Comments on fluoroquinolone toxicity by LG Lindsay, a Levaquin ( Levofloxacin ) victim.

Comments posted by LG Lindsay:

Fluoroquinolone (FQ) research articles are written in technical language that is gibberish to lay people who are not schooled in biochemistry, the genome and in molecular engineering.  Further, professional-grade research articles are generally available online only from fee-based medical research clearing houses.  Accordingly, FQ-poisoned “floxies” are screwed on both counts.  Firstly, a floxie cannot describe or fathom the nature of quinolone toxicity syndrome (QTS) because s/he is not conversant with its technology and mechanism of poisoning, and cannot articulate QTS in syntax that is understandable and acceptable to front-line medical practicioners. Secondly, even if a floxie could decrypt the technology, a floxie would have to roll the dice and hunt with his/her checkbook to find a for-fee research article that pertains to QTS. It’s the proverbial hunting for a needle in the haystack.  Separately, there is an economic disincentive that stifles profit-seeking pharmaceutical companies from making any disclosure whatsoever that might adversely effect sales. Pharmaceutical research, development and marketing survives as an on-going enterprise in an economic system that takes no prisoners. In this regard big pharma is no different than other legal corporate entities whose duty lies with increasing their shareholders’ larder while limiting their  liability.  It’s that simple. Short of a clear, verifiable test by which a causal chain can be established between FQs and QTS — whose causality is clear on its face to plumbers, butchers and candlestick makers —- QTS will continue to rumble through unopposed and occasionally wreak havoc with  the sick and medicated.  There’s really no stopping it unless floxies can enlist the help of biochemical, genetic and molecular researchists who can explain succinctly FQ technology and its downside association with QTS.

You know the drill.  Daily we scroll through dozens or hundreds of on-line articles of unknown quality that are written in specialized, arcane language of technologists.  Someone pays for generating these research articles.  It’s NOT floxies who originate and underwrite FQ research.  We’re not really sure who underwrites FQ researchists whose identities and motivation are hidden beneath soporific, sophmoric and vaguely reassuring nonprofit names that are reminiscent of lobbying firms on “K” Street in Washington, DC that routinely advocate legislation to legitimate their clients’ inalienable right for succor and liability-free profits.

And, so, we remain thirsty patients drilling frantically through scientific bolsons that remain just out-of-reach on the internet.  We pray to wrest a few drops of moisture from medical aquifers whose salvation and knowledge remain hidden deep underground and seemingly impregnable to our blunt drill.

I offer exhibit “A” (below) or  ”how I tried to penetrate fee-free research into the effects of fluoroquinolones upon dogs.”  Yup, that’s right, how FQs adversely effects canines.  It’s the only research I found that I vaguely could understand.  I’m not sure whether it says a lot about me, about dogs, about the pharmaceutical industry or about pharma-researchists.  But it says a lot about the human condition.  

“A Fluoroquinolone Induces a Novel Mitogen-Encoding Bacteriophage in Streptococcus canis”

Kindly enter the URL
and witness how FQs induce a  new way to unleash chemical messengers that trigger cell division among proteins in viruses that, in turn, infect and destroy bacteria. (See the researchists’ discussion below.***)  So, here’s how it works: The guy in a white lab coat chemically tricks viruses to grow and multiply and then invade and kill bacteria cells.  But wait, according to the above-ref. article the FQs sometimes induce “recognized emergence of canine streptococcal toxic shock syndrome (STSS) and necrotizing fasciitis (NF).” Holy shit!  After Dr. Frankenstein starts cranking on a glow-plug that zaps the hapless suffering doggie in his care with a tincture of one-too  many “bacteriophages,” the targeted bacteria wither and go tits-up while sending the dog into shock and (ready for this?) into “necrotizing fasciitis (NF).” (Does NF remind you of the FDA’s black box warning about reported tendonitis and ruptures at the Achilles heal where the tendons melt-away and snap?)  All the ususal suspect and commonplace bacteria causing prostatitis or pelvic floor pain or UTIs have now become “flesh-eating” bacteria, and while the retard under Frankensteins’s direction can now piss without pain, damn it, the little bastard cannot stand up on his own two (or four) feet which have turned to goo!  You see that I have “anthropomorphized” the dog’s experience and minted it as human experience.  The dog arrives sick and departs sicker (so much for the “dog with two dicks,” this poor dog might emerge in shock because his pecker fell-off post treatment.)  The vet conversely arrives with empty pockets and leaves with jingle.  That’s my take on this one decrypted research article about a dog who started out with streptococcus bacterium, possibly a little anal itch, and ended up shocked and half-dead with flesh-eating bacteria gobbling up his pecker (just kidding!).  Imagine a dog trying to communicate his post-treatment condition to a veternarian, and you rightly understand how difficult it is for a floxie to communicate his CNS symptoms to a doctor, half of whose three-year residency expenses (according to a recent article in the New York Times) were underwritten by drug companies, who was never trained or equipped to deal with the unintended consequences of PhDs who speak in gibberish and play Frankenstein for employers who hide more half-baked research in numberless cybervaults than they unleash for profit on their unwary and gushing consumers.

