Part 152

It is, however, from the constant presence of the bacteria in infected wounds, and their distribution through the tissues, that the argument in favor of connecting septic symptoms with the bacteria has been mainly deduced. Here the ground is sufficiently solid, and, judged by ordinary laws of scientific evidence, the pathological importance of the microspores {997} may be regarded as established. To be sure, we find them in tongue-scrapings of healthy individuals, but tongue-scrapings are poisonous if injected into the tissues. That they do not ordinarily prove so in the mouth is no more singular than that woorari can be swallowed with impunity. Tiegel has endeavored to show that round bacteria are found normally in the internal organs of the body; but Koch states that he has on many occasions examined normal blood and normal tissues by means which prevented the possibility of overlooking bacteria, or of confounding them with granular masses of equal size, and that he has never in a single instance found organisms.

It is stated that bacteria are sometimes absent from the blood withdrawn during life in septic diseases. As, however, their constant presence has been confirmed in the vessels and glomeruli of the kidneys, it is fair to assume that those organs, acting as filters, must have received the colonies observed in them from the general circulation.

The difficulty of obtaining bacteria from the blood in many cases during life in septic diseases does not, however, as was once supposed, invalidate the theory of their pathogenic importance. Septicæmia is at present employed as a collective term for a number of processes which may occur singly or in combination with one another. When a relatively large quantity of a putrid fluid is injected into the veins of an animal, death follows from the action of a chemical poison (sepsin). The blood during life rarely displays the presence of bacteria, the latter disappearing in the circulation. In animals thus poisoned blood does not possess infectious properties. This form is termed putrid intoxication. That the poison in these cases is, however, produced by the bacteria is shown by experiments of Gutmann, who demonstrated that bacteria from a drop of putrid blood cultivated in Cohn's solution developed in the fluid a poison which, when injected into the veins of dogs, occasioned death with all the symptoms of putrid intoxication. Still more conclusive were the experiments of Koch. This observer injected four drops of putrid blood beneath the skin of mice. The latter died in from four to eight hours. There were no bacteria in the blood, and the blood was not infectious. When, however, a single drop was injected, the mice often remained unaffected, but in a third of the cases they became ill after twenty-four hours, death occurring in from forty to sixty hours. The blood during life communicated the same disease to other mice, and bacilli were always present in large numbers. In these cases the dissolved poison in the fluid injected was too small in amount to destroy life, and death resulted only after a period of incubation as a consequence of the multiplication of bacilli in the blood and in the tissues.

In another class of cases Koch experimented, not with putrid blood, but with a fluid produced by macerating a piece of mouse-skin in distilled water. Of this he injected a syringeful into the back of a rabbit. The result was peritonitis, swelling of the spleen, gray wedge-shaped patches in the liver, and in the lungs were found dark-red patches the size of a pea, devoid of air--all appearances in harmony with what is designated as pyæmia. Oval micrococci were found in great numbers {998} everywhere throughout the body. But the point of special interest in the present connection is the fact that wherever these micrococci come in contact with the red blood-corpuscles the latter stick together and become arrested in the minute capillary network. The thrombi thus formed are further enlarged by the deposition of micrococci, which multiply, block up individual capillary loops, and invade contiguous tissues. In the blood-current itself, however, the micrococci do not increase in numbers, and cannot always be found in the circulation upon a single examination, but Doléris assures us that in puerperal fever by repeated trials, especially after a chill, he has never failed to demonstrate their presence.

As to the exact manner in which these minute bodies exercise their pernicious influence, whether they operate mechanically, or whether they produce a virus in the process of nutritive activity, or whether, as is probable, both suppositions are correct, must be decided by future investigations. It is enough for us to note that the connection between sepsis and bacteria is intimate and vital.

