THE EFFECTS OF TRANSITION MILK ON GROWTH AND HEALTH OF 

NEONATAL CALVES 

 

By 

 

Brandon Van Soest 

 

 

 

 

 

 

 

 

 

 

 

A THESIS 

Submitted to  

Michigan State University  

in partial fulfillment of the requirements 

for the degree of 

 

Animal Science—Master of Science 

2020 

 
 

THE EFFECTS OF TRANSITION MILK ON GROWTH AND HEALTH OF 

ABSTRACT 

 

NEONATAL CALVES 

 

By 

 

Brandon Van Soest 

 

 

Our objective was to determine if feeding transition milk (TM, milkings 2-4 after 

calving) during the first 4 d of life would improve health, GIT development, and growth of 

calves. We conducted 2 studies. In study 1, 105 Holstein heifer calves on a commercial dairy 

farm were assigned to 1 of 3 diets (n=35/diet): milk replacer (MR), transition milk (pooled and 

pasteurized), or a 50:50 blend of milk Replacer and colostrum replacer (MCR). Calves were fed 

1.9 L of MR, TM or MCR 3 times/d for 3 d. After 3 d, calves were fed and managed similarly. 

Treatment did not alter health scores. Compared to MR, TM and MCR increased BW by 56 d 

and had lower haptoglobin concentration in plasma. Utilizing NRC equations (2001), one third 

of the difference in BW gain was accounted for by caloric differences. In study 2, we fed 23 

Holstein bull calves MR or TM (pooled milkings 2, 3, and 4 kept separate and not pasteurized). 

Calves were in 6 blocks, with each block containing 4 calves born within a 12-h period.  Calves 

were fed 3 times/d for 4 d, given bromodeoxyuridine to label cells synthesizing DNA on d 5, and 

euthanized 130 mins later. Compared to MR, TM doubled BW gain and nearly doubled most 

morphological measures in all sections. In all sections, labeling with bromodeoxyuridine was 

increased 50% by TM compared to MR indicating that TM increased cell proliferation compared 

to MR. TM also improved health scores compared to MR. We conclude that feeding TM for 3 d 

after colostrum using this feeding program improves indicators of health, development, and 

growth. Whether feeding extra MR to account for energy differences with TM would have 

achieved similar results is not clear. 

 

ACKNOWLEDGMENTS 

There are many people I owe thanks to for assisting me in completing my degree. For 

starters, I would like to thank Dr. Michael VandeHaar for accepting me into his lab to pursue a 

master’s degree. He challenged, mentored and critiqued me to help me develop over the 2 years I 

have called Michigan State University my home.  

Secondly, I would like to thank Dr. Miriam Weber Nielsen for assisting in my thesis 

research projects with the planning and support throughout the past 2 years. I also would like to 

send my appreciation out to the remaining members on my guidance committee Dr. Adam 

Moeser and Dr. Angel Abuelo Sebio who invested their time and input towards my thesis. Your 

support, wisdom, and expertise were critical to the success of my research. Special thanks to Dr. 

Adam Moeser for allowing me to conduct work in your laboratory – it was a privilege to learn 

from and collaborate with your group. 

Also, thanks to Jim Liesman for helping with my statistical models and experimental 

design; Dave Main, Cara Robison, and Julie Moore for investing countless hours teaching me a 

diverse array of laboratory techniques, supplying support and supplies to assist in the completion 

of my research. Additional thanks are owed to the Nobis and De Saegher family and farm 

employees for allowing me to run a research trial at your farm and supplying calves. 

My parents and family deserve a huge thank you for the support, motivation through the 

past 6 years as I pursued my goals in the animal industry. Lastly, I want to thank the guys at 

ADM nutrition, fellow grad students, friends, and bible study group for supporting, praying and 

encouraging me as I have been away from home for the past 2 years, but still keeping in touch 

and checking in on my progress. 

 

 

iii 

 

 

TABLE OF CONTENTS 

LIST OF TABLES ......................................................................................................................... vi 

LIST OF FIGURES ...................................................................................................................... vii 

KEY TO ABBREVIATIONS ...................................................................................................... viii 

CHAPTER 1: REVIEW OF LITERATURE: NEONATAL CALF GROWTH, HEALTH, AND 
DEVELOPMENT AND THE ROLE OF COLOSTRUM AND TRANSITION MILK ............... 1 

ABSTRACT ................................................................................................................................ 1 

INTRODUCTION ...................................................................................................................... 2 

COLOSTRUM AND TRANSITION MILK .............................................................................. 3 

GUT MORPHOLOGY AND DEVELOPMENT ....................................................................... 6 

IGF-1 and Growth Hormone ................................................................................................... 8 

Lactoferrins ............................................................................................................................. 9 

Leptin .................................................................................................................................... 10 

Interaction ............................................................................................................................. 11 

B Lymphocytes and T Lymphocytes .................................................................................... 11 

INTENSIVE MILK FEEDING STRATEGIES ....................................................................... 12 

Body Growth ......................................................................................................................... 13 

Gastrointestinal Development ............................................................................................... 14 

HAPTOGLOBIN AND LIPOPOLYSACCHARIDE BINDING PROTEIN ........................... 15 

FUTURE INSIGHTS ................................................................................................................ 15 

CONCLUSIONS....................................................................................................................... 16 

APPENDIX ................................................................................................................................... 17 

REFERENCES ............................................................................................................................. 19 

CHAPTER 2: EFFECTS OF TRANSITION MILK AND MILK REPLACER 
SUPPLEMENTED WITH COLOSTRUM REPLACER ON GROWTH AND HEALTH OF 
DAIRY CALVES ......................................................................................................................... 32 

ABSTRACT .............................................................................................................................. 32 

INTRODUCTION .................................................................................................................... 33 

MATERIALS AND METHODS .............................................................................................. 35 

STATISTICAL ANALYSIS .................................................................................................... 37 

 

iv 

RESULTS AND DISCUSSION ............................................................................................... 38 

CONCLUSION ......................................................................................................................... 40 

APPENDIX ................................................................................................................................... 41 

REFERENCES ............................................................................................................................. 45 

CHAPTER 3: EFFECTS OF TRANSITION MILK ON EARLY LIFE GROWTH, HEALTH, 
AND INTESTINAL DEVELOPMENT OF DAIRY BULL CALVES ....................................... 49 

ABSTRACT .............................................................................................................................. 49 

INTRODUCTION .................................................................................................................... 50 

MATERIALS AND METHODS .............................................................................................. 52 

RESULTS ................................................................................................................................. 57 

DISCUSSION ........................................................................................................................... 60 

CONCLUSION ......................................................................................................................... 63 

APPENDIX ................................................................................................................................... 65 

REFERENCES ............................................................................................................................. 84 

CHAPTER 4: CONCLUSIONS & IMPLICATIONS .................................................................. 88 

 

 

 

 

 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

 

 

v 

LIST OF TABLES 

 

Table 1 The Shift in Milk Profile .................................................................................................. 18 

Table 2 Composition of Diets Fed to Calves on Days 2 to 4 ........................................................ 42 

Table 3 Biomarkers of Inflammation and Health Scores.............................................................. 43 

Table 4 Initial Body Weight, Weaning Weight and Gain for Calves Fed Diets. .......................... 44 

Table 5 Composition of Experimental Diets ................................................................................ 66 

Table 6 Average Body Weight Gain, Predicted Gain, and Feed Intake ....................................... 67 

Table 7 Small Intestine morphology (mm, Standard Error) ......................................................... 68 

Table 8 Bromodeoxyuridine Labeled Cells, B Cell, and T Cell Counts in the Small Intestine 
(mean, Standard Error).................................................................................................................. 69 

Table 9 Average pH of Gastrointestinal Tract Digestive Contents .............................................. 70 

Table 10 Abomasa Content ........................................................................................................... 71 

Table 11 Average Health Scores................................................................................................... 72 

Table 12 Blood Metabolites analyzed at 1100 hr before feeding treatments ............................... 73 

 

 

 

 

 

vi 

LIST OF FIGURES 

 

Figure 1 H & E Stained Small Intestine for Morphological Measures ......................................... 74 

Figure 2 Bromodeoxyuridine Labeled Cells in Small Intestine .................................................... 76 

Figure 3 B Cell and T Cell Staining in Ileum ............................................................................... 78 

Figure 4 Serum IgG Concentration ............................................................................................... 79 

Figure 5 Serum Total Protein Concentration ................................................................................ 80 

Figure 6 The Change in Plasma NEFA on d 3 Across a Feeding (2 hrs post feeding)................. 81 

Figure 7 The Change in Plasma Glucose on d 3 Across a Feeding (2 hrs post feeding). ............. 82 

Figure 8 The Change in Plasma Insulin on d 3 Across a Feeding (2 hrs post feeding). ............... 83 

 

 

 

 

vii 

KEY TO ABBREVIATIONS 

 

ADG= Average Daily Gain 

DM= Dry matter 

GH= Growth hormone  

GIT= Gastrointestinal tract 

IgA= Immunoglobulin A 

IGF-1= Insulin-like growth factor 1 

IGF-2= Insulin-Like growth factor 2 

IgG= Immunoglobulin G 

IgM= Immunoglobulin M 

ME=Metabolizable energy 

 

 

 

viii 

CHAPTER 1: REVIEW OF LITERATURE: NEONATAL CALF GROWTH, HEALTH, 
AND DEVELOPMENT AND THE ROLE OF COLOSTRUM AND TRANSITION MILK 

 

 

ABSTRACT 

Feeding high-quality, first milking colostrum within the first hours of life provides the 

neonate with passive immunity as its own immune system develops. Research shows additional 

benefits to feeding colostrum in the first few days of life other than improved health and 

immunity such as growth and organ development. As concern grows regarding antibiotic use in 

livestock, nutritional interventions are being investigated for solutions to minimize antibiotic use. 

Transition milk is the milk from the second through the fifth milkings after calving and has a 

profile that is intermediate between colostrum and whole milk. Thus, like colostrum it contains 

more bioactive components such as immunoglobulins, hormones, and growth factors than whole 

milk but in decreasing quantities as the gland transitions to synthesizing whole milk.  Recent 

studies suggest that feeding colostrum more than just one time promotes proliferation and 

reduces apoptosis of the epithelial cells in the small intestine, presumably because of bioactive 

compounds and nutrients. This increase in proliferation and decrease in apoptosis has generally 

been coupled with increased small intestinal development, improved health, and increased 

weight gain of the calf. Further research is needed to determine the effects transition milk has on 

health, intestinal development, and growth of neonatal calves in early life in comparison to 

feeding milk replacer following colostrum. This review addresses the current knowledge of 

feeding additional colostrum and transition milk on development of the immune system, 

gastrointestinal tract, and overall skeletal growth of calves.  

 

1 

INTRODUCTION 

Calves are highly susceptible to disease in the first 4 weeks of life, with enteric disease 

common in the first week followed by respiratory disease (Svensson et al., 2003, Hulbert, 2016). 

Early life stressors result in immunosuppression as glucocorticoid concentrations increase 

resulting in elevated susceptibility to infectious diseases (Concordet and Ferry, 1993; Anderson 

et al., 1999). According to USDA NAHMS (2007), 7.8% of all calves die before weaning in the 

United States with 25% of preweaned heifers affected by scours and bloat, and another 16% 

treated for pneumonia. Worldwide the mortality risk for calves within the first 48 hours of life 

ranges from 3 to 9% (Compton et al., 2017), while in Germany 17% of calves die before 

reaching 6 months of age (Tautenhahn, 2017). The common practice in the dairy industry is to 

separate calves from their dams soon after birth, resulting in dependency on farmers to supply 

high quality colostrum for passive immunity. Calves that experience disease are more likely to 

have increased age at first calving and produce less milk, protein, and fat during their first 

lactation (Heinrichs and Heinrichs, 2011).  

Viral, parasitic, and bacterial scours are also accompanied by weight loss partially due to 

the inflammation of the gastrointestinal tract (GIT) and apoptosis of villi cells in the small 

intestine (Connor et al., 2017).  Connor et al. (2017) reported that calves infected with 

Cryptosporidium parvum had damaged and reduced number of villi within the small intestine. 

Bovine colostrum contains many important hormones and growth factors that promote 

development and regeneration of the small intestine (Uruakpa et al., 2002) assisting in the repair 

of the GIT following inflammation. These nonnutritive components i.e. hormones and growth 

factors are found dispersed among the casein, whey, and fat fractions of the colostrum (Ontsouka 

et al., 2003). Onsouka et al. (2003) also determined that the majority of IGF-1, IGF-2, insulin, 

 

2 

prolactin, and other peptides were observed in the cisternal fraction when being milked out 

which is important during collection. 

The majority of GIT development is focused on the rumen where the consumption of 

solid feed initiates the ruminal fermentation. Regarding GIT development, this review will focus 

on the first few days to weeks looking at the small intestinal changes and what may promote 

development. 

Another key factor in raising healthy calves is access to sufficient supply of nutrients. 

