1. Many patients and health care workers are profoundly ignorant about how to interpret a Western Blot. If a person has one “fingerprint band,” they have Lyme disease. These specific bands are the 18, 23, 25, 31, 34, 39, 83 or 93. The lab can be a junk lab that invests nothing to optimize their kit, but if one of these bands is positive even onceLyme is present. IGeneX has the best Western Blot in the world. No other lab has invested so much for so long to create the best test. If your clinician wants to first use an ELISA, simply run. To put it bluntly, the ELISA test as a screening tool is useless, missing even the most obvious PCR positive patients.

2. Ten years of Lyme treatment is not acceptable. The practitioner who follows a year-after-year IV treatment approach is not “up-to-date.” These so called “cure” treatments often merely lower body loads or decrease symptoms without fully eradicating all the different types of infectious agents.

3. Some treatments are simply useless. For example, the use of hyperbaric oxygen (HBOT), for tick infection treatment, fails. The use of HBOT in mice is not applicable. To prove this, I decided to perform a self-funded study examining HBOT benefits on Lyme, Babesia, Ehrlichia and Bartonella. After 120 treatments at 2.4 atmospheres for 90 minutes each, all participants still had clear positive findings for all four infections. There is no validity to the claim that HBOT “kills” Lyme disease. I have talked to the late Dr. Fife in detail and carefully evaluated the HBOT research of Dr. Robert Lombard. I love this treatment for many medical problems, but it is not a tick infection cure. The last time I published this information, an HBOT owner retaliated with verbal attacks on a public forum. She was obviously biased. She offered no independent research to support her marketing.

4. Ignoring new data leads to treatment failures. For example, I have published many new books on advanced tick-borne infections, all showing new critical information. For some “Lyme-literate” physicians, it took educated patients throwing a copy at them before they read our new information, and by then, years had already passed…

5. Some health care workers believe in a Lyme literate Pope or President, but no such expert exists. Sure, some offer useful information from past investigations. However, no one has mastered 2010 tick-borne medicine and all the newest co-infection information.

6. I have been asked by a number of physicians to share my new findings. Most ask because they are ill themselves. I have asked them to stop treating themselves, and to do an hour consultation with very extensive labs. Most have refused. Tragically, what they could have learned by fixing themselves would have translated into real help for their patients.

7. Current treatment recommendations are all too often profoundly flawed. IV treatments are often used without a herbal or synthetic antibiotic cyst buster. The most common treatment for Babesia is 750 mg/teaspoon of Mepron taken twice a day. The most commonly used Babesia herbal cures are artemisinin or artesunate (for example, Zhang Artemisia from Heprapro.com). The latter involves a standard dose of one capsule three times a day — yet all four of the approaches listed above fail even after long trials.

8. The flaw in all Bartonella treatment is the lack of one-year blinded follow-up studies. I have found that Levaquin, Rifampin, Zithromax, doxycycline, Mycobutin, Cumunda, Banderol and Rife machines, at various frequencies and power, may lower body load and lead to initial feelings of improvement. None of these treatments leads to Bartonella cure.

9. The current testing for Babesia, Bartonella and Ehrlichia is markedly flawed. Some DNA or PCR tests processed by an East Coast lab can miss a positive infection ten times. If you need to do ten urine or blood samples to show a positive, this is not functional. Some labs are only fair at tissue PCR testing, when the tissue has clear Lyme, Babesia and Bartonella that can be visualized in the tissue microscopically. This is a diagnostic disaster. Amazingly, some use large national labs to do manual examination of red blood cells to look for Babesia and Bartonella. I have never seen a large national lab detect Babesia or Bartonella in over 1,000 manual smears. In patients with certain Babesia and Bartonella, no large national lab captured these infections even once. I repeatedly offered to assist them in improving their technology by linking them with hematology experts in tick infections. They did not care that their manual smears were worthless, and I was repeatedly ignored.

10. The knowledge base about both Bartonella testing and treatment borders on catastrophic. Bartonella is one of the most common infections in the world. Calling it a “co-infection” is nonsense. If anything, Lyme is the “co-infection.” Bartonella is found in vast numbers of common vectors including dust mites, fleas, flea feces, pet saliva, ticks, etc. Amazingly, it can turn off or lower antibodies to Lyme disease, Babesia, Ehrlichia, Anaplasma and even itself. Bartonella floats in blood and also enters all blood vessel walls without causing a fatal fever, and indeed, actually lowers fevers. It is the ultimate stealth infection. It turns off antibodies, fevers and immune function defense chemicals as it damages organs in anywhere from 20-60 different ways.

11. The use of fixed “protocols” or “procedures” in the treatment of tick infections is sadistic medicine. Why? It treats each ill human person as a machine that is built the same and has the exact same problems, which in turn objectifies a patient and flirts with the sociopathic. We see this mind set in serious criminals, molding people into “things” in an effort to fit their rigid perceptions of the world. To force a unique human body, with a unique infection cluster, and a unique biochemical response, into a blanket protocol is the equivalent of the objectification of the patient. It is junk “mill medicine,” plain and simple.

12. Since Bartonella turns off the production of antibodies to infections like Babesia microti or Babesia duncani and Lyme disease, I suggest that this infection must be considered in all initial consults. I would suggest learning the 40 skin patterns made by Bartonella or Bartonella/Lyme mixed infections that are made by increased tissue and blood vessels. It is also useful to know the indirect labs associated with Bartonella alone, or Bartonella with Babesia, such as IL-6, IL-1B, TNF-a, ECP, and VEGF. We discuss clinical patterns from lab results of these infections in a Babesia 2009 Update book.

13. Some patients have very few Babesia protozoa parasites, but they cause serious trouble in the body. Their small numbers cause them to be missed in a visual a FISH exam or a PCR test.

14. If your lab does not test for new species such as Babesia duncani or the many other documented species of Babesia or Bartonella that infect humans, than you cannot rule out these infections with a “negative result.” One way to decrease treatment failures is to use a new medical trick to detect stealth Babesia, whose presence can cause ongoing fatigue, headaches, weight gain and Lyme treatment failure, to name a few.

The “trick” is simple: A patient takes at least two Babesia killing medications such as Mepron, artesunate or Malarone (given for the proguanil). These medications are used for ten days at a dose you and your physician feel is worth the risk, and usually at least one will kill a few Babesia parasites.

Approximately ten to fourteen days later a second ECP level is taken to compare to the baseline. If the ECP pops up significantly, it is usually a sign of Babesia die off. Eosinophils are releasing ECP, possibly injecting Babesia debris. ECP is produced to kill parasites.

An alternative or added option is to wait five weeks and have the patient tested for antibodies to microti or duncani. One youth patient with profound illness was finally diagnosed in this manner, and after three weeks of triple Babesia treatment had significant clinical improvement for the first time in six years. Stealthy low volume Babesia is a common problem in tick and flea infection treatment. Talented health care workers commonly miss these red blood cell parasites, but this trick usually causes them to show up and can save someone from years of failed treatment.

15. The Bartonella testing of most national labs is useless. It is stunning to read so called “sages” reporting a patient does not have Bartonella because a large lab has found negative antibodies. First, they do not understand that Bartonella turns off its own antibodies, so these large labs only check for one (or two) species that infect humans, and their cut-off titers are unrealistically high. Thankfully, IGeneX Bartonella FISH testing will be available approximately July/2009 to everyone but citizens of New York State .

16. Infections and inflammation decrease insight. Tick-borne infections routinely destroy insight and lead to a personality change and/or rigid resistance to testing. This is largely due to an impaired frontal lobe (the part of the brain involved in self-awareness). Examples of decreased insight are shown in the following situations:

o Some feel they are cured when they are only improved.

o Others intentionally go to practitioners using inferior labs.

o Some refuse to be tested with eccentric resistance.

o Positive results are amazingly dismissed with a wave of the hand.

17. Some patients feel their trouble is mold alone, without any tick-borne infections. They cannot believe both are important, and both can be present. Indeed, either could be “the last straw.” Some patients get ill after a flood, large leak or some other water intrusion problem. They feel they are ill only because of mold mycotoxins that form 36-48 hours after water intrusion into drywall, insulation, carpeting and other dust or cellulose-filled materials. The EPA reports 30% of USA structures have indoor mold. Some of these indoor molds have war-grade chemicals on their surface. When the tomb room of the last King of Poland, Casimir IV was opened in Paris in 1973, ten of the twelve scientists present died. One survivor had expertise in mold and subsequently found three toxic mold species.

18. Given the average of 40,000 – 120,000 inhalations per week while residing in a moldy location, it is no wonder some are not easily cured of tick and flea infections. This significant factor was the catalyst for my decision to write two mold remediation books.

We have also known since the 1880′s that dust and high humidity leads to mold and bacteria growth indoors. Their presence makes Lyme disease much more difficult to cure.

19. Lyme has at least one surface biotoxin, the patented BbTox1. Patients with 15/16–6/5–51 HLA patterns probably are unable to remove Lyme biotoxins (R. Shoemaker) and require a binder, like cholestyramine, which has been used to bind biotoxins since the 1970′s.

20. Many patients who have had tick-borne infections have very high inflammation levels. Therefore, all starting doses of medications or herbs should be very low and gradually raised to higher levels with liver-protecting substances. Starting at full dosing in a “medically sensitive” patient is chemical battery. Massive die-offs can be confused with allergic reactions and can cause panic attacks, shortness of breath, chest pain and severe migraines. This sloppy, one-size-fits all approach, is common in large practices in which a few major “protocols” are routine.

21. Medical “Band-Aids” are often required to save a job, a marriage and to care for children. They are often a highly useful component of care. Pain, fatigue, severe insomnia, depression and anxiety often are increased with the die-off or presence of the infections carried in deer ticks. Band-Aid treatments are often useful and helpful. I treat people who run companies, schools, very large families and professional teams. They want to sleep 13 hours per day. They need stimulants for a period of time. The use of natural or synthetic stimulant options is discussed in The Diagnosis and Treatment of Babesia. Patients do not benefit from sleep in excess of 8 hours. It may just serve to get them fired!

22. If you have healthcare workers who do not feel comfortable being aggressive with treatment and diagnosis of all the top tick and flea infections, you are at the wrong place. If your healthcare provider has not spent 1,000 hours learning this complex emerging area of medicine requiring a great deal of study, find someone who is serious about it, and not someone “doing you a favor” by simply running a few tests

23. Some relapse due to treatment fatigue. Meaning, you have been treated for many years and are fed up. You have done IV antibiotics or IV nutrients, you have taken 40 pills per day, you have tried a wide range of specialized treatments, and now you tired of it all. You can now function at 80% of your baseline. You are at the end of your treatment rope. This is what happens when someone does not treat you fully and effectively at the beginning of your treatment. You can get treatment fatigue. Consider a short treatment break, and discuss this frankly with your health care provider. Do not confuse cure with improvement.

24. The treatment approach that leads to cure is not the same dose that leads to stunning organisms. A cure is not a mere reduction in bacteria load. For example, using Bicillin once a week with no cyst buster will never cure you of Lyme disease because it does not remove cysts. So years after receiving this treatment, your cancer-fighting cells, marked by some as the CD57 level, may be under 90. This is one good test that is possibly specific for Lyme disease or at least tick-borne infections. (The C3a and C4a tests are definitely not specific for Lyme).

25. Cynical relatives, friends or other health care workers can defame Lyme experts, and convince patients to drop healthcare workers who are helping. They usually use “the money” argument or “the speed of your recovery” argument to cut you off from someone sincerely trying to help you. If you have been battling for years with multiple infections, you will not be cured in four months.

26. In recent seasons the existence of a Lyme biofilm has been proposed. Organizations with millions in grants and research money have never addressed this issue. We know that many spirochetes have biofilms. Indeed, many spirochetes in your mouth are known to cause biofilms, and they are believed to limit antibiotic effectiveness.

I am currently working on a textbook that addresses the many options for attacking biofilms. No article or book exists that explores the twenty plus ways I would propose to beat a Lyme biofilm. It is believed by some professionals that highly specific enzymes (or one mineral) can undermine a Lyme biofilm. Yet enzymes are like keys, and no single enzyme is a proven “key” to undermining a Lyme biofilm.

27. Self-treatment is easy to pursue. Many experts are expensive, and their level of expertise may be uncertain. The Internet seems to offer many effective options. Some health care providers seem too narrow. Others are open to virtually everything. So you get in a medical boat and push yourself out to sea. You read like crazy. You try a, b and c. You read testimonies of hundreds of patients. You try a wide range of non-prescription options. Some days, weeks or months you feel better. Other weeks, you are not so good. You are upset. You ask yourself, “Why do I have to do all the work and learning?” This is not a good place. People exist who have already explored virtually all of the things you are going to explore in the next ten years. You need a mentor. Many

28. In many of my books and many Internet sites you can read about preventing flea and tick bites. You do not need to be re-infected with Bartonella, Lyme, Babesia or any other infection. So learn the basic steps to protection in about thirty minutes of reading.

29. Tick and flea-borne infections cause isolation. They ruin relationships due to fogginess, poor insight, depression, various addictions, rage, anxiety, extreme hostility, and refusing to get treatment, and they can sometimes provoke violence. Bartonella is likely the worst cause of these problems, but Lyme and Babesia and their die offs can also increase these problems. Isolation leads to decreased treatment options. It can ultimately lead to divorce and the loss of family relationships and friendships. This, in turn, leads to decreased resources and support while ill. Isolated humans, as Mother Teresa often said, are the poorest beings on earth.

About the Author:

Dr. Schaller is the author of 27 peer-reviewed journal articles and is one of the most prolific LL MD’s in the world. He is the author of 25 books and has published many recent books on tick-borne infections. He is a full-time self-funded researcher with a part-time private practice in the United States . For more information about Dr. Schaller, or to access free articles on topics including the one mentioned in this article, please visit www.personalconsult.com.

If you are reading this, please also read Dr Schaller’s first article “Reasons for Lyme Treatment Failures,” or you may not experience the improvement you desire. It can be found on many sites including this free link:

 http://www.personalconsult.com/articles/jamesschallermd.html

Our average patient has been to 10-50 smart, sincere and concerned physicians, but they have not returned to their baseline level of functioning.  We also inherit many treatment failures, which allow us to see by indirect and direct diverse types of testing what worked or failed before they came to us.

 1.     The notion of “Lyme Disease” is a 1990’s notion.  If a clinician uses advanced, direct and highly important indirect testing to look for the increasing number of infections carried by deer ticks, it is clear that organisms besides Lyme are present routinely in deer ticks.  The idea that deer ticks only carry one infection is a disaster.  Deer ticks carry multiple bacteria, parasites, and viruses. For example, Bartonella is far more common than Lyme disease.

 2.     There is no correct starting dose for virtually any medication.  I was asked years ago by two top editors to write an article on “sensitive and careful dosing in clinical practice.”  They noticed within my various papers we were pointing out the need for tailored dosing instead of chemical battery. For example, all medications should   begin with a first dose that is below a full tablet or capsule, because sometimes it is 20x more effective than normal. Always start with a fraction of the lowest dose pill and this can be increased over a mere 24 hours.

 Further, one never should increase or start two treatments at once. This is chaos, and causes confusion over the reason for a side effect or a good benefit. Also, if a patient develops uncomfortable feelings, either from the die off of an organism or from medication side effects, they become demoralized, and the cause is unclear with many treatments. Simply, no two people have even been treated by me the same from start to finish, and this is why a cure book on all major tick-borne infections cannot be published.

 3.     Is the new explosion of so-called “Lyme Literate” or LL-MD experts really trained to do more than basic screening?  Generally when I am trying to pursue an expertise in any aspect of tick and flea borne infections, I spend years engaged in full-time reading on the topic and try to talk with the leaders around the world who know the most on the topic.  Unfortunately, as of 2010, “Lyme Literate” really means that you have gone to a couple conferences, learn the basics from the last five to ten years, and some also shadow one or two physicians for days to a week while they see patients—both are good experiences.  Both are a good starting place, but does not make one “tick-infection literate” in any serious manner. Finding someone that knows how to use a wide range of labs which will check for a direct and indirect presence of the infections from tick, who has read thousands of articles, and consults with physicians and scientists regularly for success and failures along with finding new solutions is extremely rare in the world. Yet we do need every screening healer we can get!

