Streptococcus Equi Subsp Zooepidemicus Research Articles

Endogenous Type I-C CRISPR-Cas system of Streptococcus equi subsp. zooepidemicus promotes biofilm formation and pathogenicity.

Streptococcus equi subsp. zooepidemicus (SEZ) is a significant zoonotic pathogen that causes septicemia, meningitis, and mastitis in domestic animals. Recent reports have highlighted high-mortality outbreaks among swine in the United States. Traditionally recognized for its adaptive immune functions, the CRISPR-Cas system has also been implicated in gene regulation, bacterial pathophysiology, virulence, and evolution. The Type I-C CRISPR-Cas system, which is prevalent in SEZ isolates, appears to play a pivotal role in regulating the pathogenicity of SEZ. By constructing a Cas3 mutant strain (ΔCas3) and a CRISPR-deficient strain (ΔCRISPR), we demonstrated that this system significantly promotes biofilm formation and cell adhesion. However, the deficiency in the CRISPR-Cas system did not affect bacterial morphology or capsule production. In vitro studies showed that the CRISPR-Cas system enhances pro-inflammatory responses in RAW264.7 cells. The ΔCas3 and ΔCRISPR mutant strains exhibited reduced mortality rates in mice, accompanied by a decreased bacterial load in specific organs. RNA-seq analysis revealed distinct expression patterns in both mutant strains, with ΔCas3 displaying a broader range of differentially expressed genes, which accounted for over 70% of the differential genes observed in ΔCRISPR. These genes were predominantly linked to lipid metabolism, the ABC transport system, signal transduction, and quorum sensing. These findings enhance our understanding of the complex role of the CRISPR-Cas system in SEZ pathogenesis and provide valuable insights for developing innovative therapeutic strategies to combat infections.

Magnolol attenuates macrophage pyroptosis triggered by Streptococcus equi subsp. zooepidemicus

Streptococcus equi subsp. zooepidemicus (SEZ) is a zoonotic bacterial pathogen that causes life-threatening infections and various diseases such as meningitis, endocarditis and pneumonia. With the use of antibiotics being severely restricted in the international community, an alternative to antibiotics is urgently needed against bacterial. In the present study, the herbal extract magnolol protected mice against SEZ infection, reflected by increased survival rate and reduced bacterial burden. A pro-inflammatory form of cell death occurred in SEZ-infected macrophage. Magnolol downregulated the expression of pyroptosis-related proteins and reduced the formation of cell membrane pores in infected macrophages to suppress the development of subsequent inflammation. We further demonstrated that magnolol directly suppressed SEZ-induced macrophage pyroptosis, which partially protected macrophages from SEZ infection. Our study revealed that magnolol suppressed inflammation and protected mice against SEZ infection, providing a possible treatment for SEZ infection.

Characterization of AI-2/LuxS quorum sensing system in biofilm formation, pathogenesis of Streptococcus equi subsp. zooepidemicus.

Streptococcus equi subsp. zooepidemicus (SEZ) is an opportunistic pathogen of both humans and animals. Quorum sensing (QS) plays an important role in the regulation of bacterial group behaviors. The aim of this study was to characterize the LuxS in SEZ and evaluate its impact on biofilm formation, pathogenesis and gene expression. The wild-type SEZ and its LuxS mutant (ΔluxS) were examined for growth, biofilm formation, virulence factors, and transcriptomic profiles. Our results showed that LuxS deficiency did not affect SEZ hemolytic activity, adhesion or capsule production. For biofilm assay demonstrated that mutation in the luxS gene significantly enhances biofilm formation, produced a denser biofilm and attached to a glass surface. RAW264.7 cell infection indicated that ΔluxS promoted macrophage apoptosis and pro-inflammatory responses. In mice infection, there was no significant difference in mortality between SEZ and ΔluxS. However, the bacterial load in the spleen of mice infected with ΔluxS was significantly higher than in those infected with SEZ. And the pathological analysis further indicated that spleen damage was more severe in the ΔluxS group. Moreover, transcriptomics analysis revealed significant alterations in carbon metabolism, RNA binding and stress response genes in ΔluxS. In summary, this study provides the first evidence of AI-2/LuxS QS system in SEZ and reveals its regulatory effects on biofilm formation, pathogenicity and gene expression.

