Archive for the ‘Treatment’ Category

Tick Time Bomb: Why Experts Predict High Tick Activity in 2021

https://www.prevention.com/health/a36558703/tick-time-bomb-summer-2021/

Experts Predict Summer 2021 Will Be a ‘Tick Time Bomb’—Here’s How to Stay Safe

“We are already seeing more ticks this season than last year.”
By Korin Miller

ticks

RBKOMARGETTY IMAGES
  • Experts predict summer 2021 will be a “tick time bomb.”
  • Due to a mild winter, most parts of the country are already seeing more ticks this season than last year, as the tiny insects thrive in humidity.
  • Here’s how to protect yourself from tick bites, which can lead to various illnesses including Lyme disease.

Every summer, we hear the same warning: It’s going to be a bad year for ticks. But entomologists (a.k.a. insect experts) say that 2021 could live up to that message. In fact, The Weather Channel even referred to this year as a “tick time bomb.”

Robert Lockwood, associate certified entomologist for Ehrlich Pest Control, says experts are already noticing a thriving tick population in 2021. “Due to the mild winters and climate change, we are already seeing more ticks this season than last year,” he says.

Why does a wet winter matter? Ticks thrive in humidity. As a result, “regions that experienced wetter and warmer winters will have higher tick populations this spring and summer,” says Ben Hottel, Ph.D., technical services manager for Orkin.  (See link for article)

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For more:

  • https://madisonarealymesupportgroup.com/2018/11/07/ticks-on-the-move-due-to-migrating-birds-and-photoperiod-not-climate-change/
    • Climate-change researchers overlooked and did not take into account established populations of I. scapularis found in the late 1960’s in the upper Midwest, as well as at Manitoba in 1991, in their climate change model maps. The faulty climate change maps are devoid of any ticks in those areas – yet experience shows otherwise.
    • Climate change models overlook the fact that deer ticks were established in northwestern Ontario, southern Manitoba and were already in central Canada prior to 1970. What they predict to happen in the future has already happened in Canada. Their oversight caused a skewed rate of tick expansion and a miscalculation of northward projected movement.
    • Warmer winters are in fact lethal to I. scapularis(black-legged) ticks. In fact, overwinter survival dropped to 33% when the snow melted. This has been substantiated by other researchers as well.
    • The climate change model actually reflects migratory flight not warmer futuristic temperatures.
    • What is important to tick expansion is photoperiod, which is innate and can not be altered by climate.  Black-legged ticks require 14 hours of daylight to molt. If ticks can’t molt, they can’t move on to their next life-cycle.

      “The hypothesis that I. scapularis ticks will expand further north in the Prairie Provinces because of climate change is not only unscientific, but deceiving.”  John Scott, Independent tick researcher

More on tick prevention:

Category:

Activism, Ticks, Treatment

COVID Doctor: Big-Gov/Big-Pharma Suppression of Ivermectin Cost 500,000 Lives

**UPDATE Aug. 21, 2021**

Due to denial, suppression, and censorship of ivermectin by mainstream medicine, our corrupt public health ‘authorities’, and bought-out media, people are now forced to self-treat with ivermectin using animal medicine, causing a surge in poisonings.  (This type of thing happens in Lyme-land as well for the same reasons)

https://thenewamerican.com/covid-doctor-big-gov-big-pharma-suppression-of-ivermectin-cost-500000-lives/?

COVID Doctor: Big-Gov/Big-Pharma Suppression of Ivermectin Cost 500,000 Lives

by Selwyn Duke
COVID Doctor: Big-Gov/Big-Pharma Suppression of Ivermectin Cost 500,000 Lives
Photo: RapidEye/iStock/Getty Images Plus

Last month, renowned physician Dr. Peter McCullough lamented that thousands of lives have been lost because the medical establishment has refused to create an “official treatment protocol” for COVID-19. Now another doctor is expressing similar sentiments, saying the World Health Organization (WHO) has purposely suppressed data on drug ivermectin’s effectiveness at treating the disease because the health authority is in Big Pharma’s pocket.

It’s a trespass that has cost a half million lives, contends critical-care physician Dr. Pierre Kory — and he calls the act “criminal.” As the World Tribune reports:

In a recent Zoom call, Dr. Pierre Kory of the Front Line COVID-19 Critical Care Alliance outlined numerous details showing the World Health Organization (WHO) knowingly suppressed data on the effectiveness of ivermectin against the virus in order to benefit the vaccine interests of Big Pharma.

