Parasitic Infections of the Brain 

By Eleyna Poteet

Recent studies have suggested that parasites make up over 50% of animal life on Earth, and are therefore very important to understand. Some parasites cause infections in the brain, and can even modify the behaviors of the host. So, what are some neurological diseases that can be caused by parasites? 

Neurocysticercosis 

         Neurocysticercosis is a common parasitic disease that occurs when infected with the encysted larval stage of the helminth parasite Taenia solium (Loker and Hofkin 2015). These parasites can cause infection through the consumption of undercooked pork or water that is contaminated with the parasitic eggs (Siddiqua and Habeeb 2020). Taenia solium has two infectious forms: the adult (intestinal tapeworm) form, and the larval (cysticercus) form. Infection with the adult tapeworms causes minor symptoms and is referred to as Taeniasis. However, infection with T. solium larvae is more serious because the cysts are often formed in the central nervous system, causing neurocysticercosis. The symptoms of neurocysticercosis include headache, dizziness, vision problems, dementia, and seizures (Siddiqua and Habeeb 2020, Loker and Hofkin 2015). Neurocysticercosis is also the leading cause of acquired epilepsy in the world, and seizures occur in 50%-80% of patients that develop cysts of the brain (Loker and Hofkin 2015, Siddiqua and Habeeb 2020). It is a leading health problem in many areas of the world, including India, Latin America, and Asia. It is becoming more prevalent in other areas as well due to travel and migration (Siddiqua and Habeeb 2020).

How is Neurocysticercosis transmitted? 

Taenia solium has an indirect lifecycle, meaning that it requires more than one host. The intermediate hosts, in which the parasite develops somewhat but does not sexually reproduce, are pigs. The definitive hosts, in which the parasite fully develops and usually sexually reproduces, are humans (Siddiqua and Habeeb 2020). Eggs are consumed by pigs fecal-orally who come into contact with infected feces; this is common because the eggs can survive for long periods of time in the environment (“Taeniasis”). The eggs, or oncospheres, hatch in the animal’s intestine and invade the intestinal wall. They then migrate to the muscle tissue and develop into cysticerci (sac-like stage of the larva). Humans become infected by consuming undercooked meat containing these cysticerci. At this stage, the parasite may either develop into an adult tapeworm (only in humans), or lodge itself along the central nervous system, causing neurocysticercosis (Loker and Hofkin 2015, Siddiqua and Habeeb 2020, “Taeniasis”). 

Treatments for Neurocysticercosis 

Neurocysticercosis, like many other parasitic diseases, is treated with multiple pharmacological methods. Antiparasitic drugs like Niclosamide and Praziquantel are used to try to kill any adult T. solium tapeworms. Niclosamide is often preferred because it does not provoke any brain cysts that are not yet showing symptoms, and can therefore help prevent further symptoms worsened by treatment. Symptoms of neurocysticercosis can be treated using steroids, along with antiepileptic drugs if seizures are occurring (Loker and Hofkin 2015).

Toxoplasmosis 

Toxoplasmosis is a common disease that is the result of infection by the protozoan parasite Toxoplasma gondii. Infection occurs by consumption of undercooked meat containing cysts, exposure to infected cat feces, or sometimes from mother to child during pregnancy (”Toxoplasmosis”). Healthy individuals with strong immune systems usually experience mild flu-like symptoms, including body aches, fever, headache, and fatigue (“Parasites”, ”Toxoplasmosis”). However, immuno-compromised individuals may have more severe symptoms, including headache, confusion, poor coordination, seizures, blurred vision, and lung problems (”Toxoplasmosis”). Some studies also suggest that Toxoplasmosis could even potentially have effects on human behavior, personality, and psychomotor performance (Flegyr 2007). It is thought to infect 40 million Americans at any given time, due to the fact that many people experience little to no symptoms unless they have weakened immune systems (“Parasites”).  

How is Toxoplasmosis transmitted? 

