CASE NOTES


Fern Intoxication in Sheep and Cattle

Bruce Watt, District Veterinarian, Condobolin RLPB
Erika Bunker, Pathologist, NSW DPI

Posted Flock & Herd February 2011

Introduction

Of the 107 genera of ferns in Australia, at least five contain species which are toxic. The most significant are Cheilanthes (Rock and Mulga ferns), Pteridium (Bracken ferns) and Marsilea (the Nardoos). The active principles in ferns are ptaquiloside, a potent radiomimetic and carcinogen, and a thiaminase. While not regarded as among the most important causes of death and production loss in NSW, ptaquiloside is ranked as the most important in Tasmania, second most important in Victoria and third most important in Queensland. Marsilea induced thiamine deficiency causes serious but intermittent losses in NSW, ranks 18th on the list in Queensland and 10th on the list in the Northern Territory (McKenzie, 2002).

Toxic principles

Short term ingestion of large doses of ptaquiloside causes bone marrow aplasia. Undifferentiated stem cells seem to be most affected. The sequence of haematological change reflects the production time and life span of the blood cells. Thrombocytopenia occurs first followed by leucopenia. Due to the long life span of red blood cells and longer persistence of red cell precursors in the marrow, the mechanism of anaemia in the first place is thrombocytopenic haemorrhage rather than aplastic. There is at best a perfunctory regenerative response. Thrombocytopenia manifests as haemorrhage from mucosal and serosal and prolonged bleeding after venipunture or wounds. The blood loss is not as serious as with defects in secondary haemostasis and the anaemia is also not as severe. Generally animals succumb to the sequelae of leucopenia (bacterila infections, bacterial infarcts) rather than anaemia.

Ingested long term in low doses, ptaquiloside is a potent carcinogen causing a base substitution within the DNA. Thiaminase I catalyses the decomposition of thiamine and the most common manifestation of thiaminase induced thiamine deficiency is polioencephalomalacia.

Ptaquiloside is most concentrated in bracken fern, but the concentration is highly variable both within the structures of the plant, and depending on season and location (and presumably strain of fern) (Smith et al, 1988). Cheilanthes species may also contain toxic quantities of ptaquiloside (Smith et al, 1989).

Thiaminase is most concentrated in nardoo with moderate amounts in rock fern and lesser amounts in bracken fern.

Disease syndromes

Five (and perhaps six) clinically distinct fern toxicity syndromes are described in sheep and cattle. These are:

i. Haemorrhagic disease

Haemorrhagic disease is the acute manifestation of ptaquiloside poisoning. It is a disease of young cattle grazing either Pteridium or Cheilanthes, although it has been reported in sheep. The symptoms of this disease reflect the radiomimetic properties of ptaquiloside, which causes alteration or cessation of cell division within bone marrow and intestinal epithelium. Ptaquiloside may also damage mast cells causing histamine release leading to capillary fragility, intestinal ulceration and laryngeal oedema (Radostits et al, 2000).

Calves weaned onto country with bracken fern are most susceptible to haemorrhagic disease. It has however been recorded in older cattle.

Rock fern poisoning is also most frequently seen in calves of at least 2-3 months of age on their mothers or young weaned cattle. In inland southern Australia, Cheilanthes responds rapidly to summer rains and the disease occurs three to four weeks later. Crossing (1969-70) reported losses in calves sent on agistment in rock fern infested country.

Calves with acute ptaquiloside poisoning become dull and ‘tucked up.’ They may walk with a weak, swaying or stilted gait and may have swollen joints. Salivation which is often copious is either blood stained or brown. Bleeding may be noticed from other body orifices or in the urine. Haemorrhages are frequently observed in the oral, nasal or vaginal mucosa and under the sclera. Ventral oedema may also be observed (Beckett, 1984).

Sheep seem to be much more resistant than cattle to the radiomimetic effects of ptaquiloside. Australian reports are few and experimental induction of the disease has generally been unrewarding (Jubb et al, 1992). Sunderman (1987) reported a case in Western Australia in mature wethers which were drought fed in a paddock heavily infested with common bracken and little else. The bracken had a high proportion of young fronds which are known to be more toxic than mature foliage. Onset of the disease was much slower than that seen in young cattle. Illthrift was seen two months after exposure and the first deaths occurred shortly after. Seven months later 120 of 450 sheep had died.

