Chapter 14.

Sudden death

Enterotoxaemia (pulpy kidney) | Infectious necrotic hepatitis (Black disease) | Malignant

oedema | Other clostridial diseases | Clostridial vaccines | Anthrax | Other causes of sudden
death | Recommended reading

Return to Sheep Health & Production Index

Enterotoxaemia (pulpy

Under particular dietary conditions, Clostridium perfringens type D proliferates in the small
intestine and produces toxins, the principal one being the necrotizing, highly lethal, epsilon
toxin. Absorption of this toxin leads rapidly to diarrhoea, convulsions and death. Death may
occur so quickly that the diarrhoea is never exhibited.
The conditions which lead to the proliferation of the organism in the intestine are complex. A
common factor in many outbreaks is that the sheep are offered a diet to which they are not
accustomed. Before ruminal flora adapt to the changed diet partially digested food may spill
into the intestine and, if that food includes starch, Cl perfringens may proliferate using the
starch as a substrate. The fact that starch is a preferred substrate for this organism leads to
the association between the disease, lush feed conditions and individual animals with high
growth rates. The disease also occurs under pasture conditions which are anything but lush,
for reasons which are not always clear.
The epsilon toxin produces a profuse diarrhoea, stimulation and then depression of the CNS.
Damage to the vascular endothelial cells in a variety of organs leads to some characteristic
necropsy findings.
Clinical signs of animals acutely affected include clonic convulsions, frothing and sudden
death. If they survive more than a few hours there will be a pasty diarrhoea, staggering,
opisthotonus and convulsions or, more commonly, struggling. Older sheep may survive for
longer (24 hours) and some may even recover.

Necropsy findings

The disease is most frequently diagnosed by necropsy. Putrefaction occurs quickly. In

animals examined soon after death, necropsy findings provide reliable diagnostic evidence of
the disease.
There is an excess of straw-coloured pericardial fluid, lung oedema with froth and
haemorrhages in the endocardium, epicardium and parietal peritoneum. The intestinal
contents are creamy, particularly if death was rapid. ’Pulpy kidney’ is not a particularly useful
sign because the ’pulpiness’ is in fact a more rapid than usual autolysis.
Glycosuria virtually always occurs and is a consequence of hepatic glycogenolysis and
extreme hyperglycaemia. The finding of glycosuria is a useful contribution to diagnosis but not
completely pathognomic; glucose is fermented in urine within hours of death. (Note that
glycosuria is not a sign of enterotoxaemia in cattle.)
Brain histopathology is particularly useful; often there are symmetrical areas of haemorrhage,
oedema and softening, particularly in the basal ganglia but also in other areas.

Control by husbandry procedures

Outbreaks of enterotoxaemia are often controllable by changes to the management of the

affected mobs which alter the dietary predispostion to the disease. Exercise, a change of
pasture or diet, particularly to one with more roughage, will often stop deaths dramatically. In
lambs, tailing and marking and the check in growth rate which accompanies the procedures
will usually stop an outbreak. In the case of prime lambs over eights of age, weaning will
serve the same purpose.
The results of attempts to control enterotoxaemia in this way are not always successful, or the
procedures necessarily practicable. Antiserum is commercially available and is effective in
preventing the disease, but only for a few weeks. Antiserum is of no use in treatment of
clinical cases of enterotoxaemia.

Control with immunization

A commercial vaccine containing epsilon toxoid of Cl perfringens type D is available from

several manufacturers. In describing the use of the vaccine, there are some conventions
which are normally observed for describing the first and subsequent administrations of the
product.
Dose of vaccination Name used to describe
1 Primary
2 Secondary
3 First booster
4 Second booster

The protection afforded by one vaccination is short-lived. Complete protection will, therefore,
only come from carefully timed, repeat doses of vaccine. The timing varies with the quality of
protection desired.

