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.
The causes have not been determined conclusively. Circumstantial evidence strongly suggests that necrotic ear syndrome is due to trauma (fighting) and subsequent bacterial invasion of the damaged tissue. Another potential factor that may contribute to the problem is inadequate dietary lysine levels in the feed, although no scientific data exist to prove this assumption.
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 β-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 the 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.
The nature and extent of clinical signs 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 made based on the appearance of the affected ears.
Tincture of iodine, applied topically bid for 1 wk, has reduced the incidence and severity of the disease. Antibacterial drugs administered in the feed are effective in some herds but not in others. Lack of effectiveness could be due to drug resistance. In cases of antibacterial ineffectiveness, specimens should be collected aseptically from the deep aspect of the ulcerative lesions for culture and sensitivity testing. Traumatizing events should be minimized. Management practices (ventilation, location and functioning of waterers, pen design, group size, mixing) and proper levels of dietary lysine should be checked and corrected if deficiencies are detected. Proper immunization against porcine circovirus type 2 is important to reduce the frequency of ear necrosis on farms. (Also see Health-Management Interaction: Pigs.)