Bacterial Resistance, Infection and Chronic Fatigue Syndrome: Fighting Infections Pt. I
This is the first of a second series of posts dealing with remission strategies from infections. The contents will apply regardless of which infection model you believe causes Chronic Fatigue Syndrome. The usual models are:
- A bacterial infection in the body (tissue, bone marrow, blood) – for example: Lyme, Mycoplasma, Rickettsia
- A viral infection – for example: EBV, HHV6
- An alteration of the microbiome (mouth and intestinal bacteria)
Bacteria are adapting continuously in order to survive. In this blog I’ll describe some of the tricks they use to evade the immune system. Whether you try antivirals, prescription antibiotics, herbs, or probiotics, unfortunately these tricks often allow the bacteria to survive. In subsequent posts I will describe methods that can be used to outsmart these bugs.
Evasion by Mutation
Some pathogens evolve very rapidly once they get inside the body, either by random mutation or probably more commonly by borrowing RNA fragments from other pathogens.
If they reproduce quickly (within a day or two) slight variations of the original infection may have been produced. Because anti-infectious agents often work by attaching to a section of the bug, if the shape of the pathogen has changed they may no longer be able to attach to it. Think of an antibiotic as a key and a section of the pathogen as a lock the key fits into; if the key is bent or a small part of it is filed down or if there is sand in the lock, the key will no longer work in the lock. This “shape-shifting” is the best known way for antibiotic resistance to occur.
A Few Mutations Away From a Deadly Bird Flu
Under The Dome
Another method of resistance used by organisms on the defense all over the world is to cluster together to expose as little surface area to attack as possible. Pathogens, like many other living things, can cluster together forming colonies (or even cities :)) in the body. When pathogens clump together the anti-infectious agent will only be able to kill off the outer edge of the colony. In other cases, the infections produce a kind of glue that catches whatever is floating by creating a wall of flotsam and jetsam.
Watch fire ants build a different kind of colony that is able float on the water in the video below.
Fire Ant Colony Able to Float on Water
In both cases, we end up with something like a domed city. The dome keeps the infection inside, mostly isolated from what’s outside, but allows enough small openings that it can grab the resources (food) it needs to survive and through which it can dump its toxins. A biofilm may further prevent antibiotics from reaching a bacterial infection.
The Rip van Winkle Approach: Resistance by Hibernation
Infections often have a complex life cycle, one stage of which is hibernation. A segment of the pathogen population can turn themselves off so thoroughly that anti-infection agents don’t recognize them. This kind of resistance generally applies to just 0.01-2% of a pathogen population.
If the immune system is weak and the pathogen has a good food supply, even if the non-hibernating bugs are wiped out, once the hibernating bugs wake up they can rapidly restore the infection.
Results of recent advances in DNA analysis suggest infections and medical conditions may often produce a distinctive bacterial signature in the gut (the microbiome). Researchers have been able to determine the type of infection in some cases by analyzing the gut flora. In addition, pathogens can trigger the gut flora to produce factors the pathogen needs to reproduce, and to stop producing factors that assist the immune response.
This suggests that gut flora manipulation may be an important tool in assisting the immune response to fight off pathogens.
Exploiting the Body’s Means of Dealing with Infections
The human body has a variety of tricks to deal with infections. The core concept is to contain the infection until the immune system is able to manufacture the cells in needs to eliminate it.
Think of an infection as an invader establishing a beachhead in the body. The body will to do everything that it can to prevent the invader moving further in: it will destroy bridges, fell trees across roads, etc. In terms of our biology these mechanisms include:
While these tricks slow the infection moving into the body, they can also be exploited by the infection to subvert the immune response.
Resistance by Inflammation
Some pathogens are adept at turning the defenses the body throws up against them to their advantage. One purpose of inflammation is to prevent the spread of an infection until the immune system can be mobilized to address it, but these same measures that block the spread of an infection can also interfere with immune factors or antibiotics reaching the infection.
Resistance by Fibrin
Inert material called fibrin forms meshes over pathogens in order to slow the spread of an infection, but that mesh also inhibits the immune agent’s ability to get at the infection. A precursor to fibrin called soluble fibrin monomer allows the body to quickly create fibrin when needed. If this occurs in some people with ME/CFS – as some research suggests it might – they could end up with thick blood, misshapen red blood cells, and a difficult to reach infection.
Vascular constriction is another defense mechanism that infections can turn around and use to prevent immune agents from reaching them. Blood vessels that are overly constricted may admit only the essential foods that the infection needs and let the toxins it produces get out.
If the infection exploits enough of the options listed above it can become deeply established in the body. Getting rid of it may require systematically negating the pathogens tricks. In upcoming posts I will supply a simple cookbook recipe I’ve used to deal each item on this list to reduce infections.
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