© Glass, E.N. et al (2000) Clinical and Clinicopathologic Features in 11 Cats with Cuterebra Larvae Myiasis of the Central Nervous System. http://neuro.vetmed.ufl.edu/neuro/Journal_Club/Articles/myiasis_art.htm
Feline cuterebrosis
Etiology
Native species of rodents and lagomorphs in the Americas are the typical hosts of Cuterebra spp. larvae.
Although these bot flies are relatively host specific, they occasionally parasitize other native and introduced mammals (including domestic animals and humans), an affliction termed cuterebrosis. Cuterebra spp. larvae generally cause benign, subcutaneous lesions (warbles), but when infesting domestic cats, they can invade the eyes, respiratory tract, and cerebral tissues, causing severe, and in some cases fatal, injury. Despite more than two dozen published reports of feline cuterebrosis, the type (rodent- or lagomorph-infesting) or species-parasitizing domestic cats has rarely been determined.
Cats with CNS cuterebrosis are usually young to middle-aged animals with access to the outdoors, often presenting with signs during the months of July, August, and September. This time of year coincides with the portion of the life cycle of Cuterebra in the United States when larvae migrate through true and aberrant host tissues. A recent history of upper respiratory disease is common. The apparent association between upper respiratory disease and CNS cuterebrosis likely reflects entry and passage of larvae through the nasal passage to the cribriform plate before entry into the CNS. This route of entry of Cuterebra into the feline brain is supported by the discovery of a Cuterebra larva in the cribriform plate of the cat (deLahunta, personal communications). Clinical case studies and reviews of feline non-suppurative meningoencephalitis also have described a prodromal upper respiratory disorder. Although an unknown viral agent was suggested as the initiating agent, Cuterebra larval migration may have been the underlying causative factor. The small size of the lst- and 2nd-stage larvae (1.4 mm and 5-10 mm long, respectively) and difficulties encountered with removal and inspection of nervous tissue hinder identification and localization of these parasites.|
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Cuterebra larva surgically removed from a cat. Courtesy of Dr. Stephen White |
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Many cats with CNS cuterebrosis present during the months that coincide with the occurrence of idiopathic vestibular syndrome. The striking similarity in months of presentation suggests the possibility of a common etiologic agent. Unfortunately, results of post mortem examination of cats with idiopathic vestibular syndrome rarely are available because most affected cats partially or completely recover within a few weeks. Although the clinical signs of CNS cuterebrosis and idiopathic feline vestibular syndrome are dissimilar, both disorders may be caused by Cuterebra larvae migration because both occur during similar months of the year and usually affect cats with exposure to the outdoors. Idiopathic feline vestibular syndrome may be caused by migration of the small Cuterebra larvae through the ear canal to the portion of the peripheral vestibular apparatus responsible for the clinical signs seen in this disorder. The results of this retrospective study are compatible with such an association and warrant additional clinical investigation.
Alterations in thermoregulation in cats with intracranial cuterebrosis have been described previously. Most cats in the present study had abnormal body temperatures. This may reflect involvement of the hypothalamic thermoregulatory centre or increased temperature associated with an inflammatory response induced by larval migration, antigens, proteolytic enzymes, or some unknown toxin.
Peripheral eosinophilia often is observed in young cats with ecto- or endoparasitism, but less than 20% of the cats have peripheral eosinophilia. Therefore, lack of eosinophilia does not exclude a diagnosis of CNS cuterebrosis. Three of the cats had an increased globulin concentration, which may reflect an immune response to Cuterebra migration or acute-phase protein production in response to tissue injury or larval antigens or toxins.
The histopathologic association of CNS cuterebrosis and feline ischemic encephalopathy has been described previously. Furthermore, feline ischemic encephalopathy is not recognized in countries where Cuterebra larvae are not present (eg, Australia, New Zealand), further supporting that larvae are potential agents responsible for feline ischemic encephalopathy (Farrow, personal communication, 1996).
Clinical signs
Clinical and clinicopathologic features of feline ischemic encephalopathy and feline CNS cuterebriasis are similar. These similarities include patient age, exposure to outdoors, seasonality, recent history of upper respiratory disease, lack of well-defined clinicopathologic abnormalities, and lateralizing intracranial necrological signs. Our findings, therefore, further support the previous hypothesis that the syndrome of feline ischemic encephalopathy is caused by CNS cuterebriasis.
