Parasitic Disease of the Bovine Nervous System

Bovine Neurologic Diseases

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Parasitic Disease of the Bovine

Nervous System T. w. Schillhorn van Veen, *

Although the morbidity of parasitic diseases of the nervous system is low, the mortality is often high, and the diagnosis is more often made at postmortem examination than on the farm or in the field. In general, parasitic disease in the nervous system is caused by either (1) direct trauma caused mainly by migrating parasites or (2) indirect vascular changes that are associated primarily with blood parasites or rickettsiae. PARASITES CAUSING DIRECT TRAUMA

Various parasites migrate incidentally or specifically in the nervous system. Tapeworm larvae, such as Echinococcus cysts, 13 Coenurus cysts, 5 or cysticerci, are occasionally found in the brain but rarely cause clinical disease. Most cases occurring in cattle are incidental postmortem observations. Nematode larvae, however, are more important, as are Hypoderma larvae. Migrating Nematodes Most of the migrating nematodes are either ascarid, metastrongylid, or filarid larvae. Toxocara and Baylisascaris, which are commonly found in other domestic animals, do not affect the nervous system of cattle; the majority of such larvae are caught and resorbed in the intestinal wall or liver. The common metastrongylid, Parelaphostrongylus tenuis, the meningeal worm of white-tailed deer, does not clinically affect the deer, but migrating larvae cause considerable problems in other ruminants such as moose ('moose sickness"), sheep, and goats. Cattle are rarely affected, which is in part related to grazing habits and in part to their natural resistance to this parasite.

* Professor

of Veterinary Parasitology, Departments of Microbiology and Public Health and Large Animal Clinical Sciences, Michigan State University College of Veterinary Medicine, East Lansing, Michigan

Veterinary Clinics of North America: Food Animal Practice-Vol. 3, No.1, March 1987

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Setaria spp. are normally located in the peritoneum. However, immature stages may wander in the brain and spinal cord. Setaria digitata larvae are commonly incriminated as the cause of cerebrospinal nematodiasis in d eer 3 and horses in Asia and have been suspected in nervous disease in cattle. 14 This cerebrospinal filariasis appears to be particularly common in eastern Asia, where it is known as "kumri. " Spinal Hypodermosis During their migration from the site of infection to the skin, the larvae of Hypoderma bovis migrate along the peripheral nerves to the spinal canal. In the spinal canal, the larvae rest for a period to 2 to 3 months, mainly in the epidural fat. Their metabolic activity appears to be fairly low during this period, and reaction of host to parasite is rarely detectable. If the Hypoderma larvae are killed during this time, however, the inflammatory response of the host may be so extensive that the pressure on the spine may lead to detectable clinical signs. The majority of the Hypoderma larvae are located in the caudal parts of the spinal canal (L1 or lower) and only rarely in the thoracic parts or in the brain. 2 The postmortem diagnosis can be made by opening the spinal canal and close (histopathologic) examination of inflammatory lesions (Fig. 1). The clinical signs vary from a stiff gait to severe ataxia and weakness. The onset of the signs generally occurs 2 to 7 days after systemic insecticidal treatment (with organophosphates or ivermectin). Under normal conditions, these signs are transient, and less than 2 per cent of a herd may require attention. Affected animals are reluctant to move, and under conditions of extreme cold in winter, recovery from the disease may be delayed and some animals may die. The disease has to be differentiated from organophosphate poisoning. Generally, the latter occurs within a few hours after treatment or exposure, and certain clinical signs characteristic of organophosphate poisoning such as nervousness, salivation, bloat, and diarrhea are uncommon in spinal hypodermosis.

Figure 1. Inflammatory reaction around Hypoderma larvae (x) in cauda equina of a gOO-pound steer treated with a systemic organophosphate in February. The arrows indicate spinal cord. (Photograph courtesy of Animal Health Diagnostic Laboratory, Michigan State University.)

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Treatment is rarely necessary and is restricted to supportive therapy.4 Spinal hypodermosis can easily be prevented by avoiding the use of organophosphates or ivermectin after the cutoff date for grub treatment for the particular region. CENTRAL NERVOUS SYSTEM DISEASE ASSOCIATED WITH TICK-TRANSMITTED AGENTS

Of the four major central nervous system diseases associated with ticks, three occur mainly in the tropics; the fourth, tick paralysis, also occurs in the United States. Cowdriosis or Heartwater Disease Although this disease originates and mainly occurs in Africa, it has spread to some of the Caribbean Islands and could, with respect to the presence of suitable intermediate hosts, invade the United States. The disease is caused by Cowdria ruminantium, a rickettsial organism transmitted by Amblyomma ticks. It is suggested that the organism initially develops in reticuloendothelial cells of lymph nodes of the ruminant host and later invades the endothelial cells of blood vessels. The small (1 to 2 f..Lm) rickettsiae in the endothelial cells may alter the permeability of the capillaries, leading to transudate and edema. Transudates are commonly seen in the pericardial and pleural cavities. The main lesions in the brain are congestion and petechiae; larger hemorrhages may be seen in the meninges or the brain itself. The clinical signs vary. In peracute cases, the animal dies with or without showing nervous signs. In other, developing cases, the animals are febrile for 3 to 4 days and then show nervous signs that may begin as an increased alertness, twitching of eyes, ears, or Hluscles, teeth grinding, and, later, an unsteady gait with high-stepping of front legs and head pressing (Fig. 2). In the final stages of the dis-

Figure 2. Depression and paralysis in cowan hour before she died due to heartwater disease (Cowdria ruminantium).

