My father might have gotten “floxed” but I have no way to know for sure.
At age ≈94, still reasonably sound of mind (and even of body, for his age), he got sepsis or some similarly nasty disease. He was in a rehab place for several weeks, getting continuous IV in his arm, but I was never able to find out just what was going in there. His wife said he was getting a pain-killer and an antibiotic.
During his time in the rehab, he became disoriented, delirious, and was having hallucinations. Also, his speech became progressively more slurred and limited, until he didn’t even speak in sentences but only in occasional brief phrases, so slurred it was hard to understand what he said.
His wife claimed it was the antibiotics that were doing this to him. She never explained why she thought it was the antibiotics and not the pain drugs. (I would have thought the pain drugs were probably opioids that would have him all spaced out, but only temporarily.) His wife also insisted that she knew what those drugs were, but every time I asked, she didn’t know.
Anyway, he recovered from the infection after a few weeks and went home. However, he never recovered his mind. He lived another year and a half, during which time his wife had to tend to him extensively. His speech remained slurred and very limited; he needed help to move from one part of the apartment to another; help toileting; needed to be spoon-fed; etc.
I would very much like to know what drugs he was given. I would like to know if any staff, or his doctor, even observed his deteriorating mental condition and thought it noteworthy enough to make a note in his record. I wonder if they were giving him Cipro. I wonder what might have caused his rather sudden and significant mental decline in such a short time, while he was there.
Fluoroquinolone antibiotics are thought to be GABA-A receptor inverse partial agonists (see this paper), which would account for symptoms of insomnia, anxiety, and psychosis seen in some patients who take this class of medications, since blocking GABA function generally results in increased excitatory neurotransmission. In susceptible individuals, such as those who display a great deal of GABA-tolerance from chronic use of ethanol or benzodiazepines, this effect could be magnified further, as could concomitant use with certain NSAID medications. This paper ranks ofloxacin the lowest in blocking GABA mediated Cl- potentials, however. Given that GABA-A receptors are pentameric ion channels with varying composition (in varying parts of the brain to a degree), it’s hard to draw firm conclusions as that study didn’t identify the receptor subtype, which is thought to be important. Alternatively, use of at least certain fluoroquinolones at the same time as theophylline or caffeine can dramatically increase exposure to those agents, which serve to block inhibitory adenosine receptors in the brain.
It honestly wouldn’t surprise me, since dextroamphetamine is thought to be much more potent centrally than levoamphetamine is, as is escitalopram (which is dextrorotatory) vs it’s levorotatory enantiomer. It’s probably an oversimplification, but it could be that dextro-rotatory compounds may function as better channel blockers (dextroofloxacin for GABA-A, dextroamphetamine for DAT/NAT, es(dextro)citalopram for SERT), or it could be random coincidence.
As for Bactrim, Clinical Neurotoxicology, speculates that due to it’s inhibition of dihydrofolate reductase, the trimethoprim component could result in a deficit of tetrahydrobiopterin, though the sulfamethoxazole could play a role as well as it inhibits dihydropteroate synthetase earlier in the folate pathway, which is necessary for the first step in the biochemical pathway between tyrosine and dopamine. While it binds with greater affinity to bacterial enzymes, vs the human versions, high enough doses could produce enough of an effect in pre-disposed individuals to reduce neurotransmitter synthesis. If so, folate supplementation may actually help in that regard.
Does this imply that, if I use a lot of Ibuprofen (which I do), and if furthermore I have a background of benzo addiction and dependency (which I do), then I’m at elevated risk for having adverse reactions to fluoroquinolones?
And some of those adverse reactions, according to the horror stories, are severe to the point to debilitating, and irreversible. What is the mechanism by which permanent neurological damage is done? There are also stories of long-term peripheral neuropathies as well; it’s not only CNS damage.
I’ve already advised my doctor that I don’t consent to the use of any fluoroquinolones, and he noted it in my chart, which probably won’t be noticed if I’m ever in the hospital or ER and treated by any other doctors. Anyway, with your explanation, do I now actually have some good reason to think that I should really avoid these neurotoxic drugs?
