关于 Neisseria meningitidis

The Gram-negative species Neisseria meningitidis (Nme) belongs to the β-subgroup of proteobacteria^[1]. In 1887, Weichselbaum  was the first to identify the meningococcus from the cerebrospinal fluid of a patient with meningitis^[2]. Nme is only rarely pathogenic, causing invasive meningococcal disease (IMD)^[3]. Nme normally colonises the nasopharyngeal epithelium in humans and is transmitted by aerosolised droplets or contact with infected fluids such as saliva. IMD occurs when the meningococcus crosses the nasopharyngeal epithelium and enters the bloodstream, resulting in the rapid onset of septicaemia and/or meningitis^[4].

MLST was originally developed for the meningococcus but is now widely used for numerous bacterial pathogens^[5]. Strains can be grouped into different sequence types (STs) based on the multilocus sequence typing method on seven genes (abcZ, adk, aroE, fumC, gdh, pdhC, pgm)^[6].  STs sharing four or more common alleles are grouped into a single clonal complex named after the putative “ancestral” ST^[7]. The earliest typing scheme developed for the meningococcus was based on agglutination reactions against the polysaccharide capsule using immune rabbit serum. On this basis, thirteen serogroups were defined (A, B, C, D, E, H, I, K, L, W, X, Y, and Z), the majority of disease is caused by organisms expressing one of six capsule types namely A, B, C, W, X, and Y and belonging to one of eleven clonal complexes (cc1, cc4/5, cc8, cc11, cc18, cc32, cc41/44, cc103, cc269, cc334, and cc461). These clonal complexes are termed the hyperinvasive (or hypervirulent) lineages. Hyperinvasive lineages are most frequently associated with disease, while carriage lineages such as cc53 are associated exclusively with carriage. Other lineages, including cc22, cc23, cc60, cc162, cc174, cc213, cc364, and cc4821, exhibit weaker associations with disease^[8].

Beta-lactam antibiotics (including penicillin, ampicillin, and ceftriaxone), fluoroquinolones (such as ciprofloxacin), and chloramphenicol have all been used as empirical treatment for IMD, with ceftriaxone being the usual antibiotic of choice^[9]. Treatment of IMD will generally not result in the dissemination of resistant variants into the population.

Vaccination is a primary means of prevention and control for IMD. There are two types of meningococcal vaccines commonly in use: conjugate polysaccharide vaccines, of which a quadrivalent vaccine covering MenACWY (brand names Nimenrix, Menactra, and Menveo) is most commonly used, and outer-membrane-vesicle-based multivalent protein vaccines (brand names Bexsero and Trumenba), which are used primarily to control MenB disease since the MenB capsule is an autoantigen^[10].

The most important virulence factors of the meningococcus related to oro-nasopharyngeal colonisation include the immunoglobulin A1 (IgA1) protease and the anti-phagocytic polysaccharide capsule, as well as a series of epithelium-binding bacterial adhesins. The IgA1 protease, which is most important in previously exposed individuals, is a site-specific serine protease. It cleaves the antibody molecule at the hinge region, separating the Fab and Fc regions, thereby preventing expulsion of the pathogen via mucociliary clearance, favouring attachment to respiratory epithelium. In addition to its primary function of counteracting phagocytosis, the polysaccharide capsule of the meningococcus repels mucus, also hindering mucociliary clearance^[11].

收集的数据

---

数据来源

---

收集日期

Samples collection date:

---

宿主来源

Samples host information:

---

血清型(Serotype）

Serotype information:

---

菌株MLST

Samples MLST information:

---

进化分支(Phylogroup)

Samples phylogroup information:

---

毒力基因

Samples Virulence information:

---

抗性基因

Samples Resistance information: