Page 1097 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition
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1072                                       CHAPTER 10



  VetBooks.ir  the CNS, where the infection may localise in any  Differential diagnosis
                                                          Given that EPM may mimic almost any other neu-
           area, with the exception of the peripheral nerves.
           As with all neurological disease, the locations of
                                                          extensive.
           infection determine the clinical presentation and,   rological disease, the list of diagnostic rule-outs is
           given the potential multifocal CNS distribution of
           the parasite, a wide range of clinical signs may be  Diagnosis
           evident. It appears that some types of immunosup-  A  definitive  ante-mortem  diagnosis  cannot be
           pression and stress (such as weaning) may alter the   achieved by clinicopathological means and most
           likelihood of invasion of the CNS and the devel-  often a clinical diagnosis of EPM is reached based on
           opment of neurological disease after oral ingestion   an accumulation of data. Important considerations
           of sporocysts.                                 in reaching a diagnosis are relevant history and com-
                                                          patible clinical signs, clinical progression, laboratory
           Clinical presentation                          and other diagnostic aids, exclusion of other possible
           EPM is renowned for its diversity of clinical signs,   causes, and response to treatment. Laboratory and
           as a result of lesions of varying size and severity in   other diagnostic aids have been divided into three
           any part of the CNS. The onset of signs may be   categories: (1) positive serology titres for  S.  neu-
           insidious or acute. Spinal cord involvement occurs   rona  antibodies,  which  supports  the  diagnosis;  (2)
           in most cases, while only 5% of cases are reported   negative titres, which tends to exclude the diagno-
           to show evidence of brain disease. Other than neu-  sis; and (3) tests that support alternative diagnoses
           rological signs, there are no other syndromes asso-  and thus indirectly exclude a diagnosis of EPM.
           ciated with EPM. The disease course is also highly   The main problem with CSF antibody detection is
           variable, with progression over hours or years pos-  that inadvertent contamination of the sample with
           sible, or a waxing and waning of signs over extended   serum antibodies is common and can produce false-
           periods. The prevalence of different neurological   positive results. Many researchers suggest analy-
           signs varies to some extent between reports, but the   sis of CSF and serum for antibodies using surface
           trend, in decreasing order, is: spinal cord lesions   antigen ELISAs and producing a ratio to determine
           (causing ataxia, paresis, proprioceptive deficits and/  active infection. For detection of N. hughesi, there is
           or spasticity, usually asymmetrical), muscle atro-  an ELISA based on surface antigens and an indirect
           phy, CN deficits (from brainstem lesions) and (least   fluorescent antibody test using whole tachyzoites.
           likely) central/cerebral signs (e.g. seizures). Rarely,   Detection of S. neurona antigen by PCR is highly
           EPM may be the cause of acute onset tetraparesis   suggestive, although positive results are uncom-
           and recumbency. Regions of hypalgesia, hyper-  mon in affected animals because of the intracellu-
           aesthesia and increased sweating can also be seen.   lar nature of the organism. However, because of the
           Horses may present with urinary incontinence,   high sensitivity, a negative result is often considered
           associated with damage to the sacral spinal cord   more significant, making it highly unlikely that the
           segments. Full ‘cauda equina syndrome’ signs have   horse has the disease. The poor specificity of serum
           also been reported, where there is incontinence and   and CSF testing has forced many clinicians to use
           paralysis of the bladder, rectum, anus and penis,   other criteria, such as a response to treatment, to
           and sensory loss to the tail and perineum.     allow them to make a retrospective diagnosis. Post-
             Where  CN  deficits  are  present,  there  is  often   mortem analysis may be required for a convincing
           associated muscle atrophy (e.g. lingual or mastica-  diagnosis (Fig. 10.25).
           tory muscles [see Fig. 10.4]). These types of EPM
           cases usually have an insidious onset and may appear  Management
           as a singular syndrome. They do not normally prog-  The use of anticoccidial medication is recommended
           ress beyond complete and permanent atrophy of the   for the treatment of EPM. Traditional treatment
           muscle affected.                               has centred around the use of combinations of
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