Approximately 15% to 40% of beef cows have intramammary infection in one or more mammary glands in most surveys.493-495 Coagulase-negative staphylococci are the predominant isolates, but Staphylococcus aureus is found in 7% to 10% of samples. Streptococci and corynebacteria are isolated occasionally, as are gram-negative bacteria. Milk from infected glands has significantly higher SCC than milk from uninfected glands,493 but somatic cell counting is not usually performed in beef herds. Clinical mastitis occurs sporadically and is diagnosed and treated as for dairy cows when economically feasible; most mild clinical mastitis cases probably go unrecognized.
The prevalence and etiologic agents of intramammary infection in prepartum beef heifers are similar to those in lactating beef cows.493,496 In contrast to dairy cattle, clostridia are the predominant bacteria found in the teat canal of beef cattle, followed by Bacillus species and staphylococci.497
Several modes of mastitis transmission have been proposed for beef cattle. Flies are believed to serve as vectors for staphylococci. This may explain the higher prevalence of intramammary infection in the front glands of beef heifers than the rear glands, because flies on the front glands are less accessible by the tail. Fly-induced scabs on the teats of beef heifers have been shown to harbor staphylococci.493 Calves may also serve as vectors by transmitting oropharyngeal organisms to the teats or carrying bacteria-laden milk from teat to teat. Unsanitary housing conditions probably increase the risk of infection with environmental pathogens.498 As with dairy cows, poor udder conformation and teat injuries may predispose to mastitis.
Several studies have demonstrated numeric or significant decreases (up to 40 kg) in weaning weights of calves from beef cows with subclinical mastitis.493-495 This probably results from reduced milk production. The adverse effect on weaning weight appears to increase with the number of infected glands.494 In most cases the cost associated with reduced weaning weight is unlikely to justify antibiotic treatment. Selective intramammary antibiotic treatment at weaning based on CMT reaction has been suggested, but CMT score is unlikely to be an accurate predictor of infection. Sanitary housing conditions, appropriate stocking density, and good fly control should help minimize mastitis risk in beef cattle.
Mastitis is an uncommon problem in horses, partly because of the small size and inguinal location of the udder, which minimizes exposure to environmental pathogens. Little research has been done on the prevalence of subclinical mastitis in horses, but it is not recognized to be a serious problem. In one study, no pathogens were grown from the milk of 11 mares sampled repeatedly during the first 2 months of lactation, and average SCC was less than 50,000/mL at most sampling times.499
Clinical mastitis occurs sporadically in lactating and nonlactating mares; signs range from mild to severe. The most common clinical mastitis pathogen is Streptococcus zooepidemicus, but a variety of aerobic bacteria have been isolated from the milk of affected mares.5,500 In a retrospective study of 28 cases, gram-negative bacteria (coliform bacteria, Pseudomonas, Actinobacillus, Pasteurella) were isolated from 42% of milk samples.5 Streptococci and staphylococci constituted most of the gram-positive isolates. Rarely, mastitis is caused by nonbacterial pathogens. For example, one mare developed unilateral mastitis as a component of disseminated coccidioidomycosis.501 Verminous mastitis has even been reported.502
Clinical signs of mastitis in horses include an enlarged, firm, warm, painful mammary gland and edema of the udder and surrounding tissues. The mare resists milking, and secretions are abnormal in appearance (color, viscosity, consistency). About half of all mares with clinical mastitis are systemically ill, with signs such as fever, tachycardia, tachypnea, anorexia, depression, or agalactia. The mare may be reluctant to move or may adopt an abnormal gait to minimize contact between the hindlimb and the painful gland. Sedation or anesthesia is necessary to achieve a thorough examination of the udder and collection of milk in some horses.500
Culturing of the milk is required to identify definitively the causative pathogen of equine mastitis and confirm that antibiotic selection is appropriate. However, bacteria can often be observed on cytologic examination of the milk.5,503 A differential diagnosis for a firm, enlarged, painful mammary gland is adenocarcinoma, particularly if the udder skin is ulcerated and the secretion is serosanguineous.504 With adenocarcinoma, neoplastic cells may be seen during cytologic examination of the secretion, or a mammary biopsy may be required. Because bacterial mastitis and adenocarcinoma can occur simultaneously, it is important to reevaluate mares that do not respond as expected to antibiotic treatment. A differential diagnosis for agalactia in mares is fescue toxicosis. With fescue toxicosis, the udder is not inflamed, and mares may sweat profusely, have prolonged gestation, or give birth to weak or dysmature foals.505
Treatment of bacterial mastitis in horses consists of intramammary and systemic antibiotics to combat infection; NSAIDs to reduce pain, inflammation, and fever; and fluids to correct dehydration. Hot packing, hydrotherapy, and frequent stripping of the affected gland are empirically justified supportive measures but may be difficult to accomplish. Furosemide can be administered if edema is substantial.
