Pathology Associated with Rations

Abstract

After the excellent series of presentations we have just heard, it is possible that this discussion, "Pathology Associated with Rations," is mistitled and perhaps misdirected. The previous speakers have very competently directed their attention to what might be described as the "anatomy of the ration." Perhaps it would be more appropriate for us to get involved with what might be described as the "pathology of the ration." This play on words, "pathology of the ration," versus "pathology associated with the ration" may sound redundant However, when we consider that by definition "pathology is the study of the molecular, tissue, or organismal response of the living body when exposed to injurious agents or deprivations" (20) and attempt to connect this definition with a ration, we have established a unique premise:

That a "normal" feed, "usually" fed, supposedly furnishing nutrients in proportions and amounts as to properly nourish a cow for a given 24-hourperiod (15), can produce a harmful effect in the cow. It may be more pertinent to look for the lesion in the ration rather than in the cow; to some extent, we'll try to do this.

When discussing this association, the ration as an agent of pathologic change in the dairy cow, there are several rather basic factors that must be reiterated:

1. The ruminant emerged approximately 60million years ago and evolutionally developed tissue systems that were necessary to successfully colonize high-fiber, low-nitrogen environments (14)-environments high in cellulose. Hence, under a comparatively uncomplicated dietary regimen, ruminants became sophisticated biological fermentation-recycling factories; they prospered, dependent on microbiological populations for cellulose digestion and enhanced protein metabolism.

Despite this relatively long phylogenetic history, the ruminant has been domesticated for only 7000to 8000 years, and with regard to the dairy cow, highly productive only within very recent history. In the United States, dairy cow numbers progressively increased between the years 1850 and 1940, reaching a peak of over 24 million animals. Following this period, cow numbers have progressively declined. Despite this trend, there occurred nearly a 2,000-pound increase in average milk production between the years 1960 and 1966; this increase was approximately equal to the total improvement in production that occurred between1906 and 1930 (13). Certainly much of this production increase can be attributed to improved breeding and feeding practices. However, during this same period of improved production, certain gastro-intestinal and metabolic disorders have increased in incidence and, with respect to feeding practices, a popular idea has evolved-that we are excessively "pushing" our dairy cows for production.

1. The diverse microbiological populations of the rumen must be adapted to chemical, physical, and quantitative alterations in the ration (substrate).
2. Rumen fermentation, ideally, should be continuous and, optimally, uniform (13). Implementation of this consideration is accomplished, in part, through frequent but uniform ration intake (substrate renewal). It has been demonstrated (14), in sheep, that when the same ration, at the same total quantity, was fed in four feedings, as opposed to one or two feedings per day, there resulted:
3. a reduction in the range of intra-ruminal pH.
4. a progressive reduction in the number of rumen bacteria.
5. a progressive increase in the number of rumen protozoa.
6. increased digestibility of the ration.
7. an increase in the amount of protein stored.
8. a reduction of free ammonia levels in the rumen.
9. It must also be recalled that the end products of rumen fermentation include the energy sources for the cow: the volatile fatty acids, acetic, propionic, and butyric. It can be anticipated that these acids will normally be present in rumen fluid, when rations are fed, that include large amounts of highly digestible roughage, at molar percentages of approximately 65% acetic, 20% propionic, and15% butyric (13).
10. The lactating dairy cow is under a production burden that predisposes to energy-deficit disorders. A lactating cow may, as a consequence of lactose synthesis, lose two to four pounds of glucose daily(11). In order to maintain homeostatic mechanisms, this loss must be offset by adequate dietary intake.
11. Pathologic alterations need not be grossly discernible.

With these factors in mind, we can begin to examine some abnormal (pathologic) conditions in the dairy cow, whose incidence may be rather dramatically influenced by the composition of the ration and/or its physical structure and/or the way it is fed. These abnormal states could conceivably involve a my1iad of conditions ranging from simple indigestion to torsion of the abomasum, including, as well, the metabolic-deficiency disorders. To discuss each in the detail necessary to fulfill the definition of "pathology" (20) would be excessively time-consuming. I would prefer, therefore, to select certain disorders and use these as models to illustrate, in a practical way, the possible connections between the ration and the inducement of a pathologic condition.