More than Lyme: Tick study finds multiple agents of tick-borne diseases
COLUMBIA UNIVERSITY’S MAILMAN SCHOOL OF PUBLIC HEALTH
IMAGE: THREE PRIMARY HUMAN-BITING TICK SPECIES PRESENT ON LONG ISLAND WERE EXAMINED IN THIS STUDY. LEFT — BLACKLEGGED TICK ALSO KNOWN AS THE DEER TICK, MIDDLE — THE AMERICAN DOG TICK,… view more
CREDIT: SANTIAGO SANCHEZ-VICENTE, STONY BROOK UNIVERSITY
In a study published in mBio, a journal of the American Society for Microbiology, Jorge Benach and Rafal Tokarz, and their co-authors at Stony Brook University and Columbia University, reported on the prevalence of multiple agents capable of causing human disease that are present in three species of ticks in Long Island.
Tick-borne diseases have become a worldwide threat to public health. In the United States, cases more than doubled, from 22,000 in 2004 to more than 48,000 in 2016, according to the U.S. Centers for Disease Control. Tick-borne diseases range from subclinical to fatal infections with disproportionate incidence in children or the elderly. Moreover, some infections can also be transmitted by blood transfusions and cause severe disease in patients with underlying disorders. While public attention has focused on Lyme disease, in recent years, scientists have uncovered evidence that ticks can carry several different pathogens capable of several different tick-borne diseases, sometimes in a single tick.
In the new study, researchers collected ticks from multiple locations throughout Suffolk county in the central and eastern part of Long Island, where seven diseases caused by microbes transmitted by ticks are present. In total, they examined 1,633 individual ticks for 12 separate microbes. They found that more than half of the Ixodes (deer ticks) were infected with the Lyme disease agent, followed by infections with the agents of Babesiosis and Anaplasmosis. Importantly, nearly one-quarter of these ticks are infected with more than one agent, resulting in the possibility of simultaneous transmission from a single tick bite.
Notably, the lone star tick, a species originating from the southern U.S., has expanded its range, possibly fueled by climate change. This study documents that the invasive lone star tick is abundant in Long Island, and that it is a very aggressive tick that can transmit a bacterium that causes a disease known as Ehrlichiosis. The lone star tick has also been implicated in cases of a novel form of meat allergy, and the immature stages can cause an uncomfortable dermatitis.
“Polymicrobial infections represent an important aspect of tick-borne diseases that can complicate diagnosis and augment disease severity,” says corresponding author Jorge Benach, PhD, Distinguished Professor at the Department of Microbiology and Immunology at the Renaissance School of Medicine at Stony Brook University. “Some of the polymicrobial infections can be treated with the same antibiotics, but others require different therapies, thus enlarging the number of drugs to treat these infections.”
“In evaluating tick-borne infection, more than one organism needs to be considered,” says senior author Rafal Tokarz, PhD, assistant professor of epidemiology in the Center for Infection and Immunity at the Columbia Mailman School of Public Health, and a graduate of the Department of Microbiology and Immunology at Stony Brook University. “This study emphasizes the need to focus on all tick-borne diseases, not just Lyme.”
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The first author is Santiago Sanchez, a post-doctoral fellow in the Department of Microbiology and Immunology at Stony Brook University. Teresa Tagliafierro from Columbia and James Coleman from Stony Brook are co-authors of the study.
This study was funded by a grant from the National Institutes of Health to Benach. Support was also provided by the Island Outreach Foundation in Blue Point, NY, to the Stony Brook Renaissance School of Medicine. Support from the Steven & Alexandra Cohen Foundation (CU18-2692) was provided to Tokarz.
Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.
Patients with Bartonella species infection (bartonellosis) complain of a variety of nonspecific vision problems that can affect every function of the eye. Making diagnosis and treatment decisions even more difficult, these problems can be caused by a variety of other pathogens and diseases. Fortunately, many peer-reviewed case publications, especially in ophthalmology journals, are available that describe both common and uncommon eye symptoms caused by bartonellosis.
Documented links between Bartonella species infection and vision problems focus on Bartonella henselae (cat scratch disease) and Bartonella quintana (trench fever). B. henselae is associated with contact with animals and vectors, especially cats and fleas, while B. quintana is associated with body lice. Additional species implicated include B. elizabethae and B. grahamii.
Overview
The eye consists of structures that focus light on nerve receptors at the back of the eye, nerves that feed into the optic nerve which connects to the brain, and a blood supply that connects through a central artery and vein into the body’s blood circulation. Bartonellosis can affect each of these parts of the eye.
