glabrata

Fluoroquinolone Antibiotics and Systemic Fungal Infections – A Real Problem

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Assignment – write about how fluoroquinolone (Cipro/Ciprofloxacin, Levaquin/Levofloxacin, Avelox/Moxifloxacin and Floxin/Ofloxacin) use can cause deadly systemic fungal infections.

It has been a difficult assignment for me to complete because I have read so much about the havoc that fluoroquinolones wreak on cells – they deplete mtDNA, cause chromosomal abnormalities, disrupt the balance of minerals within cells, cause oxidative stress, etc. All of these effects of fluoroquinolones cause harm to those who take them. So, it has been difficult for me to shift modes, from thinking that the damage mechanism for fluoroquinolones is cellular damage, to noting that damage can be done by systemic fungal infections that take root after the fluoroquinolones have killed all of the good bacteria in the gut. It’s not an either/or situation though. Fluoroquinolones can cause cellular damage AND they can kill all of the good bacteria in the gut, leaving the person who takes the fluoroquinolone susceptible to systemic fungal infections. Fungal infections are one of the many chronically harmful effects of fluoroquinolone antibiotics.

All broad-spectrum antibiotics can cause fungal infections. The “use of antimicrobials is the main reason for the loss of the normal flora and its replacement by potentially pathogenic microorganisms, such as gram-negative aerobic bacilli and Candida species.” This is another reason that I am struggling with this post.  I have written multiple posts going over how fluoroquinolones are categorically different from all the other antibiotics. (They are more similar to chemotherapy drugs than they are to penicillin.) None of the other classes of antibiotics cause a chronic syndrome that includes destruction of all connective tissue throughout the body – including tendons, muscles, cartilage, etc. None of the other classes of antibiotics damage all the nervous systems – including the central, peripheral and autonomic nervous systems. Fluoroquinolones do.

Again, it’s not an either/or situation though. It is possible that some of the symptoms of fluoroquinolone toxicity stem from systemic fungal infections, while others stem from cellular damage. Symptoms like fatigue, brain-fog, food intolerances, etc. that occur both with fluoroquinolone toxicity and candida-related complex may be the result of fungal infections in those who are suffering from fluoroquinolone toxicity or they may be a result of mitochondrial damage, or both. Fluoroquinolone toxicity and candida-related complex are not mutually exclusive diseases. In fact, there may be a huge amount of overlap between the two. It was noted in an article entitled Levofloxacin and Moxifloxacin Increase Human Gut Colonization by Candida Species that fluoroquinolones, “significantly increase the concentration of Candida species in the human gut.  Hence, these agents should be used with caution in patients at risk for systemic fungal infections.” Patients at risk for systemic fungal infections include those who are immunocompromised, on corticosteroid drugs and other risk factors. In addition to causing cellular damage, fluoroquinolones also open the door for colonization of candida in the gut of those who take them.

Perhaps I shouldn’t downplay the severity of fungal infections. It is not “just” a fungal infection, just like an adverse reaction to a fluoroquinolone is not “just” a side-effect – both are chronic syndromes. They are not a light matter. If a systemic fungal infection takes hold, it can be deadly – and often is.  Debra Anderson noted in her post “Glabrata – A Deadly Post Fluoroquinolone Risk You’ve Never Heard Of” that 67-90% of diagnosed blood borne glabrata cases are fatal. Debra’s glabrata infection was brought on by a combination of steroids and fluoroquinolone antibiotics. The steroids weakened her immune system, the fluoroquinolones killed all of the good bacteria in her gut that were keeping the candida at bay, and the glabrata (a kind of candida) took over. She is fighting a tough battle. It’s a battle for her life and it is nothing to trivialize. Debra is one of two “floxie” friends of mine who are battling glabrata. The other friend has recently received a diagnosis of terminal from her doctor, she has entered hospice care and she does not expect to last much longer.

