Lacy’s Internship Paper, Lutheran

Exempla Lutheran Medical center

Meningitis

Internship Research Paper #1

Lacy Zimmerman

3/10/2011

 

 

Dr. Hays

 

 

 

On February 9, 2011 a young female was admitted to the ER because she was presenting with severe headaches, neck stiffness, high fever, vomiting and light intolerance. The staff suspected bacterial meningitis; therefore a lumbar puncture was performed in order to confirm this hypothesis. This paper will discuss the causes, symptoms, diagnosis, treatment, prevention and prognosis of meningitis, with an emphasis on bacterial meningitis.

Bacterial meningitis is a disease characterized by the inflammation of the meninges that cover the brain and spinal cord. Bacterial meningitis is typically caused by three main bacteria; Hemophilus influenzae (45%), Neisseria meningiditis (25%), and Streptococcus pneumoniae (10%) (1). It affects approximately 3 out 100,000 people in the United States (1). Meningitis can also be caused by viruses such as Herpes simplex virus , Varicella zoster virus and Mumps virus , or other various microorganisms (1).

Bacterial meningitis is commonly caused by a bacterial infection that begins in the skin that eventually penetrates into the blood. The bacteria circumvent the skin’s defenses by entering through a wound or via insect bites, most specifically mosquito bites. Once colonized in the skin, the bacteria enter the blood stream and eventually cross the blood-brain barrier to enter the central nervous system which includes the brain and the spinal cord (2).

By the time bacteria reach the meninges, they have triggered an immune response within the host causing massive inflammation and cytokine release (1,2,3). Cytokines are chemical signals released by host T-helper cells when it recognizes non-self antigens such a bacteria and their products. The cytokines released by T-helper cells include interleukin-1, interleukin-6, interleukin-8, tumor necrosis factor-alpha, and interferon-gamma (3). These cytokines stimulate the inflammatory response by dilating blood vessels to increase blood flow, increasing capillary permeability, as well as activating the coagulation pathway. Many of these cytokines also act as chemoattractants to bring additional phagocytes to the area of infection (4). Increased capillary permeability can cause fluid to leak out of the blood stream resulting in cerebral edema (swelling) that can put pressure on the brain and spinal cord resulting in the loss of some central nervous system function. This has the ability to cause cognitive deficits or loss of motor control, both of which may have restored function once inflammation is reduced.

As stated before, a lumbar puncture is a means to diagnose meningitis. A lumbar puncture is performed by inserting a needle between the 3 rd and 4 th lumbar vertebra until it pierces into the spinal canal where a sample of cerebrospinal fluid (CSF) can be obtained (5). The fluid sample is sent out for laboratory examination to confirm the presence, as well as the identity of the microorganism responsible for causing the disease.

Immediate antibiotic treatment is necessary when bacterial meningitis is suspected, and a regimen of broad-scope antibiotics must be administered even in positive lab results have not come back yet. Early antibiotic administration is vital to the effective treatment of meningitis and also helps reduce the likeliness of permanent damage to the central nervous system such as hearing loss, epilepsy, and behavioral problems (2). If treatment is not administered in a timely manner, bacterial meningitis can quickly progress into a systemic blood infection called sepsis, which is a much more fatal disease. If left untreated, the mortality rate is nearly 100% (1). With antibiotic treatment, bacterial meningitis has a mortality rate of 26.3% (1,2).

Penicillin G is the most effective antibiotic treatment against bacterial causes of meningitis but ceftriaxone, cefuroxime and ceforaxime may also be used (5). All of these antibiotics are able to pass into the blood-brain barrier to attack the causative agent.

Viral meningitis is much less severe than bacterial meningitis and only requires supportive therapy such as fluid administration (5). Typically, the body is able to clear viral meningitis infection on its own. An antiviral drug called acyclovir may be administered, but its effectiveness is questionable (5). Corticosteroids can be administered in all cases in order to reduce the immune system response by working to block tumor necrosis factor-alpha from activating immune cells (3,4).

Meningitis is relatively communicable; therefore it is necessary for all recent contacts of the infected patient receive preventative medication. Rifampin, ceftriaxone, and ciprofloxacin are administered orally for approximately 14 days (1).

Due to the severity of bacterial meningitis, effective vaccines have been developed against most of the causative agents, and are recommended for at risk age groups. Menomune is a quadrivalent polysaccharide vaccine that provides immune resistance to N. meningiditis serogroups A, C, Y, and W135 (5). Menactra is also a quadrivalent polysaccharide vaccine but is conjugated to a diphtheria toxoid for a stronger immune response against N. meningiditis . N. meningiditis vaccinations are recommended for children ages 11-18, all college freshmen living in a dormitory, and any other person age 2-55 that has an increased risk due to immune failure or genetic predispositions (5). A vaccination against H. influenzae is routine in many countries and helps protect against meningitis (5). Immunization against mumps reduces the number of cases caused by Mumps virus (5). Various other immunizations are available against most of the microorganisms that cause meningitis.

Although meningitis is not a very common disease, it has the ability to become fatal very quickly and should be taken seriously. Meningitis can be caused from anything from bacteria to viruses, each with its respective treatment regimen. With prompt identification and treatment, patients have a fairly promising prognosis and will go on to lead normal lives, free of future complication.

REFERENCES

•  Rosenstein N., Perkins B., Hughes J. Meningococcal Disease. New England Journal of Medicine. 2001. 344: 1378-1388.

•  British Medical Association. Bacterial Meningitis in Emergency Departments. The Western Journal of Medicine. 1991. 155(3): 288-289.

•  Zajdowicz S. Pathogenic Microbiology Lecture Handouts. Metropolitan State College of Denver. 2011.

•  Salyers A., Whitt D. Bacterial Pathogenesis: A Molecular Approach . ASM Press. 2002.

•  Center for Disease Control and Prevention. Bacterial Meningitis.2011. www.cdc.gov