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  Discussion on Meningeal worms of deer or llamas
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Member:
vickiann

Posted on Friday, Feb 11, 2011 - 1:58 pm:

Dr. O,

I see that llamas get meningeal worms that can be transmitted by exposure to deer DrOppings.

Can horses pick up this type of parasite too?

Are there any parasites or diseases that llamas or deer can give to horses?
Moderator:
DrO

Posted on Saturday, Feb 12, 2011 - 9:01 am:

Hello Vicki,
The meningeal worm, Parelaphostrongylustenuis, normal host is the white tailed deer and can cause disease in aberrant hosts which we think is confined to ruminants and not horses. The term "any disease" covers a very broad range and I am sure there are some, sarcoptic mange and staph infections come to mind, but in general these two species do not share parasites and diseases.
DrO
Member:
vickiann

Posted on Saturday, Feb 12, 2011 - 9:13 am:

Thanks very much Dr. O.

Good news!
New Member:
mdelton

Posted on Sunday, Feb 13, 2011 - 1:29 pm:

I have been give different information on this.

I was told that P. Tenuis can be ingested by horses and migrate to the brain. That is what the diagnosis of what happened to my 4 yr old was. Mainly by process of elimination I admit but the only definitive test is necropsy. He was tested negative for everything else they could think of. This was diagnosed at Cornell and last weekend, I attended a lecture by a vet from New Bolton who specializes in neurological cases and she said the same thing.

Please advise.

Mary
Member:
vickiann

Posted on Sunday, Feb 13, 2011 - 4:47 pm:

Troubling: https://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=246116
Moderator:
DrO

Posted on Sunday, Feb 13, 2011 - 7:30 pm:

Hello All,
MDelton, I cannot find any report of such a occurence in a horse, what is the basis of the diagnosis of your horse.

Vicki, good job I have not seen such a report and it does not appear on PUBMED. But the ability of extremely unusual things to crop up when dealing with biological cases always causes me to hedge on such questions. HOwever I would not let one report in the history of the world to trouble me, you might as well start worrying about being struck by a meteor. You should be much more worried about lightening.
DrO
Member:
vickiann

Posted on Sunday, Feb 13, 2011 - 11:26 pm:

Nonetheless, you may find the following interesting:

https://www.respe.net/system/files/documents_journalEVS_vol29.pdf Presently emergent? (associated with cervical scoliosis, mentions migration to brain)
(See the abstract on first page in blue box then page 3, P. tenuis)

Update on equine neurologic diseases (Proceedings)

Aug 1, 2008
By: Thomas Divers, DVM, DACVIM, DACVECC
CVC PROCEEDINGS

(After speaking of P. Tenuis, this article expands to discuss EPM and other disorders -- more links on P. Tenuis cases after this article)

In the field of equine neurology, there has been the discovery of a few new disorders, in addition to some newer diagnostics, and/or therapeutics.

Parelaphostrongylus tenuis infection in young horses is a recently reported neurologic disease of horses. In areas of North America that routinely diagnose P. tenuis in small ruminants and camelids, infection in the horse should be considered and will be seen!. The clinical sign of acute onset scoliosis is nearly diagnostic for the equine disease. Affected horses have been 6 mo-3 years of age. The parasite appears to have a migratory predilection in the horse for the dorsal gray column of the cervical and sometimes thoracic cord. If the lesion extends three or more vertebral segments, acute onset scoliosis with the head deviated away from the lesion side will occur. Hypalgesia to analgesia will be found on the affected (convex) side over the affected segments. There may be very mild ataxia and paresis of the limbs on the affected side. In the few cases we have performed CSF collection and evaluation on, the results were unremarkable, unlike P. tenius in small ruminants and camelids. The signs are characteristic enough in horses in an endemic area to make the diagnosis. Initially, there is no pain in manipulation of the neck, but after several weeks, arthritic changes develop. Treatments have included high doses of ivermectin and steroids, but lesions have been so advanced that successful treatment does not seem possible. Some clients have worked with physical therapists to provide exercises and braces in hopes of a return to normalcy, but this has been uniformly unsuccessful.

