Sepsis and septic shock vary in presentation with multiple factors, host response, and the invading microbes. Fever or hypothermias, tachypnea, and tachycardia often herald onset of sepsis, the inflammatory response to microbial invasion. When counterregulatory control mechanisms are over -whelmed, often as the microbes move from a local site to invade the bloodstream, homeostasis rnay fail, and dysfunction of major organs may supervene (severe sepsis). Further failure of counterregulatory mechanisms leads to septic shock, which is characterized by hypotension as well as organ dysfunction. As sepsis progresses to septic shock, the risk of dying increases substantially. Early sepsis is usually reversible, whereas patients with septic shock often succumb despite aggressive therapy.
Septic response triggered when microorganisms spread from skin or GI tract into contiguous tissues. Localized infection may then lead to bacteremia or fungemia. Microbes can also be introduced into bloodstream directly from such routes as venous access lines. In some cases, however , no primary site of infection is apparent. Septic response occurs when invading microbes have circumvented host's innate and acquired immune defenses. Lipopolysaccharide (LPS) (endotoxin) is the most potent gram-negative bacterial signal molecule. Septic response involves complex interaction among microbial signal molecules, leukocytes, humoral mediators, and vascular endothelium. Many of the characteristics of sepsis (fever, tachycardia, tachypnea leukocytosis, myalgias, somnolence) are produced by release of tumor necrosis factor α. Intravenous fibrin deposition, thrombosis, and disseminated intravascular coagulation (DIC) are important features of septic response. C5a and other products of complement activation may promote neutrophil reactions such as chemotaxis, aggregation, degranulation, and oxygen-radical production. The underlying mechanism of tissue damage is widespread vascular endothelial injury, with fluid extravasation and microthrombosis that decrease oxygen and substrate utilization by affected tissues. Nitric oxide is a mediator of septic shock.
For NM, primary focus is usually a subclinical nasopharynx infection. Shortly after adherence to nasopharyngeal mucosa, encapsulated NM are transported through nonciliated epithelial cells in large, membrane-bound vacuoles. Within 24 h NM are observed in submucosa in close proximity to local immune cells and blood vessels. NM gain access to circulation; invading NM may either be killed or multiply and initiate bacteremic stage. Hematogenous dissemination seeds the skin and meninges. Signs/ symptoms of systemic disease appear concurrently with meningococcemia, preceding symptoms of meningitis by 24 to 48 h. Edema, infarction of overlying skin, and extravasation of RBC are responsible for the characteristic macular, papular, petechial, hemorrhagic, and bullous lesions. Similar vascular lesions occur in the meninges and in other tissues. Systemic meningococcal infection is primarily a bacteremic disease; NM exhibits marked trophism for meninges and skin, and to a lesser degree for synovia, serosal surfaces, and adrenal glands. NM replicate at a rapid rate; within hours, patient may deteriorate from good health to irreversible shock, marked hemorrhagic diathesis, and death. In chronic meningococcemia, usually during periodic fevers, rash, and joint manifestations, NM can be isolated from the blood; unusual host-parasite relationship is central to this persistent infection.
* fever or low body temperature
* rapid breathing
* chills and shaking
* rapid heartbeat
* decreased urine output
* confusion or delirium.
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