Patients with bartonellosis-related eye problems may have symptoms in other organs as well that can help clarify whether the eye symptoms are caused by bartonellosis. Ophthalmologists and other physicians look for these additional signs because all of the eye conditions that can be caused by bartonellosis can be caused by a variety of bacteria and viruses, as well as other health conditions including autoimmune disorders.
It can be difficult to narrow down the possible causes of bartonellosis. Sometimes patients can’t remember any events that would have exposed them to Bartonella species. Other times the event, such as a cat scratch, may have occurred weeks to a month or more before symptoms appear and the patient may not think there is a connection. It can take detailed questioning by physicians to identify the possibility of Bartonella species exposure.
Structural Eye Symptoms
The most common way bartonellosis is seen in the eye is called Parinaud oculoglandular syndrome (POGS). About five percent of patients with acute cat scratch disease have this syndrome, which is characterized by follicular conjunctivitis (pink eye) with swollen lymph nodes nearby. It is often accompanied by a fever, and there may be bumps on the eyelid. Other symptoms known to be caused by bartonellosis, such as endocarditis (swelling of the inner lining of the heart), may also indicate that bartonellosis should be suspected.
Conjunctivitis results in easily seen inflammation of the usually white part of the eye (Source: CDC).
Inflammation of the middle layer of the structure that surrounds the eyeball is called uveitis. Uveitis causes redness of the eye and can cause light sensitivity, pain and floaters. Uveitis is sometimes associated with bartonellosis.
While case reports of eye symptoms caused by bartonellosis generally describe a sudden-onset condition, one case report describes a woman who had symptoms of bartonellosis in various body organs for more than five years, including chronic conjunctivitis (pink eye). She had multiple tests and treatments over that time including a Bartonella species test that was positive but considered nonspecific. It was only after other treatments didn’t work that antibiotics were administered. The antibiotics resolved her various symptoms.
Neurological Eye Symptoms
Neuroretinitis, an inflammation of the optic nerve head, occurs in about 2% of people with cat scratch disease (acute Bartonella henselae infection). Two-thirds of cases of neuroretinitis are caused by bartonellosis.
Neuroretinitis is usually characterized by sudden, complete vision loss and swelling that creates a star pattern in the macula (the light-sensitive tissue at the back of the eye that feeds information into the optic nerve). Though this is the typical case of neuroretinitis caused by bartonellosis, it can vary greatly. It can cause changes such as seeing odd shapes or colors Furthermore, case reports have included people who lose their vision with no other symptoms, have blurry vision with a headache, and more.
Treatment can usually, but not always, restore vision, but it can take months to resolve and there can still be long-term consequences. Complications can also occur. In one case, a child was diagnosed with neuroretinitis. Treatment was started six weeks after the diagnosis, but his vision in one eye got worse. After treatment, a full-thickness macular hole was discovered. The hole was monitored and resolved after six months.
Vascular Eye Symptoms
The eye has an important network of tiny blood vessels that provide nourishment to the tissue, but unnecessary growth of new capillaries can lead to a range of symptoms such as vision problems. Vasoproliferation (irregular growth of new blood vessels) may be more common in immunocompromised people, such as those being treated with chemotherapy products. These symptoms can be observed on the skin and in the liver and spleen and may also occur in the eye.
Tiny blood vessels in the eyes supply nutrients to cells. In the above image, larger retinal blood vessels can be seen (Source: NIH).
Vasoproliferative symptoms seem to be caused by vascular endothelial growth factor (VEGF) stimulated by bartonellosis. More research on the relationship between VEGF and bartonellosis is needed. Meanwhile, anti-VEGF agents have been used to treat vasoproliferative eye symptoms.
Conclusion
Bartonellosis can affect every part of the eye, and symptoms can be sudden and severe. Diagnosis and treatment decisions are complicated by other pathogens and diseases that can cause similar symptoms. It is important for patients and physicians to be aware of any prior animal or insect exposure that may indicate Bartonella infection. Considering additional systemic symptoms of bartonellosis may also help to clarify the diagnosis.
Learn more about bartonellosis and the testing that Galaxy Diagnostics offers here.
