cipro adverse reactions

How Many Doctors Does it Take to Fix the Shower? A Tale of Fluoroquinolone Injury

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I don’t know much about plumbing, I’ll admit it. I‘m not afraid to use a plunger, or take the lid off the toilet to jiggle the parts on the inside. I am also a master at pouring Drano in a clogged pipe. Usually this level of expertise is enough to solve the majority of my problems. However, when things get complicated, jiggling the handle just won’t do. Luckily there is a person with the technical know-how to fix most everything that my plunging skills won’t. Just one phone call away and I’ve got him. The plumber.

Plumbers can handle all sorts of issues. They arrive, do whatever magic it is that gets everything in running order again, charge a fee, and leave us happily using the facilities.  But imagine this. When the plumber arrives, instead of fixing your shower issue, he (or she) takes a cursory glance. Maybe he quickly turns the faucet on while you try to explain the problem.  He doesn’t really listen, but still pinpoints the issue right away.  “Your problem is the showerhead. You need a new one.” Perhaps you argue that this may be true, but what about the drain?  “Well, I only diagnose showerheads.  You are going to need to call a drain guy to fix your drain.”  Huh?  Well, OK.  At least go ahead and fix the showerhead.  “Oh, I can’t fix that. You need the showerhead guy for that.  I just diagnose showerheads.  I don’t fix them.”

Ridiculous right?  Of course it is.  But this is essentially what happens when we venture into the medical world with any complaint more complicated than the sniffles. Take my experience. In the last 5 months an adverse reaction to a fluoroquinolone antibiotic (Cipro) has caused my husband’s body to go haywire. Going to our family doctor my husband had a myriad of complaints (some that came right after the prescription, some that came later). These included tendon and body pain, nerve pain, tingling and buzzing nerves, insomnia, depression (can’t think why), chemical and food sensitivities, a persistent rash, and other issues which I am not at liberty to share publicly.

My husband’s doctor did what doctors are trained to do. He consulted the checklist.

Primary Physician Checklist:

  1. Throw more drugs at the problem (in this case NSAIDs for inflammation).
  2. Perform tests to eliminate “serious” issues (MS?  Fibromyalgia? Arthritis? No, no, no. Fluoroquinolone/Cipro toxicity?  Yes. This seems serious enough to us, despite our doctor never having heard of such a thing.)
  3. Refer to specialists.

Fluoroquinolone Side Effects Aren’t Impressed by Checklists

The Physician’s Checklist is a three pronged approach that got us exactly nowhere. Which is not at all surprising because the logic behind this all too common approach is deeply flawed. The implicit reasoning is that a patient can be divided into individual body parts and systems, each one with an associated specialist. For the body and tendon pain, a rheumatologist. For the nerve pain, tingling, and buzzing, a neurologist. For the rash, a dermatologist. For the foot pain, a podiatrist. For the crazy B6 and B12 blood test results, a nutritionist. For the depression, a therapist. Although we haven’t been to an endocrinologist, an allergist, or a gastroenterologist, I’m sure we could get an appointment quickly. Referring to specialists is something our primary care physician does very well. It’s the last thing on his checklist after all.

The problem that should be obvious here (besides our doctor’s total ignorance of side effects from fluoroquinolones) is that nowhere in this process has my husband been treated as more than the sum of his parts. None of these doctors talk to each other.  (For good reason perhaps. Would another doctor have patience with a neurological diagnosis of “it’s probably static on the line” with a prescription for “you can try the meds I prescribe to my diabetic patients, or not”?)  Why, for example, is my husband intolerant to foods, supplements, and medications that used to cause him no issue?  Aren’t these symptoms possibly related, both to each other and to other symptoms?  Also, why are the majority of his issues concentrated on the left side of his body? His rash is on his left leg.  His foot pain is in his left foot.  His nerve issues are most pronounced in his left leg and left temple. His left big toenail has a discoloration that is not present on the right toe…  None of our doctors have found this at all remarkable or interesting. Perhaps we would do better if doctors divided themselves by body regions.  We could go see the “leftologist” and have better luck.