We don’t have enough data to say definitively. The NSAID-Quinolone interaction shows up in Facts and Comparisons as well as Lexi-comp, but in both cases the recommendation is to monitor therapy. The data is somewhat conflicting, and it suggests that, at least in humans, it may just be that NSAIDs are increasing Cmax, AUC, and decreasing Tmax for the quinolones by reducing clearance of the drug. Other factors which would pre-dispose are renal insufficiency, a history of seizure or other neurological disorder, and high doses of either agent.
In regard to your history with benzodiazepines, we don’t know. Despite decades of use, we’re still not exactly sure why some individuals end up with a chronic withdrawal syndrome, while others don’t. There doesn’t appear to be any overt neurological damage in those suffering from chronic withdrawal, but it is possible that we just don’t have the ability to resolve to the level necessary to see it (in a living human, at least) if it is there.
Some of the horror stories are indeed scary, but remember, much like how the news media can skew the perception of a reported phenomenon to make it look worse than it actually is, so too can horror stories about medical problems, because they often fail to report pertinent details necessary to make an informed judgement.
Assuming permanent neurological damage occurs following long-term and/or high-dose use of benzodiazepines (which is still not conclusively determined), over-active excitatory nerve transmission has a tendency of throwing neuronal calcium homeostasis out of whack and generating free radicals, both of which can induce damage to, and if severe or rapidly-developing enough to overcome neuroprotective factors, apoptosis of, the nerve cell. This would apply whether we are talking CNS or PNS (or, I suspect, the often forgotten, but oh so important, ENS, for that matter).
Honestly, I wish I could give you a yes or no answer. I don’t see a problem with you not wanting to receive quinolones as an antibiotic of first choice, if other options are feasible/available, but at the same time, all drugs have the potential to be dangerous, and if a quinolone was necessary to save your life, I wouldn’t want you to refuse it altogether based on what little we know so far. It is one tiny piece of the puzzle you can discuss with your healthcare team to better provide care specifically for your circumstances, but it’s not the only piece. While it sounds like your regular doctor is fine with not putting you on these medications, you have to remember, that in a situation like a visit to the emergency room, you (or your medical power of attorney) have to be an advocate for yourself. If you feel that strongly, you have to make your beliefs known. Ideally, the practitioner in question will listen to your concerns and find a reasonable alternative, if one exists.
Just popping into this thread to mention to the women who had antibiotics for UTIs: a type of sugar called D-mannose has kept me off the antibiotics for over a year now. I’m not sure how it works, but an explanation I read likened it to working like velcro in the bladder. The shape of the D-mannose sugar molecules bind to the bacteria floating in the bladder. When you pee, the bacteria adhered to the sugar molecules get flushed out too. It is relatively cheap at approximately $12USD for a month’s supply.
I was having UTIs at least monthly and suffered through repeat courses of antibiotics and doctor bills, not to mention excruciating pain and the odd kidney infection. A daily dose of D-mannose has brought that down to one course of antibiotics in the last year. Which coincided with an episode of vigorous sex, dehydration and a missed dose, so I was really pushing my luck.
I am feeling so evangelical about D-mannose (and forever thwarting the special hell that is a UTI) that I may need to start a thread on it one day. It is one of the few ‘dietary supplements’ I have ever found to work as advertised.
I’m so glad to find this thread. I kept thinking it was just me and my messed up central nervous system that caused this reaction.
I will say, though, that acidophilus did really help the nausea part. You take it a couple hours before each dose, and then again a couple hours afterwards. Ginger was also useful.
With that, all I was left with was the nervous energy, which, once I channeled it into doing something, wasn’t so bad. So that’s my tip for you guys.
Also, my mom is going through all this stuff right now. I’m still trying to get her to at least try my recommendations, but she’s too nervous to do anything extra.
