Archive for the ‘Uncategorized’ Category

Babesia Widespread in Canada & it’s High Tolerance to Therapy

Human Babesiosis Caused by Babesia duncani Has Widespread Distribution across Canada.

Scott JD, et al. Healthcare (Basel). 2018.


Human babesiosis caused by Babesia duncani is an emerging infectious disease in Canada. This malaria-like illness is brought about by a protozoan parasite infecting red blood cells. Currently, controversy surrounds which tick species are vectors of B. duncani. Since the availability of a serological or molecular test in Canada for B. duncani has been limited, we conducted a seven-year surveillance study (2011⁻2017) to ascertain the occurrence and geographic distribution of B. duncani infection country-wide. Surveillance case data for human B. duncani infections were collected by contacting physicians and naturopathic physicians in the United States and Canada who specialize in tick-borne diseases. During the seven-year period, 1119 cases were identified. The presence of B. duncani infections was widespread across Canada, with the highest occurrence in the Pacific coast region. Patients with human babesiosis may be asymptomatic, but as this parasitemia progresses, symptoms range from mild to fatal. Donors of blood, plasma, living tissues, and organs may unknowingly be infected with this piroplasm and are contributing to the spread of this zoonosis. Our data show that greater awareness of human babesiosis is needed in Canada, and the imminent threat to the security of the Canadian blood supply warrants further investigation. Based on our epidemiological findings, human babesiosis should be a nationally notifiable disease in Canada. Whenever a patient has a tick bite, health practitioners must watch for B. duncani infections, and include human babesiosis in their differential diagnosis.

Establishment of a continuous in vitro culture of Babesia duncani in human erythrocytes reveals unusually high tolerance to recommended therapies.

Abraham A, et al. J Biol Chem. 2018.


Human babesiosis is an emerging tick-borne disease caused by apicomplexan parasites of the genus Babesia. Clinical cases caused by Babesia duncani have been associated with high parasite burden, severe pathology and death. In both mice and hamsters, the parasite causes uncontrolled fulminant infections, which ultimately lead to death. Resolving these infections requires knowledge of B. duncani biology, virulence, and susceptibility to anti-infectives, but little is known and further research is hindered by a lack of relevant model systems. Here, we report the first continuous in vitro culture of B. duncani in human red blood cells. We show that during its asexual cycle within human erythrocytes, B. duncani develops and divides to form four daughter parasites with parasitemia doubling every ~22 h. Using this in vitro culture assay, we found that B. duncani has low susceptibility to the four drugs recommended for treatment of human babesiosis, atovaquone, azithromycin, clindamycin and quinine, with IC50 values ranging between 500 nM and 20 μM. These data suggest that current practices are of limited effect in treating the disease. We anticipate this new disease model will set the stage for a better understanding of the biology of this parasite and will help guide better therapeutic strategies to treat B. duncani-associated babesiosis.


For more on Babesia:

My husband and I both had Babesia.  Thankfully, that is one we are symptom-free from, but we treated for an entire year.  Dr. Horowitz states it’s one of the most tenacious coinfections he treats.

We used:

  • Mepron (750mg/5ml two times a day)
  • Allergy Research Brand Artemisinin (500mg 2X/day)
  • An intracellular such as one of the following:

*azithromycin (Zithromax) 500mg twice a day
*clarithromycin (Biaxin) 500mg  twice a day
*doxycline 100mg 2 pills twice a day
*minocycline 100mg  twice a day

Wise treatment overlaps.  It works synergistically and it helps prevent tolerance.

Babesia treatment is typically 3 weeks on, 1 week off.  I believe we pulsed the Artemisinin MWF.  This is a particular potent form and will give you a metallic taste in your mouth.  To read about it:  (I am not affiliated with any products or services).  I was thankful for the pulsing as I had heart-attack type herxes and the breaks from those were welcome!

See Babesia Treatment link above for a symptom check-list you can print and fill out.







New Blog Series: Breaking Down the TBDWG Report to Congress

Last month we were excited to see the first report to Congress from the Tick-Borne Disease Working Group. This post kicks off a series that will break the report down into sections based on the group’s major findings. The series will run through the month of December here on the Galaxy Diagnostics blog.

