Pathogenicity Of Streptococcus Research Articles

Streptococcus cristatus bacteremia in a patient with poor oral hygiene: a case report

BackgroundStreptococcus cristatus is a member of the Mitis streptococcus group. Like other members of this group, it resides on mucosal surfaces of the oral cavity. However, little is known about its ability to cause disease as there are only a handful of cases in the literature. Two of these cases involved infective endocarditis with significant complications. However, these cases involved additional microbes, limiting the inferences about the pathogenicity of Streptococcus cristatus.Case presentationA 59-year-old African American male with end-stage cryptogenic cirrhosis and ascites presented with fatigue and confusion. A paracentesis was negative for spontaneous bacterial peritonitis, but two separate blood cultures grew Streptococcus cristatus. Our patient had a history of dental caries and poor oral hygiene, which were likely the source of the infection. Echocardiograms revealed new aortic regurgitation, indicating “possible endocarditis” per the Modified Duke Criteria. However, since his clinical picture and cardiac function were reassuring, we elected against treatment for infective endocarditis. He was treated for bacteremia with a 2-week course of cephalosporins consisting of 8 days of ceftriaxone, transitioning to cefpodoxime after discharge. Despite having end-stage liver disease, our patient did not experience any significant complications from the infection.ConclusionA patient with end-stage cirrhosis and poor oral hygiene developed bacteremia with an oral bacterium called Streptococcus cristatus. Unlike previous cases in literature, our patient did not meet criteria for a definitive diagnosis of infective endocarditis, and he experienced no other complications from the infection. This suggests coinfectants may have been primarily responsible for the severe cardiac sequelae in prior cases, whereas isolated Streptococcus cristatus infection may be relatively mild.

Regulation of (p)ppGpp and Its Homologs on Environmental Adaptation, Survival, and Pathogenicity of Streptococci.

Most streptococci are commensals, pathogens, or opportunistic pathogens for humans and animals. Therefore, it is important for streptococci to adapt to the various challenging environments of the host during the processes of infection or colonization, as well as to in vitro conditions for transmission. Stringent response (SR) is a special class of adaptive response induced by the signal molecules (p)ppGpp, which regulate several physiological aspects, such as long-term persistence, virulence, biofilm formation, and quorum sensing in bacteria. To understand the roles of SR in streptococci, the current mini-review gives a general overview on: (1) (p)ppGpp synthetases in the genus of Streptococcus, (2) the effects of (p)ppGpp on the physiological phenotypes, persistence, and pathogenicity of streptococci, (3) the transcriptional regulation induced by (p)ppGpp in streptococci, and (4) the link between (p)ppGpp and another nutrient regulatory protein CodY in streptococci.

Антибіотикорезистентність збудників стрептококозу поросят і телят

Антибіотикорезистентність збудників стрептококозу поросят і телят

P176 A case of acute urticaria and angioedema from an underlying bacterial infection

The relationship between infection and spontaneous urticaria/angioedema has been reported. Although classically attributed to viral infections, bacterial infections, notably Helicobacter pylori, staphylococcus and streptococcus pathogens have been documented.

Rapid identification of <I>Streptococus agalactiae</I> and <I>Streptococus iniae</I> with duplex PCR assay

Streptococus agalactiae and S. iniae are two common pathogens of fish Streptococcus diseases. Symptoms of disease caused by both Streptococcus pathogens were quite similar, and it was difficult to distinguish the two pathogens from each other directly from the symptoms. Therefore it is necessary to develop a rapid identification method in order to control the disease effectively and rapidly. According to the cfb gene sequence of S. agalactiae and 16S rRNA gene sequence of S. iniae, two pairs of primers were designed and synthesized, and a rapid duplex PCR assay for identification of S. agalactiae and S. iniae was established by optimization of amplification conditions. A 474 bp fragment specific for S. agalactiae and a 296 bp fragment for S. iniae were produced, but no product was amplified from the other common pathogenic bacteria of fish such as Aeromonas hydrophila and Pseudomonas aeruginosa. The method is quite sensitive, and can detect a template concentration as low as 3.2×10-3 ng/μL for S. agalactiae and 3.0×10-2 ng/μL for S. iniae, respectively. A total of eleven pathogen samples collected from pond-cultured tilapia in Guangdong and Hainan provinces were analyzed by duplex PCR. Sequencing and BLAST analysis revealed that all the sequences were cfb gene of S. agalactiae. Results of molecular identification were consistent with the previous results of biochemical assays. The double PCR method would provide a sensitive and accurate method for rapid identification of S. agalactiae and S. iniae.

