Archive for the ‘Transmission’ Category

Congenital Babesiosis in Two Infants

Congenital Babesiosis After Maternal Infection With Borrelia burgdorferi and Babesia microti
Saetre K, Godhwani N, Maria M, Patel D, Wang G, Li KI, Wormser GP, Nolan SM.
Journal of the Pediatric Infectious Diseases Society, online first 2017 Sep 16.


We describe the cases of 2 infants with congenital babesiosis born to mothers with prepartum Lyme disease and subclinical Babesia microti infection.

The infants both developed anemia, neutropenia, and thrombocytopenia, and 1 infant required red blood cell transfusion. Both infants recovered with treatment.

Additional studies are warranted to define the optimal management strategy for pregnant women with early Lyme disease in geographic areas in which B microtiinfection is endemic.


For more on Babesia:

Epstein-Barr Virus – A Key Player in Chronic Illness Barr Virus: A Key Player in Chronic Illness

Epstein-Barr Virus: A Key Player in Chronic Illness

by Dr. Bill Rawls
Posted 11/3/17

So, you’re experiencing symptoms of tiredness, achiness, sore throat, and possibly swollen lymph nodes and low-grade fever that just won’t go away.

You’ve Googled your symptoms, and mononucleosis pops up as a likely possibility. But if you’re well beyond college age, mononucleosis isn’t very common.

Chronic fatigue syndrome, fibromyalgia, and even Lyme disease are other possibilities you might have entertained, especially if you have symptoms beyond those mentioned above. But then you came across something called reactivated Epstein-Barr virus, which fits your symptoms to a tee.

If you are aware that Epstein-Barr virus (EBV) is the cause of mononucleosis, you may be wondering: What’s the difference between chronic reactivated EBV and mononucleosis? And beyond that, what makes chronic reactivated EBV chronic — and how does it play into other chronic illnesses?

To find out, read on to learn more about this complex and convoluted microbe called Epstein-Barr virus and what can make it a long-term troublemaker.

Almost Everyone Has EBV

Let’s start with the fact that EBV is much more common than you might imagine: >95% of world’s population has been infected with it.

Another interesting fact is that it’s a herpes-type virus. Yep, you read that right: EBV is a close relative of genital herpes. Known technically as Human Herpesvirus 4 (HHV-4), it’s #4 on the list of nine different herpes-type viruses that can infect humans.

Herpesviruses are composed of strands of DNA inside an envelope. After initial infection, they stay dormant in tissues indefinitely, but can reactivate if immune system functions become depressed.

In other words, if you’ve ever been infected with a herpesvirus like EBV, you will always carry it in your tissues.

EBV Can Spread Like Wildfire

The majority of people become infected with EBV as infants or young children. The virus spreads primarily by oral route via saliva. To enter the body, it infects mucous membranes lining the mouth, throat, and stomach. From there, the virus infects B cells, the type of white blood cell that produces antibodies. It also infects T cells and natural killer cells, but to a lesser extent. Infected white blood cells transport EBV throughout the body.

In this active phase, called the lytic phase, the virus takes over the machinery of infected cells to generate new viruses. This is when people are most symptomatic and contagious.

The virus spreads remarkably easily, especially in children. It is most typically spread by people who are infectious, but don’t know it — daycare workers, babysitters, grandmothers with big wet kisses. Following that, infected children rapidly pass it along to other children.

Which is a really good thing — because if you get it as an infant or young child (remember to thank your grandmother), you typically don’t get very sick at all. In fact, it’s unlikely that you would even remember the infection.

It’s only if you don’t get EBV at a young age and then get exposed later in life when your immune system is suppressed that you’re at risk for developing the form of EBV called mononucleosis.

Known as kissing disease, infectious mononucleosis (IM) is spread by intimate contact with someone shedding the virus. It typically occurs in young adults who haven’t been exposed early in life. It usually catches the person off guard when immune system functions are depressed, such as during the stress of high school or college.

Compared to EBV occurring in childhood, IM is much more severe: Common symptoms include sore throat, fever, severe fatigue, and swollen lymph nodes. It can drag on for months and be quite debilitating.25

Whether the initial encounter with EBV occurs as an innocuous infection as a child or as debilitating mononucleosis as a young adult, the host’s immune system eventually gains ground and the infection is contained.

The virus, however, is not eradicated. It persists inside memory B cells, a type of white blood cell that retains “memory” of an infection for future reference — except in this case, the cells are sabotaged into storing the actual virus. Memory B cells infected with EBV accumulate in lymphoid tissue and nerve tissue, and stay there for a lifetime.

This dormant state is referred to as the latent phase.9, 6, 12, 23Traditionally, people in the latent phase weren’t considered noninfectious. But with all the daycare workers, teachers, grandmas, and college students actively shedding the virus without knowing it, it’s become clear that someone can be very infectious without being ill. In fact, recent evidence supports that people often actively shed virus from tonsillar tissues without having significant symptoms.23

Either way, whether EBV is completely dormant or infectious without symptoms, the virus generally doesn’t cause any significant problems as long as immune system functions are robust. You can carry it for a whole lifetime and not know it — as most people do.

However, allow the immune system to become disrupted — by stress, poor diet, and other key factors I’ll explore below — and EBV can reactivate, causing symptoms similar to the mononucleosis, but much worse.4

Reactivated EBV Can Become Chronic

Chronic reactivated EBV is like mononucleosis from hell.

Symptoms of reactivated EBV include severe chronic fatigue, chronic achiness, chronic sore throat and irritation of mucous membranes, swollen lymph nodes, and a range of debilitating neurological symptoms. Symptoms can wax and wane for years. Severe cases can include evidence of liver dysfunction, immune suppression, and anemia.1

The most plausible explanation for why chronic reactivated EBV is so severe and unrelenting is that it’s not just EBV that’s at play.

This is where things get both interesting and complicated.