It was reported that the sheep suffered weight loss, lethargy, depression, exercise intolerance and anaemia. Some sheep developed diarrhoea and later, anorexia. Post-mortem findings were consistent with the disease in cattle. Haematology in sheep showed some interesting differences to cattle. The sheep were anaemic whereas cattle normally die before becoming anaemic. In cattle the neutrophil fraction is selectively suppressed whereas in sheep both lymphocytes and neutrophils were depressed.

ii. Bovine Enzootic Haematuria

Bovine enzootic haematuria is a chronic manifestation of ptaquiloside toxicity and reflects its carcinogenicity. It normally occurs worldwide after two to three years of rock fern or bracken ingestion and so is a disease of older cattle. It has also been recorded in sheep but is rare. McKenzie (1978) reported that in Queensland the disease was associated with the grazing of both Pteridium (on the coast) and Cheilanthes (inland).It was seen in both dairy and beef cattle and most were 4 to 6 years of age. Owners observed failure to thrive and /or the passing of dark brown to red urine. The haematuria was initially irregular but worsened in time. Some cattle became profoundly anaemic with haematocrits down to 10% and depressed plasma protein levels. Affected cattle, on post-mortem, showed pale tissues, depleted fat reserves, and often ascites and oedema. A spectrum of bladder tumours ranging from adenomas to haemangiosarcomas were found with associated inflammation congestion and oedema.

iii. Gastro-intestinal neoplasia

Alimentary tract neoplasia has been observed in cattle and sheep grazing bracken over a long period of time. It has been reported in the UK, South America and Kenya. Carcinomas of the oral cavity, nasopharynx, oesophagus and rumen have been reported in both species. As with the bladder tumours, there may be an association with the papilloma virus and the fern toxin, quercetin as a co-factor, at least in cattle (Smith, 2004).

iv. Retinal degeneration (bright blindness)

Progressive retinal atrophy occurs in sheep grazing bracken in northern England and has been experimentally reproduced by long term (176 days) bracken ingestion. This syndrome has not been reported in sheep in Australia suggesting that an additional factor is involved. The disease is accompanied by leucopenia.

While this syndrome has not been reported in Australian sheep, Slattery (unpublished) investigated a case of sudden blindness in weaned calves grazing in a native grass paddock in which the gullies were infested with Cheilanthes. Retinal degeneration was confirmed histologically.

v. Polioencephalomalacia

Deaths in sheep grazing Nardoo have been observed for many years. During the floods of Gwydir basin in 1974-5, 2,200 deaths were recorded of 57,000 sheep on 13 farms. The sheep showed clinical signs of polioencephalomalcia and this was confirmed histologically (Pritchard and Eggleston, 1978). Three quarters of affected sheep responded to 200 mg of thiamine subcutaneously. Only cases recumbent for more than 24 hours failed to respond. Slattery (1999) subsequently reported sporadic cases of polioencephalomalacia in sheep grazing Nardoo around gilgais and lagoons and in weaned calves also grazing Nardoo around gilgais (Slattery pers. com.).

Polioencephalomalacia was also reported in a flock of merino wethers on the southern tablelands, grazing on a pasture containing both Bracken fern and Rock fern. One of the sheep examined before death was comatose, the other showed opisthotonos and incoordination. On post-mortem and histopathology the only abnormality detected was in the CNS and was consistent with polioencephalomalacia (Chick et al, 1981). Seven weeks after introduction to the pasture 30 of 480 were found dead. Deaths continued at an average of 3 per day for the next month. At this time the whole mob was treated with 200 mg of thiamine subcutaneously and the deaths were arrested.

vi. Acute cardio-pulmonary failure in sheep

Sheep are not as susceptible to haemorrhagic disease as are cattle. Beckett (1984) reported that sheep poisoned by Cheilanthes were subject to sudden collapse while being mustered. Some recovered and some died rapidly. The disease was observed two or more weeks after summer storms. Affected sheep were febrile and in respiratory distress. Some sheep exhibited black diarrhoea and haematuria.

Affected sheep exhibited a normal red and white cell picture with no coagulation defects. On post-mortem sheep showed pulmonary oedema, patchy cardiomyopathy and enlarged, congested kidneys.

In horses and pigs the acute form of the disease has neurologic and cardiac components which are believed to be due to thiamine deficiency (Jubb et al, 1992). Chick (pers comm.) did not observe this syndrome in experimentally induced or field cases of nardoo poisoning in sheep, suggesting that the toxic principle is not solely thiaminase. Ptaquiloside may be the additional toxic principle. However Cheilanthes also contains high concentrations of thiaminase and some components of the disease in sheep may be thiamine responsive.

