Gram Negative Septicemia

Septicemia is a common nosocomial illness, with an estimated 400,000 cases occurring in the United States each year. Approximately 30% of of the cases are caused by Gram-negative bacteria. Endotoxin release by Gram-negative bacteria can lead to shock and death.

Symptoms

The symptoms of septicemia include violent shaking chills and fever, often accompanied by anxiety and rapid breathing. If septic shock develops, urine output drops, the respirations and pulse become more rapid, and the arms and legs become cool and dusky colored.

Causative Agents

Probably because they possess endotoxin, Gram-negative bacteria are more likely to cause fatal septicemias than other infectious

28.2 Bacterial Diseases of the Blood Vascular System 719

agents. Shock is common, and despite treatment, only about half of all people afflicted with this kind of infection survive. Cultures of blood from these patients usually reveal facultative anaerobes such as the enterobacterium Escherichia coli. Among the aerobic, Gram-negative rod-shaped bacteria encountered in septicemia are organisms commonly found in the natural environment, such as Pseudomonas aeruginosa. Some of the Gram-negative organisms causing septicemia are anaerobes. For example, Bacteroides sp., which make up a sizable percentage of the normal flora of the large intestine and the upper respiratory tract, cause many septicemia cases. ■ enterobacteria, p. 282 ■ Pseudomonas, pp. 272,697

Pathogenesis

Septicemia almost always originates from an infection somewhere in the body other than the bloodstream—a kidney infection, for example. Alterations in normal body defenses as the result of medical treatments, such as surgery, placement of catheters, and medications that interfere with the immune response, may allow microorganisms that normally have little invasive ability to infect the blood. Endotoxin is released from the outer cell walls of Gram-negative bacteria growing in a localized infection or in the bloodstream. Unfortunately, antibiotics that act against the bacterial cell wall can also enhance the release of endotoxin from the organisms. These antibiotics are typically used in treating Gram-negative bacterial infections. ■ endotoxin, p. 475

Many of the body's cell types, especially tissue macrophages and circulating leukocytes, respond defensively to endotoxin, just as they do to many other foreign substances, but the response to endotoxin is particularly intense. This exaggerated response to endotoxin has been considered to be a type of hypersensitivity, but the reaction of endotoxin with toll-like receptors might well be involved. ■ toll-like receptors, p. 381

The response of the body cells to endotoxin is appropriate for localizing Gram-negative bacterial infections in tissues and killing the invaders. When localization fails and endotoxin enters the circulation, however, it causes the nearly simultaneous triggering of macrophages throughout the body and a cascade of harmful events (figure 28.3). Although macrophages normally are of central importance in body defense, they also play a key role in septic shock.

The interaction of endotoxin with macrophage cell membrane causes the cell to synthesize and release cytokines such as tumor necrosis factor and interleukin-1, among others. Tumor necrosis factor (TNF) is released from macrophages within minutes of exposure to endotoxin. TNF has diverse effects, one of which is a change in the setting of the body's thermostat, causing the temperature to rise. TNF also causes circulating polymorphonuclear neutrophils (PMNs) to adhere to capillary walls, leading to large accumulations of these inflammatory cells in tissues such as the lung, which have large populations of macrophages. Experimentally, antibody against TNF gives substantial protection against endotoxic shock. ■ cytokines, p. 379

Interleukin-1 (IL-1) is another cytokine released from macrophages. Besides acting with TNF to cause fever and the release of leukocytes from bone marrow, it has many other effects. One potentially harmful action is to cause the release of enzymes from polymorphonuclear leukocytes.

720 Chapter 28 Blood and Lymphatic Infections

SHOCK IMPAIRED O2 EXCHANGE

Decreased muscle tone of heart and arteries

Fever Increased adhesiveness of PMNs Increased leakage of plasma from blood vessels

SHOCK IMPAIRED O2 EXCHANGE

Fever Increased

Decreased muscle tone of heart and arteries

Cytokines released

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  • stefan
    What is the causative agent of septicema?
    8 months ago

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