Temporohyoid osteoarthropathy is now one of the more common neurologic disorders we see in the horse. Since 2000, we have examined 24 horses with this condition. The etiology of this arthritic disease is unknown, but previous otitis interna/media is generally blamed. A small number of cases have active infection (mostly gram positive cocci and one case aspergillus). The disease is most common in middle age horses, youngest being 3 years of age, and approximately 40% have bilateral disease, although the clinical signs are almost always unilateral. The signs are variable with some horses having behavioral signs associated with being ridden or while eating; these are likely signs of pain. Acute onset of neurologic signs are believed to occur when the fused T-H joint fractures. Fractures may be associated with sudden movements of the head and have been repoted in horses being tubed or after dental procedures. Clinical signs are those associated with cranial nerve VII and/or VIII dysfunction. Diagnosis is by signs, endoscopy of the guttural pouch, radiographs or computed tomography. CSF can be inflammatory in approximately 25% of cases and in a rare case, septic (consider Staph aureus). Treatment goals are directed towards decreasing inflammation and infection, if present, and preventing complications, of which exposure keratitis is perhaps the greatest. Approximately 50% of the horses return to use. Unfortunately, we are not able to predict clinical response at the time of the initial diagnosis! We have routinely recommended a ceratohyoidectomy for both patient comfort and to prevent further fractures at the fused T-H joint(s).

Diagnosis of cervical vertebral compressive myelopathy (CVCM) continues to be an area of investigation. Intra-vertebral ratios on plain cervical films has proven to be the screening test of choice for most clinics, but sensitivity and specificity of the test are variable between clinics/radiologist reading the films, and there is poor correlation between the site of the abnormal ratio and the lesion site. Since the site of cord compression is often inter-vertebral rather than intra-vertebral in horses, an additional inter-vertebral measurement has been recommended. The inter-vertebral measurements more accurately reflect specific site(s) of compression and location and number may affect decisions to proceed with a myelogram and possibly surgery. Recently, we have even questioned the accuracy of the 50% reduction in the dorsal myelographic column for diagnosis of CVCM. Accuracy of this criteria seems to vary with vertebral site, C5-C7 being most accurate. Measurement of the reduction in dural diameter at the inter-vertebral sites in comparison to adjacent mid-vertebral body dural diameter might be more accurate for compression in the mid-cervical region.

Additional diagnostics for EPM have been recently published. If veterinarians are only testing serum as a screening test for EPM, the IFA test may be the preferred test. Titers > 160, with compatible history and clinical signs indicate a moderate or higher probability of EPM. Racing and western performance horses have been found to be at increased risk of EPM. Intermittent treatment of at risk horses has been evaluated as a means of preventing CNS infection with S. neurona. Administration of ponazuril every 7 days has some efficacy. This time frame corresponds with recent research that investigate the kinetics of S. neurona invasion in the horse.

Recently, we have described a synDrOme of symmetrical tetraparesis and ataxia and cervical pain associated with epidural hematoma (no known trauma) at C5-C6. The onset is acute and severity of signs are often 3 to 4/5 ataxia. Cause of the hematoma is unproven, but should be included in the differential diagnosis of horses with these signs. Pathophysiology, diagnosis, treatment, and prognosis will be discussed. Additional equine neurologic diseases that appear on PubMed since 2006 and will be discussed include ivermectin toxicity, hyperammoniaemia, equine motor neuron disease, fluphenazine adverse effects, and traumatic brain injury.

References

Cohen N.D. et al. A multicenter case-control study of risk factors for equine protozoal myeloencephalitis. J Am Vet Med Assoc 2007;231(12):1857-1863.

Duarte, P.C., Ebel E.D., Traub-Dargatz, J., Wilson, W.D., Conrad, P.A., and Gardner, I.A. Indirect fluorescent antibody testing of cerebrospinal fluid for diagnosis of equine protozoal myeloencephalitis. Am J Vet Res 2006;67(5):869-876.

Elitsur, E., Marsh, A.E., Reed, S.M., et. al. Early migration of Sarcocystis neurona in ponies fed sporocysts. J Parasitol 2007;93(5):1222-1225.

Feary, D.J., Magdesian, K.G., Aleman, M.A., and Rhodes, D.M. Traumatic brain injury in horses: 34 cases (1994-2004). J Am Vet Med Assoc 2007;231(2):259-266.

Hahn, C.N., Handel, I., et.al. Assessment of the utility of using intra- and intervertebral minimum sagittal diameter ratios in the diagnosis of cervical vertebral malformation in the horse. Vet Radiol Ultrasound 2008;49(1):1-6.

Levine, J.M., Adam, E., MacKay, R.J., Walker, M.A., Frederick, J.D., and Cohen, N.D. Confirmed and presumptive cervical vertebral compressive myelopathy in older horses: a retrospective study (1992-2004). J Vet Intern Med 2007;21(4):812-819.

