Cuterebral myiasis / Feline ischemic encephalopathy
Feline ischemic encephalopathy (FIE) was first described by Dr. Alexander de Lahunta in the 1970s. Affected cats had an acute onset of clinical signs related to forebrain dysfunction and necropsy of affected cats revealed gross and histologic signs of vasculitis and thrombosis of the middle cerebral artery. Several years later, histologic analysis of some affected cats revealed Cuterebra larvae body parts in the area of the middle cerebral artery.
Cuterebra are bot flies that are found most commonly in the eastern United States. The flies lay their eggs near rabbit and other small rodent burrows in the spring and early summer. The eggs hatch with the warmth of the passing rabbit/rodent and the first instar larva attaches to the fur of a passing animal. The larva enters the rabbit/rodent via a body orifice (e.g., mouth, nose), penetrates the mucosa, and then migrate through the subcutaneous tissues to the skin. Here, the larvae molt into a second instar and then third instar larva. The third instar larva creates localized swelling, and a breathing hole may be visible in the skin. It emerges from the skin in the Fall and becomes a pupa to overwinter. The adult fly emerges the following spring.
Cats become parasitized by sniffing around animal burrows. The larvae can pass through the life cycle as above, but they can also stay within the nasal cavity or migrate to other tissues, such as the brain, spinal cord (rare), eyes, and oral cavity. The theory for intracranial cuterebral myiasis is that the larvae migrate into the brain through the cribriform plate (or possibly ear canal) into the subarachnoid space or brain parenchyma. Five characteristic histologic changes have been reported in the brain of affected cats, including parasitic tracks, superficial laminar cerebrocortical necrosis, cerebral infarction, subependymal rarefaction and astrogliosis, and subpial astrogliosis. Many of these lesions are not associated with the parasitic tracks leading to the theory that the larvae secrete a toxic substance into the CSF that damages that parenchyma. This presumptive toxin may normally facilitate the passage of the larvae through the subcutaneous tissues during their migration. Vasculitis and thrombosis are less common, and cerebral infarction may be the result of vasospasm of the middle cerebral artery secondary to this presumptive toxin or subarachnoid hemorrhage.
The clinical signs of FIE occur only in outdoor cats, primarily in the late Summer or early Fall months when the Cuterebra eggs hatch. Clinical signs are often asymmetrical in nature. The most common clinical signs are mental dullness, cortical blindness, and behavior changes, but other reported signs include seizures, contralateral weakness and non-neurological signs (e.g., sneezing).
Neurologic exam findings are usually consistent with forebrain dysfunction but are not specific to cuterebral myiasis. Vestibular signs are sometimes observed.
Definitive diagnosis requires histopathological analysis of brain tissue, but a strong presumptive diagnosis can be made based on the history (forebrain signs in the late Summer to Fall in cats in the eastern US) combined with advanced imaging and cerebrospinal fluid analysis.
Routine blood tests (CBC, serum biochemical analysis) may be normal or show only mild changes, such as eosinophilia, leukocytosis, or neutrophilia). Advanced imaging (MRI preferred over CT) may show parasitic track lesions, signs of cerebral infarction, or cerebrocortical lesions. CSF may be normal to mildly inflammatory. Elevated protein content and mixed pleocytosis, sometimes with the presence of eosinophils, are relatively common.
Treatment of cuterebral myiasis is largely supportive. Phenobarbital or another anticonvulsant should be administered to cats with seizures. Whether to treat the patient for the parasite itself is a bit controversial as killing the larvae may induce an allergic inflammatory response that may be worse than being left untreated.
To reduce the risk of allergic response, the following treatment plan has been reported, although data are lacking concerning efficacy and safety. These drugs have not been labeled for this use, so owner consent is required.
Give the following once daily for three consecutive days:
- Diphenhydramine 4 mg/kg intramuscularly about 1-2 hours before giving ivermectin
- Ivermectin 200-500 microgram/kg subcutaneously
- Methylprednisolone sodium succinate 30 mg/kg intravenously
Additionally, give the following:
- Oral prednisone 5 mg per cat twice daily for 14 days
- Enrofloxacin 22.7 mg per cat once daily for 14 days
Author’s note: Although enrofloxacin has been recommended by some in the protocol above, I no longer use this medication in cats due to the risk of blindness. I typically administer clindamycin instead (10 mg/kg PO q12h for 1 month). Additionally, I typically prescribe a tapering course of prednisoLOne (better absorption in cats than prednisone) at 0.5 mg/kg PO twice daily for 7 days, once daily for 7 days and then every other day for 7 days.
The prognosis for recovery is fair to guarded. Many cats survive the condition, but residual neurologic deficits are possible.
- Glass EN, Cornetta AM, deLahunta A, et al. Clinical and clinicopathologic features in 11 cats with Cuterebra larvae myiasis of the central nervous system. J Vet Intern Med 1998;12:365-8.
- Hendrix CM, Cox NR, Clemons-Chevis CL, et al: Aberrant intracranial myiasis caused by larval Cuterebra infection. Compend Contin Educ Pract Vet 1989;11:550-9.
- James FMK, Poma R. Neurological manifestations of feline cuterebriasis. Can Vet J 2010;51:213-5.
- McKenzie BE, Lyles DI, Clinkscales JA. Intracerebral migration of Cuterebra larva in a kitten. J Am Vet Med Assoc 1978;172:173-5.
- Rissi DR, Howerth EW. Pathology in practice. Ischemic encephalopathy caused by aberrant migration of a Cuterebra larva. J Am Vet Med Assoc 2013;243:493-5.
- Williams KJ , Summers BA , de Lahunta A. Cerebrospinal cuterebriasis in cats and its association with feline ischemic encephalopathy. Vet Pathol 1998;35;330-43.
Last updated by NeuroPetVet on August 14, 2016.