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PubMed1995

[A clinical study of six cases of toxic shock-like syndrome by group A Streptococcus].

We have encountered six cases with toxic shock-like syndrome (TSLS) by Group A Streptococcus since 1978. Every patient had from the onset flu-like symptoms or high fever and immediately developed some of the following clinical signs: hypotension, acute renal failure, disseminated intravascular coagulation (DIC), and adult respiratory distress syndrome (ARDS). Three of the six patients died with rapid clinical courses and three survived. As for the surviving patients, early administration of antibiotics and anti-DIC therapy were effective. Streptococcus pyogenes were isolated from the blood in five of the patients, ascites from another, and necrotizing tissue in one patient. The serovars of the isolated strains were typed as T1/M1 in three, T8 in one, and T28 in another. The toxin-type of the strains were typed as B in four and B + C in one. Though there have been few reports of TSLS before 1992 in Japan, it is supposed that many TSLS cases may have potentially occurred.

Aged↗
PubMed1997

[Clinical study on penicillin insusceptible/resistant Streptococcus pneumoniae in the elderly patients].

Clinical features of respiratory infection in the elderly with penicillin insusceptible (31 cases) and resistant (7 cases) Streptococcus pneumonia (PSSP/PRSP) are compared to those with penicillin sensitive S. pneumoniae (PSSP) (29 cases). Incidence of bacteremia and pneumonia was higher in the PSSP group. PISP/PRSP tend to be isolated from patients with bronchitis underlaid with chronic pulmonary disease without statistic significance. Efficacy of the penicillins and 1st and 2nd generation cephem was satisfactory except in only one case of pneumonia with PISP which needed an alternative choice to the 3rd generation cephem. Now a day the degree of resistance is not so high and the available antibiotics are sufficient for the treatment of pneumococcal infection in the elderly patients. However, the wide use of oral cephems and certain new quinolones which do not have enough activity against Streptococcus pneumoniae may increase resistance. In which case, continuous surveillance and clinical caution against this resistant strain is necessary.

Aged↗
PubMed2002

[M protein gene (emm) typing of Streptococcus pyogenes].

T-agglutination typing and M protein gene (emm) typing were determined on the isolates of Streptococcus pyogenes taken from patients in Osaka and neighboring districts during 1996-2000. A total of 701 isolates were classified to 15 kinds of T types and type untypable. In all isolates, T 12 was revealed as the most dominant serotype, followed by T1, T4 and T2. The isolation rates of T 12 strains were high through these five years, and these of T1 or T4 strains formed epidemic waves showing the peak to be from 1997 to 1999 and 1998 to 2000, respectively. These of T2 strains were high in 1996 and 1997 and decreased rapidly. In 2000 T2 strain has not been detected. A total of 304 isolates were examined for emm typing. We are able to determine the emm type of all isolates including T-untypable (UT) isolates and to classify 21 kinds of emm types. T1, T2, T4, T6, T9, T11, T12, T22, T25 strains exhibited one T-type and emm type pattern association respectively such as T1/emm1, T2/emm2, T4/emm4, T6/emm6, T9/emm9, T11/emm11, T12/emm12, T22/emm22, T25/emm75. Whereas T13 strains had varied T/emm pattern associations such as T13/emm73, T13/emm77, T13/emm101. Similarly, T28, TB3264, UT had varied T/emm pattern associations. emm28 and emm87 were seen in T28, emm89 and emm94 in TB3264, emm2, emm12, emm22, emm58, emm75, emm77 and emm112 in UT. The emm typing method did not require many kinds of M typing antisera, and were successful by using the two highly conserved primers to amplify the emm gene and direct sequencing. Therefore, this method was a useful tool for typing Streptococcus pyogenes isolates.

Antigens, Bacterial↗
PubMed2006

[A case of severe necrotizing cellulitis caused by group G Streptococcus dysgalactiae subsp. equisimilis].