The Tick-Borne Disease Working Group was established by the 21st Century Cures Act, signed into law in 2016. More than 300 pages long, the Act was a sweeping response to many issues in health care brought up from within health care businesses and by members of the public. Some of these health care issues had touched legislators personally, including tick-borne disease.

The working group is a diverse collection of federal and public individuals who came together to combine information from many areas of expertise.  Federal members include representatives of major institutions in health care including the Food and Drug Administration (FDA), the U.S Department of Health and Human Services (HHS) and even the Department of Defense (DoD). Public members include representatives from major research institutions, independent specialists, scientists, and patient advocates. In total, 65 people representing a variety of stakeholders serve on either the main working group or one of the six sub-committees.

The report they have developed was paid for by the people of the United States and belongs to everyone. We have attached to this post the “Core Values to Achieve One Shared Vision” graphic and the patient stories. You can share these pages to raise awareness of tick-borne disease in your community.

The core values statement responds to many of the frustrations patients have had about how tick-borne disease awareness, diagnosis, and treatment are approached by the public health and health care provider communities. Patients have often expressed a sense that they are not being heard and that their health care issues are not being properly addressed, resulting in increased economic burden and a feeling of helplessness.

In this report, the working group clearly states that a renewed collaborative ethos incorporating the experiences and expectations of patients is required to move forward. The values they cite are: respect, innovation, honesty & integrity, excellence, compassion, collaboration, and accountability.

Future posts in this series will discuss issues related to disease surveillance and access to care as well as how the elements of the report come together to look toward improved prevention efforts.

The full report can be accessed here. At that link you can also find out more information about the working group and find a link to the full text of the 21st Century Cures Act.

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Everything That’s Known About Ehrlichiosis

Epidemiology of Ehrlichiosis


Ehrlichiosis is a disease caused by several Gram-negative obligate intracellular bacteria that are transmitted by a tick vector. The frequency of ehrlichiosis is increasing, which is ascribed to the increased awareness and diagnostic availability, as well as the expansion of regions populated with the most common tick vector – Amblyomma americanum (also known as the Lone Star tick).

Lone Star Tick (Amblyomma americanum). Image Credit: Melinda Fawver / Shutterstock

Symptoms of the disease usually include fever, anorexia, headache and myalgia, with a relatively low incidence of rash (present only in 20% of affected individuals). The knowledge of disease epidemiology is vital, as early recognition may prevent a large number of cases (and thus avoid rare fatal outcomes).

Generally, the median age for acquiring ehrlichiosis is 51-53 years, while Caucasian males are the most commonly affected group. Even though cases of the disease are found year-round, the greatest number is observed between May and August, which coincides with periods of abundant populations of ticks and human open air recreation.

Epidemiology of Human Monocytic Ehrlichiosis

Human monocytic ehrlichiosis (caused by the species Ehrlichia chaffeensis and Ehrlichia canis) was initially described in 1986, and almost three thousand cases have been reported to the U.S. Centers for Disease Control and Prevention (CDC) in the last three decades. Even though the average incidence of this disease in the United States is 0.7 cases per million inhabitants, this estimation is based on passive surveillance and probably represents substantial underestimation of the actual incidence.

For example, in one seroprevalence study conducted on children it was demonstrated that 20% of infected individuals from endemic areas had detectable antibodies to Ehrlichia chaffeensis, without any previous history of apparent clinical disease. This is in line with the finding that more than two-thirds of all infections with causative agents of human monocytic ehrlichiosis are either without any symptoms or minimally symptomatic.

Akin to other tick-borne illnesses, the distribution of arthropod vectors and reservoirs in vertebrates highly correlates with the disease occurrence in humans. The predominant zoonotic cycle of Ehrlichia chaffeensis is comprised of infected white-tailed deer as the reservoir and Amblyomma americanum as the tick vector, both prevalent across southcentral and southeast United States.

This tick also has three feeding stages (known as larval, nymph and adult stages), and each developmental representative feeds only once. Transstadial transmission of Ehrlichia can be seen during nymph and adult feeding, because larvae are uninfected. Unlike some other species (most notably Rickettsia), Ehrlichia cannot be maintained via trans-ovarial transmission pathway.

