Transition Cow Diseases

Luciano Caixeta, DVM PhD

College of Veterinary Medicine, University of Minnesota

Summary

1. Recognize and understand the pathogenesis of the most common transition cow diseases.
2. Be able to explain at a level understandable by a non-technical person how transition cow diseases occur and how to prevent it.
3. Design treatment and monitoring protocols for the most common transition cow diseases.

Introduction

The transition from late gestation to early lactation is an extremely challenging period for the modern dairy cow because of the rapid increase in energy and mineral demands for fetal growth, and colostrum and milk production. The pursuit of a more efficient production system led the dairy industry to prioritize selection for milk yield over other traits, exacerbating those metabolic problems faced by dairy cows. As a consequence, dairy cows are at greatest risk of developing diseases and involuntary culling during the periparturient period. Therefore, a good understanding of the metabolic challenges faced by dairy cows and their physiological adaptations is important to a dairy veterinarian in order to design and implement management strategies to control and prevent metabolic diseases during the periparturient period.

Content

Hypocalcemia (Milk Fever)

What is it?

Hypocalcemia, also known as Milk Fever or Parturient Paresis, is a disease that causes acute to peracute flaccid paralysis. The disease is caused by low blood calcium concentrations and occurs mainly in recently mature (3+) cows with 1-3 days of calving. Clinical disease incidence is around 1% while subclinical cases are more frequent with incidence estimates ranging from 25-73%.

How to recognize it?

Hypocalcemia is usually seen within 72 hours of parturition and has 3 stages. Stage 1 is often unobserved and lasts approximately an hour. The cow will still be ambulatory but show signs of hypersensitivity, restlessness, and excitability. She will be mildly ataxic, have muscle tremors, tachycardia, open mouthed breathing, may bellow, and may not urinate or defecate. Stage 2 lasts 1 to 12 hours and is characterized by sternal recumbency as the cow cannot stand due to flaccid paralysis. She will be depressed, dull, lethargic, have tachycardia and weak heart sounds, decreased rumen contractions, bloat due to abomasal and GI hypomotility, decreased temperature, cold extremities, and a lateral, “S” shaped kink in the neck. Stage 3 is the most serious as a cow will die if not treated within a few hours. The cow will have a loss of consciousness progressing to coma, be unable to maintain sternal recumbency, have extreme muscle flaccidity and severe bloat, a rapid weak heartbeat, no peripheral pulses, cold extremities, and no response to stimuli.

Pathogenesis

Hypocalcemia is caused by acute calcium deficiency. During the periparturient period, a sudden increase in calcium demands due to colostrum and milk production as well as the accelerated fetal growth cause a rapid decrease in blood calcium levels. Normally, parathyroid hormone is released to increase renal calcium absorption, bone resorption, and kidney vitamin D synthesis (which in turn increases calcium absorption in the gastro-intestinal tract). All these adaptations are necessary to maintain blood calcium homeostasis around parturition. When these metabolic adaptations fail, or are not as extensive as necessary, blood calcium levels decrease and dairy cows show signs of hypocalcemia.

How to treat?

Milk fever cases should be treated with 500 mL of 23% calcium gluconate IV and followed by the administration of 2 oral calcium bolus given 12 hours apart. It is important to emphasize that oral calcium bolus should not be administered if cows do not respond to the calcium IV treatment. In milk fever cows, failing to raise after treatment with IV calcium is a signal that normal muscular function has not been reestablished and cows may choke on the calcium bolus if treatment is given to cows while they are still down.

