What do hyaluronidase and kinase have in common

Additional Medical Flashcards. Term Four general classes of virulence factors. Term What variable is used to quantify virulence? Definition LD 50 number of microbes needed to kill half of an infected population.

Term Main difference between primary and secondary virulence factors? Term Adhesins are usually what kind of macromolecule lipis, protein, etc. Definition Usually proteins, but can be sugars too. Term Function of adhesins. Definition Determine specificity of infection. Term Main extracellular enzymes that constitute virulence factors. Term Purpose of hyaluronidase and collagenase as virulence factors.

Definition Chew through hyaluronic acid and collagen in extracellular matrix to facilitate invasion and spread. Term Purpose of coagulase and kinases as virulence factors. Term Major pathogens with coagulase and kinases. Term Major pathogens with hyaluronidase and collagenase. Definition Staphylococcus aureus. Term What is the function of staphylokinase?

Definition Chews through clots to help spread infection. Term What extracellular enzymes are used to digest extracellular matrix? Term Deadly fungus with antiphagocytic capsule.

Definition Cryptococcus neoformans. Term Composition of bacterial and fungal capsule. Definition Non-immunogenic polysaccharides. Term How do capsules help bacteria evade immune system? Definition Capsules are made of non-immunogenic polysaccharides; ie, they aren't recognized by the host's immune system, so macrophages and neutrophils don't detect them. Term What type of virulence factor is Streptococcus pyogenes' M protein? Definition Antiphagocytic. Term Leukocidins have what function?

Definition Destroy phagocytic white blood cells. Term Is LPS an endo- or exotoxin? Definition Endotoxin. Definition Gram-negative LPS is anchored to the outer cell membrane. Term Cytotoxins, neurotoxins, and enterotoxins are examples of endo- or exotoxins? Definition Exotoxins. Term Where do exotoxins typically act on the host's cells? Term Inflammation and immune responses are typically in response to endo- or exotoxins?

Definition Endotoxins. Term Main difference between endo- and exotoxins. Definition Exotoxins are secreted by the pathogen; endotoxins ie, LPS is part of the pathogen's structure. Term Etiologic agent of typhoid fever. Definition Salmonella typhi. Term Etiologic agent of salmonellosis. Definition Salmonella typhimurium. Term Do pathogens usually have one or several virulence factors? Definition Several. Term How is Staphylococcus aureus transmitted?

Definition Airborne. Term Is S. Definition Gram-positive. Term Species of Staphylococcus that is normal flora of nose. Definition S. Term S. Term Staphylococcus virulence factors. Term Extracellular enzyme virulence factors of Staphylococcus.

Term Antiphagocytic virulence factors of Staphylococcus. Term Toxins produced by Staphylococcus. Term Are pathogenic Streptococci Gram-negative or Gram-positive? Term Major pathogenic species in genus Streptococcus.

Term Other name for group A, beta-hemolytic Streptococcus. Definition Streptococcus pyogenes. Term Pathogenic species of Streptococcus that is alpha-hemolytic.

Evading the immune system is also important to invasiveness. Bacteria use a variety of virulence factors to evade phagocytosis by cells of the immune system. For example, many bacteria produce capsules , which are used in adhesion but also aid in immune evasion by preventing ingestion by phagocytes. The composition of the capsule prevents immune cells from being able to adhere and then phagocytose the cell.

In addition, the capsule makes the bacterial cell much larger, making it harder for immune cells to engulf the pathogen Figure 8. A notable capsule-producing bacterium is the gram-positive pathogen Streptococcus pneumoniae , which causes pneumococcal pneumonia, meningitis, septicemia, and other respiratory tract infections. Encapsulated strains of S. Some pathogens can also produce proteases to protect themselves against phagocytosis. As described in Adaptive Specific Host Defenses , the human immune system produces antibodies that bind to surface molecules found on specific bacteria e.

This binding initiates phagocytosis and other mechanisms of antibacterial killing and clearance. Proteases combat antibody-mediated killing and clearance by attacking and digesting the antibody molecules Figure 8. Figure 8. Phagocytes then bind to the antibody, initiating phagocytosis. In addition to capsules and proteases, some bacterial pathogens produce other virulence factors that allow them to evade the immune system.

