Remember that the "rare" frequency of adverse reactions stated in
the pharmaceutical package inserts is usually always grossly
underrated. The statistics provided by the manufacturers are a gross
manipulation of biased clinical trials, and are totally unreliable. For a
better assessment of your chances of getting seriously ill, consider
the table above instead. The recent experience with the U.S. postal
workers (treated with up to 60 days of ciprofloxacin) presents figures
very similar to those in table 1.
We have talked with nearly 50 people who thought that their
quinolone’s treatments had been successful and without any adverse
effect that reported having had their first time of severe bouts of
tendinitis or neurological problems a few weeks or months after the
quinolone treatment and therefore had not linked them with the drug.
The same can be said about neurological disorders. Taking into
consideration all the facts, nearly all of them now believe that que
cipro or levaquin they took is the cause of their insomnia, peripheral
neuropaties and musculoskeletal problems.
Observation:
For long or high dose treatments, the adverse reaction rate reach 100% of
patients. Many people are unaware that their illness is a manifestation of
quinolone toxicity.
There are persons that after one single pill develop a very acute
reaction that normally matures into an intermediate reaction (see
later) that lasts for 2 years on average. That should be studied by
scientifical groups because perhaps it would give some clues in the
search for an understanding of this disorders.
WHY HAS THIS REPORT BEEN WRITTEN
There is little or no medical information publicly avalaible via the
internet for the general population that deals with the practical side
of adverse reactions to quinolone antibiotics.
The only real information avalaible to date come the support groups
sustained by sufferers. (We strongly recommend visiting the
webpages www.fqresearch.org, www.drugvictims.org and
www.medicationsense.com ) (Those sites belong to their owners and do
not have any relationship with the authors of this report).
Nearly all the medical investigations in progress are not
comprehensive. The researchers in charge have a sheer lack of
knowledge about the real and true facts of this syndrome. Many
investigations are very superficial, nearly anecdotal, and only look
after a publishable paper, so that statistics of activity in the scientific
group remain high in the annual report. There are myriad scopelimiting
articles, all of which have contributed to extensive data, plus
many, many instances of scientific evidence supporting the great
damage that quinolones inflict upon people, but there is not a single
comprehensive study about the adverse effects caused by
quinolones.
No consistent clinical studies can be found that put the real figures of
adverse effects where they really are. There is not a single study that
shows the true extent of the damage caused by these antibiotics.
There are multiple causes for this lack of proper investigation:
.. The pressure exerted by drug manufacturers, the propaganda
they spread in medical circles, and the counter-studies that they
promote, most of which are unscientific creations of well paid
doctors that show “evidence according to their personal
experience" of maximum beneficial activity of the antibiotic
and their “negligible” adverse effect profile. We can even see
irresponsible and badly educated doctors prescribing and
recommending quinolones for children, when currently there is
overwhelming evidence that quinolones cause lesions of
extreme severity in inmature persons.
.. The delayed onset of symptoms is perhaps the most important
fact that is universally ignored by doctors. Many researchers
only monitor patients while they are on the medication and in
some isolated cases "up to a month later.” The vast majority of
disorders appear up to a year and a half later and are therefore

QUINOLONE ANTIBIOTICS TOXICITY. Dec 2003
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never linked with the real cause.
.. The lack of knowledge and preparation of the doctors that
prescribe them and the aspect that doctors nearly always dismiss
their patient’s complaints, and their refusal to admit any link
between the severe and long lasting pathologies and their causal
agent: the quinolones. The ignorance of doctors about the
toxicity of quinolones is simply appalling, irrational and
unjustifiable. Many doctors are handing out lifelong misery to
their patients and destroying their lives forever.
This report will help the non-medical population know more about
the true and real-life nature of quinolones. It can also be a call for the
caring doctor to promote a more critical approach and perform
unbiased professional research prior to prescribing quinolones.
We need to convince the medical class that:
.. Until better antibiotics are developed, a defectively designed
drug like a quinolone antibiotic should be restricted to
emergency, or life or death cases, but never used as a first line
of treatment. Quinolones are not an antibiotic in the traditional
sense, but a toxic chemotherapeutic agent, with very severe and
long-lasting adverse effects.
.. Thousands of affected people need help, and adequate research
is urgently needed in order to determine the mechanisms by
which these drugs cause their damage, and how to limit their
effects.
It is a shame that patients and victims once again have to write
reports like this, placing themselves years ahead of their doctors. In
ten years time the essential information contained in this report is
already common knowledge for thousands of persons, it will be
"discovered" by the medical class and then become accepted
knowledge. Too late for too many. Is this the medical class that we
deserve?
Reminding:
Half of the quinolone antibiotics marketed in the last twenty years have
been withdrawn from the market because of its great toxicity.
HOW HAS THIS REPORT BEEN WRITTEN
We have spent five years studying the floxing syndrome (QTS),
especially from the point of view of severe neuropaties, muscular
and joint disorders, with specific emphasis on the healthy, young,
active and athletic population.
We have challenged ourselves with blind trials using placebos and
active agents but always stayed away from potent drugs or
supplements. We have kept detailed diaries for years with tens of
thousands of entries recording ongoing symptoms and our attempts
at regaining basic movement, fitness, and athleticism. We have
probed and pushed ourselves through pains, endurances, and tests of
many kinds, varying as few factors as possible in each trial, so that
results could be of use. We have had more than a hundred MRIs
(magnetic resonance image), dozens of CATs (computerized axial
tomography), plain radiographs, three phase gammagraphies,
dopplers, echographies, electromyographies, nerve conductivity
tests, ultrasound tests, and hundreds of blood, urine, stool, and hair
tests along with many other diagnostic tests as well as a few
biopsies.
We have talked to hundreds of people suffering from this syndrome.
We have used logical methodologies to draw most conclusions.
Obviously, from observation, repetition and comparison alone, we
cannot aim to discover the mechanism of damage, or the elusive
clues for a healing protocol.
But, all in all, we, as many others, have demonstrated once more and
beyond any doubt, the extensive and devastating effects of quinolone
antibiotics and the unethical behaviour of the FDA and other western
agencies that are dominated by the manufacturer's lobbies who
routinely do not protect the people's health as they should, resulting
in the increase of financial profit for the laboratories and
pharmaceutical companies.
ARE YOU POISONED BY A QUINOLONE
ANTIBIOTIC?
If you have taken a course of any quinolone or fluoroquinolone
antibiotic (Cipro, Levaquin, Floxin, etc…) you have been chemically
poisoned. Depending on individual conditions, and the dosing and
lenght of the treatment, the intoxication will range from very mild
and asymptomatic to very severe and disabling.
In a minority of cases the, reaction is noticed immediately by the
patient. In a vast number of cases, most symptoms, or at least the
most severe ones, emerge weeks or months after the completion of
the quinolone treatment.
Many people can take a 7-day course of quinolone antibiotics
without perceiving any adverse effects. Their cartilage, tendons,
nerves and small veins and arteries have been directly damaged but
not enough to make them symptomatic. That is the case of many
sedentary people who deeply damage their joints as a result of
repeated but short courses of quinolones. But the fact remains
unknown to them since they are asymptomatic, and they do not use
their joints beyond the pain threshold. Later in life, it manifests as
early osteoarthritis, collagenous deterioration, or nervous system
failures. In any case, this paper is not intended for these people.
Many of us were healthy young athletes in perfect health with solid
rock knees and hips prior to taking quinolones but now have become
crippled persons, with our cartilages half destroyed, our eyes barely
functional, our bodies aching since several years ago and our whole
lifes stolen from us by a medical class that now turn its back on us.
For those that have developed symptoms like the ones described
later, first of all, they have to check if they have ingested any
quinolone antibiotics during the last three or four years. The damage
caused by the quinolone antibiotics becomes evident at a point in
time that ranges between the moment of the treatment itself and up
to eighteen months later. If your symptoms fit with any of the
cathegories listed later in this article, and you have taken
fluoroquinolones in the past, then a quinolone induced intoxication
might well be behind many or all of your recent physical problems.
This report could help assist you in getting a diagnosis.
SOME MEDICAL TERMS AND INFORMATION
The report has intentionally a non medical character. However, it is
necessary that you become familiar with a few technical facts
regarding the floxing syndrome. Some are exposed along the report,
when they are needed. A brief introduction to the general aspects of
an adverse drug reaction is included here.

