CASE NOTES


Significant Miscellaneous Problems

Chris Bourke, Principal Research Scientist (Poisonous Plants)
Orange Agricultural Institute, Forest Rd Orange NSW

Posted Flock & Herd February 2011

Introduction

Miscellaneous poisonous plant problems are potentially a confusing array of unrelated syndromes. To simplify the situation I have subdivided them into mycotoxin and non-mycotoxin associated problems and then grouped each one according to its major clinical presentation.

1. A clinical classification of significant mycotoxin poisoning syndromes

a) Those causing motor nervous effects

  1. Penitrem-like toxins = Aspergillus clavatus (farm fodder sprouted barley)
  2. Fumonisins = Fusarium verticillioides (F. moniliforme)
    equine leucoencephalomalacia
    ruminant kidney & liver disorders
  3. Paspalitrem type ergot alkaloids = Claviceps paspali
  4. Lolitrems = Fungal endophytes of Perennial ryegrass
  5. Tunicamycin-like group of syndromes
    Agrostis avenaceae (Blow away grass) plus Rathayibacter toxicus
    Polypogon monspeliensis
    (Beard grass) plus Rathayibacter toxicus
    Lolium rigidum
    (Annual ryegrass) plus Rathayibacter toxicus
    Water damaged cereal grains plus unknown actinomycete

b) Those causing autonomic nervous effects

  1. Ergotamine type ergot alkaloids = Claviceps purpurea
    hyperthermia, ill thrift, deaths, gangrene
  2. Ergovaline type ergot alkaloids = Fungal endophytes of Fescue and Perennial ryegrass
    hyperthermia, ill thrift
  3. Slobbers toxin = Rhizoctonia leguminicola (Red or white clover hay or pasture)
    excessive salivation, lacrimation, urination and defaecation

c) Those causing gastrointestinal effects

  1. Trichothecenes (DON (vomitoxin), T2, Macrocyclics eg verrucarins, roridins etc) = Fusarium spp, Cephalosporium spp, Myrothecium spp, Stachybotrys spp, Trichoderma spp etc
  2. Mitchell grass toxin (Astrebla lappacea) = Corallocytostroma ornicopreoides fungus

d) Those causing liver effects

  1. Phomopsins = Phomopsis sp (Diaporthe toxica)
  2. Aflatoxins = Aspergillus flavus + others
  3. Sporidesmin = Pithomyces chartarum (facial eczema)
  4. Drechslera campanulate (Pyrenophora semeniperda) plus fodder oats

e) Those causing vascular effects

  1. Patulin = Penicillium spp, Aspergillus spp
    Cerebral oedema, pulmonary oedema, haemorrhages
  2. Coumarins converted to Dicoumarol = fungal activity in hay eg Meliolotus officinalis (yellow sweet clover), possibly some Medicago, or Trifolium spp, definitely Anthoxanthum odoratum (sweet vernalgrass)
    Dicoumarol is both anticoagulant and makes blood vessel walls leak.

f) Those causing reproductive effects

  1. Zearalenone = Fusarium graminearum = oestrogenic effects
  2. Helminthosporium biseptatum plus Romulea rosea (Onion grass) = possibly abortion or suppression of ovulation or conception.

g) Those causing kidney effects

  1. Ochratoxins = Aspergillus ochraceus, Penicillium verrucosum = kidney, liver, GI

h) Those causing respiratory effects

  1. 4-Ipomeanol = Fusarium solani on sweet potato tubers (Ipomoea batatus)

2. A clinical classification of miscellaneous plant poisoning syndrome

a) Those causing motor nervous effects

  1. Tree lucerne / tagasaste (Chamaecytisus proliferus var palmensis) = staggers, or neonatal leukodystrophy, or query hepatic & nephrotic necrosis

b) Those causing autonomic nervous effects

Robinia pseudoacacia (black locust tree) = depression, paresis, diarrhoea, dilated pupils, cardio-respiratory difficulties

