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Description
Neosporosis is the disease caused by the intracellular protozoa Neospora caninum. The dog is the definitive host, cattle are the intermediate host and other mammalian species may act as incidental hosts. In the past N. caninum has been confused with T. gondii because they are similar morphologically, but advancements in detection methods have made the two distinguishable.
The sexual phase of replication takes place in the gastrointestinal tract of dogs, oocysts are passed in the faeces which then develop into sporozoites and are infective to dogs and cattle.
Transplacental infection results in congenital infection of puppies which is the most typical presentation of the disease. More than one puppy in a litter may be affected, although this may not occur simultaneously. Successive litters can be affected, therefore a dam whelping an infected litter should not be allowed to breed again.
Other methods of infection include ingestion of sporulated oocysts from dog faecal matter and ingestion of tissue cysts in the tissues of intermediate or incidental hosts, for example bovine placenta. The clinical syndrome associated with infection is primarily neuromuscular and is a result of the organism replicating in tissues. Other organ systems may also be affected which may result in pneumonia, ulcerative dermatitis and hepatitis.
In some animals with a chronic or subclinical infection, administration of glucocorticoids results in activation of neospora in tissue cysts and clinical disease.
Signalment
Neosporosis has been reported worldwide; puppies are most frequently affected and hunting dogs are also over represented.
Diagnosis
Clinical Signs
Young dogs:
- Ascending paralysis
- Muscle atrophy
- Rigid limbs, affecting hind limbs more than forelimbs
- Dysphagia
- Ataxia
- Death
Older dogs:
- Seizures
- Tremors
- Cerebellar disease
- Myocarditis
Laboratory Tests
Haemotology and biochemistry findings are usually non specific but depend on the systems affected; myositis may result in elevations in CK and AST. Changes in CSF include increases in protein and nucleated cell count, predominantly mononuclear but with some neutrophils. Presumptive diagnosis can be made on clinical signs and elimination of differential diagnoses such as distemper and toxoplasmosis. Definitive diagnosis is made on identification of the organism in tissues or CSF, or by the detection of oocysts in the faeces by a floatation method or PCR. N. caninum can be differentiated from T. gondii by PCR, immunohistochemistry and electron microscopy.
Treatment
Treatment with trimethroprimsulfadiazine and pyrimethamine, or repeated doses of clindamycin hydrochloride have been successful in some cases. Treatment should be started before the signs have progressed to extensor rigidity.
Prognosis
The prognosis is poor. Animals presenting with severe neurologic signs have a grave prognosis.
References
- Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition) Merial
- Nelson, R.W. and Couto, C.G. (2009) Small Animal Internal Medicine (Fourth Edition) Mosby Elsevier
- Tilley, L.P. and Smith, F.W.K.(2004)The 5-minute Veterinary Consult (Third edition) Lippincott, Williams & Wilkins