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News INFECTION | +60 articles

Xorkoth

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Wow, that first article is amazing. Iboga has anti-HIV properties? I knew it was the most powerful medicine I've ever taken (for my mind), but apparently it could help cure AIDS as well.
 

mr peabody

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Philadelphia

Stemming the increase in HIV infections

by Heather Yakin | Apr 9, 2019

While overdose deaths declined last year in Philadelphia, HIV infections increased. Last week, the Philadelphia Department of Public Health released data that show an increase in new HIV infection since 2016 after a decade of decline. The increase has been attributed to infections among people who inject drugs — 59 of whom were newly diagnosed with HIV in 2018, double the number of people who were diagnosed in 2016. Bucks County has been experiencing a similar increase.

These alarming statistics should sharpen the focus of the city’s and state’s response to the opioid crisis. While there has been a large push to increase access to naloxone — a medication to reverse opioid overdoses — and to increase access to quality treatment, the state still lags behind others when it comes to access to unused syringes. According to the Centers for Disease Control, 19 states allow needle exchanges while three other states allow exchanges in limited circumstances.

Injection drug use is often referred to as a risk factor for HIV and hepatitis C. But it is in fact the lack of access to sterile unused syringes that is driving these new infections — not drugs themselves.

Syringe-exchange programs, where people who inject drugs can discard their used syringes and get new, unused ones, are a recommended strategy to prevent HIV infections both by the CDC and Surgeon General Dr. Jerome Adams. And yet, they are still technically illegal under Pennsylvania’s drug paraphernalia law.

In the past two sessions of the General Assembly, bills that would allow for syringe exchange were introduced in the House. Both went nowhere. Rep. Ed Gainey, a Democrat from Allegheny County, is planning to reintroduce a syringe-exchange bill and is currently circulating a co-sponsorship memo.

In a meeting with The Inquirer’s editorial board in the fall, Gov. Tom Wolf expressed his support of syringe-exchange programs. He should push for a syringe-exchange bill to pass in Harrisburg this session.

In Philadelphia, Prevention Point in Kensington is operating as the sole syringe-exchange program since 1992 under the authority of a municipal executive order.

The increase in HIV infection rate is a signal that it is time for a second program in Philadelphia. Prevention Point opens pop-up exchanges all over the city in specific times but having another exchange also would connect people to other services.

Even better, the city should support opening a supervised-injection site in South Philadelphia, which is experiencing an increase in overdose deaths, that also would operate as a syringe exchange. The site could be a hub to increase the use of PreP, a daily pill that reduces the chances of contracting HIV among people who inject drugs — a population that Health Commissioner Dr. Thomas Farley says is hard to reach because they avoid traditional services.

The new data are a reminder that reducing overdose death is not the only outcome that we should follow as we assess our response to the opioid crisis. Even when this crisis is behind us, the consequences for some will be lifelong unless we act to prevent further harm.

 
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mr peabody

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Infographic: Viruses on the Brain

Ashley Yeager Mar 1, 2019

Pathogens can take various routes to pass the blood brain barrier and damage cells.

Some viruses can enter the body through the nose and mouth and move to the brain by replicating and spreading through the olfactory bulbs; the lingual nerve, which runs down the jawline and into the tongue; or the vagus nerve, which travels through the neck and thorax to the stomach.

1555191151421.png

Crossing blood-brain barrier

When interacting with the nervous system, viral particles can cross the blood-brain barrier directly or through infection of endothelial cells (below, left), or they can use a Trojan horse approach (center), infecting monocytes that cross the barrier before replicating and bursting out of the white blood cells once inside the brain. Alternatively, some viruses do not cross the blood-brain barrier but invoke an immune response that may spur cytokines or chemokines to breach the divide (right).

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Brain damage

Once inside the brain, viruses can infect cells or their myelin sheaths and kill them (below, left). Viruses don’t necessarily have to enter the brain to cause damage, though. They can also spark an immune response that activates microglia, which then consume otherwise healthy neurons (right).

1555191353491.png


 
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mr peabody

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A global map that predicts the risk of dengue in endemic countries. A higher FOI (orange-red) indicates a higher rate of infection.

Releasing artificially-infected mosquitoes could reduce global dengue cases by 90 percent

by Imperial College London | Medical Xpress | 29 Jan 2020

This is the finding of a team of international scientists, led by Imperial College London, and including researchers from the University of California and University of Florida.

The Imperial team, based at J-IDEA, the Abdul Latif Jameel Institute for Disease and Emergency Analytics, created the first ever global map of dengue transmission intensity—which is a measure of how easily dengue is transmitted from person to person.

Using this map, the researchers predicted the global effectiveness of two interventions to combat dengue—vaccination and the release of 'infected' mosquitoes unable to transmit the virus between people.

Scientists infect mosquitoes in the laboratory with a type of naturally-occurring bacteria called Wolbachia, which prevents the virus replicating in the insect. In carefully-controlled trials, releasing these modified mosquitoes in areas heavily affected by dengue has been linked to a 70 per cent reduction in cases, though scientists caution this has to be confirmed in larger trials.

The study was published in the journal Science Translational Medicine, and funded by the Medical Research Council, National Institute for Health Research, the National Institute of General Medical Sciences, and the Department for International Development.

Dr. Lorenzo Cattarino, lead author of the research from the MRC Centre for Global Infectious Disease Analysis, said: "Dengue is a leading cause of illness and death among children across the globe. Our research not only produces the first world map of dengue transmission, but can act as a tool to inform the World Health Organisation, local governments and policy makers on the effectiveness of prevention strategies, such as the release of Wolbachia-infected mosquitoes and vaccination programmes."

Dengue is a viral infection that infects over 100 million people each year. According to the latest estimates, around half of the world's population are thought to be at risk. The virus is spread by mosquitoes, and causes fever, headache, muscle and joint pain. In some cases, it can lead to a life-threatening condition called haemorrhagic fever which is a leading cause of death and serious illness among children in some Asian and Latin American countries.

There is no specific treatment for the disease, and prevention centres around avoiding mosquito bites—for instance using insecticides and reducing areas of standing water where the insects can breed, such as plastic containers.

However two methods of preventing infections have recently emerged that show promise of combatting the disease. A vaccine is now licensed for use against dengue, which works by reducing the intensity of subsequent dengue infections. There are four different types of dengue and therefore people can catch the disease four times. However, the vaccine can only be used in people previously infected with dengue (and thus requires people to be tested for dengue first). This is because the vaccine may prime a person's immune system to 'over-react' to a subsequent dengue infection if they haven't encountered the virus before, making the disease more severe.

Another method of prevention is disabling mosquitoes' ability to transmit the virus, by infecting them with the bacteria Wolbachia.

This bacteria is found naturally in around 60 per cent of insect species, including some mosquitoes, butterflies and moths.



Previous laboratory research has shown mosquitoes infected with Wolbachia do not transmit dengue, as the bacteria stops the virus replicating inside the insect.

In carefully controlled trials, scientists are now purposefully infecting the mosquito species that carry dengue—called Aedes aegypti—with Wolbachia, and releasing them into areas infected with dengue.

The trials suggest the bacteria does not pose a threat to animals or people in the areas where the mosquitoes are released.

Using data from these laboratory and mathematical modelling studies, the scientists behind the latest study used their map to predict this approach could eliminate nearly all dengue cases worldwide.

