[Streptococcus agalactiae (Streptococcus group B): clinical and bacteriological aspects].
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The cellular locations of deacylated lipoteichoic acid (dLTA) and lipoteichoic acid (LTA) were examined in late-exponential-phase cells of a serotype III strain of Streptococcus agalactiae (group B streptococci [GBS]) isolated from an infant with late-onset meningitis and compared with a fresh clinical isolate of Streptococcus pyogenes (group A streptococci [GAS]). LTA and dLTA were found to be associated with the protoplast membranes of both organisms, with only dLTA found in mutanolysin cell wall digests. Both organisms released dLTA during growth, but only the GAS released substantial levels of LTA into the culture medium. However, penicillin treatment (5 micrograms/ml for 60 min) of GBS resulted in the recovery of LTA in cell wall digests as well as in the culture medium. These results suggest that under normal growth conditions, the hydrophobic region (glycolipid) of LTA remains associated with the cytoplasmic membrane of GBS and unavailable for hydrophobic interactions at the cell surface with epithelial cells. In contrast, release of LTA into the environment by the GAS allows the fatty acid moieties to interact with hydrophobic domains on the surface of epithelial cells. These results may help explain the marked differences in the specificity of binding between these two major streptococcal pathogens for human fetal and adult epithelial cells.
Chromosomal genotypes of 128 isolates of six serotypes (Ia, Ib, Ic, II, Ic/II, and III) of Streptococcus agalactiae (group B Streptococcus) recovered predominantly from human infants in the United States were characterized by an analysis of electrophoretically demonstrable allelic profiles at 11 metabolic enzyme loci. Nineteen distinctive electrophoretic types (ETs), representing multilocus clonal genotypes, were identified. Mean genetic diversity per locus among ETs of isolates of the same serotype was, on average, nearly equal to that in all 19 ETs. Cluster analysis of the ETs revealed two primary phylogenetic divisions at a genetic distance of 0.65. A single clone (ET 1) represented by 40 isolates expressing type III antigen formed division I. Division II was composed of 18 ETs in three major lineages diverging from one another at distances greater than 0.35 and included strains of all six antigenic classes. The type III organisms in division I produce more extracellular neuraminidase and apparently are more virulent than the type III strains in division II, which are related to strains of other serotypes that cause disease much less frequently. The existence of this unusually virulent clone accounts, in major part, for the high morbidity and mortality associated with infection by type III organisms.
We have established an experimental murine model to gain insight into the pathogenicity and clinical features of type IV group B streptococcus (GBS) infections. Adult CD-1 mice were challenged intravenously with 10(7) type IV GBS cells, inducing systemic invasion. Most of the animals were able to clear the infection from the blood, brain, and lungs within 2 weeks and from the spleen and liver within 1 month. However, the animals were unable to clear the microorganism from the joints and kidneys during the 60-day observation period. About 80% of the mice challenged intravenously with type IV GBS manifested early septic arthritis, which evolved from an acute exudative synovitis to permanent lesions characterized by irreversible joint damage and ankylosis. Induction of persistent septic arthritis was dependent on the number and viability of microorganisms inoculated and was unrelated to the strain of type IV GBS and the growth phase of the inoculum. Type-specific antibodies of both immunoglobulin M and G classes could be detected by agglutination and enzyme-linked immunosorbent assay from days 7 and 14, respectively; immunoglobulin G antibodies persisted for more than 40 days. Complexes of antibodies and group- and type-specific antigens were detected in mouse sera 24 h after infection and persisted up to day 22. These results were obtained an experimental model of type IV GBS chronic infection with early development of septic arthritis, which could be useful in future studies of pathogenicity and immune mechanisms involved in the host resistance to this microorganism.
A Streptococcus agalactiae isolate of bovine origin was cultured in broth; log-phase cells were washed and radioiodinated and subsequently extracted at low pH in the presence of a nonionic detergent. A protein antigen was purified from concentrated extract by ultracentrifugation, gel filtration, and ion-exchange chromatography. The molecular weight of the protein was estimated at 31,800. The agglutinogenic character of the protein indicated its localization at the cell surface.
