Wednesday, April 25, 2012

Peng Peng the Transgenic Lamb

Long time no post!

I thought I'd pass along this cool piece of news. Apparently Peng Peng, a very cute lamb, was cloned in such a way, using C. elegans genes, that he produces greater quantities of polyunsaturated fats or"good fats."

It was only last summer that the Chinese released news that they'd managed to alter dairy cows to produce human milk. Some pretty cool stuff going on. Check out the video link.

Also, has anyone seen any actual publishings on this? What exactly is handmade cloning and how does it differ from classical approaches to cloning?

Saturday, December 15, 2007

The Paranoia of North America

I work in a Seafood Department for Thrifty Foods; while I've been there I've been able to first hand experience the combined paranoia of companies, employees and the general populace. The company I currently work for has always been proud of being very strict with sanitation, amongst other things.
As most people know, Thrifty's was recently sold to a larger company named Sobe's. About a year ago, in preparation for the sale, they brought in a policy called "Standard Operations and Procedures" (or SOPs for short). SOPs are guidelines on how to clean and sanitize everything, keep food in optimal conditions and what Johnson Diversey chemicals are needed for different situations. While I am all for improvements but it seems to me that, for the most part, when most companies bring in sanitation procedures their main goal is to achieve protection from lawsuit and a feeling of safety for customers. Examples of this can be seen with Thrifty Foods SOPs.
Bacteria is a vital part of life and species of bacteria exist almost everywhere, including in and on larger organisms such as pigs, cows, fish and humans. Bacteria also can exist in the food we eat and the liquids we drink. Digestion of certain types of bacteria can be beneficial or benign, even with small doses of pathogenic bacteria. Food sickness can occur if pathogenic bacteria align against the walls of the intestines and excrete harmful toxins. Most pathogenic bacteria optimal growth temperature is around room temperature, so by decreasing the foods temperature you decrease the growth rate of possible bacteria, which in turn lessens the risk of foodbourne illness.
There are positives to SOPs when it comes to reducing the risks of foodbourne illnesses, for example: regulation in how often temperature of cooling devices are checked and surfaces of tables, counters and tools are cleaned. Sometimes the paranoia of lawsuits can hinder the ability to protect people from pathogens. One example with Thrifty's is if someone asked for their meat to be wrapped with a bag of ice to keep it cold and away from optimal growth temperature, we can not do that for them, in fear of the customer using the ice in something causing cross contamination.
Another example paranoia in the world of food poisoning is the theory that we, first world citizens, are weakening our immune system by cutting off the everyday pathogens our bodies evolved with. The sanitation process may be great for cutting off severe cases but weak cases can make one stronger in defending against future attack. This is noticeable when people on vacation visit poorer countries that do not have the same sanitation systems put in place
and the vacationers get sick off of food that would not harm a local.
For the most part I believe that the regulations we put in place helps us but our standards can be hurt by the bureaucracy of our society. It's also pleasant to believe that these sanitation processes protect us from cases of upset stomachs to rarer and more extreme cases of fatality, but in the end there's always the possibility that we are weakening our defenses in the fight for the survival of the fittest.

AIDS: A Man Made Drug?

As far back as my knowledge of AIDS can take me, acquired immune deficiency syndrome (AIDS) is a disease caused by an infection with the human immunodeficiency virus (HIV). HIV is an RNA retrovirus that infects the CD4 T lymphocyte, a cell type essential for adaptive immunity. This infection can usually last for up to twenty years before the population of CD4 T cells diminish completely leading to a collapse in the immune system. HIV has a nucleoprotien core surrounded by a lipid envelope derived from the host cell. When HIV infects a cell, the RNA genome is first copied into a complementary DNA by reverse transcriptase, then integrated into the genome of the host cell to form a provirus. The provirus uses the transcriptional and translational machinery of the host cell to make viral proteins and RNA genomes, which are assembeled into new infection virions.