References
Kalogeropoulos, C. et al. (2011). Bartonella and intraocular inflammation: A series of cases and review of literature. Clinical Ophthalmology, 5, 817-829. doi:10.2147/OPTH.S20157 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3130920/
Woo, M. et al. (2018). A case of retinal vessel occlusion caused by Bartonella infection. Journal of Korean Medical Science, 33(47), e297. doi:10.3346/jkms.2018.33.e297 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6236082/
Fairbanks, A. M. et al. (2019). Treatment strategies for neuroretinitis: Current options and emerging therapies. Current Treatment Options in Neurology, 21(8), 36. doi:10.1007/s11940-019-0579-0 https://www.ncbi.nlm.nih.gov/pubmed/31278547
Michel, Z. et al. (2019). Multimodal imaging of two unconventional cases of Bartonella neuroretinitis [epub ahead of print]. Retinal Cases & Brief Reports. doi:10.1097/ICB.0000000000000893 https://www.ncbi.nlm.nih.gov/pubmed/31348120
Gunzenhauser, R. C. et al. (2019). The development and spontaneous resolution of a full-thickness macular hole in Bartonella henselae neuroretinitis in a 12-year-old boy. American Journal of Ophthalmology Case Reports, 15, 100515. doi:10.1016/j.ajoc.2019.100515 https://www.ncbi.nlm.nih.gov/pubmed/31341998
Toumanidou, V. et al. (2017). Neuroretinitis secondary to Bartonella henselae in a patient with myelinated retinal nerve fibers: Diagnostic dilemmas and treatment. Ocular Immunology and Inflammation, 27(3), 396-398. doi:10.1080/09273948.2017.1409357 https://www.ncbi.nlm.nih.gov/pubmed/29283743
Mabra, D. et al. (2018). Ocular manifestations of bartonellosis. Current Opinion in Ophthalmology, 29(6), 582-587. doi:10.1097/ICU.0000000000000522 https://www.ncbi.nlm.nih.gov/pubmed/30124532
Beckerman, Z. et al. (2019). Rare presentation of endocarditis and mycotic brain aneurysm [epub ahead of print]. The Annals of Thoracic Surgery. doi:10.1016/j.athoracsur.2019.06.073 https://www.ncbi.nlm.nih.gov/pubmed/31425670
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**Comment**
Another great article by Galaxy Lab. Please read the following article for more information on Bartonella, as various strains are suspected to be transmitted by ticks, mites, various flies and spiders, and other modes, and it is far more prevalent than thought: https://madisonarealymesupportgroup.com/2016/01/03/bartonella-treatment/ Fifteen species of gram-negative aerobic Bartonella are known to infect humans; however Dr. Ricardo Maggi’s statement is quite telling, “This case reinforces the hypothesis that any Bartonella species can cause human infection.”
Summary: Understanding how parasites ‘hack’ the brains of their hosts may provide new insights into decision making and behavior.
Source: Frontiers
Imagine a parasite that makes an animal change its habits, guard the parasite’s offspring or even commit suicide. While mind-control may sound like something out of a science fiction movie, the phenomenon is very real — and has spawned a new field, neuro-parasitology. As outlined in an article published in Frontiers in Psychology, understanding how parasites “hack” their host’s nervous system to achieve a particular goal could provide new insights into how animals control their own behavior and make decisions.
“Parasites have evolved, through years of co-evolution with their host, a significant ‘understanding’ of their hosts’ neuro-chemical systems,” explains one of the article’s authors, Professor Frederic Libersat from Ben-Gurion University of the Negev in Israel. “Exploring these highly specific mechanisms could reveal more about neural control of animal behavior.”
The article describes some of the sophisticated, cunning and gruesome ways that various parasites outwit and exploit their insect hosts.
One method is to affect how an insect navigates. The spores of one parasitic fungus, for example, invade an ant’s body, where the fungus grows and consumes the ant’s organs while leaving the vital organs intact. The fungus then releases chemicals that cause the ant to climb a tree and grip a leaf with its mouthparts. After emerging from the ant’s body, the fungus releases spore-filled capsules that explode during their fall, spreading the infectious spores over the ground below. By forcing the ant to climb a tree, the fungus increases the dispersal of the falling spores and the chance of infecting another ant.
Similarly, a parasitic hairworm causes infected crickets to seek out water — where they drown. The cricket’s suicide enables the worms to enter an aquatic environment for reproduction.
In another type of interaction, called “bodyguard manipulation,” the parasite forces the infected insect to guard its young. One such parasite is a wasp, which injects its eggs into a caterpillar by stinging it. Inside the live caterpillar, the eggs hatch into larvae, which feed on the caterpillar’s blood. Eventually, as many as 80 larvae emerge from the caterpillar’s body before forming cocoons to complete their growth into adult wasps.
However, wasp larvae are vulnerable to predators in their cocoons. To scare potential predators away, one or two larvae remain in the caterpillar and control its behavior through an unknown mechanism, so that it acts aggressively towards predators — thereby protecting the cocoons.
