![](https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEine33PxpES00_ZdQz3gl927Xp9jc15XdEdjO9zD3wbksBKGSm2LDkcGuf97H9BwIERTKWJgWlM8TaCAKgWsQRgd4ZnqZIfnbAaE4xuIizy6qw_0YjxjeuHVVq2JNLSyvVSJmAekW7vOHo/s200/termite2_190_126.jpg)
If only wood could be converted to biofuels, there would be no need to wait a million years for the trees to be buried and become oil. Wood is indeed convertible to useful chemicals, because termites do it every day, causing $1 billion of damage every year in the United States. But to live on a diet of wood is challenging, not least because wood contains so little nitrogen. So how do termites do it?
The trick lies in a cunning triple symbiosis, a team of Japanese scientists report in Friday’s issue of Science. In the termites’ gut lives an amoeba-like microbe called a protist, and inside each protist live some 10,000 members of an obscure bacterium.
The microbes in the termites’ gut are very hard to cultivate outside their termite host and so cannot be studied in the lab. The Japanese scientists, led by Yuichi Hongoh and Moriya Ohkuma at the RIKEN Advanced Science Institute in Saitama, have cut through this problem. They extracted the protist’s bacteria directly from a termite’s gut, collected enough to analyze their DNA, and then decoded the 1,114,206 units of DNA in the bacterium’s genome.
By comparing the DNA sequence of the bacterium’s genes with other decoded genes already in public databases, the Japanese team was able to figure out what each gene did. It could then reconstruct all the biochemical reactions of which the bacterium is capable, as shown in the figure above.
They found that in the bacterium’s biochemical repertoire is the ability to convert nitrogen (shown as N2 , to the right of center in the figure) into ammonium and hydrogen. Unlike nitrogen, which is very unreactive, ammonium is easily incorporated into biochemical reactions.
The bacterium can also import urea (shown in the yellow border, at 5 o’clock), a waste product produced by its protist host. Since it takes a lot of energy to fix nitrogen, the bacteria probably use urea as their main nitrogen source as long as their host is making enough, and switch to nitrogen as a backup, the Japanese scientists say.
The overall process whereby this troika of species makes a meal of wood is shown in the graphic at left: the termite chews the wood into particles that are absorbed by the amoeba. The amoeba breaks down the cellulose of the wood and gets the nitrogen it needs from its bacteria. The net result is that the two microbes digest wood into sugars and other nutrients of use to the termite.
Dr. Caroline Harwood, an expert on microbes and biofuels at the University of Washington, Seattle, said the new research was a “ tour de force of genome sequencing” that “solves the mystery of where the termite gets its nitrogen.” Understanding how the termite’s gut microbes digest cellulose would be of major significance for biofuels, she said, and the Japanese group’s whole genome approach could further this goal.![](https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg3D4DvAwKRPJ9JOpLFwO4cwpF_JUmHCLmHduzEOdjJJb4z7QtRSCgoMs9ZIY9tNUlVISt3_ZqXrbZBILaq-aEFfNXL8EtQxzNcQFtlO1d7GYfSYJYKxkkm5ZIKVlD-q7EkCK8wu5ks98E/s200/termite600.jpg)
![](https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj7V85drFwcYCoZLNCNEiT02nFV5Re9NklV4TRwtR_9UgorhgDqLLxtXLegu7AygNFQMsMZyzohAaApJiMigFKFF9LM5CmyNISs8r6wPGuTsU4Y60CiYIoW9c-iENmGiNOJ2f3LOFYQ8Tc/s200/5117_1_amoebaone_190x126.jpg)
![](https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjp4WzWQzpyUN9nRY_mlWTi4z54hfa8RO895oNUTixpu7Dm38jpoeIcoGdRoZRj43fSUezNAjV-BeYDqadps9nYueJfT1MU3GmO17Q8Abr4GMbfhK6xl0-AO0SKGbLE_MduY2Y4NVCYL5E/s200/24amoeba_1-190.jpg)
After producing superlatives like the world’s biggest statue of a jackrabbit and the nation’s most unpopular modern-day president, Texas can now boast what may be its most bizarre and undoubtedly its slimiest topper yet: the world’s largest known colony of clonal amoebas.
