Targeting Bacterial Gas Defenses Allow for Increased Efficacy of Numerous Antibiotics ScienceDaily (Nov. 17, 2011) � Although scientists have known for centuries that many bacteria produce hydrogen sulfide (H2S) it was thought to be simply a toxic by-product of cellular activity. Now, researchers at NYU School of Medicine have discovered H2S in fact plays a major role in protecting bacteria from the effects of numerous different antibiotics.
In the study led by Evgeny Nudler, PhD, the Julie Wilson Anderson Professor of Biochemistry at NYU School of Medicine, researchers found evidence that H2S acts as a general defense mechanism against oxidative stress, the process through which many antibiotics kill bacteria.
This information provides the basis for developing new techniques to suppress this universal bacterial defense mechanism and make bacteria more susceptible to antibiotics at lower doses. It also paves the way for reversing antibiotic resistance in human pathogens such as Staphylococcus, Pseudomonas, E. coli, and many others.
The study's findings were published online on November 17 edition of Science.
"Surprisingly little has been known about H2S biochemistry and physiology in common bacteria" said Dr. Nudler. "We are excited about the potential impact this research may have on the growing problem of microbial resistance. These findings suggest a conceptually new approach, an adjuvant therapy that targets bacterial gas defenses and thus increases the efficacy of many clinically used antibiotics."
More specifically, the study showed that integrated mechanism of H2S-mediated protection against oxidative stress also protects against antibiotics. The research provides direct support for the emerging concept of the pro-oxidative action of many antibiotics.
In addition, the study demonstrates that bacteria that generate both H2S and nitric oxide (NO) simultaneously, such as B. anthracis (a causative of anthrax), cannot survive without both gases, even under normal growth conditions. One gas makes up for the lack of the other and at least one of them is essential.
In a previous study Dr. Nudler and his colleagues demonstrated that NO plays a similar role in protecting bacteria from antibiotics (Science September 9, 2009). However, because NO is present in only a limited number of bacteria while hydrogen sulfide synthesis occurs in essentially all bacteria, the practical implications of this new finding is extremely wide-ranging.
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9 But he said to me, �My grace is sufficient for you, for my power is made perfect in weakness.� Therefore I will boast all the more gladly about my weaknesses, so that Christ�s power may rest on me. Posts: 1445 | From Poconos, PA | Registered: Jul 2004
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Hydrogen sulfide gas can be bound with pink bismuth (i.e. Pepto Bismol). I wonder if this would be helpful to take with antibiotics?
Posts: 929 | From Massachusetts | Registered: Oct 2007
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Interesting study. Thanks for posting Sherry. -------------------------------------------
In small doses pepto bismol is probably ok, but bismuth is actually toxic in large doses.
And it can be absorbed via the G.I. tract especially if you have a leaky gut.
Hubby took low doses for about a week once to try to calm nausea or G.I. pain -- anyway it just so happened that he did a chelation challenge test and had elevated levels of bismuth.
And the combination of the EDTA plus bismuth caused increased seizure-like activity and aggravated his movement disorder issues.
There is an old Townsend Letter for Doctors article about treating lyme with IV bismuth in Mexico. And at least one U.S. doc is in prison I think for allegedly killing a patient with this treatment.
Bea Seibert
Posts: 7306 | From Martinsville,VA,USA | Registered: Oct 2004
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Well, obviously, killing a patient with a treatment is not good! However, if bismuth could provide a more total kill, it may eliminate the need for taking antibiotics long-term.
It turns out there is already some research done in this area, so I think this is worth looking at:
The effect of antibiotics and bismuth on fecal hydrogen sulfide and sulfate-reducing bacteria in the rat
Hiroki Ohge1,*, Julie K Furne2, John Springfield2, Taijiro Sueda3, Robert D Madoff1, Michael D Levitt2
Article first published online: 9 JAN 2006
DOI: 10.1016/S0378-1097(03)00748-1
Abstract
Colonic bacteria produce the highly toxic thiol, hydrogen sulfide. Despite speculation that this compound induces colonic mucosal injury, there is little information concerning manipulations that might reduce its production. We studied the effect of antibiotics and bismuth on the production of hydrogen sulfide in rats.
Baseline fecal samples were analyzed for hydrogen sulfide concentration and release rate during incubation and numbers of sulfate-reducing bacteria. Groups of six rats received daily doses of ciprofloxacin, metronidazole, or sulfasalazine for one week, and feces were reanalyzed.
Bismuth subnitrate was then added to the antibiotic regimens. While sulfide production and sulfate-reducing bacteria were resistant to treatment with ciprofloxacin or metronidazole, bismuth acted synergistically with ciprofloxacin to inhibit sulfate-reducing bacteria growth and to reduce sulfide production.
