scholarly journals A Narrative Review of the W, X, Y, E, and NG of Meningococcal Disease: Emerging Capsular Groups, Pathotypes, and Global Control

2021 ◽  
Vol 9 (3) ◽  
pp. 519
Author(s):  
Yih-Ling Tzeng ◽  
David S. Stephens

Neisseria meningitidis, carried in the human nasopharynx asymptomatically by ~10% of the population, remains a leading cause of meningitis and rapidly fatal sepsis, usually in otherwise healthy individuals. The epidemiology of invasive meningococcal disease (IMD) varies substantially by geography and over time and is now influenced by meningococcal vaccines and in 2020–2021 by COVID-19 pandemic containment measures. While 12 capsular groups, defined by capsular polysaccharide structures, can be expressed by N. meningitidis, groups A, B, and C historically caused most IMD. However, the use of mono-, bi-, and quadrivalent-polysaccharide-conjugate vaccines, the introduction of protein-based vaccines for group B, natural disease fluctuations, new drugs (e.g., eculizumab) that increase meningococcal susceptibility, changing transmission dynamics and meningococcal evolution are impacting the incidence of the capsular groups causing IMD. While the ability to spread and cause illness vary considerably, capsular groups W, X, and Y now cause significant IMD. In addition, group E and nongroupable meningococci have appeared as a cause of invasive disease, and a nongroupable N. meningitidis pathotype of the hypervirulent clonal complex 11 is causing sexually transmitted urethritis cases and outbreaks. Carriage and IMD of the previously “minor” N. meningitidis are reviewed and the need for polyvalent meningococcal vaccines emphasized.

2020 ◽  
Vol 8 (11) ◽  
pp. 1675
Author(s):  
Stephen A. Clark ◽  
Ray Borrow

Reduction in the transmission of Neisseria meningitidis within a population results in fewer invasive disease cases. Vaccination with meningococcal vaccines composed of high weight capsular polysaccharide without carrier proteins has minimal effect against carriage or the acquisition of carriage. Conjugate vaccines, however, elicit an enhanced immune response which serves to reduce carriage acquisition and hinder onwards transmission. Since the 1990s, several meningococcal conjugate vaccines have been developed and, when used in age groups associated with higher carriage, they have been shown to provide indirect protection to unvaccinated cohorts. This herd protective effect is important in enhancing the efficiency and impact of vaccination. Studies are ongoing to assess the effect of protein-based group B vaccines on carriage; however, current data cast doubt on their ability to reduce transmission.


Author(s):  
Mark McMillan ◽  
Abira Chandrakumar ◽  
Hua Lin Rachael Wang ◽  
Michelle Clarke ◽  
Thomas R Sullivan ◽  
...  

Abstract Background Invasive meningococcal disease (IMD), caused by Neisseria meningitidis, leads to significant morbidity and mortality worldwide. This review aimed to establish the effectiveness of meningococcal vaccines at preventing IMD and N. meningitidis pharyngeal carriage. Methods A search within PubMed, Embase, Scopus, and unpublished studies up to 1st February 2020 was conducted. Results After removal of duplicates, 8565 were screened and 28 studies included. Protection was provided by meningococcal C vaccines for group C IMD (odds ratio (OR) 0·13 [95% CI, 0·07-0·23]), outer membrane vesicle (OMV) vaccines against group B IMD (OR 0·35 [0·25-0·48]), and meningococcal ACWY (MenACWY) vaccines against group ACWY IMD (OR 0·31 [0·20-0·49]). A single time series analysis found a reduction following an infant 4CMenB program (incidence rate ratio, 0·25 [0·19-0·36]). Multivalent MenACWY vaccines did not reduce carriage (relative risk [RR] 0·88 [0·66-1·18]), unlike monovalent A (RR 0·73 [0·61-0·85]), and C vaccines (RR 0·50 [0·26-0·97]). 4CMenB vaccine had no effect on group B carriage (RR 1·12 [0·90-1·40]). There was also no reduction in group B carriage following MenB-FHbp vaccination (RR 0.98 [0.53-1.79]). Conclusions Meningococcal conjugate C, ACWY, and OMV vaccines are effective at reducing IMD. A small number of studies demonstrate that monovalent C and A conjugate vaccines reduce pharyngeal N. meningitidis carriage. There is no evidence of carriage reduction for multivalent MenACWY, OMV, or recombinant meningococcal B vaccines, which has implications for immunisation strategies. Registration PROSPERO CRD42018082085


2016 ◽  
Vol 54 (7) ◽  
pp. 1774-1781 ◽  
Author(s):  
Areej Alhhazmi ◽  
Donna Hurteau ◽  
Gregory J. Tyrrell