Now...this is what we are taught but I cant help but think how did this begin? It was not until I had a long interesting conversation with a guy I met in Thailand that I was told of the major conspiracy theories on how HIV came to I started surfing the net to see what i could find. A rather shocking quote I found was spoken by Pentagon Spokesperson Dr. Donald MacArthur on June, 6 1969, he said "Within the next five to ten years, it would probably be possible to make a new infective microorganism which could differ in certain important aspects from any known disease-causing organism.  Most important of these is that it might be refractory to the immunological and therapeutic processes upon which we depend to maintain our relative freedom from infectious disease.  A research program to explore the feasibility of this could be completed in approximetly five years at a total cost of $10 million" (HB 15090 pg 129) Hmmm, HIV did appear approximetly 5 to 10 years later and is the first and only disease to fulfill such a definition. This epidemic, as most believe, did not start in Africa.  Actually, the first AIDS cases were found in Manhattan in 1979. The epidemic in Africa did not begin until the fall of 1982.  I ask myself how could a supposed black heterosexual African epidemic transform itself into an exclusively white young homosexual mens disease in Manhatten?  As soon as the government sponsored gay hepatitis B experiment (1978-1981) ended in Manhatten in 1981 the epidemic became official. The first cases of AIDS in gay men appeared in Manhatten in 1979, soon after the gay experiment began in Manhatten NY. Dr. Theodore Strecker's research of the literature indicates that the National Cancer Institute (NCI) in collaboration with the WHO made the AIDS virus in their laboratories at Fort Detrick (now NCI).  They combined the deadly retroviruses, bovine leukemia virus and sheep visna virus, and injected them into human tissues cultures.  The result was the AIDS virus, the first human retrovirus known to man and now believed to be 100 percent fatal to those infected. All these different conspiracies make me believe that we need to research and investigate into possible man made diseases to expose the responsible and make sure this kind of thing (if it happened this way) will not be done again.


Microbial War

First it was hamburger, then municipal water, apple cider, swimming in the lake, the day-care center, the petting zoo ...... and now, spinach. Humans have been contracting foodborne infectious diseases in many environments and products. For example, last year the toxin, known as Shiga toxin- producing Escherichia coli was found in bagged spinach that implicated the illnesses of mild intestinal disease to severe kidney complications to over one hundred people, mostly affecting children under the age of eighteen.

“If you survived the Shiga toxin and the after-effects of food poisoning you may have been the innocent victim of a battle for survival between predator and prey.”

The bacterial ciliated protozoan Tetrahymena (shown left in picture) is fifty times the size of its bacteriophage (bacteria that carry a virus) competitor; however, it is vulnerable to the toxin-encoding virus-Shiga (Stx) the bacteria carry in their DNA (shown right in picture).

The bacteria may carry around these viral hitchhikers because the Shiga toxin (Stx) gene might give the bacterial host an equalizer against bacterial predators, like Tetrahymena. To test this idea, reasearchers exposed an E. coli stain that did not carry the Shiga toxin to the eukaryote, Tetrahymena and as predicted, the bacteria were eaten. Whereas, when the bacteria containing the toxin-encoding virus- Shiga, some produced the toxin and killed the Tetrahymena; therefore, allowing the remaining bacteria to spread because there were fewer Tetrahymena eating them.

The Shiga toxin kills by binding to a receptor on the surface of a Tetrahymena and performs endocytosis to release the toxins, which cause irreversible damage to ribosomes and thereby promoting cell death. The bacteriophage induces the toxin release due to the presence of Tetrahymena by activating an S.O.S response. Scientists are working on identifying the danger signals involved in triggering the response, which can have implications for treating patients.

"When you give antibiotics to patients infected with the Shiga-toxin-producing bacteria, it may make them even sicker" he said. "That's because in the process of killing off the bacteria, the SOS response causes even more toxin to be released to do even more damage."

In recent studies, the Shiga-toxin was not effective at killing some Tetrahymena's, due to the development of resistance of the toxin by the Tetrahymena; therefore, there may be a treatment method that would give human cells the ability to become resistant to the toxin, too.

Researchers believe that the microbial war between the bacteriophage and their predators may play a role in the treatment of patients with this toxin.

"We have a very mammalian way of thinking about this and it's wrong. We are a very small part of the entire ecology of the planet and just because something can hurt us doesn't mean that's why it's there."



Excenel - not all its cracked up to be?

