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, and weak piglets, as well as respiratory disease in pigs. 1 , 2 According to the latest classification, PRRSV is classified into the genus Porartevirus , family Arteriviridae , and order Nidovirales . 3 – 5 Based on genetic and antigenic analysis
mitigating inflammation related to routine husbandry practices, like dehorning in cattle 4 , 5 and castration in swine. 6 , 7 Castration is a procedure performed in piglets that inflicts tissue damage and inflammation. Even though there are several
C ommercial swine facilities around the globe commonly castrate male piglets to prevent unwanted breeding, reduce aggression, and improve meat quality. 1 – 3 Castration is typically performed in the first week of life on nearly all male piglets
intestinal function of piglets during the weaning transition. Berkeveld et al 8 determined that citrullinemia can be used as a longitudinal marker of intestinal function during the early postweaning period, but that study was performed under experimental
E nterotoxigenic Escherichia coli (ETEC) is the main pathogen causing E coli diarrhea in newborn piglets. 1 – 4 Diarrhea has been a major cause of mortality and morbidity according to National Swine Surveys in the United States. Although
T he castration of male suckling piglets is still an important issue in livestock farming. All over the world castration is commonly practiced primarily ensuring constant meat quality 1 and reducing the risk of boar taint, 2 but also minimizing
Abstract
Objective—To determine the effects of oral administration of tilmicosin in piglets experimentally infected with Actinobacillus pleuropneumoniae.
Animals—Forty 3-week-old specific-pathogen free piglets.
Procedure—Piglets were assigned to 1 of 4 groups as follows: 1) uninfected sham-treated control piglets; 2) infected untreated piglets that were intratracheally inoculated with 107 CFUs of A pleuropneumoniae; 3) infected treated piglets that were intratracheally inoculated with A pleuropneumoniae and received tilmicosin in feed (400 ppm [µg/g]) for 7 days prior to inoculation; or 4) infected treated piglets that were intratracheally inoculated with A pleuropneumoniae and received chlortetracycline (CTC) in feed (1,100 ppm [µg/g]) for 7 days prior to inoculation. Bronchoalveolar lavage (BAL) fluid and lung tissue specimens of piglets for each group were evaluated at 3 or 24 hours after inoculation. For each time point, 4 to 6 piglets/group were studied.
Results—Feeding of CTC and tilmicosin decreased bacterial load in lungs of infected piglets. Tilmicosin delivered in feed, but not CTC, enhanced apoptosis in porcine BAL fluid leukocytes. This was associated with a decrease in LTB4 concentrations in BAL fluid of tilmicosin-treated piglets, compared with untreated and CTC-treated piglets, and also with a significant decrease in the number of pulmonary lesions. Tilmicosin inhibited infection-induced increases in rectal temperatures, as measured in untreated and CTC-treated piglets. Pulmonary neutrophil infiltration and prostaglandin E2 concentrations in the BAL fluid were not significantly different among groups at any time.
Conclusions and Clinical Relevance—Oral administration of tilmicosin to infected piglets induces apoptosis in BAL fluid leukocytes and decreases BAL fluid LTB4 concentrations and inflammatory lung lesions. (Am J Vet Res 2005;66:100–107)
History The owner of a farrowing to finish swine system reported an increase in mortality rates of piglets in the final third of the nursery phase. The farm was a certified swine breeding farm, had a negative status for porcine reproductive
Abstract
Objective—To evaluate the ultrastructural changes and localization of encephalomyocarditis virus (EMCV) and viral pathogenesis in the myocardium of experimentally infected piglets.
Animals—Eight 20-day-old piglets.
Procedure—Six piglets were inoculated oronasally with 5 ml (106 median tissue culture infective dose/ml) of EMCV suspension, and 2 were used as uninfected controls. Piglets were euthanatized or died between postinoculation days 1 and 3. Samples of heart tissue from all piglets were evaluated histologically, by virus isolation, and by use of immunohistochemistry and electron microscopy.
Results—All infected piglets had gross or microscopic lesions of interstitial myocarditis. immunohistochemically, EMCV antigen was detected in the cytoplasm of cardiac muscle cells, Purkinje fibers, and endothelial cells and in the nucleus of cardiac muscle cells and Purkinje fibers. Ultrastructural lesions were characterized by degeneration and necrosis of cardiac muscle cells and Purkinje fibers. Virus was present intracytoplasmically in cardiac muscle cells, Purkinje fibers, and endothelial cells of capillaries and intranuclearly in cardiac muscle cells. The cell membranes of the Purkinje fibers and endothelial cells had distinct protrusions that contained virus particles. In control piglets, no lesions were found, and no EMCV antigen was detected.
Conclusion and Clinical Relevance—Localization of EMCV intracytoplasmically or intranuclearly in various myocardial cells may well reflect the sites of viral proliferation. The presence of virus particles in cell membrane protrusions and in vacuoles within the lumen of capillaries indicates that virus is released not only by disintegration of the host cell but also via exocytosis. (Am J Vet Res 2001;62:1653–1657)
History On a commercial pig farm housing 2,000 commercial crossbred sows and boars (Large White x Landrace) and with a history of repeated breeding from the same boar, an increase in mortality among 1-week-old piglets related to the presence
