Skills to Develop
- State why it might be of an advantage for a bacterium trying to colonize the bladder or the intestines to be motile.
- Describe specifically how certain bacteria are able to use motility to contact host cells and state how this can promote colonization.
- Briefly describe why being extremely thin and being motile by means of axial filaments may be an advantage to pathogenic spirochetes.
- Give one example of how a nonmotile bacterium may be able to better disseminate within a host.
- Give a brief description of how a bacterium may use toxins to better disseminate from one host to another.
- Read the description of Helicobacter pylori and match the bacterium with the description of the organism and the infection it causes.
The mucosal surfaces of the respiratory tract, the intestinal tract, and the genitourinary tract constantly flush bacteria away in order to prevent colonization of host mucous membranes. Motile bacteria can use their motility and chemotaxis to swim through mucus towards mucosal epithelial cells. Many bacteria that can colonize the mucous membranes of the bladder and the intestines, in fact, are motile. Motility probably helps these bacteria move through the mucus between the mucin strands or in places where the mucus is less viscous. Examples of motile opportunists and pathogens include Helicobacter pylori, Salmonella species, Escherichia coli, Pseudomonas aeruginosa, and Vibrio cholerae. Once bacteria contact host cells they can subsequently attach, and colonize. (Attachment will be discussed in the next section.)
- Movie of motile Escherichia coli with fluorescent labelled-flagella #1 Courtesy of Dr. Howard C. Berg from the Roland Institute at Harvard.
- Movie of motile Pseudomonas from YouTube.
For example, Helicobacter pylori , the bacterium that causes most gastric and duodenal ulcers, produces urease, an enzyme that breaks down urea into ammonia and carbon dioxide. The ammonia neutralizes the hydrochloric acid in the stomach. In addition, the urease is thought to alter the proteins in the mucus changing it from a solid gel to a thinner fluid that the bacteria are able to swim through by way of their flagella, and subsequently use adhesins to adhere to the epithelial cells of the mucous membranes. To further help protect the bacterium from the acid, H. pylori produces an acid-inhibitory protein that blocks acid secretion by surrounding parietal cells in the stomach. Bacterial toxins then lead to excessive production of cytokines and chemokines , as well as mucinase and phospholipase that damage the gastric mucosa. The cytokines and chemokines, in turn, result in a massive inflammatory response. Neutrophils leave the capillaries, accumulate at the area of infection, and discharge their lysosomes for extracellular killing. This not only kills the bacteria, it also destroys the mucus-secreting mucous membranes of the stomach. Without this protective layer, gastric acid causes ulceration of the stomach. This, in turn, leads to either gastritis or gastric and duodenal ulcers.
YouTube movie of a video endoscopy exam showing duodenal ulcers caused by Helicobacter pylori.
Highlighted Bacterium: Helicobacter pylori
Click on this link, read the description of Helicobacter pylori, and be able to match the bacterium with its description on an exam.
Planktonic Pseudomonas aeruginosa uses its polar flagellum to move through water or mucus and make contact with a solid surface such as the body's mucous membranes (Figure 5.1.1). It then can use pili and cell wall adhesins to attach to the epithelial cells of the mucous membrane. Attachment activates signaling and quorum sensing genes to eventually enable the population of P. aeruginosa to start synthesizing a polysaccharide biofilm composed of alginate. As the biofilm grows, the bacteria lose their flagella to become nonmotile and secrete a variety of enzymes that enable the population to obtain nutrients from the host cells. Eventually the biofilm mushrooms up and develops water channels to deliver water and nutrients to all the bacteria within the biofilm. As the biofilm begins to get too crowded with bacteria, quorum sensing enables some of the Pseudomonas to again produce flagella, escape the biofilm, and colonize a new location.
Figure 5.1.1: Development of a Biofilm by Pseudomonas aeruginosa. Planktonic Pseudomonas aeruginosa use their polar flagella and chemotaxis to swim towards host mucous membranes. Pili then bind to host cell receptors for initial but reversible bacterial attachment.
Because of their thinness, their internal flagella (axial filaments), their corkscrew shape, and their motility (Figure 5.1.2), spirochetes are more readily able to penetrate host mucous membranes, skin abrasions, etc., and enter the body. Motility and penetration may also enable the spirochetes to penetrate deeper in tissue and enter the lymphatics and bloodstream and disseminate to other body sites. Spirochetes that infect humans include Treponema pallidum , Leptospira , and Borrelia burgdorferi ).
Figure 2: Spirochete Axial Filaments
- Movie of motile Borrelia bergdorferi, the spirochete that causes Lyme disease. From You Tube, courtesy of CytoViva.
- Movie of motile Borrelia bergdorferi, the spirochete that causes Lyme disease.
Along a different line, many bacteria produce enzymes such as elastases and proteases that degrade the extracellular matrix proteins that surround cells and tissues and make it easier for those bacteria to disseminate within the body. For example, Streptococcus pyogenes produces streptokinase that lyses the fibrin clots produced by the body in order to localize the infection. It also produces DNase that degrades cell-free DNA found in pus and reduces the viscosity of the pus. Both of these enzymes facilitate spread of the bacterium from the localized site to new tissue.
Staphylococcus aureus, on the other hand, produces surface adhesins that bind to extracellular matrix proteins and polysaccharides surrounding host cell tissue, including fibronectin, collagen, laminin, hyaluronic acid, and elastin. S. aureus proteases and hyaluronidase then dissolve these components of the extracellular matrix providing food for the bacteria and enabling the bacteria to spread.
Finally, as will be seen later in this unit under toxins, some bacteria produce toxins that induce diarrhea in the host. Diarrhea is also a part of our innate immunity to flush harmful microbes and toxins out of the intestines. On one hand, diarrhea is an advantage to the body because it flushes out harmful microbes and toxins. On the other hand, it is beneficial for the bacterium inducing the diarrhea because it also flushes out a good deal of the normal flora of the intestines and this reduces the competition for nutrients between normal flora and pathogens. In addition, diarrhea enables the pathogen to more readily leave one host and enter new hosts through the fecal-oral route.
Bacteria have to make physical contact with host cells before they can adhere to those cells and resist being flushed out of the body. Motile bacteria can use their flagella and chemotaxis to swim through mucus towards mucosal epithelial cells. Because of their thinness, their internal flagella (axial filaments), their corkscrew shape, and their motility, certain spirochetes are more readily able enter lymph vessels and blood vessels and spread to other body sites. Many bacteria produce enzymes that degrade the extracellular matrix proteins that surround cells and tissues and help to localize infection, making it easier for those bacteria to spread within the body. Some bacteria produce toxins that induce diarrhea in the host enabling the pathogen to more readily leave one host and enter new hosts through the fecal-oral route.
Dr. Gary Kaiser (COMMUNITY COLLEGE OF BALTIMORE COUNTY, CATONSVILLE CAMPUS)