People often carry other herpesviruses in addition to EBV. The list includes Herpes simplex types 1 and 2 (oral and genital herpes), varicella-zoster virus (causing both chickenpox and shingles), cytomegalovirus (CMV), HHV-6 types a and b, HHV-7, and HHV-8.

Though they are all related, each of these viruses infects the body in a different way — therefore they cause slightly different symptom profiles. In important ways, they are all are remarkably common:

They stay dormant in tissues and can be reactivated just like EBV.

If disruption of a person’s immune functions allows reactivation of multiple herpesviruses at once, symptoms can be severe and highly variable.

But that isn’t the end of the story.

Many people with chronic Lyme diseasefibromyalgia, and chronic fatigue syndrome are found to have reactivation of EBV, along with other herpesviruses and a list of other microbes including Mycoplasma, Bartonella, Chlamydia, and new microbes added to the list every day.

This strongly suggests that reactivation of EBV is likely not EBV alone.

The Connections Between EBV and Chronic Illnesses Are Many

Scientists are just beginning to explore the link between chronic EBV and other chronic illnesses, but one of the most well-researched is EBV’s relationship with multiple sclerosis (MS). Many studies have defined a variety of different mechanisms by which the virus could initiate and perpetuate MS — not enough to define EBV as the sole cause of MS, but highly suggestive that it does play a role in the illness.10

Similarly, studies have shown high viral loads of active EBV in a high proportion of patients with a variety of autoimmune diseases, including rheumatoid arthritis, systemic lupus erythematosus, Sjögren’s syndrome, and autoimmune thyroiditis.14 Again, a strong link, but not enough to suggest absolute cause of EBV alone.

And that’s not the end of the multi-microbe connections.

Recent evidence has suggested that EBV and HHV-6a might together play a role in MS.29 MS has also been linked to a variety of different microbes including, but not limited to, Chlamydia pneumoniae,35, 37 Mycoplasma sp., Spherula insularis, and paramyxovirus.14, 36

Autoimmune diseases have also been linked to a variety of microbes, including EBV, but also additional herpesviruses; other viruses including Parvovirus; a protozoan called Toxoplasmosis; and bacteria including Mycoplasma, Yersinia, and others commonly associated with chronic Lyme disease.14

Often referred to as stealth pathogens, the microbes mentioned and many others share similar stealthy characteristics:

  • They have the ability to live inside cells.
  • They infect white blood cells and are carried throughout the body, especially to areas of inflammation.
  • They can persist in a dormant state.
  • They are master manipulators of the immune system.
  • They can exist in healthy people without causing illness.
  • They are present in all populations of the world.

The deeper you dig, the more connections you find between chronic illnesses and stealth microbes. But after a while, you begin to appreciate that it’s not as much the microbes causing problems as it is disruption of the host’s immune functions that allows those microbes to flourish.

In other words, a person could be harboring a variety of stealth microbes — EBV, CMV, HHV-7, Borrelia, Bartonella, Mycoplasma, Chlamydia, and others — and not be ill as long as their immune system functions are robust.

Let immune system functions falter, however, and like a pot boiling over on the stove, the microbes erupt and cause illness.

Chronic Immune Dysfunction Is Triggered by the Perfect Storm

I came to see chronic illness differently than most other physicians because of my personal struggle overcoming chronic Lyme disease.

My experience taught me that the microbes are always there — I had likely harbored mine since childhood. It’s not until a perfect storm of factors comes together to disrupt immune functions that a person becomes ill. For me, that perfect storm was caused primarily by years of chronic sleep deprivation associated with every-other-night obstetrics on-call-duty and eating a poor diet on the run, but there were other minor stress factors as well.

My recovery did not progress until I started addressing the underlying chronic immune dysfunction.

As I shifted my practice toward caring for individuals with chronic illness, I began to see similar patterns in my patients — not necessarily the same stress factors that I had experienced, but stress factors that disrupt immune functions just the same. I began cataloging them and, interestingly, I reached a limit of just 7 categories of stress factors that are associated with chronic illness.

As astounding as it may sound, I came to the conclusion that the causes of all chronic illnesses can be traced back to these 7 factors that I came to call System Disruptors. I’ve been testing this theory for more than 10 years and always find it to be reliable. I’ve also discovered solid scientific support for my theory.

The 7 System Disruptors are:

1. Poor diet. We live in a world saturated with artificially manipulated foods. Regular consumption of these foods disrupts all systems of the body.

2. Toxins. The modern world is saturated with artificial toxins. Toxins disrupt all healing systems of the body.

3. Emotional stress. Continually running from the proverbial tiger inhibits digestion, suppresses immune function, disrupts sleep, and sets the stage for chronic illness.

4. Physical stress. Cumulative trauma, excessive heat or cold causes damage to the body, but living a sedentary life can be just as harmful.

5. Oxidative stress. Every cell in the body is continually generating free radicals as a byproduct of energy production. Free radicals damage internal components of cells. Inflammation is also a type of free radical damage.

6. Artificial radiation. Normal background radiation from the sun, solar system, and the earth itself are now amplified sources of radiation that saturate the modern world.

7. Microbes. The effects from this system disruptor set the stage for chronic illness.

For every patient with chronic illness, I can always trace back to a perfect storm of factors that came together to cause the person’s illness. What type of chronic illness they ended up with depends on three factors:

  • The person’s genetics — which determines risk, but not whether an illness will occur
  • The variety of different low-grade stealth pathogens the person has collected through life
  • How System Disruptors contribute to immune dysfunction, which allows low grade pathogens with stealthy characteristics to flourish and upset the balance of the microbiome and homeostasis in the body

Diagnosing and Treating Chronic EBV Isn’t Black and White

To help identify chronic EBV, start by trying to rule out infectious mononucleosis. By definition, IM is an acute infection with EBV alone, and there are antiviral agents (such as acyclovir, ganciclovir, and vidarabine) that work extremely well for IM and other acute infections of herpes-type viruses, so it’s worth doing testing to define IM over reactivated EBV.