They also modelled the effectiveness of the Sanofi Pasteur dengue vaccine if used in all areas affected by dengue, and found the number of dengue cases could be reduced by up to 30 per cent. This is because the vaccine reduces the probability of becoming severely ill, rather than virus transmission.

The team highlight caveats in their study. The predictions assume the effectiveness of the mosquitoes in small-scale trials will be replicated on a global scale, and that the diagnostic test for dengue screening, which is recommended before the vaccine can be administered, is 95 percent accurate. The researchers add that the two interventions were modeled separately.

Professor Neil Ferguson, co-lead author of the research, and head of Imperial's Department of Infectious Disease Epidemiology said: "Until now, gauging the effectiveness of control strategies for dengue, such as vaccine and Wolbachia-infected mosquitoes, has been limited by the lack of data on transmission across large geographical regions. The creation of this freely available global map of transmission, and the likely impact of control measures, will help identify strategies to reduce the number of people affected by the disease. The cost-effectiveness of these strategies can also be assessed, which is particularly important when most areas affected by dengue are in lower income nations."

 
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mr peabody

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Candida Auris: The fungus nobody wants to talk about

by Matt Richtel of The New York Times | April 8, 2019

In 30 years, I’ve never faced so tough a reporting challenge — and one so unexpected. Who wouldn’t want to talk about a fungus?

Last year, I began spade work on a series of articles about drug-resistant microbes: bacteria and fungi that have developed the ability to evade common medicines that we have used for decades.

Early on, I stumbled onto a compelling example. A woman in Alaska named Sari Bailey woke up one morning with green and yellow gunk coming out of her ear. Her doctor told her it was an ear infection and prescribed antibiotics. They didn’t work. Turns out she had a drug-resistant infection that rooted on her mastoid bone, just behind the ear. It nearly killed her and required multiple surgeries to clear.

Her experience showed the pronounced risk of these tenacious bugs and seemed like a good way to draw readers into a story about a very complex scientific topic. But I needed more details, and I needed context: How common was this? What was the science behind it?

When I went looking for answers, I hit my first curious wall. A hospital in Alaska declined my request to speak with a local doctor who has a lot of experience treating people with drug-resistant infections, including another woman who had been hospitalized for seven months fighting a drug-resistant staph infection.

Getting turned away is just another day at work for a reporter. But what made this incident unusual is that, in my experience, the medical community is generally eager to get the word out about public health issues.

From this germ of an observation grew one of the most curious aspects of our series: The rise in resistant bugs is cloaked in widespread and chronic secrecy.

As our reporting continued, we discovered it was common for hospitals, doctors and public health agencies to clam up when it came to talking about their troubles with resistant bugs, though they widely acknowledged the existence of the problem and even encouraged our efforts. This disconnect was at its most extreme when the issue turned to the subject of the first article in our series, which was published online on Saturday — Candida auris.

C. auris is a drug-resistant fungus that has emerged mysteriously around the world, and it is understood to be a clear and present danger. But Connecticut state officials wouldn’t tell us the name of the hospital where they had had a C. auris patient, let alone connect us with her family. Neither would officials in Texas, where the woman was transferred and died. A spokeswoman for the City of Chicago, where C. auris has become rampant in long-term health care facilities, promised to find a family and then stopped returning my calls without explanation.

There were rays of light. The State of New York, where many have died, told us they tried to connect us with families of people who had fallen ill, as did a Brooklyn branch of Mount Sinai Hospital. But one after another withdrew. “They’ve backed out,” a hospital official told my colleague Andrew Jacobs when we were hours from an interview with relatives of a C. auris patient who had died.

My emails to a researcher about C. auris in India, which has dealt with many cases, went unanswered, and that soon became common — emails and calls just not returned. We put a call-out on the New York Times website asking to speak to families affected by C. auris, recognizing this came with the risk of tipping off others to our work, and got nary a bite.

We came to realize that the secrecy surrounding C. auris was a big part of the story. A doctor in Spain wrote me that the hospital didn’t want bad press by seeming to be a hotbed of the fungus. I got the same message from a doctor in England. One doctor in New York told me that "patients, and their families, don’t like being associated with the illness, as if they had a scarlet letter — “A” for auris."

The stakes are growing. The issue goes well beyond that one fungus. Ms. Bailey’s bacterial infection continues to plague her. "This week, she will have her gallbladder removed, thanks to complications from multiple courses of antibiotics and steroids used to treat her vexing infection," her family said.

As we prepare to move ahead with more articles on drug resistance, we understand that we are tackling an issue that is so scary, it feels easy for some people to ignore, less frightening to bury.

If our series gets more people talking, that would be a victory.

 
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mr peabody

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Lyme Disease: The CDC’s greatest coverup

Collective Evolution | April 24, 2019

Lyme disease, do you have it? If you did, you probably wouldn’t know – unless you’re one of the chronic sufferers that have had to visit over 30 doctors to get a proper diagnosis. Lyme disease tests are highly inaccurate, often inconclusive or indicating false negatives.

Why? Because this clever bacteria has found a way to dumb down the immune system and white blood cells so that it’s not detectable until treatment is initiated. To diagnose Lyme properly you must see a “Lyme Literate MD (LLMD),” however, more and more doctors are turning their backs on patients due to sheer fear of losing their practices! Insurance companies and the CDC will do whatever it takes to stop Chronic Lyme Disease from being diagnosed, treated, or widely recognized as an increasingly common issue.

Lyme is considered by the medical field to “only” transmit by way of a tick infected with bacteria. However, the CDC itself admits it is under-reported, and believes there are between 300,000 to half a million new cases each year. That makes Lyme disease almost twice as common as breast cancer and six times more common than HIV/AIDS. Where are all of these new cases coming from?

When Lyme isn’t detected in the early stages, it becomes Chronic Lyme, a condition which the CDC and IDSA both deny even exists. They will continue to deny it, because if there’s one thing insurance companies hate, it’s chronic disorders they have to spend time and money treating. Therefore, a panel with ties to insurance companies gathered to write up official Lyme guidelines that assure patients are only allowed a few weeks of antibiotic treatment and are not to be diagnosed with Chronic Lyme Disease (even if clear symptoms persist and invade the nervous system). Over half of the panelists who wrote the IDSA Lyme guidelines announcing that Chronic Lyme is not real — including the panel chairman — have obvious conflicts of interest including financial interests in drug companies, diagnostic tests, and patents, as well as consulting agreements with insurance companies. Researchers and scientists with evidence in support of Chronic Lyme were intentionally excluded from the panel. Because of these unjust Lyme guidelines, insurance companies have the “right” to deny coverage for the treatment of long-term Lyme disease. Doctors have even lost their practices for successfully diagnosing and treating Chronic Lyme, as shown in the film Under Our Skin. In the case of Dr. Joseph Jemsek of North Carolina, he not only lost his license, but also his livelihood. Dr. Jemsek can no longer practice simply because he gave antibiotics to Chronic Lyme sufferers, and was then sued by BCBS for 100 million dollars, following which he had to declare bankruptcy.

Connecticut Attorney General Richard Blumenthal has investigated the IDSA panel members for possible violation of antitrust laws and conflicts of interest.

