Page 824 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

Gastrointestinal system: 4.2 The lower gastrointestinal tr act 799

VetBooks.ir Management cases on the farm and recent changes in pasture use
are risk factors. Clusters of cases are not uncommon.
Management varies with the inciting cause. Specific
treatments in cases when a cause has been identified
weather conditions and parasite burden may affect the
are described elsewhere. Management of idiopathic It has been suggested that changes in feed, pasture,
cases is frustrating. In the absence of specific clinical GI microflora and allow for C. botulinum growth and
signs treatment for a presumed impaction with fasting toxin production.
and large volume, frequent enteral fluids for 2–3 days The pathophysiology is still unclear but there is a
may be rewarding. A variety of other treatments can widespread neuroanatomical distribution of degen-
be attempted including diet change, change in loca- erative neuronal lesions, with the autonomic and
tion, deworming and antiulcer treatment. Deworming enteric nervous systems being the most consistently
with moxidectin (0.4 mg/kg p/o) is often attempted. and severely affected. The severity of the disease and
Provision of a diet consisting of ready access to good- the gross pathological findings are largely deter-
quality hay or pasture with minimal grain or pelleted mined by the extent of enteric neuronal loss. The
ration can be attempted. Alternatively, some horses cause remains elusive but current research is focused
will respond to elimination of hay from the diet by on the potential role of either C. botulinum neurotox-
switching to a complete pelleted feed. Nutritional ins or ingested pasture-derived mycotoxins.
analysis and consultation are recommended.
Clinical presentation
Prognosis Acute, subacute and chronic forms are recognised.
The prognosis is highly variable and depends on the Clinical signs of the acute form are predominately
inciting cause. It ranges from very good (i.e. EGUS) depression, anorexia and mild to moderate colic.
to very poor (i.e. GI neoplasia, grass sickness and Affected horses are initially in good body condi-
intestinal adhesions). Overall, this is a frustrating tion. Borborygmi are decreased/absent and progres-
condition in many cases because an aetiology is often sive abdominal distension develops. Muscle tremors
not identified. are common and may be severe, particularly over
the shoulders, triceps, flank and quadriceps. Patchy
GRASS SICKNESS (EQUINE sweating is common in all forms of the disease
DYSAUTONOMIA, MAL SECO) (Fig. 4.123). Tachycardia may be severe and higher

Definition/overview
Equine grass sickness (EGS) is a geographically 4.123
important debilitating and frequently fatal cause of
GI disease. EGS has been most widely reported in
the UK, but it is also present in several mainland
European countries and South America, where it is
termed ‘mal seco’. There are anecdotal reports of
EGS in North America and Australia.

Aetiology/pathophysiology
It is a polyneuropathy affecting both the central and
peripheral nervous systems. There is increasing evi-
dence supporting the role of Clostridium botulinum type
C. EGS is a seasonal disease, with case occurrence
peaking in April and June in the northern hemisphere. Fig. 4.123 Horse with subacute grass sickness
Virtually all affected horses are grazing animals, often showing marked patchy sweating, muscle
in good condition, with the risk of disease highest fasciculations and a mild tucked-up abdomen.
in horses aged 2–7 years. Previous identification of (Photo courtesy Graham Munroe)