3d. Pathogenic bacteria are invariably associated with puerperal fever, and to them the infectious qualities of the disease are due. I have been explicit regarding the evidence concerning bacteria in septic diseases, because it places the question of the infectious group of puerperal fever cases in the following position: Experiences occurring clinically, as well as those produced upon animals, teach us that certain lesions and symptoms, similar to those we are accustomed to regard as characteristic of puerperal fever, results from septic poisoning. In a large class of cases, however, the connection between childbed fever and sepsis has been deduced rather from analogy than direct proof. For those who chose to regard such as due to a specific poison peculiar to the puerperal state there was really no objection. If, however, bacteria are characteristic of septic poisoning, the question presents itself in a different light, and we have to inquire whether, in the less obvious cases, bacteria are present in puerperal fever in the proportions and groupings that we find them in other diseases due to putrid infection. Now, it is precisely proof of this nature that has recently been abundantly rendered.

Waldeyer, Orth, Heiberg, and Von Recklinghausen found the tissues and lymphatics of the parametria filled with pus-like masses, which consisted, in addition to pus-cells, chiefly of bacteria. Bacteria swarmed in the fluid of the peritoneal cavity. In one case examined by Waldeyer six hours after death, while the body was still warm, the peritoneal exudation was like an emulsion, and furnished an abundant deposit which consisted almost entirely of bacteria. Orth injected ten minims of peritoneal fluid from a woman dead of puerperal fever into the abdomen of a rabbit. As the animal was dying he broke up the medulla oblongata, and found in the peritoneal fluid enormous quantities of these {999} organisms. In puerperal fever round bacteria have been likewise found, though in less quantities, in the lymphatics of the diaphragm and in the fluids of the pleura, the pericardium, and the ventricles of the brain. In post-mortem examinations of fresh subjects the serous fluids, withdrawn under proper precautions, do not contain round bacteria except in cases of septic infection. Orth found in the purulent contents of the vessels of the funis, in children who died of sepsis, precisely the same formations as existed in the exudations of the mother.

Doléris, in a remarkable essay already referred to, published in 1880, furnishes not only conclusive evidence of the presence of bacteria in the various tissues and serous cavities of women dying of puerperal fever, but has added the evidence of their pathogenic character by cultivating them apart in sterilized fluids, and by reproducing in animals, by means of subcutaneous injections of the isolated bacteria, the infarctions, the blood-changes, and the suppurative processes of the original disease.

So far, the generic term bacteria has been employed to indicate the disease-germs which are the active agents of infection in puerperal fever. It is not, however, intended to assume that the germs of septic processes are all identical, or that they all produce precisely the same pathological conditions. Koch, indeed, maintains that a distinct specific bacterial form is found in such closely-allied affections as pyæmia, septicæmia, gangrene, and erysipelas, the different forms possessing, however, this link in common--viz. that they are alike generated in putrefying media. Singularly enough, the bacterium termo and the bacterium commune--to which the fetidity of matters undergoing putrefaction is due--are in themselves harmless. They are rapidly destroyed in the circulation, and are not inoculable. Fetid discharges from wounds are not therefore necessarily dangerous. The putrid odor serves a useful purpose, as it gives warning of the existence of conditions which favor the development of life-destroying organisms; but the latter may develop without the concurrence of the forms which give rise to putrefaction--a fact of considerable importance in view of the common belief that septic infection is excluded by the absence of fetid odors.

In puerperal fever Doléris found the prevailing pathogenic organisms consisted of bacilli or rods, and micrococci or round bacteria in the varieties of micrococci, simple points; diplococci, double points; and chains or wreaths. The bacilli he regarded as the source of acute, rapid septicæmia, while pus-production was associated with the multiplication of the round bacteria, and especially of the diplococci.

4th. The presence of germs in puerperal fever serves not only to fix cases hitherto doubtful in the category of septic diseases, but affords the most satisfactory explanation of the protean phenomena of puerperal fever itself.

We have seen, from both Koch's and Gutmann's experiments upon animals, that death may occur independently of bacteria by the rapid absorption of a chemical poison developed in a putrefying fluid. Clinical experiences, such as the speedy death sometimes observed when retained coagula or portions of placenta undergo decomposition within the uterine cavity, renders it probable that similar cases of putrid intoxication are {1000} not unknown in puerperal women, though, so far, the anatomical demonstration of the fact has not been furnished.

