Lyme disease, science, and society: Camp Other
Showing posts with label disease. Show all posts
Showing posts with label disease. Show all posts

Saturday, April 14, 2012

6 Commentary: On Dr. Phil, Lyme Disease, And "Faking It".

Yesterday a segment about chronic Lyme disease aired on the Dr. Phil Show. There's been much discussion about this episode online throughout the Lyme disease patient community, and so far comments by the hundreds have been posted rapid fire to Dr. Phil's web site about chronic Lyme disease.

I am in support of seeing more coverage on Lyme disease and patients with persisting symptoms, but I am not in support of seeing the angle of hypochrondria or "faking disease" being mentioned - even in passing - in relationship to Lyme disease.

The issue of whether or not a patient is faking their symptoms came up during an interview with a 25 year old model, Stephanie, who is experiencing unusual attacks and symptoms - and who has been accused of behaving this way in order to get attention.

While I do not know all the details of Stephanie's medical history, I would be one of the last people to accuse her of faking her symptoms to get attention. I say this in part because if she has suffered with these symptoms for five years* and hasn't been getting out much due to her condition - then like myself, she's probably discovered that after that period of time other people will stop inviting you to events. Some may not even visit.

Being a model equates with an active social life, attending events, and self-promotion. Getting plenty of attention lands you work. Becoming sick and spending most of your time at home kills your career and leads to isolation. There is little to gain there, and any initial sympathy which might be gained wears thin after the first several months. People will move on without you.

Having suffered the personal costs of isolation due to chronic illness myself, I have sympathy for her situation. And I am appalled that the first thing Dr. Phil would ask was not what evidence she had that she was suffering from Lyme disease - but to ask whether or not she was faking her symptoms.

While I disagreed with her method of self medicating, it is clear to me that she has been suffering. I've never experienced what she is calling seizures - however, earlier in my illness I had episodic attacks of severe pain which would cause me to curl up, wince, and yell with pain.

The pain was so intense there was nothing else I could do. It often happened when I was alone in bed and everyone else was out of the house. If someone wanted to accuse me of a payoff for my behavior, it wasn't coming.

It seems to be a running theme over time - this concept that if one is ill with a condition that is not easily understood or for which tests have not been well developed - then somehow the patient's symptoms must be "all in their head," or the patient must be "making it all up".

And that if a patient behaves in an unusual manner, accusations fly that they must be acting out, with others suggesting that "perhaps they have a psychological problem," or  "perhaps they just want attention."

I can't think of how many times I've heard these statements made about someone with certain medical conditions - usually conditions where the person physically appears normal to others at least some portion of the time, and isn't showing an overt sign of illness or injury.

Patients with a broken leg or weeping sores are not accused of hypochrondria or of "faking it". When a physical symptom is a daily constant and is taking time to heal, it's a concrete visual reminder to others that a person is not well.

But if someone has lesions on their brain, only their radiologist who took the MRI saw it. No one else can see them.

If someone has extreme fatigue, only they know what the experience is like to be feeling the heavy weight of that burden on their body all the time - while everyone else just sees them as someone who lies on a sofa or in bed all day and might judge them as being lazy.

If someone winces in pain at someone else turning on a lamp or children talking and laughing animatedly, everyone else may see them as being overly sensitive without knowing the experience of the person for whom sounds seem three times louder and light five times brighter.

People understand what they themselves have experienced, and people understand what they can see. Many people joke about using the Missouri license plate motto as their own personal mantra: Show me. They don't believe in something's existence unless they can see it or experience it firsthand.

But anyone with an ounce of scientific reasoning and logic can see that just because one cannot see something or experience it firsthand does not mean it doesn't exist. One can detect the presence of some agent or phenomenon through indirect detection. Much like antibodies in a blood test, one can determine infection is present without detecting the causative organism itself.

In the mid-1800s, doctors and others believed that patients' exposure to bad air in hospitals are what lead to infection in wounds. Washrooms for doctors' hands and patients' wounds were not available. Washing hands before seeing a patient was not considered necessary to avoid infection - the idea never entered one's mind.

One doctor, Dr. Joseph Lister, learned about Louis Pasteur's research that rotting and fermentation could occur under anaerobic conditions if microbes were present. By learning more about Pasteur's hypothesis as to what could prevent rotting and how this might apply to infections, Lister decided to conduct his own experiments. Even though he could not see the microbes themselves he could see the results of his research: antiseptics prevented infections in wounds fron taking hold.  

Lister went on to encourage doctors he supervised to wash their hands before surgery and use antiseptics - even though at the time doctors thought it was unnecessary and a joke at first. Nonetheless,  as time went on, others began to adopt his practices and went on to prevent many cases of infection and sepsis.

For centuries, scientists hypothesized that extrasolar planets existed. But it is difficult to directly detect them. Most extrasolar planets are detected through indirect detection methods such as measuring radial velocity or the Doppler method, by observing the drop in brightness emitted by a distant star due to a planet's transit in front of its disk, and by using several other methods. In astronomy, one can observe a number of planetary bodies' presence through the use of inference. By looking at different stars, we can infer something about the planets orbiting them - even if we can't see the planets with our own naked eye - or in some cases, even with a telescope.

These are just two examples where inference leads to association and discovery.

But here we are, in 2012, and it seems that the power of inference is somehow broken in doctors and neighbors who leap to the conclusion about patients who have symptoms they do not understand or which they have trouble offering an official diagnosis.

Like the doctors who believed patients were getting infections from bad air in the hospital without any particular data to support their conclusion - some doctors today are making snap judgments that patients' symptoms are due to their own neurotic imaginings.

The truth is, it might not be that easily determined why it is some patients are having the symptoms they do.

Instead of saying these three words, "I don't know," when there is no quick answer as to why a patient has particular symptoms, some doctors readily fall back on a psychological cause. Often without any particular training in psychology. Often without any psychological and neurological testing of the patient in front of them. Often without any rule-outs to determine if some underlying medical condition could be contributing to their patient's symptoms.

And sometimes, even with training, there is a risk their diagnosis is wrong. Because if one doctor looks through the same lens of his own area of specialization every day, sometimes it's difficult to consider presentations from a different angle.

While the debate about the cause continues, the recent outbreak of a strange rash of illnesses in upstate LeRoy, New York, could be one example of making a snap judgment based on a psychological condition.

