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A T WILSON

Publications and source records attributed to A T WILSON.

At least 19 recordsLinked to original sources

THE CELLULAR ANTIGENS OF GROUP A STREPTOCOCCI; IMMUNOELECTROPHORETIC STUDIES OF THE C, M, T, PGP, E4, F, AND E ANTIGENS OF SEROTYPE 17 STREPTOCOCCI.

The immunoelectrophoretic characteristics of the known cellular antigens of serotype 17, Group A streptococci have been presented. These include C, M, T, and polyglycerophosphate. In addition, three hitherto undescribed antigens of serotype 17 have been encountered. The F antigen occurs in most serotype 17 strains, has a faster electrophoretic mobility than M, appears in acid, distilled water, and other extracts of harvested cells, is released from the cells in large quantity into the culture medium during growth when the pH is maintained at 7.3 or over, is probably protein in nature, and may play a minor role in mouse virulence of serotype 17 strains. Its antibodies do not confer bactericidal power on human blood. The E antigen is serotype-specific and is closely associated with the M antigen. The suggestion is made here that E is a part of the M molecule, acquiring independent electrophoretic mobility when separated from the rest of the M molecule by acid hydrolysis and carrying an antigenic determinant serologically distinct from the determinant on the rest of the M molecule. E can be recognized only by immunoelectrophoresis. Its role, if any, in virulence has not been established. The third antigen, E(4), is a non-serotype-specific antigen found in most serological groups and types of hemolytic streptococci. It is serologically related to polyglycerophosphate, but its chemical nature has not been determined. It appears to be unrelated to virulence.

Animals↗

The occurrence of two M antigens in certain group A streptococci related to type 14.

A strain of Group A streptococcus previously considered to belong to Type 14 was shown to have two immunologically distinct M antigens, designated Type 14 and Type 51. Most strains having the Type 14 M antigen were found to have also the Type 51 M antigen, and are considered to belong to Type 14-51. Four strains had the Type 51 M antigen without the Type 14 M antigen and one strain had the Type 14 M antigen without the Type 51 M antigen. The failure of a variant to produce the known M antigen of the parent strain does not necessarily mean that the strain is M(-), because a second M antigen may be present as was the case in several strains described here.

Antigens↗

The relative importance of the capsule and the M-antigen in determining colony form of group A streptococci.

Evidence is presented showing that the surface configuration of Group A streptococcal colonies depends largely on whether or not the cocci form a capsule. Strains which form capsules during growth on agar produce mucoid or matt colonies. Strains that do not form capsules during growth on agar produce glossy colonies. Whether or not M antigen is formed by the growing cocci appears to have no direct effect on surface configuration of the colony, although there is an indirect and partial association between M production and the mucoid-matt variant state and between M deficiency and the glossy variant state.

Autoantigens↗

Fate of non-virulent group A streptococci phagocytized by human and mouse neutrophils.

The fate of non-virulent group A streptococci phagocytized in vitro has been investigated by destroying the phagocyte with electric current and observing whether the liberated cocci multiply. Human and mouse peripheral blood neutrophils quickly injure ingested cocci, the time required to produce 50 per cent non-survival of chains being 8 and 6(3/4) minutes, respectively.

Animals↗

Diphosphopyridine nucleotidase as an extracellular product of streptococcal growth and its possible relationship to leukotoxicity.

Among 170 streptococcal strains, there were encountered 98 that yielded culture supernates which caused splitting of diphosphopyridine nucleotide (DPN). All of the latter belonged to Group A, C, or G. Release of DPNase accompanied the growth of diverse antigenic types of Group A streptococci, and data on the frequency of DPNase-producing strains for certain types are given. In contrast, cultures representing 3 species of yeasts and 42 species of bacteria other than streptococci of the Lancefield groups were examined for the presence of DPNase as an extracellular product of growth, but in none of these was the enzyme detected. Of the Group A streptococci examined, 41 strains had pedigrees suggesting that they were the etiologic agents of acute glomerulonephritis, and 39 of these were found to produce DPNase. There is an association between capacity of streptococi to form DPNase and capacity to kill leukocytes. A possible mechanism of leukotoxicity is suggested.

Bacteria↗

The leukotoxic action of streptococci.

FOLLOWING PHAGOCYTOSIS OF CERTAIN STREPTOCOCCI HUMAN NEUTROPHILS UNDERGO A RAPID DISINTEGRATION: the leukotoxic reaction. Monocytes and eosinophils are similarly injured, as are polymorphonuclear cells of rabbit and guinea pig blood. The leukotoxic injury is not produced by culture filtrates of leukotoxic cocci nor does it follow phagocytosis of heat-killed cocci. The leukotoxic effect does not appear to be due to action of any presently known streptococcal product. The distribution of leukotoxicity among streptococci is not random, for it was found in all strains tested of certain types of group A (6, 12), and was absent from almost all strains of other types (5, 14, 30). Still other types (3, 4) had both leukotoxic and non-leukotoxic representatives. The injury was also produced by some group C and G strains. Often the streptococci that cause leukocyte death remain alive and proliferate in the cellular debris, but sometimes they are injured by the phagocyte before the latter disintegrates and are unable to proliferate on the slides. The capacity of a strain of streptococcus to injure leukocytes does not necessarily confer virulence on it. This is thought to be because a chain of streptococci, having survived its sojourn in a leukocyte it has killed, is still susceptible to phagocytosis by a fresh leukocyte, and serial phagocytoses may continue until the chain has been exposed sufficiently to the unfavorable intracellular environment to be, itself, killed. Whether leukotoxicity plays a role in naturally occurring streptococcal disease is unknown. The high incidence of leukotoxicity in Type 12 strains suggested that it might be involved in acute hemorrhagic nephritis, but if so there must be other factors since leukotoxic strains are present in types and groups not now known to be associated with nephritis.

Animals↗