Archive for the ‘Viruses’ Category

Co-Infection Patterns in Wisconsin Black Legged Ticks Show Associations Between Viral, Eukaryotic & Bacterial Microorganisms

https://www.ncbi.nlm.nih.gov/m/pubmed/30037148/

Co-Infection Patterns in Individual Ixodes scapularis Ticks Reveal Associations between Viral, Eukaryotic and Bacterial Microorganisms.

Cross ST, et al. Viruses. 2018.

Abstract

Ixodes scapularis ticks harbor a variety of microorganisms, including eukaryotes, bacteria and viruses. Some of these can be transmitted to and cause disease in humans and other vertebrates. Others are not pathogenic, but may impact the ability of the tick to harbor and transmit pathogens. A growing number of studies have examined the influence of bacteria on tick vector competence but the influence of the tick virome remains less clear, despite a surge in the discovery of tick-associated viruses.

In this study, we performed shotgun RNA sequencing on 112 individual adult I. scapularis collected in Wisconsin, USA. We characterized the abundance, prevalence and co-infection rates of viruses, bacteria and eukaryotic microorganisms.

We identified pairs of tick-infecting microorganisms whose observed co-infection rates were higher or lower than would be expected, or whose RNA levels were positively correlated in co-infected ticks. Many of these co-occurrence and correlation relationships involved two bunyaviruses, South Bay virus and blacklegged tick phlebovirus-1. These viruses were also the most prevalent microorganisms in the ticks we sampled, and had the highest average RNA levels.

Evidence of associations between microbes included a positive correlation between RNA levels of South Bay virus and Borrelia burgdorferi, the Lyme disease agent. These findings contribute to the rationale for experimental studies on the impact of viruses on tick biology and vector competence.

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**Eukaryotes are protozoans or parasites which includes worms (nematodes/helminths)**

Mainstream medicine has yet to take into account the synergistic effect of all of the pathogens found within a tick upon human suffering.  So far they continue to believe this is a one pathogen/one disease/one drug paradigm, hence the mono-therapy of doxycycline as their answer to this 21st century plague.

Until this changes, we are doomed.

Tularemia: Hunting Dogs as Possible Vectors

http://outbreaknewstoday.com/tularemia-hunting-dogs-possible-vectors-infectious-disease-59510/

Tularemia: Hunting dogs as possible vectors for the infectious disease 

Press Release

January 20, 2018

Tularemia is an infectious bacterial disease that is life-threatening for rodents, rabbits and hares, but which can also infect humans and dogs. While contact with contaminated blood or meat makes hunters a high-risk group, the frequency of infections among hunting dogs has not been much studied. Researchers from Vetmeduni Vienna have now confirmed a relevant prevalence of infections in Austrian hunting dogs following a serological study in which seven percent of the animals tested positive. This could lead to more intense debate as to whether the often asymptomatic animals represent an additional risk of infection for people.

The frequence of Dogs infected with Tularemia pathogens is higher than previously thought. (Photo: Elli Winter/moorhunde.de)
The frequence of Dogs infected with Tularemia pathogens is higher than previously thought. (Photo: Elli Winter/moorhunde.de)

Tularemia, also known as rabbit fever, is an infectious disease that is usually lethal for wild animals such as rabbits, hares and rodents. As a zoonotic disease, however, it also represents a serious health risk for people. Tularemia is caused by various subtypes of the pathogenic bacteria Francisella tularensis, which can be transmitted by biting and stinging insects or directly through contaminated hay, infected blood and other fluids. The raw meat of diseased animals is also associated with a high risk of transmission of the pathogens, which can infect dogs as well as other animals.

Austrian hunting dogs infected more frequently than previously thought

Without secondary disease, however, dogs usually exhibit no or only few symptoms and tend to have a high natural resistance to low levels of the bacteria. As a result, little attention has been paid to dogs in scientific study. Nevertheless, there are theories that canines may act as interim hosts and a further source of infections. Like hunters, dogs can come into direct contact with infected animals (e.g. when retrieving the game). The prevalence of infections among these animals is therefore an important question to be answered.

Scientists from the Research Institute of Wildlife Ecology at Vetmeduni Vienna for the first time investigated blood samples from 80 Austrian hunting dogs from rural areas known to be endemic for tularemia.

“After two independent analyses, five dogs clearly tested positive,” says first author Annika Posautz.

The study thus showed that dogs in those areas of Austria in which rabbit fever is endemic, i.e. in which it regularly occurs, show a more frequent rate of infection.

Risk of transmission from infected dogs possible, but not confirmed

“The frequency of about seven percent shows that hunting dogs can also become infected regularly. As vectors of the disease, even without symptoms, the animals must also be considered unexpected carriers,” Posautz adds.

Clear scientific evidence is still missing, however, the researchers say. Other factors, such as age – young dogs could come into more frequent contact with game for training purposes – or the question whether dogs represent a potential source of infection for people, must be addressed in future studies.

The blood samples were tested using two different agglutination tests to detect antigens on the surface of the bacteria or antibodies produced by the immune system. “Agglutination works by specifically clumping these proteins to make them visible under the microscope. In the case of suspected tularemia, more than one of these tests is necessary due to the possibility of cross-reactivity with other pathogens. If all tests are positive, the disease can be confirmed without a doubt. This was the case with five animals,” the researcher says.

Related: 

Canna-Pet

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**Comment**

I purposely left the “related” section at the bottom as a clear reminder that Tularemia has been bioweaponized.  This isn’t theoretical, it’s fact.

For more:  https://madisonarealymesupportgroup.com/2016/10/25/of-rabbits-and-men/

Tularemia, brucella, certain Rickettsia’s, numerous viruses, some chlamydia’s, and of course mycoplasma have all been weaponized.

