Continuing education – Voortgesette opleiding
Water intoxication in cattle
a
a
a
E M Njoroge , J M Maribei , P N Mbugua and S M Njiru
a
ABSTRACT
Water intoxication is a condition that is common in cattle, and has also been reported in
other domestic animals and man. A comprehensive description of the condition is lacking.
For a better understanding of the condition, this paper reviews work that has been reported
previously by various authors.
Key words: adult cattle, calves, milk, salts, water intoxication.
Njoroge E M, Maribei J M, Mbugua P N, Njiru S M Water intoxication in cattle. Journal of the
South African Veterinary Association (1999) 70(4): 177–179 (En.). Faculty of Veterinary Medicine, University of Nairobi, PO Box 29053, Nairobi, Kenya.
INTRODUCTION
Water intoxication is a condition that
occurs when excessive quantities of water
are ingested by very thirsty animals3. It
commonly occurs in animals that have
been subjected to severe exercise or high
environmental temperatures16.
Water intoxication was first reported
as a distinct syndrome in man28. Subsequently, naturally occurring cases have
been reported in man12,17,25, sheep1, pigs19,
camels27, calves2–7,10,11,13,16,18,24,26,29 and adult
cattle8. Calves are the most commonly
affected animals3.
ANIMALS AFFECTED
In cattle, the condition has been reported to occur in all ages, but it is more
common among calves 2–10 months of
age and is most frequent in calves 3–5
months of age2,7,8,29. All breeds of cattle are
affected. The condition has no sex predilection.
PREDISPOSING FACTORS
A number of factors predispose calves
to water intoxication15. Young bucket-fed
calves usually drink excessive quantities
of water if it is offered to them in the
manner in which they usually receive
their milk. Under such circumstances, the
limit of their consumption is apparently
governed not by satiety, but by the physical limit of capacity of the gut. Another
predisposing factor is the high ruminal
capacity to hold ingested water as compared with total body size.
Chronic subclinical dehydration aca
Faculty of Veterinary Medicine, University of Nairobi,
PO Box 29053, Nairobi, Kenya.
Received: March 1999. Accepted: September 1999.
companied by increased environmental
temperature, exercise or increased body
water loss due to diarrhoea or fever also
predisposes calves to water intoxication.
Calves in an oliguric state or those that fail
to rapidly develop diuresis after water
overloading have a higher predisposition
to water intoxication than normal calves.
More recent findings indicate that
failure to provide calves with both water
and salts2* from as early as 2 weeks of age
to weaning predisposes them to water
intoxication20,22. Under experimental conditions, calves raised solely on milk from
2 weeks of age to weaning developed the
condition while those raised on milk,
water and salts did not. The salts used in
the experiment included many minerals.
However, the authors did not determine
the role that each mineral component of
the salt played in prevention of water
intoxication.
Age has also been reported to predispose animals to the condition14. Haemoglobinuria is found most frequently in
calves 3–5 months of age.
In adult cattle, the most common
predisposing factor is chronic subclinical
dehydration due to prolonged failure of
water supply, accompanied by increased
environmental temperature. They develop chronic oliguria and fail to rapidly
develop diuresis after water overloading8.
HISTORY
In Kenya, a similar case history is given
by farmers in almost all cases reported
*The salt (Maclik Super®, Unga Feeds, Kenya) used had
the following constituents: NaCl 27 %; Ca 18.51 %; P
11.00 %; Mg 3.00 %; Fe 0.50 %; Cu 0.16 %; Mn 0.40 %;
Zn 0.50 %; S 0.40 %; Co 0.02 %; I 0.02 %; Se 0.0015 %;
Mo 0.0002 %.
0038-2809 Jl S.Afr.vet.Ass. (1999) 70(4): 177–179
(Clinical Records, Large Animal Clinic,
Clinical Studies Department, University
of Nairobi). Animals are exposed to a
water source where they drink ad libitum
after a long period of restriction and they
then start voiding ‘bloody’ urine. The
farmer may report having raised calves
on milk or milk substitutes alone, without
access to additional water, followed by
either unlimited water supply or an automatic water source7,8,29. One or 2 calves are
usually involved on small-holder farms,
while several may be involved on large
beef and dairy farms29. In adult cattle, the
commonly reported cases involve beef
herds raised on rangelands that have had
no water supply, followed by excess
supply8.
CLINICAL SIGNS
In a group of calves, water intoxication
may be manifested in all or only a few of
the animals2,9,18,29. Clinically, the condition
is characterised by haemoglobinuria and
nervous signs. The nervous signs include
hyperaesthesia, muscular tremors, nystagmus and lethargy20,22. Mild cases recover in 3–4 hours. In severely affected
animals, lethargy may progress to
depression and coma, and death occurs in
24–48 hours11,15,20,22. In some cases haemoglobinuria is the only clinical sign observed22,29; in others, the nervous signs
predominate and haemoglobinuria is not
detected7,9. Additional signs include hypothermia, salivation, severe ruminal
tympany, colic, diarrhoea, arrhythmia,
oedema of the eyelids and erection of
body hair7,11,15,20.
In adult cattle, water intoxication is
manifested clinically by haemoglobinuria. Other signs present in calves are
rare. Unlike camels27, bloody diarrhoea
and abortion have not been recorded in
cattle.
PATHOGENESIS
After drinking too much water, animals
develop a state of positive water balance.
The excess water circulating in the body
leads to haemodilution. In cases of water
intoxication in both calves and adult cattle
under experimental conditions, a sharp
drop in plasma Na+ concentration due to
haemodilution has been reported21,22. This
leads to increased absorption of water
177
down a concentration gradient into the
cells. Cellular hydration occurs and in
organised tissues, the cells increase in
turgidity; this is evident in the brain,
where oedema occurs, causing nervous
signs3,22,23. In unorganised tissues, particularly the erythrocytes, hypotonicity of the
blood leads to lysis of the cells and the resulting haemolysis may cause severe
anaemia and haemoglobinuria3,22–24. In
calves, haemoglobinuria has also been
attributed to fragility of erythrocytes. The
osmotic fragility of erythrocytes has been
found to be higher in calves suffering
from water intoxication than those that
do not suffer from the condition22. In
adult cattle, fragility of erythrocytes has
not been reported to play a role in the
pathogenesis of water intoxication.
POST MORTEM LESIONS
In both calves and adult cattle, the
carcass is usually in poor condition and
shows severe ruminal tympany 8,22,23 .
Grossly, there may be fluid in both the
abdominal and thoracic cavities. The fat
in the coronary grooves of the heart may
be gelatinous. The urinary bladder
usually contains red urine. The kidneys
appear dark. In calves, the sulci on the
surface of the brain are flattened, indicating a degree of oedema. This has not been
reported in adult cattle. Unlike in the
camel, rupture of the abomasum has not
been observed in either calves or adult
cattle. Ruptured abomasum has been
reported to be the only significant post
mortem finding in camels27.
Microscopic changes have been reported
only in calves. Histological examination
reveals oedema and haemorrhage of the
brain parenchyma23. Cerebral veins and
venules are congested and fill the
Virchow-Robin spaces. The kidney may
show marked lymphocytic infiltration of
the cortex and fibrosis around the capillaries. The renal medulla may have areas
of haemorrhage and congested capillaries. The epithelial cells of the kidney
tubules contain fine, red granules. The
urinary bladder may have areas of
oedema, both beneath the stratified
mucosa and in the muscular layer23.
DIAGNOSIS
Diagnosis of water intoxication is based
on age incidence, history of free access to
water after a period of restriction, rapid
onset of nervous signs and mortality,
haemoglobinuria and the finding of pulmonary oedema at necropsy7,22. Confirmatory diagnosis is achieved by elimination of other diseases that cause nervous signs and haemoglobinuria in cattle
and, retrospectively, by response to treatment.
178
DIFFERENTIAL DIAGNOSES
Water intoxication needs to be distinguished from other diseases that cause
nervous signs and haemoglobinuria.
Numerous diseases and intoxications can
cause nervous signs in cattle of various
ages. Babesiosis is the most usual cause of
haemoglobinuria in adult cattle, and may
sometimes be observed in calves.
TREATMENT
Hypertonic saline (5 %) given intravenously has been recommended for treatment of water intoxication9. However, this
is effective only in mild to moderate cases.
In severe cases, use of both 5 % dextrosesaline solution intravenously and a tranquilliser such as acetylpromazine has
been found to achieve a better response in
calves11,22.
PREVENTION
Prevention of water intoxication can be
achieved by provision of salts and water
ad libitum to calves from as early as 2
weeks of age. The salts may be provided
as blocks or powder licks for the calves to
lick ad libitum22.
WATER INTOXICATION AND SALT
POISONING
Whereas water intoxication results from
a state of positive water balance within
the body, salt poisoning occurs when
excessive amounts of salt are ingested or
animals have been drinking saline water
without access to fresh water. The salt
ingested causes irritation of the gastrointestinal tract. This is manifested as diarrho e a w i t h m u c o u s i n t h e f a ec es ,
depression of body temperature, abdominal pain and anorexia. Some salt is absorbed and may cause involvement of
central nervous system. The signs in this
case are similar to those of water intoxication in calves. However, a nervous syndrome due to salt poisoning is present in
both calves and adult cattle, while that
due to water intoxication is common only
in calves. Haemoglobinuria is the most
common clinical sign in cases of water
intoxication but has not been reported in
salt poisoning. In salt poisoning, the
plasma Na+ is elevated while in water
intoxication it is lower than in healthy
animals.
