Chapter 15: Microbial Mechanism of Pathogenicity
Pathogenicity is the ability to cause disease by overcoming host defenses, whereas virulence is the degree of pathogenicity.
Pathogens can gain entrance to the human body and other hosts through several avenues, which are called portals of entry.
Other microorganisms gain access to the body when they are deposited directly into the tissues beneath the skin or into mucous membranes when these barriers are penetrated or injured.
This route is called the parenteral route.
The potency of a toxin is often expressed as the LD50 (lethal dose for 50% of a sample population).
For most pathogens, this attachment, called adherence (or adhesion), is a necessary step in pathogenicity.
The attachment between pathogen and host is accomplished by means of surface molecules on the pathogen called adhesins or ligands that bind specifically to complementary surface receptors on the cells of certain host tissues.
M protein is found on both the cell surface and fimbriae.
It mediates attachment of the bacterium to epithelial cells of the host and helps the bacterium resist phagocytosis by white blood cells.
The M protein thereby increases the virulence of the microorganism.
These bacteria use fimbriae and an outer membrane protein called Opa to attach to host cells.
The waxy lipid (mycolic acid) that makes up the cell wall of Mycobacterium tuberculosis also increases virulence by resisting digestion by phagocytes, and the bacteria can even multiply inside phagocytes.
Coagulases are bacterial enzymes that coagulate (clot) the fibrinogen in blood.
Bacterial kinases are bacterial enzymes that break down fibrin and thus digest clots formed by the body to isolate the infection.
Hyaluronidase is another enzyme secreted by certain bacteria, such as streptococci.
Another enzyme, collagenase, produced by several species of Clostridium, facilitates the spread of gas gangrene.
Collagenase breaks down the protein collagen, which forms the connective tissue of muscles and other body organs and tissues.
There are some pathogens with the ability to produce enzymes, called IgA proteases, that can destroy these antibodies.
Some pathogens can alter their surface antigens, by a process called antigenic variation.
The microbes produce sur- face proteins called invasins that rearrange nearby actin filaments of the cytoskeleton.
To obtain iron, some pathogens secrete proteins called siderophores.
Siderophores are released into the medium, where they take the iron away from iron-transport proteins by binding the iron even more tightly.
Once the iron-siderophore complex is formed, it is taken up by siderophore receptors on the bacterial surface.
Then the iron is brought into the bacterium.
In some cases, the iron is released from the complex to enter the bacterium; in other cases, the iron enters as part of the complex.
Toxins are poisonous substances that are produced by certain microorganisms.
The capacity of microorganisms to produce toxins is called toxigenicity.
The term toxemia refers to the presence of toxins in the blood.
Intoxications are caused by the presence of a toxin; not by microbial growth.
Exotoxins are produced inside some bacteria (mostly gram- negative) as part of their growth and metabolism and are secreted by the bacterium into the surrounding medium or released following lysis.
Membrane-disrupting toxins that kill phagocytic leukocytes (white blood cells) are called leukocidins.
Membrane-disrupting toxins that destroy erythrocytes (red blood cells), also by forming protein channels, are called hemolysins.
Hemolysins produced by streptococci are called streptolysins.
Superantigens are antigens that provoke a very intense immune response.
They are bacterial proteins that combine with a protein on macrophages; this non-specifically stimulates the proliferation of immune cells called T cells.
Shock refers to any life-threatening decrease in blood pressure.
Shock caused by bacteria is called septic shock.
The visible effects of viral infection are known as cytopathic effects (CPE).
Some virus-infected host cells produce substances called alpha and beta interferons.
The toxin is contained in sclerotia, highly resistant portions of the mycelia of the fungus that can detach.
The toxin itself, ergot, is an alkaloid that can cause hallucinations resembling those produced by LSD (lysergic acid diethylamide); in fact, ergot is a natural source of LSD.
Several other toxins are produced by fungi that grow on grains or other plants.
For example, peanut butter is occasionally recalled because of excessive amounts of aflatoxin, which has carcinogenic properties.
Aflatoxin is produced by the growth of the mold Aspergillus flavus.
When ingested, the toxin might be altered in a human body to a mutagenic compound.
A few mushrooms produce fungal toxins called mycotoxins.
Examples are phalloidin and amanitin, produced by Amanita phalloides (A-man- ̄i-tah fal-LOI-de ̄z), commonly known as the deathcap.
A few species of algae produce neurotoxins.
For example, some genera of dinoflagellates, such as Alexandrium, are important medically because they produce a neurotoxin called saxitoxin.
Just as microbes enter the body through a preferred route, they also leave the body via specific routes called portals of exit in secretions, excretions, discharges, or tissue that has been shed.
Portals of exit let pathogens spread through a population by moving from one susceptible host to another.
The most common portals of exit are the respiratory and gastrointestinal tracts.