Toxoplasma gondii is an obligate intracellular parasite that is transmitted vertically through contaminated food or water (Mendez and Koshy 2017). The definitive hosts, in which the parasite can reproduce and complete its life cycle, are cats; T. gondii can also infect most warm-blooded animals, like rodents, birds, and humans, and use them as intermediate hosts (Mendez and Koshy 2017, “Parasites”). Cysts are shed through the feces of cats and are passed on to other species upon ingestion of water, soil or plants contaminated with the infectious oocysts. The oocysts (life stage 1) will transform into their tachyzoite stage (life stage 2) shortly after being ingested and migrate to different parts of the hosts body, including muscle tissue and the central nervous system. After lodging in the hosts tissues, the tachyzoites will develop into cyst bradyzoites (life stage 3) that can once again infect other organisms if the host animal is eaten. If a human becomes infected, the parasite forms tissue cysts in the skeletal muscle, cardiac muscle, eyes, and brain. (Mendez and Koshy 2017, “Parasites”, ”Toxoplasmosis”).  

 

Does Toxoplasmosis cause mind control in rodents? 

Rodents can become infected with T. gondii upon exposure to cat feces, and the parasite can migrate throughout the rodents’ body and into the brain. T. gondii needs to end up back inside of a cat to complete its lifecycle, and therefore alters the brain chemistry of the rodent to achieve its goal (Vyas et al. 2007). Typically, rodents are repelled by the smell of cat urine and will steer clear at any sign of it; however, T. gondii blocks the rat’s aversion to cat urine, increasing the likelihood that the rat will become prey and that the parasite can reproduce within the bowel of the cat (Vyas et al. 2007).  

Primary Amebic Meningoencephalitis: The Brain Eating Amoeba

Perhaps one of the most well-known parasites is Naegleria fowleri, the brain eating amoeba. This single-celled parasite is free-living and is also microscopic, and can be found in warm freshwater (rivers, lakes, and hot springs) (“Naegleria”, Loker and Hofkin 2015). This parasite gained its infamous name of the brain eating amoeba because it consumes the nervous tissue of infected individuals, causing primary amebic meningoencephalitis. (Loker and Hofkin 2015). To become infected, an individual has to come into contact with the parasite through the nasal passage, usually by sniffing contaminated water. The parasite then migrates through the nasal passage and gains access to the central nervous system (Loker and Hofkin 2015). While infection of N. fowleri is rare, there have been a handful of high profile cases in news headlines over the past decade (Grace et al. 2015, “Naegleria”). The CDC reports 145 known cases in the United States between 1962 and 2018, with at least one known case in 2019. All but four of these cases were fatal (“Naegleria”).

Treatment and Survival

Primary amebic meningoencephalitis is difficult to diagnose for multiple reasons. The symptoms of infection, including headache, fever, nausea, vomiting, seizure, and hallucinations, are similar to symptoms of bacterial meningitis (“Naegleria”). The disease also progresses rapidly, with death occurring between 1-18 days after symptoms begin. For these reasons, diagnosis of infection is usually made after death occurs (Grace et al. 2015, “Naegleria”). Infected individuals who survived were diagnosed promptly and treated with miltefosine, a broad-spectrum antimicrobial, along with cooling the body down below its normal temperature (“Naegleria”).

What Can You Do to Prevent a Parasitic Infection of the Brain?

            After learning the ways in which some brain-affecting parasites can infect humans, individuals can exercise precaution by thoroughly cooking meat, frequently cleaning their pet’s litter boxes, frequently washing their hands, and avoiding dunking their head underwater in high-risk areas!

References 

Flegyr, J., Effects of Toxoplasma on Human Behavior . Schizophrenia Bulletin 3, 757-760  

(2007).  

Grace, E., Asbill, S., Virga, K. Naegleria fowleri: Pathogenesis, Diagnosis and Treatment

Options. Antimicrobial Agents and Chemotherapy 11, 6671-6681 (2015).

Loker, E.S., Hofkin, B.V. (2015). Parasitology: A Conceptual Approach. Garland Science.

Mendez, O.A., Koshy, A.A., Toxoplasma gandii: Entry, Association, and Physiological

Influence on the Central Nervous System. PLoS Pathogens 7 (2017). 

Naegleria fowleri. CDC. https://www.cdc.gov/parasites/naegleria/index.html.

Parasites: Toxoplasmosis. CDC. https://www.cdc.gov/parasites/toxoplasmosis/.  

Siddiqua, T., Habeeb, A., Neurocysticercosis. Saudi Journal of Kidney Diseases and

Transplantation 31, 254-258 (2020).

Taeniasis. CDC. https://www.cdc.gov/parasites/taeniasis/biology.html.

Toxoplasmosis. Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/toxoplasmosis/symptoms-causes/syc-20356249.  

Vyas, A., Kim, S-K., Sapolsky, R.M., The Effects of Toxoplasma Infection on Rodent Behavior

are Dependent on Dose of the Stimulus. Neuroscience 2, 342-348 (2007).  

