The Behavior of Virulent and Avirulent Staphylococci in the Tissues of Normal Mice

Isotopic labeling of plasma proteins in vitro by tissues from staphylococcal-infected and control mice was examined, using autoradiography of immunoelectrophoretic patterns. The results indicate that in infected animals there is hyperactivity of liver tissue in producing albumin, α- and ß-globulins, and of spleen tissue in producing immune globulins. The observed increase in labeling of some proteins by tissues from infected mice is to a large extent correlated with an increase of these proteins in the serum.

Section: Discussionmentioning

confidence: 99%

Plasma Protein Formation in Vitro by Tissues From Mice Infected With Staphylococci

Williams

Asofsky

Thorbecke

1963

“…These findings are consistent with previous studies of the pathogenicity of staphylococci for mice. Experimental models employing staphylococci in mice require either the intravenous injection of at least 10 6 organisms or intraperitoneal injection with the supplementary use of mucin before progressive infection occurs (18,19).…”

Section: Discussionmentioning

confidence: 99%

The Influence of Influenza Virus Infection on Exogenous Staphylococcal and Endogenous Murine Bacterial Infection of the Bronchopulmonary Tissues of Mice

Sellers

Schulman

Bouvier

et al. 1961

It is well recognized that representatives of three bacterial genera, Staphylococcus, Streptococcus, and Hemopkilus, which are frequently present in the upper respiratory tract of man, have only a limited capacity to produce a primary pneumonia in adults. When pneumonia induced by one of these microorganisms does develop in an adult, it arises almost invariably in association with influenza virus infection or preexisting morphologic abnormalities of the bronchopulmonary structures. This situation is quite unlike that seen with Pneumococcus which has the capacity to initiate a primary pneumonia in the absence of influenza viral infection.The mechanism by which influenza influences staphylococcal, streptococcal, or influenza bacillus pneumonia has been the subject of relatively few studies in laboratory animals in the 28 years that have elapsed since the first isolation of influenza virus. Human studies have usually not employed the methods of quantitative bacteriology and have been complicated by the widespread use of antimicrobial agents.In 1941, Glover (1) noted the spontaneous occurrence of Group C streptococcal pneumonia in ferrets infected with influenza A virus. He demonstrated the increased * This investigation was supported, in part, by research grants E-635 and E-1595 from the National Institute of Allergy and Infectious Diseases, Public Health Service; and by grants from the Pfizer Foundation; from the Committee on Medical Research of the American Tmdeau Society, medical section of the National Tuberculosis Association, with assistance from the Iowa Tuberculosis and Health Association and the Greater Hartford Tuberculosis and Public Health Society. 238INFLUENZA VIRUS pathogenicity of this combination and the inability of streptococci to induce the disease in the absence of the viral infection. Later, Francis and DeTorregrosa (2) found that strains of H. influenzae produced extensive lethal pneumonia in mice previously infected with influenza virus. It was necessary for influenza virus infection to precede the introduction of bacteria; simultaneous inoculation of the two agents or of H. influenzae alone resulted in no bacterial disease. Similar results were noted with strains of beta hemolytic streptococci. Carlisle and Hudson (3,4), also demonstrated the synergism of a combination of beta hemolytic streptococci and influenza A virus.Harford and others (5) observed that pneumococci introduced intrabronchially were cleared from the normal mouse lung with great efficiency. Even when influenza virus had been present 24 hours and multiplication of virus had begun, disappearance of the pneumococci was not impeded. When pneumococci were introduced after 5 days of influenza, however, they multiplied and produced extensive disease. This suggested the operation of some factor concerned with the influenza viral lesion which did not appear until after more than 24 hours of viral infection. Harford considered this factor to be pulmonary edema fluid and has reported a number of experiments which support this concept...

“…These strains were those used extensively by Cohn and Morse and were kindly supplied by these investigators. They are characterized below:--Sm~h Strain.--This strain of Staphylococcus aureus was isolated in 1930 from a human case of osteomyelitis and has been maintained in the laboratory of Dr. Ren~ J. Dubos because of its consistent pathogenicity for mice (5). This strain was coagulase-positive, produced yellow pigment and hemolysins, fermented mannite, and was lysed by bacteriophages 44A and 42E.…”

Section: Methodsmentioning

confidence: 99%

Further Observations on the Behavior of Staphylococci Within Human Leukocytes

Rogers

Melly

1960

Recent studies by Cohn and Morse have indicated that pathogenic strains of staphylococci are not phagocytosed in systems containing rabbit serum and polymorphonuclear leukocytes in the absence of specific, thermostable opsonin (1). These studies have further suggested that both pathogenic and non-pathogenic strains of staphylococci are equally susceptible to rapid destruction within the cytoplasm of rabbit leukocytes once phagocytosis has been accomplished.Previous studies in our laboratory have demonstrated that there are significant differences in the intracellular disposition of coagulase-positive and coagulase-negative staphylococci following ingestion by human leukocytes (2). Pathogenic, coagulase-positive strains appear to survive within the cytoplasm of human granulocytes while non-pathogenic coagulase-negative strains are rapidly destroyed following ingestion. Observations on the course of staphylococcal bacteriemia in rabbits performed in our laboratory have also suggested that the survival of pathogenic strains within rabbit polymorphonuclear leukocytes may play a role in the persistence of staphylococci in the rabbit blood stream (3,4).In view of the findings of Cohn and Morse, studies on the behavior of staphylococci within human leukocytes have been extended, and the factors in human serum which promote phagocytosis have been explored. The present paper reports these observations. This study supports the thesis that a specific opsonin is required for prompt phagocytosis of pathogenic staphylococci in siliconed glass systems. Human polymorphonuclear leukocytes, like rabbit granulocytes, do not phagocytose coagulase-positive staphylococci in such in vitro systems in the absence of a specific serum factor. The intracellular fate of staphylococci ingested by human leukocytes appears to differ, however, from the fate of staphylococci within