Cattle that die of salt poisoning show
marked congestion of the mucosae of the
omasum and abomasum. Fluid faeces
that are dark in colour may be present.
Treatment of salt poisoning involves
removal of the toxic feed or water and
provision of fresh water in small quantities. In cases of nervous involvement,
treatment is similar to that for water
intoxication in calves with nervous signs.
REFERENCES
1. Abdelrahim A I, Hagir B S, Talgeldin M M
and Shommein A M 1985 Acute water
intoxication in sheep in Sudan. Revue
d’Élevage et de Médecine Veterinaire des Pays
Tropicaux 38: 180–184
2. Ascoli E W 1936 Water intoxication in
calves. Veterinary Record 48:1082
3. Blood D C, Radostits O M 1989 Veterinary
medicine, a textbook of the diseases of cattle,
sheep, pigs, goats, and horses (7th edn).
Baillière Tindall, London
4. Dolci G 1957 L’emoglobinuria parossistica
da sovraccarico idrioc del vitello. Goz vet,
Milano 4: 18–20
5. Fernegel E 1936 Paroxysmal haemoglobinuria in young calves. Inaugural dissertation, Hanover: 53, abstracted in Veterinary
Bulletin 11: 113
6. Gibbons W J 1965 Water intoxication. Modern Veterinary Practice 40: 84
7. Gibson E A, Counter D E, Barnes E G 1976
An incident of water intoxication in calves.
Veterinary Record 98: 486–487
8. Gray T C 1970 Dehydration and water intoxication of range cattle. Journal of the
American Veterinary Medical Association 157:
1549–1556
9. Hannan J 1965 Water intoxication in calves.
Irish Veterinary Journal 19: 211–214
10. Harvey F T 1936 Water poisoning in calves.
Veterinary Record 48: 641
11. Harwood D G 1976 Water intoxication in
calves. Veterinary Record 99: 76
12. Helwig F C, Schulz C B, Kuhn H P 1938
Water intoxication. Journal of the American
Medical Association 110: 644–645
13. Hornbogen F 1938 Blood picture in experimentally produced haemoglobinuria in
calves. Inaugural dissertation, Berlin
14. Jain N C 1986 Schalm’s veterinary hematology
(4th edn). Lea and Febiger, Philadelphia
15. Kirkbride C A, Frey R A 1967 Experimental
water intoxication in calves. Journal of the
American Veterinary Medical Association 151:
742–746
16. Lawrence J A 1965 Water intoxication in
calves. Journal of the South African Veterinary
Association 36: 377–378
17. LeQuesne L P 1954 Post operative water
retention. Lancet 266: 172
18. Llewellyn-Jones H 1936 Excess of water as a
cause of haemoglobinuria. Veterinary Record
48: 1056
19. Lu W H, Xie Q R, Zhao T L, Yang R Y, Dong F
L, Fen S W, Lu H Z, Zhou Q 1984 Water intoxication in pigs. Journal of Veterinary Science, Technical No. 4: 15–19
20. Maribei J M, Njoroge E M, Mbugua P N 1998
Clinical manifestation of experimental
water intoxication in calves. Indian Journal of
Animal Science 68: 531–532
21. Mielke H 1979 Elicitation of increased
diuresis, and of water intoxication induced
by diuresis inhibition, by oxytocin and
vasopressin in lactating cows. Archiv für
Experimentelle Veterinärmedizin 33: 569–593
22. Njoroge E M 1993 Studies on experimental
water intoxication in calves. MSc thesis,
University of Nairobi
23. Njoroge E M, Maribei J M, Mbugua P N 1997
Pathological changes of calves suffering
from experimental water intoxication.