Of the 14 panel authors of the first edition guidelines: 6 of them or their universities held patents on Lyme or its co-infections, 4 received funding from Lyme or co-infection test kit manufacturers, 4 were paid by insurance companies to write Lyme policy guidelines or consult in Lyme legal cases, and 9 received money from Lyme disease vaccine manufacturers. Some of the authors were involved in more than one conflict of interest.

Strong evidence of sexual transmission

The bacteria that causes Lyme disease is Borrelia burgdorferi, a type of corkscrew-shaped bacteria known as a spirochete. The Lyme spirochete is a cousin to Treponema pallidum, the spirochete that causes syphilis.

Dr. Alan MacDonald, MD who appears in the documentary ‘Under Our Skin’, says in the film that he found found Borrelia (Lyme) DNA in 7 out of 10 postmortem Alzheimers patients’ brains. This makes perfect sense, since syphilis, its cousin, also invades the brain in tertiary or neurosyphilis. Dr. Klinghardt, MD stated that he’s “never had a single patient with Alzheimer’s, ALS, Parkinson’s Disease or Multiple Sclerosis who tested negative for Borrelia.”

Why are so many people suffering from Lyme disease and its allegedly associated chronic disorders, such as Alzheimers and ALS? A new study suggests that just like its spirochete cousin that causes syphilis, Lyme disease may be sexually transmitted. The study was presented at the annual Western Regional Meeting of the American Federation for Medical Research, and an abstract of the research was published in the January issue of the Journal of Investigative Medicine.

The study — presented at the annual Western Regional Meeting of the American Federation for Medical Research — a collaborative effort by an international team of scientists — tested semen samples and vaginal secretions of three groups of patients to investigate whether passing Lyme disease to a partner through unprotected sex is a possibility. The study observed control subjects without evidence of Lyme disease, random subjects who tested positive for Lyme disease, and married heterosexual couples engaging in unprotected sex who tested positive for the disease. The presence of B. burgdorferi and identical strains of the bacterium were of particular interest to the researchers in unprotected sex in spouses.

The control subjects were found to test negative for the bacterium in semen samples or vaginal secretions, as expected by the researchers. The researchers found traces of B. burgdorferi in the vaginal secretions of all women with Lyme disease. In contrast, approximately half of the men with the disease tested positive for the bacterium in semen samples. In addition, one of the heterosexual couples with Lyme disease were found to have identical strains of the bacterium in their genital secretions.

One researcher in the study notes, “There is always some risk of getting Lyme disease from a tick bite in the woods. But there may be a bigger risk of getting Lyme disease in the bedroom.”

“Our findings will change the way Lyme disease is viewed by doctors and patients,”
said Marianne Middelveen, lead author of the study. “It explains why the disease is more common than one would think if only ticks were involved in transmission.” But will this actually change the way Lyme disease is viewed? Or will the money funneled in by insurance companies and vaccine manufacturers continue to blind and corrupt IDSA board members?

The study was a joint effort by a team of scientists which included dermatologists, molecular biologists, microbiologists, internists, and family practitioners. The most revealing aspect of the study, in my opinion, is the fact I mentioned earlier: one of the heterosexual couples with Lyme disease showed identical strains of the Lyme spirochete in their genital secretions. “The presence of the Lyme spirochete in genital secretions and identical strains in married couples strongly suggests that sexual transmission of the disease occurs,” said Dr. Mayne.

Gestational transmission from mother to child

A North Carolina State University researcher has discovered that Bartonella (a common Lyme co-infection) can be passed to unborn babies, causing chronic infections and possibly birth defects. Dr. Ed Breitschwerdt and his research group tested blood and tissue samples taken over a period of years from a mother, father and son who had suffered chronic illnesses for over a decade. Autopsy samples from their daughter–the son’s twin who died shortly after birth–contained DNA evidence of B. henselae and B. vinsonii subsp. berkhoffi infection, also found in the other members of the family.

Multiple strains of Lyme?

In 2002, W.T. Harvey, an MD from Houston, began finding large numbers of chronically ill Borrelia burgdorferi PCR- and seropositive patients in the area around his home and practice. Houston, Texas is declared a zoonotically “non-endemic” area, so he set out to understand just how this epidemic was occurring. W.T. Harvey had no competing financial interest (as the CDC and IDSA do) and received no grants when writing his study on Lyme.

“In order to understand this finding prior to sufficient data availability, we chose to examine critically the currently accepted but troublesome ‘Lyme disease’ concepts,” Harvey’s study reads.

“Our method was to analyze each foundation ‘Lyme disease’ premise within the context of available medical and veterinary literature, then to reconstruct the disease model consistent with the preponderance of that data. We find the present conceptualization of the illness seriously truncated, with a high likelihood of two distinct but connected forms of human B. burgdorferi infection. The yet-unrecognized form appears to have a broader clinical presentation, wider geographic distribution, and vastly greater prevalence. We conclude that ‘Lyme disease’ currently acknowledges only its zoonosis arm and is a limited conceptualization of a far more pervasive and unrecognized infection state that must be considered a global epidemic.”

Could you have Lyme from your pets?

Suzy Cohen of suzycohen.com is a registered pharmacist and best-selling author. When she graduated from pharmacy school in 1989, she believed that medication was the answer to helping patients get healthy. When that didn’t always work, she began to do some serious research. In one article addressing the truth about Lyme, she writes:

“Most Lyme sufferers have pet cats and dogs, they are not aware that their pets gave it to them. But it happens like this, your pets go out into the yard to do their duty, and ticks jump on them, especially in May and June, their breeding season but any time of the year is possible. Your pet totes these ticks into your house and then you cuddle with your pet. The ticks get on you, and numb your skin. They are teeny tiny, about the size of a poppy seed and you’ll never know you got bit. They like every part of your body, but especially warmer areas, like armpits for example. You may never know. Sometimes the Lyme can happen from a cat scratch or bite. When I ask pet owners about their pets, they go into a bit of denial, because of the great love they have for pets. But you have to realize pets, for as delightful as they are, are tick taxis. If you have Lyme, and get bit again by your pet, you are potentially introducing new coinfections or re-innoculating yourself with more Lyme organisms. It explains why some people just can’t get well, or get setbacks even under treatment.”

Borrelia spirochetes have been found in the urine of infected dogs, among several other animals. Studies on mice have found that the spirochetes in urine remained viable for 18-24 hours and concluded that “urine may provide a method for contact non-tick transmission of B. burgdorferi in natural rodent populations particularly during periods of nesting and/or breeding.” Evidence for direct contact transmission has been demonstrated in mice. These findings suggest that further research is needed to evaluate alternate methods of Lyme transmission, such as by the urine of infected animals to humans.

Conclusion

“Lyme is one of the many microbes that has entered our system. And I feel as a physician that things are getting to a degree that’s serious. We’re watching other mammals die out and just think, ‘well, I’m glad it’s not me.’ However, as our environment becomes increasingly polluted, so do our bodies. And then we grow bugs [parasites, pathogens] in us that are not compatible with human life anymore.” – Dr. Klinghardt, MD

 
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mr peabody

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HPV is particularly concerning for sexual minority men due to the high prevalence of HIV
and smoking in this community and the low HPV vaccination rates overall among men.


Young men are unaware of the risks of HPV infection

Rutgers University | Medical Xpress | 11 Feb 2020

Young sexual minority men—including those who are gay, bisexual, queer or straight-identified men who have sex with men—do not fully understand their risk for human papillomavirus (HPV) due to a lack of information from health care providers, according to Rutgers researchers.