A group of young women (and as it turned out later, one young man who didn't know them) in high school began exhibiting strange behavior last year. They have had unusual tics and verbal outbursts similar to those found in Tourette's syndrome.

They were taken to various medical professionals to be interviewed and examined, and the initial diagnosis which was offered was "conversion disorder". Conversion disorder used to be previously known as "hysteria", and before Freud used the term, hysteria was associated with people who were malingerers, had weak nerves, or had some meaningless disturbances. No reason for these behaviors was ever given back then beyond having poor character or a weak constitution.

Today, conversion disorder is not the same thing. It's not thought to be due to malingering or feigning illness - it is a genuine psychiatric disorder which is not related to any underlying neurological or infectious cause and is rooted in extreme stress and anxiety. One could argue it is a physiological and biochemical response to stress.

But given its psychological origins, some parents disagreed with this diagnosis outright - and feeling that their own kids could not have this disorder, they sought second opinions. With further investigation into biological causes for their symptoms, one doctor diagnosed a young woman in neighboring Corinth, New York, with Lyme disease and is apparently evaluating some of the students from LeRoy.

Today, months after the original outbreak, debate over what exactly is the cause of all these students' unusual symptoms has continued. One physician who treated some of the girls classified the disorder as PANDAS, related to streptococcal virus. Some of the girls got better under treatment for PANDAS. Some have not. Some doctors do not even think all the students suffer from the same condition as their individual presentations are somewhat different.

Where can anyone rest with this, with the knowledge that people that exhibit unusual behavior may not have it "all in their heads" and are not "making it up"?  And that similar symptoms might stem from different causes?

One must appreciate that sometimes it takes time to sleuth out the proper diagnosis. But one must also begin to appreciate that it is way past time to stop discriminating against people and labeling their motives and essential character as human beings if they engage in unusual behavior - whether it began with a traumatic experience or a tick bite.

Even if it turns out some of these young women have a disorder which was triggered by extreme stress, that does not mean they are faking it. It would be a genuine medical problem that requires treatment, just as PANDAS and Lyme disease need treatment.

From the infectious disease angle, this is not the only item to hit the news in recent months which brought up discussion about the possible relationship between bacteria and behavior.

Researcher Jaroslav Flegr has been investigating the relationship between infection with toxoplasmosis in people and their behavior, and already found some significant relationships. The psychological symptoms caused by toxoplasmosis are usually more subtle, so far, than what has been observed in these young women with tics and vocalizations - but they are further evidence that it is not always going to be clear if we alone are driving our behavior - or if a visiting microbe onboard is.

Other mental illnesses have been investigated for an infectious cause, such as schizophrenia - and various viruses and microbes have been implicated in or associated with its development.

Regardless of whether one diagnoses a patient with a psychological disorder or a physical condition, all of this should make us stop for a moment and think about how we as a society think about mental and physical illness in this country:  The gap between what is a biologically-based illness and what is a psychologically-based illness is closing and becoming blurred. With this change, greater acceptance and understanding of those with symptoms which affect them cognitively, neurologically, and psychologically is bound to occur.

It's been a long slow climb to work to remove the stigma that comes with mental illness in the United States. And it continues in part because of a tendency to believe that everyone has control over their own behavior. Tied very intimately to that idea is a belief that everyone has control over their bodies as well. Which is nice and a comforting thought to have, and most people who are completely healthy live with the privilege of this experience without ever experiencing anything else.

But once you have become incredibly ill, it becomes clear just how much is not under one's control. If you get into a car accident and have a spinal injury that is obvious to everyone, no one can ever tell you how long it will take to completely heal from your injury. Often it isn't clear if you'll completely heal at all.

The same applies to people who have been affected mentally - and not by choice, any more than the person who injures their spine in an accident. People who were healthy and "had it all together" can fall victim to an infection, genetic and environmental factors, temporary or permanent side effects of prescription medication, a car accident, or other traumas which leave them both physically and mentally affected.

The results are not something that is "all in their head" - if that phrase is meant to apply to an idea of them imagining it. On the contrary, having an infection or trauma which affects your brain is literally "all in your head" - and is in no way, shape, or form, imagining it. It is a harsh reality one must live with every day. It will mean not having control over your behavior and reactions to certain stimuli such as noise, light, the sense of touch, music, scents, the taste of certain foods, and then some.

To the outside observer, these reactions may seem strange. And even by the person having them, they are, and they are often aware their own reactions are atypical. But to the person who is living with them, it is what they have to live with and work around.

Antibiotics or other medications may bring their reactions under control and help. It may make life more predictable for those affected and those close to them who witness their behavior. And if anything, people who observe the change which occurs under such treatment over time should grasp that their symptoms have been due to their being ill and not because they were trying to get attention.

In regards to the practice of telling patients that a condition is imaginary, I have hoped that by 2012 we would have gotten much further by now and stopped this practice.  That we wouldn't be seeing young women in the prime of their lives with careers and hopes for the future lose all that and be told that their symptoms are only about trying to get attention by being sick.

It reminds me of stories of doctors who accused women back in the late 1800's of suffering from "hysteria" when they may have had multiple sclerosis. It reminds me of stories of doctors who accused patients in the 1980's through the present that it was "all in their heads" when they have CFS/ME. It reminds me of stories of doctors who today are saying those with chronic Lyme disease are "faking it" and aren't really sick - or perhaps they are depressed.

No doubt, depression can be a serious and debilitating condition in its own right which requires medical treatment and cannot be solved just by pulling oneself up by one's own bootstraps. We've moved beyond some of the stigma attached to depression and understand today that it is not a sign of poor character or laziness. But let's be sure to not confuse one disease or condition with another just because some of their symptoms overlap.

All this said, it is clear to me after having done extensive research on Lyme disease that everyone who has persisting symptoms related to Lyme disease after a tick bite and its initial treatment is not well. It's not "all in our heads"- even if for some of us the damage may be literally in our heads.

Lyme disease affects each of us somewhat differently - some of us have more neurological, cognitive, and/or psychological manifestations of disease than others. Given the pathogenesis of this disease, these differences should be no surprise: without early treatment during the acute stage, Borrelia bacteria disseminates throughout the body and can affect different organs and tissues - and at times, affects the nervous system, too.