Mackay, R.J., Tanhauser, S.T., Gillis, K.D., Mayhew, I.G., Kennedy, T.J. Effect of intermittent oral administration of ponazuril on experimental Sarcocystis neurona infection in horses. Am J Vet Res 2008;69(3):396-402.

Orsini, J.A. (ed). Clinical Techniques in Equine Practice: Neurology. 2006;5(1).

Mohammed, H.O., Divers, T.J., Summers, B.A., and de Lahunta, A. Vitamin E deficiency and risk of equine motor neuron disease. Acta Vet Scand 2007;49(1):17.

Tanabe, M., Kelly, R., de Lahunta, A., Duffy, M.S., Wade, S.E., and Divers, T.J. Verminous encephalitis in a horse produced by nematodes in the family protostrongylidae. Vet Pathol 2007;44(1):119-122.

https://vet.sagepub.com/content/44/1/119.full

Acquired cervical scoliosis attributed to Parelaphostrongylus ...
15 Aug 2006 ... Recently, 6 cases of acquired cervical scoliosis in horses were linked to P tenuis migration through the dorsal gray column of the cervical ...avmajournals.avma.org/doi/pdf/10.2460/javma.229.4.562 - Similar
(A couple of different Vet journal sites mention these 6 cases but I cannot access the information, just the notation).


https://ddr.nal.usda.gov/bitstream/10113/45069/1/IND44411509.pdf (detailed regarding intraocular P.Tenuis case)
Member:
vickiann

Posted on Monday, Feb 14, 2011 - 9:15 am:

Here is article that may have failed to open:

Expand+Verminous Encephalitis in a Horse Produced by Nematodes in the Family Protostrongylidae
M. Tanabe,
R. Kelly,
A. de Lahunta,
M. S. Duffy,
S. E. Wade and
T. J. Divers
Dr. M. Tanabe, Antech Diagnostics, 17672-B Cowan Avenue, Irvine, CA 92614 (USA). E-mail: mika.tanabe@antechmail.com.
Next SectionAbstract
Parasitic granulomatous eosinophilic inflammation was observed in the central nervous system (CNS) of a 6-month-old Arabian colt from New York state. Inflammation was associated with eggs, larvae, and adult nematodes in the cerebellum. Nematodes had histological characteristics of the superfamily Metastrongyloidea. The presence of dorsal-spined larvae in the CNS was further indicative of infection with a nematode in the family Protostrongylidae. Infections were most compatible with Parelaphostrongylus tenuis but specific diagnosis was not possible. This is the first definitive report of a protostrongylid nematode infection in a horse.

CNSdorsal-spined larvaehistopathologyhorsesMetastrongyloideanematodesparasitic encephalomyelitisParelaphostrongylus tenuis
Parasitic migratory encephalomyelitis is a rare but important cause of neurologic disease in horses. Metazoan parasites identified from the equine central nervous system (CNS) include nematodes (Strongylus vulgaris, S. equinus, Angiostrongylus cantonensis, Halicephalobus gingivalis, Setaria spp., and Draschia megastoma) and fly larvae (Hypoderma spp.).9 We identified parasitic nematodes in the CNS of a young horse in New York state. Nematode morphology and its occupation of the CNS were most compatible with the meningeal worm, Parelaphostrongylus tenuis. The northeastern USA has a high density of white-tailed deer (Odocoileus virginianus) that have a high prevalence of P. tenuis infection. This neurotropic nematode causes a debilitating neurologic disease in cervids,1, 6 ovids,1 bovids,1, 5, 12 and camelids.1 Recently, Van Biervliet et al. identified a Metastrongyloidea nematode in the CNS of a horse,11 but specific identification of the parasite was not possible. Here we present the first definitive report of protostrongylid nematodes in the CNS of a horse.

A 6-month-old male Arabian horse had acute onset of an abnormal gait and held its head to the right. There was no history of pyrexia or systemic illness. The colt was born in New York state and had not traveled to other states. Clinical signs persisted following treatment with dexamethasone, and the horse was referred to the Cornell University Hospital for Animals. Clinical examination revealed marked spastic tetraparesis and ataxia in all four limbs. The head and neck were held to the right side. A C1 to C5 lesion was suspected. Cerebrospinal fluid contained mildly increased protein (116 mg/dl, normal range 5–100 mg/dl) and 1200 cells/μl (58% lymphocytes, 40% neutrophils, 2% macrophages, and a few eosinophils and erythrocytes). Cervical radiographs were suspicious for subluxation at the atlanto-occipital joint. Computed tomography (CT) examinations were normal except for a mild atlanto-occipital joint subluxation, and a light weight cast was applied as treatment for the subluxation. The foal was unable to stand on recovery from anesthesia for the CT scan and struggled violently to attempt to stand. The patient was humanely euthanized and a necropsy was performed.