Testing for IM looks for antibodies to the virus; the presence of different types of antibodies can distinguish between IM and reactivated EBV. But testing for IM isn’t always straight-forward — mononucleosis-like syndromes can also occur with other herpesviruses (CMV, HHV-6), other viruses (typically adenoviruses), and a protozoan called Toxoplasma gondii.26 In other words, many different viruses can cause viral syndromes similar to EBV.

If you have all the symptoms of chronic reactivated EBV, then the likelihood of EBV being present is quite high, along with other microbes.

As for treating chronic reactivated EBV, because there are antiviral agents that work well for IM, you might expect that chronic EBV would also respond to antivirals.

Unfortunately, antivirals don’t work for chronic EBV.

Scientists have sorted out the technical reason for this. Antiviral agents work by blocking DNA polymerase, an enzyme the virus uses to replicate inside cells. Latent or chronic EBV infection, however, does not require DNA polymerase for the virus to replicate — therefore, current antiviral agents are ineffective against chronic EBV infection.1

Other conventional therapies, including steroid therapy (prednisone) and immunosuppressive drugs, have been used to treat chronic EBV infection, but success has been limited.1These therapies can inhibit the destructive processes of a disrupted immune function, but they have no capacity to restore normal immune function.

Lots of researchers are also looking at vaccines against EBV. The problem is that characteristics of the virus vary greatly across different geographical areas, making it difficult to create a single vaccine.8

Other methods of eradicating EBV being contemplated by conventional medical science include: B-cell depletion with monoclonal antibodies (targeting EBV-infected B cells with immunoglobulins) and new types of antiviral drugs.11, 16, 20

Focusing all efforts on eradicating EBV, however, is short-sighted. The bottom line: The underlying problem is chronic immune dysfunction, and you will not start getting well until normal immune system functions are restored.

There’s A More Practical Approach to Regaining Wellness

Remember, EBV doesn’t cause problems unless immune system functions have been disrupted.1, 14, 20, 23 Therefore, any solution must address restoring normal immune system functions in order to suppress whatever microbes may be present and flourishing.

First and foremost is minimizing the 7 System Disruptors. Following an optimal diet and making some lifestyle modifications to promote a healing environment in the body is essential for overcoming chronic EBV or any other chronic illness.

Modern herbal therapy should be the cornerstone of any restorative approach. Herbal extracts have incredible abilities, including:

  • Reducing destructive inflammation
  • Enhancing natural killer cells and other aspects of the immune system necessary to control microbes like EBV
  • Balancing hormone systems in the body that have been disrupted by chronic illness
  • Suppressing stealth microbes directly to restore balance in the microbiome

While many herbs have been found to suppress EBV, EBV is rarely found in isolation — chronic immune dysfunction always allows a variety of low-grade stealth pathogens to flourish. Therefore, a comprehensive regimen of herbal extracts is necessary.

Some effective herbal extracts for restoring immune function, balancing the microbiome, and suppressing viruses such as EBV include:

Generally most people will respond to restorative solutions alone. Drug therapy is only necessary if severe or extreme illness is not responding to the restorative therapies. It is, however, important to maintain an ongoing working relationship with your medical provider during your entire recovery.

Ultimately, all of this is great news for those with chronic reactivated EBV: It means the power to take back control of your health and feel better is in your hands. By learning how to limit the System Disruptors in your life, you’ll start to strengthen your immune function so you can live in harmony with microbes like EBV.



Unfortunately, I had to learn about this through my daughter who had severe EBV that lingered and ultimately led to the removal of her tonsils as well as using LDI/LDA therapy:

Being in Wisconsin, an epicenter for Lyme, our LLMD is also who we take our children to – just in case, God forbid, they should become infected.  Our LLMD believes, as Dr. Rawls, that immunoconfusion, or a perfect storm of events overwhelming the immune system, is behind many chronic diseases.  Retraining the immune system to recognize friend vs foe is behind LDA/LDI treatment and can often help many chronic conditions.  It certainly has helped my daughter, who is also hypothyroid, hypoglycemic, and suffers from severe endometriosis.  EBV nearly destroyed her liver.

I can attest to having to learn the importance of diet, hormones, stress, environmental toxins, and microbes.  It is crucial to find a practitioner(s) who is versed in this approach to tease out your imbalances through proper testing and clinical diagnosis.  As with Lyme, much testing isn’t helpful and requires an experienced eye and listening ear to help you uncover your personal pitfalls.  Most doctors are not trained in hormone therapy and with the chemically laden environment we live in, this is most unfortunate as many suffer from serious hormonal imbalances and mineral/vitamin deficiencies.  Doctors are taught to fear hormones when they are naturally occurring substances in the body that often need supplementing due to environmental factors.  I’m of course advocating for bioidential hormones – as close to nature as possible; however, for those of you suffering with endometriosis that makes your life unbearable, please read this unique approach which gave my daughter her life back:

For more:


1. Cohen J. Optimal Treatment for Chronic Active Epstein-Barr Virus Disease. Pediatr Transplant. 2009 Jun; 13(4): 393–396.
2. Joo E et al. An Adult Case of Chronic Active Epstein-Barr Virus Infection with Interstitial Pneumonitis. Korean J Intern Med. 2011 Dec; 26(4): 466–469.
3. Kang M, Kief E. Epstein–Barr virus latent genes. Exp Mol Med. 2015 Jan; 47(1): e131.
4. Jha H, Pei Y, Robertson E. Epstein–Barr Virus: Diseases Linked to Infection and Transformation. Front Microbiol. 2016; 7: 1602.
5. Tsao S et al. The role of Epstein–Barr virus in epithelial malignancies. J Pathol. 2015 Jan; 235(2): 323–333.
6. Paschale M and Clerici P. Serological diagnosis of Epstein-Barr virus infection: Problems and solutions. World J Virol. 2012 Feb 12; 1(1): 31–43.
7. Shen Y et al. Understanding the interplay between host immunity and Epstein-Barr virus in NPC patients. Emerg Microbes Infect. 2015 Mar; 4(3): e20.
8. Tzellos S and Farrell P. Epstein-Barr Virus Sequence Variation—Biology and Disease. Pathogens. 2012 Dec; 1(2): 156–175.
9. Iizasa H et al. Epstein-Barr Virus (EBV)-associated Gastric Carcinoma. Viruses. 2012 Dec; 4(12): 3420–3439.
10. Lassmann H et al. Epstein–Barr virus in the multiple sclerosis brain: a controversial issue—report on a focused workshop held in the Centre for Brain Research of the Medical University of Vienna, Austria. Brain. 2011 Sep; 134(9): 2772–2786.
11. Pender M and Burrows S. Epstein–Barr virus and multiple sclerosis: potential opportunities for immunotherapy. Clin Transl Immunology. 2014 Oct; 3(10): e27.
12. Stanfield B and Luftig M. Recent advances in understanding Epstein-Barr virus. Version 1. F1000Res. 2017; 6: 386.
13. Gru A et al. The Epstein-Barr Virus (EBV) in T Cell and NK Cell Lymphomas: Time for a Reassessment. Curr Hematol Malig Rep. 2015 Dec; 10(4): 456–467.
14. Lossius A et al. Epstein-Barr Virus in Systemic Lupus Erythematosus, Rheumatoid Arthritis and Multiple Sclerosis—Association and Causation. Viruses. 2012 Dec; 4(12): 3701–3730.
15. Rowe M, Fitzsimmons L, and Bell A. Epstein-Barr virus and Burkitt lymphoma. Chin J Cancer. 2014 Dec; 33(12): 609–619.
16. Martorelli D et al. Exploiting the Interplay between Innate and Adaptive Immunity to Improve Immunotherapeutic Strategies for Epstein-Barr-Virus-Driven Disorders. Clin Dev Immunol. 2012; 2012: 931952.
17. Houldcroft C and Kellam P. Host genetics of Epstein–Barr virus infection, latency and disease. Rev Med Virol. 2015 Mar; 25(2): 71–84.
18. Draborg AH, Duus K, and Houen G. Epstein-Barr Virus in Systemic Autoimmune Diseases. Clin Dev Immunol. 2013; 2013: 535738.
19. Rac J et al. Telomerase Activity Impacts on Epstein-Barr Virus Infection of AGS Cells. PLoS One. 2015; 10(4): e0123645.
20. Pender M. The Essential Role of Epstein-Barr Virus in the Pathogenesis of Multiple Sclerosis. Neuroscientist. 2011 Aug; 17(4): 351–367.
21. Dittfeld A et al. A possible link between the Epstein-Barr virus infection and autoimmune thyroid disorders. Cent Eur J Immunol. 2016; 41(3): 297–301.
22. Chen XZ et al. Epstein–Barr Virus Infection and Gastric Cancer
A Systematic Review. Medicine (Baltimore). 2015 May; 94(20): e792.
23. David A. Thorley-Lawson. EBV Persistence—Introducing the Virus. Curr Top Microbiol Immunol. 2015; 390(Pt 1): 151–209.
24. Iwakiri D. Epstein-Barr Virus-Encoded RNAs: Key Molecules in Viral Pathogenesis. Cancers (Basel). 2014 Sep; 6(3): 1615–1630.
25. Dunmire SK, Hogquist KA, and Balfour HH. Infectious Mononucleosis. Curr Top Microbiol Immunol. 2015; 390: 211–240.
26. Krupka JA et al. Infectious mononucleosis-like syndrome with high lymphocytosis and positive IgM EBV and CMV antibodies in a three-year-old girl. Cent Eur J Immunol. 2017;42(2):210-212.
27. Collin V, Flamand L. HHV-6A/B Integration and the Pathogenesis Associated with the Reactivation of Chromosomally Integrated HHV-6A/B. Viruses. 2017 Jun 26;9(7).
28. Warren-Gash C et al. Association between human herpesvirus infections and dementia or mild cognitive impairment: a systematic review protocol. BMJ Open. 2017 Jun 23;7(6):e016522.
29. Fierz W. Multiple sclerosis: an example of pathogenic viral interaction? Virol J. 2017 Feb 28;14(1):42.
30.Enquist LW, Leib DA. Intrinsic and Innate Defenses of Neurons: Détente with the Herpesviruses. J Virol. 2016 Dec 16;91(1).
31. Hutt-Fletcher LM. The Long and Complicated Relationship between Epstein-Barr Virus and Epithelial Cells. J Virol. 2016 Dec 16;91(1).
32. Siddiquey MN et al. Anti-tumor effects of suberoylanilide hydroxamic acid on Epstein-Barr virus-associated T cell and natural killer cell lymphoma. Cancer Sci. 2014 Jun;105(6):713-22.
33. Cekanaviciute E et al. Gut bacteria from multiple sclerosis patients modulate human T cells and exacerbate symptoms in mouse models. Proc Natl Acad Sci U S A. 2017 Sep 11. pii: 201711235.
34. Berer K et al. Gut microbiota from multiple sclerosis patients enables spontaneous autoimmune encephalomyelitis in mice. Proc Natl Acad Sci U S A. 2017 Sep 11. pii: 201711233.
35. Ivanova MV et al. Role of Chlamydia in Multiple Sclerosis. Bull Exp Biol Med. 2015 Sep;159(5):646-8.
36. Libbey JE, Cusick MF, Fujinami RS. Role of pathogens in multiple sclerosis. Int Rev Immunol. 2014 Jul-Aug;33(4):266-83.
37. Sriram S et al. Detection of chlamydial bodies and antigens in the central nervous system of patients with multiple sclerosis. J Infect Dis. 2005 Oct 1;192(7):1219-28. Epub 2005 Sep 2.
38. Buhner S. Herbal Antivirals, Natural Remedies for Emerging & Resistant Viral Infections. Storey Publishing. Copyright 2013.