This supply of nutrients is to prevent or combat disease and sicknesses while maximizing growth 

potential and encouraging natural behaviors. In the past 20 years, there are no indications of 

major developmental impairments of formula-fed children (Bernt and Walker, 1999) or calves 

when colostrum is fed in a timely manner (Quigley and Drewry, 1998). Intensive milk feeding 

strategies ensure the calf never experiences a period of hunger while providing access to milk 

essentially all day long. Intensive feeding increases body growth, organ growth and metabolic 

activity. 

 

COLOSTRUM AND TRANSITION MILK 

 

Colostrum is formally known as the first collection of milk following calving with the 

subsequent milkings (2 through 5) considered transition milk. Starting with milking 6 following 

calving, collections are categorized as whole milk. Colostrum IgG content is historically 

perceived as the most important factor of its quality. Colostrum also contains proteins, essential 

and non-essential amino acids, fatty acids, lactose, vitamins and minerals, lactoferrin, steroid 

hormones, thyroid hormones, insulin-like growth factors, insulin, prolactin, nucleotides, 

polyamines and enzymes (Foley and Otterby, 1978; Koldovsky, 1989; Campana and 

Baumrucker, 1995). The concentration of these compounds found in colostrum changes over the 

 

3 

first 3 days of lactation to that found in regular whole milk (Table 1, Foley and Otterby, 1970; 

Parrish et al., 1948; 1950). Typically, the bioactive and growth-promoting components of 

colostrum and transition milk are not found in high concentrations in whole milk or milk 

replacers (Grütter and Blum, 1991; Campana and Baumrucker, 1995).  

Using a proteomics approach, Le et al. (2015) showed that the proteomes of colostrum 

and whole milk overlap 74% suggesting similar secretion consistencies. However, this study also 

reported higher concentrations of proteins within milk coupled with cell division and 

proliferation in day 0 and decreasing out to day 9. In turn enzyme-associated protein 

concentrations rose from day 0 to day 9. Le et al. (2011) observed 24 different proteins 

upregulated in colostrum compared to mature milk providing additional health benefits and 

growth. Concentrations of 15 of these 24 proteins were elevated in transition milk as well (Fahey 

et al., 2019). In the first 2 days after birth neonatal calves absorb 90% of consumed nutrients as 

well as absorbing IgA, IgM, IgG, IGF-1, lactoferrin, lysozymes and other growth factors from 

colostrum (Parrish et al., 1953). The immunoglobulins absorbed are essential for their passive 

immune function while the lactoferrin aids in bacteriostatic activity of the gastrointestinal tract 

by competing for iron to bind with that microorganisms need for growth (Lönnerdal, 1985; 

Goldman et al., 1994; Schanler, 1989). 

 Even in this period of “open” gut, some studies suggest little to no absorption of insulin, 

IGF-1, Long-R3-IGF-1, and prolactin occurs suggesting localized effects within the small 

intestine (Grütter and Blum, 1991; Baumrucker et al., 1994; Hammon and Blum, 1998). 

Lactoperoxidase increases steadily from colostrum to milking 4 and then gradually drops, 

suggesting that it also might be important to the neonate (Korhonen et al., 1977; Fahey et al., 

2019). Fahey et al. (2019) concluded the antimicrobial protein, lactoperoxidase, would assist the 

 

4 

passive immunity the neonate absorbs in the first week of life supporting the practice of feeding 

transition milk. Past this window near birth these large bioactive molecules such as growth 

hormone (GH) are not directly absorbed. Feeding additional colostrum had no influence on GH 

concentration in the blood during the first week of life (Grütter and Blum, 1991; Baumrucker et 

al., 1994; Hadorn et al., 1997). Feeding additional insulin mirrored this as Grütter and Blum 

(1991) suggest insulin is either not absorbed or insulin is being retained in the liver.  

 

Increased colostrum feeding during the first 3 d increases concentrations in the blood of 

total protein, globulin, triglyceride, cholesterol, and insulin while influencing protein and fat 

metabolism for the first week in calves (Kühne et al., 2000). When Kühne et al., (2000) replaced 

colostrum with increased amounts of milk replacer fed, no differences were seen in metabolic 

and endocrine traits and intestinal absorption capacity. The weight gain difference they observed 

for colostrum fed groups compared to the calves fed milk replacer was attributed to high energy 

and protein intake. The lack of weight gain in the milk replacer fed groups resulted from reduced 

energy and protein consumption, as well as the lacked non-nutritional growth-promoting 

compounds that promote GIT development (Burrin et al. 1992, 1996). Burrin et al., (1995) 

observed that feeding colostrum promoted protein synthesis in skeletal muscles of pigs compared 

to the piglets fed formula. Similar results were observed in calves’ skeletal muscle which were 

speculated to result from the insulin consumed in the colostrum (Hammon et al., 2012; Sadri et 

al., 2017). Hammon and Blum (1999) fed colostrum and observed individual plasma free 

essential amino acids increase greater at day 1 than observed in milk replacer. With continued 

feeding of colostrum out to day 3 the essential amino acid concentrations remained higher than 

just colostrum at the first meal. Traditionally, colostrum is fed for its passive immune factors 

 

5 

protecting the calf from bacterial illness as well as initiating intestinal epithelial cell growth, and 

differentiation (USDA, 2008). 

 

GUT MORPHOLOGY AND DEVELOPMENT  

 

While in the pre-ruminant stage, the small intestine is of great importance as it is the 

primary source of digestion, absorption and exclusion. Neonatal calves are born with relatively 

mature gastrointestinal tracts, but they require morphological and functional changes from 

colostrum’s nutrient and non-nutrient components (Blum, 2006). Throughout milk feeding GIT 

growth is at its greatest rate. Shown in rats, the crypt hyperplasia is elevated 10-fold greater 

before weaning than after weaning (Cummins and Thomson, 2002). Slightly mixed results have 

been published regarding the effects of colostrum on the gut, but most of the results suggest 

increasing the development and benefiting the calf when colostrum is fed to calves. Widdowson 

et al. (1976) was first to show colostrum promoted increased development and function of the 

GIT in neonatal calves. Yang et al. (2015) fed calves either colostrum, transition milk or whole 

milk at the first feeding and found that the calves receiving colostrum had the greatest increase in 

villus length and width, crypt depth, villus height to crypt depth ratio and mucosal thickness 

throughout the small intestine and whole milk calves were the least developed. The transition 

milk calves had increased small intestinal development when compared to whole milk, but still 

had poorly developed GIT. This reaffirms that feeding colostrum for the first feeding is essential 

for GIT development, while transition milk had a similar but weaker stimulation of GIT 

development.  

The elevated concentrations of growth factors and hormone within colostrum, mentioned 

previously, are potentially the stimuli for the small intestinal and villus growth and development 

(Blum, 2006; Steinhoff-Wagner et al., 2014). Blum (2006) showed the amount of colostrum 

 

6 

consumed correlates with the villus size within the small intestinal mucosa. The initial feeding of 

colostrum is important, but calves feed additional colostrum experienced further development 

compared to those that received milk replacer. He also suggested the colostrum was reducing the 

rate of apoptosis of the epithelial cells, thus increasing the life span of the cells allowing for 

overall longer villi. Blättler et al. (2001) observed that the crypt regions contained the 

overwhelming majority of the proliferating cells in response to colostrum. This comes with little 

surprise as new mucosal epithelial cells originate within the crypts and migrate along the 

epithelial surface towards the villi ends (Johnson, 1988). Roffler et al. (2003) provided evidence 

that the further developmental advantages observed from colostrum are likely due to non-nutrient 

bioactive compounds. They observed increased villus growth in calves fed colostrum compared 

to a milk-based formula with similar concentrations of protein and energy. This resulted in 

promotion of villus growth in the colostrum fed calves. These results indicate the colostral 

hormones and (or) peptides are involved with stimulating the growth of the mucosal layer of the 

small intestine in neonatal calves. This increased development in villus length, villus width and 

crypt depth from colostrum feeding explains the increase in the absorption capacity as total 

surface area in the intestine is increased. Many studies show xylose absorption was increased in 

calves fed colostrum compared with milk replacer (Baumrucker et al., 1994b; Hammon and 

Blum, 1997a; Sauter et al., 2004). Some studies did not see the crypt depth increase to 

correspond to the villus development. Those studies suggested a negative feedback control in the 

small intestine epithelial cell during development (Bühler et al., 1998; Blättler et al., 2001). The 

amount of colostrum consumed enhanced villi growth in the proximal small intestinal more than 

in the distal small intestine (Bühler et al., 1998; Blättler et al., 2001). Feeding of milk replacer 

 

7 

instead of colostrum in early life results in looser feces, suggesting a slightly impaired GIT 

(Hardorn et al., 1997; Zanker, 1997; Kühne et al., 1999). 

 

As stated previously, large molecules such as insulin, IGF-1, and many other proteins are 

poorly absorbed, even in the first 24 hours of life. For the protein factors within the colostrum 

and transition milk to benefit the neonate, they must first survive digestion and retain biological 

functionality and then have appropriate receptors to impact the GIT. Pierce et al. (1964) found 

that the newborn calf has reduced secretion of gastric acid compared to an adult which may help 

prevent degradation of the proteins. Receptors for IGF-1, IGF-2, growth hormone, insulin and 

other bioactive compounds are located throughout the small intestine of neonatal calves where 

colostrum modifies expression and binding capacity (Blum, 2006; Hammon et al., 2013). The 

ability of these bioactive compounds to survive, bind, and keep functionality allows for the 

localized benefit to the calf’s GIT.   

 

IGF-1 and Growth Hormone 

 

Blättler et al. (2001) suggested that growth factors, rather than the nutrients, within 

colostrum are responsible for increasing cell proliferation within the small intestine. Studies 

across many species (pigs, rats, and humans) including calves have shown that feeding insulin or 

IGF-1 to neonates increased intestinal mucosa proliferation (Baumrucker et al., 1994). The 

largest supply of available amounts of IGF-1 are in colostrum (Campana and Baumrucker, 

1995). IGF-1 is known for its effects on promoting growth as it is produced in many tissues 

throughout the body, but mainly in the liver especially in 8-day old calves (Cordano et al., 1998). 

IGF-1 has no significant absorption within the GIT (Vacher et al., 1995), but can survive within 

the small intestine despite the digestive nature of the organ (Xu et al., 2002). Receptors for IGF-1 

 

8 

are located on the epithelial cells, fibroblasts, endothelia and smooth muscle of the GIT (Burrin 

et al., 1996; Howarth, 2003). The number of receptors varies along the GIT sites and is 

influenced by age and nutrition. IGF-1 enhances mucosal, submucosal and muscularis 

thicknesses, sodium and glucose absorption, lactase synthesis, as well as cell proliferation 

(Alexander and Carey, 1999; Burrin et al., 2001). Roffler et al. (2003) saw no differences in 

crypt cell proliferation or villus growth in the small intestine when feeding either a milk replacer 

with or without supplemental IGF-1. This indicates IGF-1 alone is not solely responsible for the 

increased development and growth of the small intestine. The quantity of colostrum consumed 

does not alter plasma growth hormone concentrations (Hammon and Blum, 1997b). Growth 

hormone was injected for seven consecutive days in neonatal calves resulting in increasing crypt 

depth, but no small intestinal villi developmental differences were observed (Bühler et al., 1998). 

Plasma concentrations of IGF-1 decreased less during the first week of life in calves receiving 

colostrum (which contains IGF-1) than in those receiving isoenergetic and isoprotein milk 

replacer (which would not contain IGF-1; Rauprich et al., 2000). IGF-1 concentrations are 

reduced when low levels of nutrients are supplied to the growing neonate (Thissen et al., 1994). 

 

Lactoferrins 

 

As previously mentioned, lactoferrins are elevated in colostrum and have several 

biological activities. They can act as antimicrobials, immunomodulation, affect intestinal cell 

apoptosis rate, and in humans prevent colon cancer (Van der Strate et al., 2001). Supplementing 

lactoferrin to calves decreases villus size within the jejunum, increases the size of Peyer’s 

patches in the ileum, and increases plasma IgG concentrations in neonatal calves (Prgomet et al., 

2006). Cells cultured in the presence of all-trans-retinoic acid increased apoptosis and reduced 

 

9 

cell proliferation (Purup et al., 2001). When lactoferrin interacted with all-trans-retinoic acid, it 

blocks apoptosis and allows cell proliferation to occur (Baumrucker et al., 2002). At birth calves 

are vitamin A deficient and have low concentrations of lactoferrin, but once fed colostrum the 

plasma concentrations of both are dramatically increased stimulating protein synthesis (Blum et 

al., 1997; Muri et al., 2005; Zanker et al., 2000). Schottstedt et al. (2005) found that 

supplementing vitamin A and lactoferrin to neonates increased growth and development of the 

ileum and colon and increased villus growth, maturation of epithelial cells, and size of Peyer’s 

patch follicles. 

 

Leptin 

 

Leptin is secreted by the mammary gland at a higher rate at the beginning of lactation 

into colostrum and the concentration declines in mature milk (Chilliard et al., 2001). Plasma 

leptin concentrations are elevated in mice and rats that are breastfed compared to formula fed. 

