Afarensis is a 3.5-2.8 million year old hominin from the Kada Hadar member of the Hadar formation in the Middle Awash, Ethiopia. He is approximately 41 inches tall, weighs approximately 60 pounds and has a cranial capacity of a whopping 410 cc (approximately). Afarensis is currently considered to be transitional between apes and humans and displays some traits of both. Since he spends a lot of time on the couch watching monster movies, some observers question whether he is an obligate biped (although no one has observed him climbing a tree). He also has a blog called 
By now, most of us are familiar with MRSA or methicillin resistant Staphylococcus aureus. The staph bacteria is pretty common on human skin but doesn't become a problem until it finds an entry through the flesh [afarensis had an old scar from a car accident get infected with staph, fortunately not MRSA, and spent about four days in the hospital last summer] at which point it becomes a problem. MRSA is mainly found in hospitals, although there have always been a number of cases where the person had never visited a hospital. Recent research may have uncovered why. According to Science Daily MRSA use amoeba to evade measures designed to halt their spread:
Scientists from the University of Bath have shown that MRSA infects and replicates in a species of amoeba, called Acanthamoeba polyphaga, which is ubiquitous in the environment and can be found on inanimate objects such as vases, sinks and walls.As amoeba produce cysts to help them spread, this could mean that MRSA maybe able to be ‘blown in the wind’ between different locations.
This is where it gets really interesting. Apparently, by infecting the amoeba first the MRSA becomes more virulent:
Evidence with other pathogens suggests that pathogens that emerge from amoeba are more resistant to antibiotics and more virulent. “This makes matters even more worrying,” said Professor Brown. “It is almost as though the amoeba act like a gymnasium; helping MRSA get fitter and become more pathogenic.
In other words by they become more virulent by adapting to the amoeba defense system. There are evolutionary implications (and this study refutes the claims of those who say evolutionary theory does not contribute to the practice of modern medicine):
“In many ways this may reflect how this kind of pathogenic behaviour first evolved. A good example is the bacterium that causes legionnaires disease. Probably it was pathogenic long before humans and other animals arrived on the evolutionary scene. Even today, it has no known animal host.“The most likely reason is that Legionella and many pathogens learned their pathogenicity after sparring with single-celled organisms like amoeba for millions of years. Because our human cells are very similar to these primitive, single-celled organisms, they have acquired the skills to attack us”.
As the researchers who performed the study point out effective control of MRSA requires a better understanding of it's ecology including it's interactions with other organisms. Which sounds like a promising are for future research...I'd almost give up writing about old bones and dirt for the opportunity to go back to school and study the issue...
Comments
This is really fascinating stuff. The connection between host-pathogen interactions (like Staph-human) and bacteria vs. eukaryotic predators (amoeba eat bacteria) are very interesting. The Legionella example (as well as mycobacteria, the agents of leprosy and tuberculosis) are really fascinating. I'd have to read the article, but if this holds up, it could be a major finding (you have to be a bit wary; a good test would be too see if you can find environmental amoeba with staph in them). This is something a lot of microbiologists (read: me!) are getting interested in.
Posted by: Paul Orwin | February 28, 2006 8:35 PM
From Science Daily:
I can't think of a reason for it to be any different in "wild" amoeba, but life is stranger than fiction, so yeah that's something that needs more testing. The abstract to the paper can be found here unfortunately I don't have access - but would love to read it if anybody out there scrounges up a copy??Posted by: afarensis | February 28, 2006 9:44 PM
Wild amoeba (and wild S. aureus) are very different from laboratory strains. This has been a classic problem in studying invasive infectious disease. When you set up an assay, you design it so the phenotype is easily detected. However, the assay conditions may be far from reality. Simply put, amoeba in the wild may be better at digesting the Staph. This is too complex for a comment, so I may save it for an animalcules, but the activity of our immune system is very similar to the way that amoeba and other phagocytic protozoan predators attack their prey. But the interplay is complex, and highly strain variable (on both the predator and prey side). So, being able to do it in a lab is nifty, but is only a first step (as I'm quite sure the experimenters will acknowledge).
Posted by: Paul Orwin | February 28, 2006 11:13 PM
DOH! Pardon the Homer moment and thanks for the info. Makes it even more interesting. I do think the point about the way amoeba attack prey is what the Science Daily article was trying to get at with the bit about more virulent strains emerging from amoeba more virulent which sounds like selection in action to me. I do hope you do something for Animalcules with it...I find the subject fascinating.
Posted by: afarensis | February 28, 2006 11:30 PM