Archive for the ‘Mycoplasma’ Category

Is Your Child Crazy, or Sick? Mental Illness vs. Medical Disorder

Is your child crazy, or sick? Mental illness vs. medical disorder




Can Lyme Disease Lead to Bladder Problems?

Can Lyme Disease Lead To Bladder Problems?

Lyme disease can cause many disparate symptoms over the course of its progression. It’s often called ‘The Great Imitator’ because many of its generalised symptoms resemble the symptoms of other, more prominent chronic conditions. This makes it very difficult to diagnose, and misdiagnosis rates are suspected to be extremely high. Compounding this is the fact that chronic Lyme is not widely recognised as a legitimate disorder. Despite many thousands of people suffering from long-term Lyme symptoms, hugely different from the accepted acute symptoms, the condition remains an outlier. Therefore, patient and doctor education on Lyme disease in all its forms is not as good as it should be. Many symptoms fall by the wayside because of this, and either go uninvestigated or misdiagnosed. Bladder issues might not be the first thing you associate with Lyme disease; but can Lyme disease cause bladder problems?

What is Lyme disease?

Lyme disease was christened in the town of Old Lyme, Connecticut, in 1975. This is relatively recent for a major disease, which speaks of its insidious nature. Lyme is caused by the bacteria Borrelia burgdorferi, which is spread to humans via the deer (or black-legged) tick in America, and the castor bean tick in Europe. Ticks are conduits of disease-causing bacteria, and often carry many different strains simultaneously. However, not every tick carries Borrelia burgdorferi and not every tick bite from those that do will result in Lyme.

Although the disease is often associated with America, particularly the north-eastern states, it is a global issue. Lyme rates remain alarmingly high in Europe as well as the U.S., with global warming compounding the issue. As the global temperature increases, ticks are able to live longer and migrate further, thereby increasing the instances of Lyme all over the world.

Image by Meli1670 on Pixabay: Despite many thousands of people suffering from long-term Lyme symptoms, the condition remains an outlier.

Acute vs. Chronic Lyme

The initial symptoms of Lyme present much like the flu. They manifest a day or two after the tick bite, and often involve a headache, fatigue, aches and fever – standard flu symptoms. The calling card of Lyme is a distinctive bullseye-shaped rash, which is present at the site of the bite in the majority of cases. If this is present, Lyme can be conclusively diagnosed. However, it is often overlooked, as many times people don’t realise they’ve been bitten. If treated with antibiotics, acute Lyme can be resolved rapidly and successfully for many patients. However, if that window is missed, Lyme will progress to its chronic long-term form, bringing with it a whole host of new, problematic symptoms.

Chronic Lyme represents an interplay between infection symptoms and inflammation symptoms. The former is caused by the underlying Borrelia infection, while the latter is caused by the body’s exaggerated response to the persistent bacteria. Because of this, a wide spectrum of symptoms is possible, varying in severity depending on the patient. The highly resistant Borrelia bacteria can travel and infect various parts of the body, including the neurological system and the pulmonary system.

Can Lyme disease lead to bladder problems?

Can Lyme disease affect your bladder? Some experts say it might. Bladder conditions might seem inferior to more severe issues relating to the brain and heart. But anyone who’s suffered from bladder pain can testify that it’s not a symptom to be taken lightly. The uniform name for frequent urination, bladder pain and inflammation is interstitial cystitis (IC), although a diagnosis of this disorder often means that the root cause is unknown. So does Lyme disease cause interstitial cystitis?

Lyme specialists are claiming there is a frequent crossover between Lyme symptoms and bladder issues, although not many studies have been conducted on this apparent link. There is seemingly also a connection between stomach issues, a common complaint of Lyme patients, and bladder problems. An animal study, conducted in 2006, found that in rodents, Borrelia burgdorferi is most often found in the bladder. While this and the anecdotal evidence are intriguing, it remains an unexplored area in the field of Lyme disease.

Image by Qaudronet_Webdesign on Pixabay: Can Lyme disease cause frequent urination? Some experts are suggesting it might.

