Archive for the ‘Transmission’ Category

Chronic Toxoplasmosis: Debilitating, Stealth, Underdiagnosed

https://articles.mercola.com/sites/articles/archive/2022/09/16/chronic-active-toxoplasmosis

By Dr. Mercola

Sept. 16, 2022

Story at-a-glance

  • At least one third of all people on Earth are infected with the parasite Toxoplasma gondii, averaging from 11-20% in the United States to 50% and higher in some Western European countries
  • The parasite has been implicated in ocular issues, schizophrenia, epilepsy, Alzheimer’s disease and various other neurological disorders, as well as in heart disease, pneumonia, recurrent headaches, even cancer; it is also known for causing psychological changes in its hosts
  • While the official word is that most toxoplasma infections are harmless and asymptomatic, the impact of the parasite could be much more devastating than the current mainstream medical convention presumes; it may also be cross-reacting with the spike protein and possibly contributing to the mystery of “long COVID”
  • According to recent research and clinical evidence, toxoplasma tissue cysts, previously considered harmless in immunocompetent patients, are capable of causing major health issues without converting to the cell-blasting form
  • Commonly used antibody tests can only detect antibodies for the “tachyzoite” (cell-blasting) form of the parasite but not the “bradyzoite” (tissue cyst) form
  • Dr Uwe Auf der Straße in Germany has done an important clinical investigation of the parasite, and his findings could shed light on “mystery” symptoms in many patients

Toxoplasma gondii, an intracellular protozoan organism, is a very “successful” parasite with extremely diverse host base and sophisticated, almost diabolical, methods of survival and proliferation.

It is found worldwide and is capable of infecting most warm-blooded animals as intermediate hosts, including people. It has also been found in some cold-blooded animals, such as fish. Its final hosts, inside which the parasites can sexually reproduce, are felines, including domestic cats. In the environment, toxoplasma can be found in soil, water, and other substances that have come in contact with the parasite, such as fertilizers.

At the moment, the predominant medical opinion is that at least one third of all people on Earth are in some way infected with this parasite1,2 averaging from 11-20% in the United States to 50% or higher in a number of Western European countries, for example in Germany.3 In Germany, the frequency of positive Toxoplasma detection increases from about 20% in the group of 18-29 year-olds, up to 77% in the group of 70-79 year-olds and for over 79 year-olds the frequency is 84%.4

The commonly known infection routes for people are eating uncooked meat, drinking contaminated water, or accidentally ingesting the parasite after cleaning a cat litter box.

While the official word is that most infections are harmless and asymptomatic, the impact of the parasite could be much more devastating than the current mainstream medical convention gives it credit for.

A few physicians and researchers who have been looking into Toxoplasma are challenging the conventional view on several counts. And while a number of “bombshell” scientific works on the topic have been published, the new discoveries have not yet made their way into the everyday medical practice.

It is extremely important that more doctors and researchers look into this right now — especially given the fact that an encounter with the spike protein has been shown to amplify latent or slow-developing biological malfunctions in people, and thus it is possible that “spike protein assisted” Toxoplasma may be wreaking havoc in many unsuspecting patients and contributing significantly to the mysterious “long COVID” or its injection-induced manifestation.

Toxoplasma Life Cycle

With a degree of oversimplification, there are three main forms in which this parasite exists during different phases of its life cycle. They are known as oocysts (eggs), tachyzoites (the actively proliferating adult form), and bradyzoites (tissue cysts).

The sexual reproduction of Toxoplasma gondii occurs within feline hosts. The cycle starts when the host ingests oocysts (“eggs”) or eats an animal infected with bradyzoites (tissue cysts).

Upon ingestion of the cysts, their protective wall is dissolved by proteolytic enzymes in the stomach and small intestine to release bradyzoites. The free bradyzoites then penetrate epithelial cells lining the small intestine where they proliferate to form new generations that can undergo sexual and asexual cycles. Following fertilization of the female gametes, a wall starts to form around the oocysts. The oocysts are then released to the environment along with feces.

Depending on the environment, it usually takes several days for the oocysts in feces to become infectious. Infectious oocysts can survive for up to several years in soil etc., until they are ingested by an intermediate host. Once they are ingested, their protective shield is also dissolved by proteolytic enzymes thus releasing the eggs into the intestine of the intermediate host.

They then penetrate epithelial cells lining the small intestine where they undergo a form of asexual reproduction to form tachyzoites. The newly formed tachyzoites then spread and actively penetrate other cells of the intermediate host where they are surrounded by a parasitophorous vacuole protecting them from the hosts’ immune system.5

The interesting thing about the parasitophorous vacuole is that the parasite uses a part of the membrane of the invaded host cell’s to form it, with the purpose of “hiding” from the host’s immune system.6

From there tachyzoites disseminate throughout the body and reach immunologically protected sites including brain, retina and fetus. In vitro studies revealed that tachyzoites can invade astrocytes, microglia and neurons of the mouse brain with subsequent formation of tissue cysts within these cells.7,8,9,10,11

As they continue dividing, tachyzoites ultimately cause the cell to break, releasing as many as 32 tachyzoites that then infect new cells. However, that activity usually attracts the attention of the immune system, which ultimately slows down tachyzoite multiplication. In response, the tachyzoites convert into bradyzoites (tissue cysts).12

In doing so, they change their surface structure nearly completely, which is a “major factor in the parasite’s strategy of survival” since the host’s immune system identifies microorganisms according to their surface structure, and by modifying its surface structure, toxoplasma increases its chance of successfully tricking the host’s immune system.13,14,15

The tissue cysts are common in a number of body tissues and organs including the eyes, cardiac muscle, neural tissue, and various visceral organs where they can last for the hosts’ entire lifetime.16

Houston, We Have a Problem

The general medical consensus (challenged by a small group of doctor and researchers) is that while the most active form of Toxoplasma, known as “tachyzoites” (the one that multiplies very fast and blasts host cells), can cause significant health issues, predominantly in immunocompromised hosts, the tissue cyst form (“bradyzoites”) is mostly innocuous, and, once the parasite succumbs to the attack by the host’s immune system and retreats into its tissue cysts, it just quietly sits inside those intracellular cysts and does very little.

