To all health care professionals - i need help!?!
Question: I'm doing a paper for my anatomy & physiology class on meningitis. One thing i have to explain is the physiological, anatomical, or histological process leading to the disorder.
I just don't really understand WHAT these processes are, exactly, and how I would explain them...
I only need to choose one of the three, and I don't know which one to choose. I'm thinking anatomical might be the easiest, but I'm not sure if I can really write a whole paragraph on it.
Help please!?
best answer gets all the points =]
Answers: I'm doing a paper for my anatomy & physiology class on meningitis. One thing i have to explain is the physiological, anatomical, or histological process leading to the disorder.
I just don't really understand WHAT these processes are, exactly, and how I would explain them...
I only need to choose one of the three, and I don't know which one to choose. I'm thinking anatomical might be the easiest, but I'm not sure if I can really write a whole paragraph on it.
Help please!?
best answer gets all the points =]
Pathophysiology
Three major pathways exist by which an infectious agent (ie, bacteria, virus, fungus, parasite) gains access to the central nervous system (CNS) and causes disease.
Initially, the infectious agent colonizes or establishes a localized infection in the host. This may be in the form of colonization or infection of the skin, nasopharynx, respiratory tract, gastrointestinal tract, or genitourinary tract. Most meningeal pathogens are transmitted through the respiratory route, as exemplified by the nasopharyngeal carriage of Neisseria meningitides (meningococcus) and nasopharyngeal colonization with S pneumoniae (pneumococcus).
From this site, the organism invades the submucosa by circumventing host defenses (eg, physical barriers, local immunity, phagocytes/macrophages) and gains access to the CNS by (1) invasion of the bloodstream (ie, bacteremia, viremia, fungemia, parasitemia) and subsequent hematogenous seeding of the CNS, which is the most common mode of spread for most agents (eg, meningococcal, cryptococcal, syphilitic, and pneumococcal meningitis); (2) a retrograde neuronal (ie, olfactory and peripheral nerves) pathway (eg, Naegleria fowleri, Gnathostoma spinigerum); or (3) direct contiguous spread (ie, sinusitis, otitis media, congenital malformations, trauma, direct inoculation during intracranial manipulation).
Certain respiratory viruses are thought to enhance the entry of bacterial agents into the intravascular compartment, presumably by damaging mucosal defenses. Once inside the bloodstream, the infectious agent must escape immune surveillance (eg, antibodies, complement-mediated bacterial killing, neutrophil phagocytosis). Subsequently, hematogenous seeding into distant sites occurs, including the CNS. The specific pathophysiologic mechanisms by which the infectious agents gain access into the subarachnoid space remain unclear.
Once inside the CNS, the infectious agents likely survive because host defenses (eg, immunoglobulins, neutrophils, complement components) appear to be limited in this body compartment. The presence and replication of infectious agents remain uncontrolled and incite a cascade of meningeal inflammation. This process of meningeal inflammation has been an area of extensive investigation in recent years that has led to a better understanding of meningitis pathophysiology.
Key advances in the pathophysiology of meningitis include the pivotal role of cytokines (eg, tumor necrosis factor-alpha [TNF-alpha], interleukin [IL]