This specialization is now the cornerstone of western medicinal practice. And under ideal conditions, it saves lives. For example, if you have a strange spot on your skin, where else would you want to go but to Stanford’s “Pigmented Lesion and Melanoma Clinic”? An entire clinic of the most well renowned doctors in the world, whose sole focus is diagnosing and treating spots like yours. Yes, that is truly great. However, doctors have become so very specific in their field of expertise, that they most often do not have the knowledge, time (or frankly the interest) to look outside of their own domain. (Looked at in a different way, they treat melanoma, not people.)  Humans are intricate creatures. Our health is a complex and elaborate system that is not divisible into discreet elements.  Sometimes a spot is skin cancer. Sometimes it’s a hormonal imbalance.  Sometimes it’s a side effect of medication. When our health becomes complicated, our specialists are rarely equipped to look beyond the bits and pieces and treat an entire person.

Modern general practitioners have become, in many cases, little more than the gatekeepers to these special specialists. When health concerns becomes complex, there is another professional to direct the patient to. This creates a situation in which nobody is truly responsible for treating the whole patient. Had my husband taken the conflicting advice of every specialist he visited he would, with no diagnosis whatsoever, have treated irritated nerves with pain medication, aching tendons with pain medication, injured feet with pain medication, insomnia with sleeping pills, depression with anti-depressants, ulcer-like stomach pains (caused from accepting the pain meds early on) with proton-pump inhibitors.  And the rash?  The treatment recommendation for that was a fluoroquinolone antibiotic. Specifically, Cipro. The same fluoroquinolone drug that started this whole mess.

There is No Such Thing as a Fluoroquinolone Toxicity Specialist

The one tangible outcome from visiting these various specialists is the gravity that it lends to my husband’s situation. The prevailing thought from people seems to be, “Well, it must be very serious if he has seen specialists!”  Close on the heels of this thought is the question of whether we have yet seen the right specialist. We live in Silicon Valley so people’s inevitable question is, “Well, have you been to Stanford?”  I guess Stanford is where people go when they are serious about getting well.  (Not like us, we’re satisfied with misery?)  This question is well meaning. But it clearly shows that people have an ingrained trust in the way our medical system runs (insurance issues not withstanding). If you have not been helped, it must be because you haven’t been to the right specialist yet.  The specialist with the most education. The expert. Surely a Stanford neurologist can cure my husband’s nerves, a Stanford rheumatologist can soothe the body pain, a Stanford podiatrist can fix the feet, a Stanford dermatologist can cure the rash, and a Stanford therapist can make everything cheery again. It’s not the system that’s the problem.  It’s the individuals within the system.

This isn’t logical and I no longer believe it. I don’t accept that our two options are that groups of specialists looking at small parts of the whole can fix each of those parts independent of one another, and if not, we’re hopeless. Surely our multitude of doctors can aspire to do better than this, but it seems not. Ultimately we were helped by one visit to a specialist.  It was the nutritionist who finally was at all useful.  She essentially said, “I don’t know how to help you. You need to see a naturopathic doctor, and research alternative medicine.”  This is ultimately what we have decided to do.  We will have to go outside the mainstream to find a health professional that sees patients as whole humans. We refuse to be treated any longer as a mismatch of thrust together parts. The plumber could do better.

We Need Your Help

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter. 

Image credit: Mike Bitzenhofer, via Flicker; CC 2.0;  https://creativecommons.org/licenses/by-nc-nd/2.0/

This article was published previously on Hormones Matter in December 2013.

Glabrata – A Deadly Post Fluoroquinolone Risk You’ve Never Heard About

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I would like to share information on a little known, rare infection that all too often is overlooked or misdiagnosed, by the medical profession. It is an infection that shows no mercy to its victims and is deadly  in 67 to 90% of the cases, depending upon the severity of the infection. It is called Candida Glabrata (C.Glabrata), and I, like thousands of other victims, have had to learn the harsh realities of what this infection is capable of. I have also learned that it is an infection that our medical profession knows little about and our scientific community knows even less about how to beat it. In 2007, it was listed as the fourth leading cause of bloodstream infection in United States hospitals. The fact that the medical professionals know so little about how one contracts C. Glabrata, who gets it and when to look for it, persuaded me to speak out about this, so others do not suffer as I am.

What is C. Glabrata?

First C. Glabrata is a fungus from the Candidias family, which is the same family of candidias albican  (the yeast infection that most people are familiar with), however, there are several other forms in the Candidias family. These other forms are actually known as non-albicans and they are much more serious types of fungi. There are approximately five different species in this category with Glabrata being the most serious form.

