What Is Your Diagnosis?

Allison B. Ward Department of Clinical Sciences, College of Veterinary Medicine, Kansas State University, Manhattan, KS 66506.

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 DVM
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Johnny R. Cross Neurology Section, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104.

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 DVM, DACVIM
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Eric N. Glass Neurology and Neurosurgery, Red Bank Veterinary Hospital, 197 Hance Ave, Tinton Falls, NJ 07724.

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 MS, DVM, DACVIM
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Alexander de Lahunta Department of Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.

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 DVM, PhD, DACVIM, DACVP

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History

A 5-year-old spayed female Yorkshire Terrier was referred for evaluation because of acute onset of left-sided epistaxis, hypersalivation, and neurologic signs following a 2-week history of nonproductive sneezing. On neurologic examination, the dog had a dull mentation and was circling to the left and falling to the right. Loss of facial sensation was evident. Pupil size and light responses were normal. The menace response was absent on the right. The dog had ventrolateral strabismus in the left eye and slow postural reaction responses on the right thoracic limb and right hind limb. On the basis of neurologic examination findings, lesion localization was multifocal intracranial with a left prosencephalic component.

Blood gas values and results of a coagulation profile and serum biochemical analysis were within reference limits. A CBC revealed leukocytosis (23.7 × 103 WBCs/μL; reference range, 5.3 × 103 WBCs/μL to 19.8 × 103 WBCs/μL) with mature neutrophilia (22,000 neutrophils/μL). No improvement was noticed with 3 days of treatment with metronidazole, doxycycline, ondansetron, hetastarch, hypertonic saline (7% NaCl) solution, mannitol, and a lactulose enema.

On day 4 of hospitalization, a CSF sample was obtained from the cerebellomedullary cistern. Cytologic evaluation revealed a high nucleated cell count (86 cells/μL; reference range, 0 to 5 cells/μL) and high RBC count (564 RBCs/μL; reference limit, 0 RBCs/μL). The cellular composition consisted of a mononuclear pleocytosis with 18% nondegenerative neutrophils, 40% lymphocytes, 34% large monocytes, and 8% eosinophils. The protein concentration was high at 189 mg/dL (reference range, 10 to 40 mg/dL). Magnetic resonance imaging of the brain was performed (Figure 1).

Figure 1—
Figure 1—

Dorsal T2-weighted (A), dorsal T1-weighted (B), postcontrast dorsal T1-weighted (C), and transverse gradient echo (D) MRI images of the brain of a 5-year-old female spayed Yorkshire Terrier that had had a 2-week history of nonproductive sneezing and was evaluated because of acute onset of left-sided epistaxis, hypersalivation, and neurologic signs. Echo time, repetition time, and spin echo, respectively, were as follows: panel A, 89.4 ms, 3,517 ms, and 3.0 mm/3.5 mm; panel B, 11.0 ms, 500 ms, and 3.0 mm/3.5 mm; panel C, 14.0 ms, 500 ms, and 3.0 mm/3.5 mm; and panel D, 17.0 ms, 500 ms, and 3.0 mm/3.5 mm.

Citation: Journal of the American Veterinary Medical Association 241, 6; 10.2460/javma.241.6.693

Determine whether additional imaging studies are required, or make your diagnosis from Figure 1then turn the page

Diagnostic Findings and Interpretation

Magnetic resonance imaging of the brain was performed with a 1.5-T magnet. Sagittal (T1-weighted before and after administration of gadolinium dimeglumine at a dose of 0.1 mmol/kg [0.045 mmol/lb], IV), transverse (T2-weighted, fluid attenuated inversion recovery, diffusion-weighted, gradient echo, and apparent diffusion coefficient), and dorsal (T2-weighted and T1-weighted before and after gadolinium dimeglumine administration) plane images of the brain were obtained.

A single, tract-like lesion is seen from the left nasal cavity extending caudally through the cribriform plate, left olfactory bulb, left frontal lobe, ventral temporal lobe, and left occipital lobe (Figure 2). The lesion involves the caudate nucleus, hippocampus, internal capsule, and external capsule. The continuity of the lesion is most easily seen in the dorsal plane T2-weighted images, and it has heterogenous hyperintensity on T2-weighted images and predominantly isointensity with small hyperintense foci on T1-weighted images. Extensive areas within and around the tract lesion that are hypointense on T1-weighted images, are hyperintense on T2-weighted images, and do not suppress on fluid attenuation inversion recovery sequences (data not shown) are considered most consistent with vasogenic edema. Areas of hyperintensity on both T1- and T2-weighted images most likely indicate the subacute (1 to 6 weeks' duration) degradation of blood products or protein and thus a breakdown of the blood-brain barrier and inflammation. Similarly, the mild heterogenous contrast enhancement seen throughout the lesion also suggests a disruption of the blood-brain barrier integrity or increased local blood flow and thus inflammation. Gradient echo sequences reveal a susceptibility artifact supportive of multifocal areas of chronic hemorrhage within the lesion extending from the nasal cavity to the occipital lobe (dorsal plane images not provided).

