Publications by authors named "Shakeel Mowlaboccus"

14 Publications

  • Page 1 of 1

Molecular characterisation of fosfomycin-resistant Escherichia coli urinary tract infection isolates from Australia.

Clin Microbiol Infect 2021 May 3. Epub 2021 May 3.

Murdoch University, 90 South Street, Murdoch, Western Australia, 6150, Australia; Fiona Stanley Hospital, PathWest Laboratory Medicine WA, Murdoch, Western Australia, Australia.

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http://dx.doi.org/10.1016/j.cmi.2021.04.029DOI Listing
May 2021

Australian Group on Antimicrobial Resistance (AGAR) Australian Enterococcal Sepsis Outcome Programme (AESOP) Annual Report 2019.

Commun Dis Intell (2018) 2020 Sep 15;44. Epub 2020 Sep 15.

Antimicrobial Resistance and Infectious Disease (AMRID) Research Laboratory, Murdoch University, Murdoch, Western Australia, Australia; Department of Microbiology, PathWest Laboratory Medicine-WA, Fiona Stanley Hospital, Murdoch, Western Australia, Australia.

From 1 January to 31 December 2019, thirty-nine institutions around Australia participated in the Australian Enterococcal Sepsis Outcome Programme (AESOP). The aim of AESOP 2019 was to determine the proportion of enterococcal bacteraemia isolates in Australia that were antimicrobial resistant, and to characterise the molecular epidemiology of the isolates. Of the 1,361 unique episodes of bacteraemia investigated, 95.2% were caused by either (51.4%) or (43.8%). Ampicillin resistance was not detected in but was detected in 91.1% of . Vancomycin non-susceptibility was detected in 0.1% of and in 41.8% of . Overall, 45.4% of harboured and/or genes. For the / positive isolates, 49.1% harboured genes only and 50.6% genes; 0.3% harboured both and genes. The percentage of bacteraemia isolates resistant to vancomycin in Australia is substantially higher than that seen in most European countries. consisted of 78 multilocus sequence types (STs), of which 75.0% of isolates were classified into six major STs containing ten or more isolates. All major STs belong to clonal cluster (CC) 17, a major hospital-adapted polyclonal cluster. The predominant STs (ST1424, ST17, ST796, ST80, ST1421, and ST78) were found across most regions of Australia. The most prevalent clone was ST1424, which was identified in all regions except the Northern Territory and Western Australia. Overall, 51.4% of isolates belonging to the six predominant STs harboured or genes. In 2019, AESOP has shown that enterococcal bacteraemias in Australia are frequently caused by polyclonal ampicillin-resistant high-level gentamicin-resistant or which have limited treatment options.
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http://dx.doi.org/10.33321/cdi.2020.44.72DOI Listing
September 2020

Australian Group on Antimicrobial Resistance (AGAR) Australian Staphylococcus aureus Sepsis Outcome Programme (ASSOP) Annual Report 2019.

Commun Dis Intell (2018) 2020 Sep 15;44. Epub 2020 Sep 15.

Antimicrobial Resistance and Infectious Disease (AMRID) Research Laboratory, Murdoch University, Murdoch, Western Australia, Australia; Department of Microbiology, PathWest Laboratory Medicine-WA, Fiona Stanley Hospital, Murdoch, Western Australia, Australia.