“It’s criminal,” Kory said. “It’s literally criminal.” The drug “could have saved half a million lives this year if it had been approved.”

The WHO, Kory contends, is simply taking part in the tactics of a time-worn “Disinformation Playbook.” The term was coined by the Union of Concerned Scientists 50 years ago to describe the strategies corporations have developed over decades to “attack science when it goes against their financial interests.”

According to the Tribune, this disinformation strategy has five parts:

1. The Fake – Conduct counterfeit science and try to pass it off as legitimate research.

2. The Blitz – Harass scientists who speak out with results reviews inconvenient for industry.

3. The Diversion – Manufacture uncertainty about science where little or none exists.

4. The Screen – Buy credibility through alliances with academia or professional societies.

5. The Fix – Manipulate government officials or processes to influence policy inappropriately.

“In the full Zoom call, since removed by YouTube but available on Bitchute , Kory describes how the five tactics have been deployed against the scientific findings on ivermectin,” the Tribune continues. “One example is the corruption of leading medical journals, whose editors refuse to allow ivermectin studies to advance to peer review. The most egregious institutional participant, however, is the WHO.”  (See link for article)

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**Comment**
 
Please read this important article in full.  If you have the time, also watch the videos. The monkeys are rolling out of the barrel one by one and this information must be shared widely because it’s truly a wide-spread problem which doesn’t only concern the issue of COVID.
 
This article also explains why Lyme/MSIDS patients have suffered for over 40 years. The same exact 5 parts deployed in the disinformation playbook have been and are currently being used for tick-borne illness (TBIs).  
Dr. Kory states 500,000 lives could have been saved and Dr. McCullough states 85% of the lives lost could have been saved.
The question begging to be asked is: I wonder how many lives could have been saved of those with tick-borne illness if they were allowed appropriate anti-microbial treatment that treated ALL the pathogens for the duration of time needed?

Interestingly, the article mentions USSR’s Lysenkoism, and that the problem is worsened “when there’s an unhealthy nexus between science and state.”  These same words have been uttered by microbiologist Sin Hang Lee due to the fact the CDC has suppressed  direct testing methods for Lyme disease.  He also filed a “Stay of Action” against the Pfizer COVID “vaccine,” due to the faulty PCR tests used in the trials.

Lee is far from alone.  Lyme advocate Carl Tuttle recently gave ample evidence that the CDC is lying to the public about Lyme disease.

If a silver lining exists to the COVID ‘pandemic’ it’s that blatant corruption is finally being acknowledged and exposed. Perhaps this awareness will help suffering patients understand the need to seek specialists that have separated themselves from this corrupt paradigm and truly desire to help patients.

For a great read from New York Times best-selling author and journalist Michael Capuzzo who detailed the manner in which Ivermectin came to be used to treat COVID-19, and simultaneously subjected to global censorship despite its incredibly high success rate at treating the virus:  https://covid19criticalcare.com/wp-content/uploads/2021/05/The-Drug-that-Cracked-Covid-by-Michael-Capuzzo.pdf

Ivermectin is “what the world desperately needs now,” according to Dr. Pierre Kory, one of the founding members of the FLCCC. But although the desperate need is present, governing health bodies apparently seem intent on ensuring that the drug is not known, Capuzzo reveals. 

For more:  https://www.lifesitenews.com/news/prominent-physicians-scientists-believe-u.s-doctors-group-deserves-nobel-prize-for-finding-most-powerful-covid-19-killer-known-to-science

 

Category:

Activism, Treatment, Viruses

Lyme Spirochetes in an Autopsied Brain Despite Treatment

The following article is based off the study, posted here.

https://www.lymedisease.org/lyme-spirochetes-autopsied-brain/

LYME SCI: Lyme spirochetes in an autopsied brain (despite treatment)

By Lonnie Marcum

An important new study from Tulane University found Lyme bacteria in autopsied brain tissue of a woman who had been aggressively treated with antibiotics.

“These findings underscore how persistent these spirochetes can be in spite of multiple rounds of antibiotics targeting them,” says Dr. Monica Embers, of Tulane.

Dr. Embers’ team collaborated with Dr. Brian Fallon, of the Lyme and Tick-Borne Diseases Research Center at Columbia University Irving Medical Center.

In their study, published in Frontiers in Neurology, the researchers performed an in-depth autopsy on the brain tissues of an elderly woman who had been previously treated for neurological Lyme disease.