Absolute protection

Protection of lambs to 14 weeks of age

Vaccination of ewes such that they receive a secondary vaccination or booster in the last two
weeks of pregnancy will provide passive protection of all lambs to 8 weeks of age, but less
than 100% of all lambs will still be protected by maternal antitoxin at 14 weeks of age.
Estimates of the proportion of lambs protected vary from 30% to 40%[1][2][3][4] depending on
the timing of the ewes’ vaccination history and where one considers the protective level of
serum antitoxin to lie between 0.1 and 0.25 [5][6].
For absolute protection, vaccination of lambs should, therefore, commence before they are
eight weeks of age if the ewes received a secondary or booster vaccination in late pregnancy,
earlier if the ewes did not. Vaccination of lambs can be done within a few days of birth and is
effective. Colostral antibodies do not appear to prevent the development of the lamb’s
immune response to active immunisation but very high levels of passively acquired antitoxin
may reduce the response.
Thus, if lamb marking is performed eight weeks after the start of lambing when most lambs
are 5 to 7 weeks of age, secondary or booster vaccination of the ewes two weeks before
lambing starts and vaccination of the lambs at marking will virtually guarantee their
continuous protection to 14 weeks of age. All lambs will remain protected for 6 to 8 weeks
after their primary vaccination; 80% will remain protected after a further 8 to 10 weeks[7].

Protection of lambs beyond 14 weeks of age

To maintain continuous, complete protection, a secondary vaccination should be given within

six to eight weeks of the primary dose. It is effective in raising titres to a high level if given two
weeks or more after the primary vaccination, but not if given after only one week[8]. The
period between primary and secondary doses can be extended to 15 weeks[2] or, probably,
longer, based on experiences with other immunogenic agents. As the period between the two
initial doses lengthens, however, an increasing proportion of the flock becomes susceptible to
the disease. The usual manufacturer’s recommendation that at least four weeks intervene
between primary and secondary doses appears to be based on avoiding any possible
interference with maternally derived antitoxin by the time of the secondary vaccination.
The duration of immunity following secondary vaccination is probably 15 weeks for 90% of the
flock, but only 50% are still protected at 24 weeks. Some reports suggest shorter periods of
protection. In Figure 14.1, note the wide range in immune responses and the increase with
time in the number of susceptible animals. The minimum protective level here is considered to
be 0.15 units/ml of serum (from Jansen, 1967a).

Protection to 1 year of age

Vaccination of ewes in late pregnancy and lambs at 8 and 14 weeks of age will ensure
virtually complete protection of all lambs to seven months of age. Each booster vaccination
given to animals under 1 year of age will afford a further four months protection to 100% of
the flock and five to six months protection to 80% of the flock.

Protection beyond 1 year of age

Booster vaccinations given at least 1 year after the primary vaccination lead to prolonged
immunity of 1 year’s duration at least. Further boosters given to animals in their third year of
life will produce an immunity of at least 3 years’ duration[7].

Minimum effective protection

An alternative aim to complete protection is the protection of sheep only at those times of the
year and at those ages which present the greatest risk of disease. Most deaths from
enterotoxaemia occur in animals between 2 weeks and 18 months of age. It is more common
during seasonal conditions which favour rapid growth and in British breed and British breed-
Merino cross sheep, rather than straight-bred Merinos[9].
On any property, therefore, it may be possible to devise a vaccination program which requires
less intense treatment than that affording absolute protection. For example, if enterotoxaemia
causes the deaths of lambs before weaning, booster vaccination of ewes in late pregnancy
and vaccination of lambs at marking only may completely resolve the problem. If deaths at
hogget age occur, one vaccination early in life (coinciding with marking or weaning) and a
secondary vaccination before the risk period some months later may be appropriate.
Unless deaths from enterotoxaemia are occurring before ten weeks of age there appears to
be no justification for vaccination of ewes annually and in late pregnancy. Many of the
recommendations to do so stem from experiences with British breed sheep and their crosses
in this and other countries under more intense systems of management than are common in
Australia[10].