Regarding the weaponization of tick pathogens: https://www.lymedisease.org/lymepolicywonk-questioning-governments-role-lyme-disease-make-conspiracy-theorist/

Some state Lyme (borrelia) has also been bioweaponized:

For a lengthy but informative read on the Lyme-Biowarfare connections: CitizensAlert_Bob13 (Scroll to page 44 to see an executive summary. Please notice the names of Steere, Barbour, Shapiro, Klempner, and Wormser, the first four are affiliated with the CDC Epidemic Intelligence Service (EIS). Wormser, lead author of the fraudulent Lyme treatment guidelines, lectures as an expert on biowarefare agents and treatments).

Everyone keeps yammering about climate change despite the fact ticks are extremely ecoadaptive but nobody is talking about ticks tweaked in a lab with bioweaponized pathogens.

https://madisonarealymesupportgroup.com/2018/02/27/tularemia-infected-ticks-found-on-sorrento-valley-trail-in-ca/

https://madisonarealymesupportgroup.com/2018/03/07/hantavirus-tularemia-warnings-issued-in-san-diego-county/

Herpes Viruses Implicated in Alzheimer’s Disease

https://www.the-scientist.com/news-opinion/herpes-viruses-implicated-in-alzheimer-s-disease-64246#.W1VYqg-Tels.linkedin

Herpes Viruses Implicated in Alzheimer’s Disease

SAM GANDY, ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI

Herpes Viruses Implicated in Alzheimer’s Disease

A new study shows that the brains of Alzheimer’s disease patients have a greater viral load, while another study in mice shows infection leads to amyloid-β build up.

Jun 21, 2018, Anna Azvolinsky

 

The brains of Alzheimer’s disease patients have an abnormal build up of amyloid-β proteins and tau tangles, which, according to many researchers, drives the ultimately fatal cognitive disease. This theory is being challenged by a newer one, which posits that microbes may trigger Alzheimer’s pathology.

Two new studies, using different approaches, further bolster this pathogen theory. Analyzing the transcriptomes of post-mortem brain samples from patients with Alzheimer’s disease, one group of researchers finds that two strains of human herpesvirus are significantly more abundant than in the brains of people of the same age without Alzheimer’s disease. Gene networks in the brains of Alzheimer’s patients with these strains are also rewired such that disease-related genes are differentially expressed compared to controls.

In the other study, another team of investigators observed in mouse models and in a three-dimensional human neuronal cell culture that a Herpseviridae infection could seed amyloid-β plaques. 

“These two papers add to a weight of evidence that viruses—and pathogens in general—must now be seriously considered as causal agents in Alzheimer’s disease,” Chris Carter, who studies the genetics and epidemiology of Alzheimer’s and other neurological disorders at Polygenic Pathways in the U.K., tells The Scientist.

Over three decades, there have been accumulating data from human studies suggesting that certain microbes, namely, viruses bacteria and fungi, may trigger or promote Alzheimer’s pathology in the aging brain. 

See “Do Microbes Trigger Alzheimer’s Disease?

The Mount Sinai group initially set out to mine their RNA and DNA sequencing data from Alzheimer’s brain samples for drug targets. Then they found these viral sequences that were difficult to ignore. “I recently gave a talk that I titled, ‘I went looking for drugs but all I found was these viruses,’” study coauthor Joel Dudley, a genomics researcher at the Icahn School of Medicine at Mount Sinai, tells The Scientist.

In their study of elderly human brains, Dudley and the team from Mount Sinai sequenced more than 1,400 post-mortem brain samples, finding the first evidence that human herpesviruses 6A (HHV-6A) and 7 (HHV-7) are in greater abundance in regions of the brain including the superior temporal gyrus, anterior prefrontal cortex, and dorsolateral prefrontal cortex.

These data suggest that multiple pathogens, and not just these viruses, likely contribute to Alzheimer’s disease. 

—Chris Carter, Polygenic Pathways

Using RNA and DNA sequencing data, the team computationally generated regulatory network models that implicated the presence these viruses in altering the activity of genes linked to Alzheimer’s risk.

The researchers turned to one of the microRNAs, miR-155, found in their analysis to be suppressed by HHV-6A in the human samples, to see what the functional consequence is of this interaction. They homed in on miR-155 because it was a novel microRNA and because it had been previously linked to herpes viruses. When they knocked out the gene for miR-155 in a mouse model of Alzheimer’s disease, the animals’ brains had larger amyloid plaques and higher levels of amyloid-β compared to the mouse model with a wildtype MIR155 gene.

“Conceivably, the viral proteins are acting as transcription factors that control expression of Alzheimer’s risk genes,” coauthor Sam Gandy, a professor of neurology who specializes in Alzheimer’s disease at Mount Sinai, writes in an email to The Scientist. “Perhaps this viral dysregulation of Alzheimer’s genes that we see promotes the Alzheimer’s pathology of amyloid beta aggregation, inflammation and tau tangles,” he says.

The results, published today (June 21) in Neuron, could pave the way to new intervention strategies. “If established that these viruses indeed play a role in the development of Alzheimer’s, retroviral agents should be tested as a potential therapy,” says Dudley.

In the other study, available as a preprint on the Cell website and in Neuron July 11, Rudolph Tanzi and Robert Moir, both researchers at Harvard Medical School and Massachusetts General Hospital, and their colleagues tested how amyloid-β in the brain—which these labs previously found to be an antimicrobial—reacts to herpes simplex virus 1 (HSV1), HHV6A, and HHV6B. These strains all tend to integrate into the genomes of neurons. They found that in a culture of human neuronal cells, amyloid-β could prevent HSV1 infection and can bind and aggregate the HSV1 and HHV6 viruses. Mice infected with HSV1—which can cause encephalitis—that also had genetically elevated amyloid-β expression were protected against encephalitis, but also had increased amyloid deposits.

“These studies further add to the steadily increasing number of papers that support a microbial role in Alzheimer’s disease,” Ruth Itzhaki, a molecular neurobiologist at the University of Manchester in the U.K. who studies the link between viruses and the development of Alzheimer’s disease, writes in an email to The Scientist.

