Page 1096 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

Nervous system 1071

VetBooks.ir Diagnosis EQUINE PROTOZOAL
MYELOENCEPHALITIS
A definitive ante-mortem diagnosis of neurobor-
reliosis in horses is challenging and it is possible
that the disease is overdiagnosed in areas with high Definition/overview
seroprevalence. Diagnosis is based on geographi- EPM is a common cause of neurological disease in
cal area, clinical signs, ruling out other causes for certain areas. A diverse range of clinical signs can be
the clinical signs and a positive ELISA titre or a encountered.
positive Western blot test for B. burgdorferi. The
magnitude of antibody titres has no relationship Aetiology/pathophysiology
to the likelihood of clinical disease. Additionally, Sarcocystis neurona appears to be the causative agent
treated and untreated horses may stay seroposi- in most cases, although some cases have been
tive for months or even years, and at this time it is linked to Neospora hughesi. The Virginia opossum
not known whether this indicates subclinical per- (Didelphis virginiana) is the only definitive host for
sistent infection or serial exposure to the organ- S. neurona in the USA, while a related opossum
ism. The time from infection to seroconversion (Didelphis albiventris) carries S. neurona in South
is 3–10 weeks, the great limitation of serological America. Armadillos, raccoons and the striped
tests being that they are unable to distinguish skunk have been identified as natural intermedi-
between active infection and subclinical exposure. ate hosts. No definitive host has yet been identi-
Therefore, positive test results should be inter- fied for N. hughesi. Horses are considered accidental
preted with caution. A PCR test is available for aberrant intermediate hosts for S. neurona and only
detecting the spirochaete. It can be performed on asexual parts of the life cycle have been identi-
tissue (including skin and muscle), ticks, synovial fied histologically, indicating that the infection in
fluid or whole blood. horses can be considered non-contagious and that
they are dead-end hosts.
Management The disease occurs in areas in which the caus-
Treatment consists of oxytetracycline (5–6.6 mg/ ative organism and its host are found (i.e. North and
kg i/v q12 h or q24 h for 7 days) or oral doxycy- South America). Cases have occurred all over the
cline (10 mg/kg p/o q12 h for 7 days). Treatment is world in horses that have been imported from the
often continued for a month, but this is empirical. USA, often many months to years after arrival. The
Recurrence of clinical signs is often reported after seroprevalance of the disease has been reported at
treatment is discontinued. Other supportive treat- 26–60%, but the incidence of new disease has been
ments, including chondroprotective agents and non- reported to be up to 0.51%, indicating that develop-
steroidal anti-inflammatory drugs (NSAIDs), should ment of disease is uncommon following exposure to
also be considered. the causative agent. A number of risk factors have
Prevention in endemic areas involves the preven- been associated with the development of clinical
tion of tick exposure and prolonged tick attachment, disease. One study noted a higher incidence in the
together with early antimicrobial treatment fol- spring, summer and autumn, and increased inci-
lowing Ixodes exposure. Insecticidal sprays are not dence in animals between 1 and 5 years of age, ani-
approved for use in horses and there is no commer- mals living in wooded terrain and if EPM had been
cially available vaccine at this time, although ponies diagnosed on the property previously.
have been protected against experimental infection Horses are infected by ingestion of sporocysts in
by the use of a vaccine. food or water that has been contaminated by faeces
from the definitive host. Sporocysts may excyst in
Prognosis the small intestine, resulting in the release of spo-
The prognosis is good if appropriate treatment is rozoites into the bloodstream as a cell-associated
provided. parasitaemia. There is haematogenous spread to