From 1 January to 31 December 2019, 39 institutions around Australia participated in the Australian Sepsis Outcome Programme (ASSOP). The aim of ASSOP 2019 was to determine the proportion of bacteraemia (SAB) isolates in Australia that are antimicrobial resistant, with particular emphasis on susceptibility to methicillin and on characterising the molecular epidemiology of the methicillin-resistant isolates. A total of 3,157 bacteraemia episodes were reported, of which 79.8% were community-onset. 18.5% of were methicillin resistant. The 30-day all-cause mortality associated with methicillin-resistant SAB was 14.0%, which was not significantly different from the 14.3% mortality associated with methicillin-susceptible SAB (p = 0.9). With the exception of the β-lactams and erythromycin, antimicrobial resistance in methicillin-susceptible was rare. However, in addition to the β-lactams, approximately 36% of methicillin-resistant (MRSA) were resistant to ciprofloxacin, 34% to erythromycin, 13% to tetracycline, 9% to gentamicin and 4% to co-trimoxazole. When applying the EUCAST breakpoints, teicoplanin resistance was detected in two isolates. Resistance was not detected for vancomycin and linezolid. Resistance to non-beta-lactam antimicrobials was largely attributable to two healthcare-associated MRSA clones: ST22-IV [2B] (EMRSA-15) and ST239-III [3A] (Aus-2/3 EMRSA). ST22-IV [2B] (EMRSA-15) is the predominant healthcare-associated clone in Australia. Eighty percent of methicillin-resistant SAB, however, were due to community-associated clones. Although polyclonal, approximately 71.4% of community-associated clones were variously characterised as ST93-IV [2B] (Queensland CA-MRSA), ST5-IV [2B], ST45-V [5C2&5], ST1-IV [2B], ST30-IV [2B], ST78-IV [2B] and ST8-IV [2B]. Community-associated MRSA (CA-MRSA), in particular the ST45-V [5C2&5] clone, have acquired multiple antimicrobial resistance determinants including ciprofloxacin, erythromycin, clindamycin, gentamicin and tetracycline. The multiresistant ST45-V [5C2&5] clone accounted for 12.7% of CA-MRSA. As CA-MRSA is well established in the Australian community, it is important that antimicrobial resistance patterns in community- and healthcare-associated SAB are monitored, as this information will guide therapeutic practices in treating sepsis.
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http://dx.doi.org/10.33321/cdi.2020.44.71DOI Listing
September 2020

Identification and characterisation of fosfomycin resistance in Escherichia coli urinary tract infection isolates from Australia.

Int J Antimicrob Agents 2020 Oct 31;56(4):106121. Epub 2020 Jul 31.

Murdoch University, 90 South Street, Murdoch, WA 6150, Australia; Fiona Stanley Hospital, PathWest Laboratory Medicine WA, Murdoch, WA, Australia.

Of 1033 Escherichia coli urinary tract infection isolates collected from females >12 years of age in Australia in 2019, only 2 isolates were resistant to fosfomycin with a minimum inhibitory concentration (MIC) of >256 mg/L. Despite having different multilocus sequence types, the two isolates harboured an identical plasmid-encoded fosA4 gene. The fosA4 gene has previously been identified in a single clinical E. coli isolate cultured in Japan in 2014. Each fosfomycin-resistant isolate harboured two conjugative plasmids that possessed an array of genes conferring resistance to aminoglycosides, β-lactams, macrolides, quinolones, sulfonamides and/or trimethoprim.
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http://dx.doi.org/10.1016/j.ijantimicag.2020.106121DOI Listing
October 2020

Australian Group on Antimicrobial Resistance (AGAR) Australian Staphylococcus aureus Sepsis Outcome Programme (ASSOP) Annual Report 2018.

Commun Dis Intell (2018) 2020 Mar 16;44. Epub 2020 Mar 16.

Antimicrobial Resistance and Infectious Disease (AMRID) Research Laboratory, Murdoch University, Murdoch, Western Australia, Australia; Department of Microbiology, PathWest Laboratory Medicine-WA, Fiona Stanley Hospital, Murdoch, Western Australia, Australia.

