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At least 19 recordsLinked to original sources
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↗
PubMed1961

The influence of influenza virus infection on exogenous staphylococcal and endogenous murine bacterial infection of the bronchopulmonary tissues of mice.

Mice infected with a non-mouse-adapted Asian strain of influenza A virus suffered an impaired capacity to destroy or remove staphylococci introduced by the respiratory route. This temporary inhibition of local defense mechanisms was of 7 to 10 days' duration. The persistence of staphylococci in the lung following influenza did not appear to alter the nature of the pathologic reaction to influenza virus. The presence of influenza virus infection in the respiratory tract of the mouse did not alter the fate of intravenous staphylococci in the lung or other organs. In 40 to 50 per cent of mice with influenza, purulent bronchopneumonia and infection with Pasteurella and Hemophilus of murine origin were noted. A minority of control animals evidenced such infection. The administration of antimicrobials to which the murine bacteria were susceptible prevented both the appearance of the endogenous infection with Pasteurella or Hemophilus and the purulent sequelae to influenza virus infection. The true picture of uncomplicated bronchopulmonary influenza virus infection was thus separated from the combined virus-bacteria effect otherwise encountered.

Animals↗
PubMed1951

Studies on endemic pneumonia of the albino rat. IV. Development of a rat colony free from respiratory infections.

A colony of albino rats was developed from three breeders (not germ-free) originally delivered by Cesarian section and artificially reared in the laboratories of Professor James A Reyniers. The colony has been maintained under quarantine since June, 1948, in the absence of any demonstrable involvement of the respiratory tract or of the middle ears. At autopsy pleuropneumonia-like organisms, Streptobacillus moniliformis, and the virus-like agent associated with endemic pneumonia were not recoverable from the lungs or the nasal passages of 81 young and adult rats. During the same time interval the morbidity rate of pneumonia in another rat colony known to be free from infectious catarrh was 51 per cent while the incidence of infection with the virus-like agent approached 100 per cent.

Animals↗
PubMed1953

On the nature of bacteremia in experimental pneumococcal pneumonia in the dog. I. Relationship of natural pneumococcidal-promoting activity of the serum to blood invasion.

IN A STUDY OF THE RELATIONSHIP OF NATURAL ANTIPNEUMOCOCCAL IMMUNE SUBSTANCES TO THE INCIDENCE AND COURSE OF BACTEREMIA IN DOGS WITH EXPERIMENTAL PNEUMOCOCCUS PNEUMONIA THE FOLLOWING FINDINGS CAME TO LIGHT: (1) In non-bacteremic animals, natural immune substances, as measured by the pneumococcidal-promoting action of the serum, continue to be present in relatively undiminished concentration throughout the course of the infection. (2) With the advent of bacteremia these immune properties of the blood tend to decrease or disappear, depending on the degree of bacteremia and the length of the disease course, but in certain instances they persist despite the presence of large numbers of circulating pneumococci. (3) Disappearance of natural immune substances from the blood during bacteremia is followed by their reappearance upon cessation of the bacteremia. (4) Bacteremic blood containing antipneumococcal immune substances and a sufficient quantity of leucocytes is capable of destroying in vitro relatively large numbers of pneumococci and will often sterilize itself. (5) The sequence of bacteremia first, then diminution and disappearance of humoral immunity excludes this antipneumococcal action of the blood as being the principal inhibitor of blood invasion. These observations have been interpreted as indicating that the bacteremic state consists of a constant escape of pneumococci from the pulmonary lesion and an attempt on the part of the body to compensate for the depletion of circulating immune substances resulting from their progressive immobilization by the pneumococci and their products. Thus, the loss or retention of humoral immune substances in the presence of bacteremia would appear to depend on the rate at which the body can provide new supplies of antibodies and on the number of pneumococci being discharged into the circulation. While the pneumococcidal action of the blood may not be sufficient to prevent the occurrence of bacteremia our study provides ample evidence that it exerts a potent restraining effect on the increase in numbers of pneumococci in the circulation.

Animals↗
PubMed1953

On the nature of bacteremia in experimental pneumococcal pneumonia in the dog. II. Disappearance of pneumococci from the circulation in relation to the bactericidal action of the blood in vitro.

