St George Veterinary Practice

12027 Carnarvon Hwy, St George

After Hours : 0417 731 077


Pimelea Poisoning of Cattle.


S.A. Duigan,

St George Veterinary Practice

12029 Carnarvon Highway, St George, Qld, 4487

A Perspective from St George, 59 years after initial reports of this disease were made from the town of St George and surrounding districts.



            Pimelea poisoning of cattle, formerly known as St George disease, is a cruel, debilitating and costly disease. It causes chronic heart failure, anaemia, wasting and/or the presence of diarrhoea. The economic impact is at best decreases in live weight gain and reproductive potential, or more seriously, death of the affected beasts. Major outbreaks are witnessed every 10-15 years or so when climatic factors favour growth of the native plant, Pimelea.


The Plant and The Toxin


            The genus Pimelea (Family Thymelaeceae) contains about 80 species native to Australia, although only a few have been implicated in causing disease in cattle (Kelly & Seawright, 1978). The three main species of interest in the Maranoa region are Pimelea trichostachya, P simplex and P. elongata (DPI survey, 1990). Pimelea trichostachya appears to be the most common species seen around the St. George district (field observation). A similar disease, caused by species of Pimelea, is seen in Northern South Australia, known as Maree Disease.

These species are slender herbaceous annuals up to 50-75cm tall. The leaves are alternate and the flowers occur in spikes up to 15cm long in the mature plant and are positioned at the terminal ends of branches. The small flowers and the flower stalks are covered with long silky hairs (Dowling & McKenzie, 1993).



Pimelea trichostachya


            These plants favour lighter, less fertile soils, such as sandy loams or light red clay soils (MLA, 2006). They are found in four Australian states:- Western and Central Queensland, New South Wales, South Australia and Western Australia. Pimelea spp seeds remain viable in the soil for up to two years. They are light and fluffy and likely to be easily carried via wind and dust (Pegg et al, 1994). Pimelea germinates during the cooler months of autumn and winter and flowers in spring (Dowling and McKenzie, 1993).

In 1975 a toxic compound similar to Huratoxin, found in other native Australian species was identified in Pimelea plants (Kelly & Seawright, 1978). By 1979, the irritant diterpenoid orthoester, Simplexin, was systematically isolated from Pimelea simplex and P trichostachya (Freeman et al, 1979). Irritant diterpenes have also been recognised for their skin irritant, purgative and cocarcinogenic properties (McKenzie, 2001). Chemical structure


The toxin is very potent in cattle and as little as 40-60mg whole dried plant per kg body weight given orally each day, is sufficient to produce the entire range of symptoms reported in the field (Kelly & Seawright, 1978). The most toxic part of the plant is the flower and nearby stem (MLA/Agforce Forum; McKenzie, 2006). It appears that the toxin is viable in not only the living plant, but also remains stable in dead and decaying plant matter (Kelly & Seawright, 1978).


Conditions of Poisoning


Favourable growing conditions for Pimelea are:-

  1. Previous summer rainfall below average
  2. Minimal pasture competition, ie after overgrazing or during drought,
  3. Winter rainfall and
  4. A dry spring  (Qld DPI survey, 1990; McKenzie, 2006; MLA, 2006) 

Thus, to some extent, Pimelea poisoning shows a seasonal occurrence. Incidences of poisoning are most frequent from August to December, however, new cases occur throughout the year (DPI Survey, 1990). This is due to the stable nature of the toxic components in the dead plant. Decaying fragments land on surrounding pasture and are involuntarily ingested by cattle. So, toxicity is seen in the complete absence of viable or visible plants (Kelly & Seawright, 1978).

Cattle rarely ingest Pimelea plants by choice due to its unpalatable nature (Dowling & McKenzie, 1993). So poisoning usually occurs by 1. eating fragments of the decaying plant that have contaminated surrounding pasture; 2. when, in the absence of available feed, cattle are forced to eat anything available (Kelly & Seawright, 1978), or 3. when the Pimelea plant is growing in the middle of a clump of grass, Buffel for instance. It is also believed that intoxication may occur via inhalation of this decaying plant matter (Dowling & McKenzie, 1993). It is likely that the majority of this inhaled toxin is bound to mucous in the caudal nasopharyngeal region and swallowed (McKenzie, 2001).

            Although poisoning is restricted to areas of suitable habitat (soil type and climatic requirements), it would appear that this area is increasing. Soil disturbance, previous over stocking and converting enterprises from previous sheep to cattle grazing are all leading to an increased incidence of poisoning (MLA, 2006). Moreover, altered annual rainfall patterns cause an increase in Pimelea growth and deplete competitive pasture species.

