Bacterial Pathogenesis - Online Tutor, Practice Problems & Exam Prep

Bacterial pathogenesis involves four key steps: exposure, adherence, invasion, and multiplication. Initially, pathogens enter the host through portals like the respiratory tract. Successful adherence requires specific adhesins that bind to host cell receptors. Following adherence, pathogens invade host tissues, often using mechanisms like induced endocytosis, allowing them to evade the immune system. Finally, multiplication leads to local, focal, or systemic infections, causing damage and symptoms. Understanding these processes is crucial for developing effective treatments and preventive measures against infectious diseases.

Intro to Bacterial Pathogenesis

In this video, we're going to begin our lesson on bacterial pathogenesis, or how some bacteria can cause disease. The term pathogenesis refers to the process of disease development or infection inside of a host. Bacteriopathogenesis generally involves four important steps that we'll briefly discuss below, but then go into more detail as we move forward in our course. The very first step of bacterial pathogenesis is going to be exposure to the pathogen. This means that the person, like for example, Doctor Klutch here, needs to be exposed to the pathogen, and that exposure could potentially come from another infected person who may sneeze or cough.

After exposure, the second step is the adherence of the bacterial pathogen to the skin or mucosa, which is a critical step for pathogenesis. If the pathogen cannot adhere, then it will ultimately be eliminated from the body and will not be able to cause disease. Adherence is crucial, and the pathogens can adhere to our skin or mucosa, for example. Here, what we're showing you is the bacteria adhering to the mucosa, specifically to the mucus or mucus membranes.

The third step is invasion through the epithelium. In this process, the bacteria can make its way into the epithelium, the epithelial cells, or these cells here that are on the border or perimeter. In some cases, they may remain here, while in other cases, they may make their way into the bloodstream or invade a different type of tissue.

The fourth step is the multiplication of the pathogen, the replication of the pathogen inside the host. You can see that over here, the pathogen is now multiplying and creating many identical versions of itself, which would lead to signs and symptoms and Doctor Klutch starting to feel sick.

We'll talk a lot more about each of these steps as we move forward, but for now, this here concludes our brief introduction to bacterial pathogenesis. I'll see you all in our next video.

All of the following are phases of bacterial pathogenesis except which of these answers?

• A. Bacterial pathogens are destroyed by neutrophils and macrophages of the immune system.
• B. Bacterial pathogens are transmitted from an infected host to a healthy susceptible host.
• C. Bacterial pathogens multiply inside of the infected host.
• D. Bacterial pathogens invade the host's tissues and cells.

1) Exposure to Pathogen

In this video, we're going to talk about the first step in bacterial pathogenesis, which is exposure to the pathogen. And so once again, the very first step in bacterial pathogenesis is going to be exposure to the pathogen or an encounter pathogen that is going to result in an infection. This is because the pathogen not only must be encountered, but it must enter into the host tissues via what's known as a portal of entry. A portal of entry can be defined as specific locations where the host tissue cells are directly in contact with the external environment, allowing a pathogen in the external environment to enter into the body. Examples of portals of entry include the skin, mucous membranes, and parenteral routes, which involve the pathogen being directly injected into the body or the pathogen bypassing the skin and mucus and entering into the body via sites of broken protective barriers, such as cuts in our skin or open wounds.

The most common portal of entry for pathogens tends to be the respiratory tract, just being inhaled through our respiratory system. For example, the spread of COVID-19 mainly infects using a portal of entry of the respiratory tract. If we take a look at our image down below, we can see that there's an image here focused on the exposure to the pathogen. What you'll notice here is that Doctor Klutch is being exposed to the pathogen when this infected person sneezes or coughs. You can see that Doctor Klutch is going to be exposed to these pathogens. However, not all exposures are going to result in an infection. This is because the pathogen has to be able to enter via a portal of entry, like for example, perhaps Doctor Klutch's nose. Over here, what we are showing you is a zoom in of Doctor Klutch's nose. You can see that these microbes are entering via the portal of entry through the nose and the respiratory tract. Then, you can see the pathogen is now within Doctor Klutch's respiratory tract and is going to be exposed to the nasal mucus membrane.