From 1 January to 31 December 2018, thirty-six institutions around Australia participated in the Australian Sepsis Outcome Programme (ASSOP). The aim of ASSOP 2018 was to determine the proportion of bacteraemia (SAB) isolates in Australia that are antimicrobial resistant, with particular emphasis on susceptibility to methicillin, and to characterise the molecular epidemiology of the methicillin-resistant isolates. A total of 2,673 bacteraemia episodes were reported, of which 78.9% were community-onset. A total of 17.4% of isolates were methicillin resistant. The 30-day all-cause mortality associated with methicillin-resistant SAB was 17.1% which was not significantly higher than the 13.6% mortality associated with methicillin-susceptible SAB (p = 0.1). With the exception of the β-lactams and erythromycin, antimicrobial resistance in methicillin-susceptible was rare. However in addition to the β-lactams approximately 42% of methicillin-resistant (MRSA) were resistant to erythromycin, 36% to ciprofloxacin and approximately 13% resistant to co-trimoxazole, tetracycline and gentamicin. When applying the EUCAST breakpoints teicoplanin resistance was detected in two isolates. Resistance was not detected for vancomycin and linezolid. Resistance to non-beta-lactam antimicrobials was largely attributable to two healthcare-associated MRSA clones: ST22-IV [2B] (EMRSA-15) and ST239-III [3A] (Aus-2/3 EMRSA). The ST22-IV [2B] (EMRSA-15) clone is the predominant healthcare-associated clone in Australia. Seventy-eight percent of methicillin-resistant SAB episodes in 2018 were due to community-associated clones. Although polyclonal, approximately 76.3% of community-associated clones were characterised as ST93-IV [2B] (Queensland CA-MRSA), ST5-IV [2B], ST45-VT [5C2&5], ST1-IV [2B], ST30-IV [2B], ST78-IV [2B] and ST97-IV [2B]. Community-associated MRSA, in particular the ST45-VT [5C2&5] clone, has acquired multiple antimicrobial resistance determinants including ciprofloxacin, erythromycin, clindamycin, gentamicin and tetracycline. The ST45-VT [5C2&5] clone accounted for 11.7% of CA-MRSA. As CA-MRSA is well established in the Australian community, it is important that antimicrobial resistance patterns in community- and healthcare-associated SAB are monitored, as this information will guide therapeutic practices in treating sepsis.
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http://dx.doi.org/10.33321/cdi.2020.44.18DOI Listing
March 2020

Australian Group on Antimicrobial Resistance (AGAR) Australian Enterococcal Sepsis Outcome Programme (AESOP) Annual Report 2018.

Commun Dis Intell (2018) 2020 Mar 16;44. Epub 2020 Mar 16.

Antimicrobial Resistance and Infectious Disease (AMRID) Research Laboratory, Murdoch University, Murdoch, Western Australia, Australia; Department of Microbiology, PathWest Laboratory Medicine-WA, Fiona Stanley Hospital, Murdoch, Western Australia, Australia.

From 1 January to 31 December 2018, thirty-six institutions around Australia participated in the Australian Enterococcal Sepsis Outcome Programme (AESOP). The aim of AESOP 2018 was to determine the proportion of enterococcal bacteraemia isolates in Australia that were antimicrobial resistant, and to characterise the molecular epidemiology of the isolates. Of the 1,248 unique episodes of bacteraemia investigated, 93.5% were caused by either (54.2%) or (39.3%). Ampicillin resistance was not detected in but was detected in 89.4% of . Vancomycin non-susceptibility was not detected in but was reported in 45.0% of . Overall 49.3% of isolates harboured vanA or vanB genes. Of the / positive isolates, 52.9% harboured genes and 46.2% genes; 0.8% harboured both and genes. The percentage of bacteraemia isolates resistant to vancomycin in Australia is substantially higher than that seen in most European countries. consisted of 59 multilocus sequence types (STs) of which 74.4% of isolates were classified into six major STs containing ten or more isolates. All major STs belong to clonal cluster (CC) 17, a major hospital-adapted polyclonal cluster. The predominant STs (ST17, ST1424, ST796, ST80, ST1421, and ST262) were found across most regions of Australia. The most predominant clone was ST17 which was identified in all regions except the Australian Capital Territory and the Northern Territory. Overall, 55.8% of isolates belonging to the six predominant STs harboured or genes. The AESOP 2018 study has shown that enterococcal bacteraemias in Australia are frequently caused by polyclonal ampicillin-resistant high-level gentamicin-resistant - or -harbouring which have limited treatment options.
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http://dx.doi.org/10.33321/cdi.2020.44.19DOI Listing
March 2020

Sulfamethoxazole/trimethoprim resistance overcall by VITEK® 2 and BD Phoenix™ in community-associated MRSA and MSSA.

J Antimicrob Chemother 2019 12;74(12):3639-3641

Antimicrobial Resistance and Infectious Diseases Laboratory, School of Veterinary Life Sciences, Murdoch University, Murdoch, Western Australia, Australia.

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http://dx.doi.org/10.1093/jac/dkz361DOI Listing
December 2019

Structural and biochemical insights into the disulfide reductase mechanism of DsbD, an essential enzyme for neisserial pathogens.