Smallwood et.al

Helminthic Therapy; Could Worm Infections Help with Inflammatory Diseases?

By Brenna Graber 

Parasitic relationship with Social Constructs of Medicine

In the late 1980’s, researcher David P Strachan proposed a theory that claimed personal cleanliness has gone too far which has encouraged an increase in diagnosed allergies or inflammatory diseases (Strachan 1989). Since then this concept has been repeatedly studied and is now known as the “hygiene hypothesis”. One area where this hygiene hypothesis is readily studied today would be how humans have a co-evolutionary and beneficial relationship with small parasitic infections (Lorimer 2019).

            Previously,  parasites have resided in people for a long periods of time  with little to no serious medical issues (Smallwood et. al 2017). In western medicinal practices we have set a precedent that objectifies parasites to a strictly harmful and invasive relationship  when indeed human relationships with certain parasites are mutualistic (Lorimer 2019). A mindset like such, coupled with increased hygiene which reduces exposure to these organisms, has led to an absence of an important contender to the human microbial ecosystem.

Helminthic Therapy: How it works.

Today some researchers are beginning to discover that the administration of a small worm load of helminths can be beneficial in combating multiple different

inflammatory diseases such as allergies and arthritis (Lorimer 2019). Helminths can stimulate immune responses that aid in inflammation.

Within the immune system, there are two responses; (1) Th-1 and (2) Th-2. When the body gets infected with a helminth, it ignites a Th-2 immune. While in the human body, helminths secrete different materials that the body recognizes as non-self which then activates cytokines IL-4,IL-5,Il-10,and IL-13 (Smallwood et. al).Cytokines are numerous proteins that work together and communicate in order to activate an immune response from the body. At the same time, regulatory T-cell development is occurring which promotes a cloaking effect by releasing regulatory cytokines like IL-10 and transforming growth factor (Beta). The body defending itself against the helminth cloaks the inflammation process.

Helminths such as hookworms, specifically propagate the activation of total immunoglobulin-E and activation of the innate immune systems like mast cells basophils and eosinophils. Immunoglobulins are antibodies found in the body that work to disarm whatever is infecting the body, in this case it would be the hookworm. Meanwhile, both basophils and eosinophils are white blood cells which increase in numbers during an infection. All of these processes result in a decrease of  inflammation by way of disease because the immune system is distracted by the helminth’s presence (Smyth et. al 2017).

What helminths are or have been used for treatment?

            The phyla or different kinds of helminths include roundworms, flatworms and flukes (trematodes). Most of the helminths that are used to treat inflammatory diseases are the nematodes (roundworms) and hook worms (Smallwood et. al). Specific hookworms have been organized into a table per disease,  being treated (in people) by Smallwood et al. 2017:

Inflammatory bowel disease:

●      Schistosoma mansoni

●      Heligmosomoides polygyrus

●      S. cercariae

●      Schistosoma japonicum

●      S. mansoni

●      Anisakis simplex

●      Acanthocheilonema viteae

Multiple Sclerosis:

●      S.mansoni

●      T.spiralis

●      Fasciola hepatica

●      S. japonicum

Type 1 diabetes:

●      S.mansoni

Rheumatoid arthritis:

●      S.mansoni

●      S.japonicum

●      A.viteae

●      H.polygyrus

Systemic lupus erythematosus

●      A.viteae

From other articles (Lorimer 2019):

Allergies:

●      A. caninum

●      N.americanus

●      H.diminuta

What’s Next for Helminthic treatment?

Most recent research is working to synthesize the reaction the human body has when interacting with helminths. This would be administering a pill that contains synthetic molecules that replicate helminth ability. The idea is to reduce the risks, discomfort and chance of infection while still embracing the therapeutic benefit (Lorimer 2019).

Those Opposed?

Other researchers argue that by synthesizing this relationship, some benefits will be lost that are provided by the whole helminth organism. These same researchers claim that synthetics like pills could also lead to drug dependency and potentially resistance. Instead they encourage the safety and naturally occurring benefits of helminthic therapy through monitored and safe administration of the helminths (Lorimer 2019).