Treatment

While not always practical the appropriate treatment for haemorrhagic disease includes bone marrow stimulants, blood transfusions and broad spectrum antibiotics. Mildly affected cases will recover spontaneously if the source of toxin is removed. It has been suggested that the platelet and leucocyte count can provide a guide to prognosis. Polioencephalomalacia responds to early treatment with thiamine at 5-10 mg/kg.

Management and prevention

Graziers with rock fern infested paddocks need to be alert to either not grazing susceptible livestock, especially young cattle in those paddocks, or removing them within two weeks of rain following a dry spell. Rock fern is susceptible to cultivation but this is often not practical as it often grows on rocky hills with skeletal soil.

Bracken control is outside the expertise of the authors. Herbicides and cultivation play a role. Occasional heavy grazing with lower risk livestock such as sheep may be warranted. Graziers should be aware of the risk of weaning young cattle onto bracken infested paddocks.

Nardoo grows prolifically on floodplain country after flooding. Graziers with country which grows nardoo need to be aware of this intermittent risk and either avoid grazing paddocks at risk or have thiamine on hand.

Human health implications

The risks of nardoo consumption are part of Australian legend and may have exacerbated the congenital or acquired stupidity of Bourke and Wills.

Bracken fern is consumed as a delicacy in Japan. Ptaquiloside is passed in milk and presents a public health risk (Smith, 2004). Studies in Brazil and Japan have found epidemiological evidence of an association between the human consumption of bracken fern (Japan) or ptaquiloside contaminated milk (Brazil) and alimentary tract cancers. Australian milk is probably of low risk due to dilution and the limited grazing of dairy cows on infested pastures. Most at risk in Australia are people milking their own cow in bracken or rock fern infested areas.

Case report

Two cases of probable Rock fern poisoning in calves at foot

Introduction

Rock or Mulga fern (Cheilanthes tenuifolia), grows throughout central western NSW on country which has little or no cultivation history. It is most commonly seen on rocky or skeletal soils. It responds quickly to spring, summer or autumn rains and can be prominent soon after rain.

It has a reputation for causing serious but sporadic mortalities in young cattle and sheep. Deaths usually occur after rain which has followed a dry spell. Rock fern, an erect perennial, may be the first green feed and clearly appeals to susceptible stock.

History

Case 1.

In 1998, this owner from Tottenham in central NSW lost 6 of 21 Hereford calves of 3-6 months of age while still on their mothers. The cattle were grazing in bare paddocks and losses occurred after autumn rain. Rock fern poisoning was diagnosed.

In early September, 2003 this owner found 12, 2-3 month old calves dead in a 400 hectare native perennial pasture paddock. The calves were in a mob of 55 Hereford cows and (originally) 53 calves. The owner immediately moved the cattle into a paddock of 320 ha with 120 acres of arable country (near the water source) and 200 ha of open grazing country with some Rock fern. As the owner was moving the cattle he noticed another sick calf which died two days later. The calf was noted to be dull, lethargic, with brown saliva flowing from its mouth, diarrhoea with a trace of blood and blood stained urine. On 15 September, 2003 the calves were marked and seemed healthy. On the 25 September, 2003, 5 more dead calves and three sick calves were found.

As I was absent from the district, one of the dead calves was submitted to the RVL, Orange on 26 September, 2003. (ON03/4927/EB).

Case 2.

The owner from Trundle in central west NSW called because he found 4 dead calves in a mob of 76 mature Angus cows with two week to three month old calves at foot. The cattle had been running in an uncleared hilly paddock for two months, but were moved onto a stubble paddock two weeks prior. The owner, who previously owned a property north -west of Condobolin, suspected anthrax, in part because the cows had been vaccinated but the calves had not. There is no history of anthrax on this property. At the time of the first property visit anthrax was excluded on a peripheral blood smear. A sick calf was also noticed in the paddock.

Clinical findings

Case 1.

Two, eight week old Hereford heifer calves were examined. Both were dull, lethargic and in poor condition and with rough coats. Both had pale mucous membranes, rapid shallow respiration and were febrile. Both calves had brown saliva staining the lower jaw. The first calf had petechial haemorrhages in the vaginal mucosa and traces of blood from the right nostril, while the second had ecchymotic haemorrhages in the oral mucosa.

Case 2.

