History

A 1-year-old male neutered domestic shorthair cat was evaluated for acute development of circling and dull mentation. One week prior, the patient was seen by a referring veterinarian for these clinical signs and treated with clindamycin (12.5 mg/kg, PO, q 12 h) for possible toxoplasmosis. The patient clinically improved initially, then declined again 2 days before presentation. Prior to acute development of neurologic signs, the patient had no known medical history, was current on vaccines, and was historically an indoor-outdoor cat.

On presentation, the patient was ambulatory with a left-sided hemiparesis, left-sided proprioceptive deficits, blindness in the left eye, absent left menace response with intact direct and consensual pupillary light reflexes oculus uterque (OU), compulsive circling to the right, and dull mentation. General physical examination revealed the patient to be 5% dehydrated with pale mucous membranes, bradycardia, and moderate hypotension.

Assessment

Diagnostic Plan

A CBC and serum chemistry profile were performed to obtain a baseline of the patient’s hematologic status and identify evidence of systemic disease. Blood pressure monitoring was performed to monitor hypotension and response to therapy. Thoracic radiographs were obtained to rule out thoracic disease (metastasis, lymphadenopathy, or infection). Brain MRI followed by CSF analysis was completed in attempt to connect the patient’s neurologic deficits with a specific neurologic lesion.

Diagnostic Test Findings

Results of the CBC, serum chemistry panel, and thoracic radiographs were unremarkable. Brain MRI was performed with a 1.5-T unit (Vantage Atlas 1.5-T MR Scanner; Toshiba America Medical Systems Inc). Precontrast imaging sequences (sagittal T2-weighted, transverse T2-weighted, T2 FLAIR, T2*, T1-weighted, diffusion weighted imaging) and postcontrast imaging sequences (T1-weighted images in the sagittal, transverse, and dorsal planes) were obtained.

Magnetic resonance imaging revealed a T2-weighted and FLAIR hyperintense, T1-weighted hypointense L-shaped linear track within the brain parenchyma extending from the right frontal lobe immediately adjacent to the cribriform plate cranially to the right caudate nucleus caudally, then turning left and continuing through the thalamus into the left temporal lobe. Surrounding the primary lesion was poorly defined, wispy T2-weighted and FLAIR hyperintensity affecting primarily the white matter consistent with edema. Following administration of 1.1 mL of gadoteridol, IV (gadolinium-based contrast agent), the track was moderately ring contrast enhancing with a central hypointense region. The meninges along the right frontal lobe were mildly thick and moderately contrast enhancing. Within the right caudal nasal cavity, there was a focal region of contrast enhancement with a small amount of fluid present (Figure 1).

View Full Size

Sagittal (A), dorsal (B), and axial (C) postcontrast T1-weighted images of the brain. A linear L-shaped hypointense lesion with a strong contrast-enhancing rim is seen extending from the right frontal lobe cranially to the right caudate nucleus caudally, then turning left and continuing across the thalamus into the left temporal lobe (filled white arrows), suggestive of a migrating Cuterebra larval tract. There is also focal meningeal enhancement adjacent to the right frontal lobe (white arrowhead) and a focal region of fluid accumulation and contrast enhancement within the right caudal nasal cavity (asterisk). Axial T2-weighted (D) and FLAIR (E) images show poorly defined, perilesional hyperintensity affecting primarily the white matter (open arrows), consistent with edema.

Citation: Journal of the American Veterinary Medical Association 261, 6; 10.2460/javma.22.10.0465

• Download Figure
• Download figure as PowerPoint slide

Cerebrospinal fluid collected from the cerebellomedullary cistern revealed an elevated protein concentration (28 mg/dL; reference rage, < 25 mg/dL) and a high normal nucleated cell count (4 cells/µL; reference range, < 5 cells/µL). Cytology revealed approximately 11% eosinophils, 2% medium mononuclear cells, and 87% small lymphocytes; no infectious organisms were identified. The mild inflammation and eosinophils identified on CSF cytology in conjunction with the MRI findings were most consistent with a clinical diagnosis of verminous encephalopathy caused by aberrant Cuterebra larval migration.