Epidemiology of Human Granulocytic Anaplasmosis

In the 1990s certain patients from Wisconsin and Michigan with a history of tick bite presented with a febrile illness similar quite similar to human monocytic ehrlichiosis. These cases were characterized by inclusion bodies in granulocytes rather than agranulocytes (monocytes), which is why this syndrome was initially named human granulocytic ehrlichiosis. After recent reclassification of Ehrlichia phagocytophilum to the genus Anaplasma, the disease has been renamed to human granulocytic anaplasmosis.

The annual number of human granulocytic anaplasmosis cases exceeds those of human monocytic ehrlichiosis, with an incidence case rate of 1.6 per million inhabitants in the U.S. As with Ehrlichia chaffeensis, different serosurveillence studies evince that asymptomatic disease is quite common. The disease is primarily caused by Anaplasma phagocytophilum.

This disease is seen in Europe as well, where the majority of cases is found in central Europe (e.g. Slovenia) and Scandinavian countries (e.g. Sweden), though individual reports have come from other countries as well. Nonetheless, there is limited knowledge as to the exact epidemiological features and implicated animal reservoirs in Europe.

Different ticks transmit human granulocytic anaplasmosis in different continents; Ixodes scapularis and Ixodes pacificus are the predominant tick species in the United States, Ixodes ricinus in Europe, while Ixodes persulcatus transfers the infectious agent in Asia. Small mammals (such as White-footed mouse and Dusky-footed wood rat) are primary reservoirs of the disease.

Epidemiology of Ehrlichia ewingii

The epidemiology of Ehrlichia ewingii is usually addressed separately as there are certain problems with this species, such as the absence of specific serological tests and the lack of adequate reporting systems. What we do know is that most infections have been observed in immunosuppressed patients (after organ transplantation) and in those infected with human immunodeficiency virus (HIV).

The primary vector for Ehrlichia ewingii is the Lone Star tick, as for Ehrlichia chaffeensis. Most human cases of the disease have been documented in Missouri, Oklahoma and Tennessee in the United States, although infection has been described in dogs and deer throughout the range of the tick that transmits the disease, suggesting that the infection with this specific species might be even more widespread.

Pathophysiology of the Disease

Infection with bacterial species causing ehrlichiosis occurs when the extracellular infectious form of the organism is taken up by the host cell. These infectious forms are either the elementary body or the dense core, and are taken up by the cell via a process known as endocytosis. Once inside the cell, the infecting organism divides and matures until it forms a reticulate body/reticulate core, and then a morula; these are then redifferentiated again into an elementary body/dense core so it can leave the infected host cell and spread further.

During this process, Ehrlichia and Anaplasma utilize a range of immune evasion mechanisms, such as suppression of apoptosis in host cells, down-regulation of recognition receptors in the host that could enable clearance of the infection, as well as modulation of cytokine and chemokine responses. Some species have a preference for granulocytic cells (Anaplasma phagocytophilum and Ehrlichia ewingii), while others target mononuclear phagocytes (Ehrlichia chaffeensis and Ehrlichia canis)

Furthermore, multisystem involvement is also a potential consequence, as microorganisms are found in the spleen, bone marrow, lymph nodes and peripheral blood. In fact, all the clinical manifestations are thought to be a result of a host inflammatory response to disseminated infection, rather than because of direct bacteria-induced damage.

Clinical Presentation

Patients with ehrlichiosis (regardless of the putative organism) clinically present with fever, chills, severe headache, confusion, malaise, nausea, vomiting, and generalized body aches. Respiratory symptoms such as cough may also be observed, but they are more common in adults than in  children.

Symptoms are typically seen one to two weeks following a tick bite, with a median of nine days. The problem with tick bites is that they are usually painless, and therefore many people do not even remember being bitten. Due to immune suppression, secondary infections (usually caused by cytomegalovirus or fungi) are also frequent in severely diseased patients.

In approximately one-third of individuals with ehrlichiosis there is a visible rash that is maculopapular or petechial. The rash is more commonly observed in children and typically develops five days after fever ensues. If present, the rash typically spares the palms, soles and the face.

Akin to rickettsial infections, central nervous system involvement may occur in up to 20% of affected individuals, including dangerous manifestations like meningoencephalitis. Moreover, in some patients the disease may advance to acute respiratory distress syndrome or a shock-like presentation coupled with bleeding disorders and cardiovascular instability.