Even if one does not believe in a model of chronic infection after initial antibiotic use, there is no reason to doubt that someone affected by this disease would have some damage done by its presence. This damage can lead to all kinds of problems of varying frequency and duration - damage which doctors should be well aware of and be attentive to just as they would for other medical conditions.

The effects of Lyme disease on people - particularly disseminated and late stage Lyme disease - are real and variable. Even if it becomes a post-infectious autoimmune condition, the damage done is real. The resulting symptoms need to be dealt with effectively. Medical societies and professionals need to step up to the plate and recognize them rather than write them off as imagined.


Related items of interest:


Dr. Phil Show In Three Parts - See the entire segment on Chronic Lyme disease.
Emory University Center for Ethics on an explanation that psychiatric illness is not imagined but a real condition - plus a mention that there is growing evidence of a biological basis for psychiatric disorders.
Economist on the pros and cons of toxoplasmosis.

* Stephanie, when interviewed on the show, stated she has had symptoms on and off for five years. According to her Twitter account and other online resources, she had a turn for the worse beginning in October 2011 and has been consistently ill since November 2011. So she hasn't yet been seriously symptomatic for the same period of time I was - let's hope she isn't.

Image Credit: 
Sick Girl, 1910 (Poland) - From commons.wikipedia.org under US-PD license.





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Friday, April 22, 2011

0 The Friday Four

In this week's Friday Four, we'll look at antimalarial trees that are threatened with extinction but may yet be saved to make natural medicine, how our own bacteria use immune cells to help save us from bad infections, a six-fold risk of death from C. diff in patients with IBD, and genetically engineering mosquitoes so that they have less ability to spread disease.


1) Antimalarial trees in East Africa threatened with extinction

Source link: http://www.sciencedaily.com/releases/2011/04/110420211758.htm

Olea europaea Africana -
African wild olive - antimalarial tree
ScienceDaily (2011-04-21) -- Research released in anticipation of World Malaria Day finds that plants in East Africa with promising antimalarial qualities -- ones that have treated malaria symptoms in the region's communities for hundreds of years -- are at risk of extinction. Scientists fear that these natural remedial qualities, and thus their potential to become a widespread treatment for malaria, could be lost forever.

Comments:

According to this article, researchers at the World Agroforestry Centre (ICRAF) and the Kenya Medical Research Institute (KEMRI), Common Antimalarial Trees and Shrubs of East Africa, are documenting and studying 22 of the region's malaria-fighting trees and shrubs which have been found to be antimalarial by both traditional medicinal practitioners and scientists.

Time is running out for these trees, though, because of deforestation and overexploitation for medical use without replacing the trees and cultivating new ones, but scientists are preserving them in a genebank as well as a nursery.

Here is one thing I want all alternative medicine lovers to be aware of, and it saddens me, too. The article states:
"Today, the world's newest, most-effective therapeutic treatment for malaria also comes from a plant, the Artemisia annua shrub. However, access to malaria therapies based on artemisinin compounds remains low -- around 15 percent in most parts of Africa and well below the World Health Organizations' 80 percent target. Additionally, the malaria parasite's ability to resist artemisinin is already beginning to emerge in Southeast Asia."
Here is our note of humility, humanity...

Mother Nature is in charge. She always was, and we will be one step behind her. Get a bacterial infection, then take an antibiotic, then the bacteria grows resistant to the antibiotic. Get an infection, then take an herb, then the bacteria grows resistant to the herb, too.

It's evolution in action, and there's nothing we can do to stop it. All we can hope to do is keep up, and try to maintain balance. But Mother Nature is crafty. Beautiful, mysterious, and creative, and has many tricks up her sleeve.

So just because it's an herb doesn't mean a parasite or bacteria won't develop resistance to it.

This aside: I really hope these scientists can protect and save as many of these trees as they can from destruction. It sounds like they are working hard on this problem. If they do, they may have in their hands future treatments for not only malaria but babesia, too.

Additional Sources:
http://www.worldagroforestrycentre.org/
http://www.kemri.org/

2) Learning to tolerate our microbial self: Bacteria co-opt human immune cells for mutual benefit

Source link: http://www.sciencedaily.com/releases/2011/04/110421141632.htm

B. fragilis
ScienceDaily (2011-04-22) -- The human gut is filled with 100 trillion symbiotic bacteria which we blissfully live with, although they have many features similar to infectious bacteria we react against. What decides whether we ignore -- or fight? In the case of a common "friendly" gut bacterium, Bacteroides fragilis, researchers have discovered the surprising answer: The decision is not made by us, but by the bacteria, which co-opt cells of the immune system for our benefit ... and theirs.

Comments:

So these scientists discovered that these friendly bacteria in mice, B. fragilis, can control regulatory T-cells in their immune system. These T-cells, by the way, are what protects our immune systems from attacking our own cells - they are basically anti-autoimmune cells.

B. fragilis can "trick" the immune system into activating these regulatory T-cells so they themselves will not get attacked.

How does this happen? The bacteria produces a molecule that receptors (called Toll-like receptors) on the regulatory T-cells pick up. When these regulatory T-cells get this "message", they suppress T helper 17 cells. By shutting those cells down, the bacteria is able to colonize the intestines.

This is not usually how Toll-like receptors are thought of - they are thought of as being part of a chain of communication in the immune system that works to get rid of bacteria - not keep it alive.

Question to my readers: What is the relationship between Toll-like receptors and Borrelia burgdorferi in people?

I'll give you time to research it if you don't know the answer, and will tell you next week.

Original Reference:
June L. Round, S. Melanie Lee, Jennifer Li, Gloria Tran, Bana Jabri, Talal A. Chatila, and Sarkis K. Mazmanian.The Toll-Like Receptor 2 Pathway Establishes Colonization by a Commensal of the Human MicrobiotaScience, 21 April 2011 DOI:10.1126/science.1206095

3) C. difficile increases risk of death 6-fold in patients with inflammatory bowel disease

Source link: http://www.eurekalert.org/pub_releases/2011-04/icl-cdi041911.php

Patients admitted to hospital with inflammatory bowel disease face a sixfold greater risk of death if they become infected with Clostridium difficile, a new study has found.

Comments:

The It-Could-Be-Worse News: A review published in 2010 estimated the overall mortality rate for patients with C. difficile to be 6 per cent.