Plasma leptin concentrations in preruminal calves and lambs are highly influenced by nutrient 

density and related to fat accretion rates more than with mass of body fat (Blum et al., 2005). In 

this study, feeding colostrum helped maintain a constant level of plasma leptin after birth where 

formula fed calves experiences a decrease. Leptin receptors have been discovered in the intestine 

(Ahima and Flier, 2000). Wolinski et al. (2003) observed in pigs that orally administered leptin 

contributed to development within the small intestine. In rodents, leptin increased intestinal mass 

and increased carbohydrate and amino acid absorption (Alavi et al., 2002). 

 

 

10 

Interaction 

Feeding colostrum extract powder instead of just a single growth-promoting peptide 

resulted in greater stimulation of small intestine proliferation and development (Roffler et al., 

2003). This suggests there are potential additive effects or interactions between multiple growth-

stimulating components of colostrum which enhance the proliferation and growth of the 

intestinal cells. Odle et al., (1996) and Blum and Baumrucker (2002) concluded that growth 

factors in the natural form of colostrum have different effects than individually administering 

growth factors due to potential synergistic or antagonistic properties. 

 

B Lymphocytes and T Lymphocytes  

B and T lymphocytes play a large role in the intestine as they are constantly surveying 

antigens and presenting them to other immune cells for activation. B lymphocytes also play a key 

role in production of antibodies for specific antigens and retain memory of those antigens for 

future incidences. Insoft et al. (1996) considers the intestine to be the largest immune organ in 

the body as it continually deciphers potentially harmful antigens from those of benefit. During 

the first 5 days of life, calves experience significant changes in intestinal lymphocyte population. 

Increased proliferation and decreased apoptosis results in increased T lymphocytes in both 

Peyer’s patches and epithelia with no change in B lymphocyte concentrations in the ileum 

(David et al., 2003). The feeding of colostrum when compared to milk replacer resulted in a 

decline in proliferating cells in both lymphoid follicles and Peyer’s patches B-lymphocytes 

(Norrman et al., 2003). Intestinal T lymphocytes tended to decline in colostrum fed calves in this 

study. Barrington and Parish (2001) suggested colostrum is essential for passive immunity while 

 

11 

it prevents calves from developing their active immune system potentially promoting gut 

development. This conclusion is also supported in a study where colostrum deprived calves 

started producing antibodies sooner as well as peaked higher in antibody concentrations than 

calves fed colostrum (Banks and McGuire, 1989). Norrman et al. (2003) concluded the immune 

system of calves deprived of colostrum compensated for the lack of immunoglobulins by 

maturing and starting to function sooner than that of calves receiving passive aid from the 

colostrum immunoglobulins and other bioactive components.  

 

INTENSIVE MILK FEEDING STRATEGIES 

 

Managing nutrient intake throughout the preweaning period has proven key to 

successfully rearing calves coupled with long lasting effects on health and production later in life 

(Khan et al., 2011; Ballou, 2012; Davis Rincker et al., 2008). Intensive milk feeding strategies 

target a daily milk intake of 20% of body weight in preweaned calves, trying to mimic ad libitum 

feeding, where on average the target is only 10% of body weight (Khan et al., 2011; Jasper and 

Weary, 2002; Schiessler et al., 2002). Commonly, increasing solid feed intake promptly in the 

preweaning period while reducing milk feeding is the target strategy (Huber, 1969; Kertz et al., 

2017). Feeding elevated levels of milk, especially in the first 3 weeks of life where low levels of 

concentrate are consumed, maximizes total DM intake while the GIT is still underdeveloped. 

Many studies have demonstrated that limiting liquid milk prevents calves in the first week of life 

from expressing their natural behavior of suckling, causing hunger and stress (Miller-Cushon and 

DeVries, 2015; Jensen and Holm, 2003; 2008; Borderas et al., 2009).  

 

Intensive feeding programs target unrestricted feed access all day to prevent calves from 

experiencing hunger. When feeding elevated milk replacer diets, an accepted target to feed is 1.6 

kg DM/day with 8.4 Mcal ME/day and 350 g protein/day to ensure the calf has what it needs to 

 

12 

maximize growth (Schäff et al., 2016). Intensive feeding programs are designed to simulate what 

beef calves may consume while having all day to nurse on their dams (Egli and Blum, 1998; 

Schiessler et al., 2002). Calves restricted with milk in the first week of life are unable to consume 

enough dry feed to compensate for the energy difference the intensive milk fed calves would 

receive. Schäff et al. (2016) and others observed at weaning the intensive milk program would 

not meet nutritional requirements from solid feed if milk was reduced quickly. To prevent loss of 

weight in intensive milk fed calves, individual weaning by intake of concentrate or delayed 

weaning age with step down weaning is implemented to reduce the stress at weaning (Eckert et 

al., 2015; de Passillé and Rushen, 2016). Not only are there welfare benefits to the elevated level 

of nutrition, but growth and endocrine benefits as well. 

 

Body Growth 

 

Feeding elevated milk replacer with around 30% DM of protein resulted in increased 

body growth (both fat and muscle) in the preweaning period compared to calves receiving 

restricted milk (Smith et al., 2002; Geiger et al., 2016). This should come with little surprise, 

calves that are limited nutritionally cannot consume enough energy for both maintenance and 

equivalent levels of growth as those receiving more nutrients. Calves with intensive feeding also 

experienced increased growth in the small intestine, mammary gland, thymus, and pancreas 

(Brown et al., 2005a; Prokop et al., 2015; Geiger et al., 2016; Soberon and Van Amburgh, 2017; 

Koch et al., 2019). This elevated nutrition also results in greater metabolic activity in both 

muscle, fat and rumen tissues (Naeem et al., 2012; Leal et al., 2018).  This growth benefit is 

supported by the stimulation of the somatotropic axis allowing growth hormone, IGF-1 and IGF-

 

13 

binding proteins to affect organ development and body growth (Brown et al., 2005b; Schäff et 

al., 2016; Frieten et al., 2018; Haisan et al., 2018).  

 

Gastrointestinal Development 

 

Calves fed intensive milk feeding increase intestinal development, both size and 

absorption capacity, compared to restricted feeding (Geiger et al., 2016; Koch et al., 2019). The 

level of nutrients supplied also impacts the rate of development of the intestine and its immunity 

(Khan et al., 2011; Hammon et al., 2019). Hammon et al. (2019) suggests that elevated nutrients 

assist in maturation of the intestinal tract and stabilize the microbiome, thereby reducing diarrhea 

in preweaned calves. Elevating nutrition in early weeks of life assists in resolving diarrhea 

quicker preweaning, as well as increased resistance to illness post weaning when compared with 

restricted feeding programs (Ballou et al., 2012). With the small intestine benefiting from the 

intensive milk feeding, the rumen is delayed in development as solid feed intake is suppressed 

from the large energy supply from milk (Baldwin et al., 2004; Khan et al., 2011). Khan et al. 

(2011) observed calves receiving milk at 20% of body weight prior to weaning had increased 

rumen development and dry feed intake during weaning, resulting in improved rumen function 

when compared to calves fed milk at 10% of body weight.  

 

In the first few weeks of life, calves consume low levels of concentrate, and they also 

have immature forestomaches to digest solid feeds (Drackley, 2008; Khan et al., 2016). Rauba et 

al. (2019) indicated that protein and ME from starter affected growth more than that of milk 

replacer. In contrast, de Paula et al. (2017) saw no differences in feed efficiency before and after 

weaning for calves fed milk replacer at intensive or restricted intakes. Based on that study, it 

seems likely that calves fed restricted amounts of milk replacer consume more concentrate to 

 

14 

compensate for the reduced nutrients from milk. Feeding ad libitum milk replacer for the first 6 

weeks compared to restricted feeding increased carcass weight and milk consumption by week 9, 

while having no difference on concentrate intake (Schäff et al., 2018). Korst et al. (2017) 

observed similar results, ab libitum fed calves had elevated ADG compared to restricted fed 

calves while consuming the same amount of concentrate during the first 4 weeks of life. No 

research, to my knowledge, has examined colostrum feeding rate and its effect on starter intake. 

In a period where the rumen and forestomach are not developed, I would not expect to see a 

decline in starter intake in calves receiving colostrum or transition milk instead of milk replacer 

for the first 3 or 4 days of life.  

 

 

HAPTOGLOBIN AND LIPOPOLYSACCHARIDE BINDING PROTEIN 

Haptoglobin and lipopolysaccharide binding protein (LBP) are both acute phase proteins. 

Haptoglobin binds to hemoglobin to prevent iron loss and therefore acts as an antioxidant; in 

addition, this binding also gives it antibacterial activity (Wassell, 1999).  IL-6 type cytokines 

induce haptoglobin synthesis. Elevated concentrations of serum haptoglobin indicate increased 

inflammation (Wang et al., 2001). Increased LBP concentration is also an indication for 

inflammatory response to bacterial infection. Orro et al. (2011) showed elevated concentrations 

of LBP are associated with respiratory infection. Concentrations of LBP in the first 2 weeks are 

naturally elevated and typically decrease and stabilize by week 3 or 4 in healthy calves (Orro et 

al. 2008). 

 

FUTURE INSIGHTS 

In human studies, the feeding of breastmilk to infants and its effects on the neonatal 

intestinal development alter the microbiome and maturation of the immune response by the 

 

15 

neonate, presumably because of immune cells in colostrum (Molés et al., 2018). The potential 

effect that colostrum feeding may have on the microbiome is being investigated for its 

importance in calf nutrition (Malmuthuge and Guan, 2017). As stated previously, studies have 

shown benefits in the preweaning from elevated plane of nutrition, but little is known on long 

term effects on the liver, immune system, culling rates, metabolic disease, and etc. Epigenetics 

and postnatal nutritional programing have been studied in humans along with other species 

(Guiloteau et al., 2009). In neonatal calves, Faber et al. (2005) demonstrated feeding just 2 L 

more of colostrum immediately following birth can result in healthier and more productive cows 

long term.  

 

CONCLUSIONS 

 

Many studies indicated the necessity of feeding colostrum in a timely manner on day 1 of 

life for its transfer of passive immunity. Little is known about the impact transition milk could 

have when fed after colostrum and before whole milk or milk replacer.  Feeding transition milk 

was a common practice before milk replacers became popular; this mimicked the cow-calf beef 

industry where the dam raises her calf. Transition milk and colostrum contain many similar 

hormones, bioactive components and can benefit growth and development of the neonate. 

Transition milk and colostrum promote increases in body weight, gut development, and better 

health. Intensified milk feeding programs show similar benefits with further development of 

organs, higher weight gain and improved health. Little research has combined the inclusion of 

elevated feeding of colostrum or transition milk with maintained intensive milk feedings to 

maximize the calves’ potential in growth in the preweaning stage. Further investigation is needed 

on the long-term effects of extended transition milk feeding on productivity and longevity within 

the herd.  

 

16 

 

 

 

 

 

 

 

 

 

 

 

 

APPENDIX 

 

 

 

 

 

 

 

 

 

 

 

17 

Table 1 The Shift in Milk Profile 

 

Colostrum  Transition milk  

Milk 

 

(milking postpartum) 

1 

2 

3 

IgG (g/100 mL)1 

7 

13 
4 
3.1 
2.5 

23.9 
6.7 
14.0 
4.8 

18 
5.4 
8.4 
4.3 

4.2 
4.2 
2.5 
3.9 

14 
3.9 
5.1 
3.8 

1.1 
2.4 
1.5 
4.4 

 
Milking # postpartum 
Total solids (%)1 
Fat (%)1 
Total protein (%)1 
  Casein (%)1 
  Albumin (%)1 
Immunoglobulins (%)1 
 
Lactose (%)1 
Vitamin A (μg/100 mL)1 
Vitamin E (μg/g fat)1 
Lactoferrin (g/L)2 
Insulin (µg/L)2 
Prolactin (µg/L)2 
Growth Hormone (µg/L)2 
IGF-I (µg/L)2 
Table 1 shows the data from 1Foley and Otterby, (1978) and 2Blum and Hammon, (2000) studies 
showing the shift in concentrations of the components making up the different milkings. 

190 
76 
0.86 
35 

0.5 
0.09 
0.06 
5.0 

113 
56 
0.46 
16 

150 
< 1 
105 

295 
84 
1.84 
65 

280 
1.4 
310 

34 
15 
0.00 
1 

15 
< 1 
< 2 

0.9 
6.0 
3.2 
2.7 

180 
0.5 
195 

 

 

 

 

 

 

 

 

 

 

 

18 

 

 

 

 

 

 

 

 

 

 

 

 

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19 

 

 

 

 

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CHAPTER 2: EFFECTS OF TRANSITION MILK AND MILK REPLACER 

SUPPLEMENTED WITH COLOSTRUM REPLACER ON GROWTH AND HEALTH 

OF DAIRY CALVES  

 

Brandon Van Soest*, Faith Cullens†, Michael J. VandeHaar*, and Miriam Weber Nielsen*  

 

*Department of Animal Science, and 

†Michigan State Extension, Michigan State University, East Lansing 48824 

 

ABSTRACT 

Transition milk (TM, defined here as the second through fourth milkings after calving) 

supplies additional fat, protein and immunoglobulins to the calf compared to traditional 20:20 

milk replacer at industry suggested feeding rates (~14% solids). Our objective was to determine 

if 9 feedings of TM on d 2 through 4 of life increases growth rate and overall health of calves. 

