Horizontal Gene Transfer

In the past, it has been widely accepted that “new biological functions, such as antibiotic resistance, in bacteria and other microbes arise primarily through the process of gene duplication within the same organism,” (Treangen, T.J. & Rocha E.P.C., 2011). However, current research suggests that bacteria evolve new abilities primarily by obtaining genes from other bacteria. Bacteria are able to survive in extreme and various environmental conditions because of their ability to quickly modify their genes. According to Treangen and Rocha (2011), this modification of proteins takes place either by “duplication processes followed by slow functional specialization,” in the same way as large, multi-cellular organisms, or by “acquiring different genes directly from other microbes,” also known as horizontal gene transfer.

Recent attempts to simulate the evolution of the genetic code (using the same DNA bases but with different associations of codons and amino acids) through traditional mechanisms were not successful. The code was not shared among all organisms and none of the codes evolved to reach the optimal structure of the actual code (Hunter, 2010). When the scientists simulated horizontal gene transfer of the genetic code, species could successfully exchange genetic material and swap parts of the genetic code and readily discovered the overall optimal structure. This optimal structure became universal among all organisms in the simulation.

While Horizontal Gene Transfer has been studied since 1975, new findings in HGT could change the way scientists view and study biological networks and protein evolution in microbes. It also raises the question of whether eukaryotes evolve in the same way.

References:

http://www.newsdesk.umd.edu/global/release.cfm?ArticleID=2322

http://darwins-god.blogspot.com/2010/11/did-horizontal-gene-transfer-create.html

http://www.the-scientist.com/news/display/57962/

A possible solution to disastrous oil spills

Oil Eating Microbes

~Beth Morris

Imagine that there are tiny organisms in the ocean that eat crude oil. According to German microbiologist, Dietman Pieper, there is such an organism. Though it is clear that these microbes can and do degraded massive amounts of petroleum; off the Gulf of Mexico they have been known to consume much as two Exxon-Valdez oil spills within a year’s time through natural leaks from the earth’s basin. This process is better known as bioremediation. Scientist states that approximately 1,700 out of about 5,000 genes of microbes are capable of consuming oil. Though there are many different qualities to crude oil such as methane and benzene, each microbe serves a specific purpose and can only degrade one particular particle of the oil. Though if the bacteria work as a whole, they can band together and degrade an oil spill. What happens in the process is the microbes take from the plumes of oil, oxygen and hydrocarbons and digest them into CO₂. There was debate as to whether these bacteria could perform properly in cold water, such like the Gulf of Mexico. It has been found that the certain microbes living in the Gulf reproduce at a faster rate than they would in a warmer climate. The microbes work more quickly on plumes that contain less dense crude. For example, the Exxon Valdez oil spill contained heavier oils than did the BP spill, which is seemingly why the BP spill disappeared from the ocean more quickly.

"There is no compound, man-made or natural, that microorganisms cannot degrade,” says Terry Hazen, head of the ecology department at the Lawrence Berkeley National Laboratory in California. In 1981an organism was created in a laboratory to mirror a strain of Pseudomonas. This was designed in effort to do the “oil-eating dirty work of four species in one”. However, nothing works as well as microbes found naturally in the ocean. Scientist continue to research new fields one of which is metagenomics. This field explores the DNA of the bacterial community within its natural habitat. Through this research, Biologist J. Craig Venter has discovered approximately 2,000 species in an area that was believed to harbor very little life. The sea, however continues to challenge researchers with its “complex and uncontained” mass, as they push forward to understand this amazing ecosystem.

http://www.onearth.org/article/tiny-critters-that-eat-oil

http://www.scientificamerican.com/article.cfm?id=scientists-break-down-oil

http://news.sciencemag.org/sciencenow/2010/08/bacteria-are-gobbling-gulf-oil.html

Growth Inhibition of Three Strains of E. Coli Via Certain Probiotic Strains of Lactobacillus

Most of us probably recognize E. Coli as the culprit of many outbreaks resulting from food borne contamination.  Perhaps one would recall a 1996 outbreak in Japan in which over 6000 primary school children were infected with E. Coli 0157, 1000 of whom were hospitalized for anything from hemorrhagic colitis (bloody diarrhea), to hemolytic uremic syndrome (kidney failure); or a 2002 outbreak in the U.S. associated with contamination of ground beef.  Currently, there is no vaccine for the particular strain of E. Coli 0157:H7, however, aside from following basic steps of hygenic prevention of the diseases caused by enterovirulent strains of E.Coli, alternatives are being explored.