This here concludes our lesson on the very first step in bacterial pathogenesis, exposure to the pathogen. We'll get to talk about the other three steps of bacterial pathogenesis as we move forward in our course. So I'll see you all in our next video.

During the Covid-19 pandemic, individuals around the world were advised to wear masks covering their nose and mouth. Why is this medical advice important for decreasing the spread of the SARS-CoV-2 virus?

• A. Face masks cover the openings to our respiratory system, which is the portal of entry for the SARS-CoV-2 virus.
• B. Face masks cover the openings to our respiratory system, which is the portal of exit for the SARS-CoV-2 virus.
• C. Face masks cover the openings to our digestive system, decreasing the entry of opportunistic pathogens.
• D. A and B.
• E. A and C.
• F. All of the above.

2) Adhesion to Host

In this video, we're going to talk about the second step in bacterial pathogenesis, which is adhesion to the host. After pathogen exposure and entry of the pathogen at the portal of entry, the pathogen must then properly adhere to the host. Adhesion is the ability of the pathogen to bind to host cells by using adhesion factors or adhesins. These adhesins are simply molecules on the surface of pathogens that bind to very specific receptors on the host cells. These adhesins can be found on bacterial pili, fimbriae or flagella. It is important to note that the Adhesin Receptor Binding is actually very very specific, and it ultimately controls the cell type that the Pathogen will adhere to and the tissue that the pathogen will cause disease in. This means that a pathogen will only be able to cause disease if it has the appropriate adhesins to bind to very specific host cell receptors. Without these very specific adhesins, they will not be able to adhere, and then they will not be able to cause disease.

If we take a look at our image down below, we can see an image focused on adhering or adhesion to the host cell. Notice once again we have our portal of entry; we have our microbe entering via our portal of entry, and there are two different microbes entering here. We have the green microbe entering right here and then we have the blue microbe entering right here. On the nasal mucus membranes, we have the green pathogen and the blue microbe. If we zoom in further into this particular region, the green pathogen has the appropriate adhesins to bind to this very specific host receptor. These host receptors are down below here, and the adhesins are these little molecules sticking off right around here. Because this green microbe has the appropriate adhesins to bind to the host cell receptors, it is going to be able to attach and adhere. However, notice that the blue microbe has a different set of adhesins. Because adhesion receptor binding is very specific, this blue microbe is not going to be able to bind. The turn away arrow here means that it will not be able to bind to the host cell receptors, and this means that this microbe will not be able to adhere and will not be able to cause an infection. Perhaps this microbe would need to make its way to a different set of cells, whose receptors are going to be compatible with these particular adhesins. Adhesion to the host is a critical step in bacterial pathogenesis.

This here concludes our brief lesson on this topic and we will be able to talk about the other steps of bacterial pathogenesis as we move forward. See you all in our next video.

Which of the following is not true about adhesin molecules?

• A. Adhesin molecules are receptors on the host cell's surface that allows pathogens to enter the cell.
• B. Adhesin molecules are found on pili, fimbriae, and flagella of bacterial pathogens.
• C. Adhesin molecules allow a bacterial pathogen to attach to the surface of the host's cells.
• D. Adhesin molecules bind to receptors on the surface of the host cell.

