CASE NOTES

Brassica toxicity

John Evers, District Veterinarian, Young RLPB

Posted Flock & Herd February 2011

Introduction

I have seen sporadic mortalities in sheep grazing a range of Brassica/Cruciferous species since 1994 in the Young District. Losses have been seen on grazed-off Canola crops during drought conditions in 1994 and 2002; on spray-grazed Wild Radish (Raphanus raphanistrum); and on forage Brassica during early summer of 2004.

Canola is of course a winter oilseed crop typically sown in May. In drought years a decision to cut or graze it off for fodder is made at the end of September.

Forage Brassica is sown in September/October and after an 8-12 week period is used for high intensity summer grazing. It was first grown in the District in the late 1980's and is resilient and productive green forage for sheep.

When you consider the range of toxic compounds identified in these plants it is not surprising that problems occur. However, in my experience the specific cause of these mortalities is poorly defined. In addition, photosensitisation on forage Brassica is a common problem. The nett result is that at times some producers are reluctant to graze these crops (similar to the Lucerne /Redgut situation).

According to my reading the range of potentially toxic compounds in Brassica species includes

Glucosinolates — organic substances that are metabolised to produce goitrogenic thiocyanates and thiones; and isothiocyanates that cause gut irritation. I have not seen either goitre or significant scouring.
In addition, other metabolites — especially nitrile compounds — can produce tissue damage, including liver and kidney.
S-Methyl-L-Cysteine Sulfoxide (SMCO) — is a rare form of amino acid whose metabolic products in ruminants cause haemolytic anaemia. It is closely related to the haemolytic agent in the Onion family (which has previously been reported in the Riverina). It is described in the literature as a significant problem overseas but I have not seen any evidence for this syndrome at Young.
Nitrates — high levels are recorded in Brassica forage resulting in Nitrite intoxication and methaemoglobinaemia. I have seen this once on self-sown Canola as a typical day 1 Nitrate ’crash’ but samples from sporadic cases of mortality are negative.
Cyanogenetic Glycosides — these plants are said to contain the precursors for cyanide poisoning but rarely deliver. I would agree from my experience but occasional HCN intoxication should not be discounted.

History

The common syndromes I see when these plants are grazed by sheep are

1 Sporadic Death Syndrome — seen frequently in mobs of sheep grazing failed Canola crops , particularly as they reach full flowering stage. Occasional losses are seen on self-sown plants in Canola stubbles. In late 2004 similar outbreaks were seen on forage Brassica crops (contrary to my previous general experience). I have also seen one typical outbreak on a heavy infestation of Wild Radish that was spray-grazed by a mob of Merino wethers.

The common scenario is onset of sporadic sudden deaths commencing about 5-7 days or more after grazing commences. It is worth noting that Brassica spp. are quite unpalatable and will generally be one of the last species consumed. Owners do not observe any symptoms prior to death and at autopsy I can’t detect clinical cases in the mob. The mortality rate is low (under 1%) but cumulative losses of 3%-4% over a couple of weeks force owners to remove the affected mob and losses cease.

2 Photosensitisation — seen frequently in sheep grazing forage Brassica crops but not on Canola. This is usually a mild syndrome (’Rape Scald’) reported several weeks after introduction. It generally presents as scaly ears with dry necrosis and occasional ear loss. Obvious symptoms may occur in 10%-30%. Occasionally more severe outbreaks of what appears to be a hepatogenous photosensitisation occur with typical ’bighead’ symptoms requiring immediate intervention.

Despite the fact that sheep are predominately used to graze off Canola crops and Forage Brassica is used to grow out lambs, the absence of reports involving cattle appears to be significant.

Results

Autopsy findings in the sporadic death cases are not remarkable and quite consistently reveal moderate to severe pulmonary congestion; sub-epicardial petechial haemorrhages; and some visceral congestion. There is no evidence of haemolysis or anaemia; aqueous humour is nitrate negative; and the thyroid gland is not enlarged. I presume the cause of death is acute cardio-respiratory failure.

Ad hoc histopathology from a few cases has been unrewarding but a more structured investigation might shed some light. Mostly the post-mortem is to exclude other causes so a diagnosis of ’Brassica Poisoning’ gets me by.

Discussion

While sporadic mortalities on Brassica species can be relatively easily designated as ’Brassica Poisoning’ it would be of some interest to know more about the pathogenesis.

Some of the technical information is confusing, eg, glucosinlate levels are increased in young leaves; seeds; under moisture stress and with higher sulphate levels but SMCO levels are increased in mature leaf material and effects aggravated by low phosphate levels/intake. Obviously failed Canola crops are moisture stressed but I couldn’t say that for Forage Brassica crops receiving 60 mm/month in November/December 2004.

Some interesting aspects are

Susceptibility of sheep compared to cattle
Canola toxicity compared to Forage Brassica photosensitisation
Is this a cumulative intoxication process?
Variation from the syndromes reported elsewhere, eg: haemolytic anaemia; goitre; pulmonary emphysema; polioencaphalomalacia; gastroenteritis. Perhaps others see these syndromes?

All this aside, recommendations can be made to reduce the risk of intoxication. Measures I recommend are

not putting hungry stock straight onto Brassica/Canola stands
compliance with the recommended pregrazing intervals for Forage Brassica varieties (although this is probably of more agronomic than veterinary significance)
trying to graze failed Canola crops before full flowering
daily observation
immediate removal if multiple mortalities or severe photosensitisation is observed
4-5 day rotations on/off (a la Lucerne/Redgut) if a mortality syndrome develops.

References

Veterinary Medicine — Radostis, Gay, Blood, Hinchcliff — 9th Edition 2000
Animal Health in Australia Vol 2 — Chemical and Plant Poisons — AA Seawright 1982
PGF Proceedings No 103 — Veterinary Clinical Toxicology 1987
PGF Proceedings No 350 — Gross Pathology of Ruminants 2003 — RA McKenzie
Auld BA and Medd RW — Weeds — An illustrated botanical guide to weeds of Australia