History

A 9-year-old spayed female miniature Dachshund dog was presented in August 2020 for evaluation of a 10-day history of reverse sneezing followed by development of unilateral epistaxis and acute-onset seizures. The dog had otherwise been healthy, with no previous neurological issues.

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Approximately 10 days before presentation, the dog began reverse sneezing multiple times per day. Signs remained consistent for 9 days, until 24 hours before presentation, when the patient developed unilateral epistaxis from her left naris. She was brought to her family veterinarian on the morning of presentation, where she had a generalized tonic-clonic seizure lasting approximately 1 minute, with autonomic signs. She was administered a sustained-release cefovecin sodium (Convenia; 8 mg/Kg, SC, once) as well as an anti-inflammatory dose of prednisone (0.5 mg/Kg, PO, q 24 h for 5 days) before being discharged to the care of her owners. Following discharge, the dog had a second generalized tonic-clonic seizure at home approximately 3 hours later.

She was subsequently presented to the emergency service at our referral hospital for further evaluation. On presentation, the patient was sneezing during physical examination, with mild unilateral epistaxis from the left naris.

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Assessment

Diagnostic test findings

Serum biochemistry revealed a mild increase in liver enzymes, with an ALP of 157 U/L (reference range, 22 to 143 U/L) and ALT of 110 U/L (reference range, 19 to 107 U/L). A CBC and thoracic radiographs were unremarkable.

The dog underwent general anesthesia for a head MRI, and various image sequences were obtained as follows: T2-weighted dorsal, sagittal, and transverse planes; transverse sections FLAIR; T2* GRE; STIR, diffusion-weighted imaging, and apparent diffusion coefficient map; T1-weighted pre- and postcontrast (IV gadolinium) planes (1.5-T MRI; Signa Explorer software, version 25.1; General Electric Medical Systems) of the dog’s head was performed (Figure 1). The MRI revealed bilateral T2-hyperintense, contrast-enhancing epithelium in the nasal passages, consistent with bilateral rhinitis, as well as a poorly defined hypointense structure (roughly 8.4 X 5.4 X 20 mm) in the left nasal passage (Figure 2). There was also moderate T2 hyperintensity predominantly affecting the gray matter of the right olfactory and frontal lobe, with associated mild left-sided midline shift. Moderate leptomeningeal contrast enhancement was also seen affecting the rostral half of the brain, worse on the right. Cerebrospinal fluid analysis was performed, which revealed a predominance of nondegenerate neutrophils, but a normal cell and protein count. To further investigate the T2-hypointense structure in the left nasal passage, rhinoscopy was also performed while the patient was anesthetized. A Cuterebra larva was removed when scoping the left nasal passage. This was later molecularly identified as a Cuterebra cf abdominalis larva (522 bp; GenBank Accession No. OQ352274) via PCR and sequencing targeting the partial cytochrome oxidase c subunit 2 of the mitochondrial DNA. Based on these diagnostic results, the working diagnosis was nasal cuterebriasis with associated meningoencephalitis, suspected to be secondary to aberrant larval migration.

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A—Sagittal T2-weighted (T2W) image of the head, with visible T2W hyperintensity of the frontal and olfactory lobes. B—Transverse T2W image of the brain at the level of the frontal and olfactory lobes. Moderate T2W hyperintensity predominantly affecting the gray matter of the frontal and olfactory lobes, most prominent on the right, can be seen. A mild left midline shift is also present. C—T2W FLAIR sequence, with similar hyperintensity affecting the frontal and olfactory lobes, lateralized to the right. D—Transverse T1-weighted and contrast image showing moderate leptomeningeal contrast enhancement affecting the rostral portion of the brain, lateralized to the right.

Citation: Journal of the American Veterinary Medical Association 261, 7; 10.2460/javma.23.02.0079

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A—Dorsal T2W image showing the poorly defined, T2W hypointense material against the lateral wall of the left nasal passage. B—Transverse T2W image also demonstrating the suspected foreign material in the left nasal passage. Inset—Cuterebra cf abdominalis larva obtained from rhinoscopy of the left nasal passage.

Citation: Journal of the American Veterinary Medical Association 261, 7; 10.2460/javma.23.02.0079

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Comments

Reported cases of canine cerebral cuterebriasis are limited; therefore, treatment options were considered based on a review of feline cases by James and Poma.¹ Treatment with ivermectin was initiated at a dose of 0.4 mg/kg, SC, every 24 hours for a total of 3 days. Dexamethasone was also administered at a dose of 0.1 mg/kg, IV, every 24 hours to reduce an inflammatory response during treatment. Diphenhydramine was administered at 4 mg/kg, IM, roughly 1 to 2 hours before each ivermectin dose to reduce the risk of type I hypersensitivity-like reaction that had been previously reported.^2–4 Antiseizure treatment with phenobarbital at a maintenance dose of 3 mg/kg by mouth every 12 hours had also been initiated on admission. Antibiotic treatment was not prescribed, as the patient received sustained-release cefovecin sodium before the referral. The dog continued to do well in the hospital and was discharged to the care of her owners on phenobarbital, and on prednisone (approx 1 mg/kg, PO, q 24 h), to return for a recheck 2 weeks later. A serum biochemistry repeated at discharge revealed a worsened increase in liver enzymes, with an ALP of 795 U/L (reference range, 22 to 143 U/L) and ALT of 487 (reference range, 19 to 107 U/L) as well as a mild hypoalbuminemia of 21 g/L (reference range, 29 to 43 U/L) and elevated creatinine kinase of 1,249 U/L (reference range, 40 to 255 U/L).