 4.     Routine speed IV treatment of most new patients is an error. Some individuals treating Lyme disease do a fairly rapid assessment and quickly put all of their patients on an I.V. like they are running a mill. It is almost as if they say “It is nice to meet you, let’s get you started on your I.V. quickly.”  There are many problems with this approach and far too many to discuss here, but the first problem is that the volume of spirochetes that can die with an invasive I.V. could be too many, due to the release of Lyme debris and/or Lyme biotoxins, such as Botox I can increase inflammation.  It also ignores the fact that Bartonella, with increasing numbers of human species found yearly suppresses immunity.  IV treatment will never be as effective as it could be when used alone without the use of new 2010 selected Bartonella treatments that are clearly proven to work when used alone or in combination.  Meaning, IV and all other types of Lyme treatment work profoundly better if one or more new Bartonella treatments are used. We find new such treatments every few seasons.  As previously stated in my first Townsend article on the Reasons for Lyme Treatment Failure, the most common treatments for Bartonella come from a mere 25 basic Bartonella treatment articles or infection handbooks. They lead to relapse even when they appear to work for a variable periods of time.  

 I.V. gall bladder emergencies are too frequent. One reason some insurance companies do not want to do prolonged I.V. treatment is because of gallbladder emergencies.  I am fairly stunned that the only thing given to protect the gallbladder and liver with the use of I.V. medications is Actigall, and some do not prescribe anything when giving I.V. treatment. Many have little knowledge of advanced ways to protect the liver, and yet use liver stressing treatments.  For example, any dose of azithromycin, Mepron, Malarone, Diflucan or IV or injected muscle antibiotics can stress the liver, and low doses that do not stress the liver may lead to residual infections.

 5.     Following the guidelines of practitioners with famous names, university titles or organization leadership positions is an error in judgment.  If you are famous or have a title or “chair” or are high in an organization, the more brutally busy the healer can be, sometimes working 12hours virtually every day.  So this healer can never read high volumes of new material published this season. Therefore, no organization, government agency, web site or person has the definitive, updated information on tick-infection medicine in the USA or the world. No single organization or group of organizations can provide people with authoritative instruction in how to treat an individual profoundly unique patient. 

 6.     All guidelines for medicine are flawed and outdated within one month of publication.   The explosion of new published material and non-published discoveries by hundreds of international healers make guidelines mere suggestions.

 Hundreds of thousands of articles are published every few months.   In our practice, we have only published five percent of what we have found.  Similarly, many fellow researchers I know also have limited time to publish their discoveries. 

 Further, the great philosopher of science, Kuhn, has shown that there are so many variables that impact all scientists that the notion that any group of physicians can give unbiased pure scientific recommendations is impossible. Obvious guideline errors are present in all current tick and flea-borne infection guidelines. 

 Different guidelines have outrageously specific treatment plans which are not even appropriate for cars, which in this current age have different types of oil and different amounts of recommended oil.  The human body when it is infected with a cluster of tick infections is a billion times more complex than any automobile.  Some guidelines use highly dated doses from studies that are fifteen years old.  Other guidelines do not even mention infections such as persistent human atypical Bartonella, which has vastly more vectors than Lyme disease, or Babesia and based on years of full-time reading, suppresses the immune system in highly specific ways that some guideline agencies and groups seem to totally ignore. 

 7.  A complete lack of meaningful knowledge of the immense magnitude and danger of Bartonella. This stealth bacteria has over ten different ways to infect you, and not merely a few types of ticks. It kills and harms every organ and decreases fevers and immune defenses, and does not fully respond to the top ten “published” traditional or alternative treatments. In one case report it appears that Bartonella turned off all the antibodies to five tick-borne infections, including its own antibody titer levels. In this medical family they self treated with a new Bartonella agent and this resulted in an explosion of western blot Lyme disease bands and all major deer tick infection antibody titers suddenly rose to profound levels because the immune system was no longer suppressed against them by Bartonella. Therefore, merely by the use of this newly uncovered Bartonella treatment, all of these patients negative labs at a large national lab, turned positive after being repeatedly negative.

 8.   The use of fetish, “favorite” medications, herbs or new “discovered” causes of prolonged illness. Of course, any healer studying traditional or progressive medications is serving all.  My appeal in this criticism is not to reject the fine work done by at least two hundred people internationally on traditional antibiotics, protozoa medications, anti-virals, herbs used for a wide range of infections, essential oils, and at least fifty progressive alternative treatments. 

However, like the experience of falling in love, when one love becomes all you think about, this is not optimal medicine when you fall in love with a few treatments.  

For example, minocycline, tetracycline, clarithromycin, rifampin, azithromycin, HBOT, Rife, special saunas, ozone, IV nutrients to “boost immunity,” chelation, confused detox formulas, Artemisia derivatives, essential oil combinations, IV medications, various weak alcohol based herbal programs, various energy machines, and a hundred other options found in chat rooms and Lyme disease “information” sites, are not meant to be the sole or primary style of all patient treatment. Carpenters use select tools at select times for select needs. Nevertheless, with my thanks for the above passion of those that promote these and hundreds of others of treatments, they have to pass blind rigorous simple direct and indirect testing to show they work, and very few know how to do such testing. I feel it is an error to only use an antibiotic which has limited mechanisms for killing bacteria.

I have published the most current textbook on Artemisia derivatives, including Artemisinin (qinghaosu) and many other toxic forms that should be avoided. And yet, despite being the most recent practical clinical book on the topic, based on a year of full-time study with Chinese consultants and WHO consultants, it has been ignored by some who have little herbal training or reading. Why?

The final approach that is worthy of mention is the “I only do natural treatments” approach.  Unfortunately when I interview some of these individuals many of whom are quite smart and well read, they are aware of allopathic medication side effects, but not the toxic components of the herbs they are using.  Individuals using essential oils, including those that prescribe them, usually have never read a book on the various toxicities and safety concerns of essential oils.  Some of them have excellent effects and others can provide help, but also have side effect risks and others should never be used internally at all in anything more than a minimal dose. 

 9.  The “new” yearly or bi-yearly cause of Lyme disease treatment failures is possibly wrong. I was appreciative that a few brilliant researchers found that the Bb Lyme spirochete had a biofilm in recent years–useful. But I was actually stunned this was felt to be new, since spirochetes routinely have biofilms, and dental spirochetes have immense research going back many years on biofilm promoting dental disease. A review of the major world literature shows about 25 treatment options to handle biofilms. No one has offered more than a small number of basic options to beat this problem. Perhaps it increases treatment relapses and failures, but that is not what I usually see.

 10.   Rejection of top thought leaders because of cost.  When I think back over the hundreds of physician’s, PhD’s, herbal experts, nurses, alternative healing practitioners and even poorly educated addicts who I treated decades ago, it is clear to me, that while none of them was perfect, all have helped me  immeasurably.  Currently at least 50 physicians are defamed for their fees when treating tick borne infections which can end their entire career. 

The same applies to bonding with a healer.  I often seek the wisdom of people that may be annoying, irritable, tired, simplistic, insulting, or confusing. But the fact of the matter is virtually every healer I have known, regardless of specialty, philosophy and ideology, has taught me a lesson that helps patients.  I have literally seen patients decide to go with physicians who have virtually no knowledge of tick-borne disease, because they were “caring and friendly.”

 Further some want a “local” physician, as if geography is the same as expertise and knowledge. 

 The appeal of many smart patients is to tell you this: it takes many appointments to get better, and there is no better use of any income than on your health and the health of your loved ones, instead of wasting it on healer after healer who is sincere, but does not have a complete passion to master these illnesses, and a good track record of improving lives, including very ill patients. A mere few sessions usually will not cure all your tick-borne infections.

 11.      The use of herbal treatments without solid follow-up by direct and indirect means.  Currently, one finds herbs that are mixed in grain alcohol with 1/50^th the potency of a capsule, that are supposedly cures to tick-borne disease.  In our examination of these inherited treatment failures, we have not found these low potency alcohol based herbs cure.  Others offer high priced herbs and “know” they are successful, and often recommend one size for all adults living on the earth.  Often their understanding of advanced herbal processing, standardization and the multiple chemicals in any herb is limited.  In any event, in our outcome studies we have found that these herbs at best may limit body infection volume slightly.  It is profoundly important to use effective herbs with a tailored specialized dosage for each individual or you are merely experiencing “mill medicine.”  If you are self treating with herbs or by a healer, if they promote “one size fits all” you are accepting health care inferior to dog medicine. 

 12.   Advice from Web sites and chat rooms usually does not apply to you. No two people are ever to be treated the same. To seek advice on the Internet is a concern of most physicians and healers.  Sometimes you can find mature balanced support from those who are healthy, but not new advanced and solid credible information for your medical care. Many leaders in tick-infection medicine report they are quoted incorrectly, and that the information is often wrong, sometimes dangerous and wastes time and money.  

BIOGRAPHY

James Schaller, MD has been elected by his physician peers a “Best Doctor in America .”

He has published more books on tick infections than probably any physician in history. Perhaps this is why he treats patients from all over the world.  

He is the author of 26 books and 27 papers published in highly respected peer-reviewed medical journals on topics covering ten areas of medicine.

He is the author of:

Babesia Update 2009: A Cause of Excess Weight, Migraines and Fatigue? A Common Reason for Failed Lyme Disease Treatment

The Health Care Professional’s Guide to the Treatment and Diagnosis of Human Babesiosis: An Extensive Review of New Human Babesia Species and Advanced Treatments

Artemisinin, Artesunate, Artemisinic Acid and Other Derivatives of Artemisia Used for Malaria, Babesia and Cancer

The Diagnosis, Treatment and Prevention of Bartonella: Atypical Bartonella Treatment Failures and 40 Hypothetical Physical Exam Findings; A Laboratory Guide to Human Babesia Hematology Forms.

Mold Illness and Mold Remediation Made Simple: Removing Mold Toxins from Bodies and Sick Buildings

When Traditional Medicine Fails, Your Guide to Mold Toxins

A.D.D., Irritability and Oppositional Disorders: Cutting Edge Solutions Sincere Therapists and Doctors Miss

Suboxone: Take Back Your Life From Pain Medications

Copyright James Schaller, MD 2010. This short article may be posted on any site and forwarded as desired, but only on sites that do not defame or criticize the contents.

Dr. Jones Update- Monday, April 5, 2010

Dr. Charles R. Jones is facing an immediate and overwhelming financial burden due to fines and costly sanctions placed on him by the Connecticut Medical Examining Board. What we are sadly witnessing is the persecution of a Lyme-treating doctor for his successful approach in fighting this complex and controversial disease that very few in the medical field will adequately address.

FROM THE OFFICE OF DR. JONES AND HIS DEDICATED STAFF-  We extend a special thank you to all and want you to know we continue to do all we can to be here for you and the children.  Dr. Jones has been fighting very hard to keep going.  Now he needs your support, each and everyone of you!   If you could take one minute every day to help him we would be grateful!

UPDATE FROM GOVERNOR’S OFFICE-  The Governor’s office stated today that Dr. Charles Ray Jones situation isn’t something the Governor “typically” looks into, however, with your continuing efforts we may be able to encourage her to take a closer look at the repeated targeting and prosecution of Dr. Jones.  It’s up to you to make this happen!

ONGOING ACTIONS-  Please continue contacting Governor Rell every day until she takes steps to stop the ongoing actions against Dr. Jones.  Parents and children who are visiting Dr. Jones office are writing notes and drawing pictures to encourage the Governor to help them.  They need your help.

Contact information for Governor M. Jodi Rell:

Phone Toll-Free:  1-800-406-1527

Email Governor.Rell@ct.gov

Send mail to- Governor M. Jodi Rell

Executive Office of the Governor

State Capitol

210 Capitol Avenue

Hartford, Connecticut 06106

NEW ACTIONS-  LET THE MEDIA KNOW!  Please contact a Connecticut newspaper (Letter to the Editor) with your concerns about Lyme disease and the continuing targeting of Dr. Jones.  Remember many papers have word limits (200 or less) and you must send original letters.

CT Residents- to find a newspaper in your area, see the link below.  

http://www.50states.com/news/conn.htm

If you live outside of Connecticut please contact one of the following papers.

NEW HAVEN REGISTER- letters@nhregister.com

CONNECTICUT POST- edit@ctpost.com

GREENWICH TIMES- letters.greenwichtime@scni.com

DANBURY NEWS TIMES- Letters@newstimes.com

HARTFORT COURANT-  Submit your letter on this form:

http://www.courant.com/about/thc-letters,0,2338372.customform

For information and facts concerning Dr. Jones situation:

http://www.lymerights.org/Letter_from_Dr__Jones_Feb_2010.pdf

HOW TO DONATE TO THE LEGAL DEFENSE FUND:  There is no doubt Lyme Disease has drained us financially.  Many of us have had to refinance homes, exhaust college and retirement funds and borrow from family and friends.  It is with sensitivity to this reality that we are asking you to join us in contributing to this effort in what ever way you can.  The deadline for paying the $10,000.00 fine is approaching fast (April 15, 2010) and there are mounting legal fees that need to be paid to keep Dr. Jones legal defense intact.

To donate- write “Penalty or Gift” in the memo field of your checks.  Payable to:  Pullman & Comley Trust Account-for Dr. Charles Jones

Mail to:  Elliott B. Pollack, Esquire

c/o Pullman & Comley, LLC

90 State House Square

Hartford, CT 06103-3702

PayPal instructions are posted here:

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http://www.personalconsult.com/BabesiaUpdate2009-Ebook.pdf

http://www.personalconsult.com/articles/updated-babesia-textbook.html

Further, Bartonella and Lyme disease are not rare or casual infections, and cause some fatigue and body aches, and virtually all of the criteria for these syndromes. The latter infection Lyme, according to the patents and grant requests of many infection leaders, is very damaging. Below are some very basic thoughts from a respected researcher who is only commenting on Lyme disease. If I injected 100 people with Babesia, I wonder how many would be dealing with crippling fatigue. As it is, we cannot use hamsters to grow some Babesia strains because it kills them.

I guess Babesia is not a fluffy little trivial infection.

*******************

Fibromyalgia, Chronic Fatigue Syndrome and Lyme Disease

by Bonnie Gorman RN

Dr Sam Donta presented a comprehensive, compassionate, cutting-edge lecture to Mass. CFIDS/FM Association members on November 3rd, 2002. His topic was “The Interface of Lyme Disease with CFS and FM: Diagnostic and Treatment Issues.” Dr. Donta is a nationally recognized expert on Lyme disease. He is the Director of the Lyme Disease Unit at Boston Medical Center and a Professor of Medicine at BU Medical School. He is a bacteriologist and an infectious disease specialist, who views CFS and FM from that vantage point. He is also a consultant to the National Institutes of Health (NIH), and presented at NIH’s scientific meetings on CFS research.

What does Lyme disease have to do with CFS and FM you might be asking? Some people believe that Lyme disease may be one of the causative factors in both CFS and FM. Others believe that some CFS and FM patients are really misdiagnosed chronic Lyme disease patients and vice versa. Some believe that there is no such thing as chronic Lyme disease, instead these patients actually have CFS or FM. We asked Dr. Donta to help sort all this out.

 Parallel Symptom Patterns

Dr. Donta presented the symptom lists for chronic Lyme disease, chronic fatigue syndrome (CFS), fibromyalgia (FM), and Gulf War Illness (GWI). He pointed out the similarities between them, and found there were few differences. He has treated hundreds of patients with these illnesses. He found that CFS and GWI have identical symptoms, and FM is only distinguished by a positive tender point exam, that is often positive in CFS and GWI as well. Clinically it is almost impossible to distinguish or differentiate these illnesses. He has concluded that chronic Lyme disease is remarkably similar to CFS, FM, and GWI. These multi-symptom disorders have similar symptom patterns consisting of fatigue and neurocognitive dysfunction, along with numerous other symptoms that probably relate to altered neurological function. Musculoskeletal symptoms may be more frequent in FM and in some patients with chronic Lyme than in CFS, but the definition of CFS and GWI also includes muscle aches (myalgias) and joint aches (arthralgias).