A recent epidemiology study adds real-world credence to the microbial link to Alzheimer’s. A population study in Taiwan examined more than 33,000 individuals and found that those with a herpes simplex virus infection had a 2.5-fold greater risk of developing Alzheimer’s disease. The study authors found that in those people treated with antiherpes medications, the 2.5-fold risk dropped back down to baseline. 

“The conclusion you can draw is that the antiherpes medication reduced the risk of Alzheimer’s by keeping the herpes infection in check,” says Moir.

Itzhaki agrees. This study and two others, also from Taiwan, appear to link HSV1 causally to Alzheimer’s disease, she writes. “Despite various shortcomings, these Taiwan studies are the essential first steps to a proof that a microbe could be the cause of a non-infectious disease, in this case, Alzheimer’s.” Itzhaki and a colleague wrote about these studies recently in a commentary, which aimed to interpret the “important and surprising Taiwan data” on the effectiveness of the antiviral treatment, Itzhaki tells The Scientist.

Carter cautions that the new reports should not be interpreted to mean that there is likely a single, unique Alzheimer’s pathogen, if there is one at all. “These data suggest that multiple pathogens, and not just these viruses, likely contribute to Alzheimer’s disease. It is also likely that the pathogens may vary between Alzheimer’s patients.”

The Mount Sinai team will now be verifying whether HHV6 and HHV7 are actually integrated into the genomes of Alzheimer’s patients’ brains and testing for the presence of HHV6 and HHV7 in the bloodstream and central nervous system of Alzheimer’s patients. They would like to do a study comparing living patients and controls to see if the link they observed between the viruses’ presence and changes in gene regulation related to Alzheimer’s holds up.

Tanzi’s and Moir’s labs are focusing on the role of the brain microbiome in Alzheimer’s disease. Comparing the brains of older and younger individuals, including those with Alzheimer’s, their preliminary evidence shows that the brain microbiome—which contains hundreds of bacterial and fungal species—is shifted and linked to pro-inflammatory activity. “It’s analogous to what happens with the gut microbiome in individuals with irritable bowel syndrome,” says Moir. “Our model right now is that it’s not just a single microbe, but a disturbance in the brain microbiome that can lead to Alzheimer’s disease.”

B. Readhead et al., “Multi-scale analysis of independent Alzheimer’s cohorts finds disruption of molecular, genetic, and clinical networks by human herpesvirus,” Neurondoi.org/10.1016/j.neuron.2018.05.023, 2018.

W.A. Eimer et al. “Alzheimer’s disease-associated β-amyloid is rapidly seeded by herpesviridae to protect against brain infection,” Neuron, in press, July 12, 2018.

Correction (June 21): We removed two sentences in paragraph seven. One noted the prevalence of virus in diseased brains, but did not note that the prevalence is the same in control brains. The other sentence misstated the regions of the brain where the viruses were in greater abundance compared to control brains and stated these brain regions were linked to Alzheimer’s disease. The Scientist regrets the error.

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**Comment**

  1.  Lyme/MSIDS patients often have viral involvement – particularly herpes strains
  2. The role of bacteria, viruses, and fungus is important and likely includes the very things Lyme/MSIDS patients have and are being treated for.
  3. This article points out another reason to take treatment for Lyme/MSIDS seriously.  If left unchecked, Lyme/MSIDS can possibly be a perfect storm for Alzheimer’s later.

For more:  https://madisonarealymesupportgroup.com/2017/01/18/a-bug-for-alzheimers/

https://madisonarealymesupportgroup.com/2016/06/09/alzheimers-byproduct-of-infection/

https://madisonarealymesupportgroup.com/2016/11/17/antibiotics-and-alzheimers/

https://madisonarealymesupportgroup.com/2016/06/03/borrelia-hiding-in-worms-causing-chronic-brain-diseases/

https://madisonarealymesupportgroup.com/2018/03/25/a-brief-history-of-neuroborreliosis-research-dementia-an-inside-look-at-two-researchers/

https://madisonarealymesupportgroup.com/2017/06/10/the-coming-pandemic-of-lyme-dementia/

https://madisonarealymesupportgroup.com/2016/11/17/alzheimers-lyme/

Dr. David Baewer discusses arboviruses & Lyme:  https://madisonarealymesupportgroup.com/2016/06/07/dr-david-baewer-coppe-labs/ Coppe Labs, in Wisconsin, provides advanced testing for leukotropic herpesviruses: EBV, CMV, HHV-6A and HHV-6B, as well as tick-borne pathogens, and their tests distinguish between latent and active infections.

 

 

Stories of PANDAS

https://abcnews.go.com/video/embed?id=56729630“>https://abcnews.go.com/video/embed?id=56729630  (Go here for News Story.  There are two parts.)  

What is PANDAS, the disorder some doctors say can cause extreme behavioral changes in kids?

Alexia Baier was an eager-to-learn, 4-year-old girl beginning pre-K in a suburb outside of Chicago. She thrived academically — counting, painting and playing with other children.
But five months after starting pre-K, she was infected with a bacteria that several millions of people get every year, according to the Centers for Disease Control and Prevention. The bacteria, group A strep, caused Alexia to get strep throat, a condition children usually recover from easily with treatment.
After 10 days of antibiotics, the infection disappeared but so did Alexia’s bubbly personality. Within two days after completing antibiotics, Alexia began showing behavioral changes at home and eventually at school. She suddenly became defiant and explosive.
“It was a lot of screaming, a lot of hitting and kicking adults,” said school principal AJ McCree. “When we would try and keep her safe in an isolated area, she would continue to elevate and elevate.”

Alexia’s mother, Vanessa Baier, couldn’t believe the shocking change.

“They had to call in the social worker, the psychologist, the principal. It was like a Tasmanian devil running through the classroom,” she said.

Holding back tears, Baier said she wondered: “What am I doing wrong?”

It was a four-month-long emotional roller coaster dealing with the toll on the family’s personal life and a lack of answers from the medical community until Alexia started threatening violence against others, including herself. She even attacked her mother.