A Rutgers study published in the Journal of Community Health, examined what young sexual minority men—a high-risk and high-need population—know about HPV and the HPV vaccine and how health care providers communicate information about the virus and vaccine.

About 79 million Americans are infected with HPV, with about 14 million becoming newly infected each year, according to the Centers for Disease Control and Prevention. As a sexually transmitted infection, HPV can lead to several types of cancer, including anal and penile cancer, and is particularly concerning for sexual minority men due to the high prevalence of HIV and smoking in this community and the low HPV vaccination rates overall among men.

"Particularly in light of the decades-long focus on gay men's health care as HIV care, there is a missed opportunity for HPV prevention in the community," said study co-author Caleb LoSchiavo, a doctoral student at the Rutgers School of Public Health.

The researchers, who are members of the Rutgers School of Public Heath's Center for Health, Identity, Behavior and Prevention Studies (CHIBPS), analyzed interviews with sexual minority men in their early 20s in New York City and determined they knew little about HPV infection—including transmission, signs, symptoms and cancer risk—and vaccination.

They also found that the men did not prioritize HPV vaccination due to the incorrect perception that HPV is an issue that exclusively or primarily affected women.

"Everyone who is sexually active—regardless of gender, sexual orientation, partners' genders, relationship or marital status—should talk to their doctor about receiving the HPV vaccine to prevent a future generation who may develop HPV-related cancers, such as cervical, oral and anal cancer, as we have seen emerging in Baby Boomers and Gen-Xers," said Perry N. Halkitis, Rutgers School of Public Health dean, CHIBPS director, and PI of the study.

The U.S. Food and Drug Administration has expanded the use of HPV vaccine to people between the ages of 27 to 45. Originally, it was prescribed for those between the ages of 9 to 26.

In the study, researchers found that health care providers rarely discuss HPV and the HPV vaccine with patients who are young sexual minority men, and when they do, their communication is often inadequate in conveying potential risks of HPV and benefits of vaccination.

"Clinicians have a direct role in expanding the availability of LGBTQ-competent healthcare," said lead author Jessica Jaiswal, an assistant professor at the University of Alabama, and CHIBPS affiliate. "By learning about sexual minority men's diverse health needs and routinely offering the HPV vaccine, we can move toward a health promotion model and not only a disease prevention model."

 
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mr peabody

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Newly discovered antibiotic offers hope for treating MRSA

by Victoria Forster | Forbes | March 28, 2018

A new class of antibiotics chemically related to Vitamin A have shown early promise by killing MRSA in mice.

The research reported today in Nature and led by researchers at Brown University, used an assay which tested the ability of 82,000 synthetic compounds to stop MRSA from killing tiny worms called C.elegans. They identified almost 200 promising compounds that eradicated the bacteria, while not killing the worms, and chose two to move forward with due to previous evidence they might be useful antibiotics.

Eleftherios Mylonakis, MD, leader of the study from the Medical School of Brown University said: "We are very optimistic about the way these compounds function. They target the membrane, a very finely tuned part of the bacteria which is very susceptible to targeting by drugs."

Two percent of healthy people carry MRSA in their noses, with one in three carrying some form of staphylococcus bacterium which isn’t antibiotic resistant, but MRSA poses a huge threat to those who have compromised immunity and can spread quickly in healthcare settings such as hospitals.

The most recent estimates aree that there are over 70,000 MRSA infections and 9,000 related deaths each year in the U.S., more deaths than from HIV. New treatments, and, more importantly, new treatments which MRSA does not easily evolve resistance to, are urgently needed and the current rate of progress on these treatments is simply not fast enough to tackle the speed of evolution of drug-resistant bacterial infections.

"Pharma companies have mostly abandoned this type of research, which has been devastating for the development of new antibiotics," said Mylonakis.

Mylonakis is, unfortunately right. The development of new antibiotics has been hugely hampered by the exit of multiple, large pharmaceutical companies from the field, often determining it simply not profitable enough. However this may be changing, with a recent study published in the British Medical Journal indicating more focus, albeit a lot more scope for improvement.​
 
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Patients with superbug Candida auris shed large amounts of it from their skin

By Helen Branswell | STAT | June 24, 2019

New research on Candida auris confirms what scientists have both suspected and feared: Hospitalized patients who carry the fungus shed large amounts of it from their skin, contaminating the environment in which they are being treated and leaving enough of it to infect others later on.

The superbug, Candida auris, is highly resistant to many existing antifungal drugs. It’s also resistant to regular cleaning methods, making hospital outbreaks incredibly difficult to stop.

C. auris acts more like bacteria than fungi, which do not normally cause hospital outbreaks. Its relatively recent emergence as a hospital-acquired infection has researchers scrambling to find out even the most basic information about it, like how it moves from patient to patient.

The new work was conducted by scientists from the Centers for Disease Control and Prevention in conjunction with colleagues from the Chicago Department of Public Health. It was presented Sunday at the annual conference of the American Society for Microbiology in San Francisco.

“As we’re struggling to control this organism, the reality is we don’t know how it’s spreading from person to person. We know that it does. But mechanistically we don’t know how. And so what this study was about was trying to identify the mechanism of how it can get from one person to the other,” said Joseph Sexton, a scientist with the CDC and the lead author of the work. “If we don’t understand how it spreads, we’re not going to be able to intervene.”

Before members of the team could conduct the study, they had to figure out a way to quantify how much of the fungus was present in any one place — a basic step in studying many pathogens, but not easy to do with C. auris, said Johanna Rhodes, an epidemiologist at Imperial College London. Rhodes, who studies C. auris, was not involved in the CDC research.

“A lot of us have been scratching our heads as to how the heck do you do this?” Rhodes said of the task of trying to devise a way to quantify amounts of the fungus. “It doesn’t have the standard set of genes that you would expect to find. It’s just such a weird bug.”

She was excited to learn of the CDC’s work — both the development of the quantification methods and the findings of the study on transmission of C. auris. Lots of people studying the fungus have assumed what the CDC team found, but it’s critical to actually have data, she said.

“We’ve all kind of said, ‘Yeah, we think this is it. We think this is what happens.’ But they’ve done the work,” said Rhodes. “It’s fundamental in our understanding of how this is actually spreading.”

The CDC and Chicago scientists studied 28 patients in an outbreak in what is called a ventilator-capable skilled nursing facility in Chicago. Facilities like these offer long-term care to very sick patients who are typically on ventilators, machines that breath for them. These are patients who are bed-bound.

The facility first discovered a patient carrying C. auris in March 2017. But by the time the study was done, 71% of the patients on the floor where ventilated patients are cared for were colonized with C. auris — meaning they carried it on their skin.

C. auris is an infection that is associated with patients with complex medical problems and compromised immune systems; it is generally not considered a risk to the average healthy person. But it can significantly complicate the care of people who are in intensive care units or other areas of hospitals that involve advanced care. About a third of patients who have tested positive for C. auris die, though it’s sometimes unclear if the infection was the cause of death.

The CDC-led team took skin swabs from 28 patients in the Chicago facility, swabbing their armpits and groins, which are among the places bugs that live on human bodies are often found.

They also tested a variety of surfaces in patient rooms — bed railings, doorknobs, and windowsills.

Their hypothesis was that if patient shedding was responsible for spread, they would find more of the fungus in the rooms of patients who had more of it on their skin. And indeed, they found the rooms inhabited by patients with lots of C. auris on their skin were the most contaminated with the fungus.