Group G streptococcus (GGS) is infrequently associated with severe invasive soft tissue infection and toxic shock syndrome. A 74-year-old woman with a history of lymphedema of the lower extremities after surgical and radiation therapy for uterine cancer and diabetic mellitus and admitted for swelling of the right leg, fever, and dyspnea. She presented with shock and necrotizing cellulitis of the right lower extremity. Laboratory tests showed leukocytepenia, acute renal and liver dysfunction, and muscle damage. She rapidly developed multiple organ failure and necrotizing cellulitis. A swab from skin vesicle, throat, and blood culture grew Group G Streptococcus dysgalactiae subsp. equisimilis. Despite endotoxin hemoadsorption therapy, administration of antibiotics, and intravenous immunoglobulin, she died 9 days after admission due to toxic shock syndrome caused by GGS. The M-protein gene (emm) typing of GGS isolated from both blood and skin lesion showed stG 485.0. Three virulence genes, sagA, slo and skcg, were detected from GGS isolated from them.

Aged↗
PubMed2006

[A case of thoracic empyema with gas formation associated with Streptococcus dysgalactiae subsp. equisimilis].

A 63-year-old woman suffering from dyspnea since 1 week earlier underwent a combination therapy of oral corticosteroid and ciclosporin for rheumatic arthritis. Chest radiography showed plural effusion with gas formation in the right thorax. Empyema was diagnosed based on the specimen from pleural effusion. After a chest tube was emplaced to remove and wash out pus, antibiotics were started and empyema improved immediately. Streptococcus dysgalactiae subsp. equisimilis, but not aerobic bacilli, was detected from the pus by repeated culture. Insofar as we know this is the first case of empyema with gas formation associated with Streptococcus dysgalactiae subsp. equisimilis.

Empyema, Pleural↗
PubMed2005

Genome analysis reveals pili in Group B Streptococcus.

Pili are essential virulence factors in many Gram-negative bacteria; however, they have not been described in most important Gram-positive pathogens. While screening the sequence of multiple genomes of Group B Streptococcus, we identified protective antigens that formed high molecular weight polymers. Immunogold electron microscopy revealed that the structures have a pilus-like form. These large structures have gone unrecognized in decades of studies of Group B Streptococcus.

Animals↗
PubMed1984

Monoclonal idiotope vaccine against Streptococcus pneumoniae infection.

A monoclonal anti-idiotope antibody coupled to a carrier protein was used to immunize BALB/c mice against a lethal Streptococcus pneumoniae infection. Vaccinated mice developed a high titer of antibody to phosphorylcholine, which is known to protect against infection with Streptococcus pneumoniae. Measurement of the median lethal dose of the bacteria indicated that anti-idiotope immunization significantly increased the resistance of BALB/c mice to the bacterial challenge. Antibody to an idiotope can thus be used as an antigen substitute for the induction of protective immunity.

Animals↗
PubMed2006

Mutations in penicillin-binding protein (PBP) genes and in non-PBP genes during selection of penicillin-resistant Streptococcus gordonii.

Penicillin resistance in Streptococcus spp. involves multiple mutations in both penicillin-binding proteins (PBPs) and non-PBP genes. Here, we studied the development of penicillin resistance in the oral commensal Streptococcus gordonii. Cyclic exposure of bacteria to twofold-increasing penicillin concentrations selected for a progressive 250- to 500-fold MIC increase (from 0.008 to between 2 and 4 microg/ml). The major MIC increase (> or = 35-fold) was related to non-PBP mutations, whereas PBP mutations accounted only for a 4- to 8-fold additional increase. PBP mutations occurred in class B PBPs 2X and 2B, which carry a transpeptidase domain, but not in class A PBP 1A, 1B, or 2A, which carry an additional transglycosylase domain. Therefore, we tested whether inactivation of class A PBPs affected resistance development in spite of the absence of mutations. Deletion of PBP 1A or 2A profoundly slowed down resistance development but only moderately affected resistance in already highly resistant mutants (MIC = 2 to 4 microg/ml). Thus, class A PBPs might facilitate early development of resistance by stabilizing penicillin-altered peptidoglycan via transglycosylation, whereas they might be less indispensable in highly resistant mutants which have reestablished a penicillin-insensitive cell wall-building machinery. The contribution of PBP and non-PBP mutations alone could be individualized in DNA transformation. Both PBP and non-PBP mutations conferred some level of intrinsic resistance, but combining the mutations synergized them to ensure high-level resistance (> or = 2 microg/ml). The results underline the complexity of penicillin resistance development and suggest that inhibition of transglycosylase might be an as yet underestimated way to interfere with early resistance development.