Lyme Disease Symptoms

Flu-like illness, fever, malaise, fatigue, headache, muscle aches (myalgia), and joint aches (arthralgia), intermittent swelling and pain of one or a few joints, “bull’s-eye” rash, early neurologic manifestations include cognitive disorders, sleep disturbance, pain, paresthesias (including numbness, tingling, crawling and itching sensations), as well as cognitive difficulties and mood changes. The only symptom difference in Lyme disease is the expanding circular rash with a clearing area and center resembling a “bull’s eye.” He pointed out that Lyme has multiple types of rashes and half of the rashes are not typical, they may not even include the “bull’s eye” rash. They can appear from two day after the bite, then go on for a week or so. Patients who are infected may not develop or see the rash, and may not develop any future symptoms. In studies, only one third of the patients were actually aware of their tick bites.

30-50% of acute Lyme disease patients went on to develop chronic Lyme disease. Additionally, some previously asymptomatic patients may reactivate their infection following various stressors such as trauma, surgery, pregnancy, coexisting illness, antibiotics treatment, or severe psychological stress. The Lyme vaccine can also reactivate their infection. Similar triggers such as trauma, surgery etc. are known to precipitate CFS, FM and GWI as well. This is not a new phenomenon with infectious diseases. We know infectious diseases (i.e. TB) will reactivate after illnesses or surgery — any stressor. Dr. Donta reported on the effects of gender on host susceptibility in Lyme disease, CFS, FM and other multi-symptom diseases. In all these disorders, women appear to be more affected than men, usually at about 2:1 ratios. He noted that neural cells contain estrogen and progesterone receptors, and that herpes viruses can utilize estrogen receptors to gain access to the reservoir in the cell nucleus. Treatment of chronic Lyme disease also seems to be gender-dependent to some degree, with men generally having more speedy and complete recoveries compared to women. He concluded that gender relationships are known for a number of infectious diseases, so it would not be surprising that such a relationship exists for chronic Lyme disease, CFS, FM and other multi-symptom disorders.

Etiology

Lyme Disease: A distinct difference between Lyme disease, CFS and FM is that the origin of Lyme is clear. Lyme disease is caused by spirochetal bacteria transmitted by the bite of an infected deer tick. This bacteria is the Borrelia burgdorferi bacteria. It was identified in the late 1900s in Europe . The US was late to recognize what Europe had described. Lyme disease was not formally identified by the CDC until 1977 when arthritis was observed in a cluster of children in and around Lyme , CT. Since that time Lyme disease has been identified in many states. The CDC reports that it causes more than 16,000 infections per year in the US . Some researchers feel that the prevalence is higher than that.

CFS and FM: Dr. Donta feels that Lyme disease is an important cause of CFS and FM. In addition to Lyme, there are a number of other possible causes. The evidence is still circumstantial though. Epstein-Barr virus (EBV), the major cause of infectious mononucleosis, continues to be debated as a cause of CFS. It is uncertain whether EBV can cause symptoms other than fatigue, such as myalgias and arthralgias that are not seen during acute or reactivated EBV infection in patients who are being immunosuppressed, but it remains possible that EBV could cause one type of chronic fatigue disorder. There are also other herpes viruses i.e. HHV6 that are being evaluated as potential culprits.

Dr. Donta reported that recently recognized species of Mycoplasma (Mycoplasma fermentans, Mycoplasma genitalium) have been implicated in CFS, FM and GWI. These same bacteria have also been implicated as causative agents of rheumatoid arthritis, based on PCR-DNA evidence in patients with these disorders in which 50 percent are found to have the DNA of the Mycoplasma in circulating white blood cells, compared to 5-10 percent of a normal population. Whether the presence of this DNA represents past exposure or ongoing infection remains to be resolved. No long-term studies have yet been performed in patients with CFS and FM to determine whether the finding of Mycoplasma DNA persists over months or years or whether such patients have any evidence of other infection such as Lyme disease or infection with Chlamydia species.

Central Nervous System Involvement

Dr. Donta reported that in Lyme disease, the nervous system seems to be the primary target for the bacteria causing the disease. Patients with Lyme disease express many neurologic symptoms such as pain, paresthesias including numbness, tingling, crawling and itching sensations, as well as cognitive difficulties and mood changes. Even the joint pains and occasional arthritis appear to be neuropathic in origin, as anti-inflammatory agents such as ibuprofen and other nonsteroidal anti-inflammatory drugs (NSAID) have little if any effect on the pain. Experimental evidence from animal models also affirm the localization of B. burgdorferi DNA to the nervous system. Dr. Donta postulates that the disease mechanisms could involve inflammatory responses, autoimmune responses or toxin-associated disruption of neural function. Any inflammatory responses appear to be weak, and there is no compelling evidence that Lyme disease is a result of immunopathologic mechanisms.

Commenting on his research, Dr. Donta speculated that if they are correct, and lyme bacteria is a nerve toxin that interferes with the transmission of the nerve impulse, then that is all you need to impede the normal flow of information. There is a lot of cross-talk in the nervous system. This toxin will decrease that cross-talk causing delayed responses resulting in cognitive problems — the brain fog so commonly described in all these multi-symptom disorders.

Although the disease pathways for other possible causes of CFS and FM have not been defined, Dr. Donta postulates that the central nervous system would appear to be a logical target for other pathogens or other disease processes. These illnesses clearly affect the brain and are bound to cause many neurological manifestations. Any changes in immunologic function would not appear to be sufficient to explain the various symptoms, and are likely to be secondary to other disease processes.

He feels we have been thinking too simplistically about finding whole organisms replicating in chronic diseases. It is highly likely that there is no single cause for these illnesses. It’s more likely that there are multiple causes — different organisms causing the same final set of symptoms. Researchers need a better algorithm to study these fatiguing illnesses. We need to be more inclusive, rather than trying to separate the illnesses. Sometimes in medicine, if an illness is too complex to study, research interest dwindles. We have the technology to do the research, but there hasn’t been the will and the momentum to get it done.

Clinical Diagnosis

Dr. Donta reiterated that the diagnosis of Lyme disease is primarily based on clinical grounds, just as with CFS and FM. Once other disorders are ruled out, the combination of symptoms over months is sufficient to make a presumptive clinical diagnosis. The diagnosis of Lyme is made easier if a typical rash is present during the early phase of infection. After that, it is difficult to distinguish the flu-like illness that can occur a few weeks later, or can recur over a number of months.

Dr. Donta reported that some patients develop severe headaches and an aseptic (infection free) meningitis, which frequently is diagnosed instead as viral meningitis. If a Bell ‘s palsy occurs (drooping of one side of the face), the possibility of Lyme disease is likely. If an unprovoked arthritis occurs, causing swelling of a single joint, especially the knee, but sometimes more than one joint, then the possibility of Lyme disease should also be given high consideration.

He emphasized that it is the chronic phase of the disease that causes most problems for physicians and patients, because of the lack of objective signs and the presence of so many symptoms that it causes some doctors to attribute psychological reasons for the patients’ symptoms. Many patients then receive a diagnosis of CFS or FM, when they may have underlying chronic Lyme disease as the cause of their symptoms.

Diagnostic Tests

Tests for Lyme disease, like tests for other infectious diseases, are often confusing and circumstantial, and their analysis and interpretation has often been flawed. In infectious diseases you do a Western blot test to see if you have a specific reaction. Western blot separates out proteins antigens of an organism you are looking for. It tells you if a person has been exposed. It is not a direct measurement of the organism. It is a measurement of whether the person has antibodies to it. Antibody tests are useful in the early stages of illness as with other acute infectious illnesses. Once the illness is in a chronic phase, antibody tests are not useful.

Just as viruses change from year to year, we know the Lyme bacteria mutates. There are a number of organisms that can shift their surface protein in a matter of hours and that is how they evade detection and patients test negative. These organisms attach themselves to proteins and conceal themselves — creating a cloaking mechanism that defies detection. This allows them to get where they want to go — the nervous system. Once they are inside a cell, the immune system can’t see them.

That said, Dr. Donta explained that lab tests have been helpful is some patients with Lyme disease, especially those with arthritis, in whom there are stronger antibody responses than in those with the chronic, multi-symptom form of Lyme. The criteria for the laboratory diagnosis has been patterned after the arthritic form of the disease, and not the chronic form; as a result, there are many physicians who are misinformed about the test’s lack of value in chronic Lyme disease. The Lyme Western Blot is helpful when it shows reactions against specific proteins of B. burgdorferi, but can be negative in 25-30 percent of patients who otherwise have chronic Lyme disease.

PCR-DNA tests for Lyme in blood, urine and spinal fluid are rarely positive, most likely because the bacteria and their DNA are not present in those body fluids, but inside nerve cells. Additionally, PCR-DNA studies are very easy to contaminate.

In chronic Lyme disease, the MRI exam of the brain is positive in about 10-20 % of patients. It can show some white spots (unidentified bright objects- UBO) in various areas, similar to those seen in multiple sclerosis (MS), a neurologic disease of unknown cause that has some overlapping symptoms with Lyme disease, CFS and FM, such as the numbness and tingling or paresthesias. (There are also positive MRI findings in CFS and FM patients as well.)

Dr. Donta reported that the brain SPECT scan shows some changes in blood flow to various parts of the brain, primarily the temporal (cognitive processing) and frontal (mood) lobes in about 75 percent of patients with chronic Lyme disease. Patients with CFS have also been reported to have some brain SPECT scan changes, frequently involving the occipital lobe. No comparative studies have been made among patients with chronic Lyme disease, CFS and FM. The mechanisms underlying these changes remain to be defined, but may be due to a mild vasculitis (inflammation of blood vessels) or to a signaling problem within the nerve network of the brain in those specific areas. It is promising that these changes are reversible in most patients treated with antibiotics that appear to be effective in treating the chronic Lyme disease. These MRI changes are often slow and may take a year to reverse themselves.

These are covert organisms we are dealing with. We need more direct detection methods for blood, spinal fluid and other body fluids. How do you detect organisms in spinal nerve roots or brain? Right now we can’t. Nobody is going to biopsy patients. We need an illness registry so we can do direct detection studies, particularly of the brain, after death.

Treatment: Persistence Pays Off

Dr. Donta reported that there are lots of drugs that are active against the Lyme bacteria in the test tube, but the big question is whether the drug can get to the bacteria? Lyme bacteria lives in the cells of the nervous system, perhaps other cells. Dr. Donta has experimented with various intracellular-type antibiotics. He reviewed his journey through various antibiotics. After listening to his patients he decided that some antibiotics were better than others. He then looked at clarithromycin (Biaxin) and azithromycin (Zithromax) which he found had powerful activity against Lyme bacteria in a test tube. But the antibiotics, by themselves, did not seem to do any good. He found that you need to change the cellular pH (the degree of acidity or alkalinity), making it more or less acidic, to maximize the effectiveness of the antibiotic. This allows the antibiotic to work better i.e. doxycycline seemed to work better when the pH was higher. Dr. Donta has experimented with various agents to adjust pH i.e. amantadine (used to treat flu) and plaquenil (used to treat malaria). He just submitted proposals to NIH to study various agents to determine which is most effective.

Dr. Donta emphasized that the most important aspect of treatment is that it must be long-term — 12-18 months, sometimes 24-36 months. This length is not unusual in the treatment of infectious diseases i.e. TB. In the first few months of treatment patients can expect an adverse reaction, symptoms will increase and you’ll feel worse. You need to be able to hang in through this period, and allow 3-6 months of a treatment trial to determine if it is working. The earlier in the disease process that you start on treatment, the more successful it is. The more chronic the condition the less successful it is, and you’ll need to treat over a longer period of time. This treatment resulted in substantial improvement and cures in 80-90% of patients with chronic Lyme disease. There are 10-20% who do not respond — generally those with a strongly positive Lyme test.

Dr. Donta reported that similar results have been found in some patients with CFS and FM of unknown cause, supporting the hypothesis that some patients with CFS and FM have an underlying infection responsive to those antibiotics. Antibiotic trials in CFS and FM have been limited to one month, a duration that is inadequate to properly evaluate the potential of certain antibiotics to have a positive effect on the disease. Additional studies, examining both potential etiologic agents of CFS and FM as well as treatment trials should lead to a better understanding of both the cause and treatment of patients with CFS and FM.

Q & A

Q: If the Lyme lab tests are inadequate and the symptoms are the same as CFS and FM, why not just treat all CFS and FM patients with the Lyme protocol?

A: You want to be conservative with your medicines. I think we have enough info now to tell CFS and FM patients to consider going on a 3-6 month trial of antibiotics and see if you’re better. Consider all the other meds you are already taking that just treat symptoms and not the cause of your illness. They all have side-effects that can be hazardous. Is it worth it to you to consider a primary treatment aimed at a cause? There will be resistance from some MDs. They need to be educated. Your primary MD will need to consult an LD specialist re the treatment protocol.

Q: Do patients with Lyme disease also have bowel and bladder problems like interstitial cystitis (IS) and irritable bowel syndrome (IBS)? How are they affected by treatment?

A: Yes, many patients with Lyme have IS and IBS. He was surprised how much the bowel disorders affected treatment. Tetracycline generally helps the IBS. Plaquenil can sometimes irritate the bowel.

Q: I have received different results for the western blot Lyme test. Why?

A: Lyme test results are not reproducible from one lab to the next. You will get different findings from different labs. The western blot is not a great test for Lyme since the responses to Lyme bacteria are already very small responses.

Q: I’ve been sick for 15 years with CFS and my Lyme test was negative. Is there any value in treating now?

A: If the test was negative but you have the complex of symptoms and there is no other obvious answer, why not give antibiotics a try.

Q: I had the Lyme vaccine then got Lyme symptoms. Why?

A: Lyme vaccine was pulled from the market because it was causing reactions and reactivating a slow onset of Lyme disease.

Q: What are the ocular problems in Lyme?

A: He sees optic neuritis, similar to that seen in atypical MS patients.

Q: Is there any Lyme connection to cutaneous lymphoma?

A: He has looked closely for any cancer/ Lyme associations, but has not seen many.

Q: Is there a connection with thyroid problems?

A: Thyroid problems are a very common co-existing condition with Lyme, as they are with CFS.

Q: How do I differentiate itching from allergic reactions?

A: The same sensory nerve fiber pathways that carry pain carry itching, numbness, tingling etc. Rash is common symptom. Rashes could be caused by medications, especially if they are body-wide. Is it an allergic reaction or hypersensitivity reaction? Get a complete blood count (CBC) with differential. Eosinophils will be elevated if allergic reaction. If not, then it’s a hypersensitivity reaction. Treatments are similar.

Q: How do we get funding for research to advance these illnesses?

A: He stressed how important it is to combine advocacy and research efforts. Ultimately it will be a political solution. Get active legislatively in DC. The CFS Coordinating Committee is a very good forum. Lyme does not have anything like that. Groups need to work together, not fight with each other. There should be a coalition of all these groups. We also need to show insurance companies the benefits of primary treatment to patients, as well as to insurer’s bottom line.

www.canlyme.com/fibrocfslyme.html

DR. SCHALLER NEITHER SUPPORTS NOR OPPOSES THIS INFORMATION.

March 25, 2009

Dear Esteemed Guidelines Review Panelists,

I am a Lyme patient, mother of two Lyme infected adults, award-winning author, advocate and medical researcher who probably acquired Lyme congenitally. However after our most recent tick bites, my family was forced to wait 13 years for an accurate diagnosis of Lyme disease despite nearly 100 physician and ER visits. This unnecessary delay occurred despite the fact that I removed ticks from myself and my then toddlers and we had bull’s-eye rashes and other acute Lyme symptoms. Over time, I progressively lost physical ability to the point of being unable to walk, work, drive, think, use the left side of my body, etc. I suffered intractable pain for years. My family and I were sick all of our lives because no doctors would touch the words “Lyme disease”. One physician told me behind closed doors he was “not allowed to diagnose” Lyme patients, or put the words “Lyme disease” in patient charts for fear of reprisals. I spent 10 days at the Mayo clinic in Rochester , MN whereby I was refused Lyme testing despite my symptoms and lengthy medical history. Repeatedly I heard “there is no Lyme in Wisconsin ” which was patently ridiculous. Indeed your panelist Yale’s Dr. Paul Duray performed tick surveys on WI military bases around the time my family was most recently bitten (in the 1990s). Reports indicated that areas of WI were Lyme endemic at that time. Note I lived just 2 hours from one of those endemic bases. It is felt that my parents, siblings, and probably children also have Lyme, acquired congenitally. Many of us have been re-bitten and have active Lyme infections and progressing symptoms despite repeated antibiotic treatments.

