Calf Mortality

Tremendous increase in cow/buffalo cost, hence organized farms are focusing to maintain progeny. Dairy herd replacement can be attained by improved management strategies like lower calving intervals, higher calving rates, reduced still born and pre-weaned calf mortalities and fewer non pregnant heifers. Such strategies can increase the number of replacement heifer calves in the herd from current 15% to over 35%, this will allow farmers to increase their herd sizes through natural increases.

But the main and most important constraint is the neonatal calf mortality. Neonatal calf mortality varies from 8.7 to 64 per cent throughout world. Martin and Wiggins (1973) estimated that 20% calf mortality resulted in reduction of 38% profit of a livestock farm. Neonatal calf mortality in the first month of age is accounted to be 84 per cent of the total mortality (Jenny et al.1982) and is particularly high in the third week of life (Umoh.1982). According to Afzal et al. (1983) the mortality in cattle and buffalo calves ranged from 29.1% to 39.8%. Furthermore, 25% average early calf mortality hardly provides any chance for regular replacement of low production animals.

A minimum mortality rate of 5% is usually acceptable to dairy farm standard managemental conditions. Scope of the subject is beyond the article so this is an attempt to cover important issues.

Mortality of neonatal calves was attributed to conditions like diarrhea and pneumonia (Shimizu and Nagatoma., 1978). However, environmental and managemental factors hasten the occurrence of such conditions (Khan and Khan, 1991). There is a definite association between the type of housing, feeding, managemental practices, weather conditions, external and internal parasitic infestation and bacterial infections especially those causing septicemia and enteritis with calf mortality (Blood et al.1994).

Broadly the causes of calf mortality can be divided into two

It includes all the microbes mainly bacteria and viruses.  The most commonly found microbes are

Rotavirus-The virus specially attacks the epithelium of small intestine of young calf. The virus replicates in intestinal epithelial cells near the tips of villi. Infected cells are desquamated. As epithelial cells are lost from the tips of villi, the desquamated cells are replaced by cuboidal, then flattened squamous epithelial cells. Some villi may remain denuded and stroma of villi becomes internally infiltrated with leukocytes.

Coronavirus-The virus has an affinity for epithelial cells of the villi of the small intestine. Replication of the virus in these cells is accompanied by loss of epithelium and blunting of the villi. In the colon, surface epithelial cells are also attacked, with loss of surface cells and cystic dilation and accumulation of cellular debris in underling crypts.

Incidence of coronavirus in neonatal calf diarrhea is slightly lower than rotavirus

Enterotoxigenic Escherichia coli-E. coli produces enterotoxic and septicemic colibacillosis in young calves

In enterotoxic colibacillosis, the pathogenic E. coli adhere to the mucosa and proliferate in the lumen of intestine, producing a potent enterotoxin, which stimulate excessive secretion of fluid from intestinal mucosa (Moon.1972). This loss of fluid causes the principal sign (diarrhea) and often leads to dehydration and high rate of death in the neonatal calves.

In septicemic colibacillosis, the organisms invade the host possibly through the oral cavity, respiratory system, pharynx, or umbilicus and produces and endotoxin that apparently causes the lesions. Unless the enterotoxic form occurs simultaneously, the bacteria do not reach to the small intestine, thus diarrhea or intestinal lesions do not occur (Jones et al.1983). Calves that are deficient in immunoglobulins are mostly susceptible to this form of colibacillosis (White et al 1986).

Salmonella and cryptosporidium-Salmonella infections are most frequent and of great concern to young animals. These rod-shaped, gram negative organisms are usually motile and produce gastroenteritis with nausea, vomiting, cramps and diarrhea (Jones et al 1983), salmonella in neonatal calves (28 days old) produces diarrhea in 1 to 12 per cent calves and morbidity up to 20 per cent.

Cryptosporidium occurs in diarrheic calves and more than 10 per cent of all the scouring calves excrete cryptosporidia at the same time as rotavirus. Sings are usually unapparent but chronic diarrhea has been associated with cryptosporidiosis especially in neonatal calves (Pohlenz et al. 1976).

Pneumonia-Two types of pneumonia namely, proliferative and exudative are prevalent in calves (Trigo et al.1982).The causative organisms are Pasteurella multocida ,Pasteurella hemolytica ,staphylococcus epidermis Streptococci, Pseudomonas aeuroginosa ,Mycoplasma bovis ,Corynaebacterium pyogenes , E. coli , Coronavirus , Herpesvirus1 and pestivirus .

