Neisseria meningitidis
Jimmy Rolufs

Figure 1.  Neisseria meningitidis scanning EM

Neisseria meningitidis, also known as meningococcus, is a parasitic, aerobic, Gram-negative, nonmotile, coccal bacterium that is responsible for causing meningitis and meningococcal septicemia, a serious condition that causes hemorrhaging of the skin.  Symptoms of meningitis were first noted in 1805 but it was not isolated until 1887 by Weichselbaum. The colonies of N. meningitidis appear smooth, moist, and glistening.

At an ultrasonic level N. meningitidis has a prominent polysaccharide capsule not seen in the gonococcus. The capsule is antiphagocytic and is an important virulence factor is meningococcal disease. It is most often cultivated in a peptone-blood base medium in a moist chamber containing 5-10% carbon dioxide. The media must be incubated at 37oC prior to inoculation as the organism is very susceptible to temperatures above or below 37oC, a unique trait among bacteria. The bacterium also tends to undergo rapid autolysis after death both in vitro and vivo accounting for the endotoxin, called lipooligosaccharide, during septicemia and meningitis.

Figure 2. Skin rash caused by meningococcal septicemia

N. meningitidis tends to colonize in the posterior nasopharynx of humans who are the only known host. Meningococcus inhabits the human nasopharynx without causing a detectable disease. This carrier state may last for a few days to a few months which is important because it provides a reservoir for meningococcus infection but also stimulates host immunity.  Those who are colonized are carries of the pathogen and can transmit the disease to non-immune individuals. Transmission is often from person to person in aerosol form as a sneeze. It is noted however that it is not airborne but actual transmission is in the little drops of mucosa which take residence in the mucosal membranes of those exposed. Infection occurs when the bacteria cross the mucosal barrier and enter the bloodstream. After entry into the bloodstream how the bacteria enters the central nervous system through the blood brain barrier to affect the brain is still not understood.

Current research is being done on N. meningitidis of the regulation and differential expression of gdhA encoding NADP specific glutamate dehydrogenase in clinical isolates. This study is focusing on differentiating highly virulent strains from those that are not highly virulent. Another study is focusing on the type IV pilus retraction regulated by the PilC proteins in an effort to understand why N. meningitidis is able to have twitching motility.

From the efforts of research with N. meningitidis there are currently two vaccines available to prevent meningococcal disease in the United States. Menactra is for people age 11 to 55 and Menomune is for people outside this age range and travelers. However N. meningitidis has 13 clinical subgroups 6 of which are responsible for almost all meningitidis cases and there is not vaccine for sub group B, one of the six. These vaccines also have problems of their own having a short duration of action because they do not produce memory T cells. To the right is a structure of a known antibody and the binding site. The bacteria have the ability to change this binding site avoiding the attention of the immune system.

References:
http://www.cdc.gov/std/Gonorrhea/lab/Nmen.htm
http://microbewiki.kenyon.edu/index.php/Image:Neisseria.jpg
http://bioinfo.bact.wisc.edu/themicrobialworld/mmeningitis.htmlhttp://en.wikipedia.org/wiki/Neisseria_meningitidis

*Disclaimer - This report was written by a student participaring in a microbiology course at the Missouri University of Science and Technology. The accuracy of the contents of this report is not guaranteed and it is recommended that you seek additional sources of information to verify the contents.

 

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