Economically optimal protection

Vaccination of sheep is practiced primarily to increase the financial success of sheep raising.
Vaccination has a cost, in terms of the purchase and storage of vaccine, the labour required
to administer it and the losses in production associated with any untoward effects of
vaccination. Vaccination programs which afford complete protection to all sheep which are
considered at risk, but for which the risk of enterotoxaemia is low, may not be economically
justified.
There are several parameters to consider when estimating the risk of death from
enterotoxaemia. Firstly, seasonal conditions influence the likelihood of an outbreak and the
frequency of suitable conditions may vary from farm to farm. Secondly, management factors,
including the choice of maternal and sire breeds influence the probability of an
enterotoxaemia outbreak. Thirdly, when an outbreak does occur, it usually only affects one
age group within the flock and the mortality rate is commonly 5% to 10%(9). The variable
morbidity may be due to differences in individual animals’ genetic susceptibility, growth rate or
immune status. Immunity may stem from natural exposure, one or more immunisation
treatments earlier in life, a combination of both or, in the case of lambs, persistence of
colostral protection. 20% of unvaccinated animals in Western Australian flocks have
protective levels of antitoxin[11].
Similarly, following vaccination, fewer than 100% of animals are protected and the duration of
protection varies between animals. The cost-benefit of vaccination against enterotoxaemia
must be calculated on the basis of the improvement in protection afforded by vaccination, the
risk of losses and the cost of vaccination. For example, in a prime lamb flock, reliance on
colostral protection following booster vaccination of ewes in late pregnancy may leave some
lambs susceptible to enterotoxaemia between 15 weeks of age and sale. The improvement in
protection provided by a vaccination of lambs at 8 weeks of age may not be justified after
considering the cost of vaccination, the risk of any enterotoxaemia in lambs of that age, the
small proportion of the flock which loses its maternal protection and the damage done to skins
and carcases by the injection[3][4].
A computer program has been developed to aid decision making for disease prevention in
livestock and can be used to explore the economic rationale of clostridial vaccination. The
program is called VAX-N-OMICS and is supported by an ’Agnote’ from the NSW Department
of Agriculture and Fisheries[12]. The results from a run with this program for one particular
scenario are reported in Figure 14.2.
Producers often make the decision to risk some losses from enterotoxaemia for the sake of
timing the administration of vaccine to coincide with other husbandry procedures, such as
lamb marking. Considering the cost of labour for mustering and the often marginal cost-
benefit of vaccination, such a policy is usually rational, as demonstrated in the ’break-even’
table in Figure 14.2.
As will be discussed below, epsilon toxoid is now virtually always sold in combination with
other vaccines, particularly tetanus toxoid and CLA vaccine. The extra protection afforded by
these components of the vaccine must also be considered when evaluating the cost-benefit of
enterotoxaemia vaccination.

Enterotoxaemia caused by Cl perfringens types A,B,C and E

Type A has been recorded as causing a highly fatal haemolytic disease in sheep. Type A
produces more alpha toxin than other types; this toxin is haemolytic. It also is associated with
wound infections, causing gas gangrene. Type B causes an enterotoxaemia of lambs under 3
weeks of age - Lamb dysentery. The disease is uncommon in Aust. Toxins involved are
(alpha,) beta and epsilon.
Type C causes Struck in UK - an enterotoxaemia with haemorrhagic enteritis and peritonitis
affecting adult sheep, usually when feed is abundant. Type B produces alpha and beta toxins.
Type E is reported as causing enterotoxaemia in lambs. It produces the iota toxin.
Figure 14.1 the decline in epsilon antitoxin titre in sheep receiving secondary and first
booster doses of enterotoxaemia vaccine.

Infectious necrotic hepatitis (Black disease)

A fatal, peracute intoxication caused by Cl novyi type B which proliferates in the liver following
tissue damage which produces an anaerobic environment. This anaerobic environment is
most often produced by migrating immature F hepatica.
Spores of Cl novyi are continuously ingested by grazing animals where black disease occurs
and some spores cross the intestinal wall and populate reticuloendothelial cells - including
those in the liver. Immature flukes leave tunnels about 5 mm in diameter which are
surrounded by necrotic zones. Any latent spores in these necrotic zones become vegetative,
produce toxins which extend the necrotic areas and further multiply.
The disease occurs mainly in adult sheep and less frequently in young sheep and goats.
Morbidity rates are usually low (5% to 10%) but the disease is always fatal. It occurs in most
areas where liver fluke occurs and is most likely to be seen when sheep are ingesting
metacercariae - summer and autumn.
Clinical signs are rarely observed. The course of the illness is only a few hours and sheep are
usually found dead with no signs of struggling. At necropsy, rapid putrefaction is obvious and
variably other signs :