Contrary to the milk fever cases, supplementation with i.v. calcium to dairy cows with subclinical hypocalcemia is not recommended. A team of researchers in California demonstrated that i.v. supplementation of calcium to dairy cows with subclinical hypocalcemia determined a long term decrease in blood calcium concentration. In these animals, blood calcium concentration reached levels even lower than their baseline 6 hours after treatment. Moreover, blood calcium concentration remained lower than the levels measured in cows that did not receive any IV calcium. Since dairy cows with subclinical hypocalcemia do not show clinical signs and cow-side measurements of blood calcium concentrations are cost prohibitive, subclinical hypocalcemia is rarely diagnosed in commercial farms. Despite that, the prophylactic administration of 2 oral calcium bolus (first bolus immediately after calving and second bolus 12 hours later) to lame and high producing cows (lactation > 2) contributes to minimize the risk of the development of milk fever. It has been established that the administration of calcium bolus to these groups of cows (approximately 51% of the animals in an average dairy in the United States) can determine a return on investment of 180% ($1.80 of return for each $1.00 invested).

Decision tree for the treatment of dairy cows with hypocalcemia during early lactation.

Prevention

Hypocalcemia can be prevented at the herd level by feeding a negative Dietary Cation-Anion Difference (DCAD) diet during the close-up dry period. This diet will cause compensated metabolic acidosis which allows the tight binding of parathyroid hormone to receptors, making the cow more responsive to the parathyroid hormone and preventing milk fever. A negative DCAD diet can be achieved by reducing potassium levels in the diet by reducing the amount of alfalfa silage fed and replacing it with low potassium forages such as corn silage or straw or by adding anionic salts. Cows can also be given a low calcium diet during the pre-partum period to prevent hypocalcemia, however, this strategy is very hard to accomplish because of the calcium content of forages. Lately, the use of mineral binding feed additives (i.e., synthetic zeolite A)  have been investigated. This feed additive is capable of adsorbing dietary calcium (and other cations and some anions) making it unavailable for absorption which in turn trigger metabolic adaptations to shift calcium metabolism to elevate circulating calcium concentrations. In high-risk individuals hypocalcemia can be prevented by a prophylactic treatment of calcium given subcutaneously or orally at calving and again 12 hours later (as mentioned in “how to treat'' section).

Hyperketonemia

What is it?

Hyperketonemia (also known as ketosis and/or subclinical ketosis) happens when the levels of ketone bodies in the blood are elevated. The disease is associated with decreased reproductive performance and other periparturient diseases such as hepatic lipidosis, displaced abomasum, metritis, and hypocalcemia. Hyperketonemia is most common in the first 6 weeks postpartum, with a higher incidence in older and obese cows.

How to recognize it?

Clinical signs include decreased appetite, depression, and decreased production. To diagnose the disease ketone bodies can be tested in blood, urine, or milk. Blood β-hydroxybutyrate (BHB) is the least volatile ketone body and is a useful measurement. For disease diagnosis and herd screening programs a cut-off of >1.2 mmol/L is commonly used.

Pathogenesis

The pathogenesis of hyperketonemia is not entirely understood. It is thought that low blood glucose is caused by the increased energy demand for milk production in early lactation (negative energy balance) that results in fat mobilization. Lipids are mobilized from adipose tissue and higher concentrations of circulating non-esterified fatty acids (NEFA) are detected in dairy cows during early lactation. Circulating NEFA can be used by various tissues as energy source and, as a source of preformed fatty acids by mammary gland, thus, the higher concentration of fat in milk of early lactation animals.  Nonetheless the majority of the circulating NEFA, approximately 25%, is taken up by the liver where it can be completely oxidized in the tricarboxylic acid cycle to produce ATP or partially oxidized to ketone bodies that can be used as energy source by extrahepatic tissues. NEFA taken in excess of liver oxidative capacity are repackaged into TG which are then exported at inherently low rates as very low density lipoprotein or stored in the liver leading to the occurrence of fatty liver.

Fates of mobilized fatty acids in the dairy cow.

How to treat?

Treatment for hyperketonemia consists of 300 mL propylene glycol given orally once daily for 3-5 days. This serves as a glucose precursor to shift metabolism away from lipid oxidation. If hyperketonemia is secondary to another disease that must also be addressed. A small minority of cases will present with neurologic signs (referred to as “nervous ketosis”). These should be treated additionally with a one-time bolus of 500 mL 50% dextrose solution intravenously.