Per mainstream medial convention, the vulnerable demographics are immunocompromised patients who can succumb to acute toxoplasmosis and develop potentially lethal inflammation of the brain (or become victims of a “reactivation,” where tissue cysts convert back to the fast-proliferating form, to the same effect), and newly infected pregnant women.

However, recent research has shown that bradyzoites, the toxoplasma tissue cysts, are not innocuous at all, and that they do reproduce inside the cysts and can cause inflammation and other issues without converting to tachyzoites, including in otherwise immunocompetent patients.

What complicates the issue even further is that nearly all commercially available tests (antibody blood tests and even PCR tests), are specific to the cell-blasting tachyzoite form of toxoplasma and do not detect the presence of tissue cysts.

And if that is the case — we are looking at a potentially large number of people ailing from “chronic active toxoplasma” that cannot be diagnosed by any of the commonly used methods. As a result — especially given that toxoplasma loves living in the brain — their very real and possibly exhausting physical disease may be classified or psychosomatic or straight out psychiatric.

They could be suffering from slow-developing brain inflammation, autism-like symptoms, dementia-like symptoms, or even pulmonary and heart issues — and the doctors might not even be looking in the direction of toxoplasma or ruling it out, based on negative antibodies.

(In its active form, the parasite has been implicated in ocular issues,17 heart disease,18 pneumonia,19 recurrent headaches,20,21 even cancer22 — as well as in addiction, schizophrenia, epilepsy, Alzheimer’s disease, and various neurological disorders.23,24,25 And even in its latent form, it is believed to cause psychological changes in its hosts, ranging from entrepreneurial26 to suicidal tendencies.27

Among the researchers doing groundbreaking research in Toxoplasma are Dr. Jaroslav Flegr in the Czech Republic, Dr. Robert Yolken and Dr. Vernon Carruthers in the U.S., Dr Uwe Auf der Straße in Germany, and others.

The Work of Dr. Uwe Auf der Straße in Germany

Dr Uwe Auf der Straße is a GP in Germany and the author of the book titled, “Shadow Disease Chronic Active Toxoplasmosis.”28 Here is what he has to say about the “limits of our current laboratory medicine”:

“The current medical opinion is still that a negative IgM excludes an active toxoplasmosis and thus the need of a therapy. Due to research having hinted repeatedly of a significant effect of bradyzoite activity, and due to my own observations, I definitely cannot agree with that.

Tests only react to tachyzoite-specific antibodies and the sensitivity of a standard test system in case of an initial infection is only 81.8%.29 Basic research has done further substantial work which questions the accuracy of Toxoplasma antibody assays.

‘The currently available solid phase immunoassays were developed in the 1970’s to detect strains which were circulating at that time and there are strong indications, that … standard assays may substantially underestimate the prevalence of Toxoplasma infection in a population and its effect on health and disease.’30

Further it has been proven that, in cases of a Toxoplasma infection, tachyzoite–specific IgG, IgM and even PCR can render negative results.31,32,33

In a chronic active course of the disease, reliability of our currently used lab methods has not been proven and these are most likely not suitable to detect Bradyzoites or their activity, let alone the cyst burden.

Research still focuses predominantly on acute rather than chronic toxoplasmosis and it is only a general assumption, that cases with chronically active courses of the disease as presented here could be diagnosed by using the usual antibody assays – to my knowledge this has never been proven.

The number of Toxoplasma carriers without detectable tachyzoites antibodies, who can potentially become ill from a chronic active toxoplasmosis based on an increased activity within the cysts is unclear.

From my observations it can be assumed that the number is significant, otherwise there would not appear so many younger patients in my case collection (about 40%), who suffer from a chronic active toxoplasmosis without any detectable tachyzoite antibodies.

If the immune system ceases to produce Tachyzoite antibodies after some years, the disease will no longer be detectable in the blood. This does not mean that the Toxoplasma in the cysts are inactive.

There are numerous indications that an increased activity in the cysts can trigger a symptomatic illness, since, contrary to older assumptions, bradyzoites do not rest, but can be active and can reproduce and cause illness. This refers to the findings of Fergusson et al. (1989), McLeod et al. (2008) and Watts et al (2015).”34,35,36

Dr. Uwe Auf der Straße has observed that there was no significant difference in observed symptoms between his patients with positive antibody tests and his patients with negative antibody tests in whom he suspected chronic active toxoplasmosis, based on the preliminary diagnostic method he developed and ruling out other illnesses that can produce similar symptoms. (He also took into consideration their positive reaction to toxoplasma therapy.)

“I am convinced that a significant activity within the cysts, predominantly of the bradyzoites, is the decisive reason for the illness in both groups of patients who all have inconspicuous IgM values with regards to tachyzoites, and whose IgG values, if indeed there are any, don’t show any direct correlation to the severity of the illness.

The clinical pictures in both groups are identical, and the toxoplasmosis therapy is even more effective in group B [negative antibody tests]. The bradyzoites, the activity of which we cannot measure, are currently underrated strongly, and our established laboratory values produce only a pretended security.