Necropsy examination revealed mild subluxation of the atlanto-occipital joint on the left side with elongation of the left alar ligament. There was considerable edema of the epidural fat surrounding C1, but no hemorrhage or discoloration was identified. The calvaria and cervical vertebrae were grossly normal, and no malformation was identified. No other gross abnormalities were recognized in other organs. The entire brain and segments of spinal cord were fixed in 10% neutral-buffered formalin. On sectioning of the fixed brain, a mild, diffuse, dull discoloration of the cerebellar parenchyma was observed (Fig. 1). This was most prominent in the deeper aspect of the cerebellar vermis (Fig. 1). Tissues were embedded in paraffin, sectioned, and stained with HE.


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Cerebellum and pons; horse. Dull discoloration of cerebellar parenchyma.
Microscopically, the cerebellar parenchyma and the associated meninges were widely replaced by multifocal to coalescing eosinophilic granulomatous inflammation. This was most severe in the parenchyma of the cerebellar vermis and obliterated cerebellar cortex, white matter, and meninges. The exudate was composed of large numbers of epithelioid macrophages, fewer eosinophils, and multinucleated giant cells accompanying moderate astrogliosis. The affected neuropile was edematous and pale. The white matter had scattered swollen axons. In the adjacent, less affected cerebellar parenchyma, there was moderate perivascular lymphocytic and eosinophilic cuffings, expanding the Virchow-Robin spaces. The meninges were thickened with edema and lymphocytic and eosinophilic infiltration. Numerous eggs and nematode larvae were present within inflammatory exudates (Fig. 2). The eggs were approximately 21 μm in length and had a thin shell. Both developing and embryonated eggs were present (Fig. 2). The first-stage larvae (L1) were approximately 15 μm in diameter and had thin lateral alae. A posteriorly directed dorsal spine was observed anterior of the crooked tail on L1 (Fig. 3). The full length of L1 could not be determined from histologic sections. At least 1 adult female worm was present in the cerebellar parenchyma and meninges (Fig. 4). One male worm was identified in the meninges over the medulla oblongata (Fig. 5). Adult parasites had a round body with a smooth cuticle, polymyarian-coelomyarian musculature, lateral and accessory hypodermal cords, and a “strongylid” intestine composed of 3 to 5 multinucleated cells with indistinct microvilli (Fig. 4 and inset). The female parasite was 173 μm wide with paired genital tracts containing eggs and sperm (Fig. 4 inset). The male parasite was 161 μm wide and had a single genital tract containing sperm (Fig. 5).


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Cerebellum; horse. Granulomatous encephalitis with numerous developing eggs (arrow) and a few embryonated eggs (arrowhead). HE. Scale bar = 100 μm.

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Cerebellum; horse. First-stage larva with crooked tail and a posteriorly directed spine (arrowhead). HE. Scale bar = 10 μm.

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Cerebellum; horse. Granulomatous encephalitis with cross and longitudinal profiles of an adult female nematode. Inset shows higher magnification of a cross section of the worm. Note eggs and sperm in genital tracts. HE. Scale bar= 250 μm.

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Medulla oblongata; horse. A cross section of male parasite in the meninges. Asterisk indicates parenchyma of medulla oblongata. HE. Scale bar = 100 μm.
Nematodes from the colt and from a previous horse infection reported by Van Biervliet et al.11 had the characteristic “strongylid” intestine and polymyarian-coelomyarian musculature compatible with nematodes in the superfamily Metastrongyloidea.3 Within this group, only species in the families Protostrongylidae and Angiostrongylidae demonstrate neurotropism and infection of the CNS.1 The L1 in the CNS of the colt had lateral alae and crooked tails with a posteriorly directed dorsal spine. The spine is of diagnostic significance and is unique to protostrongylid nematodes.1, 2 The family Protostrongylidae parasitize ruminants predominantly, and none of these species is known to infect horses.1 This case is the first definitive report of protostrongylid nematode infection of a horse.

