Week 4: Diagnosis

Early diagnosis of meningococcal meningitis is essential for stopping the disease in its tracks.  The most common ways to diagnose this meningitis is through either a blood sample, or sample of cerebrospinal fluid (CDC, 2014).  The bacteria are most often found in those two places, as we discussed last week.  To receive a cerebrospinal fluid sample, the patient must undergo a procedure called a lumbar puncture (CDC, 2014).  The spinal cord does not completely fill the spinal column.  There is a space at the bottom of the column where a needle can enter without hitting the spinal cord.  The fluid is withdrawn from this space (CDC, 2014).

http://www.cdc.gov/meningococcal/about/diagnosis-treatment.html 

Once the sample is drawn, it is sent to a laboratory to be tested.  With the cerebrospinal fluid sample, the bacteria may be seen with a high-powered microscope.  However, to confirm if the bacteria is present, it will grow into colonies on an appropriate medium in the lab (CDC, 2014).  Growth signifies a positive test result of a bacterium, but further tests are needed to determine which one (see below).  If the patient gives a blood sample, procedures called Polymerase Chain Reaction (PCR), and/or a latex agglutination tests must be performed (WHO, 2012).  In the method of PCR, we are able to isolate specific parts of the bacterium and make million of copies of it.  This betters our chances of detection if only a few copies of the bacterium are present in the sample (CDC, 2012).  For the latex agglutination test, latex beads with parts of the assumed bacterium are dropped over the blood sample.  If their suspicion is correct, the blood sample will clump together (NIH, 2013). 

http://www.cdc.gov/meningitis/lab-manual/chpt06-culture-id.html 

The samples are further tested in order to determine what bacteria and strain they are working with. A procedure called a gram stain will be performed (CDC, 2012).  This procedure involves different dyes being poured over the bacteria.  The characteristics of the bacterium determine what dyes will be absorbed, and ultimately the color that it will be stained.  The color also helps determine the shape of the bacterium since it is easier to see (CDC, 2012).  This is important in order to determine what treatment the patient needs to receive.  Once the diagnosis is confirmed, the treatment can begin. 

http://www.cdc.gov/meningitis/lab-manual/chpt06-culture-id.html

BIBLIOGRAPHY

Centers for Disease Control and Prevention. (April, 2014). Meningococcal Disease: Diagnosis and Treatment. Retrieved from http://www.cdc.gov/meningococcal/about/diagnosis-treatment.html

Centers for Disease Control and Prevention. (March, 2012). Meningitis Chapter 10: PCR for Detection and Characterization of Bacterial Meningitis Pathogens. Retrieved from http://www.cdc.gov/meningitis/lab-manual/chpt10-pcr.html

Centers for Disease Control and Prevention. (March, 2012). Meningitis Chapter 6: Primary Culture and Presumptive Identification of Nisseria meningitides, Streptococcus pneumonia, and Haemophilus influenza. Retrieved from http://www.cdc.gov/meningitis/lab-manual/chpt06-culture-id.html

National Institutes of Health, Medline Plus. (August, 2013) Latex Agglutination Test. Retrieved from                                                      http://www.nlm.nih.gov/medlineplus/ency/article/003334.htm

World Health Organization. (November, 2012). Meningococcal Meningitis. Retrieved from                                                               http://www.who.int/mediacentre/factsheets/fs141/en/

Week 3: Etiology and Pathophysiology

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

Week 2: Epidemiology

Since Meningococcal Meningitis can strike rapidly, and unexpectedly in healthy individuals, disease surveillance systems have been put into place to monitor its variance.  The bacterium does not only cause meningitis.  In fact, the cases of people who contract the bacterium, meningitis only occurs in about 47% (CDC, 2012).  This data has been displayed in the graph below.  To better understand this epidemiological data, I will be showing you the epidemiology of Meningococcal disease itself, rather than the symptom of meningitis.  Disease surveillance is much higher for the disease, rather than it’s characteristics.  The rate of this disease has been declining in the United States over the last 20 years.  This is mainly in response to a new vaccination.  From 2005-2001, there were an estimated 800-1,200 cases of meningococcal disease that occurred annually in the United States (Baker, 2013).  This means that there were only about 0.3 cases per 100,000 individuals.  Since the vaccine was recommended in 2005, incidence had declined by 64%, which is reflected in those rates (Baker, 2013).

 http://www.cdc.gov/vaccines/pubs/pinkbook/mening.html

Who:

Age groups that are at the highest risk are those under the age of 1, and then a peak begins again around the age of 16-21 (CDC, 2014).  Infants have a more difficult time fighting off infections like this one.  This is the same case for elderly adults.  The adolescent and young adult ages are at risk due to how this disease is transmitted.  Transmission occurs from person to person through close respiratory secretions or saliva.  It is around this age that individuals are likely to kiss others, share eating utensils, and share drinks.  5-10% of adults are carriers of the bacterium (Cohn, MacNeil, 2014).  This means they have the bacteria yet do not display any symptoms.  This is critical to understand because transmission can occur without knowing it.    

 http://www.cdc.gov/meningococcal/surveillance/index.html

Where:

Almost all cases of Meningococcal  disease and the corresponding meningitis are sporadic, meaning they occur on their own without warning.  However sometimes, outbreaks can occur in small communities, schools, colleges, prisons, military corridors, and other small populations.  An outbreak is defined as multiple cases in a community of institution over a short duration of time.  These outbreaks occur due to the simple transmission of disease from living, or working, in tight quarters (Baker, 2013).  This bacterium is not only limited to the US, but is found worldwide.  Specific areas of Africa have a high incidence of Meningococcal  disease.  The area is know as the Belt of Africa and can be seen in the picture below.  In epidemic regions, incidence rates can be up to 1,000 cases per 100,000 persons (Cohn, MacNeil, 2013).  Knowing where disease rates are high is important information to travelers that can receive vaccines for preventable disease. 

 http://wwwnc.cdc.gov/travel/yellowbook/2014/chapter-3-infectious-diseases-related-to-travel/meningococcal-disease

When:

The rise in cases seems to correspond in time with that of typical flu season, around December or January of each year (CDC, 2014). The immune system is inherently low at this time, so it is easy for bacteria to swoop in and cause disease. 

Morbidity and Mortality:

Although our rates of Meningococcal disease are at a historical low, the case fatality ratio remains at 10-15%.  This means that out of all the individuals in the United States that are contracted with the disease, 10-15% of them will die.  Out of those that survive, 11-19% have long term disabilities.  These disabilities often include neurological disability, limb or finger loss, and hearing loss (Baker, 2013). 

BIBLIOGRAPHY

Baker, C., Briere, E., Clark, T., Cohn, A., MacNiel, J., Meissner, H., Messonnier, N., Ortega, I. (2013, Mar 22).  Prevention and Control of Meningococcal Disease: Recommendations of the Advisory Committee on Immunization Practices. Retrieved from http://www.cdc.gov/mmwr/preview/mmwrhtml/rr6202a1.htm

Cohn, A., MacNeil, J., (2014, April 1) Meningococcal Disease: Manual for the Surveillance of Vaccine Preventable Diseases. Retrieved from http://www.cdc.gov/vaccines/pubs/surv-manual/chpt08-mening.html

Cohn, A., MacNeil, J., (2013, August 1) Infectious Disease Related to Travel. Retrieved from                                                   http://wwwnc.cdc.gov/travel/yellowbook/2014/chapter-3-infectious-diseases-related-to-travel/meningococcal-disease

Centers for Disease Control and Prevention. (2012, May 7). Meningococcal Disease. Retrieved from                                     http://www.cdc.gov/vaccines/pubs/pinkbook/mening.html

Centers for Disease Control and Prevention. (2014, April 1) Surveillance.  Retrieved from                                                       http://www.cdc.gov/meningococcal/surveillance/index.html

Why Meningitis?

As a Senior in High School, I remember anxiously sitting in a cold, clean room at the doctor's office.  I was waiting to receive what seemed like to be a million required immunizations before I was allowed to even set foot on the University of Washington campus.  When I thought all decisions had been made, the nurse threw a ringer in the plans.  She handed me a small book filled with vivid images of lives destroyed by Meningitis.  She told me that the vaccine was optional, but highly recommended for my age group.  It did not take me 30 seconds to decide that I wanted the vaccine.  And for those of you who don't know me, I despise shots.  I had only ever heard of Meningitis, and obviously knew it was bad by the images I had just seen. However, I did not know anything else about it…

To get a better understanding of what this disease is about, it is best to understand the anatomy of the area surrounding the brain.  We all know that the brain is this big, pink, squishy mass that sits up in our skull and controls our vital functions of life.  However, the brain is protected from the outside world by multiple layers.  The most outer protection is the skin.  Underneath the skin is the hard, bony skull.  Then, the brain is essentially wrapped in three linings.  The outermost layer that is closest to the skull is called the Dura Mater.  The middle layer is called the Arachnoid.  And the layer that is stuck to the surface of the brain is called the Pia Mater.  Between the Pia Mater and the Arachnoid is a space called the Subarachnoid (sub= below) space.  In this space flows a fluid (cerebrospinal fluid or CSF) that nourishes the brain and is continuous with the spinal cord.  A good way to remember the three layers is that it is the PAD to the brain- Pia; Arachnoid; Dura.  The three layers (Dura Mater, Arachnoid, and Pia Matter) are collectively known as the Meninges (McCaffrey, P., 2014).  Below, I have attached a simplified picture of these layers for a better understanding!

http://www.hughston.com/hha/a_17_3_1.htm

In the medical field, the word you read, can often tell you the entire meaning of the condition.  The ending of a word that ends in “-itis” means “inflammation.”  Therefore, the meaning of the disease Meningitis, means “inflammation of the meninges.” Inflammation in any part of the body is a redness, swelling and heat of a specific area and is often caused by injury or infection.  Well what causes this you ask? And the answer is many things! However in the case of Meningococcal Meningitis, it is specifically caused by an infection which I will discuss in week three of my blog! 

NEXT WEEK:

I will discuss the epidemiology of Meningitis! Epidemiology tells us more about how many are affected, who is affected, and where are people most commonly affected!

BIBLIOGRAPHY

Ferincola, P. (2005). Concussion: When the Skull Isn't Enough Protection. Retrieved from http://www.hughston.com/hha/a_17_3_1.htm

McCaffrey, P. (2014) Neuroanatomy of Speech, Swallowing, and Language. The Meninges and Cerebrospinal Fluid. Retrieved from http://www.csuchico.edu/~pmccaffrey//syllabi/CMSD%20320/362unit3.html