One such investigation conducted in 2009 by researchers, Erin L. Piper and Kathryn J. Leyva explored a keen, yet perhaps seemingly simple alternative to counteracting the serious effects of two virulent strains of E. Coli: 0157:H7 and Entertoxigenic E. coli.  Piper and Leyva experimented with the growth inhibition of these strains of E. coli, (and another non-pathogenic strain, E. Coli 25922), by exposing the pathogenic bacteria to probiotic species of Lactobacillus: L. acidophilus, L. casei, L. fermentum, and L. rhamnosus.  Previous investigations had demonstrated that certain Lactobacilli produce by-products called bacteriosins and adhesive factors which provided a noticeable degree of protection from enteric pathogens.  Based on this premise, the four strains of Lactobacilli were cultured on Man-Rogosa-Sharpe broths, and introduced to the three strands of E. Coli (cultured in Tryptic Soy Broth) to "determine the inhibitory activity of Lactobaccilus spp. against each of the three strains of E. coli." 

Three separate experiments were performed, the first two of which utilized live lactobacilli inoculated with each strain of E.coli. and the third of which utilized supernatant gathered from the lactobacilli. 

None of the experiments demonstrated complete growth inhibition of any of the E.coli strains, however the degree of inhibition varied based on the method used. "Our experimental findings suggest that Entertoxigenic E. coli was strongly inhibited when exposed to live lactobacilli cells, but only partially inhibited when exposed to supernatant alone."  On the other hand, Enterohemorrhagic (0157) E. coli was "equally inhibited by exposure to live cells or supernatant."  Needless to say, while this experiment was helpful, solutions to completely avoid such diseases have yet to come to fruition and the difficulty of finding a means to eradicate such diesase serves as a continued testament to the potency of bacterial resistance to scientific defenses.

Growth Inhibition of Gastrointestinal Strains of Eschericia coli by Lactobaccilus Species; Erin L. Piper and Kathryn J. Leyva. Journal of the Arizona-Nevada Academy of Science 2009
http://www.jstor.org/stable/25702615

http://www.medicinenet.com/script/main/art.asp?articlekey=2039

http://www.jstor.org/stable/20056769

E. coli to N-Butanol

Scientists at UCLA are developing ways to produce N-Butanol for the bacteria Escherichia coli. N-Butanol is used as a "greener" substitute fuel for diesel and gasoline. For every Liter of culture medium 15-3 grams of N-Butanol was produced. The basic steps are converting aceytl-CoA to n-butanol. E. coli does not naturally produce N-Butanol, but after adding metabolic driving forces to the pathway the production increased tenfold. E. coli was used in this project because it is very easy to manipulate, and it will only produce what it is engineered to produce without any byproducts. Some companies have went so far as to take out the enzyme from the bacteria that produces n-butanol and inserted it into other microbes such as yeast. This makes it easier to grow on an industrial scale. The production of n-butanol is very limited.

The ultimate goal of the production of n-butanol is for a safer environment for everyone. "If microbes can be engineered to turn nearly every carbon atom they eat into recoverable fuel, they could help the world achieve a more carbon-nuetral transportation fuel that would reduce the pollution now contributing to global climate change" (sciencedaily.com). Reasearchers are very optimistic that they can boost the production of n-butanol two to three times what it is now, and have enough to justify scaling up to an industrial process. They are also trying to incorporate yeast into the process because it speeds up many chemicals.

http://www.sciencdaily.com/release/2011/03/110302091648.htm http://www.sciencedaily.com/release/2011/03/110317102603.htm

Bacterial infections can cause various dangerous diseases and conditions, including the necrotic Buruli ulcer, found most commonly in Africa. When antibiotics were introduced as treatment for many bacterial infections, great strides were made in reduction of morbitity and mortality. In recent years, however, some of these bacteria have become resistant to the antibacterial nature of these drugs, resulting in very dangerous infections such as MRSA (methicilline resistant Staphylococcus aureus). A new method of treating bacterial infections may be emerging through the use of French clays.

