A correct diagnosis will often automatically follow after an investigator has precisely defined the history, the clinical signs, the gross pathology, and the histopathology of a poisoning event. These four tools remain the most informative and reliable in the plant poisonings investigation tool kit and if any one of them is in any way inconsistent with the diagnosis made then it is very likely that the diagnosis is wrong.
Outbreaks of poisonous plant related photosensitisation may be primary, or they may be secondary to a primary hepatopathy. Relatively few examples of primary photosensitisation occur, only a limited number of primary hepatopathies are accompanied by secondary photosensitisation, and so far there are no examples of primary photosensitisations that are accompanied by a primary hepatopathy.
Photosensitisation results from the circulation in the skin of compounds that can become photoenergised by incident sunlight, usually by wavelengths in the visible range (ie bright sunlight). Tolerance to these compounds has little to do with individual or species differences in the rate of metabolising the offending compound. All of these compounds are predictably only slowly metabolised, which is why they cause problems in the first place. Tolerance is all about how much ability the animal has to prevent incident sunlight from reaching the blood vessels in its skin. This tolerance is directly related to skin thickness, skin density, the length and density of fibre cover present, and the degree of pigmentation in the skin. The most common potentially photosensitising compound for ruminants is phylloerythrin formed from ingested plant chlorophyll. When a compound becomes photoenergised it is capable of destroying membrane barriers, hence it can rapidly cause a cellulitis of the dermis and epidermis which results in oedematous swelling and intense itchy irritation.
Hepatopathies can be either per acute, acute or chronic. Per acute hepatopathies are characterised by ‘sudden death’ whereas chronic hepatopathies are characterised by ill thrift. The exception is a chronic hepatopathy that results in liver copper accumulations, hence the risk of subsequent sporadic ‘sudden deaths’. Acute hepatopathies in cattle can give rise to secondary hepatic encephalopathy, as can chronic hepatopathies in horses. In both cases nervous signs will dominate the clinical picture. These signs are of CNS depression, aimless wandering and reduced awareness, but animals may also display outbursts of irritability. Eventually animals become recumbent and either comatose or convulsive. For a hepatopathy to give rise to photosensitisation it would normally be expected to involve a dysfunction of the liver mechanism for processing phylloerythrin. A commonly encountered significant processing problem is that of bile duct obstruction. Many hepatopathies do not result in photosensitisation in the majority of affected animals. This fact can be used as a diagnostic aid.
Group 1. sapogenin bile duct crystals associated
Group 2. miscellaneous
Echium, Heliotropium, Amsinckia, Senecio & Crotalaria spp can all produce PA’s. Echium plantagineum and Echium vulgare are commonly encountered weeds of cultivation paddocks, herbicide treated paddocks, overstocked pastures, or fire damaged pastures in central and southern inland districts of NSW. Alkaloids are produced in all parts of the plant including seeds (which can be present as contaminants in grain purchased for stock feed use). Alkaloid production in this plant starts at the early winter rosette growth stage (0.2% DM) and gradually increases, reaching a maximum at the late spring flowering stage (1.3% DM). By mid summer alkaloid levels will have fallen dramatically down to 0.2%. The drying process itself can reduce the alkaloid content by up to 40%. Ingestion of PA’s will inevitably cause a chronic hepatopathy. Horses and cattle are the most sensitive, sheep and goats the least. British breed sheep are more sensitive than merinos. Chronic hepatopathy in horses and cattle can lead to hepatic encephalopathy hence a presentation that involves nervous signs.
Chronic hepatopathy in sheep can lead to hepatic copper accumulations hence a presentation that involves sudden death due to the haemolytic crisis that follows the sudden release of liver copper. Horses with compromised livers will handle the high nitrogen content of legume pastures poorly. Sheep with compromised livers will tend to accumulate more copper when they are on legume pastures. Chronic hepatopathy per se will eventually give rise to ill thrift in all animal species. The supplementation of sheep with molybdenum should reduce their rate of liver copper accumulation.
When merino or goat wethers are used to control Echium infestations, the group of wethers being used should be changed at least every 2 to 3 years (with Heliotropium control change them every year). Echium is easily controlled by the establishment and maintenance of competitive perennial pasture species, this process is assisted by a combination of slashing Echium infestations at flowering time and spelling the pasture, rather than by using repetitive herbicide applications.
Senecio, Echium, Heliotropium, Amsinckia, & Crotalaria spp can all produce PA’s. Senecio madagascariensis is a short lived perennial low bush. It invades overgrazed pastures and neglected cultivation paddocks on the NSW coast. Alkaloids are produced in all parts of the plant including seeds. Germination and growth typically occurs during the Autumn to Spring period, followed by drying off of the plant over summer. Peak PA production would be anticipated at flowering, with a significant reduction in alkaloid content when the plant drying off.
Ingestion of PA’s will inevitably cause a chronic hepatopathy. Horses and cattle are the most sensitive, sheep and goats the least. British breed sheep are more sensitive than merinos. Chronic hepatopathy in horses and cattle can lead to hepatic encephalopathy hence a presentation that involves nervous signs. Chronic hepatopathy in sheep can lead to hepatic copper accumulations hence a presentation that involves sudden death due to the haemolytic crisis that follows the sudden release of liver copper.
Horses with compromised livers will handle the high nitrogen content of legume pastures poorly. Sheep with compromised livers will tend to accumulate more copper when they are on legume pastures. Chronic hepatopathy per se will eventually give rise to ill thrift in all animal species. The supplementation of sheep with molybdenum should reduce their rate of liver copper accumulation. Merino wethers and fibre producing wether goats can be used to control Senecio infestations, but to minimise any animal health risk the group of wethers being used should be changed at least every 2 to 3 years.