At recheck, the patient’s neurological signs were noted to have progressed. On presentation, she was dull, but responsive. She had a mild right head turn and had a tendency to walk in wide circles to the right, with occasional circling to the left. Her left nasal septum response had returned; however, she now had bilaterally delayed hopping in the pelvic limbs. There was a marked pain response on palpation of the cervical spine as well as vocalization when moving her head to the left or right. Based on this, multifocal lesions were suspected, affecting the right thalamocortex and cervical region. Analgesic medications were started (fentanyl [2 to 6 μg/kg/h, continuous rate infusion] and gabapentin [10 mg/kg, PO, q 8 h]) and the patient was hospitalized. Following initiation of treatment with opioids, the dog’s mentation worsened. By that evening, she was very dull with reduced responses to stimuli. She was nonambulatory, her menace response was weak, and her nasal septum response was absent bilaterally. Proprioception could not be reliably assessed, and she had a marked pain response diffusely on cervical palpation. The worsening of her neurological condition during the hospitalization could be related to the analgesic medications; however, progression of an underlying disease couldn’t be excluded.

A CBC and serum biochemistry were repeated and revealed an improvement in liver enzymes, with an ALP of 261 U/L (reference range, 22 to 143 U/L), GGT of 33 U/L (reference range, 0 to 7 U/L), and ALT of 212 U/L (reference range, 19 to 107 U/L), but were otherwise unremarkable. Repeat brain MRI revealed mildly improved bilateral rhinitis. There was also similar meningoencephalitis mostly affecting the right olfactory and frontal lobes, with new mild distension of the third ventricle. The previously noted midline shift was no longer present. In the cervical spine, there was a mild protrusion of the C2-C3 intervertebral disk, along with multifocal intervertebral disk degeneration, but no other abnormalities seen. Cerebrospinal fluid analysis was difficult to interpret due to iatrogenic hemorrhage (RBCs, 200,000 X 10₉/L), the cell count was increased at 0.2 X 10₉/L, and the protein count was elevated at 0.96 g/L (reference range, < 0.45 g/L). However, we interpreted those values with caution per the severe iatrogenic hemorrhage. The CSF was also submitted for aerobic and anaerobic culture; however, there was no growth. Based on the progression of the neurological signs and evidence of persistent meningoencephalitis on MRI, a bacterial meningoencephalitis secondary to aberrant Cuterebra larval migration was suspected. A case series by Radaelli and Platt⁵ reported that only 1 of 8 of cases with bacterial meningoencephalomyelitis had positive CSF culture results, and 1 case showed bacterial growth in a blood culture (1/3 cases); therefore, it was not unexpected to find a negative culture in our case. Prognosis for dogs with bacterial meningitis is relatively unclear given very limited literature. In the same case series, a survival time of 0 to 42 days was reported. However, given the fact that only dogs with histopathologically confirmed bacterial meningitis were included, only dogs who underwent postmortem examination were selected. Regardless, the prognosis for dogs with bacterial meningitis is generally considered to be poor. The patient was started on ampicillin (22 mg/kg, IV, q 6 h) and enrofloxacin (10 mg/kg, IV, q 24 h) with hypertonic saline or mannitol to be administered as needed in case of signs of elevated intracranial pressure. After 48 hours, the dog was transitioned onto clindamycin (11 mg/kg, IV, q 12 h) after limited response to treatment to adjust antibiotic coverage. The dog was also weaned off opioids and started on acetaminophen (approx 15 mg/kg, PO, q 8 h). The patient’s mentation steadily improved. By 48 hours later, the patient was quiet but responsive, was ambulatory with a low head carriage, and was no longer circling or getting stuck in corners.

Based on progress at follow-up, corticosteroid administration was discontinued after 2 weeks, with the clindamycin and enrofloxacin continued for 6 months, until the patient’s neurological signs had plateaued. By this time, the patient had a normal mentation, though the owners noted that there were some persistent behavioral changes at home. In particular the dog no longer responded to previous commands, had occasional episodes of staring into space, and appeared to bark and whine more than previously. Phenobarbital administration was continued for 12 months following initiation, before being discontinued. At 1-year phone follow-up, no further seizures had occurred since discontinuation.