Decades ago when I was teen I was one of the rare-ish cases of a guy getting a urinary tract infection. I was given a drug that I remember as “sulfa”, which I suppose is at least similar if not the same thing as the sulfamethoxazole in the OP.
My reaction was to be highly allergic to it. My face puffed out and I looked like a white Apollo Creed in the 15th round, and the inside of my teeth itched. Benadryl cleared that up, thankfully.
Sulfa or “sulfa drug” is often a way to refer to Bactrim, yes. Mom calls it that, too. As did my sister’s doctor. (She’s one of those who became intolerant to it.)
I was prescribed Avelox once. I don’t remember exactly what happened, but I honestly feared for my life and thought I might be having heart problems. Went to the ER and everything. I now list that as a medication I’m allergic to.
I’ve taken Levaquin, Cipro, and Bactrim on more than one occasion (not at the same time) and haven’t had any adverse reactions. Beyond the normal GI/Yeast issues that can arise from taking antibiotics in general.
I find it works great (when I remember to take it). I recommended it to a friend of mine that would get a UTI every time she saw her boyfriend. She hasn’t had one since she started taking it. It is 99% flavourless. I do detect a very (VERY) slight sweetness to the water I’ve mixed it in, but that’s it. Highly recommend.
The first statin drug I was on made me ache horribly and gave me terrible constipation. So we tried a different one that, in the mix with my antidepressant (trazodone) made me so dizzy I couldn’t walk down the hall or turn my head quickly. So, we tried me on a third one (Zocor) which didn’t have the dizzy effect but landed me in urgent care with horrible constipation (and only minor muscle aches). Interestingly, the UC doc was disgusted with me because he was sure I wasn’t eating fiber because it couldn’t be anything else. With my own doc’s approval, I lowered the dose. But without her permission, I quit taking the stuff. I feel a lot better now.
The UTI went away, but a few days ago, I realized I was coming down with a sinus infection, so I started taking it again. Interestingly, I didn’t have the depressed, achy feeling I had before, but a couple days ago, I did notice an irritated area on my upper thigh, right next to my vulvar area. I thought it was the seam on a pair of pants irritating the area, so I put them in the laundry. Yesterday, the irritated area (which also happened when I took it before) came back, and overnight, it spread a bit. I now have a red, slightly itchy circle about 6 inches in diameter; I took some Benadryl and used some leftover Triamcinolone lotion (it’s a steroid I used for scalp exzema) on it. Otherwise, I feel OK so I probably won’t go to the walk-in clinic down the road like I thought about doing.
I’ve seen your abscess saga. I shouldn’t have self-treated; I should know better than to do that. Right now, I feel dopey from the Benadryl (I did go back to bed) and a bit itchy, but I’m OK.
I started taking 800-160 mg of bactrim (which was prescribed by a PA at a walk-in clinic) due to swelling around my eye from a large zit on my forehead. Took one in the evening, woke up next morning with my throat feeling very tight, slight difficulty breathing and the worst headache I have ever had in my life. Went to work and eventually went home early because I felt like I had the flu as my body & head felt horrible…felt dizzy and like I was going throw up. I continued to take dosages into the next day but also drank a lot more water…it didn’t help. The original side effects actually went away but then my throat become extremely sore and very hard to swallow food, later that next day I then found it almost impossible to urinate from extreme pain down there. Called my doctor the next day and was told to stop immediately, and consider myself allergic to bactrim…um, ok. Two days later, the pain in urinating is getting a little better but now my mouth has several open sores. I am wondering what will happen next as it has been 48 hours since I took my last dosage. Horrific drug, for me at least.
This is certainly a cautionary tale. I have never been given Bactrim, but now I am pretty sure I would ask for an alternative, if offered.
The antibiotics I have been given over the years have caused mild nausea, dry mouth, and oddly enough, excessive perspiration. All annoying, but definitely not frightening.
Three year old thread, but I’ll chime in and say that after being prescribed Bactrim earlier this year, I broke out in the dreaded rash on my scalp and feet. I now warn doctors off of giving it to me.
