| This form of laminitis is of considerable economic importance to the dairy industry as it predisposes mature cows to sole and toe ulcer, white line disease, and double sole. It has been seen in dairy cows in most developed countries and is of greatest concern in intensively managed herds. |
| Etiology: |
| The classic hypothesis for the etiology of laminitis in cattle is comparable to that of laminitis in horses (
Laminitis: Overview). High levels of carbohydrate in the rumen invoke an increase of
Streptococcus
bovis
and
Lactobacillus
spp
, which in turn lead to a state of acidosis in the rumen. It is further hypothesized that this environment is unfavorable for gram-negative organisms and, as they die, vasoactive endotoxins are released. Rumenitis is frequently associated with ruminal acidosis and a high incidence of liver abscesses. High levels of histamine in the blood have been found in the early stages of the disease. Fiber and the frequency of feeding are extremely important factors. |
| A second hypothesis involves the receptors for epidermal growth factor (EGF) that are present in the corium of the claw. Because EGF is liberated in large quantities from the GI tract that has been damaged, it could be involved in the pathogenesis of laminitis. In addition to its mitogenic effect, EGF can inhibit the differentiation of keratinocytes in vitro. Inhibited differentiation of keratinocytes of the hoof matrix is a dominant morphologic feature in the early stages of
laminitis. This hypothesis might account for the irregularities in horn production that are seen in some cases of laminitis. |
| Recent investigations have studied the role of matrix metalloproteinase activity in the pathophysiology of laminitis. The results support the hypothesis that laminitis histopathology results from an inadequate regulation of gelatinase activity, resulting in selective degradation of basement membrane components, leading to laminitis due to failure of the basement membrane-epidermis attachment. |
| In cattle, nutritional mismanagement leading to acute acidosis is still considered to be the primary cause of the condition. However, stress arising from the effects of other risk factors causes variations in the signs of the disease and must be considered when devising control protocols. |
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| Pathogenesis: |
| The pathophysiologic process causing laminitis may be summarized as a toxic influence on capillary walls that results in insufficient nutrient supply to the keratin-producing cells and synthesis of structurally incompetent keratin. It is believed that when vasoactive toxins reach the corium, the arteriovenous shunts are paralyzed. Pressure inside the claw rises, and the vessels are damaged, which allows blood or blood fluids to escape and soak into the horn claw staining it
either pink or yellow. Hemorrhagic staining of the horn tubules of the sole give a “brush mark” appearance. Increased blood pressure inside the claw (intraungular pressure) and the associated reduced blood flow is usually followed by thrombus formation. This is a characteristic feature of laminitis. Thrombi form as fine layers inside the walls (mural thrombi) of the vessels. Because of reduced blood flow, fewer nutrients reach horn-producing tissues, and horn quality
deteriorates. The blood vessels can eventually become completely blocked, causing ischemic changes followed by scar tissue formation. |
| Frequently, young animals appear to recover from laminitis. This may be because new blood vessels develop to form collateral circulation and take over the function of those that have been damaged. Nevertheless, each time an animal has a bout of laminitis, more scar tissue is formed and the animal is less able to recover from the next insult. |
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| Clinical Findings: |
| Some animals appear to walk in a deliberate, careful manner. Hemorrhages in the sole and/or white line are consistent findings but they are not present until several weeks after the start of the nutritional insult. In the long term, the appearance of sole and toe ulcers, white line disease, and double sole confirm the suspicion that subclinical laminitis is present. If the annual incidence of these diseases collectively exceeds 10% in the multiparous cows in a herd, it may be
assumed that subclinical laminitis exists. |
| Erythema and edema (puffy heel) of the skin above the coronary band and around the dewclaws in freshly calved cows may be an indication that a transitory laminitis-like insult is occurring. A prevalence of 10% is probably an indication that the cows are being introduced to concentrate too rapidly. |
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| Treatment and Control: |
| Treatment for subclinical laminitis is impractical because diagnosis in an individual animal is not possible at the time of the causative insult(s). Control depends on epidemiologic study (to determine the age of animals most severely affected and the time when the main insults are occurring) and on minimizing environmental risk factors that exacerbate the disease. The most important risk factors are: 1) The quantity and digestibility of the carbohydrate being fed—some
carbohydrates, eg, barley and wheat, are more digestible than others, eg, corn (maize). Finely ground or moist grains are more digestible than dry, cracked grain. 2) Changes in diet—slug feeding once a day is contraindicated, and the more frequently concentrates are fed the better. Sudden changes in the diet or formulation of the diet are extremely dangerous. Component-fed cows should be given ≤7.5% of their body wt in concentrates around calving. After calving, it is
safest if rations are not increased by more than 0.25 kg/day for multiparous cows and by 0.20 kg/day for primiparous cows to a maximum of 14-16 kg (30-36 lbs). 3) The quality and quantity of fiber fed—this is probably more important than the carbohydrate component of the diet. If the carbohydrate:fiber ratio is >50% carbohydrate, the animal is increasingly at risk of rumenal acidosis. If the percentage of acid detergent fiber for the complete ration is <20%, risk of
ruminal acidosis also increases. If the particle length of silage is cut too short (25% cut <5 cm long), the contribution of effective fiber is reduced. If corn silage is fed, considerable care must be taken to ensure that the energy level derived from the silage is not underestimated. The energy level varies according to stage of growth when the corn was harvested and mode of conservation. The manure should not contain fiber particles >1 cm or undigested grain. Feces
should not contain mucin/fibrin casts, be foamy, or contain gas bubbles. The feces in the same feeding group should not vary from firm to diarrhea. 4) The Cow Comfort Index (CCI)—this is measured 1 hr before milking as the proportion of animals standing. If the CCI is >20%, risk factors affecting cow comfort should be reviewed. These include stall size, adequacy of bedding and bunk space, placement of water sources, and alley widths sufficient to avoid congestion or
queuing. Time spent ruminating should be normal; rumen stasis and hypermotility should not be detectable. 5) Lack of producer knowledge and skill—a producer is 2.5 times more likely to underestimate the incidence of lameness in a herd than a skilled observer. It is critical that producers learn to recognize the major lesions and characteristics of diseases that cause lameness and keep accurate records of the incidence and causes of lameness. 6) The availability of
micronutrients from forage or pasture—this should be evaluated in herds with a lameness problem. Some minerals may be available only at marginal levels. The presence of high levels of sulfates or iron in the drinking water antagonizes the absorption of some micronutrients. 7) The level of protein, fiber, and energy content of pasture grasses—these vary considerably depending on the species of grass, the stage of its maturity, ambient temperature, and rainfall. Sudden
changes in nutrient intake are seen when cattle are introduced to fresh pasture, particularly when rotational grazing is practiced. These changes can result in grass founder. Particular attention should be paid when changing from a housing system to a pastoral system and vice versa. |
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