Genome of parasite responsible for trichomoniasis sequenced


Researchers have decoded the genetic makeup of the parasite that causes trichomoniasis, one of the most common sexually transmitted infections ( STIs ), revealing potential clues as to why the parasite has become increasingly drug resistant and suggesting possible pathways for new treatments, diagnostics and a potential vaccine strategy.

Trichomoniasis is a sexually transmitted infection that affects both men and women and results in roughly 7.4 million new cases in the United States each year, according to the Centers for Disease Control and Prevention ( CDC ).

In women, trichomoniasis infection commonly occurs in the vagina, resulting in heavy yellow-green or gray vaginal discharge, vaginal odor, discomfort during sexual intercourse and urination, irritation and itching of the genital area and, in rare cases, lower abdominal pain.
In men, trichomoniasis is most common in the urethra; however, infected men often do not have symptoms. Those that do may experience irritation inside the penis, mild discharge, or a slight burning sensation after urination or ejaculation. Symptoms in both men and women generally appear within five to 28 days of exposure to the parasite.

Both men and women with trichomoniasis have an increased susceptibility to HIV infection and may transmit HIV to their sexual partners. Pregnant women with trichomoniasis may deliver a low birthweight or premature infant. Although the prescription drugs Metronidazole and Tinidazole usually cure trichomoniasis, drug resistance has become an increasing concern.

Trichomonas vaginalis is pear-shaped with thread-like flagella that propel its movement. Once it attaches to cells lining the host's urinary or genital tract, it flattens out and begins to ingest the cells, as well as white and red blood cells, causing direct damage to the urinary and vaginal tissues and resulting in inflammation. Trichomonas vaginalis also consumes bacteria that may be present in the urinary and genital areas, including the bacteria necessary for maintaining a normal healthy environment in the vagina. As a result, women infected with trichomoniasis become more susceptible to becoming infected by HIV and other STIs.

In generating the genetic blueprint for the parasite, researchers were surprised to find such a large and highly repetitive genome comprising nearly 26,000 predicted genes as determined by computer models and previously sequenced parasitic genomes. Repetitive genes accounted for roughly 65 percent of the genome.

" Parasites generally have smaller amounts of DNA than non-parasitic organisms, but in this case, there was ten times as much DNA than we originally thought there would be," says lead author Jane M. Carlton, who led the project while at The Institute for Genomic Research ( TIGR ). Carlton is now at New York University's School of Medicine.

Although it is not entirely clear why the genome is so large and repetitive, researchers theorize that the parasite evolved over time, previously inhabiting the intestine and later moving to the urogenital tract, which resulted in increased cell size and, subsequently, a considerably expanded genome.

The researchers also discovered more than 150 instances where bacterial genes may have transferred into the parasite's genome, suggesting that bacteria may have influenced the development of the parasite's metabolism. The decoded genome also revealed 800 genes for surface proteins that likely enable Trichomonas vaginalis to adhere to cells in the urinary and genital tracts and cause infection. Additionally, the researchers were able to analyze proteins thought to be linked to the parasite's hydrogenosome, its energy source, and identified possible ways the parasite may become resistant to these medications. Understanding how Trichomonas vaginalis causes infection and developing methods to prevent it could also help curb the transmission of other STIs often found in connection with trichomoniasis, including chlamydia and gonorrhea, according to the researchers.

Source: National Institutes of Health, 2007

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