The Most Common Cause of Meningitis - Research Paper Example

Bacterial Meningitis of the of the Infection of the membranes that enclose the spinal cord and the brain istermed meningitis. It can arise from bacterial, fungal or viral infections. Meningitis caused by bacteria is known as bacterial meningitis. It is a serious ailment that can result in the death of the patient. In general, it transpires in people who undergo a head injury or among individuals with a weakened immune system. This disease predominates among children and youth. Certain adults are also susceptible to develop this infection. Those who abuse alcohol, indulge in prolonged and deep kissing, suffer from chronic ear and nose infection, and who have contracted pneumococcal pneumonia are at a higher risk of developing this disease. This ailment is characterized by high fever, headaches, increasing drowsiness, and irritability. Immediate medical attention has to be obtained, upon suspecting the presence of this disease. In general, it is advisable to undergo hospitalization. The recommended therapy is to administer antibiotics. Despite the reported 10% fatality rate of this disease, early diagnosis and treatment have ensured recovery in the majority of the patients. Bacterial Meningitis The most common cause of meningitis is bacterial or viral infection that has commenced in some other region of the body. Some examples are, the ears, sinuses, or upper respiratory tract. On occasion, meningitis results from autoimmune disorders, fungal infections, and medications. Bacterial meningitis proves to be contagious with regard to people who are in close physical contact (Johnson, 2013). The inflammation of the meninges or the membranes that enclose the spinal cord and the brain, constitutes bacterial meningitis. The cause of the inflammation is bacterial infection that can prove to be fatal. These bacteria are present in the mouth, nose, throat, and spread from an infected individual to another via coughing, osculation, or the sharing of food or beverages. This infection can also spread from an infection of the brain, ear, nose, sinus, or throat. Such infection can also be spread by a head injury or head surgery (Drugs.com, 2013). Among children and young adults, meningococcus or Neisseria meningitides, and Streptococcus pneumonia occur frequently. These are the principal causes of meningitis in the US, and there are vaccines available for Neisseria meningitides, and Streptococcus pneumonia. These vaccines have been recommended for all the people who are special risk. The bacteria tend to spread from individual to individual via coughing and sneezing (Johnson, 2013). As such, meningococcal meningitis is a disorder that transforms, quite rapidly into Neisseria meningitidis. During this process there is an invasion of the subarachnoid space of the brain, and the meninges undergo inflammation. Prior to gaining entry into the subarachnoid space, the bacteria undergo a tremendous increase in their number within the bloodstream. This is accompanied by a release of the vesicles of the outer membrane. These vesicles contain lipooligosaccharide (LOS). It has been unequivocally demonstrated that the LOS is crucial in triggering the immune response in the host (Todar, 2009). In general, several of the bacterial that produce meningitis are to be found as inoffensive nasopharyngeal organisms. These bacteria are spread among individuals, by close and prolonged contact through intimate osculation and sneezing. As such, 10% of the population carry meningococci harmlessly in the nasopharynx region. These people develop immunity within a fortnight (Donovan & Blewitt, 2009, p. 31). The rate of carrying these bacteria tends to be more among teenagers, and varies from 25% to 30%. This has been attributed to their high risk behavior, such as smoking, and intimate kissing. In the usual course carrying bacterial develops immunity to infection. However, there are certain people, in whom the bacteria is transferred through the nasopharyngeal membrane into the blood. On reaching the blood, these bacterial undergo rapid multiplication, traverse the blood – brain barrier and produce meningitis (Donovan & Blewitt, 2009, p. 31). Systematic clinical examinations and patient history are the basis of initial diagnoses of meningitis and septicemia. Meningococcal disease demands immediate treatment, and laboratory results are usually unavailable expeditiously to confirm an initial diagnosis. Mortality can be reduced by administering parenteral penciling G, prior to hospitalization (Donovan & Blewitt, 2009, p. 33). The diagnosis can be confirmed microbiologically, by extracting the causative organism from