The fimbriae of certain species of Streptococcus contain M protein , which alters the surface of Streptococcus and inhibits phagocytosis by blocking the binding of the complement molecules that assist phagocytes in ingesting bacterial pathogens. The acid-fast bacterium Mycobacterium tuberculosis the causative agent of tuberculosis produces a waxy substance known as mycolic acid in its cell envelope.

When it is engulfed by phagocytes in the lung, the protective mycolic acid coat enables the bacterium to resist some of the killing mechanisms within the phagolysosome. Some bacteria produce virulence factors that promote infection by exploiting molecules naturally produced by the host.

For example, most strains of Staphylococcus aureus produce the exoenzyme coagulase , which exploits the natural mechanism of blood clotting to evade the immune system. Normally, blood clotting is triggered in response to blood vessel damage; platelets begin to plug the clot, and a cascade of reactions occurs in which fibrinogen, a soluble protein made by the liver, is cleaved into fibrin. Fibrin is an insoluble, thread-like protein that binds to blood platelets, cross-links, and contracts to form a mesh of clumped platelets and red blood cells.

The resulting clot prevents further loss of blood from the damaged blood vessels. However, if bacteria release coagulase into the bloodstream, the fibrinogen-to-fibrin cascade is triggered in the absence of blood vessel damage. The resulting clot coats the bacteria in fibrin, protecting the bacteria from exposure to phagocytic immune cells circulating in the bloodstream.

Whereas coagulase causes blood to clot, kinases have the opposite effect by triggering the conversion of plasminogen to plasmin, which is involved in the digestion of fibrin clots. By digesting a clot, kinases allow pathogens trapped in the clot to escape and spread, similar to the way that collagenase, hyaluronidase, and DNAse facilitate the spread of infection.

Examples of kinases include staphylokinases and streptokinases , produced by Staphylococcus aureus and Streptococcus pyogenes , respectively.

It is intriguing that S. The action of the coagulase provides an important protective barrier from the immune system, but when nutrient supplies are diminished or other conditions signal a need for the pathogen to escape and spread, the production of staphylokinase can initiate this process. For example, the bacterium Borrelia burgdorferi , the causative agent of Lyme disease , contains a surface lipoprotein known as VlsE.

Because of genetic recombination during DNA replication and repair, this bacterial protein undergoes antigenic variation. Each time fever occurs, the VlsE protein in B. It is believed that this variation in the VlsE contributes to the ability B. Another important human bacterial pathogen that uses antigenic variation to avoid the immune system is Neisseria gonorrhoeae , which causes the sexually transmitted disease gonorrhea.

This bacterium is well known for its ability to undergo antigenic variation of its type IV pili to avoid immune defenses. The physician decides to order a spinal tap to look for any bacteria that may have invaded the meninges and cerebrospinal fluid CSF , which would normally be sterile. The needle is inserted and a small volume of fluid is drawn into an attached sample tube. Because meningitis can be life threatening and because the first antibiotic therapy was not effective in preventing the spread of infection, Pankaj is prescribed an aggressive course of two antibiotics, ampicillin and gentamicin, to be delivered intravenously.

Pankaj remains in the hospital for several days for supportive care and for observation. After a week, he is allowed to return home for bed rest and oral antibiotics. After 3 weeks of this treatment, he makes a full recovery. Although viral pathogens are not similar to bacterial pathogens in terms of structure, some of the properties that contribute to their virulence are similar. Viruses use adhesins to facilitate adhesion to host cells, and certain enveloped viruses rely on antigenic variation to avoid the host immune defenses.

These virulence factors are discussed in more detail in the following sections. One of the first steps in any viral infection is adhesion of the virus to specific receptors on the surface of cells. This process is mediated by adhesins that are part of the viral capsid or membrane envelope. The interaction of viral adhesins with specific cell receptors defines the tropism preferential targeting of viruses for specific cells, tissues, and organs in the body.

The spike protein hemagglutinin found on Influenzavirus is an example of a viral adhesin; it allows the virus to bind to the sialic acid on the membrane of host respiratory and intestinal cells. Another viral adhesin is the glycoprotein gp20, found on HIV. For HIV to infect cells of the immune system, it must interact with two receptors on the surface of cells.

