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This article was published in 1996
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Botulism in Dairy Cattle

Allan Glassop, District Veterinarian, Gloucester RLPB

This presentation summarises a major outbreak of Botulism in a Gloucester dairy herd, during the Spring of 1994.

Animal health records over many years, from the Gloucester RLPB district indicate that Botulism has rarely been diagnosed or suspected as a cause of cattle mortality in this area.

No doubt some isolated unreported/undiagnosed cases have occurred, particularly in drought years due to bone chewing, or possibly drinking from stagnant water supplies, but there are no records of any major outbreaks.


The herd involved has been run by the same family for over 30 years.

It is a very well managed, well bred, well fed (consultant nutritionist), up to date (overseas study tours), high producing herd, with all records on computer. Herd size is usually around 150 milkers, and the operation breeds all its own replacement heifers.


Pit silage (forage sorghum usually), plus farm-mixed concentrates consisting of barley, soybean meal, monocalcium phosphate, sodium bicarbonate, monensin, limestone, salt, vegetable oil and sometimes urea.

The concentrates are fed in the bails, and silage is fed in open troughs on a feeding pad.

The herd is also strip-grazed on kikuyu rye clover pastures.


The first case (in retrospect) occurred on 19/9/94. and the last case on 21/11/94.

A total of 43 lactating Friesian cows died, plus 3 replacement heifers.

Only 2 or 3 cows which had displayed typical clinical signs, eventually recovered.

The owner's conservative estimate of losses, based on production losses and cull value of cows was around $110,000.

A realistic estimate would be higher than this, as the real commercial value of many of the cows would 3 or 4 times higher than their cull value.

There was no age-related incidence with affected animals ranging from replacement heifers (18 months) to 10 year old cows.


Initial signs looked like early metabolic disease (e.g. hypocalcaemia) - slight hind limb ataxia, progressing to hind limb weakness, then inability to rise - cows continued to have normal bladder and bowel control at this stage, and looked bright and alert, and continued to eat. Some cows showed mild salivation.

These signs progressed over the next 1-3 days to a typical 'frog-swimming' position, marked dehydration and weight loss, occasional muscle fasciculation, marked salivation, lateral recumbency, severe respiratory difficulty, coma, and eventually death.

The one almost pathognomonic sign (even in very early cases) was a very weak or absent tongue retraction reflex, when the tongue was manually extruded from the mouth.

Only terminal cases displayed a spontaneous flaccid prolapse of the tongue.

Marked drooling and salivation was not a particular feature until later in the course of the disease.

The first couple of cases were not seen with advanced symptoms - they had been treated by the attending veterinarian as suspected hypocalcaemias but were just found dead the next day, so Botulism was not suspected.

To give credit where credit is due, the first suggestion of Botulism was made by a Brazilian vet. who happened to be visiting the practice at the time of the next case. After listening politely to comments about ketosis, non-responsive hypocalcaemia etc., he took one look at the 'frog-swimming' cow, and said - "that's botulism, we see it all the time at home".

After a check with the Brazilian/Australian dictionary, and a healthy dose of Australian scepticism, Botulism was included in the list of different diagnoses.

A rush of cases over the next few days displaying a collective range of typical Botulism symptoms, soon verified the diagnosis on clinical grounds.


- Slight ataxia and hind limb weakness

- Very weak tongue retraction reflex

- Inability to rise

- Some muscle fasciculation

- Sternal recumbency - 'frog-swimming' position

- Salivation/drooling

- Lateral recumbency

- Severe respiratory difficulty

- Death.


In this outbreak (as is common with many Botulism cases), the diagnosis could not be confirmed with 100% certainty, despite extensive laboratory examinations and tests.

Extensive and thorough autopsies were carried out on many of the carcases, with no remarkable findings.

A large range of bacto, micro, histopath and serological tests were also unrewarding.

Diagnosis was based mainly on clinical signs, and the apparent response to vaccination.

However blood samples from 2 recovered cows, and 1 cow which subsequently died, did give a positive result for the Botulism antibody ELISA test available in Western Australia - while not proving Botulism to be the cause, it shows that the cows had been exposed, and this helps to support the diagnosis.