In 2001, a French humanitarian in the Ivory Coast began treating patients with Buruli ulcer with a poultice made from clay minerals. One of these, CsAg02, has been shown to be bactericidal against the following bacteria: E. coli, ESBL E. coli, S. enterica, P. aeruginosa, and M. marinum. It has about a 1000 fold reduction effect on these bacteria: S. aureus, PRSA, MRSA, and M. smegmatis, compared to normal growth. The bacteria chosen for this study are those recommended for testing of antimicrobials in the lab, with the exception of M. marinum, which was chosen because of it's close DNA similarity to Mycobacterium ulcerans (which cause Buruli ulcers).

The cause of the bactericidal effect of CsAg02 is yet to be determined, although the physical properties of clay (such as suffocating the bacteria, etc) seem to be ruled out. One thing that was looked at were several elements such as iron, barium and strontium which are in high concentrations in this clay mineral. However, when tested independently on these bacteria, the each element seems to actually increase growth. This is assumed to occur because these elements are needed for cell growth and may be a limiting factor in typical growth medium (broth or solid agar), instead of interfearing with cellular processes by inhibiting transport mechanisms or substituting as coenzyme factors.

It seems that the creation of an inhospitable environment may be the key mechanism that kills bacteria. A proposed idea along these lines is that the transition metals present in clay minerals take part in reactions that release free radicals. These free radicals, when in the presence of oxygen, can cause oxidative stress on the bacterial cells, killing them. Although not yet fully understood, the use of clay minerals may become part of antibacterial treatment in the future.

Links:

http://www.sciencefriday.com/newsbriefs/read/152

http://jac.oxfordjournals.org/content/61/2/353.full

Photo:

http://www.squidoo.com/volcanicashclay

Fighting off the Flu with Bacteria?

For many people, bacteria seem inexplicably disgusting and we attempt to rid ourselves of bacteria, both good and harmful. However, without bacteria, the human body would fail to have a normally functioning immune system, as was discovered by scientists in 1950s. Since this discovery, the role of bacteria in the immune system development and response has been extensively studied, with the knowledge of this friendly bacterial primarily confined to the digestive system. Furthermore, a recent study provides some evidence in bacteria helping with immune system response properties in the lungs, in particular relationship with the flu.

The flu is a highly contagious respiratory illness, caused by the influenza virus. It can cause mild-severe illness, that can lead to death in highly susceptible populations who are immunocompromised such as the very young, elderly, and people with chronic diseases such as diabetes, cancer and heart disease (CDC ). Each year teams of researchers collect strains of flu circulating in the Southern Hemisphere and determine which strains will become the most virulent and contagious. With this research of newly emerging or evolving flu strains, onto the scene of infectious disease, a new vaccine is developed with the influenza strains expected cause illness. Then each fall and winter, Public Health officials urge the public to get their annual flu vaccine, in preventing the flu. However, nearly 36,000 people succumb to the flu each year, mostly the medically fragile populations, being particularly vulnerable to the flu. Now promising new research from the country's leading scientists are suggesting that bacteria play a role in preventing the flu virus from attacking the body, by helping to implement an immune response, not only in the digestive system, but in the lungs.