c) Those causing gastrointestinal effects

  1. Lippia (Phyla spp) = ill thrift
  2. Leucaena spp = ill thrift
  3. Kurrajong (Brachychiton populneus) seed pods = ill thrift, staggers, some deaths
  4. Citrullus spp (bitter melon) = diarrhoea, dehydration
  5. Cucumis spp (paddy melon) = diarrhoea or sudden death
  6. Eremocarpus setiger (doveweed) = ill thrift
  7. Euphorbia spp = ill thrift or sudden death
  8. Erythrina spp (coral tree) = excessive intakes may kill
  9. Hydrangea = gastro-enteritis
  10. Jatropha curcas (physic nut) = gastro-enteritis
  11. Ligustrum spp (privet) = gastro-enteritis or sudden death
  12. Papaver somniferum (opium poppy) = gastro-enteritis or ill thrift
  13. Prosopis spp (Mesquite) = large amounts may cause ill thrift
  14. Castanospermum australe (Black bean tree) pods = gastro-enteritis and ill thirft

d) Those causing liver effects

  1. Crofton weed (Ageratina adenophora) flowering stage
    chronic liver disease (ruminants)
    chronic respiratory disease (horses)

e) Those causing vascular effects

  1. Persea americana (avocardo) = oedema of udder, head, neck, brisket
  2. Allium spp (Onions & Garlic) tubers = haemoglobinuria and weakness
  3. Argemone mexicana (Mexican poppy) seeds = generalised oedema and weakness

f) Those causing reproductive effects

  1. Pinus spp (pine trees) = late term abortions
  2. Reseda spp (dyer’s weed) = neonatal goitre
  3. Brassica spp = neonatal goitre
  4. Sorghum spp = congenital arthrogryposis
  5. Phytoestrogens (coumestans or coumestrol)
    burr medic (Medicago polymorpha)
    subterranean clover (Trifolium subterranean)
    lucerne (Medicago sativa)
    red clover (Trifolium pratense)
    strawberry clover (Trifolium fragiferum)
    white clover (Trifolium repens) esp large leaved varieties such as Ladino.
    The content increases when these plants are at maturity or when leaves are stressed by the presence of diseases or insect attack. Do not join animals on these pastures under these circumstances or ovulation rates will be significantly depressed.

g) Those causing kidney effects

  1. Amaranthus retroflexus (Red root) = chronic kidney disease, ill thrift
  2. Terminalia oblongata (Yellow wood tree) = chronic nephritis, weakness
  3. Ventilago viminalis (Supplejack tree) = chronic nephritis, weakness
  4. Isotropis spp (Lamb poison etc) some biotypes of some species are poisonous when flowering or fruiting = acute or chronic nephropathy.

h) Those causing muscle effects

  1. Senna (Cassia) spp pods eg Coffee senna etc = muscle weakness, myoglobinuria, and diarrhoea

i) Those causing respiratory effects

  1. Crofton weed (Ageratina adenophora) flowering stage
    chronic respiratory disease (horses)
    chronic liver disease (ruminants)
  2. Lush forages with elevated levels of the tryptophan hence rumen formation of 3-methylindole resulting in ‘fog fever’ ie interstitial pneumonia, pulmonary oedema, & emphysema.

Syndromes to be presented in more detail

a) Endophytes of fescue and ryegrass
b) Ergot of rye
c) Vetch poisoning
d) Brassica poisoning
e) Lupins poisoning
f) Pimelia poisoning
g) Rock fern & bracken poisoning
h) Oxalate poisoning

a) Endophytes of Fescue and Perennial ryegrass highlights

Endophytes are fungi that live inside plants, frequently grasses. They are transmitted in the seeds of the infected plant. There is no sign of their presence when the plant is examined with the naked eye, but they can be seen microscopically using special stains. Endophytes offer the plant protection from diseases and pests and are consequently very beneficial to the plant’s survival. Endophytes come as either wild types or as specifically cultivated types. Wild endophyte toxins in Tall fescue (Festuca arundinacea), or Perennial ryegrass (Lolium perenne), or Hybrid ‘annual’ ryegrasses (Perennial x Italian ie L perenne x L multiflorum), can cause livestock problems but most of the time they do not.

