Persistence of <i>Mycoplasma synoviae</i> in hens 
after two enrofloxacin treatments 
and detection of mutations in the <i>parC</i> gene

Carrou, Jérôme Le; Reinhardt, Anita; Kempf, Isabelle; Gautier-Bouchardon, Anne V.

doi:10.1051/vetres:2005046

Cited by 30 publications

(35 citation statements)

References 39 publications

(47 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Descriptions of mechanisms involved in quinolone resistance in veterinary medicine are scarce Le Carrou et al, 2006). Reinhardt et al (2002) showed the presence of alterations on the four target genes encoding DNA gyrase and topoisomerase IV in M. gallisepticum enrofloxacin mutants.…”

Section: Resultsmentioning

confidence: 99%

In vitroantibiotic susceptibility of DutchMycoplasma synoviaefield isolates originating from joint lesions and the respiratory tract of commercial poultry

Landman¹,

Mevius²,

Veldman³

et al. 2008

Avian Pathology

View full text Add to dashboard Cite

The in vitro susceptibility of 17 Dutch Mycoplasma synoviae isolates from commercial poultry to enrofloxacin, difloxacin, doxycycline, tylosin and tilmicosin was examined. Three isolates originated from joint lesions and 14 were from the respiratory tract. The type strain M. synoviae WVU 1853 was included as a control strain. Antibiotic susceptibility was tested quantitatively using the broth microdilution test. Based on initial and final minimum inhibitory concentration values, all tested isolates were susceptible to doxycycline, tylosin and tilmicosin. Two isolates from the respiratory tract were resistant to enrofloxacin and showed intermediate resistance to difloxacin.

show abstract

Section: Resultsmentioning

confidence: 99%

In vitroantibiotic susceptibility of DutchMycoplasma synoviaefield isolates originating from joint lesions and the respiratory tract of commercial poultry

Landman¹,

Mevius²,

Veldman³

et al. 2008

Avian Pathology

View full text Add to dashboard Cite

show abstract

“…None of the susceptible strains had a change at these positions. A previous study reported that position 81 of the ParC QRDR may be implicated in En resistance in M. synoviae (6). Positions 80 and 84 of the ParC QRDR are known hot spots for En resistance in many bacteria, including mycoplasmas, and may alone or together with a mutation within the GyrA QRDR result in decreased susceptibility to fluoroquinolones (20)(21)(22)(23)(24).…”

Section: Discussionmentioning

confidence: 99%

“…Fluoroquinolone resistance occurs primarily through mutations in the quinolone resistance-determining regions (QRDRs) of the parC and/or gyrA gene (encoding the A subunits of DNA gyrase and topoisomerase IV) or the gyrB and/or parE gene (encoding the B subunits of DNA gyrase and topoisomerase IV). Topoisomerase IV (parC gene) has been suggested to be the primary target of En in M. synoviae, based on in vivo selection of strains with decreased susceptibility after experimental infection (6).…”

mentioning

confidence: 99%

Molecular Characterization of Acquired Enrofloxacin Resistance in Mycoplasma synoviae Field Isolates

Lysnyansky¹,

Gerchman²,

Mikula³

et al. 2013

Antimicrob Agents Chemother

View full text Add to dashboard Cite

The in vitro activity of enrofloxacin against 73 Mycoplasma synoviae field strains isolated in Israel and Europe was determined by broth microdilution. Decreased susceptibility to enrofloxacin was identified in 59% of strains, with the MICs ranging from 1 to >16 g/ml. The estimated MIC 50 and MIC 90 values for enrofloxacin were 2 and 8 g/ml, respectively. Moreover, this study showed that 92% of recent Israeli field isolates (2009 to 2011) of M. synoviae have MICs of >2 g/ml to enrofloxacin. Comparison of the quinolone resistance-determining regions (QRDRs) in M. synoviae isolates revealed a clear correlation between the presence of one of the amino acid substitutions Asp79-Asn, Thr80-Ala/Ile, Ser81-Pro, and Asp84-Asn/Tyr/His of the ParC QRDR and decreased susceptibility to enrofloxacin (MIC, >1 g/ml). Amino acid substitutions at positions GyrA 87, GyrB 401/402, and ParE 420/454 were also identified, but there was no clear-cut correlation with susceptibility to enrofloxacin. Comparison of vlhA molecular profiles revealed the presence of 9 different genotypes in the Israeli M. synoviae field isolates and 10 genotypes in the European isolates; only one vlhA genotype (type 4) was identified in both cohorts. Based on results of vlhA molecular typing, several mechanisms for emergence and dissemination of Israeli enrofloxacin-resistant M. synoviae isolates are suggested. Mycoplasma synoviae is an economically important pathogen of poultry, causing respiratory disease and infectious synovitis in chickens and turkeys (1). The severity of clinical manifestations of M. synoviae infection ranges from inapparent to severe and is markedly exacerbated by the presence of other bacterial or viral pathogens. In addition, eggshell apex abnormality (EAA) has been recently described as a novel presentation of M. synoviae infection (2, 3).Antibiotic treatment at the beginning of a disease outbreak is sometimes employed to reduce economic losses caused by clinical outbreaks of M. synoviae. Enrofloxacin (En), a broad-spectrum antibiotic related to the class of fluoroquinolones, has been widely used in many countries for treatment of a variety of poultry diseases, mainly those associated with Escherichia coli and Pasteurella multocida but also avian mycoplasmosis (4). However, in some countries the use of En in poultry is not permitted, mainly due to human health concerns; in the United States, En has been banned for use in poultry since 2005.Fluoroquinolones act by inhibition of DNA replication through the formation of a ternary complex with DNA and the active site of DNA replication enzymes (5). Fluoroquinolone resistance occurs primarily through mutations in the quinolone resistance-determining regions (QRDRs) of the parC and/or gyrA gene (encoding the A subunits of DNA gyrase and topoisomerase IV) or the gyrB and/or parE gene (encoding the B subunits of DNA gyrase and topoisomerase IV). Topoisomerase IV (parC gene) has been suggested to be the primary target of En in M. synoviae, based on in vivo selection of strains with decreased ...

