A long-term study looks at the secondary health issues faced by those who suffer from pelvic inflammatory disease, which about one in eight women in the U.S. contract before the age of 20

Women who suffer from pelvic inflammatory disease (PID) may be at higher risk of infertility, according to a new long-term study. about one in eight girls contract PID before the age of 20 in this country.

The inflammatory condition develops when bacteria move up from the vagina to the higher reproductive organs like the uterus, fallopian tubes, and ovaries. it used to be that most cases of PID developed as a result of sexually transmitted diseases (STDs) like chlamydia and gonorrhea, but it’s now known that other microbes like Mycoplasma genitalium are responsible for more cases.

PID can also occur after childbirth, insertion of an intrauterine device (IUD), or miscarriage. Symptoms include pain in the pelvis, vaginal discharge, fever, fatigue, menstrual problems, and pain or bleeding during or after intercourse.

The new study followed over 800 women with mild to moderate PID, who were between the ages of 14 and 38. the research team tracked how many bouts of PID the women had over a period of seven years along with their symptoms, how often they were infertile, and how often they got pregnant.

About 20 percent of the women with PID were infertile, 57 percent got pregnant, and 43 percent reported chronic pelvic pain. Women who had repeated bouts of PID were twice as likely to suffer from infertility as women whose PID never returned after being treated initially. and women with repeated episodes of PID were five times as likely to report pain as women without PID.

“The fact that close to one-fifth of these girls were already showing signs of infertility is quite alarming,” said author Maria Trent, “and might mean that the numbers will increase as these girls get older and actively try to get pregnant.”

Women should not think that PID is a thing of the past. it is very important to continue to protect oneself from STDs by using condoms. “When it comes to [pelvic inflammatory disease],” said Trend, “we must remain as vigilant as ever. Even though PID has changed over time, it is still very much a disease that can have detrimental consequences to a woman’s childbearing ability and can lead to chronic pelvic pain down the road.”

If you are concerned about PID, or STDs, it is important to go see your doctor as soon as possible for correct diagnosis and treatment.

Trent is a researcher and clinician at Johns Hopkins Children’s Center. the study was published in the September 2011 issue of Sexually Transmitted Diseases.

Image: wanchai/Shutterstock.

This article originally appeared on TheDoctorWillSeeYouNow.com, an Atlantic partner site.

February 28, 2011 17:28 PM

Scientists Find Way to use Microbes to Treat Atopic Skin Disease

SEOUL, Feb 28 (Bernama) — South Korean scientists said Monday that they have found a way to use microbes to help treat atopic skin disease that affects a large number of people around the world. the discovery by the Korea University team led by microbiology professors Park Yong-keun and Yoon Won-suck, centres on creating a small interface ribonucleic acid (RNA) or miRNA, that suppresses the CCL22RNA, cited for triggering skin inflammatory reactions, Yonhap News Agency reported. Atopic skin disease, also known as atopic dermatitis, is a irritating skin disorder that includes symptoms of itching, scaling of the skin and redness. the scientists said the miRNA was massed produced with the assistance of Salmonella bacteria that had been specifically engineered to be harmless to humans. “The Salmonella bacteria helps strengthen the potency of the treatment substance and makes it more effective in suppressing atopic conditions,” the scientists claimed, citing good test results on laboratory mice with atopic skin conditions. the findings published in the latest issue of the international Experimental and Molecular Medicine journal showed that the new material was less costly to make compared to existing treatment that utilises genetic therapy, can be made into drugs that can be swallowed, and have no known side effects. the university researchers said patents have been requested as of last year with preliminary clinical tests to be conducted in 2012. — BERNAMA

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* 19 January 2011 by AnilAnanthaswamy<newscientist.com/search?rbauthors=Anil+Ananthaswamy>* Magazine issue 2796 <newscientist.com/issue/2796> . 

Diabetes and even obesity, as well as Parkinson’s disease, might becured just by replacing the bacteria in your gut

A FEW years ago, John Gillies had trouble picking up his grandchild. Hewould stand frozen, waiting for his Parkinson’s disease to relinquishits hold and allow him to move. then in May 2008, Gillies was givenantibiotics to treat constipation, and astonishingly his Parkinson’ssymptoms abated. what on earth was going on?

Thomas Borody, a gastroenterologist at the Centre for Digestive Diseases<cdd.com.au/> in New South Wales, Australia, put Gillies onantibiotics because he had found that constipation can be caused by aninfection of the colon. “He has now been seen by two neurologists, whocannot detect classic Parkinson’s disease symptoms any more,” saysBorody.

Borody’s observations, together with others, suggest that manyconditions, from Parkinson’s to metabolic disorders such as obesity,might be caused by undesirable changes in the microbes of the gut. Ifthat is true, it might be possible to alleviate symptoms withantibiotics, or even faecal transplants<newscientist.com/article/mg20827911.100-taboo-transplant-how-new-poo-defeats-superbugs.html> using donor faeces to restore thebowel flora to a healthy state.

Borody uses faecal transplants to cure people infected by the superbugClostridium difficile, and to alleviate chronic constipation. over thepast decade, Borody has noticed that some of his patients also seeimprovements in symptoms of their other diseases, includingParkinson’s, multiple sclerosis (MS), chronic fatigue syndrome (CFS)and rheumatoid arthritis. “Some CFS patients, given a faecaltransplant, will regain their energy quite dramatically, and theirfoggy brains will get better,” says Borody.