Systemic candida has been trivialized by many though – “Conventional medical practitioners do not recognize candida-related complex as a disease.” Candida causes symptoms like  chronic congestion, sugar cravings, food intolerances, difficulty thinking / brain fog, skin rashes, reoccurring yeast and urinary tract infections, etc. There is a tendency to dismiss these symptoms as insignificant because they are difficult to measure and quantify, they are based on patient reports, and it is easy to think of them as things that everyone experiences. Who doesn’t have sugar cravings and brain fog? The fact that popular diets abound diminishing candida exist, and thus self-diagnosis is common, don’t help to encourage traditional medical practitioners to recognize the symptoms of candida-related complex. However, there are thousands of peer-reviewed journal articles noting the very real problems of candida infections. Systemic, chronic candida infections are real – and serious.

Systemic fungal infections are also serious because they are difficult to treat.  Fungi adapt quickly to anti-fungal drugs, and develop resistance to them. Candida form biofilms. Biofilms “consist of matrix-enclosed microcolonies of yeasts and hyphae, arranged in a bilayer structure. The biofilms are resistant to a range of antifungal agents currently in clinical use, including amphotericin B and fluconazole, and there appear to be multiple resistance mechanisms.”* Additionally, antifungal drugs can be dangerous in themselves. Many antifungal drugs cause kidney and liver failure, which can lead to death.

Per the article Antifungal Resistance and New Strategies to Control Fungal Infections, “At the beginning of the 20th century, bacterial epidemics were a global and important cause of mortality. In contrast, fungal infections were almost not taken into account. Since the late 1960s when antibiotic therapies were developed, a drastic rise in fungal infections was observed, and they currently represent a global health threat.” The global health threat of fungal infections is serious, and not something to trivialize. Fungal infections can be deadly, and the treatment options for getting rid of them are limited.

The causal link between antibiotics and fungal infections should be thoroughly considered by both doctors and patients before unnecessarily strong antibiotics are prescribed or administered, especially before they are prescribed in conjunction with corticosteroid drugs. It should be noted that, “use of antibiotics and immunosuppressive drugs such as corticosteroids are major factors contributing to higher frequency of fungal infections. Antibiotics and immunosuppressive drugs, by disrupting normal bacterial colonization and suppressing the immune system, create an environment within the body in which fungi can thrive.” Whether fungal infections manifest themselves in ways that are not life-threatening but do inhibit a person’s quality of life – like developing food intolerances or brain fog – or whether they become systemic and life-threatening – like bloodstream glabrata infections – they are real and should be taken seriously.

Antibiotic use has consequences. The rise in fungal infections is one of the consequences of antibiotic use.  As very strong antibiotics that also damage mammalian cells, fluoroquinolones have even more consequences than other kinds of antibiotics. Sorting out which symptoms of fluoroquinolone toxicity are a result of cellular damage and which symptoms are a result of fungal infections is not something that has yet occurred or been written up in scientific literature.  Both cellular damage and fungal infections should be taken seriously though –they are not trivial and they can be deadly.

The glabrata form of candida is particularly difficult to diagnose and treat because the fungi don’t have hyphae.  More information can be found in Debra Anderson’s article, “Without hyphae, it is very difficult to culture, biopsy or see glabrata 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.”

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Information about Fluoroquinolone Toxicity

Information about the author, and adverse reactions to fluoroquinolone antibiotics (Cipro/ciprofloxacin, Levaquin/levofloxacin, Avelox/moxifloxacin and Floxin/ofloxacin) can be found on Lisa Bloomquist’s site, www.floxiehope.com.

BCarver1 at en.wikipedia, Public domain, via Wikimedia Commons

This article was published originally on February 6, 2014. 

From Fluoroquinolone Reaction to Glabrata Infection, and Now, Lyme Disease: A Medical Nightmare

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This post is meant to inform and educate all my friends but, more specifically, the Floxies (individuals who suffer from reactions to fluoroquinolone antibiotics) about my recent health issues. This post will explain what is happening to me, but also, hopefully make others aware of this new illness and its relationship with fluoroquinolone reactions.

Recall that over the last several years I have suffered a number of conditions, exacerbated and/or induced by a reaction to fluoroquinolone antibiotics. In addition to the fluoroquinolone reactions that I experienced, last year I battled a deadly fungal infection called glabrata. Glabrata infections have become increasingly common with the use fluoroquinolones and other bactericidal antibiotics. Though I survived, I am now battling another infection; one that was likely present all along and misdiagnosed.

