Colostral IgG concentration is an important factor that affects whether calves receive sufficient passive immunity from colostrum [46]. Unfortunately, the amount of IgG in maternal colostrum varies dramatically among cows (<1-235 g/l) with 29.4-57.8% of samples that do not reach the desired amount of 50 g IgG/l [34],[47]-[49]. Colostral quality is difficult to estimate by the farmer based on produced volume or appearance of the colostrum. Use of weight at first milking as a screening test to identify bovine colostrum with inadequate IgG concentration is not justified because of the low sensitivity [50]. Somatic cell count, measured after calving, was significantly higher in cows producing colostrum of inferior quality compared with those producing high-quality colostrum [47]. For all these reasons, it is better to measure colostral IgG content indirectly by using a colostrometer (50 g IgG/l = density of 1045) or a brix refractometer (50 g IgG/l =21-22 Brix) or directly by a cow-side immunoassay kit (single line = IgG concentration >50 g IgG/l [50]-[53]. To measure colostrum quality it should be avoided to use forestripping samples for testing purposes, as these samples may overestimate the IgG concentration [54]. Colostrum collected more than 2 hours after calving significantly lowers the colostral IgG concentration [55],[56], probably because of dilutional effects and because colostral Ig diffuse passively into the cow’s systemic circulation if colostrum is not milked out as soon as possible after calving. Colostrum from cows without a dry period has a lower IgG concentration compared with colostrum from cows having a dry period of 28 or 56 days [57]. Pooling of colostrum is not advised since this is a risk factor for FPT [38]. Cows in their 3^rd or 4^th parity or older usually have significantly higher levels of IgG per liter colostrum than heifers or 2^nd parity cows [34],[47],[48] which is reflected in calves born to heifers having a greater risk for FPT than calves born to multiparous cows [32]. However, this correlation between parity and colostrum IgG concentration is not always evident [36]. Discarding colostrum from heifers is thus not advisable.

Colostrum replacement products have a highly variable performance [49],[58]-[65], and the herd veterinarian is advised to consult results of peer-reviewed controlled trials for separate products. Colostrum supplemented in milk replacer during the first 2 weeks of life (10 g IgG, bid) reduces NCD rates because of the intestinal activity of colostral antibodies and epithelial growth promoting substances [66].

Critical control points for bacterial contamination of colostrum are the harvest and storage process. Storing colostrum at ambient temperatures results in a significant increase of bacteria [67]. Fresh colostrum can be stored up to 96 hours at 4°C when potassium sorbate is added as a preservative [67]. Industry recommendations for bacterial load are limited to 100,000 colony forming units (cfu)/ml. Depending on the time of sampling or used storage method, 0-43% of colostrum samples exceed the maximum advised bacterial count of 100,000 cfu/ml [48],[67].

Pasteurizing colostrum (60°C, 60 min) can reduce bacterial load while the viscosity and the colostral IgG concentration remain within acceptable limits for feeding [68]-[72]. Higher-quality batches of colostrum suffer a significantly greater magnitude of loss of IgG as compared with lower- or intermediate- quality batches of colostrum [68],[71]. Calves fed pasteurized colostrum had significantly higher serum IgG concentrations, serum protein values, and/or a greater apparent efficiency of absorption, compared with calves fed unpasteurized colostrum [46],[72]-[75], probably explained by bacteria that bind free IgG in the gut lumen and block uptake and transport of IgG molecules across intestinal epithelial cells. Moreover, calves fed pasteurized colostrum had a significantly decreased risk for treatment for diarrhoea [46].

Administration of an oral rehydration solution (ORS) should be commenced as soon as diarrhoea starts and should be continued as long as the calf has diarrhoea.

The osmolality of an ORS is determined primarily by the concentrations of sodium and glucose. Calves fed hyperosmotic ORS solutions (600-717 mOsm/l) (HORS) have a slower abomasal emptying rate compared with calves fed iso-osmotic ORS solutions (300-360 mOsm/l) (IORS). This slower emptying rate increases the risk for bloat or abomasitis and produces a slower rate of plasma volume expansion [80],[89],[90]. Unless previously assumed, the volume present in the reticulorumen of healthy calves after intubation appears to be predominantly due to reflux from the abomasum, rather than spillage from incomplete closure of the oesophageal groove. The calculated change in abomasal volume of intubated calves approximated that one of calves that suckled their ORS [80]. In contrast, the delivery of HORS to the small intestine is slower after intubation indicating a different effect of intubation on coordinating motility between the reticulorumen, abomasum and duodenum than does suckling [80]. These effects taken together, suckling an IORS provides the fastest rate of solution delivery to the small intestine and a slightly faster rate of plasma volume expansion than does suckling or oesophageal intubation of a HORS. However, suckling or oesophageal intubation of a HORS provides the most appropriate oral solution for treating hypoglycaemic calves, because the HORS produces a larger and more sustained increase in plasma glucose concentration [80].

