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PubMed1956

The incidence and pathogenesis of myocarditis in rabbits after group A streptococcal pharyngeal infections.

Rabbits subjected to single pharyngeal infections with group A streptococci developed cardiac lesions characterized by myofiber necrosis and a non-granulocytic cellular reaction with histiocytes, lymphocytes, and Anitschkow myocytes. The histopathologic changes were demonstrable in some animals within 24 hours of inoculation, apparently were maximal 72 hours after induction of infection (at which time they were seen in the hearts of all nine rabbits studied), and thereafter healed in the course of the following 2 weeks. The extent of involvement was variable, and with healing the necrotic areas were replaced by fibrous tissue. When intradermal infections with the same organisms were produced in rabbits, cardiac lesions, indistinguishable from those observed in the pharyngeally infected group, appeared in a much smaller number of animals. The hearts of five of six rabbits sacrificed a month or more following the last of a series of streptococcal pharyngeal infections exhibited lesions characterized chiefly by fibrosis, although mononuclear cellular infiltrations were also noted. In these repetitively infected animals the presence of occasional multinucleated giant cells and a few small foci of calcification were features not encountered in the single infection group. In a second series of rabbits sacrificed 3 days after the last of three pharyngeal infections with different strains of streptococci, acute as well as more chronic changes were observed. In none of the lesions in rabbits subjected to single or multiple streptococcal infections were bacteria demonstrable, either in histologic sections or in cultures of myocardial tissue. A large number of control animals was studied concomitantly, and in only one instance was a lesion, considered comparable to those described in the streptococcal series, encountered. The implications of these findings, particularly in terms of the non-suppurative sequelae of streptococcal infections in man, are discussed.

Animals↗
PubMed1956

The endotoxic properties of lysates of group A hemolytic streptococci.

Suspensions of group A streptococci were subjected to mechanical disruption by shaking with glass beads. The supernatant solutions produced severe delayed inflammatory reactions on intradermal injection into normal rabbits. Intravenous injections caused systemic reactions characterized by fever, leucopenia, and peripheral vasomotor phenomena. These effects were more pronounced in rabbits which had previously been infected with group A streptococci. The local and generalized Shwartzman phenomena were reproduced with these crude streptococcal lysates, and the data suggest that streptococci possess an endotoxin similar to those of Gram-negative bacterial species.

Animals↗
PubMed1958

Thyroid function in experimental streptococcal pneumonia in the rat.

In order to study the effects of a severe bacterial infection on thyroid function rats were subjected to group A streptococcal pneumonia, and thyroid activity determined by measurement of the rate of discharge of I(131) from the thyroid gland. Decreased thyroid activity of moderate to marked degree was observed in the majority of infected animals. Infected animals ate less than normal animals. Since fasting leads to decreased thyroid function, I(131) release rates were measured in control animals pair-fed with infected animals and in control and infected animals force-fed a normal intake. The reduction in thyroid activity seen in acute infection was found to be partly but not entirely due to the associated voluntary food restriction. Although the adrenal glands of rats dying of pneumonia were very large, the thyroid inhibition occurring during the course of experimental pneumonia was not secondary to increased adrenocortical function since infected, adrenalectomized animals, receiving injections of cortisone, showed thyroid inhibition comparable to that observed in intact infected animals. The possible influence of the level of thyroid activity on resistance was evaluated. In two experiments a total of 80 rats in 3 groups was pretreated with propylthiouracil and injected daily with 3 dosage levels of 7-thyroxine for 3 weeks prior to inoculation. Under these conditions mortality rates in infected animals fell with decreasing levels of thyroid function. However, induced hypothyroidism was found to afford no protective effect in comparison with untreated infected animals.

Animals↗
PubMed1959

The streptokinase-plasminogen system. I. Its effect on the pathogenicity of streptococci and other organisms for mice.