Another, more recent study has provided a more concrete link in humans. This one found that voiding dysfunction (a catchall term used to describe poor coordination between the bladder muscle and the urethra) can appear as an early or late stage symptom of Lyme. Micturition (urination) disorders can subsequently occur via two paths. The first involves the Borrelia bacteria directly invading the bladder. The second occurs as a by-product of neuroborreliosis, a symptom of Lyme caused by the Borrelia bacteria breaching the blood-brain barrier and inflaming the brain. This is a serious manifestation of chronic Lyme disease, which has repercussions for many different areas of the body.

Seven out of seven patients who suffered from Lyme encephalomyelitis (inflammation of the brain) reported reflex response problems with their bladders.

While it seems conclusive to say that there is some link between chronic Lyme disease and bladder problems, most doctors won’t have the necessary Lyme education to correctly diagnose it as such. Lyme specialists (like BCA-clinic in Germany) are few and far between; and until more medical professionals are aware of the insidious dangers of chronic Lyme in all its potential forms, patients will continue to suffer sustained misdiagnoses.

Featured image by mohamed_hassan on Pixaba


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People with interstitial cystitis feel like they have a bladder infection that never goes away. It doesn’t respond to antibiotics, and urine cultures are typically negative. Because these patients are often treated repeatedly with antibiotics, however, they frequently end up having chronic urinary tract infections with antibiotic-resistant bacteria induced by taking antibiotics. The condition occurs more often in women than men at a 5:1 ratio.

I’m starting to hear from chronic Lyme patients who suffer from bladder pain and symptoms consistent with IC. I’m also hearing from men with chronic Lyme who have bladder symptoms and chronic prostatitis (chronic infection of the prostate gland).

And, interestingly, remembering back to patients from the past, sufferers of IC frequently had chronic pain in other areas of the body. Many of them also had fatigue and symptoms common to fibromyalgia and chronic Lyme disease.

And, according to Dr. Rawls, a former OBGYN,

This makes me believe there has to be a microbial connection. Borrelia, the microbe commonly associated with Lyme disease, could be a culprit. However, I would lay odds on mycoplasma and a closely related bacterium called ureaplasma. About 75% of chronic Lyme disease sufferers have been found to harbor at least one species of mycoplasma.

According to Garth Nicolson, who’s wife survived a lethal form of bioweaponized Mycoplasma,

90% of evaluated ALS patients had Mycoplasma. 100% of ALS patients with Gulf War Syndrome had Mycoplasma and nearly all of those were specifically the weaponized M. fermentans incognitus.

*One of the hallmark symptoms of Mycoplasma is fatigue*

And the bad news for us is that Nicholson’s experience has found Mycoplasma to be the number one Lyme coinfection, and similar to other coinfections can be supposedly cleared for years only to reappear when conditions are right.

His latest paper on treating Myco:

The bioweaponized form of Mycoplasma was designed to go undetected.  It doesn’t have a cell wall, making it tough to treat.

Zoonotic Diseases & Why We Are So Interested in Bats (Bartonella, Mycoplasma, & Coronavirus)

Zoonotic Diseases and Why We Are So Interested in Bats

Pathogenic Mycoplasma Infections in Chronic Illnesses: General Considerations in Selecting Conventional and Integrative Treatments

Pathogenic Mycoplasma Infections in Chronic Illnesses: General Considerations in Selecting Conventional and Integrative Treatments

Author(s)  Garth L. Nicolson
Department of Molecular Pathology, The Institute for Molecular Medicine, Huntington Beach, California, USA.


