Meningitis is a disease that occurs by having inflammation of the protective membranes covering the brain and the spinal cord, and this protective membrane is called the meninges. Inflammation of the meninges can be caused by infection, usually either through bacteria, virus, or parasites; with bacterial infection being the most serious of the conditions.
Bacterial meningitis varies according to different age groups. The most common type of bacterial meningitis in newborn babies is usually Streptococci or Escherichia coli.1 Children less than five years old can be affected by the Heamophilus influenza type B.1 (2135) Recent trauma to the skull can give the bacteria in the nasal cavity a chance to enter the meninges. An infection in the head and or neck area such as an infection to the ear (otitis media) or to the mouth (mastoiditis) can lead to meningitis in patients who have impaired immune systems.1 (2135)
A virus that causes meningitis includes: herpes, chickenpox, shingles, mumps, and HIV. Parasitic Meningitis is usually caused by an abnormal amount of eosinophils in the CSF (Cerebro Spinal Fluid) and the most common parasites are tuberculosis, syphilis, and cryptococcosis. 1 (2138)
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Infection can enter the meninges in one of two ways; either through the bloodstream or direct contact to the meninges. Viral infections can enter through the nasal cavity along the mucous surfaces, which then will break down the borders that help block the mucous membrane from the meninges. Viral infections usually precede bacterial infections which then are able to enter the subarachnoid space which is the place where the blood brain barrier is most susceptible to infections. The most interesting thing about meningitis in my opinion is the fact that the inflammation that occurs during the infections is not necessarily due to the bacteria, or virus but it is a direct result of the body's immune response. "When the immune system identifies an infection the brain cells such as astrocytes and microglia start to release large amounts of cytokines. This then makes the blood brain barrier more likely for fluid to enter causing cerebral edema. Large number of white blood cells enters the CSF, causing inflammation to the meninges and also causes a different type of edema (interstitial edema). The third step is the inflammation that occurs to the walls of the blood vessels themselves which leads to a decreased blood flow in the brain and cytotoxic edema. These three types of edema all lead to an increased intracranial pressure and the lowered blood pressure leads to brain cells being deprived of oxygen and apoptosis because blood is unable to enter the brain anymore."1 (2133)
When the infection gets into the subarachnoid space the tissue cells initiate the inflammatory response by releasing kinins, prostaglandins and histamine. These chemicals help try to increase vasodilation and permeability of the capillaries. Since with bacterial meningitis one of the main problems is that blood is unable to move in and out of the brain, these chemicals help with that problem. Leukocytes (macrophages and neutrophils) are the first white blood cells at the injured site, in this case the subarachnoid space. The neutrophils try to neutralize the bacteria while the macrophages act as phagocytes trying to engulf the bacteria and the dead cells. One of the main ways to diagnose meningitis is to test the CSF fluid for the number of leukocytes and PMN's and an increase in leukocytes would definitely show that inflammation is taking place.
With bacterial meningitis, antibiotics are administered to the patient, and once the inflammation dies down the healing process takes place. Fibroblasts begin to form a new collagen matrix which will act as the framework for new tissue cells. Proliferation occurs in the subendothelial tissues along with the neurons in the brain such as the astrocytes and the microglia. Once the inflammation of the area has been decreased the damaged area begins to make new capillaries to bring blood to the region. In the case of the meningitis; once the intracranial pressure and the edema start to disappear the revascularization of cells will start to begin and normal blood flow can be established.
"In order to diagnose meningitis you must perform a lumbar puncture, by positioning the patient usually lying on their side, applying a local anesthetic and inserting a needle into the dural sac. You can measure the pressure of the CSF using a manometer and pressure is usually between 6 and 18 cm in bacterial meningitis. The CSF sample is examined for the presence of white blood cells, red blood cells, protein, and glucose levels."2 In acute bacterial infection the CSF shows low glucose levels, and high protein levels; with the emigration and rolling of the PMN's are greater than 300/mm^3. In acute viral infections the glucose levels are normal, and the protein can either be normal or high levels; with the emigration and rolling of PMN's are less than 300mm^3. Parasitic infections causes low glucose, high protein, and PMN's less than 300/mm^3.
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The Clinical manifestations of meningitis most commonly includes: a severe headache nuchal rigidity which is tightness in the nuchal ligament in the neck that makes them unable to flex the neck, sudden high fever, altered mental status, intolerance to bright light and loud noises. 3 Treatment of bacterial meningitis is usually done by giving antibiotics; steroids can also be given to reduce the inflammatory response, and in the case of viral infection there is no specific treatment available, so treatment of the symptoms is all that can be done. Bacterial meningitis untreated is often fatal, but if it is treated then there is a low mortality rate and viral meningitis tends to resolve on its own with no fatality.
In the United States, the most common irritant that causes COPD is long term cigarette smoke, or other forms of tobacco smoke especially if the smoke is inhaled; second hand smoke and air pollution are environmental causes as well.4
"Inflammation is characteristically present in the lower respiratory tract in patients with COPD. In stable disease, pigment-laden macrophages accumulate in the respiratory bronchioles and alveoli. These macrophages are the most numerous inflammatory cells present. Similarly, neutrophils are present within the airway lumen, within airway glands, and accumulate progressively within pulmonary tissues as the disease worsens. A key emerging concept, however, is that other inflammatory cells likely also play key roles. Lymphocyte are also present in the airways, alveolar structures, vessels, and lymph nodes. Increased numbers of T-lymphocytes are associated with more severe disease. It has also been shown that the T-lymphocytes found in COPD express chemokine receptors which are considered to be markers of T helper cells. Eosinophils are also present in the airway wall in COPD and can be found in specimens and induced sputum. The presence of eosinophil-derived mediators indicates eosinophil activation. The structural cells of the lung, including epithelial and mesenchymal cells, are now recognized as producers of inflammatory mediators. It is likely that these cells play key roles in regulating the inflammatory process in COPD."5
"The diagnosis of COPD is confirmed by spirometry, a test that measures breathing. It measures the forced expiratory volume in one second; which is the greatest volume of air that can be breathed out in the first second of a large breath. Normally at least 70% of the FVC comes out in the first second. A ratio of less than normal defines the patient as having COPD. More specifically the diagnosis of COPD is made when the FEV1/FVC ratio is less than 70%. According to the ERS criteria, it is the FEV1% predicted that defines when a patient has COPD; when FEV1% is less than 88% for men, or less than 89% for women. Spirometry can help to determine the severity of COPD as well. The FEV1 is expressed as a percent of a predicted value based on a person's age, gender, height, and weight."6
Clinical manifestation of COPD includes; a persistent cough, sputum or mucus production, wheezing, chest tightness, and tiredness. But mainly the most common symptom is shortness of breath that gets worse over time, and especially during exercise. A rapid breathing rate can also be seen along with breathing through pursed lips and active use of muscles in the neck to help with breathing, especially the scalene muscles.
COPD has no cure, but it is a preventable and treatable disease. Medications used to manage this disease are usually bronchodilators and corticosteroids. The only measure that actually has been shown to reduce mortality is the cessation of smoking and supplemental oxygen. COPD usually gets worse over time and most likely will lead to death.