In cases, however, where puerperal fever has a distinct period of incubation, and progresses step by step to the fatal ending, bacteria are always found invading the tissues of the genital canal. In rare cases they pass by the Fallopian tube to the peritoneal cavity and excite salpingitis and peritonitis. More commonly from local lesions they enter the canalicular spaces of the connective tissue forming the framework of the genital canal, which is continuous with the subperitoneal connective tissue of the pelvis. From the canalicular space they enter the lymphatics. Cellulitis is excited by their presence, and the lymphatic glands become inflamed and enlarged. In pernicious forms they produce a sero-purulent oedema, which spreads rapidly with a wave-like progress after the manner of erysipelas; or in milder cases the progress of the disease-germs is arrested by the lymphatic glands or the resistance offered by the tissues themselves, and the ordinary circumscribed phlegmon is produced. By the lymphatics which accompany the vessels of the Fallopian tubes they reach the ovaries (puerperal ovaritis), and by the broad ligaments they pass to subperitoneal tissues of the iliac and lumbar regions. Through the same system they are conveyed to the great serous cavities of the body. In the peritoneum they give rise, unless death occurs too speedily, to pyæmic peritonitis, which, unlike the traumatic form, is attended with but little pain, and for which the claim has been set up that it is peculiar to puerperal fever. The wide stomata upon the abdominal surface of the diaphragm allows the facile entrance of the organisms into its lymphatics. Waldeyer found in diaphragmitis the lymphatics of the diaphragm filled with bacteria. And thus, following the lymphatic system, if we only admit that bacteria are the active agents of sepsis, the frequency, in severe types of puerperal fever, of inflammation of the serous membranes of the peritoneum, the pleuræ, the pericardium, the meninges, and the joints finds an easy explanation. Nor is it altogether accident which determines in different cases the precise serous membranes which are affected. The widespread ramifications of the lymphatic system would naturally give rise to eccentric inflammations in place of those following the apparent continuity of tissues.

The ductus thoracicus is the principal channel through which the bacteria enter the blood. It is possible that they may further obtain access into the circulation through the radicles which furnish the communications between the capillaries and the lymphatics. We have seen that bacteria are found with difficulty in the blood during life. A few hours after death they swarm in that fluid. That they do, however, enter the general circulation during life is incontestable. Steurer writes: "As the kidneys are the great filters of the human system, I never neglected to examine them, and almost invariably found micrococci filling the arterioles and glomeruli." This is in correspondence with what occurs in other septic diseases, and accounts for the albuminuria and interstitial nephritis which often supervene in the advanced stages.

The action of the bacilli upon the blood differs materially from that of the round bacteria. So soon as the latter come in contact with the red corpuscles, the corpuscles stick together and form larger or smaller clots in the blood. They then are no longer able to pass through the minute {1001} capillary networks, but are arrested in the larger or smaller vessels (Koch). The micrococci in the resulting infarctions multiply, and migrate into the vessels and cellular tissue of the neighborhood. Thus fresh foci of infection are formed. Or by their destructive action they may, when situated near the serous surfaces, penetrate into the serous cavities, and in this way indirectly occasion peritonitis, pleurisy, meningitis, and purulent inflammations of the joints. When the micrococci enter directly into the circulation, they sometimes, in passing through the heart, adhere to the endocardium and the valves, where they cause exudation and ulceration, and give rise to the so-called endocarditis ulcerosa puerperalis. The red globules of the blood undergo changes of shape, assume a stellate aspect, and rapidly disappear. The white globules are greatly increased in numbers, and the blood itself becomes nearly colorless. A certain amount of light is thrown upon these blood-changes by Doléris, who added micrococci to the fresh blood of a frog and watched the ensuing changes under the microscope. The micrococci could be seen in the act of penetrating the red globules, which thereupon lost their color and became shrunken, and, following the discharge of the organisms, which meantime had multiplied in an astonishing manner, little or nothing of the original globules remained.

