Persistent Group B streptococcus bacteremia without clinical “sepsis” in infants

Roberts, Kenneth B.

doi:10.1016/s0022-3476(76)81080-3

Cited by 13 publications

(4 citation statements)

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“…Older infants, however, apparently may respond to and effectively localize infections, often to the meninges (41). In the United States, group B streptococci cause an estimated 3000 to 9000 cases per year of neonatal infection (1), including asymptomatic bacteremia, cellulitis, conjunctivitis, ethmoiditis, hypothalamic-pituitary dysfunction, impetigo, meningitis, omphalitis, osteomyelitis, otitis media, pleural and subdural empyema, pneumonia, respiratory distress, septicemia, and sup purative arthritis (12,18,20,21,32,34,37,41,49,64,71). Though less common than neonatal infections, reported adult infections include abor tion, abscesses, arthritis, empyema, endocarditis, meningitis, myocarditis, osteomyelitis, otitis media, peritonitis, pneumonia, postpartum infections, septicemia, and urinary tract infections (19,25,40,43,51,68-70, 87,93, 96).…”

Section: Clinical Significancementioning

confidence: 99%

Group B Streptococcal Infection in Humans

Wilkinson¹

1978

Annu. Rev. Microbiol.

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Section: Clinical Significancementioning

confidence: 99%

Group B Streptococcal Infection in Humans

Wilkinson¹

1978

Annu. Rev. Microbiol.

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“…`Although Fry and Eng (2) were the first to describe three fatal group B postpartum infections and to point out the clinical importance of GBS in human infections, it was not until 1973 that GBS were firmly established as a major cause in perinatal infections (3)(4)(5)(6)(7)(8). Meanwhile a wealth of information has been accumulated and has been summarized in a number of review articles (9-11) .GBS have been isolated with increasing frequency from infants with early-and late-onset septicemia and meningitis (5, 12), but they also contributed to more infrequent infections in adults such as abortion, abscesses, bacteremia, impetigo, arthritis, septicemia, and urinary tract infections (2,5,8,(13)(14)(15)(16)(17)(18)(19)(20) .Besides the common group antigen, most strains of GBS share an extracellular protein first described in 1944 by Christie, Atkins, and Munch-Petersen, which accordingly was named CAMP factor (21). The CAMP factor causes lysis of red blood cells that contain at least 45 mol -% of sphingomyelin (22) and which have been exposed to Staphylococcus aureus #-toxin (sphingomyelinase) .…”

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confidence: 99%

“…GBS have been isolated with increasing frequency from infants with early-and late-onset septicemia and meningitis (5, 12), but they also contributed to more infrequent infections in adults such as abortion, abscesses, bacteremia, impetigo, arthritis, septicemia, and urinary tract infections (2,5,8,(13)(14)(15)(16)(17)(18)(19)(20) .…”

mentioning

confidence: 99%

Unspecific binding of group B streptococcal cocytolysin (CAMP factor) to immunoglobulins and its possible role in pathogenicity.

Jürgens¹,

Sterzik²,

Fehrenbach³

1987

The Journal of Experimental Medicine

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The protein B of group B streptococci can bind in a nonimmune reaction to Ig of the IgG and IgM classes of various mammalian species (i.e., human, mouse, rabbit, and bovine). Protein B binding involves the Fc parts of both IgG and IgM molecules. Monoclonal or polyclonal IgG or IgM and the IgM-FC5 mu fragment of human myeloma protein combined with the protein B thereby inhibiting protein B-induced hemolysis in the CAMP reaction. The protein B/Ig complex can be dissociated with 1% Triton or guanidine-HCl (6 M). Mice infected intraperitoneally with sublethal doses of group B streptococci (GBS) and that received seven repeated intravenous injections of highly purified protein B during the first 9 h of infection developed fatal septicemia within 24 h with colony counts of up to 10(8) CFU/ml in the blood. Animals treated in the same way with either PBS or trypsinized protein B recovered. The protein B itself was not pathogenic when injected into healthy mice. Tissue sections of liver or spleen from mice infected with a lethal dose of GBS revealed the presence of protein B together with large numbers of cocci when stained by the peroxidase method using specific antibodies raised against purified protein B in the rabbit.