QUINOLONE ANTIBIOTICS TOXICITY. Dec 2003
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The terms drug allergy, drug reaction and some euphemisms
(hypersensitivity, intolerance) are often used interchangeably. If we
take into account the inmune response of the patient, drug allergy
can be restricted to the reaction in which special antibodies of the
IgE type are massively released. This report does not cover allergic
reactions.
Like many other drugs, quinolones can cause an inmunologic type I
reaction, plus many noninmunologic primary pharmacologic side
effects (insomnia, restlessness, coffee intolerance) and secondary
pharmacologic side effects (thrush, leaky gut). They can also interact
negatively with many drugs. But their distinctive actions are
probably due to their direct toxicity and the subsequent inmunologic
reaction.
Drug reactions can be classified as follows:
-table 2- TYPES OF DRUG REACTIONS

-table 3- TYPES OF INMUNE REACTIONS

In most cases, there are not markers that can confirm a diagnosis, so
all serum (blood) parameters can be normal and still be suffering
from a very severe and incapacitating reaction. Only a very
specialized and very unnacessible tissue biopsy can confirm the
problem. Therefore, most diagnostics are stablished upon clinical
symptoms. In principle, the fluoroquinolone syndrome can be
classified as a TYPE III inmunological reaction, with an added
noninmunological TOXICITY.
One thing is clear: re-exposure to quinolones, after having been
floxed previously, poses a very high health risks on the patient.
Persons that become floxed twice have the worse prognosis
(expected outcome). Many people with moderate reactions to
quinolones are later exposed again to another round of the same
antibiotics by their doctors after dismissing their complaints about
pains and disorders associated to the antibiotic. The outcome is
frequently a severe reaction that lasts 3 to 5 years and permanent
lesions.
WHAT KIND OF DAMAGE DO QUINOLONE
ANTIBIOTICS CAUSE?
This class of antibiotics has very characteristic ways of causing
lesions:
.. they damage the central and peripheral nervous systems
.. they damage small veins and arteries (vascular disorder of the
vasa vasorum and vasa nervorum)
.. they impair the rebuilding and repairing capacity of tissues,
specially connective-collagenous
.. they chemically destroy important structures, like cartilage
There are many other mechanisms of quinolone assault on the
human body (for instance, liver, kidney, pancreas and heart reactions
all of which can be fatal), but they are not the focus of the present
report.
Important fact:
Pain and disability caused by quinolones is very long lasting and affects
many parts of the body. In favourable cases recovery takes several
months to years. In severe reactions pain and lesions can last for life.
HINTS AND CLUES THAT MIGHT SAVE YOUR
LIFE
Perhaps you have taken quinolones in the past and you think that
they worked well and that you did not react negatively to them.
Check the following subtle symptoms and the usual interpretations
that people make of them.
.. You had a strange bout of tendinitis, for instance in the outer tip
of the hip, normally diagnosed as trochanteric bursitis caused by
tight belts or resting on you side. The same applies to other
areas of the body, like the elbow (epicondylitis) diagnosed as an
overuse of your tennis racquet or gardening practices, but you
remember that you had never had it before.
.. It takes you longer to recover after exercise. It is not alarming
and you have not paid much attention to it.
.. You sleep worse than before; it seems normal as you have a lot
of pressure at work.
.. From time to time you have some small throbbing pains in
different parts of the body. They last only for a few seconds, so
there is nothing to worry about it.
.. It is strange but you have occasional twitching in an eyelid, or
any other part of the body. It is not painful.
.. Some nights you feel some mild itching migrating along your
body. One brief itching here and another there. It is more
intense in the scrotum or groin. Instead of identifying it as a
peripheral neuropathy you conclude that it must be your clothes
or the new soap brand, that is more irritating.
.. You feel some stiffness, especially in one or both legs, but it is
normal because you are getting older.

QUINOLONE ANTIBIOTICS TOXICITY. Dec 2003
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.. You do not tolerate coffee as well as before.
.. Your memory is not as good as it used to be. The cause may be
too many things to think about and much stress. And you are
no longer a young person.
.. There is an urge to urinate when the bladder is partially full.
Most urologists think that is due to a dysfunction associated to
benign enlarged prostate but in reality is a neurological deficit
caused by the prescriptions of quinolones that they gave you.
If you have experienced some of these symptoms since you took
your first quinolone, perhaps you have reached your first threshold
of tolerance that -once surpassed- can result in the destruction of
your life soon thereafter if you take more quinolones.
WHAT ARE THE MAIN SYMPTOMS OF BEING
POISONED BY A QUINOLONE?
For a complete list of symptoms see later in the report. A strong
reaction generates some 30 to 50 symptoms. In some cases adverse
reactions appear right after the ingestion of the antibiotic. In
intermediate and severe reactions you may start with a few
symptoms and as time passes new and debilitating symptoms arise,
specially around the second, sixth and ninth month’s marks. And in
many cases of young, very healthy and active people, the worst
lesions emerge progressively up to eighteen months or more after the
cessation of the drug (we have deducted it beyond any doubt from
various cristal-clear cases plus several rechallenges with quinolones).
Here we include the most easily recognizable and common.
Joints and muscles-neuromotor:
.. Arthralgias (pain in joints)- especially the Achilles, plantar
fascia, ankles, knees, hips, elbows, shoulders, wrists and others.
They start as early as during the antibiotic treatment, in which
case some times the floxie becomes bedridden or unable to walk
or drive for several months, requiring a wheelchair or crutches.
In other cases arthralgias show mildly at the beginning and their
intensity increases to its maximum intensity up to a year and a
half later. In this type of delayed reaction, some six hours after
strenuous exercise the symptoms may be present as acute pains
that can be excruciating if the limit of tolerance is reached. This
limit consists of the maximum exercise that a given body can
tolerate before its impaired repairing capacity is overwhelmed
by the physical demands. For the average floxed athlete, this
limit is much lower than it was before the quinolone
intoxication.
.. Acute tendinitis not responsive to conventional treatments. This
type of tendinitis is very acute at times, requiring
immobilization, and is nearly always triggered by a level of use
that was normal in the prefloxed state, or normal daily use. The
tendinitis does not respond to anti-inflammatory medication,
which in fact, can make the symptoms worse. Sometimes the
tendinitis migrates within a joint and from one joint to others. In
the first stages of the floxing, the tendinitis is predominantly
enthesitis, which is inflammation of the insertions of muscles
and tendons into the joints. In many cases they end up in
partially or fully ruptured tendons (achilles, shoulder rotators,
wrists flexors). It is a class effect of all quinolones, in other
words, all these antibiotics are very toxic for all the tendons in
the body, for everybody. For every one the quinolones cause
small and multiple lesions in the tendons, that eventually
rupture in those people unlucky enough having weak tendons,
having taken corticoids, having preexisting vascular problems
(prediabetics) or being magnesium deficient.
.. Arthritis-like symptoms. Many symptoms resemble those of
rheumatoid arthritis and other autoimmune diseases, but are
always sero-negative and with a different pattern of clinical
symptoms.
.. Osteoarthritis-like symptoms. Joints usually start to make a lot
of noise.After the intoxication, and with time, healthy cartilage
becomes softened and erosion takes place, and the illness
presents itself as a true clinical osteoarthritis. Knee cartilages
are specially targeted by quinolones, with a very high incidence
of torn menisci (inside the knee). There are many cases of
complete destruction of previously healthy joints and the patient
has to be submited to very invasive surgical procedures and or
total joint replacement. The most damaged cartilages are the
more weight bearing ones: knees, hips and low spine.
.. Increased stiffness after exercise. It takes longer to recover
from exercise, and there is a clear loss of flexibility. Soreness in
many muscles, specially legs and shoulders, with also a
predilection for the neck.
.. Very slow recovery from impacts and blows. Whenever the
affected person is hit in athletic or daily activities, the flesh
takes much longer to recover from the pain, along with
hemorrhaging and inflammation. Dark veins, hemorraghe-like
patches under the skin.
.. The skin (and other collagenous tissues) loses nearly all
capacity of recovery. A cut on the skin near an affected joint
leaves a pink scar for many months afterward whereas it would
have become unnoticed in prefloxing state.
.. Cold feet and hands.The presentation resembles Raynaud's
syndrome. In many severe cases several phalanges of fingers
turn numb or close to frozen with cold conditions that did not
cause any trouble before the floxing. Loss of sensitiviness in
hands and feet.
Central and peripheral nervous system and systemic:
.. Brain fog, depression, depersonalization, short term memory
loss, lethargy. Slurred speech. Unability to speak fluently.
Forgetting words, getting stuck in the middle of a sentence.
Some are caused by the insomnia but it is mainly a neurological
lesion of the brain.
.. Twitching, trembling, throbbing, pins and needles sensations,
and pulsating pains in muscles and joints are the hallmark of
this disease; especially in the lower legs (ankles, Achilles,
calves, and knees), but can manifest all over the body.
Fasciculations (visible crawling under the skin) of muscles, due
to denervation. Twitching is manifested earlier in eyelids and
the triangle on the back of the hand placed between the thumb
and index finger.
.. Insomnia, very acute and difficult to tackle with. Without the
aid of herbals or drugs, severely floxed people may suffer
extreme insomnia (2 to 3 hours of unresting sleep a day) for
more than two years. Over-reaction to caffeine. Anxiety,

QUINOLONE ANTIBIOTICS TOXICITY. Dec 2003
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depression, pre-seizure state. During some part of the floxing
most people experience anxiety and panic attacks (awakening
amidst strange nightmares with fear and a feeling of dying),
especially at night or when falling asleep. Headaches, especially
unilateral, or affecting one side only.
fig.1. -frequency of musculoskeletal disorders in severe reactions-

.. Vision problems. Diplopia (double vision) and other focusing
problems. Floaters (darkened points, spots, cowebs, strings..)
moving in the vitreous of the eye, flashes (small or big
wandering lights crossing your sight, some quickly others
slowly, also called ziggies if they don’t exhibit a stright path),
brilliant lights, halos and watery curtains, acute photofobia,
complete or partial loss of vision (transitory, but lasting up to 6
minutes of absolute blindness seing just solid white), blank
points, eye pain, oculaar pressure, blurred vision. Quinolones
cause degeneration of the retina, specially the outer margins.
Vision damage reach its peak about two to six months
postfloxing. Vision damages caused by quinolones have a high
ratio of irreversibility. Severe reactions have nearly always
associated some degree of damage on the vision, that is
invariably assesed by the patients as very disabling. We have
seen so many, really a great many, cases of irreversible damage
of vision, or lesions not cured by the 5th year mark, and the
distress inflicted on the sufferers, that this would on its own be
enough cause to withdraw all the quinolones from the market
for primary care treatments.
.. Diminished erectile function (semi-impotence). Difficulty to
reach hard erections. Decreased sex drive (libido) both for men
and women. Can last up to three years in severe reactions for
young people, very healthy and active sexually prefloxing.
.. Digestive problems. The quinolones damage all the nervous
network governing the intestines. Alteration of intestinal
movements. Intolerance to foods and many compounds. Bad
reactions from defectively degraded foods. Inability to absorb
some nutrients, specially minerals. Weight loss. Destruction all
of the flora and proliferation of bad fungi.
.. Violent rectal spasms, that may cause fainting. Pains of every
sort and intensity in everypart of the body: skull, lower head,
neck, jaw, shoulders, arms, back, hips, legs, ankles, fingers and
toes.
.. Trembling of a limb after sustaining tension with the muscular
groups of that limb. For instance, trembling of the leg after toeraising
for a while, or an inability to write steadily after holding
a heavy load with that hand.

fig.2. -frequency of systemic disorders in intermediate and severe reactions-
.. Heart palpitations and arrythmias, some times life-threatening.
A serious heart condition called prolongation of the QT-interval
is a class effect of all the quinolones, showing once more that
they are very defective drugs. Skipped heart beats, irregularities,
severe poundings. Some times floxies require the implantation
of pacemakers. Many thousands of people dye from heart
attacks that are not of an infarction kind but cardiopathical,
caused by deffective nerve signals. Nearly all of them are
caused by toxic compounds, like work environment hazards, or
medications, among them the quinolones.
.. Alterations of liver, kidney and pancreas enzymes and
parameters. While taking quinolones the cholesterol and
tryglicerides skyrocket up to three times their normal values, to
return to normal range in a few weeks. Quinolones also provoke
hypo and hyperglycemias as a class effect. The quinolones
accelerate the progression towards full diabetes of those
individuals with a unrecognized precondition.
Autoinmune like responses:
The main symptoms of a quinolone poisoning resemble those of
some autoimmune disorders because in acute intoxications they
cause a type of small vessel vasculitis with neurological dysfunction:
.. Dry eye, dry mouth, dry sinuses and a shift towards dry skin.
Dry eye can be measured with moisturing stripes rendering null
values in severe reactions. Sticky, gritty eyes. Dry mouth,
specially at night or when taking any vasodilator. Dry sinus
causes a lot of infections that are opportunistic due to the
compromised inmune system of the severe floxies.

QUINOLONE ANTIBIOTICS TOXICITY. Dec 2003
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.. Neurological pain that migrates throughout the body; muscular
and joint pains.
.. Cycling or relapsing of symptoms. Causing intolerance of
certain foods. Increased sensitivity to chemicals, especially to
quinolone-tainted foods (poultry, beef).
.. Many symptoms that resemble fibromyalgia, multiple sclerosis,
lupus erythematosus, rheumatoid arthritis, reactive arthritis,
vasculitis, AIDS and other diseases.
.. Skin rashes, on hands, feet, and other areas.
WHICH KIND OF ADVERSE REACTION TO
QUINOLONE ANTIBIOTICS ARE YOU SUFFERING
FROM?
Reactions to drugs vary among individuals. But there are some very
common patterns of bodily responses to quinolone intoxication.
From the study of many cases we have concluded that it is useful to
envisage a simple scale of severity of the reactions. According to it
you can have a mild, intermediate or severe reaction. Obviously
there are not clear delimitations between them and every reaction is
unique and personal, but if you can assess to which kind you could
be fitted into, you will acquire a more precise diagnosis and will be
able to address your problem accordingly.
Many people suffer acute reactions during the first days. Eventhough
they get very scared the acuteness has no direct relation with the
severity of the reaction as a whole. You will only be in a position of
making a judgement on the severity of your QTS after a few months
since the cessation of the drug, when you line up the whole list of
symptoms, their intensity and their evolution.
If your suffer a mild reaction you can expect a good recovery in 4 or
6 months. For a intermediate reaction is typical a convalescence of 1
to 2,5 years with a diminished but aceptable life quality. Severe
reactions mean a miserable living for at least 3 years plus another 2
years to get acceptable pain levels, ending up with permanent lesions
and life limitations. This article focuses primarily on severe
reactions.
Check whether you fall into one of the following categories. There is
not a clear-cut boundary between severe, intermediate and mild
reactions. On top of that everyone is different and can have, for
example, 20 symptoms belonging to the intermediate reaction level,
and 1 or more with a greater intensity, typical of a severe reaction.
-table 4- INTENSITY OF SYMPTOMS. LEVELS OF REACTION

The whole list of the adverse reactions to a typycal quinolone is
included later on this report.
Summarizing:
Many reactions are mild and INTERMEDIATE and heal in a few months or
years with no serious sequela.
For everyone there is an extremely high risk of experiencing a severe
reaction for doses of fluoroquinolones of 1.500 mg a day for 7 days
or 1.000 mg for 2 months. Severe reactions are very distinctive
because they are extremely long lasting and feature many permanent
lesions, specially in the 4 following groups:
.. neuropathies, including peripheral, central (insomnia, ...) and
autonomic (heart, intestines, ..)
.. dry damages (eye, sinus, ears, skin, mouth)
.. cartilages destruction, joint and muscle pains
.. vision lesions (floaters, blank points, retina degradation)
ALLERGIC REACTION
(It is a complete incompatibility between your body and the drug)
If you are allergic to quinolones, as soon as you take a few pills or
even one single dose, your body reacts negatively and feel one or
more of the very noticeable side effects listed in the package insert
and in this report, that normally force you to stop the treatment
inmediatly.
This is a type of allergic reaction or anaphylactic shock and is not
covered by this article.
SEVERE REACTION
(FULL IMPACT. Severe toxicity. Inmediate problems)
This report deals specially with SEVERE reactions. If the damage
caused by the antibiotic is extensive and deep, the athlete will
experience limiting pain as soon as he intends to exercise
strenuously during the course of a quinolone antibiotic or right
afterwards. In this situation, the athlete will experience some or all of
the following:
.. Tendinitis over different parts of the body. For an athlete, this
tendinitis is very similar to normal types but different in its
persistence and unresponsiveness to conventional treatments.
The joints most affected are the Achilles and ankle complex,
knees, wrists, shoulders, hips, fingers.
.. Arthralgias in the joints. Pain of different kinds, very frequently
migrating around a joint and then moving to other joints over
time. Pains are often very debilitating, requiring almost absolute
rest for months because patients cannot walk at all or more than
a few paces or stand up for long. Even if the patient is
functional, pains have a neurological root and can be very
intense and interfere with normal activities and prevent sleep.
These arthralgias evolve to osteoarthritis in many cases with
cartilage erosions.
.. Weird sensations in the muscles and joints, like tremors,
twitching of eyelids or any muscle in the body, pulsating pains,

QUINOLONE ANTIBIOTICS TOXICITY. Dec 2003
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vibrations under the skin, heat or burning sensations.
.. Vision problems. Most prominently in the form of many
floaters (dark worm or spot like) that seem to float in the
vitreous area of the eyes. Also ziggies (brilliant minute lights
that move in a zig-zag or wavy manner in your field of vision).
Curtains of watery sight in the upper part of the field of vision
that move sideways along with your eye. Waves-like in the
outer margins of the sight. Sparks (flashing lights). Photophobia
or intolerance to strong sunlight or artificial light. Difficulty in
focusing on objects, and double vision. Occasionally temporal
loss of vision. Eye pain. In many cases, some very worrisome
implications such as dry eye syndrome are also experienced.
These problems reach their peak of intensity around the sixth
month postfloxing and last for years or become a permanent
lesion, being a marker of the likelyhood of recovery (the drier
and longer, the lesser are the chances of overall recovery).
.. Restlessness, great loss of sleep quality. Anguish and anxiety
episodes. Some times panic attacks. Intolerance (great
nervousness or increasing symptoms) to concentrated coffee
(espresso) and tea. Insomnia can last more than 3 years during
which is difficult to get more than a few hours of disrupted and
bad quality sleep. Intolerance to coffee can be present for more
than 7 years.
.. Tinnitus, or ringing in the ears. Ear pressure, usually in waves
of pressure. Hypersensitivity to normal sound. Headaches, head
pressure, mainly asymmetric.
.. Myalgias (muscular pain) all over the body, or very localized in
some parts. A strong perception that everything is not normal,
because there is not a normal recuperation after exercise, and
the individual feels achy and sick. Longer and incomplete
recovery after exercise, that leaves an ever-increasing stiffness
of joints and an aching body all over in an asymmetric fashion.
.. Heart palpitations and strange pounding and throbbing.
Skipping beats. Alterations of heartbeat. Irregular heart beats
are usually more common after eating.
.. Chest pain. Heartburn.
.. Foggy mind, drowsiness, lethargy, loss of drive and power.
Need to sleep. Tiredness and intense fatigue.
.. Strange reactions and intolerance of foods, supplements, and
chemicals. Sensitivity to parfumes, health care products and
chemicals. Taste and smell perversions. Lack of smell
sensitiviness.
.. Dry eyes, dry sinuses, dry ears, dry mouth, drier skin. These are
external manifestations of a serious lesion to all the vessels that
carry vital fluids. The same damage has been done to many
other internal organs, hence the abnormal intestinal function,
food intolerances, chemical disturbances, cycling of symptoms
and general malaise. Dry eye can have serious consequences if
not treated. Dry sinuses make you proner to get infections.
.. Neuropathies in limbs, with a lot of pain with muscle wasting
and nerve involvement. In many cases they resemble muscular
injuries. For instance, a peroneal (outer leg) nerve neuropathy
can be considered a pull in the hamstring; a peroneal nerve
neuropathy can be disguised as an ankle strain, or an overuse
syndrome and so on. These neuropathies start soon and grow in
intensity for many months. In many cases it takes several years
to get a remission of these neuropathies.
.. Skin rashes, specially in distal areas (hands, ankles). Itching, all
over the body, with little intensity, plus more intense in some
specific areas (hips for instance) when taking a hot shower, plus
itching in the groin and scrotum at night when hot. Reddish or
red-blue upper eyelids. Increase in vertical ridges in nails of
toes and fingers.
.. Weight loss, probably due to muscle destruction and atrophy
and alterations in intestinal function.
.. Abnormally cold feet and hands. Fingers close to freeze in low
temperatures that do not cause any trouble to normal persons.
Lack of feeling in some fingertips. Increase in depth of vertical
ridges in finger nails.
.. Problems with foods and drinks. Your intestines are also altered
and their permeability and ability to process foods is impaired.
If you have most of the above mentioned symptoms 9 months after
drug cessation and half or more of them are very intense, then
probably you are suffering a SEVERE reaction and this report is
specially devoted to thoses cases.
INTERMEDIATE REACTION
(MEDIUM TOXICITY. Delayed colapse)
Symptoms from a quinolone antibiotic intoxication of a lesser
intensity start with mild pains during the treatment or soon
afterwards, that are of small intensity and can even pass unnoticed.
In any case, during the first months, most of the problems are
musculoskeletal and tend to resolve without complications. But some
six to fourteen months after cessation of quinolone antibiotic
therapy, the active athlete can become suddenly prostrated and
severely affected, normally in one single joint.
This is the typical list of symptoms of a person in which the worst
adverse effects are of a musculoskeletal nature:
.. Tendinitis over different areas of the body. For an athlete, this
tendinitis is very similar to normal tendinitis but different in its
persistence and unresponsiveness to conventional treatments.
The joints most affected are the Achilles and ankle complex
(posterior tibial tendon, anterior tibialis, flexors of the toes),
knees, wrists, elbows, shoulders, hips, fingers.
.. Arthralgias in the joints. Pain of different kinds, very frequently
migrating around a joint and then moving to other joints over
time.
.. Weird sensations in the muscles and joints, like tremors,
twitching of eyelids or any muscle in the body, pulsating pains,
vibrations under the skin, heat or burning sensations.
.. Medium intensity neurological symptoms like insomnia, panic
attacks, anxiety and any light side effect included in the list at
the end of the report, plus the invisible lesions like cartilage
softening.

QUINOLONE ANTIBIOTICS TOXICITY. Dec 2003
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MILD REACTION
(Low level toxicity. Supposed safe reaction. Further problems)
In these cases, apparently there are no symptoms associated with the
quinolone treatment and the individual can feel no adverse reactions
after taking a quinolone prescription, especially a short one or one
with low doses. But the quinolone takes its toll and after several
treatments spaced weeks, months, or even years apart, subtle
symptoms will begin to develop, and the sufferer will probably never
link them to the antibiotic.
These symptoms will probably be: restlessness, especially at night,
brain fog, some minor twitching, increased cool hands and feet,
slower recovery after strenuous activity, increased stiffness after
exercise. And the unavoidable erosion of cartilages will be inevitably
added to the list.
In short:
Severe reactions present with intense, long lasting joint and
neuromuscular symptoms plus eye disorders and dry mucous parts.
WHICH ARE YOUR CHANCES OF RECOVERY?
As explained before, most people recover from the quinolone
intoxications. Many do not. Everyone with intermediate and severe
reactions get permanent damage although if it can be internal and it
can remain more or less unnoticed if it does not affect much their
daily lifes (cartilages, central nervous system). Some people ends up
with permanent chronic pain, physical difficulties, heart or vision
damage or many other irreversible lesions.
Therefore, if the toxicity level is not high, that is to say, if there are
little nervous and vascular systems alterations, the average person
will probably recover, albeit with the cartilages of the weight bearing
joints slightly eroded. The athlete will enter an accelerated course of
decay because his/her cartilage will not keep up. The endurance
athlete will no longer be able to perform at a decent normal level.
For instance, in severe cases photophobia resolves in some two years
on average, focusing impairments in 2.5 years, and flashies and
floaters take many years to fade off. Another indicator of the severity
of the floxing is a dry mucous condition. If you have long lasting dry
eyes, plus dry mouth and sinus, you are no doubt suffering a severe
reaction and running the risk of ending up with quite permanent
lesions.
If the toxicity level is high, the average person might eventually get a
decent daily life similar to the one he or she enjoyed before taking a
quinolone, but with some physical limitations for repetitive and
strenuous activities. The athlete will no longer be able to return to
competition in any impact sport, and in the best case he will be
capable of enjoying biking, hiking, swimming or other sports that
put little stress on the joints. Healing and recovery time until
reaching this point is more than three years on average. There is a
concerning number of cases for which recovery seems to be elusive
after five or more years after the last quinolone pill ingested. Perhaps
during the coming years we will see the confirmation of cases of
permanent disability, or lifelong pains and misery caused by
quinolone antibiotics.
The recovery and return to acceptable levels similar but lower to
previous ones will take one and a half years on average. If the
reaction is severe, pains and limitations can last 4 to 5 years on
average or be permanent.
It is summarized as follows:
-table 5- LIFE AFTER RECOVERY

The successful recovery stories of people enduring intermediate and
mild reactions are currently overrated because many people that end
up feeling normal are still far behind a complete recovery but they
cannot tell because they are sedentary. Those persons can report that
they are cured some two years earlier than the real healing takes
place. Nobody really gets out undamaged. Although it is difficult to
trace enough people long enough to get a conclusion, it is widely
admitted nowadays that many people remain symptomatic in a
permanent, irreversible manner.
Remember:
If you suffer a severe reaction, your chances of complete recovery are
lower than 40%.
Chances of recovery are predominant for the age bracket of 20-40
years. After the age of 40 recovery can take much longer. Beyond
the fifties more permanent damages are recorded. For people above
70 years old, recovery is completely unlikely in the case of severe
reactions.
Nearly all floxies can tell when they are recovering, because at a
precise point in time they experience less problems with foods
(recovery of the toxicity and neuropaties that prevent intestines and
organs from working properly), a lower level of pains, less stiffness
and soreness, more flexibility, there is a weight gain, insomnia
improves, and they feel stronger in every sense. Then some anxiety
develops in all floxies because they all see a glimpse of normalcy at
the horizon, and would like their ordeal to stop inmdiatly after long
years of suffering. But in severe floxings on average you feel some
recovery when you are half way the reaction, that is to say, at the 2,5
year mark for a 5 year recovery period. The second part of the
floxing is more compatible with a normal life (save sports or
strenous activities) but you still cannot eat freely, you get through
many cyclings, but many neuropaties and permanent lesions (vision,

QUINOLONE ANTIBIOTICS TOXICITY. Dec 2003
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drynesses) are still present and the floxie gets concerned about the
life lost and the perspectives lying ahead.
EVOLUTION OF FLOXING SYMPTOMS
The symptoms are listed in the above paragraphs. The evolution of
the pathology is very characteristic of this syndrome. For severe
reactions, new symptoms keep emerging for up to nearly two years
after the last pill has been ingested. The worst disorders become
apparent between months 6 to 9, but others still appear up to month
20. It varies a lot with each individual, but very typically it evolves
as follows:
SEVERE REACTION
Month 1-2: (acute phase) maximum musculoskeletal symptoms; possibly
crutches or wheelchairs needed, high level of pain, and crippling
limitations.
Month 6-9: (acute phase) maximum damage, irrespective of symptoms.
Maximum vascular damage, that affects eyes, joints, heart, ears, and so
on. Erosion of cartilages can be felt and also diagnosed by physical
examination and imaging.
Month 9-30: Increasing of the symptoms, very much affected all over. Pains
all over, with soreness, stiffness. Strong feeling that something is going
really wrong and worse. New symptoms of a toxic systemic vasculitis
(see later) may arise, like dry eye, dry sinus, and abnormal reactions to
otherwise normal infections like flu or colds that lead to a trail of deeper
symptoms. If dry eye does not develop or if it is not long lasting, the
chances of overall recovery seem to be far greater. Very intense
neuropaties in legs and other areas of the body, that can be detected in
ordinary testing. Maximum muscle pains.
Month 24-36: Cycling of symptoms. Some disorders may experience an
improvement like insomnia and some central nervous issues. Panick
attacks tend to stop. Still very sensitive to any food or suplement with
constrictive properties. A little better from myalgic pains and stiffness.
Still present exercise intolerance, dry syndromes, and vision lesions.
Month 30-38: Recovery predominant, slow progress but firm. You can feel
strong and determined and your spirit might go up too. You start to see
what permanent lesions the quinolones have caused. Less neurological
pains but still twitching, fasciculations, trembling, itching and other
similar symptoms.
Month 36-60: In roughly 40% of the cases, noticeable recovery for sedentary
people (recovery is not complete but the inactivity prevents the
endurance damage to show up). Slow recovery for active people
because strenuous exercises make symptoms to reappear, endurance is
still low, and the body is not still able to recover normally after
physically demanding activity. In the remaining 60% of the severe
cases, by month 36 people feel better than a year before but are still far
away of recovery.
From the 4th year on: depending on the individual, near complete or partial
recovery is reached. Typically irreversible damages are dry eye, dry
sinus, dry ear, dry skin, floaters, blank points in vision, some
palpitations, neuropatic pains-bearable, exercise intolerance and
occassional muscular pains.
Total recovery time: ranging from 3 to 5 years or never in some
cases that end up with different permanent lesions.
INTERMEDIATE REACTION
Month 1-12: minor musculoskeletal symptoms; limited activity, incorrectly
associated with overuse, or mechanical problems. acute phase for other
minor effects.
Month 12: (acute phase, in active, athletic people only) due to accumulated
damage, peak symptoms are reached. Collapse of a joint is typical.
There are no or very mild accompanying symptoms (vision,
neurological, etc...).
Month 12-22: Recovery predominant, relatively fast progress.
Active and athletic people will see their endurance drop a lot and
they will develop osteoarthritis early, perhaps some ten years earlier
than non-floxed people, and depending on dosage.
In MILD REACTIONS, recovery is reached between moths 4 and 12
on average. In some cases they have an acute phase of up to 3
months.
In summary, on average people tend to feel well albeit partially
recovered, according to the following timing:
.. severe reactions: 4,5 years
.. INTERMEDIATE reactions: 1,5 to 2 years
.. mild reactions : a few months
Everyone behaves slightly different to the floxing because daily
habits and personal conditions can somewhat modify the evolution
of the recovery.
CLASSIFICATION CRITERIA FOR THE LOWER
LEG
(As an example, for classification purposes, we have established a scale of
severity of the tendinitis and joint problems, used to make entries in the
research diaries).
The severity of the physiological performance of any given part of a
floxed body is graded according to its functionality. For instance,
Grade 1 corresponds to the normal state, and Grade 9 to the prerupture
of tendons.
-table 6- CIPRO INDUCED TENDINITIS

QUINOLONE ANTIBIOTICS TOXICITY. Dec 2003
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A floxie is constantly moving from one grade to another, depending
on the ingestion of more drugs, activity level and time elapsed since
last ingestion of quinolone antibiotics. Cycling of symptoms keeps
floxies moving up and down the scale. In many cases, grade 1 is
never recovered again, but instead a low, functional grade is
maintained.
We have used other similar tables for neurological issues when
preparing this report.
PAIN LEVELS
Pain levels experienced throughout the floxing can range from very
low to the maximum on a 10-point scale. Pains of the maximum
severity- stabbing, jabbing, tearing, and ripping, can be felt when a
joint or limb collapses neurologically. These pains are described as
higher than passing a kidney stone or rupturing a testicle, for
instance, and can completely block the affected joint. Intermediate
pains are common with mono-neuritis in legs, arms and neck,
especially at night and with some minor movements. Low intensity
pains (that correspond to myalgias) typically spread all over and
correspond to the "normal" state of a floxie: just feeling like a person
that is 40 years older than their current age. See later for more
information on neurological pains, how can affect daily life and how
little can be done to paliate them.
IMPAIRED HEALING IN THE FLOXED BODIES
This is another very distinct characteristic of quinolone disorders, of
which every doctor is unaware. Once you think your ankle is nearly
recovered from a intermediate reaction (say in grade G2), if not
enough time has elapsed since the ingestion of the drug (less than 2
years) then only a few repetitions of an exercise with your foot
against strong resistance can bring you to Grade 9. So, returning to
normal pre-floxing levels of activity is a continuously probing (trial
and error) method, not exempt of relapse and danger.
The floxed body has been depleted of nearly all of its natural healing
capacity. To function properly, the body must continuously produce
new tissue, especially cellular matrix, collagen and fibrous cells. For
everybody, the toxicity of the quinolones kills these mechanisms, in
a dose dependent manner.
So whenever you accidentally bump a part of your body, especially
the hand or foot (more distant areas and less irrigated tissues) it takes
an abnormal amount of time to recover. Small blows that in a normal
situation would take three days to heal, can take up to three months
of healing during the acute phases. A cut in the skin around the
Achilles will take the same time to close than in any other area of the
body, but ten to twenty times longer for the scar to clear off.
When the athlete approaches grades 6, 7, 8 and 9, there is a lot of
deposition of waste in the joints and under the skin. That makes the
waste adhere to the joints and worsen the symptoms. Massage helps
to remove those deposits in most cases.
During the months that follow the acute phase, both mechanisms
(healing and rebuilding) are slowly returning to normal, especially
the quality of the rebuilding, although the healing response still
cannot keep up with the requirements of our previous (pre-floxing)
level of activity. There are many scientific reports that show
ciprofloxacin impairs the healing of broken bones and connective
tissue. Being floxed is not the best time to undertake minor surgery
that could be avoided or rescheduled for later.
So, during the acute phase it is not possible to cope with strenuous or
very repetitive activities. It is normally advised to maintain some
degree of physical activity, but always testing and probing the limits,
without surpassing them.
Quinolones make it more difficult for people to recover after
exercise, and can cause them to develop a frank intolerance or
dislike to exercise. Pains and stiffness after exercise are very
characteristic of this toxicity. That is most likely due to a chemical
damage of the fascia (connective tissue) that exists between muscles
and allows them to run smoothly and independently. These lesions
can last for many years after the floxing.
TOXICITY GUARANTEED
Apparently there are not many studies of clinical significance that
provide a wide explanation regarding the high toxicity level of
quinolones. One can find medical reports suggesting that everyone
having a bad reaction to fluoroquinolones had a previously
underlying muscular disorder. We do not favor that theory. Also,
there is no validity to the claim that all people having a reaction to
quinolones have a common flaw or genetic component that make
them more prone to suffer adverse events. The medical community
will start to understand something about fluoroquinolones when they
acknowledge that these antibiotics are just plain toxic.
Many of us have apparently not had an adverse reaction to the first
three, four, ten or even twenty courses of quinolones over several
years, but later on symptoms indicative of an adverse reaction
culminate to the point where the patient is completely intoxicated
from the quinolone. Many, many young, healthy and athletic patients
just change in a short period of time from being the idyllic human
model for every drug manufacturer, to be intoxicated for many years
or life, and then are labelled as psychotic, a hypochondriac, or
diagnosed with serious neuropathies and pains that "were just lying
dormant."
That is simply not true. The fluoroquinolones are toxic from the first
milligram. Some people have body tissues that are more resistant
than others, but everybody becomes intoxicated. Each person has
two different potential thresholds of resistance to the damage caused
by quinolones:
LOWER THRESHOLD
Has been exposed above. It is delineated by strange bouts
of tendinitis, abnormally long recoveries after exercise,
less sleep and poorer quality sleep, some small throbbing
pains in different parts of the body, occasional twitching,
feeling some stiffness, decreased tolerance to coffee, loss
of memory, specially short-term.
UPPER THRESHOLD
The symptoms that you have experienced are those
corresponding to the severe reactions, intermediate
reactions and mild reactions. It is too late to expect a rapid
resolution, and according to the level of the intoxicationlong,
hard and miserable times may lay ahead.
The toxicity of quinolones acts in two preferential ways:
.. direct chemical destruction (cartilage, cellular functions
and organs).
.. mild, long-lasting or irreversible vasculitis, with