Pathogenic Characteristics of an Infection with Canine Influenza Virus and Streptococcus equi subsp. zooepidemicus Alone or in Combination in Mice

Both Streptococcus equi subsp. zooepidemicus (SEZ) and canine influenza virus (CIV) are two important pathogens causing infectious respiratory disease in dogs and are frequently codetected in respiratory secretions. However, the clinical significance of viral/bacterial coinfection remains unknown. This study investigated the pathogenic characteristics of infection with CIV and SEZ alone or in combination in mice. Our data indicated that the severity of the disease is related to the challenge order of CIV and SEZ. Coinfection of CIV and SEZ induced higher weight loss in mice than single infection, except for the VB group (viral followed by secondary bacterial infection). Compared with the concurrent or sequential infection groups of CIV and SEZ, mice in the CIV–SEZ preincubation group exhibited more obvious weight loss, higher mortality, and significantly enhanced burden of SEZ and CIV in tissues. Interestingly, viral and bacterial preincubation before coinfection caused typical pulmonary fibrosis in mice. Correspondingly, transforming growth factor (TGF)-β was upregulated, and its canonical small mother against decapentaplegic (Smad) 2/3 signaling was noticeably induced. Further investigation indicated that the activity of the viral neuraminidase (NA) enzyme upon sialic acid was considerably increased due to the direct interaction of CIV with SEZ, which may be related to the activation of the TGF-β signaling pathway. These findings implicate an unexpected contribution of the direct interaction between CIV and SEZ to synergistic pathogenicity.

A distinct variant of the SzM protein of Streptococcus equi subsp. zooepidemicus recruits C1q independent of IgG binding and inhibits activation of the classical complement pathway

ABSTRACT Streptococcus equi subsp. zooepidemicus (SEZ) is a major equine pathogen that causes pneumonia, abortion, and polyarthritis. It can also cause invasive infections in humans. SEZ expresses the M-like protein SzM, which recruits host proteins such as fibrinogen to the bacterial surface. Equine SEZ strain C2, which binds only comparably low amounts of human fibrinogen in comparison to human SEZ strain C33, was previously shown to proliferate in equine and human blood. As the expression of SzM_C2 was necessary for survival in blood, this study investigated the working hypothesis that SzM_C2 inhibits complement activation through a mechanism other than fibrinogen and non-immune immunoglobulin binding. Loss-of-function experiments showed that SEZ C2, but not C33, binds C1q via SzM in IgG-free human plasma. Furthermore, SzM C2 expression is necessary for recruiting purified human or equine C1q to the bacterial surface. Flow cytometry analysis demonstrated that SzM expression in SEZ C2 is crucial for the significant reduction of C3b labelling in human plasma. Addition of human plasma to immobilized rSzM_C2 and immobilized aggregated IgG led to binding of C1q, but only the latter activated the complement system, as shown by the detection of C4 deposition. Complement activation induced by aggregated IgG was significantly reduced if human plasma was pre-incubated with rSzM_C2. Furthermore, rSzM_C2, but not rSzM_C33, inhibited the activation of the classical complement pathway in human plasma, as determined in an erythrocyte lysis experiment. In conclusion, the immunoglobulin-independent binding of C1q to SzM_C2 is associated with complement inhibition.

Membrane vesicle delivery of a streptococcal M protein disrupts the blood-brain barrier by inducing autophagic endothelial cell death.

M family proteins are critical virulence determinants of Streptococci. Streptococcus equi subsp. zooepidemicus (SEZ) are Group C streptococci that cause meningitis in animals and humans. SzM, the M protein of SEZ, has been linked to SEZ brain invasion. Here, we demonstrate that SzM is important in SEZ disruption of the blood-brain barrier (BBB). SEZ release SzM-bound membrane vesicles (MVs), and endocytosis of these vesicles by human brain endothelial microvascular cells (hBMECs) results in SzM-dependent cytotoxicity. Furthermore, administration of SzM-bound MVs disrupted the murine BBB. A CRISPR screen revealed that SzM cytotoxicity in hBMECs depends on PTEN-related activation of autophagic cell death. Pharmacologic inhibition of PTEN activity prevented SEZ disruption of the murine BBB and delayed mortality. Our data show that MV delivery of SzM to host cells plays a key role in SEZ pathogenicity and suggests that MV delivery of streptococcal M family proteins is likely a common streptococcal virulence mechanism.