However, the overall death rate is substantially lower in ehrlichiosis when compared to rickettsial diseases. According to the data published by U.S. Centers for Disease Control and Prevention (CDC), the mortality rates in patients who are seen by a healthcare professional due to ehrlichiosis range from 1% to 3%.

On the other hand, a large number of patients may be infected with Ehrlichia and Anaplasma, but do not come for medical evaluation; therefore, these percentages may be overestimations of mortality. Naturally, immunocompromised individuals, elderly and those previously treated with sulfonamide antibiotics are at higher risk of more severe disease.

Differential Diagnosis

Since ehrlichiosis is a multisystem disease characterized by protean manifestations (i.e. without pathognomonic and highly characteristic clinical features), the differentials are often quite broad. Initial symptoms are often generalized and somewhat vague, which is why the illness may first be diagnosed as a possible “viral syndrome” in the context of upper respiratory infection, gastroenteritis and/or meningoencephalitis.

A history of tick exposure or tick bite in the recent past can be elicited from a majority of patients, but it is important to emphasize that this feature may be absent in up to 30% of all cases. Therefore, pursuing other appropriate diagnostic procedures to confirm this disease is of the utmost importance.

Pancytopenia (i.e. an abnormally low count for all three types of blood cells) is a hallmark laboratory finding of human ehrlichiosis during the early days of the disease.

  • leukopenia (mild or moderate) in 70% of patients (with the most significant decline being in the lymphocyte population) during the first week.
  • Anemia in 50% of acute patients
  • Low platelet count
  • elevated liver transaminases

The next step towards accurate diagnosis is making blood smears from peripheral blood, cerebrospinal fluid or bone marrow, which are stained with Giemsa or Wright’s stains to detect specific bacterial structures known as morulae.

Albeit this technique is rapid, it is rather insensitive in comparison to other confirmatory tests, and particularly in immunocompetent patients who have extremely low bacterial loads in blood and body organs.

The Use of Serology

The most sensitive method of infection confirmation is a seroconversion or a 4-fold change in antibody titers during the convalescent phase of the disease.

Specific serologic testing of IgM and IgG antibodies to Ehrlichia chaffeensis or Anaplasma phagocytophilum by means of indirect immunofluorescence assay is considered the “gold standard” and thus the most frequently employed confirmatory test.

Nonetheless, serology has its limitations, and these include a negative IgG test and uninformative levels of IgM titers in 80% of affected individuals during the first week of the disease, a high false positive rate, seroconversion failures due to weak immune function, as well as alteration of antibody response because of early antibiotic treatment.

Molecular Diagnostic Procedures

Due to high specificity and sensitivity values, as well as a very rapid turnaround time, polymerase chain reaction (PCR) became the preferred test for confirming serology findings indicative of human monocytic ehrlichiosis and human granulocytic anaplasmosis.

The use of PCR is especially important in the detection of early stages of infection, when antibody levels are low or undetectable.

A large number of kits are commercially available for whole blood PCR testing, which enables rapid diagnosis in up to 85% of infected individuals. Recent advances in molecular research even allow multiplex testing that can identify several agents of ehrlichiosis from one test.

Laboratory Culture

Although the possibility of culturing Ehrlichia and Anaplasma species is also available to clinicians and researchers, the isolation of these organisms requires cell lines and typically takes 2-6 weeks of incubation.

The sensitivity of this approach for the isolation of Ehrlichia chaffeensis is very low when compared to PCR, but higher (and almost comparable to PCR) for Anaplasma phagocytophilum.

The major pitfall of the laboratory culture approach is the paucity of competent laboratories, since this technique necessitates unique and antibiotic-free cell culture methods that are not usually available in clinical microbiology laboratories.

In addition, prior treatment with doxycycline or some other antimicrobial drugs lowers the sensitivity of culture to a greater degree when compared with blood smear analysis or PCR.


This is another confirmatory technique and is especially valuable when the diagnosis is to be made before antibiotic treatment is begun, or at least within 48 hours of its initiation. It can also be applied to bone marrow and autopsy specimens.

All those factors have to be taken into account when assessing patients with suspected ehrlichiosis, which is the reason why some propose combining different diagnostic methods to increase the likelihood of early diagnosis. Naturally, clinicians always have to consider other diseases that have similar clinical and laboratory findings to ehrlichiosis.