Prevention

Prevention for hyperketonemia revolves around the proper management (nutritional and environmental) of animals around the transition period. This includes strategies such as low energy/high forage dry cow diets and managing stress-inducing factors (i.e. overcrowding) to promote feed intake. Additionally, excessively fat or thin animals should be avoided. Ionophores such as monensin fed to dry and milking cows in a premix are also effective by shifting rumen fermentation to favor propionate production.

Displaced Abomasum

What is it?

The abomasum, a component of the ruminant digestive tract, typically lies on the abdomen floor, just to the right of midline. A displaced abomasum (DA) has shifted to the left or right side, to the left is more common. While this disease can occur in any ruminant at any time, it is almost exclusively seen in dairy cows post-calving.

How to recognize it?

The most common symptoms of DA are decreased appetite and milk production in cows that have recently calved. Cows with a left displaced abomasum (LDA) may appear to have the last three ribs on their left flank “sprung out.” Diagnosis is done by auscultating pings over the displacement area (the line from tuber coxae to the point of the elbow)

Pathogenesis

The abomasum is loosely suspended by the greater and lesser omentum. This suspension allows displacement when abomasal atony, excessive production, and accumulation of gas occurs. There is no definite cause of DA, as it is a multifactorial disease with factors such as decreased dry matter intake, high concentrate diets, hyperketonemia, hypocalcemia, deep chestedness, and parturient changes in organ structure all playing a role in causing the disease.

Displaced abomasum is a multifactorial disease

How to treat?

Treatment of a DA can be conservative or surgical. Conservative treatment consists of rolling the cow to manipulate the abomasum back into position. With rolling alone there is a high recurrence, so a percutaneous, blind suture can be used to affix the abomasum to the body wall after it is in position. Surgical treatment using a variety of approaches consisting of placing the abomasum in the correct position, and suturing it to the body wall. Some of the approaches require deflating the abomasum.  

Prevention

The best prevention is to minimize risk factors, especially around parturition. It is important to minimize/promptly treat hypocalcemia, hyperketonemia, and other concurrent diseases such as metritis. Furthermore avoiding rapid and large dietary changes, feeding inconsistency, and maintaining adequate roughage in the diet are important in combination with ensuring a rapid increase in rumen volume after calving

Sub Acute Ruminal Acidosis

What is it?

Subacute Ruminal Acidosis or SARA is a ruminal fermentation disorder leading to an extended period with decreased ruminal pH (< 5.5). SARA is usually a consequence of excessive readily fermentable carbohydrates (large amounts of grain) in the diet leading to an excessive production of volatile fatty acids (VFA) in the rumen. SARA is a subtle condition in high-producing dairy herds leading to economic losses.

How to recognize it?

Measuring ruminal fluid pH can be used as a diagnostic test for the diagnosis of SARA, however, the time of day and the day to day variation of ruminal pH hinders the use of this strategy for the diagnosis of SARA. Although not practical, methods capable of monitoring ruminal pH continuously for several days would be capable of diagnosing SARA. Dairy cows do not show specific clinical signs of SARA with decreased dry matter intake and reduced milk production being two common signs of SARA. Additionally, dairy cows experiencing SARA will have reduced milk fat (< 3.2%), reduced rumination, decreased body condition score (even if intake is normal), and unexplained diarrhea. SARA has also been associated with caudal vena cava syndrome and the observation of liver abscesses in post-mortem exams. SARA is usually diagnosed at a herd level rather than at a cow level.

Pathogenesis

SARA is caused by the ingestion of diets with high concentrations of rapidly fermentable carbohydrate or insufficient effective fiber. Such diets lead to an excessive production of VFAs that can overwhelm the ability of the ruminal papillae to absorb these acids. As a consequence, this VFA accumulates in the rumen reducing ruminal pH. Once ruminal pH drops below 5.6, VFAs shift to its undissociated form facilitating the absorption of VFA across the ruminal epithelium. Lactate levels in the ruminal fluid are usually not increased in cattle with SARA. 

How to treat?

No specific treatment as ruminal acidosis is not usually detected at the time of depressed ruminal pH.