There are seven genera within the family Protostrongylidae that produce dorsal-spined larvae. Of these, species from both Parelaphostrongylus and Elaphostrongylus are known to infest the host CNS and musculature, whereas the other five genera occupy host lung exclusively.1 In this case, infection with Elaphostrongylus is considered unlikely because this genus is not known to occur in North America.8 The genus Parelaphostrongylus contains 3 species. Parelaphostrongylus odocoilei has been reported to occur in the musculature of mule deer and woodland caribou; its range is restricted to western North America. Parelaphostrongylus andersoni occurs in the musculature of white-tailed deer in the southeastern USA, New Jersey, Michigan, Wyoming, and southcentral British Columbia, and in barren-ground caribou throughout Canada.1 Parelaphostrongylus tenuis is a common parasite of the CNS of white-tailed deer throughout eastern North America.1 The width of the female worm in the colt CNS (173 μm) was compatible with the range of measurement reported for P. tenuis (120–250 μm) and P. odocoilei (141–179 μm) but not P. andersoni (92–130 μm).6 The width of the male worm (161 μm) was compatible with the range of measurement reported for P. tenuis (92–200 μm) but not with P. odocoilei (138–156 μm) or P. andersoni (87–140 μm).6 Definitive classification of protostrongylid nematodes can be made only following examination of reproductive structures from male worms. Isolation of adult nematodes from formalin-fixed tissues was unsuccessful. The etiologic diagnosis of P. tenuis, however, is supported in this case by nematode morphometry and tissue tropism, characteristic protostrongylid epizootiology, and the host's restricted travel history and geographic range.

Acquired scoliosis and dorsal gray column myelitis were observed in the previous horse with a larva of the superfamily Metastrongyloidea, and parasitic migration was proposed pathogenesis.11 In the current case, the colt did not show clinical signs of scoliosis, and parasitic migratory lesion was not observed in the spinal cord macroscopically and microscopically.

Parelaphostrongylus tenuis, also called meningeal worm or brain worm, is a common neurotropic parasitic nematode of white-tailed deer throughout eastern North America.1 Adult worms are found in the cranial subarachnoid space and in surrounding cranial venous sinuses. Eggs are deposited into the venous circulation and are carried as emboli to the lungs, where they lodge in small capillaries and become incorporated into granulomas.1, 6 The eggs hatch and release L1 that escape from granulomas, penetrate lung alveoli, and enter air ducts.1, 6 They are carried up the mucociliary escalator, are swallowed, and pass out in host feces. The L1 infect terrestrial mollusks and develop to the infective stage (L3) in this host. Deer and other hosts become infected by accidental ingestion of L3, presumably within mollusks ingested accidentally along with vegetation.6 The L3 penetrate the abdomen and migrate to the spinal cord by 10 days after infection.6 The larvae develop in the dorsal gray columns of the spinal cord, then migrate from the nerve parenchyma into the subarachnoid space of the cranium where they mature and copulate.6

Parelaphostrongylus tenuis is generally clinically silent in white-tailed deer but causes neurological disease in all other North American cervids.1, 7 Noncervid ungulates are also susceptible to P. tenuis. Debilitating neurologic disease has been reported in sheep, goats, llamas, bighorn sheep, and various types of antelopes.1 Cattle are thought to be largely resistant to infection,7 with disease reported only rarely.5, 12 Horses might be similarly resistant because parasitic neurologic disease is rare in spite of extensive pasture overlap with infected white-tailed deer. For example, prevalence of P. tenuis in white-tailed deer is reported to be as high as 86%,1 and would presumably provide ample opportunities for parasite exposure. The low incidence of infection in horses likely reflects the evolution of protostrongylid nematodes in ungulate hosts. The mechanism of resistance to P. tenuis infection in horses is unknown. It may be caused by differences associated with acidic pH around 6 of a simple stomach of grazing horses, differences in grazing habits that prohibit ingestion of L3, or differences in the horse immune response.11 It is typically regarded that less compatible hosts result in poor or failed reproduction by P. tenuis. Excluding white-tailed deer, L1 have been observed in feces from some non-white-tailed cervids4, 10 but not from ovids, bovids, or camelids.7 Neither eggs nor larvae were observed in the lung of the colt in the present study. Feces were not examined for L1. Eggs occasionally are deposited on the meninges in permissive cervid hosts and hatch to release L1. However, neither eggs nor L1 have been reported from the CNS of infected ovids, camelids, or bovids.7 Presence of protostrongylid L1 in the colt CNS is an unprecedented observation and indicates successful reproduction. It is possible that the young age of the animal played a role in establishment of infection and disease.