U.S. Army Warns About Ticks

Season of the tick continues into the fall

By Capt. Angela L. Brewer, Chief, Environmental Health Clinic, Kenner Army Health Clinic October 5, 2017

FORT LEE, Va. (Oct. 5, 2017) — Due to the milder winter last year, this summer had more ticks than usual.

And even while the fall season has begun, individuals still need to take precautions when enjoying outdoor activities while warm weather continues.

People may not realize, but most vector-borne diseases are tick-borne. Infections from these diseases are on an increase and the geographic ranges of ticks also are expanding. Reducing exposure and eliminating habitats is the best course of action to protect adults and children.

The Blacklegged tick, Lone star tick and the American dog tick cause most human diseases. Most ticks found on Fort Lee and the local area are Lone star ticks and can possibly carry diseases, such as Ehrlichiosis, Tularemia and Heartland virus. Nearly all tick-borne diseases have many of the same symptoms — fevers and chills, aches and pains and rashes around bite location. Few cases result in death, especially if quickly diagnosed and treated.

Although these are referred to as tick-borne diseases, ticks are all born disease free. The tick feeds on a host organism infected with a blood-borne pathogen. The organism is ingested into the tick thus becoming the vector of the disease. If the vector feeds on a human for its next meal, then that person could acquire the pathogen and become ill. Not all organisms are infected, and not all vectors carry diseases. If the tick is infected, the pathogen takes approximately 24 hours to “reactivate” and get into the tick’s saliva. Ticks have specialized saliva that numbs the skin and acts as a cementing agent, which is how they can get such a firm grip on a person. A tick must be actively feeding on you for several hours to transmit a disease.

Prevention strategies include personal protection, environmental modification and tick suppression. The DOD insect repellent system is the service member’s personal protection method. A properly worn uniform is the best defense. All uniforms are now pre-treated with permethrin, which kills ticks on contact. Uniforms must be worn properly with the trouser tucked inside the boots. Also, application of a DEET-based insect repellent to any exposed skin will provide an additional layer of defense.

Off-duty service members, civilians and their families can use the same principles as well. Wear long pants when in wooded or brushy areas and tuck them into high-top boots or long socks. Wear light- colored clothing so ticks can be easily spotted and brushed off. Additionally, there are permethrin treatment kits that can be purchased to treat civilian clothing. A well landscaped yard or area surrounding buildings is an example of environmental modification. A smart landscaping tip would be to make the yard less attractive to ticks. For example, short grass and bright sunlight help reduce the tick populations in yards or on golf courses. Remove leaves branches and debris that will eliminate hiding places for ticks as well as their hosts. Install some type of barrier along the perimeters of child development centers or create gravel or wood chip pathways through wooded areas. Tick suppression is simply the application of pesticides or reducing or eliminating the hosts that ticks seek for blood meals, i.e. deer.

If bitten by a tick and the skin has been broken, remove it carefully with fine point tweezers. Do not burn, apply petroleum jelly or utilize any other mythical home remedies because there is no substitute for the following proper technique. First, disinfect the surrounding area with an alcohol swab.

Next, place tweezers as close to skin as possible and grasp the insect firmly. Pull straight up slowly until the tick either comes out or breaks. The infectious material is much farther back in the tick’s body, so there is no reason to fret if the head breaks off during removal.

After removal, keep it in a clean plastic bag and store it in a cool dry place like a refrigerator. Make an appointment to take the tick to your primary care provider. The PCM has procedures in place with Environmental Health to have the tick identified and tested for the presence of diseases.

Ticks that have not broken the skin or found on pets will not be tested.
For more information, visit A kids’ resource can be found at



There’s much we don’t know and one of those things is minimal transmission time for infection for LD.  Please know multitudes have been infected in under 24 hours.  We do know Powassan virus, another TBI, can be transmitted in mere minutes:


Prevention tips:

Droplet Digital PCR Shows 60% Bb Infection Rate in Ticks and Over 50,000 Spirochetes Per Adult Tick

Validation of droplet digital PCR for the detection and absolute quantification of Borrelia DNA in Ixodes scapularis ticks


We evaluated the QX200 Droplet Digital PCR (ddPCR™, Bio-Rad) system and protocols for the detection of the tick-borne pathogens Borrelia burgdorferi and Borrelia miyamotoi in Ixodes scapularis nymphs and adults collected from North Truro, Massachusetts. Preliminary screening by nested PCR determined positive infection levels of 60% for B. burgdorferi in these ticks. To investigate the utility of ddPCR as a screening tool and to calculate the absolute number of bacterial genome copies in an infected tick, we adapted previously reported TaqMan®-based qPCR assays for ddPCR. ddPCR proved to be a reliable means for detection and absolute quantification of control bacterial DNA with precision as low as ten spirochetes in an individual sample. Application of this method revealed the average carriage level of B. burgdorferi in infected I. scapularis nymphs to be 2291 spirochetes per nymph (range: 230–5268 spirochetes) and 51,179 spirochetes on average in infected adults (range: 5647–115,797). No ticks naturally infected with B. miyamotoi were detected. The ddPCR protocols were at least as sensitive to conventional qPCR assays but required fewer overall reactions and are potentially less subject to inhibition. Moreover, the approach can provide insight on carriage levels of parasites within vectors.