Okay, 6%. I rather it'd be 0%, but 6% is a relatively small number compared to the rate of fatalities for other conditions.

The Bad News: Those most severely ill and the elderly are in a high risk for fatality from a nasty C. diff infection.

That's not good.

The Worst News: The mortality rate for IBD patients with C. difficile at 30 days was 25 per cent, compared with 3 per cent for patients with IBD alone.

25%. That's really not good.

I really don't know what to say to this other than it's scary. I hope research finds a way to prevent and cure IBD, and that we can prevent and more effectively treat C. difficile infections.

My advice:

1) Take your probiotics if you are using antibiotics. Eat yogurt  and/or take probiotics 3 hours after and before taking antibiotics daily.

2) Take Saccharomyces boulardii. There is some evidence it stops C. diff infections.

3) Avoid taking antibiotics unless it's absolutely necessary.

4) Get evaluated for Inflammatory Bowel Disease if you suspect you have it.

This not something to mess around with.

Original Reference:
 J.A. Karas et al. A review of mortality due to Clostridium difficile infection. Journal of Infection (2010) 61, 1-8.

4) 'Disease-Proof Mosquito' Could Spread Like Wildfire

Source link: http://news.sciencemag.org/sciencenow/2011/04/disease-proof-mosquito-could-spr.html

Scientists have identified several mosquito genes that, when tinkered with, decrease the mosquitoes' ability to transmit a virus or a parasite; they have also given the insects new genes that do the same.

My only comment for this is: Will we ever see a tick that is bred to not spread Lyme disease bacteria and coinfections? 

Is there anything beneficial in having any of these hosts carry these infections for anyone but the pathogenic agents? Any whatsoever at all?

No?

Then stop these pathogens in their tracks, please.
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Saturday, April 9, 2011

4 Artemisinin and cancer

Yeah, I know, I usually don't post on the weekend... well, here I am - but only for a few minutes.

I keep tripping over that Friday Four article I posted on using artemisinin to treat leukemia cells.

I wanted to see more of the research that's out there, and I found this:

Synthesis and anti-cancer activity of covalent conjugates of artemisinin and a transferrin-receptor targeting peptide. Steve Oha, Byung Ju Kim, Narendra P. Singh, Henry Lai, Tomikazu Sasaki. Cancer Letters. Volume 274, Issue 1, Pages 33-39 (8 February 2009)
Source link:http://www.cancerletters.info/article/S0304-3835(08)00668-X/abstract

Effects of artemisinin-tagged holotransferrin on cancer cells
Henry Lai, Tomikazu Sasakib, Narendra P. Singha and Archna Messay
Department of Bioengineering, Box 357962, University of Washington, Seattle, WA 98195-7962, USA Department of Chemistry, University of Washington, Seattle, WA, USA
Received 2 August 2004. Accepted 25 August 2004. Available online 23 November 2004.
Link to above abstract

Apparently Henry Lai did previous research on the use of artemisinin on cancer, in which the earlier abstract states:
"Artemisinin reacts with iron to form free radicals that kill cells. Since cancer cells uptake relatively large amount of iron than normal cells, they are more susceptible to the toxic effect of artemisinin. In previous research, we have shown that artemisinin is more toxic to cancer cells than to normal cells. In the present research, we covalently attached artemisinin to the iron-carrying plasma glycoprotein transferrin. Transferrin is transported into cells via receptor-mediated endocytosis and cancer cells express significantly more transferrin receptors on their cell surface and endocytose more transferrin than normal cells. Thus, we hypothesize that by tagging artemisinin to transferrin, both iron and artemisinin would be transported into cancer cells in one package."
More recent research that was not done by Lai includes this study on using artemisinin to treat prostate cancer:

Effect of artemisinin derivatives on apoptosis and cell cycle in prostate cancer cells.
Morrissey, Colma; Gallis, Byronb; Solazzi, Jeffrey W.a; Kim, Byung Juc; Gulati, Romane; Vakar-Lopez, Fundad; Goodlett, David R.b; Vessella, Robert L.af; Sasaki, Tomikazu. Anti-Cancer Drugs: April 2010 - Volume 21 - Issue 4 - pp 423-432
Source Link: http://journals.lww.com/anti-cancerdrugs/Abstract/2010/04000/Effect_of_artemisinin_derivatives_on_apoptosis_and.9.aspx

An excerpt from the above abstract states:
"Artemisinin is a plant-derived anti-malarial drug that has relatively low toxicity in humans and is activated by heme and/or intracellular iron leading to intracellular free radical formation. Interestingly, artemisinin has displayed anti-cancer activity, with artemisinin dimers being more potent than monomeric artemisinin. Intracellular iron uptake is regulated by the transferrin receptor (TfR), and the activity of artemisinin depends on the availability of iron."

I also found an entire chapter of a book devoted to the study of artemisinin and how it affects pathogens and cancer:

Chapter 18: The Anti-Infective and Anti-Cancer Properties of Artemisinin and its Derivatives. Christopher Paul Hencken, Alvin Solomon Kalinda and John Gaetano D’Angelo. Annual Reports in Medicinal Chemistry. Volume 44, 2009, Pages 359-37
Link (doi): doi:10.1016/S0065-7743(09)04418-2

These are only a few examples of research being done out there on artemisinin for cancer... Seems there is an increasing interest in it. I still want to do a little more digging to see where that claim about artemisinin came from Henry Lai: "It's 100 times more specific than traditional chemotherapy. In breast cancer, it's even better."

Specificity in cancer treatment would improve treatment so much and improve the odds of surviving it with fewer side effects. So I'd really like to know more about this.

Artemisinin. It's not just for Malaria and Babesia any more.
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Friday, April 8, 2011

14 The Friday Four

In this week's edition of the Friday Four, we look at the IDSA's plan to combat antibiotic resistance with a brief recap of highlights of the STAAR Act, using artemisinin and hyperbaric oxygen as a potential cancer treatment, a dangerous new tickborne virus identified in China, and creating a new antibiotic using marine bacteria.

1) Lifesaving antibiotics face doubtful future

Source link: http://www.sciencedaily.com/releases/2011/04/110407121435.htm

ScienceDaily (2011-04-07) -- To head off a health care disaster, the Infectious Diseases Society of America has developed a plan to combat deadly antibiotic-resistant "super bugs" and is rolling out the multi-pronged plan today, on World Health Day 2011.