The sick calf was observed in the paddock on 5 January, 2005. The calf was an Angus bull calf, about 3 months of age and in store condition. It was weak but alert and able to run. It had a profuse, dirty discharge from both nostrils, laboured breathing and an intermittent soft cough. It walked with a weak, swaying gait.

The calf was caught in the paddock and treated with broad spectrum antibiotics by the owner on 6th January, but died that afternoon and was post-mortemed on 7th January.

Pathology

Case 1.

The calf submitted for post-mortem was in good body condition and in moderate state of preservation. Widespread haemorrhages were observed. These included small haemorrhages in subcutaneous tissues and muscles and ecchymotic and paint brush haemorrhages on visceral and parietal pleura and peritoneum, mediastinum, mesentery and omentum. There were also endocardial haemorrhages and mucosal haemorrhages in the trachea, abomasum, intestine, renal pelvis and ureter.

There was gross evidence of multisystemic necrotising and fibrinous inflammation, consistent with bacterial infection with lesions in the pleura, peritoneum, anterior alimentary tract and liver.

Histological examination revealed bacterial colonies in necrotising and fibrinous lesions and bacterial emboli in blood vessels of the lung and liver. A feature of the lesions was the lack of neutrophilic response. Inflammatory cells accompanying bacterial colonies, fibrinous exudate or necrosis were sparse and if present consisted of mild lymphocyte and macrophage infiltrates. The bone marrow showed marked hypocellularity.

Case 2.

The calf was in good body condition but autolyzed. Sub-cutaneous tissues were pale with haemorrhages over the rib cage. There were multiple 2-3 mm haemorrhages within the abdominal musculature. The thoracic contents were autolyzed. The lungs were black either due to haemorrhage or perhaps autolysis. There were extensive haemorrhages below the pleura.

There was also a large sub-serosal haemorrhage in the wall of the caecum and the rumen.

Laboratory Findings

Case 1.

Haematology

Test Units Reference values Calf 1 Calf 2
PL protein g/L 40-75 72 73
Fibrinogen g/L 1-5 5 5
PP/Fib.   15-100 13 14
PCV % 20-50 23 >18

RBC X10 (12) /L 5-12 5.22 >4.05

Hb g/dL 6-15 7.6 >5.9

MCV fL 32-55 44 44
MCHC g/dL 26-36 33 33
MCH pg 10-17 15 15
WBC X10 (9)?L 2.6-15 2.9 2.6
Band N X10 (9)/L 0.00-0.05 0.00 0.00
Neutrophils   0.60-12.0 >0.00

>0.03

Lymphocytes   0.50-11.0 2.87 2.57
Monocytes   0.00-1.20 0.00 0.00
Eosinophils   0.00-0.70 0.00 0.00
Basophils 0-02 0.00 0.300

It was noted that there was platelet clumping and red cell crenation in both smears. It was concluded that the blood picture was of mild anaemia and a marked non-regenerative neutropenia.

Case 2.

As the sick calf was examined from a distance in the paddock no blood samples were collected. Rib sample were submitted from the calf which was post-mortemed. Unfortunately the sample was too autolyzed for conclusive pathology.

Notes on sample collection for ptaquiloside poisoning diagnosis

Diagnosis is based on collecting evidence of bone marrow depression.

REFERENCES

Beckett RJ (1984) ‘The effects of rock fern on sheep and cattle’ Phd Thesis, University of Sydney

Radostits OM, Gay CC, Bolld DC and Hinchcliff KW. (2000) Veterinary Medicine, 9th edition. p 1658.

Crossing RJ Veterinary Inspector (1969-70) p61

Jubb KVF, Kennedy PC and Palmer N. (1992) Pathology of Domestic Animals, 4th edition, p 163 ff.

McKenzie RA (1978)-Aust Vet J 54:61

McKenzie RA (2002) CD ROM Toxicology for Australian Veterinarians

Pritchard D, Eggleston, G. and Macadam, JF (1978) Aust Vet J. 54:204

Slattery S (1999) Nardoo poisoning as a sporadic condition. Aust. Sheep Veterinary Soc. Newsletter April 1999, pp 4-5

Sunderman FM (1987) —Aust Vet J 64:25

Smith BL, Embling PP, Agnew MA, Lauren DR and Holland PT (1988) NZ Vet J 36:56

Smith BL, Embling PP, Lauren DR, Agnew MP, Ross AD and Greentree PL (1989) Aust Vet J 66:154

Smith BL (2004). Bracken fern (genus Pteridium) Toxicity — a Global Problem. From: Poisonous plants and related toxins, p227-240

 


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