Broad-spectrum antibiotics should be given until results of cytologic examination or culture of the milk are available. Potentiated sulfonamides, or a combination of penicillin and an aminoglycoside, are reasonable systemic antibiotic choices. Because no antibiotics are labeled for intramammary administration in horses in the United States, intramammary infusion products for cattle are used. Infusion products containing ceftiofur, cephapirin, amoxicillin, or hetacillin are appropriate until the cause of the mastitis is determined. A commercial intramammary infusion product is preferable to a homemade solution because the latter carries a greater risk of unintentional contamination. Intramammary infusion of antibiotics can be difficult to accomplish in horses because of the small size of the teat orifice and the presence of two distinct lobes within each udder half. One or both lobes can be infected, so antibiotics must be directed appropriately. Antibiotic treatment should be continued for at least 5 days to avoid relapse.
The prognosis for survival of horses with bacterial mastitis is good; however, milk production may be transiently or permanently reduced. Fortunately, mastitis is usually unilateral, and recurrence is rare.5 Most mares respond rapidly to antibiotic treatment. Although spontaneous recovery is possible, it is unethical to withhold treatment from a mare that is ill or in discomfort. The prognosis for mammary adenocarcinoma is poor, even with surgical removal of the affected mammary gland(s) and local lymph nodes, because of the high rate of metastasis.504
As with the horse, the udder of South American camelids (SACs) is nonpendulous, has small teats, and is protected from trauma and environmental contamination by its caudal location. Because they are not reared for milk production, SACs are spared the contagious mastitis risks associated with hand or machine milking. Therefore, it is not surprising that the prevalence of mastitis is low. In a survey of 100 llamas, potential mastitis pathogens were isolated from 21% of mammary glands, with 57% of llamas having at least one infected gland; the majority of isolates were coagulase-negative staphylococci.506 However, isolation of an organism was not associated with an increase in SCC, CMT score, NAGase activity, or pH, which indicates that the organisms were not causing mastitis. None of the llamas exhibited signs of clinical mastitis, and 88% had a CMT score of 0 (negative). The SCC (direct microscopic count) was 300,000/mL or less in all cases. Therefore, CMT and SCC scores for healthy llamas are much lower than for healthy sheep and goats. Low SCC values were also found when milk from 10 llamas was tested weekly for the first 27 weeks of lactation.507 The NAGase activity and lactoferrin concentration in llama milk is higher than in sheep or cow milk, which may help protect against infection.508
Despite a low prevalence of subclinical mastitis, llamas occasionally experience episodes of acute clinical mastitis,509 most often after birthing. Treatment includes systemic and local antibiotics and antiinflammatory agents. As with the horse, intramammary antibiotic infusion is complicated by the presence of two distinct lobes per mammary gland. Because each lobe has its own teat canal and orifice, both orifices should be cannulated when infusing intramammary antibiotics. The orifices are usually too small to accommodate the cannulas on intramammary infusion products for cattle; therefore a 3.5 French tomcat catheter is recommended.4 As with other species, disinfection of the teat end and aseptic infusion techniques are essential to prevent iatrogenic infection. Broad-spectrum antibiotics should be administered until culture results are available, because both gram-positive and gram-negative bacteria have been isolated from mastitic llamas. Systemic antibiotics should be used in conjunction with intramammary antibiotics in llamas that are systemically ill. Pain should be addressed by administering NSAIDs, with fluids administered if needed. Hot packing and frequent stripping of the affected gland are empirically justified treatments that may prove difficult because many llamas resist handling of the udder. Prognosis for survival is good if mastitis is treated early, but milk production may be reduced.