A team of researchers, led by Akiko Iwasaki, an immunologist from Yale University, in New Haven Connecticut have discovered that mice treated with neomyocin antibiotics were more susceptible to the influenza virus than mice in the control group. During the study, Iwasaki and her team treated the mice with four different antibiotics that are commonly given in humans with bacterial infections and then they were infected with the flu. Then Iwasaki and her team studied the effects of bacteria, which “kick-stared the flu-fighting pathway by activating proteins involved with inflammatory defense, which activates the cytokine interleukin that triggers dendritic immune cells to migrate to lymph nodes in the lungs" (Maxmen 2011). Once in the lungs, these immune cells begin a potent attack on influenza viruses. In the mice which were treated with neomyocin antibiotics, it was found that the inflammatory initiating proteins, were not activated and the influenza virus multiplied.

Although the exact bacteria that comes into play is not completely known, according Iwasaki, it is suggested that “the bacteria involved in this response is from the Lactobacillus species, because the mice treated with antibiotics, wipes out the Lactobacillus populations that are found in the gut." With roughly 100 trillion bacteria residing on/within the human body, this study highlights the importance of friendly bacteria, not only in known studies from the benefits in the gut, but also immune response in the lungs.

Resources:

http://www.sciencenews.org/view/generic/id/71187/title/Antibiotics_may_make_fighting_flu_harder

http://www.nature.com/news/2011/110314/full/news.2011.159.html?s=news_rss

UVA Radiation Damages DNA in Human Melanocyte Skin Cells and Can Lead to Melanoma

Studies show that UVA radiation damages the DNA in human melanocyte cells, causing mutations that can lead to melanoma. Melanocytes darkens the skin to protect it from ultraviolet rays of the sun. "For the first time, UVA rays have been shown to cause significant damage to the DNA of human melanocyte skin cells," says Moon-shong Tang, PhD, professor of environmental medicine, pathology and medicine at NYU School of Medicine. "And because melanocytes have a reduced capacity to repair DNA damage from UVA radiation, they mutate more frequently, potentially leading to the development of melanoma."

Sunlight in the form of UVA radiation causes oxygen in melanocytes to damage DNA. Oxidative DNA damage adversely affects transcription and DNA replication in melanocytes. Researchers exposed lightly and darkly pigmented human melanocytes to UVA radiation and assessed DNA

damage and the capacity of these cells to repair damaged DNA. DNA damage was detected in all melanocyte cells and these cells were unable to repair the damage. Normal skin cells were also exposed to UVA light but no damage to their DNA was observed.

In humans, prolonged exposure to solar UV radiation may result in acute and chronic health effects on the skin, eye, and immune system. UVA, UVB and UVC can all damage collagen fibers and thereby accelerate aging of the skin. The Sun emits ultraviolet radiation in the UVA, UVB, and UVC bands, but because of absorption in the atmosphere's ozone layer, 99% of the ultraviolet radiation that reaches the Earth's surface is UVA.

The authors concluded that UVA-induced oxidative DNA damage in melanocytes and the inherently reduced repair capacity in these cells are the two key factors that contribute to melanoma on the skin. The authors also discovered the underlying mechanism to explain why melanoma can also develop in areas never exposed to sunlight: Because melanocytes generally have a limited capacity to repair any DNA damage, they have a higher mutation frequency rate and are more susceptible to the development of melanoma -- even without the effects of the sun.

http://www.sciencedaily.com/releases/2010/07/100701103415.htm

http://www.sciencedaily.com/articles/u/ultraviolet.htm

http://www.google.com/images?hl=en&source=hp&q=melanoma&btnG=Search+Images&gbv=2&biw=1024&bih=677

Hospital Infections: C. difficile

When going into the hospital for treatment, most don't think about coming out with a serious disease. The disease caused by the toxins of Clostridium difficile is probed by good bacteria in the intestines being weakened by antibiotics, allowing the spores of C. difficile to evolve, form colonies, and attack the lining of the large intestine. This disease affects approximately two percent of the people that are hospitalized, with favor to the geriatric population.

To test the theory that this is a hospital- obtained bacterium, a research was done on 385 cases of C. difficile from 1991- 2005. Of the 385 cases, 192 of them were obtained from a hospital setting and another 35 was obtained from nursing home. It is more likely to obtain this bacterium in a hospital, but it is also possible to get this strand of bacteria in the community, outside of a medical setting.

