How Bacteria Cause Disease


Mechanisms by which bacteria cause disease

 

Bacteria may cause illness by exploiting the following:

  • production of structures that enable the microorganism to attach to the surface at which they cause disease;
    • pili are hair-like structures that enable bacteria to stick to surfaces through a specific mechanism; fimbriae work in a similar fashion;
    • Streptococcus mutans produces large amount of extracellular slime that allow it, and other microorganisms, to stick firmly to the surface of teeth.  The acid produced my metabolism of sugars in the diet then etches the surface of the tooth to which these bacteria are stuck, initiating dental caries.
  • production of one or more toxins;
    • There are two classes of bacterial toxins: exotoxins and endotoxins;
      •   exotoxins are enzymes that are secreted by bacteria;

        "Lockjaw" is an alternative name for tetanus. It is so called because the tetanus toxin, produced by Clostridium tetani, interferes with the transmission of nerve impulses leading to a paralysis in which muscles go into spasm. The face muscles are among the first to be affected, leading to the classical "risus sardonicus" or sardonic smile, characteristic of the disease.

        Clostridium botulinum is a close relative of Clostridium tetani. It, too, produces a neurotoxin but this causes a flaccid paralysis where muscles go limp.

        Another clostridium, Clostridium difficile causes pseudomembranous colitis, associated with the use of particular antibiotics. The disease results from the activity of two toxins that damage the gut lining, causing a copious diarrhoea.

        Vibrio cholerae causes cholera in which the victim suffers such a profuse diarrhoea that stools take on the appearance of water in which rice has been boiled. This is due to the activity of cholera toxin, activating the production of cyclic AMP in gut epithelial cells.

        The genes that code for many exotoxins are located on "plasmids" -extrachromosomal circles of DNA that carry genetic information that is not essential for the survival of the bacterium. The gene that codes for diphtheria toxin is unusual - it is carried on a bacteriophage, a bacterial virus, that integrates its DNA into the chromosome of the host bacterium.
      • Endotoxin is a component of the outer membrane of Gram-negative bacteria. This structure lies beyond the cell wall. It does not have the characteristic phospholipid bilayer seen in most membranes. Rather, the inner surface comprises mostly phospholipid while the outer layer comprises a complex known as lipopolysacchride. The sugar complexes that make up the polysaccharide component provide the bacterium with its antigenic structure. The lipid in the outer layer of the Gram-negative outer membrane is a complex lipid known as Lipid A. When purified and injected into experimental subjects, this produces the generalised symptoms associated with endotoxin - low blood pressure and raised temperature. If sufficient endotoxin is present, this may cause endotoxic shock, generalised organ failure, intravascular coagulation and death.

 

  • production of "aggressins";
    • Aggressins are bacterial enzymes that, in contrast to exotoxins, typically have localised effects. Examples include coagulase, produced by Staphylococcus aureus. This catalyses the formation of fibrin from fibrinogen, causing plasma to clot. Staphylococcus aureus tends to produce defined lesions - this is because the activity of coagulase is to "wall off" the bacteria from the host defences. Another aggressin is streptokinase, produced by Streptococcus pyogenes. This aggressin digests fibrin, allowing the infecting bacteria to spread through affected tissues. Streptokinase has found a significant medical application as a clot-buster, used to treat people with a thrombosis. Other aggressins include collagenase and hyaluronidase, produced by a range of bacteria that use these enzymes to facilitate spread of infection through tissues.
  • initiating undesirable consequences of the host defences.
    • Certain pathogenic bacteria produce soluble antigens. These may then combine with antibodies to produce circulating immune complexes. Under certain conditions these can become trapped in blood vessels compromising their function. A good example of the problems that may result from circulating immune complexes is glomerulonephritis - kidney damage following an infection with Streptococcus pyogenes.
    • Rheumatic fever results from immunological cross-reactions between human tissue antigens and antigens on Streptococcus pyogenes. Following a streptococcal infection, antibodies raised against the bacterial antigens cross-react with the antigens produced by human tissue, leading to autoimmune disease.
    • The tubercle, the characteristic lesion of tuberculosis, has as a major component of the lesion mixtures of giant cells formed by the fusion of several macrophages as well as activated macrophages and lymphocytes, cells important in immune defences. Mycobacterium tuberculosis thus produces disease by over-stimulation of our immune response to infection.
 

Link to list of topics for this section

Link to the Person-to-person spread of infection page

Link to list of dental tutorial subjects


Page edited April 2006


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© John Heritage 2005, 2006


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