Holstein heifer calves on a commercial farm were randomly assigned to 1 of 3 diets (n = 

35/diet): milk replacer (MR; Purina Warm Front BOV MOS Medicated milk replacer, St. Louis, 

MO), transition milk (TM), or a 50:50 blend of milk replacer and colostrum replacer (MCR; 

Alta HiCal Colostrum Powder replacer, The Saskatoon Colostrum Company Ltd., Saskatoon, 

SK, Canada). The TM was harvested from Holstein cows on the farm, pooled and pasteurized at 

71.7 ˚C for 15 s. Nutrient composition on a dry matter (DM) basis of TM was 25.9% fat, 41.8% 

protein and 14% solids; MR was 10.3% fat, 27.8% protein and 14% solids; and MCR was 14.6% 

fat, 38.6% protein and 15% solids. All calves received IgG-enriched colostrum replacer for the 

first 2 feedings after birth. Subsequently, calves were fed 1.9 L of MR, TM or MCR 3 times per 

day for 3 d (starting on d 2). After initial diets ended, calves were fed and managed similarly. 

Body weights (d 1, 7, 14, 21, and 56), blood samples (d 1, 7, 14, and 21), and daily health scores 

 

32 

(scale of 0 to 3) were collected through weaning at 56 d. All except 1 calf achieved successful 

transfer of passive immunity with serum IgG values over 10.0 mg/mL. From birth through 

weaning, calves fed TM and MCR gained 3 kg more total body weight than those fed MR (34.2, 

34.3, and 31.3 kg). Increased metabolizable energy (using the NRC 2001) in the TM accounts for 

0.68 kg of the increased gain compared with MR. Treatment did not alter health scores for ears, 

eyes, or feces. Haptoglobin concentrations were lower in TM and MCR than in MR calves (4.63, 

3.62, and 7.54 µg/mL), whereas lipopolysaccharide binding protein concentrations were not 

different. In conclusion, compared to traditional milk replacer feeding programs, feeding 

transition milk or milk replacer with colostrum replacer for 3 d increased growth rate of calves 

throughout the preweaning period. 

INTRODUCTION 

 

Calves are highly susceptible to disease in the first 4 wk of life (Cho and Yoon, 2014), 

and 8% of preweaned heifers die from digestive and respiratory infections (NAHMS, 2011). 

Enteric diseases are common in wk 1, and respiratory diseases increase from wk 1 through 4 

(Svensson et al., 2003; Hulbert, 2016). Diarrhea and bloat affect 25% of preweaned heifers, and 

18% of calves are treated for these conditions (NAHMS, 2007 and 2011). Pneumonia affects 

18% of preweaned heifers, and 16% receive treatment for pneumonia (NAHMS, 2007 and 2011). 

Supplying calves with adequate nutrition and IgG is an essential management practice for 

newborn calves to prevent these diseases and promote calf well-being and growth.  

Milking 2 of transition milk (TM; Godden, 2008) provides 9% more solids, 65% more protein, 

and 52% more casein and varying amounts more IgG than regular whole milk. Nutrient 

concentrations drop gradually until milking 6, when TM resembles whole milk (44, 13, 5, 2 and 

2 g of IgG per L for milkings 2 through 6; Foley and Otterby, 2008). Additional feedings of 

 

33 

colostrum promote maturation of the intestine and increase digestive efficiency (Buhler et al., 

1998; Blattler et al., 2001). Increasing the number of feedings of colostrum enhances absorptive 

capacity of the GIT, as measured by increased xylose absorption (Hammon et al., 1997b). This 

increase in absorption potentially results from the observed increase in villus height, 

circumference and area in the small intestine compared to calves receiving milk replacer. Zhang 

et al. (2015) reported higher immune and enzyme associated proteins in colostrum and TM when 

compared to milk at d 9. Feeding TM promotes calf gastrointestinal health while reducing the 

risk of a poor eye, ear, and nasal scores in calves (Conneely et al., 2014). Although IgG is no 

longer absorbed into circulation after 24 h of age, (Rayburn, 2019) the IgG and other elevated 

proteins and minerals might produce localized benefits to the digestive tract (Berge et al., 2009). 

Hammon et al. (1998) found that calves receiving colostrum had increased plasma glucose and 

insulin concentrations starting d 2 of life compared to calves receiving milk replacer. Feeding 

supplemental colostrum replacer with milk replacer in the first 14 d reduced antibiotic use and 

disease prevalence in preweaned calves (Chamorro et al., 2017). Bovine colostrum has shown to 

be an alternative to antibiotics in human medicine as it contains antibacterial and antiviral 

lactoferrins and pro-inflammatory cytokines (Hagiwara et al., 2000; Furlund et al. 2012) to 

combat infectious diseases in the gastrointestinal tract (Steele et al., 2013). 

 

We hypothesized that supplementing calves from d 2 to 4 of life with transition milk or a 

blend of milk replacer and colostrum replacer will improve health scores and growth. The 

objective of the present study was to determine the effects of feeding transition milk or milk 

replacer supplemented with colostrum replacer on growth and health compared to milk replacer 

alone.  

 

34 

MATERIALS AND METHODS 

Experiment design 

This study was conducted on a commercial Michigan dairy farm averaging 9 single born 

heifer calves over 25 kg per week during the months of May through October. The ambient 

temperature varied from -4 ˚C to 35 ˚C with an average temperature of 18.5 ˚C. All experimental 

procedures were approved by the Institutional Animal Care and Use Committee of Michigan 

State University. 

 Newborn Holstein heifer calves (n=105) were fed within the first 2-6 h of life 735 g DM 

of IgG-enriched colostrum replacer diluted in 40 ˚C water to 2.84 L (Alta Gold Colostrum 

Powder replacer, The Saskatoon Colostrum Company Ltd., Saskatoon, SK, Canada; 200 g IgG). 

Any refused colostrum replacer was administered via intragastric tube. Calves received an 

additional 686 g DM powder of standard colostrum replacer (100 g IgG, Alta HiCal Colostrum 

Powder replacer, The Saskatoon Colostrum Company Ltd., Saskatoon, SK, Canada) diluted to 

1.89 L within 12 h of birth. Once the second feeding was completed, the calves were weighed 

and transferred from the maternity area to individual hutches bedded with saw dust. The calves 

were assigned to 1 of 3 treatments by birth order: 1) milk replacer (MR; Purina Warm Front 

BOV MOS Medicated milk replacer, St. Louis, MO), 2) TM, and 3) milk replacer supplemented 

with colostrum replacer (MCR; Alta HiCal Colostrum Powder, The Saskatoon Colostrum 

Company Ltd.,  Saskatoon, SK, Canada) resulting in 35 calves per treatment (Table 2). 

Treatments were fed for the first 9 feedings on d 2-4 following colostrum feedings. All feedings 

were done by the farm staff. The MR was fed at a rate of 14% solids (140 g DM powder/ L, 

27.8% CP, and 10.3% fat on DM basis) and mixed before each feeding according to the 

manufacturer’s recommendations, supplying 1.17 Mcal per feeding of 1.89 L. The TM for this 

study was collected starting 4 mo prior to the start of the trial from the same commercial dairy 

 

35 

herd the study was held. The TM was harvested at milkings 2 through 4 after calving and stored 

at -20 ˚C. Then the TM was thawed at room temperature, pooled, and pasteurized at 71.7 ˚C for 

15 s. Samples were collected before and after pasteurization for nutrient and IgG analysis. The 

TM was then measured into 1.89 L quantities, sealed in colostrum bags (Colo Quick, Bloomer, 

WI), and frozen at -20 ˚C until feeding. Prior to feeding, the bags were placed into a thaw unit 

(Calf Hero, ColoQuick, Bloomer, WI) to heat to 41 ˚C. Before pasteurization, the TM contained 

4.39% fat, 7.08% protein, 4.38% lactose, and 29.5 g of IgG per L as fed. After pasteurization, the 

TM contained 3.79 % fat, 6.10% protein, 3.81% lactose, and 1.5 g of IgG per L as fed, and was 

calculated to contain 1.44 Mcal ME per 1.89 L. The MCR diet consisted of 147 g DM of milk 

replacer and 143 g DM of the standard colostrum replacer powder per feeding. This formula was 

designed to mimic a transition milk-like diet, supplying the calves with 15 g/L IgG. The caloric 

intake of MCR was 1.28 Mcal ME per 1.89 L. Diets were fed at a constant volume without 

adjusting for individual calves’ birthweight. Calves were fed 3 times a day at 0400, 1200, and 

1800. Birth date, weight, and time; colostrum volume and time fed; and treatment were recorded. 

On d 5, after calves received their final feeding of treatment diets, all calves were managed and 

fed similarly receiving MR until weaning at d 56. Refusals were recorded by calf feeders to the 

nearest 0.473 L (1 pint) for all liquid feed until weaning. Calves were fed milk replacer as 

follows: end of treatment to 14 d of age, 0.8 kg DM /d in 3 daily feedings; 15 to 41 d of age, 1.2 

kg DM/d in 3 daily feedings; 42 to 48 d of age, 0.8 kg DM/d in 2 daily feedings; and 49 to 56 d 

of age the calves received 0.4 kg DM/d in 1 feeding. Calf starter grain mix and water were 

available ad libitum within the pen starting on d 2. Calves were disbudded by cautery between 5 

to 12 d of age by farm staff. The calves were checked daily and treated for health issues by farm 

staff following established protocols and checked once a week by the farm veterinarian.  

 

36 

Sample collection  

  

Blood was collected via jugular venipuncture using vacutainers (BD Vacutainer™ 

Venous Blood Collection Tubes: Vacutainer Plus™ Glass Serum Tube; Becton, Dickinson and 

Company; Franklin Lakes; NJ) and 21-gauge blood collection needles (Monoject ™, Kendall 

Tyco Healthcare, Mansfield, MA) at 24 to 48 h of age and at 7 ± 1, 14 ± 1, and 21 ± 1 d of age. 

Once blood samples clotted at room temperature, samples were centrifuged at 2000 RPM for 10 

min. Serum was harvested and stored at -20 ˚C. Haptoglobin and lipopolysaccharide binding 

protein (LBP) were analyzed in blood samples from d 14 and 21 (Bovine Haptoglobin ELISA 

Kit, Immunology Consultants Laboratory, Inc., Portland, OR and LBP various species kit, 

Hycult Biotech HK503 edition, Uden, The Netherlands, respectively). Observational health 

scores were recorded daily from birth up through the first 3 wk (21 d) of age. Scores were 

recorded for fecal consistency, ear disposition, and eye discharge using the Calf Health Scoring 

Chart (University of Madison- Wisconsin School of Veterinary Medicine; 

www.vetmed.wisc.edu/dms/fapm/fapmtools/calves.htm). The health events were scored on a 

scale of 0 through 3, with 0 representing normal or healthy and 3 severe or ill. Health scores for 

each animal were summed for fecal, ear and eye separately for the first 21 d of life. Once 

summed, scores were then averaged by treatment to yield final scores to compare treatments. 

 

     

STATISTICAL ANALYSIS 

Data were analyzed for statistical differences using the mixed procedure in SAS 9.4 (SAS 

Institute Inc., Cary, NC). Our model included the fixed effect of treatment and random effect of 

block with preplanned contrasts for 1) MR vs TM and MCR and 2) TM vs. MCR. Data are 

shown using a preplanned contrast. Birthweight was used as a covariate in the calculations of 

 

37 

body weight gain. Significance was denoted at P-value ≤ 0.05 and tendencies were denoted as P-

values ≤ 0.1 and > 0.05 on all main effects. 

 

Health and growth 

RESULTS AND DISCUSSION  

Treatments did not alter fecal, ear, or eye scores (Table 3). However, eye scores were 

numerically but not statistically 50% lower (P = 0.13) for calves fed TM and MCR compared to 

controls. During the study, only 17% of calves were treated and < 1% died making it difficult to 

detect any health differences observationally. When summing the scores, the maximum possible 

score a calf could receive was 63. Our average health scores were all < 8 and mortality was < 

1%, indicating that all groups had excellent health. We speculate that if the farm had experienced 

more health problems, perhaps differences among treatments would have been apparent. Both 

TM and MCR reduced haptoglobin concentrations to 4.63 µg/mL and 3.62 µg/mL respectively 

while MR was at 7.54 µg/mL (P = 0.05); and TM and MCR were not different (P = 0.59). 

Haptoglobin increases in response to inflammatory stimuli (Morimatsu et al., 1992; Nakajima et 

al., 1993); therefore, our results indicate that TM and MCR reduced overall inflammation during 

7 through 21 d of life. Haptoglobin concentrations in healthy calves have been defined as < 350 

µg/mL (Horadagoda et al., 1994) or < 50 µg/mL (Gelsinger et al., 2016), indicating that the 

calves were healthy with the average haptoglobin concentration well below both thresholds. 