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ease, the animal is unable to rise and shows opisthotonus and continuous movement of legs and jaws. Milder forms of the disease exist, varying from a transient rise in temperature to severe diarrhea. The severity of the disease depends on the virulence of the strain as well as on the level of immunity in the host. There are no reliable serologic tests available to demonstrate exposure; a capillary flocculation test, using brain extract, is only positive for a few weeks after initial exposure or reinfection. 9 The tentative diagnosis is confirmed at postmortem examination by examining brain capillaries for the presence of the rickettsial organisms. A simple technique to obtain suitable material has been described by Synge lB in live animals and by Schreuder17 at postmortelll examination. A small pinhead-size fragment of gray matter or cerebellum is placed on a slide and crushed with another slide, resulting in two smears. These are fixed and stained with Giemsa. Colonies of the organisms are found in brain capillaries. Treatment with tetracycline is fairly effective when given before the development of nervous signs. In South Africa, exotic animals or young animals under conditions of enzootic instability are vaccinated with a modified live vaccine, but the results are variable. Cerebral Babesiosis

Babesia spp., especially B. bovis, are found in blood cells in capillaries of the brain and have been incriminated as a cause of cerebral babesiosis. The pathophysiology of the condition is not quite clear. Dalgiesh reported disseminated intravascular coagulation (DIC) in splenectomized calves but not in intact calves infected with B. hovis. 6 Wright described the accumulation of un infected blood cells in brain capillaries in the early stages of a B. hovis infection. 19 This accumulation appeared to be associated with a stellate shape of infected erythrocytes with strands interconnecting them with the endothelium. This "sticking" of erythrocytes was thought to cause capillary congestion followed by stasis, degeneration of the endotheliulll, and leakage through the capillary wall. The neurons do not appear to be affected. 15 The onset and course of the disease are usually very rapid, with an increase in rectal temperature and a variety of clinical signs that may include teeth grinding, depression, incoordination, and convulsions or coma. The diagnosis requires examination of brain tissue, but often the animal has succumbed before a diagnosis can be made. Moreover, treatment with babesiacides has little effect once the central nervous system signs develop. Cere bral Theileriosis ("Turning Sickness") This sporadic disease, caused by Theileria spp., is associated with closing of the small vessels and capillaries and secondary infarction in the brain and meninges, which is often due to emboli consisting of clusters of parasitized lymphocytes.

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The clinical signs of this afebrile disease include depression, hypersensitivity, ataxia, circling, convulsions, paralysis, and often blindness. The disease is seen in areas where T. parva, T. mutans, T. taurotragi, or T. annulata is endemic. 11 This disease may last for only a few days, and the diagnosis is generally made at postmortem examination. Collection of cerebrospinal fluid, brain biopsy, hematology, and electroencephalography do not provide reliable diagnostic information. 1 At present, no effective treatment is known. Tick Paralysis Approximately 40 different tick species have been incriminated as a cause of tick paralysis in man and animals. Most commonly associated with the condition are Dermacentor spp. (especially D. andersoni), Ixodes spp. (especially I. holocyclus), and certain Rhipicephalus spp. In the United States, the condition is mainly seen in the northwest and along the Pacific coast. The nearly engorged ticks produce a toxin that causes a motor polyneuropathy. The pathophysiology varies depending on the tick species. 8 Generally, only young animals are affected. Depending on the amount of toxin, which is closely correlated to the number of engorging ticks, the signs may vary from slightly impeded motor function to complete paralysis. In the final stages of the disease, the intercostal and abdominal musculature are also paralyzed, ultimately leading to respiratory acidosis and death. Affected animals generally show increased levels of creatine kinase and liver enzymes and decreased levels of cholinesterase. 16 Removal of the ticks results in recovery. The rate of improvement is inversely related to the degree of paralysis, and severe cases may require 2 to 4 weeks before complete recovery. The condition can be prevented by tick control or by planning the calving of cattle in such a way that young animals are not exposed to ticks (for example, in tick-free paddocks and, in endemic areas, calving in fall rather than spring). OTHER PROTOZOAL INFECTIONS