Ondersterpoort Journal of Veterinary Research
64: 110–114
24. Papadaniel S 1955 Paralytic haemoglobinuria and pulmonary oedema in calves following ingestion of large quantities of
water. Delter Hellen Kten Hetair 2: 619–623,
0038-2809 Tydskr.S.Afr.vet.Ver. (1999) 70(4): 177–179
abstracted in Veterinary Bulletin 2: 76
25. Scott J C, Welch J S, Berman I B 1965 Water
intoxication and sodium depletion in surgical patients. Obstetrics and Gynaecology 26:
168–175
26. Verhoeff J 1980 Water intoxication in calves.
Tijdschrift voor Dieregeneeskunde 105: 727–
728
27. Waitumbi J N, Conor R J 1987 Beware of
watered camels. Veterinary Record 121: 407
28. Wier J E, Larson E E, Rowntree L G 1922
Studies in diabetes insipidus, water balance
and water intoxication. American Medical
Association Archives. Internal Medicine 29:
306–330
29. Wright M A 1961 Hemoglobinuria from
excess water drinking. Veterinary Record 73:
129–130
Book review – Boekresensie
The economics of animal disease control
Coordinator: B D Perry
1999. Office Internationale des Épizooties, Paris. Soft cover. 276 pp. Price 40ecu including postage. ISBN 92-9044-488-6.
One of the recurring questions – largely rhetorical –
within the veterinary fraternity in South Africa concerns
the relative impact and cost of some of the major epidemic
and endemic diseases that confront us, particularly those
caused by ticks and tick-borne diseases (TTBD). This excellent compendium of 16 papers dealing with the
economics of disease control makes 2 points on this issue.
First, that the question itself is not relevant to the debate as
far as the economics of control is concerned. The reason, as
pointed out by R S Morris in the introductory chapter, is
that the guiding principle (equimarginal returns) should
be ‘to allocate funds progressively, moving resources to
wherever the return on the next investment dollar is highest’, and away from activities that generate a lower return.
Second, if the reference list of the relevant chapter is a
reliable measure, South Africa has contributed nothing
significant to the much-studied economics of TTBD. This
is clearly not true but it may be so that South Africa’s vast
experience and knowledge in this field is not easily accessible to the international community. One suspects that
the answer lies in differences of approach – our essentially
pragmatic/trial-and-error perspective versus a more systematic and academic approach espoused by Australians
and Europeans operating in Africa. In the modern world,
where the economics of production are increasingly important and complex, we probably have a lesson to learn
from the latter group. Current plans to establish an
integrated epidemiology unit at Onderstepoort that includes capacities for impact and risk analysis makes this
compendium extraordinarily opportune from the South
African perspective.
A particularly interesting statement, also by R S Morris,
contends that the net economic benefit obtained from
investment funds directed towards controlling animal
diseases is commonly in the range of 200–1500 %, while
the yields derived from investment in other activities in
the livestock sector are commonly about 20 %. These are
the sort of data that those of us in public service need to
attract the attention of the purse-string holders.
The coordinator (B D Perry), the editorial staff of the OIE
and especially the authors themselves, have produced a
high-quality volume with an appropriate balance of subject matter. Rushton, Thornton and Otte’s chapter covering methods (partial budgets, break-even analysis,
cost/benefit analysis etc.) is the only one that deals in any
detail with the technicalities of control economics. Other
0038-2809 Jl S.Afr.vet.Ass. (1999) 70(4): 177–179
chapters are concerned mostly with the application, using
interesting examples, of control economics in both the
developing and developed world and at different geographic levels, namely regions, countries, zones within
countries and individual farms with different production
systems. For that reason very few veterinarians dealing
with production animals would not find this volume both
interesting and instructive. There are many informative
illustrations and no irritating editorial errors or inconsistencies were encountered. Two of the papers are not in
English (Spanish and French) but they do have English
summaries.
The appeal of different chapters in this volume will
depend very much on the interests of the reader. To provide some indication as to the types and range of chapters
the following are given as examples of the subject matter:
• Control and eradication of epidemic diseases.
• Endemic diseases and disease control programmes.
• Health and productivity in smallholder livestock systems in developing countries.
• Delivery of veterinary services.
• Implications of greater global trade in livestock and livestock products.
• Rinderpest control in Africa.
• Health and productivity in the commercial dairy.
• Privatising veterinary services in Africa.
The chapter on trends and predictions for global trade in
livestock and livestock products by Leslie and Upton contains important considerations for South Africa. For example, they deduce that increasing global trade in livestock
products will disadvantage net food importers while
favouring high-income countries. South Africa is, fortunately, a net food exporter but on the livestock side the
reverse is the case. We are 8th, according to tables contained in the chapter, among world importers of ovine
meat (29 600 tonnes). They also predict that grassland-fed
ruminant meat and milk is likely to capture market share
from pig and poultry producers, presumably as a result of
BSE-type issues currently troubling consumers in Europe.
For anyone involved in production animal health where
financial considerations are important (and where is that
not the case?) this volume will provide an invaluable
source of information.
G R Thomson
ARC – Onderstepoort Veterinary Institute
Pretoria
179