Treatment did not affect serum concentration of LBP when comparing MR to the TM and MCR 

or between TM and MCR (P = 0.42 and 0.68 respectively). The LBP concentrations were 5.76, 

5.27 and 5.49 µg/mL for MR, MCR and TM, respectively. Overall, treatment did not affect 

health measures, possibly due to good farm hygiene or the level of bioactive components and 

additional IgG within the diets was not adequate to elicit a benefit.  

 

38 

Both TM and MCR increased BW gain through weaning by 3.0 kg (P = 0.02; Table 4) 

with gains of 34.2 kg and 34.3 kg, compared to MR 31.3 kg. There was no difference when 

comparing TM to MCR (P = 0.9). When considering ADG, the MR calves gained 0.56 kg/d 

while TM and MCR both gained 0.62 kg/d through the preweaning period (P = 0.01; Table 4). 

Based on NRC 2001 equations, the additional energy fed compared to MR calves in the first 

week of life would account for 1.29 kg of gain in TM calves and 0.57 kg in MCR of the 3.0 kg 

difference at weaning. Once the gain was adjusted to incorporate the difference in ME, TM and 

MCR numerically increased BW gain by 2.0 kg compared to MR calves but the effect was no 

longer significant (P = 0.13). No treatment effect was observed on refusals in the 9 feedings of 

their respective treatments (9% refusals for all diets). Following d 4 until weaning (d 56), all 

treatment groups averaged below 0.44% refusals of milk replacer. We were not able to measure 

starter grain and water intake in this study and assess their potential contribution to BW gain. 

However, any differences in water, starter, or milk intake following d 4 would be treatment 

responses, not part of the treatments. Additional feedings of colostrum or TM not only supply 

additional nutrients but also other beneficial bioactive components such as IgG; insulin; vitamins 

A, E, and B12; manganese; iron; cobalt; zinc; riboflavin; and choline (Foley and Otterby, 1978). 

Transition milk is known to contain microRNAs and bioactive proteins (Van Hese et al., 2019 

and Fahey et al., 2019). Colostrum and TM promote earlier development of the intestinal tract 

(Hammon and Blum 1997; Rauprich et al., 2000; Blattler et al., 2001) and elicit localized 

immunity within the gut (Berge et al., 2009; Chamorro et al., 2017). We speculate that these 

components within TM or MCR also promoted earlier intestinal development and localized 

immunity in our TM calves, resulting in increased weight gain. We also speculate that this might 

 

39 

have longer term benefits, as increased nutrient intake accompanied by elevated growth rates can 

hasten conception and increase milk production in first lactation (Davis Rincker et al., 2011). 

 

CONCLUSION 

The present study demonstrated that feeding additional nutrients and bioactive 

compounds in the form of TM or colostrum replacer for the first 4 d of life increases growth by 

weaning along with decreasing serum haptoglobin concentrations. We conclude that feeding TM 

or MCR for the first 4 d of life can potentially improve health and increase the rate of BW gain 

of calves. Whether this increase would translate into improved performance later in life is not 

clear. Exploiting nutritional strategies to enhance calf growth in the first few days of life offers 

potential to improve weight gain and health throughout the pre-weaning period and after.   

 

 

 

 

 

 

 

 

 

 

 

 

 

 

40 

 

 

 

 

 

 

 

 

 

 

 

 

 

APPENDIX 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

41 

 

Table 2 Composition of Diets Fed to Calves on Days 2 to 4 

   

Variable  

Fat, % on DM 
Protein, % on DM 
IgG, (g/kg DM)  
ME, (Mcal/kg DM) 
Daily DM (g) intake2 
Daily CP (g) intake2 
Daily ME (Mcal) intake2 
Expected ADG (kg/d) 2 

 

MR 

10.3 
27.8 

0 

4.03 

770 

214 

3.10 

0.59 

Diets1 
   

TM 

25.9 
41.8 
10 
5.40 

862 

360 

4.65 

1.02 

MCR 

14.6 
38.6 
98 
4.47 

864 

332 

3.86 

0.78 

1Diets contained industry standard milk replacer (MR), pooled and pasteurized transition milk 
(TM) or milk replacer supplemented at a ratio of 1:1 with colostrum replacement powder 
(MCR). Composition of nutrients in MR and MCR were provided by manufacturer and TM 
composition was determined by CentralStar Lab using near-infrared spectroscopy to measure fat 
and total protein contents of unhomogenized milk.  

2Average Daily intake of DM, CP (crude protein), ME, or expected ADG during the treatment 
period (d 2-4). 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

42 

Table 3 Biomarkers of Inflammation and Health Scores 

 

Diets1 

 

P-value 

Variable 

MR 

TM 

MCR 

SEM 

MR vs. TM 
and MCR2 

TM vs. 
MCR3 

Eye4 
Feces4 
Ear4 

Haptoglobin5 

(µg/mL) 

LBP6 (µg/mL) 

0.60 
6.8 
2.4 

7.5 

5.8 

0.31 
7.8 
2.3 

4.6 

5.5 

0.30 
7.2 
2.6 

3.6 

5.3 

0.16 
0.83 
0.42 

1.40 

0.45 

0.13 
0.4 
0.9 

0.05 

0.4 

0.9 
0.6 
0.6 

0.6 

0.7 

1Diets contained industry standard milk replacer (MR), pooled and pasteurized transition milk 
(TM) or milk replacer supplemented at a ratio of 1:1 with colostrum replacement powder 
(MCR).  
2P-value the difference between MR and the 2 dietary treatments (TM and MCR).  
3P-value the difference between the 2 treatment groups (TM vs MRC). 
4Daily health scores averaged by calf for the first 21 d 
5Haptoglobin samples from d 14 and 21 
6LBP -Lipopolysaccharide Binding Protein samples from d 14 and 21 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

43 

Table 4 Initial Body Weight, Weaning Weight and Gain for Calves Fed Diets. 

 

Diets1 

 

P-value 

Variable 

MR 

TM 

MCR 

SEM 

MR vs. TM 
and MCR2 

TM vs. 
MCR3 

Birth Weight 

(kg) 

Weaning Weight 

(kg) 

Weight Gain 

(kg) 

Preweaning 
ADG (kg/d) 

36.8 

37.6 

38.7 

0.753 

0.13 

0.24 

68.1 

71.8 

73.0 

1.01 

<0.01 

31.3 

34.2 

34.3 

0.98 

0.02 

0.562 

0.616 

0.620 

0.017 

0.01 

0.7 

0.9 

0.9 

1Diets contained industry standard milk replacer (MR), pooled and pasteurized transition milk 
(TM) or milk replacer supplemented at a ratio of 1:1 with colostrum replacement powder 
(MCR).  
2P-value the difference between MR and the 2 dietary treatments (TM and MCR).  
3P-value the difference between the 2 treatment groups (TM vs MRC). 
 

 

 

44 

 

 

 

 

 

 

 

 

 

 

 

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45 

 

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48 

CHAPTER 3: EFFECTS OF TRANSITION MILK ON EARLY LIFE GROWTH, 

HEALTH, AND INTESTINAL DEVELOPMENT OF DAIRY BULL CALVES 

 

Brandon Van Soest*, Adam Moeser†, Angel Abuelo Sebio†, Miriam Weber Nielsen*, and 

Michael J. VandeHaar* 

*Department of Animal Science, and 

†Department of Large Animal Clinical Sciences, Michigan State University, East Lansing 48824 

 

ABSTRACT 

 

Colostrum stimulates gastrointestinal development by increasing cell proliferation and 

reducing apoptosis. Transition milk (TM, milk from the second through fourth milkings after 

calving) is similar to colostrum as it contains elevated nutrient levels and bioactive components 

not found in milk replacer (MR).  We hypothesize that feeding TM will stimulate intestinal 

development, improve indicators of health status, and increase BW gain compared to feeding 

MR. We tested our hypothesis on 23 newborn Holstein bull calves (11 fed TM and 12 fed MR), 

born 6 different weekends within 12 h of each other. Calves were fed 2.8 L of colostrum within 

15 min of birth, allocated to 1 of 11 blocks, randomly assigned to MR or TM treatments within 

block, and fed treatments 3 times per day. TM was collected, pooled by milking number, and fed 

at 1.89 L (255 grams DM) per feeding as follows: milking 2 at feedings 2 to 5, milking 3 at 

feedings 6 to 8, and milking 4 at feedings 9 to 12.  In this study, TM was not pasteurized and had 

an average composition of 30% fat and 39% protein on a DM basis and 20 g IgG/L. Calves fed 

MR received 275 g DM MR (21% fat and 27% protein) at all 12 feedings. Both treatments had 

average refusals of 10%. On the morning of d 5, calves were injected IV with 5 mg of 

bromodeoxyuridine per kg BW and euthanized 130 min later. Sections of the duodenum, 

 

49 

proximal jejunum, mid jejunum, and ileum were excised to evaluate morphology. With the 

additional 0.7 Mcal ME/d and additional bioactive components such as IgG, TM grew more than 

twice as fast at 0.64 kg/d compared to MR 0.25 kg/d. Compared to MR, TM nearly doubled 

villus length, villus width, villus to crypt ratio, and mucosal length in all sections. Compared to 

MR, TM increased submucosal thickness 70% in the proximal and mid jejunum and tended to 

increase submucosal thickness in duodenum and ileum. Treatment did not alter crypt depth. In all 

sections, labeling with bromodeoxyuridine was increased 50% by TM compared to MR in the 

cells along the epithelium of the crypts and within the villi, indicating that TM increased cell 

proliferation compared to MR. Health scores were improved for cough, fecal, nose, and ear in 

TM calves compared to MR, with no difference observed in eye score. We conclude that TM 

stimulates villus, mucosal, and submucosal development in all sections of the small intestine in 

the first few days of life, while also improving health indicators and increasing growth rate.    

 

INTRODUCTION 

Transition milk is defined as milkings 2-6 after calving (Godden, 2008). Feeding TM 

following colostrum increased weight gain and improved eye, ear, and nasal health scores 

compared to calves fed milk replacer after first colostrum (Conneely et al., 2014).  In my first 

study, I also found that feeding transition milk to calves improved growth rates and indicators of 

health (Chapter 2; Van Soest et al. (in review)).  

Colostrum contains a high immunoglobulin content and is thus essential for providing 

passive immunity to the neonate. Colostrum also contains bioactive compounds and nutrients in 

different concentrations than are found in milk. TM has characteristics similar to colostrum with 

elevated concentrations of IgG and bioactive compounds, including insulin-like growth factor 1, 

growth hormone, and insulin, and these concentrations gradually decrease as milk transitions 

 

50 

from colostrum to regular milk  (Blätter et al., 2001; Kühne et al., 2000; Blum and Hammon, 

2000). 

How these elevated bioactive compounds alter the physiology of the neonate and the 

development of the neonate’s immune system is not entirely clear. Norrman et al. (2003) fed 

colostrum or a formula containing similar nutrients to calves for the first 3 d of life and saw a 

reduced proliferation of immune cells in the gastrointestinal tract, fewer B lymphocytes in the 

Peyer’s Patches, and increased proliferation of immune cells in the thymus in the calves fed 

colostrum. They suggested that the immunoglobulins of colostrum may reduce the need of the 

active immune response. Blum (2006) suggested neonatal calves’ gastrointestinal tract is 

relatively mature at birth but requires morphological and functional changes from colostrum’s 

nutrient and non-nutrient components. The growth factors i.e. IGF-1 and hormones such as 

insulin and prolactin ingested with colostrum are hardly absorbed in week-old calves (Grütter 

and Blum, 1991; Hammon and Blum 1997b; Lee et al., 1995), thus suggesting that if they have 

any effect on the calf, it must be localized within the intestine. These hormones and growth 

factors within colostrum stimulate growth of the GIT and regeneration after inflammatory 

damage (Uruakpa et al., 2002). Roffler et al. (2003) demonstrated that calves fed bovine 

colostrum extract for the first 5 d of life had larger intestinal villi than those fed MR. Benefits 

from early life colostrum supplementation have also been observed in swine  (van Barneveld et 

al., 2011); piglets who consumed colostrum protein isolate grew faster, consumed more liquid 

feed, had greater feed efficiency, and more developed digestive tracts compared to piglets 

consuming a whey protein concentrate for the first 28 days of life. When comparing calves fed 

colostrum to those fed high-density MR, Kühne et al. (2000) concluded the elevated nutrients 

and bioactive and growth-promoting compounds in colostrum increased metabolic rate, growth 

 

51 

rate, and decreased incidence of loose feces. Blättler et al. (2001) demonstrated that feeding large 

quantities of colostrum, compared to MR, reduced apoptosis of mucosal epithelial cells, 

enhanced crypt fission, increased epithelial cells from crypt to villus, and increased cell 

proliferation in parts of the small intestine. They observed no differences in crypt growth in the 

first 7 d of life, but overall, their data clearly show that colostrum contains nutrients and 

bioactive compounds that enhance intestinal development.  

Because the composition of TM has similarities to colostrum, we expect that TM might 

have effects on development and health that are similar to colostrum. We hypothesized that 

feeding TM in the first 4 d of life following colostrum would promote intestinal development, 

indicators of health status, and BW gain when compared to feeding MR. This hypothesis was 

tested in newborn Holstein bull calves. 

