Strain Characterization of Streptococcus suis Serotypes 28 and 31, Which Harbor the Resistance Genes optrA and ant(6)-Ia

Abstract

Streptococcus suis causes disease in pigs and is implicated increasingly in human disease worldwide. Although most clinical cases are associated with serotype 2, infections by other serotypes have sometimes been reported. Here, we sequenced the genome of a multidrug-resistant S. suis serotype 28 (strain 11313) and a multidrug-resistant S. suis serotype 31 (strain 11LB5). Strain 11313 was apathogenic in mouse infection models, whereas strain 11LB5 displayed ganglion demyelination, meningeal thickening, congestion, mononuclear cell infiltration, massive proliferation of cortical glial cells, and bacteria (>104 CFU/g) in the spinal cord and ganglia in mice. Furthermore, immunohistochemistry found that the heavily infiltrated glial cells were astrocytes. Strain 11313 harbored the resistance genes ant(6)-Ia, erm(B), optrA, tet(l), tet(o), and strain 11LB5 harbored the resistance genes ant(6)-Ia, erm(B), tet(40), tet(o/w/32/o), aac(6′)-aph(2″). Mouse studies showed that strain 11LB5 exhibited a similar virulence to serotype 2 strain 700794, highlighting the need for surveillance of the other serotype S. suis isolates, in addition to serotype 2, in farms. This is the first report of the aminoglycoside resistance gene ant(6)-Ia in S. suis from animals. This suggests that S. suis might serve as an antibiotic resistance reservoir, which spreads the resistance gene ant(6)-Ia or optrA to other streptococcal pathogens on farms.

Epidemiology of Antimicrobial Resistance Genes in Streptococcus agalactiae Sequences from a Public Database in a One Health Perspective

“…This gene is related to resistance to aminoglycosides [ 25 ]. The presence of this gene in isolates from human diseases has peculiar importance from a One Health approach because, recently, it was also recovered from streptococci of animal origin [ 26 ], supporting the risk of a bi-directional transfer of resistance gene.…”

How Streptococcus suis escapes antibiotic treatments

“…aphA3 Aminoglycoside O-phosphotransferase [ 116 , 121 ] aac(6’)-aph(2’’) a.k.a. aacA, aphD *9 Aminoglycoside N-acetyltransferase—O-phosphotransferase [ 97 , 115 ] aac(6’)-Ie-aph(2’’)-Ia *9 Aminoglycoside N-acetyltransferase—O-phosphotransferase [ 116 ] Glycopeptides *10 Target modification vanG D-Ala-D-Ser ligase [ 117 , 121 ] vanT D-ser producing serine racemase [ 121 ] vanXY D-Ala-D-Ala dipeptidase / D-Ala-D-Ala carboxypeptidase [ 117 , 121 ] vanZ Putatively alters the binding of (lipo)glycopeptides to cells [ 122 ] Quinolones Target mutation parC *1 Topoisomerase IV (Ser79, Asp83) [ 88 , 131 , 241 ] parE *1 Topoisomerase IV (Pro278) [ 131 ] gyrA *1 DNA gyrase (Ser81, Glu85) [ 62 , 88 , 131 , 241 ] gyrB *1 …”

“…Several genes coding for ANTs have been discovered in aminoglycoside-resistant S. suis isolates. Examples include ant1 [ 62 ], ant (6´)-Ia [ 115 , 116 ], ant (6´)-Ib [ 62 ], and ant (9´)-Ia [ 116 ] (Table 1 ). AACs comprise a large group of enzymes that acetylate amino groups at different positions on the aminoglycoside.…”

“…There are four subclasses of AACs based on the position of the amino groups that are modified. The aac (6´) gene was identified in various multidrug-resistant S. suis isolates from Asia with high MIC values for aminoglycosides [ 115 , 117 ]. It is often fused to other genes coding for different aminoglycoside-modifying enzymes, for example APHs (Table 1 ), thus generating bifunctional enzymes.…”

A Virulent Trueperella pyogenes Isolate, Which Causes Severe Bronchoconstriction in Porcine Precision-Cut Lung Slices

“…Genomic DNA of T. pyogenes 20121 was extracted by a Bacterial DNA Extraction Kit (Tiangen, Beiing, China) following the manufacturer's instructions. T. pyogenes was positively identified by detecting the 16S rRNA (12) products through PCR. The virulence factors of T. pyogenes 20121 were detected by PCR (13), including hemolysin (pyolysin, PLO), collagen-binding protein (CbpA), neuraminidase (NanH and NanP), and fimbriae (FimA, FimC, FimE and FimG).…”