An amoeba growing on a fish tank in California became a giant among microbes, reaching more than an inch across. Scientists found the vast and sticky empire stretching 40 feet across, consisting of billions of genetically identical single-celled individuals, oozing along in the muck of a cow pasture outside Houston.
“It was very unexpected,” said Owen M. Gilbert, a graduate student at Rice University and lead author of the report in the March issue of Molecular Ecology. “It was like nothing we’d ever seen before.”
Scientists say the discovery is much more than a mere curiosity, because the colony consists of what are known as social amoebas. Only an apparent oxymoron, social amoebas are able to gather in organized groups and behave cooperatively, some even committing suicide to help fellow amoebas reproduce. The discovery of such a huge colony of genetically identical amoebas provides insight into how such cooperation and sociality might have evolved and may help to explain why microbes are being found to show social behaviors more often than was expected.
“It is of significant scientific interest,” said Kevin Foster, an evolutionary biologist at Harvard University who was not involved with the study. Though amoebas would seem unlikely to coordinate interactions with one another over much more than microscopic distances, the discovery of such a massive clonal colony, he said, “raises the possibility that cells might evolve to organize on much larger spatial scales.”
Thoughts of a giant organized amoeba colony can conjure up visions of the 1958 horror classic “The Blob,” but these social amoebas, a species known as Dictyostelium discoideum, a kind of slime mold, are infinitely more subtle. Microscopic and tucked away in the dirt, the billions of amoebas would have gone unnoticed by anyone driving past the pasture. Joan Strassmann, an author on the paper along with another evolutionary biologist at Rice University, David Queller, said she and a team of undergraduates searched for the species by sticking drinking straws into dirt and cow dung to retrieve materials where the amoebas might be living. In the laboratory, they spread the samples on Petri dishes and waited to see what would grow. DNA analyses later showed that the huge numbers of amoebas collected from the pasture were genetically identical.
Bernard Crespi, an evolutionary biologist at Simon Fraser University in Canada, said the study was the first to clearly demonstrate “the extreme of relatedness” in social microbes, a population of genetically identical individuals. Such a colony provides the ideal conditions to foster the evolution of behaviors like cooperation, because the more genetically similar two organisms are, the more natural selection will favor their assisting each other.
Dictyostelium, for example, can carry out stunning feats of cooperation, engaging in what’s known as suicidal altruism, a behavior in which individual amoebas come together to form a single body, with some amoebas sacrificing themselves to allow for more effective reproduction of amoebas in other parts of the body.
Scientists said that if other species were also found to have such clonal colonies, that could help explain the surprisingly widespread finding of social behaviors among microbes. But just what conditions prompt the flourishing of clones remains unclear. Scientists said it was odd to find the slime molds thriving in an open field, as they prefer enclosed forest soils. It is possible that the lumbering cows fostered the growth of the giant clone colony by spreading the amoebas through the muck, said John Bonner, professor emeritus of ecology and evolutionary biology at Princeton University.
Meanwhile, as impressive (or even threatening) as a colony of a couple billion amoebas might sound, it has turned out to be surprisingly fragile.
“Just one week later, it had rained a lot and then it basically was gone,” Mr. Gilbert said.
Apparently, such is the fleeting nature of grand amoebic phenomena, for the Texas clone is not the first to dwindle inexplicably into nothingness. Scientists say that the last traces of what at one point may have been the world’s largest individual amoeba — and the star of a highly productive research program — shriveled in their laboratory last summer until it disappeared.
Manfred Schliwa, a cell biologist at the University of Munich, first came across the organism, known as Reticulomyxa, quite by accident as it spread as a white slime across the fish tank in his office at the University of California at Berkeley where he was then a professor.
The amoeba, a blob with no defined shape, bits of which could break off to take up a life of their own, fed so heartily off stray morsels of fish food that it eventually attained the status of giant among microbes, its body reaching more than an inch across.
A single enormous cell, the amoeba was studied by Dr. Schliwa and colleagues to understand movement from one part of a cell to another, a process that was both easily visualized and carried out extremely rapidly in the big Reticulomyxa, which at its largest could house a billion or more nuclei as it constantly shuttled cell parts and whatnot across its titanic form.
