Archive for the ‘Uncategorized’ Category

Avril Lavigne on Lyme Disease Battle: “I Was in Bed for F–king 2 Years”

(Go to link for video.  Approx. 1 Min)
Avril Lavigne is opening up about her battle with Lyme disease.
The 34-year-old singer gets candid about her health, career and more in a new interview for her Billboard cover story, during which she reveals she was in bed for two years amid her Lyme disease battle. The Grammy nominee was on tour in 2014 when she started to feel fatigued and achy, which led her to ask,

“What the f–k is wrong with me?”

When the tour came to an end, one of Lavigne’s friends realized she might have Lyme disease. According to Billboard, she was encouraged to call Canadian music producer David Foster‘s then-wife Yolanda Hadid, who had also been battling Lyme disease. Hadid ended up giving Lavigne the contact information for a Lyme specialist.

Avril Lavigne, Billboard

David Needleman


“I was in bed for f–king two years,” Lavigne tells Billboard. “It’s a bug — a spirochete — so you take these antibiotics, and they start killing it.”

“But it’s a smart bug: It morphs into a cystic form, so you have to take other antibiotics at the same time,” Lavinge continues. “It went undiagnosed for so long that I was kind of f–ked.”

The Billboard interview also states that Lavigne was in bed with her mother one night during her battle, barely able to breathe, when she started to pray.

Avril Lavigne, Billboard

David Needleman


“I had accepted that I was dying,” she tells the outlet. “And I felt in that moment like I was underwater and drowning, and I was trying to come up to gasp for air. And literally under my breath, I was like, ‘God, help me keep my head above the water.'”

That became the inspiration for her song “Head Above Water,” which she released last month after about a five-year hiatus. The singer worked on the song with her ex, Chad Kroeger, who she calls “great” and who also worked on more songs with Lavigne for her upcoming album.

“The silver lining of it is that I’ve really had the time to be able to just be present, instead of being, like, a machine: studio, tour, studio, tour,” she says. “This is the first break I’ve ever taken since I was 15.”

To read more from Lavigne’s interview, pick up a copy of Billboard, on newsstands Friday.

Yolanda Hadid Reveals She’s ‘Not Feeling Good’ Again After ‘One Year of Remission’ From Lyme Disease

Yolanda Hadid Reveals She’s ‘Not Feeling Good’ Again After ‘One Year of Remission’ From Lyme Disease

The fight continues. Yolanda Hadid revealed during her speech at the Global Lyme Alliance Gala in New York City on Thursday, October 11, that she is struggling with her Lyme disease battle again after one year of remission.
lyme disease
Yolanda Hadid speaks onstage during the Global Lyme Alliance Fourth Annual New York City Gala. Dave Kotinsky/Getty Images

“What keeps me getting up every morning is my two children that also have had Lyme disease,” the 54-year-old began, referring to her model daughter Bella Hadid and son Anwar Hadid. (She is also mother of model Gigi Hadid). “Quite often, I just went to get on with my life and pretend the whole nightmare never happened. I got sick in 2000. We’re now in 2018. I had one year of remission.”

The Real Housewives of Beverly Hills alum then explained she is not quite “back where [she] started” with her illness, but she is also no longer “feeling good.”

“[I’m] just wanting to crawl in a hole and wait for it all to pass, but I also understand the higher purpose of my journey is to continue to bring awareness to this awful disease until the change is made,” Yolanda told the crowd, which included fellow Housewives Luann de Lesseps, Dorinda Medley, Sonja Morgan, Tinsley Mortimer and honored guest Ramona Singer

lyme disease
Ramona Singer, Luann de Lesseps, Tinsley Mortimer, Yolanda Hadid, and Dorinda Medley attend the Global Lyme Alliance Fourth Annual New York City Gala. Rob Kim/Getty Images

“What keeps me awake at night is not my journey the journey of my children and so many children in the world that don’t get the proper treatments that they deserve,” she continued. “Living in today’s world is hard enough as a healthy child. It’s time that we all put an end to this. If I die next week, next month, next year — this is the most, the greatest cause I have ever fought for.”

She concluded:

“Even today, I have been in treatment all day. I feel like s—t. I showed up because this has to change.”

Yolanda has been very vocal about her struggles with Lyme disease over the years, documenting her ups and downs on RHOBH for four seasons and telling her story in her 2017 memoir, Believe Me: My Battle with the Invisible Disability of Lyme Disease.




GLA Video on Lyme

Approx. 4.5 Min

This video premiered at the 2018 Global Lyme Alliance New York Gala. Watch GLA leadership and GLA-funded researchers, among others, share insights into the problem of Lyme disease and what GLA is doing to solve it.