And guess what? They found intact Borrelia burgdorferi, the agent that causes Lyme disease, inside portions of the patient’s brain as well as DNA evidence in her spinal cord.

Obviously, you can’t take brain samples from a living person. Therefore, autopsy samples, such as used in this study, can demonstrate that Borrelia can remain in human tissues even after extensive treatment with antibiotics. Such studies are essential in the effort to develop better diagnostics and treatment.

Persistent Lyme

Many academic researchers and physicians refer to the persistent symptoms of Lyme as post-treatment Lyme disease syndrome (PTLDS). But if you ask patients who are left disabled after being treated for Lyme, they will tell you it’s “chronic Lyme disease.”

Along with the difficulty of obtaining a proper diagnosis, the treatment for Lyme is complicated by the fact that the standard antibiotic is most effective when administered early in the disease.

Any delay in treatment allows the infection to spread throughout the body leading to a more severe chronic form of the disease. This chronic form of infection often necessitates stronger intravenous antibiotics, or longer-term antibiotics to clear infection. Even then, many patients remain ill.

Researchers from Tulane and Columbia universities want to develop better methods to detect and treat Borrelia burgdorferi.

Dr. Embers has been studying Lyme disease since 1998, mostly using animal models. Her early work demonstrated that at four months post-infection, neither a 28-day course of doxycycline nor a 90-day course of antibiotics (30 days IV Rocephin, followed by 60 days oral doxycycline) could eradicate Lyme disease. More recently, she found spirochetes in multiple organs after a 28-day course of doxycycline.

History of the patient

The new study focuses on a 69-year-old deceased woman who contracted Lyme disease at age 54. At the onset of her illness, she had a well-documented erythema migrans rash accompanied by severe headache, joint pain and a fever of 104º. Her standard two-tier tests for Lyme disease were positive on ELISA and both IgM and IgG Western blots.

She was prescribed 10 days of doxycycline which resolved her initial symptoms. Two years later, the patient developed many chronic symptoms consistent with late-stage Lyme disease, as well as dementia.

At age 60, the patient was treated with IV ceftriaxone for eight weeks, which led to 60% improvement in cognition and interpersonal engagement. Although oral amoxicillin was continued three times daily for the next six months, her symptoms gradually returned. Further antibiotic treatment with minocycline did not help. All the while her IgG Western blot for Lyme disease remained positive.

Over time, the patient’s visual, mental and executive functions continued to deteriorate. At age 62, a cerebrospinal fluid (CSF) study demonstrated a positive Western blot. Unfortunately, a comparison of serum and CSF by a diagnostic ELISA was not performed at that time so she did not meet the full diagnostic criteria for neuroborreliosis.

The authors suggest that the initial symptoms of the woman at age 54 (headache, high fever) indicate brain involvement at the time of the EM rash, consistent with a mild meningitis early in the disease process.

Fifteen years after the initial diagnosis of Lyme disease, she experienced severe movement disorders, sleep disorder, paranoia and personality changes leading to a clinical diagnosis of dementia with Lewy bodies. Before she died at age 69, she decided to donate her brain to Columbia University for the study of the disease.

What is dementia with Lewy bodies?

Dementia is a general term referring to an impaired ability to remember, think or make decisions that interferes with one’s ability to perform normal activities of daily living.

Symptoms can vary widely from person to person. People with dementia typically have problems with:

  • Memory
  • Attention
  • Communication
  • Reasoning, judgment, and problem solving
  • Visual perception beyond typical age-related changes in vision

Lewy body dementia (LBD) is associated with abnormal deposits of a protein called alpha-synuclein in the brain. These deposits, called Lewy bodies, affect chemicals in the brain whose changes, in turn, can lead to problems with thinking, movement, behavior, and mood.

In healthy people, alpha-synuclein plays a number of important roles in neurons (nerve cells) in the brain, especially at synapses, where brain cells communicate with each other. In LBD, alpha-synuclein forms into clumps inside neurons, starting in areas of the brain that control aspects of memory and movement. This process causes neurons to work less effectively and, eventually, to die.

Neuroborreliosis

Lyme disease can affect any organ or system of the body including the central nervous system (brain and spinal cord) and peripheral nervous system (nerves outside of the CNS). When Lyme infects the nervous system, it can result in Lyme neuroborreliosis.

Lyme neuroborreliosis (LNB) can develop anywhere from a few days post infection to several months or even years later. Neuroborreliosis can be the primary and only manifestation in some patients with Lyme disease. Approximately 15% of patients with untreated Lyme disease will develop LNB.