Later on, as if chronic illness was not enough of an insult to my family, I was forced to fight over 12 years in family court to retain custody of my children post-divorce, yet eventually lost all parental rights in short, simply because I had Lyme disease. That occurred despite expert physician witnesses and laboratory tests clearly showing my family Lyme positive, even by CDC standards. One judge said I didn’t “look sick”. One of my children ended up in a psychiatric ward for observation due to Lyme induced depression. We have lost homes, jobs, reputations, finances; filed bankruptcy, fought disability providers, and insurers just to get medications and treatments that were life-saving, covered; and most were paid out-of-pocket. I have had to endure years of oral antibiotics that do not work, fulminant symptoms, intramuscular and IV therapies, surgical operations, the loss of several organs, and CNS, joint, and brain invasion by organisms that could have been successfully treated at onset if those whom have been holding the purse strings of information censorship had been speaking the truth about spirochetal infections; instead of silencing a growing epidemic in exchange for what has appeared to be profiteering and notoriety.

I have fought hard to defend Lyme treating physicians because of what the medical boards are doing to them (pulling their licenses or other sanctions) because they dare to treat patients outside IDSA “standards” of care that are no one’s “standards” that are merely recommendations, and which clearly do not work. This is a tragic situation when our own physicians cannot treat patients in favor of insurance companies or a handful of powerful academicians who dictate medical dogma, the former without a license, the latter without practical clinical experience. Corporatized medicine serves no one except the profiteers; and certainly not the ill patient populations. Sadly, our family’s tragic situation is not unique. I contend that if rest rict ive Lyme disease medical guidelines such as those promulgated unilaterally by the IDSA in 2000 and again in 2006, which deny aspects of this illness and minimize others, are allowed to proliferate, then more families will be facing the kinds of tragic destruction, discrimination and denial that our family has unnecessarily and unjustly, but for the sake of research dollars and promoting for-profit pipelines.

I urge you to carefully consider the long-term consequences of clinical practice guidelines that are intended to serve as recommendations and not mandate for treating physicians. The current rest rict ive IDSA guidelines and processes that allow academicians to patent and profit upon technologies also allow insurance companies to deny patients a right to become healthy and whole. This is additionally disturbing when we see that some of the academicians who are also guidelines panelists have conflicts of interest including patent holdings, and are paid consultants to pharmaceutical and insurance companies and witnesses in litigation. That some of these individuals have ongoing vaccine and diagnostic test involvement; as well as a role in the establishment of “standards” and information dissemination is intensely troubling when that information denies aspects of illness, as the IDSA guidelines do for Lyme disease. It is clear that some of these parties well know the severity of this illness but patently refuse to budge on more recent opinion. Perhaps this is because they and their associates stand to lose much if they admit to the truth about this illness. How unfortunate for those ill with this disease that power, profit, and reputations appear greater than the welfare of people globally. You have a chance to change things for Lyme patients for all of history right now, but only if you choose truthfulness over ongoing censorship for profit and private agendas.

In all fairness to patients who are to benefit from current and future guidelines, we request full consensus in writing medical guidelines, even when guidelines are merely recommendations. This process must include all current research (not just that put forth by a few panelists); everyday experiences of our treating clinicians, and valuable patient input and experience and I thank you for the opportunity to provide such input at this juncture. It is my hope that this open public input period is truly meaningful and not just a token conciliatory gesture for patients whereby the end result will be to nevertheless uphold the 2006 IDSA guidelines that patients, physicians, and others clearly do not want nor accept as legitimate. We do not want or need biased, rubber-stamped, disease dismissing, for-industry guidelines that place profits above human suffering. And patients will be far more vocal about this the longer it continues to occur until these practices cease to exist and those held accountable for these practices when they occur. Illness does not equal powerlessness, and those who are ill, expect and deserve better than what we have been spoon-fed from previous clinical practice guidelines for Lyme disease and some of its panelists.

After all, we are learning the truth about this disease; from study of all available documents, and from personal experience living with these infections. From our perspective, the guidelines and some of those who have been involved with the Dearborn criteria, the guidelines formation, diagnostic and vaccine technologies, and who also are grant recipients, and patent holders, currently appear far from truthful about this growing epidemic. The current guidelines are inaccurate and reflect a desire to rest rict patient and physician access to life-saving medications and treatment processes. The unfettered censorship of our physicians by academic mandate disguised as “recommendations” is most unwelcome in the patient/doctor relationship, and the toying of our health by insurance companies who whimsically misinterpret the IDSA guidelines is as dangerous to human life as Borrelia burgdorferi is, when left untreated or undertreated.

Clinical trials and controlled studies are necessary aspects of medicine. However, the practical patient experience has been shifted to the back burner in favor of academic “expert” opinion and research funding, including by those who do not see patients, or who occasionally do but who have only a limited patient sampling with one or two symptom presentations. Adhering to unilateral thought regarding a limited number of patients in favor of controlled, funded studies over time is an unrealistic approach that is woefully out of touch with the clinical experience. An absence of “scientific” proof is not proof of absence. Physicians who treat thousands of Lyme patients were, and are summarily excluded from the IDSA guidelines process, along with a former panelist who was excused for not agreeing to the “expert” opinion of other IDSA panelists. (Experts who again, do not have practical real time experience treating patients in a clinical setting.) The patients are crying out loudly for these processes to change, for our welfare, and for the future welfare of all persons yet to be infected with this devastating illness.

To that end, one of my recent books from my Lyme “It’s All In Your Head” series, was recently released, (titled The Baker’s Dozen & the Lunatic Fringe: Has Junk Science Shifted the Lyme Disease Paradigm). I have included 10 copies, one for each panelist to receive and review during this patient input period. I have collected significant research sources, including objective peer-reviewed articles, as well as FDA, DoD, NIH, CDC, published books, CME videotapes, and other sources, and compiled them for patients, educators, physicians, panelists, and others to review. The book illustrates also the research behind this disease as previously published by many of the IDSA panelists. It clearly shows the IDSA guidelines to be at stark odds with some of the guidelines authors’ own earlier published findings. The fact that earlier claims about the severity and persistence of Lyme disease by some of these parties do not reconcile with their current guidelines recommendations leads us to question the motivations of those who have written them.

That there are tremendous potential conflicts of interest at play does not escape the public. My book helps to illustrate what some of those important connections and conflicts may be and how they may be influencing the current Lyme paradigm. It also closely examines the CDC recommendations set forth at the 1994 Dearborn MI conference that was designed to standardize testing; yet apparently simply provided unilateral opinion that appears unsupported by scientific evidence opinion that led to a.) the release of what is considered to have been an unsafe vaccine by virtue of OspA sensitivity, chronic treatment resistant arthritis of which certain panelists were aware before the vaccine was released [evidenced by research papers]; and b.) has also led to the wrongly promoted insensitive diagnostic tests incapable of detecting most patients who have Lyme disease for many reasons examined; which has thus led to c.) thousands of people like my family being misdiagnosed, undiagnosed, and improperly treated for an organism that could have easily been treated at onset that the IDSA panelists published was persisting and severe; and d.) the refusal by doctors to continue to treat patients until symptoms are gone due to rest rict ive guidelines and fear of reprisals through medical board actions; and e.) the refusal by disability and insurance companies to pay for disability and/or treatments while they conveniently cite IDSA guidelines as mandate and not recommendation in order to control profit margins.

And since the current IDSA guidelines appear written in a manner supportive of this kind of discrimination, thousands have been disabled, killed, or have ended their own lives thanks to intractable pain, severe depression, discrimination and other factors caused by Lyme disease. If there is no “illness-for-profit” paradigm in play, then there is no excuse to continue to defend guidelines that dismiss meaningful research and clinical evidence, and contraindicate access to life-saving treatments. Lyme disease is a serious epidemic that requires open-ended treatments with combination antibiotics to the benefit of patient wellness as long as, and as frequently as is necessary until symptom resolution. Treatment benefits are nonexistent under a therapeutic schedule with limited duration that abruptly ends by a predetermined calendar date. And one which then magically changes all remaining spirochetes into some “post-Lyme syndrome”, a term that is not only hyperbole and conjecture, but also complete and utter nonsense. I outline how this is so within my new book which is provided for your review.

That there are those who continue to deny the existence of an organism that has long been studied by the military in collaboration with academic institutions as a bio-weapon; and that some of these parties, after patenting the organisms and processes, now publish contrary to some of their earlier research on these same organisms, is unconscionable in the public opinion of mass majority. That some of these parties would also be allowed to patent, profit and promote these processes by developing vaccines and insensitive/ineffective diagnostic tools in order to promote a vaccine which failed; while simultaneously holding patents on tests with a greater ability to diagnose Lyme patients but refusing to develop these more accurate processes, is also unthinkable.

Patients are imploring the current panel members to reconsider carefully the input of patients, their treating physicians and the scientific facts that have been formerly ignored during previous IDSA guidelines processes. The true research evidence is in fact present and easily accessible to all who choose to read same. Lyme disease is serious, persistent, chronic and debilitating; and even previous IDSA guidelines panelists published these facts Ñ even if they choose to minimize or flatly ignore their own findings within past and current guidelines and recent publications. For that reason, I urge you to read fully, or at the very least, glance carefully at the sections in my new book that discuss testing, patenting, grant funding, the guidelines processes, persistence, testing standardization and failures, the IDSA guidelines inadequacies/errors and the earlier research published by the IDSA guidelines authors and their associates. Likewise, consider carefully all submissions by those outside the IDSA academic “club” during this public input period.

Only when you see the truth about Lyme disease, in the form of the published research, the patient and the physician clinical experience, the revelations of conflicts of interests in former panelists, and the extent by which the paradigm is exploited for profit over patient welfare can you objectively, mindfully, and responsibly create guidelines that are clearly in the best interests of the patients they are supposed to serve something for and about which, many believe that the former and current IDSA guidelines for Lyme disease have failed miserably.

It is a tragedy that patients have had to endure the kind of prejudice and censorship that we have had over the past several decades at times by the very parties who are sworn to “first do no harm”. We have trusted unfairly those in the academic world who have had the power to keep us ill in favor of research funding. We are far more educated about our illness now, with full awareness of the political and scientific issues. Sources like the film Under Our Skin, the CT Attorney General’s investigation, and books like mine are helping others to find those truths and bring them into the spotlight. You merely have to look at them and consider the impact of forcing populations to remain ill by perpetrating ongoing myths that nobody believes or is buying except for the minority, “Baker’s Dozen”.

I urge you to consider your choices carefully. Patients will no longer stand idly by and accept what we know is not truthful. With great respect for what you are about to( undertake, but with the personal experience that this disease has long afforded me through decades of dealing with same, my research work and privileges in physician and patient advocacy, I formally request that you read the content of my new book, and put the patients first in your guidelines review process. Remember to “first do no harm”. I include on the following pages some excerpts from my book to facilitate your study-a book with more than 1,060 references. I collected this over a 4.5 year period, while ill, from publicly accessible sources. My research was included in the CT Attorney General’s anti-trust investigation into the IDSA guidelines, and part of it was shared with producers of the film Under Our Skin. Of note is that my books are available and selling internationally through popular book sellers. This information is not being taken lightly by your peers or by patients and physicians the world over. And in turn we expect and request that in a similar manner, that this information not be taken lightly by the esteemed review panel.

PJ Langhoff, Hustisford , WI
Author, advocate, researcher, Lyme patient and mother of Lyme adults

This book, The Baker’s Dozen & the Lunatic Fringe: Has Junk Science Shifted the Lyme Disease Paradigm? is available from Amazon.com.

IT IS NOT DRAMATIC HERB WITH CLAIMS WITH NO RESEARCH. IT IS NOT A TRADITIONAL ANTIBIOTICS LIKE LEVAQUIN, ZITHROMAX, RIFAMPIN, MYCOBUTIN AND MANY OTHERS. PATIENTS MAY BE IMPROVED FOR A TIME, BUT EVENTUALLY RELAPSE.

SOME MEDICAL GROUPS ARE VERY CLOSED, AND IF YOU ARE NOT 65 AND STILL ILL WITH TBD, AND A LL MD FOR TWENTY YEARS, YOU CAN BE IGNORED.

THE MODERATOR DOES NOT FEEL THIS WORK BELOW SHOULD BE IGNORED, EVEN IF THE TREATMENTS ONLY HELPED FOR A SEASON. 

Do Bartonella Infections Cause Agitation, Panic Disorder, and Treatment-Resistant Depression?

James L. Schaller, MD, MAR; Glenn A. Burkland, DMD; P.J. LanghoffMedscape General Medicine. 2007;9(3):54.

Abstract

Introduction

Bartonella is an emerging infection found in cities, suburbs, and rural locations. Routine national labs offer testing for only 2 species, but at least 9 have been discovered as human infections within the last 15 years. Some authors discuss Bartonella cases having atypical presentations, with serious morbidity considered uncharacteristic of more routine Bartonella infections. Some atypical findings include distortion of vision, abdominal pain, severe liver and spleen tissue abnormalities, thrombocytopenic purpura, bone infection, arthritis, abscesses, heart tissue and heart valve problems. While some articles discuss Bartonella as a cause of neurologic illnesses, psychiatric illnesses have received limited attention. Case reports usually do not focus on psychiatric symptoms and typically only as incidental comorbid findings. In this article, we discuss patients exhibiting new-onset agitation, panic attacks, and treatment-resistant depression, all of which may be attributed to Bartonella.

Methods

Three patients receiving care in an outpatient clinical setting developed acute onset personality changes and agitation, depression, and panic attacks. They were retrospectively examined for evidence of Bartonella infections. The medical and psychiatric treatment progress of each patient was tracked until both were significantly resolved and the Bartonella was cured.

Results

The patients generally seemed to require higher dosing of antidepressants, benzodiazepines, or antipsychotics in order to function normally. Doses were reduced following antibiotic treatment and as the presumed signs of Bartonella infection remitted. All patients improved significantly following treatment and returned to their previously healthy or near-normal baseline mental health status.

Discussion

New Bartonella species are emerging as human infections. Most do not have antibody or polymerase chain reaction (PCR) diagnostic testing at this time. Manual differential examinations are of unknown utility, due to many factors such as low numbers of infected red blood cells, the small size of the infecting bacteria, uncertainty of current techniques in viewing such small bacteria, and limited experience. As an emerging infection, it is unknown whether Bartonella occurrence in humans worldwide is rare or common, without further information from epidemiology, microbiology, pathology, and treatment outcomes research.

Conclusion

Three patients presented with acute psychiatric disorders associated with Bartonella-like signs and symptoms. Each had clear exposure to ticks or fleas and presented with physical symptoms consistent with Bartonella, eg, an enlarged lymph node near an Ixodes tick bite and bacillary angiomatosis found only in Bartonella infections. Laboratory findings and the overall general course of the illnesses seemed consistent with Bartonella infection. The authors are not reporting that these patients offer certain proof of Bartonella infection, but we hope to raise the possibility that patients infected with Bartonella can have a variety of mental health symptoms. Since Bartonella can clearly cause neurologic disorders, we feel the presence of psychiatric disorders is a reasonable expectation.

 

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Reader Comments on: Do Bartonella Infections Cause Agitation, Panic Disorder, and Treatment-Resistant Depression?  

