I. BACTERIAL PATHOGENESIS

C. VIRULENCE FACTORS THAT DAMAGE THE HOST

2. Producing Harmful Exotoxins

c. Exotoxins that Damage Host Cell Membranes (Type II Toxins)

The overall purpose of this Learning Object is:
1) to learn how some exotoxins (Type II toxins) are able to cause harm by damaging host cell membranes;
2) to introduce a number of medically important bacteria that produce toxins that damage host cell membranes; and
3) to introduce how bacteria may communicate with other members of their population by quorum sensing.

LEARNING OBJECTIVES FOR THIS SECTION

In this section on Bacterial Pathogenesis we are looking at virulence factors that damage the host. Virulence factors that damage the host include:

1. The ability to produce cell wall components (Pathogen-Associated Molecular Patterns or PAMPs) that bind to host cells causing them to synthesize and secrete inflammatory cytokines and chemokines;

2. The ability to produce harmful exotoxins.

3. The ability to induce autoimmune responses.

We are currently looking at the ability of bacteria to produce harmful exotoxins.

Exotoxins (def) are protein toxins usually secreted from a living bacterium but also released upon bacterial lysis. There are three main types of exotoxins:

1. superantigens (Type I toxins),

2. exotoxins that damage host cell membranes (Type II toxins)

3. A-B toxins and other toxin that interfere with host cell function (TypeII I toxins).

We will now look at exotoxins that damage host cell membranes.

The Ability to Produce Harmful Exotoxins

b. Toxins that Damage Host Cell Membranes (Type II Toxins)


Highlighted Bacterium: Clostridium difficile

Click on this link, read the description of Clostridium difficile, and be able to match the bacterium with its description on an exam.

 

 

E-Medicine article on infections associated with organisms mentioned in this Learning Object. Registration to access this website is free.

 

For further information on bacterial pathogenesis, see the online Microbiology Web Textbook at the University of Wisconsin-Madison.

Many gram-negative and gram-positive are able to sense their own population density, communicate with each other by way of secreted factors, and behave as a population rather than as individual bacteria. This is referred to as cell-to-cell signaling or quorum sensing and most likely plays an important role in pathogenicity for many bacteria.

Quorum sensing involves the production, release, and community-wide sensing of molecules called autoinducers that modulate gene expression in response to the density of a bacterial population. When autoinducers produced by one bacterium cross the membrane of another, they bind to receptors in the cytoplasm. This autoinducer/receptor complex is then able to bind to DNA promoters and activate the transcription of quorum sensing-controlled genes.

For example, Pseudomonas aeruginosa causes severe nosocomial infections, chronic infections in people with cystic fibrosis, and potentially fatal infections in those who are immunocompromised. Its virulence depends on the secretion of a variety of harmful exotoxins and enzymes as mentioned above. If there was an isolated production of these virulence toxins and enzymes by a small number of Pseudomonas, the body's immune responses would most likely be able effectively neutralize these harmful agents with antibodies. However, through a coordination of the expression of the genes coding for these toxins and enzymes by the entire population of bacteria, P. aeruginosa appears to only secrete these extracellular virulence factors when the density of bacteria is large enough that they can be produced at high enough levels to overcome body defenses.

Other quorum sensing-controlled processes in bacteria include biofilm formation, sporulation, antibiotic production, and bioluminescence.

 

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