Modulation of Adherence, Invasion, and Tumor Necrosis Factor Alpha Secretion during the Early Stages of Infection by Streptococcus pneumoniae ClpL

Heat shock proteins (HSPs) play a pivotal role as chaperones in the folding of native and denatured proteins and can help pathogens penetrate host defenses. However, the underlying mechanism(s) of modulation of virulence by HSPs has not been fully determined. In this study, the role of the chaperone ClpL in the pathogenicity of Streptococcus pneumoniae was assessed. A clpL mutant adhered to and invaded nasopharyngeal or lung cells much more efficiently than the wild type adhered to and invaded these cells in vitro, as well as in vivo, although it produced the same amount of capsular polysaccharide. However, the level of secretion of tumor necrosis factor alpha (TNF-alpha) from macrophages infected with the clpL mutant was significantly lower than the level of secretion elicited by the wild type during the early stages of infection. Interestingly, treatment of the human lung epithelial carcinoma A549 and murine macrophage RAW 264.7 cell lines with cytochalasin D, an inhibitor of actin polymerization, increased adherence of the mutant to the host cells. In contrast, cytochalasin D treatment of RAW 264.7 cells decreased TNF-alpha secretion after infection with either the wild type or the mutant. However, pretreatment of cell lines with the actin polymerization activator jasplakinolide reversed these phenotypes. These findings indicate, for the first time, that the ClpL chaperone represses adherence of S. pneumoniae to host cells and induces secretion of TNF-alpha via a mechanism dependent upon actin polymerization during the initial infection stage.

Contributions of Pneumolysin, Pneumococcal Surface Protein A (PspA), and PspC to Pathogenicity ofStreptococcus pneumoniaeD39 in a Mouse Model

Successful colonization of the upper respiratory tract by Streptococcus pneumoniae is an essential first step in the pathogenesis of pneumococcal disease. However, the bacterial and host factors that provoke the progression from asymptomatic colonization to invasive disease are yet to be fully defined. In this study, we investigated the effects of single and combined mutations in genes encoding pneumolysin (Ply), pneumococcal surface protein A (PspA), and pneumococcal surface protein C (PspC, also known as choline-binding protein A) on the pathogenicity of Streptococcus pneumoniae serotype 2 (D39) in mice. Following intranasal challenge with D39, stable colonization of the nasopharynx was maintained over a 7-day period at a level of approximately 10(5) bacteria per mouse. The abilities of the mutant deficient in PspA to colonize the nasopharynx and to cause lung infection and bacteremia were significantly reduced. Likewise, the PspC mutant and, to a lesser extent, the Ply mutant also had reduced abilities to colonize the nasopharynx. As expected, the double mutants colonized less well than the parent to various degrees and had difficulty translocating to the lungs and blood. A significant additive attenuation was observed for the double and triple mutants in pneumonia and systemic disease models. Surprisingly, the colonization profile of the derivative lacking all three proteins was similar to that of the wild type, indicating virulence gene compensation. These findings further demonstrate that the mechanism of pneumococcal pathogenesis is highly complex and multifactorial but ascribes a role for each of these virulence proteins, alone or in combination, in the process.

Kinetics and Regulation of Erythrogenic Toxins Type A and C During Growth of Streptococcus Pyogenes

The production of erythrogenic toxins type A (ETA) and C (ETC) is described as a function of growth kinetics. Group A streptococcal strains C 203 S and NY 5 were cultivated in yeast-peptone extract, Todd-Hewitt medium and a synthetic medium. Two main growth phases occurred during growth: a first logarithmic phase and a second linear phase. These phases were separated by a short stationary interphase caused by limitation of the amino acids L-serine and L-leucine. Maximum production of ETC was observed during the logarithmic phase, it was correlated to a high level of viable cells. ETA was produced mainly during the short stationary interphase. The production of ETC is regulated by L-isoleucine. A stagnation or reduction of the concentration of viable cells was observed during the interphase. The phosphate limitation caused during streptococcal growth induced expression of the extracellular protein phosphatase and surprisingly, of a serine proteinase activity. The association between these results and the pathogenicity of streptococci is discussed.

The contribution of pneumolysin to the pathogenicity of Streptococcus pneumoniae

The antiphagocytic polysaccharide capsule of Streptococcus pneumoniae has long been been considered the principal virulence determinant of this organism. However, there is growing evidence that the toxin pneumolysin plays an important role in the pathogenesis of pneumococcal disease and may thus be a significant additional target for vaccine development.