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“…GBS pneumonia, "early-onset disease," presents on the day of birth with signs of sepsis, granulocytopenia, and respiratory distress, characterized by pulmonary hypertension and proteinaceous pulmonary edema. Early-onset disease has been compared to Gram-negative endotoxin shock (2, 3), suggesting the involvement of extracellular toxin(s) (4,5).…”

mentioning

confidence: 99%

Molecular basis for group B beta-hemolytic streptococcal disease.

Hellerqvist¹,

Sundell²,

Gettins³

1987

Proc. Natl. Acad. Sci. U.S.A.

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Group B j3-hemolytic Streptococcus (GBS) is a major pathogen affecting newborns. We have investigated the molecular mechanism underlying the respiratory distress induced in sheep after intravenous injection of a toxin produced by this organism. The pathophysiological response is characterized by pulmonary hypertension, followed by granulocytopenia and increased pulmonary vascular permeability to protein. 31P NMR studies of GBS toxin and model components before and after reductive alkaline hydrolysis demonstrated that phosphodiester residues are an integral part of the GBS toxin. Reductive alkaline treatment cleaves phosphate esters from secondary and primary alcohols and renders GBS toxin nontoxic in the sheep model and inactive as a mediator of elastase release in vitro from isolated human granulocytes. We propose that the interaction of cellular receptors with mannosyl phosphodiester groups plays an essential role in the pathophysiological response to GBS toxin.Infection with group B 3-hemolytic Streptococcus (GBS) is associated with high morbidity and mortality rates in newborn infants (1). GBS pneumonia, "early-onset disease," presents on the day of birth with signs of sepsis, granulocytopenia, and respiratory distress, characterized by pulmonary hypertension and proteinaceous pulmonary edema. Early-onset disease has been compared to Gram-negative endotoxin shock (2, 3), suggesting the involvement of extracellular toxin(s) (4, 5).We have described (6) an extensive bacterial and media component fractionation procedure, which led to the isolation of a polysaccharide toxin from the culture media of a type III group B Streptococcus. This toxin, when infused into sheep, caused pulmonary hypertension, increased vascular pulmonary permeability, changes in lung mechanics, and granulocytopenia with accumulation of granulocytes in the lung (7)(8)(9).Structural analysis of the polysaccharide component of GBS toxin has indicated a repeating unit of nine mannose residues. The determination of the structural feature of the polysaccharide essential for biological activity has been the subject of the highest priority. The data presented herein suggest that a phosphodiester residue linking a mannosyl residue to the mannan is required for pathophysiological activity of GBS toxin. Its presence and identification are based on NMR studies. Its role in inducing respiratory distress in the sheep and release of elastase from granulocytes in vitro is based on physiological data obtained with the native GBS toxin before and after reductive alkaline hydrolysis. MATERIALS AND METHODSBacterial Cultures. GBS type III cultures were initiated from the original stock inoculum (6) and stored at -70°C by incubation in Todd-Hewitt broth (THB) for 9 hr at 37°C.Sheep blood agar (SBA) plates were inoculated and incubated overnight. Several colonies were picked and grown in THB overnight, and these cultures were used for inoculation of mice.In Vivo Passage of GBS. Mice were inoculated subcutaneously with 0.3 x 109 bacteria and were sacrifi...

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Persistent Group B streptococcus bacteremia without clinical “sepsis” in infants

Cited by 13 publications

References 4 publications

Group B Streptococcal Infection in Humans

Group B Streptococcal Infection in Humans

Unspecific binding of group B streptococcal cocytolysin (CAMP factor) to immunoglobulins and its possible role in pathogenicity.

Molecular basis for group B beta-hemolytic streptococcal disease.

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