Introduction

Bartonella is an infection that may cause a rash, enlarged lymph node(s), and malaise and fatigue that resolve over several weeks.[1,2] Many animals and insects carry this infection. Bartonella has multiple vectors and infection sources including fleas, flea feces, cat licks or scratches, ticks, lice, and biting flies.[3-6] Young stray kittens are often able to infect humans due to flea feces on their paws, or through cat scratches, bites, or licks.[7-10] Bartonella is found in cities, suburbs, and rural locations,[11-14] and is an emerging infection. In recent decades, Bartonella research publications are increasing, but psychiatric disorders were underreported in the soldiers of World War I and World War II. For example, approximately 1 million soldiers in WWI were affected with Bartonella quintana,[15] but medical journals did not report much about its psychiatric manifestations.

In the last 15 years, 9 Bartonella bacteria have been identified that are known to infect humans: B henselae, B elizabethae, B grahamii, B vinsonii subsp. arupensis, B vinsonii subsp. berkhoffii, B grahamii, B washoensis, and, more recently, B koehlerae and B rochalimae.[16-20] Currently, the largest national laboratories offer tests for only 2 species[21-23] (B quintana and B henselae). Some Bartonella cases have “atypical” presentations with signs or symptoms lasting more than weeks, causing diverse medical problems. For example, Bartonella can cause vision abnormalities, prolonged fever, joint pain, lung inflammation, respiratory disease, and granulomas throughout the body. It can occasionally cause abdominal pain, liver and spleen tissue abnormalities, thrombocytopenic purpura, bone infection, papules or pustules, maculopapular rashes, arthritis, abscesses,[20, 24-30] heart tissue and heart valve problems,[31-37] and neurologic illnesses.[38-42]

Traditionally, cognitive neurology has been related to some psychiatric illnesses. A search of PubMed with “Bartonella” and the search words “depression,” “mania,” “bipolar,” “major depression,” “depression,” “anxiety,” “panic,” “panic attack,” “psychosis,” and “schizophrenia” yielded the limited journal results below:

• Depression

• Dementia

• Encephalopathy

• Violent behavior

• Confusion

• Combative behavior

• Substance abuse disorders[43-48]

Some articles link Bartonella to substance abuse. Bartonella is repeatedly linked with alcoholism in the presence of substandard living conditions. Intravenous drug users also have an elevated prevalence of antibodies to Bartonella organisms and may be at significant risk of becoming infected.[49-53] The 3 cases described below are consistent with past reports of Bartonella causing psychiatric symptoms, and add further clinical data to these past reports.

Case 1

A 41-year-old male minister was reported by his wife, best friends, and children to have undergone a personality change after a camping trip in North Carolina . After the trip, the patient described a small right-sided “aching” axillary lymph node and reported a “fever.” He removed 3 Ixodes deer ticks from his leg and shoulder. Five weeks later, he had an “enlarged and very annoying” right-sided axillary lymph node, “excessive warmth,” irritability, severe insomnia, and new-onset eccentric rage. He had new excess sensitivity to slightly annoying smells and sounds. His afternoon temperatures were 98.7-99.9¡F, which he recorded every 3 days.

The patient tested negative for Lyme disease using the Centers for Disease Control and Prevention (CDC) 2-tier surveillance testing procedure performed at Quest Diagnostics, and yet Bartonella was suspected from his unilateral lymph node symptom and Ixodes attachment. The duration of the lymph node ache was at least 5 weeks, so “atypical” Bartonella was considered in the differential. The patient was ordered an IgG and IgM B henselae along with other lab testing. The only positive result was an IgM of 1:256. A PCR test for 2 Bartonella species was negative, but positive for B henselae when repeated.

During the next 2 weeks, the patient developed serious agitation, panic attacks, and major depression. His major depression was quantified by the Inventory to Diagnose Depression (IDD) scale.[54-56] His IDD was 39. This is in the moderate to severe range, so he was diagnosed with major depression (MD). He also was found to have excess anxiety with a 29 on the Beck Anxiety Inventory (BAI) scale, using 0-7 as a functional normal range. (Judith Beck, personal communication, 1994).[57-59]

He was so agitated that during arguments with his spouse, he threw objects such as kitchen glasses, a baseball, and a chair into his home’s drywall. Previously he was unknown to use insults or to curse at people, and now he did both almost daily. He slept 8-9 hours per day, ate normally, and had normal speech speed and enunciation patterns.

A psychiatrist diagnosed him as having bipolar disorder, despite the fact that he had no genetic history or any previous history of depression or mania. The patient gained 15 pounds in 3 weeks on 1250 mg per day of valproic acid, so he was tried on lithium carbonate, 300 mg at breakfast, lunch and dinner, with 600 mg once in the evening (blood level 1.1 mEq/L). These medications had no clear clinical effect on the patient’s agitation, mood extremes, or anhedonia with hopelessness. They were stopped after a minimum of 3-week trials.

A trial of quetiapine at 12.5 mg in the morning, afternoon, and 50 mg at bedtime helped significantly for 3 weeks, but then the drug stopped controlling his agitation and other dysfunctional behaviors. A higher dose of 25 mg of quetiapine in the morning, 25 mg in the afternoon, and 100 mg at bed was successful. The patient surprisingly reported that he felt “good” and “content” on this medication at these doses.

At this point, the patient still had a large tender unilateral lymph node, fatigue, and new papules under his right arm. Various causes of persistent large unilateral lymph nodes with papules were felt to fit a diagnosis of Bartonella. Based on a consult with an infectious disease physician, the patient was treated with azithromycin 250 mg twice daily and rifampicin 300 mg twice daily with food for 2 weeks. The patient’s anxiety increased, and he experienced 5 panic attacks. He became psychiatrically worse: highly reactive, emotionally volatile, and markedly irritable. His quetiapine was increased to 50 mg at breakfast and lunch, and 200 mg once in the evening, with immediate control of his increased morbidity.

After 5 weeks on this dual-antibiotic treatment, the patient began to exhibit sleepiness. His quetiapine dose was reduced to 25 mg at breakfast and 75 mg at bedtime, with no return of agitation or mood lability.

He was still complaining, however, of right-sided axillary lymph node symptoms, so he was treated for another 3 weeks on these antibiotics. A medical literature review of PubMed looking for the ideal dose of antibiotics and duration of treatment for this suspected Bartonella infection offered no uniform results. However, the patient’s lymph node complaints ended abruptly following 8 weeks of antibiotics, and so his medications were stopped.

The patient’s psychiatric symptoms have significantly improved, and he now remains on escitalopram 5 mg and quetiapine 6.5 mg in the morning and 25 mg qhs. His personality is felt to be 90% of baseline, according to his spouse and closest friend. We suggest this man’s psychiatric problems support a Bartonella presentation. Specifically, his symptoms immediately followed a clear Ixodes attachment, a new unilateral and uncomfortable axillary lymph node appeared just after this attachment, new papules formed, and he experienced a new constant “slight fever” feeling, a low-positive Bartonella serology result, conflicting PCR results, and a positive response to 2 antibiotics from medication classes that are believed to be effective in vivo against Bartonella. Further, his emotional improvement occurred nearly simultaneous to his enlarged lymph node normalization.

Case 2

Following the adoption of 2 young cats from a shelter, a medical student reported an “unusual rash” on her thighs, consisting of 4 linear lines measuring 4-9 cm, each 0.5-1.0 cm in width, running from the top of her thigh distally. These rashes were eventually determined to be bacillary angiomatosis by a dermatologist, following the elimination of a number of other possible causes, such as Cushing’s syndrome, Kaposi’s sarcoma, and an HIV infection.

The patient had significant risk factors for Bartonella including adoption of kittens from a shelter. She reported a number of flea bites, having “flea-bombed” her apartment 2 times within the past year, and she also allowed her cats to sleep in her bed. She explained that her cats routinely licked her hands, occasionally licked her mouth, and scratched and routinely gently bit her when playing.

The patient complained of new panic attacks, profound restlessness, and depression that began around the time of her new thigh rashes. She failed to receive benefit from routine doses of benzodiazepines or standard doses of selective serotonin reuptake inhibitors. She refused a trial of tricyclic antidepressants due to cardiac concerns, and she refused a trial of mirtazapine due to weight concerns. She rejected transdermal selegiline and bupropion due to the likelihood of an absence of anxiety benefit.

The only treatments showing modest benefit (30%-40%) for this patient were escitalopram at a dose gradually increased to 30 mg per day, which is above US Food and Drug Administration-approved dosing and higher than the dosing recommended on the basis of most research on the medication, but this dose decreased her hopelessness compared with a 3-week 20-mg trial. Her IDD dropped from 34 to 23 on escitalopram on 30 mg per day. She also self-administered SAM-e (S-adenosylmethionine) at 600 mg every morning. This latter dose is below the routine dose for the treatment of major depression, which is 1200-1600 mg per day when dosed orally. The patient felt this was “helpful” for decreasing her depression.[60-65]

The patient was warned of seizure and serotonin syndrome risks with the use of 2 antidepressants, including 1 at very high dosing, but lower doses of escitalopram felt like “nothing was happening,” and she wanted doses that had benefits.[66,67]

Over 8 weeks, an increase of escitalopram decreased her residual moderate depression. She was increased to escitalopram 60 mg and SAM-e 1200 mg over 10 weeks, which resulted in a 90% remission of her depression. She had no serotonin symptoms such as myoclonus, rigidity, hyperreflexia, shivering, confusion, agitation, restlessness, blood pressure instability, fever, nausea, diarrhea, diaphoresis, flushing, or rhabdomyolysis. She did have some residual anxiety, and this was treated with clonazepam 2 mg, 1 tablet once in the morning and afternoon, and 2 qhs, with no sedation side effects.

She still had clear information-processing limitations, markedly poor memory, and the unusual need for high psychiatric dosing to gain any benefit. Her psychiatrist noted, “She may have a diffuse brain disorder, ie, undiagnosed inflammation or infectious source. Her unusual color thigh rash images seem important.” The patient’s nurse practitioner had seen a case of cat scratch fever in the past, and hypothesized that the patient had bacillary angiomatosis from Bartonella — the infectious cause of cat scratch fever.

The patient was placed on cefuroxime 250 mg twice a day and azithromycin 250 mg 3 times a day. During Week 1, the patient became increasingly sad, irritable, and hopeless, with increased panic attacks that an increase in clonazepam did not relieve. However, by Week 2 she seemed to have less depression and agitation. Surprisingly, during Week 3, on approximately Day 16, her reddish thigh rashes were gone, with residual normal skin color with irregular patterning.

Over 8 weeks, the patient’s depression and anxiety improved. She tolerated a sharp reduction in both of her medications, ie, escitalopram was lowered to 25 mg per day with a decrease of clonazepam to 1 mg once every morning, afternoon, and evening. She stopped her SAM-e entirely. She was regarded as medically cured and only scheduled for routine gynecologic exams.

After 6 months, the bacillary angiomatosis returned approximately 50%, and the patient reported a moderate return of inappropriate anger, excess interpersonal sensitivity, severe premenstrual dysphoric disorder, irritability, and sadness.

She was regarded by her physician as having a Bartonella relapse and placed on rifampicin 300 mg 3 times per day, and cefdinir 300 mg 3 times per day for 12 weeks. He then replaced the cefdinir with azithromycin 500 mg at 1-1/2 tablets a day for 6 weeks. After this treatment, the patient was back at her baseline and now only takes escitalopram 10 mg per day, with clonazepam 0.5 mg in the morning and 0.75 mg once in the evening — a fraction of the earlier doses. The family physician feels that the antibiotics were helpful, but is still uncertain of the “best” antibiotic protocol for Bartonella, based on his review of infection handbooks and Medline articles.

Case 3

A businessman from the Midwest reported failing treatment for new adult-onset social anxiety, generalized anxiety disorder, panic attacks, and MD. His IDD depression scores were 34 and 40 taken twice over the same intake week. His BAI was 29. He also had a new, moderately severe daily headache. He had been fine psychiatrically until he went on a camping and hunting trip in Florida a couple of months earlier. Following that, he experienced “flu” and “feverish” feelings for about 9 days. He also developed 3 new skin-colored papules under his left arm. He had no rashes, tick attachments, clear flea exposures, or dog or cat contact. However, he reported extensive contact with wild bush branches and leaves while hunting and walking in the woods. He also reported that he virtually never checked himself for ticks.

His camping partner was bitten by a lone star tick and treated immediately with antibiotics for Lyme or Masterson’s disease, based upon history, location, type of tick, and a new oval, pink, homogeneous ankle rash.

Our patient failed both Lab Corp ELISA and Western blot testing for Lyme according to CDC surveillance criteria, but showed a 23 band on the IgM Western blot. His manual differential blood smear reported coccobacilli attached to some red blood cells (RBCs), a rare ability for bacteria, but found in some American Bartonella species infections. The patient was negative for a Bartonella PCR, but positive for an IgG titer at 1:128. A review of some Medline articles showed the internist that Bartonella PCR testing is not always reliable. Other articles showed a high degree of reliability. He decided to treat for Bartonella based on the patient’s high tick exposure, his friend’s tick infection, the patient’s 3 new papules, the manual blood smear, and his abnormal antibody titer.

The internist treated the patient with doxycycline 100 mg twice a day for 3 weeks with no benefit other than a slight reduction in headaches. He then treated him with rifampicin 300 mg twice daily combined with trimethoprim-sulfamethoxazole at a dose of 160 mg/800 mg twice a day for 1 month.

The patient had a marked benefit from this last treatment and returned approximately 85% to his psychiatric baseline. He no longer exhibited any social anxiety, generalized anxiety disorder, or panic attacks. His MD was only mild with an IDD of 12 (borderline normal), and he was treated daily with 100 mg of sertraline.

After approximately 14 months, the patient was in a severe motor vehicle accident and required hospitalization and multiple surgeries to regain his stability. Approximately 7-12 weeks after his accident, he began to have a resurgence of all of his psychiatric symptoms. His physician diagnosed a Bartonella relapse causing a psychiatric relapse. The patient was placed on rifabutin 300 mg daily with azithromycin 250 mg twice a day.

Over 4-5 weeks, his psychiatric symptoms improved approximately 50%, so he was treated for an additional 5 weeks with remission of all psychiatric symptoms except depression, which was being treated with 100 mg of sertraline. His sertraline blood level was checked, and his steady-state sertraline level had decreased over time, so his dose was increased from 100 mg to 150 mg per day, which restored him to a normal mood.

Results

The previously discussed patients with presumed Bartonella seemed to generally require higher dosing of antidepressants, benzodiazepines, or the use of antipsychotics in order to function normally. Doses could be reduced as the presumed signs of Bartonella infection remitted following antibiotic treatment. All patients improved significantly and nearly achieved their normal, healthy baseline mental health status.

Discussion

Bartonella with psychiatric symptoms is rarely discussed in the medical literature. In this article, we have presented case studies of patients with new clear psychiatric morbidity, sudden agitation, panic attacks, and treatment-resistant depression, all possibly attributed to Bartonella. Reasonably compelling and broad data provided evidence for inclusion in this article and included: exposure to endemic areas and endemic animals such as young cats, clear tick bites or probable flea transmission, abnormal lymph nodes, a “fever,” a positive antibody test, an eventually positive PCR, axillary papules, bacillary angiomatosis rashes, the unusual need for high psychiatric dosing to gain any benefit, information-processing limitations, poor memory, and a new, moderately severe daily headache.

The presence of Bartonella-induced psychiatric symptoms should not be surprising. First, psychiatric disorders are brain disorders, and Bartonella is documented as causing many diverse neurologic brain disorders. Second, Bartonella infections are associated with RBCs, which allow small Bartonella bacteria (a fraction of the RBC size) to enter the brain’s vascular system.[68-83] These Bartonella-infected RBCs probably cause psychiatric morbidity due to brain pathology, as indicated by the fact that some Bartonella patients have neurologic disorders, such as seizures, hemiplegia, ischemic strokes, transverse myelitis, and multiple granulomatous lesions, as well as meningitis and encephalitis.[38,84,85]

Finally, with 9 species or subspecies that can infect humans, it is possible this larger number of species can produce a wider range of signs and symptoms — some of which might be psychiatric in nature. Three clinical cases had psychiatric symptoms during Bartonella infections. All 3 cases were examined retrospectively. No patient was solicited for research. None had examinations or testing in excess of what was required by their physicians in order for them to make a clinical diagnosis. As Bartonella is an emerging infection, there is no clear standard of care with antibiotic treatment, with only 1 randomized double-blind study involving a brief trial of azithromycin having been conducted.[86]

Bartonella is an emerging infection that raises more questions than answers. The frequency of psychiatric pathology due to this emerging infection is unknown, and the best in vivo treatments against Bartonella are also still emerging. A review of the literature on laboratory diagnosis and treatment in actual human patients in vivo shows that researchers do not offer uniform treatment, and most of the articles on Bartonella treatment are small and are characterized by various limitations. Therefore, we are not proposing optimal antibiotics, dosing, or treatment duration in the treatment of Bartonella. We are merely reporting the treatments used in each of these 3 cases, each of which had some support in the literature.