When C. difficile is obtained from the community, it tends to not be as serious and affect a younger generation. This is most likely because people in the community have not recently been exposed to antibiotics like those who were hospitalized, therefore the good bacteria in their intestine was not being weakened by antibiotics. C. difficile is becoming more common in both the hospital and community. Antibiotics are being used more frequently and for illness of less importance, so more people are being exposed and affected.

Following the germination of C. difficile, patients will experience very painful stomach cramps, diarrhea, severe flu- like symptoms, and in some cases, deadly inflammation of the colon. Doctors are better able to recognize C. difficile now, making it easier to treat. The CDC references that C. difficile is responsible for at least 5,000 deaths.

Current treatment methods are not as effective as they once were because C. difficile is becoming resistant to the antibiotics used to treat it. Because it is becoming resistant, researchers need to find something more versatile that will treat C. difficile and not act as a typical antibiotic. A very interesting twist is added when it was discovered that a biosensor in the blood of llamas could be beneficial to treat C. difficile.

As mentioned earlier, C. difficile generates two different toxins, TcdA and TcdB. Both of these toxins destroy the intestinal cells by binding to the carbs on their surface and prohibiting adhesion. It has been learned through research that a single- domain cell (sdAb) could break this pattern and impede the damage to the cells of the intestine. Llamas, camels and sharks have a second antibody that is much like a human antibody, but ten times smaller, which allows it to be easily manipulated into something useful. The antibody is called a heavy chain antibody, which is derived from the single domain antibody that researchers are utilizing. Besides their small size and versatility, they are optimal for use because they are low maintenance, but highly efficient.

http://www.sciencedaily.com/releases/2009/10/091026132937.htm

http://www.sciencedaily.com/releases/2011/03/110318111927.htm

http://www.sciencedaily.com/releases/2008/10/081006180511.htm

http://www.sciencedaily.com/releases/2006/12/061204093742.htm

Pathogenic Microbes Growing on Orthodontic Retainers

Our mouths are full of different types of bacteria, some of which promote oral health and some that can be toxic to our bodies and oral cavity. Researchers have recently discovered two species of microbes that are not typically found in the mouth. The two potentially pathogenic microbes, Candida, a type of yeast, and Staphylococcus including MRSA, were found in at least 50 percent of people who wear orthodontic retainers. Researchers state that Candida and Staphylococcus rarely cause health problems unless the individual's immune system is weak. However, if Candida does become pathogenic it will release dozens of different toxic substances that affect all the organs and tissues of the body causing multiple health problems. Staphylococcus, commonly referred to as Staph, causes a wide range of infections, food poisoning, and toxic shock syndrome.

The bacteria, Candida and Staphylococcus, live in biofilms on the surface of the retainer. A biofilm is a community of bacteria living together covered in a layer of slime. Biofilms are found anywhere a combination of moisture, nutrients, and a surface exists (that slimy layer on the sides of a pool or a hot tub are biofilms). Biofilms are usually so thin that they cannot be seen by the naked eye, but in certain cases they can become very thick and apparent. When this slimy film forms on the surface of the retainer it is very difficult to remove and it often has a high level of resistance to antimicrobials.

Finding these two potentially pathogenic microbes could indicate a need for the improvement of cleaning products for orthodontic retainers to eliminate the biofilms that house these toxic microbes. However, for now hygiene is the main method in reducing the transmission of these bugs. Mouthwashes and careful tooth brushing may help to keep the microbes off of the cheeks and tongue which in turn will keep it off of the retainer. It is also important to keep in mind that anyone who handles a retainer should be sure to wash their hands before and after handling.

http://www.sciencedaily.com/releases/2011/03/110315093832.htm

http://www.cs.montana.edu/ross/personal/intro-biofilms-s1.htm

http://www.textbookofbacteriology.net/staph.html

http://www.holistichealthtools.com/candida.html

The role of bacteria in periodontal disease

Healthy gums are coral pink with no bleeding, no inflammation, and a pocket depth reading of only 3 mm or less all the way around each individual tooth. Gingivitis is when your gums appear red, swollen and bleed, but typically this is due to a lack in homecare (brushing/flossing), or hormone involvement such as pregnancy. Gingivitis is the first stage of infection, but it can be reversed by maintaining regular cleanings by your dentist, goodhomecare, and other products, such as mouthwashes to decrease microbe growth.