Treatment Options for Ehrlichiosis

Ehrlichia chaffeensis and Ehrlichia canis, the causative agents of human monocytic ehrlichiosis, are susceptible to all tetracycline antibiotics and their derivatives. These drugs exhibit broad spectrum activity by binding to bacterial ribosomes and inhibiting protein synthesis by interrupting peptide chain formation. A plethora of other human pathogens (such as rickettsiae, borreliae, chlamydiae, as well as some mycobacterial and protozoal species) are susceptible to tetracyclines as well.

Treatment considerations for human granulocytic anaplasmosis are similar to those for human monocytic ehrlichiosis, with tetracyclines being very effective against Anaplasma phagocytophilum and Ehrlichia ewingii. The possibility of Babesia co-infection often has to be considered, which means monotherapy is sometimes not sufficient.

In both groups of diseases treatment response is usually rapid. Therefore, an alternative diagnosis should be considered if fever persists for more than 72 hours after the initiation of appropriate antibiotics. Even though research studies did not specifically address recommended treatment duration, many experts advocate continued antibiotics for 3-5 days after fever abates, and perhaps even longer (up to 14 days) if there were signs of central nervous system involvement.  (Please see my comment at end of article)

A particular challenge for clinicians is ehrlichiosis in pregnancy, as tetracyclines are contraindicated in this population. Antibiotic sensitivity studies show that certain anti-tuberculous drugs have bactericidal activity in vitro against Ehrlichia and Anaplasma. This is also a viable and appropriate alternative approach in pregnant women.

Since clinical experience with other drugs that show activity in vitro is lacking, there are no fixed treatment recommendations for children younger than eight years of age, as well as for individuals who are hypersensitive to tetracycline drugs. Furthermore, there is no clinical data on the potential usefulness of adjunctive corticosteroid application to suppress the inflammatory manifestations of the disease.

Pertinent Prevention Strategies

Avoiding tick bites and removing any adherent tick immediately are the first steps in disease prevention. Individuals who reside in endemic areas are advised to wear long sleeves and light colored clothing during outdoor activities, since the latter permits easier visualization of crawling ticks. Adults at high risk of tick bites should apply repellents such as N,N-diethyl-meta-toluamide (commonly known as DEET) or permethrin to prevent this.

After visiting tick-infested regions, a careful inspection of body, hair and clothes should always be done with immediate removal of attached ticks. Research studies have demonstrated that a period lasting from 4 to 24 hours after infected ticks attach to the host is possibly essential for the  successful transmission of Ehrlichia and Anaplasma. Hence, swift and thorough removal of attached ticks is of the utmost importance for preventing transmission and subsequent disease.

At the moment there are no commercially available or experimental vaccines for prevention of either human or veterinary ehrlichiosis. In conclusion, it has to be emphasized that the diagnosis of ehrlichiosis necessitates a high level of suspicion, which is why it is often made retrospectively, with potentially dire consequences for the affected individuals in rare cases.


Sources for treatment and prevention



Lyme/MSIDS patients are often coinfected with numerous pathogens making them immunocompromised.  Cortico-steroids are not recommended for this population.  Also, as a rule, ILADS (International Lyme and Associated Diseases Society) recommends longer treatment and numerous antimicrobials due to the polymicrobial nature of tick-borne illness as well as the fact many of these pathogens are persistent.

For another great read:  The author brings up a valid point about the potential of there being undiagnosed Ehrlichia behind a ME/CFS diagnosis in a subset of patients since it infects white blood cells and the mitochondria.  The article also gives helpful percentages of symptoms and the following information:

Other symptoms of ehrlichiosis can include:

  • Fever/chills and headache (majority of cases)
  • Fatigue/malaise (over two-thirds of cases)
  • Muscle/joint pain (25% – 50%)
  • Nausea, vomiting and/or diarrhea (25% – 50%)
  • Cough (25% – 50%)
  • Confusion or brain fog (50% of children, less common in adults)
  • Lymphadenopathy (47% – 56% of children, less common in adults)
  • Red eyes (occasionally)
  • Rash (approximately 60% of children and 30% of adults)