blood, cerebrospinal fluid or throat swabs. However, it is not possible to obtain organisms always, from the blood or cerebrospinal fluid. Consequently, it is necessary to commence antibiotic therapy (Donovan & Blewitt, 2009, p. 33). In addition, diagnostic procedures, such as polymerase chain reaction have the capacity to promote the detection of microbial deoxyribonucleic acid, subsequent to the administration of antibiotics. Optimal treatment and the provision of accurate epidemiological data necessarily require microbiological confirmation. Intracranial pressure and septic shock have to be identified and rectified (Donovan & Blewitt, 2009, p. 33). This requires the administration of antibiotics in conjunction with precise and incessant assessment of the patient. Patient outcomes are significantly improved when early identification, swift relocation to hospital and vigorous treatment of the complications of elevated intracranial pressure and septic shock are employed in a coordinated manner (Donovan & Blewitt, 2009, p. 33). However, in the absence of early diagnosis and treatment, bacterial meningitis can render a patient permanently disabled or even exanimate. It has several causes, such as fungi, malignancies, parasites, or viruses. Some of the causes for bacterial meningitis are Neisseria meningitides, group B Streptococcus, type b Hemophilus influenza and Streptococcus pneumonia. Subsequent to trauma, Staphylococcal infections tend to be more commonplace (Watkins, 2009, p. 620). In order to survive inside the host organism, bacterial pathogens have developed an intricate system of physiological adaptations. These pathogens should possess the capacity to infect if they are to cause disease. The requirement, in this regard, is to be able to compete for nutrients for growth. Moreover, these pathogens should possess the necessary mechanisms for defending themselves again the immune system of the host. The cellular components required for such processes are termed virulence factors (Willis & Whitfield, 2013, p. 35). Some of the virulence factors in Gram – negative pathogens are, important extracellular and surface constituents, such as flagella chemotaxis proteins, fimbrial adhesins, secreted proteins, lipopolysaccharides, and capsules. The distribution of capsules in vast and they occur among a wide range of pathogens, such as Escherichia coli, Neisseria meningitidis, Actinobacillus pleuropneumoniæ, Sinorhizobium meliloti, and in Staphylococcus aureus, Streptococcus pneumoniæ and other important Gram – positive pathogens (Willis & Whitfield, 2013, p. 35). Under the microscope, the bacterial capsule, which is an extracellular structure, portrays itself as an extensive layer that encompasses the cell. It is composed of long polysaccharide chains, which are termed the capsular polysaccharides (CPS). Characteristically, the CPS carries a negative charge, which results in a capsular layer that is abundantly hydrated. This layer, in some isolate of E. coli, has been observed to extend from the cell surface for around 100- 400 nanometers. This layer is composed of glycan chains that are greater than 200 sugars, in length (Willis & Whitfield, 2013, p. 35). It is possible for even a single species to generate an array of CPSs that exhibit structural diversity. In many cases, these CPSs constitute the basis of serotyping schemes. An instance of this scheme is the 84K (capsular) antigens of E. coli. The surface association of capsules, ensures that in many instances, these are the primarily encountered bacterial structures by the immune system, at the time of infection. Consequently, the capsule is indispensable for circumventing the immune system of the host (Willis & Whitfield, 2013, p. 35). Thus, isolates that are devoid of capsules tend to be non – pathogenic. In addition, an excessive increase in their numbers, enables the N. meningitidis bacteria to traverse the blood – brain barrier and invade the subarachnoid space. Thereafter, the defense network of the host proves unequal to the task of containing the developing infection of the cerebrospinal fluid (CSF). This is due to the paucity of safeguards in that region (Pathan, Faust, & Levin, 2003, p. 606). A study on the incidence of bacterial meningitis in the US for the period 1998 to 2007, disclosed the following information. The pathogen N. meningitidis was identified in 549 instances of bacterial meningitis. Out of these 55 had fatal outcomes (Thigpen, et al., 2011, p. 2018). With regard to children, 587 cases of bacterial meningitis had been identified by this study. N. meningitidis was deemed to the cause in 45.9% of the cases. These involved patients in the age range of 11 