BtB#1- Host parasite interaction interface

Greetings,

Recently, I had taken a break and announced that I plan to introduce certain new series additions to the blog. Other than routine posts talking about new research in microbiology under various categories, I had a couple of guest posts, Blogger's desk and more recently Lab series talking about a variety of lab related stuff. All these posts were written expecting that people reading these stuff have a certain level of basics. Surprisingly, it came to my attention that people want to see posts that are absolutely basic. I had been under the impression that the basic ideas are evident in my posts. So I'm adding a new series that will be called "Back to Basics" or BTB in short.

Everyone who is learning about Medical microbiology is aware of an array of factors called as "virulence factors", that determine the ability of the organism to successfully establish itself. Long ago, I have posted on how the textbook idea of virulence factor is not right (Link). The important basic biological question in this post is "Is the organism evolved systems so that it could be damaging to host". To answer the question let us divide the question into two segments. First, Is damaging the host an objective of the pathogen? So why does the pathogen cause harm if that is not its primary objective?

Coming to the first question. We are classically taught to think that pathogens are inherently damaging. Note that the term "Pathogen" and "Pathogenesis" is so loosely applied in literature. Well in reality, that is not its primary objective. The primary goal of the organism is simply to replicate and reproduce using resources from the host. However, the host responds in such a way as to not give up its hard earned resources for free. The counter measures and counter-counter measures that evolves from this complex interface is responsible for evolving molecules and interactions of what we call as "pathogenesis". There is a compromise that a pathogen has to make. If its too good at attacking, it will destroy the host in a time span far too less equipped for it to replicate and transmit. If it is too slug then host will get it off the system before it had a chance to do anything. And the line of balance that is in between is too thin. So, let me make the answer clear. It is not the aim of pathogen to inflict damage. There is altogether a different reason for lethality of certain pathogens.

Second question. As I already mentioned above its the interface of interactions that actually matters. Let us take the example of hemolysins since this is perhaps the most easily understood. What is the advantage to the bacteria that produce a hemolysin say in an example case of E coli? In reality secretion of hemolysin is a complicated process with a lot of dedicated machinery. In this scenario the system is actually an evolved mechanism to obtain Iron. Hemolysin breaks up the RBC so as to release the Iron molecules in it. There isn't any other vested interest for bacteria in the RBC. Subsequently bacterial molecules like enterochelin take up the Iron. Iron being a very rare precious molecule, host has also several molecules evolved to save itself from loosing that Iron. As a matter of fact there is a evolutionary pressure on both sides to develop systems that are better than the other in sequestering nutrient. This kind of defense is also known as Nutritional Immunity. But the net effect is the outcome of such an interaction, in this case hemolysis. I think that answers the second question. Another well studied example would be Urease enzyme, which is simply a mechanism to change the pH of surroundings to benefit bacterial living conditions.

I think that settles some of the confusions, that isn't traditionally explained. The ideal definition of pathogenesis would then be, "ability to defend the ability to survive the host counter mechanisms so as to enable it to reproduce" (I just made it up for clarity of thought).

Barber MF, & Elde NC (2014). Nutritional immunity. Escape from bacterial iron piracy through rapid evolution of transferrin. Science (New York, N.Y.), 346 (6215), 1362-6 PMID: 25504720