While this is a great start, there are many other pathogens to be concerned with besides Borrelia burgdorferi (Bb), the agent of Lyme Disease:, and there are many more besides the six mentioned in this article.  Bartonella has not been proven conclusively to be transmitted by ticks, but it is highly likely.  It is also a frequent coinfection and can be spread by:

Arthropod vectors including fleas and flea feces, biting flies such as sand flies and horn flies, the human body louse, mosquitoes, and ticks; through bites and scratches of reservoir hosts; and potentially from needles and syringes in the drug addicted. Needle stick transmission to veterinarians has been reported. There is documentation that cats have received it through blood transfusion. 3.2% of blood donors in Brazil were found to carry Bartonella in their blood. Bartonella DNA has been found in dust mites. Those with arthropod exposure have an increased risk, as well as those working and living with pets that have arthropod exposure. 28% of veterinarians tested positively for Bartonella compared with 0% of controls. About half of all cats may be infected with Bartonella – as high as 80% in feral cats and near 40% of domestic cats. In various studies dogs have close to a 50% rate as well. Evidence now suggests it may be transmitted congenitally from mother to child – potentially leading to birth defects.

There is much work yet to be done.






Premature Infants Develop Babesia Via Blood Transfusion

A Cluster of Cases of Babesia Microti Among Neonates Traced to a Single Unit of Donor Blood


Three premature infants in one neonatal intensive care unit (NICU) developed transfusion-transmitted babesiosis. Two of the infants developed high-grade parasitemia. All three affected infants were treated and cured with azithromycin and atovaquone. No infant required exchange transfusion. Clinicians should be cognizant that babesiosis may be acquired via blood transfusion.


Babesia is finally getting the press it deserves.  Lately there has been much on transmission by transfusion as well as deaths in patients without spleens.   “Asymptomatic individuals with Babesia infection are able to donate blood in the United States because of the lack of specific blood donation testing. Blood products collected in Babesia-endemic areas are distributed nationally; thus, clinicians in nonendemic states may fail to include babesiosis in the differential diagnosis of a patient who had a recent transfusion history and a fever of unknown origin.” Babesia spread congenitally  Death in patient without spleen   Blood-donation screening for antibodies to and DNA from B. microti was associated with a decrease in the risk of transfusion-transmitted babesiosis.  Dr. Horowitz, a nationally recognized LLMD, states Babesia is one of the most tenacious coinfections he sees in his patients and that treatment often takes 9 months to a year, particularly with those also infected with Lyme disease (borrelia).  Treatment options in this link.  When left untreated, silent babesial infection may persist for months or even years. Although treatment with clindamycin and quinine reduces the duration of parasitemia, infection may still persist and recrudesce and side effects are common. Improved treatments are needed.

Dr. Krause published in the New England Journal of Medicine that when a patient has Lyme and Babesia, Lyme is found three-times more frequently in the blood, proving Babesia suppresses the immune system.   Dr. Horowitz warns that due to this immune suppression, patients with Rheumatoid Arthritis or Lupus and are on immunosuppressant drugs, if they have Babesia, could get much worse. The strain, B. divergens, causes a higher mortality rate and more severe symptoms, and if left untreated, this strain can develop into shock-like symptoms with pulmonary edema and renal failure.


Man Dies of Babesia“>  (video here)  By Ali Gorman, R.N.  

Husband dies of disease caused by deer tick in Bucks County

 A Bucks County woman is sharing the story of how she lost her husband to a disease she’d never heard of, and is spread by ticks.

Crissy Naticchia is still in shock. Her fun-loving husband Jeff died nearly two months ago from an infection spread by a tiny deer tick.

“It’s going to be a long, hard road ahead. I mean we had so much to do. He was only 50,” she said.

In late July, Jeff came down with a fever, sweating and fatigue. At the hospital, Crissy says it took several days for doctors to make the diagnosis. It was Babesiosis.

Doctor Neil Fishman with Penn Medicine didn’t treat Jeff, but he specializes in infectious diseases.

He says Babesiosis is transmitted by the same tick as Lyme disease.

Many people infected won’t have symptoms, but for others they will.

“The problem is the disease can get very severe if people don’t have a normal immune system,” Dr. Fishman said.

That includes people on chemotherapy, transplant recipients, elderly and anyone without a spleen.

Crissy says Jeff had his spleen removed as a child, but it never caused any problems.

“In 26 years, he’d been sick maybe twice,” she said.

Now she and their children Nicole and Max are hoping to raise awareness about Babesiosis.

It’s considered reportable, and tracked by many state health departments including, New Jersey and Delaware, but not Pennsylvania.

Doctor Fishman says it’s relatively rare in the state, but could be emerging.

“As you said we are seeing more and more Lyme disease in certain parts of the state, so we may start to see an increase in babesiosis,” he said.

Crissy added, “We live in Bucks County, across from a state park, there’s ticks everywhere. I want people to know, it’s not just Lyme. There’s other horrible diseases that are carried by ticks.”

The best prevention is insect repellent with DEET, long pants or sleeves, and to check your body for ticks after you’ve been outside in a park or in the

In the case of Babesiosis, if ticks are removed within 24 hours, they can’t transmit the disease. However, there are other tick-borne illnesses that can be spread faster. (Please read comment at end of article)

It’s always a good idea to consult with your physician if you have any concerns.