Streptococcus agalactiae is presently the commonest beta-haemolytic streptococcus isolated from clinical material in this hospital. Between October 1974 and March 1975, 81 patients with such infections were seen. Seventeen had urinary tract infections, six had septicaemia, and one neonate had meningitis. Three of those with septicaemia were neonates and two died. The organism was also found to be a cause of pyogenic skin conditions in five patients. Isolates from throat swabs in 12 patients, from sputum in four, and from the female genital tract in 18 were considered part of the normal flora. Human strains of Str. agalactiae were found to be biochemically different from animal strains.
BACKGROUND: Streptococcus agalactiae increases the risk of adverse pregnancy outcomes and neonatal infections. Clindamycin is a key alternative for intrapartum prophylaxis in penicillin-allergic women, but the prevalence of clindamycin-resistant S. agalactiae is increasing, posing a significant clinical challenge. METHODS: A total of 178 strains isolated from tertiary hospitals in Jinan and Qingdao, Shandong Province, China, were characterized using antimicrobial susceptibility testing, whole-genome sequencing, multilocus sequence typing, serotyping, and analysis of resistance and virulence genes. RESULTS: All strains were susceptible to penicillin, ampicillin, linezolid, vancomycin, and tigecycline. In contrast, resistance rates to erythromycin, levofloxacin, and tetracycline were 95.5%, 60.1%, and 56.7%, respectively. Six serotypes and 15 sequence types belonging to eight clonal complexes were identified. Notable regional differences were observed. The Ib-ST10-CC12 lineage dominated in Jinan, whereas V-ST529-CC327 was predominant in Qingdao. The resistance gene mreA was ubiquitous (100%), followed by ermB (80.3%). The key virulence genes cylE, hylB, and pavA, were detected in all strains. fbsA (99.4%), the alpha protein family (98.9%), cfb (98.3%), the Pilus Island gene cluster (94.9%), and lmb (92.7%) were also highly prevalent. The two major clindamycin resistance genes, erm and lnuB, exhibited distinctly different enrichment patterns among S. agalactiae clonal complexes, despite a certain overlap in CC19 and CC327. Specifically, erm was significantly enriched in CC12 (serotype Ib), CC19 (III/V), and CC327 (III/V). In contrast, lnuB was predominantly restricted to CC19 and CC327, where it defined a unique phylogenetic subcluster. Significant differences in resistance and virulence gene profiles were observed across different clonal complexes. CONCLUSION: Clindamycin-resistant S. agalactiae in late-pregnancy women in Shandong Province, China exhibits a broad resistance spectrum, diverse molecular types, and significant regional heterogeneity. These findings underscore the need for continued surveillance and region-specific strategies for preventing neonatal S. agalactiae infections.
Streptococcus agalactiae was found to be the cause of approximately 1% of urinary tract infections in a London teaching hospital in the 2 years studied. Of the forty-eight patients with this infection, forty-three were female. In nine patients the infection followed renal transplantation while in nine others it occurred in the presence of chronic renal failure. The rest, who included seven females who developed the infection following hysterectomies, had other clinical conditions which could have predisposed to such infections. The rarity of urinary tract infection by S. agalactiae is in contrast to the high frequency with which the organism colonizes the normal urethra. Serotypes III and II were the predominant isolates in these patients with urinary tract infections; this corresponds to the distribution of the different serotypes in the genito-urinary tract of normal individuals.