Genes, Bacterial↗
PubMed2006

Mutational analysis of class A and class B penicillin-binding proteins in Streptococcus gordonii.

High-molecular-weight (HMW) penicillin-binding proteins (PBPs) are divided into class A and class B PBPs, which are bifunctional transpeptidases/transglycosylases and monofunctional transpeptidases, respectively. We determined the sequences for the HMW PBP genes of Streptococcus gordonii, a gingivo-dental commensal related to Streptococcus pneumoniae. Five HMW PBPs were identified, including three class A (PBPs 1A, 1B, and 2A) and two class B (PBPs 2B and 2X) PBPs, by homology with those of S. pneumoniae and by radiolabeling with [3H]penicillin. Single and double deletions of each of them were achieved by allelic replacement. All could be deleted, except for PBP 2X, which was essential. Morphological alterations occurred after deletion of PBP 1A (lozenge shape), PBP 2A (separation defect and chaining), and PBP 2B (aberrant septation and premature lysis) but not PBP 1B. The muropeptide cross-link patterns remained similar in all strains, indicating that cross-linkage for one missing PBP could be replaced by others. However, PBP 1A mutants presented shorter glycan chains (by 30%) and a relative decrease (25%) in one monomer stem peptide. Growth rate and viability under aeration, hyperosmolarity, and penicillin exposure were affected primarily in PBP 2B-deleted mutants. In contrast, chain-forming PBP 2A-deleted mutants withstood better aeration, probably because they formed clusters that impaired oxygen diffusion. Double deletion could be generated with any PBP combination and resulted in more-altered mutants. Thus, single deletion of four of the five HMW genes had a detectable effect on the bacterial morphology and/or physiology, and only PBP 1B seemed redundant a priori.

DNA Mutational Analysis↗
PubMed1977

Tolerant response of Streptococcus sanguis to beta-lactams and other cell wall inhibitors.

In contrast to group A streptococci or Streptococcus pneumoniae, cells of Streptococcus sanguis (group H) do not exhibit the irreversible effects of penicillin treatment, such as loss of viability or lysis. On the other hand, the same bacteria show typical effects of penicillin, such as morphological alterations, reduction in the rate of cell wall synthesis, and secretion of murein and lipoteichoic acid polymers into the medium. A novel effect of cell wall inhibitors was also noted: treatment with beta-lactams or with fosfomycin, d-cycloserine, or beta-halogeno-d-alanine caused the release of substantial amounts of glycerol lipids into the growth medium. The antibiotic "tolerance" of S. sanguis is interpreted in terms of the hypothesis that the activity of bacterial murein hydrolases is essential for the irreversible effects of cell wall inhibitors.

Alanine↗
PubMed1978

Antimicrobial susceptibility patterns of Streptococcus pneumoniae.

