CASE NOTES


Nitrate - Nitrite Poisoning

Richard Hernando, District Veterinarian, Walgett RLPB

Posted Flock & Herd February 2011

Toxin

In ruminants: nitrate NO3 ? NO2 Nitrite in the rumen. The nitrite is absorbed into the bloodstream. It is here it binds to haemoglobin to form methaemoglobin.

Methaemoglobin cannot transport oxygen therefore an affected animal dies because its body tissues are starved of oxygen. Plants with a dry matter content of 1.5% or greater of potassium nitrate (KNO3) are a danger to ruminants. This is particularly so if the stock are hungry. Livestock can become accustomed to grazing pasture with higher levels of nitrate but this must be done with care.

CONDITIONS OF POISONING

Normally a plant converts nitrate into protein however when conditions for normal growth aren’t suitable and the nitrate level in the soil is high, a plant will accumulate nitrate. Conditions that contribute to a plant accumulating nitrate include:-
1) night
2) cloudy / overcast weather
3) cold weather
4) plants are in a wilted / stressed state
5) plants have had a herbicide applied - or a combination of these.
It is important to remember that nitrate will persist in hay.

CLINICAL SIGNS

Animals that die from nitrate — nitrite poisoning often do so rapidly. Often the animals are found dead without clinical signs having been seen.

Clinical signs (of oxygen starvation) include:-
1) rapid, gasping breathing
2) cyanotic gums
3) convulsions
4) death.

Death can occur within hours of consumption of toxic plants. In some instances death is so sudden that an animal is found literally dead in mid stride.

POST MORTEM CHANGES

— Blood clots poorly and has a chocolate colour.
— Liver, kidneys and lungs are often congested.
— Non specific changes such as haemorrhages in the trachea and around the heart are also seen.

MANAGEMENT

— Prevent livestock having access to hazardous plants in the early morning and in cold and dull weather.
— Stock, especially hungry stock, should be fed hay prior to access to potentially toxic plants.
— Dairy cattle which are to be grazed on pastures with potentially toxic levels of nitrate (eg ryegrass), can be fed a ration with a greater than normal carbohydrate level which helps prevent nitrate poisoning. The carbohydrate level can be raised by increasing the grain portion of the ration to >3.5kg/day or by increasing the molasses in the ration.

TREATMENT

Obviously ‘prevention is better than cure’ however in instances where treatment is required, animals affected by nitrate — nitrite poisoning can be given methylene blue as a 1% solution in water (1g/100ml) intravenously at a rate of 1-2mg/kg bodyweight.

Approximate doses would be:-
Cattle 100 — 200 ml
Sheep 6 — 10 ml

Treatment may need to be repeated every 6 to 8 hours. Some research suggests that doses of 20 mg/kg give better results.

The nitrate content of plants can be checked via commercially available test strips. It is a simple procedure which can help prevent poisonings.

Cattle that have adapted to grazing pasture with hazardous nitrate content shouldn’t be fed feed supplements containing monensin. In these situations, these supplements have caused stock poisonings most probably due to their alteration of the activity of the ruminal bacteria.

PLANTS CAUSING NITRATE — NITRITE POISONING

— Caltrop (Tribulus terrestris)
— Capeweed (Arctotheca calendula)
— Common oats (Avena sativa)
— Heliotrope (Heliotropium europaeum)
— Lucerne (Medicago sativa)
— Mint weed (Salvia reflexa)
— Rape (Brassica napus)
— Red salvia (Salvia coccinea)
— Redroot (Amaranthus retroflexus)
— Sorghums (Sorghum species)
— Twinleafs (Zygophyllum species)
— Variegated thistle (Silybum marianum)
— Wandering Jew (Tradescantia albifiora)

CASE STUDY

Mixed farming/cropping enterprise approximately 70km south-west of Walgett. Area is black soil plains with red soil ridges running through it. Area had been drought affected for well over 12 months and very little feed left.

Owner had been drought feeding for quite a while. Fodder included hay of various types (sorghum, wheats, etc), cotton hulls, etc. Some country is low lying and swampy — very close to the Macquarie Marshes but only when adequate rain has fallen! Had a small opportunity feedlot for calves ? weaned early and tried to feed them up for feedlotter market.

Purchased sorghum hay from down south — Forbes/Cowra area. Fed sorghum hay to the feedlot calves and then fed out a number of bales to cows with young calves at foot in a back paddock.

Owner noticed 3 dead calves a few hours later and noticed a few others were ill. He quickly removed the hay from the feedlot and called me at about 7pm. I asked regarding any other stock having received any of the sorghum hay. Said that he had fed out to some other stock and would go and see them whilst I travelled to the property.

Upon arriving at the property, I found the owner in a somewhat distraught way. He said little but just told me to follow him to one of the back paddocks. In the back paddock there were 21 cows and 2 larger calves dead in the area surrounding the sorghum hay that had been fed out.

Examination of dead animals found they had dark blue / purple (cyanotic?) mucous membranes and all had died within 100 metres of the hay bales. Many of the animals appeared to have died in mid stride. Samples were collected from 10 animals and representative samples of the sorghum hay were also collected and forwarded to the Regional Veterinary Laboratory. My initial suspicion was that the sorghum hay contained high levels of prussic acid (ie. Cyanide poisoning).

Laboratory results

1. Blood smears: - showed that 5 out of 9 smears (diphenylamine blue test) were positive for nitrate.
2. Sorghum hay: showed levels of; (a) cyanide of 22mg/kg where levels are potentially toxic at 20 mg/kg. (b) nitrate at levels of 20 000 to 50 000 mg/kg where potentially toxic levels begin at 5000 mg/kg.

Results indicated a clear cut case of nitrate poisoning.

The property owner had purchased 2 road trains of the sorghum hay and therefore had to use it. In order to minimise the risk to the remaining stock and to hopefully allow them to adapt to the sorghum hay the owner purchased other hay and ‘shandied’ it with the sorghum hay. Caution was exercised when feeding out the sorghum hay and no further losses were reported.

REFERENCES

Poisonous Plants- A Field Guide (1993). Ralph M. Dowling and Ross A. McKenzie. DPI Queensland

Poisonous Plants — Handbook for Farmers and Graziers (1983). EJ McBarron. NSW Department of Agriculture.

Poisonous Plants of Australia (1974). Selwyn E. Everist. Angus and Robertson Publishers.

 


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