Meningococcemia pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Pathophysiology

• Meningococcal disease is caused by the bacterium Neisseria meningitidis, also called meningococcus.
• About 10% of people have this type of bacteria in the back of their nose and throat with no signs or symptoms of disease, called being 'a carrier'. But sometimes Neisseria meningitidis bacteria can invade the body causing certain illnesses, which are known as meningococcal disease.

Transmission

• Neisseria meningitidis bacteria are spread through the exchange of respiratory and throat secretions like spit (e.g., by living in close quarters, kissing). Fortunately, these bacteria are not as contagious as germs that cause the common cold or the flu. The bacteria are not spread by casual contact or by simply breathing the air where a person with meningococcal disease has been.
• Sometimes Neisseria meningitidis bacteria spread to people who have had close or lengthy contact with a patient with meningococcal disease. People in the same household, roommates, or anyone with direct contact with a patient's oral secretions, meaning saliva or spit, (such as a boyfriend or girlfriend) would be considered at increased risk of getting the infection.
• People who qualify as close contacts of a person with meningococcal disease should receive antibiotics to prevent them from getting the disease. This is known as prophylaxis (pro-fuh-lak-sis). The health department investigates each case of meningococcal disease to make sure all close contacts are identified and receive prophylaxis. This does not mean that the contacts have the disease; it is to prevent it.

Progression

• Shock is due to lipooligosaccharide which is a potent toxin. This toxin initiates release of inflammatory cytokines, reactive oxygen radicals, prostaglandins, arachidonic acid, complement activated products, platelet aggregating factor, and perhaps nitric oxide.
• The bacteria attach to and multiply on the mucosal cells of the nasopharynx.
• In a small proportion (less than 1%) of colonized persons, the organism penetrates the mucosal cells and enters the bloodstream.
• The bacteria spread by way of the blood to many organs. In about 50% of bacteremic persons, the organism crosses the blood–brain barrier into the cerebrospinal fluid and causes purulent meningitis. An antecedent upper respiratory infection may be a contributing factor.
• The bacteria attach to and multiply on the mucosal cells of the nasopharynx.
• In a small proportion (less than 1%) of colonized persons, the organism penetrates the mucosal cells and enters the bloodstream.
• The bacteria spread by way of the blood to many organs. In about 50% of bacteremic persons, the organism crosses the blood–brain barrier into the cerebrospinal fluid and causes purulent meningitis.
• An antecedent upper respiratory infection may be a contributing factor.

Molecular pathophysiology of meningococcemia

• The toll like receptor system (TLR) place a role in protecting the body from invasive pathogens. It also causes destruction of host in fulminent infections.
• The cell wall of Neisseria meningitidis has different types of molecules that activate the TLR system in a dose dependent manner and release inflammatory mediators which can cause organ dysfunction and meningococcemia.
• The lipopolysacchrides in the outer membrane of the organism also illicit immune response.
• Peptidoglycan, bacterial lipoprotein and genetic polymorphism also contribute to broaden the inflammatory response.
• There is a close association between the load of meningococci, being alive or dead in CSF (cerebrospinal fluid) and plasma and magnitude of inflammatory response to the patient.

Classification of clinical presentations

• They present with a wide range of clinical conditions from transient bacteremia to rapidly progressing septicemia.
• Most of them develop meningitis as meningococci invade the meninges.
• Meningococcal infections are classified into four different clinical groups based on the following conditions.

• Presence or absence of signs of septic shock.
• Presence or absence of clinical symptoms and laboratory signs of distinct meningitis.

Clinical group	Characteristic feature	Case fatality
Fulminent meningocccal septicemia	Severe persistent septic shock lasting for >24 hours or until death and minimal pleocytosis or lack of clinical signs of meningitis.	25-55%
Distinct meningitis	Marked pleocytosis or distinct clinical signs of meningitis.	10-25%
Distinct meningitis and persistent septic shock.	Marked pleocytosis or distinct signs of meningitis and severe persistent septic shock.	<5%
Mild systemic meningococcal infection	Mild meningococcemia without developing persistent septic shock or distinct meningitis.	0%

Infection

• The meningococci which gets attached to the epithelium is transported across th epithelium by parasite directed endocytosis.
• This is facilitated by the induction of specific structural changes as a consequence of altered gene expression in the cells.

Distribution

Once the meningococci enter the circulation, they survive and multiply in it causing a systemic infection.

Neisseria meningitidis IgA1 protease

• Neisseria secretes IgA1 protease which splits IgA1 at the hinge region.

References

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