Neosporosis in Animals
Neospora caninum is a microscopic protozoan parasite with worldwide distribution. Many domestic (eg, dogs, cattle, sheep, goats, water buffalo, horses, chickens) and wild and captive animals (eg, deer, rhinoceros, rodents, rabbits, coyotes, wolves, foxes) can be infected. Neosporosis is one of the most common causes of bovine abortion, especially in intensively farmed cows. Neosporosis abortion also occurs in sheep, goats, water buffalo, and camelids, although they may be less susceptible than cattle.
A second Neospora species, N hughesi, is a cause of myelitis in horses and shares clinical features with equine protozoal myelitis, which in North and South America is usually caused by Sarcocystis neurona. Infection with N hughesi has also been described in an aborted foal. A definitive host for N hughesi has not been described. This discussion covers only N caninum infection.
Neosporosis in cattle herds manifests in both endemic and epidemic abortion patterns, but it is also possible for a herd to have a high infection prevalence without a noticeable abortion problem. Both endemic and epidemic transmission patterns in cattle are positively associated with the presence and number of dogs in and around farms. Endemic abortion is mainly associated with recrudescence of latent organisms during pregnancy followed by transplacental transmission to the fetus, although occasional transmission from dogs or other canids may compound the problem. Epidemic abortion is a possible consequence of sudden large-scale transmission to pregnant cattle, presumably by ingestion of a mixed ration or water that has been contaminated with infected canine feces. The use of mixed rations in dairy herds probably accounts for the greater prevalence of neosporosis in dairy cattle than in extensively grazed beef cattle.
Dogs are definitive hosts of N caninum and are capable of shedding oocysts in feces after eating tissues of infected animals. Gray wolves, coyotes, and dingoes are also definitive hosts, and many other wild canids are suspected. Neospora oocysts have an impervious shell that enables survival in soil and water for prolonged periods after canine feces have decomposed. Intermediate hosts such as cattle become infected by ingesting oocysts. Cattle do not produce oocysts and thus do not transmit infections horizontally to other cattle, but latent infection may endure permanently in their tissues and is transmitted to canids by carnivorism.
In cattle, N caninum can be transmitted transplacentally from an infected cow to the developing fetus, an event that may occur in multiple pregnancies of the same cow. Because most congenital infections are subclinical, congenitally infected heifer calves may be retained and added to the breeding herd and, in turn, may pass infections transplacentally to their own offspring. This endogenous transplacental transmission may enable transgenerational maintenance of the parasite even if the herd does not have frequent transmission from dogs. Exogenous transplacental transmission may occur when a previously uninfected cow ingests Neospora oocysts during pregnancy and the fetus becomes infected.
Dogs have been shown to become infected by eating infected cattle (including placentas) and deer and are presumed to become infected by consuming raw meat diets, barnyard chickens, and a variety of wild animals.
Most neosporosis abortions occur in mid to late gestation. Congenitally infected calves may be born weak or with neurologic deficits. However, most congenital infections are subclinical.
In dogs, subclinical infection is the rule, although there are a greater variety of exceptions. Litters or individual puppies may develop progressive hindlimb paresis associated with polyradiculoneuritis, myositis, and muscle atrophy. Adult dogs may have encephalomyelitis, focal cutaneous nodules or ulcers, pneumonia, peritonitis, hepatitis, or myocarditis, sometimes associated with use of immunosuppressive drugs.
Because neosporosis is only one of many causes of abortion, diagnostic efforts should focus on an array of possible causes. Aborted fetuses should be submitted to a veterinary diagnostic laboratory, together with placenta and a serum sample from the aborting dam. Examination of multiple fetuses increases the odds of accurate diagnosis. If it is impractical to submit an entire fetus, as many of the following specimens as possible should be submitted to exclude other causes of abortion: aseptically collected and chilled lung, liver, spleen, and abomasal fluid; an eyeball for nitrate testing; formalin-fixed specimens of brain (even if soft), lung, thymus, liver, kidney, spleen, adrenal gland, skeletal muscle (eg, tongue and diaphragm), and placental cotyledon; serum from the aborting dam; and thoracoabdominal fluid from the fetus for serology.
A diagnosis of neosporosis abortion can be made with great confidence from the following constellation of findings:
However, such unequivocal findings are not always present. A lesion that is nearly specific for neosporosis abortion in cattle is multifocal cerebral necrosis surrounded by nonsuppurative leukocytic reaction. Confidence in the diagnosis increases with the strength of the Neospora antibody level in the aborting dam, with high seropositive reactions at the time of abortion having greater predictive value than low seropositive reactions. Neosporosis is generally excluded in seronegative dams.
Toxoplasmosis is a more common cause of abortion in sheep and goats and has lesions similar to those of neosporosis, but toxoplasmosis abortion in cattle is rare or nonexistent.
Serologic testing of multiple cows or heifers can be used as an alternative or complementary method to determine whether neosporosis is a major reproductive problem in a herd. This strategy can be helpful when investigating herds with endemic abortion problems. Serum samples should be collected from aborting dams and from an equal number of matched herdmates with normal gestation (generally ≥10 per group). Sera should be tested and classified for Neospora antibodies. If most cows in the aborting group are seropositive and few are seropositive in the normal group, then neosporosis should be suspected as a cause of abortion in the herd; this may be confirmed by statistical comparison. If most aborting cattle are seronegative, then neosporosis is unlikely to be a major problem.
Clinically affected dogs often have Neospora antibody levels much higher than levels seen in subclinically infected individuals. Biopsy of clinically affected tissues demonstrates nonsuppurative inflammation and may reveal the presence of protozoal organisms, but immunohistochemistry or PCR may be required to detect the organisms or to differentiate them from other protozoa.
Dogs with symptomatic neosporosis usually do not shed oocysts in feces, apart from rare cases associated with diarrhea. The finding of Neospora in routine fecal floats is serendipitous, because dogs typically shed oocysts for only a period of days or weeks after ingesting tissue of an infected animal. The tiny oocysts are round to slightly oval and 10–11 microns in diameter; in comparison, Giardia cysts are oblong and approximately 9 × 13 microns, and coccidia are 2–4 times the diameter of Neospora. A smooth outer contour helps to differentiate Neospora oocysts from pitted pollen grains of similar size. The oocysts are nearly identical to those of Hammondia heydorni, a closely related parasite that has not been associated with systemic disease in dogs or with abortion in ruminants. PCR may be necessary to distinguish between oocysts of N caninum and H heydorni.
There is no approved treatment for neosporosis in cattle. Clinical neosporosis in puppies has been treated with some success by prolonged (eg, 3 weeks to 2 months) administration of clindamycin (20–22 mg/kg, twice daily) or potentiated sulfa drugs (15–30 mg/kg trimethoprim-sulfamethoxazole, twice daily). Toltrazuril and ponazuril are effective in vitro, but their efficacy in clinical neosporosis has not been reported. The prognosis is negatively associated with the severity of presenting clinical signs and with delayed treatment. The prognosis is poor in puppies if disease has progressed to hindlimb paresis with atrophied, rigid limbs.
Currently, there are no available Neospora vaccines for cattle or dogs.
It is common for dairy and beef herds to have at least a small percentage of Neospora-infected cattle. Although reducing the risk of Neospora transmission is a useful goal, complete eradication from a herd is usually impractical. Contamination of feedstuffs used in mixed rations by canine feces should be avoided. Large dairies can consider erecting dog-proof fences around the area in which feedstuffs are stored outdoors, and automatic gates can be installed to facilitate the daily traffic of heavy machinery. Smaller dairy farms may be able to protect feedstuffs within traditional buildings such as barns, grain bins, and silos.
In addition to protecting feedstuffs, herds with endemic neosporosis abortions may consider not retaining heifer calves born to seropositive cows, thereby reducing the number of congenitally infected replacement heifers that enter the breeding herd. If this technique is used, seropositive dairy cows could be bred using beef semen. For seropositive cows with valuable genetics, the use of embryo transfer to Neospora-seronegative surrogates, a technique that blocks endogenous transmission, can be considered.
Dead stock, offal from home slaughter, and placentas should be discarded in a manner that prevents ingestion by dogs to reduce the risk that dogs will become infected and shed Neospora oocysts on the farm. Dogs seropositive for Neospora have reduced likelihood for future shedding of oocysts than do seronegative dogs; therefore, serologic testing of farm dogs is seldom useful.