Conclusions

Helminths have, for a long time, been seen as an invader, an organism to be exterminated. Due to this relationship that has been created by western medicine coupled with the increase of hygiene in a developed country, helminthic therapy is not an accepted treatment by the Drug and Food Administration and therefore can’t be clinically practiced (Lorimer 2019 &). This is because of shipping regulations of the parasites when they are outside the body as well as lack of research on this form of therapy (Lorimer 2019 and Smyth et al. 2017).

The future of helminthic therapy is very open. More researchers are jumping on board with this practice. However, changing the social standards of such a developed country will not be easy (Lorimer 2019).

Literature cited

Lorimer, Jamie. 2019. Hookworms Make us Human: The Microbiome, Eco-Immunology, and a Probiotic Turn in Western Health Care. Medical Anthropology Quarterly 33(1): 60-79.

Smallwood, T.B.,P.R. Giacomin, A.Loukas, J.P. Mulvenna, R. Clark, and J.J. Miles. 2017. Helminth Immunomodulation in Autoimmune Disease. Frontiers in Immunology 8:453.

Smyth, K., C. Morton, A. Mathew, S. Karuturi, C. Haley, M. Shang, Z.E. Holzknecht, C. Swanson, S.S. Lin, and W. Parker. 2017. Production and Use of Hyenolepis diminuta Cysticercoids as Anti-Inflammatory Therapeutics. Journal of Clinical Medicine 6:98.

Strachan, David P.. 1989. Hay fever, hygiene, and household size. Department of Epidemiology and Population Science, London School of Hygiene and Tropical Medicine, London WC1E &HT.

A Cell Wall for Us All

By Patric Soce

            The study of medicine arguably has been around for hundreds if not thousands of years. With so much time available, one can only think about all the advancements and remarkable discoveries made. For example, the discovery of penicillin, first discovered by Dr. Alexander Fleming in 1928 which officially started saving lives by 1942. Such a great development can only be humbled by a massive response from microorganisms increasing their bacterial resistance. The history of penicillin is a great example demonstrating the life saving capabilities of new drugs but also the underlying danger created. In his acceptance speech for the Noble Prize in medicine, Fleming warned of the emergence of bacterial resistance. Almost a century later, we now find ourselves in an “arms race” against disease causing agents often including viral, bacterial, and organismal sources. So where do we look for new treatments or therapies when applying this to parasitism?

            Often, it is easy to overlook areas of our lives and in research, I believe we have done so with the study of medicine. A severely underrepresented field in parasitology are plant immune capabilities and their application to medical practices. Consider a current cause of death for over 700,000 people today, most of which are children under five years old! The culprit, Plasmodium falciparum the parasite responsible for malaria. Virtually all cures available for malaria currently can be traced back to plant origin such as Artemisinin a terpene made by the plant Artemisia. Or quinoline alkaloids from Chinchoa bark used to make semisynthetic chloroquine to treat the bloodworm stage of Plasmodium. Surprisingly over 1,200 plants have been shown to carry antimalarial properties but because a lack of clinical trials exist, we have little to show. A term often used to describe the antiparasitic or useful substances in plants are ‘secondary metabolites’ which are non-essential to growth but useful in plant preservation.

            The plant Artemisia annua, also known as Wormwood, has an extensive medical history in our species dating back 2000 years ago in ancient china. Today it is not only used to treat malaria but also African sleeping sickness, and Chagas’ disease, both are caused by trypanosomes or blood parasites. Interestingly, wormwood extract has been shown to target and kill cancer cells within a host and is also used in the treatment of Onchocerciasis (river blindness). The secondary metabolite responsible for treatment of malaria and trypanosome infection is Artemisinin, but this is also a false statement. It is known that secondary metabolites in plants can have synergistic interactions, meaning that once two or more substances are combined, they can have a sum effect greater than their initial capability. Such is the result when a secondary metabolite of green tea (EGCG), is combined with digitonin of the Foxglove plant resulting in a severely lowered mortality rate and survival of P. berghei (malaria). The idea of synergistic interactions is often understudied and seems to be an emerging practice in the immunoparasitology field, but such is the case with developing any new medicines.

            It should be known that Artemisia is only one of many plants used and studied when measuring anti-parasitic properties. The two most well-known parasitic infections in the world include Malaria and Trypanosomiasis, they also have the largest degree of research in response to secondary metabolites. In a 2015 study by AL-Ani et al. When the bee venom melittin is combined with secondary metabolites such as carvacrol (from cilantro) a synergistic interaction is observed inhibiting microbe infection. Although this example only deals in response to bacteria, we see potential and it makes us excited. Like with developing any new medicine, a target must be chosen and although parasites are eukaryotic creatures like us, they have no deficit in this area. Possible targets of parasites include DNA/RNA, supporting structures of the cell (cytoskeleton), and the bio-membranes (cuticle) of parasites.