 

MATERIALS AND METHODS 

Animals and Treatments 

 

The Institutional Animal Care and Use Committee of Michigan State University 

approved all experimental procedures. Twenty-three Holstein neonatal bull calves were 

purchased from a commercial Michigan dairy farm 1 hour from campus.  Four calves were 

selected each week that were all born within 12 hours of each other. Calves received 2.84 L of 

colostrum testing above 23 on a Brix refractometer by esophageal tube within the first 20 

minutes of life.  After all calves for the week were born, they were transferred to the Michigan 

State University Cow and Calf Research facility. Upon arrival, calves were housed in calf 

hutches, bedded with wheat straw, and provided water ad libitum. Calves were blocked by BW 

and randomly assigned to either TM or milk replacer (MR, Purina Cold Front BOV MOS 

 

52 

Medicated milk replacer, St. Louis, MO). There were 11 calves in total assigned to TM and 12 to 

MR. The TM was collected from cows at the Michigan State University Dairy Research and 

Teaching Center (East Lansing, MI), with milkings 2, 3, and 4 collected and managed separately. 

Upon collection, TM was frozen at -20˚C, and subsequently thawed, pooled by milking, and 

refrozen in 1.89 L batches at -20˚C. The TM was sent to a commercial lab for analysis of 

composition by near-infrared spectroscopy (Table 5, Central Star Cooperative, Inc., Lansing, MI, 

USA). At time of feeding, all diets were warmed to 40˚C. All calves were bottle-fed 1.89 L of 

their respective diet three times a day: 0400 h, 1130 h, and 1800 h. Calves in the TM group were 

fed milking 2 at feedings 2-5, milking 3 at feedings 6-8, and milking 4 at feedings 9-12. MR was 

reconstituted at 14% solids and at fed at a rate of 0.275 kg DM of powder per feeding.   

Growth and Health Status 

All calves were weighed upon arrival on d 1 and just before their 0400-h feeding on d 2, 

3, and 5. Heart girth, wither height, and hip height was measured each time weights were 

collected. Observational health scores were recorded by two researchers at each feeding for all 5 

days. Scores were recorded for fecal consistency, ear disposition, eye discharge, nasal discharge, 

and cough prevalence using the Calf Health Scoring Chart (University of Madison- Wisconsin 

School of Veterinary Medicine, 2011) on a score of 0-3 with 0 representing normal or healthy 

and 3 severely ill.  

Blood Sample Collection and Analysis 

Blood samples were collected via jugular venipuncture into either BD Vacutainer™ 

Venous Blood Collection Tubes: Vacutainer Plus™ Glass Serum Tubes, K2 EDTA, or Sodium 

Fluoride and Potassium Oxalate tubes (Becton, Dickinson and Company; Franklin Lakes, NJ, 

 

53 

USA). We collected blood upon arrival on day 1; prior to their 1130 h feeding on days 2, 3, and 

5; and once 2 hours post-feeding (1330 h) on d 3. Blood was centrifuged at 1,700 × g for 15 

minutes at 4°C. The respective serum or plasma was harvested and stored at -20˚C. 

Concentrations of IgG in TM and blood and total protein in serum were measured via RID by 

Saskatoon Colostrum Co. (Saskatoon, SK Canada). Glucose, insulin, and non-esterified fatty 

acids (NEFA) were measured in plasma from d 2 and 5  from plasma collected prior to feeding, 

and d 3 prior to feeding and 2 h after (PGO Enzyme Product No. P7119; Sigma Chemical Co., 

Darmstadt, Germany; Mercodia Bovine Insulin ELISA, Uppsala, Sweden; and HR Series NEFA-

HR, Wako Pure Chemical Co., Chuo-Ku Osaka, Japan respectively).   

Euthanasia, Tissue collection, Histology, and Immunohistochemistry 

On d 5, calves received an intravenous injection of bromodeoxyuridine (BrdU) starting at 

0720 at a rate of 5 mg/kg BW using 10 mg/mL BrdU (Sigma-Aldrich, Darmstadt, Germany) 

solution to label cells in the S phase of the cell cycle.  Calves were euthanized 130 ± 4 min after 

BrdU using intravenous injection of Pentobarbital sodium (SomnaSol ™ Euthanasia-III Solution, 

Henry Schein Animal Health, Dubli, OH, USA). The intestinal tract was excised, and 4 samples 

were collected.  Duodenum was collected starting at 5 cm caudal from the pylorus and working 

downstream.  Proximal jejunum (ProxJj) was collected starting at 100 cm caudal from the 

pylorus. Middle jejunum (MidJj) was collected starting ~30 cm cranial from the collateral branch 

of the cranial mesenteric artery. Ileum was collected starting 10 cm cranial from the cecum and 

working upstream. From each section, we removed 4 cm for morphological measurements and 

immunohistochemistry and 20 cm for collection of digesta. Tissues were flushed with ice-cold 

1X PBS buffer at pH 7.4 and placed in 10% formalin solution to fix for histology. 

 

54 

To analyze tissues for B cells, T cells and incorporation of BrdU, specimens were 

processed, embedded in paraffin and sectioned on a rotary microtome at 4 m. Slides were dried 

at 56˚C, deparaffinized in xylene and rehydrated in descending grades of ethanol washes. 

Endogenous peroxidase was blocked for 30 min in 3% hydrogen peroxide in methanol bath and 

rinsed with tap and distilled water.  Sections were denatured using 4.0 M hydrochloric acid, 

rinsed, and placed in Tris Buffered Saline pH 7.4 (TBS, Scytek Labs – Logan, UT) to adjust the 

pH. Sections were retrieved utilizing 0.4% pepsin (Sigma Aldrich- Saint Louis, MO) in 0.2 N 

aqueous hydrochloric acid for 15 minutes at 37°C followed by rinses with tap water, distilled 

water, and TBS plus Tween 20 solution. Following pretreatments, standard micro-polymer 

complex staining steps were performed at room temperature on the IntelliPath™ Flex Auto 

Stainer followed by rinses in TBS buffer (Biocare Medical – Concord, CA). Sections were 

blocked for non-specific proteins and incubated for 30 min with the respective primary antibody 

for each staining procedure. BrdU used monoclonal mouse antibody (#347580, Becton 

Dickinson, San Jose, CA), B cell used rabbit antibody (#ab78237 Abcam (Epitomics), and T cell 

used polyclonal rabbit antibody (#ab5690 Abcam, Cambridge, MA). Micro-polymer (ProMark 

Mouse on Farma HRP Polymer, Biocare) reagents were incubated for 30 min followed by 

reaction development with Romulin AEC™ (Biocare) and counterstained with Cathe 

Hematoxylin (1:10Ab for BrdU and 1:5 for T and B cells). BrdU labeled cells were visualized at 

20X magnification with a light microscopy of 20 well-oriented and intact crypt-villus segments 

in the duodenum, ProxJj, MidJj, and ilium. Cells were quantified by one observer blinded to 

treatment as cells/mm of crypt epithelium and cells/mm2 of lamina propria. B and T cell slides 

were analyzed at 40x magnification on a light microscope. B cells were observed and counted in 

10 random Pyrus patches per slide and expressed as B cells/mm2. T cells were located within 20 

 

55 

well oriented crypt-villus units and counted in the epithelial on a T cells/mm of epithelium basis 

and in the lamina propria on a cells/mm2 basis.   

For hematoxylin and eosin samples, formalin-fixed tissues were embedded into paraffin 

using Sakura VIP 2000 tissue processor (Rankin Biomedical Corporation, MI, USA) and Thermo 

Fisher HistoCentre III embedding station (Thermo Fisher Scientific, Runcorn, UK).  Once blocks 

cooled, sections of 4-5 µm were cut and dried at 56°C.  Slides were removed from the incubator 

and stained with a routine Hematoxylin and Eosin method as described by Tucker et al. (2016). 

Slides were visualized at 4x magnification with a light microscopy (Leica Microsystems, 

Wetzlar, Germany).  A minimum of 20 well-oriented and intact crypt-villus units were selected 

and measured using ImageJ software (Rasband, W.S., ImageJ, U. S. National Institutes of 

Health, Bethesda, Maryland, USA), per calf per section of tissue by a blinded observer. Villus 

height and width, crypt depth, and thickness of the mucosa and submucosa were measured, and 

the villus height/crypt depth (V/C) ratio was calculated.  

Digesta 

Digesta was collected from abomasum, duodenum, ProxJj, MidJj, ileum, and cecum. The 

pH of each sample was determined using a calibrated pH probe (Thermo Fisher Scientific, 

Runcorn, UK). The digesta from the abomasum was weighed, filtered (1.5 cm filter) to remove 

curds, and the filtered-out curds were then reweighed.  

Statistical Analysis 

 

The MIXED Procedure in SAS 9.4 (SAS Institute Inc., Cary, NC) was used to analyze 

statistical differences.  We used a repeated measures model for all blood measurements and 

health scores with fixed effects of treatment and time (or day) and random effect of block with 

 

56 

the subject for repeated measure being calf within block and treatment. Our model for all other 

measures included the fixed effect of treatment and random effect of block. For BrdU time 

between injection until euthanasia was tested as a covariate but had no effect. Residuals were 

tested for normality using the Shapiro-Wilk test and homogeneity of variance was tested with 

Bartlett’s test. Insulin was log-transformed to satisfy homoscedasticity. Significance was denoted 

at P-value ≤ 0.05 and tendencies were denoted as P-values ≤ 0.1 on all main effects.  

Calf Growth  

RESULTS 

 

Compared to MR, TM more than doubled BW gain over the 5-d study (P = 0.005; Table 

6). Using the NRC (2001), calves fed TM were predicted to have higher BW gain than calves fed 

MR because TM supplied 0.75 Mcal more ME per day (4.58 Mcal/day on average for TM and 

3.83 Mcal/day for MR, Table 5). No differences were seen with initial body measures prior to 

treatment on d 1.  TM tended to increase the change in heart girth and hip height compared to 

MR (2.77 cm vs. 1.12 cm increase, P = 0.07 and 1.45 cm vs. 0.15 cm increase, P = 0.09, 

respectively). No differences were observed for change in wither height.  

Gut Measures 

 

As shown in Table 7, TM stimulated development of the gut. Compared to MR, TM 

increased villus length of the duodenum by 63%, ProxJj by 96%, MidJj by 76%, and ileum by 

52% (P ≤ 0.003 for all). TM also increased villus width 43% in the duodenum, 63% in the 

ProxJj, 60% in the MidJj, and 40% in the ileum (P ≤ 0.008 for all) compared to MR. V/C (ratio 

of villus length to crypt depth) was increased by TM compared to MR by 54% in the duodenum, 

101% in the ProxJj, 81% in the MidJj, and 48 % in the ileum (P ≤ 0.01 for all). TM increased 

 

57 

mucosa thickness in the duodenum by 37%, ProxJj by 58%, MidJj by 47%, and ileum by 33% (P 

≤ 0.013 for all) when compared to MR. Submucosa thickness was significantly increased for 

both the MidJj and ProxJj while tending to increase in the ileum and duodenum for TM vs MR. 

There were no differences observed on the crypt depths.  

 

The number of cells labeled with BrdU (Figure 2) was increased by TM in the lamina 

propria of the duodenum by 54%, ProxJj by 75%, MidJj by 121%, and ileum by 64% (P ≤ 0.01 

for all) compared with MR. TM also increased the number of BrdU-labeled cells in the epithelial 

layer of the duodenum by 40%, ProxJj by 72%, MidJj by 78%, and ileum by 56% (P ≤ 0.0001 

for all) compared with MR (Table 8). No difference was seen between diets for B cell/ mm2 in 

the Peyer’s Patches in the ileum or the T cells within the lamina propria in the ileum. TM tended 

to increase T cells within the epithelial layer of the ileum (30.6 T cells/mm vs 24.1 T cells/mm, P 

= 0.06) compared to MR. 

 

As for pH of the digesta collected from the GI tract, TM tended to reduced abomasum pH 

(2.71 vs. 3.52, P = 0.06) and MidJj pH (6.08 vs. 6.35, P = 0.09) when compared with MR (Table 

8). No differences in pH were observed for the contents of the duodenum, ProxJj, ileum and 

colon. While no differences were observed between treatments on total content weight in the 

abomasum, TM dramatically increased curd weight and percentage of curds within the 

abomasum compared to MR (524g vs. 0.0g, P = 0.0002 and 45.1% vs. 0.03%, P = 0.001, 

respectively). 

Health Measures 

 

As shown in Table 11, TM altered indicators of calf health. TM significantly reduced 

average health score per feeding for cough (0.13 vs. 0.33, P = 0.05), fecal (0.60 vs. 1.06, P = 

 

58 

0.006), nose (0.02 vs. 0.18, P = 0.05), and ear (0.26 vs. 0.62, P = 0.02) compared to MR. TM 

elevated serum IgG on d 2 (33.3 vs. 27.4 g/L, P = 0.03) and 3 (30.9 vs 25.4 g/L, P = 0.04) 

compared to MR while no differences were observed on d 5 (P= 0.21, Figure 4). This resulted in 

an interaction between treatment and day (P = 0.03). Serum total protein was increased by TM 

compared to MR over d 2 (6.6 vs. 6.1 mg/dL, P = 0.03), 3 (6.6 vs. 6.0 mg/dL, P = 0.01), and 5 

(6.5 vs. 5.8 mg/dL, P = 0.002) with all calves declining over that time period (P = 0.03), as seen 

in Figure 5.  

