Epidemiology and Clinical Signs

Coliforms are part of the normal microflora of swine. These organisms have been isolated from udder, teat, urinary bladder, and uterine discharge.⁴ Coliforms commonly are isolated from swine feces, suggesting that the source of infection may be from the sow or a contaminated, nonsanitized environment. Contamination of teats takes place within 2 hours after farrowing. Bacteria rapidly colonize the ductular or alveolar lumina of the mammary gland.

Clinical manifestations of coliform mastitis in sows include fever (40° to 42° C), anorexia, cachexia, malaise, and agalactia. The udder is erythematous and edematous. In severe cases of coliform mastitis, clinical signs may include induration and discoloration of the mammary glands, which may pit and blanch when digital pressure is applied. Sows may display behaviors indicative of high levels of pain when the gland is palpated. In some cases, constipation and mammary edema may be present. A purulent exudate often can be expressed from the nipples of affected glands, and single glands or gland complexes can be affected. Septicemia or toxemia may result in elevated respiratory and heart rates. Sows with coliform mastitis often lie in ventral recumbency and demonstrate a reluctance to allow piglets to nurse. This condition rapidly leads to lactation insufficiency, which is discussed in greater detail later in the chapter.

Diagnosis

Gross lesions of coliform mastitis are confined to the mammary gland and regional lymph nodes.¹ Postmortem findings include regional lymphadenopathy, and longitudinal sections of udders reveal scattered areas of firmness, which are gray to red in color.¹ Histologic lesions vary in severity within the same mammary gland, ranging from a small number of neutrophils in the alveolar lumina to severe purulent infiltration with necrosis. Inguinal and iliac lymph nodes may be affected with acute purulent lymphadenitis.¹ Laboratory tests used for detection of mastitis in cows are not commonly employed in sows because of the naturally elevated cell count in sow’s milk.¹ Culture of material from affected glands is difficult, and specimens are easily contaminated by bacteria on the skin of the sow or the practitioner. Contamination can be reduced by wearing sterile gloves or by surgical preparation of the udder with tamed iodine solutions. Samples should be inoculated onto sheep blood agar and MacConkey’s agar and incubated for 24 hours at 37° C. Biochemical tests can be carried out to determine the identity of the organism isolated.

Treatment and Prevention

In acute cases of coliform mastitis, aggressive therapy is indicated. Antibiotic selection should be based on culture and sensitivity results. Response to antibiotics, however, is complicated by the heterogeneous pattern of antimicrobial susceptibility of individual isolates, not only within the herd, but also in the individual sow.¹ The pharmacokinetics of antimicrobials for mastitis therapy in swine has received only limited attention. Other compounds that may be administered in conjunction with antibiotics include prednisolone (50 to 100 mg), oxytocin (30 IU), and B vitamins to stimulate the appetite.¹ It also may be helpful to administer a prostaglandin synthetase inhibitor such as flunixin meglumine. Care of the piglets may require fostering or provision of a milk substitute (discussed later under Lactation Insufficiency Syndrome).

The best preventive measures include proper hygiene, especially removal of fecal material during and after parturition.⁵ The farrowing room and sow area should be cleaned with hot water (temperature greater than 95° C), thoroughly disinfected, and allowed to dry before the sows are moved in. It is a good management practice to wash sows with a mild soap and water, with particular attention given to the mammary area, before entry into the farrowing room. If manual intervention is required during parturition, attendants should thoroughly wash their hands and arms, wear well-lubricated arm-length sleeves, and wash the perineal region of the sow before manually entry into the birth canal. All sows requiring manual assistance during parturition should be identified and treated with an effective antibiotic. Rectal temperatures should be taken two or three times a day after treatment. Those sows that demonstrate a rectal temperature higher than 40° C should be treated for 3 to 5 days.

Currently, no vaccines for prevention of mastitis are commercially available, and positive reports from the use of experimental products have been scarce. Accordingly, the most cost-effective measures for control appear to be the management factors described here.

Epidemiology and Clinical Signs

The same factors that predispose sows to the development of urinary tract infection also may increase their susceptibility to metritis. The numerous microbes that normally inhabit the porcine reproductive tract also can be found in swine manure and have the potential to be pathogens at parturition.⁵ During gestation, the uterus is under the influence of high levels of progesterone secretions. This progesterone influence results in a closed cervix, generalized immune suppression, and an increased bacterial population.⁶

Contamination of the environment along with excessive microbial proliferation can result in infection of the uterus. Metritis also can be the result of overzealous infusion practices and excessive, unsanitary manual intervention during parturition.

Cases of metritis are characterized by a necrotic, malodorous discharge that frequently will contain remnants of fetal membranes. The sow often is anorectic, febrile, and septic. Septicemia in these cases often will result in death. Milk flow is minimal, and piglet mortality rate is increased.⁵

Diagnosis

Metritis can be readily diagnosed by the appearance of a vaginal discharge and the malodorous nature of this discharge. At postmortem examination, the uterine lumen may be filled with necrotic, yellow-brownish, purulent material.⁵ Histologic evaluation generally will demonstrate edema and purulent exudate in several layers of the myometrium.⁶ Colonies of bacteria may be evident microscopically as abscesses within the myometrium. Chronic cases are characterized by a diffuse infiltration of lymphocytes and denuded endometrial epithelium.⁶ Culture of an affected uterus commonly results in isolation of E. coli, Staphylococcus aureus, or Actinomyces pyogenes.⁵

Material for uterine culture in a live animal is readily obtained if the cervix is patent. Culture specimens can be obtained using uterine swabs inserted through a vaginal speculum.⁵ Reproductive slaughter checks also may serve as an opportunity to obtain tissue and bacterial isolates during an increased incidence of metritis. Vaginal cultures provide little information owing to the high level of contamination of this area with numerous species of nonpathogenic bacteria.⁵

Treatment and Prevention

Antibiotics for therapy of the infection should be selected on the basis of in vitro sensitivity and administered systemically. Intrauterine infusions of sodium penicillin or oxytetracycline produce satisfactory concentrations of these antibiotics in the uterine lumen. Intrauterine therapy is not widely accepted. Problems of uneven drug distribution exist. Some evidence also suggests that intrauterine infusion of antibiotics with a narrow spectrum of antibacterial activity has resulted in the elimination of an individual organism (such as E. coli), only to result in the abnormal proliferation of other bacteria, which may prolong the required time for regeneration of the endometrial lining after parturition.⁷

The steps involved in the prevention of metritis are similar to those described for preventing coliform mastitis. Suspected cases of urinary tract infection or endometritis should be treated with an antibiotic selected on the basis of culture and sensitivity testing results, a history of effectiveness on the farm, or practice experience. The most important factor is proper hygiene before, during, and after parturition at a time when the cervix is open to pathogen invasion. It is critical to recognize that the fecal bacterial flora are the same etiologic agents of metritis.