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{{Short description|Species of roundworm}}
{{Italic title}}
{{Speciesbox
| name = ''Parelaphostrongylus tenuis''
| taxon = Parelaphostrongylus tenuis
| authority = [[E. C. Dougherty|Dougherty]], 1945
}}
'''''Parelaphostrongylus tenuis''''' (also known as '''meningeal worm''' or '''brainworm''') is a neurotropic [[nematode]] parasite common to [[white-tailed deer]], ''Odocoileus virginianus'', which causes damage to the central nervous system.<ref name="duffy-wildlife-diseases">
{{cite journal | vauthors = Duffy MS, Greaves TA, Keppie NJ, Burt MD | title = Meningeal worm is a long-lived parasitic nematode in white-tailed deer | journal = Journal of Wildlife Diseases | volume = 38 | issue = 2 | pages = 448–52 | date = April 2002 | pmid = 12038147 | doi = 10.7589/0090-3558-38.2.448 | s2cid = 39879199 }}</ref><ref>{{cite book| vauthors = Smith MC, etal |title=Goat Medicine|publisher=Lea & Febiger|year=1994|volume=150}}</ref><ref name="vet.utk.edu">{{cite web|url=http://www.vet.utk.edu/news/story/brain-worm-%28meningeal-worm%29-infestation-in-llamas-and-alpacas.html|title="Brain Worm" (Meningeal Worm) Infestation in Llamas and Alpacas|publisher=University of Tennessee|access-date=2013-11-14}}</ref> [[Moose]] (''Alces alces''), [[elk]] (''Cervus canadensis''), [[caribou]] (''Rangifer tarandus''), [[mule deer]] (''Odocoileus hemionus''), and others are also susceptible to the parasite, but are aberrant hosts and are infected in neurological instead of meningeal tissue. The frequency of infection in these species increases dramatically when their ranges overlap high densities of white-tailed deer.<ref name="michigan-dnr">{{cite web|url=http://www.michigan.gov/dnr/0,4570,7-153-10370_12150_12220-26502--,00.html|title=DNR - Brainworm|publisher=Michigan DNR|access-date=2013-10-24}}</ref>
The lifecycle begins in infected [[meninges|meningeal]] tissues in the central nervous system (CNS) where adult brainworms lay eggs. The eggs are dislodged from the CNS and pass into the lungs, where they hatch. The larvae are then coughed up, swallowed, and proceed through the gastrointestinal tract. Snails and slugs then serve as intermediate hosts, which are later eaten by ungulates, allowing the process to continue.<ref name="vet.utk.edu" /><ref>{{cite book | vauthors = Fowler ME | year = 1989 | title= Medicine and Surgery of South American Camelids: Llama, Alpaca, Vicuna, Guanaco | edition = First | ___location = Ames, IA | publisher = Iowa State University Press | isbn = 978-0-8138-0393-7 | url = https://books.google.com/books?isbn=0813803934 | access-date = January 18, 2017 }}{{page needed|date=January 2017}}</ref>{{page needed|date=January 2017}} Changes in climate and habitat beginning in the early 1900s have expanded range overlap between white-tailed deer and moose, increasing the frequency of infection within the moose population.<ref>{{cite journal | journal=The Journal of Wildlife Management | title = Effects of Winter Ticks and Internal Parasites on Moose Survival in Vermont, USA | first1 = JACOB | last1 = DEBOW | first2 = JOSHUA | last2 = BLOUIN | first3 = ELIAS | last3= ROSENBLATT | date = 2021 | volume = 85 | issue = 7 | pages = 1423–1439 | doi = 10.1002/jwmg.22101 | bibcode = 2021JWMan..85.1423D | url = https://wildlife.onlinelibrary.wiley.com/doi/pdf/10.1002/jwmg.22101| url-access = subscription }}</ref>
== Lifecycle ==
The lifecycle of ''P. tenuis'' is complex and multistaged.
