Meningitis: causes, symptoms, and clinical management

Introduction
Meningitis infects the meninges, the delicate membranes that house the spinal cord and the brain. It is a rare infection that can affect adults and children alike. The disease manifests in several types such as through viral, bacterial and fungal varieties. Bacterial meningitis is the most dangerous and infectious variety. It is a life threatening disease. It infects people in physical contact. Incidentally, viral meningitis is not as severe as most of the patients that develop the disease recover on their own without seeking treatment (Wang et al., 2014). Fungal meningitis is the rarest form. It occurs in people whose immune system has been compromised.
Etiology
Bacterial meningitis is caused by bacteria that enters the body and relocates to the brain and spinal cord or when bacteria invade the meninges. The point of entry can be a skull fracture, ear or sinus infection, of surgery. Bacteria that cause bacterial meningitis include Streptococcus pneumonia, (the most common cause of bacterial meningitis) Neisseria meningitides, Haemophilus infleunzae, and Listeria monocytogenes (people who have weakened immune systems are most susceptible). Bacterial meningitis is commonly caused by S pneumonia in America and other countries across the globe.The common serotypes that lead to bacterial meningitis include 4, 6B, 9V, 14, 19, 18C, and 23. Pneumococcal strain 19A is the most notable serotype that causes the disease and can attack both children and adults (Kaplan et al., 2014; Wang et al., 2014).
Viral meningitis is caused by enteroviruses which are common in late summer and early fall. Viral meningitis is however mild and clears without medication. Chronic meningitis on the other hand is caused by organisms that are slow-growing e.g. Mycobacterium tuberculosis and fungi. Fungal meningitis is uncommon with only Cryptococcal meningitis being the common form and it affects persons with immune deficiencies e.g. AIDs. Other causes of meningitis are noninfectious and include drug allergies, chemical reactions, inflammatory diseases, and some types of cancer.
Pathogenesis
The entry point for pathogens that cause meningitis is the nasopharynx or ears into the bloodstream. They pass through the endothelial cells to enter the subarachnoid space, and then penetrate the porous capillaries of choroid plexus. They may be carried by granulocytes too. Provision of sufficient nutrients for the thriving of bacteria is one of the reasons why the Cerebrospinal fluid (CSF) is an ideal medium for infection. It also houses a couple of phagocytic cells. The antibodies are also low (McGill et al., 2016). At first there is uninhibited multiplication of bacteria. At this point the bacteria can be seen and identified through cultures, smears or through Enzyme-linked immunosorbent assay detection of antigens prior to inflammation.
Bacteria carry the potential to destroy the blood capillaries and the brain directly. The toxins generated by bacteria cause neuronal apoptosis. The endotoxin produced by bacteria triggers clotting which in turn leads to disseminated intravascular coagulation. This state leads to more severe injury because of the inflammatory reaction to bacteria. The innate immune system of the brain found in the choroid.
Actually, if neutrophytes increase in number, they can damage brain nerves, vessels and tissue. Cerebral infarcts are caused by Vasculitis and clotting. This brain damage during attack by meningitis is as a result of bacterial action in part and also the reaction to bacteria by the immune response system. The brain is sufficiently wired to deal with inflammation. However, in some situations, the unbalanced defense responses can be injurious. Increased intracranial pressure from cerebral edema is the most severe and dangerous complication of bacterial meningitis. The edema could be vasogenic as a result of heightened vascular permeability, interstitial, cytotoxic of cerebral hypoxia, high complement-fixing antibody volume or a combination of all the mentioned factors (Liechti et al., 2015). High intracranial pressure on its part leads to decreased perfusion, neuronal necrosis and hypoxia/ischemia.
The relation between manifestation and pathophysiology
Pathogens causing meningitis enter the CNS by either hematogenous, a common path, or via direct extension from a site that is contiguous. Neonates can infected through maternal genital secretions that are non sterile via the placenta or from the surrounding environment. The cascading of the inflammation causes cerebral edema and heightened intracranial pressure that causes severe headache and a swelling fontanelle or reflexes that are abnormal. Cerebral edema causes a number of neurologic complications and even death. The multiplication of bacteria is remarkably fast after they enter the subarachnoidal space. The CSF bacterial elements trigger the production of a range of inflammatory mediators, which on their part promote the entry of leucocytes into the CSF. This causes fever, headache and stiff neck suddenly. Other symptoms such as nausea, photophobia, vomiting and alteration of one’s mental status also manifest.



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Specific health promotion behaviors
Being vaccinated can reduce your chances of contracting bacterial meningitis. The vaccine is safe and is used against the A, C, Y and W-135 strains. These are responsible for 70% of bacterial meningitis infections. Booster shots may be needed intermittently (McGill et al., 2016).


Safety concerns
Usually meningitis cases are not life-threatening. To prevent infection spread, children may be isolated while being treated for the initial 24 hours before the medicines take effect. Some critically ill children may need intensive care.
Children and their parents need to be supported initially because of the shock they are subjected to by the attack and the subsequent diagnosis. Because people fear meningitis, relatives and friends may worry about the possibility of developing the disease. They should be reassured that such risk is significantly low. Prophylaxis should be provided for household contacts.


Community resource for persons with meningitis
Follow up of children that have been infected and treated of meningitis is important. Some cases manifest gradual and continuous hearing loss after the meningitis attack. Coma, seizures and hydrocephalus contribute to poor treatment outcomes because of delaying the onset of the treatment.
Families will enjoy extended support after discharge. Apart from the routine health, educational and social services, the meningitis Trust and the Meningitis Research Foundation support families and provide information regarding the illness ant outcomes of treatment. If a child has been disabled, financial assistance and provision of equipment may suffice.
Although there is commonly an extended period of convalescence, most children recover fully. Some children may manifest temporary behavior change as a result of hospitalization. Nevertheless, there are also a notable number of deaths that result from bacterial meningitis infections. A few people may develop permanent problems.











References
Kaplan, S. L., Edward, M. S., Nordli Jr, D. R., & Torchia, M. M. (2014). Bacterial meningitis in children older than one month: Clinical features and diagnosis. Waltham (MA): UpToDate.
Liechti, F. D., Grandgirard, D., & Leib, S. L. (2015). Bacterial meningitis: insights into pathogenesis and evaluation of new treatment options: a perspective from experimental studies. Future microbiology, 10(7), 1195-1213.
McGill, F., Heyderman, R. S., Panagiotou, S., Tunkel, A. R., & Solomon, T. (2016). Acute bacterial meningitis in adults. The Lancet, 388(10063), 3036-3047.
Wang, A. Y., Machicado, J. D., Khoury, N. T., Wootton, S. H., Salazar, L., & Hasbun, R. (2014). Community?Acquired Meningitis in Older Adults: Clinical Features, Etiology, and Prognostic Factors. Journal of the American Geriatrics Society, 62(11), 2064-2070.