J Biol Chem 2018 10 4;293(43):16559-16571. Epub 2018 Sep 4.

From the Department of Biochemistry and Genetics, La Trobe Institute for Molecular Science, La Trobe University, Melbourne 3086, Victoria, Australia,

The worldwide incidence of neisserial infections, particularly gonococcal infections, is increasingly associated with antibiotic-resistant strains. In particular, extensively drug-resistant strains that are resistant to third-generation cephalosporins are a major public health concern. There is a pressing clinical need to identify new targets for the development of antibiotics effective against -specific processes. In this study, we report that the bacterial disulfide reductase DsbD is highly prevalent and conserved among spp. and that this enzyme is essential for survival of DsbD is a membrane-bound protein that consists of two periplasmic domains, n-DsbD and c-DsbD, which flank the transmembrane domain t-DsbD. In this work, we show that the two functionally essential periplasmic domains of DsbD catalyze electron transfer reactions through unidirectional interdomain interactions, from reduced c-DsbD to oxidized n-DsbD, and that this process is not dictated by their redox potentials. Structural characterization of the n- and c-DsbD domains in both redox states provides evidence that steric hindrance reduces interactions between the two periplasmic domains when n-DsbD is reduced, thereby preventing a futile redox cycle. Finally, we propose a conserved mechanism of electron transfer for DsbD and define the residues involved in domain-domain recognition. Inhibitors of the interaction of the two DsbD domains have the potential to be developed as anti-neisserial agents.
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http://dx.doi.org/10.1074/jbc.RA118.004847DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6204915PMC
October 2018

Differences in the population structure of Neisseria meningitidis in two Australian states: Victoria and Western Australia.

PLoS One 2017 24;12(10):e0186839. Epub 2017 Oct 24.

Marshall Center for Infectious Disease Research and Training, School of Biomedical Sciences, The University of Western Australia, Perth, Western Australia, Australia.

Neisseria meningitidis is the causative agent of invasive meningococcal disease (IMD). A recombinant vaccine called Bexsero® incorporates four subcapsular antigens (fHbp, NHBA, NadA and PorA) which are used to assign a Bexsero® antigen sequence type (BAST) to each meningococcal strain. The vaccine elicits an immune response against combinations of variants of these antigens which have been grouped into specific BAST profiles that have been shown to have different distributions within geographical locations thus potentially affecting the efficacy of the vaccine. In this study, invasive meningococcal disease isolates from the western seaboard of Australia (Western Australia; WA) were compared to those from the south-eastern seaboard (Victoria; VIC) from 2008 to 2012. Whole-genome sequencing (WGS) of 131 meningococci from VIC and 70 meningococci from WA were analysed for MLST, FetA and BAST profiling. Serogroup B predominated in both jurisdictions and a total of 10 MLST clonal complexes (cc) were shared by both states. Isolates belonging to cc22, cc103 and cc1157 were unique to VIC whilst isolates from cc60 and cc212 were unique to WA. Clonal complex 41/44 represented one-third of the meningococcal population in each state but the predominant ST was locally different: ST-6058 in VIC and ST-146 in WA. Of the 108 BAST profiles identified in this collection, only 9 BASTs were simultaneously observed in both states. A significantly larger proportion of isolates in VIC harboured alleles for the NHBA-2 peptide and fHbp-1, antigenic variants predicted to be covered by the Bexsero® vaccine. The estimate for vaccine coverage in WA (47.1% [95% CI: 41.1-53.1%]) was significantly lower than that in VIC (66.4% [95% CI: 62.3-70.5%]). In conclusion, the antigenic structure of meningococci causing invasive disease in two geographically distinct states of Australia differed significantly during the study period which may affect vaccine effectiveness and highlights the need for representative surveillance when predicting potential impact of meningococcal B vaccines.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0186839PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5655437PMC
November 2017

Clonal Expansion of New Penicillin-Resistant Clade of Neisseria meningitidis Serogroup W Clonal Complex 11, Australia.

Emerg Infect Dis 2017 08 15;23(8):1364-1367. Epub 2017 Aug 15.