In the bacillar form of septicæmia the blood is dark and has a semi-gelatinous appearance, compared by French writers to partially-cooked gooseberry jelly. The red globules, though they exhibit the various stages of deformation, are not diminished in number. The disease is further characterized by ecchymoses and minute apoplectic effusions, and by the absence of pus-formation. In the artificial septicæmia produced by Koch in mice by means of bacilli the rod-like organisms were found to enter the white corpuscles and to compass their destruction. They did not cause the red globules to adhere together, and there was no clogging of the capillary circulation. All the principal structures of the animals subjected to experiment were infiltrated with bacilli. The distribution of the latter was apparently accomplished by the blood-vessels, and not by the lymphatics, the bacilli probably effecting their entrance into the vessels by virtue of their penetrative power, in place of traversing preformed pathways. Possibly it is this action of the bacilli which causes the weakening of the vessel-walls, as evidenced by the large number of red corpuscles which pass out from them.

In puerperal fever it is rare to find either round bacteria or bacilli acting singly as the agent of infection. As a rule, both forms exist together in varying proportions, the predominant form, however, determining in general the character of the symptoms.

Thrombosis of the veins may be a physiological phenomenon, or may be due to an alteration of the blood, to weakness of the heart, or to local influences. So long as the clot remains firm its influence is limited to disturbances of the circulation. The pyæmic symptoms--viz. suppuration of the coagulum, the separation of emboli, and the formation of metastatic abscesses--are always dependent upon the presence of round bacteria. In phlebitis the latter are found in the endothelium and in the sheaths of the veins. The inflammation of the veins is followed by {1002} thrombosis. According to Doléris, micrococci derived from the blood are deposited upon the central extremities of the clots; beyond these dépôts a fresh inflammation is set up, followed by fibrinous coagulation. Thus the micrococci become imprisoned between two plugs. The same process may be repeated until a series of abscesses are formed. For a time no mischief may ensue. Finally, however, the resistance of the outworks is overcome, an embolus becomes detached, and an infectious abscess is opened into the blood--an event which is announced by an intense chill and the familiar systemic derangement.

In septic diseases death takes place from apnoea, partly from the inability of the blood-corpuscles to carry oxygen to the tissues, and partly from paralysis of the nerve-centres.

In hospital epidemics of puerperal fever diphtheritic patches situated upon the lesions of the vulva and in the course of the utero-vaginal canal are sometimes observed. Steurer found these patches were always associated with loss of substance, and were composed of disintegrated fibrin, white and red blood-globules, and colonies of round bacteria in great abundance. Morphologically, these so-called diphtheritic patches are identical with those which appear in the throat. Pallen has reported an instance of the simultaneous occurrence of puerperal diphtheritis in the mother and throat diphtheritis in the two-weeks' old child. In lying-in hospitals it is the genital organs, as the locus resistentiæ minoris, and not the throat, which are the usual points of attack.

The question as to the extent to which erysipelas and puerperal fever are cognate diseases is in a fair way to be solved by recent investigation. Orth took the contents of a vesicle from an erysipelatous patient which contained bacteria in great abundance, and employed the same for injections under the skin of rabbits. In this way he succeeded in producing in these animals a species of erysipelas malignum. In the subcutaneous oedema and affected portions of the skin he found enormous masses of bacteria, so far exceeding in quantity the amount introduced as to prove an abundant new production. Samuel produced similar results by the injection of ordinary putrid fluids containing round bacteria. An affection resembling simple erysipelas he obtained most frequently by the application of fluid to a wound torn open after the second or third day. Lukomski found that erysipelas could be produced by fluid containing micrococci even when putrefaction did not exist. The contents of erysipelatous vesicles containing no micrococci excited no morbid manifestations. Where the erysipelatous process was fresh and progressing micrococci were found in great abundance in the lymphatics and canalicular spaces. Where the process was retrogressive, there were no micrococci to be found, even in cases in which inflammation existed to an intense degree. Doléris submitted to the culture-process of Pasteur fluid obtained from vesicles which developed in the course of facial erysipelas in a man of forty years. Micrococci in chains were found in the liquids employed identical with those he had discovered in puerperal fever. In many cases I have seen an erysipelatous inflammation start from a puerperal diphtheritic ulcer {1003} upon the introitus vaginæ, and extend outward over the buttocks, the thighs, and the lower portion of the abdomen.