See reference notes (below) drawn from Wikipedia.
Necrotizing fasciitis (NF), commonly known as flesh-eating disease or flesh-eating bacteria, is a rareinfection of the deeper layers of skin and subcutaneous tissues, easily spreading across the fascial plane within the subcutaneous tissue. Type I describes a polymicrobial infection, whereas Type II describes a monomicrobial infection. Many types of bacteria can cause necrotizing fasciitis (e.g., Group A streptococcus (Streptococcus pyogenes), Staphylococcus aureus, Vibrio vulnificus, Clostridium perfringens, Bacteroides fragilis). Such infections are more likely to occur in people with compromised immune systems.[1]

Historically, Group A streptococcus made up most cases of Type II infections. However, since at least 2001, another serious form of monomicrobial necrotizing fasciitis has been observed with increasing frequency.[2] In these cases, the bacterium causing it is methicillin-resistant Staphylococcus aureus (MRSA), a strain of S. aureus that is resistant to methicillin, the antibiotic used in the laboratory that determines the bacterium’s sensitivity to flucloxacillin or nafcillin that would be used for treatment clinically.

A mitogen is a chemical substance that encourages a cell to commence cell division, triggering mitosis. A mitogen is usually some form of a protein.

bacteriophage (băktÄ“r’Ä“É™fāj’), virus that infects bacteria and sometimes destroys them by lysis, or dissolution of the cell. Bacteriophages, or phages, have a head composed of protein, an inner core of nucleic acid-either deoxyribonucleic acid (DNA) or ribonucleic acid (RNA)-and a hollow protein tail. A particular phage can usually infect only one or a few related species of bacteria; for example, coliphages are DNA-containing viruses that infect only the bacterium Escherichia coli.

A virus infects a bacterial cell by first attaching to the bacterial cell wall by its tail. In coliphages the tail is a complex protein structure consisting of a hollow contractile sheath, with a plate at the base that contains long protein fibers. The tail fibers fix the base plate to the specific receptor site on the bacterial cell wall, and the tail sheath contracts like a syringe, forcing the DNA that is inside the virus through the cell wall and cell membrane. The entire virus protein coat remains outside the bacterium.

The injected nucleic acid is the viral genetic material; it makes use of the bacterium’s chemical energy and biosynthetic machinery to produce viral enzymes, as well as more phage nucleic acid. The viral proteins and nucleic acid molecules within the bacterial host assemble spontaneously into up to a hundred new phage particles. Eventually the bacterium lyses, releasing the particles. Lysis can be readily observed in bacteria growing on a solid medium, where groups of lysed cells appear as clear areas, or plaques.

Some DNA phages, called temperate phages, only lyse a small fraction of bacterial cells; in the remaining majority of the bacteria, the phage DNA becomes integrated into the bacterial chromosome and replicates along with it. In this state, known as lysogeny, the information contained in the viral nucleic acid is not expressed. A lysogenic bacterial culture can be treated with radiation or mutagens, inducing the cells to begin producing viruses and lyse. Lysogenic phages resemble bacterial genetic particles known as episomes. Incorporated phage genes are sometimes the source of the virulence of disease-causing bacteria.

The bacteriophage was discovered independently by the microbiologists F. W. Twort (1915) and Félix d’Hérelle (1917). The phages have been much used in the study of bacterial genetics and cellular control mechanisms largely because the bacterial hosts are so easily grown and infected with phage in the laboratory. Phages were also used in an attempt to destroy bacteria that cause epidemic diseases, but this approach was largely abandoned in the 1940s when antibacterial drugs became available. The possibility of “phage therapy” has recently attracted new interest among medical researchers, however, owing to the increasing threat posed by drug-resistant bacteria. In 2006 the Food and Drug Administration approved the use of  blah blah blah

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