Antimicrobial treatment of Mycoplasma hyopneumoniae infections.

Mycoplasma hyopneumoniae (M. hyopneumoniae) is the primary agent of enzootic pneumonia, a chronic and economically important respiratory disease of pigs. Control and prevention of M. hyopneumoniae infections can be accomplished by optimization of management and housing conditions, and by vaccination. The present paper summarizes the current knowledge on the main characteristics and efficacy of antimicrobials used for the treatment of clinical M. hyopneumoniae infections, the in vitro and in vivo activities of these antimicrobials and the reported resistance mechanisms against some. Potentially active antimicrobials against M. hyopneumoniae include tetracyclines, macrolides, lincosamides, pleuromutilins, amphenicols, aminoglycosides, aminocyclitols and fluoroquinolones. Antimicrobial treatment can be administered either orally or parenterally. Based on the overall results of efficacy studies performed under experimental and/or field conditions, the majority of agents belonging to these antimicrobial classes improved clinical parameters (clinical signs, lung lesions) and reduced performance losses due to M. hyopneumoniae infection. Antimicrobials may, however, not be able to prevent infection or to eradicate the bacterium from the respiratory tract. The decision to medicate should, therefore, be considered carefully. M. hyopneumoniae shows an intrinsic resistance against ß-lactam antibiotics, sulfonamides and trimethoprim. A few reports have shown acquired antimicrobial resistance against some antibiotics, along with associated resistance mechanisms. The results of antimicrobial susceptibility testing are difficult to interpret in terms of treatment outcome, as no clinical breakpoints have been defined for M. hyopneumoniae.

Persistence of Mycoplasma synoviae in hens after two enrofloxacin treatments and detection of mutations in the parC gene.

The ability of Mycoplasma synoviae, an avian pathogen, to persist despite fluoroquinolone treatments was investigated in hens. Groups of Mycoplasma-free hens were experimentally infected with the M. synoviae 317 strain and treated twice with enrofloxacin at the therapeutic dose. The results show that the two treatments did not have any influence on this strain of M. synoviae recovery from tracheal swabs. Mycoplasmas were isolated from tracheal swab cultures, but not from inner organs such as the liver or spleen, suggesting that this strain of M. synoviae was not able to cross the mucosal barrier to disseminate throughout the host. A significant increase of the resistance level to enrofloxacin of five re-isolated mycoplasma clones, was observed after the second treatment. This increase was associated in two clones to a Ser81-->Pro substitution, found in the ParC quinolone-resistance determining region (QRDR) of DNA topoisomerase IV. This is the first time that a mutation in a gene coding for topoisomerase IV is described in M. synoviae after in vivo enrofloxacin treatments in experimentally infected hens.

Persistence of Mycoplasma gallisepticum in chickens after treatment with enrofloxacin without development of resistance.

The ability of the avian pathogen Mycoplasma gallisepticum to persist despite fluoroquinolone treatment was investigated in chickens. Groups of specific pathogen free chickens were experimentally infected with M. gallisepticum and treated with enrofloxacin at increasing concentrations up to the therapeutic dose. When M. gallisepticum could no longer be re-isolated from chickens, birds were stressed by inoculation of infectious bronchitis virus or avian pneumovirus. Although M. gallisepticum could not be cultured from tracheal swabs collected on several consecutive sampling days after the end of the enrofloxacin treatments, the infection was not eradicated. Viral infections reactivated the mycoplasma infection. Mycoplasmas were isolated from tracheal rings cultured for several days, suggesting that M. gallisepticum persisted in the trachea despite the enrofloxacin treatment. The minimal inhibitory concentration (MIC) of enrofloxacin for most of the re-isolated mycoplasmas was the same as that of the strain with which the birds were inoculated. Furthermore, no mutation could be detected in the fluoroquinolone target genes. These results suggest that M. gallisepticum can persist in chickens without development of resistance despite several treatments with enrofloxacin.