Panicum coloratum (bambatsi panic), P. maximum (guinea grass), P. miliaceum (millet panic), P. gilvum (sweet panic or hairy panic), and Tribulus terrestris are all capable of causing spasmodic episodes of a severe acute hepatopathy with secondary photosensitiation, in juvenile sheep and goats. They are less inclined to affect adult sheep and goats or cattle. Outbreaks of this hepatopathy are very spasmodic because they require a second factor to be present before toxicity can occur.
The first factor is a particular type of steroidal saponin (often diosgenin forming) produced by these plants, and the second factor is probably an unrelated hepatotoxic compound produced concurrently either by the plant or by a pasture fungus associated with the plant. When the hepatotoxin is present the liver’s ability to process the steroidal saponin is compromised and consequently insoluble sapogenin crystals are able to precipitate out into the bile ducts. This results in an acute hepatopathy with photosensitisation and death. Activity of the second factor seems to be favoured by any short rainfall event that occurs during an otherwise dry summer. For Tribulus, activity of the second factor is definitely far less in the northern parts of NSW compared to the central and southern districts. For Panicum, activity of the second factor is possibly also far less in the northern parts of the state. Histopathology on liver sections will confirm the diagnosis.
This weed is commonly encountered in heavy infestations on steep hill country along the full length of the NSW Great Dividing Range. This plant frequently causes animal health problems but veterinarians remain unaware of these problems because they are not called in to deal with the affected livestock. Control of this weed is most economically achieved by strategic grazing and many landholders will attempt this. However if this grazing is not carried out appropriately then animals will be poisoned. Affected animals experience hyperthermia and severe photosensitisation. They become extremely irritable, some may display signs of a mild hind limb paresis, and some may experience diarrhoea. Affected animals will take about 5 days to unload any ingested hypericin and require full shade during this recovery period.
St John’s wort contains the toxin hypericin, the amount in narrow leafed wort is double what it is in broad leafed wort. The amount of hypericin in the plant can be huge from mid spring to mid autumn, but there is usually far less present from mid autumn to mid spring. The plant at first appears ‘dead’ during this low hypericin period but it is actually putting out soft green basal shoots which are both palatable and necessary for the plants survival.
The most hypericin tolerant animal is a fully pigmented steer, but the most effective defoliator of wort plants is either a sheep or a goat. The most hypericin tolerant sheep is a superfine wool type merino wether carrying at least 4 months of fleece cover. Never put pregnant animals, lactating animals or juvenile animals onto wort infested pastures. Never put recently shorn sheep onto wort.
Start grazing broad leafed wort with cattle in early April, introduce sheep in early May, pull sheep out in mid October, and pull cattle out by mid November. Start grazing narrow leafed wort with cattle in late May, introduce sheep in early July, pull sheep out in mid September, and pull cattle out by late October. Use high stocking rates and graze it hard, particularly in early Spring, this will suppress the new season hypericin producing flower spike shoots and thereby extend the low hypericin safe grazing period.
Cestrum poisoning can present as a peracute hepatopathy hence deaths within hours of plant ingestion. Affected survivors will be developing an hepatic encephalopathy hence they are depressed but irritable, usually recumbent, and ultimately either comatose or convulsive. Some affected survivors may have diarrhoea. On autopsy there will be signs of liver damage together with haemorrhages throughout the carcase. Histopathology on liver from affected survivors will confirm the presence of centilobular hepatocellular necrosis, plus brain sections may demonstrate an hepatic encephalopathy.
Both Cestrum parqui plants and Xanthium spp seedlings (Bathurst & Noogoora burrs) produce very similar hepatotoxic glycosides, namely carboxyparquin and carboxyatractyloside respectively. Consequently they cause very similar clinical syndromes. Cestrum also produces small amounts of solanum glycosides and cardiac glycosides but neither of these would seem to contribute to the clinical disorder that affects ruminants eating Cestrum.
There are 29 varieties of Lantana growing along the East Coast some are very toxic to ruminants and others harmless. Red flowered forms are generally toxic but pink, orange or white forms can vary greatly in potential toxicity. Lantana foliage contains hepatotoxic triterpenes. Affected animals may die within 2 days or not until after 3 weeks. Janundice with photosensitisation on areas of unpigmented skin are common findings. Diarrhoea or constipation can occur, as can frequent urination and dehydration. Some affected survivors will have permanent liver and kidney damage hence display chronic ill thrift.
The presentation of this syndrome includes both peracute sudden deaths and less acute more protracted cases, with photosensitisation of unpigmented areas of skin, jaundice, elevated temperature, and depression. Photosensitisation is the dominant clinical sign. Cattle are affected but so far neither sheep nor horses have been. ABLD can occur within hours of entering a toxic paddock, which is usually one that contains a lot of taller dry standing pasture growth and a lot of plant litter. The annual grass, Rough’s dogs tail (Cynosurus echinatus) is usually present in the pasture and toxicity seems to occur during warm moist weather in spring or autumn.
Dr Roger Kelly (Qld vet path) reviewed liver pathology from 30 cases and he found
From this pathology review one can see that 50% of cases have liver damage that is not usually associated with photosensitisation and yet the clinical presentation typically involves photosensitisation. This would suggest to me that ABLD involves a toxin which is both hepatotoxic and a primary photosensitiser, rather than a primary hepatotoxic compound for which secondary photosensitisation is a sequela. Some primary photosensitising compounds also cause hyperthermia and this could explain the elevated body temperature in some affected animals. I would suggest that the toxin is a hydroxy anthraquinone compound, produced by a fungus, probably a Drechslera sp (ie Pyrenophora sp), and possibly on the seed heads of the grass. Experimentally prepared Drechslera spp cultures will predictably fail to reproduce the syndrome seen in the field because toxin production by many fungi changes dramatically when they are grown on artificial media.