These examples shed light on the very old and highly specific relationship between parasites and hosts. But how exactly do these parasites affect their host’s behavior?
Neuro-parasitology is still a young field, and in most cases, researchers do not yet fully understand the mechanisms involved. However, many such parasites produce their effects by releasing compounds that act on the neural circuitry of the host. Identifying and using these compounds in the lab could help scientists to work out how neural circuits control behavior.
“Because neurotoxins are the outcome of one animal’s evolutionary strategy to incapacitate another, they are usually highly effective and specific,” says Libersat.
“Chemical engineers can generate hundreds of potential neurotoxins in the lab, but these are random and often useless, whereas any natural neurotoxin has already passed the ultimate screening test, over millions of years of co-evolution.”
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Source: Frontiers Media Contacts:
Conn Hastings – Frontiers Image Source:
The image is adapted from the Frontiers news release.
Mind Control: How Parasites Manipulate Cognitive Functions in Their Insect Hosts
Neuro-parasitology is an emerging branch of science that deals with parasites that can control the nervous system of the host. It offers the possibility of discovering how one species (the parasite) modifies a particular neural network, and thus particular behaviors, of another species (the host). Such parasite–host interactions, developed over millions of years of evolution, provide unique tools by which one can determine how neuromodulation up-or-down regulates specific behaviors. In some of the most fascinating manipulations, the parasite taps into the host brain neuronal circuities to manipulate hosts cognitive functions. To name just a few examples, some worms induce crickets and other terrestrial insects to commit suicide in water, enabling the exit of the parasite into an aquatic environment favorable to its reproduction. In another example of behavioral manipulation, ants that consumed the secretions of a caterpillar containing dopamine are less likely to move away from the caterpillar and more likely to be aggressive. This benefits the caterpillar for without its ant bodyguards, it is more likely to be predated upon or attacked by parasitic insects that would lay eggs inside its body. Another example is the parasitic wasp, which induces a guarding behavior in its ladybug host in collaboration with a viral mutualist. To exert long-term behavioral manipulation of the host, parasite must secrete compounds that act through secondary messengers and/or directly on genes often modifying gene expression to produce long-lasting effects.
Parasite patients often express the psyche of the parasites – sticky, clingy, impossible to tolerate – but a wonderful human being is behind all of that.
We are all a composite of many personalities. Chronic infections outnumber our own cells by 10:1. We are 90% “other” and 10% “us”. Our consciousness is a composite of 90% microbes and 10% us.
Our thinking, feeling, creativity, and expression are 90% from the microbes within us. Patients often think, crave, and behave as if they are the parasite.
Our thinking is shaded by the microbes thinking through us. The food choices, behavioral choices, and who we like is the thinking of the microbes within us expressing themselves.
Patients will reject all treatments that affect the issue that requires treating.
Patients will not guide themselves to health when the microbes have taken over.
And, as mentioned in this article: the fungus Cordyceps hijacks the ant to propitiate itself but here again, many Lyme patients use Cordyceps to fight microbes, lower inflammation, and increase energy and oxygen: https://rawlsmd.com/herbs/cordyceps
Lyme disease is the most prominent tick-borne disease in the United States. Co-infections with the tick-transmitted pathogens Babesia microti and Borrelia burgdorferi sensu stricto are becoming a serious health problem. B. burgdorferi is an extracellular spirochete that causes Lyme disease while B. microti is a protozoan that infects erythrocytes and causes babesiosis. Testing of donated blood for Babesia species is not currently mandatory due to unavailability of an FDA approved test. Transmission of this protozoan by blood transfusion often results in high morbidity and mortality in recipients.
Infection of C3H/HeJ mice with B. burgdorferi and B. microti individually results in inflammatory Lyme disease and display of human babesiosis-like symptoms, respectively.
Here we use this mouse model to provide a detailed investigation of the reciprocal influence of the two pathogens on each other during co-infection.
We show that
burgdorferi infection attenuates parasitemia in mice while
B. microti subverts the splenic immune response, such that a marked decrease in splenic B and T cells, reduction in antibody levels and diminished functional humoral immunity, as determined by spirochete opsonophagocytosis, are observed in co-infected mice compared to only B. burgdorferi infected mice
Furthermore
immunosuppression by B. microti in co-infected mice showed an association with enhanced Lyme disease manifestations.
This study demonstrates the effect of only simultaneous infection by B. burgdorferi and B. microti on each pathogen, immune response and on disease manifestations with respect to infection by the spirochete and the parasite. In our future studies, we will examine the overall effects of sequential infection by these pathogens on host immune responses and disease outcomes.