Lyme Disease

I recently found out that I do not have Crohn’s disease, spondyloarapathy or ME as previously suspected. A tick bite to my head left me with encephalitis (swelling of the brain) and meningitis (swelling of the spine). The symptoms emerged one week after the tick bite. I was hospitalized with amnesia, hallucinations (both visual and auditory), unable to put two thoughts together to make a sentence, and had to search for words to try and tell someone what I wanted. My speech also took on a stutter that to this day can be activated by fatigue or emotions.

I had and continue to have seizures that do not respond to usual drug treatments. The seizures would leave me for hours not knowing who I was or even able to recognize my own family. I would be treated with high doses of IV steroids in an attempt to bring the swelling down. It temporarily worked, but it was a double-edged sword because, as it was bringing down the swelling, it was also unleashing a slew of infections throughout my body.

Shortly after this event, I was diagnosed with Borrelia, Bartonella, Ehrlichia, mycoplasma, chlamydia pneumonia and Babesia. For those not familiar with tick borne infections let me let you know that Borrelia is Lyme disease and Bartonella, Ehrlichia, mycoplasma and chlamydia pneumonia are just a couple of the over thirty co-infections that the tick bacteria carry. Babesia, which is the worst of them all, is a Protozoa parasite from the family of malaria. Yes, that’s right, it’s a form of malaria!

Unfortunately, I would quickly learn that a tick bite I had four years ago and that gave me the typical bullseye rash, seen in up to 70% of cases, was my first exposure to several of these infections. Why is this so important? Well, if you do not treat these infections within the first six weeks they become chronic; meaning there is no way to eradicate them from the human body. Unfortunately, the medical profession is quite ignorant about these diseases and many do not even follow the CDC guidelines. My doctor four years ago, saw the rash. I told him about the tick bite and instead, of starting treatment immediately, he decided to test me for the illness first. As many know, the CDC testing for these illnesses is extremely unreliable with very high false negative rate. My tests came back negative, and so, I was not treated. At the time, I didn’t know about the pitfalls with these diseases or that a bullseye rash was a positive all by itself.

Within months of the first bite, I would start to have all kinds of weird things happen to me from ME symptoms, to spondyloarapathy symptoms, to dysautonomia, to MCAD to trigeminal neuralgia, to vasculitis, to Crohn’s like symptoms. As time went on, the problems would only mount, as infections slowly spread from one system to another, causing inflammation, destruction, pain and weird events that even my doctors were confounded by. I lived each day in terrible pain and spent weeks upon weeks in the hospital fighting one serious problem after the next. If I had not lived through it myself, I would not have believed that one person could suffer with so many symptoms throughout their body.

Lyme Disease and Fluoroquinolone Reactions

So, let me quickly step back here for a minute, shortly after the first tick bite, I was given Cipro for a suspected small intestine infection. It was three days into the Cipro treatments that I began experiencing fluoroquinolone toxicity. Since tick infections are neurotoxic too, it is difficult to determine whether my symptoms were tick-related, fluoroquinolone-related or both.

Apparently, when the bacteria from the tick dies, it releases a neurotoxic substance into the bloodstream causing severe toxic body-wide damage. This is known as herxing. Unfortunately, herxing and fluoroquinolone toxicity look exactly alike, so it is hard to say if I was herxing or floxed or even both. Making matters more difficult, many people with Bartonella are treated with the fluoroquinolones and they then go on to get floxed as well.

It is also important to know that the symptoms of Lyme disease and many of its co-infections look and act exactly like fluoroquinolone toxicity. This is because both cause mitochondrial, connective tissue, multi-organ symptoms. So these two illnesses act as one and the same and both are deadly in time. This is why this post is more for the Floxies. However, please know that ticks carrying these infections are located in every state, city, suburb and community throughout the world.

Ticks come in several sizes from the nymph that is no bigger than a period (.) to the size of a small raisin. They live in Chicago, Phoenix, and every other state and city throughout this country. No ONE is safe from them no matter where you live and over 60% of people will never even know they were bitten by a tick because they will not find it in the seven days that it is latched on. Just imagine something as small as a period attaching itself behind your ear, in your hair, in your groin or between your toes. You would never find it! And only 50% of folks with Lyme disease recall having a rash, so many may never know until they start getting sick. For those like me that do get tested, your chances of the test being positive or accurate is very low.