Alexia Baier is seen here during a doctors visit. Vanessa Baier
Alexia Baier is seen here during a doctor’s visit.

While Baier was driving, Alexia became violent toward her mother during a trip to get milkshakes. Baier said that Alexia began asking for a second milkshake. When Baier refused, she said, she heard Alexia unbuckle her seat belt.

“I pulled over and I turned to her. As I picked my head up, she was stabbing me in the eye with my mascara wand,” Baier said.

Baier said that between the threat of self-harm and the increased violence she realized she needed to take extreme measures.

At 4 years old, Alexia was admitted to residential treatment. After nine days of observation, Baier wasn’t convinced that Alexia was getting the help she needed. She said that the doctors’ diagnosis of bipolar disorder didn’t seem right to her and that Alexia was sent home with prescriptions for stimulant and antipsychotic medications that didn’t seem to be working.

Baier said the medication made her daughter a zombie and she was still having explosive moments.

“I was not in denial. The only thing that I kept questioning is, ‘But why did this suddenly come on? Wouldn’t I have seen signs? Or does bipolar just … come out of nowhere like this? And what about that strep?'” she said.

Eventually, a neuropsychologist connected the timing of the strep and immediate onset of behavioral symptoms.

Baier said that’s when the doctor asked: “‘OK, have you ever heard of PANDAS?’ [I was] definitely relieved to have some sort of diagnosis that made sense.”

Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections (PANDAS)

Some physicians believe PANDAS is the sudden onset of tics, Obsessive Compulsive Disorder-like behavior or other behavioral changes as a result of a streptococcal infection like strep throat. After a child gets strep throat, the immune system produces proteins, like antibodies, to protect itself.

However, some doctors think that in some cases, these antibodies may mistake its own immune system as foreign and actually attack the child’s own body, including the brain, triggering inflammation as a result of the misguided immune response. They say this “autoimmune” attack causes neuropsychiatric changes in the child, presenting as behavioral changes, like OCD and tic disorders. There is a wide range and severity of symptoms, with Alexia’s case on the more extreme end.

There is also the emergence of a broader umbrella term called Pediatric Acute-onset Neuropsychiatric Syndrome (PANS), which includes not only PANDAS but also symptoms thought to be caused by non-strep infections or other inflammatory disturbances to the system.

These non-strep infections include bacteria and viruses like Lyme disease, mycoplasma pneumonia or walking pneumonia, herpes simplex viruses and the common cold, according to the National Institutes of Health.

The thought is that this whole set of conditions boils down to one presumed cause: an overly active immune response that is sudden in onset but looks like OCD or behavioral problems. It’s no longer thought to be just about the strep. Experts caution, however, that many children will get strep and other infections with no resulting behavioral changes, while others experience behavioral changes without a prior infection.

Some doctors say the presentation of PANDAS is broad and can vary. The diagnosis requires two of the following symptoms, according to the National Institute of Mental Health: anxiety, emotional instability/depression, oppositional behavior like aggression, losing development in behavior, worsening of school performance, disabilities in sensory or motor capabilities as well as signs and symptoms like sleep or urinary problems or eating restrictions. A collaborative effort among different PANDAS researchers has resulted in this set of criteria.

Dr. Susan Swedo, senior investigator in pediatrics behavior and Chief of the Pediatrics and Developmental Neuroscience Branch with the National Institute of Health, has been studying PANDAS for decades and was the first, with her team, to identify PANDAS. Although she said the disorder is uncommon, she estimates it affects one in 200 or one in 500 children.

She also said that far too many of her fellow doctors don’t think PANDAS is real.

“They dismiss it. We don’t have an argument with people that think this exists and it might be rare. The argument is with people who are literally PANDAS deniers,” she said.

There is controversy over whether the streptococcal infection of PANDAS is really what causes persistent behavioral changes. Some doctors believe the sequential onset of strep throat and these changes could be coincidental.

Dr. Donald Gilbert, professor of child neurology at the University of Cincinnati and the director of two clinics at Cincinnati’s Children Medical Center, told ABC he believes “the majority of those who believe they have PANDAS just have regular OCD or regular old tics.”

Gilbert said that even if PANDAS is a legitimate diagnosis, it is most likely extremely rare and overdiagnosed. He is not alone in those beliefs.

PHOTO: Dr. Susan Swedo of the National Institute of Mental Health first identified PANDAS as a behavior disorder in children 20 years ago.
ABC News
Dr. Susan Swedo of the National Institute of Mental Health first identified “PANDAS” as a behavior disorder in children 20 years ago.

Swedo acknowledged that some doctors may be over-treating but said on a whole the disorder is underdiagnosed countrywide. She said that’s in part because of the number of fellow physicians who do not believe in the diagnosis of PANDAS. This makes it hard, she said, for families to find physicians willing to treat the condition.

However, some national medical organizations remain unconvinced that PANDAS is real, citing the lack of unduplicated or quality studies.

The American Academy of Pediatrics “Red Book,” a guide used by many pediatricians for infectious diseases like streptococcus, contains its stance on PANDAS.

According to the AAP Red Book, the evidence for PANDAS has relied on only a small number of patients and the authors have concluded that there is not a specific enough relationship between group A strep and the neuropsychiatric disorders to suggest treatment with antibiotics or any other therapy.

The American Academy of Pediatrics suggests management not by pediatricians, but by specialists like child psychiatrists, behavioral and developmental pediatricians or child neurologists.

The AAP states that management of any specific symptoms of OCD and tic disorders should be left to the specialists. Although some researchers and clinicians believe that treatments including antibiotics and certain immunotherapy may help “children with symptoms suggestive of PANDAS or PANS”, the AAP says there aren’t enough studies to prove this yet.