Other modes of transmission

Ehrlichia chaffeensis has been shown to survive for over a week in refrigerated blood. Therefore these bacteria may present a risk for transmission through blood transfusion and organ donation. It has also been suggested that ehrlichiosis can be transmitted from mother to child, and through direct contact with slaughtered deer. (14, 15)

Summary of Ehrlichiosis

As you can see from this nifty table, much is UNKNOWN.  This right here is another example of research begging to be done.  The results would be practical, effectual, and essential in treating patients – unlike climate data which will only line the pockets of research institutions.  Remember Zika?  It caused a media blitz with research being done everywhere.  As you can see from this article, Ehrlichia can be deadly and is spreading.  Why no news and research?

For more:

Review of Literature on Fibrosing Skin Condition Due to Lyme

Acrodermatitis chronica atrophicans in children: Report on two cases and review of the literature.

Maraspin V, et al. Ticks Tick Borne Dis. 2019.


Acrodermatitis chronica atrophicans is a late manifestation of European Lyme borreliosis and is characterized by high levels of borrelial IgG antibodies, slowly expanding skin redness usually beginning on distal parts of extremities, and corresponding histologic findings. It very rarely develops in children. The main prerequisite for the diagnosis is clinical suspicion. In the present article we report on two children with acrodermatitis chronica atrophicans and on the findings of a PubMed literature search on acrodermatitis chronica atrophicans in childhood, published in the past three decades.



Acrodermatitis chronica atrophicans (ACA) is a fancy way of saying long-term persistence of Borrelia infection in the skin.  

Not a lot is known about this condition but what is known is that lack of adequate or appropriate treatment of early Lyme leads to the condition.  Borrelia’s ability to change antigens thereby messing up the immune response doesn’t help matters either.

As to the “3 stages of Lyme,” folks can jump from stage to stage with no particular rhyme or reason:

One little girl within 4-6 hours after tick bite couldn’t walk or talk:

Please see for a slide-show of pictures.  Swelling and a bluish red coloring of the skin are fairly classic symptoms along with numbness, burning, tingling, muscle weakness, and Babinski sign (a reflex movement of the big toe upward instead of downward when the plantar aspect of the foot is stroked, a manoeuvre used to test injury to, or diseases of, the upper motor neurons).

The Medscape article also points out that other genospecies of borrelia have been known to cause ACA. They also point out ACA is often under diagnosed.

Please read this before taking the author’s advice about treatment length:  Then don’t forget the possible involvement of coinfections:  For the first time, Garg et al. show a 85% probability for multiple infections including not only tick-borne pathogens but also opportunistic microbes such as EBV and other viruses.

I’m glad articles like these are coming out.  In order for researchers and mainstream medicine to believe something it has to be published.  But just because something hasn’t been published doesn’t mean it doesn’t exist.  

December 2018 Support Group Meeting


Our next support meeting:

When:  Saturday, December 1, 2018

Where:  East Madison Police Station, 809 S. Thompson Dr., Madison, WI

Go here for parking instructions:


Neuropsych Disorders in Kids: An Interview with Co-Founder of The Stanford PANS Clinic – Dr. Kiki Chang


​Dr. Kiki Chang, is a child psychiatrist with over 22 years of experience in working with younger children, adolescents, adults and families. Formerly, Dr. Chang was Professor of Psychiatry and Behavioral Sciences at Stanford University School of Medicine and co-founder of the Stanford PANS Clinic. 
His specialty is working with youth and young adults who have or are at risk for serious mood disorders, such as depression or bipolar disorder as well as PANS/PANDAS and related neuropsychiatric disorders. Dr. Chang will be presenting a webinar August 27, 2019 for Continuing Medical Education Credit.

Thank you to Dr. Chang for allowing Foundation For Children With Neuroimmune Disorders president and founder, Anna Conkey to interview him. 

How did you first learn of PANS/PANDAS and what motivated you to begin treating children with PANS/PANDAS?

I first became interested when I realized that some patients who were referred to me for consultation with presumed bipolar disorder had an unusual onset and/or course.  These patients were also treatment resistant to standard treatments for bipolar disorder.  I discovered that many of them either met PANS criteria or had a periodic mood disorder that included elements of catatonia, or unusual mental status changes.  It made sense that underlying immunologic factors were at least partially responsible.  These patients responded to immunomodulatory treatments rather than typical psychotropics.