            Kelly & Seawright (1978) stated that all classes and ages of cattle appear to be affected equally by Pimelea intoxication. However, field reports and discussion with the producers losing cattle seem to point to recently introduced cattle and newly weaned calves, as the most commonly and most severely affected (field observation). In particular, cattle with the greatest energy drain, eg lactating cows or bulls during joining periods, always seem to suffer heavily. Research from the nineties suggests that previous exposure to Pimelea toxins in homebred cattle does not confer any protective advantage (D’Occhio, MLA Forum, 2006).




There are three recognised mechanisms by which Pimelea causes toxicity in cattle. Firstly, the irritant nature of diterpenoid orthoesters from Pimelea makes them extremely inflammatory to the lining of the gastrointestinal tract, leading to persistent diarrhoea (McKenzie, 2001). There is some blood loss in the faeces (Kelly & Seawright, 1978).

Secondly, Simplexin and other diterpenes isolated from Pimelea spp., are strong vasoactive substances (Kelly, 1975c). They achieve this by potent activation of Protein Kinase C (Pegg et al, 1994). This class of chemicals has a six membered C-ring that, although not identical in structure, is stereospatially equivalent to the natural protein kinase C activator, diacylglycerol (DAG; Pegg et al, 1994). Protein Kinase C is found in most tissues and is involved in a wide range of physiological functions including modulation of ion transport, secretion and exocytosis, gene expression, cell proliferation and importantly here, smooth muscle contraction (Pegg et al, 1994).

The bovine pulmonary vasculature is unique in that both arteries and venules as small as 20 micrometer diameter have a distinct muscular coat (Pegg et al, 1994).. Presumably Simplexin binds in the DAG binding site on the pulmonary venule wall, stimulating the action of PKC, thus, causing sustained constriction of pulmonary venules and impeding venous return from the lungs to the heart (Pegg et al, 1994). Increased right ventricular pressure and dilatation of the right side of the heart follows the congestion in the lungs (McKenzie, 2001).

            The third mode of action of poisoning is by expansion of plasma volume. Total plasma volume may increase as much as 178% and the total blood volume by 100% and is believed to be due to expansion of sinusoidal blood vessels throughout the body in conjunction with the associated heart failure (Kelly & Seawright, 1978). The extra plasma volume results in haemodilution of red blood cells and as there is no regenerative erythropoietic response, the animal becomes anaemic (Kelly, 1975c). Once the anaemia is severe enough (PCV 13%), then a rapid erythropoiesis ensues (Kelly, 1975b). Faecal loss of blood is not thought to contribute significantly to anaemia (Kelly & Seawright, 1978).


Clinical Signs


            Diarrhoea is normally the first sign of Pimelea poisoning, commencing within a few days of ingestion, and may eventually progress to dysentery (Kelly & Seawright, 1978). Cattle soon lose condition and become depressed (McKenzie, 2001). Affected animals have an inability to withstand stress and usually marked exercise intolerance develops. Cattle can die suddenly during exertion such as moving onto less affected pasture or simply trying to get to feed and water (Kelly, 1975c).

Prominent, distended jugular veins and an obvious jugular pulse are commonly seen in affected cattle (Kelly, 1975c). Dependent subcutaneous oedema develops and is mostly localised to the submandibular and/or brisket regions. However, ventral oedema may extend caudally to the udder in females or to include the entire preputial sheath in males. Swelling can also include ventral extremities (usually forelimbs) and a generalised anasarca has been documented in severely affected cases (McKenzie, 2001). These circulatory symptoms are usually not evident for at least 3 weeks although severe acute intoxications may be fatal before more specific “classical” signs develop (Kelly & Seawright, 1978). Producers note that mortality is not always related to clinical signs and that cattle can be in good condition and still suffer fatal congestive heart failure (Producer Discussion; MLA Forum Roma. September 2006)



A. 3 yr Braford cow, January 2003. Note             B. Mature cow, September 2006. Note

good Buffel coverage.                                          body condition, oedema and tail position     

                                                                            (severe scours).       


Mucous membranes become pale and the animal develops anaemia, presenting as normocytic, normochromic and initially without an accompanying compensatory erythropoietic response (Kelly & Seawright, 1978). Severely intoxicated animals usually show a panleucopaenia in which the lymphocyte counts are often reduced more than the neutrophils although these animals do not appear to be immunologically compromised (Kelly & Seawright, 1978).




