Necrotic ear syndrome in swine presents with large erosive lesions at the margin of the pinnae. The lesions start as a superficial vesicular dermatitis and progress to exudative and crusted areas. Lesions may slowly heal or progress to ulcerative, necrotic lesions. Initial superficial lesions often show Staphylococcus hyicus. The deep ulceration and necrosis have been attributed to the presence of deep beta-hemolytic streptococcal infection resulting in cellulitis, vasculitis, thrombosis, ischemia, and necrosis. Ear biting is a common inciting factor, and proper management practices and vaccination against porcine circovirus type 2 reduce the incidence of ear necrosis.
Pigs with necrotic ear syndrome have unilateral or bilateral necrosis of the pinnae, are unthrifty, and commonly develop septic arthritis or die from secondary bacterial septicemia. The condition occurs sporadically in weaned and growing pigs under all management systems, particularly when challenged with endemic diseases that may influence feed intake.
Etiology, Transmission, and Pathogenesis of Necrotic Ear Syndrome in Swine
The causes of necrotic ear syndrome have not been determined conclusively. Three hypothesis are currently considered: 1) damage of the epidermis due to Staphylococcal exfoliative toxins; 2) occlusion of small blood vessels; and 3) ear biting with subsequent beta-hemolytic streptococcal infection
Histologic and microbiologic findings suggest that the aggressive, erosive to ulcerative lesion is due to secondary bacterial infection. In the early phases of the disease, large numbers of Staphylococcus hyicus and low to moderate numbers of beta-hemolytic streptococci are found in the surface exudate; later, during the ulcerative and necrotic stage, large numbers of the streptococci are found deep in the lesion. It is hypothesized that S hyicus colonizes the traumatized tissue, which prepares the way for highly invasive streptococci that induce the changes that lead to ulceration and necrosis. Efforts to reproduce the disease by experimental inoculation of the two organisms have been unsuccessful. Spirochetes have also been found in skin samples from ear lesions using silver stain, and Treponema spp were amplified and sequenced from DNA prepared from ear lesion scrapings and broth cultures. However, the primary role of spirochetes in causing ear necrosis in pigs is unknown at this time. Moreover, porcine circovirus type 2 infection may contribute to ear necrosis, because controlling the infection through systematic vaccination has been reported to reduce the frequency of ear necrosis on farms.
Clinical Findings, Lesions, and Diagnosis of Necrotic Ear Syndrome in Swine
The nature and extent of clinical signs of necrotic ear syndrome depend on the severity of the local lesion and development of secondary bacterial septicemia. Thus, a spectrum of signs, including unthriftiness, anorexia, fever, septic arthritis, collapse, and death, may be seen.
Mild lesions consist of superficial scratches covered with thin, dry, brown crusts. Mild edema or erythema may be present near the scratches. In more severe cases, thick, brown, moist crusts cover deep ulcers. In the most severe cases, there is extensive necrosis. The lesions evolve from mild, superficial dermatitis to severe, deep inflammation with exudation, ulceration, thrombosis, and necrosis. In mild cases, resolution occurs with no loss of ear tissue; in severe cases, the margins, tips, or even the entire pinna may be lost.
Diagnosis is based on the appearance of the affected ears.
Management and Control of Necrotic Ear Syndrome in Swine
Avoidance of trauma
Proper management
Vaccination
Ear biting has been strongly associated with the incidence of necrotic ear syndrome. Avoiding trauma and controlling superficial lesions with topical antiseptics such as iodine may stop progression.
Proper management practices (ventilation, location and functioning of waterers, pen design, group size, mixing) should be followed, and proper levels of dietary lysine should be checked and corrected if deficiencies are detected. ( See also page Health-Management Interaction: Pigs.)
Proper immunization against porcine circovirus type 2 is important to reduce the frequency of ear necrosis.
Key Points
Lesions of necrotic ear syndrome in swine may begin as superficial dermatitis in areas of the trauma, most commonly by biting among piglets at weaning.
Early lesions (vesicles, bullae, erosions) are superficial and often associated with Staphylococcus hyicus infections.
Superficial lesions may progress to deeper lesions (ulceration and necrosis) and are often associated with beta-hemolytic streptococci.
Deep lesions can progress to sloughing of the pinnae and systemic involvement.
Vaccination for porcine circovirus 2 has been associated with reduced incidence of necrotic ear syndrome.
For More Information
Pejsak Z, Markowska-Daniel I, Pomorska-Mól M, Porowski M, Kołacz R. Ear necrosis reduction in pigs after vaccination against PCV2. Res Vet Sci. 2011;91(1):125-8.
Park J, Friendship RM, Poljak Z, DeLay J, Slavic D, Dewey CE. An investigation of ear necrosis in pigs. Can Vet J. 2013;54(5):491-5.
Richardson JA, Morter RL, Rebar AH, Olander HJ. Lesions of porcine necrotic ear syndrome. Vet Pathol. 1984;21(2):152-7.