None of these cases offers certain proof of a Bartonella infection, but we raise the possibility that these patients had Bartonella infection and that it had an impact on their mental health.

Conclusion

We note that the number of Bartonella species that infect humans currently outpaces the number of Bartonella species that can be tested by top national labs. Some antibiotics seem to have an effect, but dosing and duration are not clearly established or indicated by a broad literature review. Further, clinical improvement and the cessation of symptoms do not always signify complete eradication. That is, it may be possible for a patient to relapse due to a significant medical stress to the body or a decrease in immune system capacity. Of greatest importance, we believe that Bartonella can enter the brain and cause not only well-documented neurologic disorders, but also some psychiatric disorders as well.

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James L. Schaller, MD, MAR, Director, Professional Medical Services of Naples , Naples and Tampa , Florida

Glenn A. Burkland, DMD, Associate Clinical Professor, Temple University School of Dental Medicine, Philadelphia , Pennsylvania

P.J. Langhoff, science research assistant and medical writer, Hustisford , Wisconsin

Disclosure: James L. Schaller, MD, has disclosed that he has received unrest rict ed research grants from Forest , Cephalon, Wyeth, BioRay, Vitacost.com, www.QMedRx.com, Zeneca, and AstraZeneca. He is a medical advisory board consultant with stock ownership and stock options in Nutraceutical Sciences Institute. He is also the inventor of a nutraceutical transdermal bioidentical antidepressant with a patent pending.

Disclosure: Glenn A. Burkland, DMD, has disclosed no relevant financial relationships in addition to his employment.

Disclosure: P.J. Langhoff has disclosed no relevant financial relationships in addition to her employment.

Disclosure: James L. Schaller, MD, and P.J. Langhoff have disclosed that they are currently preparing a textbook on Bartonella infections. 

]]> http://lymeinfo.wordpress.com/2009/04/13/bartonella-causes-depression-anger-panic/feed/ 5 lymeinfogroup http://lymeinfo.wordpress.com/2009/04/13/mold-illness-biotoxins-mycotoxins-sick-buildings/ http://lymeinfo.wordpress.com/2009/04/13/mold-illness-biotoxins-mycotoxins-sick-buildings/#comments Mon, 13 Apr 2009 02:51:31 +0000 lymeinfogroup http://lymeinfo.wordpress.com/?p=75 ]]> Mold Illness, Biotoxins, Mycotoxins and Sick Buildings

Dr. James Schaller is the writer of three co-authored books and is a certified mold remediator and investigator. This is stunning rare mix of science and practical knowledge. He can notice in 5 minutes junk mold testing and junk remediation in reports. He tries to read closely to old and emerging experts in remediation and building defect science. Dr. Schaller is a full-time researcher and part-time clinician working as a pioneer in mold illness. However, with 27 books and 27 peer-reviewed journal articles, mold illness is not his only interest or a medical fetish.

Two of his most recent highly respected books, written with master builder and biochemist Dr. Gary Rosen, and do not take weeks to read. They have real-world images, and are not mere wordy abstraction texts. These books avoid boring narcissistic autobiography, the “discovery” of “new” treatments known by others for years or even decades, and do not force biochemistry into highly rigid and narrow thinking, which wastes immense patient time and money.

These books show the issue with mold is what we have known for a very long time — the danger of mycotoxin “powder chemicals” on the spores.

Aspergillus has many species. In my ERMI work, in which this test looks for 36 EPA chosen species by DNA in dust for a mere $200.00, I am finding a significant amount of Aspergillus fumigatus. which has many biotoxins to harm humans and their pets.

Here is a small sample of some applicable articles.

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[Article in Polish]

Buczyńska A, Cyprowski M, Piotrowska M, Szadkowska-Stańczyk I.

Załdad Srodowiskowych Zagrozeń Zdrowia, Instytut Medycyny Pracy im. prof. J. Nofera, Łódź. alina@imp.lodz.pl

BACKGROUND: The aim of the study was to quantitatively and qualitatively identify moulds occurring in the air of selected office rooms. MATERIAL AND METHODS: The study was conducted in the wintertime inside four office rooms with moisture trace and one control room. To assess mycological contamination of the air, triple samples were directly collected on Petri dishes (Malt Extract Agar medium) using a Burkard air sampler. Qualitative evaluation of moulds was based on the microscopic view and morphological features of colonies. RESULTS: Total number of moulds determined in the air of office rooms did not exceed the level of 4 x 10(2) cfu/m3. The highest concentration of moulds (3.44 x 10(2) cfu/m3) was found in the room that was also used as an archive. It was over tenfold higher than in the control room (0.33 x 10(2) cfu/m3). The qualitative analysis of moulds showed the presence of 15 species. Some of them, including Aspergillus fumigatus, Aspergillus versicolor, Aspergillus ochraceus, Cladosporium spp., Penicillium spp. and Alternaria spp., are recognized as potential health hazards to workers due to the production of mycotoxins and allergic reactions. CONCLUSIONS: The archive was the only room, where concentration of moulds slightly exceeded the reference value. To protect the health of workers who perform their duties in this place, the documents, which are an ideal place of mould growth, should be moved to a separate room. Respiratory complaints reported by workers could be associated with concentrations and species of moulds found in the office rooms under study.

Publication Types:

• English Abstract

PMID: 18421934 [PubMed - indexed for MEDLINE]

2: Mycologia. 2007 Nov-Dec;99(6):804-11.

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Association of ergot alkaloids with conidiation in Aspergillus fumigatus.

Coyle CM, Kenaley SC, Rittenour WR, Panaccione DG.

Division of Plant & Soil Sciences, West Virginia University, P.O. Box 6108, Morgantown, West Virginia 26506-6108, USA.

Ergot alkaloids are mycotoxins that affect the nervous and reproductive systems of exposed individuals through interactions with monoamine receptors. They have been studied more widely in ergot fungi and grass endophytes but also are found in Aspergillus fumigatus, an opportunistic human pathogen that reproduces and disseminates exclusively through conidia. The ergot alkaloids festucla-vine and fumigaclavines A, B and C are present in or on conidia of A. fumigatus. Cultures of the fungus that are free of conidia are difficult to obtain, obscuring comparisons of conidia versus vegetative hyphae as sources of the ergot alkaloids. To create conidiation-deficient strains of A. fumigatus we manipulated the bristle A gene (brlA), which controls vesicle formation or budding growth necessary for conidiation in Aspergillus spp. Disruption of brlA in A. fumigatus, via homologous recombination, resulted in a nonconidiating mutant that produced bristle-like structures instead of conidiophores and conidia. Moreover the disrupted strain failed to produce ergot alkaloids as verified by HPLC analyses. Complementation with a wild-type allele restored conidiation and ergot alkaloid production. These results suggest that ergot alkaloids are not produced within the vegetative mycelium of the fungus and are associated directly with conidiation.

Publication Types:

• Research Support, U.S. Gov’t, Non-P.H.S.

PMID: 18333504 [PubMed - indexed for MEDLINE]

3: Ann Agric Environ Med. 2007 Dec;14(2):229-32.

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Mycological flora on tree fruits, crust, leaves and pollen Sorbus domestica L.

Kacániová M, Fikselová M.

Department of Microbiology, Slovak University of Agriculture in Nitra, Faculty of Biotechnology and Food Sciences, Tr. A. Hlinku 2, 949 71 Nitra, Slovak Republic. kacaniov@afnet.uniag.sk

Plant-microbial interactive relations with respect to determine mycoflora of the Sorbus domestica L.–fruits, crust, leaves and pollen were studied in 2 Slovak regions. On the fruit samples the genera Alternaria, Botrytis, Cladosporium, Mucor and Penicillium occurred, on the leaves the genera Alternaria, Cladosporium and Penicillium prevailed and on crust the genera Alternaria, Cladosporium, Penicillium and Trichoderma appeared to be dominant, respectively. Isolates from the Sorbus domestica L. fruits were present by 11 genera and 13 species of microscopic fungi and isolates from pollen such as Alternaria, Botrytis, Cladosporium, Penicillium, Mycelia, Mucor and Trichoderma appeared to be the most frequently occurring genera. On the basis of further taxonomic determination, from the genera Aspergillus were isolated and identified representatives of species A. clavatus, A. fumigatus, A. niger, A. ochraceus, A. terreus. It is necessary to point out that the isolated genera Aspergillus and Penicillium are considered as the most important producers of mycotoxins.

Publication Types:

• Research Support, Non-U.S. Gov’t

PMID: 18247456 [PubMed - indexed for MEDLINE]

4: Int J Food Microbiol. 2008 Feb 29;122(1-2):85-92. Epub 2007 Nov 29.

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Mycoflora and ochratoxin A producing strains of Aspergillus in Algerian wheat.

Riba A, Mokrane S, Mathieu F, Lebrihi A, Sabaou N.

Laboratoire de Recherche sur les Produits Bioactifs et la Valorisation de la Biomasse, Ecole Normale Supérieure de Kouba, BP 92 16050 Vieux Kouba, Alger, Algeria.

Wheat is a basic staple food for very large segments of the population of Algeria. The aim of this study is to analyse ochratoxin A (OTA)-producing mould and OTA-contaminated wheat. To evaluate the mycoflora and the potential for OTA production by Aspergillus strains, a total of 85 samples of wheat destined for human consumption were collected from two regions in Algeria (Tizi Ouzou and Setif) during the following phases: preharvest, storage in silos, and after processing. The mean value counts of fungi ranged from 275 to 1277 CFU g(-1). The dominant genus was Aspergillus, predominantly A. flavus, A. niger and A. versicolor. The other isolated species were A. ochraceus, A. alliaceus, A. carbonarius, A. terreus, A. fumigatus, A. candidus and Aspergillus spp. The occurrence and the levels of the genus Penicillium, Fusarium, Alternaria and Mucor were substantially lower than those of Aspergillus. The storage in silos shows high levels of Aspergillus (66 to 84%), especially A. flavus, but A. niger and other fungi were isolated at relatively low percentages. Equal distribution of the fungal contamination into the bran, flour and semolina fractions was observed from Flour Mill and Semolina Mill. The genus Aspergillus remained present at high levels at several phases of the production process. In addition, the ability to produce OTA by 135 isolates belonging to eleven species of Aspergillus and 23 isolates of Penicillium spp. was analyzed using fluorescent detection-based HPLC. Thus, it was found that 51 isolates (32.3%) were ochratoxigenic. All isolated strains of A. ochraceus (12) and A. alliaceus (6) produced OTA at concentrations ranging from 0.23 to 11.50 microg g(-1). Most of the A. carbonarius strains (80%) were OTA producers (0.01 to 9.35 microg g(-1)), whereas A. terreus (50%), A. niger (28%), A. fumigatus (40%), A. versicolor (18%) and Penicillium spp. (21.7%) were low level producers (0.01 to 0.07 microg g(-1)). The concentration of OTA was determined in 30 samples of wheat. OTA was detected in 12 (40%) of the samples at levels ranging from 0.21 to 41.55 microg kg(-1).

PMID: 18083262 [PubMed - indexed for MEDLINE]

5: Food Chem Toxicol. 2007 Dec;45(12):2420-5. Epub 2007 Jun 22.

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Toxigenic fungi and mycotoxins in mature corn silage.

Richard E, Heutte N, Sage L, Pottier D, Bouchart V, Lebailly P, Garon D.

Groupe Régional d’Etudes sur le Cancer, GRECAN-EA 1772, Université de Caen Basse-Normandie, Centre François Baclesse, Avenue Général Harris, BP 5026, 14076 Caen Cedex 05, France.

To investigate the exposure of livestock and farm workers to mycotoxins during the last months of silage use, the mycoflora and the mycotoxins in a mature silage (11-months-old) were studied. A multimycotoxin method was developed to evaluate the toxigenic in vitro ability of fungal strains. The screening of potentially toxigenic fungi isolated from the mature silage showed that six Fusaria (Fusarium culmorum, Fusarium equiseti, Fusarium graminearum, Fusarium oxysporum, Fusarium solani and Fusarium verticillioides) and one Aspergillus (Aspergillus fumigatus) were able to produce mycotoxins on nutrient agar. Seven major mycotoxins (aflatoxin B(1), citrinin, deoxynivalenol, fumonisin B(1), gliotoxin, ochratoxin A and zearalenone) were also searched in the corn silage by high-performance liquid chromatography coupled to mass spectrometry (HPLC-MS). Among the three mycotoxins (citrinin, gliotoxin and deoxynivalenol) detected in the silage, gliotoxin, a strongly immunosuppressive mycotoxin, occurred in the mature silage at level up to 877 ppb, which was associated with the presence of A. fumigatus in the silage.

Publication Types:

• Evaluation Studies
• Research Support, Non-U.S. Gov’t

PMID: 17655998 [PubMed - indexed for MEDLINE]

6: J Leukoc Biol. 2007 Oct;82(4):839-48. Epub 2007 Jul 11.

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Effects of Aspergillus fumigatus gliotoxin and methylprednisolone on human neutrophils: implications for the pathogenesis of invasive aspergillosis.

Orciuolo E, Stanzani M, Canestraro M, Galimberti S, Carulli G, Lewis R, Petrini M, Komanduri KV.

Department of Oncology, Transplant and Advances in Medicine, University of Pisa, Italy. orci@sssup.it

Aspergillus fumigatus (AF) is a ubiquitous mold and the most common cause of invasive aspergillosis (IA) in immunocompromised patients. In stem cell transplant recipients, IA now occurs most frequently in the setting of therapy with corticosteroids, including methylprednisolone (MP). We showed previously that gliotoxin (GT), an AF-derived mycotoxin, induces apoptosis in monocytes and dendritic cells, resulting in the suppression of AF-specific T cell responses. We examined the ability of GT to induce apoptosis in polymorphonuclear leukocytes (PMN) and assessed GT effects on important neutrophil functions, including phagocytic function, degranulation, myeloperoxidase activity, and the production of reactive oxygen species (ROS). In contrast to its effects on monocytes, PMN remained resistant to GT-mediated apoptosis. Although many essential neutrophil functions were unaffected, GT inhibited phagocytosis and also induced a decrease in ROS generation by PMN. In contrast, MP therapy potentiated ROS production, suggesting a mechanism that may facilitate tissue injury in IA. Distinct from its effects on untreated PMN, GT augmented ROS production in MP-treated PMN. Our results suggest that although GT may suppress the adaptive immune response, GT may also serve to increase PMN-mediated inflammation, which is likely to play an important role in tissue destruction in the setting of IA.

Publication Types:

• Research Support, N.I.H., Extramural
• Research Support, Non-U.S. Gov’t

PMID: 17626149 [PubMed - indexed for MEDLINE]

7: Eukaryot Cell. 2007 Sep;6(9):1562-9. Epub 2007 Jun 29.

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Gliotoxin is a virulence factor of Aspergillus fumigatus: gliP deletion attenuates virulence in mice immunosuppressed with hydrocortisone.

Sugui JA, Pardo J, Chang YC, Zarember KA, Nardone G, Galvez EM, Müllbacher A, Gallin JI, Simon MM, Kwon-Chung KJ.

Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20892, USA.

