Abstract
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.
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 mm 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
View of the spinal cord with 1 longitudinal section and 2 cross-sections of nematodes (arrowheads; 4×). Perivascular lymphohistiocytic inflammation is present near the nematode sections. Bar = 1.0 mm.
View of a tangential section of the nematode in the spinal cord (60×). Bar = 100 μm.
View of the cross-sections of the nematodes in the spinal cord (60×). 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 procyonis 8 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.
Acknowledgements. 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.