"altruistic" antibiotic resistance...,

WorldScience | Confronting at­tack by an­ti­bi­otics, some bac­te­ria help each oth­er out—and un­for­tu­nately for us, they’re bet­ter off for it, re­search­ers have found.

Though a small frac­tion of pathogens in a col­o­ny may have evolved the abil­ity to re­sist a drug or class of drugs, these “su­per bugs” were found to help their more vul­ner­a­ble peers by over-pro­duc­ing a drug-fighting sub­stance.

Pre­vail­ing wis­dom held that an­ti­bi­ot­ic re­sistance works only on an in­di­vid­ual lev­el: a bac­te­ri­um ac­quires a muta­t­ion that con­fers pro­tec­tion against a drug, al­low­ing it to sur­vive and re­pro­duce. Even­tu­al­ly, as vul­ner­a­ble bac­te­ria die, the mu­tan­t's stronger prog­e­ny re­pop­u­late the col­o­ny. This basically reflects how evolution is believed to work in all species: mem­bers that are “fit­ter” or bet­ter adapt­ed to pre­vail­ing con­di­tions spread their genes through the po­pu­lation at the ex­pense of other mem­bers.

But the new stu­dy, to ap­pear in the Sept. 2 is­sue of the re­search jour­nal Na­ture, in­di­cates there are al­so popula­t­ion-wide changes in the bac­te­ri­al com­mun­ity at work. Faced with an on­slaught of an­ti­bi­otics, re­sistant Esch­e­rich­i­chia coli mi­crobes pro­duce—at an en­er­gy cost to them­selves—a pro­tein mol­e­cule that seeps in­to the com­munal broth and trig­gers a slew of pro­tec­tive mech­a­nisms in their non-re­sistant neigh­bors.

The study comes from re­search­ers at the How­ard Hughes Med­i­cal In­sti­tute in Chevy Chase, Md.

genome surprise!!!

Wired | The ebola virus is one of the nastiest pathogens known to man. It corrodes blood vessels and stops clotting, leaving most of its human victims bleeding to death through their pores. And guinea pigs — along with opossums, wallabies and insect-eating bats — have it in their genes.

A genomic hunt for virus genes traced sequences to Ebola and the closely related Marburg virus in no fewer than six vertebrate species. Echoes of the less-gruesome borna virus family appeared in 13 species, including humans. The genes appear to have been mixed in about 40 million years ago, and have stuck around ever since.

“Some of these sequences have been conserved,” and that’s almost certainly not a coincidence, said cell biologist Ann Marie Skalka of the Fox Chase Cancer Center. “We speculate that some of these must have provided an evolutionary advantage.”

Skalka specializes in RNA viruses, which unlike most common viruses are made from single strands of primitive genetic material, rather than DNA.

Common viruses, better known as retroviruses, insert their DNA into the genomes of infected cells. They hijack its function and, should the cell survive, leave pieces of themselves behind. Retroviral leftovers have accumulated for hundreds of millions of years in animal genomes; they account for about 8 percent of the human.

RNA viruses, however, were long thought to leave no leftovers. They float outside a cell’s chromosomes, hijacking its machinery from afar and ostensibly leaving genomes intact. But that assumption proved wrong. Fist tap Nana.

interspecies quorum sensing?