All of the railings on beds housing patients with C. auris tested positive for the fungus. Even the railings of two beds that contained patients who didn’t have C. auris were contaminated. Sexton said study of the patient flow on the ward revealed the beds had previously been inhabited by patients who were C. auris-positive. “So we know that they’re not doing a good enough job disinfecting the bed,” he said.

Surprisingly, three-quarters of the windowsills were also contaminated with the fungus. That was unexpected — until the team realized that windowsills were used as de facto shelves in these rooms.

“If there is a takeaway it could be …. ‘Hey, we really need to pay attention to the bed and these other areas that the patient is in contact with,’” said Sexton.

 
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An image of the HIV virus taken with transmission electron microscopy.

Researchers successfully eliminate HIV from mice genome using CRISPR

by Naia Carlos | Tech Times | 3 July 2019

Scientists have successfully removed HIV-1 DNA from mice genome, marking a huge milestone in the search for a cure to the HIV infection in humans.

To achieve this feat, researchers from the Lewis Katz School of Medicine at Temple University and the University of Nebraska Medical Center used the gene editing tool CRISPR-Cas9 in combination with an experimental drug to clear out the virus from the animal genomes. It's an innovative technique that may be the path to finding a cure for the deadly infection, although further research will likely be necessary moving forward.

"Our study shows that treatment to suppress HIV replication and gene editing therapy, when given sequentially, can eliminate HIV from cells and organs of infected animals," said study author Kamel Khalili, PhD in a press release.

CRISPR, ART work together to flush out HIV

Current treatment for HIV makes use of a technique known as antiretroviral therapy or ART, which prevents the virus from replicating. However, it does not actually eliminate HIV from the body. HIV integrates itself into the genomes of cells in the immune system, where it can hide dormant and out of reach of antiretroviral medication, which means that it's capable of rebounding and replicating to cause the development of AIDS.

In the study published in the journal Nature Communications, the research team used a new gene editing system using CRISPR-Cas9 technology in conjunction with a recently developed technique of ART called long-acting slow-effective release or LASER ART, which targets viral pockets where the virus may be lying dormant and lowers HIV replication for extended periods of time.

Previous research by Khalili and his team showed that gene editing cannot purge HIV from genomes on its own, but by combining it with the new antiretroviral drug, the researchers hoped it would become more effective.

According to Khalili, "the team wanted to see if LASER ART could suppress the replication of HIV long enough to allow the CRISPR-Cas9 to get rid of all the cells of viral DNA."

How they did it

To see whether the combination of CRISPR and LASER ART technology would be effective against HIV, the researchers engineered mice to produce human T cells that are susceptible to HIV infection. This would allow long-term infection as well as latency induced by ART. When the mice were infected, they were treated with LASER ART followed by CRISPR-Cas9.

Findings showed that there was complete elimination of HIV DNA in roughly one-third of the infected mice.

"The big message of this work is that it takes both CRISPR-Cas9 and virus suppression through a method such as LASER ART, administered together, to produce a cure for HIV infection," Khalili said. "There is now a clear path for researchers to follow up with trials in non-human primates or even clinical trials on humans within the year."

 
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In this photo, a patient uses an oral test for HIV. Free mail-order
HIV tests for high-risk men offer a potentially better strategy for
curbing the spread of HIV as compared with usual care.


Free home HIV test helps detect more infections

by Lindsey Tanner | Medical Xpress | Nov 18 2019

Mailing free home HIV tests to high-risk men offers a potentially better strategy for detecting infections than usual care.

That's according to a U.S. government study that resulted in many more infections found—including among friends with whom recipients shared extra kits.

The yearlong experiment recruited 2,600 men from online social network and music sites. Those who signed up were sent four free test kits but could order more. Many did and shared them.

Overall, 25 infections were detected in the self-testing group, versus 11 in men who just got links to local services. Even more infections—34—were detected among friends of those who shared tests.

Over 70% of participants who learned of positive results sought treatment.

 
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Deadly measles outbreak spreading like wildfire in Democratic Republic of Congo

Measles outbreak in DRC has killed 6,000 in the last year*

Medical Xpress | Jan 7 2020

Measles has killed more than 6,000 people in the Democratic Republic of Congo since January, the world's worst outbreak and nearly triple the toll in the country's Ebola epidemic, the World Health Organization said Tuesday.

DR Congo declared its latest measles epidemic in June, and last September the country launched an emergency vaccination campaign to counter the outbreak.

In 2019, more than 18 million children under the age of 5 were vaccinated across the DR Congo, the WHO said in a statement.

Around 310,000 suspected cases were reported during the year, it said.

WHO said an additional $40 million in emergency funds was needed from donors for a six-month immunisation plan for children to help curb the epidemic.

Efforts to halt the spread of both Ebola and measles are hampered by a lack of access, weak health care and unrest across the country, especially in the east.

Measles is a highly-contagious disease caused by a virus that attacks mainly children. The most serious complications include blindness, brain swelling, diarrhoea, and severe respiratory infections.

The rapid spread of measles in DRC has garnered far less attention than the Ebola epidemic that has also been raging in the east of the country since August 2018. That outbreak has killed more than 2,230 people.

*From the article here :
 
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Ebola now curable after new drug trials in DRC!

by Sarah Boseley | The Guardian | 12 Aug 2019

Test results for two new drugs in the Democratic Republic of Congo have shown good survival rates for ebola patients when treated quickly.

Ebola can no longer be called an incurable disease, scientists have said, after two of four drugs being trialled in the major outbreak in the Democratic Republic of the Congo were found to have significantly reduced the death rate.

ZMapp, used during the massive Ebola epidemic in Sierra Leone, Liberia and Guinea, has been dropped along with Remdesivir after two monoclonal antibodies, which block the virus, had substantially more effect, said the World Health Organization and the US National Institute of Allergy and Infectious Diseases, which were co-sponsors of the trial.

The trial in the DRC, which started in November, has now been stopped. All Ebola treatment units will now use the two monoclonal antibody drugs.

“From now on, we will no longer say that Ebola is incurable,” said Prof Jean-Jacques Muyembe, the director general of the Institut National de Recherche Biomédicale in DRC, which has overseen the trial. “These advances will help save thousands of lives.”

One of the biggest obstacles in fighting the year-long DRC outbreak, the second biggest ever and now with 2,800 cases, has been the reluctance of those who fall sick to seek treatment.

It has not helped that the chances of survival have been low – up to 70% of those infected in the DRC have died. Muyembe said many people saw family members go into an Ebola treatment centre and come out dead.

“Now that 90% of their patients can go into the treatment centre and come out completely cured, they will start believing it and building trust in the population and community,” he said.

Anthony Fauci, the director of the US NIAID, said the overall mortality of those given ZMapp in the trial in four centres was 49% while that of Remdesivir was 53%. A monoclonal antibody drug made by Regeneron had the lowest overall death rate, at 29%, while the monoclonal antibody 114 made by Ridgeback Biotherapeutics had a mortality rate of 34%.

But the results in people who arrived at a treatment centre soon after they became sick, rather than staying at home, were even more impressive – with death rates of 24% on ZMapp, 33% with Remdesivir, 11% with 114 and just 6% with Regeneron’s drug.

