KETOSIS IN A FRESHENED DAIRY COW


You are called out to a small dairy operation in Central Virginia to examine five of the operator's cows out of a herd of 60 head.  The cows freshened about two weeks ago and are now back in the business of producing milk.  The operator has called you in because he expects his production to be in the neighborhood of 60 pounds of milk per day per cow, but these five cows have been putting out less and less for the past five days. Furthermore, they've been losing condition in spite of eating their ration. Just today, three of the smaller ones started to tremble and stumble around when brought to the parlor for milking. The entire herd is up-to-date on vaccinations, including rabies, they all eat the same rations, they're all pastured on the same ground, and housed in the same barn.

A physical examination shows you that the five cows you're there to see are thinner than the ones producing normally.  All of them seem depressed, and the smallest ones, are camped in and look unsteady on their feet.  One is noted head-pressing in the corner of her pen.  You notice a strong acetone odor on the breath of the three cows who seem the most affected. You have a pretty good idea what this might be so you take a urine sample for a quick confirmation.  You also take a small blood sample to test its glucose level.


DIAGNOSIS

These five cows have developed ketosis, a ruminant metabolic disorder that often affects high producing dairy cows (bovine ketosis) and ewes in late pregnancy (pregnancy toxemia).  It typically affects dairy cows in negative energy balance during periods of high milk.  Ewes are most commonly affected in the days prior to parturition and when they're carrying twins or triplets.  (In case of multiple pregnancies the energy demands of the fetuses cause metabolic derangements in the mother.)

The most common etiology of ketosis in both cattle and sheep is fairly straightforward: high demand for energy depletes the body's supply of free and stored glucose, dietary intake can't keep pace with demand, and the body begins to use fatty acids and ketone bodies as its fuel source. 

Lipolysis depletes the body's fat stores and results in rapid loss of body condition, particularly in cattle.  Further, mobilization of lipids leads to accumulation and metabolism of free fatty acids in the liver, often resulting in excessive retention of lipid by the hepatocytes (fatty degeneration). Hepatic insufficiency secondary to the degeneration can lead to a spiral of more metabolic derangements. Ketosis presents in two major forms, wasting and nervous

The wasting form involves mobilization of fat stores and loss of body condition. The nervous form involves the effects of ketones on the central nervous system. The presence of high levels of ketones leads to trembling, ataxia, and erratic behavior. 

Ketosis is further classified according to its root cause and by its clinical presentation; in cattle they're classified as follows:

1. Primary ketosis

This form is seen in cattle with high body condition on good quality feed.  In this case, the cows are eating but are not meeting their energy demands and a negative energy balance results.  High protein content, low digestibility, insufficient dry matter intake, and genetic predisposition are all factors in this form of ketosis.

2. Secondary ketosis

In this case, the cows are not eating well due to another disease or condition that prevents them from meeting their intake requirements.  Ulcers, a displaced abomasum, mastitis, or other painful conditions can all can put a cow off feed during a period of high demand, resulting in ketosis.

3. Starvation ketosis

Cattle in poor condition on poor quality feed simply can't energy demands through diet, so the cow mobilizes what little fat she has to meet her needs.

Ketosis may also result from specific nutritional deficiencies or high butyrate levels in silage.


Sheep experience similar forms of ketosis but they will typically show clinical signs in late pregnancy, not in early lactation.  The classifications used for sheep are as follows:

1. Primary pregnancy toxemia

Ewes typically experience a decrease in feed intake in the last two months of pregnancy, putting them at risk of negative energy balance.  If these sheep are stressed at this stage (by shearing, crutching, or transportation), the result may be the onset of ketosis.  Sheep with decreased liver function are also at higher risk for the disorder.

2. Secondary pregnancy toxemia

As with cattle, this is a condition caused by a separate disease that causes the ewe to go off feed, resulting in negative energy balance.

3. "Fat ewe" pregnancy toxemia

In this case, the ketosis is caused by a decrease in feed intake due to excess intra-abdominal fat compressing the rumen.  The ewe can't consume enough to maintain its body weight and negative energy balance results.


This low power image shows a field of hepatocytes that are heavily infiltrated with lipid. As you can tell from the higher-magnification image, things are much worse than in the relatively mild case of Willow the obese cat. The hepatocytes are so distended that their cytoplasm is barely visible, forced to the margins of the cell membranes by the sheer volume of fat within the cells. The normal, regular architecture of the liver has been so badly distorted that the venous and biliary supply has almost certainly been compromised.

The lipid inclusions of some hepatocytes are sequestered in several small vacuoles. This allows staining of cytoplasm between the vacuoles, lending a "webby" appearance to the tissue. This sample is so completely infiltrated with fat that at first glance it resembles a field of brown fat more than it does liver!

The dark, basophilic "dots" are the nuclei of the hepatocytes, displaced to the margins of the more distended cells, giving an appearance similar to an adipocyte's "signet ring." Cells that are not as fully infiltrated have a cloudy appearance where their multiple vacuoles overlap.

If this sort of damage is extensive and prolonged, hepatocytes begin to die. Necrotic cells become an inflammatory stimulus and hepatitis and cirrhosis (scarring) will result. The liver function can be compromised to the point of causing total liver failure, which means death.

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