Increasing atmospheric concentrations of methane have led scientists to examine its sources of origin. Ruminant livestock can produce 250 to 500 L of methane per day. This level of production results in estimates of the contribution by cattle to global warming that may occur in the next 50 to 100 yr to be a little less than 2%. Many factors influence methane emissions from cattle and include the following: level of feed intake, type of carbohydrate in the diet, feed processing, addition of lipids or ionophores to the diet, and alterations in the ruminal microflora. Manipulation of these factors can reduce methane emissions from cattle. Many techniques exist to quantify methane emissions from individual or groups of animals. Enclosure techniques are precise but require trained animals and may limit animal movement. Isotopic and nonisotopic tracer techniques may also be used effectively. Prediction equations based on fermentation balance or feed characteristics have been used to estimate methane production. These equations are useful, but the assumptions and conditions that must be met for each equation limit their ability to accurately predict methane production. Methane production from groups of animals can be measured by mass balance, micrometeorological, or tracer methods. These techniques can measure methane emissions from animals in either indoor or outdoor enclosures. Use of these techniques and knowledge of the factors that impact methane production can result in the development of mitigation strategies to reduce methane losses by cattle. Implementation of these strategies should result in enhanced animal productivity and decreased contributions by cattle to the atmospheric methane budget.

Methane emissions from cattle.

In addition to the bacteria in the rumen there are many larger (5–250/mm long) organisms which at various times have been designated protozoa Of these the ‘ovals’ (Quin’s and Eadie’s) are now known to be large bacteria (Orpin, 1976) and the ‘flagellates’ Neocallimastix frontalis, Piromonas communis and Sphaeromonas communis are the zoospores of phycomycete fungi (Orpin, 1977a, b) There are genuine flagellates in the rumen, eg Trichomonas spp, Monoceromonas sp and Chilomastix sp, but almost nothing is known about their metabolism (Jensen and Hammon, 1964) The largest, most obvious and most important protozoa are the ciliates, of which there are two groups both in the subclass Trichostomatia The so called ‘holotrich’ protozoa belong to the order Vestibuliferida and the entodiniomorphs to the order Entodiniomorphida, suborder Entodiniomorphina and family Ophryoscolecidae As the properties and metabolism of these two protozoal groups are different, they will be considered separately below

The Rumen Protozoa

Microbial protein synthesis and flows of nitrogen fractions to the duodenum of dairy cows.

http://www.commoditieslawyers.com/uploads/1/1/2/8/11280347/1.2.1.2_pdf_of_link_to_acidosis.pdf

Ruminal acidosis in beef cattle: the current microbiological and nutritional outlook.

Since the first reports of satellite cells in 1961, considerable knowledge has accumulated concerning their phylogenetic distribution and their location, morphology, and function. There is no doubt that satellite cells are capable of undergoing mitosis and that they have considerable motility. These cells function as the progenitors of the myofiber nuclei that must be added during normal (postnatal) growth of muscle. In muscle undergoing or attempting to undergo regeneration, the satellite cell functions as a myogenic stem cell to produce myoblasts that line up and fuse within the scaffolding of the remnant basal lamina or migrate into the interstitium to produce neofibers . A number of problems remain to be solved concerning the regulation of satellite cell function. At this time it is equivocable whether or not the presumptive myoblast and the satellite cell are functionally identical and at the same stage of myogenic differentiation. Apparently there is species variation in terms of the ability of myotubes from embryonic myogenic cells and satellite cells to synthesize protein. The mechanism(s) by which a wide variety of stimuli activate satellite cells is not known, nor is the mechanism(s) by which satellite cells become inactive during the latter stages of growth and adulthood known. Mitogenic factors are present in damaged muscle; but the specific characteristics of these factors and their mechanism of activation are also unknown. Hormones are certainly involved in the regulation of proliferation and differentiation of myogenic cells, but whether presumptive myoblasts and satellite cells or their myotubes respond similarly to hormones in culture has not been adequately examined. Greater understanding of these mechanisms will increase the possibility of total muscle recovery from severe injury or disease. Such knowledge would also have particular application to the production of meat animals and to a greater understanding of the growth process in general.

The muscle satellite cell: a review.

Eight bull calves (four Holsteins and four Ayrshire calves with mean birth weight of 38.8 kg) were ruminally cannulated at 3 d of age and allocated to one of two weaning programs. All calves were fed colostrum for 3 d after birth and milk until weaning. Calves in the conventional-weaning program were fed a starter diet from 3 d of age and weaned at 6 wk of age. In the early-weaning program, calves were fed a highly palatable pre-starter diet from 3 d of age until they consumed 227 g/d, and then fed a mixture of pre-starter (227 g) and starter diet ad libitum. Calves in this group were weaned at 4 wk of age. Ruminal samples were collected at 3 and 7 d, then weekly thereafter through 8 wk and at 10 and 12 wk of age to assess microbial activity. Calves in the early-weaned group had a higher concentration of total ruminal volatile fatty acids at an earlier age than the calves in the conventional-weaning program. This was accompanied by a trend toward higher lactate concentrations and lower ruminal pH in the early-weaned group during their first 4 wk of age. Lactate and ammonia concentrations decreased with calf age. The total anaerobic bacterial counts increased slightly with calf age, whereas Streptococcus bovis and facultative bacterial populations decreased with calf age. Amylolytic, proteolytic, lactobacilli, lactate-utilizers, cellulolytic and methanogenic bacterial populations increased progressively in both groups. Cellulolytic and methanogenic bacteria were present in both groups at 3 d of age. No protozoa were detected in calves of either group. In general, the most significant changes in bacterial populations and metabolic activity in both groups occurred between 4 and 6 wk of age. Although calves in both groups had similar patterns of bacterial development, calves in the early-weaning program tended to have high ruminal microbial activity at an earlier age than the conventionally weaned calves.