The presence of pathogenic mycoplasmas in various chronic illnesses and their successful suppression using conventional and integrative medicine approaches are reviewed. Evidence gathered over the last three decades has demonstrated the presence of pathogenic mycoplasma species in the blood, body fluids and tissues from patients with a variety of chronic clinical conditions: atypical pneumonia, asthma and other respiratory conditions; oral cavity infections; urogenital conditions; neurodegenerative and neurobehavioral diseases; autoimmune diseases; immunosuppressive diseases; inflammatory diseases; and illnesses and syndromes of unknown origin, such as fatiguing illnesses.
Only recently have these small intracellular bacteria received attention as possible causative agents, cofactors or opportunistic infections or co-infections in these and other conditions. Their clinical management is often inadequate, primarily because of missed diagnosis, under- and inadequate treatment and the presence of persister or dormant microorganisms due to biofilm, resistence and other mechanisms.
Pathogenic Mycoplasma species infections have been suppressed slowly by anti-microbial and integrative treatments, resulting in gradual reductions in morbidity, but not in every patient. Even if mycoplasmas are not a cause or an initial trigger for many chronic illnesses, they appear to play important roles in the inception, progression, morbidity and relapse of chronic illnesses in rather large patient subsets. Ignoring such infections can result in failure to achieve eventual patient recovery, even with application of potentially curative treatments.
As Dr. Breitshwerdt is the Bart Guru, Dr. Nicolson is the Mycoplasma King.  Both are involved intimately with pathogens that have changed their lives.  We owe these men a great debt as without their expertise and fortitude, we would be completely in the dark.  To read about Dr. Nicolson’s experience with bioweaponized Mycoplasma read the provocative book, “Project Daylily.”  I notice that he dedicated this article to his deceased wife who survived a lethal mycoplasma infection.
Please refer to the full-length article in the link at the top of the story but I’ve highlighted a few things below on how Mycoplasma evades the immune system as well as effective treatment.  There’s much, much more in the full-length article you should understand.
According to Dr. Nicolson, 80% of Lyme/MSIDS patients also have Mycoplasma.
CFS/ME patients according to PCR have various mycoplasmas.
Excerpt from section 2 on Host Response Systems:
Pathogenic mycoplasmas can evade immune recognition and destruction by undergoing rapid surface antigenic variations [7] [27]. Even with their slow intracellular growth rates, by rapidly altering their cell surface antigenic structures as well as modulating host immune responses, pathogenic mycoplasmas can evade host surveillance mechanisms [7] [27]. This helps explain the chronic nature of mycoplasmal infections and the inability of hosts to completely suppress pathogenic mycoplasmal infections via host responses that are effective against other more rapidly growing bacteria [27].
Excerpt from 4.12 Fatiguing Illnesses:
The most common fatiguing illness is chronic fatigue syndrome (CFS) or myalgic encephalomyelitis. This is an unexplained, long-term, persistent illness characterized by disabling fatigue plus additional signs and symptoms [98] [99]. Most if not all patients with CFS show evidence of chronic viral and bacterial infections (reviewed in [45] [47] ). In fact, the odds ratio for the presence of chronic infections was calculated to be 18.0 (p < 0.001), suggesting that CFS patients have a very high probability of multiple chronic infections [100]. The most commonly found infections (by PCR of blood monocytes) were various pathogenic species of mycoplasmas [100] [101].  M. pneumoniae was the most common mycoplasma species found, followed by M. fermentans, M. hominis, and M. penetrans [101].
Excerpt from Section 5 Treatment of Pathogenic Mycoplasmal Infections:
In many cases mycoplasmal infections are not the definitive infection that defines the condition. An example of this is chronic Lyme disease, a complex clinical condition with Borrelia species as the prominent infectious agent but with other bacterial, parasite, and viral components as co-infections [47] [119] [120] [121]. Pathogenic mycoplasmal co-infections are important in such multiple infection diseases, being present in up to 80% of chronic Lyme diseases cases [120] [122].
Excerpt from Section 5.1 Antimicrobial Treatments:

The conventional antimicrobial treatments of pathogenic mycoplasmal infections usually involve systemic therapy with oral antibiotics, but the choice of antibiotic(s) depends to a certain degree on the mycoplasma species being treated. Since mycoplasmas do not have a cell wall, antibiotics that act on cell wall synthesis are ineffective [2] [3] [7] [40] [50] [59] [124] [125]. Instead, mycoplasmas are treated with anti-microbials that attack their metabolism, replication, synthetic machinery or other specific bacterial targets. Since most mycoplasmas and ureaplasmas are generally sensitive to tetracyclines (doxycycline, minocycline, among others), with some notable exceptions, these should be considered for frontline treatment, and quinolones (ciprofloxacin, sparfloxacin, levofloxacin, ofloxacin, among others) [125] [126] [127] [128] , as alternative treatment. However, M. pneumoniae and M. genitalium strains are especially sensitive to macrolides (azithromycin, clarithromycin, erythromycin, among others), whereas M. hominis strains are usually resistant [126] [127] [128]. Ureaplasmas are moderately susceptible to macrolides [127] [128]. M. hominis and Ureaplasma urealyticum are generally more resistant to tetracyclines than other species [129] [130] , and M. hominis strains have been observed to be resistant to quinolones [131]. Some discussion of these antimicrobials and their uses in treating pathogenic mycoplasmal infections in chronic illnesses can be found in [132] [133] [134].

Treatment of pathogenic mycoplasma infections with oral antibiotics generally involves daily or pulsed treatment, such as every-other-day administration, at the maximum dose recommended for a particular antibiotic [132] [133] [134] [135]. Due to the cyclic nature of mycoplasmal proliferation some organizations recommend every-other-day antibiotic regimens [135].

Another important consideration is antibiotic resistance, which can occur during treatment [132] [138]. A major problem has been the shifting minimum inhibitory dose concentrations required to treat mycoplasmal infections with antibiotics, such as treatment of M. genitalium infections with oral tetracyclines [139]. This requires increasing dose levels or shifting to a different antibiotic regimen [132].

In most chronic illness patients pathogenic mycoplasma infections do not respond quickly to anti-microbial therapy, so long-term therapy must be considered [123] [132] [133] [135].

When antibiotics are used to treat pathogenic mycoplasmal infections, Jarisch-Herxheimer reactions (J-H reactions) usually occur [132] [141]. These are observed as temporary increases in the severity of signs and symptoms, and J-H reactions generally involve fevers, chills, muscle aches, fatigue, skin rashes, pain and other signs and symptoms related to cytokine release [141].

In most patients this has required prolonged treatments that have resulted in very slow recoveries, often requiring a year or more of treatment [48] [121] [123] [132] [133].

There are some alternative procedures that can increase the in vivo effectiveness of antimicrobial therapies. One method that has been used to increase the effectiveness of antibiotics has been the use of agents that increase the penetrability or the intracellular activities or effectiveness of antibiotics or other drugs. For example, the anti-malarial drug Plaquenil (hydroxychloroquine) has been used to alkalize intracellular compartments and improve antimicrobial entry and cytotoxic effects [121] [132] [145].


For more:, also known as Mono, is an infection that triggers Guillain-Barre as well as mycoplasma and cytomegalovirus.

Molecular Prevalence of Bartonella, Babesia, and Hemotropic Mycoplasma Species in Dogs With Hemangiosarcoma from Across the United States

2020 Jan 10;15(1):e0227234. doi: 10.1371/journal.pone.0227234. eCollection 2020.

Molecular prevalence of Bartonella, Babesia, and hemotropic Mycoplasma species in dogs with hemangiosarcoma from across the United States.


Hemangiosarcoma (HSA), a locally invasive and highly metastatic endothelial cell neoplasm, accounts for two-thirds of all cardiac and splenic neoplasms in dogs. Bartonella spp. infection has been reported in association with neoplastic and non-neoplastic vasoproliferative lesions in animals and humans. The objective of this study was to determine the prevalence of Bartonella spp. in conjunction with two other hemotropic pathogens, Babesia spp. and hemotropic Mycoplasma spp., in tissues and blood samples from 110 dogs with histopathologically diagnosed HSA from throughout the United States. This was a retrospective, observational study using clinical specimens from 110 dogs with HSA banked by the biospecimen repository of the Canine Comparative Oncology and Genomics Consortium. Samples provided for this study from each dog included: fresh frozen HSA tumor tissue (available from n = 100 of the 110 dogs), fresh frozen non-tumor tissue (n = 104), and whole blood and serum samples (n = 108 and 107 respectively). Blood and tissues were tested by qPCR for Bartonella, hemotropic Mycoplasma, and Babesia spp. DNA; serum was tested for Bartonella spp. antibodies.