2) Non Infectious causes

Immunoglobulin-Immunoglobulins are acquired by the offspring through the agency of colostrum. In colostrum, immunoglobulins present are IgG1, IgM, IgA and IgG2, however, IgG1 is predominant representing 80 per cent of the total immunoglobulins absorbed by the neonatal calf (Blom.1982). Immunoglobulins from the colostrum absorb into the circulation from the small intestines of the neonatal calf by a process micropinocytosis (Blood et al.1982). Maximum absorption occurs within the first 6-8 hours after birth (Blom.1982). The amount of antibodies from individual females shows differences due to breed, nutritional status and parity. Season, geography, and sex is also known to influence passive transfer of colostral immunoglobulins in calves (Sangwan et al.1985). During absorptive period, competition between microorganisms and immunoglobulins does occur for intestinal receptors for transportation to the circulation. Intestinal bacteria produce malabsorption syndrome by occupying immunoglobulins receptors resulting in hypo or agammaglobulinemia in neonatal calves (Snodgrass et al.1986) Colostral immunoglobulins present in the intestine and subsequently absorbed in to the circulation protect neonatal calves against enteric and respiratory disease and even from leg injuries (Norheim et al.1986). High mortality and morbidity due to diarrhea, pneumonia and other diseases occurs in immunodeficient calves (Braun et al.1983). Calves without adequate circulating IgG1 are four time more likely to die and twice as likely to become ill than calves with adequate circulating immunoglobulins (White  et al.1986).

Season-Season has a significant effect on the calf mortality (Fink.1980) as well as on the absorption of immunoglobulins inneonatal calves. In temperate climates the mean serum IgG1 concentrations were lowest in winter born calves and increased during the spring and early summer,perhaps this is the reason that higher mortality rates of 69.6 and 15.36 per cent had been observed in winter born buffalo calves than 39.4 and 5.97 per cent in summer born calves (Sharma et al.1984).

Parturition problems and parity-Dystocia in the dams increases the rate ofmortality in neonates. About 50 per cent calves are lost atparturition due to dystocia (6). Dystocia is mainly due toabnormal presentation of calf especially backward andbreech presentation. Incidence of dystocia is higher(5.6%) in primiparous dams than (0.9%) in multiparousdams and is also significantly higher (p<0.01)when the calf is male (57.6%) but lowered (42.4%) whenthe calf is female (Patterson et al.1986). Persistent hymen in heifers is animportant condition which delays the delivery of the youngone in naturally bred heifers (Ahmad et al.1986). According to Jenny andhis colleagues, stillborn calves are more likely to dieas compared to normal delivered calves. Stillbirths varywith the parity of the dam and season of the year. In primiparous cows and during winter, stillbirthswere higher than in multiparous cows and summerseason. There is another factor i.e., sex which increasesthe rate of stillbirths in male calves (Szenci et al.1982).As parturition problem decreases with age and parityof the dam, the amount of colostrum available and concentration of colostral immunoglobulins increases.

Studies conducted by Odde.(1988), manifested immune status to be better in calves from multiparous than primiparous dams. When there is better immune status of calf, its survival will not be affected by the gastrointestinal or respiratory diseases.

Sex and birth weight of calf-Mortality is higher in male 25.5%) than in female(13.9%) neonatal calves (Kaushik et al.1980), reason for this higher mortalitymight be due to serum immunoglobulins, requiredfor the protection from different diseases during neonatallife, absorb less in male (20.69 mg/ml) than female (25.12mg/ml) calves. Competition between microorganismsand immunoglobulins for a common intestinal receptordoes occur in early few hours of life (Staley et al.1985), due to this competitionmale calves become more immunodeficient thanfemale calves, therefore, former calves (59.42%) aremore prone to bacterial diseases than later (50%) neonatalcalves. Stillbirths as well as dystocia problems aremore common when male calves are involved. The birth weight had a significant effect on mortality.Calf mortality decreases gradually with increase in birthweight and minimum (21.1%) in calves weighing41 kg and above at birth.Similar observationsabout birth weight of calves have been reported by Singhet al. There is also difference of opinion, as Verma etal.  reported non significant effect of birth weight ofcalves on calf mortality. Male calves had a significanthigher (37.2 kg) body weight than female (33.7 kg) calves(Bellows et al.1987), perhaps this is the reason that dystocia is morecommon when the sex of the calf is male.

Management and miscellaneous factors-In calf houses, poor ventilation, overcrowding, no regular cleaning and disinfection predispose various diseases of calves, especially of respiratory tract leading to high calf mortality. Tympani and milk indigestion also play an active role in the neonatal calf mortality. Absorption of immunoglobulins continue up to 48 hours in calves, but maximum absorption occurs within the first 6- 8 hours of life (Blom.1982), if feeding of colostrum is delayed from this period, it results in hypo or agammaglobulinemia in calves. Compared to hand feeding, suckling is a greater source of absorption of colostral immunoglobulins, therefore, it is generally recommended to allow calf to suckle its mother for the first two days post-partum. Calves kept in pens develop arthritis, tendovaginitis or abscesses and even fractures and those develop naval joint illness had a poor survival rates (Britney et al. 1984). Mortality of calves can be reduced by rearing them on elevated and perforated floors (Simensen.1982). Similarly naval disinfection and removal of mucous from the mouth and nose reduces mortality and morbidity rates in calves (Fink.1980).

