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I read the wikipedia article about Neisseria meningitidis, and it says that

N. meningitidis is a part of the normal nonpathogenic flora in the nasopharynx of up to 5–15% of adults

In some cases however, it infects the bloodstream, creating a Meningococcemia disease which is highly lethal. It may also create a meningococcal meningitis.

The article also says that this disease is somewhat infectious. Not as infectious as common cold, but it is known to cause epidemics in Africa and Asia.

My question is: How can it be so abundant in its non-pathogenic form (up to 15% of adults) yet cause epidemics? It seems that it's transmitted from nose to nose somehow and doesn't cause a disease, yet when it does cause a disease it also causes a disease upon transmission.

It's not like a strain of E. coli that may cause disease in immunosuppressed individuals yet is a part of normal microbiota for other people. Because then it wouldn't cause epidemics, since the majority of the population is immune to it as evidenced by the fact that it's part of their microbiota.

Does N. meningitidis mutate to become pathogenic? Do the nasal strain and the pathogenic strain have different genotypes?

I tried searching for an answer but didn't find any.

Thank you very much.

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  • $\begingroup$ Welcome to Biology.SE! This seems like an interesting question, but I would note that 5-15% is not "the majority of the population" ... β€”β€”β€” You may benefit from taking the time to go through the tour and the help pages starting with How to Ask questions effectively on this site. Thanks! 😊 $\endgroup$ – tyersome Nov 2 '19 at 17:46
  • $\begingroup$ If you can come up with a well supported (referenced) answer to your question I encourage you to post it as an answer here. β€”β€”β€” The wikipedia article on epidemics may be of interest. You also might want to read up on epidemiology and opportunistic pathogens β€” many "infections" by disease causing organisms can be asymptomatic (e.g. typhoid). $\endgroup$ – tyersome Nov 2 '19 at 18:06
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It's not like a strain of E. coli that may cause disease in immunosuppressed individuals yet is a part of normal microbiota for other people.

Well, actually, it is kind of like that.

The answer is complicated, but can be boiled down to, virulent serotypes of Neisseria meningitidis infect susceptible populations. For the short answer, just read between the highlighted boxes.

Invasive meningococcal disease results from the interplay of: (1) microbial factors influencing the virulence of the organism, (2) environmental conditions facilitating exposure and acquisition, and (3) host susceptibility factors favoring bacterial acquisition, colonization, invasion, and survival.

Virulent serotypes have capsules that help them evade detection and destruction; they have an outer envelope that helps them invade and infect susceptable individuals.

The virulence (14) of N. meningitidis is influenced by multiple factors: capsule polysaccharide expression, expression of surface adhesive proteins (outer membrane proteins including pili, porins PorA and B, adhesion molecules Opa and Opc), iron sequestration mechanisms, and endotoxin (lipooligosaccharide, LOS). N. meningitidis also has evolved genetic mechanisms resulting in a horizontal genetic exchange, high frequency phase, antigenic variation, and molecular mimicry, allowing the organism to successfully adapt at mucosal surfaces and invade the host.

The most susceptible populations are infants/babies (most frequently), young children and unvaccinated young adults (during outbreaks). These are the populations most likely to have no to low antibodies against the bacteria.

The meningococcus remains a common cause of bacterial meningitis in children and young adults in the USA (132), now mostly affecting children less than 2 years of age (102, 133). Two-thirds of meningococcal disease in the first year of life in the US occurs in infants less than 6 months of age (134). Worldwide, the rates of meningococcal disease are also highest for young children due to waning protective maternal antibody, but in epidemic outbreaks, older children and adolescents can have high rates of disease. Fifty percent of cases in infants in the US are due to serogroup B; serogroup C is mostly seen in adolescents and serogroups B and Y in older adults. Even though peak incidence occurs among infants and adolescents; one-third to one-half of sporadic cases are seen in adults older than 18 years.

Carrier state isn't lifelong or even year long, in fact, it can last as little as a few weeks.

When approximately 10% of individuals from the general population at any time were carrying N. meningitidis in the nasopharynx (Cartwright et al., 1987), the carriage rate was shown to be <3% in children younger than 4 years and increased to 24–37% in the age-group 15–24 years... Then carriage rates decrease to less than 10% in older age-groups.

and

Meningococcal carriage increases rapidly among university students in the first month of the academic year and much of this increase probably occurred during the first week (Neal et al., 2000). The study, performed at the University of Nottingham, UK, showed the carriage rate increased in the first week of term from 6.9 % on day 1, to 11.2 % on day 2, to 19.0 % on day 3 and to 23.1 % on day 4. High social mixing probably caused this increase.

Carrier state is influenced by protective antibodies, local mucosal factors, and lower virulence of the bacteria in carriers. Smokers, for example, are more likely to be carriers than non-smokers. The type of N. meningitidis also influences carrier vs. infected individuals.

In Norway, approximately 9% of the carriage isolates belonged to two of the known hypervirulent clonal complexes...

That is, of 100 carriers, less than 10% carry a very virulent type. Non-virulence or low-virulence is the norm.

A non-virulent strain can become virulent to others by sharing of DNA.

Because of mixed colonization with other bacteria and because of its duration, the carrier state is an ideal condition for horizontal gene transfer between different strains of meningococci, and between meningococci and other commensal bacterial species. The human nasopharynx may harbour diverse pathogenic bacteria, like N. meningitidis, H. influenzae, S. pneumoniae, as well as non-pathogenic bacteria, such as N. lactamica and the moraxellae.

Again, carriers ave protective antibodies.

Immunity to invasive meningococcal disease is dependent upon the presence of serum immunoglobulin G (IgG) which elicits bactericidal activity toward the infecting organism. Infants may be protected from meningococcal disease by the presence of maternal IgG which is obtained passively during gestation and lactation. Maternal immunity will be replaced by acquired immunity. Exposure to non-pathogenic Neisseria and other cross-reacting species in the nasopharynx increases the level of specific antibodies during childhood (Sanchez et al., 2001, 2002; Troncoso et al., 2000).

And

Carriage of commensal Neisseria, especially N. lactamica, is associated with a high titre of antibodies against N. meningitidis. Highly homologous structures are present in N. lactamica and N. meningitidis (Troncoso et al., 2000, 2001). Sera from mice immunized with N. lactamica and boosted with N. meningitidis have been shown to kill meningococci.

...Mucosal immunity is not able to prevent the colonization of the nasopharynx by meningococci, but it plays an important role in preventing the invasion of epithelial cell (Griffiss, 1995).

If that answers your question, that's what I hoped for, because the rest is a mystery to me. But remember, you aren't a lifelong carrier. You might be a weekslong carrier, and every exposure to a non-virulent serotype increases your immunity.

Neisseria meningitidis: Biology, Microbiology, and Epidemiology
Neisseria meningitidis: an overview of the carriage state

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  • $\begingroup$ Thank you for your answer. I'll have to reread it a few more times and also explore the sources your referenced before accepting though. Thank you very much for such a detailed answer. $\endgroup$ – iliar Nov 4 '19 at 22:49

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