A couple of things:  the lack of a spleen was this man’s undoing.Risk factors for severe disease include:

Do not have a spleen (up to 20% mortality)
Weak immune system (AIDS, corticosteroid therapy, malignancy with therapy, multiple stealth microbe infections at one time)
Elderly (>50 years old, especially with health problems)

As to removing a tick within 24 hours not transmitting Babesia – well that’s a crock of hooey.  Show me the studies and I will find a hundred people who defy them.
The claims that removal of ticks within 24 hours or 48 hours of attachment will effectively prevent LB are not supported by the published data, and the minimum tick attachment time for transmission of LB in humans has never been established.
Additionally ticks carry many other diseases including tick-borne encephalitis, human granular ehrlichiosis, babesiosis, bartonellosis, and others. The attachment times for transmission of many of these are unknown, though there is evidence that some are transmitted very quickly.
The challenge with these studies, and there are many, is that most placed multiple ticks on multiple rodents. Multiple ticks may be transmitting different pathogens. It has also been shown that ticks feeding on mice coinfected with B. microti and B. burgdorferi were twice as likely to become infected with Bb compared to B. microti, suggesting that coinfection can amplify certain pathogens – which is another reason to only use one rodent and one pathogen to separate out multiplying factors that muddy the waters. Also, rarely do studies record the titer of both tick and host – again, making it nearly impossible to determine what’s what. It was also noted that transmission times are unknown for many pathogens.
**And as always: if you are the ONE person who contracted Lyme Disease in 10 minutes, all these numbers are essentially meaningless. The frightening truth is that these numbers, along with geographical information regarding tick habitats, are often used against patients. It is beyond time for doctors to listen, educate themselves, and treat patients with the respect they deserve – not to mention it’s time for them to treat patients clinically and not based on tests that are wrong over half the time and with the knowledge that ticks are spreading everywhere and bringing the pathogens with them. (In other words, throw the maps away!)
The review essentially gives the following transmission times for various pathogens. Again, please know these numbers are not definitive and many, many cases have proven this fact.
Take each and every tick bite seriously and don’t mess around and take a “wait and see approach.” There is too much at stake.
 There is so much we don’t know for certain and peoples’ lives are at stake.  To claim to be all knowing would be foolish.  Far better to plainly state, “Ticks are nature’s dirty needles.  The quicker you properly get that sucker off the better, as there is much we don’t know about transmission times!”  

Night at the Blood Sucking Creature Museum

A museum of blood-sucking nightmares: the US National Tick Collection

Posted: Sep 15, 2017 9:18 AM CDT

Susan Scutti, CNN –


To get to the US National Tick Collection, visitors to the campus of Georgia Southern University must descend into the bowels of the Math/Physics Building, where sunlight is absent and locked doors with unpronounceable signs prohibit entry.

Curator Dr. Lorenza Beati, a smiling woman in wire-rimmed glasses and blue jeans, a woman who radiates the same vibe as a kindly, eccentric aunt, welcomes anyone who has daring enough spirit.

Inside the collection, an elaborate camera for shooting closeups of ticks has made its home in a cramped room. It has a strobe-light effect to capture precise images of individual ticks splayed on white backgrounds, and as she operates the camera, Beati’s palce face appears in shadow and light.

She leads the way to a large abandoned-looking space where retro scientific fume hoods, glass beakers and microscopes reside. A narrow hallway is made even more congested by filing cabinets lining both walls. In turn, they are crammed with dusty files and yellowed correspondence from another century.

The main room of the collection is a brightly lit, cheerful place with coloring books and temporary tick tattoos available for the youngest visitors, and immaculate white-metal cabinets holding countless drawers.

Open the drawers to find bottles upon bottles of tick specimens, an endless variety of small, dark forms permanently suspended within clear liquid — a science-fantasy version of prison or hell, depending on a visitor’s horror movie associations.

A trip through tick world

The national tick collection is part of the Smithsonian Institution and is the world’s largest, by every account. Housed at Georgia Southern University in Statesboro since 1990, the collection contains over a million specimens representing 96% of the world’s 900 recognized tick species, including all those found in the United States.

“We keep our ticks preserved in 90% ethanol,” Beati says, emphasizing the word “we.” When kept in ethanol, specimens can last hundreds of years, she says. Dry ticks pinned like butterflies have been known to last 200 years; these should keep even longer.

The collection’s birthplace was Rocky Mountain Laboratories in Hamilton, Montana, in 1905. Some of the specimens are historical artifacts — ticks found on presidents’ dogs or on animals shot by Teddy Roosevelt — but it doesn’t take a fancy pedigree to wow Beati.

“To me, the most basic dog tick can be interesting,” says Beati, also an associate professor of biology at Georgia Southern. All ticks are blood-feeders — that’s their only food, she explains. Some will feed on any of the many terrestrial vertebrates, a category that includes birds, reptiles, mammals and amphibians. Yet other ticks are finicky eaters, such as the rat snake tick, which feeds only on the blood of that particular serpent.

To most of us, ticks may appear to be just another bug, but this is not the case. Unlike insects with segmented bodies that include distinct heads, thoraxes and abdomens, ticks are more like “a unique bag containing all their organs,” Beati says. “Ticks are not insects; they are arachnids.”

With eight legs, they are closely related to spiders and scorpions. Ticks are also mites, a diverse subclass of arachnids. “Ticks are probably the group of mites best known because they transmit diseases,” Beati says.

In fact, the core of the collection was formed in 1905 when scientists discovered that ticks could transmit illness, she explains.

First reaction of visitors

The ancient Egyptians used large ticks with bright, colorful spots on their backs as inspiration for jewelry, Beati says. African ticks feed on large animals and so become the most decorated and most colorful — in some cases, a pure gold hue — among their species, she explains.

Children from the Statesboro area who make the trek to the collection, shepherded by their teachers, often love the colorful ticks, Beati says. They also like the big ticks, those reaching a size of three-quarters of an inch or more.

” ‘Can ticks explode?’ That’s one of the questions they have, because they see them so big,” Beati says. “No. Ticks cannot explode. They know when to stop.

“Ticks are never a favorite of anyone. Usually the first reaction — it’s always, ‘Bew, what are these things?!’ But when we show them how diverse ticks are, how important they are for public health, they become more interested,” she says.

She herself took to ticks only after learning more about them.

“I’m an M.D., and I started studying parasitology in Switzerland, and the specialty of the laboratory where I was studying parasitology was vectors — so all the attributes that transmit diseases to humans or domestic animals, and in particular, ticks,” Beati, a Swiss native, says. “They were discovering at that time Lyme disease in Europe. So it was a really hot topic.”