mBio | ABSTRACT Otitis media (OM) is among the leading diseases of childhood and is caused by opportunists that reside within the nasopharynx, such as Haemophilus influenzae and Moraxella catarrhalis. As with most airway infections, it is now clear that OM infections involve multiple organisms. This study addresses the hypothesis that polymicrobial infection alters the course, severity, and/or treatability of OM disease. The results clearly show that coinfection with H. influenzae and M. catarrhalis promotes the increased resistance of biofilms to antibiotics and host clearance. Using H. influenzae mutants with known biofilm defects, these phenotypes were shown to relate to biofilm maturation and autoinducer-2 (AI-2) quorum signaling. In support of the latter mechanism, chemically synthesized AI-2 (dihydroxypentanedione [DPD]) promoted increased M. catarrhalis biofilm formation and resistance to antibiotics. In the chinchilla infection model of OM, polymicrobial infection promoted M. catarrhalis persistence beyond the levels seen in animals infected with M. catarrhalis alone. Notably, no such enhancement of M. catarrhalis persistence was observed in animals infected with M. catarrhalis and a quorum signaling-deficient H. influenzae luxS mutant strain. We thus conclude that H. influenzae promotes M. catarrhalis persistence within polymicrobial biofilms via interspecies quorum signaling. AI-2 may therefore represent an ideal target for disruption of chronic polymicrobial infections. Moreover, these results strongly imply that successful vaccination against the unencapsulated H. influenzae strains that cause airway infections may also significantly impact chronic M. catarrhalis disease by removing a reservoir of the AI-2 signal that promotes M. catarrhalis persistence within biofilm.

IMPORTANCE Otitis media (OM) is one of the most common childhood infections and is a leading reason for antibiotic prescriptions to children. Chronic and recurrent OM involves persistence of bacteria within biofilm communities, a state in which they are highly resistant to immune clearance and antibiotic treatment. While it is clear that most of these infections involve multiple species, the vast majority of knowledge about OM infections has been derived from work involving single bacterial species. There is a pressing need for better understanding of the impact of polymicrobial infection on the course, severity, and treatability of OM disease. In this study, we show that communication between bacterial species promotes bacterial persistence and resistance to antibiotics, which are important considerations in the diagnosis, prevention, and treatment of OM. Moreover, the results of this study indicate that successful preventive measures against H. influenzae could reduce the levels of disease caused by M. catarrhalis.

gut intelligence

Video - humorous probiotic propaganda.

organelle | Just as the diversity of commensal microbiota and other conditions of intra-cellular, organ and metabolic health dramatically affect both our mental function and our immune system, our planet has similar features and capacities which until very recently depended upon extant biodiversity for their robust protective, relational, nutritive and prophylactic activity.

The shocking and incredibly sudden damage we have inflicted upon biospheric diversity (primarily at the scale of animals and ecosystems) has severely impacted planetary health and healing, creating in effect a exploding crisis in which protections which have long been active have suddenly and egregiously disappeared. The biodiversity we’ve erased previously acted as shock-absorbers, communications and intelligence assets, and an immunity system.

We should pause to note that Earth’s experience of time differs dramatically from our own, and to her only some few heartbeats have passed, while for us it has been 500 years. Effectively, she is in shock, and her temperature will fluctuate wildly, her inner clock has gone haywire, and she shall certainly shiver, shake and bleed. Her heartbeat, metabolic status and ‘blood pressure’ are also fluctuating wildly.

The results of these events are feeding back into every species on the planet — since we are not ‘part’ of Earth, but instead living instances of Earth. This then feeds back into the planet, and the resultant reflexive cycle creates a recursively expanding nightmare with terrifying consequences including but not limited to ‘auto-immune’ disorder on a planetary scale. This means simply ‘the elements of her body will attack each other, failing to recognize itself as self’ —just as we have done to the other species of the world.

The biodiversity which required millenia to establish cannot be ‘healed’ — it is gone and there is no ‘pill’ or ‘therapy’ that can replace it. In fact, if history is any measure, what will happen once the various nations realize what they are up against is the wholesale erasure of the remaining resources in the hope of stockpiling survival assets for specific groups of people and nations. A part of this activity is sure to include another infamous facet of human capacity: the wartime ‘denial of assets to the enemy’ move which stipulates that assets one cannot acquire for themselves or allies be destroyed or poisoned so that others cannot use them against you. This is not the future I am speaking of, but the present.

Could it be that as we annihilated the anciently conserved commensal bacterial symbionts in our own guts with antibiotics and other toxins, we set ourselves up to become omnicidal maniacs who could no longer recognize ourselves in the eyes and bodies of the creatures and ecosystems that comprise our most ancient and treasured symbionts?

