The larvae of some ascarid roundworms, including Toxocara spp of dogs and cats and Baylisascaris spp of mustelids, can cause CNS disease.
Nervous disorders, frequently associated with ascarid infection in young dogs, may be due to focal lesions in the CNS caused by the death of aberrant arrested larvae of T canis. Toxocara larvae may also invade the eye and cause ocular larva migrans in people.
Baylisascaris procyonis is the ascarid found in the small intestine of raccoons. It causes larva migrans in both wild and domestic animals in North America and is usually associated with the production of clinical CNS disease. More than 90 species of wild and domesticated animals have been identified as being capable of serving as paratenic (transport) hosts harboring B procyonis larvae. Some species, including opossums, skunks, cats, pigs, sheep, and goats, appear to be marginally susceptible or resistant to the neurologic migration. The parasite has been associated with the production of cerebrospinal nematodiasis in people, particularly children; it also has been implicated as a cause of ocular larva migrans.
Dirofilaria immitis is often referred to as the canine heartworm but can also infect cats and ferrets. As adults, these parasites usually infect the right ventricle and the pulmonary artery and its fine branches. D immitis has been recovered from a variety of aberrant sites, including the CNS of its definitive hosts and the anterior chamber of the eye. (Also see Heartworm Disease.)
Elaeophora schneideri, a filarid of the carotid arteries and its branches, is common in mule deer, primarily in western North America. Microfilariae accumulate in the skin of the head and face; intermediate hosts are tabanid horseflies. Larvae develop in arteries of the leptomeninges before migrating to the carotids. Infection is usually asymptomatic in normal definitive hosts. In wapiti, moose, white-tailed deer, sheep, and goats, worms in the arteries cause degeneration and loss of the endothelium and accumulation of plasma proteins and platelets on and within the intima. Thrombosis, infiltration of the intima, and fibroblastic proliferation may eventually result in occlusion and ischemic necrosis in associated tissues. Necrotic lesions associated with occlusion of leptomeningeal arteries are commonly found in the brain. Neurologic signs include blindness, head deviation, circling, ataxia, and paralysis (also see Elaeophorosis).
Setaria digitata is found in Asia and is a common parasite of the peritoneal cavity. Microfilariae are found in the blood; mosquitoes are intermediate hosts. Details of development in the normal host are unknown. In cattle, clinical signs do not appear to develop. In horses, goats, and sheep, the developing worms invade the CNS and cause motor weakness, ataxia, lameness, drooping eyelids or ears, and lumbar paralysis. Lesions include focal malacia and degeneration of axis cylinders and myelin sheath in all regions of the CNS.
Setaria cervi has been reported on the leptomeninges of deer in Europe and in the former USSR, often in association with Elaphostrongylus cervi. Setaria spp have also been found in the CNS of horses. The significance of these findings is unclear.
Filarids may also parasitize avian species. Splendidofilaria quiscula is found in the cerebral hemispheres of grackles (Quiscalus quiscua) and other birds in North America. Paronchocerca helicina is found in the cranial leptomeninges of the snake bird (Anhinga anhinga) in the USA.
Angiostrongylus cantonensis is a common parasite of the pulmonary arteries of rats in southeast Asia and the south Pacific. Terrestrial, aquatic, and amphibious snails and slugs are intermediate hosts. Paratenic hosts are freshwater prawns, land crabs, coconut crabs, and planarians. Larvae invade the cerebrum and develop in the neural parenchyma for ~2 wk, then enter the subarachnoid space and migrate, ~1 mo after infection, to the pulmonary arteries via the venous system. Neurologic signs are rare in rats with light to moderate infections, but circling, cannibalism, and paraplegia may develop in heavy infections. In endemic areas, people frequently acquire infections by consuming raw or undercooked intermediate or paratenic hosts. In people, this parasite may produce a fatal eosinophilic meningoencephalitis. In Australia, A cantonensis has produced an ascending paralysis in puppies. It may be an incidental parasite in dogs.
Gurlita paralysans is found in the spinal veins of cats and has reportedly produced a high incidence of paralysis. It may be an incidental parasite in cats.
Elaphostrongylus cervi is a common parasite of the skeletal musculature of Rangifer and Cervus spp (reindeer and elk) in the holarctic region, especially Eurasia. It is transmitted through terrestrial snails and slugs and apparently develops for a time in the CNS before migrating to the muscles. Infection is associated with lumbar weakness, paresis, and paralysis in cervids in Sweden and in the former USSR.
Parelaphostrongylus tenuis is found in the subdural space and venous sinuses of the cranium of white-tailed deer in eastern North America. Eggs reach the lungs in the venous blood and develop into larvae, which pass up the bronchial tree and out with the feces. Infective larvae, acquired from terrestrial snails and slugs as the deer feeds, invade the spinal cord and develop for several weeks in the dorsal horns of the gray matter; then, they invade and mature in the subdural space. The infection is usually asymptomatic in white-tailed deer. However, P tenuis causes pathology in the CNS of various cervids (moose, caribou, wapiti) and antelope, llamas, sheep, and goats. In these hosts, the parasite produces considerable trauma in the CNS. In addition, eggs deposited in the neural tissue provoke marked inflammatory reactions. Clinical signs consist of lumbar weakness, ataxia, lameness, stiffness, circling, abnormal positions of the head, and paralysis. Signs vary in onset and character in individual animals. Temporary remissions are typical.
Skrjabingylus nasicola and S chitwoodorum are found in the frontal sinuses of mustelids, especially mink, weasels, and skunks. Larvae acquired from terrestrial snails and slugs develop for a time in the gut wall, then migrate to the spinal cord. They move on to the leptomeninges to the brain and along the olfactory tracts to the cribriform plate, which they penetrate to reach the frontal sinuses. Their presence on the leptomeninges elicits hemorrhage and leptomeningitis. In heavy infections, some subadult worms may invade the brain and cause neurologic signs, including paralysis.
Halicephalobus deletrix is a free-living soil rhabditiform associated with soil and decaying vegetation in the host's environment. This nematode has been reported in the CNS of horses and people. It may reach the CNS through wounds contaminated by soil that contain these nematodes or through abscesses in the oral and nasal cavities. The nematode multiplies in the CNS and is highly destructive of neural tissues. Pathogenicity in the CNS can be attributed to trauma caused by activities of the parasites; the role of excretory and secretory products is unknown. Also, the parasites may transport pathogenic microorganisms to the CNS. Clinical signs are related to the location of and lesions produced by the parasite. Signs resemble viral encephalitis and include motor weakness, ataxia, head deviation, circling, depression, blindness, drooping of the ear or eyelid, loss of the herding instinct, and paralysis. Lesions consist of vasculitis, hemorrhagic necrosis, and malacia.
Migrating larvae of strongyles (perhaps Strongylus vulgaris) have been reported in the CNS of horses. Larvae of Stephanurus dentatus rarely invade the CNS of pigs. Larvae of Trichinella spiralis were found in the brain in a fatal case of trichinosis in a person. Larvae of Strongyloides stercoralis may invade the brain of experimentally infected animals. Gnathostoma spinigerum has been found rarely in the CNS of people. Eustrongylides ignotus implanted subcutaneously in rats and chickens migrated to the CNS and caused death of the host.
Last full review/revision July 2013 by Charles M. Hendrix, DVM, PhD