Dairy cattle frequently develop physiologic edema of the udder during the periparturient period. Other large animals are affected less frequently. Physiologic udder edema must be differentiated from pathologic edema, which can accompany mastitis and diseases of other body systems. Physiologic udder edema is symmetric, is cool to the touch, and pits on palpation. It can be limited to the udder or extend cranially along the ventrum or into the perineal region. In contrast, the edema that accompanies mastitis is more focal, is asymmetric, and is accompanied by abnormal milk and an inflamed mammary gland. Intermandibular and brisket edema, which are often observed in cows with congestive heart failure or severe hypoproteinemia, do not occur in cows with physiologic udder edema.
In most cases, physiologic edema is of little consequence and resolves spontaneously after parturition. However, treatment is recommended if the udder becomes excessively large and heavy, because this threatens the integrity of the udder suspensory apparatus and predisposes to teat injury and mastitis. Severe edema also can hinder ambulation or impair milking or nursing of the teats. If the edematous udder impinges on the skin of the thigh, moist dermatitis and secondary infection may develop, and the skin may slough; this condition is referred to as udder scald.
The mechanism(s) of physiologic udder edema is uncertain. Supplementing the ration of prepartum dairy cows with high concentrations of sodium or potassium salts significantly increases the incidence and severity of edema.510 However, serum biochemical values and fractional clearance of electrolytes are similar in affected and nonaffected cows.511 Increased capillary hydrostatic pressure (resulting from changes in mammary blood flow and intramammary pressure that occur around parturition) might be involved, as might incompetent valves in the cranial superficial epigastric veins draining the udder. Cows with udder edema have higher blood pressure in the cranial superficial epigastric veins than do unaffected cows, and blood pressure is inversely related to mammary blood flow.512 Poor udder suspension can also predispose to physiologic udder edema.
First-calf heifers and high-producing cows are at greatest risk of developing udder edema. Other risk factors are not well documented. In a case-control study of heifers in Florida, the risk of udder edema increased as height of the heifer increased, was higher if calving occurred in winter than in summer, and was higher if the fetus was male rather than female.513 Heifers with udder edema in the first lactation were more likely than unaffected heifers to develop edema in subsequent lactations.513
Treatment of udder edema includes preventing excessive salt intake and administering a diuretic. In the United States, furosemide is labeled for use in dairy cows, has 48-hour milk-withholding and slaughter-withholding times, and is the diuretic of choice for treating udder edema. In one study, high cranial superficial epigastric venous pressure in cows with udder edema was reduced by IV administration of furosemide (500 mg), but not hydrochlorothiazide (250 mg) or acetazolamide (500 mg).512 Repeated administration of furosemide for several days should be avoided, but if repeated dosing is necessary, cows should be monitored for signs of electrolyte imbalance. Although corticosteroids have been recommended for treatment of udder edema, their efficacy is questionable. Prepartum milking reduces the severity of edema514 but also decreases colostral immunoglobulin concentration at calving, so an alternative source of colostrum is needed. Increased milking frequency, udder massage, exercise, and hydrotherapy are empirically justified treatments for udder edema. Udder supports are available for cows with excessively pendulous or heavy udders.
It is not uncommon to observe blood in postpartum mammary secretions. Small vessels may rupture as a result of trauma or in conjunction with udder edema. The milk is usually light pink to red or brown and may contain blood clots. Antibiotic treatment is not indicated. Bloody milk can also accompany severe clinical mastitis or gangrenous mastitis, both of which have a poor prognosis, but physical examination of the animal will identify these conditions.
