Delayed reactions to Fluoroquinolones (FQs) are complex to say the least.  However if we look at how drugs damage the mitochondria we can get a good idea how this process works, especially antibiotics.

In the book “Drug Induced Mitochondrial Dysfunction”(2008 Wiley) they discuss antibiotic mitochondrial toxicity. In the book it states that mitochondrial protein synthesis is more closely related to bacterial endosymbiont than cytoplasmic protein synthesis. “As a result, antibiotics that bind to the bacterial ribosome and target bacterial protein synthesis may also bind to the mitochondrial ribosome and inhibit mitochondrial protein synthesis.”

It is important to note that “toxicity caused by inhibition of mitochondrial protein synthesis is not immediately observed. Mitochondria turn over slowly in many tissues. Depending on the degree of inhibition, time is required for the amount of mitochondrial machinery and the ability to synthesize ATP fall below a pathogenic threshold value.” (DIMD; page 465) This delayed reaction can make connecting the adverse symptoms to an environmental exposure (like a medication or chemical) very difficult as it happens slowly, over time, as mitochondrial function falls below a critical threshold and the individual then becomes symptomatic.

In a nutshell, certain antibiotics such as fluoroquinolones, damage the mitochondria. Because mitochondria turn over slowly in many tissues it takes some time for the damages to become evident.  It is only after they reach a critical point (the ability to synthesize ATP fall below a pathogenic threshold), does the damage become evident.

The amount speed, severity, and location of the damage in the body depends on many factors, such as how much initial toxicity was present, health of the person at the time of the initial onslaught, and their genetic makeup, to name a few.