Properties of high and low density subpopulations of group B streptococci: enhanced virulence of the low density variant

Håkansson, Stellan; Bergholm, Ann-Marie; Holm, Stig E.; Wagner, Barbara; Wagner, Manfred

doi:10.1016/0882-4010(88)90035-6

Cited by 26 publications

(19 citation statements)

References 17 publications

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“…Furthermore, in an in vivo study, low-buoyancy strains with small amounts of capsule became highly encapsulated and established bacteremia after 5 days of inoculation. Our studies with S. iniae indicate that commensal strains do not cause bacteremia up to 5 days following injection and capsule expression is not evident even in virulent strains (data not shown) (15). Although we have not observed mucoidy in our studies, S. iniae was originally described as an encapsulated organism (27), and mucoid colonies, characteristic of encapsulation, were reported in a fish infection model (8).…”

Section: Discussioncontrasting

confidence: 40%

“…We have noted that disease-associated strains of S. iniae display a high buoyancy (turbid) in broth culture, whereas commensal strains have a low buoyancy, forming a granular precipitate (unpublished data) as described for the type strain (ATCC 29178) (27). For GBS, buoyancy in broth culture is directly related to the level of capsular polysaccharide expression (15,16). Furthermore, in an in vivo study, low-buoyancy strains with small amounts of capsule became highly encapsulated and established bacteremia after 5 days of inoculation.…”

Section: Discussionmentioning

confidence: 99%

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Streptococcus iniaeVirulence Is Associated with a Distinct Genetic Profile

et al. 2001

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Streptococcus iniae causes meningoencephalitis and death in commercial fish species and has recently been identified as an emerging human pathogen producing fulminant soft tissue infection. As identified by pulsedfield gel electrophoresis (PFGE), strains causing disease in either fish or humans belong to a single clone, whereas isolates from nondiseased fish are genetically diverse. In this study, we used in vivo and in vitro models to examine the pathogenicity of disease-associated isolates. Strains with the clonal (disease-associated) PFGE profile were found to cause significant weight loss and bacteremia in a mouse model of subcutaneous infection. As little as 10 2 CFU of a disease-associated strain was sufficient to establish bacteremia, with higher inocula (10 7 ) resulting in increased mortality. In contrast, non-disease-associated (commensal) strains failed to cause bacteremia and weight loss, even at inocula of 10 8 CFU. In addition, disease-associated strains were more resistant to phagocytic clearance in a human whole blood killing assay compared to commensal strains, which were almost entirely eradicated. Disease-associated strains were also cytotoxic to human endothelial cells as measured by lactate dehydrogenase release from host cells. However, both disease-associated and commensal strains adhered to and invaded cultured human epithelial and endothelial cells equally well. While cellular invasion may still contribute to the pathogenesis of invasive S. iniae disease, resistance to phagocytic clearance and direct cytotoxicity appear to be discriminating virulence attributes of the disease-associated clone.

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Section: Discussioncontrasting

confidence: 40%

Section: Discussionmentioning

confidence: 99%

Streptococcus iniaeVirulence Is Associated with a Distinct Genetic Profile

et al. 2001

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“…Decreased buoyancy, decreased surface negative charge, and increased hydrophobicity as measured in our S. iniae ⌬PGM mutant are changes consistent with diminished expression of a polyanionic surface capsule. Direct correlations between buoyancy, degree of encapsulation, and animal virulence have been demonstrated for group B Streptococcus (14), group A Streptococcus (43), and Streptococcus equi (3). Of particular interest, ⌬PGM mutants of S. pneumoniae lacking surface capsule are avirulent in mice (16).…”

Section: Discussionmentioning

confidence: 99%

Streptococcus iniae Phosphoglucomutase Is a Virulence Factor and a Target for Vaccine Development