Periodontal disease happens when gingivitis progresses. Symptoms include swollen, red, puss, bleeding or pocket depth readings greater than 4 mm. If home care is not adequate then plaque will remain on teeth and if left long enough it will calcify and turn into calculus (Also known as tartar). These bacteria continue to hibernate below the gum line in the “natural pocket” space. The bacteria then continue to multiply and can be destructive to the Periodontal ligaments, causing the gums to recede, and then the supporting structure of bone is destroyed. Having periodontal disease also means having a constant low grade infection in the body. Dental research is on the rise about its affects to your overall health.

Online research shows there are many types of microbes living in your mouth with bacteria being the most abundant. There are over 100 million in every milliliter of saliva from more than 600 different species. Not all bacteria in the mouth are harmful but most are killed by either stomach or saliva enzymes. However, certain bacteria are responsible for periodontal disease and tooth decay. Some examples of the bacteria found in mouth are: Streptococcus Mutans, which is known to digest sugars and starches in foods and produce acids which dissolve tooth enamel. This is a gram positive bacterium that grows under anaerobe, and aerobe conditions, and is part of the normal flora of the mouth. S.mutans is one bacterium that has receptors that aids in adhesion to teeth. This bacterium sits on teeth and causes tooth decay. Another different type of bacteria that is associated with periodontal disease is Porphyromonas gingivalis. P. Gingivalis is a rod shaped gram negative anaerobe found in periodontal lesions and is associated with adult periodontal diseases such as gingivitis, periodontal infections and mouth abscesses.

According to American Academy of periodontology research, there is an association between periodontal disease and chronic inflammatory conditions, diabetes, cardiovascular disease and Alzheimer's disease. Having a healthy mouth and managing inflammation and bacteria will not only help reduce periodontal disease but help manage overall health. Periodontal disease and bacterial decay can be easily prevented with good daily oral hygiene and regular visits with the dentist. Dentists have products such as mouthwashes, chewing gums, sprays and toothpastes that can regulate PH, and control harmful bacteria from sticking to your teeth and gums,therefore causing damage.

References used:

http://www.brighthub.com/science/genetics/articles/45935.aspxwww.perio.org/consumer/mbc.top2.htm

http://www.denniskunkel.com/DK/Bacteria/26708A.html

http://www.perio.org/consumer/mbc.top2.htm

Diagram used:

http://www.umm.edu/patiented/articles/whatsymptomsofperiodontaldisease0000242.htm

Why Low Birth Weight Is Linked to Obesity Later in Life

Infants with low birth weights are more likely to struggle with obesity problems later in life. Why? The findings from the research show that newborn babies are programmed to overeat at the level of stem cells before birth when the mother has deprived nutrition. Their work with laboratory animals found that newborns with low birth weight had fewer neurons in the area of the brain that controls food intake than those with a normal birth weight. The researchers noted that previous studies have shown that babies that have a low birth weight and then experience an accelerated "catch-up" growth are at increased risk for health problems later in life, such as obesity, heart disease, type 2diabetes, high blood pressure and osteoporosis. "This study demonstrates the importance of maternal nutrition and health in reducing obesity," said Dr. Mina Desai. “Obesity and its related diseases are the leading cause of death in our society, yet we have few effective strategies for prevention or treatment. These studies suggest maternal nutrition could play a critical role in preventing obesity and related disease." In addition to obesity, the findings of altered brain (neural stem cells) development suggest that fetal growth restriction may be associated with cognitive and/or behavioral alterations.

