I. BACTERIAL PATHOGENESIS

B. VIRULENCE FACTORS THAT PROMOTE BACTERIAL COLONIZATION OF THE HOST

4. The abilty to compete for iron and other nutrients

The overall purpose of this Learning Object is:
1) to learn how the ability to compete for iron and other nutrients plays a role in bacterial pathogenicity by promoting colonization; and
2) to introduce several examples of medically important bacteria that successfully compete for iron and other nutrients in order to promote colonization.

LEARNING OBJECTIVES FOR THIS SECTION

In this section on Bacterial Pathogenesis we will be looking at virulence factors that promote bacterial colonization of the host. The following are virulence factors that promote bacterial colonization of the host .

1. The ability to use motility and other means to contact host cells.
2. The ability to adhere to host cells and resist physical removal.
3. The ability to invade host cells.
4. The ability to compete for iron and other nutrients.
5. The ability to resist innate immune defenses such as phagocytosis and complement.
6. The ability to evade adaptive immune defenses.

We will now look at the ability of bacteria to compete for iron and other nutrients.

Virulence Factors that Promote Bacterial Colonization of the Host

4. The Ability to Compete for Iron and Other Nutrients

Often the ability to be pathogenic is directly related to the bacterium's ability to compete successfully with host tissue and normal flora for limited nutrients. One reason the generation time (def) of bacteria growing in the body is substantially slower than in lab culture is because essential nutrients are limited. In fact this is a major reason why the overwhelming majority of bacteria found in nature are not harmful to humans.

To be pathogenic, a bacterium must be able to multiply in host tissue.The more rapid the rate of replication, the more likely infection may be established. Pathogens, therefore, are able to compete successfully for limited nutrients in the body. Generally bacteria compete for nutrients by synthesizing specific transport systems or cell wall components capable of binding limiting substrates and transporting them into the cell. A good example of this is the ability of bacteria to compete for iron.

As we will see later in Unit 4 under nutritional immunity, the body makes considerable metabolic adjustment during infection to deprive microorganisms of iron. Iron is essential for both bacterial growth and human cell growth. Bacteria synthesize iron chelators - compounds capable of binding iron - called siderophores. Many siderophores are excreted by the bacterium into the environment, bind iron, and then re-enter the cell. Others are found on the cell wall where they bind iron and transport it into the bacterium.

Meanwhile, the body produces iron chelators of its own (transferrin, lactoferrin, ferritin, and hemin) so the concentration of free iron is very low. The ability of bacterial iron chelators to compete successfully with the body's iron chelators as well as those of normal flora may be essential to pathogenic bacteria.

Some bacteria produce in addition to their own siderophore, receptors for siderophores of other bacteria in this way take iron from other bacteria. Furthermore, a number of pathogenic bacteria are able to bind human transferrin, lactoferrin, ferritin, and hemin and use that as their iron source. For example, Neisseria gonorrhoeae (inf), Neisseria meningitidis (inf), and Haemophilus influenzae (inf) are able to use iron bound to human transferrin and lactoferrin for their iron needs, while pathogenic Yersinia species are able to use transferrin and hemin as iron sources. Borrelia burgdorferi (inf) doesn't even use iron as a cofactor, but instead uses manganese. Furthermore, a number of bacteria are able to produce exotoxins that kill host cells only when iron concentrations are low. Perhaps in this way the bacteria can gain access to the iron that was in those cells.

For further information on bacterial pathogenesis, see the online Microbiology Web Textbook at the University of Wisconsin-Madison.

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