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In the previous section, we explained that some pathogens are more virulent than others. This is due to the unique virulence factor s produced by individual pathogens, which determine the extent and severity of disease they may cause. A pathogen’s virulence factors are encoded by genes that can be identified using molecular Koch’s postulates. When genes encoding virulence factors are inactivated, virulence in the pathogen is diminished. In this section, we examine various types and specific examples of virulence factors and how they contribute to each step of pathogenesis.
As discussed in the previous section, the first two steps in pathogenesis are exposure and adhesion. Recall that an adhesin is a protein or glycoprotein found on the surface of a pathogen that attaches to receptors on the host cell. Adhesins are found on bacterial, viral, fungal, and protozoan pathogens. One example of a bacterial adhesin is type 1 fimbrial adhesin , a molecule found on the tips of fimbriae of enterotoxigenic E. coli ( ETEC ). Recall that fimbriae are hairlike protein bristles on the cell surface. Type 1 fimbrial adhesin allows the fimbriae of ETEC cells to attach to the mannose glycans expressed on intestinal epithelial cells. [link] lists common adhesins found in some of the pathogens we have discussed or will be seeing later in this chapter.
| Some Bacterial Adhesins and Their Host Attachment Sites | |||
|---|---|---|---|
| Pathogen | Disease | Adhesin | Attachment Site |
| Streptococcus pyogenes | Strep throat | Protein F | Respiratory epithelial cells |
| Streptococcus mutans | Dental caries | Adhesin P1 | Teeth |
| Neisseria gonorrhoeae | Gonorrhea | Type IV pili | Urethral epithelial cells |
| Enterotoxigenic E. coli (ETEC) | Traveler’s diarrhea | Type 1 fimbriae | Intestinal epithelial cells |
| Vibrio cholerae | Cholera | N-methylphenylalanine pili | Intestinal epithelial cells |
The presence of bacteria in Michael’s blood is a sign of infection, since blood is normally sterile. There is no indication that the bacteria entered the blood through an injury. Instead, it appears the portal of entry was the gastrointestinal route. Based on Michael’s symptoms, the results of his blood test, and the fact that Michael was the only one in the family to partake of the hot dogs, the physician suspects that Michael is suffering from a case of listeriosis.
Listeria monocytogenes , the facultative intracellular pathogen that causes listeriosis, is a common contaminant in ready-to-eat foods such as lunch meats and dairy products. Once ingested, these bacteria invade intestinal epithelial cells and translocate to the liver, where they grow inside hepatic cells. Listeriosis is fatal in about one in five normal healthy people, and mortality rates are slightly higher in patients with pre-existing conditions that weaken the immune response. A cluster of virulence genes encoded on a pathogenicity island is responsible for the pathogenicity of L. monocytogenes . These genes are regulated by a transcriptional factor known as peptide chain release factor 1 (PrfA). One of the genes regulated by PrfA is hyl , which encodes a toxin known as listeriolysin O (LLO), which allows the bacterium to escape vacuoles upon entry into a host cell. A second gene regulated by PrfA is actA, which encodes for a surface protein known as actin assembly-inducing protein (ActA). ActA is expressed on the surface of Listeria and polymerizes host actin. This enables the bacterium to produce actin tails , move around the cell’s cytoplasm, and spread from cell to cell without exiting into the extracellular compartment.
Michael’s condition has begun to worsen. He is now experiencing a stiff neck and hemiparesis (weakness of one side of the body). Concerned that the infection is spreading, the physician decides to conduct additional tests to determine what is causing these new symptoms.
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