Due to the high prevalence of infection and the issues of congenital transmission and transmission through blood transfusion, the issue of concurrent infection and what it does to animal and human health is of paramount importance.
Ticks are one way tularemia can be spread. Rabbits are another.
By Briana Zellner
Ticks can be hosts to many different infectious diseases including Lyme disease and Rocky Mountain spotted fever. However, you may not be familiar with another important tick-borne disease called tularemia.
Tularemia, or rabbit fever, is caused by the bacterium Francisella tularensis (F. tularensis). F. tularensis can cause life-threatening infections that often are misdiagnosed as the flu.
If antibiotic treatment is not started early, tularemia can be fatal or can result in life-long health problems, including kidney and liver damage.
During the Great Depression era (1930s), there were over 10,000 cases of tularemia per year in the U.S., linked to either rabbit hunting or tick bites. Today, about 250 tularemia cases are reported each year in the U.S. Worldwide, there are thousands of tularemia cases each year. F. tularensis can be carried or cause disease in over 3,000 different animals.
Tularemia transmission
In addition to ticks, humans can become infected by eating or drinking contaminated food or water, being bitten by infected mosquitoes or flies, handling infected animal carcasses, or even inhaling air contaminated with the bacteria (mowing over an infected rabbit burrow/nest). These different infection routes can cause different disease symptoms, making tularemia extremely difficult to diagnose.
If quickly diagnosed, tularemia can be treated with antibiotics. However, there is no vaccine to prevent tularemia disease.
As a researcher in Dr. Jason Huntley’s lab at the University of Toledo College of Medicine and Life Sciences, I study how F. tularensis infects and causes disease. Using this information, our lab also works to develop new therapeutics and vaccines to prevent tularemia.
Every day we are exposed to millions of bacteria on our skin, in our lungs, and in our digestive tract. Luckily, we have specialized immune cells in our body that recognize invading bacteria, engulf, and kill them. These immune cells signal to other cells to alert them that the body is under attack so that infections can be quickly cleared.
Unfortunatley, F. tularensis is very good at avoiding these immune cells. In fact, F. tularensis actually can invade and replicate inside immune cells and many other cell types.
The bacteria have specialized proteins on their surface that allow them to invade and survive inside human cells. The bacteria also have a unique protective barrier, called the cell wall, which prevents them from being killed by our immune system.
The cell wall is a very important component of these bacteria. Think of it like a suit of armor or a bullet-proof vest designed to protect these bacterial invaders. If the armor is damaged or missing, the invaders are much more vulnerable to attack.
When immune cells encounter F. tularensis, they try to attack the bacteria and cause chinks in the armor. However, F. tularensis is very good at quickly repairing these chinks, infecting other cells, and reproducing to extremely high numbers – causing life-threatening disease.
Tularemia’s bacterial armor
Our lab has identified over 50 bacterial armor genes that allow F. tularensis to infect human cells and cause disease. Although these genes work together to protect the bacteria from our immune attack system, I have been able to use genetic tools to precisely delete only one armor gene to study.
I have found that these modified bacteria cannot replicate inside immune cells or cause disease in animals. When I examine these modified bacteria by electron microscopy, I have shown that they have abnormal cells walls – chinks in their armor.
Most importantly, I have recently shown that these modified bacteria can be used as a vaccine to protect animals from tularemia, similar to the modified chickenpox and measles, mumps, rubella (MMR) vaccines that are currently used.
Although I am a long way from testing this vaccine in humans, the potential to prevent human tularemia is exciting. In addition, because very little is known about the cell wall of F. tularensis, my project has provided new information about how we can develop new drugs to attack F. tularensis and potentially other bacteria.
Briana Zellner is a Ph.D. student in the Department of Medical Microbiology and Immunology in The University of Toledo College of Medicine and Life Sciences Biomedical Science Program. For more information, contact Briana.Zellner@rockets.utoledo.edu or go to utoledo.edu/med/grad/biomedical. This article was originally published in The Toledo Blade.
Tularemia, in aerosol form, is considered a possible bioterrorist agent that if inhaled would cause severe respiratory illness. It was studied in Japan through 1945, the USA through the 60’s, and Russia is believed to have strains resistant to antibiotics and vaccines. An aerosol release in a high population would result in febrile illness in 3-5 days followed by pleuropneumonitis and systemic infection with illness persisting for weeks with relapses. The WHO estimates that an aerosol dispersal of 50 kg of F. tularensis over an area with 5 million people would result in 25,000 incapacitating casualties including 19,000 deaths.
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