Group B streptococci (GBS) cause severe invasive disease in both neonates and adults. Understanding the epidemiology of GBS provides information that can include determining disease prevalence rates in defined populations and geographic regions, documenting the success of GBS screening programs, and understanding antimicrobial susceptibility patterns. In Alberta, only neonatal invasive GBS (iGBS) disease is notifiable to health authorities. We performed a surveillance study of iGBS in Alberta, Canada, from 2003 to 2013. Over the 11-year period, the disease incidence rate increased from a low of 3.92 cases/100,000 population to a high of 5.99 cases/100,000 population. The capsular polysaccharide serotypes (CPSs) found were CPS III (20.3%), CPS V (19.1%), CPS Ia (18.9%), CPS Ib (12.7%), CPS II (11.1%), CPS IV (6.3%), and nontypeable GBS (9.4%). Rates of early-onset disease (0 to 7 days) increased from 0.15 cases/1,000 live births (in 2003) to 0.34 cases/1,000 live births (in 2013). Rates of late-onset disease (>7 to 90 days) also rose, from 0.15 cases/1,000 live births (in 2003) to 0.39 cases/1,000 live births (in 2013). Alberta also experienced an increase in CPS IV isolates, from 2 cases (in 2003) to 24 cases (in 2013), of which the majority werehvgApositive (86.6%). The predominant sequence type (ST) in 2013 was ST459. Erythromycin resistance rose from 23.6% to 43.9% (in 2013). Clindamycin resistance also increased, from 12.2% to 32.5%. In summary, Alberta, Canada, has experienced an increase in GBS disease; the increase includes both neonatal and adult disease. CPS IV cases also notably increased during the surveillance period, as did resistance to erythromycin and clindamycin.


2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Sarah Teatero ◽  
Erin Ramoutar ◽  
Allison McGeer ◽  
Aimin Li ◽  
Roberto G. Melano ◽  
...  

2019 ◽  
Vol 209 (2) ◽  
pp. 95-108 ◽  
Author(s):  
Beata Młynarczyk-Bonikowska ◽  
Anna Majewska ◽  
Magdalena Malejczyk ◽  
Grażyna Młynarczyk ◽  
Sławomir Majewski

AbstractNeisseria gonorrhoeae is an etiologic agent of gonorrhoea, one of the most common sexually transmitted diseases caused by bacteria. For many years, infections caused by N. gonorrhoeae were considered to be relatively easy to treat; however, resistance has emerged successively to all therapeutic agents used in treatment of the disease, e.g., penicillin, ciprofloxacin or azithromycin. Currently, the global problem is the emergence and a threat of spread of N. gonorrhoeae strains resistant to extended-spectrum cephalosporins (ESC), such as injectable ceftriaxone and oral-used cefixime. Especially, dangerous are multi-resistant strains resistant simultaneously to ESC and azithromycin. Three strains with high-level resistance to azithromycin and resistant to ESC were first time isolated in 2018. Moreover, in 2018, the first ESBL was described in N. gonorrhoeae and that makes the threat of appearing the ESBL mechanism of resistance in N. gonorrhoeae more real, even though the strain was sensitive to ceftriaxone. Molecular typing revealed that variants resistant to ESC occurred also among strains belonging to epidemic clonal complex CC1 (genogroup G1407) distinguished in NG-MAST typing system. The G1407 genogroup, in particular the ST1407 sequence type, is currently dominant in most European countries. The presence of different mechanisms of drug resistance significantly affects clinical practice and force changes in treatment regimens and introduction of new drugs.


2005 ◽  
Vol 134 (2) ◽  
pp. 377-383 ◽  
Author(s):  
K. H. DYET ◽  
D. R. MARTIN

An epidemic of meningococcal disease caused by serogroup B meningococci expressing the P1.7-2,4 PorA protein began in New Zealand in 1991. The PorA type has remained stable. Different porB have been found in association with the P1.7-2,4 PorA, although type 4 has been most common. The clonal origins of B:P1.7-2,4 meningococci isolated from cases during 1990 to the end of 2003 were analysed. In 1990, the year immediately preceding the recognized increase in disease rates, all three subclones (ST-41, ST-42, and ST-154) of the ST-41/44 clonal complex occurred among the five isolates of B:P1.7-2,4. The two sequence types, ST-42 and ST-154, continued to cause most disease throughout New Zealand. Isolates belonging to subclone ST-41 were mostly identified early in the epidemic and in the South Island. 16S rRNA typing indicated that isolates belonging to the subclones ST-41 and ST-154 share a common ancestor, with those typing as ST-42 more distantly related with some genetically ambiguous. It is possible that ST-41 and ST-154 may have evolved one from the other but evolution to ST-42 is more difficult to explain. It is possible that one or more of the ST types could have been introduced into New Zealand prior to the first detection of clinical cases in 1990. Genetic diversity may have occurred during carriage in the community.


2001 ◽  
Vol 20 (2) ◽  
pp. 221-227 ◽  
Author(s):  
Seth H. Pincus ◽  
Stephen R. Lepage ◽  
Robert F. Jung ◽  
Jennifer G. Massey ◽  
Mahesh Jaseja

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