show abstract

“…Thus, it is more probable that M. suis developed tetracycline resistance mechanisms. In a study of M. synoviae, an increase in resistance to enrofloxacin could be demonstrated after several in vivo treatments of experimentally infected hens (27). However, when we used a microarray-based detection assay used to screen for antibiotic resistance genes in gram-positive The presence of M. suis within porcine erythrocytes nonetheless has significant clinical implications.…”

Section: Discussionmentioning

confidence: 99%

Mycoplasma suis Invades Porcine Erythrocytes

et al. 2009

View full text Add to dashboard Cite

Mycoplasma suis belongs to the hemotrophic mycoplasma group and causes infectious anemia in pigs. According to the present state of knowledge, this organism adheres to the surface of erythrocytes but does not invade them. We found a novel M. suis isolate that caused severe anemia in pigs with a fatal disease course. Interestingly, only marginal numbers of the bacteria were visible on and between the erythrocytes in acridine orange-stained blood smears for acutely diseased pigs, whereas very high loads of M. suis were detected in the same blood samples by quantitative PCR. These findings indicated that M. suis is capable of invading erythrocytes. By use of fluorescent labeling of M. suis and examination by confocal laser scanning microscopy, as well as scanning and transmission electron microscopy, we proved that the localization of M. suis was intracellular. This organism invades erythrocytes in an endocytosis-like process and is initially surrounded by two membranes, and it was also found floating freely in the cytoplasm. In conclusion, we were able to prove for the first time that a member of the hemotrophic mycoplasma group is able to invade the erythrocytes of its host. Such colonization should protect the bacterial cells from the host's immune response and hamper antibiotic treatment. In addition, an intracellular life cycle may explain the chronic nature of hemotrophic mycoplasma infections and should serve as the foundation for novel strategies in hemotrophic mycoplasma research (e.g., treatment or prophylaxis).Mycoplasma suis is a member of the family Mycoplasmataceae. This organism belongs to a group of uncultivable highly specialized bacteria which parasitize the surface of erythrocytes of a variety of mammals (34). These species represent a distinct new cluster in the genus Mycoplasma and have been given the trivial name hemotrophic mycoplasmas (HM). Infections with HM are identified clinically by overt life-threatening hemolytic anemia or by subtle chronic anemia characterized by infertility, immune suppression, and greater susceptibility to infections (34). It is noteworthy that organisms that morphologically resemble HM have also been detected in the blood of humans (1,8,42,50).M. suis causes febrile acute icteroanemia in pigs (IAP), which is accompanied by high numbers of M. suis cells in the blood, as confirmed by microscopy as well as by PCR (18,21,34). Clinical symptoms are successfully cured by treatment with tetracycline. Nevertheless, once pigs are infected with M. suis, they remain lifelong carrier animals and therefore are epidemiologically important (19). Chronic M. suis infections result in reproductive disorders in sows, growth retardation in piglets, and increased susceptibility to respiratory and enteric infections in feeder pigs. M. suis occurs worldwide, and chronic IAP, in particular, is of major economic importance (19).Contrary to the well-established clinical picture of IAP (i.e., high morbidity and low mortality), we recently observed an increased incidence of acute IAP in feed...

show abstract

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

Cited by 30 publications

References 39 publications

In vitroantibiotic susceptibility of DutchMycoplasma synoviaefield isolates originating from joint lesions and the respiratory tract of commercial poultry

In vitroantibiotic susceptibility of DutchMycoplasma synoviaefield isolates originating from joint lesions and the respiratory tract of commercial poultry

Molecular Characterization of Acquired Enrofloxacin Resistance in Mycoplasma synoviae Field Isolates

Mycoplasma suis Invades Porcine Erythrocytes

Contact Info

Product

Resources

About