PARAMETERS THAT CAN BE CHANGED BY THE USER

Description Current value

Vaccine cost 12 c/dose
Labour cost for vaccination 6 c/dose
Percentage of lambs given booster vaccination 100%
Vaccine efficacy 70%
Minimum average lamb value $10
Vaccine efficacy 70%
Maximum average lamb value $30
Minimum % clostridial losses 0.0%
Maximum % clostridial losses (max=25%) 10.0%

Enter new value or press <ENTER> to leave value unchanged:

Press <ESC> to return to the menu.
BREAK-EVEN POINT (% deaths prevented)
The table below sets out the break-even point for a vaccination program for a range of lamb
values and vaccination costs.
Average lamb value is the average value of lambs in the flock and the vaccination cost is the
total cost of vaccination (vaccine plus labour) using a range of costs around your selected
figures.
The break-even point is the average percentage of lambs that must be saved to cover the
total cost of the program.

VACCINATION AVERAGE LAMB VALUE

 Cost $10 $15 $20 $15 $30
$0.14 4.0% 2.7% 2.0% 1.6% 1.4%
$0.16 4.6% 3.1% 2.3% 1.9% 1.6%
$0.18 5.2% 3.5% 2.6% 2.1% 1.8%
$0.20 5.8% 3.9% 2.9% 2.3% 2.0%
$0.22 6.3% 4.2% 3.2% 2.6% 2.1%

For: Vaccine= 12 c/dose Labour= 6 c/dose Efficacy= 70 % 100 % of lambs receiving booster
vaccination.
Press <P> to print hard copy or any other key to continue .......

EXPECTED RETURNS ($/head)

The table below sets out the expected returns (average profit or loss ($ per lamb) after costs
are deducted) from a vaccination program for a range of lamb values and disease incidences.
Average lamb value is the average value of all lambs in the flock, and the % deaths prevented
is the expected long term average percentage of clostridial deaths per year in an
unvaccinated flock.
% Deaths preventes Average lamb value
$10 $15 $20 $15 $30
0.00 -0.36 -0.36 -0.36 -0.36 -0.36
2.00 -0.22 -0.15 -0.08 -0.01 -0.06
4.00 -0.08 0.06 0.20 0.34 0.48
6.00 0.06 0.27 0.48 0.69 0.90
8.00 0.20 0.48 0.76 1.04 1.32
10.00 0.34 0.69 1.04 1.39 1.74
For: Vaccine= 12 c/dose Labour= 6 c/dose Efficacy= 70 %
100 % of lambs receiving booster vaccination.
Press <P> to print hard copy or any other key to continue .......

Figure 14.2 : Results from a run with ’VAX-N-OMIC’. The parameters entered are an
attempt to estimate the cost-benefit of giving a primary and secondary vaccination with
5-in-1 vaccine to lambs. The expected protection rate averaged over the ensuing 12
months is 70%. If lambs are worth $20, and the death rate is reduced by 2% by
vaccination, the return from vaccination is -$0.08 per lamb. The cost of vaccination
(including labour) would need to fall to $0.14 per injection to break-even (from
Sergeant, 1992).

• marked subcutaneous venous congestion (hence the name), straw coloured fluid in
serous cavities, often blood tinged in the abdomen
• the liver is generally engorged and will have at least one area of necrosis, 1 to 2 cm
diameter, often under the capsule of the diaphragmatic surface but they may be
within the deeper liver parenchyma apparent only after serial slicing of the liver
• impression smears of sections taken from the periphery of liver lesions examined by
fluorescent antibody will confirm the presence of large numbers of Cl novyi - care
should be taken in interpreting such results from animals dead more than a few hours