Toxoplasmosis, which is commonly associated with cerebral lesions in other animals, rarely affects the brain of cattle. Cerebral Trypanosomiasis Involvement of the central nervous system, which is commonly seen in human sleeping sickness, is uncommon in bovine trypanosomiasis. Masake describes a disseminated non suppurative meningoencephalitis in cattle experimentally inoculated with Trypanosoma congolense and T. brucei. 12 Field observations on cerebrospinal trypanosomiasis are rare, but a 9-day-old calf infected with T. theileri and showing central nervous system signs has been reported. 9

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Nervous Coccidiosis This syndrome, which is associated mainly with Eimeria zuernii and E. bovis infections, is not due to the presence of these coccidia in the brain or spinal cord but to secondary changes occurring with intestinal coccidiosis. The pathophysiology is not clear; antibody-antigen reactions, autointoxication, and a loss of electrolytes have been suggested as possible mechanisms. In the United States, the majority of cases occur during winter in calves or in weanlings, often within weeks of a stressful period. Affected animals show muscle tremors, strabismus, tetanic spasms, convulsions, and sometimes blindness. The clinical signs and the reported improvement after treatment with electrolytes and parenteral magnesium, calcium, and dextrose suggest that loss of electrolytes and minerals does play a role in the pathophysiology of this disease. 7 The latter treatment is, of course, a supplement to treatment for coccidiosis in general, which involves the use of sulfonamides or amprolium. Prevention of coccidiosis, by husbandry methods or by feeding of coccidiostats, eliminates the risk of this nervous system syndrome.

REFERENCES 1. van Amstel SR: Bovine cerebral theileriosis. Some aspects of its clinical diagnosis. In Proceedings of the XII World Congress on Diseases of Cattle, Amsterdam, pp 981-985. 2. Belli P, Laval A: Apparition de troubles paralytiques enzootiques sur des broutards charolais faisant l'objet d'une infestation massive par des larves d'hypodennes. Rev Med Vet 132:62-66, 1981. 3. Bohme LK, Supperer R: Untersuchungen ueber Setarien (Nematoda) bei heimischen Wiederkauern und deren Beziehung zur "epizootischen cerebrospinalen Nematodiasis". Z Parasitenk 17: 165-174, 1955. 4. Brown FG: Toxicological hazards in warble fly eradication programmes. Vet Paras itoI 3:265-270, 1977. 5. Clegg FG, Bayliss JB: Coenurus cerebralis as a cause of hydrocephalus in the ox. Vet Rec 70:441-442, 1958. 6. Dalgiesh RJ, Dimmock CK, Hill MWM et al: Babesia argentina: Disseminated intravascular coagulation in acute infections in splenectomized calves. Exp Parasitol 40:124-131, 1976. 7. Fanelli HH: Observations on nervous coccidiosis in calves. Bovine Pract 18:50-53, 1983. 8. Gothe R, Kunze K, Hoogstraal H: The mechanisms of pathogenicity in the tickparalyses. J Med Entomol 16:357-369, 1979. 9. Grunert E, Andresen P: Zentralnervose Storungen mit lethalen Ausgang bei einem mit Trypanosoma theileri infizerten Saugkalb. DTW 77:304-306, 1970. 10. Ilemobade AA: Study of heartwater and the causative agent, Cowdria ruminantium (Cowdry, 1925) in Nigeria. Thesis, Ahmadu Bello University, Zaria, Nigeria, 1976. 11. Khanna BM, Kharole MU, Dhar S, et al: Histologic studies in cerebral theileriosis of calves infected with Theileria annulata. Indian J Parasitol 6:91-94, 1982. 12. Masake RA, Nantulya VM, Akol GWO, et al: Cerebral trypanosomiasis in cattle with a mixed Trypanosoma congolense and T. brucei infection. Acta Trop 41:237-246, 1984. 13. Medda A: Echinococcosi cerebrale nei bovine. Profilassi 12:12-24, 1939.

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14. Mohiyuddeen S: Enzootic bovine paraplegia in some Malnad tracts (hilly and heavy rainfall region) of Mysore State with particular reference to cerebrospinal nematodiasis and its probable cause. Indian J Vet Sci 26:1-19, 1956. 15. Rogers RJ: Observations on the pathology of Babesia argentina infections in cattle. Aust Vet J 47:242-247, 1971. 16. Schniewind A, Gothe R, Neu H: Zur Pathophysiologie der durch Rhipicephalus evertsi evertsi (Neuman, 1897) induzierten Zeckenparalyse der Schafe. Berl Munch Tierarztl Wochenschr 96:81-85, 1983. 17. Schreuder BEC: A simple technique for the collection of brain samples for the diagnosis of heartwater. Trop Anim Health Prod 12:25-29, 1980. 18. Synge BA: Brain biopsy for the diagnosis of heartwater. Trop Anim Health Prod 10:45-48, 1978. 19. Wright IG: An electron microscopic study of intravascular agglutination in the cerebral cortex due to Babesia argentina infection. Int J Parasitol 2:209 -215, 1972. A-12 Veterinary Clinical Center College of Veterinary Medicine Michigan State University East Lansing, Michigan 48824