Gliotoxin is an immunosuppressive mycotoxin long suspected to be a potential virulence factor of Aspergillus fumigatus. Recent studies using mutants lacking gliotoxin production, however, suggested that the mycotoxin is not important for pathogenesis of A. fumigatus in neutropenic mice resulting from treatment with cyclophosphomide and hydrocortisone. In this study, we report on the pathobiological role of gliotoxin in two different mouse strains, 129/Sv and BALB/c, that were immunosuppressed by hydrocortisone alone to avoid neutropenia. These strains of mice were infected using the isogenic set of a wild type strain (B-5233) and its mutant strain (gliPDelta) and the the glip reconstituted strain (gliP(R)). The gliP gene encodes a nonribosomal peptide synthase that catalyzes the first step in gliotoxin biosynthesis. The gliPDelta strain was significantly less virulent than strain B-5233 or gliP(R) in both mouse models. In vitro assays with culture filtrates (CFs) of B-5233, gliPDelta, and gliP(R) strains showed the following: (i) deletion of gliP abrogated gliotoxin production, as determined by high-performance liquid chromatography analysis; (ii) unlike the CFs from strains B-5233 and gliP(R), gliPDelta CFs failed to induce proapoptotic processes in EL4 thymoma cells, as tested by Bak conformational change, mitochondrial-membrane potential disruption, superoxide production, caspase 3 activation, and phosphatidylserine translocation. Furthermore, superoxide production in human neutrophils was strongly inhibited by CFs from strain B-5233 and the gliP(R) strain, but not the gliPDelta strain. Our study confirms that gliotoxin is an important virulence determinant of A. fumigatus and that the type of immunosuppression regimen used is important to reveal the pathogenic potential of gliotoxin.

Publication Types:

• Research Support, N.I.H., Intramural
• Research Support, Non-U.S. Gov’t

PMID: 17601876 [PubMed - indexed for MEDLINE]
PMCID: PMC2043361

8: Int J Med Microbiol. 2008 Apr;298(3-4):319-27. Epub 2007 Jun 15.

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Gliotoxin production by clinical and environmental Aspergillus fumigatus strains.

Kupfahl C, Michalka A, Lass-Flörl C, Fischer G, Haase G, Ruppert T, Geginat G, Hof H.

Faculty for Clinical Medicine Mannheim, University of Heidelberg, Institute for Medical Microbiology and Hygiene, Theodor-Kutzer-Ufer 1-3, D-68167 Mannheim, Germany. claudio.kupfahl@imh.ma.uni-heidelberg.de

The mycotoxin gliotoxin is produced by fungi of the genus Aspergillus, including the important human pathogen Aspergillus fumigatus. Gliotoxin exerts a broad spectrum of immunosuppressive effects in vitro and is detectable in the sera of patients suffering from invasive aspergillosis. In order to correlate the pathogenic potential of A. fumigatus with the ability to produce gliotoxin and to investigate the taxonomic distribution of gliotoxin-producing Aspergillus strains among clinical isolates, a total of 158 Aspergillus isolates comprising four different species (A. fumigatus, n=100; A. terreus, n=27; A. niger, n=16; A. flavus, n=15) were collected from different medical centers (some originating from probable cases of aspergillosis) and from environmental samples in Germany and Austria. Remarkably, gliotoxin was detected in most culture filtrates of A. fumigatus of both clinical (98%) and environmental (96%) origin. The toxin was also detected, with decreasing frequency, in culture filtrates of A. niger (56%), A. terreus (37%), and A. flavus (13%). The highest gliotoxin concentrations were detected in A. fumigatus strains of clinical (max. 21.35 microg/ml, mean 5.75 microg/ml) and environmental (max. 26.25 microg/ml, mean 5.27 microg/ml) origin. Gliotoxin productivity of other Aspergillus species was significantly lower. Culture supernatants of A. fumigatus strains lacking gliotoxin production showed a significantly lower cytotoxicity on macrophage-like cells and T-cells in vitro. In contrast, lack of gliotoxin production in the other Aspergillus species tested had no significant influence on the cytotoxic effect of culture supernatant on these immune cells.

PMID: 17574915 [PubMed - indexed for MEDLINE]

9: Microbiology. 2007 Jun;153(Pt 6):1677-92.

Related Articles, Links

Aspergillus flavus: human pathogen, allergen and mycotoxin producer.

Hedayati MT, Pasqualotto AC, Warn PA, Bowyer P, Denning DW.

Department of Medical Mycology and Parasitology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran.

Aspergillus infections have grown in importance in the last years. However, most of the studies have focused on Aspergillus fumigatus, the most prevalent species in the genus. In certain locales and hospitals, Aspergillus flavus is more common in air than A. fumigatus, for unclear reasons. After A. fumigatus, A. flavus is the second leading cause of invasive aspergillosis and it is the most common cause of superficial infection. Experimental invasive infections in mice show A. flavus to be 100-fold more virulent than A. fumigatus in terms of inoculum required. Particularly common clinical syndromes associated with A. flavus include chronic granulomatous sinusitis, keratitis, cutaneous aspergillosis, wound infections and osteomyelitis following trauma and inoculation. Outbreaks associated with A. flavus appear to be associated with single or closely related strains, in contrast to those associated with A. fumigatus. In addition, A. flavus produces aflatoxins, the most toxic and potent hepatocarcinogenic natural compounds ever characterized. Accurate species identification within Aspergillus flavus complex remains difficult due to overlapping morphological and biochemical characteristics, and much taxonomic and population genetics work is necessary to better understand the species and related species. The flavus complex currently includes 23 species or varieties, including two sexual species, Petromyces alliaceus and P. albertensis. The genome of the highly related Aspergillus oryzae is completed and available; that of A. flavus in the final stages of annotation. Our understanding of A. flavus lags far behind that of A. fumigatus. Studies of the genomics, taxonomy, population genetics, pathogenicity, allergenicity and antifungal susceptibility of A. flavus are all required.

Publication Types:

• Research Support, N.I.H., Extramural
• Research Support, Non-U.S. Gov’t
• Review

PMID: 17526826 [PubMed - indexed for MEDLINE]

10: Mycopathologia. 2007 May;163(5):249-60. Epub 2007 Mar 28.

Related Articles, Links

Occurrence of ochratoxin A and ochratoxigenic mycoflora in corn and corn based foods and feeds in some South American countries.

Magnoli CE, Astoreca AL, Chiacchiera SM, Dalcero AM.

Departamento de Microbiología e Inmunología, Facultad de Ciencias Exactas Físico Químicas y Naturales, Universidad Nacional de Río Cuarto, Ruta Nacional 36, km 601, Rio Cuarto, 5800, Cordoba, Argentina. cmagnoli@exa.unrc.edu.ar

Cereals and cereal- derived products constitute the base of human and animal feeding in South American countries. This review attempts to give an overview of the ochratoxin A (OTA) occurrence and potential sources of OTA contamination in those products. The environmental conditions as humidity and temperature in the colonization of the substrates by Aspergillus section Nigri isolated from corn kernels were also discussed. The available information on the ochratoxigenic mycoflora and OTA presence in corn, corn based food and feed is limited. Only few surveys have been carried out in Argentina, Ecuador and Brazil; which showed that Aspergillus niger aggregate and A. ochraceus species would be the main source of OTA. It’s possible to emphasize that, the species A. carbonarius has not been isolated from these substrates and Penicillium verrucosum was isolated only from pig feeds of Argentinean samples in low percentage. Studies about the ecophysiology of ochratoxigenic fungi and OTA occurrence are in progress in Latin America to reduce the impact of this toxin in the food chain.

Publication Types:

• Research Support, Non-U.S. Gov’t
• Review

PMID: 17390233 [PubMed - indexed for MEDLINE]

11: BMC Microbiol. 2007 Jan 23;7:5.

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Verruculogen associated with Aspergillus fumigatus hyphae and conidia modifies the electrophysiological properties of human nasal epithelial cells.

Khoufache K, Puel O, Loiseau N, Delaforge M, Rivollet D, Coste A, Cordonnier C, Escudier E, Botterel F, Bretagne S.

Laboratoire de Parasitologie-Mycologie, Hôpital Henri Mondor (AP-HP), Université Paris 12, and UMR BIPAR 956, Créteil, France. k_khoufache@yahoo.fr <k_khoufache@yahoo.fr>

BACKGROUND: The role of Aspergillus fumigatus mycotoxins in the colonization of the respiratory tract by conidia has not been studied extensively, even though patients at risk from invasive aspergillosis frequently exhibit respiratory epithelium damage. In a previous study, we found that filtrates of A. fumigatus cultures can specifically alter the electrophysiological properties of human nasal epithelial cells (HNEC) compared to those of non pathogenic moulds. RESULTS: We fractionated the organic phase of filtrate from 3-day old A. fumigatus cultures using high-performance liquid chromatography. The different fractions were tested for their ability to modify the electrophysiological properties of HNEC in an in vitro primary culture model.The fraction collected between 20 and 30 min mimicked the effects of the whole filtrate, i.e. decrease of transepithelial resistance and increase of potential differences, and contained secondary metabolites such as helvolic acid, fumagillin, and verruculogen. Only verruculogen (10(-8) M) had effects similar to the whole filtrate. We verified that verruculogen was produced by a collection of 67 human, animal, plant and environmental A. fumigatus isolates. Using MS-MS analysis, we found that verruculogen was associated with both mycelium and conidia extracts. CONCLUSION: Verruculogen is a secondary metabolite that modifies the electrophysiological properties of HNEC. The role of these modifications in the colonization and invasion of the respiratory epithelium by A. fumigatus on first contact with the epithelium remains to be determined.

Publication Types:

• Research Support, Non-U.S. Gov’t

PMID: 17244350 [PubMed - indexed for MEDLINE]
PMCID: PMC1797047

12: Microbes Infect. 2007 Jan;9(1):47-54. Epub 2006 Dec 12.

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Gliotoxin from Aspergillus fumigatus affects phagocytosis and the organization of the actin cytoskeleton by distinct signalling pathways in human neutrophils.

Coméra C, André K, Laffitte J, Collet X, Galtier P, Maridonneau-Parini I.

INRA UR 66 Laboratoire de Pharmacologie et Toxicologie, 180 chemin de Tournefeuille, 31931 Toulouse Cedex 9, France. christine.comera@toulouse.inserm.fr

Gliotoxin is a mycotoxin having a considerable number of immuno-suppressive actions and is produced by several moulds such as Aspergillus fumigatus. In this study, we investigated its toxic effects on human neutrophils at concentrations corresponding to those found in the blood of patients with invasive aspergillosis. Incubation of the cells for 10min with 30-100ng/ml of gliotoxin inhibited phagocytosis of either zymosan or serum-opsonized zymosan without affecting superoxide production or the exocytosis of specific and azurophil granules. Gliotoxin also induced a significant re-organization of the actin cytoskeleton which collapsed around the nucleus leading to cell shrinkage and the disappearance of filopodia. This gliotoxin-induced actin phenotype was reversed by the cAMP antagonist Rp-cAMP and mimicked by pCPT-cAMP indicating that it probably resulted from the deregulation of intracellular cAMP homeostasis as previously described for gliotoxin-induced apoptosis. By contrast, gliotoxin-induced inhibition of phagocytosis was not reversed by Rp-cAMP but by arachidonic acid, another member of a known signalling pathway affected by the toxin. This suggests that gliotoxin can affect circulating neutrophils and favour the dissemination of A. fumigatus by inhibiting phagocytosis and the consequent killing of conidia.

Publication Types:

• Research Support, Non-U.S. Gov’t

PMID: 17196420 [PubMed - indexed for MEDLINE]

13: Alkaloids Chem Biol. 2006;63:45-86.

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Ergot alkaloids–biology and molecular biology.

Schardl CL, Panaccione DG, Tudzynski P.

Department of Plant Pathology, University of Kentucky, Lexington, KY 40546-0312, USA.

EA have been a major benefit, and a major detriment, to humans since early in recorded history. Their medicinal properties have been used, and continue to be used, to aid in childbirth, with new uses being found in the treatment of neurological and cardiovascular disorders. The surprisingly broad range of pharmaceutical uses for EA stems from their affinities for multiple receptors for three distinct neurotransmitters (serotonin, dopamine, and adrenaline), from the great structural diversity of natural EA, and from the application of chemical techniques that further expand that structural diversity. The dangers posed by EA to humans and their livestock stem from the ubiquity of ergot fungi (Claviceps species) as parasites of cereals, and of related grass endophytes (Epichloë, Neotyphodium, and Balansia species) that may inhabit pasture grasses and produce toxic levels of EA. Further concerns stem from saprophytic EA producers in the genera Aspergillus and Penicillium, especially A. fumigatus, an opportunistic pathogen of humans. Numerous fungal species produce EA with a wide variety of structures and properties. These alkaloids are associated with plants in the families Poaceae, Cyperaceae, and Convolvulaceae, apparently because these plants can have symbiotic fungi that produce EA. Pharmacological activities of EA relate to their specific structures. Known as potent vasoconstrictors, the ergopeptines include a lysergic acid substituent with an amide linkage to a complex cyclol-lactam ring structure generated from three amino acids. Simpler lysergyl amides and clavines are more apt to have oxytonic or psychotropic activities. One of the lysergyl amides is LSD (5), the most potent hallucinogen known. The EA biosynthetic pathway in Claviceps species has been studied extensively for many decades, and recent studies have also employed epichloës and A. fumigatus. The early pathway, shared among these fungi, begins with the action of an aromatic prenyl transferase, DMATrp synthase, which links a dimethylallyl chain to L-tryptophan. When the dmaW gene encoding DMATrp synthase was cloned and sequenced, the predicted product bore no identifiable resemblance to other known prenyl transferases. The dma W genes of Claviceps species are present in clusters of genes, several of which also have demonstrated roles in EA biosynthesis. In many other fungi, dma W homologues are identifiable in otherwise very different gene clusters. The roles of DMA Trp synthase homologues in these other fungi are probably quite variable. One of them is thought to prenylate the phenolic oxygen of L-tyrosine, and another catalyzes the unusual reverse prenylation reaction in the biosynthesis of fumigaclavine C(10), an EA characteristic of A. fumigatus. The second step of the EA pathway is N-methylation of DMATrp (12) to form 13, which is then subjected to a series of oxidation/oxygenation and reduction reactions to generate, in order, chanoclavine-I (16), agroclavine (19), and elymoclavine (6). Shunt reactions generate a wide variety of other clavines. Two epimerizations occur in this pathway: one from 12 to 16, the other from 16 to 19. Further oxidation of 6, catalyzed by the cytochrome-P450 CloA, generates lysergic acid (1). An unusual NRPS complex, lysergyl peptide synthetase (LPS), is responsible for linking 1 to three hydrophobic L-amino acids to generate the ergopeptide lactams. The LPS complex includes two polypeptides, one (LPS 2) possessing a single module for activation of 1, and the other (LPS 1) possessing three modules, each specifying one of the L-amino acids. Variations in LPS 1 sequences are associated with variations in the incorporated amino acids, leading to differences between strain chemotypes, and even multiple ergopeptines within strains. For example, C. purpurea P1 produces two distinct ergopeptines (ergotamine (4) and ergocryptine (Table I)), each of which is believed to be generated by multiple LPS 1 subunits encoded by separate, but related, genes (lpsA1 and lpsA2). The main ecological roles of EA in nature are probably to protect the fungi from consumption by vertebrate and invertebrate animals. The EA produced by plant-symbiotic fungi (such as epichloë endophytes) may protect the fungus by protecting the health and productivity of the host, which may otherwise suffer excessive grazing by animals. The EA, at levels typical of plants bearing these symbionts, can negatively affect the health of large mammals as well herbivorous insects. Some clavines have substantial anti-bacterial properties, which might protect the fungus and, in some cases, their host plants from infection. However, the fact that a large number of epichloë, and even several Claviceps species, produce no detectable EA indicates that the selection for their production is not universal. An unfortunate fact for many livestock producers is that some of the most popular forage grasses tend to possess EA-producing epichloë endophytes. Such endophytes are easily eliminated, but confer such fitness enhancements to their hosts that their presence is often preferred, despite the toxic EA. The future looks promising for continued interest in EA. Research continues into their pharmacological properties, medicinal uses, and structure-function relationships. New clavines and lysergic acid derivatives are identified regularly from new sources, such as marine animals. Also, programs are well underway to modify or replace epichloë endophytes of forage grasses in order to produce new grass cultivars that lack these toxins.