Blood Measures 

 

TM tended to increase plasma NEFA during the entire study (P=0.07) with a day effect 

(P = 0.015) where d 2 was significantly higher for TM compared to MR (370 vs. 288 mmol/L , P 

= 0.04). No differences were detected on the other days pre-feeding. On day 3, TM increased 

plasma NEFA concentration compared to MR from pre to post-feeding  (Figure 6, TM: 264 

mmol/L pre to 334 mmol/L post vs. MR: 220 mmol/L pre to 206 mmol/L post, P=0.0045 Max SE 

is 29). No treatment effects were observed for glucose, but there were day and treatment by day 

effects (Figure 7, P = 0.005 and P = 0.0007, respectively). Glucose concentration decreased from 

d 2 through d 5 for calves fed MR but did not decrease for calves fed TM (MR: 6.33, 5.16, and 

4.72 mmol/L vs. TM 5.66, 5.61, and 5.83 mmol/L; Max SE is 0.3). On d 3 both treatments had 

little overall changes, but TM tended to have higher glucose concentrations compared to MR 

(5.61 mmol/L pre to 5.66 mmol/L post vs. MR: 5.16 mmol/L pre to 5.05 mmol/L post, P = 0.06; 

Max SE is 0.28). Feeding TM tended to increase plasma insulin concentrations from d 2, 3, and 5 

compared to MR (TM: 410, 515, and 549 µg/L vs MR: 1476, 353, and 207 µg/L; P = 0.09; Max 

SE is 131). On d 3 both treatments had an increase in plasma insulin following feeding, but no 

 

59 

treatment differences were observed (Figure 8; TM increased by 455 µg/L vs MR increased by 

378 µg/L; P = 0.21). 

Growth and health 

DISCUSSION 

 

In this study, we found that calves fed TM grew 0.4 kg/d more than calves fed MR. One 

third of this increase could be accounted for by the difference in nutrient composition for TM 

compared to MR. We suggest that some of the benefit of TM must be due to improvements in 

intestinal development and (or) health.  

 

All calves received high-quality colostrum within the first 20 minutes of life at the 

commercial farm ensuring successful transfer of passive immunity of > 10 mg/ml IgG (Jaster, 

2005). The first feeding of treatment was offered between 6 and 24 hours of birth. Because TM 

also contains IgG, the calves fed TM received more IgG than those fed MR. Although these IgG 

would have been less efficiently absorbed, absorption extends out to 24 h after birth (Chigerwe et 

al., 2008); essentially no absorption of IgG occurs after 24 h (Weaver et al. 2000).  Blood 

samples collected between 6 and 12 h on d 1, before calves were fed treatments, IgG 

concentrations in blood were not significantly different (P=0.12), even though the reported mean 

was 24% greater for TM than MR calves. On d 2 and 3, calves fed TM had higher concentrations 

of IgG in blood, which could have resulted from the IgG in TM. Total serum protein followed 

the same trend as IgG but remains significantly different out to d 5. Additional feedings of 

colostrum have shown mixed results in studies when it comes to diarrhea prevalence. Berge et 

al., (2009) saw a decrease in diarrhea with increased IgG supply from colostrum suggesting a 

localized effect at the level of the gut lumen. In contrast, Nocek et al. (1984) found that feeding 

colostrum for 45 d resulted in higher prevalence of scours compared to milk replacer. Conneely 

 

60 

et al. (2014) found that eye, ears, and nasal health scores are improved with increased feedings of 

TM compared to feeding MR. In the current study, calves fed TM had reduced average health 

scores by nearly half of that of calves fed MR for fecal consistency and ear score. The number of 

observations of coughing was reduced by 65% and nasal discharge by 13% in TM calves 

compared to MR. This improvement in fecal observational health scores suggests the 

immunoglobulins or bioactive components in TM supply additional protection in the gut from 

potential infectious bacteria (Chapter 2; Van Soest et al. (in review)). Along with the improved 

observational health from feeding TM, the number of T cells were increased in the epithelium of 

the ileum. This increase in epithelial T cells potentially could prevent illness at the level of the 

GIT. Norrman et al. (2003) saw a reduction in the number of B cells in Peyer’s patches in calves 

fed colostrum vs. formula, but not in the number of T cells in the ileum.  Our study observed no 

differences in the number of B cell within Peyer’s patches. Our results agree with David et al. 

(2003) where the number of B cells in Peyer’s patches was similar for calves were fed colostrum 

and calves fed MR.  David et al. (2003) speculated that even with the reduced apoptosis and 

increase proliferation observed in Peyer’s patches of calves fed colostrum compared to MR, the 

number of B cells did not increase due to migration out of the Peyer’s patches.  

Intestinal development  

 

In our study, we found that TM increased gut development, as indicated by several 

different measures.  These findings are consistent with studies that have shown that feeding 

colostrum increases development of the small intestine as indicated by changes in depth of 

crypts, length and width of villi, and thickness of mucosa and submucosa compared to feeding 

bulk tank milk or MR (Blum, 2006; Blättler et al., 2001). Presumably, the increased development 

is due to the high concentrations in colostrum of hormones, growth factors, and cytokines that 

 

61 

alter proliferation, migration, differentiation, and longevity of epithelial cells, as well as 

digestion, absorption, and development and function of the immune system (Blum and 

Baumrucker, 2008). In our study, calves fed TM had increased villus width and length in all 4 

sections of the small intestine while having no differences in crypt depth compared to MR which 

agrees with what Blättler et al. (2001) observed. We observed increased epithelial cell 

proliferation of the crypt and villi in all sections of the small intestinal tract when Blättler et al. 

(2001) only observed differences in the duodenum and jejunum when feeding colostrum 

compared to MR. The potential difference of our study from that of Blättler et al. might be due to 

differences in quantity, composition, and processing of the diets; whereas Blättler et al. fed 6 

feedings of reconstituted colostrum extract powder, we fed 11 feedings of unpasteurized TM 

from milkings 2 through 4. Blättler et al. (2001) suggests the increased villi length and 

unchanged crypt depth could result from the migration of epithelial cells to the villus tips from 

the crypt coupled with reduced apoptosis. This increased development of the small intestine 

likely results from all of the bioactive compounds and nutrients found in colostrum or transition 

milk, making it complicated to supplement individually. Various bioactive components affect the 

GIT differently depending on the location of their receptors (Cordano et al., 1998; Georgiev et 

al., 2003; Ontsouka et al., 2004; Krüger et al., 2005). Some of these peptide hormones such as 

insulin have the potential of being absorbed, as has been shown in neonatal pigs (Xu et al., 

2002). IGF-1 is capable to survive and remain active in the GIT in calves (Koldovsky et al. 

1989); this further supports localized effects that are mediated by specific receptors in epithelial 

cells, fibroblasts, endothelia and smooth muscle in the GIT (Howarth, 2003). This localized 

stimulus from different components of TM could partially explain the increased development of 

calves fed TM compared to MR.     

 

62 

 

We observed both a day and treatment by day effect of treatments on blood glucose 

(Figure 7, P = 0.005 and P = 0.0007, respectively). Blood glucose concentrations of calves fed 

MR over the 5-d study declined but they remained consistent in calves fed TM; perhaps this was 

related to the increased GIT development of TM calves. As the MR calves were growing, 

perhaps gut development could not satisfy the demand for glucose, so blood glucose 

concentrations dropped. In contrast, perhaps the TM calves, with more developed GIT, were able 

to absorb enough glucose to maintain blood glucose concentrations. Overall, there are no 

treatment effects observed on blood NEFA concentration. We are unsure of the reason for the 

elevation of NEFA concentrations on d 2. This elevation in blood NEFA concentration on d 2 

observed in MR calves may have resulted from travel, refusals, or insufficient energy supply 

from MR causing mobilization of fat from stores. Blood insulin concentrations of calves 

mirrored the changes in glucose concentration. We again observed a day and treatment by day 

effect of treatments on blood insulin (Figure 8, P<0.0001 for both). Insulin concentrations 

persisted at a constant level in calves fed TM while decreased in calves fed MR. We are unsure 

the reason for the elevation of blood insulin in calves fed MR as it does not coincide with an 

extreme level of glucose on d 2.  

CONCLUSION 

 

Feeding TM in the first week of life following colostrum improved gut development, 

indicators of health status, and growth compared to feeding MR. Calves fed TM gained 0.64 kg/d 

compared to 0.25 kg/d for calves fed MR. A portion of this difference can be attributed to TM 

calves receiving 0.7 Mcal more ME per day, while the rest might result from the increased small 

intestinal development or improved health. The small intestine of calves fed TM had increased 

villi length, villi width, mucosal thickness, submucosal thickness, villi/ crypt ratio, and epithelial 

 

63 

cell proliferation than calves fed MR; thus, we conclude that TM enhanced intestinal 

development. Feeding TM decreased health scores, elevated IgG concentrations in blood, and 

increased the number of T cells in the epithelium of the ileum compared to feeding MR; thus, we 

conclude TM potentially improves variables associated with health status. We speculate an 

elevated plane of nutrition and the presence of nutrients and bioactive compounds found in TM 

enhanced intestinal development and immune function and therefore improved growth and 

health in the first week of life. We further speculate that the improved gut development and 

health would have carry-over benefits and enhance health and growth for most of the critical first 

3 weeks in the life of a calf.   

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

64 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

APPENDIX 

 

65 

Table 5 Composition of Experimental Diets 

  

 

Diet 

TM1 

Milking 

Milking 

Milking 

Item 
Feedings2 
IgG (g/kg DM) 
ME3 (Mcal/kg DM) 
% Protein (DM) 

% Fat (DM) 

2  
2-5 

217.5 

5.53 

50.7 

27.3 

3  
6-8 

94.4 

5.09 

38.6 

33.4 

4  
9-12 

46.6 

5.09 

34.0 

36.7 

MR 

 

2-12 

0 

5.26 

26.6 

20.6 

% DM 
14.0 
1The composition of TM (transition milk) changed with each milking. 

14.9 

17.6 

15.3 

2Feeding 1 was colostrum 

3ME was calculated using NRC 2001 equations. Enthalpies of 9.2, 5.7, and 3.95 were used for 
fat, protein, and lactose, respectively. GE (gross energy) was multiplied by 0.97 and 0.96 to 
determine ME. 

 

 

66 

Table 6 Average Body Weight Gain, Predicted Gain, and Feed Intake 

Treatment 

  

Variable 

Birth Weight (kg) 
Milk Fed (L/d) 

Milk Refusal (L/d) 
ME consumed2 (Mcal/d) 
Predicted ADG1 (kg/d) 
ADG All 5 d (kg/d) 

Initial Heart girth (cm) 
Initial Hip Height (cm) 

Initial Wither Height (cm) 

Δ Heart girth (cm) 
Δ Hip Height (cm) 

TM 

41.2 

5.67 

0.66 

5.05 
0.81 

0.64 

79.5 
80.0 

76.8 

2.77 
1.45 

MR 

42.3 

5.67 

0.58 

4.22 
0.58 

0.25 

81.3 
80.8 

76.8 

1.12 
0.15 

Δ Wither Height (cm) 
1Predicted ADG calculated using NRC 2001 for first week of life 

0.00 

0.71 

P-Value 

TRT 

0.4 
- 

0.6 

0.001 
0.002 

0.005 

0.12 
0.5 

0.9 

0.07 
0.09 

0.28 

2 ME consumed post colostrum during trial (feedings 2-12) 

 

 

 

67 

Table 7 Small Intestine morphology (mm, Standard Error) 

 
Item 
Villus Length (mm) 

Duodenum 
Proximal Jejunum 
Mid Jejunum 
Ileum 

 

Villus Width (mm) 

Duodenum 
Proximal Jejunum 
Mid Jejunum 
Ileum 

 

Crypt Depth (mm) 

Duodenum 
Proximal Jejunum 
Mid Jejunum 
Ileum 

 

Villus/Crypt ratio 

Duodenum 
Proximal Jejunum 
Mid Jejunum 
Ileum 

 

Mucosal Thickness (mm) 

Duodenum 
Proximal Jejunum 
Mid Jejunum 
Ileum 

 

Sub Mucosal Thickness (mm) 
Duodenum 
Proximal Jejunum 
Mid Jejunum 
Ileum 

 
 

 
 

 
 

 
 

 
 

 

 

 

 

 

Treatment 

MR 

 

0.504 ± 0.058 
0.609 ± 0.047 
0.568 ± 0.058 
0.536 ± 0.044 

 
 

0.0977 ± 0.0096 
0.0891 ± 0.0086 
0.0942 ± 0.0090 
0.105 ± 0.0093 

 
 

0.338 ± 0.023 
0.356 ± 0.020 
0.332 ± 0.019 
0.310 ± 0.022 

 
 