Fifty clinical isolates of Streptococcus pneumoniae received by the Streptococcus Laboratory of the Center for Disease Control from August 1976 through March 1977 and 50 pneumococcal strains retrieved from 13- to 16-year storage (originally isolated October 1961 through December 1964) were tested for susceptibility to 10 antimicrobial agents by disk-agar diffusion and agar dilution tests. No appreciable differences in susceptibility patterns were apparent between the two groups, and, except for one isolate, all were highly susceptible to every drug tested except gentamicin. This single isolate required higher drug concentrations to inhibit macroscopic growth and had corresponding decrements in zones of disk inhibition with penicillin, ampicillin, and cephalothin. An additional 43 pneumococci recently received from various areas of the United States and Canada were screened by a disk agar diffusion method for penicillin resistance. Four of these isolates had penicillin zone diameters <30 mm, and subsequent agar dilution test results showed that the penicillin minimum inhibitory concentrations were elevated with these organisms. Antimicrobial susceptibility patterns of pneumococci to antimicrobials other than penicillin and its analogs have not changed substantially in over a decade. However, due to the emergence of strains with decreased susceptibility to penicillin, the screening test for penicillin resistance in pneumococci, especially in isolates from spinal fluid and blood, could be clinically useful as an aid in selecting optimal therapy.

Cephalosporinase↗
PubMed1978

Effect on antibiotics on protease production by a viridans streptococcus.

A viridans streptococcus (Streptococcus MG intermedius 974) isolated from a confirmed case of subacute bacterial endocarditis was studied for the production of extracellular proteases during exponential growth and after penicillin (0.10 mug/ml) and/or streptomycin (20 mug/ml) treatment. Exponentially growing cultures produced a variety of extracellular proteases, as determined by the elution profiles of active proteins from Sephadex G-100 and Sepharose 4B columns. Examination of supernatant fluids from cultures of S. MG intermedius treated with penicillin or streptomycin for 12 h indicated a reduction of at least 50% in the number of different proteolytic species produced. However, some of the proteases produced by the cultures during penicillin or streptomycin treatment had significantly higher specific activities when compared with proteases produced by exponentially growing cells. The combination of penicillin and streptomycin further reduced both the number and the specific activities of the extracellular proteases on a cell dry weight basis.

Anti-Bacterial Agents↗
PubMed1980

Mutational loss of sensitivity to mutacin GS-5 in Streptococcus pyogenes: characterization of a mutant deficient in receptor protein.

By means of a stepwise selection procedure, mutants capable of growing in the presence of relatively high multiplicities of a bacteriocin from Streptococcus mutans GS-5 were obtained from a sensitivie strain of Streptococcus pyogenes. Mutacin-neutralizing activity of cell extracts containing receptor protein was examined in one variant that adsorbed 1/6 the amount of bacteriocin adsorbed by the parent strain under conditions equivalent to "saturation." Partially purified receptor protein from both parent and mutant cells neutralized an equivalent amount of bacteriocin on a weight-to-weight basis, indicating that in vitro there was no significant difference in affinity for the mutacin between the respective receptor fractions. Cell extracts from the mutant, solubilized by treatment with trichloroacetic acid, neither neutralized mutacin activity nor interfered with receptor protein-mediated mutacin neutralization in vitro. The mutant phenotype may thus represent a cell surface density of receptor protein which results in the adsorption of sublethal amounts of mutacin. The mutant retained its sensitivity to other mutacins, e.g., those produced by strains LM-7 and BHT of S. mutans, and did not differ from wild-type cells with respect to either detergent sensitivity (sodium lauryl sulfate and Triton X-100) or to inhibition by penicillin, rifampin, bacitracin, erythromycin, and tetracycline.

Bacterial Proteins↗
PubMed1984

Infection caused by vancomycin-resistant Streptococcus sanguis II.

A patient with bacteremia caused by vancomycin-resistant Streptococcus sanguis II is presented. This rare occurrence suggests that vancomycin may not be a completely reliable antibiotic in the treatment of infections due to viridans species of the genus Streptococcus. Gram-positive isolates from blood and otherwise sterile body fluids should be tested for susceptibility to vancomycin.

Anti-Bacterial Agents↗
PubMed1988

High-level resistance to gentamicin in clinical isolates of Streptococcus (Enterococcus) faecium.

