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Sonja Opper Take Home #6 10/30/13 Meningitis is an inflammation of the membrane that surrounds the brain and spinal cord, known as the meninges. It is suspected that as early as the age of Hippocrates, meningitis has been recognized as a disease. The first recorded major outbreak of was in Geneva in 1805. In 1887 Anton Weichselbaum was the first to report that a bacterial agent was the cause of meningitis. In 1906 and “antiserum” was developed by the American scientist, Simon Flexner and decreased the mortality rate of meningococcal disease. In 1946 penicillin was reported to be successful in treating meningitis. Symptoms of the disease are a sudden onset of fever, stiff neck, rash and a headache (Meningitis, 2013). Other symptoms include nausea, vomiting, sensitivity to light and confusion. Symptoms develop from three to seven days after exposure. Each year in the United States, approximately 4,100 cases of bacterial meningitis are reported. Of the 4,100 cases, around 500 cases were fatal (Meningitis, 2013). Risk factors associated with bacterial meningitis are age and close living quarters. Infants are at high risk for meningitis. Infants do not have an established immune system and therefore are a desirable host for bacteria such as Escherichia coli and Listeria monocytogenes. Living in a community setting also increases the risk of developing meningitis. Infectious diseases spread quickly through large groups when in a confined space. For this reason it is required for students entering colleges and individuals entering the military to be vaccinated for meningitis. Common agents that cause meningitis are viruses, bacteria or other microorganisms. Common bacteria that cause meningitis are Neisseria meningitides, Haemophilus influenza, Streptococus pneumonia, group B Streptococcus, Listeria monocytogenes, Escherichia coli and Neisseria meningitides (Meningitis, 2013). Haemophilus infulenzae is an opportunistic pathogen, residing in the host until the immune system is weakened. H influenza sticks to the host cell by trimeric autotransporter adhesins. These proteins, found on the outside wall of the gram negative bacteria allow it to adhere to the cell walls of the host. The bacteria “sticks” to an extracellular portion of the cell such as a collagen fiber which will eventually allow the bacteria access to the cell (Linke, 2006). Neisseria meningitides is a Gram-negative diplococcus bacterium that commonly causes meningitis. The cell also uses trimeric autotransporter adhesins to infect cells of the host. The bacteria is an opportunistic pathogen that infects the host when the immune system is impaired. Streptococus pneumonia is also an opportunistic pathogen found in the respiratory tract. Its virulence factors include pneumolysin, an anti-phagocytic capsule and adhesins. The vaccination for S. pneumonia consists of polysaccharides found in the capsule and on the surface of the bacteria (Verma, 2012). Listeria monocytogenes is a food-borne pathogen. L. monocytogenes is Gram-positive that can live within the host’s cells. It achieves this by explosive polymerization of actin filaments. Penicillin or ampicillin can be used to kill L. monocytogenes (Ramaswamy, 2007). The mechanism of infection is through the mucosal lining of the nasal passages. From there the bacteria enter the bloodstream of the host and enter the cerebral space near the subarachnoid space where the blood brain barrier is weakened. The inflammation that ensues is a response of the immune system. The inflammation of the meninges puts pressure on the brain which deprives brain cells of oxygen causing cell death (Meningitis, 2013). Antibiotics commonly given to cure meningitis are chloramphenicol and ampicillin. These two antibiotics are commonly administered before the lumbar puncture test comes back with the positive result for meningitis. Because the inflammation is extremely damaging to the central nervous system, the antibiotics are administered before the disease progresses anymore. Antibiotics initially worsen the inflammation because as the bacteria are killed, more polysaccharides are released from the membranes, causing a greater response from the immune system (Meningitis, 2013). Chloramphenicol is a protein synthesis inhibitor and ampicillin is a cell wall inhibitor. With two different cidal mechanisms, one or both will kill the infectious bacteria (Ramaswamy, 2007). The vaccine for meningitis has been available in the United States since the 1970’s. The vaccine contains polysaccharides found on the outside of the bacteria that commonly provoke an immune response. Transmission of bacteria that cause meningitis can be transferred by contact with mucosal linings of an infected person. Behaviors such as sneezing or kissing can transfer the bacteria (Verma, 2012). Long-term effects of meningitis consist of loss of certain brain functions. Because the pressure put on the brain causes cell death, some functions of the brain are impaired after the patient heals. Many patients experience hearing loss, memory loss and personality changes as a result of meningitis. Works Cited Meningitis. (2013, March). Retrieved 10 30, 2013, from Center for Disease Control and Prevention: http://www.cdc.gov/meningitis/index.html Linke D, Riess T, Autenrieth IB, Lupas A, Kempf VA (2006). "Trimeric autotransporter adhesins: variable structure, common function". Trends Microbiol 14 (6): 264–70. Verma R, Khanna P (2012) Pneumococcal conjugate vaccine: A newer vaccine available in India. Hum Vaccin Immunother 8(9). Ramaswamy V, Cresence VM, Rejitha JS, Lekshmi MU, Dharsana KS, Prasad SP, Vijila HM. (02 2007). "Listeria – review of epidemiology and pathogenesis."