S J Mattingly's research while affiliated with University of Texas Health Science Center at San Antonio and other places

... Although no evidence of peptidoglycan turnover was obtained in the experiments described above, it seemed possible that turnover could occur during unbalanced growth conditions, such as during cell wall thickening induced by inhibition of protein synthesis (22,23), during inhibition of peptidoglycan synthesis, or during recovery from such inhibitions. In view of electron microscopic observations of the apparent shedding of large pieces of cell wall (34), it seemed particularly appropriate to examine the effects of physiological stresses on peptidoglycan turnover. ...

... On the basis of this assumption, the pregnant mouse model would fit well for a comparative evaluation of virulence of bovine and human GBS isolates. In this regard, our findings were not as clear-cut as those previously reported (10, 13, 17, 19), thereby necessitating a reevaluation of the virulence of bovine isolates. Further studies involving a greater number of strains would permit researchers to choose between the lethality in nonpregnant mice or the abortive model reported here, but in our opinion, abortion and placental colonization constitute a suitable mouse model for the examination of GBS virulence and possibly for the evaluation of immunological protection against these organisms. ...

... Estudios posteriores demostraron que esta CAV posee varias características que le confieren una elevada virulencia, tales como valores elevados de productos extracelulares, como antígeno de tipo III, hialuronidasa y proteasa [35][36][37] . Una característica única de los aislamientos que pertenecen a esta CAV es su incapacidad para crecer a 40 ºC en medios con alto contenido de fosfato 20,[38][39][40] . Varios estudios realizados en el centro de México han demostrado la existencia de esta clona 38,41 . ...

... The repeating unit structure of GBS type III polysaccharide is illustrated in Fig. 1. Although previous investigations have suggested the capsular polysaccharide is linked to peptidoglycan in the cell wall (17,18), the nature of the attachment of the capsular polysaccharide to the GBS cell wall has not been clearly defined. In this study, we present evidence to show that the type III GBS capsular polysaccharide is covalently linked via a phosphodiester bond and a linker oligosaccharide to Nacetylglucosamine residues of the disaccharide repeating unit of cell wall peptidoglycan, while the group B antigen is linked to N-acetylmuramic acid. ...

... Usually, the entrance into the stationary phase is accompanied by a decrease of enzyme activity that may be a consequence of protease secretion. Such a feature of neuraminidase production is shared by some streptococci from group A and B, Streptococcus oralis, and Pseudomonas aeruginosa (Milligan et al. 1977;Davis et al. 1979;Straus and Portnoy-Duran 1983;Byers et al. 2000;Ghazaei et al. 2010a, b). Although quite rare, in some Arthrobacter strains, maximum neuraminidase production occurs during the lag-phase with a significant reduction of enzyme activity as bacteria enter the exponential phase (Flashner et al. 1977). ...

... The transcriptomic analysis in GBS strengthens the conserved role of CodY as a global regulator of metabolism, with genes encoding functions involved in the uptake of amino acids and oligopeptides subjected to the highest level of regulation. As genes required for the biosynthesis of precursors of most amino acids, including BCAAs, are missing in the genome of GBS, this bacterium relies on transporters and peptidases for amino acids metabolism (Milligan et al., 1978;Glaser et al., 2002). The capacity to take up exogenous oligopeptides is particularly important to support growth in amniotic fluid, which contains only low amounts of free amino acids (Mesavage et al., 1985;Samen et al., 2004). ...

... We found the hlyB gene to be present within 80% of both carriage and invasive disease isolates. Associations have been made between elevated production of this enzyme and neonatal disease within type III isolates [64], however, other studies have observed invasive disease caused by isolates lacking this gene [65]. ...

... In these studies, however, the organisms were regarded as minor pathogens, although several of the strains appeared as pure isolates. Despite the demonstration that viridans streptococci are capable of elaborating potentially toxic and damaging extracellular proteases that may cause apparent clinical disease (9), most microbiology laboratories do not identify these organisms in clinical specimens to the species level because of their uncertain role in the pathogenesis of the diseases in which they are found, as well as the difficulty in identifying viridans streptococci with conventional biochemical tests. Since the introduction of schemes for species identification (10,11), the S. milleri group of viridans streptococci have received attention because of their frequent isolation from various suppurative infections (12)(13)(14)(15), but there are only a few reports describing the clinical features of pleuropulmonary diseases caused by species of viridans streptococci other than those of the S. milleri group (16)(17)(18). ...

... Our microarray analysis identified a large number of genes involved in sugar uptake and metabolism as being upregulated in the Dclp strains. Among these were the genes encoding enzymes responsible for the biosynthesis of IPS, a glycogen-like polymer that serves as a storage form of carbohydrate (DiPersio et al., 1978). The synthesis of IPS has been implicated in enhanced survival of S. mutans and has been shown to contribute to caries formation (Gibbons & Socransky, 1962;Spatafora et al., 1995;van Houte et al., 1970). ...

... Likewise, the reversal of the killing capacity of neutrophils by the addition of iron or iron compounds would suggest that iron-binding proteins play an essential role in the bactericidal activity of polymorphonuclear leukocytes (5,6,8). These effects are distinct from the traditionally studied bacteriostatic phenomenon of iron deprivation by ironchelating molecules (reviewed in reference 12). ...