A range of other tests were undertaken:

Attempts to culture Cl. botulinum from tissue samples, gut contents, feed samples and water samples were negative.

Mouse inoculation tests using a range of samples were also negative.

Even Botulism antigen ELISA tests (carried out by Queensland D.P.I.) on tissues, gut contents, feed and water samples, were all negative.

Trying to demonstrate Botulism toxin from various samples, is like looking for the proverbial needle in the haystack, so it is not surprising that all these tests were unrewarding.


- Clinical signs

- Demonstration of toxin

- Mouse inoculation

- Botulinum Ag ELISA

- Botulinum Ab ELISA

- Demonstration of bacteria

- Response to vaccination.


Treatment of early cases with milk-fever type treatments gave no response, and in some cases appeared to hasten death.

Various supportive treatments proved to be of little use.

Removing suspect feed sources from the ration made no apparent difference, nor did cleaning water troughs (which did contain a thick bottom-layer of grain and vegetable material!), and changing water sources.

Vaccination of all at-risk stock was the obvious solution, but because of severe drought conditions across much of Qld and NSW, vaccine was virtually unobtainable.

After dozens of phone calls, some vaccine (about 1 month expired) was obtained from a reseller in Qld.

The first vaccinations were started on 14/10/94, and booster shots were given 12-14 days later, as and when more vaccine could be sourced. Some of the vaccine was bivalent C and D, some was only Type C. - we just used whatever we could get, on the first cows into the bails!


Traditionally, 4 common sources of toxin are described:

1. Bone chewing especially under conditions of P deficiency during drought.

2. Contamination of feed with decomposing organic matter e.g. rodents, birds etc.

3. Rotting organic material in stagnant water supplies.

4. Toxico-infectious Botulism, from germination of ingested spores, and subsequent growth of Cl. Botulinum in the gut.

A large number of possible sources of toxin were considered in this case, but no definite source could be identified despite extensive and expensive testing.

Some of the possible sources were:

1. Pit silage contaminated by rodent/rabbit/bandicoot carcases.

2. Imported soybean meal (ex. U.S.A.).

3. Used cooking oil, added to the ration as an energy source.

4. Contaminated water supplies, as cattle watered from a variety of sources, including a clean river, almost stagnant dams containing decaying plant material, and troughs containing a layer of decaying grain and hay on the bottom.

5. Feed mill/mixer contaminated by rodent carcases (e.g. snake case in Qld.)

6. Toxico-infectious Botulism, due to growth of Cl. Botulinum, in the gut - possibly triggered by ration changes.

None of these possible sources could be confidently identified as the cause.

The pit silage was (and still remains) the first choice, but the farm has been making and feeding silage the same way for 30 years without any previous problems. Numerous silage samples could not demonstrate any Botulism bacteria or toxin. Also, to the best of the owner's knowledge, the 3 replacement heifers which died, did not have access to silage.

One epidemiological observation of interest, first observed by the owner and supported by Dave Gardiner's (V.O. Maitland) computer records was that the deaths seemed to occur in 3 distinct 'waves', each 'mini-outbreak' following an increase in the soybean content of the ration. Again extensive testing of the soybean meal failed to demonstrate bacteria or toxin.

Graph of botulism deaths in dairy

Dave Gardiner's hypothesis is that the problem was not caused by ingestion of preformed toxin, but by the growth of ingested spores/bacteria in the gut, triggered by the increasing % of soybean meal in the ration.

Each change in soybean content involved an approximate 30% increase in quantity.

No dry cows were affected during the outbreak.

The herd owner is still in business, largely only because he had a large number of replacement heifers coming on, and he was able to rebuild herd numbers relatively quickly.

Considerable quantities of silage (particularly round-bale silage) are used on the coast every year. It is quite common and unavoidable to collect a few rabbits and bandicoots when cutting silage crops, so one of the $64 questions arises:- 'Should we recommend routine Botulism vaccination for herds feeding Silage'????

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