strains were mainly type 15/16 and 2, respectively. In contrast, most of the 400 carrier strains belonged to serotypes other than 2 or 15/16, or were non-typable, and most strains were sensitive to sulphadiazine. Among the resistant group B and C carrier strains there were more type 2 and 15/16 strains than would have been expected from the average. The virulence markers: serogroup A, B and C, serotype 2 and 15/16, and resistance to sulphadiazine, coexist in more carrier strains than would be expected if the distribution of these markers was random.

Treatment of agar-grown meningococci with dilute hydrochloric acid and suspension in saline after washing gave a preparation suitable for meningococcal serotyping by staphylococcal coagglutination with monoclonal antibodies. The monoclonal antibodies available for use and attached to protein A on the staphylococci were directed against the serotype protein antigens 2a, 2b (class 2), 15 (class 3) and the subtype protein antigens P1. 2 and P1. 16 (class 1). Ninety per cent of systemic strains and thirty-four per cent of a collection of carrier isolates, both from Norway late 1981/early 1982, were typable. The serotype antigen 15 alone or in combination with P1. 16 or P1. 16 alone were detected in about 85 per cent of the systemic strains. The quality of the whole-cell meningococcal antigen was important for the test to be easily read.

Variation in nine enzymes in 152 isolates of Neisseria meningitidis from Norway (118 from blood or cerebrospinal fluid of patients with systemic disease and 34 from the pharynx of healthy carriers) was analysed by starch-gel electrophoresis. All nine enzymes were polymorphic and the number of allozymes (electromorphs) identified per locus ranged from 3 to 12, with a mean of 6.1. Among the 152 isolates, 55 unique combinations of electromorphs (electrophoretic types, ETs) were distinguished. Twenty ETs were represented among the carrier isolates and 37 among the systemic isolates; hence, only two ETs were found in both groups of isolates. ET-5 was identified 67 times among the 118 systemic isolates (58%), indicating an association of this ET with invasiveness; ET-5 was also the most common type among the carrier isolates (18%). Genetic similarity between ETs was analysed by pairwise comparison of all 55 ETs with respect to the number of electromorphs by which they differed. No evidence of a general genetic difference between carrier and case isolates was found. Two well-defined clusters of ETs were observed, each including one of the two most common ETs identified among the systemic isolates (ET-5 and ET-37), together with isolates differing from them only at one or two loci. All isolates of ET-5 and ET-37, as well as their closely related variants defined by the similarity matrix, were resistant to sulphonamide, independent of their antigenic characteristics and isolation site. The extensive allozyme variation among isolates of the same serogroup demonstrated the limited value of serogrouping as an epidemiological tool. All but one isolate of serotype 15:P1.16 were electrophoretically similar, as were all the 2a:P1.2 isolates. The 15:P1.15 isolates, however, were genetically heterogeneous. The distribution of alleles in genotypes identified among the systemic isolates indicated that genetic recombination may occur in natural populations of N. meningitidis.

In cell free extract from Neisseria meningitidis an enzyme has been found which catalyses the oxidation of L-malate to oxaloacetate in the absence of pyridine nucleotides, using ferricyanide as electron acceptor. The enzyme was found to be particle-bound, as determined by sucrose gradient centrifugation. Activity corresponding to this enzyme was demonstrated in extracts from all strains tested of selected Neisseria species. In contrast to the large differences in NAD-linked malate dehydrogenase activity among the species, the interspecies variation of the pyridine nucleotide independent oxidation of malate was not sufficiently distinct to be useful for classification purposes.

Neisseria elongata subsp. glycolytica strain 6171/75 is closely similar to the type strain of N. elongata, M2, as regards DNA base composition, fatty acid content and electrophoretic mobility of two glutamate dehydrogenases, one of which showed a reaction of identity with the corresponding enzyme from M2 in double immunodiffusion in agar. The strain showed genetic homologies with strain M2 in genetic transformation at a level suggesting species identity, and with N. meningitidis at a lower level. No affinity to Moraxella species or "false neisseriae" was demonstrated, with the exception of a production of a few transformants in the 6171/75 recipient by DNA from Kingella kingae. The strain showed the same pattern of associated variation of colony type, fimbriation and competence in transformation as that found in other Neisseria and Moraxella species. After continuous subcultivation for some time some clones of the strain appeared to have lost the ability to produce acid from glucose.

Using standardized laparoscopy technique, fluid was aspirated from the pouch of Douglas, from the Fallopian tubes and from ovarian cysts in 85 cases with clinical diagnosis of pelvic inflammatory disease (PID). The concentration of doxycycline in the aspirates was measured after oral ingestion of 200 mg of doxycycline (Vibramycin). A therapeutic level was achieved in the tubes and in ovarian cysts within a few hours, and on continuation of the treatment these values followed the plasma concentration closely, still being within the therapeutic range 24 hours after the final dose. The clinical effect was excellent, 94% (60/64) of the cases with verified PID being cured by doxycycline.