Malignant oedema
This name embraces severe wound infections of the subcutaneous tissues and intoxications
caused by a variety of clostridial organisms - including Cl septicum most commonly, Cl novyi
type A, Cl chauvoei, Cl perfringens type A and Cl sordellii. (Cl novyi type A was previously
Cl oedematiens.)
’Swelled head’ is the special case of malignant oedema which occurs in rams and is usually
caused by Cl novyi type A (type B toxoid is protective). Blackleg is caused by Cl chauvoei but
is an infection of muscles.
The disease follows introduction of the organism and the production of at least a small area of
anaerobic necrosis. Wounds caused by shearing, marking, mulesing, fighting, vaccination or
’crow pick’ can lead to clostridial infection. Lambed ewes, particularly if there has been
dystocia, can develop malignant oedema of the perineal area.
Clinical signs develop with 12 to 48 hours of wounding and include local swelling, crepitus,
heat and redness, the signs varying on the infecting organism. Cl novyi produces oedema
rather than gaseous swelling leading to severe oedema of the face, throat and neck.
At necropsy, the oedema fluid may be thin or gelatinous. Gas is present, except with Cl novyi
infections, when the fluid is gelatinous, clear and odourless. Cl perfringens and Cl sordellii
infections produce a putrid odour.
The longer course of this disease allows the possibility of treatment - and penicillin can be
used. Success is only likely in very early cases or when used prophylactically (for example,
after assisting ewes at lambing).

Other clostridial diseases

Blackleg

Mainly a disease of cattle but also occurs in sheep. Caused by Cl chauvoei.

Bacilliary haemoglobinuria

Has been reported overseas in sheep, but mainly cattle. Caused by Cl novyi type D more
commonly called Cl haemolyticum.

Braxy (Bradsot)

Caused by Cl septicum, which infects the abomasal wall and produces a fatal toxaemia.
Occurs when sheep are grazing heavily frosted pastures. Has occurred in Tasmania.

Clostridial vaccines

In relation to the previous discussion of important clostridial diseases of sheep, the following
vaccines are available :
Pulpy kidney ATPT[13] Cl perfringens type D
Black disease and Swelled head ATPT Cl novyi type B
Malignant oedema (some forms) ATPT Cl septicum
FICl chauvoei
In addition, for diseases not causing sudden death :
Tetanus TPTCl tetani
Botulism ATPTCl botulinum type D
and for less important diseases of sheep:
Blackleg ATPT Cl chauvoei
ATPT Cl septicum
FI Cl chauvoei
Commonly used combinations include :
3-in-1 vaccine PK, Tet, CLA
6-in-1 vaccine PK, Tet, Mal Oed, Black dis, B Leg, CLA
(CLA vaccine is available with most commercial clostridial combinations and adds little to the
cost.)
Where any of malignant oedema, swelled head or black disease are a risk, vaccination with
6-in-1 vaccine should be considered - for example, rams are at risk of swelled head and are
valuable, it is rational to ensure they are well protected by vaccination. Where those diseases
do not occur with a significant incidence, vaccination with only 3-in-1 should be considered.

Anthrax

Most cases of anthrax in sheep are peracute with sheep dying within 1 to 2 hours of first
showing signs. Characteristically, there are discharges of tarry blood from all orifices.
The disease is caused by Bacillus anthracis. It is apparent in smears of blood from animals
dead from anthrax as gram positive rods which stain well with methylene blue - a
distinguishing feature from clostridia. Spores form when the organisms are exposed to
oxygen and the spores can survive in soil for many years. Animals are infected when spores
enter the body by ingestion or through wounds. Soil, water or infected feeds (meatmeal,
bonemeal) or bones from anthrax carcases provide sources of infection. In outbreaks, spread
occurs from animals dead of the disease. The carrier state does not occur.
Within Australia, the disease occurs frequently only in NSW and Victoria and in NSW occurs
most frequently between October and April. Within NSW, the higher rainfall country of the
tablelands and slopes are practically free of the disease.
The disease is readily transmissible to humans, causing respiratory, alimentary or cutaneous
forms of anthrax. Fortunately, the cutaneous form is most common and responds to treatment
with antibiotic therapy.

Diagnosis

When investigating sudden deaths of sheep or cattle, particularly in anthrax endemic areas,
much care should be taken to avoid opening the carcase of animals dead from anthrax.
Effective protective clothing should be worn for any necropsy which has a possibility of
sudden death.
Characteristic signs of death from anthrax include tarry blood discharges from any orifices,
striking absence of rigor mortis and rapid gaseous decomposition. In such cases, a blood
sample should be collected from a superficial vein. A smear is made, air dried, fixed and
stained with aqueous polychrome methylene blue.
If a necropsy is undertaken, there are a number of changes characteristic of anthrax. The
blood does not clot, there are ecchymotic haemorrhages in many organs, blood tinged serous
fluid in body cavities, severe enteritis and enlargement of the spleen with liquefaction of its
contents.
Anthrax must be differentiated from other causes of sudden death of sheep, particularly
blackleg amongst the clostridial diseases discussed and from some of the following causes of
sudden death.

