Today we have to take a look back to our discussion in week
one. But now I am going to help you
understand what causes meningococcal meningitis, and how the meningitis comes
to be. Three conditions need to be
present in order for the disease to occur. 1) You must be exposed to the
pathogen. 2) You must acquire a strain
that can cause disease. 3) The bacteria must be able to invade
(Manchanda, Gupta, Bhalla, 2006).
The most prominent offender in this case is the bacterium Nisseria meningitides (Hoffman, Weber,
2009).
This bacterium can sit inside of a human who does not even realize
it. The most common place for the
bacteria to sit is in the nasal cavity. As
we also discussed before, this bacteria can travel from person to person by
sneezing, kissing, sharing drinks, and other ways that swap saliva. Then sometimes, that bacteria finds the
perfect host, such as one with damaged lining of the respiratory tract. Just like cars, there are multiple models of
the bacteria. Serogroups A, B, and C
contain capsules around itself and are the most likely to cause damage
(Manchanda, Gupta, Bhalla, 2006). If the
bacteria has the ability to work its way into the blood stream, it can multiply
to increasingly high numbers. By way of
the blood, the bacteria can travel to the brain and leak out, reaching the
layers of the meninges surrounding the brain as well as spinal cord (Pathan,
Faust, Levin, 2003).
As soon as the bacteria enter the blood, the body realizes
that something is not right. The body is
able to detect the bacterium’s endotoxin.
The body’s inherent response is to attack these foreign invaders
(Pathan, Faust, Levin, 2003). Our
natural defenders, the immune system, try’s to swoop in and get rid of the
offender. Our body’s best way to destroy
these unwanted bacteria is through regulated processes of inflammation. The endotoxin continues to send red flags to
the immune system, which allows inflammation of the meninges to continue
(Hoffman, Weber, 2009). The bacteria
also cause microvascular damage due to its presence in the bloodstream that the
immune response that occurs. This damage
includes increased ability for blood to exit the vascular system, improper constriction
and dilation of arteries, the loss of the ability for blood to clot, and decreased
heart function (Pathan, Faust, Levin, 2003).
The impaired central nervous system (brain and spinal cord)
can be seen as a result of both direct invasion of the meninges, and a location
receiving the septic blood by the vascular permeability (Pathan, Faust, Levin,
2003). Many individuals develop a raised
pressure inside of the brain due to the inflammatory process and edema that is
occurring. Since the skull is a hard
container, and the brain is squishy, the brain shifts in order to make room for
this new pressure. Many of these
patients are at risk for loss of consciousness and decreased blood volume being
able to reach the brain, which contains the oxygen that we need for the brain
to survive (Pathan, Faust, Levin, 2003).
Here is a link to a video animation of the process! Below
are also scholar articles that are more in depth to the Pathophysiology of the
disease! https://www.youtube.com/watch?v=j3SdmgYBs4E
BIBLIOGRAPHY:
Hoffman, O., Weber, R. (November, 2009). Pathophysiology and
Treatment of Bacterial Meningitis. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3002609/
Manchanda, V., Gupta, S., Bahalla, P., (2006) Meningococcal
Disease: History, epidemiology, pathogenesis, clinical manifestations, diagnosis, antimicrobial susceptibility, and prevention. Retrieved from http://www.ijmm.org/article.asp?issn=0255- 0857;year=2006;volume=24;issue=1;spage=7;epage=19;aulast=Manchanda
Pathan, N., Faust, S., Levin, M. (2003). Pathophysiology of
Meningococcal Meningitis and Septicemia. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1763171/pdf/v088p00601.pdf
Shipley, C. (October, 2012) Bacterial Meningitis Video. Retrieved
from https://www.youtube.com/watch?v=j3SdmgYBs4E
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