Milk fever (parturient paresis or hypocalcemia) is a metabolic disorder primarily affecting high-producing dairy cattle, typically within the first 72 hours after calving. The condition is characterized by a rapid and severe drop in the cow’s blood calcium levels. This severe hypocalcemia impairs nerve and muscle function, often leading to the cow being unable to stand. The onset of lactation places an immense physiological demand on the animal, requiring a swift regulatory response to prevent sudden calcium depletion.
Understanding the Physiological Mechanism
The fundamental cause of milk fever is the failure of the cow’s homeostatic system to mobilize calcium quickly enough to meet the demand of colostrum production immediately following calving. Colostrum contains a highly concentrated amount of calcium, which rapidly drains circulating calcium from the bloodstream. The body defends against low blood calcium by secreting parathyroid hormone (PTH). PTH stimulates the bone to release stored calcium and increases dietary calcium absorption from the gut via Vitamin D activation.
This hormonal response takes time to execute, creating a lag period where blood calcium concentration plummets below a functional threshold. This failure is often exacerbated in older cows, whose ability to resorb calcium from bone diminishes with age. The resulting hypocalcemia directly affects muscle contraction and nerve signaling, leading to clinical signs of weakness and paralysis.
Addressing the Contagion Concern
Milk fever is not a contagious disease; it is a nutritional and metabolic disorder. It cannot be transmitted from one animal to another through contact or environmental exposure, unlike infectious diseases caused by viruses, bacteria, or parasites. The disorder stems entirely from a cow’s internal imbalance of calcium regulation relative to the sudden demand of milk production.
The perception of contagion may arise because multiple animals in a herd can experience milk fever simultaneously. This clustering is due to shared risk factors, such as the synchronized physiological stress of calving and uniform dietary management. When management practice or feed formulation is suboptimal, it predisposes all susceptible cows to the same metabolic failure. The simultaneous occurrence reflects common management challenges, not disease transmission.
Acute Treatment Protocols
Immediate intervention is necessary once a cow shows clinical signs of milk fever, such as tremors, unsteadiness, or the inability to rise. The standard acute treatment involves the slow, intravenous (IV) administration of a calcium solution, typically 500 milliliters of 23% calcium gluconate. This IV delivery provides a rapid influx of calcium directly into the bloodstream, quickly restoring levels needed for muscle function. The solution must be administered slowly, usually over five to ten minutes, while monitoring the cow’s heart rate to avoid cardiac complications.
If the cow is still unable to stand after a few hours, a second treatment may be administered, often utilizing a multi-mineral solution containing magnesium and phosphorus alongside calcium.
Once the cow is standing and alert, follow-up care is provided using oral calcium boluses or gels. These oral supplements are absorbed slowly and help sustain elevated calcium levels until the cow’s natural homeostatic mechanisms fully engage. Administering oral treatments only after the cow is standing prevents the risk of aspiration due to impaired swallowing reflexes.
Long-Term Dietary Prevention
Since milk fever is a predictable metabolic event, long-term prevention focuses on meticulous nutritional management during the dry period, particularly in the two to three weeks before calving. The most effective strategy involves manipulating the Dietary Cation-Anion Difference (DCAD) in the pre-calving diet. DCAD measures the balance between positively charged ions (cations like potassium and sodium) and negatively charged ions (anions like chloride and sulfur) in the feed.
The goal is to formulate a diet with a negative DCAD by adding anionic salts, such as ammonium chloride or magnesium sulfate, to the ration. A negative DCAD induces a mild, compensated metabolic acidosis, priming the body to mobilize calcium effectively. This slight acidification increases the responsiveness of tissues to parathyroid hormone, allowing the cow to efficiently draw calcium from bone and increase intestinal absorption once calving occurs.
To ensure the anionic diet is working, the urine pH of the pre-calving cows must be monitored regularly. A successful negative DCAD diet should lower the urine pH into a target range, typically between 6.2 and 6.8 for Holsteins, or 5.8 to 6.3 for Jerseys. If the urine pH remains high (above 7.0), the diet is not acidic enough, and more anionic salts may be needed. This proactive nutritional approach, implemented for 10 to 21 days before calving, significantly reduces the incidence of milk fever by preparing the cow’s system for the massive calcium drain of lactation.