Chapter 11 Udder and teat disorders

Blind quarters 203

Mastitis 204

Summer mastitis 204

Acute mastitis 205

Chronic mastitis 206

Mastitic changes in milk 207

Blood in milk 207

Mastitic milk 207

Introduction

The dairy cow is bred and fed to produce large volumes of milk. With the metabolic stress of high performance and the physical effects of being milked and handled two or three times daily, it is not surprising that the udder and teats are subject to a wide variety of disorders. The primary disease, mastitis, is of worldwide economic importance and much money is spent on its prevention, treatment and control. The first part of the chapter deals with mastitis in lactating and dry cows, and describes changes that may be seen in milk. The second part illustrates teat lesions, including a wide variety of viral infections, notably bovine herpes mammillitis, cowpox and pseudocowpox, vesicular stomatitis, and fibropapillomas (warts). Other systemic diseases that also affect the teats, e.g., foot-and-mouth disease, are covered elsewhere (p. 221).

Because of their anatomical position, especially in cows with pendulous udders, teats are vulnerable to injuries, eczema, and other physical influences. These problems are considered in the third part of this chapter, although changes associated with photosensitization are covered elsewhere (3.5). The final part of the chapter includes miscellaneous conditions of the udder.

Congenital conditions

Supernumerary teats

Clinical features

supernumerary teats are a congenital condition. They may be found between the front and rear teats, and/or attached to the udder behind the rear teats (11.1), or to the base or side of one of the main teats, where they can interfere with milking. They are typically, shorter than normal teats, and have thinner walls. They may connect to the sinus of an existing teat, or, more commonly, have a separate supernumerary gland.

11.1 Two supernumerary teats behind rear teats

Management

as such teats are unsightly, may interfere with milking, and can develop mastitis, they are normally removed with curved scissors early in life. Care is necessary to identify the correct teat.

Blind quarters

Clinical features

blind quarters in heifers with nonpatent teats can be either congenital or acquired. There are two congenital forms, one in which there is a total absence of the teat canal, but the teat fills with milk, and less commonly a second where there is a persistent membrane between the teat cistern and canal at the teat base, and no milk can be palpated in the teat. The acquired form, when a thickened central core is palpable in the teat canal, may be caused by undetected summer mastitis (11.2) or trauma from being suckled as a calf (2.14). The associated quarter may be swollen immediately postpartum due to accumulated milk, but this later regresses to be smaller than the other quarters. In mature cows a blind quarter may occasionally arise from chronic mastitis in the previous lactation, although in many animals a prolonged dry period often results in self-cure. Visible unevenness of quarters occurs in around 60% of milking animals, varying with age, stage of lactation, and mastitis history.

11.2 Summer mastitis: left hind quarter and teat thickened in heifer (Charolais)

Mastitis

Summer mastitis

Definition

this form of mastitis, typically seen in nonlactating cows and heifers, invariably leads to extensive parenchymal damage and loss of the quarter. An infectious condition commonly involving Arcanobacterium pyogenes and many other possible organisms, it is transmitted by the sheep head fly, Hydrotaea irritans. Some cases may occur in lactating cows secondary to teat sphincter trauma.

Clinical features

this endemic form of suppurative mastitis, with a characteristic foul odor, typically occurs sporadically in mid–late summer in Europe, because the vector H. irritans is active during July–September. Mild cases become only slightly ill, whilst the more severely affected cows are dull, pyrexic, and anorexic. They may abort, or produce weakly calves at term. Acute, untreated cases may die. Very few quarters recover, although cases are very occasionally mild enough to pass unrecognized until calving, when the affected quarter is nonfunctional (“blind”) and the teat is palpably thickened. Occasionally summer mastitis is seen in a bull or a young calf.

The Charolais heifer in 11.2 is an early case, showing distension of the left hind quarter, which was typically hard and sore, with a prominent, turgid teat. In more advanced cases, the infection may burst through the udder, as shown in the right hind quarter in 11.3. A thickening of the central teat canal was palpable, the quarter was very hard, and yellow pus with a pungent odor was discharging from the teat and udder.

11.3 Sumer mastitis: suppurative mastitis in dry cow has burst through skin

Management

parenteral treatment with antibiotics possibly and NSAIDs will reduce the systemic effects. Local antibiotic treatment of the quarter is rarely successful, but frequent stripping or surgical drainage using a longitudinal teat incision may prevent udder abscessation.

Control

dry cow therapy with longacting intramammary antibiotics, internal teat sealants, fly repellents, and keeping cattle away from known fly areas, or housing them during the period of risk. In high-risk areas fly repellents should ideally be applied to the udder weekly.

Acute mastitis

Peracute and acute mastitis are most commonly seen in the first few weeks after calving and are often the result of periparturient immune suppression. Disease may result from recrudescence of dormant dry period infections, or from new intramammary infections during lactation. Cases can occur throughout lactation at a lower frequency. In most cases peracute mastitis with toxemia results from coliform infections. Similarly, in acute mastitis, environmental organisms such as coliforms (e.g., Escherichia coli) or Streptococcus uberis are frequently involved. Immune suppression occasionally leads to acute disease from “contagious” mastitis organisms such as staphylococci, which are carried on the skin or in the udder of affected cows and transmitted to other cows during milking.