Unfortunately, we shall now we shall see firsthand what ‘multiple sudden opportunistic infections’ look like at the scale of a world, rather than that of a person, or a people.

gut instinct

Video - hookworm lifecycle papermation.

Guardian | The research that so excited Lawrence was a development of the so-called "hygiene hypothesis". This theory, first developed by David P Strachan in the British Medical Journal in 1989, suggests that many of the "modern" illnesses that have grown exponentially in industrialised western countries – allergies, asthma, type 1 diabetes, Crohn's disease, irritable bowel syndrome, multiple sclerosis and possibly rheumatoid arthritis and autism, and others – are the result of inappropriate autoimmune responses. The development of chlorinated drinking water, vaccines, antibiotics, and the sterile environment of early childhood have, the argument goes, as well as preventing infection also upset the balance of the body's internal ecology. Inflammatory responses that evolved through millions of years in the certain presence of "old friends" – parasites and bacteria – have been thrown wildly out of kilter in their absence, causing autoimmune illnesses, in which the body's immune system turns on itself, and oversensitivity to harmless antigens such as pollen, or dust, or cats, or particular food groups.

The story that most interested Lawrence was the ongoing research of Professor David Pritchard, an immunologist at Nottingham University. While in the field in Papua New Guinea in the late 1980s, Pritchard noted that patients infected with the Necator americanus hookworm were rarely subject to the whole range of autoimmune-related illnesses, including hay fever and asthma. In the years since, Pritchard had developed a thesis to support this observation through painstaking clinical trials (which began after he infected himself with 50 hookworm). The thesis proved that hookworm, in small numbers, seemed able to regulate inflammatory immune responses in their hosts. (Dr Rick Maizels, at Edinburgh University, has subsequently identified the process – involving the white T-cells in the blood that regulate immunity – that allowed this to happen.)

"When I read that stuff," Lawrence recalls, "everything immediately made sense to me. In our obsession with cleansing and sterility, with the eradication of parasites, we had thrown the baby out with the bath water. The central idea is that our bodies have an internal ecosystem. One of the ironies of this, to me, is that everyone is concerned about biodiversity in the outside world, and saving the rainforest, but we've also screwed up the biodiversity inside us."

And so Jasper Lawrence set out on what became a compulsive and somewhat desperate quest. Despite the fact that perhaps one billion people in the world still live with hookworm, getting infected in the developed western world is not an easy thing. The drift of our culture has long been to eradicate parasites – or "symbions", as Lawrence prefers. To begin with, he tried to get accepted as a participant on one of the various studies investigating the phenomenon. But when that proved fruitless he determined to go to Africa and become infected.

Prior to this trip, he recalls, he contacted "all the clever people I knew who worked in medicine. I sent them all the research and asked them their opinion. They all said the same thing: 'Yes, it appears safe, but I would not advise you to do this; you need to wait 20 or 30 years for all the studies to come in. For a molecule to be identified and a drug to be tested…'"

You don't have to talk to Lawrence for long to realise he is not a man who might be prepared to wait 20 or 30 years for anything. Instead, he took a plane to Cameroon.

The life cycle of Necator americanus is not an attractive one. Hookworm infiltrate a new human host when larvae, hatched in human excrement, penetrate the soles of the feet, enter the bloodstream, travel through the heart and lungs and are swallowed when they are coughed up from the pharynx. Only in the small intestine do they mature into adults (just under 1cm long), where they can live an average of five years latching on to the intestinal wall, siphoning off tiny amounts of blood, and – this is the crucial part – "regulating the volume" of immune responses. They mate inside the host, with females laying up to 30,000 eggs per day, up to 50m eggs during a lifetime, which pass out in faeces. In the tropics, in places where there is an absence of both toilets and shoes, extreme cases of hookworm kill 70,000 people a year, and afflict many others with anaemia; they exacerbate malnutrition and stunted growth in children. There are crucial caveats to these scare stories, however. Hookworm cannot and do not replicate in the gut. They are not infectious. In small numbers they are considered harmless, and very easily eradicated. And their life cycle is fatally interrupted by the introduction of either shoes or plumbing.