1.63 ± 0.13 
1.76 ± 0.10 
1.80 ± 0.20 
1.90 ± 0.20 

 
 

0.848 ± 0.074 
0.964 ± 0.062 
0.899 ± 0.065 
0.841 ± 0.053 

 
  

0.171 ± 0.022 
0.110 ± 0.012 
0.119 ± 0.011 
0.133 ± 0.013 

TM 

 

0.824 ± 0.060 
1.190 ± 0.048 
1.004 ± 0.059 
0.812 ± 0.045 

0.140 ± 0.0099 
0.146 ± 0.0089 
0.150 ± 0.0092 
0.146 ± 0.0096 

0.336 ± 0.023 
0.346 ± 0.020 
0.324 ± 0.019 
0.313 ± 0.023 

2.52 ± 0.14 
3.55 ± 0.11 
3.27 ± 0.20 
2.81 ± 0.21 

1.159 ± 0.078 
1.522 ± 0.063 
1.323 ± 0.067 
1.121 ± 0.055 

0.232 ± 0.023 
0.218 ± 0.012 
0.196 ± 0.012 
0.159 ± 0.013 

68 

 
P-value 

 

0.003 

<0.0001 
<0.0001 

0.001 

 
 

0.008 

<0.0001 
<0.0001 

0.006 

 
 

0.9 
0.7 
0.8 
0.9 

 
 

0.0007 
<0.0001 
<0.0001 

0.01 

 
 

0.01 

<0.0001 
0.0001 
0.004 

 
 

0.08 

<0.0001 
0.0005 

0.09 

Table 8 Bromodeoxyuridine Labeled Cells, B Cell, and T Cell Counts in the Small Intestine 
(mean, Standard Error) 

 
Item 
Lamina Propria BrdU labeled 
cells1 
Duodenum (Cells/mm2) 
Proximal Jejunum (Cells/mm2) 
Mid Jejunum (Cells/mm2) 
Ileum (Cells/mm2) 
 

Epithelium BrdU labeled cells3 
Duodenum (Cells/mm) 
Proximal Jejunum (Cells/mm) 
Mid Jejunum (Cells/mm) 
Ileum (Cells/mm) 
 

Treatment 

TM 

MR 

 

 
 

1011 ± 83 
  969 ± 63 
1122 ± 60 
  901 ± 59 

71.1 ± 2.3 
85.3 ± 2.2 
85.0 ± 1.5 
70.1 ± 3.3 

 

653 ± 80 
555 ± 61 
507 ± 57 
548 ± 58 

 
 

50.9 ± 2.2 
49.7 ± 2.1 
47.8 ± 1.5 
44.9 ± 3.1 

 

P-value 

 

0.01 

0.0006 
<0.0001 
0.0005 

 
 

<0.0001 
<0.0001 
<0.0001 
0.0002 

 
 

 
 

Immune cells4 
B cells (Cells/mm2) 
T cells (Cells/mm2) 
T cells (Cells/mm) 
1 Cell count of Cells/mm2 of the respective section of the small intestine within the cross section 
of the microscope slide 

811 ± 81 
24.1 ± 2.4 

996 ± 85 
30.6 ± 2.5 

4698 ± 602 

3432 ± 574 

 
 

0.16 
0.15 
0.06 

3 Cell count of Cells/mm of the respective section of the small intestine within the cross section 
of the microscope slide  

4 Cell count of either Cell/mm or Cell/mm2 within the ileum epithelium or lamina propria, 
respectively, within the cross section of the microscope slide 

 

 

69 

Table 9 Average pH of Gastrointestinal Tract Digestive Contents 

 

Treatment 

P-Value 

pH Variable 

TM 

MR 

TRT 

Abomasum  
0.06 
Duodenum  
0.43 
Proximal Jejunum 
0.52 
Mid jejunum  
0.09 
Ileum 
0.97 
Colon 
0.96 
1 Max SE is the largest standard error across treatment  

2.71 
5.09 
5.54 
6.08 
6.99 
5.60 

3.52 
5.42 
5.38 
6.35 
6.98 
5.61 

 

Max 
SE1 

0.3 
0.3 
0.2 
0.1 
0.1 
0.1 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

70 

Table 10 Abomasa Content 

  

Treatment 

P-Value 

TM 

MR 

Variable 
Total content weight (g) 
Curd weight (g) 
% Curds 
1 Max SE is the largest standard error across treatment  

1280 
524 
45 

800 
0.0 
0.0 

TRT 

0.19 
0.0002 
0.001 

 

Max 
SE1 

230 
40 
5.1 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

71 

Table 11 Average Health Scores 

  

Treatment 

 

P-Value 

Health Variable1 
Cough 
Fecal 
Nose 
Ear 
Eye 

TM 
0.119 
0.56 
0.165 
0.241 
0.07 

MR 
0.322 
0.983 
0.190 
0.576 
0.04 

Max 
SE2  TRT  Day 
0.09 
0.01 
0.05 
0.02  0.004 
0.5 
0.03 
0.02 
0.39 
0.02 
0.02  0.007 
0.001  0.27  0.009 

TRT* 
Day 
0.9 
0.8 
0.6 
0.2 
0.9 

 

 

 

 

 

 

1 Scores on a scale of 0-3 (0 being healthy, 3 being ill). Scores were taken 3x a day and then 

averaged across the study for each calf. 

2Max SE is the largest standard error across treatment and day 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

72 

Table 12 Blood Metabolites analyzed at 1100 hr before feeding treatments 

Glucose  
(mmol/L) 

 

 

Max 
SE1 

TM  MR  P-value 
0.4 
5.66 
0.17 
5.61 
5.83 
0.001 

6.33 
5.16 
4.72 

2 
3 
5 

  TM  MR  P-value 
410  1476  <0.0001 
 
0.4 
514 
 
549 
0.07 
 

353 
207 

0.3 
0.3 
0.3 

Insulin 
(µg/L) 

 

NEFA 

(mmol/L) 

 

Max 
SE1 

131 
131 
131 

  TM  MR  P-value 
0.04 
 
0.27 
 
0.9 
 

370  288 
264  220 
268  272 

Max 
SE1 

29 
29 
29 

 
Day 
 (pre 
feeding) 

 

1Max SE is the largest standard error across treatment and day 

 

73 

Figure 1 H & E Stained Small Intestine for Morphological Measures 

 

 

74 

 

Figure 1 (cont’d) 

Light micrographs of hematoxylin and eosin (H and E) stained duodenum (TM: A and MR: B), 
proximal jejunum (TM: C and MR: D), mid jejunum (TM: E and MR: F), and ileum (TM: G and 
MR: H) sections of neonatal calves fed either transition milk (TM) or milk replacer (MR) for the 
first 4 days of life. Observation was done at 4x magnification. TM calves have increased 
morphological measures other than crypt length. 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

 

75 

Figure 2 Bromodeoxyuridine Labeled Cells in Small Intestine 

 

76 

 

Figure 2 (cont’d) 

Light micrographs of Bromodeoxyuridine (BrdU) stained duodenum (TM: A and MR: B), 
proximal jejunum (TM: C and MR: D), mid jejunum (TM: E and MR: F), and ileum (TM: G and 
MR: H) sections of neonatal calves fed either transition milk (TM) or milk replacer (MR) for the 
first 4 days of life. Observation was done at 20x magnification. TM had larger inclusion of BrdU 
stained cells in all sections. 

 

 

 

 

 

77 

Figure 3 B Cell and T Cell Staining in Ileum 

Light micrographs of B and T cell stained ileum sections of neonatal calves fed either transition 
milk (TM) or milk replacer (MR) for the first 4 days of life. Observation was done at 40x 
magnification for B cells and 20x magnification. No difference was observed in B cell stained 
peyer’s patches in ileum or T cells in the laminal propria. TM increased T cells in epithelium of 
villi.  

 

 

 

 

 

 

 

 

78 

Figure 4 Serum IgG Concentration 

The (**) indicates P ≤ 0.05 and (*) indicated P ≤ 0.1 but P > 0.05 when comparing between 

treatment at that time point. The error bars here indicate the SE. 

 

 

 

 

 

 

 

 

 

 

79 

 

Figure 5 Serum Total Protein Concentration 

**

**

**

)
L
d
/
g
m

(
 
n
i
e
t
o
r
P
m
u
r
e
S

 

6.9

6.7

6.5

6.3

6.1

5.9

5.7

5.5

2

3

4

5

Days of Life

TM

MR

 

The (**) indicates P ≤ 0.05 and (*) indicated P ≤ 0.1 but P > 0.05 when comparing between 

treatment at that time point. The error bars here indicate the SE. 

 

 

 

 

 

 

 

 

 

 

 

 

 

80 

Figure 6 The Change in Plasma NEFA on d 3 Across a Feeding (2 hrs post feeding). 

)
L

/
l

o
m
m

(
 
n
o

i
t

a
r
t

 

n
e
c
n
o
C
A
F
E
N
m
u
r
e
S

 

**

385

335

285

235

185

135

85

11 hr

15 hr

TM

MR

 

The (**) indicates P ≤ 0.05 and (*) indicated P ≤ 0.1 but P > 0.05 when comparing between 

treatment at that time point. The error bars here indicate the SE. Calves were fed at 1130 hr. 

 

 

 

 

 

 

 

 

 

81 

 

 

Figure 7 The Change in Plasma Glucose on d 3 Across a Feeding (2 hrs post feeding). 

 

n
o

i
t

a
r
t

 

l

n
e
c
n
o
C
e
s
o
c
u
G
m
u
r
e
S

 

* 

6.25

6

5.75

5.5

5.25

)
L

/
l

o
m
m

(

5

4.75

4.5

11 hr

15 hr

TM

MR

 

The (**) indicates P ≤ 0.05 and (*) indicated P ≤ 0.1 but P > 0.05 when comparing between 

treatment at that time point. The error bars here indicate the SE. Calves were fed at 1130 hr. 

 

 

 

 

 

 

 

 

 

 

 

 

82 

Figure 8 The Change in Plasma Insulin on d 3 Across a Feeding (2 hrs post feeding). 

/

)
L
g
µ
(
 
n
o

i
t

a
r
t

n
e
c
n
o
C
n

 

i
l

u
s
n

I
 

m
u
r
e
S

1285

1085

885

685

485

285

85

11 hr

15 hr

TM

MR

 

The (**) indicates P ≤ 0.05 and (*) indicated P ≤ 0.1 but P > 0.05 when comparing between 

treatment at that time point. The error bars here indicate the SE. Calves were fed at 1130 hr. 

 

 

 

 

 

 

 

 

 

 

 

83 

 

 

 

 

 

 

 

 

 

 

 

 

REFERENCES 

 

 

 

 

 

 

 

 

 

 

 

84 

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87 

CHAPTER 4: CONCLUSIONS & IMPLICATIONS 

 

In our studies, we observed growth benefits to calves supplemented additional bioactive 

compounds and nutrients during the first week of life. In the first study, little to no differences 

were observed when pasteurized and pooled transition milk (from milkings 2-4) or milk replacer 

supplemented with colostrum replacer were fed in the first 9 feedings after colostrum on growth, 

health scores and blood health indicators. The pasteurized transition milk and colostrum replacer 

supplemented milk replacer increased ADG in the preweaning period as well as decreased 

plasma haptoglobin. The pasteurization process of the transition milk destroyed most of the IgG 

and reduced the fat, protein and lactose concentrations. Transition milk still had a higher caloric 

ME compared to colostrum supplement milk replacer and milk replacer. The colostrum 

supplemented milk replacer had the highest IgG and intermediate amount of ME.  Therefore, I 

suggest that both additional bioactive compounds and ME are beneficial to calves in the first 

week of life. 

 

In the second study, we observed similar results as our previous study by feeding 

unpasteurized transition milk to increase ADG during the first week compared to milk replacer 

when fed for 11 feedings. Transition milk fed calves also experienced improved health scores, 

increased IgG and total serum protein and more developed small intestines. The improvement in 

GIT development perhaps influenced the glucose concentrations to remain constant in the 

transition milk fed calves when compared to the milk replacer fed calves who decreased in blood 

glucose concentrations. Increased epithelial T cells in the ileum were also observed in calves fed 

transition milk.  

 

88 

 

As farmers strive to increase weight gain of preweaned calves and minimize the use of 

antibiotics and decrease incidences of illness, my studies show that feeding transition milk for 

either 9 or 11 feedings could potentially improve calf health. More research is needed to know 

the optimal quantity and number of feedings of transition milk to optimize the health and growth 

benefits.  Since the first study lacked starter intake measures, observing the impact transition 

milk intake on starter intake should be investigated. Additional research should also be 

conducted to examine if the enhanced development of the GIT in calves fed TM compared to 

MR results in greater digestibility while calves are fed milk or even after calves are fed similar 

diets.  Researchers should also determine if these improvements in GIT development, health, and 

growth rate in early life might also decrease breeding age and increase subsequent milk 

production. A cost vs benefit analysis should be included in these studies. In summary, future 

research is needed to explore all potential benefits of feeding TM to calves in the short and long 

term. 

 

89