JVDI Advertisement
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Journal of Veterinary Diagnostic Investigation Vol. 21 Issue 3, 400-402
Copyright © 2009 by the American Association of Veterinary Laboratory Diagnosticians
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Snook, E. R.
Right arrow Articles by Bauer, R. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Snook, E. R.
Right arrow Articles by Bauer, R. W.

Case Reports

Verminous myelitis in a pit bull puppy

Eric R. Snook1, David G. Baker and Rudy W. Bauer

Correspondence: 1Corresponding Author: Eric R. Snook, Department of Pathobiological Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70803. esnook{at}vetmed.lsu.edu


    Abstract
 TOP
 Sources and manufacturers
 Abstract
 References
 
A 10-week-old, male pit bull dog presented to the referring veterinarian with hind limb paresis and epaxial muscle atrophy. No spinal lesions were identified at gross necropsy; however, histologically there was marked granulomatous myelitis in the spinal cord between T13 and L2 with occasional, intralesional nematode larvae. Based on morphologic characteristics, the nematode larvae were identified as Strongyloides spp., possibly Strongyloides stercoralis.

Key Words: Aberrant parasite migration • larval migration • spinal cord • Strongyloides

A 10-week-old, male pit bull puppy presented to the referring veterinarian with hind limb paresis. Neurologic examination resulted in a neuroanatomic diagnosis of a T13–L2 spinal cord lesion. The animal was euthanized, and a full necropsy was performed. The only abnormalities observed at necropsy were bilateral pale and atrophic longissimus dorsi muscles. Fecal flotation was negative for parasite eggs or larvae. Based on the antemortem localization of the possible spinal cord lesions, representative sections of the spinal cord were trimmed between T12 and L2 and placed in 10% neutral buffered formalin. Tissues were processed routinely, embedded in paraffin, sectioned at 5 µm, and stained with hematoxylin and eosin.

Randomly throughout the gray and white matter of the spinal cord, there were areas of granulomatous inflammation characterized by aggregates of macrophages, multinucleated giant cells, and small numbers of scattered neutrophils. The gray matter was multifocally vacuolated, and the meninges contained small numbers of neutrophils, plasma cells, and lymphocytes. Multifocally throughout the neutropil between T13 and L2, there were occasional sagittal or oblique sections of nematode larvae (Fig. 1). Measurements were taken of several larval sections (Figs. 2, 3). Larvae measured 34.7–54.3 µm wide (mean = 45.4 µm), but because the longitudinal section was incomplete, it was not possible to accurately measure the length of the worm. Examination of sagittal and longitudinal sections revealed platymyarian musculature and an indistinct intestine. In a tangential section of the parasite, the parasite appeared to have a forked tail; however, this may also be sectioning artifact. Based on these morphologic features, the larvae were most consistent with a Strongyloides sp.1,6


Figure 01
View larger version (153K):
[in this window]
[in a new window]

 
Figure 1 View of the spinal cord with 1 longitudinal section and 2 cross-sections of nematodes (arrowheads; 4x). Perivascular lymphohistiocytic inflammation is present near the nematode sections. Bar = 1.0 mm.

 

Figure 02
View larger version (164K):
[in this window]
[in a new window]

 
Figure 2 View of a tangential section of the nematode in the spinal cord (60x). Bar = 100 µm.

 

Figure 03
View larger version (167K):
[in this window]
[in a new window]

 
Figure 3 View of the cross-sections of the nematodes in the spinal cord (60x). Bar = 100 µm.

 
Infective third-stage larvae of some members of the superfamily Rhabditoidae, including Strongyloides spp. and Caenorhabditis elegans, are known to possess tripartite forked tails (Viney ME, Lok JB: 2007, Strongyloides spp. In: WormBook, ed. The C. elegans Research Community. Available at http://www.wormbook.org. Accessed on December 22, 2008).6 Although multiple sections of spinal cord from other regions were examined, nematode larvae were only identified between T13 and L2 (histologically and with a dissection microscope). Small, occasional glial nodules were scattered within the neutropil in decreasing numbers away from the primary lesion.