Comments: I don't know why this is considered the latest news on ScienceDaily... this plan is basically a repeat of all that is found in the STAAR Act.

I wrote about the IDSA's 2010 testimony to the House Committee back in early January. I posted about it on Lymenet, too.

Did anyone notice back then? I sure hope people notice now.

I'll repeat here what I wrote back in January:
This act should be more familiar to you all, because the STAAR Act stands for "Strategies to Address Antimicrobial Resistance".


Taken from the final 2010 report from the IDSA to the House Committee on Energy and Commerce Subcommittee on Health:


"The STAAR Act strengthens existing efforts by establishing an Antimicrobial Resistance Office (ARO) within the HHS Office of the Assistant Secretary of Health. The Director of ARO will serve as the director of the existing interagency task force. The Act also establishes a Public Health Antimicrobial Advisory Board (PHAAB) comprised of infectious diseases and public health experts who will provide much-needed advice to the ARO Director and task force about antimicrobial resistance and strategies to address it. The STAAR Act will strengthen existing surveillance, data collection, and research activities as a means to reduce the inappropriate use of antimicrobials, develop and test new interventions to limit the spread of resistant organisms, and create new tools to detect, prevent and treat drug-resistant “bad bugs.”" 
And that's just part of it, really - you ought to read the entire report.

One of the IDSA's broader goals beyond this act is to institute a special fee called "the Antibiotic Innovation and Conservation Fee" on every course of antibiotics used by doctors and veterinarians in the future - both to acquire money for funding new antibiotic development - and to encourage restricted and judicial use of the antibiotics remaining in use. And then there is also the proposal for an "antibiotic stewardship program" which will be intended to track and reduce usage of antibiotics as well as lower medical cost.

This is one of the reasons I mention the issue of needing more research into the issue of persistence, and that it can't wait. It already couldn't wait, but now it becomes a more important issue. If persistence is proven, then long-term use of antibiotics to treat Lyme disease beyond the standard minimum would be accommodated - but if it isn't, then with the passage of the STAAR Act, if the proposed antibiotic stewardship program passes along with it - could affect Lyme disease patients on long-term antibiotics a lot.

How far will this act go, and how does one determine what the "inappropriate use of antimicrobials" actually is?

I'm in support of stopping antibiotic use on healthy livestock and think antibiotic use can be cut back for ear infections and acne. I'm in support of hospitals practicing more safe hygiene controls and using UV irradiated keyboards - if not UV-C doused rooms between patients - to reduce the spread of potentially deadly MRSA and C. difficile. I see the value of the STAAR Act  - especially in reducing the spread of resistant organisms and funding new antibiotics - the world desperately needs new antibiotics, including Lyme disease patients. Even better, I'd like to see development of technology that stops infection in its tracks without the use of antibiotics - thus avoiding the concern over resistance entirely. In the meantime, though? I have concerns this act could potentially be a strike against Lyme disease patients in getting ongoing treatment. It all depends on the implementation.

2) Kill Cancer Naturally - With Hyperbaric Oxygen and Artemisia Annua L. aka Artemisinin

Artemisia Annua or
"Sweet Annie"

ScienceDaily (Apr. 4, 2011) — An environment of pure oxygen at three-and-a-half times normal air pressure adds significantly to the effectiveness of a natural compound already shown to kill cancerous cells, researchers at the University of Washington and Washington State University recently reported in the journal Anticancer Research.




Link: http://www.sciencedaily.com/releases/2011/04/110404142813.htm

Comments:  And you thought Artemisinin was just for Babesia and Malaria treatment... In the future it might be used to treat cancer - only time will tell.

Seriously, someone needs to do more research using hyperbaric oxygen chambers. This could be something useful - and it should be easy enough to test on human volunteers under the supervision of a medical professional.

Note, though, that this study wasn't on actual people with cancer - it is a study in which the researchers used artemisinin or high-pressure oxygen alone on a culture of human leukemia cells. Results on cancer cells in vivo in people who sit in hyperbaric oxygen chambers may differ - this is something that needs to be tested in the future.

They found out that using either the artemisinin or the oxygen reduced the cancer cells' growth by 15 percent. But if they used them in combination - over a 48 hour period after 90 minutes of high-pressure oxygen - the cancer cells' growth was reduced by 38 percent. That's an over 50 percent increase in artemisinin's effectiveness.

Henry Lai, UW research professor of bioengineering, said that, "Artemisinin is a promising low-cost cancer treatment because it's specific, it's cheap and you don't have to inject it. It's 100 times more specific than traditional chemotherapy. In breast cancer, it's even better."

Is that true? A 100 times more specific? How? Where is he getting this information from? I want to know.

At any rate, it would be interesting to hear more about this and see further studies.

[ Side note: Science Daily's write up mentions that the FDA has approved the use of hyperbaric oxygen therapy chambers for Lyme disease - when that is not true. HBOT has only been approved for the use of 13 indications, and Lyme disease is not one of them - treatment with HBOT for Lyme disease is considered an off-label use or experimental. ]

Publication source:
Yusuke Ohgami, Catherine A. Elstad, Eunhee Chung, Donald Y. Shirachi, Raymond M. Quock, Henry C. Lai.Effect of Hyperbaric Oxygen on the Anticancer Effect of Artemisinin on Molt-4 Human Leukemia Cells.Anticancer Research, 2010; 30: 4467-4470 [link]

3) New Tickborne Virus In China Has High Mortality Rate

Source link: http://www.scienceagogo.com/news/20110222214117data_trunc_sys.shtml

Writing in the New England Journal of Medicine, scientists explain how a previously unknown and dangerous virus carried by ticks has been responsible for seasonal outbreaks of the disease in six of China's most populated provinces.

The newly discovered pathogen has been dubbed 'Severe Fever with Thrombocytopenia Syndrome virus'. It has been placed in the Bunyaviridae family, along with the hantaviruses and Rift Valley Fever virus.

Symptoms include high fever and gastrointestinal disorder; the mortality rate was initially estimated at 30 percent.

Comments:  This is scary. I think between the TBE in Europe and this, my next vacation will be at McMurdo station.

