Page 919 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition
P. 919
894 CHAPTER 5
VetBooks.ir (a) include amiodarone, anabolic steroids, azathioprine,
carbamazepine, cyproheptadine, erythromycin,
isoniazid, NSAIDs, omeprazole, paracetamol, peni-
cillin, phenobarbitone, phenothiazines, phenytoin,
rifampin, sulphonamides and tetracyclines. It may be
prudent to use such agents with care in horses known
to be suffering from hepatic damage and monitoring
biochemical markers of liver injury when such drugs
are used, especially for long durations.
Excessive iron intake results in deposition of
haemosiderin in the liver where it may cause oxida-
tive damage and hepatotoxicity. Haemosiderosis
is the term generally used for benign iron accumu-
lation whereas haemochromatosis implies pathologi-
cal effects. Iron accumulation and toxicity may be
(b)
associated with iron-rich supplements in an acute
or chronic fashion. Some forages can be remark-
ably high in iron, usually when quantities of soil are
included into the forage during grass cutting, and
also some natural water sources can be high in iron
oxide. Genetic storage disorders are possible but
poorly characterised in horses.
Mycotoxins are common in an equine diet, espe-
cially in preserved forages, although mycotoxicosis
associated with fresh pasture plants (e.g. clovers) is also
suspected. Outbreaks of hepatic disease are seen fre-
quently in horses in the absence of known toxic plant
or drug exposure, and forage-associated mycotoxico-
sis is commonly suspected in such cases. Aflatoxins
are perhaps the best known hepatomycotoxin and
have been associated with ingestion of contaminated
forage and corn. Fumonisins are also hepatomycotox-
ins that may be present in forage and corn, although
they are better known for causing cerebral damage
in horses. Seasonal variations in clinical or subclini-
cal liver disease in horses may be associated with
introduction of feeds or forages and/or production of
mycotoxins within the dietary constituents. Moisture
is required for fungal growth and low temperatures
tend to stimulate mycotoxin synthesis.
Clinical presentation
There are no clinical signs specific for, or sugges-
Fig. 5.19a, b Other hepatotoxic plants: (a) Trifolium tive of, hepatotoxicity per se. Most cases are initially
hybridum (alsike clover); (b) Xanthium strumarium detected showing typical clinical signs of hepatic
(cocklebur) in mature (top) and cotyledonary stages insufficiency (see above) or possibly seen showing
(bottom). signs of vague and non-specific illness (e.g. poor