Buchanan¹,

et al. 2005

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Streptococcus iniae represents a major health and economic problem in fish species worldwide. Random Tn917 mutagenesis and high-throughput screening in a hybrid striped bass (HSB) model of meningoencephalitis identified attenuated S. iniae mutants. The Tn917 insertion in one mutant disrupted an S. iniae homologue of a phosphoglucomutase (pgm) gene. Electron microscopy revealed a decrease in capsule thickness and cell wall rigidity, with ⌬PGM mutant cells reaching sizes ϳ3-fold larger than those of the wild type (WT). The ⌬PGM mutant was cleared more rapidly in HSB blood and was more sensitive to killing by cationic antimicrobial peptides including moronecidin from HSB. In vivo, the ⌬PGM mutant was severely attenuated in HSB, as intraperitoneal challenge with 1,000 times the WT lethal dose produced only 2.5% mortality. Reintroduction of an intact copy of the S. iniae pgm gene on a plasmid vector restored antimicrobial peptide resistance and virulence to the ⌬PGM mutant. In analysis of the aborted infectious process, we found that ⌬PGM mutant organisms initially disseminated to the blood, brain, and spleen but were eliminated by 24 h without end organ damage. Ninety to 100% of fish injected with the ⌬PGM mutant and later challenged with a lethal dose of WT S. iniae survived. We conclude that the pgm gene is required for virulence in S. iniae, playing a role in normal cell wall morphology, surface capsule expression, and resistance to innate immune clearance mechanisms. An S. iniae ⌬PGM mutant is able to stimulate a protective immune response and may have value as a live attenuated vaccine for aquaculture.With increased development of intensive operations, disease has become a significant hurdle to the profitable culture of fish and shellfish. Streptococcal infections in fish, in particular those produced by the pathogen Streptococcus iniae, have increased markedly with intensification of aquaculture practices (37). S. iniae causes a fatal meningoencephalitis and is associated with large-scale mortality in a wide variety of marine and freshwater cultured fish species, as well as in wild species (5,39,46). More than 30 species of fish have documented susceptibility to S. iniae disease, including trout (10), yellowtail (19), tilapia (39), barramundi (6), and hybrid striped bass (HSB) (11). S. iniae is distributed globally and is estimated to cause yearly economic losses of hundreds of millions of dollars. Occasionally, S. iniae can cause serious zoonotic infections in humans who injure themselves while handling infected fish (20,42).Relatively little is known of the genetics of S. iniae or of the pathogenic mechanisms underlying its virulence. Here, we describe a severely attenuated mutant of S. iniae, identified through random transposon mutagenesis and direct screening for virulence in HSB. Analysis of the transposon insertion site revealed a disruption of an open reading frame (ORF) with similarity to bacterial phosphoglucomutase (pgm) genes. The enzyme phosphoglucomutase (PGM) interconverts glucose-6-phosphate an...

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“…An abundantly encapsulated low density (LD) phase variant of GBS was processed from the reference strain GBS 090 Ia Colindale by repeated gradient centrifugation [4]. The strain is a kind gift from Stellan Håkansson, University of Umeå, Sweden.…”

Section: Bacteriamentioning

confidence: 99%

Lung Function and Bacterial Proliferation in Experimental Neonatal Pneumonia in Ventilated Rabbits Exposed to Monoclonal Antibody to Surfactant Protein A

Herting

Strayer

Jarstrand

et al. 1998

Lung

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Surfactant protein A (SP-A) increases the resistance of surfactant to inhibition by plasma and other proteins. In a previous study we found that a monoclonal anti-SP-A antibody (R 5) increased the sensitivity of surfactant to inhibition by fibrinogen in vivo and in vitro. SP-A has been shown to stimulate microbial phagocytosis and killing by alveolar macrophages. We hypothesized that using R 5 to inactivate SP-A in an animal model mimicking congenital group B streptococcal (GBS) pneumonia might result in increased bacterial proliferation and a deterioration in lung function. Newborn near term rabbits were delivered by Cesarean section, anesthetized, tracheotomized, and ventilated for 5 h in a plethysmograph system allowing measurement of dynamic lung-thorax compliance. Postnatally the animals received one intratracheal injection (5 ml/kg) of R 5, nonspecific IgG, or normal saline. At 30 min all animals received a standard dose of an encapsulated GBS strain by intratracheal injection. The number of bacteria (mean log10 CFU/g lung +/- S.D.; CFU = colony forming unit) was evaluated in lung homogenates. Histologic lung sections were judged by light microscopy. Bacterial proliferation was similar in rabbits treated with the monoclonal antibody (9.33 +/- 0.39; n = 14) and in control animals receiving saline (9.16 +/- 0.35; n = 14) or nonspecific IgG (9.26 +/- 0.31; n = 11). No significant differences were noted on the histologic analysis or in measurements of lung function. We conclude that intratracheal instillation of a monoclonal anti-SP-A antibody did not increase bacterial proliferation in GBS-infected newborn rabbits. These findings suggest that SP-A does not play an important role in protection against encapsulated GBS strains in the neonatal period.

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Properties of high and low density subpopulations of group B streptococci: enhanced virulence of the low density variant

Cited by 26 publications

References 17 publications

Streptococcus iniaeVirulence Is Associated with a Distinct Genetic Profile

Streptococcus iniaeVirulence Is Associated with a Distinct Genetic Profile

Streptococcus iniae Phosphoglucomutase Is a Virulence Factor and a Target for Vaccine Development

Lung Function and Bacterial Proliferation in Experimental Neonatal Pneumonia in Ventilated Rabbits Exposed to Monoclonal Antibody to Surfactant Protein A

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