Neurological Lyme can affect many parts of the nervous system alone or in various combinations resulting in:

  • Lyme meningitis – inflammation of the membranes that cover the brain/spinal cord.
  • Lyme encephalitis – inflammation inside the brain
  • Lyme myelopathy – inflammation of the spinal cord
  • Lyme cranial neuritis – inflammation of the cranial nerves
  • Lyme neuropathy – inflammation of the peripheral nerves
  • Bannwarth’s syndrome – “terrible triad” of meningitis, cranial neuritis and painful neuropathy.

Lyme encephalitis is a common manifestation in LNB patients who receive delayed or inadequate treatment for Lyme disease.

Common symptoms of LNB include facial palsy, headache, stiff neck, vertigo (dizziness), cognitive dysfunction, memory or concentration problems, mood changes, sleep disturbances, or paresthesias (numbness and tingling.)

The symptoms of LNB and dementia depend on which portions of the brain are affected as follows:

  • The cerebral cortex—controls many functions, including information processing, perception, thought, and language
  • The limbic cortex—plays a major role in emotions and behavior
  • The hippocampus—essential to forming new memories
  • The midbrain and basal ganglia—involved in movement
  • The brain stem—where all10 pairs of cranial nerves originate, also important in regulating sleep and maintaining alertness
  • Brain regions— important in recognizing smells (olfactory pathways), and hearing (auditory pathways)

Some signs of LNB that overlap with signs of dementia may include:

  • Getting lost in a familiar neighborhood
  • Using unusual words to refer to familiar objects
  • Forgetting the name of a close family member or friend
  • Forgetting old memories
  • Not being able to complete tasks independently

How Lyme persists

Unlike typical bacteria, Borrelia has the ability to evade the immune system by propelling itself to different areas of the body, changing its outer surface proteins and shapeshifting—mechanisms that also help the bacteria resist standard antibiotics.

Prior research has pointed to persistent infection as the cause of chronic Lyme disease including research by Fallon at Columbia University, Embers at Tulane University, Lewis at Northeastern University, Baumgarth at University of California, Davis, Zhang at Johns Hopkins University, Aucott at Johns Hopkins University, Novak at Harvard Medical School and many others.

Multiple studies in both animals and humans over several decades have demonstrated both inflammation and persistence of Borrelia in the nervous system following doxycycline treatment.

Using three highly sensitive methods of detection validated with nonhuman primate samples at Tulane National Primate Research Center, the research team concluded that at the donor’s time of death, her central nervous system still harbored intact spirochetes in spite of aggressive antibiotic therapy for Lyme disease at different times throughout her illness.

The researchers employed the use of immunofluorescence staining to image the spirochetes, polymerase chain reaction or PCR to detect the presence of B. burgdorferi DNA, and RNAscope to determine whether the spirochetes were viable.

The authors summarize the patient’s “initial good response to the IV ceftriaxone suggests a microbial infection was being treated, or that inflammation was dampened. The decline thereafter suggests either that persister Borrelia were present that are now known not to remit with standard antibiotic therapy, that an irreversible neurodegenerative process had been triggered by the prior B. burgdorferi infection, or that an unrelated neurodegenerative disorder was present at the same time as the presumed B. burgdorferi CNS infection.”

Future directions

Dr. Ember’s says the team plans to continue to investigate further tissues from other patients who have elected to donate. She hopes this study “brings more awareness to the ability of Borrelia to persist, even with extensive antibiotic therapy.”

As far as treatment, Embers believes, “we need to find something that works at all phases of the infection from acute to chronic.” She says her team is currently “collaborating with several groups to identify better treatments, be it combination therapy, targeted therapy with small molecule inhibitors, or immune boosting. All of the above!”

In light of this study, perhaps governing health agencies should reconsider the IDSA’s one-size-fits-all recommended treatment for Lyme disease. The growing body of evidence demonstrating Borrelia’s ability to survive a short course of of antibiotics, proves we need to move towards a more individualized approach to Lyme treatment.

LymeSci is written by Lonnie Marcum, a Licensed Physical Therapist and mother of a daughter with Lyme. In 2019-2020, she served on a subcommittee of the federal Tick-Borne Disease Working Group. Follow her on Twitter: @LonnieRhea  Email her at: lmarcum@lymedisease.org.