Lyme Disease Stats

This illness has become this century’s greatest plague as the numbers of people infected continue to grow by unbelievable rates. The CDC estimates 300,000 people are infected a year, but the ILADS which keeps better logs estimates the number to be closer to one million a year.

The death rate is in the thousands to hundreds of thousands a year. And those numbers do not reflect those who die from Alzheimer’s, ALS, MS, Parkinson’s, and several other diseases that are now being looked at by Harvard and Duke Universities as being symptomatic diseases of Lyme.

Lyme Disease and Neurodegenerative Disease

It has long been speculated that Lyme mimicked neurodegenerative disease processes, along with over 310 other diseases, but recent studies done on the brains of those deceased by these illnesses has shown a stunning revelation. Autopsy studies have found that a very large percentage (sometimes 100% ) of ALS, Parkinson’s and Alzheimer’s  have borrelia in the brain. (These finding were discussed in the movie: Under our Skin. Other good videos to watch on the topic include those by Dr. Richard Horowitz ). Because of these findings, many individual studies have since been done on these groups, by treating Alzheimer’s, MS and ALS patients for Lyme and co-infections. The studies were mind blowing. All groups responded immediately to the drugs, better than they did to any of the standard treatment drugs used to treat those conditions.

Unfortunately, they will never be cured because there is no medicine available today that is able to eradicate these infections from the body. Nevertheless, the progression of their diseases and their symptoms were reduced and that potentially bought them years more with better quality of life. This has been such an amazing discovery that Duke University just built and opened the first building totally dedicated to studying these infections, with the hopes of finding better testing, vaccines, and effective treatments. Seriously though, we are decades away from answers. So for now, those who are not infected must take all precautions with their animals and children, even in your own backyard. Those that are infected must get early diagnosis and better treatment. This means our government MUST look at all the studies and stop following the bought for IDSA guidelines, so that we can educate our doctors everywhere on how to spot it and how to treat tick born infections.

Calls for More Lyme Disease Research

Recently, there were marches across the country that very few news media chose to cover. There were big time athletes, actors, and rock stars that have had their lives nearly wiped out by this illness. Several are still fighting for their own lives, but are also taking up fight for this disease. Some of the more well-known people with Lyme Disease include: Yolanda Foster (the Beverly Hills Housewives), Ashley Olsen (actress from Full House), Avril Lavign (Pop rocker) and the list goes on. Many of these people are also facing the fact that their children are also infected because they were either bitten or it was passed during birth. Yes, that’s right these infections can be passed through the womb, as well as, through breast milk and blood. The CDC is just now beginning to address the nation’s blood supply, because 40% of those infected with Babesia were infected after a blood transfusion. This is a serious plague that is infecting our nation and our human existence. According to the CDC there are more people being diagnosed yearly with these infections than HIV and breast cancer combined!!! And as the global warming keeps ramping up the numbers are growing exponentially each year.

The Cost of Treating Lyme Infections

So, what is the average cost of treating Lyme and its co-infections? Well,  it estimated to be around $1.3 billion per year. This situation is being likened to the AIDS epidemic and those of us that are sick and fighting for our lives have to somehow find ways to speak out so that our government changes its attitudes and people lives can be saved.

My Health

I am fighting a losing battle at this time. What makes it worse, is that I had underlying conditions that have only complicated the illness and weakened my body. I will never be able to eradicate the Lyme infections from my body. Our hope is to slow them down and buy me some more time, but so far I have been losing the battle. The malaria symptoms appear to be overtaking me at this point.

My only blessing is that I have doctors that are working diligently to find a way to slow them down and keep me going. God bless Dr. Delacruz who even takes time on Sunday to call me and check in and let me know that he is praying every day for me. Unfortunately, every day is an unGodly struggle with pain, and I have been bed ridden now since June of this year.

My entire GI system has now gone into failure and my vascular system is quickly following. The malaria is to blame for this at this point. We are going start, yet another round of treatments, but as this infection grows stronger, the higher the risk of death is from the treatment. So far, the treatment has left me fighting fungal infections and SIBO as well as the herxing. We are forced to do everything by IV at this point, including my feedings. This is going to be a rough week, as we once again start a new regime of drugs. Since I literally just got out of the hospital a few days ago, I’m not looking forward to this. Now you know the fight I’m in and what I’m up against.