Prevention

Since treatment is difficult the main goal is prevention. Diet formulation and feed bunk management are essential in the prevention of SARA. Avoiding abrupt introduction of fresh cows to high concentrate diets will enable the ruminal bacterial population and ruminal papillae to adapt  in order to digest and absorb VFA. Additionally, the feeding of adequate effective fiber will stimulate rumination and the production of saliva buffering ruminal pH. It is important to point out that the incorporation of long fiber can lead to more cases of SARA if the forage particles are long enough to allow for sorting. Feeding a total mixed ration lowers the risk of SARA because it decreases the chances of a large grain meal. Providing a free-choice buffer as a supplemental source of buffer to the buffer already contained in the diet is beneficial to individual cows.

Metritis

What is it?

Metritis is one of the most common diseases of dairy cows postpartum. Metritis the inflammation of the uterus as a response to a bacterial infection.  Prevalence of metritis on farms range from 8%-40% with an average prevalence in US herds around 20%. Uterine diseases have been reported to cost over $650 million annually to the dairy industry in the United States.

How to recognize it?

Metritis is recognized based on the identifical of clinical signs during physical examination of fresh cows. The primary signs of metritis are enlarged and flaccid uterus with fetid and watery red-brownish discharge during the first 21 days in milk. Non-specific signs associated with metritis cases include depressed attitude and decreased feed intake. Although common, up to 80% of the cows with metritis do not have fever.

Pathogenesis

Dairy cows have anatomical barriers preventing uterine contamination with environmental bacteria, however, around parturition the birth canal dilates enabling the invasion of bacteria ascending from the environment and animal’s skin and feces. Recent culture-independent studies demonstrated that aerobic and anaerobic bacteria are present in the uterine lumen of all cows immediately after parturition. Escherichia coli, Trueperella pyogenes, Bacteroides spp, and Fusobacterium necrophorum, especially strains possessing specific virulence factors, have been described as the main pathogens initiating and sustaining postpartum uterine contamination and disease. Although the etiology of uterine diseases is mainly attributed to bacterial infection, bacterial contamination alone is not sufficient for the development of metritis. Reduced immune function and impaired regulation of inflammation are components in the pathogenesis of uterine diseases. The metabolic changes preceding parturition result in a systemic immunosuppression in dairy cows around calving. This weak immune response and failure to clear bacterial infection in a timely manner is associated with the development of uterine disease. Additionally, suboptimal inflammatory responses are problematic with physiologic and pathologic inflammation of the uterus being different in magnitude, regulation, duration and timing.

How to treat?

Metritis usually responds to systemic administration of antimicrobials with or without non-steroid anti-inflammatory drugs. Supportive therapy is also helpful. Cephalosporin and penicillin are the antibiotics appropriate for systemic treatment because they are active against the common pathogens causing metritis and reach therapeutic levels in the uterus. Intrauterine administration (uterine infusion) of antibiotics is not recommended.

Prevention

The goal of prevention is to minimize risk factors. This is accomplished by 2 key management areas. First is maintaining good hygiene, always providing dry and clean bedding at calving. The second measurement to prevent uterine diseases is to minimize negative energy balance and stress are crucial. To minimize stress avoid pen moves, segregate animals by lactation group (generally most important to have 1st lactation cows separated from 2nd and greater lactation), avoid overcrowding (especially in close- up cow and fresh cow areas), and monitor and improve cow comfort.

Retained Placenta

What is it?

Retained placenta or RP is defined as the failure of expulsion of fetal membranes by 24 hours after parturition. Incidence ranges between 5% to 15%. Incidence of RP is higher in older animals. Risk factors include abortion, stillbirth, multiple birth, dystocia, and uterine torsion. RP is also associated with infectious disease, heat stress, hypocalcemia and with induced parturition. Cows with retained placenta are more likely to developer of postpartum diseases (i.e., metritis, ketosis, mastitis, etc.).

How to recognize it?