References

Gadila SKG, Rosoklija G, Dwork AJ, Fallon BA and Embers ME (2021) Detecting Borrelia Spirochetes: A Case Study With Validation Among Autopsy Specimens. Front. Neurol. 12:628045. doi: 10.3389/fneur.2021.628045

Personal communication with Monica Embers, PhD.

 

Category:

Lyme, research, Treatment

Can Lyme Disease & Bartonella Trigger Eating Disorders?

https://www.lymedisease.org/lyme-bartonella-eating-disorders/

Can Lyme disease and Bartonella trigger eating disorders?

May 12, 2021

by Daniel A. Kinderlehrer MD

There are quite a few reviews in the medical literature documenting the neuropsychiatric conditions associated with Lyme disease, and most of them include the general category of “eating disorders.”  But when I searched for case histories, I could find only one, published in 1992.

Pachner et al. described a 12-year-old boy who initially presented with right knee swelling and tested positive for Lyme disease.1 He was treated with doxycycline for 30 days and his knee was better.

However, two months later, he became depressed and restricted his food intake, compulsively exercised, and lost 31 pounds. He still tested positive for Lyme disease and was treated with IV penicillin for two weeks, and soon thereafter he was no longer depressed, he ate normally, and gained weight.

This month, I published a case study about a second case of anorexia nervosa in association with Lyme disease.2 It is important to distinguish between simple anorexia, or loss of appetite, which is common with many medical conditions and infections, and anorexia nervosa, which is a disorder characterized by the obsessive need to lose weight by refusing to eat.

My patient Diane was raised in upstate New York, which is highly endemic for Lyme disease. In fact, she had multiple tick bites as a youngster with no known illness.

However, she did have some issues that stood out: at two years old she began screaming and pulling her hair out—a condition termed trichotillomania. This gradually morphed into generalized anxiety and irritability.

Food restrictions

When she was 14, Diane had another tick attachment that was not treated, and she developed fatigue, frequent sore throats, impaired cognition, and worsening depression, anxiety and irritability. At 15,  she began restricting her food intake and purging after meals.

This led to an admission to an eating disorder unit, where she was diagnosed with anorexia nervosa. She went in and out of the inpatient facility and an outpatient eating disorder program several times without success. She was also making serious suicide threats. Her mother is a savvy nurse and had her tested for Lyme disease. It was positive.

When I first met Diane, she was 16. She was refusing to eat and had a nasogastric tube in place, through which she received her nutrition. She maintained that she was still overweight and needed to restrict her diet—she was 5’6” and weighed 125 lbs. During her physical exam, I noticed Bartonella striae on her thighs—reddish striations that look like stretch marks, but not in the normal skin planes. Diane interpreted these as stretch marks, which further supported her belief that she was overweight.

Diane tested positive for Babesia and Mycoplasma in addition to Lyme disease. She tested negative for Bartonella, but the striae are virtually diagnostic for that microbe.

Bartonella and psychiatric symptoms

In a study posted in December 2020, Dr. Ed Breitshwerdt and colleagues described 29 patients with mental health issues who tested positive for Bartonella. Twenty-four of them developed skin rashes at the same time they developed neuropsychiatric symptoms. Most of those skin changes look the same as the ones on Diane.3The Bartonella striae are caused by new blood vessel formation in layers of the dermis, and biopsies of the striae have demonstrated Bartonella bacteria.4

We treated Diane with three months of intravenous ceftriaxone and a total of one year of oral antibiotics. Her eating disorder has stayed in remission for three years. It is interesting that when Diane began Bactrim, which attacks Bartonella, she had a Herxheimer reaction in which she again refused to eat. This suggests that Bartonella was triggering her eating disorder.

Traditionally, the etiology of anorexia nervosa is considered to be a combination of genetic and environmental factors, such as dysfunctional home circumstances, a history of emotional trauma and modern Western culture’s emphasis on thinness.5-8

PANDAS and PANS

However, there are several reports in the medical literature that describe the role of infections in the etiology of eating disorders.9-14 There is also a higher risk of eating disorders in children and adolescents with autoimmune disease.15 When you connect infection with autoimmunity, one of the outcomes is autoimmune encephalitis—i.e. PANDAS or PANS.