Dr. Schliwa, still mystified by the demise of the big-amoeba-that-couldn’t, said he hoped at some point to obtain a new wild Reticulomyxa, though under natural conditions the organism is much smaller and lives in the soil, making it difficult to spot. In fact, like the colony of social amoebas, the giant amoebas could be everywhere underfoot without anyone’s noticing.
“I used to joke,” Dr. Schliwa said, “that there might be a giant organism in the soil spanning the entire continent and whenever you dig up a shovelful you get a piece of it.”
So where will the next giant amoeba be found hiding? Dr. Schliwa points out that the original discovery of the amoeba-to-end-all-amoebas was made in the 1940s by a researcher named Ruth N. Nauss. She discovered the species in a New York City park.
2009 H1N1 Vaccination Recommendations
With the new H1N1 virus continuing to cause illness, hospitalizations and deaths in the US during the normally flu-free summer months and some uncertainty about what the upcoming flu season might bring, CDC's Advisory Committee on Immunization Practices has taken an important step in preparations for a voluntary 2009 H1N1 vaccination effort to counter a possibly severe upcoming flu season. On July 29, ACIP met to consider who should receive 2009 H1N1 vaccine when it becomes available. The 2009 H1N1 vaccination recommendations are available at http://www.cdc.gov/mmwr/preview/mmwrhtml/rr58e0821a1.htm.
2009 H1N1 VaccineEvery flu season has the potential to cause a lot of illness, doctor’s visits, hospitalizations and deaths. CDC is concerned that the new H1N1 flu virus could result in a particularly severe 2009-2010 flu season. Vaccines are the best tool we have to prevent influenza. CDC hopes that people will start to go out and get vaccinated against seasonal influenza as soon as vaccines become available at their doctor’s offices and in their communities. The seasonal flu vaccine is unlikely to provide protection against 2009 H1N1 influenza. However a 2009 H1N1 vaccine is currently in production and may be ready for the public in the fall. The 2009 H1N1 vaccine is not intended to replace the seasonal flu vaccine – it is intended to be used along-side seasonal flu vaccine.
CDC’s Advisory Committee on Immunization Practices (ACIP), a panel made up of medical and public health experts, met July 29, 2009, to make recommendations on who should receive the new H1N1 vaccine when it becomes available. While some issues are still unknown, such as how severe the flu season, the ACIP considered several factors, including current disease patterns, populations most at-risk for severe illness based on current trends in illness, hospitalizations and deaths, how much vaccine is expected to be available, and the timing of vaccine availability.
The groups recommended to receive the 2009 H1N1 influenza vaccine include:
Pregnant women because they are at higher risk of complications and can potentially provide protection to infants who cannot be vaccinated;
Household contacts and caregivers for children younger than 6 months of age because younger infants are at higher risk of influenza-related complications and cannot be vaccinated. Vaccination of those in close contact with infants younger than 6 months old might help protect infants by “cocooning” them from the virus;
Healthcare and emergency medical services personnel because infections among healthcare workers have been reported and this can be a potential source of infection for vulnerable patients. Also, increased absenteeism in this population could reduce healthcare system capacity;
All people from 6 months through 24 years of age
Children from 6 months through 18 years of age because cases of 2009 H1N1 influenza have been seen in children who are in close contact with each other in school and day care settings, which increases the likelihood of disease spread, and
Young adults 19 through 24 years of age because many cases of 2009 H1N1 influenza have been seen in these healthy young adults and they often live, work, and study in close proximity, and they are a frequently mobile population; and,
Persons aged 25 through 64 years who have health conditions associated with higher risk of medical complications from influenza.
No shortage of 2009 H1N1 vaccine is expected, but vaccine availability and demand can be unpredictable and there is some possibility that initially, the vaccine will be available in limited quantities. So, the ACIP also made recommendations regarding which people within the groups listed above should be prioritized if the vaccine is initially available in extremely limited quantities. For more information see the CDC press release CDC Advisors Make Recommendations for Use of Vaccine Against 2009 H1N1.