Control Measures

Proper calf care begins before the calf is even born. Dairy cows in the dry period are offered mineral and vitamin mixes in order to prevent issues associated with deficiency in both the cow and the calf. Some of these issues include retained fetal membranes (RFM), lazy calving, calving difficulty (dystocia), milk fever, calf death and poor calf health. For example maternal deficiency of trace minerals and Vitamin E in late pregnancy can compromise the immune system of the calf. This may increase susceptibility to scour, pneumonia, navel-ill, joint-ill, etc. It is generally advised to feed dry cow mineral and vitamins for approximately six weeks pre-calving. This is in order to combat deficiencies in the total dietary intake.

Never overcrowd close-up pens. Maternity pens should be single use to minimize the spread of disease. The dam should be clean before she goes into the pen because the calf may nuzzle her in search of colostrum. Be prepared to remove the calf from the dam and maternity pen immediately to avoid disease transfer. This happens primarily through "manure meals" via nose dives into the bedded pack while attempting to stand, sucking on the cow´s manure-laden body searching for colostrum, or ingesting manure-contaminated colostrum. The dam should be up-to-date on booster vaccinations. These vaccinations allow her to transfer passive immunity through colostrum to her calf.

Simple management procedures such as ensuring adequate intake of good quality colostrum within the first 12 hours of life, housing and good hygiene to minimize disease transfer, providing clean drinking water, developing appropriate feeding protocols to encourage early rumen development and paying closer attention to climate control and animal health can all lead to improved calf vigour and performance. Good record keeping is also important so farmers can more easily identify susceptible calves and quickly treat potential problems.

After delivery, attention shifts to thenewborn calf. Process the calf by stimulatingit to breathe, check its generalhealth status and dip the navel in astrong (7%) iodine tincture solution. Remove the calf from the dam andprovide a clean, dry resting surface toensure its hair coat stays dry, helpinginsulate against the cold ground, low airtemperatures and sudden temperature changes. Provide at least 6 inches ofbedding as a cushion to minimize physicaltrauma. House calves in individualpens to reduce the spread of disease.A sound colostrum program is essentialin raising healthy calves, whichare born without an immune system.Colostrum allows a calf to develop animmune system, protecting it fromdisease until it can produce its ownantibodies within four weeks. Becausecolostrum is essential to a healthy calf,be prepared to feed colostrum 24 hoursa day, seven days a week. Feed high quality(at least 50 grams immunoglobulinsper liter) fresh, refrigerated, orfrozen colostrum from a second or laterlactation Johne´s-negative cow. If colostrumis not available, feed a colostrumreplacement product with 50 or moregrams of immunoglobulins per liter.

After the colostrum´ s period, whole milk should be provided to the calf until 15 days of age @ a level of 1/8th to 1/10th of the calf'´s body weight. (see Table 3). Milk replacer can be fed along with the whole milk provided that it has a certain composition of nutrients. It is not advisable to completely substitute whole milk with milk replacer. Milk and/or replacer should be offered to the calf on at least two occasions per day. The milk and/or replacer should be served at body temperature (38-39^ºC).

Table 1: Feeding of the calf

At two weeks of age, the calf should be introduced to good quality green feed and concentrates, as a calf starter (Table 3). This stimulates the rumen to grow and function properly. By following the feeding schedule in Table 8 a daily gain of 0.35 kg can be expected in Murrah calves.

*first 3 to 4 days, feed colostrum.

**ensure a smooth and gradual change to milk replacer

Calf starter mixture-Typical calf starter mixture should have the following Ingredients

Buffalo calves fed with Stover´s of maize, bajra and oat cannot meet their nutrient requirements and are often in negative energy and protein balance. However, feeding the calves with treated Stover´s with a urea-molasses-salt complex both enhances the palatability of the Stover´s as well as the digestibility and nutrient value.

Combinations of Practices like proper care of dam during last phase of pregnancy, intensive care of calf after birth, improved managemental practices and veterinary aid in emergency will help you to prevent the problem to a large extent.

Afzal M, Javed MH, Anjum AD : Calf mortality: Seasonal pattern, age distribution and causes of mortality. Pakistan Vet J, 3:30-33, 1983.