Fescue is predominantly a summer growing plant and the ryegrasses predominantly spring and autumn growing plants. Seed retaining ‘autumn saved’ pastures are typically fescue pastures not ryegrass pastures, since the latter will have dropped its seed by this stage. The seed of endophyte plants can be very high in endophyte toxins and consequently it poses the highest livestock risk. However when these plants are grazed very hard the butt of the plant may be ingested and this can be just as high in endophyte toxins as the seed head. Both of these situations can be managed around once they are understood.

Wild endophytes that occur in Australian Tall fescue and Perennial ryegrass can produce an ergot alkaloid called ergovaline. In addition endophytes in PRG can also produce a toxin called lolitrem B. Toxin producing endophyte activity is very seasonal within a year and very variable from year to year. Toxin production tends to kick off in Nov-Dec, peak in Feb-March, and turn off in May-June. A wet spring followed by a dry summer and autumn will favour higher toxin production levels. The highest risk period for potentially toxic egovaline levels is generally around Jan-Feb and for lolitrem B around March-April.

Toxic levels of ergovaline can cause a group of clinical signs collectively referred to as ‘Summer ill-thrift’ and toxic levels of lolitrem B can cause the syndrome known as Ryegrass Staggers (covered elsewhere under ‘staggers syndromes’). The signs of ‘Summer ill-thrift’ occur together as a single syndrome but some commentators give this a more negative spin by presenting each clinical sign in isolation as though it were a separate disorder.

If either Tall fescue or Perennial ryegrass, in the seeding growth stage, is fed to livestock during cold winter weather, in the form of autumn saved pasture paddocks or as silage or as hay, then it is possible for the ergovaline toxin that it contains to cause a form of peripheral gangrene called ‘Fescue foot’. This problem is very rarely seen in Australian livestock, and so far it has only ever occurred with Tall fescue plant material not with Perennial ryegrass.

Endophyte toxin effects in livestock will usually only occur when animals are either grazing very, short pastures, for example in cell grazing or crash grazing systems, or very tall mature pastures that have set seed, for example autumn saved pastures. Silage and hay that has been made from seeding growth stage endophyte infected grass pastures can also be toxic. The ensiling process will only reduce ergovaline levels by up to 20% but sun curing cut pasture prior to hay baling can reduce levels by up to 70%. Nitrogen fertilisation of at risk pastures should be delayed till late autumn because late summer applications can cause up to a 100% increase in ergovaline levels in subsequent weeks.

Ergovaline induced ‘Summer ill-thrift’ is a transient syndrome the severity of which is directly related to the amount of ergovaline ingested in the total mixed daily diet. As ergovaline levels rise livestock reduce their voluntary ingestion of those plants and eat more of alternative species. Therefore the measured amount of ergovaline in an endophyte carrying grass sample from a mixed pasture can give a false indication of the overall pasture toxicity risk. Whereas in New Zealand the fescue or ryegrass component of a pasture may be 80 to 100% this is generally not the case in Australia. In fact in northern New South Wales the perennial ryegrass component of pastures is usually less than 20%. If 80 to 100% of a pasture consists of endophyte infected plants then it becomes much more difficult for the livestock grazing it to switch to grazing alternative species, hence the risk of toxicity will be higher.

The anti wild endophyte grass pastures people frequently speak about so called subclinical or hidden livestock health and production effects. This is really a bit of nonsense since all of the potential effects of endophyte toxins can be either seen or measured. The determining factor for toxic effects is the total amount of toxin present in each kg of the total dry matter ingested off a pasture, by each animal, each day.

For ergovaline and sheep, the ingestion of < 0.8 mg ergovaline per kg of dry matter causes no effects. Ingestion of somewhere between 0.8 and 1.2 mg by sheep may cause inappetence, hence a consequent transient decrease in weight gain and milk production. When the ingestion level reaches 2.0 mg or greater, mild diarrhoea may occur, hyperthermia (hence increased salivation and respiration) may occur, and a degree of true agalactia (a direct reduction in milk production) may be experienced. Compensatory weight gain will follow as soon as the ergovaline intake declines. The corresponding ergovaline values for cattle are < 0.4, between 0.4 and 0.8, and 1.2 mg or greater respectively. The values for horses are < 0.4, between 0.4 and 0.6, and 1.0 mg or greater respectively. It remains a possibility that ruminants suffering from a significant ergovaline induced hyperthermia may be at risk of death should they be denied access to shade for more than 3 consecutive hours on a bright sunny day. No cases have so far been reported for endophyte affected animals but they have been reported for animals affected by ergot of rye hyperthermia.