            Necropsy findings vary according to severity and duration of illness and with the particular symptoms that were exhibited prior to death. Acutely intoxicated animals may be seen to literally drop dead with very little time for pathophysiological changes to develop (Kelly & Seawright, 1978). Affected animals are usually in poor body condition and have minimal fat reserves, which are replaced by oedema if anything (Kelly, 1975a). Hydrothorax and moderately congested lungs are present while ascites is absent. Hydrothorax occurring in the absence of ascites in this type of cardiovascular collapse is a relatively rare occurrence (Kelly & Seawright, 1978). The right ventricle is usually dilated, without hypertrophy of the cardiac muscle (Kelly, 1975a). Myocardial necrosis is often seen and is attributed to prolonged anaemia plus increased plasma volume (Kelly & Seawright, 1978).

The liver is grossly engorged due to retention of blood (Kelly, 1975a). It appears swollen, has a deep purple discolouration and is spongy with the vast excess of blood that has accumulated in hugely dilated periportal sinusoids; a condition described as peliosis hepatis (McKenzie, 2001). These large distended sinusoids and lakes of blood lined by stretched hepatocyte plates are especially prominent in subcapsular tissue, where they may become thrombosed (Kelly & Seawright, 1978). Corrosion casts of severely affected livers show that there is ready communication between portal and hepatic veins via these enlarged vascular spaces (Kelly & Seawright, 1978). Capillary dilatation of other organs with a sinusoidal type circulation, such as kidneys, adrenal cortex, spleen and bone marrow is also common (Kelly, 1975c). Lymph nodes are oedematous & show depletion of lymphoid tissue (Kelly & Bick, 1976).

Abomasal ulceration was detected on autopsy of calves experimentally intoxicated with Pimelea (Kelly, 1975b,c). Congested intestines are seen in acutely poisoned animals (Dowling & McKenzie, 1993). However, considering the severity of the diarrhoea suffered by these animals, microscopic examination of the gut reveals remarkably little pathology (Kelly & Seawright, 1978).



Animal Species Affected


In horses and sheep the syndrome has historically been believed to be restricted to severe gastrointestinal irritation. There are none of the other chronic symptoms seen in cattle (Kelly & Seawright, 1978). This is because sheep and horses lack the powerful smooth muscles in the pulmonary venule walls that are present in cattle (McKenzie, 2001).

However, recently there have been reports of horses exhibiting cardiovascular signs due to Pimelea (McKenzie; MLA Forum, 2006). In the Maree district in 2002, a horse with access to Pimelea simplex, showed typical signs of Pimelea intoxication. Clinical signs included severe oedema of the head, neck and brisket and post mortem and histology showed liver pathology to be typical of that documented in cattle (Weaver, 2002).




There is no recognised specific therapy. Desperate circumstances call for desperate measures and some producers have, anecdotally, taken to slashing brisket swellings to release the accumulated fluid. Treatment at present revolves around management of stock and affected pasture.

Severely affected animals can recover if nursed and removed from the source, however, it will be a very protracted recovery time. Avoiding exercise by providing food and water and minimising stress are very important to recovery. Less severely affected animals may recover more quickly if simply given something else to eat (Kelly, 2006; pers com). Dietary supplementation especially with high protein additives such as cotton seed and silage appears to be favourable with producers (Producer Discussion; MLA Forum, 2006). It seems to be a general consensus amongst producers that urea supplementation exacerbates the condition. This is possibly due to increasing dry matter intake as cattle eat everything in sight so will probably graze closer to the ground.

Immunisation of cattle with a protective immunogen against Simplexin was attempted by CSIRO and the University of Central Queensland but was not successful (Pegg et al, 1994). Immunised cattle produced antibodies to the toxic components of Pimelea but no protection from poisoning was observed.

Supportive symptomatic therapy for heart failure with diuretics may be justified with valuable animals, eg bulls (McKenzie, 2005). Various clients of ours have trialled this with possible short term gain, although no scientific data exists. The loop diuretic, Frusemide, (Frusemide 50mg/ml; Ilium) at a dose of 5-10mls IM once or twice daily (as per label instructions for cattle) temporarily decreases the load on the heart. The mechanism of action, although not fully established, increases renal excretion of water and electrolytes (Plumb, 2002). In some animals this may give some short-term reprieve such as allowing movement to hospital pens/paddocks or abattoirs.