On average, people who fall ill are not turning up at a treatment centre for four days, said Dr Michael Ryan from the World Health Organization. This reduces their chances of survival and makes it likely that the virus, spread through bodily fluids, will be transmitted to their families.

“The numbers might change,” said Fauci. “Not all the data has been accumulated.” The two monoclonal antibodies will both now be used in every treatment centre in DRC.

Fauci paid tribute to all of those involved in the trial in four towns: Beni, Katwa, Butembo and Mangina. NGOs including International Medical Corps and Médecins Sans Frontières “put their lives on the line every day to care for patients in extremely difficult conditions in the area where the outbreak is occurring,” he said.

Clinical trials in epidemic conditions are hard – even more so in Ebola outbreaks, where medical staff have to wear protective suits and all patients must be isolated.

“This trial – the first-ever multi-drug randomised trial for Ebola – has happened despite such highly complex and challenging circumstance,” said Dr Jeremy Farrar, the director of Wellcome and the co-chair of the WHO Ebola therapeutics group. “A long-running outbreak like this takes a terrible toll on the communities affected and it is a sign of just how difficult this epidemic has been to control that there have already been enough patients treated to tell us more about the efficacy of these four drugs.”

"The trial will have saved lives,"
he said. The next phase should reveal more about which of the two works best in certain settings. “The more we learn about these two treatments, and how they can complement the public health response, including contact tracing and vaccination, the closer we can get to turning Ebola from a terrifying disease to one that is preventable and treatable. We won’t ever get rid of Ebola but we should be able to stop these outbreaks from turning into major national and regional epidemics,” he said.

 
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Is CBD a superbug antibiotic?

by Kathleen Doheny | WebMD

Cannabidiol, or CBD, already being researched and used for anxiety, insomnia, epilepsy and pain, may be the next superbug fighter for resistant infections, a new study suggests.

"The researchers tested CBD against a wide variety of bacteria, including bacteria that have become resistant to the most commonly used antibiotics," says Mark Blaskovich, PhD, senior researcher at the Centre for Superbug Solutions at the Institute for Molecular Bioscience at the University of Queensland in Australia.

The development is important, as antibiotic resistance is reaching dangerously high levels, according to the World Health Organization.

What the research shows

CBD is a non-psychoactive compound taken from cannabis and hemp; it does not produce the high that regular marijuana does. To date, the FDA has only approved CBD for treating rare and severe forms of seizure, although it is promoted for many other health benefits.

Blaskovich presented the research Sunday at the American Society for Microbiology annual meeting. The research includes work in test tubes and animal models. Research presented at meetings should be viewed as preliminary until published in a peer-reviewed medical journal.

"The first thing we looked at is CBD's ability to kill bacteria," he says. "In every case, CBD had a very similar potency to that of common antibiotics."

The researchers tested the CBD against some strains of staphylococcus, which cause skin infections, and streptococcus, which cause strep throat.

They compared how effective CBD was compared to common antibiotics, such as vancomycin and daptomycin. "We looked at how quickly the CBD killed the bacteria. It's quite fast, within 3 hours, which is pretty good. Vancomycin (Vancocin) kills over 6 to 8 hours."

The CBD also disrupted the biofilm, the layer of ''goop'' around bacteria that makes it more difficult for the antibiotic to penetrate and kill.

Finally, the lab studies showed that "CBD is much less likely to cause resistance than the existing antibiotics," Blaskovich says.

"CBD is selective for the type of bacteria," he says.

He found it effective against gram-positive bacteria but not gram-negative. Gram-positive bacteria cause serious skin infections and pneumonia, among other conditions. Gram-negative bacteria include salmonella (found in undercooked foods) and E. coli (the cause of urinary tract infections, diarrhea, and other ailments), among other bacteria.

In another study, also presented at the meeting, the researchers tested topical CBD to treat a skin infection on mice. "It cut the number of bacteria after 48 hours," Blaskovich says, "although it did not clear the infection." That research is ongoing.

Perspective

Brandon Novy, a microbiology researcher at Reed College in Portland, OR, calls the study findings ''very promising,'' since the results show the bacteria were not able to form resistance to the CBD, and since the bacteria were not able to form a biofilm.

Both findings are important. "The biofilm is an important part of the whole infection process," he says. "It helps the bacteria attach to whatever surface or host and survive."

At the same meeting, Novy presented a preliminary study, finding that CBD also looks promising to fight some gram-negative infections.

"It is an important study that deserves to be followed up on," says Amesh Adalja, MD, an infectious disease doctor and senior scholar at the Johns Hopkins Center for Health Security.

*From the article here :
 
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Surge in chemsex parties fueling a fresh HIV epidemic in European cities, doctors warn

by Kate Kelland | The independent | 13 Sep 2019

A surge in “chemsex” parties, where some people spend days getting high on drugs and having sex with scores of partners, is refueling epidemics of HIV in European towns and cities, doctors say.

Despite much higher risks of contracting the virus that causes AIDS, as well as other sexually transmitted infections (STIs), users search online “hook-up” apps like Grindr for tags such as “high and horny” or “party and play” to find others wanting drug-heightened and often anonymous and unprotected sex.

The result, AIDS experts say, is that in cities across Europe, HIV is spreading rapidly – leading to concentrated epidemics in hard-to-reach groups.

“Chemsex is very pervasive now – it’s a growing phenomenon,” said Rusi Jaspal, a professor of psychology and sexual health at De Montfort University in Leicester who has been studying the spread of HIV and the chemsex scene.

At a London conference hosted by the International Association of Providers of AIDS Care (IAPAC), the group’s president Jose Zuniga, described chemsex as "a challenge of proportions we cannot fully comprehend at this time.”

Chemsex is characterised by the use of drugs such as crystal meth, mephedrone and GHB, or gamma-hydroxybutyric acid, to enhance sexual arousal, performance and pleasure.

A subset of chemsex is known as “slamsex”, where partygoers self-inject drugs rather than taking them as pills or via pipes.

"The drugs reduce inhibitions and increase feelings of horniness or lust,” Mr Jaspal said, "and contribute to “a perfect storm” in groups with high HIV rates for the virus to spread."

In a small study published in 2014 of people attending HIV clinics in England and Wales, 30 per cent of HIV-positive men surveyed reported chemsex in the previous year, and 10 per cent said they had engaged in slamsex.

Ignacio Labayen de Inza, a chemsex specialist who works at several UK clinics and online as a counsellor says “things have got much worse” since then.

“It’s not just a UK thing,” he told Reuters. “It’s in Amsterdam, Berlin, Munich, Rome, Kiev, Moscow, Helsinki – and in many of what people call ‘gay destinations’, like Ibiza, Torremolinos, the Canary Islands.”

A Spain-based study last year found that of almost 750 HIV-positive men surveyed, 60 per cent reported having unprotected anal sex and 62 per cent had been diagnosed with an STI. Rates of infections and high-risk sexual behaviour were higher among the 30 per cent who reported having engaged in chemsex or slamsex.

Globally, the fight against HIV and AIDS has made dramatic progress in the past decade. According to the UNAIDS agency, 1.7 million people were newly infected with HIV in 2018, a 16 per cent drop since 2010, driven mostly by reducing HIV rates in Africa.

But progress is stalling and the epidemic is tightening its grip in key groups. UNAIDS says more then half of new HIV cases in 2018 were in minority or marginalised groups such as men who have sex with men, transgender people and sex workers.