For all animal species lolitrem B ingestion levels of between 1.8 and 2.0 mg of lolitrem per kg of dry matter per day can result in signs of ryegrass staggers. In most years the total amount of toxin present in each kg of total dry matter ingested off a typical New South Wales fescue or perennial ryegrass containing mixed pasture will be less than 1.2 mg for ergovaline and 1.8 mg for lolitrem B, consequently ‘Summer ill-thrift’ and ‘Ryegrass Staggers’ are only very occasionally encountered, and ‘Winter Lameness’ is a very, very, rare event.

From the animal health and production information provided above it would not be hard, if it suited your purposes, to present a very negative spin on wild endophyte carrying PRG pastures. However there is very little evidence from Australian pastures that the potential livestock problems associated with PRG are anything more than an occasional nuisance that can be managed around. That said, the New Zealand based commercial pasture seed industry, its Agresearch New Zealand pasture research co-operators, and individuals within the Victorian Dept of Primary Industries have chosen to put a doom and gloom spin, on the speculated potential livestock problems that may or may not occur, on Australian wild endophyte carrying PRG pastures. I can only assume that they are well intentioned in their current enthusiasm for replacing wild endophyte PRG with expensive, tailor made, trademarked, endophyte selected, PRG varieties. In NSW at least this enthusiasm would seem to be misplaced.

In my experience it is better to manage around an existing but predictable low risk pasture plant livestock problem than it is to replace the plant with new varieties that may or may not remove some current livestock problems only to replace them with a different set of new ones. All of the major selected pasture plant species grown in southern Australia come with some degree of livestock risk. The best approach is to understand the risk and manage around it. For example 30 years of phalaris plant breeding has still not produced a livestock safe phalaris variety, despite the hopes, promises, enthusiasm and best intentions of all of those involved in this process. The good news is that 30 years on research directed at the phalaris livestock problems themselves has established a much greater understanding of the problems and as a consequence much better pasture management strategies to avoid them.

b) Ergot of rye highlights

Ergot of rye (Claviceps purpurea) is a fungal infection of the seed head of grasses belonging to the rye family and some cereals. A common host is Annual Ryegrass (Lolium rigidum) a grass of cultivation paddocks in the wheat belt of NSW. The infected seeds become black and swollen and are called ergots. These can be ingested when pasture is grazed or as contaminates of grains in feed lot rations. Cattle and horses are much more susceptible to poisoning than sheep. Ergots contain the alkaloid ergotamine, and contrary to popular belief they do not cause a nervous syndrome in livestock, the so-called ‘nervous ergotism’ of humans.

Toxic levels of ergotamine cause a group of clinical signs collectively referred to as ‘Summer ill-thrift’. In addition, if either ergot infected Annual or Perennial ryegrass, in the seeding growth stage, is fed to livestock during cold winter weather, either as autumn saved pasture paddocks or as silage or as hay, then it is possible for the ergotamine toxin that it contains to cause a form of peripheral gangrene of the lower limbs that results in severe lameness. In the Australian environment this form of ergotism is extremely rare. Reproductive effects of ergot alkaloids are poorly documented but they may potentially interfere with the establishment of pregnancy or alternatively, cause late term and neonatal problems.