It is difficult to develop reliable bradyzoite-specific tests, since bradyzoites reveal themselves only rarely to the immune system and only lead to a limited antibody production.”37

“Thankfully, basic research has begun to address this problem, and there are new and promising methods being developed, with the aim of getting a grip on this problem and reveal hitherto not detectable toxoplasma presence and even to determine the cyst burden.”38

Toxoplasma and the Mind

According to Kathleen McAuliffe, author of the book “This Is Your Brain on Parasites,”39 researchers have noticed a strong correlation between toxoplasma infection and schizophrenia and other mental disorders in humans. She also notes studies where anti-psychotic drugs inhibited toxoplasma in vitro.

In fact, the mind-controlling ability is Toxoplasma’s “trademark.” I wrote about it earlier in the article titled, “Don’t Underestimate Mind-Controlling Parasites.”

To quote Dr. Uwe Auf der Straße again, whose book I can’t recommend enough, “symptoms comprise an increased risk for the occurrence of schizophrenia40,41,42,43 psychoses44 or aggressive behaviour, also a doubling of the risk for accidents in cases where Toxoplasma antibodies have been detected.45

Explanations for that may point to the mentioned behavioural changes and the decreasing psychomotor resilience46 due to Toxoplasma infections. It is scary that even an increase in the number of attempted suicides has been correlated with antibody detection in toxoplasmosis.”47,48

“It fits this bill that toxoplasmosis infected rats are known to lose all fear of cats. They literally seek them out in broad daylight, to be eaten in the end, a behaviour that is very advantageous for the spreading of Toxoplasma, but not so good for the rat. The consequence is clear.

When the host is ‘ripe’ and contains many bradyzoite – cysts, it is simply more useful for the parasite when dead instead of alive, particularly if the death is caused by a cat. Death by car accident or suicide are thus somehow “inappropriate”, but can be regarded as a somewhat macabre continuation of such behavioural disturbances in the present.”

Many Tricks of Toxoplasma

The tricks of this parasite are endless. For example, it knows how to hijack the host’s macrophages — and instead of being destroyed by a macrophage,49 take over it and use it as a temporary home to transform into the active form and then use it as a cab to travel around the host’s body!

According to the accepted view, the release of actual “eggs” from the ingested oocysts into the host’s system happens due to the processes in the host’s digestive system. However, a study came out showing that the process can happen in the absence of digestive factors, and that the parasite can not only survive but also transform into its most active form inside macrophages, after being “eaten”:

“Our results show that the oocyst internalization kinetics can vary among a given population of macrophages, but similar processes and dynamics could be observed. Most of the cells manipulate oocysts for ~15 min before internalizing them in typically 30 min … Liberated sporozoites within macrophages then differentiate into tachyzoites within 4-6 h following oocyst-macrophage contact.”

Another paper, titled, “Inhibition of nitric oxide production of activated mice peritoneal macrophages is independent of the Toxoplasma gondii strain,” shows that Toxoplasma is capable of inhibiting nitric oxide production. Nitric oxide, that plays an important role in immune response50,51 and is frequently mentioned in the context of COVID.

It’s an “enzyme that is expressed in activated macrophages, generates nitric oxide (NO) from the amino acid L-arginine, and thereby contributes to the control of replication or killing of intracellular microbial pathogens.”52

The overall mechanism that the parasite uses to invade host cells is beyond of the scope of this article but if you are curious, you can check out the paper titled, “How does Toxoplasma gondii invade host cells?” If you want to learn more about how it modulates host cell’s responses, there is another technical paper titled, “Toxoplasma gondii Modulates the Host Cell Responses: An Overview of Apoptosis Pathways.”

And if you want to learn more about Toxoplasma and brain blood barrier, you can read this paper, “Toxoplasma gondii and the blood-brain barrier.”

Toxoplasma and the Spike Protein: A Possible Connection?

According to Dr. Uwe Auf der Straße, a patient could be potentially simultaneously infected with Toxoplasma and with one or more other pathogens, some of the them kicking in as opportunistic infections.

In that case, the clinical picture may be even more confusing, and the condition of the patient may be more severe, even though Toxoplasma is capable of causing enough trouble if it manages to sufficiently proliferate — whether in its active form or inside the tissue cysts — all on its own.

Dr. Uwe Auf der Straße’s book was published in 2019, so there is nothing about COVID in the book — but it is not illogical to presume that when a person with latent or relatively slowly developing Toxoplasma encounters the spike protein, whether it’s from infection or from the COVID injection, it may create a “perfect storm” and kick Toxoplasma in high gear, creating debilitating and/or mysterious symptoms, resulting in vaccine injury or “long COVID.”53

If the percentage of people with chronic active Toxoplasma is as high as Dr. Uwe Auf der Straße suspects, it is also not illogical to assume that due to the deficiencies in the current diagnostic standards and tools, a lot of people suffering from chronic active Toxoplasma may not be properly diagnosed, and their maladies may be attributed to psychosomatic factors or remain a medical mystery.

An additional complication is that “atypical mixed forms of the known Toxoplasma strains, which are significantly more aggressive than the previously known Toxoplasma strains have been detected in Germany, and this might happen worldwide.”54,55,56

Anecdotally, per Dr. Uwe Auf der Straße, patients with chronic active toxoplasma could experience increased irritability where they “blow up” out of nowhere even though they realize that there is no good reason and don’t feel good about being so irritable — as well as anxiety or depression, with men more prone to irritability, and women more prone to anxiety and depression.

At the same time, also anecdotally, increased irritability has been observed in some recipients of the COVID injection. And while there can be lots of factors causing mood changes, it could be something to look into.

Curiously, there is an overlap between the list of natural remedies that have been studied as potentially treatments against toxoplasma and showed improvements — and the list of “alternative” COVID and “long COVID” treatments.57,58,59,60 Due to the tremendous complexity of the issue and the fact that myriads of factors impact our immune response and reactions to treatments, further investigation of the correlation by honest and curious is urgently needed.

Conventional toxoplasma treatments are considered effective in treating tachyzoites but there is no known conventional treatment for the tissue cyst form.61

Better Diagnostics: Some Hope

According to Dr Uwe Auf der Straße, in his practice, he found one particular testing method to be more reliable than the conventional ones:

“The Lymphocyte-Transformation-Test (LTT) has made my work on Toxoplasmosis easier in the last months, but is not (yet) used for the diagnose of toxoplasmosis on a wider scale. By means of this test, we can detect activity of our immune system’s T-lymphocytes, which react specifically towards certain pathogens.

While the immune system is dealing with certain pathogens, T-lymphocytes become specifically reactive to this pathogen, and the intensity of this reactivity can be measured pathogen-specifically.”

“This is measurable for about 4 weeks, and thus the LTT mirrors the current activity of pathogens. A more than threefold elevated stimulating index (SI) indicates, that specific T-cells are present in the blood and thus an active confrontation of the immune system and the tested germ takes place.

A validation concerning chronic active toxoplasmosis has not yet been performed, but according to both Dr. Hopf-Seidel and my own experiences with patients suffering from a chronic active toxoplasmosis, it is most likely more sensitive than the Toxoplasma IgM.”

Dr Uwe Auf der Straße also speaks highly of the work of Dr. Yolken’s team:

“I consider a new approach of the scientific group led by Professor Yolken in Baltimore to be promising. A paper on this approach has been published in June, 2018.62 The scientists used a known detection method (a Western blot test) for the detection of Toxoplasma proteins, which also give proof of the presence of Toxoplasma.

Of 25 patients, who were suffering from severe psychic disorders, 3 patients (8.2%) were diagnosed as positive with Toxoplasma IgG. Four times as many, 12 patients (35.3%) were then diagnosed with Toxoplasma by detection of Toxoplasma protein in their blood.

The detection of these proteins seems to offer a significantly more sensitive method to diagnose toxoplasmosis than the usual available antibody tests. Until this can be used as a routine procedure, the tests will have to be examined in further studies.”

“The same group of scientists is currently developing another highly-sensitive method, which can detect Toxoplasma cysts in every stage of the disease. This concerns the MAG1 antigen, which occurs in great numbers inside the bradyzoite cysts and in their outer membrane. Antibodies which are directed against this MAG1 antigen can be detected in the laboratory.

The scientist could prove in mice that the amount of MAG1 antibodies detectable in the blood showed a significant correlation to the amount of bradyzoite cysts inside the brain. It was also shown that in case of negative MAG1 antibody detection, no bradyzoite cysts were found.

This marker could possibly be used as a scale for a chronic infection and for the burden with bradyzoite cysts in the future. This would be a huge step for laboratory diagnostics and for affected patients even more so.”

“Another approach is that clues for a disturbed metabolism in patients with Chronic Fatigue Syndrome (CFS) are being investigated intensively. In 2016 it was proven that CFS patients share anomalies in 20 metabolic pathways of their mitochondria.63 One might picture mitochondria best as our cells’ power plants.

The intensity of the illness in CFS patients negatively impacts the activity of the metabolic pathways and the quantity of metabolites, which result from the mitochondria’s work. This “shutdown” of the metabolism has been interpreted as a shifting of the mitochondrial metabolism into “survival mode.”

Toxoplasma can also very severely affect the mitochondria,64 and the intensity of affliction is probably related to the strain of Toxoplasma which has infected the patient.65 It would be of utmost interest if the deviations in mitochondria metabolism during a chronic active toxoplasmosis might resemble those detected in ME/CFS patients, as there is strong overlap in the symptoms of both diseases. They might even be identical in some cases.”

Conclusion

It is possible that due to imperfect diagnostics and insufficient understanding of this parasite in the medical community, a lot of people with chronic active toxoplasma remain undiagnosed or diagnosed incorrectly, and suffer profoundly from the lack of proper treatment.

It is also possible that Toxoplasma is a significant factor, contributing to complications from spike protein toxicity. I believe that understanding this issue is important. It requires time and attention of researchers and doctors, and my prayer is for solid knowledge to come, and for the “mystery” suffering to end.

About the Author

To find more of Tessa Lena’s work, be sure to check out her bio, Tessa Fights Robots.

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For more:

Toxoplasmosis causes many mental issues and psychiatrist E. Fuller Torry believes that 75% of schizophrenia is associated with infections, with Toxo a significant portion.  https://madisonarealymesupportgroup.com/2016/05/21/toxoplasmosis/

Tickease Founder On Dangers of Ticks, What We Need to Know About Prevention

https://www.wideopenspaces.com/tickease-founder-on-ticks/

TickEase Founder Dan Wolff on Dangers of Ticks, What We Need to Know About Prevention


 

Dan Wolff, aka: “Tick Man Dan,” wore a tie emblazoned with images of ticks to his wedding. He regularly wears shirts and even a wristwatch with pictures of the arachnids on them. He has two tattoos of the creepy, blood-sucking pests permanently inked onto his left leg. He even goes on tick hunting expeditions, and he keeps jars of them around his home. This may strike some people as weird, but for Wolff, they’re conversation starters on a subject he’s passionate about. Plus, it’s part of how he makes his living. Tick Man Dan’s mission is simple: to educate the public on the dangers posed from the diseases and parasites carried by ticks, and to promote his brand, TickEase. The company makes a set of specialty tweezers designed by Wolff himself that are meant specifically for the removal of ticks and their nymphs once embedded in a person.

When I spoke to Wolff via Zoom from his home in Massachusetts, I learned more about ticks in one 40-minute sitting than I had learned my whole life. We spoke about TickEase and their Tick-Kits, proactively preventing issues, and his general enthusiasm for these tiny creatures that are capable of causing such big problems.  (See link for article)

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SUMMARY:

  • Out of necessity, Wolff created Tickease when he couldn’t find a good tick removal device – particularly for an embedded nymph (which is as small as a poppy seed).
  • Unfortunately Wolff regurgitates the “warmer weather gets more ticks” mantra – essentially propelling the ‘climate change’ myth regarding tick and disease proliferation. 
    • Ticks are marvelously ecoadaptive and can survive virtually all weather by burrowing under leaf litter and snow – and anything else they can find. 
    • The repeated mantra of “climate change”, wildlife proliferation, and surburban sprawl ignores the very real spreading of ticks by our own government who has experimented on ticks for decades.
    • Willy Burgdorfer, the “discoverer” of Lyme disease was a researcher at the Rocky Mountain laboratory where he weaponized ticks by force-feeding them numerous pathogens.
  • Ticks can be active year-roundproving their ecoadaptability.  They can go into a dormant state called diapause due to a anti-freeze-like substance in their bodies which actually feeds the Lyme bacteria.
  • Wolff found ticks can wake up fast with a feeding frenzy if there are periods of cold interrupted by a sudden increase in temps. Please watch this short video demonstrating how quickly this can happen.
  • Wolff dispels the myth that it takes 36 hours for ticks to transmit Lyme.  (It can happen in a few of mere hours)
  • He also points out that viruses can be transmitted in minutes and that ticks carry far more than just Lyme.
  • When removing a tick, do not agitate it or get the contents of the abdomen on you.

For more:

 

Deer Keds, Flying Ticks?

https://www.iamexpat.de/expat-info/german-expat-news/tick-season-germany-look-out-flying-ticks

Tick season in Germany: Look out for “flying ticks”

Excerpts:

Ticks can cause similar problems amongst humans, spreading diseases like tick-borne encephalitis (TBE) and Lyme disease, as well as some other, lesser-known diseases like babesiosis and boutonneuse fever. In 2019, a Hyalomma tick even infected a man in North Rhine-Westphalia with typhus.

Beware of “flying ticks”

Between July and October, the deer louse fly is also active in Germany. Sometimes known as a “flying tick”, these critters make a beeline for their target and then shed their wings when they land, burrowing down, biting and sucking blood from their victims. The ticks usually target animals, but attacks on humans have been recorded. They prefer to bite humans on the scalp or neck and can cause allergic reactions and even heart infections.

Deer louse flies are usually found in forests in the summer and autumn. It is recommended to thoroughly check any pets after walks in case they have been bitten by ticks. Ticks can be located using a flea comb and removed with adhesive tape or washed away. Any animal that has been infested with ticks should be bathed and washed.

(See link for article)

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The deer ked (Lipoptena cervi) mainly parasitize elk and deer but also bite humans.  It is unknown whether it serves as a vector for transmission but the following have been detected:

Remains of L. cervi have been found on Otzi, the Stone Age mummy.

Read the following on the deer fly (200 species in the Chrysops genus):

While male deer flies collect pollen, female deer flies feed on blood, which they require to produce eggs.[4] Females feed primarily on mammals. They are attracted to prey by sight, smell, or the detection of carbon dioxide. Other attractants are body heat, movement, dark colours, and lights in the night. They are active under direct sunshine and hours when the temperature is above 22 °C (71.6°).[4] When feeding, the females use scissor-like mandibles and maxillae to make a cross-shaped incision and then lap up the blood. Their bite can be painful. Anti-coagulants in the saliva of the fly prevents blood from clotting and may cause severe allergic reactions. Parasites and diseases transmitted by the deer fly include tularemia, anthrax, anaplasmosis, equine infectious anemia, hog cholera, and filiariasis. DEET is not an effective repellent.[2]

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https://www.sciencedaily.com/releases/2019/05/190531135826.htm

New records show spread of parasitic deer flies across the United States

Date:
May 31, 2019
Source:
Penn State
Summary:
With flattened bodies, grabbing forelegs and deciduous wings, deer keds do not look like your typical fly. These parasites of deer — which occasionally bite humans — are more widely distributed across the US than previously thought, according to entomologists, who caution that deer keds may transmit disease-causing bacteria.

With flattened bodies, grabbing forelegs and deciduous wings, deer keds do not look like your typical fly. These parasites of deer — which occasionally bite humans — are more widely distributed across the U.S. than previously thought, according to Penn State entomologists, who caution that deer keds may transmit disease-causing bacteria.

“It was more or less known where deer keds are found, but very broadly,” said Michael Skvarla, extension educator and director of the Insect Identification Lab in the Department of Entomology at Penn State. “We don’t know if deer keds transmit pathogens (disease-causing microorganisms), but if they do, then knowing where they are at more precisely could be important in terms of telling people to watch out for them.”

The researchers collated records of the four North American deer ked species and produced the most detailed locality map of these flies to date, documenting ten new state and 122 new county records. The researchers published their results in a recent issue of the Journal of Medical Entomology. They also provided an illustrated species-identification key.