Lots of great info here.  Correcting Senator Blumenthal, Lyme is not an epidemic, it’s a literal pandemic.

Also, there are reasons the map showing Lyme isn’t entirely blacked out:  1)  The CDC maps are notoriously faulty 2) We are only talking about Lyme (borrelia) 3) There are many other pathogens involved in this nightmare that need to be factored in as well and recognized by main-stream medicine, surveillance, researchers, and the media.  These pathogens singularly are serious but when coupled with Lyme are deadly.

Throw these maps out!  Historically maps have been used against seriously ill patients for decades.  They have been denied diagnosis and treatment due to a piece of paper.

This tick border thing is a man-made constructed paradigm that has never been accurate, but it’s fit the CDC/NIH/IDSA narrative. (go to page 6 and read about Speilman’s maps which are faulty but have ruled like the Iron Curtain.)  According to independent Canadian tick researcher, John Scott, Ticks and Lyme are NOT propelled by climate change but by migratory birds and other reservoirs who do not refer to maps in their travels!

For more:



Multilocus Sequence Typing of Clinical Borreliella Afzelii Strains: Population structure and Differential Ability to Disseminate in Humans

Multilocus sequence typing of clinical Borreliella afzelii strains: population structure and differential ability to disseminate in humans.

Gallais F, et al. Parasit Vectors. 2018.


BACKGROUND: Lyme borreliosis in humans results in a range of clinical manifestations, thought to be partly due to differences in the pathogenicity of the infecting strain. This study compared European human clinical strains of Borreliella afzelii (previously named Borrelia afzelii) using multilocus sequence typing (MLST) to determine their spatial distribution across Europe and to establish whether there are associations between B. afzelii genotypes and specific clinical manifestations of Lyme borreliosis. For this purpose, typing was performed on 63 strains, and data on a further 245 strains were accessed from the literature.

RESULTS: All 308 strains were categorized into 149 sequence types (STs), 27 of which are described here for the first time. Phylogenetic and goeBURST analyses showed short evolutionary distances between strains. Although the main STs differed among the countries with the largest number of strains of interest (Germany, the Netherlands, France and Slovenia), the B. afzelii clinical strains were less genetically structured than those previously observed in the European tick population.

Two STs were found significantly more frequently in strains associated with clinical manifestations involving erythema migrans, whereas

another ST was found significantly more frequently in strains associated with disseminated manifestations, especially neuroborreliosis.

CONCLUSIONS: The MLST profiles showed low genetic differentiation between B. afzelii strains isolated from patients with Lyme borreliosis in Europe.

Also, clinical data analysis suggests the existence of lineages with differential dissemination properties in humans.



This research highlights why thousands of patients remain undiagnosed. CDC two-tiered testing tests for ONE STRAIN of borrelia.  ONE.  There are 300 strains and counting worldwide.

It also shows how the differences between strains matter.  In this study, some strains were associated with the EM rash, while others were associated with disseminated symptoms – particularly neuroborreliosis.

Huh.  Guess we weren’t making it all up after all.
Could someone give the memo to the CDC, NIH, & IDSA?









Basketball Star Pushing for Lyme Cure

Great interactive article in link above on stats, prevention, symptoms, and the Elena Delle Donne Charitable Foundation.

Case of Recurrent Fever & Multiple Splenic Infarcts (& Why Short Treatment Duration Often Doesn’t Work for Babesia)  (See comment at end of article)

An 85-Year-Old Man With Recurrent Fever and Multiple Splenic Infarcts

Shuker, Orel, MSc; Subran, Mala, MBBS; Hardie, Rochelle, MBBS; Ghitan, Monica, MD; Chapnick, Edward K., MD; Lin, Yu Shia, MD

Infectious Diseases in Clinical Practice: September 2018 – Volume 26 – Issue 5 – p 300–302
doi: 10.1097/IPC.0000000000000643

An 85-year-old man with a history of benign prostatic hyperplasia, hyperlipidemia, and Guillain-Barré syndrome in 1989 presented in September 2017 for the third time in 2 months with intermittent fever, chills, and night sweats. In July, he presented with a 5-day history of intermittent fever, with a temperature of 103°F and chills. The urinalysis and chest x-ray were normal, and 2 sets of blood cultures showed no growth. A computed tomography (CT) scan of the abdomen and pelvis was performed (Fig. 1A). The leukocyte count was 4200/μL (69% neutrophils), hemoglobin (Hb) 11.0 g/dL, and platelet count 63,000/μL. Patient received 3 days of azithromycin and was discharged with 2 days of oral cefpodoxime and azithromycin to complete a 5-day course of treatment.