Characterization of Streptococcus equi subsp. zooepidemicus isolates containing lnuB gene responsible for the L phenotype.

Within the framework of the β-hemolytic streptococci surveillance carried out by the National Reference Laboratory from Uruguay, three putative Streptococcus equi subsp. zooepidemicus (SEZ) were received from different health centers. Being these the first reports associated with human infections in Uruguay, the objective of this work was to confirm their identification, to determine their genetic relationship and to study their antibiotic susceptibility. Using four different methods, they were identified as SEZ, a subspecies which has been described as the etiologic agent of rare and severe zoonosis in a few cases in other countries. The three isolates presented different pulsotypes by PFGE; however, two of them appeared to be related and were confirmed as ST431 by MLST, while the remaining isolate displayed ST72. Their resistance profile exhibited an unexpected feature: despite all of them were susceptible to macrolides, they showed different levels of resistance to clindamycin, i.e. they had the so-called "L phenotype". This rare trait is known to be due to a nucleotidyl-transferase, encoded by genes of the lnu family. Although this phenotype was previously described in a few SEZ isolates, its genetic basis has not been studied yet. This was now analyzed by PCR in the three isolates and they were found to contain a lnuB gene. The lnuB sequence was identical among the three isolates and with many lnuB sequences deposited in data banks. In conclusion, for the first time in Uruguay, three SEZ isolates recovered from non-epidemiologically related cases of human invasive infection were identified. Moreover, this is the first report about the presence of a lnu gene in the S. equi species, revealing the active lateral spread of the lnuB in a new streptococcal host.

Protection Efficacy of Monoclonal Antibodies Targeting Different Regions of Specific SzM Protein from Swine-Isolated Streptococcus equi ssp. zooepidemicus Strains.

Streptococcus equi subsp. zooepidemicus (SEZ) has a wide host spectrum, including humans and domestic animals. The SEZ-caused swine streptococcicosis outbreak has occurred in several countries, and the swine-isolated strains usually have specific S. zooepidemicus M-like (szm) gene types. In this study, we found that the production of this specific szm gene (SzM protein) was an effective vaccine candidate. It could provide better protection with a 7-day interval immune procedure than the traditional vaccine strain ST171 and attenuate the strain ΔsezV against swine-isolated hypervirulent SEZ infections. According to this outcome, we developed monoclonal antibodies (McAbs) targeting the variable and conserved regions of this SzM protein, respectively. These McAbs all belong to the IgG1 isotype with a κ type light chain and have opsonophagocytic activity rather than agglutination or complement activation functions. We estimated the protection efficiency of the McAbs with 3 different passive immunotherapy programs. The anti-conserved region McAb can provide effective protection against swine-isolated SEZ infections with only the inconvenient immunotherapy program. It also partially works in preventing infection by other SEZ strains. In contrast, the anti-variable region McAb is only adapted to protect the host against a specific szm type SEZ strain isolated from pigs, but it is flexible for different immunotherapy programs. These data provide further information to guide the development of derived, genetically engineered McAbs that have potential applications in protecting hosts against swine-isolated, hypervirulent SEZ infections in the future. IMPORTANCE The swine-isolated SEZ, with its specific szm gene sequence, has impacted the pig feeding industry in China and North America and has led to serious economic loss. Though the SzM protein of SEZ has been proven to be an effective vaccine in preventing infection, most previous studies focused on horse-isolated strains, which have different szm gene types compared to swine-isolated strains. In this study, we developed the McAbs targeting the conserved and variable regions of this SzM protein from the swine-isolated hypervirulent strains and evaluated their protection efficiency. Our research provided information for the development of chimeric McAbs or other genetically engineered McAbs that have potential applications in protecting pigs against hypervirulent SEZ infections in the future.