What makes Glabrata so serious is the fact that it is only one of a few fungi that do not have hyphae, which are like the tenticles. Without hyphae, it is very difficult to culture, biopsy or see under a microscope. Due to the fact that it cannot be easily diagnosed, it is usually is not discovered in a person until they are very sick and by then it is a race against time to save the individual. The other problem with fungi without hyphae is that they are able to morph and adapt for survival. This means they have the ability to live in both alkaline and acidic environments. This is the part that makes them so deadly, because we only know how to kill fungus by changing the PH balance of the environment to basically make the living conditions unconducive to their life cycle. So, when you have a fungus like C. Glabrata that cannot be easily detected, diagnosed and then treated, you have what is known by the CDC as a deadly fungal infection.

The History of Glabrata

The fortunate thing about Glabrata is that it is a very rare form of fungus that is almost never seen in the general population. It was discovered during the 80’s when the AIDs population came to awareness. Prior to that, it had never been found in humans. Once the HIV population became infected, the fungi were impregnated in hospitals all over the country. Through the 90’s, the only people identified with this infection were the critically ill and immune compromised population, end stage HIV or end stage cancer patients in ICU units. With compromised immune systems these patients had no resistance to the fungus, and unfortunately, the mortality rate was 100%.

By the early 2000’s a new population of people were beginning to show up with C. Glabrata, only now it had moved beyond the immune comprised HIV and end-stage cancer patients. A study in 2010, found that 73% of C. Glabrata cases occurred in patients previously given fluoroquinolones. This new, previously healthy group of people falling ill to Glabrata had all been treated with a broad spectrum fluoroquinolone antibiotic often in conjunction with a steroid. Steroid treatment alone is a risk factor for the C. Glabrata infection. According to my current physicians, when fluoroquinolones are combined with steroids, the risk for contracting C. Glabrata increases significantly.

Research shows that the fluoroquinolones wipe out all gut flora (good and bad). When combined with immunosuppressive steroids, the patient’s ability to fight bad bacteria and fungus is compromised. When all the gut flora are killed, the first flora to grow back are those that are the strongest and most resilient. Much like weeds in your garden, fungus and bad bacteria grow at a faster rate and are stronger mutants than the good bacteria. If the patient was also prescribed steroids, their own immune system can no longer come in to fight off the bad gut flora. This leaves the gut vulnerable to serious infections especially fungal ones like Glabrata. Fluoroquinolones are one of the most potent gut flora destroyers on the market. There is no other class of antibiotics that so totally annihilate gut flora to the level that the fluoroquinolones do. Combining fluoroquinolones with steroids is a recipe for disaster.

In sum, there are only four ways to develop a C. Glabrata infection, end stage HIV, end stage cancer, patients with neutropenia – a genetic or chemo-induced condition that limits white blood cells needed to protect the body from fungal invasion – or by using a broad spectrum antibiotic, like the fluoroquinolones combined with a steroid.

Diagnosing Glabrata – Why So Many Victims of Glabrata Die

Glabrata is very difficult to diagnose, leaving the infection to take hold before it is recognized. The Glabrata fungus does not have hyphae and does not present like all other forms of candidias. This fungus does not produce a white cheesy like curd discharge from the gut / stool, vagina or penis. Instead, it produces a milky white to grayish thin discharge, often seen with bacterial infections. It also produces minor to severe swelling of the tissues and erythema (redness). The infection causes horrific burning (often described as grinding glass into the tissues and then pouring acid on them) with very little itching.

In the early stages, before a doctor thinks to look for C. Glabrata, the infection is frequently misdiagnosed as a bacterial infection. The patient is put on antibiotics; often the same antibiotics that created the susceptibility to the infection to begin with. When these fail again and again, the doctors are often at a loss as to what is going on, especially if the person was a young, healthy individual prior to being given antibiotics with steroids. Since most physicians have been trained to only look for Glabrata with HIV or seriously ill cancer patients, they never think to look for it. It usually takes until the person becomes critically ill with the infection before they realize that it is a fungal infection, at which point the doctor will order specific tests looking for a non albican fungus. In more than half of all cases of Glabrata it is not realized until autopsy. These are not like other fungal tests because they have to be grown in special agar (petry dishes) and then stained with special stains and then looked at under high powered microscopes. The final drawback is that this fungus needs 6 to 8 weeks to grow out, which costs precious time that most patients do not have.

