Triggers for dormant E.coli release: Antibiotic dose levels

Asexual Survival Characteristics (E.coli)

Say you start off with a strain called x...

If you kill all of x with an antibiotic, then there are no x survivors, and if you were to again be infected with x (as a fresh contamination), and took the same antibiotic, there could be no increase in the resistance of x. It would be just like the first time, and they would be all killed.

But this is where natural selection comes in. E.coli are asexual organisms with natural variation in the genetic makup of some of the bacteria in every colony. In effect E.coli are genetic clones of each other, but there are occasional mutations that produce genetic variation, giving the variation different survival capabilities. For example, although some of the mutations will have poor survival capabilities, some E.coli in every colony may be able to survive unusual heat, cold, toxin levels, antibiotic attack, or high acidity or alkalinity. They pass on these survival characteristics to their progeny.

Doctors attempt to fight the resistance of E.coli by varying the antibiotics used, and by increasing antibiotic dose levels to compensate for the resistance effect, but this only exasperates the problem as the E.coli become increasingly resistant, even to broad-spectrum antibiotics. The result is seriously resistant E.coli that only something that defeats the E.coli in another way (like Waterfall D-Mannose) can get rid of from your body.

Variant E.coli and Antibiotic Resistance

The mechanism of E.coli antibiotic resistance is that one or more natural E.coli variants, (lets call it variant xy), survives the antibiotic attack. For example, by not succumbing to fluorine poisoning. So the antibiotic kills off all x colonies, and xy is left to multiply and establish colonies of it's own, passing on its resistance to fluorine (or whatever toxin the antibiotic utilised) to its duplicates. Most of the xy colonies will be xy type variant, and we already know that xy variant can survive the antibiotic that killed all its x brothers. It's a born survivor. You can't use what you used to kill x, to kill xy - at least not at the same dose levels or not for the same treatment length. So you'll need a longer course of antibiotics or at a stronger dose level to kill xy. And don't forget, xy will have its own variants. Somewhere, there will be an xz variant that can survive these bigger doses.

Lets look at the logic again: We know for a fact that E.coli builds up resistance to any antibiotic used against it. It can only do that if some of the bacteria survive the antibiotic attack. If your second episode of cystitis is simply a fresh contamination of the same E.coli that you were previously contaminated with, we are not talking about mutated survivors of the antibiotic, we are talking about the plain old original bug again, so the same dose level of the same antibiotic will work as well as it did before. However, that is not how the course of repeated cystitis attacks works. Typically, infection becomes more and more frequent. Patients go back for more antibiotics. Doctors find that the same dose level doesn't work, so they increase the dose levels, and increase the number treatment days. Or they vary the antibiotic. Gradually, they have to move on to big hitting fluorotoxins like Ciprofloxacin. See Business Week Cipro: Now for the Downside

Thus, increasing resistance could not happen if the cystitis were the result of fresh E.coli contamination of non-resistant bugs through faecal contamination or introduced through a sexual partner, or by any other route. Resistance occurs because of survival of the fittest - survival from a previous contamination.

Logic therefore tells us that resistant E.coli is left in the bladder after treatment with antibiotics. Fact tells us that it's detectable six weeks later in 35% of women. A year later it has recurred in half of all antibiotic treated women.

"Although antibiotics initially sterilize the urine in almost all patients, bacteriuria recurs in approximately one-half by one year." Approach to the Patient with Asymptomatic Bacteriuria, Thomas Fekete, MD,Professor of Medicine and Microbiology, Temple University School of Medicine.

Less detectable, but still present, are E.coli living behind biofilms in the bladder, because they don't show up in urine tests. [Proof!]

Also see: Dynamic interactions between host and pathogen during acute urinary tract infections.

Implications and Avoidance

From the fact that if you are suffering from repeat episodes of cystitis, E.coli are probably living in your bladder, dormant or not, it is apparent that it is more difficult to avoid than it would be if the problem were simply cross-infection, or poor hygiene. And anyway, once you've had an episode or two of cystitis you'll be obsessively clean. What we've found is that there can be a number of triggers that lead to the next episode - a number of triggers that lead to the reactivation of dormant E.coli already in the bladder, or the release of E.coli pods from behind biofilms in the bladder (the biofilms are made of the same stuff as your bladder wall.)

The triggers for dormant E.coli release and causes of fresh contamination also differ, although there is some crossover. Whatever caused that very first infection, it is what makes new or apparently new that is important to sufferers.

Triggers for dormant E.coli release:

• Previous history of infection and antibiotic use. The more recent the use of antibiotics, the greater the probability that an infection is caused by dormant E.coli being released.
• Dehydration (allows high concentration of uric acid. E.coli seems able to sense when conditions are right for multiplication. It thrives in an acid environment, and even releases its own acid.) Beware of drinking too much coffee or alcohol. If you have a dry mouth, you are probably dehydrated.
• Acidic urine through drinking acidifying drinks like orange juice or cranberry. Cranberry tablets have the same effect. (Although they contain a small amount of D-Mannose, this is not enough to stop infections. The acidifying effect just makes E.coli infections worse, although cranberry can be useful for Proteous infections.)
• Sexual intercourse or other stimulation of the bladder, such as by vigorous exercise. This can even trigger long-dormant E.coli pods to begin releasing E.coli into the bladder, for example, even if you have not had sex for ten years, you can get 'honeymoon cystitis' when you next have sex.
• Various spices with properties that allow them to get into the urine and act as an irritant.

Antibiotic dose levels

With dormant E.coli release, taking the same level of antibiotic over the same period as your previous infection is unlikely to clear the problem, and will make the infection more resistant through the process of natural selection. Taking a higher or longer dose of antibiotics is likely to clear the current episode of cystitis, but produce more resistant dormant E.coli, making your next episode even harder to clear.