The patient was readmitted to the hospital 4 days later with fever of 104°F associated with chills and sweating. Intravenous vancomycin, cefepime, and metronidazole were given. The leukocyte count was 7800/μL, Hb 11.0 g/dL, and platelet count 386,000/μL. Blood cultures and CT of the abdomen and pelvis were negative. The patient was discharged from the hospital on day 4 without antibiotics when fever subsided.

In mid-September, 2 months after the initial presentation, the patient was readmitted to the hospital for recurrent fever for 10 days, with worsening fatigue, malaise, and anorexia. The leukocyte count was 6100/μL, Hb 7.6 g/dL, and platelet count 130,000/μL, with lactate dehydrogenase 849 U/L, alanine aminotransferase 53 U/L, aspartate aminotransferase 70 U/L, and alkaline phosphatase 41 U/L. The erythrocyte sedimentation rate was 115 mm/h, and C- reactive protein was 10 mg/dL. Blood cultures and echocardiogram were normal. Repeat CT scan of the abdomen and pelvis is shown in Figure 1B. The patient denied travel outside New York. He is originally from Greece and has lived in Brooklyn, NY, for 50 years. He did not recall any insect or tick bites, and no other family members had a similar illness. The patient denied any dental procedures in the past year. Patient’s home medications were finasteride and pravastatin. What is your diagnosis?

Part 2

Diagnosis: Babesia Infection Caused by Babesia microti

Our patient presented with intermittent fever of unknown origin, and tick-borne disease was not included in the differential diagnosis initially. Thus, peripheral smears for parasites were not done in his previous 2 admissions. The initial CT scan showed a normal liver and spleen size (Fig. 2A). A subsequent CT scan 2 months later revealed numerous new splenic infarcts with hepatosplenomegaly (Fig. 2B). As mentioned, blood cultures and echocardiogram were nondiagnostic. On further questioning, the patient recalled that he had visited family in Greenport, Long Island, for the fourth of July weekend, 5 days prior to the onset of his febrile illness. Peripheral blood smear showed intraerythrocytic and extraerythrocytic ring inclusions consistent with babesiosis (Fig. 3) with 0.3% parasitemia. Polymerase chain reaction for Babesia microti was positive. Our patient was immediately started on azithromycin plus atovaquone, and the temperature normalized within 48 hours. He was discharged home on hospital day 7.

Splenic infarction is a rare complication of Babesia infection. To date, only 2 cases of splenic infarction in association with Babesia infection in humans have been published in the literature.1 Interestingly, azithromycin as monotherapy at a higher dose resulted in a significant reduction in Babesia parasitemia and prolongation of survival when compared with controls in hamster models.2 Our patient’s initial improvement in fever and thrombocytopenia after his first hospitalization was likely due to azithromycin therapy. There has been evidence of drug resistance to azithromycin-atovaquone with relapse of Babesia infection in immunocompromised patients after initial exposure to azithromycin as monotherapy.3 However, our patient remained afebrile and has been doing well 3 months after completion of a 10-day course of azithromycin plus atovaquone therapy.

Babesiosis is a tick-borne infection caused by intraerythrocytic protozoa of the genus Babesia, transmitted by the Ixodes tick. Babesia microti is the most predominant strain in the Northeastern and upper Midwestern region of the United States.4 The most common route of transmission is via direct inoculation from Ixodes scapularis ticks. Blood transfusion and rarely transplacental transmission have also been documented.4 The peak acquisition of disease occurs between May and September. Although tick activity and tick-borne diseases are common in warmer months, I. scapularis is active throughout the year, when ambient-air temperature is greater than 4°C (40°F).5 Thus, babesiosis should be considered and investigated appropriately even during the months not typical for increased tick activity.

Clinical manifestations of Babesia infections are variable, depending on the Babesia species and the immune status of the host. Clinical presentation of babesiosis includes febrile hemolytic anemia due to parasite-mediated lysis of red blood cells in the circulation.6 Babesia infections may induce cycles of disease by varying antigen expression and by displaying new outer-surface proteins during the disease course. The antigenic variants are referred to as serotypes and prevent the elimination of the protozoa by the immune system. This may contribute to the recurring nature of relapsing fever.7

