Serious infections in adults due to group B streptococci

Bayer, Arnold S.; Chow, Anthony W.; Anthony, Bascom F.; Guze, Lucien B.

doi:10.1016/0002-9343(76)90329-6

Cited by 169 publications

(51 citation statements)

References 18 publications

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“…Septic GBS arthritis in nonpregnant adults was considered extremely rare (5,18) until the early 1980s, when two independent studies stressed that its incidence seemed to be increasing (17,34). This trend has been confirmed by recent studies in which GBS infection was found to account for 7 to 10% of all diagnosed cases of bacterial arthritis (7,22).…”

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Toll-Like Receptor 2 Deficiency Is Associated with Enhanced Severity of Group B Streptococcal Disease

et al. 2009

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Group B streptococcus (GBS) has been recognized as an ever-growing cause of serious invasive infections in nonpregnant adults, in particular, in association with severe underlying diseases. The most common manifestations include primary bacteremia, urinary tract infections, pneumonia, meningitis, peritonitis, and osteoarticular infections. Toll-like receptor-2 (TLR2) mediates host responses to gram-positive bacteria. TLR2 function was investigated in murine GBS-induced sepsis and arthritis in wild-type (wt) and TLR2-deficient (TLR2 ؊/؊ ) mice. Mice were infected with different doses of GBS (10 7 , 5 ؋ 10 6 , or 10 6 CFU per mouse). Mortality, appearance of arthritis, GBS growth in the organs, and local and systemic cytokine and chemokine production were examined. TLR2؊/؊ mice showed earlier and higher mortality rates and increased incidence and severity of arthritis than wt mice at all the infecting doses employed. Histopathological analysis of the joints confirmed clinical observations. TLR2 ؊/؊ mice exhibited a higher microbial load in blood, kidneys, and joints than wt animals. In vitro experiments performed with peritoneal polymorphonuclear cells and macrophages showed a significantly lower bactericidal ability of cells from TLR2 ؊/؊ mice. Increased systemic and local levels of interleukin-1␤ (IL-1␤), IL-6, tumor necrosis factor alpha, macrophage inflammatory protein-1␣ (MIP-1␣), and MIP-2 accompanied the more severe development of sepsis and arthritis in TLR2 ؊/؊ mice. In conclusion, the lack of TLR2 was associated with an impaired host resistance to GBS infection, likely due to a diminished bacterial clearing and a consequent enhanced inflammatory response.

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Toll-Like Receptor 2 Deficiency Is Associated with Enhanced Severity of Group B Streptococcal Disease

et al. 2009

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“…There is a difference in the level of susceptibility, however, with group A streptococci being more susceptible than group B (3,10). It has also been reported that a longer period of time is required for penicillin to begin killing cultures of group B than of group A (13).…”

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Synergism, killing kinetics, and antimicrobial susceptibility of group A and B streptococci

Baker¹,

Thornsberry²,

Facklam³

1981

Antimicrob Agents Chemother

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“…Group B disease is known to occur in other compromised hosts including diabetics (4,8), patients with liver disease, and ones with renal failure (4). Moreover, we have demonstrated that acutely stressed neonates with group B streptococcal sepsis or meningitis often develop neutropenia (6) and have PMN chemotactic and bactericidal abnormalities (19).…”

Section: Discussionmentioning

confidence: 99%

“…Both healthy and term neonatal PMNs have defective chemotactic activity (13,16) which would partially explain the abnormality observed. Of interest is the fact that diabetic individuals who have an increased incidence of group B streptococcal infections (4,8) also have defects in PMN chemotactic activity (1 1, 12).…”

Section: Discussionmentioning

confidence: 99%

Functional Leukocyte Administration in Protection against Experimental Neonatal Infection

1980

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SummaryStudies have shown that human neonates who develop group B streptococcal sepsis usually lack opsonic antibody (Ab) to their infecting strain and that these neonates may also have impaired polymorphonuclear leukocyte (PMN) function. The present study was designed to determine the efficacy of administration of PMNs or opsonic Ab-contPining serum in protecting against group B streptococcal infection in a newborn rat model. After intraperitw neal (IP) injection of -5 x 106 streptococci, animals received separate IP injections of saline, serum lacking opsonic antibody (Ab negative), Ab positive serum or washed adult human PMNs (2 x 106). The mortality rate in 55 neonatal rats infected with group B streptococci who received saline or Ab negative serum was 91%. In contrast, 40 animals who received adult human PMNs at the time of inoculation had a survival rate of ! N% (P < 0.001).Human serum containing opsonic antibody also provided significant protection against mortality in this model (survival rate 51%, P < 0.001). Leukocvtes from normal term neonates. stressedbemates, or ones pietreated with cytochalasin B offered less protection than did functional adult human cell (P < 0.001). SpeculationThis study provides evidence for polymorphonuclear leukocyte (PMN) dysfunction as another risk factor in group B streptococcal disease and suggests that fully functional PMNs are required for protection. Furthermore, this model involving the administration of human PMNs to an animal appears to have the potential for the in viw evaluation of PMN function in neonates and other compromised hosts. (2) have demonstrated the absolute requirement of specific antibody for significant opsonization of group B streptococci. In previous studies, we have shown that human neonates who develop group B streptococcal sepsis usually lack opsonic antibody to their infecting strains (10) and that these neonates may also have impaired polymorphonuclear leukocyte function (19). Inasmuch as opsonization and phagocytosis represent the most important host defense mechanisms in clearing the body of these bacteria, the present study was designed to determine the effects of passively supplying functional human polymorphonuclear leukocytes (PMNs) or serum containing opsonic antibody in protecting against group B streptococcal infection in a newborn rat model. METHODS PREPARATION OF ORGANISMSGroup B streptococci type I11 were isolated from the blood and cerebrospinal fluid of infected infants. The strains were cultured at 37°C in Todd-Hewitt broth (Difco Laboratories, Detroit, MI), washed and concentrated in phosphate-buffered saline by centrifugation to contain 5.0 X 10' to 1.0 X lo9 colony-forming units per ml, as previously described (10, 17). NEONATAL RAT INFECTIONSSprague-Dawley outbred pregnant female rats (Holtzman) were obtained one wk before delivery. When tested, maternal rat serum did not appear to contain signif~cant opsonic activity against most of the strains we used. The neonatal progeny less than 24 hr-old were randomly assigned to gro...

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Serious infections in adults due to group B streptococci

Cited by 169 publications

References 18 publications

Toll-Like Receptor 2 Deficiency Is Associated with Enhanced Severity of Group B Streptococcal Disease

Toll-Like Receptor 2 Deficiency Is Associated with Enhanced Severity of Group B Streptococcal Disease

Synergism, killing kinetics, and antimicrobial susceptibility of group A and B streptococci

Functional Leukocyte Administration in Protection against Experimental Neonatal Infection

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