Alexia Baier is awarded ‘Student of the Month’

Today, Alexia is 8 and, her parents say, doing a lot better. After receiving the diagnosis of PANDAS from a neurologist three years ago, she was placed on different antibiotics for the streptococcus bacteria, took steroids and had her tonsils and adenoids removed.

She does have occasional flare-ups but they are quickly treated with antibiotics, according to the family. Alexia improved behaviorally and was even awarded “Student of the Month” out of her entire school. With the return to a sense of normalcy, the family decided to turn their scary experience into an opportunity for advocacy.

For Alexia and her family, their experience with PANDAS was enough for them to join the fight with other families to pressure Illinois to become the first and only state so far requiring insurance companies to financially support PANDAS treatment. The law was passed and signed into law in Illinois in July 2017.

Constant research continues and supporters of PANDAS hope that the policy, financial support and health-care stance on this issue will shift and improve along with understanding. They say this will require the collaborative work of both critics and supporters of PANDAS.

To learn more about PANDAS, click here for more information.

ABC News’ Neha Chaudhary contributed to this story.

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For more on PANDAS/PANS:  

https://madisonarealymesupportgroup.com/2018/01/05/scary-side-of-childhood-strep/

https://madisonarealymesupportgroup.com/2017/06/30/child-with-lymemsidspans-told-by-doctors-she-made-it-all-up/

https://madisonarealymesupportgroup.com/2017/10/09/today-is-panspandas-awareness-day/

https://madisonarealymesupportgroup.com/2017/04/11/hidden-invaders-infections-can-trigger-immune-attacks-on-kids-brains-provoking-devastating-psychiatric-disorders/

https://madisonarealymesupportgroup.com/2017/10/08/misdiagnosed-how-children-with-treatable-medical-issues-are-mistakenly-labeled-as-mentally-ill/

https://madisonarealymesupportgroup.com/2018/02/21/why-therapy-isnt-enough-when-you-have-ocd-and-pans-pandas/

https://madisonarealymesupportgroup.com/2017/10/01/panspandas-steroids-autoimmune-disease-lymemsids-the-need-for-medical-collaboration/

https://madisonarealymesupportgroup.com/2018/03/14/dr-frid-children-lyme/

https://madisonarealymesupportgroup.com/2015/10/06/november-dr-brown-on-msids-pandas-pans/  (According to Dr. Brown, 80% of his PANS & Autistic patients have Lyme/MSIDS)

Misdiagnosed with bipolar disorder, girl had PANS:  https://www.mercurynews.com/2014/04/19/misdiagnosed-bipolar-one-girls-struggle-through-psych-wards-before-stanford-doctors-make-bold-diagnosis-and-treatment/

 

Tickborne Diseases – Confronting a Growing Threat

https://www.nejm.org/doi/full/10.1056/NEJMp1807870

Tickborne Diseases — Confronting a Growing Threat

Catharine I. Paules, M.D., Hilary D. Marston, M.D., M.P.H., Marshall E. Bloom, M.D., and Anthony S. Fauci, M.D.

July 25, 2018, at NEJM.org.

Every spring, public health officials prepare for an upsurge in vectorborne diseases. As mosquito-borne illnesses have notoriously surged in the Americas, the U.S. incidence of tickborne infections has risen insidiously, triggering heightened attention from clinicians and researchers.

nejmp1807870_f1

Common Ticks Associated with Lyme Disease in North America.

According to the Centers for Disease Control and Prevention (CDC), the number of reported cases of tickborne disease has more than doubled over the past 13 years.1 Bacteria cause most tickborne diseases in the United States, and Lyme disease accounts for 82% of reported cases, although other bacteria (including Ehrlichia chaffeensis, Anaplasma phagocytophilum, and Rickettsia rickettsii) and parasites (such as Babesia microti) also cause substantial morbidity and mortality. In 1982, Willy Burgdorfer, a microbiologist at the Rocky Mountain Laboratories of the National Institute of Allergy and Infectious Diseases, identified the causative organism of Lyme disease, a spirochete eponymously named Borrelia burgdorferi. B. burgdorferi (which causes disease in North America and Europe) and B. afzelii and B. garinii (found in Europe and Asia) are the most common agents of Lyme disease. The recently identified B. mayonii has been described as a cause of Lyme disease in the upper midwestern United States. Spirochetes that cause Lyme disease are carried by hard-bodied ticks (see graphic), notably Ixodes scapularis in the northeastern United States, I. pacificus in western states, I. ricinus in Europe, and I. persulcatus in eastern Europe and Asia. B. miyamotoi, a borrelia spirochete found in Europe, North America, and Asia, more closely related to the agents of tickborne relapsing fever, is also transmitted by I. scapularis and should be considered in the differential diagnosis of febrile illness occurring after a tick bite.

Patterns of spirochete enzootic transmission are geographically influenced and involve both small-mammal reservoir hosts, such as white-footed mice, and larger animals, such as white-tailed deer, which are critical for adult tick feeding. The rising incidence and expanding distribution of Lyme disease in the United States are probably multifactorial, but increased density and range of the tick vectors play a key role. The geographic range of I. scapularis is apparently increasing: by 2015, it had been detected in nearly 50% more U.S counties than in 1996.

Lyme disease’s clinical manifestations range from relatively mild, nonspecific findings and classic erythema migrans rash in early disease to more severe manifestations, including neurologic disease and carditis (often with heart block) in early disseminated disease, and arthritis, which may occur many months after infection (late disease). Although most cases are successfully treated with antibiotics, 10 to 20% of patients report lingering symptoms after receiving appropriate therapy.2 Despite more than four decades of research, gaps remain in our understanding of Lyme disease pathogenesis, particularly its role in these less well-defined, post-treatment symptoms.