The vital role of covS in the establishment of Streptococcus equi subsp. zooepidemicus virulence

Streptococcus equi subsp. zooepidemicus (SEZ) is an important zoonotic agent. Here, a virulence-attenuated strain M35246 derived from natural variation of wild-type SEZ ATCC35246 was found. M35246 showed a deletion of 25 contiguous genes as well as a loss-of-function mutation in covS. Subsequently, a 25-gene-deleted strain (ΔPI), a covS-mutant strain (McovS), and relevant complementary strains were constructed and investigated. M35246 and McovS were significantly less encapsulated and exhibited poorer anti-phagocytic capacity compared to wild-type SEZ. McovS was significantly more sensitive to β-lactams, aminoglycosides, macrolides, and lincosamides than wild-type SEZ. M35246, McovS, and ΔPI exhibited an increase in median lethal dose (LD50) in mice by 105, 105, and 5 times when compared to wild-type SEZ, respectively. Neither M35246 nor McovS were isolated from mice 48 h after being challenged with approximately 2 000 times the LD50 of wild-type SEZ. Transcriptome analysis showed that 668 significantly differentially expressed genes existed between McovS and wild-type SEZ. Numerous virulence factor-encoding genes and anabolic-related genes in McovS that were involved in anti-phagocytosis, capsule formation, pathogenicity, and antibiotic resistance were downregulated significantly relative to the wild-type strain. This study revealed that the CovS plays a vital role in the establishment of SEZ virulence.

BifA Triggers Phosphorylation of Ezrin to Benefit Streptococcus equi subsp. zooepidemicus Survival from Neutrophils Killing.

Streptococcus equi subsp. zooepidemicus (SEZ) ATCC35246 can invade the brain and cause severe neutrophils infiltration in brain tissue. This microorganism can survive and reproduce to an extremely high CFU burden (108–109/organ) under stressful neutrophils infiltration circumstances. The aim of this research is to explore the mechanism of the SEZ hypervirulent strain with its specific bifA gene which avoids being eliminated by neutrophils in the brain. We isolated the primary mouse neutrophils to treat SEZ WT and bifA gene defective (ΔBif) strains. The ΔBif strain had a weakened function of defending against neutrophils killing in vitro. The interaction between BifA and ezrin proteins in neutrophils were identified by co-IP and immunoblot. In neutrophils, the BifA interacts with ezrin and triggers the phosphorylation of ezrin at its Thr567 site in a PKC-dependent manner, then the excessive elevation of phosphorylated-ezrin recruits Dbl and activates Rac1. Since the Rac1 is closely relevant to several critical cellular functions, its abnormal activation will lead to neutrophils dysfunction and benefit to SEZ survival from neutrophils killing. Our findings reveal a novel consequence of BifA and ERM family protein (for ezrin, radixin, moesin) interaction, which happens between BifA and ezrin in neutrophils and contributes to SEZ survival in the brain. BifA should be considered as a potential target for drug development to prevent SEZ infection.

MiR-223-3p contributes to suppressing NLRP3 inflammasome activation in Streptococcus equi ssp. zooepidemicus infection

Streptococcus equi subsp. zooepidemicus (SEZ) is an essential pathogen in a range of species, causing a worldwide variety of diseases, such as meningitis, endocarditis, and septicaemia. Studies have shown that microRNAs (miRNAs), which regulate target genes at the post-transcriptional level, play an important regulatory role in the organism. In this study, the infection of J774A.1 murine macrophages with SEZ up-regulated NLRP3 inflammasome and downstream pathways accompanied by miR-223–3p down-regulation. Through computational prediction and experimental confirmation, we have shown that miR-223–3p directly targets the NLRP3 mRNA. Consequently, overexpression of miR-223–3p suppressed NLRP3 inflammasome activation and downstream pathways in response to SEZ infection. The miR-223–3p inhibitor exhibited the opposite effect, causing hyperactivation of NLRP3 inflammation activation and downstream pathways. Additionally, we further demonstrated that miRNA-223–3p inhibited the secretion of IL-1β and IL-18 by regulating the NLRP3/caspase-1 pathway. Furthermore, intravenous administration of miR-223–3p significantly decreased inflammation in mice in response to SEZ. In conclusion, our results demonstrated that miR-223–3p contributes to suppressing the NLRP3 inflammasome activation in SEZ infection, contributing novel evidence to identify a therapeutic target for treating SEZ.