Aberrant parasite migration to the spinal cord in dogs is rare. Literature searches reveal that most reports are of Spirocerca lupi and Angiostrongylus spp. migration but also include Baylisascaris procyonis8 or Dirofilaria immitis.2 In the current case, the larvae appear to be from the superfamily Rhabditoidae based on histomorphology. Genera of the superfamily Rhabditoidae have been reported to infect the central nervous system of horses and humans. Parasite genera found in this geographic location include Strongyloides and Halicephalobus (syn. Micronema).3 Dogs in the southeast United States are commonly infected with Strongyloides stercoralis. Infection is established when infective third-stage larvae (L3) penetrate the skin or are ingested. If infection occurs by skin penetration, larvae travel via the blood to the lungs where they penetrate the alveoli, travel up the trachea, are swallowed, and mature in the small intestine.10 If infection occurs via ingestion, larvae travel directly to the small intestine, where they mature. Adult parthenogenetic females release embryonated eggs in the host intestine. Eggs hatch, releasing L1, which are passed in the feces and develop into additional infective L3 in the environment. Alternatively, larvae develop into nonparasitic (free-living) adult male and female worms that produce additional free-living generations, or larvae, which develop into infective L3.9 In some cases, however, hatched larvae may remain in the intestine and develop into infective L3. These may penetrate the intestinal mucosa and disseminate to internal organs, a condition known as "hyperinfection." Organs to which L3 may disseminate include those of the central nervous system.7 In immunocompromised humans, dissemination occurs with overwhelming infections.2,8,10

Although spread of Strongyloides in humans is typically secondary to immune compromise, there was no evidence of concurrent disease that may have rendered the pit bull puppy in the present study susceptible to aberrant migration. Bone marrow and lymphoid tissue appeared within normal limits histologically; however, whether the immune cells were functioning correctly in vivo cannot be determined based upon histologic evaluation.GoGoGo


    Acknowledgments
 
The authors are very appreciative to histotechnologists Cheryl Crowder, Hal Halloway, and Kendra Shultz for their technical expertise and invaluable assistance in preparing the numerous serial sections necessary in this case.


    Sources and manufacturers
 TOP
 Sources and manufacturers
 Abstract
 References
 
From the Department of Pathobiological Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA. Back


    References
 TOP
 Sources and manufacturers
 Abstract
 References
 

  1. Chitwood M., Lichtenfels 1972 Parasitological review: identification of parasitic metazoan in tissue sections. Exp Parasitol 32 407 519.[Medline]
  2. Cooley A.J., Clemmons R.M., Gross T.L. 1987 Heartworm disease manifested by encephalomyelitis and myositis in a dog. J Am Vet Med Assoc 190 431 432.[Medline]
  3. Gardiner C.H., Koh D.S., Cardella T.A. 1981 Micronema in man: third fatal infection. Am J Trop Med Hyg 30 586 589.[Abstract/Free Full Text]
  4. Genta R.M., Walzer P.D. 1989 Strongyloidiasis. In: Parasitic infections in the compromised host Genta R.M., Walzer P.D. 463 525 Marcel Dekker New York, NY
  5. Kothary N.N., Muskie J.M., Mathur S.C. 1999 Residents' teaching files: Strongyloides stercoralis hyperinfection. Radiographics 19 1077 1081.[Free Full Text]
  6. Little M.D. 1966 Comparative morphology of six species of Strongyloides (Nematoda) and redefinition of the genus. J Parasitol 52 69 84.[Medline]
  7. Morgello S., Soifer F.M., Lin C.S., Wolfe D.E. 1993 Central nervous system Strongyloides stercoralis in acquired immunodeficiency syndrome: a report of two cases and review of the literature. Acta Neuropathol 86 285 288.[Medline]
  8. Rudmann D.G., Kazacos K.R., Storandt S.T., et al. 1996 Baylisascaris procyonis larva migrans in a puppy: a case report and update for the veterinarian. J Am Anim Hosp Assoc 32 73 76.[Abstract]
  9. Schmidt G.S., Roberts L.S. 1985 Order Rhabditata: pioneering parasites. In: Foundations of parasitology, 3rd ed. 463 468 Times Mirror/Mosby College Publishing St. Louis, MO
  10. Walker M.D., Zunt J.R. 2005 Neuroparasitic infections: Nematodes. Semin Neurol 25 252 261.[Medline]




This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Snook, E. R.
Right arrow Articles by Bauer, R. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Snook, E. R.
Right arrow Articles by Bauer, R. W.


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS