Neospora caninum is a microscopic protozoan parasite with worldwide distribution. Many domestic (eg, dogs, cattle, sheep, goats, horses, chickens) and wild animals (deer, 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 South American 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. The life cycle of N hughesi is unknown. Discussion in this chapter deals only with 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 endogenous transplacental transmission, 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. Wild canids also are suspected to be, and coyotes have been confirmed as, definitive hosts. 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 endures 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 the majority of congenital infections are subclinical, congenitally infected heifer calves may remain in the breeding herd and in turn may pass infections transplacentally to their own offspring. This endogenous transplacental transmission enables 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.
Abortion can occur throughout gestation. Nonsuppurative inflammation is the main lesion in aborted fetal tissues. 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, or myocarditis.
Diagnosis of Bovine Abortion
Because neosporosis is only one of many causes of abortion, diagnostic efforts should focus on an array of possible etiologies. 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 rule out 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: 1) lack of other etiologic agents; 2) nonsuppurative inflammation in multiple fetal organs especially including the brain, heart and skeletal muscle; 3) immunohistochemical or PCR detection of Neospora in fetal tissues; and 4) Neospora seropositivity of the dam or fetus. 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 ruled out in sero-negative dams.
Toxoplasmosis, which is common in sheep but rare or nonexistent in cattle, causes abortion with identical fetal lesions.
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 or more 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.
Diagnosis of Canine Neosporosis
Clinically affected dogs often have Neospora antibody levels that are much higher than levels observed 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. The finding of Neospora in routine fecal floats is serendipitous, because dogs typically only shed oocysts for 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. A smooth outer contour helps to differentiate them from pollen grains of similar size. Neospora oocysts are nearly identical to oocysts 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 dogs is treated with prolonged administration of clindamycin or potentiated sulfa drugs. 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.
The level of efficacy of a killed N caninum vaccine for cattle, commercially available in the USA since 1998, is unclear. Currently, there are no other available Neospora vaccines.
The majority of dairy and beef herds contain 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 that are 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 dogs from eating them, in order to reduce the risk that dogs will become infected and shed Neospora oocysts on the farm. Dogs that are seropositive for Neospora have reduced likelihood for future shedding of oocysts compared with seronegative dogs; therefore, serologic testing of farm dogs is seldom useful.
Despite its similarity to Toxoplasma, Neospora infection has not been clearly associated with any human disease. Laboratory workers should guard against inoculation, which caused fetal lesions in parenterally inoculated primates.
Last full review/revision March 2012 by Milton McAllister, DVM, PhD, DACVP