Susan Swedo initially described children who developed mental health issues following a streptococcal infection and coined the term PANDAS—Pediatric Autoimmune Neuropsychiatric Disease Associated with Streptococcal Infection.16,17 In particular, these kids had OCD, anxiety, and other mood and behavioral disorders. It wasn’t long before Sokol and Gray described anorexia nervosa in patients with PANDAS.18

Once it became clear that multiple microbes can trigger a PANDAS-like syndrome, the name was changed to Pediatric Acute-onset Neuropsychiatric Syndrome (PANS). The primary criteria for PANS established at the First PANS Consensus Conference include OCD or severely restricted food intake.19

Neuroinflammation

The dots are now connected. An infection can cause an autoimmune reaction that results in neuroinflammation—autoimmune encephalitis—that can manifest not only in OCD and other neuropsychiatric symptoms, but also trigger anorexia nervosa.

Diane probably had a PANS-like syndrome. When she was younger, she had trichotillomania (hair pulling), which has similarities to OCD. This was followed by anxiety and irritability.

When  she had yet another tick attachment at age 14, her symptoms worsened.  This exposed her to reinfection or to additional tick-borne pathogens.

It is noteworthy that Diane had four tick-borne infections: Lyme disease, babesiosis, mycoplasmosis and bartonellosis. In my clinical experience, Mycoplasma and Bartonella are the most likely pathogens to trigger PANS-like syndromes, and both of these have been documented as causing PANS.20-22 Wouldn’t it be a good idea if all patients with anorexia nervosa were screened for tick-borne infections and PANS?

With this in mind, Dr. Nancy Brown and I tested a group of adolescents in a residential treatment center who were suffering from severe mental health issues. In the next installment I’ll describe what happened with that study.

In the meantime, it’s good to keep in mind that PANS is not just for kids. Adults also suffer from autoimmune encephalitis with severe neuropsychiatric symptoms. And the onset is not always sudden—often the onset is gradual or stuttering. I suggest we change the name to Microbe-induced Autoimmune Neuropsychiatric Syndrome (MANS).23

Read the case study here.

Dr. Daniel Kinderlehrer is an internal medicine physician with a private practice in Denver, Colorado, devoted to treating patients with tick-borne illness. He is the author of  Recovery From Lyme Disease: The Integrative Medicine Guide to the Diagnosis and Treatment of Tick-Borne Illness.