Combination antibiotic�bismuth therapy could provide insights into the importance of sulfide and sulfate-reducing bacteria in both human and animal models of colitis and have clinical utility in the treatment of antibiotic-resistant enteric pathogens.
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I think the question would be how long/how much would be needed to facilitate more complete killing of the bugs. But the article below outlines some of the dangers of allowing hydrogen sulfide to go unchecked in the body.
The ME/CFS doc mentioned below has found hydrogen sulfide gas in patients with ME/CFS, with higher levels corresponding to severity of illness -- it would be interesting to see if this is similar with Lyme (he does testing and is in Belgium):
ME/CFS breakthrough - Hydrogen sulfide as a central mechanism
23 June 2010 ABSTRACT OF UPCOMING JOURNAL ARTICLE � Preliminary Draft The De Meirleir research team will also publish a journal article on their work. The following draft was disseminated via the CO-CURE listserv May 28 2009.
Research on Extremely Disabled M.E. Patients Reveals the True Nature of the Disorder By Kenny De Meirleir(1), Chris Roelant(2), Marc Fremont(2), Kristin Metzger(2), Henry Butt(3)
(1) Vrije Universiteit Brussel & HIMMUNITAS foundation, Brussels, Belgium (2) Protea Biopharma, Brussels, Belgium (3) Bioscreen & Bio 21, University of Melbourne, Melbourne, Australia
In this study we compared totally bedridden patients (Karnofski score 20-30) with less ill ME patients (Karnofski score 60-70), family controls, contact controls and non-contact controls.
EBV, HHV6 and Borna virus titers were not different in the three groups. Plasma LPS distinguished the groups, with the highest values in the bedridden patients.
LPS [lipopolysaccharide] is a strong activator of the immune system, and high plasma concentrations suggest a hyperpermeable gut. There are many possible causes for this, but a lack of 'local' energy production is one of them.
In a separate study (In Vivo, in press) we observed intestinal overgrowth of Gram positive D/L lactate-producing bacteria which are also known to produce H2S [hydrogen sulfide] in presence of certain heavy metals as a survival defense mechanism.
We therefore hypothesized that the urine of the bedridden ME patients would contain more H2S derived metabolites than the less ill and the controls. Using a proprietary simple color change urine test this hypothesis was confirmed.
In the extremely ill, urine added to the yellow color reagent immediately turns dark blue, whereas in the less ill the reaction is slower and in the controls no reaction occurs.
Being a potent neurotoxin, H2S induces photophobia, intolerance to noise, mitochondrial dysfunction by inhibition of cytochrome oxidase, and depresses the cellular immune system and induces neutropenia and low numbers of CD8+ lymphocytes.
Its effects, at least in part explain the clinical condition of the severely disabled ME patients.
Furthermore the effects of the bacterial H2S induces increased ROS production by the liver and retaining of heavy metals particularly mercury in the body.
The latter is also neurotoxic, induces apoptosis, and interferes with the aerobic metabolism. Chronic increased production of H2S by intestinal bacteria leads to build-up of mercury in the body as proven by a Zn DTPA/DMPS challenge test.
Finally in 20% of the ME patients (in the severely ill) we found, using a special luminescence technique, aberrant prions which also interfere with the energy metabolism.
These patients have gone on to develop A.P.D. (aberrant prion disease � patent pending). These aberrant prions give rise to a transmissible disorder. 10% of the A.P.D. patients have very high prion counts in their saliva and can directly transmit it to others.
APD patients can transmit these proteins via blood and likely also through sexual contact which then can give rise to slowly developing aberrant prion disease.
In a separate experiment 40 healthy blood donors were screened for A.P.D. One individual tested very positive, indicating that apparently healthy individuals can already be carriers and that blood transfusion carries the risk of transmitting A.P.D.
In conclusion, ME is a disorder which is caused by increased endogenous H2S production. For the latter many factors can be present.
Because of the effects of H2S in the body a chain of events will develop which have more and more negative effects on the aerobic metabolism and depression of the immune system leading to more and more infections and reactivation of endogenous viruses.
In its final stage aberrant transmissible prions develop which put the patients in a total energy depleted state.
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sparkle7
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re: In a separate study (In Vivo, in press) we observed intestinal overgrowth of Gram positive D/L lactate-producing bacteria which are also known to produce H2S [hydrogen sulfide] in presence of certain heavy metals as a survival defense mechanism.
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It seems everything I'm reading these days relates to heavy metal toxicity...
Thanks for posting!
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