To test a possible link between the gut and Parkinson’s disease, Borodyand neurologist David Rosen of the Prince of Wales Private Hospital inSydney are embarking on a pilot study, hoping to recruit people withboth constipation and Parkinson’s. The plan is first to treat them withantibiotics and eventually with faecal transplants. They hope bothfaecal transplants and antibiotics will treat gut infection and henceParkinson’s.

Rosen is cautious: “I wouldn’t for one minute be suggesting that thisis the next cure,” he says. But the idea that Parkinson’s could becaused by bacteria dovetails with work by neuroanatomists Heiko Braakand Kelly Del Tredici at the University of Ulm in Germany.

In 2003, Braak and Tredici showed that damage to the nervous system inParkinson’s progresses from the vagus nerve in the lower brain stem tothe higher regions of the brain and eventually to the cerebral cortex.They also found damage in the enteric nervous system, which controlsthe gastrointestinal (GI) tract and communicates with the brain via thevagus nerve. this discovery prompted them to suggest that Parkinson’smight be caused by a bug that breaks through the mucosal barrier of theGI tract and enters the central nervous system via the vagus nerve(Journal of Neural Transmission, DOI: 10.1007/s00702-002-0808-2<dx.doi.org/10.1007/s00702-002-0808-2> ).

So what about the dramatic improvements seen in people with autoimmunediseases, such as rheumatoid arthritis, after faecal transplant?Borody’s hypothesis is that an infection of the colon releases antigensinto the bloodstream, which trigger an immune response. Unlesssomething is done to completely clear the colon of the antigen, theimmune response is relentless, eventually leading to systemicinflammation that manifests itself as an autoimmune disease.

Interpreting Borody’s results requires extreme caution. However, thereis evidence from animal models that intestinal microbes can influenceautoimmunity. for instance, Alexander Chervonsky<biomed.uchicago.edu/common/faculty/chervonsky.html> of theUniversity of Chicago and colleagues have linked microbes in the gut totype 1 diabetes, an autoimmune disorder caused by the destruction ofinsulin-secreting pancreatic cells. over 80 per cent of a particularbreed of engineered mice that are kept germ-free develop type 1diabetes. When the same mice were dosed with a cocktail of bacteriasimilar to those present in the human gut, only 34 per cent of the micedeveloped type 1 diabetes, suggesting a connection between gut floraand autoimmune diabetes (Nature, DOI: 10.1038/nature07336<dx.doi.org/10.1038/nature07336> ).

Researchers are becoming increasingly aware of the link between gutflora and autoimmunity, says Arthur Kaser, an expert on inflammationand intestinal flora at the University of Cambridge. for instance, micedesigned to develop autoimmune diseases do so in some labs but not inothers. The discrepancy is down to differences in the intestinal floraof the mice. “Intestinal microbiota has a dramatic effect on [what] wecurrently consider as autoimmune disease,” says Kaser.

Evidence for such links in humans is also growing: Anne Vrieze of theAcademic Medical Center in Amsterdam, the Netherlands, and colleaguesstudied 18 obese men with metabolic syndrome, a collection of symptomsthat includes low insulin sensitivity. The group received faecaltransplants – either of their own stool or stool from lean, healthydonors.

The results of this first double-blind trial were presented at theannual meeting of the European Association for the Study of Diabetes inStockholm, Sweden, in September. The researchers found that, six weeksafter the infusions, insulin sensitivity improved significantly in thenine men who received donor stool.

Gut flora has also been linked to obesity. over the past five years,Jeffrey Gordon <gordonlab.wustl.edu/> of Washington Universityin St Louis, Missouri, and colleagues have shown that there are markeddifferences in the gut flora of obese and lean individuals. Theiranalysis suggested that the microbes in obese individuals are releasingnutrients from food that would have remained undigested in leanindividuals. Importantly, they showed that transferring the microbiotafrom obese mice into lean mice caused the lean mice to put on weight(Nature, DOI: 10.1038/nature05414<dx.doi.org/10.1038/nature05414> ).

So can you reverse obesity in humans by transferring gut microbes fromlean people into obese people? It’s a question that Alex Khoruts<med.umn.edu/gi/faculty/khoruts/home.html> , at theUniversity of Minnesota Medical School in Minneapolis, hopes to answer.He is planning a trial in which obese people will be given faecaltransplants, either of their own faeces or samples taken from lean,healthy donors. “The idea is to alter the composition of colon flora,and see whether it has an impact on obesity,” says Khoruts.

“This is absolutely exciting,” says Kaser. But he insists that we arefar from understanding the nature of the microbes that populate ourbody – after all, the colon alone contains nine times as many bacterialcells as there are human cells in the body. And we don’t yet know whatconstitutes “healthy” colon flora. this will make it difficult tojustify any large-scale adoption of faecal transplants, he adds. Ifintestinal bugs are indeed causing autoimmune diseases, “you don’t wantto treat one disease and introduce another”, says Kaser.

Nonetheless, he is convinced that human microbiota will becomeincreasingly important in our understanding of disease. “Textbooks willhave to be rewritten when we consider the contribution of intestinalmicrobiota,” he says. “We have an elephant in the room that has not yetbeen appreciated.”[Issue 2796 of New Scientist magazine] <newscientist.com/issue/2796>* from issue 2796 <newscientist.com/issue/2796> of NewScientist magazine, page 8-9.