During a 14-month period beginning in July 1986, three distinct clinical isolates of Streptococcus (Enterococcus) faecium demonstrating high-level resistance (MIC, greater than 2,000 micrograms/ml) to gentamicin, kanamycin, tobramycin, and streptomycin were recovered from individual patients at one institution. Combinations of ampicillin with any of these agents failed to show bactericidal synergism. By filter-mating techniques, high-level gentamicin resistance could be transferred into a susceptible recipient of the same species at frequencies as high as 1 x 10(-4); transfer into Streptococcus faecalis JH2-7 occurred at lower frequencies (less than 2 x 10(-7). Aminoglycoside substrate profile analysis of clinical isolates as well as of laboratory-derived cured strains and transconjugants revealed 2"-aminoglycoside phosphotransferase and 3'-aminoglycoside phosphotransferase (III) phosphorylating enzymes, AAC-6' acetylating activity above that attributable to the intrinsic activity characteristic of S. faecium, and a streptomycin adenylylating enzyme. All three isolates carried a 51-megadalton plasmid. Curing of this plasmid or conjugative transfer into susceptible recipients was associated with the loss or acquisition of high-level gentamicin resistance, respectively. Loss of high-level gentamicin resistance was also observed when curing techniques resulted in a decrease in the size of this plasmid equivalent to a 10-megadalton deletion. Transferable, high-level resistance to gentamicin and other aminoglycosides, which was previously recognized in S. faecalis, has now emerged in clinical isolates of S. faecium, with the attendant concerns for possible spread.

Ampicillin↗
PubMed1993

Chromosomally mediated high-level gentamicin resistance in Streptococcus mitis.

Four blood culture isolates of Streptococcus mitis were found to be resistant to penicillin (MIC, 16 to 32 micrograms/ml) and gentamicin (MIC, 128 or 1,000 micrograms/ml), and the two antibiotics demonstrated a lack of in vitro synergy. As shown by polymerase chain reaction assays, the structural gene known to encode high-level gentamicin resistance in Enterococcus faecalis, Enterococcus faecium, and Streptococcus agalactiae was also present in all four S. mitis strains. Attempts to isolate plasmids were unsuccessful, but an oligonucleotide probe derived from the gentamicin resistance gene hybridized to distinct restriction fragments of genomic DNA, suggesting that the resistance genes in these strains are integrated into the bacterial chromosome.

Chromosomes, Bacterial↗
PubMed1996

Identification of the tetracycline resistance gene, tet(O), in Streptococcus pneumoniae.

Five isolates of Streptococcus pneumoniae resistant to tetracycline but lacking tet(M) were studied. The tetracycline resistance gene, tet(O), was detected for the first time in the pneumococcus. The gene was amplified and sequenced and found to share 99% nucleotide sequence identity and 99, 99, and 98% deduced amino acid sequence identity with the tet(O) resistance genes of Streptococcus mutans, Campylobacter coli, and Campylobacter jejuni, respectively.

Amino Acid Sequence↗
PubMed1997

mefE is necessary for the erythromycin-resistant M phenotype in Streptococcus pneumoniae.

Recently, it was shown that a significant number of erythromycin-resistant Streptococcus pneumoniae and Streptococcus pyogenes strains contain a determinant that mediates resistance via a putative efflux pump. The gene encoding the erythromycin-resistant determinant was cloned and sequenced from three strains of S. pneumoniae bearing the M phenotype (macrolide resistant but clindamycin and streptogramin B susceptible). The DNA sequences of mefE were nearly identical, with only 2-nucleotide differences between genes from any two strains. When the mefE sequences were compared to the mefA sequence from S. pyogenes, the two genes were found to be closely related (90% identity). Strains of S. pneumoniae were constructed to confirm that mefE is necessary to confer erythromycin resistance and to explore the substrate specificity of the pump; no substrates other than 14- and 15-membered macrolides were identified.

Anti-Bacterial Agents↗