‘Summer ill-thrift’ starts as inappetence hence a secondary transient decrease in weight gain and milk production. When the ergot ingestion level increases further mild diarrhoea, hyperthermia (hence increased salivation and respiration), and a degree of true agalactia (a direct reduction in milk production), may be experienced. Compensatory weight gain follows as soon as ergotamine intake declines. The most striking clinical sign associated with ergot of rye poisoning is hyperthermia. Affected animals will seek shade, stand in water and be reluctant to travel when mustered. If hyperthermic animals are deprived of adequate shade for more than 3 consecutive hours on bright sunny days they are at great risk of dropping dead. This problem is typically seen in feed lot situations when the grain supply is unknowingly contaminated with ergot of rye and the pens are not shade protected.

c) Vetch poisoning highlights

Lush green vetch pastures can cause a dermatitis-ill thrift syndrome in cattle. Affected animals develop signs of a patchy pruritic dermatitis, conjunctivitis, diarrhoea, fever, inappetence, weight loss, respiratory distress, and haematuria. This is a multi-system disorder that involves eosinophilic granulomatous inflammation and vasculitis. The liver, kidney, skin, gut and lungs are all affected.

Vetch seeds, when eaten in large quantities, can cause an acute fatal nervous disorder. This may be caused by the amino acid L-canavanine or it may involve per acute ammonia toxicity, it remains unclear.

Vicia sativa var dasycarpa and Vicia villosa var dasycarpa refer to the same plant, Namoi woolly pod vetch, and along with Vicia villosa var villosa (Russian or Hairy vetch) and Vicia benghalensis (Poppany vetch) can cause the poisonings outlined above. Initial reports by Panciera in the USA spoke of three different vetch syndromes but the clinical evidence indicated only two. A recent report by Suter (2002) in Victoria has speculated that Vicia sativa (vetch) hay may have the potential to cause cyanide poisoning in cattle, and so this could be a third option. Cattle affected when grazing vetch will develop signs of a patchy pruritic dermatitis, conjunctivitis, diarrhoea, fever, inappetence, weight loss, respiratory distress, and haematuria.

d) Brassica poisoning highlights

Raphanus raphanistrum (Wild radish, wild turnip), Canola (Brassica x napa), and Forage brassicas (Brassica spp) such as chou moellier, cabbage, broccoli, turnips etc can in some situations be poisonous to livestock. The risk increases when brassicas are flowering and setting seed, or when they have been affected by drought, or frost, or when they put out fresh growth after rain.

The Brassica syndromes are:

Brassicas can also cause photosensitisation, bloat, nitrate poisoning, and oxalate poisoning.

The Brassica toxins are:

e) Lupins poisoning highlights

There are two main types of lupins, Lupinus albus and Lupinus angustifolius. The former has a large seeded, high alkaloid selection (> 3% alk) called ‘Lupini bean’ which is used for human consumption, and a low alkaloid selection (< 0.03% alk) which is used (along with L. angustifolius) as stock feed. Both species of Lupinus are susceptible to infection by the Phomopsis (now Diaporthe toxica) fungus. Lupin seed is very high in protein hence nitrogen and therefore can potentially cause peracute ammonia toxicity in ruminants.

Consequently three forms of fatal poisoning are possible with lupins; alkaloid poisoning, phomopsin poisoning, and per acute ammonia toxicity. The first and the last look very similar and present with nervous signs, the phomopsin problem presents as a typical acute hepatopathy. Phomopsin toxicity is far more commonly encountered than either of the other two problems

f) Pimelia poisoning highlights

Pimelia comprises a group of unpalatable annual herbs found in western NSW, southern Qld and northern SA. Poisoning can occur from direct ingestion of fresh plant, usually during spring, or it can occur following the accidental inhalation of dry fragments of the plant in paddock dust usually during summer. Two syndromes are possible, one is a fatal form of intense diarrhoea following the ingestion of the plant, and the other is a syndrome called St George disease following the inhalation of dried plant fragments. The former syndrome is probably caused by diterpenoids of the prostratin type and the latter by diterpenoids of the simplexin type.

St George disease cases present with signs of congestive heart failure. This results from the chronic pulmonary blood vessel constriction that is caused by simplexin. Affected animals develop large oedematous swellings of the brisket and lower jaw, are typically in poor condition and may or may not have concurrent diarrhoea.

g) Rock fern & bracken fern poisoning highlights

Both Cheilanthes seiberi (Rock or Mulga fern) and Pteridium aquilinum var esculentum (Bracken fern) cause similar poisoning problems. Both can produce thiaminases and ptaquilosides but different populations (or biotypes) of plants within each genus vary in terms of the quantities of each compound that they can produce. Consequently the type and severity of a poisoning event will vary greatly from place to place.