            When targeting the DNA or RNA of a parasitic infection, two methods are available to us by secondary metabolites, alkylation, and intercalating. Alkylation is the process of molecules forming double bonds with individual DNA bases, this double bond then inhibits the process of DNA replication causing death. A secondary metabolite that does such, originates from the Birthwort flower and is a known carcinogen called Aristolochic acid. Just as with wormwood, birthwort flower has an extensive history being a traditional medicine whose usefulness correlates with concentration. An Intercalating molecule like Berberine from the Barbary bush most often causes mutations in DNA replication (frameshift/deletion) resulting in death (of the parasite). This is achieved by insertion of the molecule between complementary base pairs further stabilizing the double helix. And when targeting cellular proteins or structures, we need to pick key moments in the cell cycle typically during division. Colchicine, a substance produced by the flower species Colchicum has an affinity for microtubules and can prevent formation by adhering to tubulin, leading to the prevention of cell division. Other methods like this target key steps in division and ironic enough, can stop division by preventing the degradation of the microtubules. Because parasites often do not have lungs or gills, they must exchange gas through their skin, and knowing this we have found our next target, the bio-membrane. In order to harm the membrane, we only need to disturb it enough to affect the level of permeability used to contain and prevent certain molecules entering the parasite. And you bet there is a secondary metabolite capable of this, usually involving terpenes and phenylpropanoids!

            As most of us probably learned as children; if you play with fire, you are going to get burned. In this case, we are not necessarily playing with fire, but taking and altering naturally produced molecules (most of which are toxic) for our own uses. Just as eukaryotic plant cells utilize a cell wall, perhaps we can integrate a cell wall into ourselves (metaphorically). This “cell wall” for us would most likely contain a variety of secondary metabolites utilizing their unique synergetic interactions to cure any disease, especially the parasitic! Hopefully now we understand how many different methods are available when combating parasites and the importance of naturally occurring molecules available. But the problem is presented as we are still in the human “arms race” against disease, a war technically against nature.

References

Current Status of Malaria. (2011, September 24). MALARIA.COM | Malaria Information, Research and News. https://www.malaria.com/questions/malaria-current-status

Editors of Encyclopaedia Britannica. (1998, July 20). Aristolochiaceae. Encyclopedia Britannica. https://www.britannica.com/plant/Aristolochiaceae

Issam, A. A., Zimmermann, S., Reichling, J., & Wink, M. (2015). Pharmacological synergism of bee venom and melittin with antibiotics and plant secondary metabolites against multi-drug resistant microbial pathogens. Phytomedicine, 22(2), 245-255.

Markel, H. (2013, September 27). The real story behind penicillin. PBS NewsHour. https://www.pbs.org/newshour/health/the-real-story-behind-the-worlds-first-antibiotic

National Cancer Institute. (2019, January 14). Aristolochic acids - cancer-causing substances. https://www.cancer.gov/about-cancer/causes-prevention/risk/substances/aristolochic-acids

Nootriment. (2019, December 20). Artemisinin effects, health benefits and uses. World Health Source, LLC. https://worldhealthsource.com/artemisinin-effects-health-benefits-and-uses/

Phillips R. S. (2001). Current status of malaria and potential for control. Clinical microbiology reviews, 14(1), 208–226. https://doi.org/10.1128/CMR.14.1.208-226.2001

Wink, M. (2012). Medicinal plants: a source of anti-parasitic secondary metabolites. Molecules, 17(11), 12771-12791.

Invasion of the Brain Worm, Parelaphostrongylus tenuis, a threat to the survival of the Moose species in North America.

By Kaysey Ferris

Background: Parelaphostrongylus tenuis (Brian worm) is a species of parasitic roundworm that have a threadlike structure. These parasites are commonly found within white-tailed deer populations. However other species are susceptible including moose, elk, caribou, mule deer, fallow deer, bighorn sheep, pronghorns, domestic sheep, goats, llamas, camels, guinea pigs, and to a lesser extent domestic cattle. Humans are not at risk of contracting this parasite.

History: The effects of Brain worm in moose was first reported in Minnesota in 1912, followed by two major declines in the moose population, the first from 1925-27 and the second occurring in 1933-34. A meningeal worm was identified as the main contributor to the disease in 1963, and later classified as Parelaphostrongylus tenuis in 1971.