This is Monique. She was born with some very serious conditions that forced her to spend her first couple months in a specialized horse clinic. Since, she has recovered to the point were she can now support herself and stabilize her metabolism without her mothers milk. The major problems leading up to this point in time have left her immune system suppressed and therefore susceptible to many common bacteria that can be found around a wet climate barn yard. It was no surprise that the "cold" that circulated briefly around the several other young horses, would reach Monique. But when the symptoms of her "cold" progressed far worse than those of the other horses, she was put on Excenel to help her get over the infection that was developing in her lungs.

Excenel is an antibiotic common among large animals that falls under Cephalosporins. Cephalosporins of this generation are classified as bactericidal, acting to inhibit the mucopeptide synthesis of the bacterial cell wall and creating an osmotically sensitive cell. They are different generations of chephalosporins, each with their own specificities and developed resistancies. For example, 1st generation Cephalosporins are more effective towards gram-positive bacteria such as S.intermedius and S.aureas (to name only two), and are consistently resisted by Streptococci, Enterococci, Methicillin-resistant Staphylococci, and Pseudomonas. 3rd generation cephalosporins are much broader spectrum with few recognized or tested resistant bacteria, while some antibiotics of the 3rd generation have proved particularly effective against Pseudomonas. Excenel is a new generation cephalosporin antibiotic used particularly in horses for its abilities against S.equi and Streptococcus zooepidemicus involved in common respiratory infections. Sounds promising right?

Wrong! Monique was given Excenel intramuscularly for a month straight, twice as long as Excenel advertises, but still, her symptoms persisted. A broad spectrum bactericidal drug that triggers common pathogens to horses should have worked well with Monique's suppressed immune system! What went wrong?

When a sterile swab was taken of Monique's mucus, Pseudomonas as well as S.aureus were isolated. Other forms of gram-positive mannitol fermenting Staphylococci were also present (could it have been possibly S.equi) as well as some very interesting other bacteria that could not be analyzed. The evidence of both S.aureus and Pseudomonas indicates the inevitable resistance factor. Has the bacteria causing the problem become resistant? It could be!

With the mucus sample we were able to take a look at the raw evidence through making a simple slide. The slide showed lots of puss, a very effective way to prevent antibiotics from reaching target areas of infection. Puss protects the bacteria causing the infection by acting as a barrier between antibiotics and the site of infection. Could this explain why such a highly regarded drug has failed in Monique's case? Possibly.

Monique was in a specialized hospital for months. Within the sterile walls of any medical institution, bacteria are discouraged in as many ways as possible creating a selective pressure. Many hospitals today are facing the man made circumstance of MRSA, Methicillin resistant Staphylococci. Recall that for first generation cephalosporins MRSA are resistant. Could it be that Monique actually suffers from something more than a common respiratory bacterial infection? Could she have contracted MRSA somewhere in the hospital? The other horses she has come in contact with have recovered meaning that she has most likely not contracted MRSA.

Monique's case is very complicated and no serious conclusions can be drawn without further extensive testing, however, some theories from micro biology 202 can be applied. The antibiotic was unable to penetrate the infection causing bacteria due to resistance factors or the antibiotic was unable to localize the infection site due to prevention variables. The possibility of MRSA exists but is unlikely. Excenel did not work and continues to not work. The veterinarians are now looking into some other options such as a tracheal flush. The bacteria that is causing the problem has evidently proved its virulence and therefore the next step is for the veterinarians to culture the bacteria from the lower respiratory track and examine the real "enemy". Email for updates!
Dr.Margret Clarins (JDF vet)
Veterinarians hand book of drugs (trust me - this is not a hand book)
Linda Scotten (Instructor at Camosun College) (THANK YOU!!)

Hendra is such a pretty name.

There has been an onslaught of (quasi)movies in the last few years which focus on the impending doom we may one day face from zombies/vampires/global warming. While these flicks often temp our tender imaginations, it would seem the most realistic threat we may one day face comes from bite sized flying rodents.

Back in 1994 a strange thing happened. A strange virus was discovered at a horse stable, where it had killed 13 horses, and one human. The source of the outbreak was hard to pinpoint because of the rapid emergence and retreat of the pathogen, but after some clever sleuthing the case unfolded. The virus was found to stem from contact with bats, and further testing found consistent ( albeit low) traces of the virus in local bats. The virus was named “Hendra”, for the small town in Australia it was first discovered in, and although it has never risen to the fame of ebola or the plague it shares many traits with these two known killers.