Ruminal microbial development in conventionally or early-weaned calves

Intraruminal administration of lasalocid or monensin (1.3 mg/kg body weight) effectively prevented in glucose- or corn-induced lactic acidosis in cattle. Administering the antibiotics for 7 days before experimentally inducing acidosis with corn (27.5 g/kg body weight), effectively prevented acidosis, while 2 days' were sufficient to prevent glucose-induced acidosis (12.5 g/kg body weight). The different responses observed in the two trials probably stemmed from the difference in amounts of carbohydrate used to induce acidosis. Antibiotic-treated cattle had higher rumen pH values and lower L(+) and D(-) lactate concentrations that control cattle that received no antibiotics. Ruminal VFA in control cattle decreased, while total VFA and the molar proportion of propionate increased in antibiotic-treated cattle after grain engorgement. Control cattle exhibited classic signs of acidosis, such as lowered blood pH; increased blood lactate, particularly D(-) isomer; hemoconcentration, and depleted alkali reserve with a pronounced based deficit. Antibiotic-treated cattle exhibited no signs of systemic acidosis.

Prevention of lactic acidosis in cattle by lasalocid or monensin.

Diaminopimelic Acid Content of Feeds and Rumen Bacteria and Its Usefulness as a Rumen Bacterial Marker

Thirty-six steers (148 to 500 kg) divided into six equal groups were used in a toxic syndrome study of lasalocid and monensin given as a single oral dose. One group was given a placebo, a second group received monensin (25 mg/kg body weight) and the other four groups received lasalocid at 1, 10, 50 or 100 mg/kg body weight (bw). No toxic signs developed in cattle given placebo or lasalocid at 1 or 10 mg/kg bw dose. The earliest toxic signs were muscle tremors, tachycardia and rumen atony. After 24 h, the cattle were dehydrated, anorectic and had diarrhea. Deaths occurred between d 1 and 22.5 in the groups receiving lasalocid at 50 and 100 mg/kg bw and monensin. Altered values in blood leucocytes, erythrocytes, hemoglobin, hematocrit, total protein, albumin, creatinine, urea nitrogen, total bilirubin, creatine kinase, lactic dehydrogenase, calcium, chloride and inorganic phosphate occurred 1 d after dosing: urine pH and specific gravity also changed 1 d after dosing. Maximum changes occurred at d 3. Most of the changes were indicative of dehydration rather than specific organ damage.

Lasalocid toxicity in cattle: acute clinicopathological changes.

Summary Four rumen-fistulated Holstein steers were fitted with cannulas for the collection of portal, jugular and carotid blood. In addition, the thoracic duct of one steer was cannulated for the collection of lymph. Steers were given .125, .25 or .5 g urea/kg body weight 16 hr after a previous feeding. Within 5 min after the administration of the .5-g dose, rumen ammonia increased from 9.7 to 32.0 mg/lO0 ml, rumen pH from 6.47 to 7.87; portal blood ammonia from 1.02 to 8.01 mg/lO0 ml, carotid blood ammonia from .18 to 1.17 mg/lO0 ml and jugular blood ammonia from .13 to .36 mg/100 ml. Lymph ammonia increased from .22 to .32 mg/100 ml within 15 minutes. The .125- and .25-g doses of urea produced proportionate changes. In a second experiment, three Jersey cows were given .5 g urea/kg body weight, and the rates at which urea appeared in carotid and jugular blood were determined. Only small amounts of urea appeared in carotid and jugular blood during the first 5 min after dosing, but the concentrations then increased slowly but progressively. We concluded that because carotid blood ammonia concentration increased so rapidly after dosing with urea, ammonia must leak past the liver, and it is therefore unlikely, that there is a liver threshold for ammonia which must be exceeded before ammonia will reach the carotid artery. The marked difference in ammonia concentrations in carotid and jugular blood suggests that the

S. J. Galitzer

Papers

Ruminal microbial development in conventionally or early-weaned calves

Prevention of lactic acidosis in cattle by lasalocid or monensin.

Diaminopimelic Acid Content of Feeds and Rumen Bacteria and Its Usefulness as a Rumen Bacterial Marker

Lasalocid toxicity in cattle: acute clinicopathological changes.

Ammonia toxicity in cattle. V. Ammonia concentration of lymph and portal, carotid and jugular blood after the ingestion of urea.