QUINOLONE ANTIBIOTICS TOXICITY. Dec 2003
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neuropathic after effects.
Obviously, you will not find many doctors willing to admit these two
phenomena do actually occur. But the sooner more research is
conducted in that direction, the further we will advance in terms of
understanding the problem.
The following section of the report deals with some of the most
important problems caused by quinolones.
THE VASCULAR CONNECTION
This point of the report is a hypothesis on the ultimate cause of the
floxing syndrome. We cannot aim to discover anything of medical
importance. But we can argue about some ideas that correspond well
with t our experiences, the clinical symptoms and that allow us to
favor some habits and avoid others in our daily lives, with some
basic understanding about the why and why not.
Although it is not generally accepted, we think that one of the main
damaging paths used by fluoroquinolones is vascular. There are
many scientifical papers that relate vasculitic events induced by
quinolones but they are presented as exceptional happenings.
However, the quinolones provoke unfailingly a specific sort of
vascular lesion.
Arteries are composed of 3 layers. The intima is composed of the
endothelium and underlying subintimal connective tissue. The media
is composed of the internal and external elastic lamina surrounding
the smooth muscle. The adventitia lies at the outermost area
comprised of connective tissue in which nerve fibers and vasa
vasorum (small vessels) are dispersed.
The vasa vasorum exist within the substance of the end organs.
These vasa vasorum include the capillaries, that are approximately
the size of a red blood cell and they do not have the media layer. The
very small vessels that surround and supply the nerves are called
vasa nervorum.
The quinolone antibiotics either alter the capillaries permeability, or
induce the deposition of immunological complexes inside them, or
cause a spasm-like narrowing of their ducts. In any case, the result is
the same. Small vessels in muscles, skin, nerves, heart, brain and
other organs are deprived of blood flow (ischemic), or now having
lesions, and they die or do not work properly. Therefore, in this
report we define vasculitis as an inflammation of the vessel walls
with vascular damage or attendant tissue injury.
What nobody knows and requires much more research are the factors
that determine the duration of disease, the type of tissues involved
and their damage, as well as how to target therapies at inflammation
without interfering with healing.
Accumulation of inflammatory cells in the vessel wall is the common
feature of vasculitis, although it is not well understood how tissue
damage occurs. It is widely admitted that there is a three-stage
process:
.. initiation of the injury
.. recruitment of inflammatory cells and tissue damage
.. regulation of the immune response.
Quinolone vasculitis is a systemic vasculitide (so called because of
their multiorgan nature). Inflammation and damage can be transient
or more permanent. The alterations in coagulation and vasomotor
tone result from local damage to the endothelium as well as intrinsic
components of the cytokines that are released through the process.
Drug toxicities are among the causes and processes strongly
associated with vascular injury. Immune complexes with certain
immuno-chemical characteristics activate a complementary cascade
that induces neutrophil mediated damage to the vessel wall. The
presence of granulocytes is usually associated with fibrinoid necrosis
as would be expected on the basis of their release of toxic enzymes
during inflammation. Necrosis in the vessel wall is a large
contributor to scarring and the delayed sequelae present in some
cases of vasculitis like the quinolone-induced vasculitis.
Normally, quinolone vasculitis appears some time after exposure,
and is a link in the chain of adverse events that take place for months
on end. All of the vasculitides are likely secondary to some form of
inflammatory stimulus, usually infectious or toxic, like in our case.
In quinolone vasculitis the underlying real cause either cannot be
identified (no doctor is willing to admit that quinolones are the direct
cause of vascular disorders) or has long since been cleared by the
host, leaving only a chronic or recurrent inflammation centering on
the vasculature.
Overall, vasculitis secondary to a defined infection or toxin is clearly
the most frequently encountered vasculitis and an important etiology
in peripheral nerve vasculitis. Toxins as a cause of vasculitis are
increasingly established. Because quinolone vasculitis is so varied in
its presentation and clinical pace, early identification may be
difficult. In this vasculitis, neuropathies are frequent, occurring in
80%-100% of patients. Mononeuropathy multiplex is the most
distinctive pattern, although nerve alterations of other kinds are very
common too (twitching, throbbing, pins and needles, numbness,
sensory polyneuropathies). See the paragraph devoted to
neuropaties.
There is the issue of diagnosis. The diagnosis of vasculitis is
fundamentally an invasive process. Identification of inflammatory
cells that diminish the delivery of blood to tissue is a critical feature.
Furthermore, the numerous causes that may result in vasculitis can
often be distinguished only at the cellular level. Histological studies
characterizing lesions on the basis of the infiltrating cells may
provide information on both the mechanisms inducing inflammation
and predict the sequelae of the lesions. There is an urgent need to
determine the underlying mechanism for appropriate treatment.
For most floxies the blood studies may be entirely normal. There is
no serological test that confirms or excludes a vasculitis. Quinolone
vasculitis is:
.. seronegative (non-ANCA, negative SSA, SSB, anti-Sm, normal
anticardiolipine, antiphospholipid, soft muscle markers,
halotypes....)
.. drug-induced, non-abating with drug withdrawal, and typically
reaches its acute phase many months after drug discontinuation.
.. not responsive to any known treatment; very long lasting or
permanent.
So, in summary, blood ducts spread in smaller and smaller conducts,
called arterioles and venioles. The real ends of them reach every part
of the body and the red blood cells have to circulate through them
almost in single row. The former ducts bring the oxygen and the
nutrients and the latter ones collect the by-products and CO2 (carbon
dioxide) resulting from cell activity.
There are zones with very little arteriole and veniole supply:
cartilages, tendons, nerves and connective tissue. Due to the
vasculitis caused by quinolones, the inner diameter of the conducts is

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narrowed. The result is that the vessels cannot correctly supply the
tissues or take away the waste. The consequences are:
.. lack of blood supply (injury to vasa nervorum) in nerves that
cause intense neuropathy like numbness, tremors, twitching,
tingling, and neuritis.
.. lack of blood supply to cartilage, in addition to the toxic assault,
causes necrotizing, and erosion with osteoarthritis in weightbearing
joints.
.. lack of blood supply in tendons and overuse with daily
movements causes tendinitis.
.. heart arrythmias, palpitations, poundings, that last for years and
in some cases require the implantation of a pacemaker. Many
deaths have been associated with quinolone-induced
cardiopathies.
.. poly-myositis and muscle destruction are frequently seen in
severe reactions.
.. lack of blood supply in the extremely narrow ocular vessels
causes sparkling, zig-zagging, wandering small lights. Floaters
are a result of dying cells due to lack of blood supply. Many
floxies get ischemic areas in the outer margins of the retina.
Optic neuritis is very common.
.. temporary and complete loss of vision, occurring in some cases
from month 5 to month 13th: lack of irrigation of the eyes.
.. lack of blood supply near the skin in the more distant areas of
the body and a tendency to have cool feet and hands
This vasculitis seems to be an autoimmune disease and for short
treatments is responsive to most conventional treatments such as
corticosteroid therapy, immunosuppressive drugs, and the like. In the
case of a severe reaction, long-term treatments with corticoids are
contraindicated (increase very much the likelihood of experiencing a
tendon rupture) and also ineffective.
The search for a non-invasive marker for vasculitis remains
disappointing. Some of the most effective treatments for quinoloneinduced
toxicity are substances with a strong vasodilation activity or
active blood thinners. On the other hand, substances with
vasoconstrictive properties are nearly always detrimental for floxies
and induce relapses, an increase of symptoms and delayed
recoveries.
Remember:
Your problems after the reaction are the tip of the iceberg. The quinolones
have damaged in different degrees all your body systems.
VASCULITIC RASHES
Many severe cases of intoxication by quinolones have a skin rash
present. There is a predilection for the distal ends of the limbs: hands
and feet. The following picture is an example of a vasculitic rash
induced by ciprofloxacin in a young athlete.

