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This article was published in 1996
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Some Observations and Comments on Fireweed Toxicosis of Cattle on the Mid-North Coast of NSW

AJ Glassop, District Veterinarian, Gloucester RLPB

Pyrrolizidine alkaloids in plant species such as Senecio, Crotolaria, Echium and Heliotropium, are potentially hepatotoxic for cattle.

After Bracken Fern, Fireweed is arguably the most common toxic weed in native and improved pastures on the Mid-North coast.

Fireweed is an aggressive invader of pasture, particularly when dry conditions reduce competition from other species, or where soil is disturbed for pasture sowing or renovation. It survives, flowers and sets seed under extremely dry conditions, when other plant species are dying from lack of moisture. It can set seed almost all year round, although the main flowering period is during the cooler months.

Senecio madagascariensis, an introduced species of Fireweed, is the dominant species along coastal NSW and South-East Queensland. In the past, S. madagascariensis has been confused with closely related forms of the Australian native Fireweed (S. lautus), which comprise only a minor part of the Fireweed population of coastal NSW.

Senecio lautus has caused cattle losses in Queensland, and only botanical experts can differentiate S. lautus from S. madagascariensis.

This presentation of some field observations from a variety of cases of S. madagascariensis toxicosis diagnosed in the Gloucester RLPB district over the last few years, is to remind field veterinarians that Pyrrolizidine Alkaloidosis can produce a variety of clinical syndromes.

On the Mid-North coast, there has been an increase in the number of cases of Pyrrolizidine Alkaloidosis diagnosed in cattle during recent years. It seems the main reason for this are:

1. Increased exposure of cattle to Fireweed, due to drought conditions.

2. We're looking harder and investigating more cases of ill-thrift and subsequent death.

3. A recognition of the range of histological hepatic lesions produced in S. madagascariensis toxicosis.

In early cases, P.A. was often not considered as a differential diagnosis where periacinar hepatic necrosis fibrosis was the only finding the diagnosis in these cases was 'toxic hepatopathy' (consider aflatoxicosis, gossypol toxicity, congestive heart failure, Noogoora Burr, Poison Peach, Lantana etc.)

However periacinar hepatic fibrosis (so-called 'veno-occlusive' disease) is now recognised as a chronic manifestation of Pyrrolizidine Alkaloidosis in cattle (Cook et al. 1994).

Demonstration of sulphur-bound pyrrolic metabolites in liver tissue confirmed these cases, and fireweed toxicosis became a more common diagnosis.

Cases have occurred in all parts of the district, in cattle of all ages, most breeds, at any time of year and under all types of feed conditions, but because deaths were usually sporadic, many probably went uninvestigated and undiagnosed. P.A. has been diagnosed at autopsy on over 35 properties in this district in recent years.

Most properties involved have lost only 1 or 2 head, the biggest loss in this district being 15 head on one particular property - this is only small compared to losses of 50+ head, reported on some properties in Queensland.

'Background' liver damage from P.A.s may be found in cattle that have died from other unrelated causes, so the overall economic losses caused by Fireweed (due to sub-clinical hepatopathy), are impossible to quantify.

CLINICAL SIGNS

Signs are extremely variable, ranging from chronic ill-thrift, to sudden death in fat animals that had appeared ill only in the 24 to 48 hours prior to death.

The usual clinical picture of Fireweed toxicosis associated with liver fibrosis, is characterised by illthrift, sometimes scouring, emaciation and eventual death OR in milder cases, just vague illthrift and poor growth rates.

In my experience, jaundice is rarely a clinical observation, even in cases with severe liver damage. Some cases show CNS signs associated with an hepatic encephalopathy; these signs include ataxia, staggering, blundering through fences, aggressiveness and apparent blindness.

Some cases have been sudden deaths in fat animals in opportunity feedlots, where the animals have been on feed for 60-70 days - with definitely no access to Fireweed in that time!

Other cases have been in yearling stud Friesian heifers on prime Kikuyu / rye / clover pasture with absolutely no Fireweed present - BUT these heifers had been on agistment in Fireweed infested paddocks some 3-4 months previously.

It has previously been recognised that cattle exposed to P.A.s in Fireweed, may not show signs of toxicosis until as long as 6-12 months (or more) after exposure. Possibly the alkaloids are stored in hepatocytes, and not metabolised to the toxic sulphur-bound pyrrolic metabolites until some later stage.

NECROPSY FINDINGS

Chronic illthrift cases have a marked hepatic atrophy - a small firm liver with a palpable consistency of 'tyre-rubber', and often with a silvery slightly-mottled sheen on the cut surface. The gall bladder is often enlarged and full of dark tacky bile. Many cases have excessive pale-straw coloured fluid in the abdominal cavity - the quantity of this transudate may be up to 10 litres or more.

Sudden death cases often display a slightly enlarged liver with an obvious mottled appearance on the cut surface. This mottling can sometimes extend to a very striking two-toned tan and brown 'jigsaw' pattern on the cut surface. In some cases ecchymotic and petechial haemorrhages may be found in various parts of the carcase, but this is not a constant finding.

DIAGNOSIS

One consistent finding in cases where hepatopathy has been suspected and pre-mortem bloods have been submitted, is a significant elevation of GGT levels (up to 3-4 times normal). Other liver enzymes (AST, ALPetc.) and bilirubin, are not consistently elevated.

Pathologists at RVL Wollongbar describe 3 main changes in cattle livers in S. madagascariensis toxicosis:

1. Megalocytosis

2. Portal fibrosis/biliary hyperplasia

3. Periacinar fibrosis (often myxomatous and often bridging from periacinar to periportal areas.

Some, or all of these changes may be present - NOT ALL CASES SHOW ALL CHANGES.

The typical histological change is of a marked periacinar myxomatous fibrosis ('veno-occlusive' disease - as it may totally occlude the central vein) often bridging across the lobule to areas of periportal fibrosis.

Megalocytosis (enlargement) of hepatocytes, with karyomegaly (enlarged nuclei) may be prominent. Karyomegaly is often also present in kidney sections.

Demonstration of sulphur-bound pyrrolic metabolites in fixed liver tissue is evidence of exposure to P.A.s, but by itself does not conclusively diagnose death form Pyrrolizidine Alkaloidosis.

An interesting observation is that I have never seen visible evidence of cattle eating or even nibbling mature Fireweed plants, and I have never diagnosed a case in a paddock of 'wall to wall' Fireweed (see slides).

The obvious assumption is that cattle avoid eating mature Fireweed, but the young seedlings may be the culprits - accidentally ingested with pasture? more palatable?, higher alkaloid content?

PLANT STUDIES

During 1994, monthly collections were made of plant samples of S. madagascariensis from 2 sites at Taree and 1 at Wollongbar, and of S. lautus from 2 sites at Rockhampton. The aims were to determine the concentration of alkaloids in the plants, and whether those varied with stage of growth, time of year or seasonal conditions.

Final results from these studies are not available, but some preliminary observations are interesting.

Initial analyses showed the NSW samples had much lower concentration of alkaloids than the Queensland samples (0.03% D.M. compared to 0.1 - 0.5% D.M. in Qld. samples), and these concentrations were below those generally accepted to be necessary to result in hepatic damage. However further investigations now indicate that S. madagascariensis contains different alkaloids to S. lautus, and that the limited assay method was not detecting the S. madagascariensis alkaloids.

The economic impact of Fireweed (S. madagascariensis) on cattle production is not clear. It is an unpredictable cause of disease that is usually sporadic, but can, as in recent drought years, cause more dramatic problems.

Because of its usually sporadic occurrence and because of the wide range of other disease conditions which can result in illthrift, it is likely that most cases of Pyrrolizidine Alkaloidosis due to S. madagascariensis are never diagnosed.

REFERENCE

Cook RW, GIN PA, Fraser GC, Boulton JB (1994): Periacinar hepatic fibrosis in cattle - the distinctive 'veno-occlusive' lesion of Pyrrolizidine Alkaloidosis. Proceedings Aust. Soc. for Veterinary Pathol. - Canberra.


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