In Western Australia, Neisseria meningitidis serogroup W clonal complex 11 became the predominant cause of invasive meningococcal disease in 2016. We used core-genome analysis to show emergence of a penicillin-resistant clade that had the penA_253 allele. This new penicillin-resistant clade might affect treatment regimens for this disease.
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http://dx.doi.org/10.3201/eid2308.170259DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5547816PMC
August 2017

Acquisition of the capsule locus by horizontal gene transfer in Neisseria meningitidis is often accompanied by the loss of UDP-GalNAc synthesis.

Sci Rep 2017 03 14;7:44442. Epub 2017 Mar 14.

School of Biomedical Sciences, University of Western Australia, Perth, Australia.

Pathogenic meningococci have acquired a 24 kb capsule synthesis island (cps) by horizontal gene transfer which consists of a synthetic locus and associated capsule transport genes flanked by repetitive Regions D and D'. Regions D and D' contain an intact gene encoding a UDP-galactose epimerase (galE1) and a truncated remnant (galE2), respectively. In this study, GalE protein alleles were shown to be either mono-functional, synthesising UDP-galactose (UDP-Gal), or bi-functional, synthesising UDP-Gal and UDP-galactosamine (UDP-GalNAc). Meningococci possessing a capsule null locus (cnl) typically possessed a single bi-functional galE. Separation of functionality between galE1 and galE2 alleles in meningococcal isolates was retained for all serogroups except serogroup E which has a synthetic requirement for UDP-GalNAc. The truncated galE2 remnant in Region D' was also phylogenetically related to the bi-functional galE of the cnl locus suggesting common ancestry. A model is proposed in which the illegitimate recombination of the cps island into the galE allele of the cnl locus results in the formation of Region D' containing the truncated galE2 locus and the capture of the cps island en bloc. The retention of the duplicated Regions D and D' enables inversion of the synthetic locus within the cps island during bacterial growth.
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http://dx.doi.org/10.1038/srep44442DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5349592PMC
March 2017

Temporal Changes in BEXSERO® Antigen Sequence Type Associated with Genetic Lineages of Neisseria meningitidis over a 15-Year Period in Western Australia.

PLoS One 2016 29;11(6):e0158315. Epub 2016 Jun 29.

Marshall Centre for Infectious Disease Research and Training, School of Pathology and Laboratory Medicine, University of Western Australia, Perth, Australia.

Neisseria meningitidis is the causative agent of invasive meningococcal disease (IMD). The BEXSERO® vaccine which is used to prevent serogroup B disease is composed of four sub-capsular protein antigens supplemented with an outer membrane vesicle. Since the sub-capsular protein antigens are variably expressed and antigenically variable amongst meningococcal isolates, vaccine coverage can be estimated by the meningococcal antigen typing system (MATS) which measures the propensity of the strain to be killed by vaccinated sera. Whole genome sequencing (WGS) which identifies the alleles of the antigens that may be recognised by the antibody response could represent, in future, an alternative estimate of coverage. In this study, WGS of 278 meningococcal isolates responsible for 62% of IMD in Western Australia from 2000-2014 were analysed for association of genetic lineage (sequence type [ST], clonal complex [cc]) with BEXSERO® antigen sequence type (BAST) and MATS to predict the annual vaccine coverage. A hyper-endemic period of IMD between 2000-05 was caused by cc41/44 with the major sequence type of ST-146 which was not predicted by MATS or BAST to be covered by the vaccine. An increase in serogroup diversity was observed between 2010-14 with the emergence of cc11 serogroup W in the adolescent population and cc23 serogroup Y in the elderly. BASTs were statistically associated with clonal complex although individual antigens underwent antigenic drift from the major type. BAST and MATS predicted an annual range of 44-91% vaccine coverage. Periods of low vaccine coverage in years post-2005 were not a result of the resurgence of cc41/44:ST-146 but were characterised by increased diversity of clonal complexes expressing BASTs which were not predicted by MATS to be covered by the vaccine. The driving force behind the diversity of the clonal complex and BAST during these periods of low vaccine coverage is unknown, but could be due to immune selection and inter-strain competition with carriage of non-disease causing meningococci.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0158315PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4927168PMC
July 2017

The role of oxidoreductases in determining the function of the neisserial lipid A phosphoethanolamine transferase required for resistance to polymyxin.