Distribution: Parelaphostrongylus tenuis are currently found within eastern and central Canada stretching into eastern and central North America. However as white-tailed deer populations continue to grow and move into new areas, the range of this parasite expands as well.

Key Words: L1-L4 larvae stages 1-4, Definitive host: supports the adult or sexually reproductive form of a parasite, Intermediate hosts: required by the parasite to undergo development to reach sexual maturity.

Transmission: The life cycle of P.tenuis takes place over 82 to 91 days. Within its definitive host a white-tailed deer, the life cycle begins when an infected intermediate gastropod host (snail or slug) is consumed during grazing. The intermediate hosts obtain the original infection when L1 larvae penetrate the foot of a gastropod. These larvae grow into their L3 stage within the gastropod over a three to four-week period but require a definitive host to complete their life cycle. During digestion the larva are released and will penetrate the abomasal wall of the stomach within 10 days after ingestion. They then travel from the peritoneal cavity along lumber nerves into the central nervous system. Once they enter the neural tissue, development into their L4 stage occurs within the dorsal horns of the spinal cord. After about 25 days the L4 larvae migrate from the neural tissue to the subdural space were the they develop into their adult stage.

As adults, P.tenuis will migrate to different areas of  the brain and spinal cord to deposit their eggs. This includes areas such as the venous sinuses within the cranium, the meningues, and the venous circulation (an interconnected system of veins and sinuses) where the eggs are moved to the heart and lungs. Eggs that are lodge into the lungs develop into fibrous nodules and embryonate into the first larvae stage, L1. The L1 larvae then move to the alveoli (tiny air sacs) in the lungs which allow for rapid gaseous exchange, where they are coughed up into the mouth and swallowed, and later released from the deer in the mucous coating of their feces. An image of the life cycle is proved in figure 1 below.

Figure 1 Life cycle of P.tenuis

Impact on Moose: Within an abnormal host such as a moose, they will become infected the same way as a white-tailed deer. However, the nematodes (roundworm) damage the nervous tissue through inflammation, manipulation, or mechanical destruction. This damage leads to a wide range of abnormal behaviors exhibited by the animal with a neurological disease. These symptoms include weakness, loss of coordination, head tilt, apparent blindness, circling, loss of fear, depression, inability to feed, weight loss, and finally paralysis and death. Moose populations in certain areas of North America have diminished by almost 50 percent. Brian worm is one factor believed to have contributed to this decline. This is due to the parasites ability to infect and kill moose of various ages of either sex.

Diagnosis: A definitive diagnosis cannot be determined from just witnessing the abnormal behaviors in an animal that is suspected of being infected. There also needs to be a necropsy (animal autopsy) were the presence of adult P.tenuis is confirmed within the spinal cord or the brain.

Importance: Even though P.tenuis causes little to no harm within white-tailed deer, it dose pose a danger to multiple species outside of their normal host. Due to their altered state of behavior, infected animals such as moose pose a danger to both themselves and humans. P.tenuis infections are also always fatal within abnormal hosts causing great damage to local populations that live alongside white-tailed deer.  

Treatment: Currently there is no form of drug treatment for P. tenuis once they have entered the central nervous system. Studies are currently underway involving the use of antihelmintics drugs (antiparasitic drugs) to manage infections in captive white-tailed deer.

Management:  According to researchers the white-tailed deer population has increased from about 500,000 in the early 1900s to about 30 million today. As this population continues to grow and spread into new areas it carries the parasite with it. Since there is no drug treatment or cure for P.tenuis the best way to manage infections in both normal and abnormal hosts is to control wild white-tailed deer populations and monitor their health.

References:

Murray W. Lankester. (2018). Considering Weather-Enhanced Transmission of Meningeal Worm, Parelaphostrongylus Tenuis, and Moose Declines. Alces : A Journal Devoted to the Biology and Management of Moose, 1.

Lankester, M. W. (2010). Understanding the Impact of Meningeal Worm, Parelaphostrongylus Tenuis, on Moose Populations. Alces, 46, 53–70.

Eating snake meat can lead to infection with pentastomes ("tongue worms").

Emerging cases of visceral pentastomiasis in the Democratic Republic of Congo were diagnosed as infection by several species of pentastomes. A link to the article in Emerging Infectious Diseases is here.