  • Bartonella spp. DNA was amplified and sequenced from 73% of dogs with HSA (80/110)
  • hemotropic Mycoplasma spp. DNA was amplified from a significantly smaller proportion (5%, p<0.0001)
  • Babesia spp. DNA was not amplified from any dog

Of the 100 HSA tumor samples submitted,

  • 34% were Bartonella PCR positive (32% of splenic tumors, 57% of cardiac tumors, and 17% of other tumor locations)
  • Of 104 non-tumor tissues, 63% were Bartonella PCR positive (56% of spleen samples, 93% of cardiac samples, and 63% of skin/subcutaneous samples).
  • Of dogs with Bartonella positive HSA tumor, 76% were also positive in non-tumor tissue.
  • Bartonella spp. DNA was not PCR amplified from whole blood.

This study documented a high prevalence of Bartonella spp. DNA in dogs with HSA from geographically diverse regions of the United States. While 73% of all tissue samples from these dogs were PCR positive for Bartonella DNA, none of the blood samples were, indicating that

whole blood samples do not reflect tissue presence of this pathogen.

Future studies are needed to further investigate the role of Bartonella spp. in the development of HSA.



And here, we see exactly what patience experience in reality: negative blood tests but positive tissue samples.  Dr. Ericson has found Bartonella in tissues directly by where a PICC line was removed:

This is true not only for Bartonella but for Lyme as well as all of the coinfections.  Doctors that rely only on testing are missing patients right and left.

Please spread the word.


Live Q & A Webinar: Lyme Coinfections 11/19

Live Webinar: Ask Dr. Rawls
Join Dr. Bill Rawls for this new LIVE WEBINAR on Tuesday, November 19th, at 8pm ESTfor a new LIVE Q&A webinar about Lyme Disease Coinfections.

If you have questions about diagnosing and treating common Lyme coinfections including Epstein-Barr, Bartonella, Mycoplasma, Babesia, and Candida, you don’t want to miss this webinar.

Topics covered by Dr. Rawls during the webinar will include:

  • What are the telltale signs of a Lyme coinfection?
  • Do you need to know which coinfection(s) you have before seeking treatment?
  • Are there any reliable tests for Lyme and coinfections?
  • What are the best herbal and natural remedies for Lyme coinfections?
  • How can you tell for certain when Lyme and coinfections are gone?
  • Numerous other insights and answers throughout the live Q&A with Dr. Rawls

Submit your top Lyme coinfection questions after you register, and Dr. Rawls will try to answer as many as possible.

Plus, we will announce an exclusive offer for webinar attendees.

Reserve Your Seat Now »
We look forward to seeing you there!

P.S. If you have questions about the webinar, please reply to this email or call us at 800-951-2414.


Tickborne Triggered Seizure Disorder – A Case Study

October 16, 2019


Tickborne Triggered Seizure Disorder: Case Study of a Teenager with New Onset Seizure Disorder and the Neurological Impact of Tickborne Diseases

The Neurological impact of Bartonella and Rickettsia

This next case study is of an 18-year-old female who was adopted at the age of 5. Her adoptive mother described her as a malnourished premature baby who eventually received good foster care. This young lady was diagnosed with a growth hormone deficiency that was left untreated in her country of origin at the age of two. By the age of five, she was adopted and moved to the US with her American family. She was fully immunized twice, diagnosed with hypothyroidism and inadequate growth. By this time, an Endocrinologist was onboard and treating her thyroid and growth deficiencies. She seemed to rebound, reaching puberty by the age of 13. Life was stable for some time until January of 2016. She was nearly sixteen years old and developed sudden neuropsychiatric symptoms with acute confusion, severe obsessive-compulsive disorder, frequent urination, insomnia, auditory hallucinations, severe sensory issues, leg tremors and eventually catatonia.  Given her acute changes, her mother rushed her to the Emergency Room for evaluation. EEG was negative and she was hospitalized for apparent acute psychosis treated with Risperdal and Ativan.