For one thing, it’s fast paced and lethal. There was nothing to be done for the infected horses, and of the two humans who showed symptoms, only one survived. Since this outbreak over a decade ago, Hendra, and its relative Nipah have repeatedly struck with deadly results, resulting in a swarm of research. Nipah has proved to be the more dangerous of the two, killing 105 humans, and resulting in the culling of over a million pigs in Malaysia in 1999.

The term “zoonosis” is another item connecting Hendra and Nipah, to the Plague, and Ebola. It refers to a pathogen which is harbored in animals, and then crosses over to affect humans. Approximately sixty percent of human infectious diseases start this way, ranging from common strains of influenza to West Nile Fever. Could zoonosis inspire our fear to the degree that zombies have? Maybe not, but it’s a more realistic enemy to be sure.


National Geographic, Octover 2007, pg82-85.

The Forgotten Fungus

When reports first came out about the “deadly fungus” the newspapers were flooded with articles pertaining to Cryptococcus gatti. Nowadays, the newspapers only occasionally report on the “forgotten fungus”.

On June 6, 2002 the B.C. Centre for Disease Control issued a health advisory, including possible symptoms of the disease, as to the emergence of Cryptococcus on Vancouver Island. Cryptococcus is a microscopic yeast that is found in the air, trees and soil of Vancouver Island and is responsible for disease in humans and animals in British Columbia since 1999. Cryptococcus is found throughout the world, in Southern California, Australia, Central and South America, Africa, India, South-east Asia and Spain, but is new to Canada. It is not known exactly how the Cryptococcus fungus came to be in British Columbia but it is suggested that imported tropical plants are to blame or that it may have always existed here and is now prevailing due to climate or environmental changes (ie increased air borne concentrations due to drier than normal summers). Either way, it has been considered the world’s largest outbreak of Cryptococcal disease ever identified.

Cryptococcal disease is caused by the inhalation of the air borne fungal spores that can be carried via wind many kilometers from the source. The disease cannot be transferred human to human or from animal to human and vice versa, it is not contagious. Once in the lungs, Cryptococcus gatti can cause pneumonia, meningitis, lung nodules, and can affect the central nervous system. The incubation period is anywhere from 2 to 9 months and initial symptoms can include headaches, night sweats, fever, prolonged cough, and weight loss in humans and runny noses, coughs, lumps under the skin, changes in personality, blindness, and seizures in animals. Cryptococcal disease can be diagnosed in humans and animals by using an antigen test and if detected early enough, can be treated with antifungal medication.

There is no vaccine for Cryptococcus and no recommended precautionary measures to avoid the disease. Nor are there any fungicides or chemicals to apply to the trees for protection. However, knowing the symptoms and alerting your doctor or veterinarian is helpful in early diagnosis and treatment. It is reported that even in central Vancouver Island areas, doctors and veterinarians are not very familiar with the disease and outside of B.C. most physicians are not aware that Cryptococcus gatti may be responsible for infection. On a more positive note, not everyone who breathes in the airborne spores becomes sick. Areas of Vancouver Island where the fungus was first located remain open to the public and none of the people who regularly work there have ever reported serious illness. The risk of contracting the disease is very low considering the amount of exposure and confirmed cases in the past. Thus, the benefits of getting outside and remaining active should strongly out way the risk of infection.

Although Cryptococcus gatti is responsible for what has been considered the world’s largest outbreak of Cryptococcal disease ever identified, it has failed to capture the attention of the media. Even in central Vancouver Island where the fungus is most prevalent, there is very low coverage. It is estimated that Cryptococcus gatti has had less than one fifth the coverage West Nile has received, and West Nile has yet to even spread into British Columbia. The majority of the 176 confirmed cases from 1999-2006 are linked to Vancouver Island, however, by the end of last year 6 cases where confirmed on the lower mainland with absolutely no link to the island. Though it has not had the media coverage it perhaps should have, the expansion of Cryptococcus gatti shows it is a fungus to be reckoned with.