Effects of oral administration of tilmicosin on pulmonary inflammation in piglets experimentally infected with Actinobacillus pleuropneumoniae.
OBJECTIVE
To determine the effects of oral administration of tilmicosin in piglets experimentally infected with Actinobacillus pleuropneumoniae.


METHODS
Forty 3-week-old specific-pathogen free piglets.


METHODS
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 10(7) CFUs of A pleuropneumoniae; 3) infected treated piglets that were intratracheally inoculated with A pleuropneumoniae and received tilmicosin in feed (400 ppm [microg/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 (1100 ppm [microg/gl) 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
Oral administration of tilmicosin to infected piglets induces apoptosis in BAL fluid leukocytes and decreases BAL fluid LTB4 concentrations and inflammatory lung lesions.
Nerland
Erin M
EM
Department of Biological Sciences, Mucosal Inflammation Research Group, University of Calgary, Calgary, AB T2N 1N4, Canada.
LeBlanc
Justin M
JM
Fedwick
Jason P
JP
Morck
Douglas W
DW
Merrill
John K
JK
Dick
Paul
P
Paradis
Marie-Anne
MA
Buret
Andre G
AG
D000189:Actinobacillus Infections / Q000188:drug therapy / Q000503:physiopathology / Q000662:veterinary*; D016977:Actinobacillus pleuropneumoniae; D000821:Animal Feed; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use*; D017209:Apoptosis / Q000187:drug effects; D015232:Dinoprostone / Q000096:biosynthesis; D007962:Leukocytes / Q000187:drug effects; D007975:Leukotriene B4 / Q000096:biosynthesis; D018942:Macrolides / Q000627:therapeutic use*; D009195:Peroxidase / Q000096:biosynthesis; D010587:Phagocytosis / Q000187:drug effects; D018410:Pneumonia, Bacterial / Q000188:drug therapy / Q000662:veterinary*; D013552:Swine; D013553:Swine Diseases / Q000188:drug therapy* / Q000503:physiopathology; D015645:Tylosin / Q000031:analogs & derivatives* / Q000627:therapeutic use*
D000894:Anti-Inflammatory Agents, Non-Steroidal; D018942:Macrolides; D007975:Leukotriene B4; D009195:Peroxidase; D015232:Dinoprostone; C052319:tilmicosin; D015645:Tylosin