The inhibitory effect of sodium polyanethol sulfonate (0.05%) upon growth of Neisseria meningitidis was found to be neutralized by adding gelatin (l.1%) to the growth medium. The neutralizing effect was demonstrated in solid medium, as well as in nutrient broth for blood cultures. The findings parallel those of Wilkins and West (6) regarding gelatin neutralization of the inhibitory effect of sodium polyanethol sulfonate on Peptostreptococcus anaerobius.

Strains of Neisseria meningitidis responsible for an epidemic of meningococcal disease occurring in Norway since the mid-1970s and for recent increases in the incidence of disease in several other parts of Europe have been identified by multilocus enzyme electrophoresis as members of a distinctive group of 22 closely related clones (the ET-5 complex). Clones of this complex have also colonized South Africa, Chile, Cuba, and Florida, where they have been identified as the causative agents of recent outbreaks of meningococcal disease. There is strong circumstantial evidence that outbreaks of disease occurring in Miami in 1981 and 1982 were caused in large part by bacteria that reached Florida via human immigrants from Cuba.

The catabolism of glucose in selected Neisseria species was studied by radiorespirometry. The Entner-Doudoroff and pentose phosphate pathways were operating in all species, the greater part of the substrate being routed through the former, somewhat dependent on the medium used. Acetate was oxidized via the tricarboxylic acid cycle. In all species, a fraction of the triose was recycled through fructose phosphates to glucose 6-phosphate. Phosphate inhibited the oxidation of acetate. In media devoid of phosphate and sodium (N. meningitidis and N. gonorrhoeae) or of phosphate and potassium (other saccharolytic Neisseria), the conversion of triose to pyruvate was inhibited. In these media the catabolism of glucose proceeded slowly, and no substrate was used for biosynthetic purposes. The results point to a difference in the regulation of glucose metabolism in pathogenic and non-pathogenic Neisseria.

The restriction endonuclease fingerprinting technique was applied to meningococcal DNA in an attempt to identify individual strains of Neisseria meningitidis B15 (serogroup B, serotype 15), which causes approximately 90% of cases of meningococcal disease in northern Norway. Thirty representative strains (10 each from asymptomatic pharyngeal carriers, patients with septicemia, and patients with meningitis) were investigated with the restriction endonucleases Hind III and Eco RI. The 10 carrier strains showed a remarkable heterogeneity of fingerprints that rendered each strain easily distinguishable from the others. The 10 strains from the blood and the 10 from the cerebrospinal fluid showed similar but not identical restriction patterns. The results obtained with the two endonucleases were in perfect agreement. Our data suggest that a large number of different B15 clones are present in the population of northern Norway, but that only one single clone causes invasive meningococcal disease.

The genetic structure of populations of Neisseria meningitidis was examined by an analysis of electrophoretically demonstrable allelic variation at 15 structural genes encoding enzymes in 688 isolates. Variation among strains in serogroup and serotype has little relationship to the complex structure of populations revealed by enzyme electrophoresis, which involves 14 major lineages of clones diverging from one another at more than half their genetic loci. Clones of one of these lineages, the ET-5 complex, have been identified as the causative agent of recent outbreaks and epidemics of meningococcal disease in Europe, South Africa, Latin America, and the United States. There is evidence that organisms of the ET-5 complex reached Florida via human immigrants from Cuba.

The catabolism of pyruvate and acetate is selected Neisseria species was studied by radiorespirometry. Both substrates were oxidized via the tricarboxylic acid cycle. N. elongata and the "false neisserias" (N. catarrhalis, N. ovis and N. caviae) did oxidize acetate in the absence of other substrates. This can be explained if it is assumed that these species have glyoxylic acid cycle activity. In the "true neisserias" other than N. elongata, acetate was oxidized only in the presence of glutamate, indicating that these species do not possess a glyoxylic acid cycle.

Characteristics of 67 strains of Neisseria meningitidis causing systemic disease in Norway during the winter 1981-82 are reported and related to clinical manifestations. Included in the study were also pharyngeal isolates of meningococci collected in the same period from 35 healthy military recruits. The strains were examined for serogroup, serotype as determined with monoclonal antisera (against antigens 2a, 2b, 12, 15 and 16), and sulfonamide susceptibility. Predominating in the systemic disease material were serogroup B, serotype 15, 16 (or 15), and sulfonamide-resistant strains. This complex of characteristics also appeared to be associated with the severity of manifestations (septicemia and death). The material of meningococci from healthy carriers unassociated with cases of disease was clearly different; these strains were typically non-groupable, non-typable and sulfonamide-sensitive. The full combination of traits usually seen in strains causing systemic disease was rare in carrier isolates. The results are discussed in relation to the epidemiological development of meningococcal disease in Norway.

The catabolism of glutamate and fumarate was studied by radiorespirometry in selected Neisseria species. The tricarboxylic acid cycle is functioning in all species tested, in spite of the known absence of in vitro malate dehydrogenase activity in N. meningitidis, N. gonorrhoeae and N. cinerea. The results imply a pyridine nucleotide independent oxidation of malate. The oxidation of glutamate is less complete in the presence of phosphate. In N. meningitidis, N. perflava, N. flava, N. subflava and N. lactamica the catabolism of fumarate was slow and incomplete in the absence of glutamate.