Differences in the Accessory Genomes and Methylomes of Strains of Streptococcus equi subsp. equi and of Streptococcus equi subsp. zooepidemicus Obtained from the Respiratory Tract of Horses from Texas.

ABSTRACTStreptococcus equi subsp. equi (SEE) is a host-restricted equine pathogen considered to have evolved from Streptococcus equi subsp. zooepidemicus (SEZ). SEZ is promiscuous in host range and is commonly recovered from horses as a commensal. Comparison of a single strain each of SEE and SEZ using whole-genome sequencing, supplemented by PCR of selected genes in additional SEE and SEZ strains, was used to characterize the evolution of SEE. But the known genetic variability of SEZ warrants comparison of the whole genomes of multiple SEE and SEZ strains. To fill this knowledge gap, we utilized whole-genome sequencing to characterize the accessory genome elements (AGEs; i.e., elements present in some SEE strains but absent in SEZ or vice versa) and methylomes of 50 SEE and 50 SEZ isolates from Texas. Consistent with previous findings, AGEs consistently found in all SEE isolates were primarily from mobile genetic elements that might contribute to host restriction or pathogenesis of SEE. Fewer AGEs were identified in SEZ because of the greater genomic variability among these isolates. The global methylation patterns of SEE isolates were more consistent than those of the SEZ isolates. Among homologous genes of SEE and SEZ, differential methylation was identified only in genes of SEE encoding proteins with functions of quorum sensing, exopeptidase activity, and transitional metal ion binding. Our results indicate that effects of genetic mobile elements in SEE and differential methylation of genes shared by SEE and SEZ might contribute to the host specificity of SEE.IMPORTANCE Strangles, caused by the host-specific bacterium Streptococcus equi subsp. equi (SEE), is the most commonly diagnosed infectious disease of horses worldwide. Its ancestor, Streptococcus equi subsp. zooepidemicus (SEZ), is frequently isolated from a wide array of hosts, including horses and humans. A comparison of the genomes of a single strain of SEE and SEZ has been reported, but sequencing of further isolates has revealed variability among SEZ strains. Thus, the importance of this study is that it characterizes genomic and methylomic differences of multiple SEE and SEZ isolates from a common geographic region (viz., Texas). Our results affirm many of the previously described differences between the genomes of SEE and SEZ, including the role of mobile genetic elements in contributing to host restriction. We also provide the first characterization of the global methylome of Streptococcus equi and evidence that differential methylation might contribute to the host restriction of SEE.

Zoonotic infection and clonal dissemination of Streptococcus equi subspecies zooepidemicus sequence type 194 isolated from humans in Thailand.

Streptococcus equi subsp. zooepidemicus (SEZ) is a zoonotic pathogen associated with diseases in a wide range of animals as well as in humans. SEZ sequence type (ST) 194 strains have been associated with outbreaks in China, the USA, and Canada and have caused high mortality in pigs. Nevertheless, human infection by this ST has never been reported. This study conducted a retrospective analysis of 18 SEZ strains from human patients in Thailand during 2005-2020. The study revealed clonal dissemination of ST194 with the identical pulsotype in human patients throughout Thailand. Clinical manifestation was mainly septicemia (61.1%), while 72.2% had a history of eating raw pork products. There were six fatal cases (33.3%). Antimicrobial susceptibility testing revealed that all strains were susceptible to penicillin, ampicillin, cefotaxime, erythromycin, levofloxacin, clindamycin, chloramphenicol, tetracycline and vancomycin. Virulence-associated genes, including bifA, szM, szP, sdzD, spaZ, and fszF, were present in all tested strains. Some representative genes in four pathogenicity islands found in the swine outbreak SEZ-ATCC35246 (ST194) strain were detected in these SEZ strains. Whole-genome sequencing analysis of three representative SEZs in this study revealed no acquired antimicrobial-resistant genes and they contained the same virulence factors. The single-nucleotide polymorphism phylogenetic tree demonstrated that the current strains were clustered with swine ST194 strains. The results should be highlighted as a public health concern, especially to those who may directly or indirectly have contact with livestock or companion animals or have consumed raw meat products as risk factors for infections with SEZ.