PLoS One 2014 12;9(9):e106513. Epub 2014 Sep 12.

School of Pathology and Laboratory Medicine, and The Marshall Center for Infectious Diseases, Research and Training, University of Western Australia, Perth, Western Australia, Australia.

The decoration of the lipid A headgroups of the lipooligosaccharide (LOS) by the LOS phosphoethanolamine (PEA) transferase (LptA) in Neisseria spp. is central for resistance to polymyxin. The structure of the globular domain of LptA shows that the protein has five disulphide bonds, indicating that it is a potential substrate of the protein oxidation pathway in the bacterial periplasm. When neisserial LptA was expressed in Escherichia coli in the presence of the oxidoreductase, EcDsbA, polymyxin resistance increased 30-fold. LptA decorated one position of the E. coli lipid A headgroups with PEA. In the absence of the EcDsbA, LptA was degraded in E. coli. Neisseria spp. express three oxidoreductases, DsbA1, DsbA2 and DsbA3, each of which appear to donate disulphide bonds to different targets. Inactivation of each oxidoreductase in N. meningitidis enhanced sensitivity to polymyxin with combinatorial mutants displaying an additive increase in sensitivity to polymyxin, indicating that the oxidoreductases were required for multiple pathways leading to polymyxin resistance. Correlates were sought between polymyxin sensitivity, LptA stability or activity and the presence of each of the neisserial oxidoreductases. Only meningococcal mutants lacking DsbA3 had a measurable decrease in the amount of PEA decoration on lipid A headgroups implying that LptA stability was supported by the presence of DsbA3 but did not require DsbA1/2 even though these oxidoreductases could oxidise the protein. This is the first indication that DsbA3 acts as an oxidoreductase in vivo and that multiple oxidoreductases may be involved in oxidising the one target in N. meningitidis. In conclusion, LptA is stabilised by disulphide bonds within the protein. This effect was more pronounced when neisserial LptA was expressed in E. coli than in N. meningitidis and may reflect that other factors in the neisserial periplasm have a role in LptA stability.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0106513PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4162559PMC
May 2015

Attachment and invasion of Neisseria meningitidis to host cells is related to surface hydrophobicity, bacterial cell size and capsule.

PLoS One 2013 6;8(2):e55798. Epub 2013 Feb 6.

School of Pathology and Laboratory Medicine, The University of Western Australia, Perth, Western Australia, Australia.

We compared exemplar strains from two hypervirulent clonal complexes, strain NMB-CDC from ST-8/11 cc and strain MC58 from ST-32/269 cc, in host cell attachment and invasion. Strain NMB-CDC attached to and invaded host cells at a significantly greater frequency than strain MC58. Type IV pili retained the primary role for initial attachment to host cells for both isolates regardless of pilin class and glycosylation pattern. In strain MC58, the serogroup B capsule was the major inhibitory determinant affecting both bacterial attachment to and invasion of host cells. Removal of terminal sialylation of lipooligosaccharide (LOS) in the presence of capsule did not influence rates of attachment or invasion for strain MC58. However, removal of either serogroup B capsule or LOS sialylation in strain NMB-CDC increased bacterial attachment to host cells to the same extent. Although the level of inhibition of attachment by capsule was different between these strains, the regulation of the capsule synthesis locus by the two-component response regulator MisR, and the level of surface capsule determined by flow cytometry were not significantly different. However, the diplococci of strain NMB-CDC were shown to have a 1.89-fold greater surface area than strain MC58 by flow cytometry. It was proposed that the increase in surface area without changing the amount of anchored glycolipid capsule in the outer membrane would result in a sparser capsule and increase surface hydrophobicity. Strain NMB-CDC was shown to be more hydrophobic than strain MC58 using hydrophobicity interaction chromatography and microbial adhesion-to-solvents assays. In conclusion, improved levels of adherence of strain NMB-CDC to cell lines was associated with increased bacterial cell surface and surface hydrophobicity. This study shows that there is diversity in bacterial cell surface area and surface hydrophobicity within N. meningitidis which influence steps in meningococcal pathogenesis.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0055798PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3566031PMC
August 2013