The first interaction involves binding between gp and the CD4 cellular marker that is found on some essential immune system cells. However, before viral entry into the cell can occur, a second interaction between gp and one of two chemokine receptors CCR5 and CXCR4 must occur. Table 6 lists the adhesins for some common viral pathogens and the specific sites to which these adhesins allow viruses to attach.

Antigenic variation also occurs in certain types of enveloped viruses, including influenza viruses, which exhibit two forms of antigenic variation: antigenic drift and antigenic shift Figure 9. Antigenic drift is the result of point mutations causing slight changes in the spike proteins hemagglutinin H and neuraminidase N. On the other hand, antigenic shift is a major change in spike proteins due to gene reassortment. This reassortment for antigenic shift occurs typically when two different influenza viruses infect the same host.

The rate of antigenic variation in influenza viruses is very high, making it difficult for the immune system to recognize the many different strains of Influenzavirus. Although the body may develop immunity to one strain through natural exposure or vaccination, antigenic variation results in the continual emergence of new strains that the immune system will not recognize.

This is the main reason that vaccines against Influenzavirus must be given annually. Figure 9. Antigenic drift and antigenic shift in influenza viruses. The resultant virus possesses a mixture of the proteins of the original viruses. Influenza pandemics can often be traced to antigenic shifts. You have recently identified a new toxin. It is produced by a gram-negative bacterium. It is composed mostly of protein, has high toxicity, and is not heat stable. You also discover that it targets liver cells.

Based on these characteristics, how would you classify this toxin? Skip to main content. Microbial Mechanisms of Pathogenicity. Search for:. Virulence Factors of Bacterial and Viral Pathogens Learning Objectives Explain how virulence factors contribute to signs and symptoms of infectious disease Differentiate between endotoxins and exotoxins Describe and differentiate between various types of exotoxins Describe the mechanisms viruses use for adhesion and antigenic variation.

What kind of pathogen causes listeriosis, and what virulence factors contribute to the signs and symptoms Pankaj is experiencing? If so, how might this explain his new symptoms? Two types of cell death are apoptosis and necrosis. Visit this website to learn more about the differences between these mechanisms of cell death and their causes. Click this link to see an animation of how the cholera toxin functions.

Click this link to see an animation of how the botulinum toxin functions. Think about It Describe how exoenzymes contribute to bacterial invasion. Explain the difference between exotoxins and endotoxin. Name the three classes of exotoxins. Think about It Name at least two ways that a capsule provides protection from the immune system.

Besides capsules, name two other virulence factors used by bacteria to evade the immune system. For another explanation of how antigenic shift and drift occur, watch this video. Think about It Describe the role of adhesins in viral tropism. Explain the difference between antigenic drift and antigenic shift. Exoenzymes and toxins allow pathogens to invade host tissue and cause tissue damage. Exoenzymes are classified according to the macromolecule they target and exotoxins are classified based on their mechanism of action.

Bacterial toxins include endotoxin and exotoxins. Endotoxin is the lipid A component of the LPS of the gram-negative cell envelope. Exotoxins are proteins secreted mainly by gram-positive bacteria, but also are secreted by gram-negative bacteria. Bacterial pathogens may evade the host immune response by producing capsules to avoid phagocytosis, surviving the intracellular environment of phagocytes, degrading antibodies, or through antigenic variation. Viral pathogens use adhesins for initiating infections and antigenic variation to avoid immune defenses.

Influenza viruses use both antigenic drift and antigenic shift to avoid being recognized by the immune system. Multiple Choice Which of the following would be a virulence factor of a pathogen?

Cytopathic effects, such as inclusion bodies and syncytium formation, are the visible signs of viral infections. Bacteria such as E. Polio is transmitted by ingestion of water contaminated with feces containing polio virus. What portal of entry does polio virus use? Sign in. Chapter 15 Cards. Helpfulness: 0. Set Details Share. Grade levels: College: First year.

Subjects: microbiology. What do hyaluronidase and kinase have in common? They are both enzymes involved in evading host defense. According to your Concept Map, which of the following organisms exhibits antigenic variation? Shiga toxin is more lethal than staphylococcal enterotoxin.