In summary, our observations confirm that horses are susceptible to encephalitis from infection by nematodes in the family Protostrongylidae. Specific identification of the nematodes was not possible but features of parasite morphology, their anatomical location, and epizootiology were most compatible with P. tenuis. Our observations suggest that horses might be susceptible to infection and disease caused by P. tenuis. Protostrongylid nematode infection should be included as a differential diagnosis for instance of neurologic disease in horses in endemic area of eastern North America.

Previous SectionNext SectionAcknowledgements
The authors thank Alexis Wenski-Roberts and David M. Fitzgerald for assistance with photographs. We also appreciate the revision of this manuscript by Dr. Cynthia X. Bacmeister.

© 2007 American College of Veterinary Pathologists
Previous Section References
1.↵ Anderson RC
Anderson RC
Anderson RC: The superfamily metastrongyloidea. In: Nematode Parasites of Vertebrates, Their Development and Transmission, ed. Anderson RC, 2nd ed., pp. 129–172. CABI Publishing, Oxon, UK, 2000 2.↵ Anderson RC, Chaubaud AG, Willmott SAnderson RC, Chaubaud AG, Willmott S: CIH keys to the nematode parasites of vertebrates. No. 5. Keys to genera of the superfamily Metastrongyloidea. Commonwealth Agricultural Bureaux, Farnham Royal, England, 1978 3.↵ Chitwood M, Lichtenfels JRChitwood M, Lichtenfels JR: Identification of parasitic metazoa in tissue sections. Exp Parasitol 32: 407–519, 1972 CrossRefMedlineOrder article via InfotrieveWeb of Science4.↵ Duffy MS, Greaves TA, Burt MDDuffy MS, Greaves TA, Burt MD: Establishment of adult Parelaphostrongylus tenuis, patent infections, and acquired immunity after experimental infection of white-tailed deer (Odocoileus virginianus) and red deer (Cervus elaphus elaphus). J Parasitol 90: 245–254, 2004 CrossRefMedlineOrder article via Infotrieve5.↵ Duncan RB Jr, Patton SDuncan RB Jr, Patton S: Naturally occurring cerebrospinal parelaphostrongylosis in a heifer. J Vet Diagn Invest 10: 287–291, 1998 FREE Full Text6.↵ Kontrimavichus VL, Delyamure SL, Boev SN
Kothekar VS
Kontrimavichus VL, Delyamure SL, Boev SN: Metastrongyloids of domestic and wild animals. In: Fundamentals of Nematology, ed. Kothekar VS, Vol. 26, pp. 94–156. Oxonian Press, New Delhi, 1985 7.↵ Lankester MW
Samuel WM, Pybus MJ, Kocan AA
Lankester MW: Extrapulmonary lungworms of cervids. In: Parasitic Diseases of Wild Mammals, ed. Samuel WM, Pybus MJ, Kocan AA, pp. 228–278. Iowa State University Press, Ames, Iowa, 2001 8.↵ Lankester MW, Fong DLankester MW, Fong D: Distribution of elaphostrongyline nematodes (Metastrongyloidea: Protostrongylidae) in Cervidae and possible effects of moving Rangifer spp. into and within North America. Alces 25: 133–145, 1989 9.↵ Lester GLester G: Parasitic encephalomyelitis in horses. Compend Contin Educ Prac Vet 14: 1624–1630, 1992 10.↵ Samuel WM, Pybus MJ, Welch DA, Wilke CJSamuel WM, Pybus MJ, Welch DA, Wilke CJ: Elk as a potential host for meningeal worm: implications for translocation. J Wildl Manage 56: 629–639, 1992 CrossRef11.↵ Van Biervliet J, de Lahunta A, Ennulat D, Oglesbee M, Summers BVan Biervliet J, de Lahunta A, Ennulat D, Oglesbee M, Summers B: Acquired cervical scoliosis in six horses associated with dorsal grey column chronic myelitis. Equine Vet J 35: 86–92, 2003 MedlineOrder article via InfotrieveWeb of Science12.↵ Yamini B, Baker JC, Stromberg PC, Garndiner CHYamini B, Baker JC, Stromberg PC, Garndiner CH: Cerebrospinal nematodiasis and vertebral chonDrO-dysplasia in a calf. J Vet Diagn Invest 9: 451–454, 1997 FREE Full TextCiteULikeComploreConnoteaDel.icio.usDiggRedditTechnoratiTwitterWhat's this?

