Treating Scour in Calves
Scour is the most common disease in young calves and, as a result, is the greatest single cause of death in calves, accounting for almost 50% of all calf deaths in the UK1. One in seven dairy breed calves and one in thirteen beef breed calves are believed to die as a result of scour during the rearing phase in the UK each year1. Scouring calves have a major impact on the economic viability of farms, with economic losses due to treatment costs, labour costs and calf mortality. The Scottish Agricultural College (SAC) estimate an average cost of £44 per calf, excluding the cost of calf mortality.
Figure 1. Main causes of scour in neonatal calves in the UK (VIDA 2012)
All of these pathogens can be found in faecal samples from perfectly healthy calves but poor environmental and management practices can predispose animals to the development of disease:
Presence of pathogens in scour does not always equate with disease:
Potential pathogens are present in healthy animals as well as diseased animals
Shedding of pathogens in the scour can be intermittent in healthy and diseased animals
Many scour outbreaks are caused by a mixture of infections
This can present a diagnostic challenge for the practitioner when relying on faecal samples. Therefore it is recommended to take several samples from animals showing signs of diarrhoea, and several samples from those not showing clinical signs. Organisms present in both groups are less likely to be causing clinical signs.
The pathology of neonatal diarrhoea can be broadly classified into three mechanisms:
Increased secretion of electrolytes and bicarbonate from gut cells proximally in the small intestine. Water follows into the gut lumen. This hypersecretion overwhelms the absorptive capacity of the colon, and diarrhoea results. This pathological mechanism is caused by E. coli. Enterotoxinogenic serotypes bind to specific receptors in the small intestine causing increased sodium, chloride and bicarbonate secretion in to the lumen. This results in rapid dehydration. The receptors in the small intestine are only present for the first few days of life, hence E. coli diarrhea is only usually seen in very young calves.
Pathogens such as Rotavirus, Coronavirus and Cryptosporidia cause intestinal villous atrophy, reducing the small intestine’s ability to absorb nutrients. There is also loss of surface enzymes and transport mechanisms. This results in the presence of undigested lactose in the colon, which ferments. Fluid and electrolytes are drawn into the colon.
Causes can include rapidly changing milk replacer brand, changing from waste milk to milk replacer, and stressors such as transport, weather, vaccinations, dehorning, etc. This results in a failure of adequate milk digestion in abomasum. It is the end result of an oversupply of undigested milk nutrients in the intestines which overwhelms their absorptive capacity. Pathogens use the extra nutrients to multiply which can predispose to pathogenic scour.
No matter which is the inciting pathogenesis, the result is diarrhoea, dehydration, weakness, acidosis and electrolyte imbalance which can eventually lead to shock, coma and possibly death.
Oral rehydration therapy
For neonatal calf diarrhoea, oral rehydration therapy is the single most important therapeutic measure and is usually successful if instigated immediately after diarrhoea has developed.
The main functions of oral electrolytes are to address the following consequences of scour:
When should you treat with electrolytes?
Calves can lose 5 to 10% of their bodyweight as water within the first day of scouring. Fluid loss in excess of 8% requires intra-venous fluid therapy, and over 10% loss can result in death. This makes daily calf monitoring and quick treatment essential. The amount of water lost by scouring calves can be estimated by skin tenting, gum condition, attitude, and ability to stand or suckle (Table 1).
Table 1. Clinical symptoms that help evaluate amount of dehydration in calves.
Adapted from: Can Vet J. (1989); 30(7): 577–580. A retrospective study of the relationship between clinical signs and severity of acidosis in diarrheic calves. Jonathan M Naylor.
Fluid deficit = % of dehydration X body weight
This deficit needs to be administered in addition to fluids necessary for maintenance requirements (50ml/kg/day). As a general rule of thumb, ongoing losses in diarrhoea are estimated between 1 to 4l/day depending on faecal consistency.
The calf’s gastro-intestinal tract must be at least partly functional to be able to administer oral fluids safely. If the calf has ileus, fluids pool in the forestomach, which can lead to bloat and rumenal acidosis. Calves with any sort of suckle reflex/chewing action can safely tolerate oral fluids.
Anorexic, depressed, dehydrated, recumbent, bradycardic calves require intravenous fluid therapy.
What should the oral rehydration solution contain?
The main components to consider when selecting the correct formula are:
Bicarbonate precursors, e.g. acetate, propionate
Amino acids eg. glycine, glutamine
Rehydration depends on sodium absorption: active transport of sodium into intestinal interstitium creates an osmotic gradient. Water follows the sodium, and together they expand the extracellular fluid. Sodium absorption is a passive process, and depends on coupling with movement of actively absorbed or secreted solutes, for example, glucose, amino acids or volatile fatty acids such as acetate/propionate. Therefore if sodium was provided without the addition of these other molecules, either small or no net absorption of sodium would occur. Inclusion of sodium at a rate of 90-130 mmol/l is recommended2.
These are added to decrease metabolic acidosis and aid with absorption of sodium. They include bicarbonate, citrate, lactate, acetate or propionate. Pure bicarbonate would alkalinise the abomasum to a higher degree than propionate and acetate and therefore may have a deleterious effect on milk clotting in the abomasum. Inclusion of alkalinizing agents at 60 to 80 mmol/l is recommended2.
Correction of acidosis has traditionally been achieved by adding alkalinising substances. However, recently there has been growing interest in the strong ion difference (SID) of electrolyte solutions as this is related to efficacy of a product to promote alkalinisation. In practice, both theories are important. The product selected must deliver an excess of strong cations (Na+) relative to the concentration of strong anions (Cl-):
SID = [Na+] + [K+] – [Cl-]
[x] = concentration of x
A minimum SID of 60-80 mEq/L is recommended3.
Glucose provides an energy source and is transported into the intestine on a one to one ratio with sodium, helping sodium absorption. Glucose should be provided at a concentration of at least 100mmol/l4.
In a normal animal, most potassium reserves lie within the intracellular fluid. As the body tries to compensate for acidosis, intracellular potassium ions are exchanged for H+ ions which leads to hyperkalaemia (not correlated with intracellular fluid stores). Hyperkalaemia is usually resolved with reversal of acidosis. However, increased faecal losses of potassium during an episode of diarrhoea cause net depletion of intracellular stores of potassium; hence the inclusion of potassium, ideally at a concentration of 10-30mmol/lin oral rehydration therapy2.
Amino acids such as glycine and glutamine facilitate absorption of sodium via co-transport. Glutamine is an important nutrient of rapidly dividing cells such as enterocytes. Starvation begins to adversely affect the villi within 2-4 days of diarrhoea starting. Inclusion of glutamine has benefits in aiding to rapidly correct plasma volume, improving recovery from hyponatraemia and metabolic acidosis, and restoration of normoglycaemia5.
Solutions with higher osmolality provide greater nutritional support. However, oral rehydration solutions with excessively high osmolalities (>650mOsm/l) slow abomasal emptying, which is a risk factor for abomasal bloat, and could increase severity of diarrhoea by increasing net secretion into the lumen of intestine. An osmolality of 400-600 mOsm/l is recommended3.
A concentration of 40-80 mEq/l is recommended3.
Table 2. Comparison of Norbrook products