to 17 years. The fatality rate was 6.9% for this group. In the context of adults, 1083 cases of bacterial meningitis were identified by this study. The overall fatality rate among adults was determined to be 16.4%. A linear increase in the fatality rate was discerned, and the increase was seen to increase with increasing age (Thigpen, et al., 2011, p. 2021). A number of effective vaccines have been developed and deployed on a large scale. However, the rate of human mortality and illness, due to Neisseria meningitidis, Group B Streptococcus, Hæmophilus influenzæ and Streptococcus pneumoniæ continue to be a cause for deep concern. This has been accompanied by a residual disease burden resulting from bacterial meningitis, which has become apparent due to several continuing or emergent pathogens. Some of these pathogens are Escherichia coli, Staphylococcus aureus, Salmonella spp and Mycobacterium tuberculosis (Bottomley, Serruto, Sáfadi, & Klugman, 2012, p. B78). The contemporary world has to make concerted efforts to reduce bacterial meningitis. To this end, organizations, such as the Gates Foundation, WHO, PATH and GAVI can assume a leadership role, in order to ensue better deployment of vaccines. Another desired intervention would be the introduction of polymerase chain reaction based detection techniques for identifying bacterial pathogens in the CSF and blood (Bottomley, Serruto, Sáfadi, & Klugman, 2012, p. B84). The administering of antibiotic therapy, during the early stages of bacterial meningitis infection can prove to be very effective in saving life and reducing suffering. There is considerable ambiguity regarding the effectiveness of the new antibiotics in curing this infection, due to the absence of clinical data to establish their value. The incomplete results obtained in the different medicines being utilized for dealing with bacterial meningitis, makes it obvious that this infection presents a daunting therapeutic challenge (van de Beek, Brouwer, Thwaites, & Tunkel, 2012, p. 1693). Notwithstanding the immunization program, meningitis is an ailment that will persist in afflicting the populace. Some of the reasons behind this are that a few of the children may not have undergone the entire course of the program, whilst the members of older groups may have not benefitted from it. There is also the possibility of individuals acquiring this disease, by means of an infection that has not been taken into consideration by this vaccination program. This makes it imperative to be always vigilant in recognizing the symptoms of this dread disease, and to brook no delay in addressing it (Watkins, 2009, p. 621). Despite the rapidity of its occurrence, and its propensity to cause death, bacterial meningitis need not be viewed with terror. This disease can be cured if immediate diagnosis and treatment, preferably in a hospital setting, are provided to the patient. Prevention is always preferable to treatment. Therefore, people should improve their nasopharyngeal hygiene and take serious steps to develop a strong immune system. References Bottomley, M. J., Serruto, D., Sáfadi, M. A., & Klugman, K. P. (2012). Future challenges in the elimination of bacterial meningitis. Vaccine, 30(Supplement 2), B78 – B86. Donovan, C., & Blewitt, J. (2009). An overview of meningitis and meningococcal septicaemia. Emergency Nurse, 17(7), 30 – 37. Drugs.com. (2013). Bacterial Meningitis In Children. Retrieved August 25, 2013, from CareNotes: http://www.drugs.com/cg/bacterial-meningitis-in-children.html Johnson, K. (2013, March 30). Understanding Meningitis – the Basics. Retrieved August 25, 2013, from WebMD: http://www.webmd.com/brain/understanding-meningitis-basics Pathan, N., Faust, S. N., & Levin, M. (2003). Pathophysiology of meningococcal meningitis and septicaemia. Archives of Disease in Childhood, 88(7), 601 – 607. Thigpen, M. C., Whitney, C. G., Messonnier, N. E., Zell, E. R., Lynfield, R., Hadler, J. L., . . . Schuchat, A. (2011). Bacterial Meningitis in the United States, 1998 – 2007. The New England Journal of Medicine, 364(21), 2016 – 2025. Todar, K. (2009, December 31). Meningococcal Meningitis. Retrieved August 28, 2013, from The Microbial World: http://textbookofbacteriology.net/themicrobialworld/meningitis.html van de Beek, D., Brouwer, M. C., Thwaites, G. E., & Tunkel, A. R. (2012). Advances in treatment of bacterial meningitis. Lancet, 380(9854), 1693 – 1702. Watkins, J. (2009). Bacterial meningitis. Practice Nursing, 620 – 621. Willis, L. M., & Whitfield, C. (2013). Structure, biosynthesis, and function of bacterial capsular polysaccharides synthesized by ABC transporter – dependent pathways. Carbohydrate Research, 35 – 44. Read More