Meanwhile, tickborne viral infections are also on the rise and could cause serious illness and death.1 One example is Powassan virus (POWV), the only known North American tickborne encephalitis-causing flavivirus.3 POWV was recognized as a human pathogen in 1958 after being isolated from the brain of a child who died of encephalitis in Powassan, Ontario. People infected with POWV often have a febrile illness that can be followed by progressive and severe neurologic manifestations, resulting in death in 10 to 15% of cases and long-term sequelae in 50 to 70% of survivors.3 An antigenically similar virus, POWV lineage II, or deer tick virus, was discovered in New England in 1997. Both POWV subtypes are linked to human disease, but their distinct enzootic cycles may affect their likelihood of causing such disease. Lineage II seems to be maintained in an enzootic cycle between I. scapularis and white-footed mice — which may portend increased human transmission, because I. scapularis is the primary vector of other serious pathogens, including B. burgdorferi. Whereas only 20 U.S. cases of POWV infection were reported before 2006,3 99 were reported between 2006 and 2016. Other tickborne encephalitis flaviviruses cause thousands of cases of neuroinvasive illness in Europe and Asia each year, despite the availability of effective vaccines in those regions. The increase in POWV cases coupled with the apparent expansion of the I. scapularis range highlight the need for increased attention to this emerging virus.

The public health burden of tickborne pathogens is considerably underestimated. For example, the CDC reports approximately 30,000 cases of Lyme disease per year but estimates that the true incidence is 10 times that number.1 Multiple factors contribute to this discrepancy, including limitations in surveillance and reporting systems and constraints imposed by available diagnostics, which rely heavily on serologic assays.4 Diagnostic utility is affected by variability among laboratories, timing of specimen collection, suboptimal sensitivity during early infection, imperfect use of diagnostics (particularly in persons with low probability of disease), inability of a single test to identify coinfections in patients with acute infection, and the cumbersome nature of some assays. Current diagnostics also have difficulty distinguishing acute from past infection — a serious challenge in diseases characterized by nonspecific clinical findings. Moreover, tests may remain positive even after resolution of infection, leading to diagnostic uncertainty during subsequent unrelated illnesses. For less common tickborne pathogens such as POWV, serologic testing can be performed only in specialized laboratories, and currently available tests fail to identify novel tickborne organisms.
Such limitations have led researchers to explore new technologies. For example, one of the multiplex serologic platforms that have been developed can detect antibodies to more than 170,000 distinct epitopes, allowing researchers to distinguish eight tickborne pathogens.4 In addition to its utility in screening simultaneously for multiple pathogens, this assay offers enhanced pathogen detection, particularly in specimens collected during early disease. Further studies are needed to determine such assays’ applicability in clinical practice.

Nonserologic platform technologies may also improve diagnostic capabilities, particularly in identifying emerging pathogens. Two previously unknown tickborne RNA viruses, Heartland virus and Bourbon virus, were discovered by researchers using next-generation sequencing to help link organisms with sets of unexplained clinical symptoms. The development and widespread implementation of next-generation diagnostics will be critical to understanding the driving factors behind epidemiologic trends and the full clinical scope of tickborne disease. In addition, sensitive, specific and, where possible, point-of-care assays will facilitate appropriate clinical care for infected persons, guide long-term preventive efforts, and aid in testing of new therapeutics and vaccines.

In the United States, prevention and management of tickborne diseases include measures to reduce tick exposure, such as avoiding or controlling the vector itself, plus prompt, evidence-based treatment of infections. Although effective therapies are available for common tickborne bacteria and parasites, there are none for tickborne viruses such as POWV.

The biggest gap, however, is in vaccines: there are no licensed vaccines for humans targeting any U.S. tickborne pathogen. One vaccine that was previously marketed to prevent Lyme disease, LYMErix, generated an immune response against the OspA lipoprotein of B. burgdorferi, and antibodies consumed by the tick during a blood meal targeted the spirochete in the vector.5 Nonetheless, the manufacturer withdrew LYMErix from the market for a combination of reasons, including falling sales, liability concerns, and reports suggesting it might be linked to autoimmune arthritis, although studies supported the vaccine’s safety. Similar concerns will probably affect development of other Lyme disease vaccines.5

Historically, infectious-disease vaccines have targeted specific pathogens, but another strategy would be to target the vector.5 This approach could reduce transmission of multiple pathogens simultaneously by exploiting a common variable, such as vector salivary components. Phase 1 clinical trials are under way to evaluate mosquito salivary-protein–based vaccines in healthy volunteers living in areas where most mosquito-borne diseases are not endemic. Since tick saliva also contains proteins conserved among various tick species, this approach is being explored for multiple tickborne diseases.5

The burden of tickborne diseases seems likely to continue to grow substantially. Prevention and management are hampered by suboptimal diagnostics, lack of treatment options for emerging viruses, and a paucity of vaccines. If public health and biomedical research professionals accelerate their efforts to address this threat, we may be able to fill these gaps. Meanwhile, clinicians should advise patients to use insect repellent and wear long pants when walking in the woods or tending their gardens — and check themselves for ticks when they are done.
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**Comment**

While this article repeats much of the same verbiage that’s been repeated for years, particularly the vaccine push, they are ignoring the following:

  1. Many TBI’s are congenitally transmitted:  https://madisonarealymesupportgroup.com/2018/06/19/33-years-of-documentation-of-maternal-child-transmission-of-lyme-disease-and-congenital-lyme-borreliosis-a-review/https://madisonarealymesupportgroup.com/2018/07/24/congenital-transmission-of-lyme-myth-or-reality/https://madisonarealymesupportgroup.com/2018/02/26/transplacental-transmission-fetal-damage-with-lyme-disease/
  2. There is a real probability of sexual transmission:  https://madisonarealymesupportgroup.com/2018/02/06/lyme-in-the-southern-hemisphere-sexual-transmission/https://madisonarealymesupportgroup.com/2017/02/24/pcos-lyme-my-story/
  3. While they mention Ehrlichia, Anaplasma, Rickettsia, and Babesia, there are many other players that are hardly getting a byline.  For a list to date:  https://madisonarealymesupportgroup.com/2017/07/01/one-tick-bite-could-put-you-at-risk-for-at-least-6-different-diseases/.  This is an important issue because to date the medical world is looking at this complex illness as a one pathogen one drug illness when nothing could be further from the truth.  No one has done any research on the complexity of being infected with more than one pathogen.  It will reveal the CDC’s guidelines of 21 days of doxy to be utter stupidity.
  4. Also, worth mentioning is that only a few of these are reportable illnesses so there is absolutely no data on how prevalent any of this is.  Surveillance is a real problem.
  5. Regarding what ticks are where….this ancient verbiage needs to change.  Ticks are moving everywhere.  This is on record in numerous places:  https://madisonarealymesupportgroup.com/2018/07/16/ticks-that-carry-lyme-disease-are-spreading-fast/https://madisonarealymesupportgroup.com/2018/07/10/we-have-no-idea-how-bad-the-us-tick-problem-is/https://madisonarealymesupportgroup.com/2018/07/22/citizen-scientists-help-track-tick-borne-illness-exposure/
  6. No tick is a good tick.  They all need blood meals and have the potential to transmit disease.  
  7. This article is silent about the Asian Longhorned tick that propagates itself by cloning and can drain cattle of their blood.  Found in six states so far it was recently found on a child in New Jersey:  https://www.northjersey.com/story/news/environment/2018/07/24/bergen-county-nj-child-may-first-carrying-longhorned-tick-us/825744002/.  Word in the tick world is it had NOT bitten the child and tested negative for pathogens.  What is concerning is that it is known to transmit SFTS virus and Japanese spotted fever in Asia. This story is a reminder that this tick is NOT just a livestock problem and that a normal child going about a normal day with NO contact with livestock had this tick on her.  Another clear reminder that it is foolish to put any of this in a box.
  8. They need to emphasize that the “classic erythema migrans rash” while indicative of Lyme, is unseen or variable in many patients.
  9. Constraints in testing is a true problem but an even bigger problem is untrained and uneducated medical professionals.  This stuff may never test clearly.  Get over it.  Get trained to know what to look for!
  10. The Lyme vaccine was a bust.  It still is.  Unless safety concerns are dealt with we want nothing to do with any vaccine.
  11. All I know is that mosquitoes and Zika get more attention that this modern day 21st century plague that is creeping everywhere and is a true pandemic.  It still isn’t being seriously dealt with or researched.  What research is being done is same – o – same -o stuff we already know.  Study the tough stuff – the unanswered questions or things that are just repeated as a mantra for decades.
We need answers out here not repeated gibberish that isn’t helping patients.
Afterthought:

The one thing I didn’t deal with that I will point out now is this regurgitated number in the NEJM article of 10-20% of patients moving on to chronic/persistent Lyme. The following informative article written by Lorraine Johnson points out this number to be considerably higher which corresponds to my experience as a patient advocate: https://madisonarealymesupportgroup.com/2018/07/22/lyme-costs-may-exceed-75-billion-per-year/. Excerpt below:

Besides the staggering financial cost to this 21st century plague, this paper, based on estimates of treatment failure rates associated with early and late Lyme, estimates that 35-50% of those who contract Lyme will develop persistent or chronic disease.

Let that sink in.

And in the Hopkins study found 63% developed late/chronic Lyme symptoms.

For some time I’ve been rankled by the repeated CDC statement that only 10-20% of patents go on to develop chronic symptoms. This mantra in turn is then repeated by everyone else.

While still an estimate, I’d say 35 to over 60% is a tad higher than 10-20%, wouldn’t you? It also better reflects the patient group I deal with on a daily basis. I can tell you this – it’s a far greater number than imagined and is only going to worsen.

 

 

Oklahoma-Ehrlichiosis Central

https://www.tulsaworld.com/news/local/oklahoma-is-ehrlichiosis-central-and-common-lone-star-ticks-which/article_408eed87-5b3e-5b3e-a829-9d7802ad578b.html

Oklahoma is ‘Ehrlichiosis Central,’ and common lone star ticks, which carry it, are ‘most active’ now

Flu-like illness spread via tick

By Kelly Bostian Tulsa World

July 4, 2018

Oklahoma ticks

The female lone star tick (left) is easily identified by the pronounced white dot or star in the center of her back. The species’ male is on the right. Courtesy/Rick Grantham, OSU

Correction: An infobox with this story contained incorrect numbers for tick-borne illnesses in Tulsa County. It has been corrected.

__________________________________________________________________________

Texas may be the Lone Star State, but late June through August is prime time for the real lone star to shine in Oklahoma — the lone star tick, that is.

Chances are this summer you have heard of someone in your circle of Oklahoma friends — or someone who knows someone — who has come down with ehrlichiosis (sounds like “air-leaky hoses).”

Along with the spotted fevers (rickettsioses), it is one of the most common tick-borne diseases in Oklahoma. It is primarily shared to Oklahomans through the lone star tick (the one with the white spot on its back), and the heat of summer is the time the lone star tick is most active, according to Oklahoma State University entomologist Justin Talley.

“We’ve had two people in our building and some in other departments come down with it recently, as well,” he said. “A lot of ticks are out right now, and it seems to be getting passed around for some reason, but that’s also pretty typical. We’ve always had it here in Oklahoma.”

The flu-like bacterial infection is passed from “reservoir species” such as white-tailed deer and coyotes through the lone star tick to humans.

While northeastern states are the prime areas for Lyme disease, Oklahoma is Ehrlichiosis Central.

“When you look at the Centers for Disease Control data, there are three states that are the hotbed for it: Oklahoma, Missouri and Arkansas,” Talley said.

It can prove fatal if left untreated, especially for very young or elderly patients. Fatal cases are not limited to but most often hit children younger than 10 and people over 70, Talley said.

“The summer is definitely a problematic time of year. Highest risk is April to October, but we really encourage people to be aware of tick-borne diseases like ehrlichiosis year around and statewide,” said Rachel Clinton, epidemiologist with the state Department of Health Acute Disease Service. “Each year we continue to see a lot of cases statewide.”