Once the demand for vaccine for the prioritized groups has been met at the local level, programs and providers should also begin vaccinating everyone from the ages of 25 through 64 years. Current studies indicate that the risk for infection among persons age 65 or older is less than the risk for younger age groups. However, once vaccine demand among younger age groups has been met, programs and providers should offer vaccination to people 65 or older.
![](https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj06IB5LIgTK7F1FdQUEd_fiTKbO7uZIZRFqF4QWR9hV__2RRpkW6K_Acf2vdXjTPINoPJxfdoCIYdOZNFfZYqFgogmuUS_taP7msslnBB1gzkqcQgslwpYX3mHD1-oFDZLiQvsCrbUNVs/s200/200px-AntigenicShift_HiRes.png)
Nomenclature
The various types of influenza viruses in humans. Solid squares show the appearance of a new strain, causing recurring influenza pandemics. Broken lines indicate uncertain strain identifications.
Influenza A virus strains are categorized according to two proteins found on the surface of the virus: hemagglutinin (H) and neuraminidase (N). All influenza A viruses contain hemagglutinin and neuraminidase, but the structures of these proteins differ from strain to strain, due to rapid genetic mutation in the viral genome.
Influenza A virus strains are assigned an H number and an N number based on which forms of these two proteins the strain contains. There are 16 H and 9 N subtypes known in birds, but only H 1, 2 and 3, and N 1 and 2 are commonly found in humans AND swine, or otherwise known as, pigs.
The Spanish flu, also known as La Gripe EspaƱola, or La Pesadilla, was an unusually severe and deadly strain of avian influenza, a viral infectious disease, that killed some 50 million to 100 million people worldwide over about a year in 1918 and 1919. It is thought to be one of the most deadly pandemics in human history. It was caused by the H1N1 type of influenza virus. The 1918 flu caused an unusual number of deaths, possibly due to it causing a cytokine storm in the body. (The current H5N1 bird flu, also an Influenza A virus, has a similar effect.)The Spanish flu virus infected lung cells, leading to overstimulation of the immune system via release of cytokines into the lung tissue. This leads to extensive leukocyte migration towards the lungs, causing destruction of lung tissue and secretion of liquid into the organ. This makes it difficult for the patient to breathe. In contrast to other pandemics, which mostly kill the old and the very young, the 1918 pandemic killed unusual numbers of young adults, which may have been due to their healthy immune systems mounting a too-strong and damaging response to the infection.
The term "Spanish" flu was coined because Spain was at the time the only European country where the press were printing reports of the outbreak, which had killed thousands in the armies fighting World War I. Other countries suppressed the news in order to protect morale. Influenza A virus subtype H2N2#Russian flu for the 1889–1890 Russian flu
The more recent Russian flu was a 1977–1978 flu epidemic caused by strain Influenza A/USSR/90/77 (H1N1). It infected mostly children and young adults under 23 because a similar strain was prevalent in 1947–57, causing most adults to have substantial immunity. Some have called it a flu pandemic, but because it only affected the young it is not considered a true pandemic. The virus was included in the 1978–1979 influenza vaccine.
Illustration of influenza antigenic shift.
Main article: 2009 flu pandemicIn the 2009 flu pandemic, the virus isolated from patients in the United States was found to be made up of genetic elements from four different flu viruses – North American swine influenza, North American avian influenza, human influenza, and swine influenza virus typically found in Asia and Europe – "an unusually mongrelised mix of genetic sequences." This new strain appears to be a result of reassortment of human influenza and swine influenza viruses, in all four different strains of subtype H1N1.
Preliminary genetic characterization found that the hemagglutinin (HA) gene was similar to that of swine flu viruses present in U.S. pigs since 1999, but the neuraminidase (NA) and matrix protein (M) genes resembled versions present in European swine flu isolates. The six genes from American swine flu are themselves mixtures of swine flu, bird flu, and human flu viruses. While viruses with this genetic makeup had not previously been found to be circulating in humans or pigs, there is no formal national surveillance system to determine what viruses are circulating in pigs in the U.S.
On June 11, 2009, the WHO declared an H1N1 pandemic, moving the alert level to phase 6, marking the first global pandemic since the 1968 Hong Kong flu.