Specific binding of the 1251-labeled human S protein (vitronectin) which has been shown to be identical with serum-spreading factor, was observed with group A, C, and G streptococci as well as with Staphylococcus aureus and Escherichia coli. The specific binding of S protein to group A, C, and G streptococci was high, whereas the binding to S. aureus and E. coli cultures was moderate. In contrast, group B streptococci and a number of other bacterial species tested did not interact with S protein. The binding of S protein to bacteria was saturable and could be inhibited only by unlabeled S protein but not by albumin. Trypsinization and heat treatment of bacteria destroyed the S-protein binding capacity for group G streptococci, S. aureus, and E. coli but not for group A and C streptococci. Likewise, unlabeled human fibronectin and heparin inhibited the binding of labeled S protein to group G streptococci, S. aureus, and E. coli, but did not influence the binding to group A and C streptococci. Double-reciprocal plots of S-protein binding to group G streptococci indicated that fibronectin inhibited the binding in a, competitive manner, while heparin acts in a noncompetitive manner. Moreover, the binding of S protein to G streptococci could be partially inhibited by the synthetic peptide Gly-Arg-Gly-Asp-Ser, which contains the cell attachment site of S protein. Trypsin-treated S protein had similar binding activity as untreated S protein for group G streptococci, S. aureus, and E. coli, but showed reduced binding to group A and C streptococci. The present data are indicative of two different types of bacterial binding sites in S protein. The binding to group G streptococci, S. aureus, and E. coli is mediated in part through a domain in the S protein containing the sequence Arg-Gly-Asp, whereas a different site is responsible for the binding to group A and C streptococci.

A small plasmid of 3.95 kb, encoding resistance to chloramphenicol (Cm) was detected in three of 33 Staphylococcus hyicus strains. The plasmid in each of the three strains was indistinguishable by Southern-blot hybridization and restriction enzyme analysis. It was shown by curing and by transformation to specify resistance to Cm. A preliminary restriction map of the plasmid, designated pSC2, is presented. Chloramphenicol acetyltransferase was demonstrated by enzyme assay and by SDS-PAGE of cell-free lysates of pSC2 transformants.

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Actinomyces pyogenes and Arcanobacterium haemolyticum were further characterized. A. haemolyticum, in contrast to A. pyogenes, gave synergistic hemolytic reactions with streptococci of serological group B and inhibited staphylococcal beta-hemolysis. A. pyogenes and A. haemolyticum had a number of common, as well as distinctly different enzymatic properties, useful for their characterization. Extracts from A. pyogenes reacted with antiserum against streptococci of serological group G in contrast to those from A. haemolyticum.

The objective of this review on the investigation of "cara inchada" in cattle (CI), pursued over the last 30 years, was to elucidate the pathogenicity of the disease and come to proper conclusions on its etiology. CI has been widely considered to be of nutritional origin, caused primarily by mineral deficiency or imbalance. However, the disease consists of a rapidly progressive periodontitis, affecting the periodontal tissues at the level of the premolars and molars during the period of tooth eruption generally starting in young calves. The disease led to great economic losses for farmers in central-western Brazil, after the occupation of new land for cattle raising in the 1960s and 1970s. The lateral enlargement of the maxillary bones of affected calves gave the disease the popular name of "cara inchada", i.e., swollen or enlarged face. The enlargement was found to be due to a chronic ossifying periostitis resulting from the purulent alveolitis of CI. Black-pigmented non-saccharolytic Bacteroides melaninogenicus, always together with Actinomyces (Corynebacterium) pyogenes, were isolated in large numbers from the periodontal lesions. B. melaninogenicus could be isolated in small numbers also from the marginal gingiva of a few healthy calves maintained on CI-free farms. "In vitro"-assays showed that streptomycin and actinomycin, as well as the supernatants of cultivates of actinomycetes from soils of CI-prone farms, applied in subinhibitory concentrations to the bacteria tested, enhanced significantly (up to 10 times) the adherence of the black-pigmented B.melaninogenicus to epithelial cells of the bovine gingiva. The antibiotics are apparently produced in large quantities by the increased number of soil actinomycetes, including the genus Streptomyces, that develop when soil microflora are modified by cultivating virgin forest or "Cerrado" (tree-savanna) for the first time for cattle grazing. The epidemiology of CI now provides strong evidence that the ingestion with the forage of such antibiotics could possibly be an important determinant factor for the onset and development of this infectious periodontitis. The antibiotic enhanced adherence of B.melaninogenicus to the sulcus-epithelium of the marginal gingiva, is thought to allow it to colonize, form a plaque and become pathogenic. There is experimental evidence that this determinant factor for the development of the periodontitis is present also in the milk of the mothers of CI-diseased calves. It has been shown that the bacteria isolated from the periodontal CI-lesions produce enzymes and endotoxins capable of destroying the periodontal tissues. The epidemiology of CI, with its decline in incidence and its disappearance after several years, could be explained by the fact that the former equilibrium of the microflora of the once undisturbed virgin soil has been reached again and that the number of antibiotic producing actinomycetes has been anew reduced. By this reasoning and all the data available, CI should be considered as a multifactorial infectious disease, caused primarily by the anaerobic black-pigmented non-saccharolytic Bacteroides melaninogenicus, always together with the micro-anaerobic Actinomyces pyogenes. Accordingly, the onset and development of the infectious periodontitis is apparently determined by ingestion with the forage of subinhibitory concentrations of antibiotics produced in recently cultivated virgin soils. This hypothesis is supported by the recent observation of renewed outbreaks of CI-periodontitis in former CI-prone areas, following fresh cultivation after many years. The infectious nature of CI is confirmed by trials in which virginiamycin was used efficiently for the oral treatment of CI-diseased cattle. Previously it has been shown, that spiramycin and virginiamycin, used as additives in mineral supplements, prevented CI-periodontitis.