How pathogenic bacteria can enter the body

Streptococcus pneumoniae; note the presence of the capsule surrounding the bacteria

Via Science Daily, a report on how Streptococcus pneumoniae, a relatively innocuous bacterium that can cause conjunctivitis, is able to increase in virulence by breaching our bodies defenses. Researchers at a division of Harvard Medical School recently published in the medical journal PLoSONE, and described a novel enzyme made by virulent isolates of this bacterium.

The human body has two broad classes of surfaces which face the external world; our skin and our mucous membranes. Skin represents a formidable barrier to microorganisms, as the dry and salty environment inhibits the growth of most pathogens. Additionally, the dense, dead outer layers act as a physical barrier to microbial penetration. Mucous membranes, such as those that line the conjunctiva of the eye, the oral cavity, the gastrointestinal tract, and many other sites, presents a moist, nutrient rich environment that would at first glance promote the growth of microorganisms. The secretion of mucus however presents as significant a barrier to entry as the dry layers of skin; consequently the active secretion of mucus is essential to prevent colonization by pathogenic microorganisms. 

Purification of ZmpC by column chromatography

Mucus secretions are composed of two types of proteins called “mucins.” The sticky properties of mucin solutions trap microorganisms, and the cells which line the mucous membranes actively move trapped microbes before they can penetrate into tissue and cause disease. The researchers cultured virulent (or more able to cause disease) isolates of Streptococcus pneumoniae in the presence of mucin-secreting cells.

What they found was that these isolates of the bacterium were significantly more able to break down mucin in comparison to less-virulent isolates of the same organism. The assay that they used to identify the enzyme responsible for this property was very straightforward: the ability to release mucin from human cells was measured in bacterial protein samples, and the protein responsible for the activity was identified from the S. pneumoniae genome.  The protein has been named ZmpC, and disease causing isolates of the bacterium possess the gene, while non-disease causing isolates do not.

So the mechanism for virulence becomes easy to understand. The bacterium secretes an enzyme that breaks down the sticky mucin layers on our membranes, and is able to gain access to the tissue underneath it. This mechanism then provides a possible therapeutic approach to treating infections by these isolates. One could apply a competitive inhibitor which mimics how mucin binds to the active site on the ZmpC enzyme, preventing the ability of the organism to degrade the sticky barrier. Such a compound could easily be administered in aerosol form.


About ycpmicro

My name is David Singleton, and I am an Associate Professor of Microbiology at York College of Pennsylvania. My main course is BIO230, a course taken by allied-health students at YCP. Views on this site are my own.

Posted on March 10, 2012, in gross, Microbes in the News, Wash your hands!. Bookmark the permalink. 2 Comments.

  1. I find this article fascinating in that it amazes me that bacteria which are basically simple prokaryotic cells are able to change and create new ways to make us sick and defend themselves against antibiotics. I was impressed in chapter 10 by the various ways that bacteria resists antibiotics. For example how certain bacteria will completely stop making folic acid, which is what allows sufonamides to be effective against them, and begin absorbing folic acid from the environment, thus rendering sulfonamides ineffective against them. I just think considering these are one celled organisms and the fact that they can create these multiple forms of resistance by creating ways to eliminate what our bodies are doing and our antibiotics are doing to stop them is almost respect worthy, though making our lives in the medical field harder. I know many multi-celled organisms that are put to shame by bacterias’ many forms of creativity.

    • One of the major themes in our chapter in infectious disease is that genetically very similar microorganisms can vary wildly with respect to their ability to cause disease in the human body. See for instance, this post about the Black Death from last fall. The upshot of that paper is that isolates of Yersinia pestis that accounted for many millions of deaths a few centuries ago is not all that different from the organism today.

      Streptococcus pneumoniae actually has a long history with this topic as well, and was used in one of the first experiments to demonstrate that genetic information regarding virulence could be transferred between bacteria. Frederick Griffith beautifully demonstrated that avirulent strains of S. pneumoniae could become lethal when mixed with the DNA from virulent strains. This experiment did not prove that DNA was the hereditary material, but was one of the foundation experiments that led to that conclusion a decade later.

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