3) Invasion into Host Tissues

In this video, we're going to talk about the 3rd step in bacterial pathogenesis, which is invasion into the host cell or into the host tissues. Once a pathogen has adhered to the host, it will then either find a way to invade the inside of a host cell or just enter into the surrounding host tissues. Invasion of the inside of a host cell allows a pathogen to reduce competition for nutrients and to hide in order to avoid the immune system. Invading the inside of a host cell can be beneficial for the pathogen. The invasion into most types of host cells involves one of two potential mechanisms of induced endocytosis, which is when the bacterial cell tricks, "host cells" to perform endocytosis or to endocytose even when that host cell typically would not perform endocytosis. We'll talk a little more about this as we go along. This induced endocytosis can occur via the pathogen coming into contact with epithelial cells and secreting effector proteins that cause membrane ruffling, which occurs with the cell's actin, part of the cell's cytoskeleton. Membrane ruffling can be defined as a rearrangement of the actin filaments. This rearrangement in the host cell results in membrane ruffles, which are essentially wrinkles that ultimately enclose the bacterial cell and bring the bacterial cell into the host cell, resembling endocytosis, but not quite exactly the same. The other way is by standard endocytosis where the pathogen expresses surface proteins that bind to receptors on the host cell and the pathogen is then engulfed into the host cell.

If we take a look at this image below, we can get a better idea of how invasion into the host cell can occur. On the left, we have some pathogens that have adhered, and on the right, pathogens that have invaded the host cells. Here we're showing you two different pathways. We have the top pathway here in red and the bottom pathway in blue, both facilitating the invasion inside the host cell. The first path that the pathogen could take is through membrane ruffling. The pathogen will secrete effector proteins which are taken in by the host cell. These effector proteins ultimately cause the actin filaments to rearrange in this membrane ruffling. You can see that the membrane starts to wrinkle up and ruffle, and ultimately, what happens is that the pathogen is brought towards the inside of the host cell. Once the pathogen is inside, it has less competition for nutrients allowing it to survive and thrive better and also to avoid the host's immune system. It can be advantageous for pathogens to invade inside host cells.

The other way the pathogen could invade inside the host cell is by being engulfed through regular endocytosis. The surface proteins on the surface of the bacteria bind to host cell receptors. Upon binding to the bacterial surface proteins, the host cell receptors induce standard endocytosis and the pathogen is engulfed. The pathogen then makes its way into the host cell where it has less competition for nutrients and can avoid the host's immune system. Ultimately, the host cells have been invaded and the cells are now inside the host cell. If they're not going to remain inside the host cell, they can then continue to make their way into the host tissues.

This concludes our brief lesson on the invasion of the pathogen into the host cell or the host tissues and we'll be able to get some practice applying these concepts and then talk about the 4th and final stage of bacterial pathogenesis as we move forward. So I'll see you all in our next video.

The process by which infectious agents are ingested by host cells is termed

• A. Exocytosis.
• B. Pinocytosis.
• C. Endocytosis.
• D. Phagosome fusion.

Which of the following is not a method bacterial pathogens use to invade host cells in pathogenesis?

• A. Pathogens induce the host cell to engulf them.
• B. Pathogens breaks apart outside of the cell, are phagocytosed, then reassembles once within the host cell.
• C. Host cell membrane rearranges after the pathogens bind to the host cell's surface.
• D. The pathogens express surface proteins that allow them to bind to the host cell and begin endocytosis.

4) Multiplication (Colonization) Inside Host

In this video, we're going to talk about the 4th step in bacterial pathogenesis, which is the multiplication of the pathogen or colonization of the pathogen inside the host. After a pathogen enters the inside of a host cell or the host's tissues, it will begin to multiply or colonize inside the host and start damaging the host by causing an infection. Pathogens can cause three types of infections that we have listed below: local infections, focal infections, or systematic infections.

Local infections, as their name implies, are confined to a relatively small, localized area of the body, usually near the portal of entry. On the other hand, focal infections typically start off as localized infections but then spread to different parts of the body. Focal infections cause infections in multiple different areas of the body, usually by using the bloodstream. The third type is a systematic infection, characterized by an infection that disseminates or spreads widely throughout the entire body, making it systemic or affecting the entire body.

If we take a look at our image below, we are focusing on the colonization of the host. On the far left, we depict a local infection. A local infection remains within a small area of the body. For example, if there is a cut, the pathogen may enter via the cut and multiply and colonize this specific region of the body without spreading if it is a local infection. The next type we discuss is the focal infection, which may start as a local infection but then spreads to a different area of the body. In this example, we show an infected tooth cavity that may contain specific microbes. These microbes may travel to a different location in the body, potentially leading to endocarditis, an infection of the heart's lining and valves. Notice that the focal infection is capable of spreading to a different region of the body.

