Acidosis is the most common nutritional disorder in the feedlot. A large amount of highly fermentable feeds, such as cereal grains, consumed in a short amount of time can result in the production of more lactic acid than can buffered by the rumen. This results in water from the circulatory system being drawn into the rumen (body becomes dehydrated) and pronounced changes in the blood Ph. Signs will usually be acute or sub-acute. Survivors of acute acidosis may have chronic problems such as fungal rumenitis, liver abscesses, bloat, and founder or laminitis.
Acute acidosis: Animals that are not adapted to readily fermentable feeds are more susceptible to acidosis (sometimes called grain overload) than animals that have been carefully adjusted. However, even animals conditioned to full feed can be susceptible under some conditions such as feed changes and temporary restrictions in feed availability. Acutely affected animals will usually develop signs within 12-24 hours of overeating. They will be completely off feed, depressed and unwilling to move, weak, and dehydrated. They may appear blind, grind their teeth, grunt, and occasionally kick at their belly. Fullness and distension of the abdomen (rumen) may be observed. A foul smelling diarrhea may be observed unless the condition is so acute that the animal dies before it can develop.
In severe cases animals will lie down, unable to rise. They generally lie quietly with their head tucked to the side. Body temperature may be subnormal and the pulse is weak. Death usually occurs within a few hours after the animals go down.
Animals that survive may suffer from damaged ruminal lining and destruction of rumen microflora leading to a fungal overgrowth of the rumen and death. Some deaths may occur as long as 3 weeks after a herd episode of overeating and acidosis. Less severe rumen lining damage may lead to liver abscesses and growth impairment. Laminitis, or founder, may follow acute acidosis, and evidence of subacute laminitis in the form of overgrown and deformed hooves may be present 30-60 days later.
Subacute acidosis: Animals with less acute and severe signs may still eat but may not consume as much as normal or be off feed for only a short time. The only overt signs of subacute acidosis may be reduced gains and the presence of diarrhea in the form of flat gray stools. Because rumen lining damage may still occur in the absence of severe signs, these animals may develop chronic rumen damage and liver abscesses.
Weather conditions can cause fluctuations of intake of an otherwise acceptable ration. Storm conditions can cause cattle to consume a greater amount of feed before and after the storm. Muddy conditions which can alter feed intake. A drop in barometric pressure can indicate oncoming storm conditions. Conditions that promote intake of the regular ration in a shorter amount of time can cause acidosis. Hot, humid weather will cause cattle to eat a greater proportion of their feed at night, rather than during the day.
Improper mixing of feed can cause acidosis. As previously discussed improper bunk management can be a cause of acidosis. Only occasional cleaning of water troughs will also affect intake. Inclusion of an ionophore may help reduce intake fluctuations.
Treatment-Acute Acidosis: If cattle are noticed soon after consuming large amounts of grain and before they drink water, problems may be avoided by keeping them away from water for up to 24 hours (Baker et al., 1983). Some common treatments are oral administration of mineral oil and/or sodium bicarbonate along with activated charcoal, anti-endotoxin therapy, and surgical emptying of the rumen in some cases.
Bloat occur when rumen gas production exceeds the rate of gas elimination. Gas then accumulates causing distention of the rumen. The skin on the left side of the animal behind the last rib may appear distended.
Although bloat is often classified as being either pasture or feedlot bloat, it is probably more accurate to identify it as being either free-gas bloat or frothy bloat. Frothy bloat is more common in cattle eating legumes or lush grass than in feedlot cattle. Free-gas bloat is more common in feedlot cattle.
Frothy Bloat: In situations of foamy or frothy bloat, gas production is not greatly increased but the gases are trapped in the foam. Frothy bloat in feedlots usually develops slowly over several weeks and often become chronic. Poloxalene is an effective "deformer" for frothy bloat.
Free-Gas Bloat: Many of the same factors causing acidosis are associated with free-gas bloat. Therefore proper bunk management and other preventative measures should be practiced for prevention of bloat.
Treatment: Free-gas bloat can usually be relieved by inserting a 3/4" rubber hose into the rumen via the esophagus. If "hosing" does not give immediate relief, a defoaming agent (poloxalene) should be administered through the hose to break the surface tension of the ingesta. A pint of mineral oil is also a defoamer. Drenching should be avoided because of the danger of inhalation by the bloated animal which can cause immediate death or lead to pneumonia. A trocar should be used as a last resort. Chronic bloaters should be shipped for slaughter.
Many factors contributing to acidosis and bloat also affect the incidence of liver abscesses and founder.
Abscessed Livers: Some cattle are genetically more prone to liver abscesses. Irregular feed intake or sickness can also contribute to an increased incidence of abscessed livers. Continuous use of low level antibiotics such as chlortetracycline, oxytetracycline, and tylosin can be very effective in control of liver abscesses with animals on a high grain diet. Approved combinations of ionophores and antibiotics are now available.
Founder: Founder is usually associated with abrupt changes from high roughage to high grain diets. Typical signs of founder are lameness and long hooves. Brahman-type cattle appear to be more susceptible to founder when fed high grain diets.
The animal that dies later in the feeding period represents greater loss to the feeder. Causes of sudden death include:
Necropsy of dead animals is crucial to define the cause of death and prevention plan strategies. A recent study has indicated a majority of these deaths are caused by bloat and pneumonia and that more frequent observation may reduce many such deaths.
The term "urinary calculi" describes mineral deposits in the urinary tract (Emerick and Wohlgemuth, 1985). These deposits may block the flow of urine in male cattle. Prolonged blockage generally results in rupture of the urinary bladder or urethra, releasing urine into the surrounding tissues or abdomen. This produces the condition referred to as "water belly. Two types of urinary calculi predominate in cattle and sheep: (1) the phosphatic type formed principally under feedlot conditions and (2) the siliceous type occurring mainly in range animals.
Clinical Signs: Animals afflicted with urinary calculi may at first appear restless with frequent straining in an unsuccessful attempt to urinate. They may repeatedly stamp their feed and kick at the abdomen. In some cases when urinary blockage is not complete, urine may dribble slowly from the sheath. After complete blockage of urine flow, the bladder or urethra finally ruptures releasing urine into the body cavity and surrounding tissues. At this stage the animal may show a complete loss of appetite and stand quietly or lie down. A ruptured urethra results in a large swelling under the skin in front of the scrotum.
Phosphatic Urinary Calculi: A high phosphorus level and calcium-phosphorus imbalances promote this type of urinary calculi. Lower water consumption by animals during the winter is believed to be an important reason for the higher urinary calculi incidence associated with that season. Hard water is often blamed for the occurrence of urinary calculi. However, calcium and magnesium that constitute the "hardness" of water have been found to promote protection against phosphatic urinary calculi. The best prevention method to maintain a 2:1 to 1.2:1 calcium to phosphorus ratio.
Foot rot is not a nutritional disorder but preventative measures are available via feeding. Chemotherapeutic agents used in feed include: zinc methionine (ZinproTM), oxytetracycline, chlortetracycline. However, these products are not a replacement for keeping lots clean and dry.