Human zoonotic infectious disease caused by Streptococcus equi subsp. zooepidemicus

Streptococcus equi subsp. zooepidemicus (SEZ) is a highly contagious infectious organism that causes disease in horses. SEZ is seldom isolated from humans; however, zoonotic infections are occasionally reported in individuals exposed to horses and other livestock. Herein, we report three human cases of SEZ in individuals, one with direct horse contact and two among individuals who had eaten raw horse meat. The phylogenetic tree showed that the genotypes of SEZ isolates from two of the cases on Jeju Island, South Korea, were similar to those of isolates from the United Kingdom and the United States of America.

A streptococcal Fic domain-containing protein disrupts blood-brain barrier integrity by activating moesin in endothelial cells.

Streptococcus equi subsp. zooepidemicus (SEZ) is a zoonotic pathogen capable of causing meningitis in humans. The mechanisms that enable pathogens to traverse the blood-brain barrier (BBB) are incompletely understood. Here, we investigated the role of a newly identified Fic domain-containing protein, BifA, in SEZ virulence. BifA was required for SEZ to cross the BBB and to cause meningitis in mice. BifA also enhanced SEZ translocation across human Brain Microvascular Endothelial Cell (hBMEC) monolayers. Purified BifA or its Fic domain-containing C-terminus alone were able to enter into hBMECs, leading to disruption of monolayer barrier integrity. A SILAC-based proteomic screen revealed that BifA binds moesin. BifA’s Fic domain was required for its binding to this regulator of host cell cytoskeletal processes. BifA treatment of hBMECs led to moesin phosphorylation and downstream RhoA activation. Inhibition of moesin activation or moesin depletion in hBMEC monolayers abrogated BifA-mediated increases in barrier permeability and SEZ’s capacity to translocate across monolayers. Thus, BifA activation of moesin appears to constitute a key mechanism by which SEZ disrupts endothelial monolayer integrity to penetrate the BBB.

Identification of novel genes associated with anti-phagocytic functions in Streptococcus equi subsp. zooepidemicus

The anti-phagocytic abilities of bacteria often affect bacterial pathogenicity. Here, random mutant library of Streptococcus equi subsp. zooepidemicus (SEZ) was constructed using transposon mutagenesis. After careful screening, 30 transposon mutants with different transposon insertion sites were identified by conducting quantitative phagocytosis and insertion-site confirmation assays, whose anti-phagocytic abilities were significantly reduced relative to the wild-type strain. Insertion sites of 19 strains were monocistronic, including genes coding membrane proteins, transporters, and enzymes with unknown pathological function, such as sadM, adhP, purD, guaA, alpha-galactosidase coding gene, ABC transporter permease coding gene, metallo-beta-lactamase coding gene, and three secreted enzyme coding genes spuZ, slaB, and endoS, as well as known virulence factor coding genes, such as hasA and szM. The insertion sites of another 11 strains were polycistronic. We focused on four monocistronic-mutant strains: MhtpZ, MspuZ, MslaB, and MendoS. The anti-phagocytic abilities of not only the mutants that were precoincubated with the recombinant proteins, but also the complement strains were significantly more pronounced than those of all four corresponding mutants. The polyclonal antiserum against SlaB or EndoS also significantly decreased the anti-phagocytic capacity of wild-type SEZ. All four mutants exhibited significantly decreased viability in whole blood and reduced lethality in mice relative to the wild-type strain. Thus, we identified a variety of new anti-phagocytic factors, particularly multiple SEZ secreted enzymes. These factors are instrumental in the phagocytic resistance of SEZ in the absence of opsonin. Our results provide a framework for further studies of SEZ pathogenesis and relevant vaccine development for novel potential targets.