The team harnessed citizen science — collection of data by the public — to gather deer ked records from the U.S. and Canada. In addition to scouring museum databases and community websites like BugGuide and iNaturalist, the team distributed deer ked collection kits to hunters as part of the Pennsylvania Parasite Hunters community project. The researchers also collected flies directly from carcasses at Pennsylvanian deer butcheries.

“I really like using citizen science information,” said Skvarla. “It often fills in a lot of gaps because people are taking photographs in places that entomologists may not be going. Deer keds are the perfect candidate for citizen science. They’re easy to identify because there’s only four species in the country and because they’re mostly geographically separated. And as flat, parasitic flies, they’re really distinctive. You couldn’t do this with a lot of insect groups because they’d be too difficult to identify from photographs.”

The European deer ked, Lipoptena cervi, thought to have been introduced from Europe, previously was reported to occur throughout the Northeast region. The researchers newly report this species from Connecticut, Rhode Island, Vermont, and as far south as Virginia. In Pennsylvania, it occurs throughout the state, with 26 new county records.

The researchers also describe new records of the neotropical deer ked, L. mazamae, from North Carolina, Tennessee and Missouri — increasing its range further north and east than had previously been reported.

In western North America, two deer ked species, L. depressa and Neolipoptena ferrisi, are found from British Columbia through the U.S. and into Mexico — and as far east as South Dakota. The researchers newly report these species from Nevada and Idaho.

Deer keds are usually found on deer, elk and moose, but occasionally bite humans and domestic mammals. Although several tick-borne pathogens — including bacteria that cause Lyme disease, cat scratch fever and anaplasmosishave been detected in deer keds, it is unknown whether they can be transmitted through bites.

“In Pennsylvania you have a lot of hunters,” said Skvarla.

“Deer keds can run up your arm while you’re field dressing a deer and bite you. If these insects are picking up pathogens from deer, they could transmit them to hunters. With two million hunters in the state, that’s not an insignificant portion of the population. We don’t want to scare people, but people should be aware there is the potential for deer keds to transmit pathogens that can cause disease.”

The researchers will next screen hundreds of deer keds for pathogens. They will also dissect some insects to screen the salivary glands and guts separately. According to Skvarla, this approach will give a good indication of whether deer keds could transmit pathogens through bites, or whether the bacteria are merely passed through the gut after a blood meal.

In Pennsylvania, after deer keds emerge from the soil each fall, they fly to a host and immediately shed their wings, usually remaining on the same host for life. Females produce just one egg at a time — it hatches inside her, and she feeds the growing larva with a milk-like substance. When the larva is almost fully developed, it drops to the soil and forms a pupa, eventually emerging as a winged adult. If disease-causing bacteria are transmitted from mother to offspring, newly emerged flies could pass on pathogens to hosts. Pathogens could also be spread when bacteria-harboring flies jump between animals in close contact.

The other researcher working on this project was Erika Machtinger, assistant professor of entomology at Penn State.

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https://www.mdedge.com/dermatology/article/171732/infectious-diseases/deer-ked-lyme-carrying-ectoparasite-move

Deer Ked: A Lyme-Carrying Ectoparasite on the Move

Lipoptena cervi, known as the deer ked, is an ectoparasite of cervids traditionally found in northern European countries such as Norway, Sweden, and Finland. Although rarely reported in the United States, this vector recently has been shown to carry Borrelia burgdorferi and Anaplasma phagocytophylum from specimens collected domestically. Importantly, it has been suggested that deer keds are one of the many disease-carrying vectors that are now found in more expansive regions of the world due to climate change. We report a rare sighting of L cervi in Connecticut. Additionally, we captured a high-resolution photograph of a deer ked that can be used by dermatologists to help identify this disease-carrying ectoparasite.

Practice Points

  • There are many more disease-carrying arthropods than are routinely studied by scientists and physicians.
  • Even if the insect cannot be identified, it is important to monitor patients who have experienced arthropod assault for signs of clinical diseases.

Case Report

A 31-year-old man presented to the dermatology clinic 1 day after mountain biking in the woods in Hartford County, Connecticut. He stated that he found a tick attached to his shirt after riding (Figure). Careful examination of the patient showed no signs of a bite reaction. The insect was identified via microscopy as the deer ked Lipoptena cervi.

Comment

Lipoptena cervi, known as the deer ked, is an ectoparasite of cervids traditionally found in Norway, Sweden, and Finland.1 The deer ked was first reported in American deer in 2 independent sightings in Pennsylvania and New Hampshire in 1907.2 More recently deer keds have been reported in Massachusetts, New York, Pennsylvania, and New Hampshire.3 In the United States, L cervi is thought to be an invasive species transported from Europe in the 1800s.4,5 The main host is thought to be the white-tailed deer (Odocoileus viginianus). Once a suitable host is found, the deer ked sheds its wings and crawls into the fur. After engorging on a blood meal, it deposits prepupae that fall from the host and mature into winged adults during the late summer into the autumn. Adults may exhibit swarming behavior, and it is during this host-seeking activity that they land on humans.3

Following the bite of a deer ked, there are reports of long-lasting dermatitis in both humans and dogs.1,4,6 One case series involving 19 patients following deer ked bites reported pruritic bite papules.4 The reaction appeared to be treatment resistant and lasted from 2 weeks to 12 months. Histologic examination was typical for arthropod assault. Of 11 papules that were biopsied, most (7/11) showed C3 deposition in dermal vessel walls under direct immunofluorescence. Of 19 patients, 57% had elevated serum IgE levels.4