These rashes tend to resolve spontaneously, but signal serious
reactions to quinolones.
In all, about 15% with severe or intermediate adverse reactions to
quinolones actually develop a vasculitic rash.
-Picture 1- The points marked as "B" are red points, like pustules but with no
secretion. The point marked as "C" is a purple type of hematoma.
NEUROLOGICAL IMPLICATIONS
The longest lasting damages from quinolones are perhaps the
neurological alterations. Neurotoxicity is a common feature of all
quinolones since such adverse reactions have been described with all
derivatives so far known. Some research suggests that they are due
to the neuromuscular blocking effects of quinolones. Maybe they are
secondary (a consequence) of the vasculitic mechanism.
Neuropathies are a prominent feature of the toxic vasculitides. The
reasons for this frequency are not immediately clear. The rich blood
supply and the capacity of nerves to function reasonably well with
anaerobic (no oxigen) metabolism normally render the nerve
relatively resistant to ischaemia (disruption of blood supply). The
immediate cause of the vasculitic neuropathies is inflammation or
deposition of inmuno complexes that eventually harden, thicken, and
develop scar tissue, decreasing the diameter and impeding blood
flow with occlusion of the vasa nervorum resulting in ischaemia of
the peripheral nerve that end up damaged or dead. This category of
nerve damage, in which isolated nerves in different areas are
damaged, is called mononeuropathy multiplex or multifocal
mononeuropathy.
On top of that, nearly all the floxies have peripheral neuropathy.
Peripheral neuropathy describes damage to the peripheral nervous
system, the vast communications network that transmits information
from the brain and spinal cord (the central nervous system) to every
other part of the body and viceversa. Because every peripheral nerve
has a highly specialized function in a specific part of the body, a
wide array of symptoms can occur when nerves are damaged. Some
people may experience temporary numbness, tingling, and pricking
sensations (paresthesia), sensitivity to touch, or muscle weakness.
Other floxies, particularly in severe reactions, may suffer more
extreme symptoms, including burning pain (especially at night, very
exacerbated by heat), muscle wasting, paralysis, or organ or gland
dysfunction. People may become unable to digest food easily,
maintain safe levels of blood pressure, sweat normally, or experience
normal sexual function.
Some forms of neuropathy involve damage to only one nerve and are
called mononeuropathies that in many cases are difficult to recognize
properly and thus are diagnosed as normal musculoskeletal lesions.
Sometimes two or more isolated nerves in separate areas of the body
are affected-called mononeuritis multiplex. Often though, multiple
nerves affecting all limbs are affected-called polyneuropathy. Toxic
drug-induced neuropathy usually involves nerves on both sides of
the body, although not always symmetrically (many floxies get far
more rigid and painful on one side), and pain is a common symptom.

QUINOLONE ANTIBIOTICS TOXICITY. Dec 2003
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The neuropaties that we experience are predominantly asymmetrical
and they migrate around certain areas of the body, with a marked
predilection for lower limbs and distal areas (hands, feet).
In short, quinolones damage both central and peripheral nervous
systems. It is very typical to feel pin and needles sensations, as well
as throbbing pains, numbness, trembling, fasciculations (crawling
under the skin), tremors, twitching, and neurological pains migrating
all along the body. In most floxings the associated pain typically
does not respond to simple analgesics, and can become chronic and
may interfere with sleep (more intense in hot areas of the body) and
be present also at rest. Neuropathic pain is difficult to control and
can seriously affect emotional well-being and overall quality of life.
As has been shown earlier, insomnia, nervousness, anxiety,
overreactions to stress, anger and anguish are also very common.
The damage is very extensive and symptoms fit well in many
neurological subdiseases like all kind of peripheral neuropaties:
mononeuritis muliplex, sensorimotor neuropaties, demyelinating
neuropaties, axonal neuropaties, autonomic nerve damage, and many
more specific disorders. Central system neuropaties affect many
organs like heart, eyes, brain and intestines.
PERIPHERAL NEUROPATHY
Peripheral neuropathy, affects a variety of peripheral nerve cells and
fibers, including sensory (temperature, touch, vibration...), motor
(muscles), and autonomic (orthostotic pressure, erection) fibers.
Most quinolone induced peripheral neuropathies affect all fiber types
to some extent. However, a single fiber type may be predominantly
or exclusively affected in some cases producing very particular
neuropaties. In some floxies, peripheral neuropathies involve single
peripheral nerves (single=mono neuropathies), or numerous
individual peripheral nerves, the so-called mononeuritis multiplex
syndrome. In addition, peripheral nerve disorders may involve the
brachial plexus, lumbosacral plexus, or a single root, that is to say,
the low spine, resulting in signs and symptoms in one limb, with
pains that can be excruciating. Most cases of floxing conform to a
polyneuropathy syndrome, which usually implies both sensory and
motor fiber involvement in a relatively symmetric fashion and
typically with a distal-to-proximal gradient of involvement (more
intense the more distant from the trunk). These conditions are termed
sensorimotor polyneuropathies, and they represent the most common
form of peripheral neuropathy.
Quinolones can induce pathologic reactions in the nerves: wallerian
degeneration, axonal degeneration, and segmental demyelination. In
wallerian degeneration, the axon degenerates distal to a focal lesion
that interrupts the continuity of the axon. This reaction often occurs
in focal mononeuropathies that result from nerve infarction as a
result of a schemic vasculitic process. The toxicity plus the ischemia
interfere with nerve metabolism. They affect the longest neurons
first, since long neurons have greater metabolic demands than short
ones. Symptoms therefore may begin in the feet, then progress up
the legs and then affect the hands. It is a typical pattern.
Axonal (rod) degeneration, starts at the most distal (distant from the
trunk) extent of the axon. Axonal degenerative polyneuropathies are
usually symmetric, and are not common in floxings. However
floxies show predominantly signs of segmental demyelination, that
refers to focal degeneration of the myelin sheath with sparing of the
axon. This reaction can be seen in focal mononeuropathies but also
in generalized sensorimotor or predominantly motor neuropathies.
Toxic segmental demyelinating polyneuropathies might be the result
of the inmunological reaction.
In those peripheral nerve disorders that are characterized by either
wallerian degeneration or axonal degeneration, prognosis (likely
outcome) is less favourable due to the fact that the axon must
regenerate and reinnervate muscle, the sensory organ, blood vessels,
and other structures before clinical recovery is noted. Recovery may
be more rapid with segmental demyelination because remyelination
is accomplished more quickly, in turn reestablishing normal
conductivity of the axon and return of function.
It is easy for the floxie to feel and describe the symptoms of his/her
peripheral neuropathy.
Sensory symptoms: Sensory symptoms include sensory loss, a sense
of numbness, tingling, prickling, and pins-and-needles sensations,
pain, thermal sensation, vibratory sense and intolerance to light
touch. Damage to large sensory fibers lessens the ability to feel
vibrations and touch, resulting in a general sense of numbness,
especially in the hands and feet. People may feel as if they are
wearing gloves and stockings, or having the foot in a cast. In most
generalized polyneuropathies, these symptoms begin in the most
distal (far from the trunk) extent of the longest sensory fibers, like
the toes and feet and then crawl their way up to the knees point in
which the disorders also starts at the fingertips spreading the process
to the upper extremities. In addition to sensory loss, patients
frequently complain of paresthesias and dysesthesias, often
characterized by a sense of numbness. Pain is a serious symptom for
many floxies. It may be described as a dull aching sensation, an
intense burning sensation or, occasionally, as intermittent lancinating
pulses of pain (called throbbing in this report).
Motor-muscle: Muscle weakness is the most common symptom of
motor nerve damage. Other symptoms may include painful cramps
and fasciculations (uncontrolled muscle twitching visible under the
skin), muscle loss, bone degeneration, and changes in the skin, hair,
and nails (these more general degenerative changes also can result
from sensory or autonomic nerve fiber loss). Impairment of motor
function typically begins with weakness in the toes, and as the
polyneuropathy progresses, ascends up the distal lower extremities to
the level of the knees, at which time motor involvement in the hands
may be observed.
In the toxic segmental demyelinating polyneuropathies, proximal
muscle (quads) weakness resulting from root
(polyradiculoneuropathy) involvement may be observed. Axonal
degenerative polyneuropathies tend to produce weakness along with
muscle atrophy, but atrophy is much less conspicuous in segmental
demyelinating polyneuropathies because in these disorders the axon
remains in continuity with the muscle, preventing denervation
atrophy. Therefore, your doctor can measure your thigs perimeter
and tell you that finds both the same size, eventhough you feel your
painful one nearly useless, soft, iddle and deprived of strenght.
The most common symptom (but not unniversal) in severe floxing
polyneuropathy is weakness in dorsiflexion of the great toe. That
disability is somehow a measure of the initial severity of the
polyneuropathy.
Autonomic nerves: Some floxies report symptoms that evidence that
autonomic fibers are also affected. Symptoms of autonomic nerve
damage are diverse and depend upon which organs or glands are
affected. Autonomic nerve dysfunction can become life threatening
when the heart begins beating irregularly (extremely common in
floxies) or there is difficulty with breathing. Other common
symptoms of autonomic nerve damage include an inability to sweat
normally (floxies notice reduced or absent sweating in the legs and

