Heat stability

Generally inactivated by heat



A distinct toxic mechanism for each

Innate immune response; a systemic response leads to fever, a dramatic drop in blood pressure, and disseminated intravascular coagulation.


Generally very potent; some are among the most potent toxins known.

Not very toxic; small amounts in a localized area lead to an appropriate response that helps clear an infection.

Damage Associated with Inflammation

The inflammatory response itself can destroy tissue because phagocytic cells recruited to the area inevitably release some of the enzymes and toxic products they contain. The life-threatening aspects of bacterial meningitis, for example, are due to the inflammatory response itself. Complications of certain sexually transmitted diseases are also due to the damage associated with inflammation. If Neisseria gonorrhoeae or Chlamydia trachomatis infections ascend from the cervix to involve the fallopian tubes, the inflammatory response can lead to scarring that obstructs the tubes, either predisposing a woman to an ectopic pregnancy or preventing fertilization altogether.

Damage Associated with Antibodies

Antibodies generated during an immune response can also lead to damaging effects by these mechanisms:

■ Antigen-antibody complexes. These complexes may form during the immune response and settle in the kidneys and joints. There they can activate the complement system, causing destructive inflammation. Acute glomerulonephritis, a complication that can follow strep throat and impetigo caused by Streptococcus pyogenes, is due to antigen-antibody complexes that settle in the kidney, eliciting a response that damages kidney structures called glomeruli. ■ acute glomerulonephritis, p. 540

■ Cross-reactive antibodies. Some antibodies produced in response to an infection may bind to the body's own tissues, promoting an autoimmune response. Some evidence indicates that acute rheumatic fever, a complication that can follow strep throat, may be due to the binding of antibodies produced in response to Streptococcus pyogenes to a normal tissue protein.

This occurs most frequently in people with certain MHC types (see Perspective 16.1). ■ acute rheumatic fever, p. 567

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