Diagnosis is accomplished by visualization of discolored, fetid membranes hanging from the vulva > 24 hours after parturition. In some cases retained fetal membranes remain within the uterus and vagina and cannot be easily observed without a thorough examination. In these cases, RP might be confused with metritis because of the presence of a foul-smelling discharge.

Pathogenesis

Retained placenta occurs when there is a decrease in neutrophil function ultimately delaying or blunting the immune response necessary to promote the detachment of the cotyledon from the caruncles in the uterus. In summary, the detachment of the placenta from the uterus is driven by the cow's immunological response and not by uterine motility.

How to treat?

There is no specific treatment for retained placentas. Untreated cows will expel membranes between 2 and 11 days. Manual removal of retained fetal membranes is NOT recommended and might be harmful. Treatment with gonadotropin-releasing hormone (GnRH), prostaglandin F2 alpha, and oxytocin does not improve placental release. Intrauterine infusion of antibiotics does not increase cure rate and antibiotics residues can be detected in milk.

Prevention

Like other transition disorders dry matter intake and stress mitigation play a critical role in preventing retained placenta. Stress reduction is accomplished by many factors, but starting with reduction in group size and improved cow comfort. Nutritional strategies to ensure adequate immune response around parturition can be helpful. Supplementation of vitamin E, selenium, beta carotene, and monensin has been found to have a positive effect.

Monitoring

When monitoring the transition period, choosing the correct monitoring measures for each area of management is paramount. In order to monitor the transition period, the following broad areas can be used as a guideline: dairy herd general information (e.g., stocking density, cow comfort, body condition scoring [BCS]), milk production during early lactation, fresh cow health and events (e.g., disease incidence and prevalence, death and culling), and feeds and feeding (i.e., feeding management). A check-list for monitoring factors associated with health and performance of transition dairy cows based on these four general areas is presented below

.

1. Dairy herd cow comfort

• Appropriate stocking density
• Bunk Space
• Access to water
• Stall design
• Comfortable and sanitary bedding material
• Heat abatement

2. Milk production in early lactation

• “Problem cows”
• Early lactation milk production

• Peak, 1st 305ME, week 4 milk

2. Fresh cow health and events

• Diseases incidence
• Death and culling within 30-60 days in milk

4. Feeds and feeding

• Routine comprehensive total mixed ration audits
• “Test-and-treat” strategy to monitor hyperketonemia in fresh cows
• Monitoring of urine pH if using anionic salts

Additional Resources

• Caixeta and Omontese - MONITORING AND IMPROVING HEALTH FROM DRY-OFF TO PR.pdf.
• Caixeta, L.S., J.A. Herman, G.W. Johnson, and J.A.A. McArt. 2018. Herd-Level Monitoring and Prevention of Displaced Abomasum in Dairy Cattle. Veterinary Clinics of North America: Food Animal Practice 34:83–99. doi:10.1016/j.cvfa.2017.10.002.
• Gilbert, R.O. 2016. Management of Reproductive Disease in Dairy Cows. Veterinary Clinics of North America: Food Animal Practice 32:387–410. doi:10.1016/j.cvfa.2016.01.009.
• McArt, J.A.A., and R.C. Neves. 2020. Association of transient, persistent, or delayed subclinical hypocalcemia with early lactation disease, removal, and milk yield in Holstein cows. Journal of Dairy Science 103:690–701. doi:10.3168/jds.2019-17191.
• Oetzel, G.R. 2017. Diagnosis and Management of Subacute Ruminal Acidosis in Dairy Herds. Veterinary Clinics of North America: Food Animal Practice 33:463–480. doi:10.1016/j.cvfa.2017.06.004.
• Ospina, P.A., J.A. McArt, T.R. Overton, T. Stokol, and D.V. Nydam. 2013. Using Nonesterified Fatty Acids and β-Hydroxybutyrate Concentrations During the Transition Period for Herd-Level Monitoring of Increased Risk of Disease and Decreased Reproductive and Milking Performance. Veterinary Clinics of North America: Food Animal Practice 29:387–412. doi:10.1016/j.cvfa.2013.04.003.