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hands, and at the same time excessive sweating confined to the head
and neck region), a partial loss of bladder control and an inability to
control muscles that expand or contract blood vessels to maintain
safe blood pressure levels. A loss of control over blood pressure can
cause dizziness, lightheadedness, or even fainting when a person
moves suddenly from a seated to a standing position (orthostatic
hypotension).
In severe floxings other autonomic symptoms include dryness of the
eyes and mouth (another marker of the severity of the floxing) and
gastrointestinal dysmotility (nerves controlling intestinal muscle
contractions often malfunction), often manifested by alternating
constipation and diarrhea or by early satiety. Many people also have
problems eating or swallowing if certain autonomic nerves are
affected. In intermediate and severe floxings in men, partial erectile
dysfunction or incontinence is one of the first autonomic symptoms.
Diagnosis. Such a vast array of presentations of peripheral
neuropathy in floxies makes precise diagnosis a challenging task and
is the reason that physicians get to different conclusions depending
on the predominance of the axon/myelin, phocal/diffuse,
symmetric/asymmetric, sensory/motor/autonomic involvement, and
adding the difficulty posed by the fact that floxies develop all of
them in different grades.
Doctors may order a set of tests to evaluate your disorder: nerve
conduction studies, needle electrode examination, brain and spine
MRI, lumbar puncture for cerebrospinal fluid analysis. Blood and
urine works can include glucose tolerance test, vitamin B12, serum
protein, anti-GM1 antibodies and anti-myelin antibodies, plus
investigations of markers of various connective disorders associated
with vasculitis. The ultimate analysis is a nerve biopsy, that when
performed with the most advanced technics by well trained
physicians can assist in the complete characterization of the lesions.
It is an invasive procedure and few floxies have undertaken it
because is mainly ordered only in severe reactions and when a
diagnosis of vasculitis or inmune reaction of other sort is being
considered. Less common are precision sensory testings, and studies
of sudomotor function, and autonomic responses to provocative
physical maneuvers.
In many cases the electrical conductivity tests render normal results,
as well as MRIs of the brain and spine, and spinal taps. But it is also
very typical that well conducted studies discover alterations in the
sensory and motor status of the nerves in many parts of the body.
Muscles also show decreased responses in electromyographic
(EMG) studies.
Other very common findings are decreased or altered signals in the
nerves that control the hands, especially the ulnar nerve. You will
know that your ulnar nerves are affected if your small and ring
fingers become numb, normally if you exert pressure around your
elbow or when bending your elbows sleeping at night. Some doctors
will tend to diagnose you as having ulnar or carpal tunnel syndrome,
but you are really suffering toxic ulnar neuritis.
Other nerves very commonly implicated are the nerves of the legs.
Pains occur predominantly in the hamstrings, lateral or medial knees,
outer gluteus, calves, quads, groin, and several areas of the ankle,
plus the toes. Many times pains mimic strains, tendinitis, muscular
fiber disruptions, sprains, but they are toxic neuritis.
Remember:
In severe reactions neurological pains can last for years and impair your
life’s quality.
In general, we have multiple peripheral nerve lesions. They can
occur sequentially and in a random fashion (now the upper left leg,
then the right ankle, ..). As said before, the earliest findings are loss
of vibratory sensation in the toes, atrophy of intrinsic foot muscles,
and reduced or absent ankle jerks. In severe reactions there are signs
of lower motor neuron lesions: weakness, more generalized atrophy
and fasciculations.
Double or triple mononeuritis dominates in intermediate reactions.
For instance, the right leg (hamstring and ankle-Achilles) plus heart
arrhythmias and perhaps an elbow epicondylitis. Multiple neuritis is
more typical of severe reactions. For instance, this includes the right
leg, plus heart disorders, plus elbow, shoulder, hips, wrists, and
above all- optic neuritis.
Optic neuritis reflects a lesion of the optic nerve and is a secondary
effect of the damage caused by the quinolones to the small blood
vessel complexes of the eye (in fact is an ischemic optic
neuropathy). The optic nerve dysfunction usually manifests with
blank spots, difficulties in focusing, and in severe cases transient
complete losses of vision with a solid white vision in one or both
eyes. These blindness episodes have been reported with
ciprofloxacin and last for some minutes, are very scaring, appear
suddenly, so they are also dangerous depending on the activity upon
which the floxie is on. These blindness events can happen
periodically up to 18 months after the treatment with ciprofloxacin
and at any time for the following years if the floxie gets a high reexposure
to quinolones through poultry ingestion for instance.
If the intoxication of the quinolones has been intermediate, these
neurological symptoms tend to dissapear in two years time on
average. If the intoxication has been severe, the neurological
disorders linger on for many years without abating, although for the
4th or 5th year mark the floxie can experience an improvement.
CONSTANT PAIN ALL OVER. MYALGIAS
Besides the neurological pains, in severe reactions constant, intense
and spread all over pains are very common. Basically they are drug
induced myopathies, again probably secondary to the vasculitic
reaction. The major symptoms in drug induced myopathies are
proximal muscle weakness (quads, hamstrings, shoulder, biceps,
triceps), increased muscle enzyme levels, electromyographic
changes and histological lesions. Quinolones induce painful
myopathies associated with neuropaties, that could be called painful
neuromyopathies. It is typical of these neuromyopaties a free period
between the beginning of the treatment and the appearance of
symptoms, and incomplete resolution after withdrawal of the
treatment.
OTHER DISORDERS YOU MIGHT EXPERIENCE
Quinolones are very toxic drugs for the liver, pancreas and kidneys.
Half of the quinolones marketed since their creation have been
withdrawn from the market because of their potentially fatal toxic
profile. Some had a marked inclination to destroy the liver
(trovafloxacin), others the heart, and all are very toxic to vital organs
as a class effect. It is not uncommon to get abnormal results in serum
tests for many months after discontinuation of the drug.
On top of the general problems that you may have due to the toxicity
of the quinolones, many people have additional problems, due to

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alterations of functions or systems that were working well but in
delicate equilibrium before taking the quinolones. For instance, if
without knowing it you suffered a little osteoarthritis because of
overuse during your endurance sports, a short leg, asymmetrical
muscle mass, lack of flexibility or the like, all of them will become
very noticeable when your floxed body cannot compensate for any
minor flaw.
When you suffer strong quinolone-induced neuropathies of the
extremities, you will experience atrophy (wasting) of the main
muscles. Sometimes it is very difficult to detect unless tested by a
professional. Muscles most frequently subject to wasting are the
tibialis anterior, soleus, gastrocnemius, vastus medialis, the other
quadriceps muscles, shoulder and forearm muscles.
Atrophy of the muscles that control a joint make this joint more
prone to injury, normally from repetitive loads. So the vicious cycle
starts: the neurological lesions waste the muscles, so joints are
overloaded, or eccentrically or abnormally loaded, and they degrade,
creating another layer of pains and disability that blends with the
previous one and that contribute to a never ending “snowball effect”
injury.
So, it is important that