Signs consistent with central nervous system (CNS) migration also have been described in cats. Recently, detailed descriptions of the histopathologic lesions of CNS cuterebrosis were reported with the suggestion of a relationship to feline ischemic encephalopathy. Histopathologic features characteristic of CNS cuterebrosis are the presence of parasitic track lesions, superficial laminar cerebrocortical necrosis, cerebral infarction, subependymal rarefaction and astrogliosis, and subpial astrogliosis. Reported cases of CNS cuterebrosis have not included clinical data that may have facilitated antemortem diagnosis.
Most cats in this study were presented with lateralizing prosencephalic neurologic signs. This finding is consistent with reports of cats with intracranial Cuterebra migration. Surprisingly, a large number of cats in this study had left lateralizing intracranial signs. A review of previously described cases of CNS cuterebriasis disclosed that more than 70% of affected cats had a left prosencephalic lesion. The reason for this lateralization remains unexplained. Approximately 25% of the cats in this study developed seizures. A recent study of cats with seizure disorders disclosed that nearly 50% of cats (n = 14) presenting for seizure activity were classified as having non-suppurative meningoencephalitis of undetermined cause. Another 20% of cats in the cited study (n = 6) had signs consistent with feline ischemic encephalopathy. Some of these cats may have had CNS cuterebriasis.
Examination of CSF collected from the cerebellomedullary cistern did not consistently disclose an inflammatory response in the 3 cats evaluated. In addition, only 1 of 2 cats with an inflammatory reaction had an increased number of eosinophils in the CSF. Thus, lack of an eosinophilic inflammatory response in the CSF presumably does not exclude a diagnosis of CNS cuterebriasis. However, CSF results were available in only a few of the reported cats and definitive conclusions about CSF analyses in CNS cuterebriasis cannot be made.
Only 1 cat in the present report had computed tomography performed. The results of that scan indicated a mottled appearance to the brain, which sometimes is seen in cats and dogs with an encephalitis. Other imaging modalities such as magnetic resonance imaging or angiography may be more beneficial in diagnosing this disease antemortem. In particular, magnetic resonance imaging has the advantage of more easily detecting damage to tissues of the CNS.
Treatment
A report of CNS cuterebriasis described the use of ivermectin in a treatment protocol for 2 cats.
Ivermectin has been shown to be effective in mice infected with Cuterebra species. One cat in this study and 3 other similarly affected cats not included in this study have been treated in our hospital for presumptive CNS cuterebriasis based on clinical findings. The cat in this study was given diphenhydramine intramuscularly (4 mg/kg), 1-2 hours before giving ivermectin subcutaneously (400 g/kg) and dexamethasone intravenously (0.1 mg/kg). The antihistamine and steroids were administered to prevent anticipated anaphylactic or allergic reactions associated with larval death from the ivermectin administration. Treatment was repeated 24 and 48 hours later. In addition, the cat was given enrofloxacin (5.0 mg/kg PO ql2h) for 14 days to help prevent bacterial infection introduced by presumed larvae migration. This cat as well as the cats not included in the study did not have any adverse reactions to the treatment and there was no progression of clinical signs. The cat in the study was euthanized 2 months after treatment because of continued inappropriate urination.
Although histopathologic findings in the cerebrum of the cat were consistent with Cuterebra larvae myiasis, no larva was recovered. Based on these findings, the above treatment may be warranted in young to middle-aged outdoor or indoor-outdoor cats presenting with peracute to acute lateralizing intracranial neurologic signs in July, August, and September in the north-eastern region of North America. Although ivermectin does not readily cross the blood-brain barrier in normal dogs and cats, it has previously been shown to be effective in treatment of various migrating fly larva within the CNS. This effect is attributed to disruption of the blood-brain barrier from migrating parasites. Although it remains uncertain whether ivermectin is effective in the treatment of CNS Cuterebra in the cat, we suggest that our treatment protocol be used when the signalment, seasonality, and acute to peracute neurologic features described herein are recognized in cats, even though ivermectin has not been approved by the US Food and Drug Administration for use in cats, except at a lower dose for use as a heartworm preventative.