¡Destruida!

25) new March 2011: http://www.jmedicalcasereports.com/content/5/1/104/abstract

They have a terrible safety record, quite disastrous. The reasons it's taken so long to become known (in some countries it's becoming known, but not Spain or the U.K!) are:

1. The adverse effects are not just sometimes, but nearly always delayed. They can start to be felt or noticed a few days, weeks, or months after exposure. (Two years in a few, rare cases.) Who , whether doctor or patient, would suspect an “antibiotic” (je je je) taken months earlier of causing completely new health problems in the present?
Molecular Pharmacology
Delayed cytotoxicity and cleavage of mitochondrial DNA in ciprofloxacin-treated mammalian cells.
http://molpharm.aspetjournals.org/content/50/5/1178.short

2. Tolerance levels. If you've previously used the same medicine or group of medicines, you don't expect to be debvastated by it next time.

3. The absurdity of the range and severity of adverse effects – hard to believe unless you know more. And people don't know more because it's hard to believe so no-one believes it so it doesn't become known!

4. Cunning/ignorant/careless misuse of language: antibiotic instead of synthetic anti-microbial; reaction instead of effect; UTI when no infection has been found..

5. The extraordinary power and influence of the pharmaceutical industry.

6. It isn't mandatory on physicians or anyone else to report adverse events. Many doctors don't even know where they're supposed to report, if they do know they seldom bother, and hardly any patients know they a right to or where. As hardly any doctors believe that the crazy horror is caused by Fqs, they don't even think of reporting it, so the ignorance continues in a vicious spiral.

Although it's truue that some people are very senstive to quins and others can take several courses before having a problem, there is no-one who cannot be damaged by them; it's a question of reaching one's limit, as far as we know (not proved, but empirically evident.) Some people are wrtecked forever by just one pill, but every day we get people arriving in the forums saying, “At last I know what's been wrong with me all these years,” and they've been “diagnosed” with a long list of maladies (depression, bi-polar syndrome, fibromyalgia, CFS ha ha, Sjrogen's (sp?) arthrosis and many more – most of which they have got, as most aren't real diagnoses, but just giving a name to a set of symptoms wiothout having a clue what caused them.) Very often, such people have been ill for 10 or 20 years or even longer and – this is the worst part – have been prescribed more fluoroquinolones since and just got iller and iller, but others are folk who've had several courses of an FQ without noticing any ill effects, then took just one tablet of the next 'scrip' and wham - the whole lot comes down on them.

Studies show that quite a short-term and low-dose exposure does damage cartilage and tendons; other studies already showed that the fibroblast production is dramatically lowered.. Well, just search anfd search, especially with Google Academic, and you can find a great many studies, more and more, coming thick and fast, now so many of us have complained and campaigned, naughty, squeaking guinea-pigs that we are. Eeeeek!

What are they?
Quinolones are not antibiotics; they are synthetic chemo-therapeutic broad-spectrum antibacterial agents. of which the first was produced accidentally 1962 as a result of alterations to a compound isolated from production of the antimalarial drug chloroquine. During the 1980s the fluorine atom was added to make fluoroquinolones, which are extremely potent, extremely fast-acting and have “excellent” penetration, including of the brain and bones. (Many of us were prescribed Fqs without even a sample analysis, not even a dipstick; many of us had no bacterial infection at all, let alone in our brains or bones.)

Antibiotics are compounds produced by bacteria and fungi which are capable of killing, or inhibiting, competing microbial species. This phenomenon has long been known; it may explain why the ancient Egyptians had the practice of applying a poultice of moldy bread to infected wounds. But it was not until 1928 that penicillin, the first true antibiotic, was discovered by Alexander Fleming, Professor of Bacteriology at St. Mary's Hospital in London.
Returning from holiday on September 3, 1928, Fleming began to sort through petri dishes containing colonies of Staphylococcus, bacteria that cause boils, sore throats and abscesses. He noticed something unusual on one dish. It was dotted with colonies, save for one area where a blob of mold was growing. The zone immediately around the mold—later identified as a rare strain of Penicillium notatum—was clear, as if the mold had secreted something that inhibited bacterial growth.
http://www.acs.org/content/acs/en/education/whatischemistry/landmarks/flemingpenicillin.html [i/]

Antibacterial chemotherapeutic agents: contemporary anti-infective chemotherapy: quinolone antibacterials https://s3.amazonaws.com/assets.prod.vetlearn.com/1a/a3a710678c11e0a3340050568d17ce/file/PV0710_zimmerman_CE.pdf

Fluoroquinolones: Then and Now
https://s3.amazonaws.com/assets.prod.vetlearn.com/1a/a3a710678c11e0a3340050568d17ce/file/PV0710_zimmerman_CE.pdf

What do they do, how do they work?
Here's a neat little video showing how FQs slaughter bacteria:

Fluoroquinolones act by inhibiting the activity of both the DNA gyrase and the topoisomerase IV enzymes. For most gram negative bacteria, DNA gyrase is the primary fluoroquinolone target. Fluoroquinolones have been shown to bind specifically to the complex of DNA gyrase and DNA rather than to DNA gyrase alone. As a result of this binding, quinolones appear to stabilize the enzyme-DNA complexes which in turn results in breaks in the DNA that are fatal to the bacterium. A second mechanism of fluoroquinolone action is shown here. With some exceptions, topoisomerase IV is the primary target of fluoroquinolone action in most gram positive bacteria such as Staphylococci and Streptococci, with DNA gyrase being a secondary target. The separation of 2 new interlinked daughter strands of circular DNA is disrupted. The final result on the bacteria, however, is the same. Bacterial replication is disrupted and the bacterium breaks apart.

Unfortunately, mitochondria are probably eveolved from bacteria that moved into or were taken into eukarytic cells to live in endosymbiosis and their DNA is similar – oops!

Molecular Biology of the Cell: The Mitochondrion
http://www.ncbi.nlm.nih.gov/books/NBK26894/

Mitochondria (singular mitochondrion) are abundant organelles present in nearly all eukaryotic cells . The main function of mitochondria is to produce adenosine triphosphate (ATP), the cellular energy source. Mitochondria are believed to be the evolutionary result of early anaerobic (nonoxygen-using) eukaryotic cells engulfing aerobic (oxygen-utilizing) bacteria, resulting in a symbiotic relationship between the two organisms. The eukaryotic cells received ATP in exchange for supplying nutrients to the engulfed bacteria, and the bacteria provided ATP and allowed the eukaryotic cell to survive in the increasing oxygen atmosphere present early in Earth's history.
http://www.biologyreference.com/Ma-Mo/Mitochondrion.html#ixzz3EJmO5oT6

http://www.newcastle-mitochondria.com/mitochondria/what-do-mitochondria-do/

It is now thought that Fqs may also cause breaks in nucleic DNA.
Here are some links forrm Google Academic about Fqs and central and peripheral nervous sytem damage: http://tinyurl.com/neec4tq

And here¡'s our friend Bob, who died in June this year, after seven years of CNS hell: http://youtu.be/Dk74NtLSqZo?list=PL5031C8B80502DD3C

Fun fun fun all the way with the gift that keeps on giving.

http://cid.oxfordjournals.org/content/32/Supplement_1/S9.full
Mechanisms of Action of Antimicrobials: Focus on Fluoroquinolones
Fluoroquinolone-Associated Tendinopathy: A Critical Review of the Literature
http://cid.oxfordjournals.org/content/36/11/1404.full
Intrinsic cytotoxic effects of fluoroquinolones on human corneal keratocytes and endothelial cells.
http://www.ncbi.nlm.nih.gov/pubmed/18157922
In Vitro Discrimination of Fluoroquinolones Toxicity on Tendon Cells: Involvement of Oxidative Stress
Fluoroquinolones: relationships between structural variations, mammalian cell cytotoxicity and antimicrobial activity
http://jpet.aspetjournals.org/content/308/1/394.full
(PMID:8652078)
Abstract
Hayem G, Carbon C
Clinique de Rhumatologie, CHU Bichat-Claude Bernard, Paris, France.
Drug Safety : an International Journal of Medical Toxicology and Drug Experience [1995, 13(6):338-342]
Type: Journal Article
DOI: 10.2165/00002018-199513060-00003
Abstract Highlight Terms
Diseases(5) Species(1)
.. Given the absence of an adequate model of tendinopathy and the poor predictivity of animal manifestations in arthropathy and cartilage lesions in humans, careful monitoring of patients during phase II and III trials and, more importantly, long term pharmacovigilance during the postmarketing period, are still strongly warranted.http://europepmc.org/abstract/MED/8652078


	"Quinolones are have been around for a while now and have a pretty good safety record." Quote from a G.P.

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