In addition to the associated dermatologic findings, the deer ked is a vector of various infectious agents. Bartonella schoenbuchensis has been isolated from deer ked in Massachusettes.7 A recent study found a 75% prevalence of Bartonella species in 217 deer keds collected from red deer in Poland.5 The first incidence of Borrelia burgdorferi and Anaplasma phagocytophylum in deer keds was reported in the United States in 2016. Of 48 adult deer keds collected from an unknown number of deer, 19 (40%), 14 (29%), and 3 (6%) were positive for B burgdorferi, A phagocytophylum, and both on polymerase chain reaction, respectively.3

A recent study from Europe showed deer keds are now more frequently found in regions where they had not previously been observed.8 It stands to reason that with climate change, L cervi and other disease-carrying vectors are likely to migrate to and inhabit new regions of the country. Even in the current climate, there are more disease-carrying arthropods than are routinely studied in medicine, and all patients who experience an arthropod assault should be monitored for signs of systemic disease.

How Ticks Ambush & Give You Lyme/MSIDS

https://www.lymedisease.org/ticks-ambush-lyme-disease-healy/

Precisely how do ticks ambush you–and give you Lyme disease?

John Eoin Healy, PhD, now retired from University College Cork, Ireland, has been researching tick biology for over 40 years. In the following article and video, he explains how questing ticks make contact with unsuspecting people and animals.

by John Eoin Healy, PhD

Various estimates indicate that up to 60% of people who contract Lyme borreliosis (Lyme disease) have no recollection of being bitten by a tick.

For those concerned about Lyme disease risk, it may be useful to explain how ticks make contact with and attach to host animals i.e. birds and mammals, including unfortunate humans.

The species of tick that transmits the Borrelia bacteria that cause Lyme disease are Ixodes ricinus in Europe, and Ixodes scapularis and Ixodes pacificus in North America. These ticks thrive in areas with woodland or heavy vegetation which provide the cool moist conditions that these ticks need to survive.

Their second vital requirement is a sufficient number of host animals (deer, cattle, sheep, goats, small mammals and birds) to ensure that ticks have hosts on which they can feed (that is, suck blood) and then reproduce. Increasing numbers of host animals such as deer will accelerate the growth of tick populations.

Ticks have limited mobility

At the risk of stating the obvious, ticks are wingless and therefore cannot fly. Neither can they run or jump. The species of tick that transmit the Borrelia bacteria that cause Lyme disease move very little laterally on the ground, that is, in the horizontal plane.

When a blood-fed larva (the first active life stage) drops from the skin of a bird or mammal, it moves directly downwards with the prospect of finding humid vegetation. There, it undergoes digestion and it moults into the next active life stage, the nymph.

If the larva happens to drop from its host onto a dry path or other unsuitable terrain, then it will most likely desiccate and die.

In the event of success, the emerged nymph will begin to seek a host. It does this by climbing vertically on whatever vegetation happens to be in the immediate vicinity.

Ticks don’t choose their location

Sometimes one may hear someone say, “Long grass is the only place you will find ticks” or, “Stay away from ferns – always ticks there” or some such warning, as if ticks choose the vegetation that they will climb. Ticks have no say in the matter – they simply climb whatever vegetational structure is available to them at the location that the previous life stage dropped from its host.

The behaviour and movements of host bird and mammal species dictate where ticks are deposited. So, a blood-fed larva will give rise to an emerging nymph, and a blood-fed nymph will produce an adult male or female. And of course, a blood-fed female will produce up to 2,000 eggs from which larvae will hatch.

I have conducted mass releases of paint-marked adult ticks in a prepared “arena” in a woodland clearing and then observed what happened. I found that the vast majority of individual ticks moved less than 2 metres from their release point, although a small number managed to travel 4 to 5 metres within 4 days.

The most interesting finding was that the majority of ticks somehow managed to locate vertical vegetation to climb within a short radius from the point of release.

Ticks have a finite fuel supply

Ticks waiting for a host to appear.

Ticks limit their horizontal movement for a very good reason – an economic one. A blood-fed larva that drops from a host has a finite energy supply of fat. Think of it as a full fuel tank. The more a tick moves, the more fuel it burns.

If it runs out of fuel before making contact with a host, then life ends for that particular tick. So, ticks have evolved a strategy to conserve their energy supplies by minimizing their movement. They climb vertically and wait … and wait … and wait.

Usually, they will position themselves at or close to the tip of a structure, whether it be a leaf, twig, bracken, grass or rush stem. Ticks can be found on vegetation from a few centimetres to almost 2 metres above ground level. When no hosts are nearby, ticks can assume a resting or “quiescent” position with front legs folded.

In the event of ticks becoming dehydrated, they will move downward into the moist vegetation mat to replenish their bodily water content, before climbing vertically once more.

Ambushing a host

Image shows a nymph and an adult female questing – front legs extended and raised. Another female is in the quiescent pose.

Ticks can detect the presence of a potential host by temperature, carbon dioxide and by various odours released from the skin of the host. Each of the front pair of legs has a specialised organ which is loaded with sensory cells for this purpose.

Once a tick detects the presence of a host animal, its behaviour changes. It will begin to move and adopt what is termed the “questing” pose.

A questing tick waves its front legs about as its scans the local atmosphere. It is most likely that it has the capability to determine the direction and distance from the approaching host although this has not been proven.

In a video clip which I shot in an infested woodland location, you can see how easily an adult female tick latches onto my finger.

The tick was initially in a quiescent position (saving energy) until I began to move my hand close to the rush stem on which it sat. Sensing my hand, and therefore a possible blood meal, it begins to quest as the video shows.