Probably most important is recognising when climatic factors favour Pimelea growth and moving cattle from the affected pasture before clinical signs develop (McKenzie, MLA Forum, 2006). This is easier said than done since shifting affected cattle usually brings about one of two events; the severe cases either roll over and die as they are being moved or else they go down and refuse to move, thus remaining on the affected pasture (Kelly pers com, 2006). Removing the source of the toxin usually reduces signs of diarrhoea very quickly, however, signs of heart failure and anaemia may persist for many months before eventual recovery or death (McKenzie, 2005). Options are maintaining a safe hospital paddock on heavier soil if possible, lot feeding, agistment, putting cattle on the road or selling.

Cattle should not be allowed to return to affected country until after significant summer rainfall that will wash away decayed Pimelea plant fragments from the pasture and facilitate biodegradation of the toxin by plant surface and soil microbes (McKenzie, 2005). Once a good pasture stand has been established in an affected paddock, cattle should be allowed to graze this country for only 5-6 weeks before spelling the paddock again. According to one of our local producers, this enables the grass population to remain competitive and minimise growth of unwanted Pimelea species (Bill King pers com, 2006). There is no instant cure to remedy decades of poor land management when faced with adverse climatic conditions that favour Pimelea germination and growth.

It is worth noting that most of this country around St George was previously sheep grazing country. Superior economic returns from producing cattle over sheep have tempted producers to shift the focus of their enterprise to the cattle market.  Since sheep suffer diarrhoea only from grazing Pimelea and don’t seem to be inflicted with the same cardiovascular signs as cattle it is feasible to suggest that a return to sheep production could overcome stock losses.

Controlling plant populations once they are established is difficult, often costly and largely dependent on weather. Reducing the grazing pressure to allow some competitive pasture growth may decrease the density of Pimelea. However, Pimelea trichostachya is reported to survive in dense growth of Buffel grass (McKenzie, 2005).   Soil disturbance, such as cultivating paddocks, is likely to encourage the growth of Pimelea (Pegg et al, 1994).

Burning pasture in successive years to destroy both plants and their seedlings may help. However, unpredictable rainfall may make this a risky procedure, plus there may be insufficient fuel loads to allow a thorough second burn. A once only burn will likely encourage germination of seeds in the subsequent growing season (Pegg et al, 1994) and thus, increase future Pimelea population densities (McKenzie, 2006).




     Lack of fuel to burn in second consecutive season.

                             September, 2006. 


 The application of effective herbicides is restricted by cost and environmental considerations. Last decade the Queensland Wheat Research Institute suggested that combinations of Atrazine, 2,4-D and Agral 60 could kill 80-90% of young Pimelea plants at a cost of approximately $9/ha. Or 2,4-D alone might be effective at approximately $6/ha (Wells, G. Unpublished data 1995). Newer selective broad leaf herbicides include, eg Glean or Ally, with improved efficacy may be preferable now. Spraying should be done while the plant is small since larger plants have decreased leaf surface area to total plant volume ratio so chemicals may not kill as effectively (Producer Discussion; MLA Forum, 2006).


Economic Importance


            ABC Southern Queensland’s Alice Platt reported the cost of Pimelea to the Southwest Queensland cattle industry as being upwards of $10 million in the early 1990’s (ABC Online, 2006). It has a multi-tiered effect in that it causes cattle deaths, decreased live weight gains and reproductive losses (MLA, 2006). For example, in a mild case of intoxication, if protracted scouring and ill-thriftiness caused a daily weight loss of 0.3kg, in one year the decrease in live weight is 109.5kg. This is a significant loss in value to the producer.

There are some staggering examples of losses around our area. One property has lost 120 head of cows in the last 6 months (at ~$500/hd = $60 000 plus calf losses) and 4 bulls. Another enterprise lost 14 bulls (at an average value of approximately $3000/hd, a financial loss of about $42 000). These are most likely conservative estimations. There is a huge risk in buying expensive animals, such as bulls, to place on country known to have Pimelea. Accepting cattle for agistment is another risky business and quite a few of my clients have had a difficult time trying to save other people’s cattle or paying for temporary treatment in severe cases.

“Old Cashmere” 35km NW of St George, is 34 000 acres of grazing country currently running approximately 200 fewer breeders (a difference of 440 Live Stock Units if 1 LSU = requirements for 450kg steer at maintenance) than in a “normal”, non-drought affected year (Bill King pers com, 2006). While most paddocks on this property are contaminated with some Pimelea, there is one paddock in particular known to cause severe intoxication of cattle. The only management difference is that it is stocked at a lower rate. There is also a marked decrease in reproductive activity in cows from this paddock compared with seven other paddocks; 66% pregnancy rate as opposed to the other paddocks averaging 91% (78-96%).

