Or will it be a secret "resonant activation" center to fight the new superbacteria?
A bacterial colony may develop a small number of cells genetically identical to, but phenotypically different from, other normally growing bacteria. These so-called persister cells keep themselves in a dormant state and thus are insensitive to antibiotic treatment, resulting in serious problems of drug resistance. In this paper, we proposed a novel strategy to 'kill' persister cells by triggering them to switch, in a fast and synchronized way, into normally growing cells that are susceptible to antibiotics. The strategy is based on resonant activation (RA), a well-studied phenomenon in physics where the internal noise of a system can constructively facilitate fast and synchronized barrier crossings. Through stochastic Gilliespie simulation with a generic toggle switch model, we demonstrated that RA exists in the phenotypic switching of a single bacterium. Further, by coupling single cell level and population level simulations, we showed that with RA, one can greatly reduce the time and total amount of antibiotics needed to sterilize a bacterial population. We suggest that resonant activation is a general phenomenon in phenotypic transition, and can find other applications such as cancer therapy.
So if we can resonate the bacteria then they are no longer dormant and can be killed off Notice the scientists are in computer science.
So the killer bacteria in dishwashers -- a black yeast -- will need to have their phenotype changed through a new resonance activation
Oops -- they are a fungi not a bacteria:
The main difference is that the bacteria are prokaryotic organisms, and fungi are eukaryotic organisms.
ScienceDaily (Nov. 28, 2011) — Bacteria and fungi are remarkably mobile. Now researchers at Tel Aviv University have discovered that the two organisms enjoy a mutually beneficial relationship to aid them in that movement -- and their survival.
Yeah so the human body has more bacteria than number of human cells. Will the NSA take notice of this? I mean the bacteria and fungi hip-hopping each other --
Fungal spores can attach themselves to bacteria, "hitching a ride" wherever the bacteria travel. And while this allows them to travel further than they would on their own, says Prof. Eshel Ben-Jacob of TAU's Raymond and Beverly Sackler School of Physics and Astronomy, it's certainly not a one-way street. Bacteria live largely in the rhizosphere -- the environment that surrounds plant roots -- where air pockets can interrupt their progress, he explains. When faced with a gap, the bacteria can drop the fungal spores to form a bridge, and continue across the chasm.
Symbiosis. The Spirochete is symbiotic with humans -- Lyme's Disease, Syphilis, AIDS -- all spirochetes possibly -- autism and alzheimers maybe who knows? Dr. Lynn Margulis on symbiosis and spirochetes
These observations can also be applied to agriculture and medicine, showing new mechanisms by which bacteria and fungi can help one another to invade new territories in the rhizosphere -- as well as in hospitals and within our own bodies
O.K. so the high temperature sanitizing dishwasher gets up to 82 degrees Celsius but it's a perfect environment for the killer black yeast:
Both Exophiala species showed remarkable tolerance to heat, high salt concentrations, aggressive detergents, and to both acid and alkaline water. This is a combination of extreme properties not previously observed in fungi.
Dude -- the UK paper has the headline wrong - they call it "deadly bacteria" but it's fungi as yeast, not bacteria.
B. burgdorferi spirochetes take up residence in tissues of people bitten by ticks that carry the bacteria in their guts and inject them via saliva. The spirochetes’ most familiar form is an agile, spiral-shaped swimmer associated with acute symptoms of Lyme disease and rapid reproduction of the bacteria. But as Margulis explains, these bacteria can “go underground” and persist for years by entering a self-protective, quiescent stage known as a spirochete round-body (RB) propagule. In this state, they better resist what scientists call “unfavorable environmental conditions” such as starvation, desiccation and exposure to antibiotics such as penicillin and deoxycillin. Chronic Lyme disease symptoms correlate with the continuous presence of reversible RB propagules in patients’ moist tissues.
What the Brorsons’ work shows is that, unlike other antibiotics, Tygecycline administered at the correct dosage and timing destroys the bacterium even when it has protected itself in this quiescent stage. Other antibiotics, if they do anything at all, simply cause B. burgdorferi to enter its RB propagule state and wait out the treatment. “Tigecycline is, so far, the only known antibiotic that destroys the Lyme disease spirochete in both the growing and the quiescent RB stages of its life history” Margulis notes.
O.K. so the symbiosis of spirochetes with humans means the spirochetes go into a dormnant state which is the purpose of resonant activation to treat -- but now they've got a new antibiotic that is effective against this dormant state
O.K. so this is fascinatingly similar to what the RIFE machine was for -- based on the argument that bacteria took up different forms -- and this is now verified that "resonant activation" from physics changes the phenotype of the bacteria -- so it turns active again and also changes form, just as RIFE argued was true!!
Margulis’s laboratory explores an evolutionary hypothesis. She and her colleagues posit that a certain spirochete genome provided an ancestral component to the earliest nucleated cells (eukaryotes). Spirochete remnant DNA hypothesized to be present in all nucleated organisms should be detectable in the proteomes of fully sequenced genomes. Simply stated, spirochete ancestors of Perfilievia
russae free-living spirochetes presented at the Berlin meeting by Galina Dubinina (Institute of Microbiology of the Russian Academy of Sciences, Moscow, Dubinina et
al., 2008) by hypothesis are the closest co-descendants of the cytoskeleton of our nucleated cell lineage (Margulis et al., 2006). We envision these (sulfide-oxidizing, 0.25 μm diameter spirochetes) are related to ancestors of cilia, sperm
tails, haptonemes and myriad other organelles of motility in nucleated organisms. If the evidence is correctly interpreted spirochete remnants have dwelled in stable symbioses in eukaryotes since their origin in the Proterozoic eon over 1000 million years ago (mya) (Hall, 2008).
Wow so AIDS may actually be caused by the symbiotic hidden form of syphilis!
Since Montagnier's work, many centers that used immunological tests not sensitive for all stages of syphilis have documented a close relationship between a history of treponematoses and HIV/AIDS (Veugelers et al., 1992; Renzullo et al., 1991; Blocker et al., 2000). Chronic syphilitics and AIDS patients, those unmistakably ill and immune suppressed, do not succumb to HIV or syphilis
directly. They die of reactivation tuberculosis (TB) and ubiquitous mycobacterium avium intracellulare (MAI group) diarrhea, and emaciation associated with refractory
bowel infections in emaciated homosexuals and in immune compromised patients generally. TB and other mycobacteria correlate with amoebic dysentery. Death
records report causes as Pneumocystis carini pneumonia, Entamoeba histolytica, Candida albicans or other “opportunistic infection” (Coulter, 1987). In sub-Saharan
Africa, the historic overuse of antibiotics and malnutrition also contribute to immune suppression. One of us (John Scythes) reports that he has not found a single documented case of an immune suppressed patient, whether HIVpositive
or -negative, who has died of complications of syphilis since HIV records began being maintained in the early 1980s. Is it possible that the narrow focus on "HIV as
the cause of AIDS", an example of scientific "misplaced concreteness" typical in explanation of evolution (Cobb, 2008), has facilitated missed diagnosis of syphilis?