The efficient spread of a pathogen via an insect vector requires that an individual insect consumes a blood meal from an infected host and transfers the pathogen to a naive host. In a few striking cases, the pathogen alters the behavior of the insect so that its transmission to a new host is more likely. An example is the bacterium Yersinia pestis, which causes bubonic plague. It multiplies in the flea’s foregut to form aggregated masses that physically block the digestive tract; during each repeated, but futile, attempt at feeding, some of the bacteria in the foregut are flushed into the bite site, thus transmitting plague to a new host (Figure 23–14).
Whereas many epithelial barriers such as the skin and the lining of the mouth and large intestine are densely populated by normal flora, others, including the lining of the lower lung and the bladder, are normally kept nearly sterile. How do these epithelia avoid bacterial colonization? A layer of protective mucus covers the respiratory epithelium, and the coordinated beating of cilia sweeps the mucus and trapped bacteria up and out of the lung. The epithelial lining of the bladder and the upper gastrointestinal tract also has a thick layer of mucus, and
Figure 23–14 Plague bacteria within a flea. This light micrograph shows the digestive tract dissected from a flea that had dined about two weeks previously on the blood of an animal infected with the plague bacterium, Yersinia pestis. The bacteria multiplied in the flea gut to produce large cohesive aggregates (red arrows); the bacterial mass on the left is occluding the passage between the esophagus and the midgut. This type of blockage prevents a flea from digesting  its blood meals, so that hunger causes it to bite repeatedly, disseminating the infection. (From B.J. Hinnebusch,
E.R. Fischer and T.G. Schwan,  J. Infect. Dis. 178:1406–1415, 1998.) these organs are periodically flushed by urination and by peristalsis, respectively, which washes away most microbes.
Pathogenic bacteria and eukaryotic parasites that infect these epithelial surfaces have evolved specific mechanisms for overcoming these protective mechanisms. Those that infect the urinary tract, for example, adhere tightly to the epithelial lining via specific adhesins, which are proteins or protein complexes that recognize and bind to cell-surface molecules on the epithelium. An important group of adhesins in E. coli strains that infect the kidney are components of the pili—surface projections that can be several micrometers long and thus able to span the thickness of the protective mucus layer; at the tip of each pilus is an adhesin protein that binds tightly to the D-galactose–D-galactose disaccharide on glycolipids on the surface of kidney cells (Figure 23–15). Strains of E. coli that infect the bladder rather than the kidney express a second kind of pilus with a different adhesin protein that binds to bladder epithelial cells. It is the specificity of the adhesin proteins on the tips of the two types of pili that is responsible for the bacteria’s colonizing of the different parts of the urinary tract.