4) New Drugs From Bugs

Source Link: http://www.sciguru.com/newsitem/7751/New-drugs-from-bugs/

bioluminescent marine
bacteria on agar
This is interesting news from the UK... Chemists from Bristol and microbial geneticists from Birmingham determined the sequence of the complete DNA content of a marine bacterium that produces the new antibiotic, thiomarinol (owned by Daiichi-Sankyo). They then identified the genes responsible for making the antibiotic on the basis of their similarity to genes that make the related but less potent antibiotic, mupirocin, which is currently used to combat MRSA (methicillin resistant Staphylococcus aureus).

They found the genes are on a relatively small, separate DNA molecule called a plasmid, which is just big enough to carry the genes for making the antibiotic plus genes to allow the plasmid to replicate autonomously in the bacterium. The plasmid thus carries genes that make both the mupirocin-like antibiotic as well a second antibiotic, holomycin, and a gene responsible for joining both antibiotics together, forming a more potent molecule.

Tests showed that by joining the antibiotics together the resulting chemical is able to inhibit the growth of MRSA strains that have become resistant to mupirocin.

Comments: Read more at the link. I think it's pretty interesting to learn about how new antibiotics are made, even though I would like to find a way to fight infection using other medications and other technologies. We really need antibiotics that don't eventually become resistant and don't cause C. difficile infections (or imbalances that lead to infections, in a number of cases) - or we need an entirely different infection-fighting approach. This development of new antibiotics in the meantime is something desperately needed worldwide, and I'm glad to see it happening - I just wonder how long it will take before clinical trials are on the horizon...

Related Publications:
A natural plasmid uniquely encodes two biosynthetic pathways creating a potent antibiotic.
D. Fukuda, A. S. Haines, Z. Song, A. Murphy, J. Hothersall, E. R. Stephens, R. Gurney, C.
Riemer, R. Marshall, R. J. Cox, J. Crosby, C. L. Willis, T. J. Simpson and C. M. Thomas,
PLoS ONE, 2011, 6, in press.

Nature Reviews Microbiology 8, 281-289 (April 2010) | doi:10.1038/nrmicro2278
Resistance to and synthesis of the antibiotic mupirocin
Christopher M. Thomas, Joanne Hothersall, Christine L. Willis, Thomas J. Simpson
http://www.nature.com/nrmicro/journal/v8/n4/full/nrmicro2278.html
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Friday, April 1, 2011

8 The Friday Four

In this edition of the Friday Four, we'll look at using bacteria itself to deliver antibiotics and treat cancer, a huge touchscreen microscope, the value of Vitamin A in B1 cell immunity, and the mystery of lateral gene transfer between Chagas disease pathogens and its host.

1) 'Bacterial dirigibles' emerge as next-generation disease fighters

Link: http://www.sciencedaily.com/releases/2011/03/110329134120.htm

Summary: ScienceDaily (2011-03-30) -- Scientists have developed bacteria that serve as mobile pharmaceutical factories, both producing disease-fighting substances and delivering the potentially life-saving cargo to diseased areas of the body. They reported on this new candidate for treating diseases ranging from food poisoning to cancer -- termed "bacterial dirigibles."

Comments:


I don't know how many people are aware how much genetic engineering already goes on. Once the industry took off... well, it took off like wildfire. It's pretty common to do exactly what is stated in this article: "...Traditional genetic engineering reprograms bacteria so that they produce antibiotics, insulin, and other medicines and materials. The bacteria grow in nutrient solutions in enormous stainless steel vats in factories. They release antibiotics or insulin into vats, and technicians harvest the medicine for processing and eventual use in people."


In this experiment, they programmed E. coli not to pump out antibiotics into a vat in some factory somewhere... No, they created a version of E. coli that could target a portion of the intestine and adhere to it, and begin sending out chemical signals that influenced the production of proteins in different cells around it.


So I'm trying to understand this. They took E. coli, the bacteria that often makes people sick, and made a version that delivers itself to a specific part of the body and is programmed to affect other cells near it. Crazy.


What if this sort of "bacterial dirigible" could seek out and find remote Borrelia burgdorferi in collagen-rich tissues, in the adventitia of the heart, and in the brain? Does this have potential for killing the remaining spirochetes that may survive the initial onslaught of antibiotics?


2) Researchers in Finland Build Giant Multitouch Microscope

This is just too cool.  I want one. I want to see my spirochetes on this sucker.  [Time 1:43]


I think Leeuwenhoek would have just about shit himself if he saw one of those...

3) In the absence of Vitamin A, the body loses immune cells that put the brakes on the earliest stages of infection


Summary: Scientists have recognized the immune-boosting capabilities of vitamin A for the better part of a century, even without fully understanding how it helps the body fight off bacteria and viruses. "Soon after its discovery, vitamin A was termed ‘the anti-infective vitamin’ and was widely used to enhance recovery; but with the introduction of antibiotics, the therapeutic use of vitamin A diminished," says Sidonia Fagarasan of the RIKEN Center for Allergy and Immunology in Yokohama, Japan.

Comments:


So these researchers fed these mice a Vitamin A-free diet, and when they did, the mice had lower levels of IgA and IgM. They were given pneumonia vaccines and produced zero response. And then, the researchers tried to transplant B1 cells from healthy mice to these deficient mice - only to find that the B1 cells deteriorated, didn't last that long, and died off over several days.


However, the good news is, they found out the stem cells in the deficient mice's bone marrow could give rise to B1 cells - but they wouldn't do it unless they had some Vitamin A.


The researchers found out that a transcription factor protein found in activated T cells (NFATc1), regulates expression of numerous important genes in B1 cells. The researchers observed reduced NFATc1 levels in the mice's deficient B1 cells, but found that expression could be largely restored if these mice were injected with ATRA, a product of cellular vitamin A metabolism. After this injection, B cells increased more than four fold in number in ten days.


Having a balanced diet is definitely important for the immune system, and being deficient in Vitamin A would be problematic. Something so simple.


Even though it sounds like a good idea to take lots of Vitamin A given the immune system benefit, it doesn't work that way: if you're deficient, you need more; if you're taking too much, you need less because it can damage your liver and by extension kidneys because of too much calcium there. (It's also bad to consume high quantities during pregnancy - it can lead to failure to thrive in newborns.)