Adults lay eggs on the dura mater (the outer layer of the meninges) of the brain or directly into the bloodstream of an infected host.<ref name="michigan-dnr" /> The eggs hatch into first-stage larvae, which travel in the bloodstream to the lungs, where they travel up the respiratory tract, are swallowed, and then pass out of the body in the mucus coating of fecal pellets.<ref name="michigan-dnr" /><ref name="ny-dec">{{cite web|url=http://www.dec.ny.gov/animals/72211.html|title=Brain worm|publisher=New York State Department of Environmental Conservation|access-date=2013-10-24}}</ref>
Gastropods such as snails and slugs feed upon the mucus coating of the fecal pellets and ingest the larvae.<ref name="michigan-dnr" /><ref name="ny-dec" /> While in the gastropod, the larvae develop into second- and third-stage larvae, which are capable of infection.<ref name="ny-dec" />
[[Category:Roundworms]]▼
[[Category:Parasites]]▼
Gastropods carrying second- and third-stage larvae may be accidentally ingested with plants, which results in the larvae being transmitted to a new host. The larvae then move into the new host's stomach wall and make their way to the CNS, as in white-tailed deer, or the brain as in other ungulates. Once in these tissues, they develop into their adult third stage of life and lay eggs to begin the cycle again.<ref name="michigan-dnr" /><ref name="ny-dec" />
== Transmission ==
Adults of ''P. tenuis'' can persist for many years in a single host, which allows for many first-stage larvae to be shed in feces.<ref name="duffy-wildlife-diseases" /><ref>{{cite journal| vauthors = Karns PD, Jordan PA |title=Pneumostrongylus tenuis in moose on a deer-free island|journal=The Journal of Wildlife Management|year=1969|volume=33|issue=2|pages=431–433|doi=10.2307/3799850|jstor=3799850}}</ref> It is quite common in many populations of white-tailed deer, which have built up a strong resistance.<ref name="michigan-dnr" /> After gastropod ingestion, moose or other deer may be hosts of the second- and third-stage worms. Moose resistance to ''P. tenuis'' is much lower than white-tailed deer, which results in a higher mortality rate.<ref name="lankester-alces">{{cite journal| last = Lankester | first = Murray W. | name-list-style = vanc | year=2010 | title=Understanding the Impact of Meningeal Worm, Parelaphostrongylus tenuis, on Moose Populations | journal=Alces | volume=46 |pages=53–70 | url = http://alcesjournal.org/index.php/alces/article/view/59/82 | access-date = January 18, 2017 }}</ref>
Infected deer density, temperature, climate conditions, and length of transmission periods all affect transmission levels.
* Areas with higher deer populations experience dramatic increases in incidental brainworm larvae consumption.<ref name="karns-wildlife-management">{{cite journal|last=Karns|first=P.D.|title=Pneumostrongylus tenuis in deer in Minnesota and implications for moose|journal=Journal of Wildlife Management|year=1967|volume=31|issue=2|pages=299–303|doi=10.2307/3798320|jstor=3798320}}</ref>
*The temperature and climate conditions of summers can regulate gastropod abundance, with hot, dry summers reducing populations and cool, dry summers increasing populations.<ref name="wasel-wildlife-diseases">{{cite journal | vauthors = Wasel SM, Samuel WM, Crichton V | title = Distribution and ecology of meningeal worm, Parelaphostrongylus tenuis (Nematoda), in northcentral North America | journal = Journal of Wildlife Diseases | volume = 39 | issue = 2 | pages = 338–46 | date = April 2003 | pmid = 12910761 | doi = 10.7589/0090-3558-39.2.338 | s2cid = 23444907 }}</ref>
*High or low gastropod populations directly affect the transmission rate of larval worms to new hosts. Hot, dry summers also reduce the survival numbers of first-stage larvae on fecal pellets.<ref name="lankester-alces" />
*Variation of transmission periods is based on the time when snow is absent from the ground. Gastropods are dormant during snow periods, thus first-stage worms cannot be transmitted to additional hosts.<ref name="lankester-alces" /> So, shorter seasons of snow are met with longer transmission periods of increased potential for transmission through the intermediate vector gastropods.
== Symptoms/clinical signs ==
Brainworm affects neurological and behavioral responses. Deer rarely show any external symptoms of'' P. tenuis'' infection due to their high acquired resistance. Moose, however, have low resistance, and may show a number of symptoms. Though infrequent, cases of moose recovering from brainworm infection have been reported. In both deer and moose, symptom severity does not necessarily vary with severity of infection.
*Infected individuals may not have any external symptoms.
*Mild symptoms may include slower movements and response time, frequent stumbling, unusually tilted head, and emaciation.
*Severe symptoms include extreme weakness, lameness, walking in circles, partial or whole blindness, loss of fear for humans, ataxia, and mortality.
Several other ungulates are susceptible to brainworm infection, including elk, caribou, mule deer, sheep, goats, llamas, alpacas, rarely cattle, and rarely horses. Severe neurological damage similar to that of infected moose is shown to occur in these species.