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Molecular Confirmation of Parelaphostrongylus tenuis Infection in a Horse With Verminous Encephalitis
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Veterinary Pathology January 1, 2007 vol. 44 no. 1 119-122
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Moderator:
DrO

Posted on Monday, Feb 14, 2011 - 7:18 pm:

I saw two horses struck by lightening last year Vicki. If it worries you, you should seperate them but currently this appears to be quite rare with the only report that I know of the one you post above.
DrO
Moderator:
DrO

Posted on Monday, Feb 14, 2011 - 7:25 pm:

Ohhh that is not right you still don't need to separate the camelids. The alpaca and llama are aberrant hosts and the life cycle is not completed in them so therefore not a risk to your horses: it is the deer that are the problem.
DrO
Member:
vickiann

Posted on Monday, Feb 14, 2011 - 7:29 pm:

I am not saying that it is not rare but veterinarians apparently seem to think that this may be an emerging problem.

This is not just about one horse as there have been more cases than that with more than one presentation.

It is not just about separating llamas and horses but deer and horses.
Member:
vickiann

Posted on Monday, Feb 14, 2011 - 7:31 pm:

Apparently we were cross posting.
Moderator:
DrO

Posted on Tuesday, Feb 15, 2011 - 7:18 pm:

Hello Vicki,
The most relevant item that fits the facts as I know them that I can find in your above posting seems to me to be:
Cattle are thought to be largely resistant to infection,7 with disease reported only rarely.5, 12 Horses might be similarly resistant because parasitic neurologic disease is rare in spite of extensive pasture overlap with infected white-tailed deer. For example, prevalence of P. tenuis in white-tailed deer is reported to be as high as 86%,1 and would presumably provide ample opportunities for parasite exposure. The low incidence of infection in horses likely reflects the evolution of protostrongylid nematodes in ungulate hosts. The mechanism of resistance to P. tenuis infection in horses is unknown. It may be caused by differences associated with acidic pH around 6 of a simple stomach of grazing horses, differences in grazing habits that prohibit ingestion of L3, or differences in the horse immune response.11 It is typically regarded that less compatible hosts result in poor or failed reproduction by P. tenuis.

I wonder if the case in the Arab foal above could be related to a possible immunodeficiency an inherited problem of Arabs. I have the utmost respect for Tommy Divers knowing him personally from my Alma Mater Georgia and attending some of his infectious disease lectures. If Tommy considers this an emerging disease my ears prick up but I don't personally see the facts behind this yet. After all he was also one of the authors responsible for the "the horse resistant" statement I quote above.
DrO
Member:
vickiann

Posted on Tuesday, Feb 15, 2011 - 7:50 pm:

Interesting. Thanks, Dr. O.

Just something for us all to be aware of and apparently some llama owners dose with Ivermectin every 30 days to control this problem but of course that may also cause more resistant strains?

Some of us who keep horses seem to have bad luck with our horses experiencing every possible problem imaginable no matter how hard we try to practice good management so we get a bit paranoid.

Probably it is best to discourage deer from frequenting our horse pastures for any number of reasons? Or would you not worry about that at all?
Moderator:
DrO

Posted on Wednesday, Feb 16, 2011 - 7:16 am:

Deer do visit my pastures and I don't worry about P. tenuis at all. If you believe this is a problem for your horses however you will need to put up very tall fences, 8 feet or higher may be required.

Mary, I am still interested in what your horses clinical signs were and what specific tests were run.
DrO
Member:
vickiann

Posted on Wednesday, Feb 16, 2011 - 5:17 pm:

I would probably worry more about black legged or deer ticks than P. Tenuis.

When I had Lance in North Carolina last trip there were deer in his pasture area frequently.

He had a black legged tick sucking on his neck just before we came home and within about 12 days or so he became very ill with what we believe was ehrliciosis. He had all the symptoms of EIA and it was a very long recovery period.
New Member:
mdelton

Posted on Friday, Feb 18, 2011 - 11:38 am:

Dr O,

I'll try to keep it short. Here goes:

Horse (3 yr old 3/4 connemara 1/4 TB) was "normal" and had been started under saddle. I bred this horse and the only time he was off the farm was to go to an in-hand breed show in Aug 09 and to the Adirondacks for a trail ride over Labor Day 09.

Towards the end of Sept, noticed he was walking with a bit of a side-to-side swagger but we thought it was because he was a 7/9 BCS. Thru Oct &Nov, I noticed he moved his hind legs very wide when he walked. He didn't trot much but I figured it was the hard ground.. He also started spooking which was unusual for him so I thought maybe there was an eye problem.