Figure 2—
Figure 2—

Same MRI images as in Figure 1. A—A continuous heterogenously hyperintense lesion can be seen from the left nasal turbinates to the left occipital lobe (white arrows). B—Areas of hyperintensity (white arrows) can be seen. C—Multifocal areas of heterogenous contrast enhancement can be seen within the tract lesion (white arrows). D—Notice the signal void (susceptibility artifact) within the lesion (black arrows).

Citation: Journal of the American Veterinary Medical Association 241, 6; 10.2460/javma.241.6.693

A tract lesion extending from the left nasal cavity to the brain strongly suggests parasite migration as the cause of the dog's clinical signs. Although a foreign body migration should be considered, the presence of eosinophils within the CSF makes it less likely. Necrotizing encephalitis, although seen in Yorkshire Terriers, was not considered a differential diagnosis because of the apparent nasal cavity involvement.

Treatment and Outcome

The dog of the present report was treated for intracranial parasitic migration with diphenhydramine (2 mg/kg [0.91 mg/lb], IM) and dexamethasone sodium phosphate (0.3 mg/kg [0.14 mg/lb], IV). Several hours later, ivermectin (400 μg/kg [181.8 μg/lb], SC) was given. Unfortunately, the patient's neurologic status continued to decline, and the dog was euthanized 7 days after initial evaluation. Necropsy revealed a gross discoloration and a softening in the position of the tract seen on MRI. On microscopic examination, the lesion consisted of a hemorrhagic necrosis with an eosinophilic, histiocytic, lymphoplasmacytic inflammation, which is consistent with histopathologic changes in confirmed cases of cerebral cuterebriasis.

Comments

Intracranial parasitic migration has been described in dogs. The most extensive literature involves dogs infected with Cuterebra spp,1 although Baylisascaris procyonis and Alaria spp have been found as well. The life cycles of the latter 2 necessitate ingestion of the organism with migration through other host tissues, including the gastrointestinal tract and the lungs. In the dog of the present report, the lack of clinical signs associated with pulmonary or gastrointestinal disease, normal findings on thoracic radiography, and lack of lesions in either the lungs or gastrointestinal tract at necropsy made Cuterebra the most likely parasite.

The Cuterebra genus of bot fly comprises > 20 species in North America. Aberrant migration occurs when an accidental host is invaded through a natural orifice. Because the most commonly suspected route of cerebral infection is through the nasal passages, upper respiratory signs precede neurologic signs, as seen in the dog of the present report.

It is theorized that as the larva burrows into brain tissue, toxins from the organism enter the CSF directly or from the parenchyma through damaged ependymal cells. These toxins are likely the cause of vascular necrosis, leading to the regionally extensive inflammation, hemorrhage, and ischemia. Analysis of CSF reveals an inflammatory response with or without eosinophilia. In the dog of the present report, mononuclear pleocytosis with a mild eosinophilic and mild neutrophilic component were most consistent with infectious (eg, fungal, protozoal, and verminous) and noninfectious meningoencephalitides (eg, idiopathic eosinophilic meningoencephalitis) or neoplasia. Advanced imaging in this case helped prioritize the differential diagnoses.

Reported MRI lesions of cerebral myiasis in dogs and humans have been shown to be hypointense to gray matter on T1-weighted images and hyperintense on T2-weighted images with heterogenous contrast enhancement,1–4 as seen in the dog of the present report. A well-visualized migration tract such as that shown here is highly suggestive of parasitic migration.

Although not commonly recognized, intracerebral cuterebriasis should be on the list of differential diagnoses for any canine patient with a multifocal neuroanatomic localization, especially if the neurologic signs are preceded by upper respiratory signs. Advanced imaging is helpful to support this diagnosis. A single, tract-like lesion that extends into the brain through the nasal passages is highly suspicious for Cuterebra migration.

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