== Diagnosis ==
Presently, a commercial antibody test that can detect ''P. tenuis'' antemortem does not exist.<ref name=":0">{{cite journal | vauthors = Mittelman NS, Divers TJ, Engiles JB, Gerhold R, Ness S, Scrivani PV, Southard T, Johnson AL | title = Parelaphostrongylus tenuis Cerebrospinal Nematodiasis in a Horse with Cervical Scoliosis and Meningomyelitis | journal = Journal of Veterinary Internal Medicine | volume = 31 | issue = 3 | pages = 890–893 | date = May 2017 | pmid = 28317172 | pmc = 5435076 | doi = 10.1111/jvim.14691 }}</ref><ref>{{cite journal | vauthors = Dobey CL, Grunenwald C, Newman SJ, Muller L, Gerhold RW | title = Retrospective study of central nervous system lesions and association with Parelaphostrongylus species by histology and specific nested polymerase chain reaction in domestic camelids and wild ungulates | journal = Journal of Veterinary Diagnostic Investigation | volume = 26 | issue = 6 | pages = 748–54 | date = November 2014 | pmid = 25274743 | doi = 10.1177/1040638714553427 | doi-access = free }}</ref> Diagnosis in deer can be conducted by analyzing fecal pellets for larval ''P. tenuis'', or ''post mortem'' necropsy to detect presence of adult ''P. tenuis'' in the brain cavity or second- and third-stage worms along the spinal cord.<ref name="duffy-wildlife-diseases" /><ref name="karns-wildlife-management" /><ref name="wasel-wildlife-diseases" /> However, brainworm larvae are difficult to distinguish from other parasitic worm species that can also be found in fecal pellets,<ref name="murray-wildlife-monographs">{{cite journal| vauthors = Murray DL, Cox EW, Ballard WB, Whitlaw HA, Lenarz MS, Custer TW, Barnett T, Fuller TK |title=Pathogens, nutritional deficiency, and climate influences on a declining moose population|journal=Wildlife Monographs|year=2006|volume=166|issue=1|pages=1–30|doi=10.2193/0084-0173(2006)166[1:PNDACI]2.0.CO;2|s2cid=17800980 }}</ref> so detection of adult worms through necropsy is recommended. Diagnosis in moose is conducted with necropsy to detect worms in the brain or spinal cord.<ref name="ny-dec" /><ref name="murray-wildlife-monographs" /> Diagnosis in horses can be conducted with postmortem samples used for polymerase chain reaction (PCR) testing.<ref name=":0" /><ref name=":1">{{cite journal | vauthors = Tanabe M, Gerhold RW, Beckstead RB, de Lahunta A, Wade SE | title = Molecular confirmation of Parelaphostrongylus tenuis Infection in a horse with verminous encephalitis | journal = Veterinary Pathology | volume = 47 | issue = 4 | page = 759 | date = July 2010 | pmid = 20581347 | doi = 10.1177/0300985810363488 | doi-access = }}</ref> Positive PCR results show evidence of ''P.'' ''tenuis'' infecting equines.<ref name=":0" /><ref name=":1" /> In veterinary patients, such as goats, an eosinophilic pleocytosis can be suggestive of ''P. tenuis'' infection.<ref name=":3">{{Cite journal |last1=Garcia |first1=Jessica |last2=Smith |first2=Joe |last3=Fry |first3=Michael |last4=Mulon |first4=Pierre-Yves |date=May 2023 |title=Clinical presentation, diagnostics, treatment, and outcome of goats diagnosed with presumptive cerebrospinal nematodiasis at a veterinary teaching hospital |journal=The Canadian Veterinary Journal |volume=64 |issue=5 |pages=419–425 |issn=0008-5286 |pmid=37138711|pmc=10150576 }}</ref><ref name="Breuer e000706">{{Cite journal|last1=Breuer|first1=Ryan|last2=Merkatoris|first2=Paul|last3=Tepley|first3=Samantha|last4=Dierks|first4=Caitlyn|last5=Klostermann|first5=Cassandra|last6=Flaherty|first6=Heather|last7=Smith|first7=Joseph|date=2019-01-01|title=Treatment of cerebrospinal nematodiasis in a Boer Buck|url=https://vetrecordcasereports.bmj.com/content/7/1/e000706|journal=Veterinary Record Case Reports|language=en|volume=7|issue=1|article-number=e000706|doi=10.1136/vetreccr-2018-000706|s2cid=86538320 |issn=2052-6121|url-access=subscription}}</ref><ref name="Smith">{{Cite journal|last1=Smith|first1=Joe|last2=Kreuder|first2=Amanda|last3=Breuer|first3=Ryan|last4=Still-Brooks|first4=Kelly|date=2019-08-12|title=Meningeal Worm Infection in Central Iowa Goat Herds II: Individual Cases and Treatment Using a Camelid Therapeutic Protocol|url=https://www.iastatedigitalpress.com/air/article/id/7188/|journal=Animal Industry Report|volume=2019|issue=1}}</ref>
== History ==