Cost of medication for symptomatic treatment needs to be considered. To reduce oedema, Frusemide retails at approximately $40 per 50ml bottle. At a dose rate of 5-10ml once or twice daily, clients are looking at $4.00-$8.00 per dose. Multiple doses may be necessary, eg “Chippeway” one 4 month old steer received 10ml daily for 5 days (one whole bottle). He did eventually recover. However, medical treatment is unlikely to be economically justifiable where large numbers are affected

The cost of additional control / management measures for Pimelea alone eg agistment, supplementary feeding, moving stock around (time/labour) has not been investigated. Producers would appreciate just having more time for other tasks and not worrying about cattle deaths or illness. Another concern mentioned by a local producer was the mental state of producers dealing with this problem. Similar to severe, protracted drought situations, the stress and increased pressure on the family unit causes increased likelihood of divorce, depression, suicide, etc.


What is being done and what still needs to be done?


Unfortunately, being native, there is little chance that any eradication campaigns will occur or likely be successful if attempted. Biological control, such as insects or fungi to specifically attack Pimelea could be considered, however, there is considerable risk of harming other native species with control measures (McKenzie, MLA Forum, 2006).

Considerable interest exists, in manipulating numbers or activities of specific populations of rumen microflora to detoxify toxic plant components ingested by grazing cattle (Weimer, 1998). Bacteria would need to adapt to produce the necessary metabolic machinery, including enzymes for biotransformation, transport proteins to shift the toxic matter into the cell plus the necessary regulatory genetic material (Weimer, 1998). Adaptation will only occur if there is selective pressure on a group of bacteria to produce this machinery, eg. the advantage of being able to metabolise the toxic plant to provide a source of energy. Therefore, the toxic plant needs to be constantly present in sufficient quantities to justify bacterial modification. Unfortunately the seasonal nature of Pimelea means that there will be part of each year when plants are not present at high enough levels and, thus, bacterial populations depending on this plant species as an energy substrate may not survive.

There is some debate amongst local producers as to whether homebred cattle are able to withstand Pimelea toxins any better than introduced cattle. It is likely that no home ground advantage exists. Yet sheep appear to have dealt with these toxins for decades. Hence, at risk cattle could be inoculated with sheep rumen fluid containing microbes, which may offer some protection (Johnston et al, 1998).

            If a suitable drug could be found with beneficial effects and no undesirable side effects, the pharmacological deactivation of Protein Kinase C might prevent its binding to pulmonary venule walls (McKenzie, 2005). Currently this seems quite unlikely (McKenzie, 2005) given the scope of functions that PKC is involved in. Alternatively, a compound to bind Simplexin, in particular its functional C-ring so altering its stereospatial similarity to DAG, would inhibit it from binding to PKC in the pulmonary venule smooth muscle and may provide an answer.        

At a recent MLA forum in Roma (September 2006), producers were encouraged to fill in a survey designed to establish the extent of the problem – both plant distribution and cattle numbers affected. Last decade when producers found themselves in a similar situation, much noise was made and funds were granted for research leading to a little further information being gleaned about this plant and the nature of the condition. The difficulty is that relatively few are affected and the problem is worse in some years than others. When the season changes and the incidence of poisoning isn’t so high, there is no pressure maintained to keep up research. Now we find ourselves in the same situation as before, namely Pimelea is abundant, alternative feed is not and cattle are dying. Hence, the need for producers, whether affected currently, previously or possibly in the future to fill out the survey and avoid going back to square one in another 10 years time.




            The toxic component of the native genus Pimelea is irritant to the intestines and causes severe congestive heart failure. The sporadic nature of Pimelea poisoning outbreaks has hindered attempts to completely purify the toxin and understand its pathophysiology. There is no recognised treatment and symptomatic medication for heart failure is only a temporary measure and partial answer at that. The most important management tool is recognising early on when climatic factors favour Pimelea growth and increase the risk of poisoning. Removing cattle from the affected pasture at this time decreases stock losses.



My sincere thanks to Ross McKenzie, Roger Kelly, Bill Aspden Sandi Jephcott and Geoff Niethe for their assistance and information. Also thanks to my colleague Blair Kennedy who’s assistance with computers is greatly appreciated.