Growth of pigs with viral and bacterial pneumonia.

摘要

Infectious pathogens that cause disease in food-producing animals allegedly impair growth and cause heavy economic losses. Therefore, to investigate how infectious pathogens impair growth in pigs a disease model that employed Mycoplasma hyopneumoniae (Mh) and Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) was established. In the first study, Mh infection resulted in pneumonic coughing and the development of lung lesions. In addition, steady-state levels of mRNA encoding tumor necrosis factor-α and interleukin (IL) 1β but not IL-6 were increased in lesioned lung tissue compared to nonlesioned tissue of the same lung. However, Mh did not depress feed intake (FI), weight gain (WG) or protein accretion (PA). Thus, the purported detrimental effects of Mh on pig growth may be highly dependent on the presence of other pathogens. To investigate this possibility, a second study involving dual infection was conducted. Pigs were inoculated with PRRSV and Mh—alone or in combination—and growth performance, and serum IL-1β and IL-6 were determined. In addition, the steady-state level of mRNA encoding myostatin (MSTN)—a negative regulator of muscle mass—was measured in skeletal muscle.; Infection with PRRSV increased serum IL-1β and IL-6, increased MSTN and mRNA in skeletal muscle, and decreased FI, WG, PA and the mass of several skeletal muscles, but neither Mh nor the Mh×PRRSV interaction were significant. The Mh-induced lung lesions, however, were 3- to 5-times greater in pigs with both Mh and PRRSV than in those with Mh alone. Correcting WG and PA for differences in FI after PRRSV inoculation showed that the reduction in FI was able to explain the decrease in WG but not the decline in PA. Serum cytokines were negatively correlated with FI, WG and PA, and positively correlated with MSTN mRNA. Myostatin mRNA was positively correlated with WG and PA. Thus, the magnitude of increases in inflammatory cytokines and MSTN following a disease challenge may be predictive of the decreases that can be expected in PA and growth. Collectively, these findings suggest that the decrease in growth in PRRSV-infected pigs may be due to an increase in metabolically active inflammatory cytokines and MSTN gene expression.