Bovine biology series
Part - 42 Life cycle (3/8)
This is our third lesson of the life cycle, the yearning for life that is reproduction.....the passing of genetic material onward.
The genetic set, the sum total of genes, is established at the time of fertilization. That is, in mammals, reproduction is accomplished by combinations of genetic material, found in DNA, in such a manner that a truly unique individual is comprised.
In biology, then, reproduction that results in syngamy is obligatory. What follows is the opposite of reduction; rather, cell differentiation and growth of a truly unique individual is begun. Soon, cells begin to find their own purpose, some becoming liver cells, some becoming heart muscle, some forming nerve ganglions, and still others epithelial cells.
What follows is quite remarkable in the womb of a mammal. Whereas a fully developed fetus is made, its organs already functioning, its metabolic machinery already processing nutrients, and its immune system already protecting the body proper.
Birth of this fetus is, of course, an obligation in that soon the weight and metabolic demand of the fetus outgrows the womb’s ability, and hence the female’s ability to sustain its rapid growth.
The logical question is what initiates parturition, the birthing process in a female mammal?
In the dairy cow, about three to four weeks before calving, the high levels of progesterone begin to subside with the increasing levels of estrogen. Remember that progesterone is absolutely required for maintenance of the fetus. Increased levels of estrogen a month before calving serves the role of preparing the uterus for calving by changing the tone of the uterus.....to an active one from the more passive, quiet one.
Certain contractile proteins are secreted so that the uterine lining, the myoepithelial cells, are ready to begin contractions for fetal delivery.
The fetus itself is responsible for this initiation of hormonal shift. Specifically, the fetal adrenal cortex secretes an increasing amount of cortisol, in turn driving the production of enzymes that convert progesterone into estrogen. Again, this hormone shift begins a month or so before calving.
As the time of calving nears, increased prostaglandin secretion by the female is begun. Prostaglandin initiates regression of the corpus luteum, which in turn reduces the level of progesterone. Prostaglandin also exerts a strong influence on the uterine musculature in preparing it for contraction in the same manner that estrogen does.
The hormone relaxin plays the role of relaxing the cervix, through which the fetus must pass at birth. This cascading of events prepare the uterus and cervix for contraction and relaxation. Another hormone, oxytocin, is secreted by the female so that strong uterine contractions can begin. This release of oxytocin begins when the uterine contractions move the fetus against the cervix itself, as if calling upon a strong contractile hormone (oxytocin) so that the fetus can be shoved through the cervix.
Prolonged gestations can be caused by many factors. Some are disease and microbial in nature, while some may cause the fetal brain to improperly develop. This in turn limits the fetal hypothalamus to signal the anterior pituitary with adrenocorticotrophic hormone (ACTH), so that the adrenal cortex can release cortisol.
The result of most of these is, of course, a womb that is not prepared for calving. The exogenous use of estrogen or prostaglandin may result in the initiation of calving, in many cases the calving process is not orderly, the fetus may be dead, the presentation may be extraordinary, the dystocia’s will obligate mechanical assistance, or the fetal membranes are retained. All in all, the process of calving is the remarkable harmony of events that all proceed in a rather orderly manner.
For as anyone present at a calving of any kind knows, we are first and always awestruck that the fetus of just nine months is as complete as it is.
Let us describe this newborn calve, just born in a calving pen or pasture. The cow has been contracting for two hours or so, and finally with six to eight forcible contractions the calf is completely separate from the cow.
First, the calf is no longer physically tied to the cow as the umbilical cord is severed. The lungs grasp for air, for the lung tissue is so much better at oxygen intake and carbon dioxide output than the umbilical cord. So the calf opens its mouth and breaths.
This is automatic in mammals, and can be a problem if any obstruction, usually liquid, is present that prevents the entry of air into the lungs.
The calf is born with a completely sterile intestine. For that reason, the cleanliness of the birthing area is of paramount importance. That is, along with that first breath of air, the environmental influence of bacteria present a challenging dilemma for the calf.
Why? Because the calf is devoid of antibodies, those circulating molecules that help destroy environmental bacteria that are present in the environment. We know full well the beneficial use of colostrum in providing what we call the passive immunity after birth by feeding colostrum. The calf gut is capable of absorbing these antibodies found in colostrum for the 12 hours or so after birth; by 24 hours this ability is gone.
Antibodies that the calf produces with a healthy immune system can soon begin their role of destroying invading environmental bacteria, but at birth, this immunity is provided by the cow via the colostrum.
The newborn calf is not a ruminant; its digestive system resembles a monogastric like humans or pigs. The milk fed is shunted or moved into the abomasum through the esophageal groove. Rennin is the predominant enzyme in the calf’s stomach, serving the role of coagulating or thickening the milk by exerting a mixing up of milk proteins. This slows the milk passage time so that its nutrients can be absorbed in the lower gut.
Over time, of course, the influence of rennin decreases as the pepsin - hydrochloric acid level increases as solid food replaces the milk. Similarly, lactase, the enzyme responsible for cleaving the milk sugar molecule into individual sugars, is replaced by amalase, an enzyme exerting influence upon sugars and carbohydrates found in solid food.
Calf scours continues to challenge calf feeders. Most cases originate with virulent strains of enterotoxic E. Coli finding their way into the calf gut. There, they proliferate in the small intestine and produce an enterotoxin.
The enterotoxic strain of E. Coli influences the movement of sodium into the small intestine and then out of the gut. In other words, a net sodium loss, putting the calf in ionic shock. Acidosis of the gut results, with the calf feeder having to get a buffer of some sort into the calf or dehydration results. A net sodium loss carries with it water; thus in calf scours, there can be net water loss as water dilutes the digesta and we see diarrhea.
E. Coli is a normal inhabitant of the calf gut. When colostrum is fed the first hours after birth, the calf is more able to deal with enterotoxic strains of E. Coli, keeping their numbers down so that the enterotoxin level is low enough that sodium cellular level is maintained; the calf is absorbing milk nutrients and gains weight.
There are two other kinds of bacteria that predominate the calf gut.....Clostridium and lactobacilli. There exists a certain balance in the calf gut with these and E. Coli. Generally, if this balance is maintained the calf is largely protected from scours. Fermentative scours can occur when excessive or indigestible carbohydrates are fed. The lactobacilli bacteria ferment this overt carbohydrate load resulting in excessive lactic acid, which irritate the intestinal lining with scours as a result.
Putrefactive scours can result in a more severe form of calf scours. As the calf grows but is still on milk, the numbers of E. Coli and clostridium bacteria are decreased in the stomach with the increasing levels of hydrochloric acid, dropping the pH level. Recall that here the milk protein is coagulated or clotted due to the action of rennin or pepsin. If this clot is not formed because plant protein is fed in a milk replacer, or too much milk protein is consumed, the abomasum is overloaded with unclotted protein. The pH is increased due a lack of hydrochloric acid to keep the digesta acidic enough.
The passage into the lower gut of undigested food provides substrate for entero-bacterial growth, as well as a more alkaline pH. The resultant toxins elicit a sodium and bicarbonate loss; water is lost from the bloodstream with the onset of diarrhea in an attempt to flush the irritant out of the body.
Viral agents can exert a tragic influence on the lining of the small intestine by damaging the villa where food absorption takes place. This damage can last the lifetime of the animal, decreasing productive ability. Vaccinating programs help alleviate these agents, specifically, for Reovirus and Coronavirus.
Finally calves are weaned at 60 to 90 days on average as solid food replaces milk diets.
Next month we examine the weaned calf until she herself calves.
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