References

  1. Pachner AR, Duray P, Steere AC. Central Nervous System Manifestations of Lyme Disease. Arch Neurol. 1989;46(7):790-795.
  2. Kinderlehrer DA. Anorexia Nervosa Caused by Polymicrobial Tick-Borne Infections: A Case Study. Int Med Case Rep J. 2021;14:279-287.
  3. Breitschwerdt, E.B.; Bradley, J.M.; Maggi, R.G.; Lashnits, E.; Reicherter, P. Bartonella Associated Cutaneous Lesions (BACL) in People with Neuropsychiatric Symptoms. Pathogens. 2020;9:1023.
  4. Maluki A, Breitschwerdt E, Bemis L, et al. Imaging analysis of Bartonella species in the skin using single‐photon and multi‐photon (second harmonic generation) laser scanning microscopy. Clin Case Rep. 2020;8(8):1654-1570.
  5. Yilmaz Z, Hardaway JA, Bulik CM. Genetics and epigenetics of eating disorders. Adv Genomics Genet. 2015;5:131–150.
  6. Tagay S, Schlottbohm E, Reyes-Rodriguez ML, Repic N, Senf W. Eating disorders, trauma, PTSD, and psychosocial resources. Eat Disord. 2014;22(1):33-49.
  7. Ferrell EL, Russin SE, Flint DD. Prevalence Estimates of Comorbid Eating Disorders and Posttraumatic Stress Disorder: A Quantitative Synthesis. J Aggress Maltreat Trauma. 2020;20:1-19.
  8. Becker AE, Fay KE, Agnew-Blais J, Khan AN, Striegel-Moore RH, Gilman SE. Social network media exposure and adolescent eating pathology in Fiji. Br J Psychiatry. 2011;198(1):43-50.
  9. Brown RF, Bartrop R, Beumont P, Birmingham CL. Bacterial infections in anorexia nervosa: delayed recognition increases complications. Int J Eat Disord. 2005;37(3):261-265.
  10. Favaro A, Tenconi E, Ceschin L, Zanetti T, Bosello R, Santonastaso P. In utero exposure to virus infections and the risk of developing anorexia nervosa. Psychol Med. 2011;41(10):2193-9.
  11. Raevuori A, Lukkariniemi L, Suokas JT, Gissler M, Suvisaari JM, Haukka J. Increased use of antimicrobial medication in bulimia nervosa and binge-eating disorder prior to the eating disorder treatment. Int J Eat Disord. 2016;49(6):542-52.
  12. Park RJ, Lawrie SM, Freeman CP. Post-viral onset of anorexia nervosa. Br J Psychiatry. 1995;166(3):386-9.
  13. Simon MW. Anorexia and failure to grow associated with Epstein-Barr virus infection. J Ky Med Assoc. 1998;96(1):13-15.
  14. Breithaupt L, Köhler-Forsberg O, Larsen JT, et al. Association of Exposure to Infections in Childhood with Risk of Eating Disorders in Adolescent Girls. JAMA Psychiatry. 2019;76(8):800–809.
  15. Zerwas S, Larsen JT, Petersen L, et al.. Eating Disorders, Autoimmune, and Autoinflammatory Disease. Pediatrics. 2017;140(6):e20162089.
  16. Swedo SE, Leonard HL, Kiessling LS. Speculations on antineuronal antibody-mediated neuropsychiatric disorders of childhood. Pediatrics. 1994 Feb;93(2):323-326.
  17. Swedo SE, Leonard HL, Garvey M, et al. Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections: clinical description of the first 50 cases. Am J Psychiatry. 1998;155(2):264–71.
  18. Sokol MS, Gray NS. Case study: an infection-triggered, autoimmune subtype of anorexia nervosa. J Am Acad Child Adolesc Psychiatry. 1997;36(8):1128-33.
  19. Chang K, Frankovich J, Cooperstock M, et al. Clinical Evaluation of Youth with Pediatric Acute-Onset Neuropsychiatric Syndrome (PANS): Recommendations from the 2013 PANS Consensus Conference J Child Adolesc Psychopharmacol. 2015;25(1):3–13.
  20. Piras C, Pintas R, Pruna D, Dessi A, Atzoril L, Fanos V. Pediatric Acute-onset Neuropsychiatric Syndrome and Mycoplasma Pneumoniae Infection: A Case Report Analysis with a Metabolomics Approach. Curr Pediatr Rev. 2020:16(3):183-193.
  21. Frankovich J, Thienemann M, Rana S, Chang K. Five youth with pediatric acute-onset neuropsychiatric syndrome of differing etiologies. J Child Adolesc Psychopharmacol. 2015;25(1):31-7.
  22. Breitschwerdt EB, Greenberg R, Maggi RG, Mozayeni BR, Lewis A, Bradley JM. Bartonella henselae Bloodstream Infection in a Boy with Pediatric Acute-Onset Neuropsychiatric Syndrome. J Cent Nerv Syst Dis. 2019;11:1179573519832014
  23. Kinderlehrer, D.A. Does Lyme Disease Cause PANS? J Biomed Res Environ Sci. 2021;2(3):126-131.

Category:

Bartonella, Lyme, research, Treatment

Case Series Shows Wide Range of Babesia Symptoms & Presentations

https://danielcameronmd.com/case-series-shows-wide-range-babesia-symptoms-presentations/

CASE SERIES SHOWS WIDE RANGE OF BABESIA SYMPTOMS AND PRESENTATIONS

babesia-symptoms

Babesia can be a serious tick-borne illness in some patients. A case series published in the Nurse Practitioner Journal demonstrates the difficulty in diagnosing the disease, as it can cause a wide range of clinical presentations. The authors focus on five cases which occurred in southeastern New Jersey, an area endemic for Babesia. All of the patients were hospitalized.

By

This case series describes a broad range of Babesia symptoms in elderly patients, making the diagnosis particularly challenging.

Case 1: A 78-year-old white female was admitted with fever, chills, lethargy, fatigue, and marked changes in sensorium. “She had a maximum temperature of 100.6° F (38.1° C); sepsis was considered for this patient,” writes Paparone, a Nurse Practitioner (NP) from the Atlantic County Health Department in Northfield, New Jersey. A tick-borne illness was considered, in part due to multiple tick bites, abnormal liver function tests, anemia, and thrombocythemia. “Peripheral smear was positive for Babesia, and she had a Babesiaimmunoglobulin M (IgM) of 1:160 and Anaplasma (previously referred to as Ehrlichia) IgM of 1:320.” [1]

The woman’s mentation and lethargy dramatically improved when treated with a combination of doxycycline, atovaquone and zithromax.

Case 2: A 90-year-old white female was admitted for rectal bleeding with a hemoglobin of 7.6 g/dL and low platelet count of 103 × 109/L. The bleeding resolved with an octreotide infusion. The woman also had fever spikes to 100° F and a positive smear for Babesia. Her illness resolved with azithromycin and atovaquone.