I also started collaborating with a pediatric rheumatologist, Dr Jennifer Frankovich, who was interested in the same patients from the other end – many of her patients with rheumatologic disorders also had psychiatric symptoms including OCD.  When we realized our shared interests and that these patients fell under the PANS rubric, we decided to join forces with Margo Thienemann and start the PANS Clinic at Stanford.

Do you ever treat children who did not have an abrupt or acute onset, and if so, do they respond similarly to children who did have an abrupt onset?

Yes I do, and not always.  Abrupt is an arbitrary but necessary concept – is it 48 hours? 72 hours?  In our 2013 Expert Consensus Diagnostic meeting we agreed on 72 hours but many kids with sub-acute onset, say one week, will still likely have the same underlying issues – it’s just that if you keep stretching out that onset time, then it becomes a gray area and muddies the research waters.  The longer and more gradual the onset, the less likely it will fit clear PANS criteria and also have the same treatment response.

How do you determine which patients with PANS would benefits from psychiatric medications and when to introduce them? 

I think our guidelines present this issue fairly well (first author Dr Margo Thienemann, JCAP 2017).  If needed, psychiatric support is always indicated – to help alleviate severe anxiety, agitation, sleeplessness, etc.  If patients are functioning OK without them, then I prefer to treat medically as long as possible before using psychotropics.  At some point, whether due to only partial treatment response medically, or other factors, psychotropics make a lot of sense.

Is there a particular class of psychotropic medication that tends to be more effective in children with PANS?

I have a particular fondness for lithium, in that for youth with severe mood disruption, including a bipolar like picture, even in a PANS context, it can be very useful.  Yes, lithium has potential side effects, but if it works, it works great.  I could go on and on about the benefits of lithium and how it is missing in our soil, water, and diets, but you probably have a word limit.

Are there any anomalies you see when treating children with PANS with psychotropic medications? 

Not sure what you mean – do you mean do SSRI’s sometimes worsen their course?  Sure, but not always.  Also antipsychotics sometimes cause EPS symptoms more so than would be expected.  Probably due to the dopamine dysregulation going on in the basal ganglia being compounded by a dopamine receptor antagonist.

Many medical providers have interpreted the JCAP treatment guidelines as step one, “Psychiatric and Behavioral Interventions,” step two, “Use of Immunomodulatory Therapies,” and step three, “Treatment and Prevention of Infections.” As one of the authors, was the intent to suggest psychiatric and behavioral interventions prior to other interventions or has this been misinterpreted? 

Yes, that would be a misinterpretation of the treatment guideline!  It’s really based on the patient’s presenting issues.  All three approaches should be considered initially.  The order depends on what’s going on with the individual patient.  If there is clear infection, then of course treat it first.  If psychiatric symptoms are severe and need urgent stabilization, then do that.  I had no idea people were interpreting the guidelines that way, I think the introduction paper to the guidelines explains the overall approach well.

Have you treated any patients with longstanding diagnoses of bipolar, schizophrenia, depression, or any mood disorders whose symptoms resolved with immunomodulatory therapies? 

Yes, on occasion.  I saw the recent report from Japan about the patient with schizophrenia whose symptoms resolved with bone marrow transplantation after a subsequently diagnosed cancer.  Absolutely make sense in SOME cases.  Great example – clozapine has a long history of working where other antispychotics have failed – for schizophrenia or bipolar disorder.  Why?  The receptor profile is similar to other atypical antipsychotics – so what sets it apart?  Well, the one main side effect people have to check for is agranulocytosis, or basically suppressing the body’s production of white blood cells.  Hmm…so a potential “side effect” is suppressing the immune system? Seems like not a coincidence to me – it probably affects the immune system in some way even when not having full suppression of neutrophil production…and that is in my opinion probably why it works when other medications don’t…that perhaps those patients have a more immune-mediated illness.

What is your approach to managing children with autism who develop neuropsychiatric symptoms? How does this differ from your approach to those without autism? 