So get a test to see if you're deficient in Vitamin A first - and if so, then it's pretty easy to find foods full of  Vitamin A.


One thing that comes to mind after reading this is that recently I've read a paper, 'The Important And Diverse Roles of Antibodies in Host Response to Borrelia' by Laroca and Benach. In it, it mentions that B1 cell or x-linked immunodeficiency leads to more severe spirochetemia with B. hermsii... B1 b cells are needed for IgM antibody response.

Source publication:

Maruya, M., Suzuki, et al. Vitamin A-dependent transcriptional activation of the nuclear factor of activated T cells c1 (NFATc1) is critical for the development and survival of B1 cells. Proceedings of the National Academy of Sciences USA 108, 722–727 (2011). http://www.pnas.org/content/108/2/722.short

4) Two new studies seek to validate the results of a retracted 2004 paper on parasite-to-host gene transfer, but skepticism lingers

Link: http://www.the-scientist.com/news/display/58093/

Do not let this bug kiss you - it can
carry Chagas disease parasites...
Summary: The microparasite that causes Chagas disease really can integrate bits of its genetic material into its host's genome, where it can then be inherited by the host's offspring, according to two studies published in PLoS ONE and PLoS Neglected Tropical Diseases (PLoS NTD).

Comments:


So this is kind of insane. Interesting and insane. The claim is being made for what might be the first documented instance of lateral gene transfer from the parasite that causes Chagas disease to not only its host but also a following vertical transfer to the host's offspring.


WTF. This is almost as far out as Lynn Margulis' claims about Borrelia burgdorferi.


These two recent studies are supposed to confirm the research found in a 2004 paper published in Cell which was later retracted. That paper showed - or supposedly showed - that University of Brasilia researchers found that T. cruzi could transfer genetic material to its rabbit, chicken, and human hosts. This sort of gene transfer - specifically of mitochondrial kinetoplast DNA (kDNA) - may contribute to the disease by disrupting host gene function and causing an autoimmune response.


Those looking at the newer research are eyeing it cautiously because of the earlier publication's retraction, which was done because Cell's staff made the determination that certain important information was missing from the paper. Speculation was that it was because identification and analysis of the specific sites of DNA integration were omitted.


I think this study and the two subsequent studies recently done will need to be repeated by another party not related to them, since this would be pretty big news if it's true. Also, someone needs to make sure their PCR methods don't create weird chimeras in passing.

Source publications:

M.M. Hecht et al., "Inheritance of DNA transferred from American trypanosomes to human hosts," PLoS ONE, 5: e918, 2010. 

A.R.L. Teixeira et al., "Trypanosoma cruzi in the chicken model: Chagas-like heart disease in the absence of parasitism," PLoS Negl Trop Dism, 5: e1000, 2011.
 

---

And here's a bonus link set for my readers who are interested in aberrant and unusual contrails in the sky:
http://www.nature.com/nclimate/journal/v1/n1/full/nclimate1078.html

Here is the study to which the above article refers:

It was posted at the source on March 29, so I reassure you that it was not an April Fool news item.
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Thursday, March 24, 2011

0 Video: Immunology Lectures from The Einstein College of Medicine

Given the volume of questions I'm getting on the immune system lately, I thought I'd post this 14 part mini series on the immune system.

Others have reported that watching this makes learning about immunology less scary and overwhelming - I haven't seen the entire series yet, but how about watching an episode or two and letting me know what you think of them?

There are slides online which accompany the lectures - these are the first session's slides:

Below is episode 1 - from there you should be able to advance to the next video in the series.

Learning more about immunology, microbiology, genetics, and molecular biology will help in understanding the research that is out there as well as patents.

All this knowledge is within reach - but requires putting the time in, and patience with one's own brain fog. I know, because I've been there... and it's a slow learning process - but learning does happen.
Read More

Friday, March 11, 2011

0 The Friday Four

In today's Friday Four, we'll look at how tuberculosis bacteria survive inside macrophages, chemotherapy drugs that kill malaria, a potential source for a new anti-inflammatory treatment, and a vascular disorder that is misdiagnosed as multiple sclerosis.

Full text of the articles and links to the sites or publications on which they are based are available at the cited locations.

1) How Tuberculosis Bacteria Manage to Survive Inside Body’s Macrophage Cells

Tuberculosis kills two million people each year. Researchers at Linköping University in Sweden are now presenting new findings that show how the bacterium that causes the disease manages to survive inside the body's macrophage cells in order eventually to blow them up and spread their infection.

ScienceDaily. Retrieved March 11, 2011,
from http://www.sciencedaily.com­ /releases/2011/03/110309073940.htm

Original source publication: http://www.expertsvar.se/english/

2) Malaria’s Weakest Link: Class of Chemotherapy Drugs Also Kills the Parasite That Causes Malaria

A group of researchers from EPFL's Global Health Institute (GHI) and Inserm (Institut National de la Santé et de la Recherche Médicale, the French government agency for biomedical research) has discovered that a class of chemotherapy drugs originally designed to inhibit key signaling pathways in cancer cells also kills the parasite that causes malaria. The discovery could quickly open up a whole new strategy for combating this deadly disease.

Science Daily. Retrieved March 10, 2011,
from http://www.sciencedaily.com­ /releases/2011/03/110308084743.htm

Original source publication:
Audrey Sicard, Jean-Philippe Semblat, Caroline Doerig, Romain Hamelin, Marc Moniatte, Dominique Dorin-Semblat, Julie A. Spicer, Anubhav Srivastava, Silke Retzlaff, Volker Heussler, Andrew P. Waters, Christian Doerig. Activation of a PAK-MEK signalling pathway in malaria parasite-infected erythrocytes. Cellular Microbiology, 2011; DOI: 10.1111/j.1462-5822.2011.01582.x

3) Engineered Protein Has Potential for New Anti-Inflammatory Treatment

Researchers from across multiple disciplines at NYU Langone Medical Center created a new protein molecule derived from the growth factor progranulin may provide the basis for new therapies in inflammatory diseases, such as rheumatoid arthritis, according to a study published in the March 10, 2011 issue of Science.