With the purpose of ascertaining the influence exerted by the pneumococcidal activity of the blood on the course of bacteremia occurring in experimental canine pneumococcal pneumonia, a study was made of the rates at which intravenously injected pneumococci disappeared from the circulation and the shed blood of diseased dogs. Preliminary studies on normal animals showed that blood containing hundreds of thousands of pneumococci per cc. immediately after injection usually became sterile or nearly so within an hour's time. Simultaneous observations carried out on the blood in vitro showed an analogous rapid disappearance of the microorganisms, although the effect was not quite as marked. Similar tests on non-bacteremic dogs with pneumonia revealed essentially the same ability of the body to dispose of large numbers of circulating pneumococci. The shed blood likewise exhibited marked bactericidal power. The occurrence of bacteremia during pneumonia did not retard greatly the rate at which injected pneumococci disappeared from the circulation, as compared with the non-bacteremic state. After several hours the numbers of circulating microorganisms were approximately the same as prior to the intravenous injection. Blood in vitro often cleared as fully as it did in vivo over the same length of time. Studies on the role played by humoral immune substances in the bactericidal action of the blood showed that while their presence was necessary for maximum killing power, and that bacteremic blood lacking humoral immune properties was rarely capable of self-sterilization in vitro, nevertheless such blood often retained considerable bactericidal potency as shown by its ability to reduce materially the numbers of pneumococci added to it. This phenomenon is discussed. The marked pneumococcidal capacity of the blood exhibited by dogs with experimental pneumococcal pneumonia and its persistence during bacteremia suggest that this constitutes the principal mechanism for limiting the degree of blood invasion. The similarity of the findings in canine and human pneumococcal lobar pneumonia is pointed out.

Animals↗
PubMed1954

The effect of adrenal steroids, corticotropin, and growth hormone on resistance to experimental infections.

Cortisone acetate, hydrocortisone, and hydrocortisone acetate depress the resistance of mice to pneumococcal and influenza viral infections, although hydrocortisone acetate is somewhat less effective than the free alcohol, when given subcutaneously. Pituitary adrenocorticotropin, even in highly purified form and in oil and beeswax, does not significantly alter the resistance of mice to these experimental infections, even when given in doses which may cause profound eosinopenia, lymphopenia, and weight loss, and which are at the limit of tolerance of the animals. Corticosterone depresses resistance to pneumococcal infections significantly, but fails to alter resistance to influenza viral infections. The findings suggest that murine adrenals may produce one of the known adrenal steroids such as corticosterone along with another steroid, or may produce a steroid other than cortisone, hydrocortisone, or corticosterone. When resistance is decreased by adrenal steroids, survival time is invariably shortened, and the effect of the steroid hormones is frequently demonstrable within the 1st day after infection with pneumococci, making it unlikely that the depression of resistance that is seen is primarily due to depression of antibody formation. A single dose of 5 mg. of cortisone may cause depression of resistance and may decrease the survival time for 3 to 6 days afterward. Growth hormone (somatotropic hormone) in highly purified form, and in the doses used, did not overcome the weight loss induced by cortisone, but the animals treated with growth hormone and cortisone regained their lost weight more rapidly than those receiving cortisone alone. Growth hormone alone caused a slight increase in the rate of gain in weight over controls. Growth hormone alone did not increase resistance to infection, and did not increase the survival time, in mice infected with either pneumococci or influenza virus. Growth hormone in various dosages failed to overcome the effect of cortisone in depressing resistance to these infections. Cortisone, hydrocortisone, corticosterone, and corticotropin did not alter significantly the titers of influenza virus attained in the murine lungs during the first 2 days after infection, but cortisone and hydrocortisone markedly delayed the rate at which virus titers declined during the subsequent 6 days. Corticosterone and corticotropin delayed the rate at which the titers declined but slightly, and growth hormone had no apparent effect, as compared with controls. Growth hormone did not overcome the effect of cortisone and hydrocortisone on viral titers. No detectable antibody was found as late as 6 days after infection, in controls or in hormone-treated animals.

Adrenal Cortex↗