Streptococcus agalactiae was identified as the cause of mastitis in a 240-cow dairy herd. Forty-five per cent of the herd had cell counts over 500,000/ml, and 28 per cent had cell counts over 1,000,000/ml. Dry cow therapy was used regularly but teat dipping had not been used for three years. The procedures at milking were modified, teat dipping was introduced, and the herd was divided into two according to cell count. The 120 cows with higher cell counts were treated with 300 mg erythromycin (Erythrocin intramammary; Sanofi Animal Health) preparation per quarter at two consecutive milkings. Towards the end of lactation, all the 90 lactating cows in the herd were again treated with erythromycin. Milk samples were collected from all the cows in the herd 12 months after the initial treatment, and S agalactiae was isolated from only one replacement heifer which had been purchased after the treatments with erythromycin. The butterfat and protein levels in the milk were compared with those of a similar, but untreated, herd for 12 months before and after therapy. The butterfat levels rose sharply after treatment, and financial assessment showed a 41 per cent return on investment in the 12 months following the treatment.
Staphylococcus aureus and Streptococcus agalactiae growth responses to metabolites of Corynebacterium bovis cultured in media containing polyoxyethylenesorbitan monolaurate, monooleate, or trioleate and milk were determined. Filter sterilized metabolites of 48-h C. bovis cultures in synthetic media were added to cultures of Staph. aureus and Strep. agalactiae. Staphylococcus aureus and Strep. agalactiae were inoculated into 12-h C. bovis milk cultures. Growth responses of Staph. aureus and Strep. agalactiae were not affected by C. bovis metabolites of synthetic media. Staphylococcus aureus growth was inhibited during logarithmic and stationary phases in milk containing mixed cultures of C. bovis compared with growth in pure Staph. aureus cultures. Streptococcus agalactiae growth curves were similar in pure and C. bovis mixed cultures. Fatty acid compositions were not different in sterile milk and milk containing bacterial cultures. Growth responses of Staph. aureus and Strep. agalactiae were not related to concentration of C. bovis metabolites or fatty acid content of media in which C. bovis were cultured.
Interbacterial coaggregation between Actinomyces viscosus indigenous to the human mouth and Streptococcus pyogenes and Streptococcus agalactiae was studied. Fifteen of twenty-six strains of Streptococcus pyogenes and thirteen of thirty-one Streptococcus agalactiae showed a coaggregation with Actinomyces viscosus strain. The results show that the coaggregation mechanism required calcium and was dependent on pH. Some coaggregations were inhibited by 0.06 M. lactose and by 1 M. NaCl.
The protein X of Streptococcus agalactiae is a surface antigen borne by a high proportion of strains isolated from bovine mastitis. We have tested the capacity of two strains of X-bearing Streptococcus agalactiae to induce mastitis in dairy cows. The reference X-strain (411.07) produced an intramammary infection with local clinical signs in the three inoculated quarters. Another X-bearing strain (443.31) of bovine origin produced infection in all 11 quarters inoculated with only 25 or 85 colony-forming units. In naive cows, strain 433.31 induced less exudation of plasma into the milk, shedding of bacteria, macroscopic alteration, and a lower somatic cell count (SCC) than did the reference strain. Only one quarter spontaneously eliminated the infection before antibiotic treatment 9 days after inoculation. The serum of all the cows contained naturally acquired or induced antibodies to the challenge strain (443.31) and possessed opsonic activity. Before inflammation occurred, the milk was almost devoid of antibody or opsonic activities. The early phase of infection was characterized by rapid multiplication of streptococci in the milk, followed by a sharp drop in bacterial counts concomitant with the onset of inflammation. Three cows immunized with protein X displayed higher SCC and bactericidal activity in milk from the inoculated quarter at the onset of inflammation than non-immunized cows. Two of the three immunized cows underwent an early and transient febrile episode and eliminated the infection.
A latex agglutination test system (Rapid Mastitis Test [RMT]; Immucell, Portland, Maine) containing reagents for the identification of Staphylococcus aureus and Streptococcus agalactiae from bovine intramammary infections was evaluated with 527 staphylococcal and 267 streptococcal isolates. The RMT Staphylococcus aureus reagent detected 94.2% of 242 Staphylococcus aureus isolates, 80% of 25 Staphylococcus intermedius isolates, and 42.8% of 21 tube coagulase-positive Staphylococcus hyicus isolates. All Streptococcus agalactiae isolates were correctly identified by the RMT Streptococcus agalactiae reagent. Cross-reactions were observed with one Streptococcus dysgalactiae and three Streptococcus uberis strains. The RMT was found to be an acceptable method for the detection of Staphylococcus aureus and Streptococcus agalactiae isolated from bovine mammary glands. The occurrence of coagulase-positive staphylococci other than Staphylococcus aureus requires biochemical testing for species level identification.