Publication Types:

• Research Support, Non-U.S. Gov’t
• Research Support, U.S. Gov’t, Non-P.H.S.
• Review

PMID: 17133714 [PubMed - indexed for MEDLINE]

14: Ann Agric Environ Med. 2006;13(1):147-61.

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Toxic micromycetes in grain raw material during its processing.

Lugauskas A, Raila A, Railiene M, Raudoniene V.

Laboratory of Biodeterioration Research, Institute of Botany, Zaliuju ezeru 49, LT-08406 Vilnius, Lithuania. lugauskas@botanika.lt

In 2003-2005 micromycetes were isolated and identified from wheat, barley, rye, buckwheat grain brought into mills or from processing enterprises. Contamination of the produced flour with micromycete propagules (cfu g(-1)), changes in micromycete diversity and abundance in the course of flour storage, preparation and baking of bread, production of groats or other food products and fodder were determined. Most attention was given to widely distributed micromycetes, known producers of toxins: Alternaria alternata, Aspergillus candidus, A. clavatus, A. flavus, A. fumigatus, A. niger, A. oryzae, A. (=Eurotium) repens, Fusarium culmorum, F. equiseti, F. graminearum, F. moniliforme, F. oxysporum, F. poae, F. sporotrichioides, Penicillium brevicompactum, P. chrysogenum, P. cyclopium, P. daleae, P. expansum, P. funiculosum, P. roqueforti, P. urticae, P. verruculosum, P. viridicatum, Phoma exiqua, Rhizomucor pusillus, Rhizopus stolonifer, Trichothecium roseum. Abilities of these micromycetes to produce secondary toxic metabolites were determined as well as possible hazard caused to people consuming the contaminated products.

Publication Types:

• Research Support, Non-U.S. Gov’t

PMID: 16841886 [PubMed - indexed for MEDLINE]

15: J Med Microbiol. 2006 Jul;55(Pt 7):913-8.

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Effect of N-chlorotaurine on Aspergillus, with particular reference to destruction of secreted gliotoxin.

Reeves EP, Nagl M, O’Keeffe J, Kelly J, Kavanagh K.

Medical Mycology Unit, National Institute for Cellular Biotechnology, Department of Biology, NUI Maynooth, Co. Kildare, Ireland. emer.reeves@nuim.ie

The fungistatic and fungicidal activity of N-chlorotaurine (NCT), a long-lived oxidant produced by stimulated neutrophils, was investigated. Physiological concentrations (75-100 microM) of NCT showed clear fungicidal activity against a range of Aspergillus isolates. Moreover, killing by NCT was significantly increased in the presence of ammonium chloride, explained by the formation of monochloramine by halogenation of ammonium. One clinical isolate of Aspergillus fumigatus was characterized for the production of the immunosuppressive agent gliotoxin, and NCT was shown to cause destruction of gliotoxin, possibly via reduction of the disulphide bridge. Because of its endogenous nature and its high antifungal activity, NCT appears to be a good choice for topical treatment of Aspergillus infections, and the results of this study further substantiate its therapeutic efficacy.

Publication Types:

• Research Support, Non-U.S. Gov’t

PMID: 16772419 [PubMed - indexed for MEDLINE]

16: J Microbiol Methods. 2006 Aug;66(2):286-93. Epub 2006 Jan 31.

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A new and rapid bioassay for the detection of gliotoxin and related epipolythiodioxopiperazines produced by fungi.

Grovel O, Kerzaon I, Petit K, Robiou Du Pont T, Pouchus YF.

S.M.A.B., Universit̩ de Nantes, P̫le Mer et Littoral РFacult̩ de Pharmacie, BP53508- 44035 Nantes cedex 01, France. olivier.grovel@univ-nantes.fr

Gliotoxin is an immunosuppressive cytotoxin produced by numerous environmental or pathogenic fungal species. For this reason, it is one of the mycotoxins which must be systematically searched for in samples for biological control. In this study, a new, rapid and sensitive method for detecting gliotoxin has been developed. This bioassay is based on the induction of morphological changes in cultured cells (human KB cell line) by gliotoxin. Interpretation of the assay can be carried out after 1 h of incubation, either by direct microscopic observation, or with an automated microplate-reader at 630 nm. The limit of detection is 18-20 ng of gliotoxin in the well, depending on the used observation method. A high degree of specificity of the detection is brought about by the ability of the reducing reactant dithiothreitol to inhibit the biological activities of epipolythiodioxopiperazines (ETPs), such as gliotoxin, by reducing their polysulfide bridge. The bioassay allows a rapid primary screening of samples and a semi-quantitative evaluation of the gliotoxin concentration in extracts. The method has been used to study the gliotoxin production by different fungal strains, allowing to highlight 3 strains of Aspergillus fumigatus producing gliotoxin in various extracts.

PMID: 16451813 [PubMed - indexed for MEDLINE]

17: J Microbiol Methods. 2006 Jul;66(1):170-3. Epub 2006 Jan 18.

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Quantification of phagocytosis of Aspergillus conidia by macrophages using a novel antibody-independent assay.

Luther K, Rohde M, Heesemann J, Ebel F.

Max-von-Pettenkofer-Institut, Ludwig-Maximilians-Universität, Pettenkofer-Strasse 9a, 80336 Munich, Germany.

The pathogenic mould Aspergillus fumigatus can cause severe infections in immunocompromised patients. Phagocytosis of inhaled conidia is an early and crucial event in the defense of A. fumigatus infections. Here we describe a novel antibody-independent assay for quantification of phagocytosis, that in this study has been applied to different Aspergillus species, but that is in principle suitable for many fungi.

Publication Types:

• Research Support, Non-U.S. Gov’t

PMID: 16412526 [PubMed - indexed for MEDLINE]

18: Acta Pharm. 2005 Dec;55(4):365-75.

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Mycotoxigenicity of clinical and environmental Aspergillus fumigatus and A. flavus isolates.

Kosalec I, Pepeljnjak S.

Department of Microbiology Faculty of Pharmacy and Biochemistry University of Zagreb, Zagreb, Croatia. ikosalec@pharma.hr

Clinical isolates of fifty strains of A. fumigatus and 30 strains of A. flavus from immmunocompromised patients from the hematological unit were analyzed for mycotoxin production and compared with the same number of environmental isolates (from soil, compost, and air). Only 9 (18%) strains of A. fumigatus produced gliotoxin in a mean concentration 2.22 mg mL-1 (range 0.5-5 mg mL-1). Aflatoxin B1 was detected in 7 (23%) isolates (range from 0.02 to 1.2 mg L-1) and aflatoxin G1 in one (3%) of clinical A. flavus isolates (0.12 mg L-1). In the group of environmental isolates, 11 (37%) were positive for aflatoxin B1 production (range from 0.02 to 1.2 mg L-1) and one for aflatoxin G1 (0.02 mg L-1). Bioautoantibiogram (“bioassay in situ”) on TLC plates against Bacillus subtilis NCTC 8236 showed that only gliotoxin-producing strains have bactericidal activity of Rf values corresponding to gliotoxin. The secondary-metabolite profiles of clinical and environmental A. fumigatus and A. flavus isolates were homogeneous, except for gliotoxin production, which was detected only in the group of clinical isolates of A. fumigatus (18%).

Publication Types:

• Comparative Study

PMID: 16375826 [PubMed - indexed for MEDLINE]

19: Acta Pharm. 2005 Dec;55(4):357-64.

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Verruculogen production in airborne and clinical isolates of Aspergillus fumigatus Fres.

Kosalec I, Klarić MS, Pepeljnjak S.

Department of Microbiology Faculty of Pharmacy and Biochemistry University of Zagreb, Zagreb, Croatia. ikosalec@pharma.hr

Among airborne aspergilli sampled in outdoor air of the Zagreb area (2002/2003), Aspergillus niger (v. Teigh.) and A. fumigatus (Fres.) were the most abundant species (20-30%), with low mean annual concentrations (0.21-1.04 CFU m-3). Higher concentrations of A. fumigatus were observed in autumn and winter (0.5-1.05 CFU m-3) than in spring and summer (0-0.4 CFU m-3). On the other hand, A. fumigatus was found to be the most frequent isolate from upper and/or lower respiratory tracts of imunocompromised patients in many studies. This species produces several mycotoxins, including the tremorgenic mycotoxin verruculogen that can be found in spores and during myceliar growth. Verruculogen production ability was tested on 30 airborne and 33 clinical isolates of A. fumigatus. In both groups, high percentage of verruculogen-producing strains was noticed (84% of airborne and 91% of clinical isolates). Verruculogen production was not significantly different in the groups of airborne isolates (0.34+/-0.16 mg mL-1), and clinical isolates (0.26+/-0.19 mg mL-1).

Publication Types:

• Comparative Study

PMID: 16375825 [PubMed - indexed for MEDLINE]

20: J Clin Microbiol. 2005 Dec;43(12):6120-2.

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Frequency and species distribution of gliotoxin-producing Aspergillus isolates recovered from patients at a tertiary-care cancer center.

Lewis RE, Wiederhold NP, Lionakis MS, Prince RA, Kontoyiannis DP.

University of Houston College of Pharmacy, Texas Medical Center Campus, 1441 Moursund St. #423, Houston, TX 77030, USA. rlewis@uh.edu

Aspergillus isolates (n = 103) collected from cancer patients were screened to determine the taxonomic distribution and quantity of gliotoxin production. Gliotoxin was detected in 93% of Aspergillus fumigatus, 75% of A. niger, 25% of A. terreus, and 4% of A. flavus cultures. Gliotoxin concentrations were highest in cultures of A. fumigatus.

PMID: 16333108 [PubMed - indexed for MEDLINE]

PMCID: PMC1317213

Larvae — are very small (about the size of a pin head) and tan. They feed in late summer, near ground level, on mice, shrews, chipmunks, voles, and other small animals. Larvae can pick up the disease from an infected animal. Peak activity: August.

First, this helpful CDC and NASD image shows the small size of deer ticks and they are not black, it is merely the color of the fonts. They inject a pain killer and an anti-histamine and an anticoagulant to allow for maximized spread of the many types of infections it carries.

It appears that about 2800 per year are infected and meet highly rigid and research oriented criteria from lab tests which have very high false negatives. And even if the kits were not dummied down to a mere two species specific proteins for the M class test, which is an virtually an anti-test, we know from one study 1/40 physicians report Lyme when all the ducks are lined up in the eccentric “real case” research criteria definition.

In my area of Florida we have vast numbers coming from New Jersey for care and to live and vacation. And many have tick and flea-borne infections like Lyme, Babesia or serious atypical Bartonella. The latter two make Lyme cure more complex, then filtered simplistic studies which exclude all the normal complex patients.

Outdoor Workers with High Positive Rates

To evaluate the spread of Lyme disease in New Jersey, we conducted a statewide cross-sectional study of Lyme disease seroprevalence in a high-risk occupational group of outdoor employees. Of the 689 employees who participated in the study, 39 (5.7 percent) were positive for antibody to B. burgdorferi, the causative agent of Lyme disease. Seroprevalence varied markedly by county; unexpectedly high seroprevalence rates were found in several northern counties (Sussex, Hudson, and Hunterdon). Furthermore, some southern counties (Atlantic, Cape May, and Ocean) with large tick populations (as measured by self-reported exposure to ticks) had low seroprevalence rates which were inversely correlated with self-reported preventive practices. These data suggest that Lyme disease, as measured by seroprevalence of antibody to B. burgdorferi, may be spreading beyond the southern portion of the state where it had been previously well documented and that preventive behaviors may play an important role in minimizing the risk of the disease.

Am J Public Health. 1990 October; 80(10): 1225Ð1229.

Lyme disease in New Jersey outdoor workers: a statewide survey of seroprevalence and tick exposure. M D Goldstein, B S Schwartz, C Friedmann, B Maccarillo, M Borbi, and R Tuccillo

SOME SAMPLE CO-INFECTION STUDIES SHOWING THAT TO IGNORE OR TO CASUALLY TEST OR TO TREAT WITH QUESTIONABLE DOSING — BAD MEDICINE

Adelson ME, Rao RV, Tilton RC, Cabets K, Eskow E, Fein L, Occi JL, Mordechai E.

Medical Diagnostic Laboratories L.L.C., 133 Gaither Dr., Suite C, Mt. Laurel, NJ 08054, USA.

PCR analysis of Ixodes scapularis ticks collected in New Jersey identified infections with Borrelia burgdorferi (33.6%), Babesia microti (8.4%), Anaplasma phagocytophila (1.9%), and Bartonella spp. (34.5%). The I. scapularis tick is a potential pathogen vector that can cause coinfection and contribute to the variety of clinical responses noted in some tick-borne disease patients.

PMID: 15184475 [PubMed - indexed for MEDLINE]
PMCID: PMC427842

3: Emerg Infect Dis. 2003 Feb;9(2):184-8.

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Endemic babesiosis in another eastern state: New Jersey.

Herwaldt BL, McGovern PC, Gerwel MP, Easton RM, MacGregor RR.

Centers for Disease Control and Prevention, Atlanta, Georgia 30341-3724, USA. bxh4@cdc.gov

In the United States, most reported cases of babesiosis have been caused by Babesia microti and acquired in the northeast. Although three cases of babesiosis acquired in New Jersey were recently described by others, babesiosis has not been widely known to be endemic in New Jersey. We describe a case of babesiosis acquired in New Jersey in 1999 in an otherwise healthy 53-year-old woman who developed life-threatening disease. We also provide composite data on 40 cases of babesiosis acquired from 1993 through 2001 in New Jersey. The 40 cases include the one we describe, the three cases previously described, and 36 other cases reported to public health agencies. The 40 cases were acquired in eight (38.1%) of the 21 counties in the state. Babesiosis, a potentially serious zoonosis, is endemic in New Jersey and should be considered in the differential diagnosis of patients with fever and hemolytic anemia, particularly in the spring, summer, and early fall.

Publication Types:

• Case Reports

PMID: 12603988 [PubMed - indexed for MEDLINE]

4: J Clin Microbiol. 1999 Jun;37(6):2051-2.

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Southern extension of the range of human babesiosis in the eastern United States.

Eskow ES, Krause PJ, Spielman A, Freeman K, Aslanzadeh J.

The Univeristy of Connecticut, Farmington, USA.

We sought evidence of babesiosis in three residents of New Jersey who were suspected of local acquisition of Babesia microti infection. We tested serial blood samples from these residents for B. microti antibodies and amplifiable DNA by using immunofluorescent antibody and PCR techniques. All three residents experienced symptoms suggestive of acute babesiosis. The sera of each of the patients reacted against babesial antigen at a titer fourfold or higher in sequentially collected blood samples. PCR-amplifiable DNA, characteristic of B. microti, was detected in their blood. These data suggest that human B. microti infections were acquired recently in New Jersey, extending the range of this piroplasmosis in the northeastern United States.

Publication Types:

• Case Reports
• Research Support, U.S. Gov’t, P.H.S.

PMID: 10325378 [PubMed - indexed for MEDLINE]
PMCID: PMC85028

5: Emerg Infect Dis. 1998 Jan-Mar;4(1):97-9.

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Prevalence of tick-borne pathogens in Ixodes scapularis in a rural New Jersey County.

Varde S, Beckley J, Schwartz I.

New York Medical College, Valhalla, New York, USA.

To assess the potential risk for other tick-borne diseases, we collected 100 adult Ixodes scapularis in Hunterdon County, a rapidly developing rural county in Lyme disease endemic western New Jersey. We tested the ticks by polymerase chain reaction for Borrelia burgdorferi, Babesia microti, and the rickettsial agent of human granulocytic ehrlichiosis (HGE). Fifty-five ticks were infected with at least one of the three pathogens: 43 with B. burgdorferi, five with B. microti, and 17 with the HGE agent. Ten ticks were coinfected with two of the pathogens. The results suggest that county residents are at considerable risk for infection by a tick-borne pathogen after an I. scapularis bite.

Publication Types:

• Research Support, U.S. Gov’t, P.H.S.

PMID: 9452402 [PubMed - indexed for MEDLINE]