Other causes of sudden death

A number of other disease conditions which have been reviewed in other sections of the
notes can, under certain conditions, cause sudden death. These include :
Salmonellosis
’Red gut
Haemonchosis
Acute fascioliasis
Hypomagnesaemia
In addition, some less common causes of sudden death include :
Bloat
Lightning strike
Exposure/hypothermia
Anaphylaxis and anaphylactoid reactions
There are a number of plant toxicoses and chemical poisonings causing sudden death,
including :
Poisoning with nitrate/nitrite, cyanogenetic and cardiac glycosides, fluoroacetates
Poisoning with lead, copper, arsenic
Blue-green algal poisoning
Green cestrum poisoning
Phalaris sudden death
Grazing of Phalaris aquatica can lead to a syndrome of sudden death or to a staggers
syndrome. The staggers syndrome is an acute, or more commonly, chronic nervous system
disorder, associated with the presence of tryptaminic alkaloids in the phalaris plant. This form
of phalaris intoxication is discussed further in the section on diseases of the nervous system.
The sudden death form of the disease has also been called the ’cardiac’ form and the
’peracute’ form.
Recent evidence suggests that phalaris sudden death is not caused by tryptamine
alkaloids[14], despite earlier evidence that it was[15]. Furthermore, outbreaks of phalaris
sudden death seem to be of at least two types. The two most apparent classifications are the
’cardiac’ form and the more recently described ’polioencephalomalacic’ form. Some forms of
sudden death appear to be difficult to classify as either of these, and may be associated with
cyanide or nitrate intoxication[16].
The cardiac form is a cardio-respiratory disorder precipitated by a disturbance of the flock,
particularly mustering, following a short period of grazing phalaris. Outbreaks are clustered in
late summer and autumn. Usually fewer than 1% of the flock at risk are affected. Affected
sheep collapse; some subsequently recover but most die. In animals examined alive the heart
is in ventricular fibrillation and, although the sheep continue to breathe, cyanosis is marked.
There are no signs of nervous system derangement clinically or at necropsy.
The polioencephalomalacic form need not be precipitated by disturbance. Sheep die rapidly
and any seen alive show blindness, depression, aimless wandering, head pressing, tremors,
opisthotonus, recumbency and convulsions or coma. The clinical signs and the necropsy
findings are very similar to the polioencephalomalacia of thiamine deficiency. If thiamine is
involved in this disease, the active chemical must be a particularly potent thiamine antagonist,
because the onset of disease can occur so soon after exposure to the pasture. The peak
incidence is autumn and early winter. Disease incidence can be high, up to 14%, but more
commonly around 5%[15].
The earlier descriptions of field outbreaks of phalaris sudden death do not distinguish
between cardiac and polioencephalomalacic forms so it is difficult to know if predisposing
conditions are similar for both. It has been observed that highly fertile soils, particularly those
improved with phosphate fertilizers and leguminous plants[17], seem to be more toxic than
less fertile ones. Deaths can occur within 2 hours of commencing grazing or as long as
several weeks after access[18]. Outbreaks are related to the sudden access of hungry sheep
to phalaris pasture, particularly pasture which has been spelled from grazing and is
shooting[19].
Prevention of mortalities by grazing management is worthwhile but no strategy can be
guaranteed. It would appear unwise to graze hungry sheep on phalaris pastures and the risk
seems to be higher if the pasture is freshly shooting and is on a soil likely to be high in
nitrogen. Wherever possible, phalaris should be continuously grazed. Intraruminal cobalt
pellets, which protect against phalaris staggers, do not protect against phalaris sudden
death[20]. Phalaris sudden death occurs on low alkaloid cultivars of P aquatica like
Sirolan[21].