Ahmad KM, Malik SH, Ahmad M, Khan A : Persistent hymen in a buffalo heifer. Pakistan Vet J, 6:48-49, 1986.

Bellows RA, Patterson DJ, Burfening PJ, Phelps DA : Occurence of neonatal and postnatal mortality in range beef cattle. II. Factors contributing to calf death. Theriogenology,28:573-586, 1987.

Bhullar MS, Tiwana MS : Factors affecting mortality among buffalo calves. Indian J Anim Sci, 55:599-601, 1985.

Blom JY : The relationship between serum immunoglobulin values and incidence of respiratory diseases and enteritis in calves. Nord Vet-Med, 34:276-284, 1982.

Blood DC, Radostits OM : Veterinary Medicine, 7th Ed, ELBS, Oxford, 1989.

Braun RK, Tennant BC : The relationship of serum globulin levels of assembled neonatal calves to mortality caused by enteric diseases. Agri-Practice, 4:14-15, 1983.

Britney JB, Martin SW, Stone JB, Curtis RA : Analysis of early calf hood health status and subsequent dairy herd survival- ship and productivity. Prep Vet Med, 3:45-52, 1984.

Fink T : Influence of type of housing, microclimate and management on health of calves. Inaugural Disser Tierarztliche Hochshule, Hannover, p 120, 1980.

Jenny BF, Cramling GE, Glaze TM : Management factors associated with calf mortality in South Carolina dairy herds. J Dairy Sci, 64:2284-2289, 1981.

Jones TC, Hunt RD : Veterinary Pathology, 5th ed, Lea and Febiger, Philadelphia, PA 19106, USA, 1983.

Kaushik SN, Gupta OP, Agarwal SC, Dass SC : Neonatal mortality in Hariana-Bos Taurus crossbreeds. Indian J Dairy Sci, 33:516-518, 1980.

Khan A, Khan MZ : Immunoglobulins in relation to neonatal calf mortality. Pakistan Vet, 11:...., 1991.

Moon WH : Pathogenesis of enteric diseases caused by Escherichia coli. Adv Vet Sci Comp Med, 18:179-211, 1974.

.Norheim K, Simensen E, Gjestang KE : The relationship between serum IgG levels and age, leg injuries, infections and weight gains in dairy calves. Nord Vet Med, 37:113-120, 1985.

Odde KG : Survival of the neonatal calf. Vet Clinics north Am Food Anim Pr, 4:501-508, 1988.

Patterson DJ, Bellows RA, Burfening PJ, Carr JB : Occurrence of neonatal and postnatal mortality in range beef cattle. I. Calf loss incidence from birth to weaning, backward and breech presentations and effects of calf loss on subsequent pregnancy rate of dams. Theriogenology, 28:557-571,1987.

Pohlenz J, Moon HW, Cheville NF, Garner FM : Cryptosporidiosis as a probable factor in neonatal diarrhea of calves. J Am Vet Med Assoc, 172:452-457, 1978.

Sangwan ML, Anand GR, Dwarkanath PK : Genetic and non-genetic factors affecting plasma immunoglobulin levels in cross bred calves. Indian J Dairy Sci, 40:140-150, 1985.

Sharma MC, Pathak NN, Hung NN, Lien NH, Vuc NV : Mortality in growing Murrah buffalo calves in Vietnam. Indian J Anim Sci, 54:998-1000, 1984.

Simensen E : An epidemiological study of calf health and performance in Norwegian dairy hers. II. Factors affecting mortality. Acta Agri Scandinavia 32:421-427, 1982.

Snodgrass DR, Terzolo HR, Campbell D, Sherwood I, Menzies JD, Synge BA : Aetiology of diarrhoea in young calves. Vet Record, 119:31-34, 1986.

Staley TE, Bush LJ : Receptor mechanisms of the neonatal intestine and their relationship to immunoglobulin absorption and disease. J Dairy Sci, 68:184-205, 1985.

Szenci O, Kiss MB : Perinatal calf losses in large production units. Acta Vet Acad Sci Hungaria, 30:85-95, 1982.

Trigo TE, Trigo TF, Hernandez LG, Ramirez CC, Berruecos VM : Pathology and bacteriology of calf pneumonia. Veterinaria Mexico, 13:131-140, 1982.

Umoh JU : Relative survival of calves in a university herd in Zaire, Nigeria. British Vet J, 138:507-514, 1982.

Verma GS, Sadana DK, Basul SB, Sharma PA : Studies on mortality in buffalo calves. Indian J Anim Sci, 50:87-90, 1980.

White DG, Andrews AH : Adequate concentration of circulating colostral proteins for market calves. Vet Record, 119:112-114, 1986.