Genetic diversity of Streptococcus equi subsp. zooepidemicus isolated from horses

Streptococcus equi subsp. zooepidemicus (SEZ) is an opportunistic and zoonotic pathogen of horses. In this study, genetic intraspecies variability of SEZ obtained mainly from respiratory and genital samples of horses was investigated by analysis of the 16S–23S rRNA intergenic spacer region (ISR) and of the 16S rRNA gene. 16S–23S ISR rRNA type A1 was predominant, although a high rate of multiple products (30.5%) was obtained. Phylogenetic analysis of the 16S rRNA gene detected three genogroups (I, II and III). 16S rRNA variable regions V1 and V2 are the most important regions for evaluating SEZ intraspecies variability, but at least V1-V5 regions should be considered to avoid mistakes. Analysis of all 16S rRNA sequences available in databases assigned human SEZ to groups I and III but not to group II. These results show a high genetic variability in SEZ collected from different specimens of horses from various regions of Italy.

First molecular characterization of Streptococcus equi subsp zooepidemicus isolates from Argentinean mares through MLST tool

First molecular characterization of Streptococcus equi subsp zooepidemicus isolates from Argentinean mares through MLST tool

Isolation, Identification and Characterization of AZO Dye reactive Violet 5R Degrading Bacterial Strains from the Textile Sludge

Three bacterial strains, Streptococcus equi subsp. zooepidemicus, Brevibacillus centrosporus and Paenibacillus azoreducens, have been isolated from the sludge samples collected from Textile Industry, Bhaluka, Bangladesh, which have the abilities to degrade Reactive Violet 5R. The decolourization rate was different for the different concentrations of the same dye. Brevibacillus centrosporus displayed a decolorization rate of 94.55%, 90.79%, 91.17% when inoculated and incubated in an SM broth containing the azo dye reactive violet 5R at 1% (v/v), 3% (v/v) and 5% (v/v) concentrations respectively for a consecutive 5 days. Paenibacillus azoreducens showed a decolorization rate of 85.63%, 86.48%, 38.81% for the 1% (v/v), 3% (v/v), and 5% (v/v) of the azo dye reactive violet 5R respective concentrations. On the other hand Streptococcus equi subsp zooepidemicus produced intriguing results where the decolorization rates were 67.78%, 21.69%, 40.10% for 1% (v/v), 3% (v/v) and 5% (v/v) respectively of the azo dye reactive violet 5R.Journal of Bangladesh Academy of Sciences, Vol. 41, No. 2, 136-143, 2017

Factors Associated with Survival in 97 Horses with Septic Pleuropneumonia.

BackgroundSeptic pleuropneumonia is a common cause of morbidity and mortality in horses, but there is limited data available regarding factors associated with survival.Hypothesis/ObjectivesTo identify factors predictive of survival in horses with septic pleuropneumonia.AnimalsA total of 97 horses with septic pleuropneumonia at 2 referral institutions.MethodsA retrospective study was performed. A diagnosis of septic pleuropneumonia was based on the presence of sepsis, pleural effusion, and positive bacterial culture from tracheal aspiration (TA) or pleural fluid (PF).ResultsThirty‐one percent of horses had a recent history of travel. Clinical signs included lethargy (78%), tachycardia (75%), tachypnea (60%), fever (43%), prolonged capillary refill time (22%), and ventral edema (14%). The most common clinicopathologic abnormality was hyperfibrinogenemia (79%). Increased serum creatinine concentration at presentation was negatively associated with survival (OR, 5.13; CI, 1.88–14.01; P = .001) and return to work (OR, 6.46; CI, 1.10–37.92; P = .034). Eighty‐four TA and 67 PF samples were submitted for culture, 98 and 84% of which were positive, respectively. The most common isolate was Streptococcus equi subsp zooepidemicus. Tracheal aspirates were more sensitive than PF for bacterial growth, but some organisms isolated from PF were not isolated from TA. Thoracotomy was positively associated with survival (OR, 0.13; CI, 0.01–0.83; P = .028).Conclusions and Clinical ImportanceIncreased serum creatinine concentration is a negative prognostic indicator and is likely a reflection of dehydration. Submission of TA and PF is recommended. Thoracotomy should be considered as a treatment for pleuropneumonia.