After her hospitalization she followed up with a well-known Neurologist who identified positive Mycoplasma and initiated a course of Azithromycin. By the fourth dose she began to return to her normal state and began sleeping again. She was treated for over a month with antibiotics and seemed stable.

There was a great deal of stress in the family, a close family member died and within two weeks she developed new onset grand mal seizures while sleeping. Another ER visit with a normal EEG at the time determined perhaps the stress and trauma of her family member’s death may have triggered the event.

In January 2018 she had another grand mal seizure early in the am. Her neurologist began medications to address. She had no additional seizure activity but noted increasing anxiety. By December 2018 she suffered another grand mal seizure.

Further evaluation by the neurologist showed negative Lyme screening only, viral panels negative, tick-borne co-infections were not obtained, thyroid studies, electrolytes and inflammatory markers were all within normal limits.

This patient presented to me in February 2019. Upon further evaluation she was found to have progressive muscle weakness, cognitive dysfunction ongoing psychiatric symptoms, tremors and noted random striae or “stretch-marks” that would appear and disappear all over her body. She stated that this had occurred since the age of fourteen.  She admitted several evaluations with psychiatric acute hospital admission for escalating neuropsychological symptoms that included visual and auditory hallucinations, compulsions, rage, emotional lability, delusions, anxiety as well as the ongoing physical symptoms. Neuropsychological meds were ineffective. The patient upon presentation was taking high dose Depakote, gabapentin and folic acid to control her seizure activity.

Initial lab work up at my office showed an IGM positive Bartonella Henselae, Lyme Western Blot with an IGM indeterminate band 23-25 and IGG positive bands 18,23-25,28,31,34,39,41,45,and indeterminate bands 58 and 66. She also showed IGG positive Rickettsia and Anaplasma. She carried one copy of MTHFR A1298C and had significant GI bacteria overgrowth with Streptococcus, Citrobacter, Proteus and Bacillus.

She was started on a course of Azithromycin and Bactrim as well as biofilm busters and herbals.  Two months later she reported significant improvements noting striae lightening, energy improvements, mood stability, resolution of hallucinations, and her sleep was improving. She noted ongoing body and hand tremors as well as struggles cognitively with word finding but was back in school full time.

We decided to continue the treatment course and repeat her bloodwork in two months as well as continue follow up with her Neurologist to monitor. By June the patient was feeling great. She began a Depakote wean with her Neurologist and graduated High School.

Her lab results showed improvements with Bartonella levels as well as GI bacterial overgrowth. Rickettsia antibodies lingered unchanged as did Lyme bands. I added to her regimen Doxycycline and Cefdinir as well as an antifungal and supportive herbals to prevent yeast.

This patient is still a work in progress, however what is important to note is her complete reversal of the neuropsychological symptoms once antibiotics were initiated as well as the ongoing, successful wean of seizure medications.

Bartonella and Rickettsia infections both have an affinity for the central nervous system. It is challenging to identify given their non-specific symptom presentation at times. Rickettsia isn’t well understood regarding brain parenchyma and central nervous system transmission. We know in mouse studies, Rickettsia and Bartonella both contribute to neuroinflammation which can contribute to acute psychological symptoms. We see this type of neurological process in classic PANS patients related to strep. Although I see the trend clinically, I don’t feel that autoimmune encephalopathy related to tick-borne infections in children and young adults is well documented.

My hope is thru case study presentations you’ll connect real world, everyday struggles of these vulnerable patients with the disease process. I strongly feel further exploration of autoimmune encephalopathy as it relates to Lyme and other Tickborne illnesses in pediatrics should be a collaborative effort with mental health practitioners and welcome those interested to contact me.


For more: (Treatment)  (Rickettsia treatment)