Note the ambushing strategy that this species has evolved – it doesn’t hunt its victim, it waits for the victim to pass close by. The smaller nymph behaves in exactly the same way.

I focused on an adult female for this video rather than a nymph simply because its size made it easier to capture on camera.

The video shows how easy it is for a tick to “jump on board” a passing human. The slightest brush of a hand, arm or leg against infested vegetation is all that is necessary.

Of course, ticks will also cling onto clothing and burrow through to the skin where they will penetrate and begin to suck blood. Bare wrists, arms and legs are the most vulnerable body parts so there is very good reason to use an appropriate tick repellent on these areas.

Light-coloured clothing makes visual detection of ticks much easier. And it is very important that clothing should be of a close weave as ticks will find this much more difficult to penetrate. I would also recommend that socks and walking boots/shoes be sprayed with repellent.

A note on adult and nymph ticks

The Ixodes ticks species that transmit Lyme disease have three active life stages – larva, nymph and adult. The general view among Lyme/tick specialists is that larvae carry very little Borrelia and so present a minimal risk to humans. Adult male ticks do not feed and so cannot transmit bacteria.

Nymphs pose the real threat. An unfed nymph is approximately 1.5 mm in size and weighs around 0.2 mg. In contrast, an unfed adult female can be 3.5 mm in length and 2 mg in weight – 10 times the weight of a nymph.

A person is much more likely to see and feel an adult tick on the skin than detect the smaller nymph. And once a tick has attached and has begun to suck blood, the smaller nymph may remain undetected for long enough to pass Borrelia into the unsuspecting victim. And of course, the small physical size and weight of the nymph explains why so many Lyme disease victims cannot recollect being bitten by a tick.

Dr. Healy’s expertise lies in the area of tick ecology, genetics, behavior and Borrelia infection rates. He has published in all of these fields. Click here for a list of his publications.

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**Comment**

While ticks can’t fly, they can blow in the wind.  I’ve seen it.

Also, ticks can transmit 19 pathogens and countingfar more than just Lyme.

And minimum attachment time has never been determined which means nobody has a clue how little of time it takes for a tick to transmit diseases to you.  Treat each tick bite as seriously as a heart attack.

Birds vs. Rodents in Transmitting Tick-Borne Pathogens

https://danielcameronmd.com/birds-rodents-transmitting-tick-borne-pathogens/

Birds vs. rodents in transmitting tick-borne pathogens

birds-tick-borne-pathogens

While white-footed mice are considered to be the primary reservoir for tick-borne pathogens, the role of birds as hosts in transmitting such infectious agents is not fully understood. A new study examines the transmission patterns in Canada between the two groups.

In their study, “Transmission patterns of tick-borne pathogens among birds and rodents in a forested park in southeastern Canada,” Dumas et al. “investigated and compared the role of breeding birds to rodents in local transmission dynamics of Bburgdorferi s.s., Aphagocytophilum and Bmiyamotoi, which are emerging pathogens in southeastern Canada.”¹

Researchers collected ticks and rodents from the Mont Saint-Bruno National Park in Quebec, an area endemic for Lyme disease. They aimed to identify:

  • Distribution of tick-borne pathogens B. burgdorferi, B. miyamotoi, and A. phagocytophylum in ticks and tick hosts;
  • Evaluate the contribution of birds as hosts to B. burgdorferi transmission compared with white-footed mice;
  • Determine risk factors for tick infestation and B. burgdorferi infectivity among hosts.

They collected 25,150 larvae, 4,177 nymphs and 232 adult blacklegged ticks.  And trapped 665 mice, 13 Eastern chipmunks, 15 Northern short-tailed shrew and one Red-backed vole.

The team found 470 (70.68%) mice, 12 (92.31%) chipmunks and 2 (13.33%) shrews infested with at least one tick. Ticks were not found on the only vole captured. Ticks collected from these small mammals were predominantly attached to the ears.

Approximately 70% of mice and 92% of chipmunks were infested with at least one tick, compared with 29% of captured birds.

Additionally, 849 birds belonging to 50 different species were captured. Researchers found ticks on 28.86% of the birds, “with the majority of these ticks removed from members of the Passerellidae (37.41%), Turdidae (31.11%) and Parulidae (17.04%) families,” writes Dumas.

How many hosts were infected with tick-borne pathogens?

When reviewing tick-borne pathogens detected in hosts tissue, the authors found 33.92% of mice were positive for Bburgdorferi, 0.48% for Bmiyamotoi and none for Aphagocytophilum.

Meanwhile, 84.62% of chipmunks were positive for Bburgdorferi, 15.38% for Bmiyamotoi and 7.69% for Aphagocytophilum.

“Pathogens were not detected in any of the bird biopsies (n = 262),” the authors point out. However, birds may not be infected but they are responsible for carrying the ticks to new areas.  They also supply a much needed meal for the ticks.

“Our results support the relevance of considering the role of hosts other than the white-footed mouse in eco-epidemiological studies of tick-borne diseases,” the authors suggest.

References:
  1. Dumas A, Bouchard C, Dibernardo A, et al. Transmission patterns of tick-borne pathogens among birds and rodents in a forested park in southeastern Canada. PLoS One. 2022;17(4):e0266527. Published 2022 Apr 7. doi:10.1371/journal.pone.0266527

For more:

For far too long, the white-footed mouse has been given too much credit for the spread of ticks and TBIs.  Many do not know that reptiles are also reservoirs.  And birds can travel great distances dropping ticks along the way that are from other parts of the globe.