Lastly, on the far right, we discuss a systematic infection. As its name implies, a systematic infection means that the entire body is going to be infected. For example, a bacterial infection of the blood spreads throughout the entire body, known as a systematic infection if spread throughout the entire body. This concludes our brief lesson on the multiplication or colonization of the pathogen inside the host, and we'll be able to get some practice applying these concepts as we move forward in our course. I'll see you all in our next video.

Multifocal tuberculosis is characterized by:

• A. A patient with a single lobe of the left lung being infected with Mycobacterium tuberculosis bacteria.
• B. A patient with damage in their lungs, vertebrae, & CNS caused by Mycobacterium tuberculosis bacteria.
• C. A patient with Mycobacterium tuberculosis bacteria circulating throughout the blood stream.
• D. None of the above.

Sickle cell anemia is a blood disorder where affected individuals have 'half-moon' shaped red blood cells. Sickle cell anemia is an example of a _________ disease.

• A. Systemic.
• B. Local.
• C. Focal.
• D. Contagious.

Bacterial pathogen Z has proteins on its surface which bind to receptors on the host cell's surface. After it is bound, the host cell engulfs the bacterium. This means that the proteins on the surface of bacterium Z are:

• A. Virulence factors.
• B. Adhesins.
• C. Able to induce endocytosis in the host cell.
• D. A and B only.
• E. A, B and C.

Here’s what students ask on this topic:

What are the four key steps in bacterial pathogenesis?

The four key steps in bacterial pathogenesis are exposure, adherence, invasion, and multiplication. Initially, pathogens enter the host through portals like the respiratory tract. Successful adherence requires specific adhesins that bind to host cell receptors. Following adherence, pathogens invade host tissues, often using mechanisms like induced endocytosis, allowing them to evade the immune system. Finally, multiplication leads to local, focal, or systemic infections, causing damage and symptoms. Understanding these processes is crucial for developing effective treatments and preventive measures against infectious diseases.

How do bacterial pathogens adhere to host cells?

Bacterial pathogens adhere to host cells using adhesion factors or adhesins. These adhesins are molecules on the surface of pathogens that bind to specific receptors on host cells. Adhesins can be found on bacterial pili, fimbriae, or flagella. The binding between adhesins and host cell receptors is highly specific, determining the cell type and tissue the pathogen will infect. Without the appropriate adhesins, pathogens cannot adhere and will be eliminated from the body, preventing disease.

What mechanisms do bacteria use to invade host cells?

Bacteria use two main mechanisms to invade host cells: membrane ruffling and standard endocytosis. In membrane ruffling, bacteria secrete effector proteins that cause rearrangement of the host cell's actin filaments, creating ruffles that engulf the bacteria. In standard endocytosis, bacterial surface proteins bind to host cell receptors, inducing the host cell to engulf the bacteria. Both mechanisms allow bacteria to enter host cells, reducing competition for nutrients and evading the immune system.

What are the different types of infections caused by bacterial pathogens?

Bacterial pathogens can cause three types of infections: local, focal, and systemic. Local infections are confined to a small area near the portal of entry. Focal infections start as localized infections but spread to different parts of the body, often via the bloodstream. Systemic infections disseminate widely throughout the entire body, affecting multiple organs and systems. Understanding these infection types helps in diagnosing and treating bacterial diseases effectively.

What is the role of portals of entry in bacterial pathogenesis?

Portals of entry are specific locations where host tissue cells are in direct contact with the external environment, allowing pathogens to enter the body. Common portals of entry include the skin, mucous membranes, and parenteral routes (e.g., cuts or wounds). The respiratory tract is a frequent portal of entry for airborne pathogens. Successful entry through these portals is the first step in bacterial pathogenesis, leading to subsequent adherence, invasion, and multiplication within the host.