Clinical features

the most prominent sign of acute mastitis is an enlarged, hard, hot and painful quarter, which may be apparent before any changes are visible in the milk. In some cases, a brown serous discharge may be seen on the surface of the affected quarter and teat, as in the lactating Friesian cow in 11.4. A section of an affected udder (11.5), shows deep red inflammation of the teat cistern and teat canal mucosa. There is prominent subcutaneous edema and the skin at the tip of the teat is congested. Changes of this nature can lead to gangrene. The yellow foci (A) in the udder parenchyma are pockets of pus. In 11.6 the teat of the affected quarter is swollen with areas of hemorrhage. There is an obvious area of gangrene affecting the udder skin, which is dry, cracked, and cold. This cow was severely ill with an eventually fatal toxemia, although in less extensive cases the necrotic portion of the udder will slough and recovery is still possible. Such cases should not be confused with udder bruising (11.7).

11.4 Acute mastitis: enlarged quarter with serous discharge on skin

11.5 Acute mastitis: inflammatory changes in teat cistern and mucosa, severe skin edema

11.6 Acute mastitis, early gangrenous changes

11.7 Bruising of udder with skin discoloration and enlarged forequarter

Advanced gangrene (11.8) leads to cold, damp teat skin. Although mastitis was limited to the left forequarter (A), the entire udder was blue, edematous, and cold to the touch. Adjacent to the affected teat is a skin slough and red exudate. The secretion from the udder was a deep port-wine color and was mixed with gas. The cow had been normal when milked 12 hours previously, indicating the peracute onset of disease. In cases of nonfatal, gangrenous mastitis the overlying skin (11.9), or even the entire affected quarter, sloughs slowly in 1–2 months.

11.8 Advanced gangrene of udder: peracute case with slough of skin around affected quarter (A)

11.9 Gangrenous mastitis: nonfatal case with massive skin slough

Management

intramammary antibiotics, combined with parenteral antibiotics, fluid therapy and NSAIDs for more acute cases. Continual stripping of affected quarters, and parenteral oxytocin allegedly improves recovery rate. Prevention depends on reducing pathogen concentration at the teat orifice and correct machine function. Environmental hygiene, correct premilking teat preparation, avoidance of mechanical trauma to the teat sphincter (11.32, 11.33), and minimization of teat end impacts are all important points. Standard texts give details.

Chronic mastitis

Definition

Streptococcus agalactiae, S. dysgalactiae, S. uberis, staphylococci, Mycoplasma, Arcanobacterium pyogenes, and other bacteria can produce a chronic mastitis, manifested as “clots” in the milk (11.14), with or without palpable udder changes.

Clinical features

the Friesian cow in 11.10 has large, hard nodules protruding from the udder, with two in the right quarter and one in the left. These are chronic, intramammary, staphylococcal abscesses. Staphylococci were cultured from the milk, which had a high cell count and gave a strongly positive reaction to the California mastitis test. Such advanced cases, which are usually unresponsive to treatment, are dangerous carriers and should be culled. If only one quarter is affected, that quarter may be dried off otherwise infection will be transferred to other quarters and other cows at milking. The Friesian cow in 11.11 had a blind quarter, having had mastitis in the previous lactation. The front left teat is slightly smaller than the others, and the associated quarter has totally atrophied.

11.10 Chronic mastitis: large nodules are chronic staphylococcal abscesses within mammary parenchyma

11.11 “Blind” quarter: front left teat and quarter atrophied

Management

treatment options are as for environmental infections. Control of contagious mastitis rests on reducing cow-to-cow spread of infection during the milking process. Milking hygiene (gloves, liners, paper towels, etc.), early detection and treatment of cases, thorough postmilking teat disinfection, correct milking machine function, dry cow antibiotic therapy, and culling are important control measures. Raised cell counts in the bulk tank milk may lead to financial penalties.

Mastitic changes in milk

Milk is thicker and more viscous during the dry period and immediately postpartum (i.e., colostrum). Its character also changes in mastitis. Although specific types of mastitic infection frequently lead to similar changes in milk, the appearance of the milk is not pathognomonic, and bacteriological examination is required to confirm the causative organism and to determine the antibiotic sensitivity.

Blood in milk

Clinical features

true blood clots are the characteristic feature of blood in milk. They may be present in slightly pink-tinged milk (11.12) or, in more severe cases, in a secretion that is almost totally red (11.13). Seen only in newly calved cows, or after trauma, the condition usually resolves spontaneously. Herd outbreaks of unknown etiology may occur.

11.12 Blood in milk: newly calved cow with isolated clots

11.13 Blood in milk: severe case

Management

no treatment has been found to be consistently useful. Incomplete milking leading to increased intramammary pressure is believed to assist in hemostasis, but as this increases the risk of a new quarter infection, prophylactic antibiotic cover should be given.

Mastitic milk

Clinical features

watery, translucent milk with occasional clots (11.14) is typical of a mild mastitis such as that caused by S. agalactiae or S. dysgalactiae. Normal milk may be totally absent in severe staphylococcal (11.15) or Arcanobacterium pyogenes infections, when the secretion consists of thick clots suspended in a clear, serous fluid. Summer mastitis (often A. pyogenes) invariably produces a thick secretion with a characteristic pungent odor.