Dec 1 '09 - He had lots of trouble standing on 3 feet for the blacksmith...very unusual. I decided that there really was something wrong so had the vet out. Soon as she saw him, she said it was neurological and I'd better get him to Cornell. Her comments were "sways while standing and walks with hypermretric gait in all four limbs".

We started him on Marquis that day and took blood for EPM test. Took him to Cornell 12/11/09 (had to wait for a safe travel day) . Took 40 min to load him because he kept leaning to the left when he walked and he'd sort of lose balance and scare himself. At Cornell, they kept him on double dose of Marquis for the next 3 weeks while more tests were done.

CBC - all levels within normal range except that AST was low (at 208 on 12/14/10 and 158 U/L on 12/23/10 where normal low limit is 212 U/L. Also phosphate was 6.6 mg/dL on 12/14/10 and 2.9 on 12/23/10 where normal is 2.1 - 4.7 mg/dL

No parasites seen in hematology.


CT scan - no abnormality detected, pre-contrast and post-contrast.

Spinal fluid was taken and showed Total protein of 26 mg/dL, RBC of 5 cells/uL, and 2 nucleated cells/uL, eosinophiles were seen and I was told that was indicative of a parasite infection; i.e. possible abberant migration to cerebellum.

He was tested for EPM (from CSF, S.neurona and N. hughesii), Encephalomy, WNV, and all tests (some by 2 different methods) were neg. Fecal showed strongyles.

He was given Vit E, mannitol, DMSO, TMZ's, dexamethasone. gastrogard. thiamine, furosemide, panacur, flunixin during his 4 week stay.

The conclusion was that he had a lesion in the cerebellum that was not detectable by CT scan and that it was probably due to migration of a parasite to the brain. I was told that the likely suspects were strongyle or P. Tenuis.

Horse was able to walk, get up and down, and was not dangerous so we did not euthanize. Since he's been home, he has either truly improved or has learned to deal well with his problem. He walks better and trots, canters, bucks, rears and does not fall down. However, he will at times still list to the left when moving.

One other problem this horse has which probably is not related but... he is very sensitive to bug bites and his belly, chest, mane get raw during the summer. I have tried everything to address this problem (certainly everything I have read on this board) and can't seem to keep it from getting worse. It's gotten worse every year and his skin gets quite thickened. I mention this because he is always itching his belly on the ground and has open sores that could be an entry point for parasites.

If I've missed anything you want to know, let me know.

Mary
Member:
mdelton

Posted on Monday, Feb 21, 2011 - 12:20 pm:

Vicki,

The article you posted about the 6 month old Arabian horse which was necropsied is certainly one of the reasons Cornell suspected a similar diagnosis with my horse.

There are a couple of symptoms I forgot to mention that we noticed before we realized that my horse was neurological.

One was that he became very wary of anything approaching him from the front, particularly at eye level. If you bent down and approached him, he was much better but if you walked towards him, he would move back quickly. He hadn't behaved like this previously.

He also had head tremors which have subsided now but if he sees something and focuses on it in the distance, sometimes his whole body will tremor.

I mentioned his spookiness whereas in the past, he would walk by something and want to go see it but now he would scoot away from it. He was particularly bad about things coming up behind him to. The eye specialist vet at Cornell thought he had lost some caudal vision. Again, this has improved since he's been home.

I turn him out with my other geldings and he can take care of himself. I also hand walk him in the indoor and walk him over poles on the ground or a small cross rail. He will jump it sometimes. I hand walk him along the road and he's fine with cars going by. He has the most trouble walking downhill and when he's turned out, he has to go down a slight hill and he still lists to the left whether he walks, trots, or canters although I think he's slightly straightet at the canter.

I inquired of the New Bolton vet when she gave her lecture about neurological problems if she knew of any horses that completely recovered. She said that most don't, (the worst ones are put down) but the improvement you will see occurs in the first 36 months and then they seem to stay the same. So I have till April 2001 to see if my horse improves any more. I'm still hopeful.
Member:
vickiann

Posted on Monday, Feb 21, 2011 - 5:58 pm:

Thanks for sharing that interesting information Mary.

I hope that you will continue to see improvement with your horse.
Moderator:
DrO

Posted on Monday, Feb 21, 2011 - 6:26 pm:

Excellent history MD and I have little to add. It appears that we will have to wait for a definitive diagnosis and I hope we have to wait a good long time. Good Luck and keep us updated.
DrO
Member:
mdelton

Posted on Wednesday, Feb 23, 2011 - 12:40 pm:

Dr. O and Vicki,

Thank you for your good wishes for my horse. I see I made some typos in my post but you read it correctly .

Mary
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