Two monoclonal antibodies produced against Streptococcus agalactiae were studied for their specificity and sensitivity. Both reacted strongly in the enzyme-linked immunosorbent assay and indirect fluorescent antibody test with S agalactiae, but did not react with other gram-positive organisms frequently found in test herds in Mississippi. A procedure for using monoclonal antibodies in the detection of S agalactiae-infected milk samples is proposed.
Streptococcus agalactiae (group B streptococci) isolates from infected infants have been demonstrated to have three- to fourfold or higher levels of cell-associated lipoteichoic acid than isolates from asymptomatically colonized infants, suggesting a role for this cell surface polymer in the relative virulence of these organisms. The present study indicates that symptomatic isolates of type III group B streptococci can be readily differentiated from asymptomatic strains by their response to various levels of phosphate in a chemically defined medium (FMC). Both classes of isolates had the same doubling time (TD of 30 to 35 min) in FMC containing 65 mM sodium phosphate. However, levels of phosphate greater than 125 mM distinguished the two classes of strains. Asymptomatic strains pregrown in 65 mM phosphate to the stationary phase rapidly initiated growth at elevated phosphate levels, while symptomatic strains initiated growth only after a prolonged incubation period (greater than 400 min). These results suggest that the physiological growth response of clinical isolates of group B streptococci to phosphate can serve as a diagnostic aid in screening potentially virulent strains in pregnant women and newborn infants.
Two out of 30 strains of Streptococcus agalactiae produced stable L phase variants when passaged on hypertonic agar containing penicillin. Streptococcal L phase variants were inoculated into six quarters of cows. The cows were observed for three months but the L phase was not reisolated and no reversion took place, the cows remaining free from streptococcal infection.
The economic benefits of treating lactating cows for Streptococcus agalactiae mastitis were studied at a large (689 milking cows) central California dairy. Postcure milk production of case cows (infected, treated, and cured) was compared with production of paired control cows (uninfected) and was matched for yield, days in milk, days in gestation, and parity. A simulation was used to plot expected lactation curves for mastitic cows (infected, not treated) with characteristics similar to those of each control cow, and these curves were compared with actual case-cow lactation curves. The difference in actual and expected production was used to calculate net economic benefits of treatment. Comparison of expected with actual production indicated a net benefit from treatment of $396/cow for cows treated in early lactation and $237 for cows treated in midlactation, but a net loss of $55 for cows treated in late lactation. Lactation number did not have a significant impact on economic benefits of treatment. In contrast to other studies indicating no economic benefit from treating mastitis during lactation, this study's positive results may have been attributable to the high cure rate (98%) and the subclinical form of mastitis being treated. Streptococcus agalactiae mastitis treatment during early and midlactation would appear to be an economically justifiable option for dairy managers.
The sensibility of 3100 Streptococcus agalactiae strains and 600 Staphylococcus aureus strains to antibiotics was examined in 1975 in the veterinary institute of the Slovak Socialist Republic by the plate diffusion test. The strains were collected from the dairy cow's milk samples. Of the Streptococcus agalactiae strains there were sensible 100% to ampicillin, 99.06% to chloramphenicol, 98.13% to erythromycin, 96.12% to oxytetracycline, 91.11% to bacitracin, 58.12% to penicillin, 23.92% to neomycin, 17.78% to streptomycin. Of the Staphylococcus aureus strains there were sensible 97.48% to erythromycin, 97.14% to chloramphenicol, 95.15% to ampicillin, 94.81% to bacitracin, 93.26% to oxytetracycline, 92.49% to neomycin, 85.37% to streptomycin and 46.02% to penicillin. The results are being more thoroughly analysed and compared in the dicussion.