Originally posted by RedBalloon
Is this microbial mutation so new, though, or is it just that we are now able to actually see, observe, and understand it with the advances in the
past 30 years?
I'm still not going to kiss a cat
LOL. Aww. It's just a kitty cat.
...What's happening is very new. Not sure if current toxoplasmis gondii is a new strain or not but much of what's out there now is new, and about to
remake the world.
Seems that many of our "interventions and activities" don't just trigger new mutations - they kill natural microbial predators at the same time. So
the predators don't evolve along with the diseases. Which means the new infectious mutations have no natural predators, and also are resistant to
antiobiotics, anti-virals and whatever we throw at them.
"As the epidemiology of waterborne diseases is changing, there is a growing global public health concern about new and reemerging infectious diseases
that are occurring through a complex interaction of social, economic, evolutionary, and ecological factors."
Crit Rev Microbiol. 2002;28(1):1-26. Emerging waterborne infections: contributing factors, agents, and detection tools. Theron J, Cloete TE.
Department of Microbiology and Plant Pathology, University of Pretoria, South Africa. PMID: 12003038
Re: Vectors, hitchhikers and mutation processes...
Animal prion infections, such as scrapie (sheep) and "mad cow disease" (cattle), have shown a pattern of horizontal transmission in farm conditions
and several ectoparasites have been shown to harbor prion rods in laboratory experiments. Fly larvae and mites were exposed to brain-infected material
and were readily able to transmit scrapie to hamsters. New lines of evidence have confirmed that adult flies are also able to express prion proteins.
Several cell types found on the human skin, including keratinocytes, fibroblasts and lymphocytes, are susceptible to the abnormal infective isoform
of the prion protein, which transforms the skin to produce a potential target for prion infection.
Int J Dermatol. 2003 Jun;42(6):425-9. Could ectoparasites act as vectors for prion diseases? Lupi O. Center for Vaccine Development, University of
Texas Medical Branch at Galveston, Galveston, TX, USA. PMID: 12786866
..So prion-related diseases can hitchhike on flies, yeast, plants, meat, bacteria, you name it. ...Looks like the "actin" protein is the key
...Actin is everywhere - virtually every living cell on earth has actin in the cytoskeleton or membrane, which is how all these new little suckers
cross species and kingdom barriers (from mammals to fungi to plants and protozoa - not supposed to happen, but it is).
"The most biologically significant property of actin is its ability to self-associate and form two-stranded polymeric microfilaments. In living
cells, these micro filaments form the actin cytoskeleton, essential for maintenance of the shape, passive mechanical properties and active motility of
eukaryotic cells. Recently discovered actin-related proteins (ARPs) appear to share a common ancestor with conventional actin. At present, six classes
of ARPs have been discovered, three of which have representatives in diverse species across eukaryotic phyla and may share functional characteristics
with conventional actin. The three most ubiquitous ARPs are predicted to share a common core structure with actin and contain all the residues
required for ATP binding. Surface residues involved in protein protein interactions, however, have diverged. Models of these proteins based on the
atomic structure of actin provide some clues about how ARPs interact with each other, with conventional actin and with conventional actin-binding
Trends Cell Biol. 1996 Jun;6(6):208-12. Actin' like actin? Mullins RD, Kelleher JF, Pollard TD. The authors are at the Dept of Cell Biology and
Anatomy, Johns Hopkins University School of Medicine, 725 N. Wolfe St, Baltimore, MD 21205, USA. PMID: 15157457
BTW and LOL - I love this stuff too. ...Are you up on RNA interference?