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, and produces large amounts of seed which is readily distributed by wind, so there is an enormous seed bank in the soil.
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 the closely related Australian native Fireweed (S.lautus), which comprises only a minor part of the Fireweed population of coastal NSW. Senecio lautus has caused significant cattle losses in Queensland, and only botanical experts can differentiate S.lautus from S.madagascariensis.
S.quadridentatus (cotton fireweed) also contains pyrrolizidine alkaloids, but has not been identified on any of the properties in this district.
This presentation of some field observations from a variety of cases of S.madagascariensis toxicosis diagnosed in the Gloucester RLPB district over several 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. Possibly the main reasons for this are:-
(1) Increased exposure of cattle to Fireweed, over a number of drought years
(2) More investigation of sporadic cases of ill-thrift and subsequent death
(3) A recognition of the range of histological hepatic lesions produced in S.madagascariensis toxicosis - apart from megalocytosis and karyomegaly of hepatocytes, portal fibrosis and biliary hyperplasia, periacinar hepatic fibrosis (so called ‘veno-occlusive’ disease) is now recognised as a chronic manifestation of Pyrrolizidine Alkaloidosis in cattle (Cook et al 1994).
Laboratory submissions have been made from all parts of the district, (at least 30 or more properties over several years), in cattle of all ages and most breeds, at any time of year and under all types of feed conditions, but because deaths were usually sporadic, many more cases were probably uninvestigated and undiagnosed. A significant number of cases seemed to occur in the winter/spring period particularly where paddocks were overstocked and feed was somewhat limited i.e. the cattle were under some degree of ‘metabolic stress’. However some cases have been diagnosed where paddock feed was relatively good.
While most properties involved have had only sporadic cases and have lost only one or two head, the biggest loss in this district was 15 head on one particular property over a three or four week period — this is only a small loss compared to losses of 50+ head, reported on some properties in Queensland.
‘Background’ sub-clinical 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), is impossible to quantify.
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 chronic Fireweed toxicosis associated with chronic 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 a hepatic encephalopathy; these signs include ataxia, staggering, blundering through fences, aggressiveness and apparent blindness.
Some more acute cases have been almost sudden deaths in otherwise healthy animals, where the animals have been on very good pasture — with little obvious presence of fireweed in the pasture at that time. These cases often demonstrate an acute liver necrosis superimposed over a more chronic liver fibrosis.
Other cases have been, for example, 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 is suspected that cattle exposed to P.A.’s in Fireweed, may not show signs of toxicosis until as long as six months (or more) after exposure. The toxic metabolites of the alkaloids cause cumulative damage to hepatocytes, so clinical expression is dependent on alkaloid dose at any one time, as well as length of exposure to alkaloids.
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, oedematous and full of dark tacky bile. Many cases have excessive straw coloured fluid in the abdominal cavity — the quantity of this transudate may be up to 10 litres or more.
Conversely, acute cases often display a slightly enlarged liver with an obvious pale mottled appearance on the cut surface. This mottling can sometimes extend to a very striking two-toned tan and red ‘jigsaw’ pattern on the cut surface. (See colour slides). Occasionally scattered petechial haemorrhages may be found in various parts of the carcase, but this is not a constant finding.
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 ten times normal). Other liver enzymes (AST, ALP etc) and bilirubin, are not consistently elevated in all cases.
Pathologists at R.V.L. Wollongbar describe 3 main changes in cattle livers in S.madagascariensis toxicosis:-
(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 necessarily 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 sometimes present in kidney sections.
A test to demonstrate the presence of sulphur-bound pyrrolic metabolites in fixed liver tissue (or in blood samples) is evidence of exposure to P.A.’s, but by itself does not conclusively diagnose death from Pyrrolizidine Alkaloidosis. However, as far as I am aware, this test is no longer available in Australia.
An interesting observation is that I have never seen visible evidence of cattle eating or even nibbling mature Fireweed plants (even in drought), and I have never diagnosed a case in a paddock of ‘wall to wall’ Fireweed (see slides). Conversely many cases have been diagnosed in paddocks where fireweed was not obviously present in profuse amounts at the time.
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?
Some years ago, monthly collections of plant samples of S.madagascariensis were made from two sites at Taree, one at Menangle and one at Wollongbar, and of S.lautus from two 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. As far as I know these studies were never finalised, but some preliminary observations were interesting.
Initial analyses showed the NSW samples had much lower concentrations 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 suggest that S.madagascariensis may contain different alkaloids to S.lautus, and that the initial limited assay method was not detecting these alkaloids. As far as I know there has been no further work done due to lack of funding.
There is no specific treatment for affected animals, but problems can be minimised by pasture improvement, rotational grazing and avoidance of overstocking.
Control of fireweed has been attempted using a variety of methods including hand weeding, herbicide application using wick-wipers to protect underlying pasture, slashing, and grazing by sheep or goats (which seem to find fireweed more palatable than do cattle, as well as being less susceptible to the toxic effects of the alkaloids).
While some of these methods may assist with short term control of fireweed density, long term control is generally less successful due to the massive seedbank present in the soil. In my opinion the most successful control of fireweed is achieved by promoting competitive improved pastures, and avoidance of overstocking.
The overall economic impact of Fireweed (S.madagascariensis) toxicosis 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 serious losses.
In reality, the number of cases diagnosed is relatively small compared to the number of cattle in the district and the amount of fireweed present in the district, but because of the usually sporadic occurrence, and because of the wide range of other disease and/or nutritional problems which can result in illthrift, it is likely that many cases of Pyrrolizidine Alkaloidosis due to S.madagascariensis are never diagnosed.
Cook R.W., Gill P.A., Fraser G.C., Boulton J.B. — Periacinar hepatic fibrosis in cattle — the distinctive ‘veno-occlusive’ lesion of Pyrrolizidine Alkaloidosis. Proceedings of Aust. Soc. for Vet. Pathol., Canberra 1994.