Exposure/hypothermia

Losses of sheep following shearing when exposed to low temperatures, rain and high wind
chill factors can be very high, particularly in summer and if the sheep have been losing weight
prior to shearing. Losses as high as 90% of the recently shorn sheep have been recorded and
mortalities can occur in sheep as long as 28 days off-shears[22].

Recommended reading

Radostits OM, Blood DC and Gay CC (1994) Diseases caused by Clostridium spp, In
Veterinary Medicine VIII edition Bailliere Tindall, p 677
[1] Hepple JR, Chodnik KS and Price EK (1959) Immunisation of Lambs against Clostridium
welchii type D Enterotoxaemia (Pulpy Kidney Disease) with a Purified Toxoid Aluminium
Treated Vet Rec 71 p 201
[2] Oxer DT, Minty DW and Leifman CE (1971) Vaccination trials in sheep with clostridial
vaccines with special reference to passively acquired Cl. welchii type D antitoxin in lambs
Aust Vet J 47 p 134
[3] Wallace GV (1963) Homologous passive protection of lambs against various clostridial
diseases N Z vet J 11 p 39
[4] Wallace GV (1964) Homologous passive protection of lambs against various clostridial
diseases - Part 2 N Z vet J 12 p 61
[5] Thomson A and Batty I (1953) The antigenic efficiency of pulpy kidney disease vaccines
Vet Rec 65 p 659
[6] Jansen BC (1960) The experimental reproduction of pulpy kidney disease Jl S Afr vet med
Ass 31 p205
[7] Jansen BC (1967a) The duration of immunity to pulpy kidney disease of sheep
Onderstepoort J vet Res 34 p 333
[8] Jansen BC (1967b) The production of a basic immunity against pulpy kidney disease
Onderstepoort J vet Res 34 65
[9] Seddon HR (1965) Enterotoxaemia of sheep and goats in Bacterial diseases, Part 5,
Volume 1 of 'Diseases of Domestic animals in Australia', revised by HE Albiston,
Commonwealth of Australia, Department of Health p 71
[10] Montgomerie RF (1961) Clostridium perfringens (Cl welchii) enterotoxaemia in the
ruminant Canad vet J 2 p 439
[11] Wilkinson FC (1981) Enterotoxaemia - Economics of vaccination University of Sydney
Post-graduate Committee in Veterinary Science, Proceedings No 58 p 67
[12] Sergeant ESG (1992) VAX-N-OMICS; A computerised decision support system for
disease prevention programs in livestock Agnote Agdex 400/684 NSW Agriculture and
Fisheries
[13] ATPT stands for Alum Treated Purified Toxoid
[14] Bourke CA, Carrigan MJ and Dixon RJ (1988) Experimental evidence that tryptamine
alkaloids do not cause Phalaris aquatica sudden death syndrome in sheep Aust Vet 65 p
218
[15] Gallagher CH, Koch JH, Moore RM and Steel JD (1964) Toxicity of Phalaris tuberosa
for sheep Nature 204 p 542
[16] Bourke CA and Carrigan MJ (1992) Mechanisms underlying Phalaris aquatica "sudden
death" syndrome in sheep Aust vet J 69 p 165
[17] Moore RM and Hutchings RJ (1967) Mortalities among sheep grazing Phalaris tuberosa
Aust J Exp Ag Anim Husb 7 p 17
[18] Fearn JT (1966) In Gallagher CH, Koch JH and Hoffman M (1966) Diseases of sheep
due to ingestion of Phalaris tuberosa Aust vet J 42 p 279
[19] Gallagher Ch, Koch MD and Hoffman H (1967) Deaths of ruminants grazing Phalaris
tuberosa in Australia Aust vet J 43 p 495
[20] Moore RM, Arnold GW and Hutchings RJ (1961) Poisoning of Merino sheep on Phalaris
tuberosa L. pastures Aust J Sci 24 p 88
[21] Kennedy DJ, Cregan PD, Glastonbury JRW, Golland DT and Day DG (1986) Poisoning
of cattle grazing a low-alkaloid cultivar of Phalaris aquatica, Sirolan Aust vet J 63 p 88
[22] Holm Glass M and Jacob H (1992) Losses of sheep followingadverse weather after
shearing Aust vet J 69 p 142