Diagnosis of ehrlichiosis can be tricky because people may think they have the flu and may not realize or recall that they were bitten by a tick up to two weeks earlier — especially people who spend a lot of time outdoors for their work or recreation, she said.

“It’s especially important for parents to check children for ticks every day, and if you’re working outdoors in a high-concentration area, you should inspect twice a day,” Clinton said. “Small children need to be looked at closely because they just don’t know they’ve been bitten. The hairline is an especially important place to look.”

Talley said the most important things are awareness, taking steps to prevent bites, and proper removal and documentation after being bitten.

“That’s the biggest thing. The lone star is the most active tick right now, especially east of I-35, Tulsa and southeast. You can go out anywhere and get one on you, even in your backyard,” he said.

Talley advised gentle, slow pulling of the tick straight away from the skin for removal, preferably just with tweezers or fingernails so as not to cause the tick to regurgitate back into the wound.

Tick-removal devices can be good, too;

“just don’t use anything that requires a twisting motion,” he said. “You want to lift it straight up, slowly, so a tool that is like a bottle-opener is OK.”  “Whatever you do, do not put a hot match or anything on the tick,” he said. “Just pull it off.”

The best thing then is to mark a calendar or put a date on a zip-seal bag, drop the tick in the bag and put it in the freezer. That can help with identifying the tick if something arises and, in rare cases, it could help solve a medical mystery.

“You can get the little brown seed tick, too, and it can be just a smaller lone star tick,” he said. “We can tell what it is under a microscope.”

Lone star ticks are not the only ticks in Oklahoma, but they are the ones most commonly associated with ehrlichiosis — as well as tularemia, southern tick-associated rash illness, the rare Heartland virus and the alpha-gal or meat allergy.

Dog ticks are the second most active now. They are most closely associated with Rocky Mountain spotted fever but also may be a vector for tularemia.

 

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More on Ehrlichosis:  https://madisonarealymesupportgroup.com/2018/03/09/dogs-ehrlichiosis/

https://www.lymedisease.org/ehrlichiosis-tick-borne-disease-no-one-heard/

More on Tularemia:  https://madisonarealymesupportgroup.com/2016/10/25/of-rabbits-and-men/

https://madisonarealymesupportgroup.com/2018/02/27/tularemia-infected-ticks-found-on-sorrento-valley-trail-in-ca/

https://madisonarealymesupportgroup.com/2018/03/07/hantavirus-tularemia-warnings-issued-in-san-diego-county/

More on RMSF:  https://madisonarealymesupportgroup.com/2018/07/10/first-rmsf-death-in-wisconsin/

https://madisonarealymesupportgroup.com/2018/06/12/georgia-mom-warns-others-after-son-contracts-rocky-mountain-spotted-fever-after-tick-bite/

https://madisonarealymesupportgroup.com/2017/10/21/mom-got-rocky-mountain-spotted-fever-while-picking-pumpkins/

More on Heartland Virus:  https://madisonarealymesupportgroup.com/2017/08/02/heartland-virus-in-arkansas/

https://madisonarealymesupportgroup.com/2016/11/01/heartland-virus-ravages-mans-body/

https://madisonarealymesupportgroup.com/2018/07/01/surveillance-for-heartland-bourbon-viruses-in-eastern-kansas/

Rutgers Racing to Contain Asian Longhorned Tick

https://www.nj.com/news/index.ssf/2018/07/this_is_how_dna_helps_rutgers_scientists_crack_the.html

It spreads SFTS (sever fever with thrombocytopenia syndrome), “an emerging hemorrhagic fever,” causing fever, fatigue, headache, nausea, muscle pain, diarrhea, vomiting, abdominal pain, disease of the lymph nodes, and conjunctival congestion, but the potential impact of this tick on tickborne illness is not yet known. In other parts of the world, this Longhorned tick, also called the East Asian or bush tick, has been associated with several tickborne diseases, such as spotted fever rickettsioses, Anaplasma, Ehrlichia, and Borrelia, the causative agent of Lyme Disease.

For a 2016 literature review on SFTS: http://infectious-diseases-and-treatment.imedpub.com/research-advances-on-epidemiology-of-severefever-with-thrombocytopenia-syndrome-asystematic-review-of-the-literature.php?aid=17986
Although the clinical symptoms of SFTS and HGA are similar to each other, but the treatment methods of the two diseases are totally different. Doctors notice that the biggest difference between the clinical symptom of SFTS and HGA is that SFTS patients generally without skin rash, the dermorrhagia is also not seriously, and few massive hemorrhage cases were reported [23]. It is also reported that SFTS patients had gastrointestinal symptoms, such as nausea, vomiting, and diarrhea, which are rarely observed in HGA patients [2]. So these differences can be used as the auxiliary basis of differential diagnosis.
At present, there is still no specific vaccine or antiviral therapy for SFTSV infection. Supportive treatment, including plasma, platelet, granulocyte colony stimulating factor (GCSF), recombinant human interleukin 11, and gamma globulin is the most essential part of case treatment [44]. Meanwhile, some measures were taken to maintain water, electrolyte balance and treat complications are also very important.
Ribavirin is reported to be effective for treating Crimean-Congo Hemorrhagic Fever (CCHF) infections and hemorrhagic fever with renal syndrome, but it is still inadequate to judge the effect of ribavirin on SFTS patients because of the study limitation without adequate parameters were investigated [45]. Host immune responses play an important role in determining the severity and clinical outcome in patients with infection by SFTSV.
For Viral treatment options: https://madisonarealymesupportgroup.com/2016/03/28/combating-viruses/

And lastly, please know ticks parasitize one another, potentially spreading all manner of diseases to humans.  This fact also shoots holes in the regurgitated mantra that only certain ticks carry certain pathogens.  If they are feasting on one another, they can potentially infect each other and then us:  https://madisonarealymesupportgroup.com/2018/03/07/tick-bites-tick-hyperparasitism/