Unfortunately, I’m not in this fight alone my husband is also infected, as is my daughter, sons and granddaughter. My youngest brother who was diagnoses with MS almost twenty years ago and who has not responded well to treatments, has now also been alerted to this. He is now looking into finding treatment for Lyme. These infections have swallowed up my family and most who are infected are struggling with trying to get and afford treatment for their children and loved ones. To see what we go through with meds and to understand the cost of these infections, I posted some of the pics of my oral drugs. This is typical for Lyme Disease patients and this does not include the numerous IV drugs that we take daily. There truly are so many drugs that they didn’t all fit on the table. Many need multiple pill carriers to remind them if they took each one. You can see picks like this posted by Avril Lavign and many other Lyme patients. This is common to anyone who gets any of these infections and unfortunately, this is life long and daily, and most, like me, will still remain very ill and go on to lose their life. We need a cure and we can’t wait neither can our infected children wait.

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This story was published originally on November 12, 2015. 

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.

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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.

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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.

Living with Ehlers Danlos is Hell

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I have Ehlers Danlos. On top that disease, I was given fluoroquinolone antibiotics and suffered a severe reaction which then lead to a rare and deadly fungal infection called Glabrata. This is what I have lived through over the three years.

Ehlers Danlos

Ehlers Danlos Syndrome (EDS) are genetic mutations that cause a lack of several types of collagen found throughout the body (skin, muscle, tendons, tissues, nerves and blood vessels). I have types I, II, & IV and crossover variations into several other forms. The type IV form that I have, also known as the vascular form, is a rare mutation form rarely ever seen (as of to date only three families including mine) and this is the most severe form that the NIH and John Hopkins has ever seen. This along with having more than one form (which is also extremely rare) has affected every part of my body and every system I have. It has left me with several other sub-illnesses, (some of them are common to all EDS sufferers and others not so common) such as hyperadrenergic dysautonomia, systemic mastocytosis, myalgic encephlamylitis (ME), pelvic congestion syndrome (PCS) and if God did not think he gave me enough to fight he threw in seronegative spondyloarthpathy with Crohns, which is seen in 35% of all female EDS patients. I also developed secondary Sjorgen’s Disease.

Ehlers Danlos plus Fluoroquinolones – Exploding Collagen

On top of all this crap I was given a fluoroquinolone drug by mistake, which is a collagen depleting drug!

After taking only four pills, my life turned upside down on a dime. I spent 64 days in the hospital fighting for my life, as my defective collagen exploded in every part of my body. Since then I have been fighting a daily battle of severe pain and organs and blood vessels that no longer know how or have the capabilities of functioning normally. It has now been almost three years since the fluoroquinolones and my body is still deteriorating.  Fluoroquinolones, as all my floxy friends know, is a nuclear bomb that slowly kills through DNA adduction and mitochondrial destruction.

The fluoroquinolones have left me with no immune system to speak of, so I am constantly fighting one infection after another. Last year, I fought the hardest battle of my life with a rare drug resistant fungal infection known as Glabrata; leaving me to spend 120 plus days in the hospital plus five months of home nursing care and daily IV’s of poison that nearly wiped out my liver. While fighting the Glabrata infection, I was also fighting the Crohn’s, liver damage, fluoroquinolone symptoms, sublexes, dislocations of my ribs from my sternum and a host of organ, nerve and blood vessel issues.

Pelvic Congestion Syndrome with Ehlers Danlos

One of the most painful issues is the pelvic congestion syndrome (PCS). The easiest way to explain this awful part of vascular EDS is to think of varicose veins the legs; the kind that when the person stands the blood begins to pool in their legs, the veins bulge out like thick blue ropes and begin to swell. After standing for a short period of time these people begin to suffer horrific pain down their legs to the point that they have to sit and put their legs up because it feels like razor blades cutting through them. Well, pelvic congestion syndrome is the exact same thing only it is the blood vessels in your abdomen. It can be the major arteries or the smaller ones known as the feeder veins, the ones that feed your organs.