Thiaminases can cause:

  1. Thiamine deficiency-PE, in sheep and horses, can occur after several weeks of plant ingestion. Affected animals develop an aimless wandering, incoordination, convulsive, staggers syndrome.

Ptaquilosides are carcinogenic and they destroy bone marrow, specifically platelet and neutrophil blood cell production. Affected animals will haemorrhage and display greater susceptibility to infectious agents. Ptaquilosides can cause:

  1. An acute haemorrhagic syndrome, usually in cattle, after several months of ingestion, hence bloody faeces, bloody nose, and submucosal haemorrhages of the mouth, rectum and vagina.
  2. A chronic haematuria syndrome, usually in cattle, after many months of ingestion, hence red urine, cystitis, anaemia and ill thrift.
  3. Chronic ingestion of Ptaquilosides by cattle has been associated with neoplasia of the bladder, and by humans with neoplasia of the oesophagus and stomach.
  4. In the UK a retinal degeneration syndrome called ‘bright blindness’ has been reported in sheep.

h) Oxalate poisoning highlights

  1. Acute soluble oxalate driven hypocalcaemia in ruminants is commonly associated with rapidly growing, young, lush, fresh pastures dominated by; Pigweed, Fat hen, Sorrel, Oxalis, Roly poly, Soda bush, Portulaca etc. The highest risk is the first day of grazing, this is because the rumen can adapt to the safe handling of large oxalate loads over about a 3 to 4 day period. The most susceptible animals are those that have been feed deprived for 24 to 48 hours. The sudden absorption of large amounts of free oxalate will precipitate blood calcium. Rapidly growing juveniles and pregnant or lactating females are at most risk. The clinical presentation is predominantly a staggers syndrome, affected animals develop a muscle weakness hence display signs of limb paresis with muscle fasciculations and eventually sternal recumbency and possibly respiratory distress.
  2. Ruminants can either metabolise some ingested insoluble calcium oxalate, or break down ingested soluble oxalates, or form insoluble calcium oxalates. When large amounts of oxalate ions are absorbed by the rumen mucosa it becomes injured and some oxalate crystals will be precipitated within the wall itself or its associated arterioles. This can result in mucosal hyperaemia and diarrhoea.
  3. Soluble oxalates respiratory syndrome in ruminants can occur when large amounts of oxalate ions are carried to the lungs and damage lung capillaries. This presents as pulmonary oedema.
  4. Soluble oxalates nephrosis syndrome in ruminants can occur with the ingestion of large amounts of soluble oxalates over a short period or lesser amounts ingested over a long period. When ultimately precipitated out as insoluble crystals in the renal tubules, this can lead to either an acute nephrosis syndrome (in cattle) characterised by recumbency and coma, or as a chronic nephrosis syndrome (in sheep) characterised by ill-thrift.
  5. Insoluble prismatic-form calcium oxalate crystals are responsible for nutritional secondary hyperparathyroidism in horses and donkeys. This is associated with the long term grazing of certain grass dominant pastures on the north coast of NSW. Potential problem grasses include; Setaria grass (Setaria sphacelate), Buffel grass (Cenchrus ciliaris), Guinea grass (Green panic, Gatton panic) (Panicum maximum), Kikuyu grass (Pennisetum clandestinum), Brachiaria / Urochloa spp (Summer grass), and Digitaria spp (Umbrella grass). Because the dietary calcium is in a water insoluble form it cannot be absorbed by the duodenum of the horse hence the animal goes into a chronic negative calcium balance. Blood parathyroid hormone levels rise, osteodystrophia fibrosa swellings develop in the jaw bone, osteoporosis develops in the long bones, erosions occur at the joint surfaces and hyperplasia of the parathyroid glands becomes evident. Animals present with a generalised lameness and ill-thrift.
  6. Insoluble needle-form calcium oxalate crystals can be responsible for an intense, severe, irritation of the buccal mucosa. This condition is associated with chewing the leaves of certain house and garden plants most notably Philodendrons (Dieffenbachia spp, Philodendron spp) and Lilies (Arum spp, Zantedeschia spp).

 


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