Tough question.  Certainly just because you are diagnosed with an autism spectrum disorder doesn’t mean you CAN’T develop a PANS condition. Some might argue that these kids might be actually MORE susceptible to such a condition, given the propensity of kids with ASD to have OC symptoms and/or tics.  My approach does not differ really for treatment, but for diagnosis there must be a clear acute onset meeting PANS criteria in order to say, yes this is PANS and let’s treat accordingly.

If you could snap your fingers and have any research on PANS completed tomorrow, what would you most like to see studied?

Egads, great question, there are so many studies I would like to see done.  I’d have to say probably first to have placebo controlled steroid trials in youth with PANS.  Clearly clinically steroids can be effective, but it would help tremendously to have this proven in a RDBCT.  Oh and having a cleaner and longer IVIG trial completed – and if positive then getting an indication so that insurance companies will all have to cover it for these kids.

_____________________  According to Dr. Brown, 80% of his PANS patients have Lyme/MSIDS.





Understanding Debilitating LD Symptoms – Podcast with Dr. Spector

Episode 43: Understanding Debilitating Lyme Disease Symptoms

Cindy Kennedy, FNP, is joined by Neil Spector, M.D., who discusses his experience with debilitating Lyme disease symptoms and how to manage them.Dr. Spector is the Sandra Coates Associate Professor of Medicine, an Associate Professor of Cancer Biology and Pharmacology and the Associate Director of Developmental Therapeutics for the Duke Cancer Institute.

Dr. Spector’s work has focused on elucidating molecular mechanisms underlying therapeutic resistance to therapies targeting the Human Epidermal Growth Factor Receptor (HER) family of receptor tyrosine kinases that are involved in the pathogenesis of breast cancer and other commonly occurring solid tumors.

He directed the translational research program that facilitated the successful development and eventual FDA approval of lapatinib (Tykerb), a small molecule inhibitor of the HER2 and EGFR tyrosine kinases, for the treatment of advanced stage HER2 overexpressing (HER2+) breast cancers.

His lab developed the first preclinical models of therapeutic resistance to lapatinib, which identified a novel mechanism of resistance that was published in the Proceedings of the National Academy of Sciences, and served as the scientific rationale for a clinical development program that led to the FDA approval of lapatinib in combination with the aromatase inhibitor letrozole as a first line therapy for patients with HER2+/Estrogen Receptor positive metastatic breast cancer.

His application of translational research to the preclinical and clinical development of lapatinib is widely regarded as a model for of how precision oncology can transform treatment of cancer patients, and facilitate the development of targeted cancer therapies.

Dr. Spector’s research collaborations with colleagues at Duke led to the first clinical trial of a HER2 kinase inhibitor (lapatinib) combined with a HER2 vaccine. He also oversaw the early phase clinical development of nelarabine, an ara-G prodrug that was FDA approved for the treatment of pediatric acute lymphoblastic leukemia. His work with Dr. Tim Haystead (Professor, Cancer Biology and Pharmacology) has led to the identification of novel small molecules that target cell pathways involved in the earliest stages of tumorigenesis, providing an opportunity to prevent breast and other cancers in high risk individuals.

Dr. Spector was recognized by his peers through his selection as a Komen Research Scholar, a group representing the top breast cancer researchers from around the world. He was the recipient of the R. Wayne Rundles Award recognizing outstanding research accomplishments by a Duke investigator, and the Wendell Rosse Teaching Award recognizing excellence in teaching as determined by Duke medical oncology/hematology fellows.

In addition to his Duke research, Dr. Spector was appointed in 2016 to serve as the National Director of Precision Oncology for the VA Healthcare System.

Dr. Spector also detailed his personal 17-year journey with Lyme disease and the life-threatening cardiac complications that ensued, leading to heart transplant in 2009 in his book, “Gone In a Heartbeat: A Physician’s Search for True Healing.”

He was recently awarded a $3.8 million grant to develop molecular targeted therapies for two tick borne illnesses, Borrelia (Lyme disease) and Bartonella.

Dr. Spector earned an undergraduate degree at the University of North Carolina-Chapel Hill and an M.D. from Rutgers-New Jersey Medical School. He completed his internal medicine residency training at Parkland Hospital, University of Texas-Southwestern Medical Center, Dallas and a Medical Oncology/Hematology/Bone Marrow Transplantation fellowship at Massachusetts General Hospital and Dana-Farber Cancer Institute, Harvard Medical School.


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