Another important route of exit is the genitourinary tract.
Pathogenicity is the ability to cause disease by overcoming host defenses, whereas virulence is the degree of pathogenicity.
Pathogens can gain entrance to the human body and other hosts through several avenues, which are called portals of entry.
Other microorganisms gain access to the body when they are deposited directly into the tissues beneath the skin or into mucous membranes when these barriers are penetrated or injured.
This route is called the parenteral route.
The potency of a toxin is often expressed as the LD50 (lethal dose for 50% of a sample population).
For most pathogens, this attachment, called adherence (or adhesion), is a necessary step in pathogenicity.
The attachment between pathogen and host is accomplished by means of surface molecules on the pathogen called adhesins or ligands that bind specifically to complementary surface receptors on the cells of certain host tissues.
M protein is found on both the cell surface and fimbriae.
It mediates attachment of the bacterium to epithelial cells of the host and helps the bacterium resist phagocytosis by white blood cells.
The M protein thereby increases the virulence of the microorganism.
These bacteria use fimbriae and an outer membrane protein called Opa to attach to host cells.
The waxy lipid (mycolic acid) that makes up the cell wall of Mycobacterium tuberculosis also increases virulence by resisting digestion by phagocytes, and the bacteria can even multiply inside phagocytes.
Coagulases are bacterial enzymes that coagulate (clot) the fibrinogen in blood.
Bacterial kinases are bacterial enzymes that break down fibrin and thus digest clots formed by the body to isolate the infection.
Hyaluronidase is another enzyme secreted by certain bacteria, such as streptococci.
Another enzyme, collagenase, produced by several species of Clostridium, facilitates the spread of gas gangrene.
Collagenase breaks down the protein collagen, which forms the connective tissue of muscles and other body organs and tissues.
There are some pathogens with the ability to produce enzymes, called IgA proteases, that can destroy these antibodies.
Some pathogens can alter their surface antigens, by a process called antigenic variation.
The microbes produce sur- face proteins called invasins that rearrange nearby actin filaments of the cytoskeleton.
To obtain iron, some pathogens secrete proteins called siderophores.
Siderophores are released into the medium, where they take the iron away from iron-transport proteins by binding the iron even more tightly.
Once the iron-siderophore complex is formed, it is taken up by siderophore receptors on the bacterial surface.
Then the iron is brought into the bacterium.
In some cases, the iron is released from the complex to enter the bacterium; in other cases, the iron enters as part of the complex.
Toxins are poisonous substances that are produced by certain microorganisms.
The capacity of microorganisms to produce toxins is called toxigenicity.
The term toxemia refers to the presence of toxins in the blood.
Intoxications are caused by the presence of a toxin; not by microbial growth.
Exotoxins are produced inside some bacteria (mostly gram- negative) as part of their growth and metabolism and are secreted by the bacterium into the surrounding medium or released following lysis.
Membrane-disrupting toxins that kill phagocytic leukocytes (white blood cells) are called leukocidins.
Membrane-disrupting toxins that destroy erythrocytes (red blood cells), also by forming protein channels, are called hemolysins.
Hemolysins produced by streptococci are called streptolysins.
Superantigens are antigens that provoke a very intense immune response.
They are bacterial proteins that combine with a protein on macrophages; this non-specifically stimulates the proliferation of immune cells called T cells.
Shock refers to any life-threatening decrease in blood pressure.
Shock caused by bacteria is called septic shock.
The visible effects of viral infection are known as cytopathic effects (CPE).
Some virus-infected host cells produce substances called alpha and beta interferons.
The toxin is contained in sclerotia, highly resistant portions of the mycelia of the fungus that can detach.
The toxin itself, ergot, is an alkaloid that can cause hallucinations resembling those produced by LSD (lysergic acid diethylamide); in fact, ergot is a natural source of LSD.
Several other toxins are produced by fungi that grow on grains or other plants.
For example, peanut butter is occasionally recalled because of excessive amounts of aflatoxin, which has carcinogenic properties.
Aflatoxin is produced by the growth of the mold Aspergillus flavus.
When ingested, the toxin might be altered in a human body to a mutagenic compound.
A few mushrooms produce fungal toxins called mycotoxins.
Examples are phalloidin and amanitin, produced by Amanita phalloides (A-man- ̄i-tah fal-LOI-de ̄z), commonly known as the deathcap.
A few species of algae produce neurotoxins.
For example, some genera of dinoflagellates, such as Alexandrium, are important medically because they produce a neurotoxin called saxitoxin.
Just as microbes enter the body through a preferred route, they also leave the body via specific routes called portals of exit in secretions, excretions, discharges, or tissue that has been shed.
Portals of exit let pathogens spread through a population by moving from one susceptible host to another.
The most common portals of exit are the respiratory and gastrointestinal tracts.
Another important route of exit is the genitourinary tract.