For some of us with Ehlers Danlos, PCS affects only one or two veins and for others, like me, it affects several or all. For me, it is the feeders and the major mesenteric artery that are damaged. Every time I am in an upright position for any length of time the blood vessels dilate and fill with blood. This puts pressure on my organs and all the nerves that surround them. So, I suffer from both organ inflammation and dysfunctional organs because of the Ehlers Danlos. I also have severe nerve pain that can only described as a screaming pain. It makes me want to jump out of my own skin and run. The pain is so bad, I want to run to the nearest ER and beg for someone to help or end my life.

Unfortunately, there is no way to fix this other than to take enough pain meds to knock me out for days. Life with Ehlers Danlos, and especially PCS, revolves around being drugged with the strongest pain meds on the market and only getting up to shower and then back to lying down flat again. It leaves me unable to walk. Many people with Ehlers Danlos are in wheelchairs, but even that has its time limits.

Ehlers Danlos Specialists – Good Luck

In an attempt to hold on, people with Ehlers Danlos reach out to other patients, looking for any help they can. We search out specialists around the country, always praying that we will find that one doctor that is going to have the miracle we need. Because this is such a rare illness and my form of it is particularly rare, there is no protocol or research to follow. We are all on our own. Every one of us with Ehlers Danlos, no matter where we live in the country, have at some point, seen the same handful of doctors and received the same response – ‘there is nothing we can do.’

My journey has lead me to specialists from Chicago to Washington DC to Michigan and to Mayo, both my doctors and I have consulted with doctors from the NIH, John Hopkins to UCLA, and of course, every one of them tells me the same thing: ‘You can’t fix this [the exploding veins]. If you try [surgery]you will surely cause more severe damage to the remaining blood vessels or the surrounding nerves, which could, and has in some who have attempted it, left them in what is known as intractable nerve pain that is not treatable.’

Surgery to Repair Veins and Arteries Damaged by Ehlers Danlos

For people with Ehlers Danlos, healing is difficult and complications to surgery are very real and dangerous; attempts to stint, remove, bypass or replace the veins only causes other veins to erupt. Surgery is a bit like a dog chasing his tail. I have seen these complications first hand in others who have tried these surgeries, but there are a few, a very few people, who have succeeded and healed.

I know the risks and have spent the last two years searching out a doctor willing to attempt to repair my veins. I have begged and pleaded him to try it on me. Surgery to fix the faulty veins is very risky. The 80% failure rate is 80% and the repeat rate, 100%, meaning additional surgeries. And yet, I am willing to pursue the surgery anyway. What else can I do? There are no other treatments. My one feeder vein, which should have the circumference of a piece of pencil lead, now has the circumference of a quarter and is only getting bigger by the month. It is a feeder vein to my lower colon and rectum and is no longer allowing the organ to function normally. The pain is beyond anything I can take, even on pain meds. It is going to blow at some point and I am not willing to go there or lose my organs, so after much consideration, and two years of working with a surgeon, we are going to go in after this vein and we’re going to clamp it off and bypass it.

This vein is embedded in not only feeder nerves to the colon and rectum, but also, a ganglion of autonomic nerves. This surgery is extremely risky. If any of these nerves are damaged in the process, I would suffer not only intractable nerve pain, but also, loss of control of the bowel or bowel paralysis. This could also happen to my bladder, which eventually may cause me to lose the colon and the rectum (or as we Cronnies like to call it a “Barbie butt”, which is where they remove it all, put a bag on your side and sew up your butt like a Barbie doll).  On top of this, because of the autonomic nerves connect there; I could lose control over my heart rate, blood pressure and respiration. With all this being said, I’m willing to take my chances.

This surgery will leave me in severe pain for about 10 to 30 days. I will be bed ridden for those 30 days. This surgery will not get me off the pain meds but should reduce them dramatically. We’re only working on one vein right now; however, we may need to work on another.

Last Saturday, I woke up to filling the toilet with blood, a sign that something else has gone wrong. I took my pain meds, took my BP and heart rate and decided I was going to live. I went to the bathroom again, again later that day and this time I bleed out so bad that even after standing up I was still trickling blood and clots down my leg. It was off to the ER again.  After several hours they could not figure out where it was coming from but my hemocrit was high enough that I did not need a transfusion, so I told them I was going home and did.