Treating Glabrata

Once Glabrata is diagnosed the next hurdle is how to treat. Currently, there are only a few drugs that have any potential to kill it: Diflucan (fluconazole), Caspofungen and Amphotericin B. Each is problematic. Diflucan has to be used at ten times the normal level for months on end, to kill C. Glabrata. Most people are unable to tolerate this course of treatment and in 99% of cases it fails and in many cases, the fluconazole induces resistance to it and other azole fungicidesCaspofungen or microfungen, are additional options. They can cause serious liver and kidney problems, leading to failure of one or both organs. These drugs work in about 70% of all cases, but again must be used for months on end and many patients are unable to tolerate the treatment.

The last drug known to kill C. Glabrata is Amphotericin B. This drug is only used when the person is on their death bed because it is so toxic that it causes acidosis within minutes of being administered. Over 90% of patients go into multi-organ failure and die within three hours of infusion (discussions with my doctors). This drug too must be used for months on end to kill it.  Amphotericin B has a 90% success rate if the patient can survive the drug itself.

In very serious and resistant cases, Flucytosine is combined with the Amphotericin B. Flucytosine is thought to open the cell walls and lets the Amphotericin B in to kill. Flucytosine is an old chemo drug that is quite potent drug. When combined Amphotericin B, the results can be deadly. These are the only drugs known to treat this fungus.

Glabrata Becomes Resistant

As if Glabrata isn’t difficult enough to diagnose and treat, the fungus is very adaptive. If the patient survives the drugs, the fungus can, and often does, become resistant to the drug that it is being treated with, leaving the person with no options to kill it. This means that you get ONE shot with a medicine because it will become resistant the second time around. Glabrata has to be killed totally. If not and it returns, there is no treatment.

But as a fungus, Glabrata does not die on contact with the medicine. Let me explain this in an easier way. Look at it like this a bacteria is like a spider or bug, when you spray it with Raid it stops dead in its tracks and dies right there where you sprayed it. With fungus it is like a weed in your yard, when you spray it with weed killer the first day it begins to droop the next day it turns brown and by the third day it falls to the ground. If you then then pull the weed up and if you did not get the roots too within a week you will have a new weed back again. Fungi work in the same way, which is why it must be treated for months on end. Fungal infections are notoriously hard to treat and some of the most deadly infections to have. This is why Glabrata is fatal in 90% of all cases.

I Have a Glabrata Infection

I have a Glabrata infection and am fighting for my life. How did I contract this deadly fungal infection? I was prescribed Cipro plus a steroid for a misdiagnosed and assumed GI infection. I had a stomach bug, likely the flu, but since I have a diagnosis of IBS and the doctor was unable to see me for four days, she suspected I had a small intestine bacterial overgrowth (SIBO). I was prescribed an antibiotic, Cipro, plus steroids. That is, I was prescribed these meds on the assumption that I had a bacterial infection. I did not.

Three days after starting Cipro, I fell ill to Cipro toxicity. My gut flora were wiped out, I just didn’t know it yet and neither did my doctors. A week later, I found out that I never had an infection and didn’t need Cipro to begin with, but it was already too late for me. In the coming months, the GI bleeds began and other GI issues that would be misdiagnosed as Crohn’s Disease and bacterial infections ensued. It was not until last month that my doctors determined that all my problems were due to a deep seeded or disseminated infection with Glabrata.

We tried the Diflucan, which failed miserably. My WBC count and neutraphil count rose and I was now in serious trouble. We put a central line in and started the microfungen. After the first seven days, my counts dropped drastically, but by day nine, I began to step backwards. The fungus was morphing to survive and was becoming resistant to the drug. We are now looking at Amphotericin B. We will give it two more weeks and then make that call but it is not looking good right now. My symptoms have begun to ramp up again. I know the odds are against me with less than a 10% cure rate, I am fighting an uphill battle but I need to win this one for my life!

Why I Am Telling My Story

Patients must understand the dangers of this class of drugs especially when combined with steroids, because many doctors do not! Fluoroquinolones are the most commonly prescribed antibiotic in the US and combining them with steroids seems to happen frequently.

Also know that 78% of the time Glabrata starts in the gut. Other times it starts in PIC and central lines. In either case, one initiated, it infiltrates the prostrate for men and the vagina for women. It has been known to seed itself any organ throughout the body. If you are suffering with an infection in any of these areas that does not respond to antibiotics and you are also suffering with GI issues, you need to ask your doctor about checking you for a fungal infection, especially if you have used a fluoroquinolone antibiotic with a steroid prior to the onset.

We Need Your Help

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter. 

 

Featured image: GMS stained skin punch biopsy demonstrating fungal spores of C. glabrata, eScholarship, University of California.

This story was published originally in December 2013.