Virchow has so far given in his adhesion to the new school as to say: "Especially in this connection are to be mentioned the diphtheritic process and the erysipelatous, especially erysipelas malignum. The granular deposit in diphtheritically affected tissues, of which I formerly spoke, has more and more proven to be of a parasitic character. What we formerly regarded as simple, organic granules, as infiltration or exudation, has since proven to be a dense aggregation of micro-organisms which penetrate into the tissues and cells to compass their destruction."

Thus we find in surgical fever, in puerperal fever, in diphtheria, and in erysipelas the presence of a common element which links them together, and which establishes the relationship which has long been recognized as existing between these various processes.

4th. The differences between surgical and puerperal septicæmia are due to differences partly structural and partly physiological in the wounded surfaces exposed to septic contamination.

A certain amount of misapprehension has arisen from the circumstance that along with many coincidences in the symptoms of puerperal and surgical fever there are observable differences which, from a purely clinical point of view, would justify a separate classification of the two affections. It will not do, however, to ignore the fact that the conditions which prevail in the parturient canal subsequent to labor have no strict analogue in the lesions which the surgeon is called upon to treat, and that therefore a complete identity as to all the clinical features of puerperal and surgical fever would hardly be within the range of possibility.

In the puerperal state it is necessary to take into account the blood-changes induced by pregnancy, the effects of shock and exhaustion in protracted labors, the frequency of hemorrhage, the deep situation of puerperal wounds, the presence of clots, decidua, and dead tissue in a state of disintegration or decomposition, the ease with which deleterious matters are absorbed by the wide lymphatic interspaces, the serous infiltration of the pelvic tissues, the exaggerated size of the lymphatics and veins, and the proximity of the peritoneal cavity.

Samuel, in speaking of the immunities and dispositions to septic poisoning, says: "The statistical frequency of septic puerperal disease is due to the length of the parturient canal, to the fact that through this long passage there must pass all the pathological and physiological excretions, and to the soiling of these parts with fingers, instruments, and secretions which have become the bearers of sepsis." He found, on the other hand, that it was extremely difficult to produce a progressive ichorous condition by daily painting an open stump with a septic fluid, though the same was readily obtained when an infinitesimal quantity of septic fluid was injected underneath a fascia.

5th. In the present state of our scientific knowledge it is necessary to admit that there is a limited number of febrile and inflammatory disturbances occurring in puerperal women, the bacterial origin of which may be fairly questioned. As illustrations of this class may be {1004} mentioned: 1. Cases of catarrhal endometritis due to errors of diet and exposure. Indeed, I have frequently, in hospital practice, been able to trace severe cases of cellulitis, pelvic peritonitis, and general peritonitis occurring in the winter season to the patient getting out of bed dripping with perspiration, and clad only in a night-dress, and going thus barefooted over a cold, uncarpeted floor to the water-closet. 2. Cases of puerperal disorders proceeding from emotional causes, the nervous system furnishing the first impulse to the disturbed action. 3. Cases of excessive vulnerability in non-pregnant women; individuals are sometimes found so susceptible that a parametritis follows a simple application of the tincture of iodine to the cervix. 4. Cases of pelvic peritonitis starting from old intra-peritoneal adhesions. 5. Cases of peritonitis and retro-peritoneal inflammations secondary to ulcerative processes in the cæcum or the descending colon. This condition is apt to be masked during pregnancy, but starts into activity during childbed as a consequence of fecal accumulation or of excessive purgation.