Case 3: A 57-year-old white male was admitted with fever, malaise, and chills. His temperature had risen to 101° F during his 5-day hospital stay. Anaplasmosis was suspected due to his elevated liver enzymes, leukopenia, and thrombocytopenia. Intravenous doxycycline, oral clindamycin and quinine were prescribed. But he tested positive for Babesia. His hospital course was complicated by acute hearing deterioration. Quinine was stopped and his treatment was changed to oral azithromycin and oral atovaquone.

Case 4: An 81-year-old white male was admitted with increasing lethargy, weakness, chills, and blurred vision. Babesia was diagnosed on peripheral smear. Anaplasmosis was suspected based on anemia and thrombocytopenia.

Subsequently, serologic studies demonstrated an Anaplasmosis IgG of 1:256, Babesia IgM and IgG of 1:320. He was discharged after a 10-day combination of azithromycin and doxycycline. There was no evidence Babesia was treated during the hospitalization.

“At discharge on day 10, [he] was switched to clindamycin orally three times a day and quinine orally three times a day because of intolerance to azithromycin, and he completed a 14-day course of therapy,” writes Paparone.

Case 5: An 85-year-old white male was admitted with intermittent recurring fevers and chills. “He had a history of hairy cell leukemia, splenectomy, atrioventricular block (pacemaker), gouty arthritis, prostatic hypertrophy, and polymyalgia rheumatica,” writes Paparone. Babesia was diagnosed with 10.4% of his red blood cells infected. He was prescribed oral azithromycin and atovaquone. Doxycycline was added due to the possibility of a concurrent tick-borne infection.

He was discharged on day 8 only to be readmitted with an inability to ambulate and generalized weakness. His peripheral smear was positive for Babesia. “Due to the persistence of parasitemia despite adequate therapy, he was changed to clindamycin,” according to Paparone. His treatment was changed back to azithromycin and atovaquone due to gastric distress and a generalized erythematous coalescing rash. A peripheral smear for Babesia was negative at 5.5 weeks.

Each of the five cases presented differently: 

  1. Fever, chills, lethargy, fatigue, and marked changes in sensorium
  2. GI bleed
  3. Fever, malaise, and chills
  4. Increasing lethargy, weakness, chills, and blurred vision
  5. Intermittent recurring fevers and chills

Co-infections 

Three of the five cases with babesia symptoms were treated for co-infections without confirmatory serologic tests. Two of three cases were treated for Anaplasmosis without serologic confirmation.

Treatment tolerance

Zithromax and atovaquone were well tolerated in a population of patients with babesia symptoms that included 4 elderly patients ranging from 78 to 90 years old. Quinine was stopped due to hearing loss in one subject. Clindamycin and quinine were stopped in a second subject due to gastric distress and a generalized erythematous coalescing rash.

There was no evidence any of the 5 subjects babesia symptoms required blood transfusions despite their anemia and thrombocytopenia. This suggests that prompt recognition of Babesia in the hospital setting might avoid the transfusions described in the literature.

Babesia was successfully treated even in their immunocompromised patient, who was treated with exchange transfusion due to persistent parasitemia. “Red blood cell exchange transfusions are recommended for cases of severe babesiosis in patients with parasitemia of 10% or greater, severe anemia (hemoglobin less than 10 g/dL), or pulmonary, kidney or liver impairment,” writes Paparone. “Exchange transfusions are used to rapidly decrease parasitemia, correct anemia, and help remove toxic byproducts produced by the infection.”

Authors’ recommendations  

“This case series illustrates the need for the NP to appreciate the variable clinical presentations of babesiosis to facilitate prompt diagnosis, provide proper therapeutic management, and avoid the poor outcomes associated with this disease.” [1]

• It is important for the NP to understand that infected patients may not recall a tick bite and that clinical presentations may not only be variable but also nonspecific, ranging from subclinical to severe.

• The possibility of co-infection with other tick-borne illnesses (Lyme disease and anaplasmosis) must be considered.

• Furthermore, the NP needs to assume an active role in patient education to affect babesiosis awareness and prevention.

Related Articles:

Case report: Delayed onset babesia

Geriatric babesia cases are rising and may require longer treatment

Babesia infection and tick-borne agents transmitted through blood supply

References:
  1. Paparone, P. and P.W. Paparone, Variable clinical presentations of babesiosis: A case series. Nurse Pract, 2017. 42(11): p. 1-7.

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Babesia, research, Treatment