Immunocompetent individuals typically have subclinical illness, associated with low-level parasitemia (<4%) and may present with a gradual onset of nonspecific flulike symptoms. Babesiosis in immunocompromised patients is often severe, with a complication rate of 40% to 60%, including acute respiratory failure, congestive heart failure, renal failure, and disseminated intravascular coagulation.8,9 Patients may present with splenic infarction as in our patient. Proposed mechanisms of splenic infarction in human babesiosis include microthrombus formation and local release of vasoactive factors caused by red blood cell lysis leading to infarcted necrosis of splenic tissue.10 Moreover, during infection, proinflammatory cytokines are released, specifically tumor necrosis factor, interleukin 1, interleukin 6, and interferon, leading to increased expression of adhesion molecules on the surface of the vascular endothelium. This in turn results in cytoadherence of the infected erythrocytes to the vascular endothelium.10 The parasitized erythrocytes also lack the deformability needed to transit the splenic sinusoids, causing their sequestration by resident macrophages and obstruction of the vascular flow within the spleen.1

Our patient presented with fever of unknown origin and new splenic infarcts secondary to Babesia infection. Our case reinforces the importance of taking a detailed history including travel history when evaluating a patient with fever of unclear etiology. Our patient did not think that it was relevant to mention during his earlier admissions to the hospital that he traveled to Greenport, Long Island (Suffolk County), for a weekend. Furthermore, babesiosis should be included in the differential diagnosis in a patient who presents with nonspecific flulike symptoms, hematological manifestations, and new splenic infarcts on radiographic imaging. Physicians should ensure timely diagnostic testing and appropriate initiation of treatment in a patient with babesiosisand splenomegaly to prevent further progression to splenic infarct or rupture, which may lead to a fatal outcome.


The authors thank Myrna Dyer from the Department of Microbiology for providing the blood smear figure and Keith Arbeeny from the Department of Radiology of Maimonides Medical Center in Brooklyn, NY, for providing the radiological imaging figures.


1. Florescu D, Sordillo PP, Glyptis A, et al. Splenic infarction in human babesiosis: two cases and discussion. Clin Infect Dis. 2008;46(1):e8–e11.

2. Weiss LM, Wittner M, Wasserman S, et al. Efficacy of azithromycin for treating Babesia microti infection in the hamster model. J Infect Dis. 1993;168(5):1289–1292.

3. Krause PJ, Lepore T, Sikand VK, et al. Atovaquone and azithromycin for the treatment of babesiosis. N Engl J Med. 2000;343(20):1454–1458.

4. Vannier E, Krause PJ. Human babesiosis. N Engl J Med. 2012;366:2397–2407.

5. Duffy DC, Campbell SR. Ambient air temperature as a predictor of activity of adult Ixodes scapularis (Acari: Ixodidae). J Med Entomol. 1994;31(1):178–180.

6. Kavanaugh MJ, Decker CF. Babesiosis. Dis Mon. 2012;58:355–360.

7. Deitsch KW, Lukehart SA, Stringer JR. Common strategies for antigenic variation by bacterial, fungal and protozoan pathogens. Nat Rev Microbiol. 2009;7(7):493–503.

8. Hatcher JC, Greenberg PD, Antique J, et al. Severe babesiosis in long island: review of 34 cases and their complications. Clin Infect Dis. 2001;32(8):1117–1125.

9. Krause PJ, Gewurz BE, Hill D, et al. Persistent and relapsing babesiosis in immunocompromised patients. Clin Infect Dis. 2008;46(3):370–376.

10. Wozniak EJ, Lowenstine LJ, Hemmer R, et al. Comparative pathogenesis of human WA1 and Babesia microti isolates in a Syrian hamster model. Lab Anim Sci. 1996;46(5):507–515.


More on Babesia:  This article put out by The Nurse Practitioner demonstrates clearly how their short treatment duration doesn’t work for immunocompromised patients, which is pretty much everyone with Lyme/MSIDS as we are typically infected with more than one thing, and even if it’s just Lyme with Babesia 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.  Despite the lack of acknowledgment, there’s a lot of us with Lyme and Babesia and even more pathogens.  

The one drug, one disease paradigm does not work with Lyme/MSIDS.
**Complex Babesiosis is associated with severe anemia and high parasitaemia levels**
**Chronic Babesiosis can trigger cardiovascular, kidney, and liver problems**

Personally, I can attest to the importance of the anti-malarial medications my husband and I were both put on. We both had chest pressure and dizziness but the headaches I had were out of this world. My heart would also flop like a fish out of water and wake me up from a dead sleep – racing. Neither of us had night sweats and we presented differently. My husband developed hyper coagulation and anemia while I did not. Heparin helped him tremendously.

If you are having heart involvement and antibiotics typically used for Lyme are not touching it, please discuss Babesia with your health care provider (and Bartonella as well!). 