ScienceDaily. Retrieved March 10, 2011,
from http://www.sciencedaily.com­ /releases/2011/03/110310141431.htm

Original source publication:
Wei Tang, Yi Lu, Qing-Yun Tian, Yan Zhang, Feng-Jin Guo, Guang-Yi Liu, Nabeel Muzaffar Syed, Yongjie Lai, Edward Alan Lin, Li Kong, Jeffrey Su, Fangfang Yin, Ai-Hao Ding, Alexandra Zanin-Zhorov, Michael L. Dustin, Jian Tao, Joseph Craft, Zhinan Yin, Jian Q. Feng, Steven B. Abramson, Xiu-Ping Yu and Chuan-Ju Liu. The Growth Factor Progranulin Binds to TNF Receptors and Is Therapeutic Against Inflammatory Arthritis in Mice. Science, 10 March 2011 DOI: 10.1126/science.1199214

4) Vascular Brain Disorder Often Misdiagnosed as Multiple Sclerosis, Study Finds

A devastating vascular disorder of the brain called CADASIL, which strikes young adults and leads to early dementia, often is misdiagnosed as multiple sclerosis, Loyola University Health System researchers report.

ScienceDaily. Retrieved March 10, 2011,
from http://www.sciencedaily.com­ /releases/2011/03/110310141431.htm

Original source publication:
R. Vázquez do Campo, S. Morales-Vidal, C. Randolph, L. Chadwick, J. Biller. CADASIL: a case series of 11 patients. Revista de Neurologia, 2011; 52: 202-210


:: PLACEHOLDER:: Comments on these articles coming soon... in the meantime, take a look - interesting stuff.
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Monday, February 7, 2011

0 Koch's Postulates

Just an FYI... for tales of xenodiagnosis...

http://en.wikipedia.org/wiki/Koch's_postulates


Koch's postulates

From Wikipedia, the free encyclopedia
Koch's postulates are four criteria designed to establish a causal relationship between a causative microbe and a disease. The postulates were formulated by Robert Koch and Friedrich Loeffler in 1884 and refined and published by Koch in 1890. Koch applied the postulates to establish the etiology of anthrax and tuberculosis, but they have been generalized to other diseases.


The postulates

  1. The microorganism must be found in abundance in all organisms suffering from the disease, but should not be found in healthy organisms.
  2. The microorganism must be isolated from a diseased organism and grown in pure culture.
  3. The cultured microorganism should cause disease when introduced into a healthy organism.
  4. The microorganism must be reisolated from the inoculated, diseased experimental host and identified as being identical to the original specific causative agent.
However, Koch abandoned the universalist requirement of the first postulate altogether when he discovered asymptomatic carriers of cholera[1] and, later, of typhoid feverAsymptomatic or subclinical infection carriers are now known to be a common feature of many infectious diseases, especially viruses such as polioherpes simplexHIV and hepatitis C. As a specific example, all doctors and virologists agree that poliovirus causes paralysis in just a few infected subjects, and the success of the polio vaccine in preventing disease supports the conviction that the poliovirus is the causative agent.
The third postulate specifies "should", not "must", because as Koch himself proved in regard to both tuberculosis and cholera,[2] not all organisms exposed to an infectious agent will acquire the infection. Noninfection may be due to such factors as general health and proper immune functioning; acquired immunity from previous exposure or vaccination; or genetic immunity, as with the resistance to malaria conferred by possessing at least one sickle cell allele.
The second postulate may also be suspended for certain microorganisms or entities that cannot (at the present time) be grown in pure culture, such as prions responsible for Creutzfeldt–Jakob disease.[3] In summary, a body of evidence that satisfies Koch's postulates is sufficient but not necessary to establish causation.


History

Koch's postulates were developed in the 19th century as general guidelines to identify pathogens that could be isolated with the techniques of the day.[4] Even in Koch's time, it was recognized that some infectious agents were clearly responsible for disease even though they did not fulfill all of the postulates.[2][5] Attempts to rigidly apply Koch's postulates to the diagnosis of viral diseases in the late 19th century, at a time when viruses could not be seen or isolated in culture, may have impeded the early development of the field of virology.[6][7]Currently, a number of infectious agents are accepted as the cause of disease despite their not fulfilling all of Koch's postulates.[8] Therefore, while Koch's postulates retain historical importance and continue to inform the approach to microbiologic diagnosis, fulfillment of all four postulates is not required to demonstrate causality.
Koch's postulates have also influenced scientists who examine microbial pathogenesis from a molecular point of view. In the 1980s, a molecular version of Koch's postulates was developed to guide the identification of microbial genes encoding virulence factors.[9]


See also


References

  1. ^ Koch Robert (1893). "Über den augenblicklichen Stand der bakteriologischen Choleradiagnose" (in German). Zeitschrift für Hygiene und Infectionskrankheiten 14: 319–333.doi:10.1007/BF02284324.
  2. a b Koch Robert (1884). "2 Die Aetiologie der Tuberkulose". Mitt Kaiser Gesundh. pp. 1–88.
  3. ^ Inglis TJ (November 2007). "Principia aetiologica: taking causality beyond Koch's postulates"J. Med. Microbiol. 56 (Pt 11): 1419–22. doi:10.1099/jmm.0.47179-0PMID 17965339.
  4. ^ Walker L, Levine H, Jucker M (2006). "Koch's postulates and infectious proteins.". Acta Neuropathol (Berl) 112 (1): 1–4. doi:10.1007/s00401-006-0072-xPMID 16703338.
  5. ^ Koch R (1893). "Ueber den augenblicklichen Stand der bakteriologischen Choleradiagnose". J. Hyg. Inf. 14: 319–33. doi:10.1007/BF02284324.
  6. ^ Brock TD (1999). Robert Koch: a life in medicine and bacteriology. Washington DC: American Society of Microbiology Press. ISBN 1555811434.
  7. ^ Evans AS (May 1976). "Causation and disease: the Henle-Koch postulates revisited"Yale J Biol Med 49 (2): 175–95. PMID 782050.
  8. ^ Jacomo V, Kelly P, Raoult D (2002). "Natural history of Bartonella infections (an exception to Koch's postulate)"Clin Diagn Lab Immunol 9 (1): 8–18. doi:10.1128/CDLI.9.1.8-18.2002.PMID 11777823.
  9. ^ Falkow S (1988). "Molecular Koch's postulates applied to microbial pathogenicity". Rev. Infect. Dis. 10 (Suppl 2): S274–6. PMID 3055197.


Further reading
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