Brassica toxicosis

o bovis

Contributor(s):

Nicola Bates

Mike Reynolds

Synonym(s): Brassic oleracea, Brassica rapa, Brassica juncea, Brassica nigra, Brassica elongata

Introduction

Cause: ingestion of brassicas, particularly with the exclusion of other fodder.
Signs: weakness, hypothyroidism, gastrointestinal signs, respiratory distress.
Diagnosis: history and clinical signs.
Treatment: supportive.
Prognosis: depends on severity of signs and the syndrome exhibited.
Brassica toxicosis is associated with a number of different syndromes with various names.
- Usually only one syndrome is present in a single animal or herd, but sometimes multiple syndromes may occur.
Brassicas can also accumulate nitrates and cause nitrate poisoning.

Toxic effects are more likely to occur when animals are fed only Brassica crops.
They are usually used as a winter feed source when other forage is unavailable.
The concentrations of glucosinolates vary with the species, variety, season and environmental conditions.

Brassicas contains S-methylcysteine sulphoxide (SMCO) which is converted during normal fermentation in the rumen to dimethyl disulphide. This is toxic to red blood cells and oxidises hemoglobin leading to Heinz body formation and hemolytic anemia .
Hemolysis of cells occurs as a result of oxidative damage.

Brassicas contain numerous glucosinolates. These sulphur-containing compounds are hydrolysed by myrosinase (an enzyme in plant tissue) or in the ruminal environment to isothiocyanates, thiocyanates, nitriles and related compounds.
- Isothiocyanates are irritant to mucus membranes and have an antithyroid effect.
- Nitriles depress growth and are toxic to the liver and kidneys.
- Thiocyanates have an antithyroid effect.
- Oxazolidine-2-thiones are related to isothiocyanates. They also have an antithyroid effect.
Effects on the thyroid include blocking tyrosine iodination an inhibition of T4 production (due to goitrin, a breakdown product of thiooxazolidine) and inhibition of thyroid iodine uptake due to thiocyanate formation.

Brassicas contain a high concentration of tryptophan which is converted in the rumen to 3-methylindole.
This binds with the protein of type I cells in the pulmonary airways resulting in acute pulmonary edema and emphysema.

Polioencephalomalacia is uncommon in ruminants grazing brassica crops. Polioencephalomalacia
The cause of brassica-induced polioencephalomalacia is unknown but may be due to the high sulphur content of brassicas.
Sulphate is reduced to sulphide in the rumen, it then reacts with sulphite and may act as a thiaminase but it is more likely that the neurotoxic effects are due to additional direct effects in the brain via lipid peroxidation. There are minimal changes in tissue concentration of thiamine.
The high sulphur content may also reduce bioavailability of copper Copper leading to copper deficiency.

The cause of the blindness is unknown. It is transient and not associated with a fatal outcome Causes of bovine blindness.

In cattle, brassica-related photosensitivity is a secondary photosensitivity associated with hepatocellular toxicity.
The identity of the toxic compounds in photosensitivity in cattle is unknown. It may be nitrile derivatives of glucosinolates.

There is limited information on the cause of brassica-related bloat.
The free gaseous bloat may be due to the rapid accumulation of free gas. Ruminal bloat

Poor health and reproductive failure in animals eating large quantities of brassicas, without other foodstuffs in the diet, is usually due to a combination of effects: anemia, low copper concentrations, irritation of mucous membranes and antithyroid effects.

This usually occurs 7-10 days after animals begin to graze, sometimes as early as 5 days or up to 4 weeks.

Toxic effects are more likely to occur when animals are fed only brassica crops.
The concentrations of glucosinolates vary with the species, variety, season and environmental conditions.
Varieties of brassica crops have been developed that are low in glucosinolates.