Alkalinizing agents commonly used in commercial ORS are bicarbonate and bicarbonate precursors, mainly acetate, propionate, citrate and phosphate. The higher assumed alkalinisation of ORS products containing bicarbonate (BORS) or citrate (CORS) when compared to solutions containing other bicarbonate precursors is confirmed by most recent studies in absolute numbers, but never significantly different [90]-[93]. High SID-fluids (≥79 mmol/l) are recommended to treat acidosis because the SID value of an ORS determines the degree of abomasal and serum alkalinisation [91],[94]. Prolongation of the in vivo clotting time is more likely to occur when larger volumes of an ORS in cow’s milk are fed, because luminal pH will initially be greater and remain greater for a longer period of time [90],[95]. From these studies it can be carefully concluded that feeding a BORS or CORS does not affect milk clotting in vivo and disagrees with general recommendations to not feed BORS or CORS concurrently with or short before/after cow’s milk to calves. The SID value and fed amount of an ORS seem to play a more important role, both in correcting dehydration and metabolic acidosis [91],[94].

It should be noted that most of the research discussed above was executed in a small number of healthy, non-diarrhoeic calves. Milk clotting, abomasal luminal pH and abomasal emptying rates could differ between diarrhoeic and non-diarrhoeic calves.

Intravenous (IV) fluid therapy should be implemented if the calf is severely dehydrated (>8%), depressed, has a weakened/absent suckle reflex or suffers from a dilated abomasum and/or intestinal hypomotility. The fluids should always be warmed e.g. by adding a coil to the IV fluid line and placing this in a bucket of hot water so that the calf does not need to use extra energy to bring the given fluid to body temperature. To sustain improved clinical status, an IV fluid therapy needs to be followed by continued ORS therapy [31],[96]. Both the jugular as the auricular veins can be catheterized for IV rehydration, but by using the ear vein, larger quantities of fluid can be given during a longer period of time in an on farm setting.

Bicarbonate requirements for IV correction of acidosis are still being calculated as follows: bicarbonate (g) = body weight (kg) × BE (mmol/l) × 0.6 (l/kg) × 0.084 (g/mmol) [86],[96]. When using this formula, metabolic acidosis was not corrected in more than half of the calves and the risk of failure to correct acidosis increased with D-lactate concentrations [86]. Calves with distinct changes in posture and demeanour thus seem to need higher doses of bicarbonate than calculated with the factor of 0.6 in the formula mentioned. However, in this study no follow-up therapy with ORS was offered, which could explain calves becoming acidotic again after 24 h. Other studies reporting treatment failures had a more severe metabolic acidosis before treatment compared with successfully treated calves [31],[96]. The formula mentioned above should only be used for estimation of buffer required for correction of incurred losses and overdosing seems more desirable than underdosing [86]. Bicarbonate can be given IV as an isotonic (IBS) or hypertonic solution (HBS). In the field it is more practical to use a HBS compared with an IBS. Rapid IV administration of an 8.4% bicarbonate formulation at 5-10 ml/kg provided an effective and safe method to improve acid-base abnormalities [31],[96]-[98]. There were no direct indications in these studies of potential adverse effects related to electrolyte concentrations, oxygen-haemoglobin dissociation curve, hypercapnia or paradoxical intracellular acidosis, as previously assumed. It can be concluded from these studies that HBS can be safely used if the speed of an IV administration does not exceed 1.25 ml/kg/min in calves not suffering from respiratory problems.

Hypoglycaemia is best addressed by giving 150 mg glucose/kg. Larger quantities of glucose should be avoided because of the risk of glycosuria. Calves that are cachectic and reluctant to drink can also be given a constant glucose infusion using the ear vein approach as discussed earlier.