Page 920 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

Liver disease 895

VetBooks.ir athletic performance or mild lethargy) where hepatic of feedstuffs, although the incidental presence of
hepatomycotoxins such as aflatoxins may be found in
insult has not yet been severe enough to decompen-
sate hepatic functions. Coincidental liver disease in
several herd-mates may be an indicator of dietary some forage samples fed to horses with no evidence
of hepatic injury. Additionally, given the typical bulk
hepatotoxins (plants, iron or mycotoxins). storage of forage compared with the small size of
samples submitted for mycotoxin analysis, there is
Differential diagnosis considerable potential for sampling error when test-
As no specific clinical indicators of hepatotoxicity ing forage samples. Nevertheless, this author has
exist, differential diagnoses include all of those to be found circumstantial evidence associating fumonsin
considered in cases of hepatic insufficiency (above). B1 contamination of forage with outbreaks of liver
disease in horses.
Diagnosis
Plant-derived hepatotoxins are usually first sus- Management
pected when clinical signs of hepatic insufficiency As mentioned above, one important action to con-
are seen alongside clinicopathological indicators of sider when investigating a horse with hepatic disease
hepatic insult and known exposure to hepatotoxic is to perform more widespread serum biochemical
plants. Blood tests are rarely specifically helpful in testing of several herd-mates, as this will commonly
the establishment of hepatotoxicity. However, pyr- demonstrate a more widespread outbreak of subclin-
roles formed following hepatic biotransformation of ical liver disease. Epidemiological considerations in
PAs have been shown to appear in the plasma and to such instances raise suspicions of exposure to a con-
bind to haemoglobin and other plasma proteins such tagious or toxic agent. Although research is ongo-
as fibrinogen via thiol groups. The stable compounds ing, there seems little current support for commonly
so formed can be identified in equine blood samples, suspecting contagious liver disease with the excep-
using chromatographic and other proteomic meth- tion of rare outbreaks of Theiler’s disease or fascioli-
ods, although such tests remain experimental rather asis. Thus toxins, perhaps from a nutritional source,
than commercially available. should be primarily suspected in most outbreaks.
With the prime exception of PAs, most hepato- Epidemiological patterns of disease within the
toxins do not lead to specific findings in liver biopsy herd might implicate certain grazing, forage or feed
specimens. The typical combination of megalocy- sources and this should then be examined closely for
tosis, biliary hyperplasia and fibroplasia are typical known toxic plants (e.g. Senecio sp.), moulding or other
of PA toxicity. Many different patterns of pathol- gross contamination. Consideration should then be
ogy may be seen following exposure to hepato- given to strategies of wholesale dietary change to
toxic drugs and chemical agents including zonal achieve avoidance of suspected nutritional sources,
or multifocal hepatocellular necrosis, lymphocytic even when the putative toxin remains unknown; for
hepatitis, cholestasis, granulomatous and even neo- example, as replacing hay feeding with commercial
plastic disease. bagged haylage or replacing homegrown grain with
To a large extent iron appears to be inevitably proprietary mixes.
accumulated in the liver of normal domesticated Examination of biopsy specimens offers clinically
horses, with mild to moderate amounts of hepatic important information, and specific pathological
haemosiderin being common in horses without findings may direct specific treatment protocols to
evidence of liver disease. Interpretation of the rel- aid recovery of suspected hepatotoxicity cases (e.g.
evance of large amounts of haemosiderin found in antifibrotic agents, anti-inflammatory drugs, phle-
the liver of horses should take into account further botomy for removal of iron, etc. [see Treatment of
signs of pathology, the horse’s age and the relative hepatic insufficiency for details]). Clearly the most
accumulation in hepatocytes versus Kupffer cells fundamentally important response to hepatotoxicity
and other macrophages. Commercially available ser- is identification and discontinuation of exposure to
vices exist for determination of mycotoxin content the toxic agent(s), although this may be difficult to