Most pregnancies last about 40 weeks. About 12 percent of babies in the United States - or 1 in 8 - are born prematurely each year. In 2003, more than 490,000 babies in the U.S. were born prematurely. The shorter the term of pregnancy is, the greater the risks of complications. In the United States, more than 60% of adults are overweight and more than 20% are obese, and about 17% of children and teens aged 2 to 19 are obese, according to backg

round information in the news release. Numerous parental influences shape the eating habits of youth including; the choice of an infant feeding method, the foods they make available and accessible, the amount of time children are left unsupervised and their eating interactions with others in the social context. Several studies suggest that breastfeeding offers a small but consistent protective effect against obesity in children.

Appetite is regulated by a close interplay between the digestive tract, adipose tissue and the brain. Studies show that children who eat a school lunch instead of a packed lunch are more likely to be obese. The same goes for children who stay inside and watch hours of TV or play video games instead of being active outside. According to the findings, 15 percent of the middle-school students were obese, but nearly all, whether overweight or not, reported unhealthy habits. More than 30 percent had consumed regular soda the previous day, and less than half remembered eating two portions of fruits and vegetables within the past 24 hours. Only one-third of students said they exercised for 30 minutes for five days in the previous week. Looking at the long-term consequences, overweight adolescents have a 70 percent chance of becoming overweight or obese adults, which increases to 80 percent if one or more parent is overweight or obese. Parents need to get more involved with their children so they can get them on right eating/exercising habits before it is too late.

http://aspe.hhs.gov/health/reports/child_obesity/

http://www.sciencedaily.com/articles/p/premature_birth.htm

http://www.foodproductdesign.com/news/2011/01/childhood-obesity-linked-to-lifestyle-choices.aspx

http://www.sciencedaily.com/releases/2011/03/110310070311.htm

HPV and Cervical Cancer

If your a woman or even a man in todays society then I'm sure you have heard of Gardasil. Gardasil is a vaccine that can protect against four types of Human Papillomaviruses (HPV).  The vaccine can protect against two types of HPV that can cause cervical cancer, cancer of the cervix, and two more types that cause genital warts. Although outside of those four types of HPV, there are more than a 150 viruses that are related. Forty types of these viruses are sexually transmitted, even through only genital contact. Types 16 and 18 cause about 75% of cervical cancer cases in women and types 6 and 11 cause about 90% of genital warts in females and males.

It has been recognized that HPV is directly related and the cause of cervical cancers. There are two types of HPV that are related to cervical cancer and these are named low-risk and high-risk types. Both of the types can create growth of abnormal cells, but the only type of HPV that leads to cancer is the high-risk type. Once those cervical cells begin to change, it can take 10-15 years before an invasive cervical cancer appears. When the cells change they become pre-cancerous and if detected early on, it can be treated before the cells become cancerous.

The problem that people have who contract HPV and who are at risk for cervical cancer, is that there are very little symptoms and it is said that symptoms do not always occur. A few symptoms include; low back pain, pain during sex, and painful urination. These symptoms can also be connected to many other conditions and therefore it doesn't mean a person necessarily has cervical cancer.

Cervical cancer is more common in woman than men and the reasons are unknown, but regardless it can be deadly.There are 30 women each day in the United States that are diagnosed with cervical cancer. In 2010 it was estimated over 12,000 women would be diagnosed with cervical cancer and and that 4,000 women would die from it.

To stop women from being victims of cervical cancer, HPV can be detected early on. HPV DNA tests are used to look for viral DNA and can detect a viral infection before abnormal cells appear. Another test used is the Pap test, which is a screening test that detects cervical cell changes. All of these tests are approved by the FDA for women but unfortunately there aren't any approved tests for men.

http://www.cancer.gov/cancertopics/factsheet/Risk/HPV

http://www.gardasil.com/hpv/human-papillomavirus/index.html?WT.mc_id=GL0ES&MTD=2

http://www.thehpvtest.com/about-hpv/cervical-cancer-faqs/?LanguageCheck=1

http://img.thebody.com/press/2008/nobel_hpv.gif