Bloody milk should be withheld from sale for human consumption. The milk usually returns to normal appearance within 1 week. However, because blood contains natural antimicrobial inhibitors, bloody milk may cause false-positive antibiotic residue test results. The IgG1 concentration of bloody colostrum is similar to that of normal-appearing colostrum, meaning it is not necessary to discard colostrum simply because it contains blood.65
About 2 weeks before parturition, the mammary gland begins producing colostrum, a process that accelerates as parturition approaches. Colostrum contains an appropriate balance of nutrients for the neonate, as well as substances that provide protection against infection and modulate development of the immune system.515,516 Of particular importance are colostral immunoglobulins, which are derived predominantly from maternal serum, by selective transport across mammary epithelial cells.517,518
In cattle, all immunoglobulin (Ig) isotypes are transported into colostrum,519 but IgG transport predominates. Mammary epithelial cells express receptors for both IgG1 and IgG2 during the periparturient period, but IgG1 receptors are more abundant and of higher affinity.518 Preferential transport of IgG1 results in an IgG1/IgG2 ratio of at least 7:1 in colostrum, compared with 1:1 in plasma.517 The IgG1 concentration of Holstein colostrum averages 40 to 80 g/L, with substantial variability among cows.520
Immunoglobulin G1 is also the most abundant Ig in the colostrum of sheep and goats, with concentrations averaging 60 to 80 g/L in sheep521,522 and 40 to 60 g/L in goats.523 Preferential transport of IgG1 over IgG2 has been demonstrated.523,524 Less is known about colostral Ig isotypes and transport in SACs,525,526 but mean colostral IgG concentration for llamas and alpacas in one report was 193 g/L,525 much higher than for small ruminants.
Equine colostrum contains IgGa, IgGb, IgGc, IgG(T), and IgA, but IgGb predominates, as is true for serum. In one study, serum-to-colostrum concentration ratios of these five isotypes were 0.06, 0.12, 0.16, 0.17, and 0.18, respectively, demonstrating that all are greatly increased in colostrum.527 Total IgG in equine colostrum is highly variable, with concentrations ranging from less than 10 to almost 400 g/L.527,528 In contrast to colostrum, IgA is the predominant Ig in equine milk.527
Neonatal ruminants are agammaglobulinemic at birth and rely on absorption of colostral IgG1 across the intestinal epithelium during the first day of life to achieve protective circulating Ig concentrations.522,529 Foals are also dependent on intestinal absorption of colostral Ig, particularly IgGb.527 Most dairy calves are hand-fed a fixed volume of colostrum by bottle, bucket, or esophageal feeder.530 Therefore, the IgG1 concentration of the colostrum is critical in determining if a sufficient mass (≥125 g/calf) of IgG1 is fed. Beef calves, small ruminant neonates, and foals usually obtain colostrum by suckling the dam, so both the amount of colostrum suckled and its Ig concentration are critical in determining if a sufficient mass of Ig is ingested.
A number of factors influence colostral IgG concentration. Colostral IgG concentration is typically lower for cows in first or second lactation than cows in third or greater lactation.65,530 In contrast, colostral IgG concentration was highest in 3- to 10-year-old mares and lower in older mares in one study.528 In sheep, yearlings had higher colostral IgG1 concentrations than older ewes.521 Beef cows typically produce colostrum of higher IgG concentration than dairy cows,531 and breed differences in colostral IgG concentration are apparent in both ruminants and horses.521,528,532,533
Differences in colostral IgG concentrations among species, or among animals within a species, probably result largely from the volume of colostrum produced. Colostral IgG concentration is negatively correlated with colostral volume in dairy cows, meaning that colostrum from high-yielding cows frequently has lower IgG concentration than colostrum from lower yielding cows.65,530
Colostral IgG concentration is highest at the first milking after parturition and declines rapidly thereafter, which means that a delay in time to first milking results in a progressive reduction in IgG concentration.534 The decline in colostral IgG concentration in horses appears to be even more rapid than in cattle.527 Intramammary infection reduces colostral yield in dairy cows but not colostral IgG concentration.535
Direct measurement of IgG concentration in colostrum is time-consuming and costly, so IgG concentration is often estimated from the specific gravity of the colostrum. In cattle, specific gravity is positively correlated with colostral protein concentration and, to a lesser extent, IgG1 concentration520,532,536; the relationship between specific gravity and IgG1 may differ among breeds of cows.532 In horses, there is also a positive correlation between colostral specific gravity and IgG concentration.528 Cattle producers frequently measure colostral specific gravity on-farm, using a commercial colostrometer. Values marked on the colostrometer do not accurately reflect actual IgG1 concentration,536 but the colostrometer can be used as a tool to differentiate very poor colostrum from excellent colostrum. Unfortunately, the appearance of bovine colostrum is not indicative of its IgG concentration.65
Transfer of colostral Ig to the neonate is discussed in Section Three of this book.
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