The bleeding had stopped as usual, but I called the doctor, and spent the day at Northwestern with my doctor trying to figure out which vein blew. We think it came from the kidney and that was a self-contained bleed; it busted open and then clotted itself off. This is not my first bleed. I am constantly in the hospital for bleeds. My doctor says I need to come in and STAY in the hospital. I looked at her and said, “I spent just over 200 days in the hospital in 2012 and over 120 in in 2013 and I’m somewhere around 50 plus this year, I’m not going in anymore unless I’m dying.” It is not that I am giving up the fight but I’m tired damn it! So, I’m living and letting God take care of the rest.

Living Chronically Ill with Ehlers Danlos: Children and Spouses

This is only one of the many things I live with daily from EDS. The saddest part of all of this is now watching my babies go through this journey. The heart break and guilt runs deep and not being able to save them from this hell, is hell itself.  All we can do is to teach them how live with this horrible disease and be guinea pigs ourselves to help find ways to eventually treat them.

The men in our lives suffer right along with us. They feel helpless during our suffering. They have to pick up the household duties on top of working, and then there are the countless ER visits, the surgeries, the endless nights sleeping in chairs next to our beds in the ER, ICU or hospital, holding our hands and praying that we will get through this one too. They too have to deal with our screaming pain that many times leaves us unable to even hold a conversation. When we reach that screaming pain level, these poor spouses know it’s going to get ugly because it is all we can do to breathe. God help them if they even breathe too loudly because we are likely to snap the F@#k off and that’s when the crazy person comes out, the kind of crazy that even their mothers never warned them about because no one ever knew that level of crazy existed. They have learned the code words for it’s a really bad day, which means make sure I have a tall glass of water, my pain pill bottle and then leave me alone until I am either drugged enough or my body has adjusted to the pain level. My poor Tom not only deals with me but also my daughter who is now experiencing the pain and fatigue on levels that are leaving her to fight the crazy nasty pain devil that comes with this illness and that’s not to mention all the problems my boys have gone through because of this disease. God love these men and any faults they may have because they are angels to go through this.

Ehlers Danlos is a genetic disease that affects every part of our bodies, it affects every system and it disables us at every turn. There is no cure or treatment, there are few doctors who even know about this illness and even fewer that are willing to treat us. We actually get turned away as soon as they find out what we have. Our pain is so severe and incapacitating that most of the time there is not much that can be done other than to put us in the hospital and sedate us into oblivion! Those with the vascular form walk around with a cloud hanging over our heads not knowing when the next bleed is going to happen and whether it will be the one that finally takes us out.

I live with aneurisms in my brain, spinal cord and mesenteric artery. They will blow eventually just like the feeder veins. Some of us take palliative care, not that we are giving up the fight but because we hope they offer us something that helps. After being a hospice nurse for nearly 20 years, I could not do this. I walked out of the hospital and have chosen not to go there anytime soon. My head just cannot comprehend that yet.

Ehlers Danlos – We Look Normal

The worst part of this disease is that from the outside we look like everyone else, so no one can see our pain or what is happening to our bodies on the inside, so very few understand what our lives are like or what it takes for us to just get dressed. They can’t understand how different we are, only those that live with us, and unfortunately, our children who are now walking our path and the other EDS sufferers. It is also hard for some to not understand how one child in a family plagued with this illness can be so sick while another who has it too only suffers some minor problems or nothing until one of their arteries burst in the 5th decade of life. This is still being researched, the only thing they do know is that it is dominant gene and the mutation is true to the family, but the symptoms vary in degrees and systems from one person to another. It is a horrific disease that robs us of our lives and hides inside so others cannot see what we live with daily. At the bottom of this page I posted a pic from the National EDS foundations site to try and make people aware of what we look like on the inside, this is what EDS does to our bodies, organs, bones, nerves. If people could see what we really look like maybe then they could understand our pain, then maybe they would not criticize but instead praise us for continuing to fight, to get out of that bed, to continue to keep living despite the destruction! For me I continue to fight for my kids, I offer myself up for research, hell I’ll be a guinea pig like so many of us Ehlers Danlos sufferers. I will continue to get my ass knocked out by this disease but I refuse to stay down. No, I will get up and I will put a smile on my face I will laugh. I will go out and join the rest of the world, because that’s what we do!!

Postscript: Debra enters surgery today, August 28, 2014. We wish her well.

Ehler's Danlos