In 1912, an unknown neurological disease affecting moose was first reported in Minnesota.<ref>{{cite journal| vauthors = Fenstermacher R, Jellison WL |title=Diseases affecting moose|journal=University of Minnesota Agriculture Exponent State Bulletin|year=1933|volume=6}}</ref> Major declines in the moose population were reported, 1925–27 and 1933–34, following the discovery of this unknown disease. In 1963, a meningeal brainworm, ''Pneumostrongylus tenuis'', was determined as the etiological agent causing neurological disease in moose. Around 1971, taxonomists reclassified it as ''Parelaphostrongylus tenuis''.<ref>{{cite journal| vauthors = Anderson RC |title=Neurologic disease in moose infected experimentally with Pneumostrongylus tenuis from white-tailed deer|journal=Pathology|volume=1|issue=4|year=1964|pages=289–322|doi=10.1177/030098586400100402|doi-access=free}}</ref><ref>{{cite journal| vauthors = Loken KI, Schlotthauer JC, Kurtz HJ, Karns PD |title=Pneumostrongylus tenuis in Minnesota moose (Alces alces)|journal=Bulletin Wildlife Disease Association|year=1965|volume=1|issue=2|page=7}}</ref><ref>{{cite book |last1=Botzler|first1=Richard G. | first2 = Richard W. | last2 = Brown | name-list-style = vanc |title=Foundations of Wildlife Diseases |publisher=Univ. of Calif. Press |year=2014 |page=62}}</ref>
White-tailed deer populations in the eastern United States are now known to be commonly infected with meningeal worm. Infection in the southeastern and western United States is less common. This disease has also been found in the Canadian provinces of Ontario, Saskatchewan, Manitoba, and Nova Scotia.<ref>{{cite book | vauthors = Benson DA, Dodds GD | date = 1997 | title = The deer of Nova Scotia. | publisher = Department of Lands and Forests | ___location = Province of Nova Scotia }} Cited in: {{cite journal | vauthors = Telfer ES | title = Continuing environmental change-An example from Nova Scotia. | journal = The Canadian Field-Naturalist | date = 2004 | volume = 118 | issue = 1 | pages = 39–44 | url = http://www.canadianfieldnaturalist.ca/index.php/cfn/article/viewFile/880/881 | doi = 10.22621/cfn.v118i1.880 | doi-access = free }}</ref> The grassland biomes of the United States and Canada apparently act as a barrier to the movement of the disease. Evidence from Canada seems to support this, since the western distribution of meningeal worm has changed little since the 1960s.<ref name="wasel-wildlife-diseases" /><ref>{{cite journal| vauthors = Bindernagel JA, Anderson RC |title=Distribution of the meningeal worm in white-tailed deer in Canada|journal=The Journal of Wildlife Management|year=1972|volume=36|pages=1349–1353|doi=10.2307/3799283|issue=4|jstor=3799283}}</ref>
== Epidemiology ==
The geographic ranges of moose and white-tailed deer were historically separate prior to the 20th century.<ref name="duffy-wildlife-diseases" /><ref name="karns-wildlife-management" /> Moose are well adapted to winter survival, whereas deer are not. They could not withstand the harsh winters in these regions of the northeastern United States and the southeastern provinces of Canada.<ref name="lankester-alces" /> Deer populations began to move into the southern portions of moose range in the early 1900s following changes in climate,<ref name="wasel-wildlife-diseases" /> logging, mining, forest fires, and increasing human development.<ref name="duffy-wildlife-diseases" /><ref name="karns-wildlife-management" /> High-quality deer habitat associated with these changes has led to dramatic increases in deer abundance in these regions.<ref name="duffy-wildlife-diseases" /><ref name="karns-wildlife-management" />
White-tailed deer are the normal host of the ''P. tenuis'' parasite and are immunologically adapted to its presence. Deer and ''P. tenuis'' have coadapted in an evolutionary arms race over time. Deer remain largely unaffected by the presence of ''P. tenuis'' because of the immunity they have built as a result of coadaptation.<ref name="michigan-dnr" /><ref name="moose-circle">{{cite journal| vauthors = Peterson B | year = 1997 | title=Moose Walking in Circles | journal = The Minnesota Volunteer | issue = September–October | pages = 24–31 | format = online pdf of print issue | url=https://webapps8.dnr.state.mn.us/volunteer_index/past_issues/issue_pdf?issue_id=112 | access-date = January 18, 2017}}</ref> The prevalence and infection rate of ''P. tenuis'' in deer is density dependent; increased rates of infection by the parasite are the result of higher deer densities.<ref name="duffy-wildlife-diseases" /><ref name="karns-wildlife-management" />
Moose populations on the southern fringes of their range have recently experienced dramatic declines. As deer encroached upon the southern fringes of moose range, they introduced the parasite to a [[Naivety#Science|naïve]] host, the moose.<ref name="murray-wildlife-monographs" /> Upon transmission of the pathogen into moose, the worm causes cerebrospinal nematodiasis, a disease of the nervous system that often results in death.<ref name="michigan-dnr" /> ''P. tenuis'' may be one factor that has contributed to moose declines in southern portions of their range. This disruption of host-pathogen dynamics due to habitat alterations has promoted the spread of this parasite to a naïve host and has potentially contributed to declines in moose abundance and productivity in regions with high deer densities.<ref name="lankester-alces" /> Continued increase in deer abundance and density in the southern fringes of moose range are predicted to facilitate sustained transmission of ''P. tenuis'' to moose. Continued transmission of deer-related parasites, coupled with low productivity, habitat degradation, and a northward shift in the moose thermoneutral zone, leads to a troubling prognosis for southern moose populations.<ref name="murray-wildlife-monographs" /> Murray et al. (2006) predict, if current trends continue, moose populations in these regions will not be viable and population declines will persist.
== Treatment ==
Currently, there is no definitive treatment for ''P. tenuis'' in mammals, though research is still being conducted''.'' The use of anthelmintics (ivermectin and fenbendazole) have been attempted in white-tailed deer. The results indicate, however, that ivermectin was ineffective against larvae that had already reached the spinal cord.<ref>{{Cite journal|last=Kocan|first=A. Alan | name-list-style = vanc |date= October 1985 |title=The Use of Ivermectin in the Treatment and Prevention of Infection with Parelaphostrongylus tenuis (Dougherty) (Nematoda: Metastrongyloidea) in White-tailed Deer (Odocoileus virginianus Zimmermann) |journal=Journal of Wildlife Diseases |volume=21 |issue=4 |pages=454–455 |doi=10.7589/0090-3558-21.4.454 |pmid=3841163 |doi-access=free }}</ref> Fenbendazole and ivermectin, combined with anti-inflammatory therapy have been used to manage infections in goats.<ref name=":3" /><ref name="Smith"/><ref name="Breuer e000706"/>
== Current and past research ==
The majority of moose brainworm research in North America has been conducted in northern Minnesota, where a historical moose population of 4,000 to 5,000 moose had declined to an estimated 1,200 individuals by 1997.<ref name="moose-circle" /> In this region, wildlife managers are challenged to predict and attempt to mitigate moose declines resulting from deer-related pathogens. Because no effective methods to prevent the transmission or infection of brainworm in moose have been found, managers have focused their efforts on decreasing deer densities in these regions.<ref name="karns-wildlife-management" /> The Minnesota DNR identified that population densities greater than 12 deer/square mile result in increased moose mortality as a result of brainworm. Managers in these areas are responsible for evaluating suitable habitat for moose and deer, as well as setting management priorities and population goals to decrease the transmission of ''Parelaphostrongylus tenuis'' in moose.<ref name="moose-circle" /> Though the main focus of research has been on white-tailed deer and moose, research has found that the guinea pig can be used as an experimental model of ''P. tenuis'' infection.<ref name=":2">{{Cite journal| vauthors = Haigh JC, Mackintosh C, Griffin F |date=2002-08-01|title=Viral, parasitic and prion diseases of farmed deer and bison|journal=Revue Scientifique et Technique de l'OIE|volume=21|issue=2|pages=219–248|doi=10.20506/rst.21.2.1331|pmid=11974612|doi-access=free}}</ref>
== References ==
{{Reflist}}
{{Taxonbar|from=Q7136712}}
{{Authority control}}
[[Category:Parasitic nematodes of mammals]]
[[Category:Nematodes described in 1945]]
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