Establishment of Infection

In order to cause disease, most pathogens must first adhere to a body surface; once they have attached, they then multiply to high enough numbers to either produce an appreciable amount of toxin or invade. In some cases, after they have colonized a surface they deliver molecules to epithelial cells, inducing a specific change in those cells.


Because the first-line defenses are very effective in removing organisms, a pathogen must adhere to host cells as a necessary first step in the establishment of infection. Microorganisms that attach to cells, however, do not necessarily cause disease. Many

466 Chapter 19 Host-Microbe Interactions members of the normal flora of the mouth and intestine adhere to cells with no ill effect whatsoever. Other factors such as toxin production and invasive ability of the microbe generally must come into play before disease results. ■ first-line defenses, p. 372

To bind to host cells, bacteria use adhesins. These are often located at the tips of pili, the filamentous protein structures found on the surface of the cell (figure 19.3; see figure 3.42). Pili used for attachment are often called fimbriae. Adhesins can also be a component of other surface structures such as the glycocalyx or various cell wall proteins (see figure 3.37). The streptococci that cause tooth decay produce a gly-cocalyx, for example, allowing them to attach to the tooth surface; other bacteria then adhere to this sticky surface, forming a biofilm. ■ pili, p. 65 ■ glycocalyx, p. 63 ■ biofilm, p. 104

The surface receptors on animal cells to which the bacterial adhesins attach are typically glycoproteins, protein molecules that have various sugars attached, or glycolipids; the adhesin binds to the sugar component of the receptor. For example, the adhesin of common pili of E. coli binds to the man-nose component of surface receptors found on cells in the intestine. Note that the surface receptor serves a distinct role for the cell that produces it; the microbe merely exploits the molecule for its own use. Neisseria gonorrhoeae adheres to mucosal epithelial cells by means of a molecule called CD46; the normal function of this molecule is to bind certain complement components, facilitating their degradation before they can trigger damage to the host cell. ■ glycoprotein, p. 29 ■ complement, p. 381

The binding of an adhesin to a surface receptor is highly specific, dictating the type of cells to which the bacterium can attach. For example, the adhesin of most strains of E. coli allows them to adhere to intestinal cells. Certain pathogenic strains, however, have various other additional adhesins that allow them to attach to cells in other tissues. Strains of E. coli that cause urinary tract infections generally produce a type of pili called P pili; these pili mediate specific attachment to cells that line the bladder. E. coli strains that cause watery diarrhea pro-

Pili with adhesins

Host cell glycoprotein receptors for pili

— Host cell membrane

Figure 19.3 Pili Attachment to Host Cell Protein adhesins of microorganisms attach to glycoprotein or glycolipid receptors on host cells. (See figure 3.42.)

Pili with adhesins

Host cell glycoprotein receptors for pili

— Host cell membrane

Figure 19.3 Pili Attachment to Host Cell Protein adhesins of microorganisms attach to glycoprotein or glycolipid receptors on host cells. (See figure 3.42.)

duce a type of pili that allows the bacteria to attach specifically to cells of the small intestine. These strains, enterotoxigenic E. coli (ETEC), are often species-specific. Some ETEC strains infect humans, whereas other strains infect only certain domestic animals. ■ enterotoxigenic E. coli, p. 615


A microorganism must multiply in order to colonize the host, a prerequisite for infectious disease. To colonize a site that is populated by normal flora, the new arrival must compete successfully with established organisms for space and nutrients, and overcome their toxic products such as fatty acids and antimicrobial compounds called bacteriocins. They also must counter the body's defenses aimed at protecting the surfaces.

IgA antibodies that recognize adhesin molecules and bind to them may prevent attachment of pathogens to the mucosal surfaces, thwarting their attempts at colonization. Microbes, however, have developed counterstrategies. These include: rapid turnover of pili, which effectively sheds antibody that has bound; antigenic variation, which can alter the type of pili produced; and IgA proteases, which cleave the antibody molecule. ■ antigenic variation, p. 187

One of the limiting nutrients for bacteria is often iron; recall that the body uses lactoferrin and transferrin to sequester iron. Some pathogens produce their own iron-binding molecules, siderophores, which compete with the host proteins; others are able to use the iron that has bound to the host proteins. ■ lactofer-rin and transferrin, p. 375

Delivery of Effector Molecules to Host Cells

Once they have colonized a surface, some bacteria are able to deliver certain molecules directly to host cells, inducing changes in those cells. This characteristic appears to be particularly common among gastrointestinal pathogens. In some cases, the compounds delivered induce changes that damage the recipient cell, such as loss of microvilli; in others, they direct the uptake of the bacterial cell, a process that will be discussed in the next section. ■ microvilli, p. 599

Gram-negative bacteria use type III secretion systems to deliver proteins to eukaryotic cells. These structures resemble short flagella and function as microscopic hypodermic needles (figure 19.4). The secretion systems and transferred proteins are often encoded by pathogenicity islands. ■ pathogenicity island, p. 212

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  • leena
    Is pilli used for the establishment of infection in bacteria?
    4 years ago

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