Also, go to the Babesia Treatment link above and print and fill out the Babesia checklist by Dr. Schaller.  These checklists are more helpful than testing.  Testing often misses cases.  

For us, treating for Babesia made a huge difference. I’m happy to report ALL of those symptoms are completely gone after a full year hitting it hard with anti-malarials. The best treatments overlap. Again, see Babesia Treatment link for ideas on what this looks like.




Understanding Disease Transmission in Ticks

Understanding disease transmission in ticks

Study may help find ways to prevent future spread of pathogens


Understanding how immune responses affect disease transmission could be the first step toward eventually developing a preventative treatment for tick-born illnesses, researchers say.
CAMERON SHEPPARD, Evergreen contributor
October 2, 2018


Research at WSU to understand how the mechanisms of tick immune systems operate could help uncover ways to affect how ticks carry and transmit diseases, many of which affect humans.

One type of tick, Ixodes scapularis, can transmit at least seven different diseases from feeding on the blood of a host, a number that is relatively high when compared to other bugs and insects that carry disease, said Dana Shaw, microbiologist and researcher at WSU.

Shaw said the I. scapularis’ high vector competency or ability to carry and transmit diseases, is what caught her attention. She wanted to study how the immune system of a tick operates to understand what mechanisms affect a tick’s ability to spread disease.

Shaw said much of what is known about the mechanisms and chemical pathways of arthropod immune systems comes from research done with Drosophila, a genus of fruit fly.

With the Drosophila, the biochemical pathway leading to an immune system response to certain gram-negative microbial infections is triggered by the presence of transmembrane peptidoglycan recognition proteins, or PGRPs.

In other words, the PGRPs are necessary to trigger an immune system response to these infections in the Drosophila.

Genome sequencing research done on the I. scapularis tick previous to Shaw’s study had indicated that transmembrane PGRPs and other downstream molecules were not present in I. scapularis ticks as they were in the Drosophila.

This led Shaw and colleagues to ask how the biochemical pathways that cause an immune response in the I. scapularis were being triggered without the presence of molecules similar to transmembrane PGRPs and other downstream molecules in the Drosophila.

Shaw’s research group is now hypothesizing that the immune response in ticks is triggered by a cellular reaction known as the unfolded protein response, or UPR.

After analyzing the transcriptional response of a sample of I. scapularis ticks, Shaw’s team found 14 genes that indicated the potential for a UPR activation in the event of an infection with the Anaplasma phagocytophilum pathogen.

In humans, it is known as known as granulocytic anaplasmosis, and can cause respiratory failure, organ failure or death in its late stages.

To test the hypothesis that UPR activation would trigger an immune response to infection, the researchers used tick cell lines that had been infected with A. phagocytophilum. Before infecting the tick cells, a sample set of cells underwent a process known as transcriptional knockdown.

Kristin Rosche, scientific assistant at WSU, said transcriptional knockdown blocks specific RNA from creating the proteins it would normally create. In this case, it was used to block the UPR genes in I. scapularis ticks.

After measuring and comparing the survivability rate of pathogens in the tick cells that had their UPR genes blocked to the tick cells that had not undergone transcriptional knockdown, it was evident that blocking the UPR did alter the infectious burden A. phagocytophilum had in the cells.

“Whether this is through an innate immune response or not is not yet known,” Shaw said. “We are still in early stages of the UPR project and we cannot draw any hard conclusions with our preliminary evidence.”

What this research may have uncovered is knowledge about a new immune signaling pathway that could affect a tick’s ability to carry and transmit pathogens.

Rosche said this research is significant because tick habitats are changing and expanding to new areas, and tick-borne diseases are difficult to diagnose and treat.

This research is a step toward developing preventatives for certain tick-borne illnesses, even if that possibility is far away.

“This research is necessary in order to have other people take the next steps,” Rosche said.



  1. We are currently at 18 and counting diseases spread by ticks:
  2. The black legged tick is not the only transmitter of disease.
  3. While this new work presents some hopeful possibilities, let us never forget that the black legged tick is not the only way people can get infected and much, much more work needs to be done on vectors and transmission.  Willy Burgdorfer, the one who first “discovered” Borrelia, burgdorferi, the causative agent of LD, became infected while working in the lab when Bb infected rabbit urine got into his eye.  Nobody talks about that inconvenient truth, or the fact there’s 33 years of data on congenital transmission:  There is evidence to suggest sexual transmission of Lyme:  This was done in 2014 and no follow up studies have been done.

Why wouldn’t research on sexual transmission be done on the most common vector borne disease?  

This is the million dollar question that remains unanswered.