From the Institute of Zoology in Neuchâtel, Switzerland, Beati’s interest in ticks led her to the World Health Organization’s Collaborative Center for Rickettsial Diseases and Arthropod-borne Bacterial Diseases in Marseilles, France, and then the US Centers for Disease Control and Prevention in Atlanta. She was working at Yale University in New Haven, Connecticut, when the opportunity to curate the tick collection arose.

Beati — whose name means “blessed”In Italian — jumped at the chance. After all, the collection is an active resource that researchers from all corners of the Earth make the trek to see.

“They compare their specimens to ours to decide whether or not they are dealing with already described species or new ones,” Beati explains.

Previously unknown ticks, then, are sometimes identified at the collection by way of these comparisons. Along with taxonomy, scientists and students work on gaining a better understanding of tick biology and tick-borne diseases.

Ticks cause “many, many diseases,” Beati says. “Lyme disease is probably the most popular in the US.” Ixodes scapularis, the deer tick, transmits Lyme.

Another “very important disease” in America is Rocky Mountain spotted fever, which is transmitted by Dermacentor variabilis, or the dog tick. This disease has spread farther than its name would suggest, Beati notes: “There were some really deadly cases of Rocky Mountain spotted fever in the Native American reservations in Arizona and New Mexico.”

“Probably the most dangerous disease transmitted by ticks is Crimean-Congo hemorrhagic fever,” she says, explaining that Hyalomma ticks found in desert areas of Africa and the Middle East transmit it.

Once one person is infected, a tick is no longer required for this illness to be passed from person to person. “You bleed, and it can be deadly,” Beati says, shaking her head sadly. “It’s a bad disease.”

Global citizens

There are different opinions about when ticks first appeared on the planet, with hypotheses ranging from 200 million to 400 million years ago, Beati says. Yet all scientists agree on one thing: Ticks have evolved to adapt to an enormous number of habitats on all continents.

“So you can find them in Antarctica, and you can find them deep in the Sahara desert,” Beati says, adding that their blood habit has led to some unique characteristics.

For example, one family of ticks “can survive without feeding for decades,” she says. “They just go dormant, and their metabolism is very slowed down, but you open the box, you blow on the box, and they start moving around, and they are fine.”

Some of these ticks have been kept alive in the laboratory for over 12 years without any food: blood.

“If you think about ticks, they are parasites, but unlike a mosquito, a tick has to feed for a long time,” Beati said. “It’s not one second and it’s gone.” Instead, a tick has to fight the host’s immune system, and so it has developed a diverse array of molecules, she explains.

“They inject anesthetics so that you don’t feel anything,” Beati says. “They inject anticoagulants so that the blood will keep flowing where they are biting and it doesn’t clog. They inject antihistamines so that you don’t feel the itch when they bite, and they also inject molecules that really fight your immune system, so you are immune-suppressed where they bite you.”

Scientists have begun work synthesizing similar molecules in their labs to use as human medicines, she says. Recent molecular work focuses on the genetic material found in ticks. In fact, tick DNA is a gold mine of information.

“DNA extracted from a tick will contain both the DNA of the tick plus the DNA of the pathogens in the tick, or the DNA of the blood of the animal that was the last host of the tick,” Beati says. “You can basically have the list of every single bacterium that goes on in a tick. In one tick, you can find hundreds and hundreds of bacteria.”

With the field of tick-related science moving very fast, “we will discover lots of new microorganisms,” she says. The newest molecular tools and techniques help scientists predict the possibility of disease. “New diseases transmitted by ticks — people call them emerging diseases — have been popping up on a regular basis,” she says.

Whether you’re a scientist or a citizen, safety remains key when you encounter — or are bitten by — a tick.

Through her eyes

Depending on the species — and how well-fed they are — female ticks “can lay thousands of eggs. Two thousand. Three thousand,” Beati says. This is why people who wade into long grass and disturb a batch of larvae may find hundreds of ticks clinging to them.

“One of the important things we tell people when they want to remove ticks is, don’t break the tick,” Beati says. She explains that if you do so, any bacteria in the tick could end up on your skin. If you have an open wound, whether from the tick bite or not, the tick juice might infect you. “So always, when you remove ticks, make sure you disinfect well your hands and your fingers.”

For a tick to grab hold of you, you have to touch them, and then they will climb on you and decide whether you are an animal they like, Beati explains. If so, they will find a place on your body where they feel comfortable enough to feed.

This is usually a “darker place where they can hide,” Beati says. “So if you find a tick crawling on you, you have a bit of time before they actually start biting you.” Even after an infected tick bites, hours may pass — up to 24 after the initial bite — before you become susceptible to disease.

*Please see my comment at end of article*

Beati herself is no stranger to their bite. It happens all the time, she says: “I actually love that. It helps me collect.” That said, not every tick she discovers in this way finds its way to a home in one of her specimen jars.

Disease may be frightening, but fear is not uppermost in Beati’s mind when she sees a tick.

“If you look at any tick under the microscope, you will find something beautiful about them,” this renowned scientist says. “They look like beautiful wood.”

0riginal story:

As to transmission time to infection: (Excellent video by microbiologist Holly Ahern)
Only 1 mouse study has been done that showed by 24 hours every tick had transmitted infection; however, animals studies have proven it can occur in under 16 hours and frequently in under 24.  NO HUMAN STUDIES HAVE EVER BEEN DONE, and no studies have determined minimum time required for transmission.  There is also the issue of partially fed ticks which can transmit more quickly as spirochetes are already in their salivary glands.  Also, Anaplasma and other tick borne infections can be spread in minutes.
One other point:  No ticks can’t fly, but they can blow in the wind.  They state they can’t drop from trees, but let’s use our gray matter for a moment.  If a tick comes off a bird or rodent in a tree, who is to say it can’t fall or drop and infect a person beneath.  Many patients insist they became infected this way. (one such story here but I’ve heard of many, many more)