Human plasminogen, plasma, or serum increased the pathogenicity of six streptokinase-positive streptococcal strains for mice. Combinations of commercial streptokinase and plasminogen or streptokinase and plasma did not usually increase mouse mortality to a greater degree than did plasminogen or plasma alone, suggesting that the maximal effective amount of streptokinase was produced by the organisms. The pathogenicity of Salmonella paratyphi (fibrinolysin variable) and a Group D streptococcus (streptokinase-negative) was not increased by plasminogen, plasma, or streptokinase, whereas a combination of streptokinase and plasminogen, or streptokinase and plasma did significantly increase mouse mortality resulting from these organisms. Combinations of certain concentrations of streptokinase and plasminogen increased the pathogenicity of a fibrinolysin-negative staphylococcal strain for mice to a greater extent than did either substance alone. The observed results provide evidence that streptokinase, by an interaction with plasminogen, contributes to the pathogenicity of streptokinase-positive streptococci.

Animals↗
PubMed1960

Relation of particle size of C polysaccharide complexes of group A streptococci to toxic effects on connective tissue.

The component of Group A streptococci which is responsible for the chronic, remittent, multinodular lesion of connective tissue is derived from the cell wall. Further evidence is given to support the essential role of the group-specific C polysaccharide in the production of this lesion. A series of particles containing the group-specific C polysaccharide was prepared, ranging in size from large cell wall fragments to the relatively small hapten. A comparison of the lesion producing capacity of the particles in this spectrum revealed that maximum toxic activity is associated with C polysaccharide complexes of intermediate size. The discussion considers colloidal properties associated with C polysaccharide complexes of a certain size, and the influence particle size has on persistence in tissue, as possible explanations of the relationship between the size of the C polysaccharide complex and its ability to produce the chronic lesion of connective tissue.

Cell Wall↗
PubMed1962

Factors involved in the induction of non-specific resistance to streptococcal infection in mice by endotoxin.

Endotoxins derived from several species of Gram-negative bacteria, while inducing non-specific resistance to typhoid bacilli in mice, failed to increase the resistance of these animals to infection with virulent strains of Group A streptococci. However, if administration of endotoxin was followed by injection of minute amounts of type-specific antiserum, a substantial degree of protection against the streptococcal pathogen was obtained. The same amount of type-specific antiserum given to the animals by itself did not have any effect on the outcome of the streptococcal infection. Fresh rabbit blood, obtained from animals pretreated with endotoxin, together with anti-M protein immune serum, was found strongly bactericidal for streptococci. These observations suggest that, at least with regard to streptococcal infection, both humoral and cellular factors are required for induction of non-specific resistance.

Animals↗
PubMed1953

Studies on the generalized Shwartzman reaction. III. Lesions of the myocardium and coronary arteries accompanying the reaction in rabbits prepared by infection with group A streptococci.

Cutaneous and systemic infections of rabbits by Group A streptococci bring about a state of preparation for, respectively, the local and generalized Shwartzman reactions, produced by intravenous injection of meningococcal or S. marcescens toxin. With maximal systemic streptococcal infections, the lesions of the generalized Shwartzman reaction do not differ from those caused by two successive intravenous injections of Gram-negative bacterial toxins. The characteristic lesions of the reaction are bilateral cortical necrosis of the kidneys, hemorrhagic necrosis in the lungs, liver, and spleen, and myofiber necrosis in the myocardium. Under optimal conditions involving the dosages of streptococci and toxin, and the time interval between the injections, a new lesion consisting of necrosis and the accumulation of fibrinoid material in the walls of the coronary arteries occurred in approximately 50 per cent of animals within 48 hours after the injection of meningococcal toxin. Fibrinoid necrosis was not observed in the arteries of tissues other than the heart. It did not occur in control rabbits injected with streptococci alone or toxin alone, nor in animals with the generalized Shwartzman reaction produced by two intravenous injections of toxin. Streptococcal bacteriemia was present at the time of death in one-third of the animals with fibrinoid necrosis. In one animal, a group of bodies resembling cocci in chains was seen within the wall of a coronary artery with fibrinoid necrosis. A series of photomicrographs to illustrate the pathological changes in the hearts and kidneys of streptococcus-infected rabbits subjected to the Shwartzman reaction is presented.

Animals↗