Treatment

Initial treatment in the hospital included placement of an IV catheter, fluid therapy (lactated Ringer solution, 10 mL/kg, IV bolus followed by continuous maintenance rate of 60 mL/kg/d, IV), and maropitant (1 mg/kg, IV, q 24 h). Following diagnosis of CNS Cuterebra larval migration, treatment with ivermectin (0.4 mg/kg, SC, q 24 h for 3 days) was initiated along with ampicillin/sulbactam (50 mg/kg, IV, q 6 h) and enrofloxacin (5 mg/kg, IV, once); enrofloxacin treatment was discontinued after the initial dose due to lack of clear indication. Dexamethasone sodium phosphate (0.11 mg/kg, IV, q 24 h) and diphenhydramine (4 mg/kg, IM, q 24 h prior to each dose of ivermectin) were administered to mitigate inflammatory reactions associated with parasite death. On day 5 of hospitalization, the patient remained stable and IV medications were discontinued; the patient was transitioned to PO medications, which were continued at home following discharge on day 6. These medications included amoxicillin/clavulanate (13.3 mg/kg, PO, q 12 h) continued for 2 months and methylprednisolone (0.64 mg/kg, PO, q 24 h) for 2 weeks, which was abruptly discontinued by the owner.

One month after discharge, the patient returned for recheck evaluation. Per owners, the patient was doing well at home aside from intermittent urination outside of his litter box and sporadic left forelimb weakness. Recheck neurologic exam revealed absent left-sided menace, intermittent inappropriate left foot placement when sitting, and persistent but improved left-sided postural reaction delays. All other neurological assessments were normal. Phone communication with owner 24-months after diagnosis revealed the patient is doing well at home.

Comments

Reports of aberrant Cuterebra larval migration to the CNS are sporadic in the veterinary literature.¹ Most cases of small mammal cuterebriasis describe infestations localized to skin and subcutaneous tissues during summer months (June through September), when Cuterebra larvae migrate through host tissue; however, aberrant larval migration has been reported in the pharynx, eye, thorax, and cribriform plate.^1–3 Neurological manifestation of CNS Cuterebra larval migration is often acute, severe, and rapidly progressive.^1–4 While the condition is reported in dogs, cats are the most commonly affected species within the veterinary population. Affected cats are typically young to middle-age with access to the outdoors and, depending on the path of brain migration, may display a variety of clinical signs such as status epilepticus, blindness, head pressing, anorexia, circling, abnormal mentation, postural reaction deficits, abnormal gait, and cranial nerve deficits.^1–3 In addition to the development of neurologic signs, many patients also have a recent history of upper respiratory tract disease likely reflecting Cuterebra migration from the nasal passage through the cribriform plate prior to burrowing through brain parenchyma.^2–4

To the authors’ knowledge, there have been a total of only 6 reported cases of aberrant Cuterebra CNS migration in dogs, but > 20 cases in cats.^1–4 Of the 6 cases in the veterinary literature that discuss this disease in dogs, only 1 survived the acute disease phase, but it required chronic management with anti-epileptic drugs to control persistent cluster seizures.¹ In general, affected cats appear to have a better prognosis than dogs; however, prognosis remains guarded to poor in most cases.¹

Definitive antemortem diagnosis of CNS cuterebriasis requires craniectomy followed by parasite identification and surgical extraction. Although reportedly attempted in 1 dog, the migrating tract and larvae were unidentified.¹ Given the invasiveness and risk of surgery, presumptive diagnosis is typically made via blood work, brain MRI, and CSF analysis.^1–4 Blood work commonly reveals a peripheral leukocytosis with eosinophilia and hyperglobulinemia consistent with parasitic or allergic disease and systemic inflammation, respectively.^2,3 Brain MRI and CSF analysis are considered high-yield diagnostics, as brain imaging often reveals the migrating Cuterebra larval track as well as secondary changes (inflammation, edema, and hemorrhage), which, combined with eosinophilic pleocytosis in CSF, is consistent with verminous encephalopathy.^1,2,

Optimal treatment of CNS cuterebriasis has yet to be determined; however, various medical management protocols have been associated with successful outcomes.^1–3 The majority of case reports involving feline cerebral cuterebriasis suggest ivermectin as the therapy of choice, and various dosages have been reported, including 0.2 mg/kg, SQ, once; 0.3 mg/kg, SQ, q 48 h for 3 treatments; 0.3 mg/kg, PO, q 14 d for 2 treatments; or 0.4 mg/kg, SQ, q 24 h for 3 treatments.^1–3 Simultaneous administration of anti-inflammatory corticosteroids, antihistamines, and/or antibiotics has also been recommended to prevent inflammatory or hypersensitivity reactions and treat infection secondary to larval migration.^1–3

In summary, CNS cuterebriasis represents a neurologic disease more common in cats than dogs, resulting in presentation during summer months with acute onset and often asymmetric, focal or multifocal, intracranial signs preceded by upper respiratory disease.³ Prognosis is overall guarded, but early diagnosis and treatment may lead to complete recovery or at least an acceptable long-term quality of life.³