"The human immunodeficiency virus that causes AIDS can’t be cured, but can be kept in check for decades with cocktails of highly effective antiviral medicines. It’s partly this advance that is behind the high-risk practice of chemsex," said Mr de Inza.

“People are not scared any more of HIV,” he said. “Many people I see say they think ‘it’s only a matter of time anyway, so I might as well have some fun’.”

Shannon Hader, deputy director of UNAIDS, says the key to limiting chemsex and its consequences is to get the right protection messages and methods to those who need them.

Encouraging use of HIV prevention drugs known as PreP, or pre-exposure prophylaxis, is one effective step, she said, and can give people who have chemsex some control over their health.

“In this epidemic, we always have to be looking for what’s coming next that we’re not addressing,” she said. “And with PreP, we need to ensure we’re not missing people in the chemsex environment.”

 
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Ibogaine an effective treatment for Hepatitis C

European Ibogaine Forum | Vienna 8 -10 September 2017

The hepatitis C virus (HCV), which is common among drug users, was first described as non-hepatitis A and non-hepatitis B virus in 1973, until it was finally identified in 1989 by genetic engineering of the hereditary material. In Central Europe, most people are now vaccinated against the hepatitis A virus and the hepatitis B virus, but there is currently no available immunisation against HCV.

Symptoms of hepatitis C include an inflammed liver, pain in the liver and increased production of liver enzymes. There are different treatment options for HCV. The standard treatment option combines interferon with ribavirin. However, this treatment option has no guaranteed success. In addition, the long treatment period of 24 to 72 weeks is unpleasant due to the numerous side effects.

In 1990, the antiviral effect of Ibogaine was reported for the first time. Since then, there have been reports of cures and documented reductions in HCV concentration after Ibogaine treatment. In 2005, Howard Lotsof filed a patent application for the use of Ibogaine and other Iboga alkaloids to treat hepatitis C and related symptoms.

The results of Ibogaine-assisted HCV therapy are promising. Repeated administration of small doses of Ibogaine HCL lowers the viral load slightly but continuously. A single staggered treatment of a high dose of Ibogaine HCl, significantly reduces the viral load of the hepatitis C genotype 3 and is favourably comparable with the interferon-ribavirin therapy. The reduction in viral load continues even after the end of the Ibogaine treatment.

In addition, Ibogaine HCL is significantly less toxic than the conventional therapy.
 However, within the pharmaceutical industry and many Western doctors, there seems to be no particular interest in alternative methods of treatment. Meanwhile, Ibogaine therapy is far more cost effective than monthly treatment with interferon-ribavirin. Unfortunately, there are no other clinical studies, only anecdotal reports.

 
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Electron microscope image of Fortaleza-strain Zika virus (red),
isolated from a microcephaly case in Brazil.


Breakthrough in Zika virus vaccine

by Elisa Black, University of Adelaide | Medical Xpress | Dec 13 2019

Researchers from the University of Adelaide have made significant advances in developing a novel vaccine against Zika virus, which could potentially lead to global elimination of the disease.

The virology team, led by Professor Eric Gowans and Dr. Branka Grubor-Bauk—based at the Basil Hetzel Institute for Translational Health Research and supported by The Hospital Research Foundation—has developed a vaccine that prevents Zika infection in pre-clinical models of the disease.

Their findings have been published today in the leading international journal Science Advances.

Zika is a mosquito-transmitted 'flavivirus' which can cause microcephaly (a birth defect where a baby's head is significantly smaller than expected) and severe birth defects in infants born to infected mothers.

The introduction of an effective vaccine for Zika will prevent infection of pregnant women and the resultant congenital effects in the unborn child.

Dr. Grubor-Bauk, senior research officer with the Adelaide Medical School, said the team had developed a novel vaccine against Zika that proved effective in mouse models.

"This is the first vaccine study that shows that a T cell-based vaccine can confer protection against a systemic Zika infection,'' she said.

"Our vaccine offers an advantage over other vaccines in development by eliminating the ongoing concerns in the field about enhancement of infection following exposure to dengue virus. This finding demonstrates for the first time that protective T cell vaccines against Zika are achievable."

"Zika virus is extremely detrimental if you're pregnant and there has been no therapy or vaccine available to date. If we can progress this work and immunise women who are of reproductive age and most at risk, we can stop the devastating effects of Zika infection in pregnancy and make a huge difference to the health of the global community."


This research, which has been years in the making, has progressed to this significant stage thanks to funding from National Foundation for Medical Research and Innovation (NFMRI) and ongoing funding from The Hospital Research Foundation.

The work was done in collaboration with eminent global vaccine researcher Prof Dan Barouch, Director of Harvard Medical School's Centre for Virology and Vaccine Research (CVVR) at Beth Israel Deaconess Medical Centre; as well as Adelaide's Prof Sarah Robertson, Director of the Robinson Research Institute, University of Adelaide; and other scientists from the universities of Adelaide, South Australia and Flinders.

"The next steps are to advance the vaccine to being ready for Phase I human clinical trials. This involves further pre-clinical studies which are vitally important to identify the most effective dosing and demonstrate protection against Zika infection in different pre-clinical models of the disease," Dr. Grubor-Bauk said.

"The goal is to de-risk and create an attractive technology with a strong IP position, for licensing or co-development with a commercial partner."

"We are grateful to The Hospital Research Foundation which has been instrumental in their support of our research over this time. We could not have reached this point without them."


The findings of this study will also greatly inform other research in the development of flavivirus vaccines by shifting the focus of vaccine development from viral envelope and antibody-based vaccines to T-cell based vaccines.

 
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Cannabis as a treatment for Tuberculosis

by Sanjai Sinha, MD | Sensi Seeds

Tuberculosis (TB) is a debilitating respiratory disease that typically results in death if untreated. Vaccination programs and modern antibiotics have successfully held TB at bay for decades in most developed societies, but new, drug-resistant strains are now emerging. Cannabis has been shown to exert antimicrobial effects on TB and similar microbes.

Tuberculosis is a microbial infection, caused by various strains of mycobacteria (primarily Mycobacterium tuberculosis). Mycobacteria require abundant oxygen to survive and replicate: M. tuberculosis colonises the lungs for this reason, and the closely-related leprosy bacterium, M. leprae, forms clusters in the epidermal and epithelial tissues—which receive oxygen from the blood, as other tissues, but can also absorb atmospheric oxygen.

Infection with M. tuberculosis typically leads to a latent (asymptomatic) infection, although 5-10% of infections lead to an active form of the disease that causes a chronic cough, rapid weight loss, and fever, and has a mortality rate of around 66% if untreated. With treatment (usually antibiotics) likelihood of death is somewhat reduced—but as the active disease is difficult, time-consuming and costly to treat, efforts to contain TB rest far more on our ability to immunise our populations against it.

Multi-Drug-Resistant Tuberculosis

MDR-TB typically occurs when ‘first-line’ antibiotic treatment courses are ceased or interrupted before the bacteria are fully eradicated. In these cases, what remains are often the most resilient forms of the bacterium—those with particularly impermeable cell walls (M. tuberculosis is known for its thick, waxy cell walls), those expressing genes encoding for drug-modifying enzymes, or those that have mutated entirely. These resilient bacteria then replicate and can be transmitted just as with normal TB—although there is evidence that MDR-TB outbreaks are less likely to arise in healthy populations, and are more common among the immunocompromised, such as HIV/AIDS patients.

Once a TB infection has become multi-drug-resistant, its mortality rate generally increases to around 80%. There are still some drugs that can treat MDR-TB, including some forms of chemotherapy, but the side-effects can be hugely debilitating. If these ‘second-line’ treatments are mismanaged, MDR-TB can become XDR-TB, or extensively-drug-resistant TB. It is estimated that 40,000 cases of XDR-TB are diagnosed each year, and it appears that prevalence is increasing: in 2008, 49 countries had documented cases of XDR-TB; now, the number of countries has risen to 91.

Although MDR-TB is rare and XDR-TB rarer still, it could be disastrous if such strains gain a foothold in the general population, as the standard BCG vaccine is not entirely effective against them (or even ‘normal’ TB, against which it is estimated to be approximately 50% effective). Thus, new vaccines and treatment options are urgently sought, and governments and international organisations across the planet are pouring money into research and development.

Hemp seed used to treat Tuberculosis in pre-war Czechoslovakia

In pre-World War II Czechoslovakia, hemp seed was routinely used as part of a treatment program for children suffering from TB. Prior to 1948 (at which point the Czechoslovakian Pharmaceutical Industry was nationalised) a product called Edezyme was available on the market; even now, a similar recipe is apparently still produced as a home remedy in some areas. Ground hemp seed is steeped in warm milk (60-80°C) for at least thirty minutes, before being pressed and filtered. Then, the mixture is administered to the patient on alternate days; each dose should consist of 375ml of milk and contain 50-80 grams of seed.

Observations recorded over almost thirty years at the Jince Sanatorium in western Czechoslovakia (now part of the Czech Republic) indicated that treatment with hemp seed milk typically resulted in significant improvements, and many successful cures—even in the absence of other medication, and in times when balanced, nourishing meals were rare. It is thought that the high content of polyunsaturated essential fatty acids found in the primary hemp seed protein, edestin, is important in the treatment of TB—it has been shown that M. tuberculosis bacteria are destroyed at faster rates when high levels of arachidonic acid are present; arachidonic acid is produced in the body via the metabolism of linoleic acid, which is found in very high levels in hemp seed.




Modern research into cannabis and TB

In the 1950s, research began to provide evidence of the significant antimicrobial properties of cannabis, and investigations into its potential use as a treatment for tuberculosis began in earnest, with promising initial results. In 1960, it was demonstrated that isolated cannabis resin inhibited growth of M. tuberculosis and various other bacterial pathogens.

Knowledge of the specific cannabinoids themselves was in its infancy (CBD and CBN had been isolated in the 1940s, but THC and other cannabinoids would not be identified until 1964), and as the world began to strengthen anti-cannabis laws in the 1960s and 1970s, research began to stagnate. However, CBD had been shown to exert specific antimicrobial properties, and as the speed of research began to pick up once more in the 1990s, renewed attention was paid to this area of investigation.

Now, research into the microbial properties of cannabis has uncovered substantial evidence that strains of drug-resistant pneumonia and MRSA are destroyed by several cannabinoids, CBC, CBG, CBD and THC. A 2011 Israeli study conducted on rats injected with M. tuberculosis in order to cause experimental autoimmune encephalomyelitis (an animal model of multiple sclerosis) showed that subsequent treatment with CBD greatly slowed the progression of the disease. The researchers concluded that this effect was mediated by CBD-induced inhibition of T-cell proliferation, a property CBD has also been demonstrated elsewhere to possess, and does not explicitly mention a direct bactericidal effect on M. tuberculosis, but it is possible that it played some role in slowing the progression of the disease.

Cannabinoids, TB, and the Th1 immune response

When an individual is infected with tuberculosis, a set of immune responses that defines the progression and outcome of the disease is triggered—this immune response differs between individuals, and for the vast majority of humans, no symptoms will ever become apparent. It is not known precisely what mechanisms determine natural immunity to TB; there are multiple different strains, and various different environmental and other factors can exert an influence.

What is known is that the Th1 immune response is vital for defence against intracellular pathogens (microbes that infiltrate and reproduce inside host cells, such as TB), and individuals that are susceptible to symptomatic TB have their Th1 immune response inhibited. In instances of Th1 suppression, the Th2 immune response kicks in—however, this response is designed to defend against extracellular pathogens (such as toxins and parasites), and when forced to attempt to defend against TB, actually allows for more rapid and effective progression of symptoms.

Cannabinoids have been demonstrated in several papers to be immune system modulators. More specifically, it is thought that they inhibit the Th1 immune response while promoting the Th2 response. Thus, in instances where activation of the Th1 immune response is crucial to fighting off an infection, as is the case with tuberculosis, it would appear that avoiding the use of cannabis would be advantageous.

It is clear that much research remains to be done on the complex relationship between the endocannabinoid system and the immune response, and on how use of cannabis may alter one’s susceptibility to or prognosis of infections with TB and similar microbial pathogens. However, the bactericidal effect of cannabinoids is certainly of interest to researchers, and as the issue of drug-resistant bacteria becomes ever more relevant, cannabis is sure to have a part to play in their control and management.


There is a shocking paucity of information available online concerning the treatment of TB with cannabis or CBD. Anyone needing more is going to have to really dig, and you should!! - pb
 
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More than 7 million new malaria cases in Burundi this year

Medical Xpress | Oct 30 2019

The World Health Organization says more than 7 million cases of malaria have been reported in Burundi this year. Officials blame the outbreak on factors including the lack of protective bed nets, problems with medicines and climate change.

The U.N. health agency says malaria has killed nearly 2,700 people this year in the East African nation and caused 64% more cases than in 2018.

The agency says there is "probably a decrease in the effectiveness of treatment, which is still under investigation." It says Burundi is ordering new medicines and planning campaigns to spray homes with insecticide and distribute bed nets.

Scientists fear warming temperatures may result in a spike in mosquitoes, which spread malaria and other diseases.

Globally, malaria sickens about 219 million people every year.

 
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Ibogaine in the treatment of Hepatitis C

by Bruce Blaus | Creative Commons

The hepatitis C virus (HCV), which is common among drug users, was first described as non-hepatitis A and non-hepatitis B virus in 1973, until finally identified in 1989 by genetic engineering of the hereditary material. In Central Europe, most people are now vaccinated against the hepatitis A virus and the hepatitis B virus, but there is currently no available immunisation against HCV.

Symptoms of hepatitis C include an inflammed liver, pain in the liver and increased production of liver enzymes. There are different treatment options for HCV. The standard treatment option combines interferon with ribavirin. However, this treatment option has no guaranteed success. In addition, the long treatment period of 24 to 72 weeks is unpleasant due to the numerous side effects.

In 1990, the antiviral effect of Ibogaine was reported for the first time, and since then there have been reports of cures and documented reductions in HCV concentration after Ibogaine treatment. In 2005, Howard Lotsof filed a patent application for the use of Ibogaine and other Iboga alkaloids to treat hepatitis C and related symptoms.

The results of Ibogaine-assisted HCV therapy are promising. Repeated administration of small doses of Ibogaine HCL lowers the viral load slightly but continuously. A single staggered treatment of a high dose of Ibogaine HCl, significantly reduces the viral load of the hepatitis C genotype 3 and is favourably comparable with the interferon-ribavirin therapy.

 
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